Emergency Cardiology 2nd Edition
Emergency Cardiology 2nd Edition
Emergency Cardiology 2nd Edition
CARDIOLOGY
EMERGENCY
CARDIOLOGY
Second Edition
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CONTENTS
Abbreviations vi
CHAPTER 2 Resuscitation 84
Appendices 239
Index 269
ABBREVIATIONS
viii
CHAPTER 1
EPIDEMIOLOGY
Coronary heart disease is the most common cause of death in the United
Kingdom. In total, 220 000 deaths were attributable to ischaemic heart
disease in 2007. It is estimated that the incidence of acute coronary
syndrome (ACS) is over 250 000 per year.
Sudden death remains a frequent complication of ACS: approximately
50 per cent of patients with ST elevation myocardial infarction (STEMI)
do not survive, with around two-thirds of the deaths occurring shortly
after the onset of symptoms and before admission to hospital. Prior to
the development of modern drug regimes and reperfusion strategies,
hospital mortality after admission with ACS was 30–40 per cent. After the
introduction of coronary care units in the 1960s, outcome was improved,
predominantly reflecting better treatment of arrhythmias. Current therapy
has improved outcome further for younger patients who present early in
the course of their ACS. The last decade has seen a significant fall in the
overall 30-day mortality rate. Most patients who die before discharge do
so in the first 48 hours after admission, usually due to cardiogenic shock
consequent upon extensive left ventricular damage. Most patients who
survive to hospital discharge do well, with 90 per cent surviving at least
1 year. Surviving patients who are at increased risk of early death can be
identified by a series of adverse clinical and investigational features, and
their prognosis improved by intervention.
EPIDEMIOLOGY 1
ACUTE CORONARY SYNDROMES
DEFINITIONS
The term ‘acute coronary syndrome’ (ACS) has been developed to describe
the collection of ischaemic conditions that include a spectrum of diagnoses
from unstable angina (UA) to non-ST elevation MI (NSTEMI) and STEMI.
Patients presenting with ACS can be classified into two groups according
to their electrocardiogram (ECG) (Figure 1.1): those with persistent STEMI
and those without (non-ST elevation ACS or NSTEACS). The treatment of
STEMI requires emergency restoration of blood flow within an occluded
culprit coronary artery. Patients presenting with NSTEACS often have
ECG changes including T-wave inversion, ST depression or transient ST
elevation, although occasionally the ECG may be entirely normal. This
group can be classified further according to the presence of detectable
levels of cardiac proteins, troponins, in patients’ serum (see below). Thus,
NSTEACS patients with undetectable cardiac troponins (UA) are
distinguished from those in whom myocardial ischaemia is severe enough
to cause myocardial necrosis, leading to troponin release into the
circulation (NSTEMI). Detection of cardiac troponin following ACS is a
strong predictor of recurrent ischaemia. However, it should be remembered
that patients with UA are still at increased risk of further events, especially
those with pain at rest or dynamic ST changes on their ECG.
ACS
ST change
Persistent
ECS T-wave inversion
ST elevation
Normal ECG
STEMI NSTEACS
Diagnosis
NSTEMI UA
2 DEFINITIONS
ACUTE CORONARY SYNDROMES
PATHOPHYSIOLOGY
PATHOPHYSIOLOGY 3
ACUTE CORONARY SYNDROMES
the release of tissue factor and the expression of the vitronectin (αvß3)
receptors leading to platelet activation and aggregation through the expression
of the glycoprotein IIb/IIIa receptor is an important event in the development
of thrombus. Platelet-rich thrombus is associated with cyclical reductions in
coronary blood flow with additional coronary vasoconstriction resulting from
endothelial disruption, and thromboxane A2 (TXA2) and serotonin production
leading to reduced nitric oxide (NO) production. Inflammatory acute phase
proteins, cytokines and systemic catecholamines stimulate the production of
tissue factor, procoagulant activity and platelet hypercoagulability.
A number of factors that can trigger the onset of ACS have been identified,
acting by initiating plaque rupture or promoting thrombus formation.
Some patients report heavy physical exertion or mental stress shortly
before the onset of ACS. Circadian variation in coagulation and
autonomic nervous system activity contribute to an increased incidence of
ACS in the morning. Irrespective of this, the risk of an individual episode
of exercise or stress precipitating the onset of ACS is low, and most
episodes have no identifiable direct triggers.
Other non-athersclerotic causes for ACS include arteritis, trauma,
spontaneous coronary dissection, thromboembolism, cocaine use and
congenital abnormalities such as anomalous coronary arteries. Patients
who present as a result of these rare causes will usually not have the
classical risk factors associated with atherosclerosis; typically the
diagnosis is not established until after coronary angiography.
Acute STEMI usually results from total occlusion of a coronary artery, with
subsequent myocardial cell necrosis occurring in as little as 15 minutes.
Continued occlusion results in a wavefront of necrosis spreading from the
subendocardium to the subepicardium. The amount of myocardial injury
depends on the duration of occlusion, the presence of collateral blood flow
and the degree of preconditioning of the myocytes to ischaemia. In animal
models, persistent occlusion of a coronary artery will usually result in
complete infarction of the area subtended after 6 hours. Subendocardial and
full thickness or transmural mycocardial infarction can be well
demonstrated with cardiac magnetic resonance imaging (MRI) using late
gadolinium enhanced images. These images correlate well with
macroscopic histological findings.
NSTEACS are usually associated with partial or transient occlusion of the
coronary artery that may result in ST depression or T-wave changes on
the ECG. Myocardial injury occurs as a result of a sudden decrease in
luminal diameter leading to reduced perfusion or due to plaque
PATHOPHYSIOLOGY 5
ACUTE CORONARY SYNDROMES
DIAGNOSIS
Presentation
Chest pain is a common reason for patients to attend hospital, accounting
for up to 5 per cent of visits to the emergency department and 40 per cent
of hospital admissions. Around 50 per cent of patients presenting with
chest pain will have an underlying ACS, requiring hospitalization and
intensive medical therapy. The remainder have other cardiac and
non-cardiac causes for their symptoms, and require a different
management approach. This section gives guidelines on diagnosing ACS,
and differentiating it from other common causes of chest pain.
The diagnosis of ACS is usually made using a combination of clinical and
ECG features. Cardiac troponin studies and functional tests can then be
used to further risk-stratify the patient. As a general principle, all patients
with symptoms that may be due to an ACS should be admitted to hospital.
These patients should preferably be admitted to a chest pain assessment
unit or heart attack centre, as those at high risk of early adverse events
need to be carefully monitored and selected for early invasive therapy.
Clinical features
Most patients with ACS present with chest discomfort; in STEMI and
80 per cent of NSTEACS this is prolonged, lasting over 20 minutes.
6 DIAGNOSIS
ACUTE CORONARY SYNDROMES
Electrocardiographic changes
The majority of patients with an ACS will have an abnormal ECG at some
stage. An initial normal ECG does not rule out the diagnosis, as ECG changes
can develop, evolve and resolve rapidly. Commonly, the first ECG performed
during the course of the presentation (often by paramedics) is the one that
shows evidence of myocardial ischaemia, prior to resolution with appropriate
pre-hospital treatment. Patients with a suggestive history and a normal ECG
should be admitted and the ECG monitored at regular intervals; if ECG
changes then develop, appropriate treatment can be initiated.
DIAGNOSIS 7
ACUTE CORONARY SYNDROMES
II aVL V2 V5
III aVF V3 V6
V1
II
V5
Figure 1. 2 Anterolateral myocardial infarc tion. Note ST elevation in leads V2–V6, I and aVL .
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
II
Figure 1. 3 High lateral myocardial infarc tion. Note the ST elevation in leads I and aVL with reciprocal changes in
the inferior leads. Coronar y angiography demonstrated a 95 per cent stenosis in a high diagonal branch.
I aVR
V1
V4
II aVL
V5
V2
III aVF
V6
V3
II
Figure 1.4 Acute inferior myocardial infarction. Note the ST segment elevation in leads facing the inferior wall
(II, III, aVF). Reciprocal changes are seen in diametrically opposed leads (I and aVL) located in the same (frontal)
plane.
I aVR V4
V1
II aVL V5
V2
III aVF V3 V6
Figure 1.5 Posterior wall myocardial infarc tion. Note the tall R waves in leads V1–V3 associated with ST
depression.
ACUTE CORONARY SYNDROMES
• Outside the chest cavity. For example, referred pain from the neck.
Pain referred from the cervical or thoracic spine will have features
of musculoskeletal chest pain.
Since acute chest pain can have many possible causes, a careful history
and comprehensive physical examination along with inspection of
the ECG and chest x-ray are mandatory in all cases where diagnostic
uncertainty exists.
INITIAL TREATMENT
Background
Patients with evolving MI often do not request medical aid until
symptoms have been present for more than 1 hour. This patient delay
occurs at the most critical time in the course of the illness, when pain is
often severe and the risk of ventricular tachyarrhythmias and cardiac
arrest is high. Therefore, any patient with chest pain suspected of having
an ACS should be urgently transferred to hospital for assessment. Transfer
should ideally take place by trained paramedics with cardiac monitoring
and resuscitation facilities and the ability to obtain an ECG en route.
Treatment and analgesia should be given en route to hospital if possible.
Transmission of the ECG to the admitting hospital in advance will allow
the diagnosis to be confirmed and allow for early initiation of further
management.
If a patient with suspected ACS arrives in hospital, rapid processing is
necessary to establish an early diagnosis and allow effective emergency
care to be instituted. An appropriately trained doctor should review
patients who present to the emergency department with possible ACS
as soon as possible. The initial assessment should be rapid, and aimed
at establishing the diagnosis, assessing the haemodynamic state and
determining suitability for reperfusion therapy. Patients with clear-cut
clinical features of STEMI with an ECG that demonstrates ST elevation
or bundle branch block should enter a ‘fast track’ system, designed to
ensure that they receive appropriate emergency care; any reperfusion
therapy required should be instituted within 90 minutes of the initial call
for medical assistance. A successful fast track system is only possible if
medical staff respond rapidly to calls from the emergency department, and
the aim should be to review patients with a suggestive history and ECG
changes within 10 minutes of their arrival.
INITIAL TREATMENT 17
ACUTE CORONARY SYNDROMES
Emergency care
The main aims for treatment of ACS are to prevent continued ischaemia,
limit myocardial damage, reduce the incidence of left ventricular
dysfunction, heart failure and death. This is achieved with early
identification of patients who require revascularization and treatment of
complications of ischaemia including arrhythmia (VF/VT and
bradycardia), heart failure and shock. Initially, in all patients with ACS,
emergency care consists of symptom relief, administration of
antithrombotic agents, and instigating reperfusion therapy as early as
possible for STEMI.
The priorities are to:
• Establish venous access with a large-bore cannula in an arm vein
providing ready access for drug administration, and institute
rhythm monitoring to aid in the rapid detection and treatment of
arrhythmias.
• Provide adequate analgesia, which is vital. Uncontrolled pain and
anxiety are associated with sympathetic activation, with resultant
detrimental effects on cardiac performance, oxygen consumption and
the arrhythmia threshold. Intravenous (IV) opioids are indicated to
provide rapid relief of pain. Intramuscular injections should be
avoided, as they have a slower onset of action, are associated with
unpredictable absorption, may cause a haematoma if thrombolytic
therapy is given, and can affect CK estimations. The agent of choice is
IV diamorphine 2.5–5.0 mg, given with an IV antiemetic. The dose
should be repeated every 5 minutes until adequate analgesia is
achieved. If repeated administration of diamorphine fails to relieve
the pain, IV beta-blockers or nitrates should be considered.
Respiratory depression produced by diamorphine can, if necessary, be
rapidly reversed by naloxone.
• Treat pulmonary oedema with IV frusemide 40–80 mg. If
pulmonary oedema is severe, an IV nitrate infusion (as detailed in
Appendix A) should be commenced.
• Consider supplemental oxygen. Hypoxia is common in patients
with evolving infarction, and may increase myocardial necrosis or
have adverse metabolic effects. Supplemental oxygen will optimize
oxygen delivery and limit ischaemia, and should be given to all
patients with breathlessness or features of heart failure. Since
hypoxia may be present in 20 per cent of patients with an initially
18 INITIAL TREATMENT
ACUTE CORONARY SYNDROMES
TREATMENT OF ST ELEVATION MI
Background
Prior to the advent of thrombolysis or primary PCI, the only means of
achieving therapeutic reperfusion in patients with evolving MI was
emergency CABG. Although no randomized trials have been performed,
good results were reported for large case series from the 1970s, with an
improvement in outcome compared to medically treated patients.
Hospital mortality in the surgically treated patients was around 5 per cent,
TREATMENT OF ST ELEVATION MI 19
ACUTE CORONARY SYNDROMES
PRIMARY PCI
The use of primary PCI to achieve reperfusion in STEMI was first
reported in 1983. Early case series suggested that primary PCI was a safe
and effective means of restoring antegrade flow in the infarct-related
artery (IRA) of a patient with STEMI. Potential advantages compared to
thrombolysis led to a series of randomized studies comparing the two
treatment modalities. Primary PCI, when performed promptly by
experienced operators, has been shown to be superior to thrombolysis.
A meta-analysis of 23 randomized trials with 7739 patients revealed a
significantly lower rate of early death (0.7 per cent vs 0.9 per cent,
p = 0.0002) in favour of primary PCI. Non-fatal reinfarction (3 per cent vs
7 per cent, p < 0·0001), and the risk of stroke (1 per cent vs 2 per cent,
p = 0.0004) were also significantly reduced. There was an increased risk of
major bleeding in the primary PCI group related to the arterial access site.
This may be minimized with newer combinations of antithrombotic
regimes and the use of the radial route for arterial access.
Benefits over thrombolysis
The efficacy of primary PCI is thought to predominantly result from
increased patency rates achieved in the IRA (90–95 per cent with primary
PCI vs 30–40 per cent with streptokinase and 50–60 per cent with
fibrin-specific agents). In addition to maintaining patency, treating the
underlying culprit plaque reduces rates of reinfarction and reintervention,
thereby reducing overall ischaemic and mechanical complications. The
lower incidence of stroke and in particular haemorrhagic stroke also
20 PRIMARY PCI
ACUTE CORONARY SYNDROMES
22 PRIMARY PCI
ACUTE CORONARY SYNDROMES
in bleeding when comparing the radial to femoral route (0.7 per cent vs
2.7 per cent in the GpIIb/IIIa groups) and when comparing bivalirudin to
GpIIb/IIIa inhibitors in patients undergoing angioplasty via the femoral
route (3 per cent vs 5.8 per cent).
Aspiration catheters are fine bore catheters which can be passed along an
angioplasty wire into the IRA. They are designed to aspirate thrombus in
order to reduce distal embolization. Several randomized trials have shown
they improve ST-segment resolution and coronary flow. A meta-analysis
of randomized trials of thrombectomy in STEMI has shown a benefit for
manual aspiration catheters with a decreased combined end point of death
and MI. This was largely driven by the TAPAS trial, which showed improved
30-day and 1-year survival in cases treated with routine aspiration prior to
stenting, even when thrombus was not angiographically detectable.
THROMBOLYSIS
Background
Despite the advent of primary PCI, thrombolysis remains the initial
treatment for a large proportion of acute STEMI patients in the UK.
Thrombolytic therapy for acute MI was first used in 1958. Debate about
THROMBOLYSIS 23
ACUTE CORONARY SYNDROMES
its efficacy continued until 1986, when the publication of the first GISSI
study clearly demonstrated the value of streptokinase. By the
mid-1990s, more than 100 000 patients had been randomized into a
series of large-scale thrombolytic trials, which have helped to optimize
the use of thrombolytic drugs. These large-scale trials have
demonstrated that:
• thrombolysis produces an important time-dependent reduction in
mortality. Treatment within the first hour after symptom onset
can prevent irreversible myocardial necrosis from progressing, and
abort an evolving infarct. Treatment within the first 6 hours of
symptom onset limits infarct size and reduces mortality by
25 per cent. Treatment between 6 and 12 hours may help to salvage
some ischaemic myocardium (particularly in the border zone of
the infarct) and reduces mortality by about 10 per cent. Over
12 hours from symptoms, PCI is the preferred treatment as it
increases the chance of successful reperfusion and it does not carry
the risks associated with late thrombolysis. Based on this first
series of trials, thrombolytic therapy reduces 1-month mortality by
17 per cent, preventing 18 deaths for every 1000 patients treated.
This mortality benefit is maintained in the long term, with 10-year
survival rates substantially improved in treated patients. Newer,
more efficacious agents have improved on these 1-month and
10-year survival figures
• mortality reduction is present regardless of age, sex or infarct site
• aspirin has an additive beneficial effect of similar magnitude to
that produced by thrombolysis, and should be given to all patients
with evolving MI
• the concurrent use of unfractionated heparin and thrombolytic
therapy has been extensively studied. There are no beneficial effects
apparent when intravenous or subcutaneous heparin is used with
streptokinase or with early rt-PA (alteplase) regimens but the risk of
bleeding complications is increased. For accelerated rt-PA and the
newer plasminogen activators, heparin [controlled by regular
activated partial thromboplastin time (aPTT) monitoring] reduces
coronary reocclusion rates, and should be given for 48 hours
• thrombolysis increases the risk of stroke in the first 24 hours after
treatment, but this is offset by the much larger reduction in cardiac
deaths with treatment. Stroke risk is greater in older patients (over
24 THROMBOLYSIS
ACUTE CORONARY SYNDROMES
THROMBOLYSIS 25
ACUTE CORONARY SYNDROMES
Inclusion criteria
Where primary PCI is not available or where an additional time delay to
primary PCI of 90 minutes or more is expected, thrombolysis should be given if:
Exclusion criteria
These continue to evolve, and are in general decreasing as our experience
with thrombolytic agents increases. At present there are few absolute
contraindications. Many are now regarded as relative, to be interpreted
within the clinical context. Criteria include:
• known coagulation disorder, including uncontrolled
anticoagulation therapy
>110 mmHg)
Complications
Allergy
Allergic reactions to streptokinase are due to the effect of pre-existing
antistreptococcal antibodies. Mild urticarial reactions are the most common
allergic response, and should be treated with 200 mg IV hydrocortisone and
10 mg IV chlorpheniramine. If a more severe reaction with bronchospasm
occurs, 250–500 mg of intramuscular adrenaline should be administered
along with nebulized bronchodilators. Major anaphylaxis is very rare
(0.1 per cent). If this occurs, with associated cardiovascular collapse, 5 mL
of 1:10 000 adrenaline IV is first-line therapy, followed by rapid volume
loading with IV plasma expanders, steroids and antihistamines. Allergic
reactions to the newer plasminogen activators are very rare.
Haemorrhage
Minor bleeding at venepuncture sites is relatively common, but rarely
requires any specific therapy other than direct compression at the site.
Major haemorrhagic episodes requiring transfusion are rare. If a major
bleed occurs consider the following action:
• stop thrombolytic infusion (or heparin)
• reverse heparin with protamine sulphate (10 mg per
1000 u heparin)
Hypotension
Hypotensive reactions to thrombolytic infusion can occur with any agent,
but are more common with streptokinase. They should be treated initially
THROMBOLYSIS 27
ACUTE CORONARY SYNDROMES
by tilting the patient’s head down and, in the case of streptokinase, the
infusion should be slowed down or, if necessary, halted for 5 minutes. It
can usually be successfully restarted when the blood pressure recovers.
Atropine 0.6 mg IV can be given if a bradycardia is also present. If the
hypotension persists and is clearly associated with the infusion, then the
drug should be stopped, and a plasminogen activator substituted for
streptokinase, as it is less likely to cause hypotension. In the case of severe
persistent hypotension, fluids and inotropes can be administered
cautiously if necessary.
Cerebrovascular events
The overall incidence of stroke is only minimally increased, since
thrombolytic therapy causes a slight increase in cerebral haemorrhages,
which is offset by a reduction in cerebral infarcts. Plasminogen activators
are associated with a greater risk of haemorrhagic stroke than
streptokinase. Stroke is more common in older patients. If a stroke occurs,
thrombolytic or anticoagulant therapy should be discontinued. A CT scan
and neurological opinion will help to determine the mechanism of the
stroke and guide therapy.
Failed reperfusion
Detection and implications of failed reperfusion
Patients treated with thrombolysis who achieve effective reperfusion have a
good prognosis, with hospital mortality rates of less than 5 per cent.
Achievement of successful reperfusion is associated with IRA patency,
restoration of rapid antegrade blood flow into a patent microcirculation and
resolution of chest pain. In a substantial proportion of patients, however,
reperfusion fails. In some of these patients the IRA is persistently occluded
by an extensively disrupted plaque or residual thrombus. In other patients
(particularly those treated late), platelet microthrombi or capillary
disruption prevent reperfusion of myocardium at the tissue level despite
restoration of blood flow in the epicardial IRA. Failure of reperfusion is
associated with continuing chest pain, extensive infarction, electrical and
haemodynamic instability, mechanical complications and a poor prognosis.
Detecting failed reperfusion in current clinical practice is based on
serial evaluation of ST segments. Persistent ST elevation occurs in about
one-third of patients, and is associated with failure of reperfusion, and
portends an adverse prognosis. Of the 1398 patients enrolled in the
INJECT trial, those with no ST resolution had a 17.5 per cent hospital
mortality, those with partial resolution a 4.3 per cent mortality and those
with total resolution a 2.5 per cent mortality.
28 THROMBOLYSIS
ACUTE CORONARY SYNDROMES
Rescue angioplasty
The REACT trial as well as meta-analysis of angioplasty strategies after
thrombolysis support the role of rescue angioplasty for STEMI patients
who fail to reperfuse after thrombolysis. The REACT trial recruited such
patients presenting within 6 hours. The criterion used to diagnose failed
reperfusion was the presence of <50 per cent resolution of maximal ST
elevation on the 90-minute post-thrombolysis ECG. The original trial
showed a significant reduction in reinfarction at 6 months in those
undergoing rescue angioplasty when compared to repeat thrombolysis or
conservative therapy (2.1 per cent vs 10.5 per cent vs 8.5 per cent).
Follow-up data at 1 year showed a sustained benefit with increased
event-free survival in the rescue PCI group. Accordingly, all patients
should have an ECG recorded 90 minutes after commencing
thrombolysis. Patients who have less than 50 per cent ST segment
resolution in the infarct zone should be considered for rescue angioplasty.
Recurrent ischaemia and early PCI after thrombolysis
Following successful thrombolytic therapy, patients are often left with a
residual high grade stenosis or an ‘inflamed’ ruptured plaque. Recurrent
ischaemia occurs in up to one-third of thrombolyzed patients, and is
associated with increased hospital mortality. Usually, early recurrent
ischaemia is related to further thrombus formation at the site of the
original unstable atherosclerotic plaque. The GRACIA-1 trial looked at
patients who were successfully thrombolysed and compared routine
angiography within 24 hours with an ischaemia-guided approach. Among
the subjects undergoing early angiography, stenting of the IRA was
performed in 80 per cent. This was associated with a significant reduction
in a combined end point of death, reinfarction or revascularization
(9 per cent vs 21 per cent at 12 months). Index hospital stay was also
significantly reduced in the early group.
Recently, another trial (TRANSFER-AMI) of 1059 patients compared
immediate transfer for PCI after thrombolysis (with tenecteplase) with
standard treatment with rescue angioplasty if required. Angiography
was undertaken at a median of 2.8 hours in the immediate transfer
group and 32.5 hours in the standard treatment group. In the standard
group, 34.9 per cent underwent early angioplasty for rescue, shock and
reinfarction. Overall, early angiography was associated with significantly
reduced recurrent ischaemia (0.2 per cent vs 2.1 per cent), as well
as a reduced combined end point of death, reinfarction, recurrent
ischaemia, new or worsening heart failure or cardigenic shock within
30 days.
THROMBOLYSIS 29
ACUTE CORONARY SYNDROMES
• ST elevation 0.5–1 mm
• ST depression 0.25–1 mm
• T-wave inversion in >2 leads
• Q waves
• left ventricular hypertrophy
• abnormal rhythm
8 7.5
4 3.7
3.4
3
2 1.7
1.0
1
831 174 148 134 50 67
0
0 to <0.4 0.4 to <1.0 1.0 to <2.0 2.0 to <5.0 5.0 to <9.0 9.0
17/50
35
30
4/21 2/9
25
I
Cardiac death/M
31/196
20
15
6/68
10
10/191 4/61
5 6/86
High risk
0
se
on
Intermediate risk
sp
0.2 1/84
re
st
Low risk
te
Trop 0.06-0.2
e
o nin <0.16
cis
T ((
g L -1
er
)
Ex
24 hours
High-risk patients
The American Heart Association/American College of Cardiology (AHA/
ACC) guidelines recommend an invasive strategy in NSTEACS in the
following situations:
• recurrent angina/ischaemia at rest or low-level exercise despite
intensive medical therapy
• signs or symptoms of heart failure or new or worsening mitral
regurgitation
• high-risk findings on non-invasive stress testing
• reduced left ventricular function (EF <40 per cent)
• haemodynamic instability
• sustained ventricular tachycardia (VT)
• PCI within the previous 6 months
• prior CABG
• high-risk score (e.g. TIMI or GRACE)
• new or presumably new ST-segment depression
• elevated cardiac biomarkers (troponin I and T).
Patients with recent PCI are likely to have a restenosis or stent thrombosis
best treated with reintervention. Prior CABG represents another subgroup
where early intervention is of benefit due to the high rate of venous graft
failure. Patients with reduced left ventricular function, acute heart failure
or previous anterior Q-wave MIs have sufficient risk to support a policy
of early angiography. Patients with extensive co-morbidities and patients
with chest pain with low-risk scores are unlikely to benefit from an
invasive strategy.
Low-risk patients
Non-invasive stress testing with a low-level treadmill exercise test (two
stages of the Bruce protocol) should be performed in patients free of
ischaemia at rest or on minimal exertion for 12–24 hours. Should patients
be discharged prior to this, symptom-limited exercise testing may be done
within 7–10 days of presentation.
Where the baseline ECG has resting ST-segment depression (>0.1 mV),
bundle branch block, left ventricular hypertrophy, an intraventricular
conduction defect, a paced rhythm, or the patient is on digoxin therapy,
stress perfusion imaging (radioisotope or MRI) or stress echocardiography
may be done to identify a substrate for ischaemia. Those that subsequently
have a positive stress test should undergo coronary angiography with a
view to revascularization.
The RITA-3 study also showed benefit for an invasive strategy with
reduced refractory angina at 4 months (4.4 per cent vs 9.3 per cent). There
Thrombocytopenia
Thrombocytopenia can occur after treatment for ACS as a result of
exposure to heparins or GpIIb/IIIa inhibitors. Heparin-induced
thrombocytopenia (HIT), is a serious, immunoglobulin-mediated
complication that often leads to thromboembolic complications. It occurs
with UFH (incidence 5 per cent) and LMWH (incidence 0.5 per cent)
usually after between 5 and 10 days of use (or sooner if there has been
previous exposure to heparins), and is associated with a 50 per cent
reduction in the platelet count or a drop to < 100 X 109 platelets/L. It should
be treated with the cessation of heparin and introduction of another
antithrombotic agent such as lepirudin or danaparoid. Bleeding
complications of HIT are rare but 50 per cent of patients with HIT develop
arterial or venous thrombosis which can be life threatening. Further
exposure to heparins should be avoided in patients who have had HIT.
GpIIb/IIIa-induced thrombocytopenia is often more profound with
platelet counts of < 50 X 109 platelets/L. It occurs more frequently with
abciximab (up to 2.4 per cent) and less with eptifibatide (0.2 per cent) and
tirofiban (0.5 per cent). The GpIIb/IIIa inhibitor and heparin should be
discontinued. Most patients remain asymptomatic and platelet counts begin
to improve within 24 hours. Platelet transfusions should be reserved for
those with bleeding. Thrombosis is rare with GpIIb/IIIa inhibitor-induced
thrombocytopenia; however, there is a higher incidence of adverse events,
due to bleeding, repeat revascularization, recurrent ischaemia and death.
Aspirin
Unless there is a contradidication, aspirin should be administered to all
patients with NSTEACS and STEMI at presentation. It should be
continued indefinitely in all patients with suspected or proven coronary
disease. Aspirin inhibits the cyclooxygenase enzyme in platelets which
leads to the formation of thromboxane A2, a potent stimulus to platelet
activation. Data from the Veterans Administration Cooperative Study, the
There are few contraindications to the use of aspirin, but it should not be
given to patients with:
Clopidogrel
Clopidogrel is a thienopyridine which blocks ADP-mediated platelet
aggregation and the activation of the GpIIb/IIIa receptor, which cross-links
platelets through fibrinogen. It was shown to be of value in NSTEACS in
the CURE trial: this randomized 12 562 patients with NSTEACS
have a faster onset and be more potent than clopidogrel. The TRITON
TIMI 38 study, undertaken in ACS patients (99 per cent undergoing PCI),
assessed prasugrel (loading dose 60 mg, followed by 10 mg maintenance)
in comparison to clopidogrel (loading dose 300 mg, followed by 75 mg
maintenance). The primary end point of cardiovascular death, non-fatal
MI and non-fatal stroke was reduced by 23 per cent at 30 days in the
prasugrel group (9.9 per cent vs 12.1 per cent, p < 0.001). The benefit was
sustained to 15 months though there was an increased risk of life-
threatening bleeding in those taking prasugrel (1.4 per cent vs 0.9 per cent,
p = 0.01). The benefits of prasugrel were more pronounced in STEMI
patients, in whom there was a 32 per cent reduction in the primary end
point, and a decreased requirement for adjuvant GpIIb/IIIa therapy with
no observed increase in bleeding.
Duration of antiplatelets
Following NSTEACS, it is recommended that DAPT, with aspirin and
clopidogrel, should be continued for at least 1 year whether treated by
PCI or medically (CURE study). For STEMI, there is strong evidence
for benefit for DAPT up to 1 month (COMMIT and CLARITY studies)
and considering the effect on NSTEACS it is reasonable to continue
DAPT for 1 year for all ACS, including STEMI. In addition, most
patients will be treated with PCI and therefore the duration will depend
on the type of stent used as well as the risk of reinfarction (which will
be dependent on other factors such as diabetes and impaired left
ventricular function) that should be weighed up against the risk of
bleeding. Patients who receive a DES need to continue DAPT for at
least 1 year, as premature cessation is strongly associated with a risk
of stent thrombosis, which carries a high mortality. This was shown in
the PREMIER study where patients with DES who discontinued
clopidogrel experienced a nine-fold higher risk of mortalty (7.5 per cent
vs 0.7 per cent, p < 0.0001). Premature discontinuation in patients
managed medically may also lead to a higher risk of death and
reinfarction. Therefore, in any patients who are going to require
Anticoagulants
As previously discussed, heparin is required for 48 hours after
thrombolysis with plasminogen activators. Heparin is not beneficial and
is not recommended as routine therapy after streptokinase. UFH was used
in the initial trials of plasminogen activators, however more recently the
EXTRACT-TIMI 25 trial showed that the use of LMWH post
thrombolysis resulted in a lower rate of reinfarction compared to UFH
(9.9 per cent vs 12 per cent, p = 0.001) at a cost of increased major bleeding
(2.1 per cent vs 1.4 per cent, p < 0.001). In meta-analyses, the use of
LMWH has been shown to be more effective than UFH in reducing
reinfarction and ischaemia in NSTEACS treated medically with no
increase in bleeding. In the SYNERGY trial, LMWH has also been shown
to be as effective as UFH in patients undergoing an early invasive strategy
albeit at an increased risk of major bleeding (9.9 per cent vs 7.6 per cent).
The increased risk of bleeding in patients undergoing PCI may have been
due to the addition of UFH while the previous dose of LMWH was still
active. In the STACKENOX trial the addition of UFH to enoxaparin
resulted in a considerable and prolonged increase in clotting parameters
(anti-Xa and anti-IIa) but had no effect on the more routinely measured
activated clotting time (ACT). Additionally, LMWH alone during PCI in
the STEEPLE trial showed lower rates of mainly femoral access site
complications. However, the use of UFH is still recommended during PCI
procedures as it is rapidly effective with a measurable change in the ACT
and it can be promptly reversed with protamine if necessary.
Bivalirudin, a direct thrombin inhibitor, is also effective in STEMI and
NSTEACS patients and can be continued during PCI. The main advantage
of bivalirudin is the reduction in bleeding compared to the use of heparin
and GpIIb/IIIa inhibitors. In NSTEACS, fondaparinux, a factor Xa
inhibitor, when given subcutaneously at a dose of 2.5 mg, was shown to be
as effective as the LMWH enoxaparin in the OASIS-5 trial. Major bleeds
were reduced by 48 per cent in the fondaparinux group, although it was
noted that there was a higher incidence of catheter-related thrombus which
did not impact on the primary end point. Therefore fondaparinux can be
recommended for NSTEACS, particularly for those at high risk of bleeding,
when intervention is likely to be delayed, or when medical management is
preferred. If patients on fondaparinux undergo PCI, it is recommeded that
they receive heparin during the procedure. Fondaparinux was also studied
in STEMI in the OASIS-6 trial involving 12 092 patients either treated with
thrombolysis, primary PCI or without any reperfusion therapy. There was
a significant reduction in the primary end point of death or reinfarction at
30 days when compared to UFH. (9.7 per cent vs 11.2 per cent, p = 0.008).
This benefit was mainly observed among patients who were not treated
with primary PCI. Even those that did not receive reperfusion therapy
without a conventional indication for UFH benefited from fondaparinux
in reducing the incidence of the primary end point. The benefits were
onserved without an increase in bleeding and stroke.
Overall, anticoagulants are recommended in all patients with ACS, but
the doses and agents used need to be carefully considered in relation to
patients’ bleeding risks.
Abciximab (ReoproTM )
Abciximab has the most data among the GpIIb/IIIa inhibitors, in
particular when used after angiography. Analysis of pooled data from three
large trials (EPIC/EPILOG/EPISTENT) including 7290 patients with ACS
receiving stenting has shown a 29 per cent reduction in late mortality
when compared to placebo. Based on the experience of the EPIC trial, the
EPILOG trial confirmed the need to reduce the bolus heparin dosing to
70 U/kg during intervention to diminish this risk. More recent data from
the ISAR-REACT 2 study have shown the benefit for abciximab in
addition to loading with clopidogrel 600 mg in NSTEACS. At 30 days,
the composite end point of death/MI/urgent target vessel
revascularization was reduced in the abciximab group by 25 per cent,
compared to placebo (8.9 per cent vs 11.9 per cent, p = 0.03). Subgroup
analysis had revealed that the benefits were isolated to those patients who
had positive troponins. Interestingly, the 1-year follow-up of
ISAR-REACT 2 has shown continued benefit in the primary end point
(23.3 per cent vs 28 per cent, p = 0.012), which now also extended to
troponin-negative patients.
The use of abciximab up-front (prior to angiography) has been studied
in a meta-analysis of 29 570 patients. The benefit of abciximab was
only observed in patients who subsequently went on to have PCI.
Based on current evidence, abciximab should be considered in the
catheter laboratory for all troponin-positive NSTEACS requiring PCI.
Among STEMI patients, the use of abciximab has been shown to be of
benefit in a large meta-analysis with 27 115 patients. However, several
of the trials did not use stents, and none of the included studies used
the higher loading dose of clopidogrel, so these studies do not really
reflect contemporary practice. Indeed, a more recent study, BRAVE-3,
showed no additional benefit on infarct size (measured by single-
photon emission CT) with abciximab when 600 mg of clopidogrel
was used. Based on the evidence, the use of abciximab for STEMI is
recommended, but not mandated, and may be reserved for patients
at low bleeding risk, who have not received adequate loading with
clopidogrel, or those with a large thrombus burden.
any clinical benefit compared to placebo. Overall, the small molecules can
be recommended for selective use in NSTEACS, but there is not enough
data to recommend their routine use in STEMI.
Beta-blockers
Beta-blockers have antiarrhythmic, anti-ischaemic and antihypertensive
properties. Small studies indicate that these beneficial effects reduce chest
pain, myocardial wall stress and infarct size in patients with STEMI. An
overview of almost 30 000 patients randomized to placebo or IV therapy
in the pre-thrombolytic era indicated that they were well tolerated,
preserved left ventricular function and reduced the incidence of
arrhythmia and early mortality.
The large COMMIT study compared the use of early IV then oral
metoprolol with placebo in STEMI patients. The metoprolol group showed
a modest reduction in reinfarction and ventricular fibrillation but no
overall benefit on mortality. More importantly, the rate of cardiogenic
shock was significantly higher in the metoprolol group. Therefore, routine
use of intravenous beta-blockers cannot be recommended for all patients
with STEMI. As maximum mortality benefit from beta-blocker therapy
is obtained in higher-risk patients, whose infarctions are complicated
by arrhythmias or heart failure; treatment should be directed to specific
problems such as ongoing chest pain, poorly controlled hypertension and
tachy-arrhythmia. However, patients should be carefully selected to avoid
those at risk of developing shock (e.g. patients with large, un-reperfused
anterior infarcts and patients with mechanical complications).
Long-term oral beta-blockers, commenced in the convalescent phase of MI,
have been evaluated in a large number of placebo-controlled trials. In a recent
meta-analysis of 82 trials enrolling more than 54 000 patients, mortality
was reduced by almost 25 per cent due to the prevention of reinfarction
and sudden death. These benefits are apparent irrespective of age, site of
infarction, and presence or absence of previous MI or complications. Serious
side effects are rare. Benefit is still apparent after several years of therapy, and
beta-blockers should therefore be continued indefinitely.
On the basis of these trial data, all patients should be considered for long-
term oral beta-blocker after STEMI. Contraindications to beta-blocker
therapy are present in around 15 per cent of patients, and consist of:
• resting heart rate <55 bpm
• second or third degree heart block
• a history of asthma.
ACE inhibitors
Activation of the renin–angiotensin system is an early compensatory
response to an evolving MI. Activation of the renin–angiotensin system
Statins
Statin therapy has been evaluated in a series of large primary and
secondary prevention trials enrolling more than 50 000 patients (CARE,
4S, WOSCOPS, AFCAPS, LIPID and most recently the Heart Protection
Study). These trials conclusively demonstrate that:
• statin therapy reduces mortality in patients with symptomatic
ischaemic heart disease by around a third
• statin therapy is safe and well tolerated
• patients of all ages and either sex benefit
Hypokalaemia
Hypokalaemia is common in patients with acute infarction, and is related
to prior treatment with diuretics or catecholamine effects on electrolyte
handling. Hypokalaemia is associated with myocardial electrical instability
(the incidence of ventricular fibrillation may be as high as 15 per cent in
infarcts associated with a serum potassium of 3.0–3.5 mmol/L, and 5 per cent
or less in infarcts associated with a potassium of 4.5–5.0 mmol/L) and
should be corrected. If serum potassium is below 4.0 mmol/L in the absence
of an important arrhythmia, then oral potassium supplements are given
(e.g. slow K, three tablets three times daily, providing approximately
72 mmol potassium daily) and potassium rechecked after 12–18 hours. If
ventricular arrhythmias occur in association with a serum potassium of
less than 4.0 mmol/L, intravenous potassium is given as detailed in
Appendix A, rechecking serum levels after 3 hours to ensure that
potassium levels have risen to greater than 4.0 mmol/L.
Magnesium therapy
A number of small studies (including LIMIT-2) suggested that routine
administration of magnesium may reduce mortality following acute
infarction by beneficial effects on heart rate, contractility, electrical
stability and platelet activity. The routine use of magnesium was therefore
examined in almost 60 000 patients in the ISIS-4 study, and this showed
that treatment had no beneficial effect on mortality. Subgroup analysis
showed no benefit even when magnesium was given early, or to patients
who did not receive thrombolytic therapy. These results were confirmed
in the recent MAGIC trial of over 6000 patients. There is therefore no
good evidence to support the routine use of magnesium in patients with
evolving acute MI. Magnesium is, however, still indicated for the
treatment of arrhythmias.
Nitrate therapy
Nitrates have a number of potentially beneficial effects (systemic
vasodilatation and coronary artery dilatation), and small early studies
suggested that their routine administration to patients with acute
infarction may reduce mortality. The ISIS-4 and GISSI-3 trials investigated
routine nitrate use in a total of almost 80 000 patients, and found no
substantial beneficial effect on mortality. Although nitrates are safe and
effective in the treatment of post-infarction ischaemia or heart failure,
they should not routinely be administered to uncomplicated patients.
Hyperglycaemia
Patients with pre-existing diabetes have an increased risk of ischaemic
heart disease, and an unfavourable prognosis following acute MI. Patients
who have no history of diabetes but an elevated glucose on admission also
have a poor prognosis. The high mortality may be related to the
occurrence of autonomic neuropathy, pre-existing ventricular
dysfunction or due to detrimental myocardial cellular changes induced by
diabetes. Additionally, sympathetic activation will induce insulin
resistance and hyperglycaemia in susceptible patients, increasing the
release of non-esterified fatty acids, which augment myocardial oxygen
consumption, depress contractility and increase the risk of heart failure.
A strategy of controlling elevated plasma glucose by insulin infusion
followed by subcutaneous injections in hyperglycaemic patients with
acute MI could prevent these adverse metabolic effects, and was
investigated in over 600 patients randomized in the DIGAMI trial.
Treatment with IV insulin infusion reduced mortality by around
40 per cent. The maximum reduction in mortality occurred in patients
who had not previously received insulin therapy, and were at low risk of
death on the basis of clinical criteria. On the basis of these trial data, it is
recommended that all patients with an admission glucose >11 mmol/L
should be commenced on a sliding scale IV insulin infusion with
the infusion rate adjusted to maintain blood glucose in the range
7–11 mmol/L, in combination with 500 mL of 5 per cent dextrose infused
over 24 hours. Oral hypoglycaemic agents should be withdrawn. The
infusion should be continued for at least 24 hours, or until the patient is
clinically stable. However, it is less clear how to manage patients in the
long term. The DIGAMI trial suggested that 3 months of tight glycaemic
control with subcutaneous insulin may improve outcomes; however, this
was not confirmed in the DIGAMI-2 trial. Therefore, tight control with
conventional oral hypoglycaemics may be of benefit where possible, and
may reduce the incidence of adverse effects due to insulin such as weight
gain and hypoglycaemia.
COMPLICATIONS OF ACS
Background
Complications following ACS are more common following STEMI.
Modern reperfusion including the increased use of PCI has resulted in
dramatic reductions of reinfarction and death over the last decade;
consequently, this has resulted in a reduction in the incidence of
post-ACS complications. In a SWISS registery of STEMI patients,
reinfarction decreased from 3.7 per cent to 0.9 per cent between the
years 2000 and 2007. This was linked with an increase in the use of PCI
from 43 per cent to 85 per cent over the same time period. However,
complications still occur and when they do arise are often related to
more extensive STEMI, where the infarct-related artery has not been
reperfused. This is more common in patients who present late, the
elderly (over 75) and those with diabetes. These patients often have
poorer left ventricular function and additionally may have extensive
coronary disease which is not easily amenable to revascularization. Left
ventricular dysfunction is directly associated with lower rates of
survival and those with extensive myocardial injury more commonly
have mechanical and arrythmic complications. In patients with severe
left ventricular dysfunction (EF <30 per cent) despite successful
revascularization for STEMI, the presence of pathological Q waves on
ECG and signs of heart failure are clinical markers of poor myocardial
recovery and prognosis. It is important to identify these patients early
so they can be monitored closely and to allow for prompt treatment
when necessary.
54 COMPLICATIONS OF ACS
ACUTE CORONARY SYNDROMES
COMPLICATIONS OF ACS 55
ACUTE CORONARY SYNDROMES
Cardiogenic shock
Background
Cardiogenic shock occurs in a small proportion of patients who
present with extensive infarction and is responsible for the majority of
in-hospital deaths. The GRACE registery data and a large Swiss registery
have shown that the incidence has recently decreased as the use of
reperfusion and in particular primary PCI has increased. This is likely
to be as a result of reducing recurrent ischaemia with use of stents and
antiplatelets, in addition to smaller infarct sizes due to accessibility of
early primary PCI and thrombolysis. Cardiogenic shock complicating
an ACS can be due to:
• infarction or ischaemia of >40 per cent of the left ventricular
myocardium leading to pump failure (85 per cent of cases)
• a potentially reversible complication leading to severe
decompensation, such as acute mitral regurgitation, ventricular
septal rupture or right ventricular infarction (15 per cent of
cases).
56 COMPLICATIONS OF ACS
ACUTE CORONARY SYNDROMES
Subgroup analysis suggested a larger benefit for younger (<75 years of age)
patients treated early (within 6 hours of diagnosis). Taken together, this
body of non-randomized and randomized trial data suggests that selected
patients with cardiogenic shock may benefit from intensive supportive
therapy combined with revascularization.
Diagnosis
A diagnosis of cardiogenic shock due to left ventricular dysfunction can
be confidently made in patients with evidence of extensive ischaemic
myocardial damage who present within 24 hours of the onset of an acute
STEMI with features of:
• hypotension (systolic BP persistently <90 mmHg)
• clinical signs of a low output sate (urine output <30 mL/h, poor
peripheral perfusion or impaired cerebration)
• evidence of raised cardiac filling pressures (the presence of clinical
or radiological pulmonary oedema implies that pulmonary artery
wedge pressure is >15 mmHg).
If there are atypical features to the clinical presentation, careful evaluation is
required to exclude treatable complications of MI. In particular, if there is:
• late onset of cardiogenic shock or an associated new murmur, the
cardiogenic shock may be due to a mechanical complication
• low blood pressure in the absence of pulmonary oedema in a
patient with inferior or posterior infarction or a negative fluid
balance, when hypotension may be due to right ventricular
infarction or hypovolaemia.
If any doubt exists as to the cause of the cardiogenic shock,
echocardiography and pulmonary artery catheterization are required. In
patients with cardiogenic shock due to severe left ventricular dysfunction
there will be extensive left ventricular hypokinesia at echocardiography in
association with a raised (>15 mmHg) pulmonary wedge pressure and a
low (<2.2 L/min/m2) cardiac index.
60 COMPLICATIONS OF ACS
ACUTE CORONARY SYNDROMES
• hypertension
• marked/persistent ST elevation.
In addition, the incidence of free wall rupture may be increased by
thrombolytic therapy, particularly if it is given late in the course of the
infarct. Intravenous beta-blocker therapy reduces the risk of free wall
rupture. Free wall ruptures present within a few days of the onset of
STEMI. The usual presentation is with a sudden acute rupture presenting
as collapse with electromechanical dissociation which does not respond to
resuscitation. In 25 per cent of cases a subacute rupture occurs, with a slower
leak of blood into the pericardial space which may produce tamponade.
Echocardiography confirms the presence of fluid in the pericardial space.
Immediate surgery should be considered, as there is a high risk of major
rupture and death occurring unpredictably.
COMPLICATIONS OF ACS 61
ACUTE CORONARY SYNDROMES
62 COMPLICATIONS OF ACS
ACUTE CORONARY SYNDROMES
COMPLICATIONS OF ACS 63
ACUTE CORONARY SYNDROMES
with LVT and heart failure. The clinical features that increase the risk of
LVA formation are:
• extensive anterior STEMI
• persistent ST elevation in the infarct zone
• heart failure.
Patients with confirmed LVA should be considered for anticoagulation to
reduce thromboembolism. In view of their concomitant left ventricular
dysfunction they should also receive adequate drug therapy, including
ACE inhibitors and aldosterone antagonists. They are at high risk of
ventricular arrhythmia and should be evaluated for an implantable
cardioverter defibrillator (ICD). If they remain symptomatic with heart
failure or develop worsening mitral regurgitation, due to negative left
ventricular remodelling, they should be considered for coronary artery
bypass surgery and aneurysmectomy.
Clinically significant deep venous thrombosis and pulmonary embolism
are now rare following uncomplicated ACS. The risks are increased in
patients with extensive complicated STEMI, particularly if prolonged bed
rest or heart failure occur. In high-risk patients, prophylactic low-dose
subcutaneous LMWH should be instituted and continued until the patient
is clinically stable and mobile.
Pericarditis
Pericarditis is an early complication associated with extensive STEMI,
usually within the first week. The clinical features of pericarditis
complicating anterior STEMI are:
• sharp central chest pain, worse with respiration, relieved by sitting
up or leaning forward but not relieved by glyceryl trinitrate (GTN)
• an associated friction rub.
In inferior STEMI a friction rub is rare, and the pain may be atypical
or radiate to the left shoulder. Progression of pericarditis to a clinically
significant effusion is rare. Treatment consists of:
• reassuring the patient about the cause of the symptoms
• pain relief with simple analgesics such as dihydrocodeine, with
non-steroidal anti-inflammatory agents reserved for patients with
persistent symptoms
• avoiding administration of anticoagulants if possible, as they may
increase the risk of progression to haemorrhagic pericardial
effusion, leading to tamponade.
64 COMPLICATIONS OF ACS
ACUTE CORONARY SYNDROMES
Sinus tachycardia
Sinus tachycardia is common after an ACS, and is often associated
with extensive anterior STEMI, sympathetic activation and an adverse
prognosis. In sinus tachycardia, each QRS complex is preceded by a
normal P wave, the QRS complexes are of normal morphology, and the
rate is normally less than 140 bpm. If sinus tachycardia is persistent and
excessive, it may cause extension of myocardial necrosis by increasing
oxygen consumption. If sinus tachycardia is persistent:
• adequate analgesia should be ensured
• heart failure should be looked for and treated
• beta-blockade should be considered if there are no
contraindications.
Atrial tachyarrhythmias
Peri-infarction AF occurs in 10–20 per cent of STEMI patients. Atrial
electrical instability or stretch leads to the development of multiple micro
re-entry circuits within the atrium leading to chaotic atrial electrical activity
which is intermittently conducted via the AV node to erratically depolarize
the ventricles. The rapid ventricular rate and loss of AV synchrony results in
a significant reduction in cardiac output and an increase in ischaemia.
Characteristic ECG features of AF are an irregular baseline due to
fibrillation waves (often best seen in V1) with completely irregular
ventricular activity. The incidence of AF is increased in patients with:
• large infarctions
• increased age
• pericarditis
• right ventricular infarction
• diabetes
• hypertension
• inotrope use.
The development of early (<24 hours) AF is usually associated with
inferior STEMI, whilst later (>24 hours) AF is usually associated with
anterior STEMI and heart failure. Mortality is more than doubled in ACS
patients who develop AF.
Idioventricular rhythm
Idioventricular rhythm is very common in STEMI patients, presenting
as a regular broad complex tachycardia with a stable QRS configuration
and a rate of less than 120 bpm. It is due to enhanced automaticity in a
ventricular focus, and is often associated with spontaneous or
therapeutic reperfusion. Idioventricular rhythm is rarely associated
with haemodynamic compromise and has no adverse effect on
mortality. Since the arrhythmia is usually well tolerated, no specific
treatment is required.
Ventricular tachycardia
Non-sustained VT (three or more consecutive ventricular beats at a rate
>120 bpm, lasting for less than 30 seconds) occurs in up to 7 per cent of
STEMI patients. When it occurs in patients with previous MI or has a
rapid rate, it may be a marker of an adverse prognosis. In most patients it is
asymptomatic, and antiarrhythmic therapy (with the exception of
beta-blockers) should be avoided. As for other non-sustained
peri-infarction arrhythmias, treatment should be directed towards
control of pain, ongoing cardiac ischaemia, heart failure and correction of
electrolyte disturbance. If episodes of non-sustained VT are frequent,
prolonged or symptomatic, and do not respond to the above measures or
beta-blockers and magnesium then amiodarone can be considered if the
corrected QT interval is normal.
Ventricular fibrillation
Ventricular fibrillation is characterized by rapid disorganized multiple
re-entrant wavelets in the ventricle, resulting in loss of co-ordinated
ventricular myocyte activity with loss of output and cardiac arrest.
Untreated, the arrhythmia is fatal, and is responsible for most
pre-hospital deaths in patients with STEMI. Most episodes occur early,
with 80 per cent occurring within 12 hours of symptom onset. If
defibrillation is performed rapidly, most episodes of VF can be
reversed, but success rate declines rapidly with time. When VF occurs
early in patients with good left ventricular function, long-term survival
is not compromised; when VF occurs late in patients with heart failure,
it is often a terminal event. The protocol for treatment of VF is detailed
in Chapter 2.
Sinus bradycardia
Sinus bradycardia (<60 bpm) is common early after ACS, particularly in
patients with inferior STEMI and vagal activation. If the heart rate is
persistently below 45 bpm or there are rate-related symptoms, a bolus of
atropine 0.6 mg IV (repeated as necessary) will increase the sinus rate. If
sinus bradycardia persists despite repeated boluses of atropine, temporary
pacing should be considered.
Right bundle branch block can occur with less extensive infarction, as
can involvement of only the anterior fascicle of the left bundle, leading
to left axis deviation. Patients who develop left bundle branch block
in combination with a long PR interval, or the combination of right
bundle branch block, left axis deviation and a long PR interval, have
suffered extensive damage to their conduction system; such patients
should be discussed with a senior colleague, as prophylactic temporary
pacing may be indicated to avert the need for pacemaker insertion in a
compromised patient if sudden complete heart block with a slow escape
rhythm develops.
II aVL V2 V5
III aVF V3 V6
II
Figure 1.8 Acute inferior myocardial infarc tion with first degree AV block.
ACUTE CORONARY SYNDROMES
II aVL
V2 V5
III aVF V6
V3
V1
II
V5
Figure 1.9 Acute inferior myocardial infarc tion with complete AV block.
ACUTE CORONARY SYNDROMES
Ventricular tachycardia
Ventricular tachycardia occurring after the first 48 hours, even if
asymptomatic or non-sustained, is an important risk factor for early
sudden death, particularly when it occurs in association with significant
left ventricular dysfunction (ejection fraction <35 per cent). Trials of class
I antiarrhythmic drugs have been uniformly disappointing, with no
beneficial effect, and some evidence of an adverse pro-arrhythmic effect.
In the late 1990s, five important trials (EMIAT, CAMIAT, MADIT,
MADIT-2 and MUST) reported, and provide some guidelines for an
evidence-based approach to management of these patients. Current
guidelines state that patients who have syncopal VT or VF without a
treatable cause (i.e. not related to their index presentation) should be
considered for an ICD for secondary prevention. Patients who are over
1 month from their index event qualify for an ICD on primary grounds if
they have an ejection fraction (EF) of <30 per cent and QRS duration of
≥120 ms or if the EF is <35 per cent with non-sustained VT on holter
Rehabilitation
After ACS, cardiac rehabilitation aims to restore patients to their optimal
physical, psychosocial, emotional and vocational status using a
multidisciplinary and multifactorial programme. Each patient needs a
programme tailored to meet individual needs. As a minimum, sessions of
medical assessment and review, education and counselling should be
offered to all patients. Patients who make a good recovery from their ACS
and have a satisfactory negative exercise test should enter a supervised
exercise programme. In patients with extensive infarction or a positive
exercise test, exercise rehabilitation should be deferred until investigation
and further treatment are completed. Patients who have important
co-morbidity may not be suitable for an exercise programme. Patients
who complete a multifactorial rehabilitation programme benefit from:
• reduced anxiety and depression
• increased chance of returning to active employment
• improved cardiovascular function and exercise capacity
The Driver and Vehicle Licensing Agency (DVLA) does not require
that patients inform them after an uncomplicated ACS, although
patients are not allowed to drive for up 4 weeks unless successfully treated
with primary PCI and the EF is ≥40 per cent, in which case driving
can commence after 1 week. After a complicated ACS the DVLA may
impose a large period of restriction, and patients should be advised to
contact the authority directly for advice. The requirements of insurance
companies are variable. Patients should seek advice from their own
insurer before recommencing driving after ACS. Patients who hold
a vocational licence to drive an HGV or public service vehicle must
contact the DVLA after an ACS. These licences will be automatically
withdrawn, but may be returned if the DVLA is satisfied with a medical
report and the results of a post-ACS exercise test (currently patients are
required to exercise for 9 minutes of the Bruce protocol, off medical
therapy, with no symptoms or ECG changes). Air travel should be
avoided for 6 weeks after an uncomplicated ACS or longer in patients
with complications. Sexual activity should be avoided early after ACS.
Patients who have a satisfactory exercise test result can be reassured that
the cardiovascular demands of intercourse are normally less than of the
exercise test, and be encouraged to return to normal activity. Patients
with significant post-MI exercise symptoms may need more specialized
psychosexual counselling.
KEY POINTS
• ACS are very common. Although modern treatment has improved
outcome in younger patients, ageing of the population results in a
continuing high prevalence of morbidity and mortality.
• Most deaths occur shortly after the onset of symptoms.
• Almost all episodes of ACS are caused by thrombotic occlusion or
partial occlusion of a coronary artery related to an unstable
atherosclerotic lesion.
• Plaque instability (reflecting enhanced inflammatory activity within
an atherosclerotic lesion) may be triggered by multiple factors.
• Initial categorization of an ACS is based on clinical evaluation
combined with analysis of the ECG.
• Cardiac troponins are highly sensitive and specific biomarkers, with
elevation confirming that irreversible myocardial necrosis has occurred.
KEY POINTS 79
ACUTE CORONARY SYNDROMES
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ACC/AHA 2007 Guidelines for the management of patients with unstable angina/
non-ST-elevation myocardial infarction – executive summary. J Am Coll Cardiol
2007; 50: 652–726.
ACE Inhibition Myocardial Infarction Collaborative Group. Indications for ACE
inhibitors in the early treatment of acute myocardial infarction. Systemic overview
of individual data from 100000 patients in randomised trials. Circulation 1998;
97: 2202–12.
Antman EM, Cohen M, Radley D, et al. Assessment of the treatment effect of
enoxaparin for unstable angina/non-Q-wave myocardial infarction. TIMI
11B-ESSENCE meta-analysis. Circulation 1999; 100: 1602–8.
Bavry AA, Bhatt DL, et al. Benefit of early invasive therapy in acute coronary
syndromes: a meta-analysis of contemporary randomized clinical trials. J Am Coll
Cardiol 2006; 48: 1319–25.
Boersma E, et al. Does time matter? A pooled analysis of randomized clinical trials
comparing primary percutaneous coronary intervention and in-hospital
fibrinolysis in acute myocardial infarction patients. Eur Heart J 2006; 27:
779–88.
Bonaca MP, et al. Antithrombotics in acute coronary syndromes. J Am Coll Cardiol
2009; 54: 969–84.
Borden WB, Faxon DP. Facilitated percutaneous coronary intervention. J Am Coll
Cardiol 2006; 48: 1120–8.
Brodie BR, Stuckey TD. Mechanical reperfusion therapy for acute myocardial
infarction: Stent PAMI, ADMIRAL, CADILLAC and beyond. Heart 2002; 87: 191–2.
Brown N, Young T, Gray D, Skene AM, Hampton JR. Inpatient deaths from acute
myocardial infarction, 1982–92: analysis of data in the Nottingham heart attack
register. BMJ 1997; 315: 159–64.
Budaj A, Yusuf S, et al. Benefit of clopidogrel in patients with acute coronary
syndromes without ST-segment elevation in various risk groups. Circulation 2002;
106: 1622–6.
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Hlatky MA. Evaluation of chest pain in the emergency department. N Engl J Med 1997;
337(23): 1687–8.
Implantable cardioverter defibrillators for arrhythmias. Review of Technology
Appraisal 11. National Institute for Health and Clinical Excellence January 2006.
Keeley EC, Boura JA, Grimes CL. Primary angioplasty versus intravenous
thrombolytic therapy for acute myocardial infarction: a quantitative review of 23
randomised trials. Lancet 2003; 361: 13–20.
Keeley EC, Boura JA, Grimes CL. Comparison of primary and facilitated percutaneous
coronary interventions for ST-elevation myocardial infarction: quantitative review
of randomised trials. Lancet 2006; 367: 579–88.
Laarman GJ, Dirksen MT. Early discharge after primary PCI. Heart 2010; 96: 584–7.
Mahon NG, O’Rorke C, Codd MB, McCann HA, McGarry K, Sugrue DD. Hospital
mortality of acute myocardial infarction in the thrombolytic era. Heart 1999; 81:
478–82.
Malmberg K, Ryden L, Efendic S, et al. Randomised trial of insulin-glucose infusion
followed by subcutaneous insulin treatment in diabetic patients with acute
myocardial infarction (DIGAMI study): effects on mortality at 1 year. J Am Coll
Cardiol 1995; 26: 57–65.
Mehta SR, et al. Early versus delayed invasive intervention in acute coronary
syndromes. N Engl J Med 2009; 360: 2165–75.
Montalescot G, Cayla G, Collet J, et al. Immediate vs delayed intervention for acute
coronary syndromes: a randomized clinical trial. JAMA 2009; 302(9): 947–54.
Morris F, Brady WJ. ABC of clinical electrocardiography. Acute myocardial infarction –
Part I. BMJ 2002; 324: 831–4.
Murphy JJ. Problems with temporary cardiac pacing. BMJ 2001; 323: 527.
Nattrass M. Managing diabetes after myocardial infarction. BMJ 1997; 314: 1497.
Noble MIM. Can negative results for protein markers of myocardial damage justify
discharge of acute chest pain patients after a few hours in hospital? Eur Heart J 1999;
20: 925–7.
Norris RM. The natural history of acute myocardial infarction. Heart 2000; 83:
726–30.
Stone GW. Angioplasty strategies in ST-segment elevation myocardial infarction: Part
I: primary percutaneous coronary intervention. Circulation 2008; 118: 538–51.
Stone GW. Angioplasty strategies in ST-segment elevation myocardial infarction: Part
II: intervention after fibrinolytic therapy, integrated treatment recommendations,
and future directions. Circulation 2008; 118: 552–66.
Stone GW, et al. Bivalirudin during primary PCI in acute myocardial infarction. N
Engl J Med 2008; 358: 2218–30.
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elevation myocardial infarction: the CRUSADE (Can Rapid risk stratification of
Unstable angina patients Suppress ADverse outcomes with Early implementation of
the ACC/AHA guidelines) bleeding score. Circulation 2009; 119: 1873–82.
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the Magnesium in Coronaries (MAGIC) trial. Lancet 2002; 360: 1189–96.
82 KEY REFERENCES
ACUTE CORONARY SYNDROMES
KEY REFERENCES 83
CHAPTER 2
RESUSCITATION
BACKGROUND
Epidemiology and physiology
Cardiovascular disease is the leading cause of death in the UK, with more
than 300 000 victims each year. Sudden cardiac death represents
approximately 25–30 per cent of all cardiovascular death, claiming an
estimated 70 000–90 000 lives each year.
Although the causes of cardiac arrest are numerous (Table 2.1), most
events in adults occur as a result of ischaemic heart disease. A number of
studies have shown a circadian pattern of cardiac arrest with the majority
of events occurring in the morning hours (6 a.m. to 12 noon) and a low
Reversible triggers
Electric shock
84 BACKGROUND
RESUSCITATION
Wolff–Parkinson–White syndrome
Long QT syndromes
Brugada syndrome
Idiopathic VT/VF
Causes of asystole
Heart block
Myocardial infarction
Hypoxia
Drugs (antiarrhythmics, beta-blockers, verapamil) especially with
pre-existing sinus node disease
‘4 Hs and 4 Ts’
Hypoxia
Hypovolaemia
Hypo/hyperkalaemia and other metabolic disorders
Hypothermia
Tension pneumothorax
Tamponade
Toxic/therapeutic disorders
Thromboembolic and mechanical obstruction
BACKGROUND 85
RESUSCITATION
incidence at night. Some data also suggest a late afternoon peak between
4 p.m. and 7 p.m. A seasonal variation in cardiac arrest is also recognized
with an increased number of cases occurring during the winter months.
Resuscitation after cardiopulmonary arrest is effective in only one in five
patients with about a third of long-term survivors having apparent motor
or cognitive deficits.
By far the most commonly encountered rhythm is ventricular fibrillation
(VF) or pulseless ventricular tachycardia (VT) occurring in more than
50 per cent of cases. With time, VF deteriorates from coarse VF to fine VF
and eventually to asystole. The prognosis is less favourable for non-VF/VT
rhythms. Independent predictors of mortality during follow-up include
increased age (>65 years), the presence of heart failure and cardiac arrest
not related to an acute coronary syndrome (ACS).
After a cardiac arrest, the only interventions that have been proven to
improve long-term survival are basic life support and early defibrillation
[immediate commencement of cardiopulmonary resuscitation (CPR)
confers a 2.7-fold increase in the rate of survival]. Therefore, the key to a
successful outcome is dependent on initiation of a rapid sequence of
events with minimal delay (Figure 2.1). Ideally, the goal of in-hospital
defibrillation should be a collapse–shock interval of less than 3 minutes.
Although data from randomized controlled trials are limited, techniques
for CPR have been standardized in recent years, and the guidelines in this
chapter are based on those published by the Resuscitation Council (UK)
and the European Resuscitation Council (ERC).
The major role of CPR is to provide some blood flow to both the
myocardium and central nervous system to allow for successful
defibrillation and resuscitation, and to preserve long-term organ function.
Although a number of theories have been proposed, the mechanism by
Intubation, venous
CPR started
Early recognition The only definitive access (central),
preferably within
and fast access to treatment for VF or ventilation,
4 minutes of collapse
emergency help pulseless VT is antiarrhythmic drugs,
to minimize brain
via 999 defibrillation intensive care
damage
support, etc.
86 BACKGROUND
RESUSCITATION
Airway
A quick inspection of the oropharynx should be performed, and any
obstructions such as food or loose dentures should be removed. Tight-
fitting dentures should be left as it helps support the soft palate. Manoeuvres
such as the head tilt, chin lift and jaw thrust can be used to ensure that the
tongue and soft tissues do not obstruct the airway. A variety of airway
adjuncts are now available on most resuscitation trolleys and include
facial masks, Guedel airways (an estimate of the size may be obtained by
selecting an airway with a length corresponding to the vertical distance
between the incisor tooth and the angle of the jaw) and nasopharyngeal
tubes (the diameter size in adults is usually 6–7 mm or the diameter of the
little finger). The tip of a nasopharyngeal tube should be visible in the
pharynx behind the tongue. For more skilled and experienced staff, the
insertion of a laryngeal mask or, ideally, an endotracheal tube can be
attempted.
Breathing
It is important to look, listen and feel for breath sounds and chest
movements. In any patient in whom breathing is inadequate or absent,
artificial ventilation must be commenced as soon as possible.
Oxygenation of the patient is the primary objective and the highest
concentration of oxygen available should be administered. This can be
achieved by using a mask with a reservoir bag, which can deliver inspired
oxygen concentrations of 85 per cent at flow rates of 10–15 L/min. Tidal
volumes of 400–600 mL are adequate to make the chest rise and are less
likely to cause gastric insufflation and aspiration. Between 1.5 and
2 seconds should be spent in the inspiratory phase.
Circulation
Until now, previous resuscitation guidelines have required the absence of
a carotid pulse to diagnose cardiac arrest and start CPR. However, times
in excess of 30 seconds are required to achieve an accuracy of 95 per cent.
As a consequence, current guidelines have de-emphasized the carotid
pulse as the sole criterion for starting CPR, and include the search for
signs of a circulation such as chest wall movement and breathing. If there
is no circulation, then chest compressions should be commenced. The heel
of one hand should be placed in the middle of the lower half of the
sternum, the fingers should be off the chest and the other hand is brought
down to rest on the back of the hand with the fingers interlocked. Vertical
downward pressure is applied to depress the sternum 4–5 cm and then the
pressure is released. A compression rate of 100 per minute using a
compression to ventilation ratio of 30:2 is now recommended for single
and multiple rescuers when ventilating non-invasively (bag and mask).
Once intubated, ventilation should continue at approximately
12 breaths/min with chest compression maintained uninterrupted for
Defibrillation
The only definitive treatment for VF or pulseless VT is defibrillation.
Although these rhythms are initially readily treatable, the chances of
successful defibrillation diminish rapidly with time and decline by
7–10 per cent per minute. In the case of a witnessed arrest especially when
a shockable rhythm has been identified, it is reasonable to attempt a
precordial thump. The thump delivers a small amount of kinetic energy,
which may be adequate to convert a fibrillating myocardium. All reported
cases of successful precordial thump occurred within 10 seconds of
VF/VT. If precordial thump is not successful or if VF/VT is more
prolonged then electrical cardioversion is required. Often, patients are not
monitored and the duration of VF/VT is unknown, in this case chest
compressions should be initiated first until the rhythm is determined.
Experimental studies have shown that interruption in chest compressions
is associated with a lower chance of survival. In addition, interruptions in
chest compression reduce the chance of successfully converting VF to
another rhythm. Therefore, unless the patient is monitored and
defibrillation can be achieved immediately after collapse, chest
compressions should be started and maintained until defibrillation is
possible. Following defibrillation chest compressions should be continued
as delay in checking for a pulse may further compromise the myocardium
if a perfusing rhythm has not been restored.
Shocks are initially started at between 150 J and 360 J with a biphasic device.
Biphasic shocks involve the polarity of the current being reversed part way
through the delivery of a shock, as a result the defibrillation threshold is
lowered and the shock energy required for successful defibrillation is
reduced. Monophasic defibrillators are being phased out as they are less
efficient at terminating VF/VT. If they are used they should be set to
360 J from the outset. The paddles should be applied firmly to the chest wall
with water-based gel pads between them and the skin. The pressure applied
should be approximately 8 kg of force and the correct positions are shown
in Figure 2.2a. The use of hands-free self-adhesive pads allows for safer
operation by allowing the operator to discharge the device without leaning
over the patient. They also allow for quick identification of rhythm
and therefore quicker defibrillation than using standard electrodes. If
defibrillation is unsuccessful in the anterolateral position, then further
attempts in the anteroposterior position (Figure 2.2b) and/or a different
cardiac pacing
defibrillator are worth trying. The positions of the positive and negative
paddles do not matter when defibrillating.
In patients with permanent pacemakers, defibrillation in the
anteroposterior position is preferable, even though modern pacemakers
are fitted with protection circuits. When defibrillation is attempted, ensure
that the electrodes are placed at least 12–15 cm from the pacemaker unit.
Pacing
Pacing can often be life saving, especially in situations where bradycardia
preceded the cardiac arrest or where bradycardia is associated with
haemodynamic intolerance following successful resuscitation. Pacing can
be attempted non-invasively or invasively, depending on the equipment
available and/or the experience of the operator.
Non-invasive (transcutaneous) pacing
Transcutaneous pacing can be easily applied, requires minimum training
and avoids the risks of central venous cannulation. Many defibrillators are
now equipped with external pacing facilities and it is important for those
involved in managing cardiac arrest to familiarize themselves with this
option. Pacing is usually carried out through self-adhesive gel pads which
can also be used for defibrillation if necessary. When used for pacing, the
device often additionally requires a 3-lead ECG (electrocardiogram) to be
attached. The ECG gain is adjusted to ensure sensing of any intrinsic QRS
complexes. The demand mode is selected and the pacing rate set to
60–90 bpm. The pacing current is set at the lowest setting and the
pacemaker turned on. The current is then slowly increased, observing the
patient, and monitored until electrical capture is seen. As the current
increases, the skeletal muscles contract and a pacing spike is seen on the
monitor. Electrical capture is recognized by wide QRS complex and a
broad T wave. A current range of 50–100 mA is usually sufficient (Figure
2.3). The presence of a palpable pulse ensures electrical capture results in
mechanical capture (myocardial contraction). Failure to achieve
mechanical capture in the presence of good electrical capture indicates
non-functional myocardium. Patients often require sedation with an IV
benzodiazepine (Diazemuls) as the procedure can be painful.
Transcutaneous pacing is only a temporary measure until transvenous
pacing can be instituted.
Transvenous pacing (box 2.1)
The resuscitation trolley should always be present and venous access
available. Bradycardia, asystole and ventricular tachyarrhythmias are
threshold has been ascertained, the output voltage should be set at three
times the threshold or 3 V, whichever is higher. This compensates for
subsequent threshold elevations due to inflammation and oedema at the
electrode–tissue interface. If in sinus rhythm, a back-up rate of 50/min is
set. If there is heart block or bradycardia, the rate is normally set at
70–80/min.
The wire is sutured firmly with a loop formed externally to minimize the
chance of inadvertent lead displacement. Finally, a chest x-ray is obtained
to exclude any complications.
Temporary venous pacemakers should be checked at least once daily for
pacing threshold, evidence of infections around venous access sites,
integrity of connections, and battery status of the external generator.
Underlying rhythm should also be assessed and recorded at these checks.
Pacing thresholds are checked by increasing the pacing rate to obtain
continuous pacing, then progressively decreasing the output voltage until
capture is lost. A sudden increase in the threshold usually indicates the
need for repositioning.
ARRHYTHMIA ALGORITHMS
Shockable rhythms (VF/pulseless VT)
This is recognized on the cardiac monitor by the presence of chaotic
fibrillation waves, due to wandering cardiac electrical activity along
continuously changing pathways (Figure 2.4a, Box 2.1) or a broad complex
tachycardia (Figure 2.4b). Defibrillation with a biphasic shock is the
definitive treatment for VF (Figure 2.5). The likelihood of survival
decreases 10 per cent for each minute of time after the onset of
uncorrected VF. Defibrillation should be performed as soon as the
diagnosis of VF is considered, with an initial shock of 150 J to 360 J,
followed by chest compressions. If pulseless electrical activity develops,
the non-shockable algorithm is followed. If VF persists, CPR is
maintained for 2 minutes, followed by assessment of rhythm and further
shocks if indicated (Figure 2.5). During CPR, an adequate airway and
oxygenation (intubating the patient only if trained or experienced) are
ensured, intravenous access obtained, and adrenaline 1 mg administered
every 3–5 minutes. Adrenaline works principally as a vasoconstrictor
(α-agonist effect) to increase the efficiency of basic life support, not as an
adjuvant to defibrillation. Adrenaline 2–3 mg (made up to a volume of
10 mL using sterile water) can be given via the tracheal tube. This should
ARRHYTHMIA ALGORITHMS 95
(a)
(b)
Figure 2.4 (a) Chaotic electrical activity of ventricular fibrillation. (b) Monomorphic VT: a rapid regular broad complex
tachycardia.
RESUSCITATION
Unresponsive?
Open airway
Look for signs of life
Unresponsive?
CPR 30:2
Until defibrillator /
monitor attached
Assess
rhythm
Shockable Non-shockable
(VF / pulseless VT) (PEA / Asystole)
During CPR:
• Correct reversible
causes (see below)
• Check electrode
1 Shock position and contact
150–360 J biphasic
or 360 J monophasic • Attempt / verify:
IV access and oxygen
• Give uninterrupted
compressions when
airway secure
• Give adrenaline every
Immediately resume 3–5 minutes Immediately resume
CPR 30:2 CPR 30:2
for 2 min • Consider: amiodarone, for 2 min
atropine, magnesium
Reversible causes
Hypoxaemia Tension pneumothorax
Hypovolaemia Tamponade (cardiac)
Hypo/hyperkalaemia/metabolic Toxins
ARRHYTHMIA ALGORITHMS 97
RESUSCITATION
then be followed by at least five ventilations to disperse the drug into the
peripheral bronchial tree and aid absorption.
Recent studies suggest that amiodarone may be superior to lidocaine in
cardioverting shock-resistant VF. In addtion there is evidence that
amiodarone increases the chance of survival to hospital for shock-
resistant VF. Therefore, it is now recommended that amiodarone be used
as the first-choice antifibrillatory agent. A dose of 300 mg IV should be
administered if VF/VT persists after three shocks. Lidocaine can be used
if amiodarone is not available though it should not be given if amiodarone
has already been used due to potential pro-arrhythmic effects of multiple
drugs. Drug doses and infusion regimens are discussed in Appendix A.
Non-shockable rhythms
These rhythms usually have a poor outcome unless a reversible cause can
be found and rapidly treated. The right side of the resuscitation algorithm
(Figure 2.5) should be followed.
Asystole
This is recognized by the total absence of any ventricular electrical activity
on the cardiac monitor. Causes are summarized in Box 2.1. The gain setting
on the monitor is set to 1 mV and the leads and electrical connections are
secured. Where possible, an additional lead should be viewed so as to avoid
missing a potentially reversible arrhythmia (fine ventricular fibrillation). If
in doubt, treatment is with defibrillation as in VF/pulseless VT. Basic life
support should be commenced for 2 minutes, during which time advanced
airway and ventilation techniques are performed, intravenous access gained
and adrenaline 1 mg given. Atropine 3 mg IV or 6 mg via the tracheal tube
(made up to a volume of at least 10 mL of sterile water) is administered. The
monitor should be closely inspected for the presence of atrial activity (P
waves), which may suggest complete heart block with ventricular asystole.
This may respond to external (transcutaneous) or transvenous pacing
depending on the skills and equipment available. If asystole persists, CPR is
continued with the administration of adrenaline 1 mg every 3–5 minutes.
The administration of higher-dose adrenaline as a single bolus is no longer
recommended.
98 ARRHYTHMIA ALGORITHMS
RESUSCITATION
• Persistent cardiac ischaemia that may have precipitated the cardiac arrest
should be looked for and treated. In particular VT/VF that is ischaemia
driven may respond to the use of an intra-aortic balloon pump.
• A portable chest x-ray should be arranged and any pneumothorax
treated.
• Left ventricular failure and hypotension should be treated, if
present. If hypotension persists consider a pulmonary artery
catheter to guide optimal fluid and inotropic therapy.
and potassium are normal. It is well documented that full recovery can
occur with resuscitation attempts of up to 9 hours.
NEW DEVELOPMENTS
Alternative techniques to standard manual CPR have been developed to
improve perfusion during CPR. Active compression–decompression CPR
(ACD-CPR) is performed with a portable device equipped with suction cup
to actively lift the anterior chest during decompression. This decreases
intrathoracic pressure, enhancing venous return for the next compression.
Randomized studies have shown equivocal benefit using this technique,
and therefore it is not recommended for routine use at present. However,
these devices may be advantageous in situations where delivering adequate
chest compressions is difficult, such as during transport. They have also
been used in several cases that allowed patients to undergo CT scanning or
even coronary angiography without interrupting CPR.
The major determinant of survival in patients with VF and pulseless VT is
the time taken for defibrillation. Consequently, there has been a natural
KEY POINTS
• CPR is a dynamic subject and therefore all health care staff involved in
patient care should be trained and kept up to date with advanced life
support protocols.
• The most commonly encountered rhythm during a cardiac arrest is VF
or pulseless VT.
• The prognosis is less favourable for non-shockable rhythms unless a
reversible cause is present.
• The only interventions that have been shown to improve long-term
survival are basic life support and early defibrillation.
• Careful post-resuscitation care is essential to maximize the chances of
a full recovery.
KEY REFERENCES
Adgey AAJ, Johnston PW. Approaches to modern management of cardiac arrest. Heart
1998; 80: 397–401.
Berg RA, Sanders AB, Kern KB, et al. Adverse hemodynamic effects of interrupting
chest compressions for rescue breathing during cardiopulmonary resuscitation for
ventricular fibrillation cardiac arrest. Circulation 2001; 104: 2465–70.
ARRHYTHMIAS
BACKGROUND
The management of cardiac arrhythmias complicating acute coronary
syndrome (ACS) is dealt with in Chapter 1. This chapter deals with the
management of arrhythmias that occur as a complication of other cardiac
and medical disorders. Optimal treatment of these arrhythmias depends
on two principles:
• inspecting the electrocardiogram (ECG) and reviewing the
clinical presentation to establish the diagnosis. This provides
information about arrhythmia mechanism and guides treatment
selection.
• assessing the effect of the arrhythmia. Patients with good cardiac
function will often tolerate arrhythmias without major
haemodynamic compromise. Patients with coexistent cardiac
impairment may be severely compromised by an arrhythmia.
Tachyarrhythmias associated with major haemodynamic
compromise usually require urgent cardioversion.
Bradyarrhythmias associated with major haemodynamic
compromise often require pacing. Patients with better tolerated
arrhythmias can be treated with drug therapy.
If there is any doubt about diagnosis or treatment, a senior colleague
should be consulted for advice.
The symptoms produced by the onset of an arrhythmia are highly
variable. In an individual with no cardiac disease, an arrhythmia may be
asymptomatic. A rapid tachyarrhythmia often produces palpitations. In
104 BACKGROUND
ARRHYTHMIAS
BACKGROUND 105
ARRHYTHMIAS
Some drugs have more than one class of action, and others such as
adenosine and digoxin cannot be classified using this simple system.
Because of the complex nature of these drugs and the potential to induce a
wide range of adverse effects, it is important to become familiar with the
use of a small number of front-line drugs. Polypharmacy should be
avoided; if the first-line therapy fails, a senior colleague should be
contacted for advice before using a second drug. The onset of an
arrhythmia is often associated with problems such as heart failure,
pulmonary infection or embolism, thyroid disturbance, hypoxia,
electrolyte imbalance or drug administration. It is important to look for
and treat correctable factors that may initiate or perpetuate an
arrhythmia.
ATRIAL FIBRILLATION
Background
AF is the most common cardiac arrhythmia (Figure 3.1). The incidence
and prevalence of AF increases with age: the prevalence is approximately
9 per cent in patients in their ninth decade.
The development of AF is associated with atrial electrical instability or
atrial distension induced by:
• hypertension
• congestive heart failure
• valvular heart disease
• ischaemic heart disease
• pulmonary infection or embolism.
Other less common causes of AF are cardiac trauma (including iatrogenic
trauma associated with cardiac surgery), metabolic abnormalities, exposure
to toxins (such as alcohol), pericardial disease or systemic infection. In some
patients, AF can arise in an otherwise entirely normal heart. This lone AF
may be due to small localized areas of electrical instability in the atrium
II
aVL V2 V5
III
aVF V3 V6
II
Figure 3.1 Atrial fibrillation is charac terized by the absence of P waves and an irregular ventricular rhy thm.
The ‘reverse tick’ deformit y of the ST segment, associated with digoxin, is best seen here in leads V5 and V6.
ARRHYTHMIAS
Treatment of post-operative AF
Post-operative AF is common, particularly among those undergoing
cardiac surgery: it is estimated to occur in up to one-third of patients
undergoing coronary artery bypass graft surgery, and is more frequent
when valve surgery is undertaken. Older patients, and those with previous
episodes of AF, are more likely to develop post-operative AF.
Post-operative AF has important implications for morbidity and
mortality, and can contribute to lengthening admissions. Episodes may
relate to electrolyte disturbances, hypoxia or infections, and treatment
should focus on these precipitants. Otherwise, episodes should be
managed as for other cases of acute-onset AF. Ideally, rhythm
management should be used for AF complicating cardiac surgery.
ATRIAL FLUTTER
In atrial flutter (Figure 3.2), the electrophysiological mechanism is
different from that of AF. In most patients with atrial flutter a re-entry
circuit in the right atrium depolarizes at a rate of 300/min in a circular
anticlockwise direction, down the lateral border of the right atrium,
through an area of slowed conduction near the tricuspid valve annulus
and back up the atrial septum. The normal AV node cannot conduct at
this rate, and commonly 2:1 AV block occurs. The electrocardiogram
shows a regular narrow complex tachycardia (in the absence of bundle
branch block) at a rate of 150 bpm. This rate may be slower in a patient
with impaired AV nodal function, or faster if sympathetic nervous system
activation is present. Atrial activity may be visible on the ECG, seen as
saw-tooth flutter waves with a rate of 300/min, best visualized in V1. The
flutter waves may only be visible during a temporary increase in the
degree of AV block induced by vagal manoeuvres or intravenous
adenosine. It is important and useful to have documentation of the
presence of flutter waves, and these procedures should be performed with
V1
aVL V5
II
V2
aVF V6
III
V3
II
Figure 3. 2 Atrial flut ter is charac terized by the undulating saw-tooth baseline (flut ter waves ) bet ween the QRS
complexes. The flut ter waves are best seen in the inferior leads and lead V1. In this case the flut ter rate is 250 bpm
and there is 4 :1 AV block.
ARRHYTHMIAS
printable ECG monitoring. Atrial flutter may degenerate into AF, or the
rhythm may alternate between flutter and fibrillation.
The onset of atrial flutter may be associated with symptoms of
haemodynamic compromise due to the rapid ventricular rate and loss of
effective atrial mechanical activity. As with AF, there is a risk of intra
atrial clot formation in atrial flutter, leading to systemic embolization, and
these patients require appropriate antithrombotic therapy as well as
arrhythmia treatment. Attempts to slow the ventricular rate using drugs
are often unsuccessful, and the aim of treatment should be to restore sinus
rhythm. Treatment depends on the clinical circumstances:
• If the arrhythmia is associated with significant haemodynamic
compromise (systolic BP <90 mmHg), or symptoms of angina,
impaired conscious level or heart failure, urgent DCC is the
treatment of choice.
• If the arrhythmia is well tolerated, an attempt can be made to
restore sinus rhythm with drug therapy, although atrial flutter is
often resistant to treatment with drugs. Class Ic antiarrhythmic
drugs may terminate atrial flutter, but can also cause a poorly
tolerated increase in ventricular rate (by slowing the flutter rate to
less than 300/min and therefore facilitating 1:1 atrioventricular
conduction at a rate greater than 150 bpm). Amiodarone has
beneficial effects on atrial electrical stability, and may terminate the
arrhythmia. In addition, amiodarone impairs atrioventricular
conduction, and this property will help to slow the ventricular rate.
We therefore recommend IV amiodarone for the treatment of atrial
flutter, using the regimen detailed in Appendix A. If amiodarone is
ineffective, the ventricular rate can be slowed with IV atenolol
5–10 mg. Anticoagulation and cardioversion can then be performed
following the same guidelines as for AF. Overdrive pacing is an
alternative treatment that is effective in restoring sinus rhythm in
70 per cent of patients. If facilities are available, a temporary pacing
wire is positioned against the lateral wall of the right atrium. A
burst of rapid atrial pacing at a rate of 400 bpm for several seconds
will usually restore sinus rhythm. Occasionally AF will be
precipitated, and this will often spontaneously revert to sinus
rhythm. If it persists, it is easier to treat than atrial flutter.
• If atrial flutter persists despite 24 hours of intravenous amiodarone,
or is resistant to overdrive pacing, DCC (often at very low energies)
has a high success rate in restoring sinus rhythm.
Treatment
Most episodes of AVNRT can be terminated by vagal manoeuvres or
intravenous drug therapy. Stimulating the vagus by a Valsalva manoeuvre,
carotid sinus massage (after excluding the presence of carotid bruits) or
activation of the diving reflex (by application of a cold stimulus to the
face) will temporarily slow AV nodal conduction and interrupt the
tachycardia circuit, terminating the arrhythmia in some patients. Some of
these techniques can be used by the patient to try to terminate an attack at
home, avoiding the need to attend hospital. Adenosine has a very short
half-life (as short as 1.5 seconds) and no significant haemodynamic side
effects. It works by transiently blocking conduction at the AV node and is
very effective at terminating AVNRT. Adenosine is given as a rapid bolus
at 3–6 mg into a proximal peripheral vein, often the cubital vein, and
immediately flushed through with 10 mL of saline. If this fails,
incremental doses of up to 18 mg can be administered. The patient should
be warned that transient facial flushing, dyspnoea and chest pain are
common, but last for less than 20 seconds.
II
aVL V2 V5
III
aVF V3 V6
II
Figure 3. 3 Wolf f– Parkinson – White syndrome. A shor t PR inter val and delta waves indicate the presence of an
accessor y pathway.
ARRHYTHMIAS
Atrial fibrillation
AF is less common in patients with accessory pathways, but can be life
threatening. The atria depolarize rapidly (350–600 impulses per minute)
during AF. In a normal individual, the AV node protects the ventricles
from this rapid erratic electrical activity. If AF occurs in a patient with an
accessory pathway that is capable of rapid anterograde conduction, rapid
atrial electrical activity can be conducted directly to the ventricles,
resulting in a very fast ventricular response that can lead to
haemodynamic collapse, or degenerate to VF. The ECG will show an
irregularly irregular rhythm with a variable QRS morphology (due to
most complexes being conducted via the pathway, leading to a broad QRS
morphology, with a minority conducted via the AV node leading to a
narrow QRS morphology).
Treatment
In patients with WPW sydrome who present with the common form of
narrow complex orthodromic tachycardia and who are not
haemodynamically compromised, initial drug therapy is appropriate. As a
general principle, drugs that predominantly block AV nodal conduction
should be avoided in patients known to have an accessory pathway. In
certain circumstances, AV nodal blocking drugs can cause tachycardia
acceleration (for instance, in patients with AF and a pathway capable of
rapid anterograde conduction). It is therefore preferable to use a drug that
acts predominantly to slow accessory pathway conduction. Intravenous
flecainide 2 mg/kg (maximum 150 mg) has a good safety profile in a
patient with an accessory pathway, and will terminate more than 80 per
cent of episodes. If flecainide fails, consult a senior colleague before
administering another drug. If the patient is haemodynamically
compromised with the tachycardia, DCC is the treatment of choice.
When AF occurs in a patient with a pathway capable of rapid anterograde
conduction, the ventricular rate can exceed 250 bpm. These rapid
ventricular rates are often associated with haemodynamic compromise or
heart failure, and urgent DC cardioversion is required. If the AF is slower
and well tolerated, a drug that slows accessory pathway conduction (such
as flecainide 2 mg/kg IV) can be used to slow the ventricular rate and
restore sinus rhythm.
Because of the inherent risk of sudden death, all patients with an
accessory pathway should be reviewed by an electrophysiologist to plan
an optimal investigation and treatment strategy. The most dangerous
pathways are those that are capable of rapid antegrade conduction from
atria to ventricles. Concealed pathways and pathways that show
intermittent pre-excitation or pre-excitation that disappears with
exercise are unlikely to be capable of rapid antegrade conduction, but
electrophysiological characterization of the conduction characteristics of
the pathway is more reliable than inspection of the surface ECG.
Ablation is highly successful and low risk, and should be considered for
all patients with an accessory pathway (the risks of long-term
antiarrhythmic drug therapy are probably greater than the procedure-
related risks of EPS and ablation).
ATRIAL TACHYCARDIA
Atrial tachycardia is relatively rare. Unifocal atrial tachycardia arises
from a single repetitively discharging area of micro re-entry or
enhanced automaticity. During the arrhythmia the ECG will usually
show a regular narrow complex tachycardia with a rate of 120–240 bpm
(Figure 3.4). Each QRS complex will be preceded by a morphologically
abnormal P wave, usually best seen in V1. An upright P wave in V1
indicates the tachycardia is due to a left atrial focus, a positive P wave in
AVL indicates a right atrial origin. The arrhythmia can arise in patients
with structural heart disease leading to atrial dilatation or dysfunction,
particularly in patients with cardiorespiratory co-morbidities, but
commonly no cause is found. Atrial tachycardia is often resistant to
drug therapy. Nodal blocking drugs will not terminate the arrhythmia,
but may slow the ventricular rate. Antiarrhythmic drugs that stabilize
atrial electrical activity (such as sotalol, flecainide and amiodarone) may
terminate the arrhythmia. If drug therapy fails, overdrive pacing or
cardioversion should be considered. Unifocal atrial tachycardias are
readily treated by ablation in suitable patients who have recurrent
symptoms.
Unifocal atrial tachycardia may arise as a complication of digoxin
toxicity. In this case, digoxin induces a variable degree of
atrioventricular block as well as triggering the discharge of an atrial
II
aVL V2 V5
III
aVF V3 V6
II
Figure 3. 4 Atrial tachycardia. Note the morphologically abnormal P waves seen best in the limb leads.
ARRHYTHMIAS
ectopic focus. The atrial rate is generally 150–200 bpm, and the degree of
atrioventricular block may fluctuate, producing an irregular ventricular
rhythm. When atrial tachycardia with variable block complicates
digoxin therapy:
• further digoxin therapy should be withheld until the arrhythmia
resolves
• beta-blockers should be given (if necessary) to slow the ventricular
rate
• potassium should be maintained above 4.0 mmol/L
• Digibind (see Chapter 8) should be considered.
DCC should be avoided, as it may induce intractable arrhythmias in a
patient with digoxin toxicity.
Multifocal atrial tachycardia most commonly arises as a complication
of respiratory disease in acutely ill elderly patients, and is characterized
by multiple atrial foci producing constant variation in the P-wave
morphology and a variable atrial rate (Figure 3.5). Therapy consists of
ensuring that the potassium level is adequate, treating the underlying
respiratory problem, and using AV nodal blocking drugs to control the
ventricular rate.
VENTRICULAR ARRHYTHMIAS
Background
A tachycardia with broad QRS complexes can be due to:
• VT
• supraventricular tachycardia in a patient with pre-existing or
rate-related bundle branch block
• supraventricular tachycardia in a patient with an accessory
II aVL V2 V5
III aVF V3 V6
II
Figure 3.5 Multifocal atrial tachycardia is charac terized by the following : a rate more than 10 0 / min ; organized,
discrete non - sinus P waves with at least three dif ferent forms in the same ECG lead ; isoelec tric baseline bet ween
P waves ; and irregular PP, PR and RR inter vals. In patients with hear t rates less than 10 0 / min, the term multifocal
atrial rhy thm is used.
ARRHYTHMIAS
Monomorphic VT
The commonest cause of monomorphic VT is ischaemic heart disease.
Monomorphic VT occurring early in the course of an ACS is usually due to
enhanced automaticity in an infarcting segment of myocardium.
Monomorphic VT occurring late after an ACS is usually associated with
re-entry in scar tissue. Less common causes include cardiomyopathy,
myocarditis, arrhythmogenic right ventricular dysplasia, valvular heart
disease, or scarring associated with cardiac surgery. Occasionally,
monomorphic VT can arise in an entirely normal heart. The occurrence of
monomorphic VT with a left bundle and right axis configuration in a patient
with a normal heart indicates that the arrhythmia is arising from the right
ventricular outflow tract. A relatively narrow QRS duration suggests that the
origin of the tachycardia lies close to the bundle of His (fascicular VT). Both
II V2 V5
aVL
III aVF V3 V6
II
Figure 3.6 Ventricular tachycardia. Note, the broad QRS duration (>14 0 ms ) , marked axis deviation (in this case
right axis deviation ) , RSr pat tern in lead V1, deep S in lead V5 and V6, AV dissociation ( best seen in lead II ) and
a fusion beat ( nineteenth QRS complex on the rhy thm strip ) .
ARRHYTHMIAS
Polymorphic VT
Polymorphic VT is characterized by repeated progressive changes in QRS
morphology and orientation, producing an appearance of twisting
Ventricular fibrillation
The commonest cause of VF is ischaemic heart disease, and it is
responsible for 90 per cent of deaths related to ACS. The emergency
management of VF is dealt with in Chapters 1 and 2. If VF occurs in the
absence of evidence of an ACS, careful investigation is required as
described for VT. All patients who survive an episode of VF not associated
with ACS should be considered for an ICD, as this is prognostically more
effective than drug therapy.
BRADYARRHYTHMIAS
Background
Bradyarrhythmias arising as a complication of ACS (particularly inferior
STEMI) are dealt with in Chapter 1. Bradyarrhythmias that are not related
to an ACS are most commonly due to idiopathic fibrosis of the conduction
system (which is more common in the elderly), although a wide range of
other cardiac conditions can occasionally be responsible. These
bradyarrhythmias may present with important symptoms that require
urgent treatment.
BRADYARRHYTHMIAS 127
Figure 3.7 Polymorphic V T. Note the frequent changes in QRS complex morphology.
ARRHYTHMIAS
Atrioventricular block
First degree heart block (prolongation of the PR interval to >200 msec)
signifies slow conduction of electrical activity from atria to ventricles
(Figure 3.8). First degree block does not cause symptoms, and can occur
in young people in association with high vagal tone. In older individuals
it may indicate the presence of underlying fibrosis in the conduction
system with a risk of progression to higher grade AV block. In second
degree block there is intermittent failure of conduction of atrial impulses
to the ventricles, manifest as a P wave not followed by a QRS complex. In
Mobitz type 1 (Wenckebach) second degree AV block, a progressive
increase in impaired conduction in the AV node occurs with each
successive sinus beat. This leads to a progressive prolongation in the PR
interval until an atrial impulse fails to be conducted, resulting in a
dropped beat. After the dropped beat, AV conduction recovers and the
sequence is repeated. Mobitz type 1 block can be a benign phenomenon
occurring in normal individuals with high vagal tone, particularly
during sleep. In the absence of high vagal tone in a younger individual,
Mobitz type 1 block is associated with a significant risk of progression to
high degree AV block with symptoms. In Mobitz type 2 second degree
AV block, impaired conduction in the bundle of His or bundle branches
leads to intermittent failure of conduction of atrial impulses to the
ventricles without preceding lengthening of the PR interval. These
patients often have associated bundle branch block and axis deviation
(bifascicular block), occasionally with associated PR interval
prolongation, reflecting extensive disease in the bundle of His. Patients
with Mobitz type 2 block have extensive conduction system disease and
are at increased risk of Stokes–Adams attacks, slow ventricular rates and
sudden death. Complete heart block occurs when there is total failure of
conduction of electrical activity from atria to ventricles (Figure 3.9).
Complete heart block can be due to disease at nodal or bundle of His
level. If the block is at nodal level, the escape rhythm that results will be
narrow complex, stable and usually fast enough to support an adequate
circulation. In patients with extensive disease in the bundle of His, the
subsidiary pacemaker will be low in the conduction system, producing a
slow, unreliable broad complex escape rhythm, with an increased risk of
major symptoms.
BRADYARRHYTHMIAS 129
II
II aVL V2 V5
III aVF V3 V6
II
Figure 3.9 Complete hear t block. There is complete AV dissociation with the P waves and QRS complexes
occurring without any relation to each other. Note the constantly changing PR inter vals.
ARRHYTHMIAS
132 BRADYARRHYTHMIAS
ARRHYTHMIAS
KEY POINTS
• Selecting the best treatment depends on the mechanism and effect
of an arrhythmia.
• QRS duration is not a totally reliable guide to the site of origin of an
arrhythmia.
• Antiarrhythmic drug therapy has many limitations (due to poor
efficacy and side effects).
• AF is common – treatment depends on the duration of the
arrhythmia and its haemodynamic effects. Atrial flutter is
relatively uncommon, and is treated in a similar fashion to AF.
• The commonest cause of recurrent narrow complex tachycardia is
AV nodal re-entry (which usually can be terminated by adenosine).
• Accessory pathways are not always associated with an abnormal
resting ECG. The commonest associated arrhythmia is a regular
narrow complex tachycardia with P waves visible between QRS
complexes; AF is rare but can be dangerous.
• A broad complex tachycardia can be due to VT, bundle branch
block or an accessory pathway. Most of these tachycardias are VT.
• Many bradyarrhythmias are well tolerated and emergency pacing
should be avoided if possible.
KEY REFERENCES
Blaauw Y, Crijns HJGM. Treatment of atrial fibrillation. Heart 2008; 94: 1342–9.
Brugada P, Brugada J, Mont L, Smeets J, Andries EW. A new approach to the
differential diagnosis of a regular tachycardia with a wide QRS complex.
Circulation 1991; 83: 1649–59.
Camm AJ, Garratt CJ. Adenosine and supraventricular tachycardia. N Engl J Med 1991;
325: 1621–9.
DaCosta D, Brady WJ, Edhouse J. ABC of clinical electrocardiography. Bradycardias
and atrioventricular conduction block. BMJ 2002; 324: 535–8.
Dancy M, Ward D. Diagnosis of ventricular tachycardia: a clinical algorithm. BMJ
1989; 291: 1036–8.
Edhouse J, Morris F. ABC of clinical electrocardiography. Broad complex
tachycardia – Part I. BMJ 2002; 324: 719–22.
Edhouse J, Morris F. ABC of clinical electrocardiography. Broad complex tachycardia –
Part II. BMJ 2002; 324: 776–9.
Esberger D, Jones S, Morris F. ABC of clinical electrocardiography: junctional
tachycardias. BMJ 2002; 324: 662–5.
Fox DJ, Tischenko A, Krahn AD, et al. Supraventricular tachycardia: diagnosis and
management. Mayo Clin Proc 2008; 83: 1400–11.
Ganz LI, Friedman PL. Supraventricular tachycardia. N Engl J Med 1995; 332: 162–73.
Goodacre S, Irons R. ABC of clinical electrocardiography: atrial arrhythmias. BMJ
2002; 324: 594–7.
Julian DG. The amiodarone trials. Eur Heart J 1997; 18: 1361–3.
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Cardiol 1997; 29: 1190–8.
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supraventricular tachycardias. Eur Heart J 1997; 18(Suppl C): C27–C32.
Murphy JJ. Problems with temporary cardiac pacing. BMJ 2001; 323: 527.
Obel OA, Camm AJ. Supraventricular tachycardia: ECG and anatomy. Eur Heart J
1997; 18(Suppl C): C2–C11.
Peters NS, Schilling RJ, Kanagaratnam P, Markides V. Atrial fibrillation: strategies to
control, combat, and cure. Lancet 2002; 359: 593–603.
Pye M, Camm AJ. Supraventricular tachycardia: a comprehensive review of the
diagnosis and management of supraventricular tachycardia. Hosp Update 1996; 22:
226–37.
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Roden DM. Risks and benefits of antiarrhythmic therapy. N Engl J Med 1994; 331:
785–91.
Van Gelder IC, Hagens VE, Bosker HA, et al. A comparison of rate control and rhythm
control in patients with recurrent persistent atrial fibrillation. N Engl J Med 2002;
347: 1834–40.
Wellens HJJ. The value of the ECG in the diagnosis of supraventricular tachycardias.
Eur Heart J 1996; 17(Suppl C): 10–20.
Wellens HJJ. Ventricular tachycardia: diagnosis of broad QRS complex tachycardia.
Heart 2001; 86: 579–85.
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control in patients with atrial fibrillation. N Engl J Med 2002; 347: 1825–33.
HYPERTENSIVE EMERGENCIES
BACKGROUND
Epidemiology
In a small proportion of patients with hypertension, an accelerated phase of
the disease may develop into malignant hypertension. This presents
clinically as a hypertensive emergency with marked elevation of blood
pressure accompanied by end-organ damage. The frequency of
hypertensive emergencies is declining due to widespread early treatment of
less severe hypertension, with contemporary incidence rates of around
1 per cent in hypertensive subjects. A hypertensive crisis is commonest in
the young black male population.
This accelerated phase may present us a medical emergency in which
the blood pressure should be reduced immediately to avoid irreversible
target organ damage. The urgent need for blood pressure control is
most acute where life-threatening complications such as an aortic
dissection or encephalopathy occur. Any hypertensive condition can
develop into a crisis, although it is commoner in secondary forms of the
disease such as with phaeochromocytoma and in renovascular
hypertension. Prior to the introduction of effective antihypertensive
therapy, less than 25 per cent of patients with malignant hypertension
survived 1 year, with a 1 per cent 5-year survival. In the current era with
renal dialysis support, 1- and 5-year survival is 90 per cent and 80 per
cent, respectively. In severe hypertension, early death is usually due to
stroke or acute renal failure. In the longer term, coronary artery disease
becomes the commonest cause of death.
Hypertensive emergencies are most common in patients with
long-standing, poorly controlled chronic hypertension, often following an
BACKGROUND 135
HYPERTENSIVE EMERGENCIES
Pathophysiology
Any cause of hypertension can lead to a hypertensive emergency
(Table 4.1). The likelihood of severe adverse effects is highest in
patients who develop a rapid increase in systemic blood pressure: the
vascular adaptation to chronic hypertension reduces the likelihood
of end-organ damage, with the corollary that in the absence of
pre-existing hypertension, a hypertensive emergency can occur at a lower
pressure. A hypertensive emergency occurs when sustained diastolic
blood pressure is above 130 mmHg leading to a risk of end-organ
damage.
The exact initiating step in a hypertensive crisis is not well understood.
There is a cascade of physiological decompensation initiated by a
critical degree of hypertension, which occurs both systemically and
locally in vascular beds. An increase in vasoreactivity occurs. The
renin-angiotensin-aldosterone system is crucial in the development of
this hyper-reactivity. Angiotensin II is a potent vasoconstrictor and
also has direct cytotoxic effects on endothelium through activation of
gene expression or pro-inflammatory cytokines such as interleukin-6
(IL-6) and the transcription factor, NF-κb. Inhibition of tissue
angiotensin converting enzyme (ACE) can prevent malignant
hypertension in transgenic mice. Systemically, there is activation of the
sympathetic nervous system, the renin-angiotensin-aldosterone system
and increased release of antidiuretic hormone. This leads to systemic
vasoconstriction and a rise in vascular resistance, as well as an increase
in circulating blood volume. Paradoxically, the baroreceptor response
to this is overwhelmed with a further increase in circulating
vasopressor hormones. Locally, free radical production and endothelin
release is associated with further endothelial dysfunction, growth
factor release and vascular smooth muscle cell proliferation
diminishing local vascular autoregulation. Progressive endothelial
dysfunction through pro-inflammatory cytokines with up-regulation
of endothelial adhesion molecules (such as E- and P-selectin) promotes
136 BACKGROUND
HYPERTENSIVE EMERGENCIES
Essential hypertension
• acute glomerulonephritis
• renal vasculitis
• haemolytic uraemic syndrome
• thrombotic thrombocytopenic purpura
Renovascular disease
Pregnancy
• eclampsia
Endocrine disease
• phaeochromocytoma
• hypheradrenalism (Cushing’s syndrome)
• renin-secreting tumours
Drugs
• cocaine abuse
• sympathomimetic abuse
• erythropoietin in haemodialysis patients
• cyclosporin A
• interactions with monoamine oxidase inhibitors (tyramine ingestion)
Autonomic hyper-reactivity
• Guillain–Barré syndrome
• acute intermittent porphyria
Neurological disease
• head injury
• cerebrovascular accident
• brain tumours
BACKGROUND 137
HYPERTENSIVE EMERGENCIES
Clinical features
Malignant hypertension is associated with a persistent diastolic pressure
of greater that 130 mmHg. Other diagnostic clinical features of malignant
hypertensive crisis include:
• hypertensive retinopathy
– haemorrhage, exudates and papilloedema (grades 3 and 4
hypertensive retinopathy)
• hypertensive encephalopathy
– headache, confusion, altered consciousness, leading to seizure
activity and coma
138 BACKGROUND
HYPERTENSIVE EMERGENCIES
CLINICAL EVALUATION
History
An accurate history of the duration and severity of any pre-existing
hypertension must be established. It is equally important to establish the
presence of end-organ damage, such as hypertensive renal disease and
cerebrovascular disease. Symptoms of target organ injury may be present:
• anterior chest pain: myocardial ischaemia, acute aortic dissection;
• posterior chest pain: aortic dissection;
• dyspnoea: acute pulmonary oedema, acute heart failure;
• altered consciousness/seizures: encephalopathy.
It is important to take a complete drug history to establish both any
pre-existing therapy and the possibility of recent drug withdrawal or
non-compliance. The recreational abuse of cocaine or other
sympathomimetic drugs should be considered.
Physical examination
• Blood pressure measurement – in both arms, erect and supine
• Cardiovascular examination – presence of heart failure (raised
jugular venous pressure (JVP), third heart sound, pulmonary
crepitations)
• Neurological examination – conscious level, visual fields, focal
pyramidal signs
• Fundoscopy – new haemorrhages, exudates and papilloedema
indicate a hypertensive emergency.
Investigations
Initial investigations:
• Biochemistry – urea, creatinine and electrolytes
• Haemotology – full blood count, including a blood film for
evidence of haemolysis
• 12-lead ECG – to exclude/confirm ischaemia, to indicate left
ventricular hypertrophy
• Chest x-ray – look for evidence of heart failure or dissection
• Urinalysis – red blood cells, protein.
Additional investigations should include:
• echocardiography
• renal ultrasound scan
• computed tomography of thorax and abdomen, and
• magnetic resonance renovascular and neuro-imaging (see below).
MANAGEMENT
The treatment of a hypertensive crisis is based on consensus rather than
on randomized controlled trials. The first principle of care is that a
hypertensive emergency patient is managed in a high-dependency
environment with withdrawal of any potential treatments that may be
exacerbating the situation. This allows for accurate and continuous
blood pressure monitoring with an arterial line. Treatment should be
initiated by the intravenous route and titrated against the
antihypertensive response. Combination therapy is preferred to achieve
an additive effect and may be tailored towards any compromise in a
particular end organ. In aortic dissection, a combination of intravenous
beta-blockade (labetalol, which is a mixed alpha- and beta-blocker)
given first followed by sodium nitroprusside is the preferred therapy. In
the presence of myocardial ischaemia, intravenous glyceryl trinitrate
140 MANAGEMENT
HYPERTENSIVE EMERGENCIES
Labetalol
This mixed alpha- and beta-adrenergic blocker is the other mainstay
of therapy in a hypertensive emergency. Although its beta-blocking
effect is weaker than conventional beta-blockers, it can be given in bolus
form at a dose of 20–80 mg in addition to an intravenous infusion of
2 mg/min.
ACE inhibition
These drugs are effective in lowering blood pressure within 15 minutes of
an intravenous bolus such as enalaprilat (1.25–5 mg), with an effect lasting
at least 4 hours. However, precipitous falls may occur in patients with
hypovolaemia or significant renovascular disease. In accelerated
hypertension, a pressure-induced natriuresis may occur, leading to the
confounding physiological situation of hypovolaemia in the setting of
hypertension.
Fenoldopam
This drug is approved for use in hypertensive emergencies. It is a
peripheral dopamine-1 receptor agonist, which peripherally vasodilates
with an additional potent vasodilating effect on renal arteries. It has a
quick onset (5 minutes) and is used at a dose of 0.1–0.6 μg/kg/min. In one
study compared with sodium nitroprusside, fenoldopam improved renal
dysfunction in severely hypertensive patients with renal impairment.
Glyceryl trinitrate
Intravenous GTN (5–100 μg/min) is of particular use where significant
coronary artery disease coexists with a hypertensive emergency. Although
not a potent therapy for hypertension itself, the restoration of the
imbalance between myocardial demand and supply through reduction in
intramyocardial wall tension, preload reduction and improved collateral
blood supply is of benefit, particularly when used in conjunction with
beta-blockade. Like sodium nitroprusside, afterload reduction is of
benefit in the presence of LVF.
A recent systematic review of 15 randomized controlled trials was unable to
find evidence that antihypertensive drugs reduced mortality or morbidity
in patients with hypertensive emergencies (there were no randomized
studies specifically addressing this issue). Further, there was insufficient
evidence to determine which drug or drug class was most effective in
reducing mortality and morbidity. Whilst there were some small differences
in degree of blood pressure lowering among classes, the clinical significance
was unclear. The review demonstrated evidence of blood pressure lowering
efficacy for nitrates, ACE inhibitors, diuretics, alpha-adrenergic
antagonists, calcium channel blockers and dopamine agonists. Nitrates
(including nitroprusside) were the most studied group, making this class of
drug a reasonable choice of therapy in hypertensive emergencies.
Phaeochromocytoma
Phaeochromocytoma arise from sympathetic ganglia derived from the
primitive neural crest with 90 per cent arising from the adrenal medulla,
10 per cent bilateral and 10 per cent malignant rather than benign. They
account for up to 0.2 per cent of hypertensive patients. These ‘tumours’,
which are essentially extreme nodular hyperplasia, may occur as part of
the familial multiple endocrine neoplasia (MEN-2) syndrome. They create
extreme fluctuations in systemic blood pressure with associated
symptoms, although the hypertension becomes persistent in half of
patients. With adrenaline as the predominant catecholamine secreted
(mainly from adrenal medullary tumours), symptoms of an increased
cardiac output with systolic hypertension, sinus tachycardia, sweating,
flushing and apprehension occur. Noradrenaline is usually the
predominant hormone (adrenal and most extra-adrenal tumours), and
there is an increased peripheral vasoconstriction with diastolic as well as
systolic hypertension with less tachycardia or palpitations. In 45 per cent,
the hypertension is paroxysmal, and often occurs in response to
anaesthesia, parturition or pharmacological stress from histamine,
caffeine, beta-blockade or glucocorticoids. Attacks have a variable
frequency, and the majority (80 per cent) last for less than an hour. Less
commonly, patients with familial tumours are normotensive.
A direct relationship between high levels of catecholamines and
myocardial injury exists with the potential for myocarditis and acute LVF.
Diagnosis is made simply through a 24-hour urine collection for urinary
metanephrines. To improve the specificity of this test, patients should
have monoamine oxidase inhibitors and mixed alpha- and beta-blockers
(labetalol, carvedilol) discontinued beforehand. The tumour may be
localized by CT scanning with the occasional need for radioisotope
localization with MIBG. Where possible, phaeochromocytoma should be
resected with careful pre- and peri-operative alpha-adrenoceptor
blockade (with intravenous phentolamine at 5–10 μg/min) to diminish
vasoconstriction and to allow intravascular volume expansion.
KEY POINTS
• In about 1 per cent of patients with hypertension, an accelerated phase
may occur as part of the progression of the disease and is commonest
in the young black male population. It is commoner in secondary
forms of the disease such as with phaeochromocytoma and in
renovascular hypertension.
• Prior to established antihypertensive therapy, less than 25 per cent of
patients with malignant hypertension survived 1 year, with a 1 per cent
5-year survival. In the current era with renal dialysis support, 1- and
5-year survival is 90 per cent and 80 per cent, respectively. Early death
tends to occur due to stroke or acute renal failure.
• Malignant hypertension is the clinical syndrome where a sudden
increased systemic blood pressure is likely to result in acute end-organ
injury. The likelihood of this may vary according to pre-existing levels
and to the rate of the acute rise, although it is accepted that a persistent
diastolic blood pressure of greater than 130 mmHg is likely to result in
vascular injury.
• The clinical features of a hypertensive crisis comprise a diastolic blood
pressure greater than 130–140 mmHg, hypertensive retinopathy,
hypertensive encephalopathy, acute renal failure and microangiopathic
haemolytic anaemia (Table 4.2).
• Hypertensive encephalopathy is an acute medical emergency
characterized by headache, irritability and an altered conscious level.
Other potential complications of a hypertensive crisis are an
intracerebral or subarachnoid haemorrhage and a thrombotic
infarction in an individual with predisposing atherosclerotic
cerebrovascular disease.
• Acute LVF is a common cardiovascular manifestation of a hypertensive
crisis. Acute aortic dissection and acute coronary syndrome may also
occur.
KEY REFERENCES
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profile, and previous case of 100 cases. Am J Public Health 1988; 78: 636–42.
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BACKGROUND
Epidemiology
Dissection of the thoracic aorta is one of the most dramatic acute medical
emergencies with serious adverse consequences if not diagnosed and treated
promptly and appropriately. It has been estimated that there are around
3 cases per 100 000 population per year, most commonly occurring in men
aged between 50 and 70 years, and more often in the black population. On
average, left untreated, 50 per cent of patients die within 48 hours (estimated
at a 1–2 per cent mortality per hour from presentation) with 70 per cent
dead at 1 week and 90 per cent dead at 3 months. Frequency peaks in the
morning, possibly related to the circadian variation in blood pressure.
The International Registry of Acute Aortic Dissection (IRAD),
established in 1996, has reported trends in the management and outcome
of the condition.
BACKGROUND 149
ACUTE AORTIC SYNDROMES
Pathophysiology
Contemporary information relating to clinical factors underlying
aortic dissection in a large group of subjects is available from the IRAD
database. Acute aortic dissection is strongly associated with systemic
hypertension (due to a sustained high intraluminal pressure) and with
advancing age, but less so with atherosclerosis per se. Cystic medial
degeneration in the aortic wall is an intrinsic feature of several
connective tissue disorders which are associated with dissection such
as Marfan’s syndrome, Ehlers–Danlos syndrome and, occasionally,
150 BACKGROUND
ACUTE AORTIC SYNDROMES
BACKGROUND 151
ACUTE AORTIC SYNDROMES
by oversewing the aortic edges, thus removing the driving force behind
the propagation of the false channel. An interposition graft may be
required in the ascending aorta to restore integrity to this section of the
dissection. If the aortic valve is competent and unaffected directly by the
dissection, it may be resuspended in the graft at the aortic valve ring or
it may require replacement with a prosthesis if disrupted.
Simultaneously, systemic blood pressure and left ventricular
contractility should be significantly reduced to remove the direct
pulsatile stress on the aortic wall.
Immediate therapy
All patients in whom a thoracic aortic dissection is suspected should be
monitored and treated in a high-dependency environment for
haemodynamic and cardiac rhythm monitoring and for central venous
access. Patients should be cross-matched for the eventuality of either
dissection or rupture and early surgery. The three initial goals of
therapy are:
lowering.
Definitive treatment
The accepted paradigm in dissection management is that surgical
treatment is superior to medical treatment in the management of type A
dissection, whereas medical therapy is superior in uncomplicated type B
dissection (see Box 5.1). This comes about through surgery preventing
progression of dissection and potentially fatal consequences. Patients with
distal dissection tend to be older with atherosclerotic vascular disease,
often with a reduced cardiac reserve, and tend to tolerate surgery less well,
favouring medical therapy. The attrition rate in patients with proximal
dissection treated surgically occurs through complications having already
occurred or through the friability of the aortic wall at surgery.
In practice, the decision to intervene in chronic dissection is based upon
evidence of progressive pathological change over time. In patients with
symptoms or signs of peripheral ischaemia, the indication for
intervention is clear. In asymptomatic individuals, intervention is
recommended for progressive aortic dilatation (>5 cm maximum
diameter), and when there is evidence of a persistent false lumen in
communication with the true lumen.
Surgery
Current practice dictates that the proximal dissection should be repaired
early to prevent extension and rupture, and to operate on distal
dissections extending proximally using cardiopulmonary bypass. Of
patients with type A dissections, the IRAD database revealed lower
30-day mortality in surgically treated patients than those treated
medically (see Clinical outcomes in aortic dissection).
The goal of surgery is to prevent progression of the dissection and to
relieve obstruction in peripheral branches: thus, the intimal tear is
excised and the origin of the false lumen excluded by proximal and
distal suturing of the edges of the aorta. A prosthetic Dacron graft may
be needed to approximate the ends of the aorta. Surgery requires a
period of deep hypothermic circulatory arrest. Where the aortic valve is
involved, the false channel is decompressed by the surgery described
above, but may still require replacement or repair. Where the aorta is
very friable, the whole ascending aorta and valve may be replaced using
a composite graft containing a prosthesis with resuturing of the
coronary arteries to the conduit. Preservation of the native aortic valve,
which avoids the complications associated with a prosthetic valve,
usually requires approximation of the two layers of dissected aortic wall
and resuspension of the commissures with pledgeted sutures. However,
prosthetic valve replacement is frequently advisable in the setting of
pre-existent valve disease or in Marfan’s syndrome to reduce the
likelihood of re-operation.
external rupture rate with IMH, which tends to run a more malignant
course than typical descending aortic dissection.
These high mortality rates have been confirmed in several other large
series. Moreover, for acute disease complicated by end-organ ischaemia,
surgical mortality exceeds 50 per cent, with a substantial risk (7–36 per
cent) of paraplegia (or paresis), dependent upon the extent of aortic
dissection and the duration of cross-clamping, amongst those who
survive. Chronic aortic dissection (presentation up to 2 weeks after the
onset of symptoms) has a higher in-hospital survival of around 90 per cent
whether they are treated medically or surgically, largely through
self-selection due to the lack of acute complications in the initial phase of
dissection.
KEY POINTS
• Acute aortic dissection in a high-mortality condition with a 48-hour
mortality of 50 per cent, with 70 per cent dead at 1 week and 90 per cent
dead at 3 months, if left untreated. With treatment, overall hospital
mortality is 27 per cent.
• Acute thoracic dissection is strongly associated with systemic
hypertension and with advancing age. Several connective tissue
disorders (of which Marfan’s syndrome is the commonest) are
associated with dissection due to cystic medial degeneration in the
aortic wall.
• There are pathological variations accounting for one-eighth of cases of
‘aortic dissection’. In penetrating atherosclerotic ulcers (PAU), no
intimal flap is demonstrable with a crater visible extending into the
aortic wall associated with haematoma within the media of the aortic
wall. IMH occurs where significant thickening or enhancement of the
aortic wall is seen in the absence of a flap or dissection.
• Aortic dissection can mimic different conditions in the evolution of
the symptoms and signs such as severe chest pain, vasovagal
symptoms and hypotension, severe hypertension, acute aortic
regurgitation, myocardial infarction, stroke, pleural effusion and
visceral infarction.
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BACKGROUND
Epidemiology
Venous thromboembolism (encompassing deep venous thrombosis
[DVT] and pulmonary embolism [PE]) is a great constant in acute
medicine with no major difference in its incidence or mortality in the past
20 years. The age- and sex-adjusted incidence rate is 117 cases per 100 000
person-years. The incidence rises particularly in those aged >60 years,
irrespective of gender, largely driven by PE.
Pulmonary embolism is a life-threatening condition associated with a
high mortality rate. There is a direct relationship between age and
mortality. In almost a quarter of patients with PE, the initial clinical
manifestation is sudden death. Mortality is at least 10 per cent in the first
few hours of presentation and exceeds 15 per cent at 3 months post
diagnosis. Unfortunately, PE is undiagnosed in many cases, and the
majority of patients with fatal PE do not have specific symptoms to aid
diagnosis. Indeed, PE occurs more frequently among patients with
alternative causes of dyspnoea, such as those with heart failure and
chronic obstructive airways disease. For example, the relative risk of PE in
heart failure patients is twice that of those without heart failure, and
increases as left ventricular systolic function declines. Furthermore, PE
patients with heart failure have higher overall mortality and readmission
rates than those without heart failure.
BACKGROUND 167
ACUTE PULMONARY EMBOLISM
168 BACKGROUND
ACUTE PULMONARY EMBOLISM
General surgery Age <40 years Age 40–60 years Age >60 years
Surgery <30 min Surgery 30–60 min Surgery >60 min
No risk factors + risk factors
Incidence (%)
Distal DVT 2% 10–40% 40–80%
Proximal DVT 0.4% 6–8% 10–15%
Symptomatic PE 0.2% 1–2% 5–10%
Fatal PE 0.002% 0.1–0.8% 1–5%
In otherwise fit patients, once more than 25 per cent of the pulmonary
vascular bed is occlusive, there is an increased afterload or pressure load
on the right ventricle leading to an increase in right ventricular systolic
pressure. With increasing pressure load, the right ventricle will dilate
(against a restrictive pericardium) with the development of functional
tricuspid regurgitation, an increased right atrial pressure and, ultimately,
cardiogenic shock. The paradoxical movement of a pressure-loaded right
ventricle leads to left ventricular diastolic dysfunction in addition to a
reduction in left ventricular pre-load through a reduced transpulmonary
blood flow. Echocardiography identifies these features with an increase in
end-systolic and end-diastolic diameters and septal flattening in both
phases of the cardiac cycle. Left ventricular end-diastolic diameter is also
reduced with significant embolism.
The mechanism of hypoxaemia in massive PE is multifactorial. It occurs
through significant ventilation-perfusion mismatch, and may also occur
due to intrapulmonary A-V shunting through areas poorly ventilated with
residual blood flow. Shunting may also occur at an atrial level where acute
right heart pressures may reverse the shunt through a patent foramen
ovale. Where the cardiac output is low, insufficient gas-exchange may
occur in the residual areas of perfusion leading to systemic further
desaturation. Hypercapnia is rare in massive PE due to tachypnoea.
Symptoms of massive PE are severe dyspnoea (not orthopnoea), syncope
and low cardiac output. Angina may occur through a combination of
hypoxaemia, tachycardia and hypotension. Central cyanosis and acute
right heart strain ensue. It may be difficult to hear a right ventricular
gallop rhythm or widely split second heart sound in the presence of
significant respiratory distress.
A differential diagnosis of acute PE includes:
• acute coronary syndrome
• acute proximal aortic dissection
• acute pulmonary oedema
• acute pneumonia
• pleurisy
• acute bronchospasm
• acute exacerbations of chronic airflow limitation
• bronchogenic carcinoma
• pneumothorax
• chest wall syndrome
• fractured rib
Investigations
12-lead electrocardiography. Although 87% of patients have an
abnormal ECG, these are largely non-specific and include anterior
T-wave changes, ST segment abnormalities and left or right axis deviation.
In the Urokinase Pulmonary Embolism Trial (UPET), 32 per cent
of patients with massive PE and 26 per cent of those with massive/
submassive PE had ECG signs of acute cor pulmonale such as the S1Q3T3
pattern, right bundle branch block (RBBB), P pulmonale or right axis
deviation. The ECG may be completely normal in younger, previously fit
patients.
Clinical Probability
V/Q scan (Probability) Highly likely Uncertain Unlikely
(80 –100%) (20 –79%) (0 –19%)
Near normal/normal 0 6% 2%
Haemoptysis 1
CT immediately available*
No Yes
Echocardiography
RV overload
CT available and
No Yes CT
patient stabilized
Heparin anticoagulation
The heparin–antithrombin III complex inactivates thrombin and, to a
lesser extent, activated factors IX and X. The efficacy of heparin in PE is
through prevention of further fibrin generation from thrombin
D-dimer
negative positive
No treatment Multidetector CT Multidetector CT
Low-molecular-weight heparin
LMWH has become the treatment of choice for venous thromboembolism.
It is produced by depolymerization of UFH leading to small molecules
capable of inhibiting activated factor X in preference to thrombin
(activated factor II). Given a longer half-life and less ancillary binding, the
anticoagulant dose is predictable after subcutaneous dosing. As the aPTT
measures antithrombin activity, LMWH, if necessary, should be
monitored by its anti-Xa activity. Its administration subcutaneously
requires less supervision and may be given once or twice daily (depending
on exact LMWH type) to give as effective a therapy as UFH in the
treatment of proximal DVT and acute PE. Its role in massive pulmonary
embolism is less well validated, however.
The use of LMWH can be problematic and it should be given with care in
patients with renal failure. Intravenous UFH, which is not renally cleared,
should be the preferred mode of initial anticoagulation for patients with
severe renal impairment (creatinine clearance <30 mL/min); it may also be
preferable among those at high risk of bleeding, as its anticoagulant effect
can be reversed quickly.
Thrombolytic therapy
Thrombolytic therapy is indicated in the treatment of massive PE (shock,
severe hypoxaemia) or PE with echocardiographic right ventricular
dysfunction. Because of its ability to promote fibrinolyis it has additional
benefit in breaking up residual deep venous thrombus and reduces the
risk of recurrent PE and chronic thromboembolism. There are several
thrombolytic agents that have been used, streptokinase, urokinase,
and the more fibrin-specific tissue plasminogen activator and reteplase,
which work through different means to activate breakdown of
plasminogen to plasmin which degrades fibrin in clot. All appear to be
equally effective and safe. Thrombolysis has been shown to resolve
thrombotic obstruction and to improve haemodynamic parameters.
However, despite the appeal, there are few data from randomized trials of
thrombolytic therapy against heparin powered to demonstrate a
difference in hard clinical outcomes.
Contraindications to thrombolytic therapy are similar to those in the
treatment of myocardial infarction. However, while most benefit is
derived when treatment is started within 48 hours of symptom onset,
thrombolysis can still be useful in patients up to 2 weeks later. Heparin
should be withheld until the aPTT is less than 2:1 after thrombolysis. The
risk of bleeding is greatest where the administration of thrombolysis is
prolonged or where vascular puncture sites are present. If persistent major
bleeding occurs, plasmin activity can be reversed by intravenous
aprotinin and fibrinogen replenished with clotting factors in fresh frozen
plasma (which will contain plasminogen).
Suggested doses for thrombolytic drugs for pulmonary embolism are:
• streptokinase 0.25–0.5 M over 15 minutes followed by 0.1 MU/h
for 24 hours
• urokinase 4400 U/kg over 10 minutes then 4400 U/kg for 12 hours
• tPA 10 mg bolus, then 90 mg over 2 hours
• reteplase two 10 U boluses 30 minutes apart
Pulmonary embolectomy
The rapid restoration of pulmonary blood flow is likely to be a major
determinant in preventing the mortality from massive PE. In the past,
surgery was considered the best means of removing significant clot load.
The vogue for surgical embolectomy even in extreme situations is
diminishing. Historically, patients in shock despite inotropic support who
continue to deteriorate and those with major contraindications to
Mechanical thrombectomy
In the modern era of percutaneous intervention, attempts have been made
to provide an alternative to surgical embolectomy. Initial techniques have
focused on retrieval devices to hold and extract a thrombus from the main
pulmonary artery in patients with massive PE. However, this approach has
been of limited success. Clot fragmentation has been described in
uncontrolled studies using a pigtail catheter. The theoretical benefit of this
approach is that the clot will fragment into a smaller vascular area as it
embolizes distally and will be more susceptible to thrombolysis. This will
reduce pulmonary artery pressure and improve transpulmonary flow in
most cases. In cases where pulmonary artery pressure remains high, this
may occur through release of vasoconstrictor hormones such as
thromboxane A2 arguing for the actual removal of clot rather than simple
embolization of it. Again, outcome data for this technique are limited.
However, newer devices are becoming available which both fragment and
aspirate clots such as the Hydrolyser™, Amplatz™ and Günther catheters.
The most promising device may be the Arrow-Trerotola percutaneous
thrombolytic device (PTD), which consists of a motor-driven 5F outer
catheter connected to a fragmentation basket which rotates at 3000 rpm.
The latest version of this device may be introduced over-the-wire through a
guide catheter into the thrombus and activated to fragment the thrombus.
KEY POINTS
• PE occurs through dislodgment of a venous thrombus from the deep
leg or the pelvic veins into the pulmonary arterial circulation. The
clinical signs of embolism are determined by the level at which the
thrombus is occlusive.
• The development of a venous thrombus is determined by Virchow’s
triad of local injury, hypercoagulability and stasis of flow.
• Venous thromboembolism is a clinical situation where the diagnosis
is more often not made than made. The clinical suspicion of a DVT
(leg swelling, calf tenderness, venous distension of subcutaneous
vessels, discolouration) should be confirmed objectively, due to the lack
of predictive accuracy in the clinical examination.
• In the presence of a suspected acute DVT, either compression
ultrasound or impedance plethysmography should be done. If
inconclusive or inadequate, venography or MRI should be done.
• In acute PE, classic symptoms are unexplained dyspnoea, pleuritic
chest pain and haemoptysis with tachypnoea in particular and
tachycardia being common signs, but all are non-specific.
• The V/Q scan is often non-specific and in one study which evaluated
the V/Q scan by pulmonary angiography or post-mortem, it was
apparent that PE was often present in the presence of non-diagnostic
scans in 40 per cent of cases.
• CTPA is limited by poorer visualization of the peripheral areas of the
lung but is associated with 95 per cent specificity and sensitivity for PE.
CTPA has the greatest sensitivity for emboli in the main, lobar or
segmental pulmonary arteries.
• The treatment of acute PE includes intravenous heparin, oxygen
supplementation and haemodynamic support with noradrenaline and
careful volume balance. In the absence of circulatory failure, a strategy
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INFECTIVE ENDOCARDITIS
BACKGROUND
Epidemiology and pathophysiology
Strictly speaking, infective endocarditis (IE) is a disease in which an
infective organism colonizes the heart valves, septal defects or mural
endocardium. However, in clinical practice the definition extends to
include infections on arteriovenous shunts, arterio-arterial shunts and
aortic coarctations, as the clinical presentation is often indistinguishable.
The infection evolves to produce a vegetation that comprises an amorphous
mass of organisms, inflammatory cells, fibrin and platelets. Following
successful treatment for IE, healing occurs by fibrosis and calcification.
Overall, there are approximately 1500 cases of endocarditis in the UK per
year, with an estimated in-patient mortality between 15 and 20 per cent.
IE can occur not only on congenital or acquired structural cardiac
abnormalities but also on normal, previously healthy valves. Traditionally,
endocarditis has been divided into acute and subacute forms. Acute
bacterial endocarditis is usually due to a virulent organism such as
Staphylococcus aureus, which can rapidly lead to complications within
days or weeks if left untreated. Subacute bacterial endocarditis is more
indolent, usually presents weeks to months after the initial infection and
is caused by organisms such as Streptococcus viridans or coagulase
negative staphylococci. This classification was initially based on untreated
disease. Since devastating complications such as valve perforation and
cerebral embolization can arise with a variety of different organisms and
bacteria are not always implicated, the term IE is more appropriate and is
now widely used.
188 BACKGROUND
INFECTIVE ENDOCARDITIS
BACKGROUND 189
INFECTIVE ENDOCARDITIS
Streptococcus viridans 50 10 8 30
Enterococci 5 8 2 6
Other streptococci 5 2
Staphylococcus aureus 20 57 15 10
Staphylococcus 5 3 33 29
epidermidis
Gram-negative 6 7 17 10
bacteria (including
HACEK group) a
Fungus 1 5 10 5
Culture negative 5 5 5 5
Diphtheroids 8 3
Mixed/Others 3 3 2 2
aThe HACEK group of organisms consists of Haemophilus species, Actinobacillus
CLINICAL PRESENTATION
The clinical syndrome of IE consists of fever, changing murmurs, septic
embolization to any organ and petechial lesions of the skin. The
diagnosis should be suspected in anyone who presents with pyrexia and
Heart murmurs are heard in 80–85 per cent of patients with IE but may
be difficult to detect or be absent in patients with tricuspid valve
involvement. Careful auscultation in full inspiration is often useful in
diagnosing right-sided murmurs. Septic pulmonary embolization from
right-sided valvular IE (frequently seen in IVDU-related IE) can give rise
to shortness of breath, haemoptysis, pleuritic chest pain and pulmonary
abscesses.
Poor prognostic factors include increased age, infection of a prosthetic
valve, patients with cardiac complications on admission, persistent sepsis,
type of organism involved (Staphylococcus, fungal and nosocomial
infections carry a higher risk than Streptococcus viridans infection), and the
presence of associated diseases such as chronic renal disease, chronic liver
disease, neoplasms and HIV.
Continued
Minor criteria
(1) Predisposition: predisposing heart condition or intravenous
drug use
(2) Fever: temperature >38.0°C
aAdiagnosis of IE is made if there are two major or one major and three
minor or five minor criteria. Possible IE is suspected if there is one major
and one minor criterion, or three minor criteria.
Adapted from Li, et al. Clin Infect Dis 2000; 30: 633–8.
Infection related
Intracardiac: Paravalvular/intracardiac abscesses
Extracardiac: Line infection, metastatic infection, mycotic aneurysms, spinal
abscess, vertebral osteomyelitis, discitis, etc.
Antibiotic resistance: seldom a cause especially if the infecting bacteria has
been cultured and sensitivity determined
Antibiotic sensitivity
Can be associated with or without a rash, eosinophilia and a rise in CRP in a
patient who had been previously doing well
Multiple organisms
Usually seen in intravenous drug abusers
Wrong diagnosis
Lymphoma, sarcoidosis, AIDS, tuberculosis, atrial myxoma, acute rheumatic
fever, autoimmune disease such as SLE, etc.
ANTICOAGULANT THERAPY
Anticoagulant therapy has not been shown to prevent embolization in IE
and may increase the risk of intracerebral haemorrhage. Patients with
prosthetic valve endocarditis who are receiving chronic anticoagulant
therapy should be allowed to cautiously continue. However, in the
presence of cerebral emboli with haemorrhage, temporary
discontinuation of anticoagulation is appropriate. In unstable patients
or in those for whom surgery is planned, warfarin can be discontinued
and replaced with unfractionated heparin, which can easily be
reversed.
Absolute Relative
PREVENTION
IE is a life-threatening disease and carries a high risk of morbidity and
mortality despite modern antimicrobial and surgical treatment. It is
therefore imperative, whenever possible, to try to prevent unnecessary
infections, especially those in high-risk groups. When determining which
patients need antibiotic cover, it is important to consider the underlying
cardiac condition (as some conditions are more often associated with
endocarditis than others), the risk of bacteraemia associated with the
particular procedure, and the likely organism that may propagate to give
rise to IE. Currently there is considerable controversy over when antibiotic
prophylaxis should be given. Recently several guidelines advising on
antibiotic prophylaxis have changed, reflecting the lack of evidence that
exists for the benefits of chemoprohylaxis. Additionally, there is evidence
to suggest that bacteraemia occurs with everyday activities such as
chewing or brushing teeth. Consequently, in the UK, the National Institute
for Health and Clinical Excellence (NICE) has published guidelines
stating that prophylaxis is not required, except where there is evidence of
active infection. This is at odds with recommendations of the AHA and
ESC. The Working Party of the British Society for Antimicrobial
Chemotherapy (BSAC) guidelines are similar to that of the AHA and ESC
and are stated below. They recommend prophylaxis for dental procedures
(involving dento-gingival manipulation) in those at high risk of
endocarditis such as patients with:
• previous IE
• cardiac valve replacement
• surgically constructed systemic or pulmonary shunt or conduit.
These patients should be given amoxycillin 3 g po, 1 hour prior to the
procedure. Those allergic to penicillin should be given clindamycin
600 mg po.
PREVENTION 199
INFECTIVE ENDOCARDITIS
KEY POINTS
• IE is a challenging medical disease, which requires a high index of
suspicion, and early diagnosis and treatment in order to be successfully
managed.
• IE can involve multiple systems and can often present in a similar way
to other conditions such as connective tissue disorders, atrial myxoma
and lymphomas, and is therefore a great mimicker.
• Although the number of cases of IE related to rheumatic heart disease
has decreased, this reduction has been balanced by an increased
incidence of IE in IV drug abusers and the elderly.
• Advances in microbiology techniques and echocardiographic imaging
(in particular, TOE) have improved the ability to diagnose IE.
• A multidisciplinary approach is necessary for decision-making during
treatment, with consultation from cardiology, cardiothoracic surgery
and the microbiology departments.
• Patients with signs and symptoms of heart failure should be considered
for early surgical intervention.
• Administration of antibiotic prophylaxis is determined by the
underlying cardiac condition as some conditions are more often
associated with endocarditis than others, the risk of bacteraemia
associated with the particular procedure, and the likely organism that
may propagate to give rise to IE.
KEY REFERENCES
AHA Scientific Statement. Infective endocarditis diagnosis, antimicrobial therapy, and
management of complications. Circulation 2005; 111: e394–e433.
Dajani AS, Taubert KA, Wilson W, et al. Prevention of bacterial endocarditis.
Recommendations by the American Heart Association. JAMA 1997; 277:
1794–801.
Durack DT. Prevention of infective endocarditis. N Engl J Med 1995; 332: 38–44.
Durack DT, Lukes AS, Bright DK. New criteria for the diagnosis of infective
endocarditis: utilization of specific echocardiographic findings. Am J Med 1994;
96: 200–9.
Greaves K, Mou D, Patel A, Celermajer D S. Clinical criteria and the appropriate use of
transthoracic echocardiography for the exclusion of infective endocarditis. Heart
2003; 89: 273–5.
Guidelines for the antibiotic treatment of endocarditis in adults: report of the Working
Party of the British Society for Antimicrobial Chemotherapy. J Antimicrob
Chemother 2004; 54: 971–81.
Guidelines for the prevention of endocarditis: report of the Working Party of the
British Society for Antimicrobial Chemotherapy. J Antimicrob Chemother 2006; 57:
1035–42.
Li JS, Sexton DJ, Mick N, et al. Proposed modifications to the duke criteria for the
diagnosis of infective endocarditis. Clin Infect Dis 2000; 30: 633–8.
Mylonakis E, Calderwood SB. Infective endocarditis in adults. N Engl J Med 2001; 345:
1318–30.
Oakley CM, Hall RJC. Endocarditis problems – patients being treated for endocarditis
and not doing well. Heart 2001; 85: 470–4.
Piper C, Korfer R, Horstotte D. Prosthetic valve endocarditis. Heart 2001; 85: 590–3.
Prophylaxis against infective endocarditis – Antimicrobial prophylaxis against
infective endocarditis in adults and children undergoing interventional procedures.
National Institute for Health and Clinical Excellence. March 2008.
DIGOXIN TOXICITY
Digoxin is commonly used in the treatment of chronic atrial fibrillation
(AF) and heart failure. More than 10 per cent of patients receiving the drug
have been found to have evidence of digoxin toxicity when admitted to
hospital. Digoxin has a narrow therapeutic index (therapeutic concentration
1–2 ng/mL or 1.3–2.6 nmol/L) with toxicity occurring with serum
concentrations >2.5 ng/mL. Serum concentration measurements must be
taken at least 6 hours after the last dose. Toxicity can occur as a result of
deliberate or accidental self-poisoning or more commonly from drug
accumulation over a period of time, particularly in the elderly and patients
with associated renal impairment. Drugs such as verapamil, captopril,
quinine, quinidine, propafenone, flecainide, amiodarone, prazosin,
spironolactone, tetracycline, erythromycin and carbenoxalone can also
increase serum concentrations and predispose to toxicity. Agents causing
hypokalaemia or intracellular potassium deficiency, hypomagnesaemia,
hypercalcaemia and hypothyroidism can increase myocardial sensitivity to
digoxin, despite satisfactory therapeutic concentrations.
Clinical presentation
Clinical features of toxicity include constitutional effects such as lethargy
and weakness; gastrointestinal effects including anorexia, nausea and
vomiting; neurological effects including confusion, weakness,
paraesthesiae and, rarely, fits and acute psychosis; ocular disturbances
including blurred vision, xanthopsia (yellow vision). Severe poisoning can
cause hyperkalaemia (by inhibiting the myocardial membrane adenosine
triphosphate (ATP) pump) and metabolic acidosis.
Digoxin toxicity can cause any arrhythmia, and various conduction
disturbances. The commonest arrhythmia and, usually, an early sign of
Management
If digoxin toxicity is suspected then the following steps should be
taken:
• stop digoxin
• correct hypokalaemia if present
• check digoxin level
• monitor cardiac rhythm and correct any sustained
For acute overdoses, oral activated charcoal should be given to absorb any
cardiac glycoside remaining in the gut and to interrupt the enterohepatic
circulation.
Ventricular ectopics, first degree AV block and AF with a slow rate but
haemodynamic stability require no special therapy except drug
withdrawal.
Clinical presentation
Early clinical features are due to the anticholinergic effects of the drug,
and include dilated pupils, dry skin, dry mouth, decreased bowel sounds
(ileus), urinary retention and tachycardia. Cardiovascular toxicity can
rapidly ensue with the development of hypotension, arrhythmias and
asystole. Toxicity results primarily from effects on the myocardial cell
action potential, direct effects on vascular tone and indirect effects
mediated by the autonomic nervous system.
TCADs can inhibit the fast-acting sodium channel and are therefore
similar to class 1A antiarrhythmic drugs. Consequently, TCADs can
impair cardiac conduction and prolong repolarization. They also have a
negative inotropic effect due to inhibition of calcium entry into myocytes.
The inhibition of sodium channels is pH dependent with acidosis
aggravating cardiotoxicity. Conversely, an increase in pH is protective by
improving cardiac conduction and reducing negative inotropic effects.
Impaired conduction in the His–Purkinje system slows propagation of the
ventricular depolarization wave, and prolongs the QRS interval. QRS
interval prolongation is the most distinctive feature of serious TCAD
overdose, and is usually seen as a non-specific conduction delay on the
electrocardiogram (ECG). A QRS duration >120 ms is a good predictor of
cardiac and neurological toxicity, whereas a QRS duration >160 ms is
predictive of ventricular arrhythmias. Prolongation of repolarization
causes an increase in QT interval, predisposing to Torsade de Pointes.
Non-uniform slowing may cause unidirectional block and re-entry
circuits to develop, analogous to ischaemic myocardium, resulting in VT;
VT may be difficult to distinguish from sinus tachycardia in the presence
of prolonged QRS and PR intervals (P waves may be obscured by the
preceding T wave). A 12-lead ECG may help reveal P waves not visible on a
rhythm strip. VF is usually a terminal rhythm that occurs as a
complication of VT or hypotension. The PR interval in TCAD overdose is
often prolonged, but second or third degree AV block is rare. Sinus
tachycardia is the most common rhythm disorder seen and is present in
more than 50 per cent of patients.
Management
Management is generally supportive, with monitoring of respiration and
cardiac rhythm. Owing to the possibility of rapid deterioration,
intravenous access is recommended. A 12-lead ECG should be obtained
because it may reveal QRS prolongation that is not evident on the single
lead of a cardiac monitor.
The anticholinergic effects may delay gastric emptying, and a large, single
dose of activated charcoal administration should be considered,
particularly if ingestion has occurred within an hour of presentation.
Any hypoxia and electrolyte or metabolic disturbances should be
corrected. Even in the absence of acidosis, if there is cardiac involvement
(QRS prolongation >140 ms, ventricular arrhythmias) or hypotension,
50 mmol sodium bicarbonate should be administered slowly (see
Appendix A). Because marked alkalosis can be physiologically
SUBSTANCE ABUSE
It is estimated that almost one in four people in developed countries have
misused recreational drugs at some time during their life. Therefore,
independent of clinical practice, most doctors will have to manage
patients with the ill effects associated with recreational drug abuse at
some point during their career. In addition to their effects on the central
nervous system, many of these agents induce profound changes in the
heart and circulation, which are responsible for a significant proportion of
drug-related morbidity. The purpose of this section is to review the
cardiovascular complications associated with some of the commonly
misused recreational drugs.
metabolized and excreted in the urine over a 2-week period. At high doses,
cocaine can impair myocardial electrical conduction and contractility by
blocking fast sodium and potassium channels and inhibiting calcium entry
into myocytes. Amphetamine and its derivative ecstasy produce indirect
sympathetic activation by releasing noradrenaline, dopamine and
serotonin from central and autonomic nervous system terminals. The
plasma half-life varies from as little as 5 hours to 20–30 hours depending
on urine flow and pH (elimination is increased in acidic urine). Compared
to cocaine, amphetamine lacks the local anaesthetic effect of inhibiting fast
sodium channels.
Clinical effects
Sympathetic activation can lead to varying degrees of tachycardia,
vasoconstriction, unpredictable blood pressure effects and arrhythmias,
depending on the dose taken and the presence or absence of coexisting
cardiovascular disease. Although hypertension is common, hypotension
as a result of paradoxical central sympathetic suppression, a late relative
catecholamine-depleted state or acute myocardial depression can occur.
Myocardial depression may be caused by ischaemia, a direct toxic effect of
the drug or mechanical complications (acute aortic rupture, tension
pneumothorax, pneumopericardium, etc.).
Management
Similar principles apply to the management of the cardiovascular
complications associated with these drugs. If the patient is agitated and
anxious, then a benzodiazepine in sedative dosages should be
administered as this can attenuate some of the cardiac and central
nervous system toxicity.
In the treatment of hypertension, beta-blockers should be avoided, as they
may be associated with unopposed alpha-mediated vasoconstriction
leading to paradoxical increase in blood pressure and coronary artery
vasoconstriction. The combined alpha- and beta-blocker drug, labetalol,
is theoretically preferable to selective beta-blockers. However, the
alpha-blocking effect is relatively weak and therefore labetalol can also
exacerbate hypertension. Hypertension can be safely managed with either
an alpha-blocker such as phentolamine or with vasodilators such as
hydralazine, nitrates and nitroprusside. When hypertensive crises lead to
the mechanical complication of aortic dissection or acute valve rupture,
emergency cardiothoracic surgery may be required.
Myocardial ischaemia should be treated initially with oxygen, aspirin and
benzodiazepine. If there is continuing ischaemia, then vasodilators such
as nitrates or phentolamine should be administered in an attempt to
reverse residual coronary artery spasm. Patients with persistent ST
segment elevation should undergo primary angioplasty. Among patients
undergoing coronary stenting, the potential of non-compliance with
antiplatelet medication should be borne in mind when choosing the type
of stent.
Clinical effects
The adrenergic effects of these drugs are usually mild and do not produce
the profound sympathetic storms seen with cocaine and amphetamine.
Symptoms corresponding to general sympathetic arousal include dilated
pupils, tachycardia, hypertension and hyper-reflexia. Although
Management
Management is usually supportive, as the majority of symptoms resolve
within 12 hours. Agitated patients should be sedated with a
benzodiazepine. The use of neuroleptic agents should be avoided as they
can intensify toxic effects. Supraventricular arrhythmias can be treated
with adenosine or verapamil. Apart from benzodiazepines,
pharmacological intervention for mild to moderate hypertension is
usually not required. Treatment for dangerously high blood pressure and
myocardial ischaemia should follow the same general principles described
for cocaine and amphetamine.
Narcotic analgesics
Pharmacology
Morphine and its semi-synthetic analogue heroin are the most commonly
misused narcotic analgesics. When used alone or in combination with
other drugs, they account for over 40 per cent of drug-related deaths.
Heroin is slowly metabolized to morphine, which has a plasma half-life of
2–3 hours.
Clinical effects
Narcotic agents act centrally on the vasomotor centre to increase
parasympathetic and reduce sympathetic activity. This effect, combined
with histamine release from mast cell degranulation, can result in
bradycardia and hypotension. Drug-induced bradycardia along with
enhanced automaticity can precipitate an increase in atrial and
ventricular ectopic activity, AF, idioventricular rhythm or potentially
lethal ventricular tachyarrhythmias. Some narcotic drugs (such as the
synthetic agent, dextropropoxyphene, a constituent of co-proxamol) have
additional sodium channel blocking effects, causing ECG QRS
prolongation, and further contributing to their pro-arrhythmic potential.
It is recognized that methadone, commonly used in treating opioid
addiction, delays cardiomyocyte repolarization, resulting in ECG QT
prolongation, which is associated with Torsade de Pointes.
Bacterial endocarditis, affecting mainly right-sided cardiac structures, is a
well-known complication of intravenous narcotic drug abuse, sometimes
Management
Initial management centres around ensuring an adequate airway,
breathing and circulation. In the presence of respiratory depression,
severe hypotension and bradycardia, administration of repeated boluses
or an infusion of a narcotic receptor antagonist, naloxone (Narcan), will
be required, as detailed in Appendix A. In severe hypotension, the
insertion of a pulmonary flow catheter may be needed to help guide fluid
and inotropic administration, and avoid inappropriate administration of
diuretics in patients with non-cardiogenic pulmonary oedema, which
requires intensive ventilatory support.
There are no useful published data to guide selection of antiarrhythmic
agents for the treatment of supraventricular and ventricular
tachyarrhythmias. In the first instance, patients should be investigated,
and hypoxic, metabolic and electrolyte deficits corrected. As the misused
drug is rapidly metabolized, the majority of arrhythmias are short lived,
and it is therefore preferable to avoid the use of antiarrhythmic agents
where possible to minimize the risk of pro-arrhythmic interactions. If
treatment is needed for supraventricular arrhythmia, conventional agents
such as adenosine, beta-blockers, verapamil and digoxin have been
recommended. Ventricular arrhythmias should be managed along
conventional lines. Persistent bradycardia may require atropine or
temporary cardiac pacing.
Clinical effects
Following inhalation, feelings of euphoria, excitement and invulnerability
can occur rapidly and are short lived. Cardiac arrhythmias are presumed
Management
Patients should be managed in a calm non-threatening environment, with
sedation if necessary. Hypoxia and chemical disturbances should be
corrected to optimize myocardial electrical stability. Haemodynamically
unstable tachyarrhythmias require prompt electrical cardioversion.
Profound bradyarrhythmias may be treated cautiously with atropine or
temporary cardiac pacing. Hypotension can be treated with intravenous
fluids, guided by a pulmonary artery catheter, if necessary. Inotropic
agents are best avoided, if possible, as they may induce refractory
ventricular tachyarrhythmias in the electrically unstable myocardium.
Calcium administration may help to reverse myocardial depression. In
patients with sustained tachyarrhythmias, beta-blockers or amiodarone
may help to combat sympathetic activation and are the antiarrhythmic
drugs of choice. Cardiac ischaemia should be managed with oxygen,
vasodilators and reperfusion treatment. Cardiomyopathies are treated
conventionally.
Cannabis
Pharmacology
Cannabis is the most widely consumed recreational drug. It has a plasma
half-life of 20–30 hours and can be detected in the urine for several days in
occasional users, and up to months in heavy users.
Clinical effects
Cannabis has a biphasic effect on the autonomic nervous system,
depending on the dose absorbed. Low or moderate doses can increase
sympathetic and reduce parasympathetic activity, producing a
tachycardia and an increase in cardiac output. In contrast, higher doses
inhibit sympathetic and increase parasympathetic activity, resulting in
bradycardia and hypotension. Reversible ECG abnormalities affecting the
P and T waves, and the ST segment, have been reported. It is not clear
whether these changes occur as a direct result of cannabis, independent of
its effect on the heart rate.
Supraventricular and ventricular ectopic activity can occur, and
arrhythmias possibly relating to cannabis use have been reported. In
patients with ischaemic heart disease, cannabis increases the frequency of
anginal symptoms at low levels of exercise and may be a trigger for the
onset of an acute MI. This is believed to occur as a result of drug-induced
increase in blood pressure, heart rate and myocardial contractility,
increasing myocardial oxygen demand.
Management
In the absence of major underlying structural heart disease, the
autonomically mediated changes in heart rate and blood pressure are
usually well tolerated and therefore no treatment is needed. Where
necessary, hypotension usually responds to intravenous fluid
administration. For significant bradycardia, atropine can be administered.
Patients presenting with unstable angina or MI should be treated
conventionally.
KEY POINTS
• The abuse of recreational drugs is common and it is inevitable
that doctors will have to manage and treat their associated ill
effects.
• Recreational drugs are complex and can induce profound changes in
cardiovascular function, both acutely and chronically.
• Recreational drugs are often taken together, which can result in
complex synergistic interactions with potentially detrimental
effects.
• A high index of suspicion with early intervention and management is
often the key to successful treatment.
KEY REFERENCES
AHA Scientific Statement Management of Cocaine-Associated Chest Pain and
Myocardial Infarction. Circulation 2008; 117: 1897–1907.
Dick M, Curwin J, Tepper D. Digitalis intoxication recognition and management. J Clin
Pharmacol 1991; 31: 444–7.
Fisher BAC, Ghuran A, Vadamalai V, Antonios TF. Cardiovascular complications
induced by cannabis smoking: a case report and review of the literature. Emerg Med
J 2005; 22: 679–80.
Ghuran A, Nolan J. Recreational drug abuse; issues for the cardiologist. Heart 2000; 83:
627–33.
Kelly RA, Smith TW. Recognition and management of digitalis toxicity. Am J Cardiol
1992; 69: 108G–19G.
Mittleman MA, Lewis RA, Maclure M, Sherwood JB, Muller JE. Triggering myocardial
infarction by marijuana. Circulation 2001; 103: 2805–9.
Osterwalder JJ. Patients intoxicated with heroin or heroin mixtures: how long should
they be monitored? Eur J Emerg Med 1995; 2: 97–101.
Toxbase (National Poisons Information Service): http://www.spib.axl.co.uk
Williams DR, Cole SJ. Ventricular fibrillation following butane gas inhalation.
Resuscitation 1998; 37: 43–5.
PERICARDITIS
BACKGROUND
Acute pericarditis is a clinical syndrome caused by inflammation of the
pericardium and characterized by chest pain, a pericardial friction rub and
electrocardiographic abnormalities. It is more common in adult males than
in women and young children. Common causes include idiopathic, viral,
bacterial, uraemia, post-myocardial infarction, trauma and neoplasms
(Table 9.1). After myocardial infarction, pericarditis can occur within
1–4 days, or, less commonly, after 1–4 weeks as part of Dressler’s syndrome,
a systemic inflammatory condition thought to result from an autoimmune
reaction to myocardial necrosis. The pericardial reaction can be purulent,
haemorrhagic, fibrinous or serofibrinous. Complications may result in
restriction of cardiac filling, either as a result of blood or fluid trapped in
the pericardial sac (cardiac tamponade) or from thickening of the
pericardium (constrictive pericarditis). These conditions may be prevented
if diagnosis and management are undertaken early.
CLINICAL FEATURES
Pericarditis often presents with sharp chest pain, localized retrosternally or
in the left precordial region, and exacerbated by breathing, coughing,
moving or lying flat. The pain often radiates to the trapezius ridge, but may
also radiate into the neck, jaw, arms, or upper abdomen and can therefore
mimic an ACS or an acute abdomen. The pain is relieved by sitting up and
leaning forward. As the pericardium is well innervated, acute
inflammation may cause intense pain and initiate vagal reflexes. There may
be a history of prodromal symptoms, which can include fever, malaise and
myalgia. Dyspnoea may occur because of splinting of the chest from pain or
because of significant accumulation of pericardial fluid (see Chapter 11).
Nocardia, toxoplasmosis
A pericardial friction rub is often present and is best heard along the left
sternal edge with the patient leaning forward. The persistence of the rub
throughout inspiration and expiration as well as when the breath is held
can help distinguish a pericardial rub from a left-sided pleural rub. Large
effusions can compress the base of the left lobe of the lung, causing an area
of dullness and bronchial breath sounds just below the angle of the left
scapula (Ewart’s sign).
DIAGNOSIS
General
Non-specific markers of inflammation including white cell count (WCC),
erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are
usually raised. Cardiac enzymes may be elevated if the inflammation
extends to the myocardium, and for this reason cardiac isoenzymes cannot
always be used to differentiate between acute pericarditis and ACS.
Cardiac troponins are frequently elevated, but do not necessarily indicate a
DIAGNOSIS 219
PERICARDITIS
Electrocardiogram
ECG changes (Figure 9.1) can occur a few hours or days after the onset of
pericardial pain and are characterized initially by concordant, concave ST
segment elevation in all leads except leads aVR, V1 and sometimes V2
(these leads show reciprocal ST depression). There is often PR segment
depression associated with ST elevation (and sometimes PR elevation with
ST depression). The following evolutionary changes then occur:
isoelectric ST segment with flattened T waves, isoelectric ST segment with
T inversion and finally reversion of T waves to normal. These changes are
different from cardiac ischaemia (Table 9.2). It should be emphasized that
they may not follow an exact sequence and some patients may present
with only ST elevation and a return to normal without T inversion.
Alternatively, T inversion may be the first sign, since the acute process was
missed. Pericardial effusion can produce low voltage QRS complexes and
electrical alternans (see Chapter 11).
Echocardiography
Echocardiography is valuable for determining the presence and size of a
pericardial effusion and monitoring progress if the effusion is drained or
treated conservatively. Furthermore, any contractile dysfunction resulting
from myocarditis can also be detected.
220 DIAGNOSIS
I
aVR V4
V1
II aVL
V5
V2
III aVF
V3 V6
II
MANAGEMENT
The first step is to establish whether the pericarditis is related to an
underlying medical problem that requires specific therapy; for instance,
uraemic pericarditis will require urgent dialysis.
Non-specific therapy consists of bed rest until pain and fever have
disappeared, and the administration of anti-inflammatory agents such as
aspirin (600–900 mg every 4–6 hours), ibuprofen (200–400 mg every
6 hours) or indomethacin (25–50 mg every 6 hours). In the randomized
COPE study, the addition of colchicine to aspirin was shown to be more
effective than aspirin monotherapy for the treatment of acute pericarditis.
The dose given was 1-2 mg during the first 24 h, followed by a
maintenance dose of 0.5-1 mg daily for 3 months. Combination therapy
was associated with quicker symptom resolution as well as a much
reduced recurrence rate. Similarly, the same combination was more
effective than aspirin alone for recurrent episodes. With the exception of
aspirin, anti-inflammatory drugs should be used cautiously in
post-infarction pericarditis as they can affect scar formation and
predispose to myocardial rupture. Some therapeutic studies have
indicated that corticosteroid treatment is associated with more frequent
recurrent pericarditis. In general, corticosteroids should be reserved for
those with underlying rheumatalogic conditions or intolerance to the
agents discussed above.
Antibiotics should be restricted to cases of purulent pericarditis and
documented antibiotic-sensitive micro-organisms. Anticoagulants should
be discontinued unless there is strong evidence for the development of
thromboembolic complications. If anticoagulants must be continued,
such as in patients with mechanical heart valves, intravenous heparin,
which has a short half-life and whose action can easily be reversed with
protamine sulphate, should be used. Patients should then be examined
closely for the development of pericardial effusion.
222 MANAGEMENT
PERICARDITIS
KEY POINTS
• There are a number of causes of acute pericarditis but idiopathic, viral
and post-MI pericarditis are the commonest.
• Occasionally the pain of pericarditis can mimic an acute abdomen or
MI; however, in the majority of cases pericarditis has characteristic
clinical and electrocardiographic features.
KEY REFERENCES
Imazio M, Bobbio M, Cecchi E, et al. Colchicine in addition to conventional therapy for
acute pericarditis: results of the COlchicine for acute PEricarditis (COPE) trial.
Circulation 2005; 112: 2012–16.
Ivens EL, Munt BI, Moss RR. Pericardial disease: what the general cardiologist needs to
know. Heart 2007; 93: 993–1000.
Maisch B. Pericardial disease, with a focus on etiology, pathogenesis, pathophysiology,
new diagnostic imaging methods, and treatment. Curr Opin Cardiol 1994; 9:
379–88.
Oakley CM. Myocarditis, pericarditis and other pericardial disease. Heart 2000; 84:
449–54.
Spodick DH. Risk prediction in pericarditis: who to keep in hospital. Heart 2008; 94:
398–9.
CARDIAC TRAUMA
BACKGROUND
In developed countries, cardiac trauma represents one of the leading
causes of death in those under the age of 40 years. Young males are more
likely to be affected than females. Road traffic accidents and physical
violence are responsible for the majority of cases, although the incidence
of iatrogenic causes as a result of intravascular and intracardiac
catheterization as well as cardiopulmonary resuscitation (CPR) is
currently rising. Advances in initial resuscitation and surgical
management mean more patients are surviving the initial insult.
Cardiac trauma is divided into penetrating and non-penetrating injuries. Both
mechanisms can lead to myocardial rupture, contusion, laceration, pericardial
insult, coronary injury, valvular damage, arrhythmias and conduction
abnormalities. Cardiac trauma is easily overlooked as attention is diverted to
more obvious skeletal and multisystem injuries. As a result, haemodynamic
instability can rapidly develop with devastating results. A high index of
clinical suspicion with the early use of diagnostic techniques is essential and is
often the key to successful management. It is important for physicians to have
a good working knowledge of cardiac trauma to enable them to diagnose the
occurrence of these conditions and manage the non-surgical components.
accidents (as the heart is compressed between the steering wheel or seat
belt, and the sternum and spine) but can also occur as the result of falls,
fights and sporting injuries. Box 10.1 summarizes the injuries that can
develop as a consequence of non-penetrating cardiac trauma.
Cardiac contusion is considered the most common injury to the heart
following blunt trauma. Cardiac contusion usually produces no significant
symptoms and can easily go unrecognized. Subepicardial and
subendocardial petechiae, bruising, haematoma, lacerations and
full-thickness myocardial damage, later followed by necrosis, fibrosis and
aneurysm formation, can occur. The key symptom is precordial pain
resembling that of myocardial infarction (MI) but unrelieved with nitrates.
Other sites of chest trauma may confuse the clinical picture, but unlike
injury to the thoracic wall, pain from cardiac contusion is not affected by
breathing. There may be inappropriate tachycardia, gallop rhythm and a
pericardial rub. The electrocardiogram (ECG) may show non-specific
ST-T wave changes (Figure 10.1), findings of pericarditis, loss of R-wave
amplitude and even pathological Q waves depending on the degree of
injury. Localized injury to the conducting system can give rise to varying
degrees of atrioventricular (AV) block, intraventricular conduction defects
or bundle branch block. Supraventricular tachycardias, atrial fibrillation
II aVL C2 C5
III aVF C3 C6
II
(a)
Figure 10.1(a) Non-penetrating cardiac injury sustained during a motor vehicular accident. Note the non-specific
ST-T wave changes. There is T-wave inversion in lead III, and flattening in II and aVF. There was notching of the
T wave in leads V3–V6. Reprinted with permission from Moriaty A. (1999) p. 578.
I
aVR V1 V4
II aVL V2 V5
III
aVF V3 V6
II
(b)
Figure 10.1(b) Repeat ECG a few weeks later demonstrates resolution of these changes. Reprinted with permission
from Moriaty A. (1999) p. 578.
CARDIAC TRAUMA
CARDIAC RUPTURE
Rupture of the free wall, interventricular septum, heart valves, papillary
muscles or chordae tendineae can occur acutely owing to the direct force
of the injury or may be delayed up to 2 weeks resulting from necrosis.
Rupture of the thoracic aorta commonly occurs at the aortic isthmus, just
below the origin of the left subclavian artery. These complications are
usually fatal. Patients may present with signs and symptoms of acute
cardiac tamponade, severe congestive heart failure with a new murmur or
haemorrhagic shock. If indicated, pericardiocentesis may be life saving.
Meticulous fluid resuscitation and early surgical intervention is the
definitive treatment for most patients.
PERICARDIAL INJURY
Trauma to the pericardium can range from contusion to laceration or
rupture allowing herniation of the heart. Clinical findings include a
pericardial friction rub and ST-T wave changes on the ECG characteristic
of pericarditis. Complications such as haemopericardium and tamponade
can occur. In the case of cardiac herniation, the heart becomes entrapped,
there may be impaired filling and occasionally compression of the
coronary arteries. There may be evidence of a displaced heart and
pneumopericardium on a chest x-ray. The ECG can show a new shift in
axis or bundle branch block. The only therapy for cardiac herniation is
surgical repositioning. Uncomplicated pericarditis can be treated with
non-steroidal anti-inflammatory agents. Recurrent pericardial effusions
associated with pericardial pain, pyrexia and a friction rub can sometimes
occur. It is similar to the post-pericardiotomy syndrome and is treated
with non-steroidal anti-inflammatory agents. Constrictive pericarditis
can occur as a late sequel and the treatment is total pericardiectomy.
COMMOTIO CORDIS
Sudden death may occur in young sport participants when a small hard
ball (such as a cricket ball) or other projectile (lacrosse ball, hockey puck,
karate kick) strikes the victim in the precordium. This phenomenon is
termed commotio cordis and affects children and adolescents 5–15 years
of age without pre-existing heart disease. It is the second most common
cause of sudden cardiac death in young athletes after hypertrophic
cardiomyopathy. Characteristically, there is no structural damage to the
thoracic cavity or heart. The causative precordial blows are often not
perceived as unusual for the sporting event involved or of sufficient
magnitude to cause death. It is believed that an appropriately timed
precordial blow, during the electrically vulnerable phase of ventricular
repolarization (15–30 ms before the T-wave peak), can induce a
ventricular tachyarrhythmia and subsequently death. At present, early
basic and advanced life support, and ensuring adequate chest protection,
are the only effective treatments against this phenomenon.
into the mediastinum and pleural space, causing haemorrhagic shock and
massive haemothorax on chest x-ray. This is commonly seen in large or
right ventricular wounds. However, if the pericardium does not permit
free drainage because its opening has been obstructed by a blood clot,
adjacent lung tissue or other structures, then blood accumulates within
the pericardial space, causing cardiac tamponade. Under these
circumstances, the chest x-ray will show a normal size cardiac silhouette,
as the acute and rapid accumulation of fluid within the pericardial space
does not allow distension of the pericardium. Echocardiography can be
useful for diagnosing pericardial effusions, foreign bodies in the heart and
intracardiac shunts.
Initial management includes securing the airway, establishing venous
access and appropriately administered intravenous fluids and blood. The
offending object should remain in situ until exploratory surgery can be
carried out. Patients who fail to respond to resuscitation and suddenly
decompensate, should undergo immediate thoracotomy and repair of any
treatable cardiac trauma. The incidence of late sequelae can be as high as
20 per cent and includes atrial and ventricular septal defects, tricuspid
and mitral valve lacerations, and coronary injury. These complications
may be missed on initial examination, only becoming apparent after a few
days or weeks because of fibrous retraction of wound edges, resolution of
oedema, ventricular enlargement and lysis of occluding clots. It is
therefore essential that all post-cardiac trauma patients are closely
monitored while in hospital and also in the outpatient clinic. Not
surprisingly, penetrating cardiac injuries are usually immediately fatal,
with the victim dying before reaching hospital.
KEY POINTS
• Cardiac trauma is a leading cause of death under the age of 40 years.
• It is divided into penetrating and non-penetrating injuries, which can
both lead to myocardial rupture, contusion, laceration, pericardial
insult, coronary injury, valvular damage, arrhythmias and conduction
abnormalities.
• It is easily overlooked and should always be considered in anyone
presenting with skeletal and multisystem injuries.
• A high index of clinical suspicion with the early use of diagnostic
techniques is essential and is often the key to successful management.
KEY REFERENCES
Anderson DR. The diagnosis and management of non-penetrating cardiothoracic
trauma. Br J Clin Pract 1993; 47: 97–103.
Bansal, MK et al. Myocardial contusion injury: redefining the diagnostic algorithm.
Emerg Med J 2005; 22: 465–9.
Jackson L, Stewart A. Use of troponin for the diagnosis of myocardial contusion after
blunt chest trauma. Emerg Med J 2005; 22: 193–5.
Moriaty A. Myocardial contusion caused by seat belt. Br J Cardiol 1999; 6: 577–9.
Westaby S, Odell JA. Cardiothoracic Trauma. London: Arnold, 1999.
CARDIAC TAMPONADE
BACKGROUND
Cardiac tamponade is an emergency clinical syndrome that occurs
when blood or fluid fills the pericardial space, raising intrapericardial
pressure and preventing ventricular diastolic filling. Consequently,
venous pressures are greatly increased, and there is a reduction in stroke
volume and cardiac output with the development of shock. The
development of tamponade relates to the rapidity of fluid accumulation
and the distensibility of the pericardium rather than the quantity of
fluid. If accumulation is rapid, or if left ventricular function is
compromised for other reasons, as little as 250 mL may be sufficient to
produce tamponade. In contrast, it may take in excess of a litre of fluid
to produce tamponade if it accumulates over a long period of time. Some
common causes of cardiac tamponade are listed in Box 11.1.
CLINICAL PRESENTATION
Patients typically present with cardiogenic shock, with hypotension,
cold-clammy peripheries, oligo-anuria and associated agitation.
Untreated, this condition can be rapidly fatal. In the setting of a more
slowly developing tamponade, patients appear less ill and may present
with anorexia, weakness and signs of biventricular failure such as
shortness of breath, peripheral oedema and hepatomegaly. There may be
an accompanying tachycardia, and the presence of pulsus paradoxus (an
inspiratory decrease in amplitude of the palpated pulse or measured blood
pressure) is supportive of the diagnosis. The jugular venous pressure
(JVP) is markedly elevated with a prominent x descent and absent y
descent. A positive Kussmaul’s sign (an inspiratory increase in the JVP) is
rare in cardiac tamponade. Its presence suggests that an organizing
Box 11
11.1 Causes of ca
carr dia c ta
tammp onade
• Malignant disease
• Post-infective pericarditis
• Rupture of the free wall post-myocardial infarction
• Uraemia
• Iatrogenic; post-diagnostic (cardiac catheterization) or
therapeutic procedures (pacemaker electrode insertion,
angioplasty, etc.), anticoagulation
• Chest trauma
• Radiation
• Hypothyroidism
• Dissecting aortic aneurysm
• Post-pericardiotomy syndrome
• Dressler’s syndrome
• Connective tissue diseases, e.g. rheumatoid arthritis, systemic
lupus erythematosus, etc.
• Idiopathic
MANAGEMENT
If haemodynamic compromise is present, intravenous fluids or inotropic
agents can be administered to maintain haemodynamic support, while
preparing the patients for pericardiocentesis (see below). Cardiac
tamponade associated with cardiac trauma or aortic dissection requires
immediate surgical intervention.
Pericardiocentesis
• Pericardial aspiration should ideally be performed with full x-ray
screening, rhythm monitoring and resuscitation facilities readily
available. Echocardiography can be used to guide pericardial
aspiration as it allows visualization of the pericardial space, the
myocardium and the aspiration needle. It can therefore give an
indication of the best line of approach.
• The patient is placed at 30–45° to pool the pericardial fluid anteriorly
and inferiorly. The patient is then connected to an ECG monitor.
• A long 18-gauge needle should be used. The V1 lead from an ECG
machine can be connected to the metal hub of the needle via a
sterile alligator clip to provide continuous monitoring from the tip
of the puncture needle.
• Although several sites have been advocated for pericardiocentesis,
the subxiphoid approach is preferred as it is extrapleural and avoids
the coronary, pericardial and internal mammary arteries. The skin
is cleaned and lignocaine infiltrated between the left side of the
xiphisternum and the adjacent left costal margin, with the point
directed towards the left shoulder, 45° to the skin.
• The needle is advanced while periodically aspirating and injecting
small amounts of lignocaine. The needle is advanced until fluid is
aspirated, indicating that the needle has reached the pericardial
space. If using ECG monitoring, ST elevation indicates that the tip
of the needle is in contact with the myocardium. Alternatively, the
injection of a few millilitres of contrast media can be used to
determine if the needle is in the pericardial space or within a
cardiac chamber. If the contrast media swirls and is rapidly
236 MANAGEMENT
CARDIAC TAMPONADE
KEY POINTS
• Cardiac tamponade is a clinical diagnosis caused by a critically
increased volume of fluid within the pericardium obstructing inflow of
blood to the ventricles.
• Consider the diagnosis in any patient in a haemodynamically collapsed
state, with a raised JVP, reduced heart sounds, low-voltage complexes
on the ECG and clear lung fields.
• Pericardiocentesis should be done only by those experienced in
performing the procedure.
KEY REFERENCES
Callahan JA, Seward JB, Nishimura RA, et al. Two dimensional echocardiographically
guided pericardiocentesis: experience in 117 consecutive patients. Am J Cardiol
1985; 55: 476–84.
Guberman B, Fowler NO, Engel PJ, Gueron M, Allen JM. Cardiac tamponde in medical
patients. Circulation 1981; 64: 633–40.
Krikorian JG, Hancock EW. Pericardiocentesis. Am J Med 1978: 65: 808–14.
239
240
A P PEN D I X A : I N T R AV EN O U S C A R D I AC D RU G REG I M EN S
Abciximab During PCI for Major and minor Half-life = 10 min IV or intracoronary bolus Thrombocytopenia occurs
ACS bleeding. but effect on 250 (g/kg followed by in 0.4–1% of patients and
Thrombocytopenia platelets up to infusion of 0.125 (g/kg/h improves within 5–10 days.
48 hours for 12 hours Readministration within 30
days is associated with a
higher risk of
thrombocytopenia (4%)
Adenosine Narrow complex Flushing, chest Half-life = 10–30 s. Initially 6 mg through a Dipyridamole potentiates
tachycardia (SVT) pain, headache, Rapidly metabolized large central or peripheral the effect of adenosine.
dyspnoea, by erythrocytes and vein followed by a flush of Methylxanthines
bronchospasm, endothelial cells 10 mL saline. If necessary (theophylline, caffeine)
nausea, excess a further 3 doses each of competitively antagonize
sinus or AV node 12 mg can be administered the adenosine receptors
inhibition every 1–2 min and therefore higher doses
(bradycardia) may be needed.
Contraindications:
asthmatics, second or third
degree AV block and sick
sinus syndrome
Adrenaline Cardiac arrest Tachycardia, Half-life = 2 min Cardiac arrest: IV = 1 mg Cautions: ischaemic heart
(epinephrine) Anaphylaxis arrhythmias, 1- and 2-receptor (10 mL of 1:10000 or 1 mL of disease, diabetes mellitus,
Inotropic support hypertension, agonist, high-dose 1:1000). Repeat as per hyperthyroidism and
hypokalaemia, -adrenergic resuscitation guidelines hypertension
hyperglycaemia, vasoconstrictive Anaphylaxis: initially,
headache, anxiety, effect IM = 0.5 mg (0.5 mL of
tremor, sweating 1:1000). Repeat after 5 min
in the absence of clinical
improvement. In some cases
several doses may be
needed. In severely ill
patients with circulatory
collapse, give IV 500 (g
(5 mL of 1 in 10 000) at a rate
of 100 (g/min with ECG
monitoring. Also give
chlorpheniramine 10–20 mg
IM/IV and hydrocortisone
100–500 mg IM/IV Inotropic
support: 5 mL of 1:1000 in
45 mL of 5% dextrose or
normal saline (this gives a
concentration of 100 (g/
mL). The usual infusion
dose ranges between
0.01 and 0.5 (g/kg/min.
Higher infusion doses
are acceptable
depending on the clinical
condition
241
242
Appendix A: (Contd)
Alteplase STEMI Minor and major Half-life = 4 min. MI: given as an accelerated At present, few absolute
(Actilyse, Pulmonary haemorrhages, Metabolized by the regimen: IV 15 mg bolus, contraindications as many
rt-PA) embolism (PE) rash, nausea and liver. Binds to followed by 0.75 mg/kg are now relative, which
vomiting fibrin-associated (maximum 35 mg) over needs interpreting within
plasminogen to form 30 min, then 0.5 mg/kg the clinical context. See
plasmin, which in (maximum 35 mg) over section on thrombolysis, in
turn breaks down 60 min. Give heparin IV Chapter 1
fibrinogen and 5000 U before commencing
fibrin rt-PA, followed by 1000 U/h
after completion of the
rt-Pa infusion. Aim for an
aPTT 50–75 s (1.5–2.5 times
control) PE: IV 10 mg over
1–2 min, followed by 90 mg
over 2 h. Maximum
1.5 mg/kg in patients
<65 kg. Give heparin as
mentioned above
Amiodarone Accessory Pulmonary fibrosis, Half-life = 25–110 During cardiac arrest: VF/ Can increase digoxin and
pathway hyper/hypothy days. Hepatic pulseless VT: amiodarone warfarin levels.
tachycardias, roidism, corneal metabolism, lipid 300 mg, made up to 20 mL Contraindications: sinus or
atrial fibrillation, microdeposits, skin soluble with with 5% dextrose (can be AV node disease (unless
atrial flutter photosensitivity extensive given peripherally). A fitted with a pacemaker)
Ventricular and discolouration, distribution in the further dose of 150 mg may iodine sensitivity,
tachyarrhythmias pro-arrhythmic effect body be given for recurrent or pregnancy, breast feeding,
Cardiac arrest (VF) recorded though rare refractory VF/VT, followed thyroid dysfunction
by an infusion of 1 mg/min (relative)
for 6 h and then 0.5 mg/min Administration via a central
to a maximum daily dose of line is preferable to avoid
2 g. Stable tacharrhythmias: thrombophlebitis during
150 mg diluted in 5% prolonged infusions.
dextrose to a volume of However, a large peripheral
20 mL given over 10 min; this line is acceptable in the
can be followed by a further short term until
dose of 150 mg if needed. arrangements can be made
Alternatively, a dose of to place a central line by
300 mg in 100 mL 5% skilled personnel
dextrose over 1 h can be
given. Follow with a
continuous infusion of
900 mg in 5% dextrose over
24 h. Maximum
recommended dose is 1.2 g
in 24 h (European data sheet
recommendation) although
current resuscitation
guidelines advocate that up
to 2 g in 24 h can be used
Atenolol Acute Hypotension, Half-life = 6–9 h. IV 2.5–10 mg at a rate of Acts synergistically with
management of bronchospasm, Excreted by the 1 mg/min digoxin to control atrial
supraventricular negative inotrope kidney, fibrillation.
tachyarrhythmias and chronotrope, cardioselective, not Contraindications: heart
(including atrial peripheral lipid soluble rate less than 60 bpm, PR
fibrillation and ischaemia interval >0.24 s, second or
atrial flutter) ACS third degree AV block,
Angina systolic arterial pressure
Hypertension <100 mmHg,
243
244
Appendix A : ( Contd )
Atropine Bradyarrhythmias Tachycardia, dry Rapidly cleared from IV 0.3–1 mg every 3–5 min Contraindications: angle
sulphate Cardiac arrest mouth, blurred the blood and is to a total of 3 mg or closure glaucoma (pupillary
(asystole) vision (difficulties distributed 0.04 mg/kg body weight. dilation can increase
with visual throughout the During resuscitation IV intraocular pressure),
accommodation), body. Incompletely 3 mg bolus (see myasthenia gravis,
urinary retention, metabolized in the resuscitation guidelines) prostatic enlargement (can
constipation liver and excreted in precipitate urinary
the urine as retention). These effects,
unchanged drug and however, are not relevant
metabolite. A to either the cardiac arrest
half-life of about 4 h situation or immediate
has been reported post-resuscitation care
Bivalirudin Anticoagulation Major and minor Half-life = 25 min. For PCI: IV bolus of Caution in renal failure
during PCI and bleeding Rapid onset of 0.75 mg/kg followed by Monitor ACT
treatment of ACS action with peak infusion of 1.75 mg/kg/h.
concentrations In medical treatment of
15 min after IV ACS: IV bolus of 0.1 mg/kg
bolus. Eliminated followed by infusion of
mainly by renal 0.25 mg/kg/h for up to
excretion 72 hours
Calcium Hyperkalaemia Bradycardias and Transient effects IV 10 mL of the 10% Avoid adding to solutions
chloride 10% Hypocalcaemia arrhythmias solution. Give slowly containing bicarbonate,
or calcium EMD arrest phosphates or sulphates.
gluconate Calcium Use separate IV access
10% antagonist
toxicity
Digoxin Rate control Anorexia, nausea, Half-life = 36 h. For atrial fibrillation, give Reduce dose in elderly and in
atrial fibrillation, confusion, Excreted mainly by 250–500 (g (orally) every renal failure. Hypokalaemia,
atrial flutter vomiting, visual the kidney. Peak 8 h for 24 h, then 125–250 hypomagnesaemia,
Heart failure disturbance. effect may take up (g daily thereafter. A hypercalcaemia, and
Arrhythmias to 2 h. Therapeutic loading dose is not hypothyroidism increase
including concentration 1–2 necessarily required for use myocardial sensitivity to
ventricular ectopy ng/mL (1.3–2.6 in mild heart failure. In digoxin. Cautious
and bigeminy, nmol/L). Toxic range renal impairment, reduce administration in patients
paroxysmal atrial >2.5 ng/mL dose.For urgent loading, with hypertrophic
tachycardia with give IV 0.5–1 mg (diluted in obstructive cardiomyopathy
block, heart block, 50 mL of 5% dextrose or and atrial fibrillation.
idioventricular normal saline) over at Contraindications: patients
rhythm, ventricular least 2 h with Wolff–Parkinson–White
tachycardia syndrome, second or third
degree AV block
245
246
Appendix A: (Contd)
Dobutamine Inotropic support Tachycardias, Half-life = 2.4 min. Given as an IV infusion Central haemodynamic
in cardiogenic arrhythmias, 1-adrenergic between 2.5 and 20 (g/kg/ monitoring recommended.
shock hypertension receptor agonist, min. Can be given Infusion can be given via a
hypokalaemia lesser 2- and peripherally. See Table A.1 peripheral line
-agonist effects for infusion rates according
to body weight
Dopamine Low doses for As for dobutamine Half-life = 5 min. Low 2.5 (g/kg/min for renal Preferable to give via a
renal perfusion doses stimulate renal perfusion. 5–20 (g/kg/min central line, since
Moderate doses dopamine receptors, for inotropic and extravasation from a
for cardiac therefore improving vasoconstrictive effects. peripheral line may cause
inotropic support renal blood flow. See Table A.2 for infusion severe ischaemic injury due
High dose for Moderate doses rates according to body to vasoconstriction
peripheral stimulate weight
vasoconstriction 1-receptors. High
doses stimulate
-receptors
Esmolol As for atenolol As for atenolol, Half-life = 9 min. Give a loading dose of IV Can increase digoxin levels
plus: confusion, Selective 1-receptor 500 (g/kg/min over 1 min and prolong the action of
thrombophlebitis antagonist. Onset of before each titration step. suxamethonium.
and skin necrosis action occurs within Use titration steps of 50, Interactions may occur with
from extravasation 2 min. Following 100, 150 and 200 (g/kg/ warfarin and intravenous
discontinuation, full min over 4 min each, morphine
recovery from stopping at the desired
beta-blockade effects therapeutic effect
occur at 18–30 min.
Metabolized by red
blood cells
Eptifibatide Treatment of Bleeding and major Half-life = 150 min. IV bolus 180 (g/kg Thrombocytopenia occurs
high-risk ACS bleeding Renal elimination followed by infusion at in 0.2–1.2% of patients
Hypotension 2(g/kg/min for up to
72h. Reduce dose if
GFR < 50
Flecainide Acute QRS prolongation, Half-life = 13–19 h. IV 2 mg/kg or maximum Contraindications: sick
termination of pro-arrhythmic, Two-thirds 150 mg over 10–30 min. sinus syndrome, left
atrial fibrillation negatively hepatically Maintenance infusion ventricular dysfunction,
Accessory inotropic,dizziness, metabolized, 1.5 mg/kg/h (in 5% intraventricular conduction
pathway visual disturbances, one-third excreted dextrose or normal saline) delay or AV block, patients
tachycardias ataxia, peripheral unchanged in the for 1 h, subsequently with a history of ACS.
neuropathy, urine reduced to 100–250 (g/ Can increase stimulation
reversible increase kg/h for up to 24 h. threshold in patients with
in liver enzymes Maximum cumulative dose permanent pacemakers,
in first 24 h = 600 mg therefore use with caution.
If QRS complex is
prolonged by 20% from
baseline, reduce dose or
discontinue, until ECG
returns to normal
Fondaparinux Medical Major and minor Half-life = 17-21 2.5 mg subcutaneously od Heparin should be given
treatment of ACS bleeding hours. Peak activity for up to 8 days during PCI to prevent
after 2 h. Renal catheter-related thrombus
elimination
247
248
Appendix A : ( Contd )
Labetalol Blood pressure As for atenolol Half-life = 3–4 h. 50 mg slow IV bolus over As for atenolol
control in High lipid solubility, 1 min, repeat after 5 min if
hypertensive not cardioselective, necessary (maximum
emergencies or -blockade effect, 200 mg). For continuous
acute aortic metabolized by the infusion, commence
dissection liver infusion rate at 15 mg/h
and every 30–60 min up to
160 mg/h. Discontinue
infusion once blood
249
250
Appendix A: (Contd)
Lignocaine Ventricular CNS side effects Effect of a single 50 mg bolus over a few Reduce concentration in
(lidocaine) tachycardia including dizziness, bolus lasts only a minutes. Can be repeated hepatic failure, congestive
Ventricular paraesthesiae, few minutes, then to a maximum of 200 mg. cardiac failure, following
fibrillation drowsiness, half-life = 2 h. Rapid Follow up with an infusion cardiac surgery and shock.
confusion, hepatic metabolism of 4 mg/min for 30 min, Cimetidine and
convulsions and then 2 mg/min for 2 h, beta-blockers can increase
respiratory then 1 mg/min over 24 h blood levels
depression, (500 mg in 500 mL 5%
hypotension, dextrose, gives a
bradycardia concentration of 1 mg/mL)
Magnesium Persistent Nausea, flushing, Excreted by the Arrhythmias: 4 mL of 50% Caution in renal failure and
sulphate ventricular hypotension, kidney magnesium sulphate liver problems
tachyarrhythmias confusion, (8 mmol) in 100 mL of 5% *The evidence to support
Polymorphic weakness, loss of dextrose or normal saline the routine administration
ventricular tendon reflexes, over 15–30 min IV. Repeat of intravenous magnesium
tachycardia arrhythmias once if necessary. MI*: in acute MI is controversial,
8 mmol bolus over 20 min, and therefore the use of
followed by an infusion of magnesium should be
65–72 mmol over 24 h restricted to the treatment
of recurrent ventricular
arrhythmias
Metoprolol As for atenolol As for atenolol Half-life = 3–7 h. IV 2.5 mg over 2–4 min. As for atenolol
Partially lipid May repeat every 5 min up
soluble, to 15 mg
cardioselective,
metabolized by the
liver
Naloxone To reverse Nausea, vomiting, Half-life = 60–90 min; Opioid overdose: 0.8–2mg The duration of action of all
respiratory sweating, therefore, short IV, repeated at intervals of opioids is often greater
depression tachycardias. Can duration of action. 2–3 min to a maximum of than that of naloxone;
induced by precipitate an Onset of action 10mg. For a continuous therefore, additional doses
opioids acute withdrawal within 1–2 min infusion: 2 mg diluted in (or a continuous IV
syndrome and following IV 500mL 5% dextrose or infusion) of naloxone may
non-cardiogenic injection. normal saline (4 (g/mL), be required. The patient
pulmonary Metabolized by the start infusion at 60% of the should be closely observed
oedema in addicts liver initial administered dose following initial reversal
per hour Use with caution in patients
with pre-existing
cardiovascular disease or in
patients receiving
cardiotoxic drugs, since
arrhythmias (VT, VF, atrial
fibrillation) can occur
Noradrenaline To improve blood Hypertension, Half-life = 3 min. Comes as a strong sterile Contraindications:
(nor pressure in headache, Except in the heart, solution (2mg/mL). Make up hypertension, pregnancy,
epinephrine) hypotensive palpitations, its action is a concentration of 80(g/mL patients on monoamine
patients by bradycardia, predominantly on by adding 4mg (2mL oxidase inhibitors. Caution
causing arrhythmias, -receptors solution) to 48mL of 5% in patients with ischaemic
peripheral peripheral dextrose, or 40mg (20 mL heart disease
vasoconstriction ischaemia, solution) to 480 mL 5%
251
252
Appendix A : ( Contd )
Propranolol As for atenolol As for atenolol Half life = 1–6 h. IV 0.5–1 mg every 5 min As for atenolol
Lipid soluble, to a maximum of
non-cardioselective, 0.15–0.2 mg/kg
metabolized by the
liver
Reteplase STEMI Minor and major Half-life = 15min. Reconstitute 10 U in 10 mL At present, few absolute
(Rapilysin, haemorrhages, and Recombinant of the solvent provided contraindications as many
r-PA) hypersensitivity plasminogen (using the filter supplied). are now relative, which
reactions (allergic activator which Give slowly over 2 min. needs interpreting within
reactions) catalyses the cleavage Administer a further 10 U the clinical context. See
of endogenous after 30 min. Give heparin section on thrombolysis, in
plasminogen to IV 5000 U before Chapter 1
generate plasmin. commencing r-PA, followed
Primarily eliminated by 1000 U/h after
by the kidney and to a completion of the second
small extent by the r-PA bolus dose. Aim for an
liver; however, no aPTT 50–75 s (1.5–2.5 times
dose change is control)
required in renal or
hepatic insufficiency
Sodium Prolonged Tissue necrosis if 50 mL of 8.4% (50 mmol/L) Do not administer via an
bicarbonate resuscitation extravasated. by slow intravenous endotracheal tube. Avoid
(pH <7.1 or base Administration can injection adding to solutions
excess � -10) result in the containing calcium chloride
generation of or calcium gluconate. Use
carbon dioxide, separate IV access
which diffuses
rapidly into cells.
This can result in a
paradoxical
intracellular acidosis;
a negative inotropic
effect on ischaemic
myocardium; a high,
osmotically active,
253
254
Appendix A: (Contd)
sodium load to an
already
compromised
circulation and
brain; and a left
shift in the oxygen
dissociation curve,
inhibiting release of
oxygen to the
tissues
Streptokinase STEMI Minor and major Half-life = 30 min. MI: 1.5 million units in At present, few absolute
Pulmonary haemorrhages, Activates 100 mL normal saline over contraindications as many
embolism (PE) hypotension, rash, plasminogen 1 h PE: 250 000 units over are now relative, which
nausea and 30 min, then 100 000 units needs interpreting within
vomiting, allergic every hour for up to 12–72 h. the clinical context. See
reactions including Monitor clotting section on thrombolysis, in
anaphylaxis, fever parameters Chapter 1
Tenecteplase STEMI Minor and major Half-life 20–24 min. Tenecteplase is dosed based This drug is not compatible
(TNKase, haemorrhages, and Derivative of human on weight and is given as a with dextrose, and therefore
TNK-tpa) hypersensitivity tissue plasminogen single-bolus injection over should not be given in the
reactions (allergic activator that binds 5 s (<60 kg = 30 mg, 60–69 kg same intravenous line. Lines
reactions) to fibrin and = 35 mg, 70–79 kg = 40 mg, containing dextrose should
converts 80–89 kg = 45 mg, 90 kg = be flushed before and after
plasminogen to 50 mg). Tenecteplase is administration. At present,
plasmin supplied as a sterile, few absolute
lyophilized powder in a contraindications as many
50-mg vial. Each 50-mg vial are now relative, which
of tenecteplase is packaged needs interpreting within
with one 10-mL vial of the clinical context. See
sterile water for injection,
255
256
Appendix A : ( Contd )
Tirofiban High-risk ACS Major and minor Half-life = 1.8 h. IV infusion of 0.4 (g/kg/ Incidence of
bleeding. Renal excretion min for 30 min followed by thrombocytopenia
Thrombocytopenia infusion of 0.1 (g/kg/min 0.4–1.9%
for 48 h. High-dose bolus
tirofiban is an IV bolus of
25 (g/kg/min over 3 min
followed by 0.15 (g/kg/min
for 18 h. Half infusion dose
if GFR < 30
Verapamil Narrow complex Sinus or AV nodal Half-life = 4–6 h. 5–10 mg over 2 min. A Contraindications:
tachycardia (SVT) inhibition. Liver metabolized. further 5 mg can be given hypotension, bradycardia,
where adenosine Negatively Active metabolite after 5–10 min second and third degree AV
is contraindicated inotropic norverapamil block, sick sinus syndrome,
or has failed cardiogenic shock, cardiac
failure, broad complex
tachycardia
<5 0a
5.1–10 1
10.1–15 2
15.1–20 3
Laboratory values
Na 135–145 mmol/L
K 3.5–5 mmol/L
Cl 95–105 mmol/L
Mg 0.75–1.05 mmol/L
Troponin T <0.05(g/L
Continued
pH 7.35–7.44
O2 saturation 93–98%
H1 36–44 mmol/L
40–75% WCC
20–45% WCC
1–6% WCC
0–1% WCC
aPTT 35–45 s
Left ventricle
Right ventricle
Aortic
Pulmonary artery
Right atrium
PR interval 120–200 ms
Formulae
American College of http://www.acc.org/ Clinical statements, ACC/AHA practice guidelines, links to other online cardiology
Cardiology journals, ECG of the month, echo of the month
British Cardiac Society http://www.bcs.com/ BCS guidelines, meetings, education and training issues
Cardiac angiograms http://www.sbu.ac.uk/,dirt/ Developed by South Bank University and contains normal and abnormal cardiac
and coronary museum/gs-sixth.html#11 angiograms
arteriograms
Cardiac arrhythmias http://www.arrhythmia.net/ Case histories, ECGs, diagnosis and management of various cardiac arrhythmias
Cardiology Compass http://www. A general overview of various cardiology procedures, image bank, links to other
cardiologycompass.com/ online cardiology journals and resources
Cardiosource http://www.cardiosource. Cardiology information resource service for cardiovascular news, clinical trials,
com/ Medline, trial acronyms, journal links (including the American College of
Cardiology journal and Current Journal Review Scan), ACC/AHA practice guidelines
Doctors.net.uk http://www.doctors.net.uk/ General medical information including cardiology forum, presentations, access
to Clinical Medicine by P Kumar and M Clark, Clinical Biochemistry by William
Marshall, Textbook of Paediatrics by Forfar and Arneil, Merck Manual of
Diagnosis and Therapy, NICE and SIGN guidelines, Clinical Risk Management,
TRIP, Hospital Medicine journal and many more useful links
Doctorsworld.com http://www.doctorsworld. General medical news, career information, a library which includes access to
com guidelines, formularies, clinical calculators, Merck’s manual, Gray’s Anatomy,
Emergency Medicine, Travel Medicine and many more
ECG library http://www.mrcppart1. Excellent collection of ECGs
co.uk/ ecgs/ecghome.html
Electronic Medicines http://emc.vhn.net Provides free access to up-to-date, comprehensive and reliable information
Compendium about prescription and over-the-counter medicines available in the UK
Emergency Medicine http://www.ncemi.org/ Extensive resource on the management of acute medical emergencies. From
on the Web e-medicine online textbooks, algorithms, calculators, nomograms, scoring systems,
tables, key journals update, online dictionaries and many other useful links
Medicdirect.co.uk http://www.dr.medicdirect. General medical resource centre. Lectures, slide library, leading edge articles,
co.uk/ main.ihtml prescribers’ journal online, drug update, career advice, clinical guidelines, clinical
tools, clinical calculators and scores, patient information and videos
Medicines and Drug http://www.digri.demon. Excellent collection of links on drug information, from general prescribing to
Information Centre co.uk/ drugs.htm individual properties, adverse reactions and interactions
265
266
Appendix C : ( Contd )
Medscape.com http://www.medscape.com/ General medical resource service with the option of receiving updates in chosen
specialty
North American http://www.naspe.org/ Heart rhythm information and resource for healthcare professionals and the
Society for Pacing and public
Electrophysiology
(NASPE)
Resuscitation Council http://www.resus.org.uk A valuable resource for providing information on resuscitation, which is updated
UK regularly. All new publications by the council are posted on the site together with
details about forthcoming events, courses, membership and, when appropriate,
important statements
The X-ray files http://www.radiology.co. A large collection of radiology cases, tutorials and useful links
uk/xrayfile/xray/index.htm
Chest http://www.chestjournal.org/
Circulation http://circ.ahajournals.org/
Heart http://heart.bmjjournals.com/
Hypertension http://hyper.ahajournals.org/
Lancet http://www.thelancet.com/
Page numbers in bold type refer to tables and boxes; those in italic to figures.
abbreviations vi-viii
lifestyle modification 78
in thrombocytopenia 40
medical therapy, adjunctive 40–53
Actrapid 258
adenosine 240
ACUITY trial 22
antiarrhythmic drug therapy 106
causes 5, 79
in supraventricular arrhythmias 211,
complications 1, 54–65
and tachycardia 122–4
62–3
and CPR 87, 95–8, 99
background 54
AFCAPS trial 50
pericarditis 64–5
thrombolysis 27
60–1
alteplase (rt-PA) 24, 25, 26, 242
definitions 2, 2
guidelines 35, 192
diagnosis 2, 6–17
American Heart Association (AHA)
diet after 78
amiodarone 68, 69, 242–3
epidemiology 1
in atrial tachycardia 120
in-hospital recovery 77
predisposing to bradycardia and
incidence 1
AV block 204
background 17
in ventricular tachycardia 126
269
INDEX
ampicillin 196
percutaneous interventional 158–60
139, 147
aortic syndromes, acute 149–66
angina
aortic valve regurgitation 152
typical/atypical 7
arrhythmia algorithms 95–9
unstable (UA) 6
asystole 98
170, 176
shockable rhythms 95–8
angioplasty
ventricular fibrillation/pulseless
balloon angioplasty 22
ventricular tachycardia 95–8
in cardiogenic shock 59
arrhythmias 104–34
facilitated 30
background 104-6
primary 211
in digoxin toxicity 203–4
rescue angioplasty 29
key points 133
anti-ischaemic agents 70
peri-infarction 65–75
prophylactic 53
background 65
antibiotics
sinus tachycardia 66
198–9
beats 65–6
in pericarditis 222
post-infarction 76–7
anticoagulants 44–5
treatment principles 104
in pericarditis 222
thrombolytic device (PTD) 183
222
in pulmonary embolism 174
antiplatelets
reference ranges 260
duration of 43–4
aspirin 19
oral 18
in acute coronary syndromes 40–1
classifications 149–50
in pericarditis 222
as consequence of non-penetrating
causes 85
diagnosis 153–5
atherosclerosis 3–4
epidemiology 149
risk factors 3–4
pathophysiology 150–1
diagnosis and assessment 108
270
INDEX
treatment 113–14
bleeding risk 40
block
emergencies
treatment 115–16
bradyarrhythmias 127–33, 212, 215
atropine 28
bradycardia, in volatile substance abuse
asystole 98
215, 216
cannabis 216
BRAVE-3 study 46
in sinus bradycardia 70
British Society for Antimicrobial
in transvenous pacing 93
200
bacteria
balloon angioplasty 22
in atrial fibrillation 109
benzodiazepines
calcium channel antagonists, NSTEACS
in transcutaneous pacing 91
calcium channel blockers 49
toxicity 205
calcium gluconate 245
contraindications 48
cardiac arrest 84–7
in phaeochromocytoma 144
cardiac ischaemia 99
pre-existing therapy 53
cardiac rupture 229
271
INDEX
causes 235
in pericarditis 15, 218
definition 234
referred 16
management 236–7
chest x-rays
background 225
in cardiac tamponade 235
236
in infective endocarditis 195
causes 225
in pericardiocentesis 237
consequences 226
chlorpheniramine 27
consequences 231
263
management 232
chronic obstructive pulmonary disease
background 56–8
CLARITY study 42, 43
diagnosis 58
clindamycin 199, 200
management 58–9
clopidogrel 19
risk factors 57
in acute coronary syndromes 41–2, 46,
(ACD-CPR) 101
management 211–12
background 84-7
coccobacilli, gram-negative 190
chest compression 87
Cockcroft and Gault formula 263
cardioversion
multi-slice (MSCT) 17, 153, 154–5
CARE trial 50
angiography (CTPA), in
carvedilol 144
pulmonary embolism 174–5, 176,
catecholamine 209
185
catheterization
conduction disturbances 71–4
aspiration catheters 23
after non-penetrating cardiac trauma
cardiac 59, 70
226
CCS-1 trial 50
after penetrating cardiac trauma 231
chest pain 6
infective endocarditis 189
non-cardiac 14–16
contrast venography 170, 171
272
INDEX
226, 230
dihydropyridine calcium antagonists 49
COX-2 inhibitors 53
dipyrimadole, in AVNRT 115
crack 208–12
110, 113, 116, 122, 208, 211
management 211–12
in tricyclic antidepressant overdose
pharmacology 208–9
208
cytomegalovirus 4
drug abuse
174
individual drugs
dalteparin 33, 37
drug use, intravenous (IVDU) 189, 191,
danaparoid, in thrombocytopenia 40
192, 194
DAVIT trials 49
drug-related cardiac problems 203–17
DEDICATION trial 22
key points 216
defibrillation 89–91, 90
133
(ICD) 64
regimens 240–56
dextropropoxyphene 213
see also substance abuse; and
diabetic retinopathy 27
individual drugs
diamorphine 18
dual antiplatelet therapy (DAPT) 22,
diazepam
Duke criteria, for diagnosis of infective
DIGAMI trials 53
digoxin 245
echocardiography
273
INDEX
transthoracic 195
family screening 101
mitral regurgitation 63
fibrinogen 45
in pericarditis 220
flucloxacillin 196, 200
electrocardiography
gestational hypertension 144–5, 147
226, 227–8
in hypertensive emergencies 142
in NSTEACS 31–2
glycoprotein (Gp) IIb/IIIa inhibitors
in thrombolysis 29
GRACIA-1 trial 29
EMIAT trial 76
gram-negative bacteria 190, 192
endocarditis 210
GUSTO trials 25, 26, 33
bacterial 213–14
enoxaparin 44
haemodynamic pressures and parameters,
enterococci 190
reference ranges 261–2
EPIC trial 45
haemopericardium 230
EPISTENT trial 45
haemoptysis 171, 185
in thrombocytopenia 40
heart block 129–32
ESPRIT study 47
complete (third degree) 71, 74, 75, 131,
EUROPA study 50
132
191
Mobitz type 1 (Wenckebach) 72, 129,
EVA-AMI study 47
132
274
INDEX
129, 132
key points 146–7
197–8
mortality 146
Helicobacter 4
in pregnancy 144–5
after streptokinase 44
specific 142–6
64, 181
142–3, 146, 147
NSTEACS patients 19
hypertensive retinopathy 138, 147
in renal impairment 39
hypokalaemia 51, 205
in myocardial infarction 24
management
in pericarditis 222
in hypovolaemia 59–60
in pulmonary embolism 178, 180–1,
in right ventricular infarction 59–60
182, 185
in thrombolysis 27–8
in thrombocytopenia 40
in substance abuse 209, 214, 215, 216
hirudin 181
impedance plethysmography (IPG) 171
HOPE study 50
infective endocarditis (IE) 188–202
HORIZONS trial 42
acute/sub acute 188
HORIZONS-AMI trial 22
antibiotics 196, 197, 198–9
risks 53
antimicrobial treatment 196–7, 197
hydrocortisone 27
clinical presentation 190–2
hydroxocobalamin 156
definition 188
hypercapnia 173
diagnosis and investigations 192–5
hypercoagulability 168
epidemiology and pathophysiology
hyperglycaemia 52–3
188–90
hyperkalaemia 203
key points 200–1
hypertension
microbiology 190
renovascular 135
risk factors 189
causes 137
INSTEAD trial 159–60
275
INDEX
INTIME-2 trial 26
low molecular weight heparin (LMWH)
intravenous drugs
embolism 176–7
regimens 240–56
lupus anticoagulant 168
ISAR-COOL trial 38
ISAR-REACT 2 study 46
McConnell’s sign 177
ischaemia
MADIT trials 76
cardiac 99
magic mushrooms (psilocybin) 212–13
isoprenaline 249
therapy 52
in transvenous pacing 93
magnetic resonance imaging (MRI)
journals 267
Marfan’s syndrome 150, 158, 164
MDPIT trial 49
Klebsiella 210
dissection 153
metoclopramide 55
labetalol 249–50
metoprolol 48, 49, 251
Lactobacillus 189
Mobitz type 1 (Wenckebach) heart block
background 54
block 72–4, 129, 132
treatment 55–6
mortality
lepirudin 181
cardiovascular disease 84
in thrombocytopenia 40
hypertensive emergencies 146
complications 169
pulmonary embolism (PE) 167
in intravenous pacing 93
musculoskeletal disorders, chest pain 15
in pericardiocentesis 236
MUST trial 76
208
myeloproliferative disorders, platelet
in ventricular fibrillation 98
aggregation in 169
LIMIT-2 study 52
acute inferior 12
LIPID trial 50
anterolateral 10
276
INDEX
classification 3
noradrenaline 209, 251–2
high lateral 11
in pulmonary embolism 179, 185
posterior wall 13
in tricyclic antidepressant overdose
myocardium
oesophageal reflux, chest pain 15
consequences of non-penetrating
ON-TARGET 2 trial 47
trauma 231
oxygen
myoglobin 9–14
in cardiac ischaemia 215
in CPR 88
naloxone 251
in myocardial ischaemia 211
213
in 169
in digoxin toxicity 205
145
permanent, after STEMI 74
in hypertension 211
in resistant ventricular tachycardia 70
NSTEACS patients 19
in Torsades de Pointes 69–70
syndromes (NSTEACS) 2, 2,
Palla’s sign 174
5–6, 9
PAMI-II trial 23
bleeding risk 39
(PAU) 160–1, 164
chest discomfort 6
penicillin 196
chest pain 32
allergy 196, 199, 200
emergency care 19
peptic ulcer disease, chest pain 15
exercise test 33
percutaneous coronary intervention (PCI)
low-risk patients 36
in NSTEACS 35, 36–8
treatment 31–2
benefits over thrombolysis 20–1
(NSTEMI) 2
early discharge after 23
53, 64
in thrombolysis 24
277
INDEX
trauma 231
pulmonary embolectomy 182–3
pericardiocentesis 236–7
pulmonary embolism (PE) 167–87
complications 223
differential diagnosis 173
definition 218
epidemiology 167
diagnosis 219–22
incidence 169
management 222–3
mortality 167
symptoms 218–19
risk factors 168–9
perindopril 50
symptoms 171–2, 185
phentolamine
arrhythmia algorithms 98–9
plaques, atherosclerotic 4, 79
PURSUIT trial 47
plasminogen activators 25
platelets
quinidine, predisposing to
aggregation 169
tachyarrhythmias 204
PLATO trial 43
radiofrequency ablation, in atrial flutter
pleura, chest pain 15
114
complications 169
reference ranges 259–62
potassium 51
renal failure, acute 139, 147
144–5
rescue angioplasty 29
PREMIER study 43
restenosis 22
PRISM studies 46
resuscitation see cardiopulmonary
propranolol 252
resuscitation
195, 199
revascularization strategies in NSTEACS
PROVE-IT trial 51
rheumatic heart disease 189
Pseudomonas 210
rifampicin 196
278
INDEX
heparin after 44
SAVE trial 50
in pulmonary embolism 182
seizures 208
stress testing 101
serotonin 5, 209
stroke risk, in thrombolysis 24–5, 28
complications 169
supraventricular arrhythmias 211, 213
sinus bradycardia 70
211, 214, 215
SMASH trial 57
syndrome 78
narrow/broad-complex 105–6
142, 147
atrioventricular nodal re-entry
(STEMI) 1, 2, 5, 17
supraventricular 205
atrioventricular block 71
Takotsubo (stress) cardiomyopathy 30–1
chest discomfort 6
tamponade see cardiac tamponade
diagnosis 8
TAPAS trial 23
73, 75
theophyllines, in AVNRT 115
pericarditis 64–5
thienopyridines
treatment 2, 19–20
in acute coronary syndromes 19, 41,
STACKENOX trial 44
in primary PCI 22
196
thrombocytopenia 40
statins 50–1, 80
thromboembolic pulmonary disease
STEEPLE trial 44
184–5
stents
thromboembolism 64
streptococci 190
exclusion criteria 26–7
279
INDEX
thrombolysis (continued)
Valsalva manoeuvre 210
failed reperfusion 28
vancomycin 196
haemorrhage 27
Vaughan-Williams drug classification
hypotension 27–8
105–6
inclusion criteria 26
venous thromboembolism 167–9,
mortality 24
185
after 29–30
ventricular arrhythmias 122–7
trials 24–5
ventricular ectopics 204
25–6
95–8, 96, 127
thrombolytic therapy
ventricular septal rupture 61–2
in myocardial infarction 24
ventricular tachyarrhythmias 210, 211,
thromboxane 209
ventricular tachycardia (VT) 76–7, 125
thromboxane A 2 5
monomorphic 69, 96, 124–6
ticagrelor 19, 43
polymorphic 69, 126–7, 128
TIMACS trial 38
pulseless 86, 89, 95–8, 96
in NSTEACS 37
in AVNRT 115
in thrombocytopenia 40
predisposing to bradycardia and AV
TRACE trial 50
in supraventricular arrhythmia
TRANSFER-AMI trial 29
214
overdose 206–8
Virchow’s triad 173, 185 168, 185
management 207–8
vitamin B12 156
TRITON-TIMI 38 study 43
vitamin K 184
troponin(s) 210
volatile substance abuse 214–15
ultrasound
Wells score 177–8, 178
atherosclerotic plaques 4
Westermark sign 174
heroin
treatment 119
195, 196
x-rays see chest x-rays
urokinase 182
xanthopsia 203
280