Normal structure and function:

Blunt cardiac injury

Pathophysiology  Rapid deceleration or direct blow to the precordium → shearing,
compression, abrupt pressure change

Clinical  Arrythmia ranging from asymptomatic (eg, PVCs) to fatal (eg,

spectrum VFib)
 Acute coronary syndrome from coronary dissection or
thrombosis
 Myocardial dysfunction ("myocardial contusion")
 Ruptured valve, septum, or ventricular wall
  Cardiac tamponade

Confirmatory  ECG, cardiac monitoring for 24-48 hours

testing  Echocardiogram; TEE is superior but more invasive so in
hemodynamically stable go for TTE.

Obesity is the greatest risk factor for HTN

Abnormal ECG is followed by observation for approximately 24 hours (eg, risk of fatal
arrhythmias), in addition to cardiac enzyme testing and echocardiography (eg, rule out
tamponade)
Congenital heart disease:

Hypertrophic cardiomyopathy in infants of diabetic mothers

Pathogenesis  Maternal hyperglycemia → fetal hyperglycemia & hyperinsulinemia
 ↑ Glycogen & fat deposition in interventricular septum → dynamic
LVOT obstruction

Clinical  Often asymptomatic

findings  May have respiratory distress and/or hypotension
 Systolic ejection murmur

Imaging  Chest x-ray: cardiomegaly

 Echocardiogram: ↑ thickness of interventricular septum, ↓ LV
chamber size

Treatment  Intravenous fluids & beta blockers to increase LV blood volume

Prognosis  Spontaneous regression by age 1

LVOT = left ventricular outflow tract.

 Coarctation of the aorta
Pathology  Thickening of tunica media of aortic arch
 Can be associated with Turner syndrome or bicuspid aortic valve

Clinical  ↑ BP & strong pulses in upper extremities

features  ↓ BP & weak pulses in lower extremities
 Neonates* (severe narrowing)
o Heart failure (eg, poor feeding, diaphoresis)
o Cardiogenic shock
 Children/adults (mild narrowing)
o Lower extremity claudication
o Palpable pulsations of intercostal vessels (collaterals)
o Secondary hypertension (upper arms)

Complications  Aortic aneurysm, dissection & rupture

 Cerebral aneurysm & subarachnoid hemorrhage

Treatment  Prostaglandin E1 for neonates with severe narrowing

 Surgical repair

*After closure of ductus arteriosus.

BP = blood pressure.

Coarctation of the aorta

Etiology  Congenital
 Acquired (rare) (eg, Takayasu arteritis)

Clinical features  Upper body

o Well developed
o Hypertension (headaches, epistaxis)
 Lower extremities
o Underdeveloped
o Claudication
 Brachial-femoral pulse delay
 Upper & lower extremity blood pressure differential
 Left interscapular systolic (aortic) or continuous (coolaterals)
murmur

Diagnostic  Supine position b/l upper BP measurment and prone b/l lower limbe
studies BP
 ECG: Left ventricular hypertrophy
 Chest x-ray
 o Inferior notching of the 3rd to 8th ribs
o "3" sign due to aortic indentation

 Echocardiography: Diagnostic confirmation

Treatment  Balloon angioplasty ± stent placement

 Surgery
 PDA-dependent congenital heart disease
 Coarctation of the aorta
 D-transposition of the great arteries
 Hypoplastic left heart syndrome
 Total anomalous pulmonary venous connection
 Tricuspid atresia
 Clinical features of Marfan syndrome
Skeletal  Arachnodactyly
 ↓ Upper-to-lower body segment ratio, ↑ arm-to-height ratio
 Pectus deformity, scoliosis, or kyphosis
  Joint hypermobility

Ocular  Ectopia lentis

Cardiovascula  Aortic dilation, regurgitation, or dissection(Usually prior to 40s)

r  Mitral valve prolapse

Pulmonary  Spontaneous pneumothorax from apical blebs

Skin  Recurrent or incisional hernia

 Skin striae

Moderate or large ventricular septal defect

Timeline Pathophysiologic changes
In utero  RV & LV pressures equal
 No significant hemodynamic consequences

Postnatal transition  ↓ PVR, ↑ SVR

 Left-to-right shunting through VSD

Infancy  RV volume overload/dilation

 Pulmonary overcirculation
 LA & LV volume overload/dilation

Late childhood  Pulmonary arterial vascular thickening (↑ PVR)

 Right-to-left shunting through VSD (ie, Eisenmenger
syndrome)
Hypertension:
Secondary causes of hypertension
Condition Clinical clues/features
Renal parenchymal  Elevated serum creatinine
disease  Abnormal urinalysis (proteinuria, red blood cell casts)

Renovascular disease  Severe hypertension with onset after age 55

 Recurrent flash pulmonary edema
 Rise in serum creatinine
 Abdominal bruit

Primary aldosteronism  Spontaneous or easily provoked hypokalemia

Pheochromocytoma  Paroxysmal hypertension with tachycardia

 Pounding headaches, palpitations, diaphoresis

Cushing syndrome  Cushingoid body habitus

 Proximal muscle weakness
 Hyperglycemia

Hypothyroidism  Fatigue, dry skin, cold intolerance

  Constipation, weight gain, bradycardia

Primary  Hypercalcemia that result in increased renin secretion,

hyperparathyroidism sympathetic hyperresponsiveness, and peripheral artery
vasoconstriction.
 Kidney stones
 Neuropsychiatric symptoms

Coarctation of the aorta  Lateralizing hypertension

 Brachial-femoral pulse delay

The risk of hypertension increases with the duration of OC use, due to increase hepatic
anginotensinogen production. Immediate discontinuation is recommedned in women who
develop HTN(5%); OCs shoul not be used in patients with HTN.

Clinical clues to renovascular disease

HTN-related symptoms  Resistant HTN (uncontrolled despite 3-drug regimen)
 Malignant HTN (with end-organ damage)
 Onset of severe HTN (>180/120 mm Hg) after age 55
 Severe HTN with diffuse atherosclerosis
 Recurrent flash pulmonary edema with severe HTN

Supportive evidence Physical examination

 Asymmetric renal size (>1.5 cm)

 Abdominal bruit(systolic-diastolic)

Laboratory results

 Unexplained rise in serum creatinine (>30%) after starting

ACE inhibitors or ARBs

Imaging results

 Unexplained atrophic kidney

 Laboratory evaluation of hypertension
Renal function  Serum electrolytes (Na, K, Ca)
tests  Serum creatinine
 Urinalysis
 Urine albumin/creatinine ratio (optional)
 Endocrine tests  Fasting glucose or hemoglobin A1c
 Lipid profile
 TSH

Cardiac tests  ECG

 Echocardiogram (optional)

Other tests  Complete blood count

 Uric acid (optional)

Isolated systolic hypertension, by increased stiffness or decreased compliance of the arterial

wall. It is associated with an increase in cardiovascular morbidity and mortality, and
management should be similar to that of primary hypertension, with lifestyle modifications and
pharmacologic therapy.

Lifestyle interventions for hypertension

Modification Recommended plan Approximate ↓

systolic BP
(mm Hg)
DASH diet Diet high in fruits & vegetables & low in saturated 11
& total fats
Weight loss Reduction of BMI to <25 kg/m2 6 per 10-kg loss
Aerobic exercise 30 minutes/day for 5+ days/week 7
Dietary sodium <1.5-2.3 g/day (response varies) 5-8
Alcohol ≤2 drinks/day in men, ≤1 drink/day in women 5
limitation
DASH = Dietary Approaches to Stop Hypertension.

Antihypertensives during pregnancy

First line  Beta blockers (labetalol)
 Calcium channel blockers (nifedipine)
 Hydralazine
 Methyldopa

Second line  Clonidine

 Thiazide diuretics

Contraindicate  ACE inhibitors

d  Angiotensin II receptor blockers
 Direct renin inhibitors
 Nitroprusside
  Mineralocorticoid receptor antagonists
(spironolactone)

Fibromuscular dysplasia
Clinical  90% women (in adults)
presentation  Internal carotid artery stenosis
o Recurrent headache
o Pulsatile tinnitus
o Transient ischemic attack
o Stroke
 Renal artery stenosis
o Secondary hypertension
o Flank pain

Physical  Subauricular systolic bruit

examination  Abdominal bruit

Diagnosis  Imaging preferred (eg, duplex US, CT Agiography, MR

Angiograpghy)
 Catheter-based arteriography

Treatment  Antihypertensives (ACE inhibitors or ARBs 1st line)

 PTA
 Surgery (if PTA unsuccessful)

Excessive alcohol intake (ie, >2 drinks/day) and binge drinking (ie, ≥5 drinks in a single sitting)
are associated with increased incidence of hypertension, higher BP, and failure to respond to
appropriate antihypertensive therapy.

Joint National Committee 8 recommendations for treating hypertension

Initiate Rx Goal blood pressure
Age ≥60 ≥150 mm Hg systolic <150/90 mm Hg
BP or
>90 mm Hg diastolic BP
Age <60, ≥140 mm Hg systolic <140/90 mm Hg
BP or
chronic kidney disease, >90 mm Hg diastolic BP

diabetes
Initial treatment Black Thiazide diuretic or CCB,
choice alone or in combination
 (ACEI/ARB, not first-line)
Other ethnicities Thiazide diuretic, ACEI, ARB, or
CCB,
alone or in combination
All ethnicities with ACEI or ARB,
chronic kidney disease alone or in combination with
other drug classes

Hypertension stages
Category & Management Comments
definition
Elevated BP Lifestyle changes Weight loss, exercise, dietary changes
(SBP 120-129; (reduced salt, alcohol in moderation,
DBP <80) DASH diet)
Stage 1 HTN Lifestyle changes An antihypertensive drug is needed if:
(SBP 130-139; ± 1 antihypertensive drug
DBP 80-89)  Comorbid DM, CKD, or ASCVD
OR
 10-year risk of ASCVD >10%

Stage 2 HTN Lifestyle changes A 2-drug combination is recommended if

(SBP ≥140; AND 1-2 antihypertensive BP is ≥20/10 mm Hg above target.
DBP ≥90) drugs However, elderly patients who are at risk
for falls due to orthostatic hypotension
may benefit from single-drug initiation
and gentle titration.

What is the TOC for RAS HTN??

Choice of antihypertensive drug for comorbid conditions
Coronary atherosclerosis  Angina pectoris: beta blocker, CCB
 Post–myocardial infarction: ACE inhibitor or ARB,
beta blocker

Heart failure with  ACE inhibitor or ARB, beta blocker, diuretic, aldosterone
reduced ejection fraction antagonist

Atrial fibrillation  Beta blocker, nondihydropyridine CCB

or flutter
Chronic kidney disease  ACE inhibitor or ARB

Gout  Losartan, other ARB, CCB (avoid diuretics)

Osteoporosis  Thiazide diuretic

 Migraine  Beta blocker, CCB

AAfriacans first line is chlorothiadone except in metabolic syndrome use CCBs

Although most cases of RAS occur in elderly men with diffuse atherosclerotic disease, it can
also occur in patients with a transplanted kidney and is commonly associated with operative
abnormalities (eg, trauma during organ procurement, abnormal suture placement), viral
infection (cytomegalovirus, BK virus), and atherosclerosis of the donor artery. Transplant
RAS typically occurs in the first 2 years after transplantation.
ACE inhibitors or angiotensin receptor blockers are indicated for initial therapy in patients
with renovascular hypertension (due to renal artery stenosis). Renal artery stenting or
surgical revascularization is reserved for patients with resistant hypertension(despite optimal
medical therapy) or recurrent flash pulmonary edema and/or refractory heart failure due to
severe hypertension.

The diagnosis of hypertension must be confirmed by one of the following:

  Ambulatory BP readings, as measured by an automatic device worn continuously by
the patient for 24-48 hours. The device monitors BP at regular intervals (eg, 15-60 min).
 If continuous ambulatory BP monitoring is not available, an acceptable alternative is
home BP monitoring done twice a day (morning and evening) for a week.
 If home BP monitoring is not possible, 3 office readings (preferably by an automated
machine while the patient is alone) at least a week apart are needed.

In contrast, if end-organ damage (eg, left ventricular hypertrophy, retinopathy, nephropathy) is

present or if the patient has a systolic BP ≥180 mm Hg or diastolic BP ≥120 mm Hg, then the
diagnosis of hypertension can be established in the office without additional confirmation, and
therapy should be started quickly.

Patients with severe hypertension or evidence of end-organ damage should be prescribed

antihypertensive therapy immediately.

Coronary heart disease:

Classification of angina
Classic  Typical location (eg, substernal), quality & duration
 Provoked by exercise or emotional stress
 Relieved by rest or nitroglycerin

Atypical  2 of the 3 characteristics of classic angina

Nonanginal  <2 of the 3 characteristics of classic angina

 Treatment of chronic stable angina
Beta blockers  Mtoprolol and atenolol
 First-line therapy
 ↓ Myocardial contractility & heart rate

Nondihydropyridine CCBs (Dialtiazem)  Alternative to beta blocker

 ↓ Myocardial contractility & heart rate

Dihydropyridine CCBs  Added to beta blocker when needed

 Coronary artery vasodilation

 ↓ Afterload by systemic vasodilation

Nitrates  Long-acting added for persistent angina

  ↓ Preload by dilation of capacitance veins

Ranolazine  Alternative therapy for refractory angina

 ↓ Myocardial calcium influx

CCBs = calcium channel blockers.

Mechanism Best for Not for

Type of stress
Exercise ECG  ↑ HR  Patients able  LBBB
test  ↑ BP to reach tHR  Pacemaker
(tHR = 85%  Patients unable to
of 220 − reach tHR
age)

Pharmacologic  Nonselective  LBBB  Reactive airway

stress test with adenosine  Pacemaker disease
adenosine( rega agonist  Patients  Patients on
denoson,  Dilates unable to dipyridamole or
apadenoson) or coronary reach tHR theophylline
dipyridamole arteries  Hoptensive patients
without ↑ HR
or BP

Dobutamine  Β-1 agonist  Reactive  Tachyarrhythmias

stress  ↑ HR ± BP airway
echocardiograp disease
hy  Patients
unable to
reach tHR

BP = blood pressure; HR = heart rate; LBBB = left bundle branch block; tHR = target HR.
 A decreased tracer uptake both at rest and with exercise (fixed defect) indicates likely scar
tissue with decreased perfusion and CAD.
 A decreased tracer uptake with stress but normal uptake at rest (reversible defect) indicates
inducible ischemia and likely CAD.

Vasospastic angina
Pathogenesis  Hyperreactivity of coronary smooth muscle

Clinical  Young patients (age <50)

presentation  Smoking (minimal other CAD risk factors)
 Avoid NSAIDs(prostacyclin) and BBs(vasoidilators)
 Recurrent chest discomfort
o Occurs at rest or during sleep
o Spontaneous resolution <15 minutes

Diagnosis  Ambulatory ECG: ST elevation

 Coronary angiography: No CAD

Treatment  Calcium channel blocker (preventive), Diltiazem

 Sublingual nitroglycerin (abortive)

CAD = coronary artery disease.

Myocardial infarction:
 Relative frequency of selected presenting
symptoms in acute coronary syndrome
Chest pain 80%-85%
Dyspnea 70%-75%
Nausea 40%-55%
Vomiting 15%-20%
Epigastric pain 10%-15%

Women, the elderly, and patients with diabetes in particular are more likely to have atypical
symptoms.
 Comparison of left ventricular and right ventricular MI
Left ventricular MI Right ventricular MI
Clinical  Pulmonary edema  Clear lungs
features  S3 & S4  Marked hypotension

ECG  Ischemic changes  Inferior ischemic changes

findings in anterior, lateral,  ST-segment elevation in V4R
or inferior leads  Bradyarrhythmias(due to SA and AVN
involvment"RCA"

Hemodynami  ↑ LV & RV  ↑ RV preload, ↓ LV preload

c findings preload  ↑ SVR
 ↑ SVR

Management  Fluid restriction  Fluid resuscitation (immediate IV saline

 Preload & bolus)
afterload reduction  Avoid preload reduction; The failing RV
 Reperfusion becomes reliant on hydrostatic pressure to
therapy force blood through the pulmonary
circulation and is highly sensitive to a
reduction in preload; nitrates, diuretics,
and opioids are best avoided because
they reduce RV preload and can
profoundly worsen hypotension.
 Reperfusion therapy
 Transient transvenous pacemaker if
bradycardia or AV block

The underlying mechanism responsible for periinfarction ventricular arrhythmias varies

according to the time elapsed since the onset of MI. Arrhythmias occurring within 10 minutes
of coronary occlusion are known as "immediate" or phase 1a ventricular arrhythmias.
Acute ischemia causes heterogeneity of conduction with areas of marked conduction slowing
and delayed activation, which in turn predisposes to reentrant arrhythmias(eg. Vfeb) is the
mcc of death. On the contrary, "delayed" or phase 1b arrhythmias occur about 10-60
minutes after acute infarction and are thought to result from abnormal automaticity.

General managment:

 Dual antiplatelet therapy (DAPT) with aspirin and P2y12 receptor blockers (eg,
clopidogrel, prasugrel, ticagrelor)
 Beta blockers
 Angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers
 HMG-CoA reductase inhibitors (statins)
 Aldosterone antagonists (eg, spironolactone, eplerenone) in patients with left ventricular
ejection fraction ≤40% who have heart failure symptoms or diabetes mellitus
Inferior wall MI

Left ventricular aneurysm

Etiology  Scar tissue deposition following transmural MI
 Clinical  Several months following MI
presentation  Heart failure & angina
 Ventricular arrhythmia (eg, ventricular tachycardia)
 Systemic embolization (eg, stroke)

Diagnosis  ECG: Persistent(in the same leads of previous MI) ST elevation, deep Q
waves

 Echocardiograph: Thin and dyskinetic myocardial wall

Mechanical complications of acute myocardial infarction

Complication Time Involved Clinical findings Echocardiogram
course coronary findings
artery
Right Acute RCA  Hypotension  Hypokinetic RV
ventricular  Clear lungs
failure  Kussmaul sign

Papillary muscle Acute RCA  Severe  Severe mitral

rupture or pulmonary regurgitation
within edema with flail leaflet
3-5  New
days holosystolic
murmur

Interventricular Acute LAD  Chest pain  Left-to-right

septum rupture or (apical  New ventricular shunt
within septal) or holosystolic  ↑ O2 level from
3-5 RCA murmur RA to RV
days (basal  Biventricular
septal) failure
  Shock

Free wall Within LAD  Chest pain  Pericardial

rupture 5 days*  Shock effusion with
to 2  Distant heart tamponade
weeks sounds

Left ventricular Up to LAD  Subacute heart  Thin &

aneurysm several failure dyskinetic
months  Stable angina myocardial wall

*50% occur within 5 days.

.
 Patients with MI can have paradoxical splitting of S2 due to delayed myocardial relaxation
and delayed closure of the aortic valve.
Whenever inferior wall MI is suspected based on ischemic changes in the inferior ECG leads,
RV involvement should be evaluated using a right-sided precordial ECG, ST-segment
elevation in lead V4R is highly accurate in confirming RVMI.

ACE inhibitors (eg, enalapril, lisinopril), cardioselective beta blockers (eg, metoprolol), and
aldosterone antagonists (eg, spironolactone) improve survival following MI, likely due to
inhibition of neurohormonal-mediated cardiac remodeling.
Aspirin,clopidogrel and heparin before PCI
Management of unstable angina &
 non–ST-segment elevation myocardial infarction
Nitrates  Caution with hypotension (eg, right ventricular
infarction)

Beta blockers  Cardioselective (eg, metoprolol, atenolol)

 Contraindicated in heart failure & bradycardia
 Intravenous for hypertensive patients

Antiplatelet therapy  Aspirin & P2Y12 receptor blocker

(eg, clopidogrel)

Anticoagulation  Unfractionated heparin, enoxaparin, bivalirudin,

or fondaparinux

Statin therapy  High intensity (eg, atorvastatin, rosuvastatin)

Coronary reperfusion  Emergent coronary revascularization (eg,

hemodynamic instability, cardiogenic shock).
 Percutaneous coronary intervention within 24 hr

ACLS:
The most critical factor determining overall patient survival is elapsed time to effective
resuscitation. This includes effective (CPR) (eg, chest compressions), prompt rhythm analysis,
and early defibrillation for patients found to be in a shockable rhythm.

Ventricular fibrillation or pulseless ventricular tachycardia (VT) should be managed with

immediate defibrillation shock. In contrast, patients with symptomatic or sustained
monomorphic VT (unresponsive to antiarrhythmics) hemodynamic instability due to a narrow or
wide QRS complex tachyarrhythmia (eg, atrial fibrillation, atrial flutter, Monomorphic VT with
a pulse) should be managed with synchronized cardioversion. Lidocaine is alternative of
Amidrone.

Immediate defibrillation is indicated in hemodynamically unstable patients with TdP. While

intravenous magnesium is the first-line therapy for stable patients with recurrent episodes of
TdP.

Patients with persistent tachyarrhythmia (narrow- or wide-complex) causing hemodynamic

instability should be managed with immediate synchronized cardioversion.
Carotid:
All patients with carotid artery stenosis should receive medical therapy with antiplatelet agents
and statins. Some evidence suggests benefit of carotid endarterectomy in asymptomatic patients
with high-grade (80%-99%) stenosis. However, asymptomatic patients with lower-grade (<80%)
lesions are managed medically.

Symptomatic carotid stenosis is defined by the occurrence of transient ischemic attack (TIA) or
stroke in the distribution of the affected artery within the previous 6 months. Carotid
endarterectomy (CEA) is recommended for symptomatic patients with high-grade carotid
stenosis (generally 70%-99% for symptomatic lesions) . However, patients with persistently
disabling neurologic deficits, 100% occlusion of the carotid artery, or life expectancy <5 years
are unlikely to benefit.

Carotid artery dissection

Etiology  Trauma; spontaneous occurrence
 Underlying contributors: HTN, smoking, CTD, OCPs

Clinical  Unilateral head & neck pain, transient vision loss

presentation  Ipsilateral partial Horner syndrome
o Ptosis & miosis without anhidrosis as the sympathetic fibers
responsible for facial diaphoresis travel along the external
carotid artery
 Signs of cerebral ischemia (eg, focal weakness)

Diagnosis  Neurovascular imaging (eg, CT angiography)

Treatment  Thrombolysis (if ≤4.5 hr after symptom onset)

 Antiplatelet therapy (eg, aspirin) ± anticoagulation

CTD = connective tissue disease; HTN = hypertension.

Aortic and peripheral artery disease:

 Acute aortic dissection
Clinical  History of HTN, genetic disorder (eg, Marfan syndrome)
presentation  Severe, sharp, tearing chest or back pain
 >20 mm Hg difference in SBP between arms

Diagnosis  ECG: normal or nonspecific ST- & T-wave changes

 Chest x-ray: mediastinal widening
 CT angiography or TEE for definitive diagnosis


Treatment  Pain control (eg, morphine)

 Intravenous beta blockers (eg, esmolol)
 ± Sodium nitroprusside (if SBP >120 mm Hg despite treatment
with BBs)
 Emergent surgical repair for ascending dissection or descending
that result in organ malperfusion

Acute aortic dissection

Clinical features  History of HTN*, Marfan syndrome, cocaine use
 Severe, sharp, tearing chest or back pain
 ± >20 mm Hg variation in SBP between arms

Complications  Stroke (carotid artery)

due to extension  Acute aortic regurgitation (aortic root/valve)
(involved structure)  Horner syndrome (carotid sympathetic plexus)
 Myocardial ischemia/infarction (coronary artery ostia)
 Pericardial effusion/tamponade (pericardium)
 Hemothorax (pleural cavity)
 Renal injury (renal arteries)
 Abdominal pain (mesenteric arteries)
 Lower extremity paraplegia (spinal arteries)

HTN = hypertension; SBP = systolic blood pressure.

*
Strongest overall risk factor.
If hemodynimically stable and no contrast allergy nor elevated creatinine go for CT with
contrast, if unstable TEE

Abdominal aortic aneurysm

Risk factors  Advanced age (eg, >60)
 Smoking, male sex, hypertension
 History of atherosclerosis or CTD

Clinical  Mostly asymptomatic

presentation  Rapid expansion
o Dull abdominal/back pain
o Distal embolization
 Rupture
o Sudden, severe abdominal/back pain ± shock
o Umbilical/flank hematoma

** Complications:
-Distal ischemia
-High-output heart failure, resulting from erosion of the AAA into the vena
cava (ie, aortocaval fistula).
-After AAA repair sigmoid ischemia (1-7%) should be suspected if bloody
diarrhea and left lower quadrant pain and tenderness, fever and leukocytosis
so check sigmoid perfusion after repair.

Rupture Retroperitoneal
 Smoking cessation
 Elective repair for size >5.5 cm (asymptomatic)
 Urgent repair for symptomatic & HD stable patients.
 Emergency repair for symptomatic & HD unstable patients.

CTD = connective tissue disease; HD = hemodynamically.

-Turner: Cardiovascular disease, including bicuspid aortic valve and aortic root dilation, places
patients at an increased risk for aortic dissection; this risk is further increased during pregnancy.
CT angiography for hemodynamically stable patients or transesophageal echocardiography
(likely in the operating room) for unstable, hypotensive patients.

incomplete rupture (ie, tear of the intima ± media), which may result in:

 Creation of a secondary, false lumen similar to aortic dissection

 Creation of an obstructive intimal flap or intramural hematoma that impedes distal blood
flow (pseudocoarctation), resulting in proximal hypertension and distal hypotension
(eg, upper extremity hypertension with diminished femoral pulses)
 Expansion of the adventitia under high-flow pressure, causing compression/stretching of
surrounding structures such as the left recurrent laryngeal nerve (eg, hoarse voice)

CT angiography of the chest is highly sensitive and specific for thoracic aortic injury and is
readily available.
Incomplete rupture should prompt emergent surgical evaluation.

Diagnosis of BTAI can be confirmed via CT angiography for hemodynamically stable patients or
transesophageal echocardiography (likely in the operating room) for unstable patients. Although
hemodynamic support (eg, fluids, blood products) is indicated in hypotensive patients, systolic
blood pressure is generally kept at <100 mm Hg to prevent injury extension and rebleeding
while awaiting emergent operative repair.

Peripheral:
Acute limb ischemia
Etiology  Cardiac/arterial embolus (eg, AF, LV thrombus, IE)
 Arterial thrombosis (eg, PAD)
 Iatrogenic/blunt trauma

Clinical 6 Ps of acute limb ischemia

features
 Pain
 Pallor
 Paresthesia
 Pulselessness
 Poikilothermia (cool extremity)
  Paralysis (late)

Management  ASAP Anticoagulation (eg, heparin)

 Thrombolysis vs surgery
 CT angio or ABI

Ankle-brachial index (ABI)

ABI = SBP of dorsalis pedis or posterior tibial artery ÷ SBP of
brachial artery
≤0.9 Diagnostic of peripheral artery disease
0.91-1.3 Normal
>1.3 Suggests calcified & uncompressible vessels*
*Other testing should be considered.

For diagnosis of PAD we use ABI(gold standard)

Arterial duplex ultrasound can be used to localize the site and severity of vascular obstruction.
However, it is less sensitive and specific than ABI for the initial diagnosis of PAD. It is
generally performed in symptomatic patients with abnormal ABI who are being considered for
interventional procedures.

CS: causes: Long bone fracture and prolonged compression or Reperfusion injury. Dx: Delta
pressure: DBP-Comp pressure if below 30.

Clinical features of compartment syndrome

Common  Pain out of proportion to injury
 Pain ↑ on passive stretch
 Rapidly increasing & tense swelling
 Paresthesia (early)

Uncommon  ↓ Sensation
 Motor weakness (within hours)
 Paralysis (late)
 ↓ Distal pulses (uncommon)

Tx: Urgent fascietomy or observation/ escharatomy if due to cicumfrential burn eschar

 Extremity vascular trauma
Clinical Hard signs
manifestations
 Observed pulsatile bleeding
 Presence of bruit/thrill over injury
 Expanding hematoma
 Signs of distal ischemia

Soft signs

 History of hemorrhage
 Diminished pulses
 Bony injury
 Neurologic abnormality

Evaluation If hard signs or hemodynamic instability

 Surgical exploration

Otherwise

 Injured extremity index; if less than 0.9 do angiography CT or

other
 CT scan or conventional angiography
 Duplex Doppler ultrasonography

Post thrombotic syndrome

Epidemiology  Chronic venous insufficiency following
acute DVT
 Most cases arise within 2 years of
thrombus

Manifestation  Leg edema, fatigue, pain, superficial

s venous dilation, venous stasis ulcers
 Often worse at the end of the day

Treatment  Exercise (eg, ankle flexion, walking)

 Compression (eg, bandages, stockings)

DVT = deep venous thrombosis.

 Chronic venous stasis
Risk factors  Obesity
 Advanced age
 Varicose veins
 History of DVT

Clinical  Leg pain (achy, heavy)

features  Edema
 Venous dilation (varicosities, telangiectasias), erythema due to
hemosiderin
 Dermatitis: erythema, pruritus, scaling, weeping
 Chronic woody induration and fibrosis and brown discoloration
 Microvascular disease, platelet aggregation, and increased expression
of proteolytic enzymes can cause chronic irregular Ulcers
Management  Dx: U/S
 Elevation
 Compression stockings
Femoral artery aneurysm. A pulsatile groin mass below the inguinal ligament is characteristic;
anterior thigh pain is due to the compression of the femoral nerve that runs lateral to the artery.
Femoral artery aneurysm is the second most common peripheral artery aneurysm after popliteal
aneurysm. It may be associated with an abdominal aortic aneurysm.

Retroperitoneal hematoma prsent with hemodynamic instability and ipsilateral flank or back
pain. Diagnosis is confirmed with non-contrast CT scan of abdomen and pelvis or abdominal
ultrasound. Treatment is usually supportive, radial approach has lower complications rate.

Chronic lymphedema
Etiology  Physical disruption of lymphatic drainage
o Lymphadenectomy, radiation
o Malignant obstruction
o Chronic inflammation (eg, recurrent cellulitis)
o Parasitic infection (eg, filariasis)
o Congenital (eg, Turner syndrome)
o Obesity

Clinical  Swelling, heaviness, discomfort

presentation  Early: soft skin, pitting edema
 Late: firm, dry & thickened skin; nonpitting edema

Treatment  Weight loss, limb elevation

 Compression bandages & physiotherapy (eg, lymphatic drainage by

massage).
 Diuretics contraindicated

Chronic lymphedema typically presents with pain, swelling, and heaviness in one or more
extremities. Patients with early disease usually demonstrate soft skin with pitting edema.
However, progressive deposition of subcutaneous collagen and adipose tissue occurs, leading
to later development of firm, thickened skin and nonpitting edema. In advanced cases, the
skin may develop a warty appearance. Inability to lift the skin on the dorsum of the second toe
(positive Stemmer sign) is highly specific for lymphedema.
Vasculitis
Kawasaki disease
 Pathophysiology &  Medium-vessel vasculitis
epidemiology  Usually affects children age <5
 ↑ Incidence in East Asian ethnicity

Diagnostic criteria  Fever ≥5 days plus ≥4 of the following:

o Conjunctivitis: bilateral, nonexudative
o Mucositis: injected/fissured lips or pharynx,
strawberry tongue
o Cervical lymphadenopathy: ≥1 node >1.5 cm
o Rash: perineal erythema & desquamation;
polymorphous, generalized
o Erythema & edema of the hands/feet, periungual
desquamation

Laboratory findings  ↑ Platelets & WBCs; ↓ hemoglobin

 ↑ Acute-phase reactants (eg, C-reactive protein)
 ↑ AST & ALT
 Sterile pyuria
 Echocardiogram at time of diagnosis and on follow up

Treatment  Intravenous immunoglobulin to decrease anerysum

development & aspirin which has no effect on anersyum
but decrease inflammation and infarction

Complications  Coronary artery aneurysms

 Ventricular dysfunction (lymphocytic myocarditis)
 Pericardial effusion

A Prolonged fevers (>14 days), delayed treatment with intravenous immunoglobulin

(IVIG), and age <1 increase the risk for cardiac complications. Most aneurysms regress
over time, and ventricular dysfunction typically improves with IVIG therapy.

Polyarteritis nodosa
Pathophysiolog  Correlation with underlying hepatitis B/C (immune complexes)
y  Fibrinoid necrosis of arterial wall → luminal narrowing &
thrombosis → tissue ischemia
 Internal/external elastic lamina damage → microaneurysm
formation → rupture & bleeding

Clinical  Constitutional: fever, weight loss, malaise
features  Skin: nodules, livedo reticularis, ulcers, purpura
 Renal: hypertension, renal insufficiency, arterial aneurysms
 Nervous: headache, seizures, mononeuritis multiplex
 Gastrointestinal: mesenteric ischemia/infarction
 Musculoskeletal: myalgias, arthritis

Diagnosis  Negative ANCA & ANA

 Angiography: microaneurysms & segmental/distal narrowing
 Tissue biopsy: nongranulomatous transmural inflammation
CT and MRI can reveal aneurysm formation or narrowing of the arterial lumen.
The diagnosis is made based on clinical features.
 Henoch-Schönlein purpura (IgA vasculitis)
Pathogenesis  Perivenular leukocytoclastic (neutrophils & monocytes) vasculitis
 Deposition of IgA, C3 & fibrin in small vessels

Clinical  Classic findings*:

manifestations o Palpable purpura/petechiae on lower extremities
o Arthritis/arthralgia
o Abdominal pain, intussusception"usually confined to the small
bowel (ileoileal) that do not reduce spontaneously often require
surgical management"
o Renal disease (similar to IgA nephropathy)
o
 Other findings: scrotal pain & swelling

Laboratory  Normal platelet count & coagulation studies

findings  Normal to ↑ creatinine
 Hematuria ± RBC casts &/or proteinuria
 Management  Supportive care (hydration & NSAIDs) for most patients
 Hospitalization & systemic glucocorticoids for severe symptoms that
not responding to analgesics or terminal renal failure

*Clinical diagnosis requires purpuric rash plus ≥2 additional classic findings.

Renal disease in HSP may not be initially evident, as in this patient with a normal urinalysis, but
it can develop months after symptom onset. Serial screening urinalyses should be performed
in HSP.
Giant cell arteritis: clinical manifestations
Systemic  Fever, fatigue, malaise, weight loss
symptoms
Localized  Headaches: located in temporal areas
symptoms  Jaw claudication: most specific symptom of GCA
 PMR
 Arm claudication: associated bruits in subclavian or axillary
areas
 Aortic wall thickening or aneurysms
 CNS: TIAs/stroke, vertigo, hearing loss

Visual  Amaurosis fugax: transient vision field defect progressing to

symptoms monocular blindness
 AION: most common ocular manifestation, pale, edematous
disc with blurred margins.

Laboratory  Normochromic anemia

results  Elevated ESR & CRP
 Temporal artery biopsy

Treatment  PMR only: low-dose oral glucocorticoids (eg, prednisone 10-

20 mg daily)
 GCA: intermediate- to high-dose oral glucocorticoids (eg,
prednisone 40-60 mg daily)
 GCA with vision loss: pulse high-dose IV glucocorticoids (eg,
methylprednisolone 1,000 mg daily) for 3 days followed by
intermediate- to high-dose oral glucocorticoids

AION = anterior ischemic optic neuropathy.

Standard initial treatment includes intermediate- to high-dose oral glucocorticoids (eg,

prednisone 40-60 mg daily); patients with early ocular symptoms (eg, amaurosis fugax, vision
blurring) should be admitted to the hospital urgently for pulse-dose parenteral glucocorticoids
(eg, methylprednisolone 500-1,000 mg daily).

Because patients with GCA require long-term (ie, >1-year) glucocorticoid therapy, which itself
carries significant risks, the diagnosis should be confirmed as soon as possible with temporal
artery biopsy. However, to minimize the risk of ION, treatment should be initiated immediately
and should not be delayed while awaiting biopsy results . Biopsy findings remain detectable up
to 30 days after the start of treatment.

***In GCA ,10%-20% of patients, is aortic aneurysm due to large-vessel involvement. Patients
with aortic aneurysm are typically followed with serial imaging studies.

Serum antineutrophil cytoplasmic antibodies (ANCA) should be checked in all patients with
suspected GPA (high sensitivity and specificity). Proteinase 3-ANCA (also known as c-ANCA)
is most commonly positive in GPA; myeloperoxidase-ANCA (or p-ANCA) is sometimes
positive, although it is more commonly positive in other ANCA-associated vasculitis (eg,
microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis [EGPA]). HIV can
increase the chance of false-positive ANCA results and should be ruled out. Patients with a
clinical presentation and ANCA studies consistent with GPA may be initiated on therapy (high-
dose corticosteroids and immunomodulators/cytotoxic agents) prior to confirmatory tissue
biopsy. Biopsy of affected cutaneous, renal, or occasionally lung tissue is preferred for the
diagnosis of GPA. In patients with GPA, nasal mucosal biopsy is associated with a high rate of
false negatives.
So antibodies, treatment then biopsy.

A pathergy test diagnoses Behçet syndrome; it involves obliquely inserting a 20-gauge needle
into the skin and checking the site 24-48 hours later for the development of a >2-mm papule.
Behçet syndrome can cause recurrent genital ulcers but they are usually small, painful, and on
the scrotum. Oral ulcers are also frequently present.

Henoch-Schönlein purpura (IgA vasculitis)

Pathogenesis  Perivenular leukocytoclastic (neutrophils & monocytes) vasculitis
 Deposition of IgA, C3 & fibrin in small vessels

Clinical  Classic findings*:

manifestations o Palpable purpura/petechiae on lower extremities
o Arthritis/arthralgia
o Abdominal pain, intussusception
o Renal disease (similar to IgA nephropathy)
 Other findings: scrotal pain & swelling due to localized vasculitis.
Blood flow to the testicles is normal or increased, and scrotal symptoms
typically self-resolve.

Laboratory  Normal platelet count & coagulation studies

findings  Normal to ↑ creatinine
 Hematuria ± RBC casts &/or proteinuria

Management  Supportive care (hydration & NSAIDs) for most patients

 Hospitalization & systemic glucocorticoids for severe symptoms

*Clinical diagnosis requires purpuric rash plus ≥2 additional classic findings.

NSAIDs = nonsteroidal anti-inflammatory drugs; RBC = red blood cell.

Cutaneous small-vessel vasculitis (ie, leukocytoclastic vasculitis) can be triggered by antibiotics
but presents as painful, raised, nonblanching, petechial or purpuric lesions (ie, palpable purpura).

Valvular heart diseases:

 Benign vs pathologic murmurs
Benign Pathologic
History  Asymptomatic  Infants: poor weight gain,
 Normal growth respiratory distress, difficulty
 No significant family history feeding
 Older children: exertional
fatigue, chest pain, syncope
 Family history of SCD or
CHD

Murmur  Early or midsystolic  Holosystolic or diastolic

characteristics  Musical or vibratory  Harsh
 Grade 1-2 intensity  Grade ≥3 intensity
 Decreases or disappears with
standing & Valsalva  Intensity persists with
maneuver* standing & Valsalva
maneuver

Other  Normal vital signs  Central cyanosis

findings  Normal S1 & S2  Loud, fixed, or single S2
 Symmetric pulses  Weak femoral pulses
 Hepatomegaly

Management  Reassurance  ECG & echocardiography

*Venous hum is a benign murmur exception that increases with standing.

CHD = congenital heart defect; SCD = sudden cardiac death.

 Prosthetic valve dysfunction
Types & causes  Transvalvular regurgitation with biosynthetic (cusp degeneration
or thrombus prevent closure)
 Paravalvular leak with mechanical (annular degeneration, IE)
 Valvular obstruction/stenosis (valve thrombus)

Clinical  New murmur (regurgitant or stenotic)

manifestations  Macroangiopathic hemolytic anemia
 Heart failure symptoms, thromboembolism

Diagnosis  Echocardiography

IE = infective endocarditis.
Tricuspid regurgitation could result from incomplete closure or damage of the valve.
 Valve replacement in aortic stenosis
Severe AS criteria  Aortic jet velocity ≥4.0 m/sec,or
 Mean transvalvular pressure gradient ≥40 mm Hg
 Valve area usually ≤1.0 cm2 but not required

Indications for valve Severe AS & ≥1 of the following:

replacement
 Onset of symptoms (eg, angina, syncope)
 Left ventricular ejection fraction <50%
 Undergoing other cardiac surgery (eg, CABG)

AS = aortic stenosis; CABG = coronary artery bypass grafting.

Antibiotic prophylaxis for secondary prevention

of rheumatic fever
Severity Duration of therapy

following last attack

Uncomplicated rheumatic fever 5 years or until age 21*
With carditis but no valvular disease 10 years or until age 21*
With carditis & valvular disease 10 years or until age 40*
*Whichever duration is longer. Intramuscular penicillin G benzathine every 3-4 weeks is
preferred.

Pulmonic valve stenosis

Etiology  Congenital (usually isolated defect)
 Rarely acquired (eg, carcinoid)

Clinical  Severe: Right-sided heart failure in childhood

presentation  Mild: Symptoms (eg, dyspnea) in early adulthood
 Crescendo-decrescendo murmur (↑ on inspiration)
 Systolic ejection click & widened split of S2
 pulmonic ejection click(high-pitch sound after S1 best heard
during expiration)
 Diagnosis  Echocardiography

Treatment Percutaneous balloon valvulotomy (preferred)

 Surgical repair in some cases



Mitral stenosis in adults

Etiology  Rheumatic heart disease (vast majority of cases)
 Age-related calcification, radiation-induced

Clinical presentation  Exertional dyspnea, orthopnea, PND, hemoptysis

 Pulmonary edema ± right-sided heart failure (eg,
LE edema)
 Atrial fibrillation, ↑ risk for systemic embolization

Diagnosis  Opening snap with middiastolic rumble at the

apex
 Echocardiography: ↑ transmitral flow velocity

Treatment  Percutaneous valvotomy or surgical

repair/replacement

LE = lower extremity; PND = paroxysmal nocturnal dyspnea.

Atrial fibrillation can induce acute decompensated heart failure in the setting of MS because
many patients with MS require the additional left ventricular filling supplied by atrial
contraction (ie, atrial kick at end-diastole) to remain compensated. Atrial fibrillation in the
setting of MS also carries an even higher thrombogenic risk than nonvalvular atrial
fibrillation, and routine anticoagulation with warfarin is indicated regardless of CHA2DS2-Vasc
score.
 Hemodynamic changes in mitral regurgitation
Acute Compensated Decompensated
MR
chronic MR chronic MR
Preload ↑↑ ↑ ↑
Afterload ↓ No change ↑
Contractile function No change No change ↓
Ejection fraction ↑↑ ↑ ↓
Forward stroke volume ↓ No change ↓
MR = mitral regurgitation.
 Surgical indications for severe chronic mitral valve regurgitation
Primary MR  Surgery if LVEF 30%-60% (regardless of symptoms)
 Consider surgery if successful valve repair*(not replacment) is highly
likely:
o Asymptomatic & LVEF >60%
o Symptomatic & LVEF <30%

Secondary MR  Medical management, valve surgery rarely indicated

*When possible, durable valve repair is favored over replacement because replacement
necessitates lifelong anticoagulation & repeat replacement is often needed after ~10 yr.

LVEF = left ventricular ejection fraction; MR = mitral regurgitation.

The 3 most common causes of aortic stenosis in the general population are senile calcific
aortic stenosis, bicuspid aortic valve, and rheumatic heart disease. A bicuspid aortic valve is
the cause of aortic stenosis in the majority of patients age <70.

Uvular pulsation (Müller's sign) may be appreciated with the high-amplitude systolic pulsation
and rapid diastolic collapse that occurs with severe aortic regurgitation.

The most common presentations of PVT include:

 Thromboembolism: left-sided (ie, mitral or aortic) PVT (which embolize to the systemic
circulation) can present as TIA, stroke, myocardial infarction, bowel ischemia, and limb
ischemia; by contrast, right-sided (eg, tricuspid) PVT may cause pulmonary embolism.
 Prosthetic valve dysfunction: usually manifesting as obstruction (stenosis) or, rarely,
regurgitation. Patients may have a new murmur or signs and symptoms of heart failure.

Transthoracic echocardiography can confirm the diagnosis of PVT, assess the degree of
thrombus, and evaluate for prosthetic valve dysfunction. To prevent PVT, patients with
prosthetic valves are kept on antithrombotic therapy. Mechanical prosthetic valves are more
thrombogenic and require anticoagulation. Bioprosthetic valves are less thrombogenic and
typically require only aspirin therapy; however, PVT can still occur.
 Aortic stenosis
Causes  Calcific disease (most common, age >70)
 Congenital bicuspid valve (younger patients)
 Rheumatic heart disease (common worldwide
but rare in developed countries)

Clinical  Dyspnea on exertion, decreased exercise

manifestation tolerance
s  Angina pectoris (severe AS)
 Syncope (severe AS)
 Heart failure (severe AS)

Physical  Crescendo-decrescendo systolic murmur best

examination heard at RUSB with radiation to carotids &
axillae
 Slow-rising (delayed) & weak carotid pulse

Management  Aortic valve replacement for severe AS

causing symptoms or LV systolic dysfunction

AS = aortic stenosis; LV = left ventricular; RUSB = right upper sternal

 border.

Cardiac arrhythmias:
Diastolic and continuous murmurs are usually due to an underlying pathologic cause, and their
presence should prompt further evaluation with a transthoracic echocardiogram. Midsystolic
murmurs in otherwise young, asymptomatic adults are usually benign and do not require further
evaluation.
Pathologic causes include sick sinus syndrome, myocardial ischemia or infarction , obstructiv
e sleep apnea, hypothyroidism, increased intracranial pressure, and medications.
.
 Sick sinus syndrome
Clinical  Elderly patients
features  Bradycardia
o Fatigue, dyspnea, dizziness, syncope
 Bradycardia-tachycardia syndrome
o Atrial arrhythmias (eg, atrial fibrillation)
o Palpitations

ECG findings  Sinus bradycardia

 Sinus pauses (delayed P waves)
 Sinoatrial nodal exit block (dropped P waves)

Treatment  Pacemaker
 +/- Rate-control medication (if tachyarrhythmias)

Digoxin toxicity cause pathognomenic atrial tachycardia (due to aautomacity(Delayed after

depolarization)) and AV block (mainly mobitz 1); if automacity in sinus node it is result in
tachycardia but if in cardiomyocyyes--cause Vtach

**New-onset right bundle branch block can sometimes be seen in pulmonary embolism.
 all patients with AFeb have TSH and T4 and TTE at diagnosis.
Lone AF, is <60 years patients with CHADVASCs 0, don't require anticoagulants

afeb post-CABG is treated with BBs or Amidrone .

Beta blockers (class II antiarrhythmics) dampen sympathetic activity and shorten the QT
interval at rapid heart rates to reduce the risk of syncope and death in patients with congenital
LQTS; this benefit is most prominent with the nonselective beta blockers, propranolol and
nadolol. Implantable cardioverter-defibrillator placement or left cardiac sympathetic
denervation are also appropriate in some high-risk patients.

Causes of QT prolongation
Acquire Electrolyte  Hypocalcemia
d derangements
  Hypokalemia

 Hypomagnesemia

Medication  Antibiotics (eg, macrolides,

induced fluoroquinolones)
 Psychotropics (eg, antipsychotics, TCAs,
SSRIs)
 Opioids (eg, methadone, oxycodone)
 Antiemetics (eg, ondansetron, granisetron)
 Antiarrhythmics (eg, quinidine,
procainamide, flecainide, amiodarone,
sotalol)

Inherite  Jervell & Lange-Nielsen syndrome (autosomal recessive)

d  Romano-Ward syndrome (autosomal dominant)

SSRI = selective serotonin reuptake inhibitors; TCA = tricyclic antidepressants.

Causes of QT prolongation
Acquired  Medications
o Macrolides & fluoroquinolones
o Antiemetics (eg, ondansetron)
o Azoles (eg, fluconazole)
o Antipsychotics, TCAs & methadone
o Class IA antiarrhythmics (eg, quinidine)
o Class III antiarrhythmics (eg, dofetilide)
 Electrolyte abnormalities (eg, ↓ Mg, ↓ K)

Congenital  Romano-Ward syndrome (autosomal dominant)

 Jervell & Lange-Nielson syndrome (autosomal
recessive) due to mutation in delayed rectifiers

TCAs = tricyclic antidepressants.

\
Vtach
Next step in evaluation is to identify the type of SVT with the use of vagal maneuvers (eg,
carotid sinus massage, Valsalva, eyeball pressure) or intravenous adenosine. Adenosine or vagal
maneuvers temporarily slow conduction via the AV node and can aid in diagnosis by unmasking
"hidden" P waves in patients with atrial flutter or atrial tachycardia. They can also cause a
transient AV nodal block and terminate AV node-dependent arrhythmias, including AVNRT and
orthodromic AVRT.

Tobacco and alcohol are reversible risk factors for premature atrial contractions. Beta blockers
are often helpful in symptomatic patients.
The left atrial stretching likely also contributes to atrial fibrosis and some degree of atrial
conduction remodeling.
Comorbidities that encourage atrial fibrillation
Precipitants of  Systemic hypertension*
atrial dilation  Mitral valve dysfunction
&/or  Left ventricular failure
conduction  Coronary artery disease (CAD)
 remodeling  CAD-related factors (eg, DM, smoking)
 Obesity & obstructive sleep apnea
 Chronic hypoxic lung disease (eg, COPD) due to beta agonist
treatment and right atrial HTN
 Atrial septal defect

Triggers of  Hyperthyroidism
increased  Excessive alcohol use
automaticity  Increased sympathetic tone
o Acute illness (eg, sepsis, PE, MI)
o Cardiac surgery
 Sympathomimetic drugs (eg, cocaine)

*Most common predisposing comorbidity. Caffeine dose not.

COPD = chronic obstructive pulmonary disease; DM = diabetes mellitus;

MI = myocardial infarction; PE = pulmonary embolism.
Atrial fibrillation
Pathogenesis  Atrial remodeling due to:
o Age-related myocardial changes(dramatically increase with
Age)
o Atrial enlargement from heart disease (eg, HTN, CAD"both
result in decreased LV output which in result cause LA
enlargment)
 Foci of rapid electrical activity:
o Commonly originate in pulmonary veins
o Alcohol intake & ↑ sympathetic drive may contribute

Clinical  Asymptomatic or palpitations ± dyspnea, fatigue

presentation  Irregularly irregular pulse
 May present with thromboembolic event (eg, stroke)

Diagnosis  ECG shows variable R-R intervals & no P waves

 Continuous ECG often needed for paroxysmal disease (because in the
beggining, only paroxysmal then continuous) then persistant then
permenant. Any Symptomatic patient needs ablation

CAD = coronary artery disease; HTN = hypertension.

Heparin is DOC during pregnancy and warfarin for valvular afeb (regardless of chadvasc score)
Multifocal atrial tachycardia
Etiology  Exacerbation of pulmonary disease (eg, COPD)
 Electrolyte disturbance (eg, hypokalemia)
 Catecholamine surge (eg, sepsis)

Clinical findings  Typically asymptomatic

 Rapid, irregular pulse
  ECG: >3 P-wave forms & atrial rate >100/min

Treatment  Correct underlying disturbance

 AV nodal blockade (eg, verapamil) if persistent

AV = atrioventricular; COPD = chronic obstructive pulmonary disease.

Unlike atrial fibrillation, MAT does not create an increased risk of atrial thrombus formation and
thromboembolism; therefore, anticoagulation is not recommended. Pharmacologic rate control
with calcium channel blockers (eg, verapamil) or cardioselective beta blockers (eg, metoprolol)
is indicated for MAT only when rapid ventricular rate leads to myocardial ischemia or
congestive heart failure or when the arrhythmia persists despite management of the underlying
disturbance. Beta blockers may worsen bronchospasm in patients with exacerbation of COPD
and should be used with caution.
Heart block:
Atrioventricular block
Clinical presentation ECG features Management
First degree Asymptomatic PR interval Observation
prolongation
Mobitz type I Usually asymptomatic Progressive PR Observation
second degree interval lengthening
followed by dropped (rarely PPM
QRS complex placement)
Mobitz type II Fatigue, lightheadedness, Constant PR interval PPM placement
second degree syncope with randomly dropped
QRS complexes
Third degree Fatigue, lightheadedness, Complete dissociation PPM placement
(complete) syncope of P waves & QRS
complexes

PPM = permanent pacemaker.

Second-degree atrioventricular block:

distinguishing features of Mobitz types I & II
Mobitz type I Mobitz type II
Level of block AV node Below AV node
(eg, His bundle)
ECG findings Progressive prolongation of Constant PR interval
PR interval followed by with randomly dropped
dropped QRS complex QRS complexes
QRS complexes Narrow Narrow or wide
Decreased vagal tone Block improves Block worsens
(eg, exercise, atropine)
Increased vagal tone Block worsens Block improves
(eg, carotid massage)
Risk of complete block Low High (indication for PPM)
AV = atrioventricular; PPM = permanent pacemaker.
Heart failure:
In
Studies of patients presenting with acute dyspnea, most patients with dyspnea due to CHF had
plasma BNP levels >400 pg/mL whereas levels <100 pg/mL had a high negative predictive
value for CHF as a cause of dyspnea. Such low values should prompt the search for noncardiac
causes of dyspnea. BNP has high senstevity >90% in contrast for other specific but not
sensetive signs like JVP LL edema ..etc.
Oxygen, IV furosamide, IV Nitroglycerine in addition to serial cardiac biomarkers and
Echocardiogaphy

Noninvasiveventilation is a cardinal in managment.

 Heart failure with preserved left ventricular ejection fraction
Causes  LV diastolic dysfunction: hypertension with concentric LVH,
restrictive cardiomyopathy, hypertrophic cardiomyopathy
 Valvular heart disease: aortic stenosis/regurgitation, mitral
stenosis/regurgitation
 Pericardial disease: constrictive pericarditis, cardiac tamponade
 Systemic disorders (high-output failure): thyrotoxicosis, severe
anemia, large arteriovenous fistula

Management  Control blood pressure & heart rate

 Address concurrent conditions: AF & myocardial ischemia
 Treat volume overload with diuretics
  Exercise training/cardiac rehabilitation

AF = atrial fibrillation; LV = left ventricle; LVH = left ventricular hypertrophy.

Prerenal acute kidney injury (AKI) can occur in volume overloaded states. That occurring in an
acute heart failure exacerbation is most likely due to cardiorenal syndrome, which involves
elevated central venous pressure leading to a reduction in renal perfusion. Decreased renal
perfusion due to reduced cardiac output also plays a role. Diuretics, typically beginning with a
loop diuretic, are first-line therapy for managing volume overload in patients with HF as
manifested by peripheral and/or pulmonary edema. In patients with HF, an elevated
BUN/creatinine ratio should not deter diuretic therapy if clinical evidence of congestion is
present.
For these reasons, PPV has a major mortality benefit (number needed to treat = 13) in
cardiogenic pulmonary edema.

Congestive heart failure (CHF) frequently causes bilateral pulmonary infiltrates on chest x-ray.
In contrast to bacterial or viral pneumonia, which cause prolonged chest x-ray findings, patients
with CHF can have rapid resolution of chest x-ray findings following diuretic administration.

HF exacerbated by NSAIDs because it causes sodium retention

Shock:
 Hemodynamic measurements in shock
Parameter Hypovolemic Cardiogenic Obstructive Distributive
shock shock shock
shock
CVP ↓ ↑ ↑ ↓
(right-sided
preload)
PCWP ↓ ↑ ↓* ↓
(left-sided
preload)
Cardiac index ↓ ↓ ↓ ↑**
(LV output)
SVR ↑ ↑ ↑ ↓
(afterload)
SvO2 ↓ ↓ ↓ ↑**
* Of note, cardiac tamponade causes prepulmonary obstructive shock as blood is unable
to fill the compressed right-sided heart chambers. Despite reduced left-sided preload,
the expected PCWP is paradoxically elevated due to external compression of the left
atrium, a rare exception when left-sided preload and PCWP are discordant.

**Cardiac index & SvO2 are usually decreased in neurogenic shock due to impaired
sympathetic reflexes.

CVP = central venous pressure; LV = left ventricular; PCWP = pulmonary capillary

wedge pressure; SvO2 = mixed venous oxygen saturation; SVR = systemic vascular
resistance.
Crystalloid solution (eg, normal saline, Ringer's lactate) is the fluid of choice to restore volume
quickly as it is as effective as albumin in terms of survival but is less costly and easier to acquire.

Crystalloid should be given as intravenous boluses (500-1000 mL) to improve systolic blood
pressure >90 mm Hg, at which perfusion is considered adequate. This is continued with close
monitoring for evidence of volume overload (eg, pulmonary edema, hypoxia) or until fluid no
longer improves the blood pressure. If the patient fails to respond or develops evidence of
volume overload without improvement in blood pressure, then vasopressors (eg, norepinephrine)
should be started to improve perfusion.
This patient's arterial blood gas is suggestive of a compensated metabolic acidosis (likely lactic
acidosis due to organ hypoperfusion); therefore, it would be reasonable to administer isotonic
saline without concern about worsening the acidosis.

Intravenous hydrocortisone can be used in septic shock but is generally started in patients who
do not respond to volume resuscitation and the initiation of vasopressors.
Myopericardial diseases:

Post–cardiac injury syndrome

Causes  Post–cardiac injury syndrome is a form of acute pericarditis that results
from immune-complex deposition in the pericardium. Causese below,
exposes the immune system to cardiac antigens and typically has a latency
period of several weeks to months.
 Myocardial infarction (ie, Dressler syndrome)
 Cardiac surgery (eg. postpericardiotomy) or trauma
 Percutaneous coronary intervention

Clinical  Latent period of several weeks to months

features  Pleuritic chest pain, fever, leukocytosis, tachypnea, tachycarida, enlarged
cardiac sillhoutte and muffled heart sounds if effusion develop.
 Dx:
 Chest x-ray: pleural effusion ± enlarged cardiac silhouette
 Echocardiography: pericardial effusion

Treatment  Colchicine monotherapy can also be effective in preventing PCIS when

administered following cardiac surgery
 Nonsteroidal anti-inflammatory drugs + colchicine
 Corticosteroids in refractory disease

Prognosis  Usually self-limited disease course

 May cause chronic/recurrent disease leading to constrictive pericarditis

Viral myocarditis
Clinical  Relatively young adults (eg, age <55)
presentatio  Viral prodrome (eg, fever, malaise, myalgias)
n  Heart failure (eg, dyspnea, orthopnea, edema), S3, holosyctolic murmer
due to mitral regurgitation
 Chest pain
 Sudden cardiac death
 Pathogenesis: inadequate immune response to a viral infection allows the
virus to invade cardiac myocytes, leading to cytotoxicity and impaired
 contractile function

Diagnosis  ECG: nonspecific

 Echocardiography: 4-chamber dilation
 Cardiac MRI: late enhancement of the epicardium
 Biopsy(Gold standards): lymphocytic infiltration, viral DNA or RNA

Treatment  Medication (eg, diuretics, ACE inhibitor, beta blocker)

 (eg, diuretics, inotropes) is typically initiated based on clinical suspicion.
In addition, patients should be monitored in the intensive care unit due to
risk of shock and fatal arrhythmias.
 Temporary ventricular assist device, if needed
 Heart transplant if no recovery

Viral myocarditis
Etiology  Coxsackievirus B, adenovirus

Clinical  Viral prodrome

features  Heart failure: respiratory distress, murmur, hepatomegaly

Diagnosis  Chest x-ray: cardiomegaly, pulmonary edema

 ECG: sinus tachycardia
 Echocardiogram: decreased ejection fraction
 Biopsy (gold standard): inflammation, necrosis

Treatment  Supportive (eg, diuretics, inotropes)

 Intravenous immunoglobulin
Rheumatic fever:
Echocardiography is part of the evaluation for acute rheumatic fever

Acute rheumatic fever

 Epidemiology  Peak incidence: age 5-15
 Twice as common in girls

Clinical Major  Joints (migratory arthritis)

features  ♥ (Carditis)
 Nodules (subcutaneous)
 Erythema marginatum

 Sydenham chorea

Minor  Fever
 Arthralgias
 Elevated ESR/CRP
 Prolonged PR interval

Late sequelae Mitral regurgitation/stenosis

Prevention Penicillin for group A streptococcal
(Streptococcus pyogenes) pharyngitis
CRP = C-reactive protein; ESR = erythrocyte sedimentation rate.

Sydenham chorea
 Pathophysiology  Preceding GAS infection
 Molecular mimicry between anti-GAS antibodies & neuronal
antigens in basal ganglia

Clinical features  Involuntary, jerky movements (worse while awake & with action)
 Hypotonia
 Emotional lability (ie, inappropriate laughing), obsessive-compulsive
behaviors
 ± Symptoms of acute rheumatic fever
 Poor execution of motor tasks due to hypotonia and intrusion of
choreic movements, which can result in intermittently weakened hand
grip (ie, milkmaid grip)
 Tics (eg, repetitive throat clearing)

Evaluation  GAS testing: throat culture, ASO & anti-DNAse B titers

 Cardiac testing: echocardiography, ECG

Treatment  Chronic antibiotics (eg, penicillin G)

 Symptomatic (antidopaminergics [eg, haloperidol])

Prognosis  Spontaneous remission

 Recurrence common
 ↑ Risk of rheumatic heart disease

anti-DNAse = antideoxyribonuclease; ASO = antistreptolysin O; GAS = group A Streptococcus.

Pharyngitis due to Streptococcus pyogenes (group A Streptococcus) is often self-resolving, as

seen in this patient. However, a 10-day course of oral penicillin is recommended to prevent
ARF. In addition, ARF can recur with increasing severity after successive group A streptococcal
infections. Therefore, patients with ARF should receive prophylactic long-acting, intramuscular
benzathine penicillin G for several years. This treatment is meant to eradicate bacterial
carriage to prevent recurrent ARF and worsening rheumatic heart disease.

Culture-positive infective endocarditis

 Staphylococcus aureus  Prosthetic valves
 Intravascular catheters
 Implanted devices (eg, pacemaker/defibrillator)
 Intravenous drug users

Viridans streptococci  Gingival manipulation

 Respiratory tract incision or biopsy

Staphylococcus epidermidis  Prosthetic valves

 Intravascular catheters

 Implanted devices

Enterococci  Nosocomial urinary tract infections

Streptococcus gallolyticus  Colon carcinoma

(formerly S bovis)  Inflammatory bowel disease

Fungi  Immunocompromised host

(eg, Candida)  Intravascular catheters
 Prolonged antibiotic therapy

Staphylococcal infection is the most common cause of healthcare-associated infective

endocarditis (IE); streptococcal infection is a common cause of community-acquired IE.

Infective endocarditis:
Infective endocarditis
Risk factors  Congenital heart disease or prosthetic valve
 Previous endocarditis
 Intravascular catheters
 Intravenous drug use

Physical  New regurgitant murmur

examination  Skin: Janeway lesions, Osler nodes
 Roth spots (eyes), splinter hemorrhages (nails)
 Splenomegaly
 ± Signs of embolic phenomenon

Diagnostic testing  Hematuria/proteinuria (glomerulonephritis)

 Positive blood cultures
 TEE > TTE for detecting vegetation

Treatment  Acute: Empiric treatment with vancomycin

  Subacute: Treatment based on culture results (ceftrixone,
pencillin)

TEE = transesophageal echocardiogram; TTE = transthoracic echocardiogram.

Blood culture then Echo

Vascular & immunologic manifestations of infective endocarditis

Vascular phenomena  Systemic emboli (cerebral, pulmonary, or splenic infarctions)
 Mycotic aneurysm
 Janeway lesions: macular, erythematous, nontender lesions on
the palms & soles

Immunologic  Osler nodes: painful, violaceous nodules seen on the fingertips

phenomena & toes
 Roth spots: edematous & hemorrhagic lesions of the retina

Mitral valve disease, usually mitral valve prolapse with coexisting mitral regurgitation, is the
most common valvular abnormality detected in patients with infective endocarditis.

Infective endocarditis—modified Duke criteria

Diagnostic criteria for IE Major criteria

 Blood culture positive for typical microorganism

(eg, Staphylococcus
aureus, Enterococcus, viridans streptococci)

 Echocardiogram showing valvular vegetation

Minor criteria

 Predisposing cardiac lesion

 Intravenous drug use

 Temperature >38 C (100.4 F)
 Embolic phenomena
 Immunologic phenomena (eg, glomerulonephritis)
 Positive blood culture not meeting above criteria

Definite IE

 2 major OR 1 major + 3 minor criteria

 Possible IE

 1 major + 1 minor OR 3 minor criteria

Clinical findings  Fever (>90%)

(frequency)  Heart murmur (85%)
 Petechiae (≤50%)
 Subungual splinter hemorrhages (<50%)
 Osler nodes, Janeway lesions (<50%)
 Neurologic phenomena (embolic) (≤40%)
 Splenomegaly (≤30%)
 Roth spots (retinal hemorrhage) (<5%)

IE = infective endocarditis.

The most appropriate next step is to obtain serial blood cultures. It is recommended that a
minimum of 3 blood cultures be obtained from separate venipuncture sites (not from a vascular
catheter) over a specified period prior to initiating antibiotic therapy to improve
microbiological yield and ensure the causative organism is identified (as this will determine
appropriate antibiotic management). In patients with acute illness, all 3 blood cultures should be
obtained over a 1-hour period before beginning empiric antibiotic therapy. Patients with stable
subacute illness (eg, general malaise with no fever) should have blood cultures obtained over
several hours, and antibiotic therapy can be delayed until the blood culture results become
available.

Transthoracic or transesophageal echocardiogram is recommended in suspected IE to assess for

the presence of vegetations and other complications (eg, valve perforation, perivalvular
abscess). However, blood cultures should be drawn before cardiac imaging studies are obtained

To confirm the diagnosis using the modified Duke criteria, blood cultures should be obtained (to
identify the causative microbe), followed by echocardiography (to identify the vegetation) if
blood cultures are positive.

Overall, the risk of IE following dental procedures in patients with acquired valvular defects due
to rheumatic fever is low, and antibiotic prophylaxis is not indicated. However, prophylaxis is
indicated in patients with a history of IE.

Streptococcus pneumoniae is a rare cause of IE. When it does occur, it typically involves the
aortic valve and has an acute presentation following an episode of pneumonia.

Ampicillin-sulbactam is generally not recommended for empiric therapy in patients with

suspected or diagnosed IE. However, it is recommended for penicillin-resistant enterococcus
and HACEK organisms once culture sensitivity results are available. Clindamycin is
occasionally used for the treatment of cellulitis due to methicillin-resistant S aureus (MRSA)
infection and also for prophylaxis against IE in high-risk patients undergoing invasive dental
procedures.

Aqueous penicillin G is the drug of choice in patients with native-valve IE due to penicillin-
susceptible Viridans streptococci.

Infective endocarditis with intravenous drug use

Pathogenesis  Injected particles cause microdamage to right-sided
valves before being filtered out by the lungs
 Microdamage facilitates bacterial attachment
 Increased risk with HIV

Clinical  Tricuspid valve most commonly affected

features  Staphylococcus aureus is the most common organism
 Septic pulmonary emboli present in up to 75% of cases
 Audible murmur may be absent in 50% of cases
 Few peripheral manifestations
(eg, splinter hemorrhages, Janeway lesions)
 Heart failure uncommon
 Common surgical indications in infectious endocarditis
 Acute heart failure (eg, aortic/mitral valve regurgitation)
 Extension of infection (eg, abscess, fistula, heart block)
 Difficult-to-eradicate organism (eg, fungus, MDR pathogen)
 Persistent bacteremia on antibiotics
 Large vegetation/persistent septic emboli
 Very high risk of embolism (eg, large valvular vegetation [>1 cm]) or persistent septic
embolization despite appropriate antibiotic therapy

MDR = multidrug-resistant.
Heart failure is the most common cause of death in patients with IE and most commonly occurs
with infection of the aortic or mitral valves

Pericardium
Acute pericarditis
Etiology  Viral (coxsackie B virus ) or idiopathic
 Autoimmune disease (eg, SLE,RA)
 Uremia (acute or chronic renal failure): no usual ECG changes because
inflammatory cells do not pentrate the myocardium, Tx: Hemodialysis (if
not responding , give NSAIDs or colchicine), but anticoagulants are CI
because of risk of hemorrhage, bcz of >50% have pericardial effusion, all
patients should undergo assessment of cardiac tamponade before dialysis
 Post myocardial infarction
 o Early: peri-infarction pericarditis(decrease the risk by early
reperfusion (<3hrs) to minimize the risk of necrosis and PIP,
occura <4 days; patients should undergo Echocardiogram )
o Late: Dressler syndrome (fever , pericarditis , pleuritis )

Clinical  Pleuritic chest pain (↓ when sitting up) that cause reffered pain to
features trapezius ridges(lower aspect of scapula) ± fever, leukocytosis,
&  Pericardial friction rub (highly specific) Triphasic: atrial, ventricular
diagnosis systole and ventricular diastole

 ECG: diffuse ST-segment elevation & PR-segment depression that

evolves to diffuse T wave inversion
 Echocardiography: pericardial effusion

Treatment  NSAIDs & colchicine "colchicine lowers the rate of recurrent

pericarditis" for viral or idiopathic etiology
 Corticosteroids are 2nd line
 Variable for other etiologie
 Avoids NSAIDs and steroids in periinfarction pericarditis because it
delayes healing.(supportive only or Aspirin)

NSAIDs = nonsteroidal anti-inflammatory drugs; SLE = systemic lupus erythematosus.

Echocardiography confirms the diagnosis and typically shows increased pericardial thickness,
abnormal septal motion, and biatrial enlargement. Diuretics can provide temporary relief, and
pericardiectomy is the definitive treatment for patients with refractory symptoms.

Cardiac Tamponade, Bottle shaped with clear lung fields.

Physical examination findings of effusion without cardiac tamponade include diminished heart
sounds on auscultation and a maximal apical impulse that is difficult to palpate.

Characteristics of cardiac tamponade

Rapidity of fluid Acute Subacute
accumulation Minutes to hours Days to weeks
Clinical signs Beck triad: hypotension, JVD, muffled heart sounds

Pulsus paradoxus (>10 mm Hg decrease in SBP with

inspiration)
Effusion volume 100-200 mL 1-2 L
Chest x-ray findings Normal cardiac Enlarged, globular cardiac
 silhouette silhouette

Cardiac tamponade
Etiology  Blood in pericardial space (eg, LV rupture, cardiac surgery)
 Pericardial effusion (eg, malignancy, infection, uremia)

Clinical  Beck triad: hypotension, JVD, ↓ heart sounds

signs  Pulsus paradoxus: SBP ↓ 10 mm Hg during inspiration

Diagnosis  ECG: low-voltage QRS complex, electrical alternans

 Chest x-ray: enlarged cardiac silhouette,* clear lungs

 Echocardiography: right atrial & ventricular collapse, IVC plethora

Treatment  Intravenous fluids to increase right-sided preload

 Drainage via pericardiocentesis or pericardial window

*Subacute but not acute tamponade.

Malignant pericardial effusion

Etiology  Common primary tumors: lung, breast, GI tract, lymphoma,
melanoma
  May be initial manifestation of malignancy or recurrence

Clinical  Progressive dyspnea, chest fullness, fatigue

features  ECG: ↓ QRS voltage ± electrical alternans
 CXR: enlarged cardiac silhouette & clear lung fields
 Echo: large effusion ± signs of tamponade (eg, right atrial collapse)

Treatmen  Acute management: pericardiocentesis, cytologic fluid analysis

t  Prevention of recurrence: prolonged drainage (eg, catheter,
pericardial window)

CXR = chest x-ray; echo = echocardiography; GI = gastrointestinal.

Cardiomyopathies:

Hypertrophic cardiomyopathy (HCM) is characterized by a systolic ejection murmur without

radiation to the carotids, and African American patients are most commonly affected.

Hypertrophic cardiomyopathy
Pathophysiology  Mutations in sarcomere protein genes (most
common)
 Autosomal dominant
 Variable expressivity/penetrance

Clinical features  Asymptomatic or identified by family screening

 Fatigue, chest pain, palpitations, syncope
 SEM exacerbated by dehydration/impaired LV filling

Diagnostic  ECG: LVH, repolarization abnormalities

evaluation  TTE: LVH, ↑LVOT gradient, SAM of mitral valve
 Exercise testing
 Family screening

Management  Avoidance of volume depletion

 BBs(atenolol/metoprolol)/CCBs or disopyramide
 Surgery if symptoms persist

Complications  Sudden cardiac death

 Heart failure
  Stroke

; SEM = systolic ejection murmur;

Effect of maneuvers on hypertrophic cardiomyopathy

Physiologic effect Left ventricular Murmur intensity
blood volume
Valsalva ↓ Preload ↓ ↑
(strain phase)
Abrupt
standing
Nitroglycerin
administration
Sustained ↑ Afterload ↑ ↓
hand grip
Squatting ↑ Afterload &
preload
Passive ↑ Preload
leg raise
(macrocytic anemia [MCV >100 µm3], thrombocytopenia, >2:1 ratio of AST, ALT).

Alcoholic cardiomyopathy is a diagnosis of exclusion in patients with dilated cardiomyopathy

and history of alcohol abuse in whom no other potential causes of cardiomyopathy (eg, coronary
artery disease, valvular heart disease) are suspected or identified. The degree of LV dysfunction
in alcoholic cardiomyopathy is directly related to the daily amount and overall duration of
alcohol intake. The primary therapy for such patients is complete abstinence from alcohol use;
this intervention is associated with improvement or normalization of LV function over time.

Stress-induced (takotsubo) cardiomyopathy

Risk factors  Postmenopausal woman
 Recent physical or emotional stressor

Clinical  Pathogenesis: may be microvascular spasm with consequent ischemia

features and myocardial stunning that leads to impaired contraction.
 Chest pain mimicking myocardial infarction
 Decompensated heart failure
 Moderate troponin elevation
 ECG: ischemic changes in precordial leads

Diagnosis  Catheterization: no obstructive CAD

  Echo: LV apical hypokinesis, basilar hyperkinesis

Treatment  Resolves in several weeks with supportive care

CAD = coronary artery disease; LV = left ventricular.

Miscellaneous:
Immune-mediated reactions are responsible for a variety of drug-induced conditions such as
membranous glomerulonephritis induced by captopril.

Holt-Oram (heart-hand) syndrome is associated with both ASD and upper-limb bone deformities
(eg, radius, carpals).

Syncope in HOCM is often multifactorial and can be due to outflow obstruction, arrhythmia,
ischemia, and a ventricular baroreceptor response that inappropriately causes vasodilation

Pulsus pardoxus in COPD and asthma is due to increased capicitance of the lung vasculature and
the restriction of heart due to compression from lung. PP is canceled in Aortic regurgitation.

Pulsus bisferiens (or biphasic pulse) refers to 2 strong systolic peaks of the aortic pulse from left
ventricular ejection separated by a midsystolic dip. It can be palpated in patients with significant
aortic regurgitation (with or without aortic stenosis), hypertrophic obstructive cardiomyopathy,
and, occasionally, large patent ductus arteriosus.

Infiltration of noncaseating granulomas leads to surrounding inflammation and can result in

conduction defects (complete AV block is most common), restrictive cardiomyopathy (early
manifestation), dilated cardiomyopathy (late manifestation), valvular dysfunction, and heart
failure. Sudden cardiac death can occur due to complete AV block or ventricular arrhythmia.

Upright tilt table testing is occasionally used to establish the diagnosis of vasovagal syncope in
patients with recurrent unexplained syncope in the absence of organic heart disease

We use CO2 in laproscope.

Peritoneal stretch receptorssense the increase in intraabdominal pressure and respond by

triggeringincreased vagal tone. Close monitoring is required as patients may develop severe
bradycardia, atrioventricular block, and sometimes asystole. The increased intraabdominal
pressure can also cause a mechanical increase in systemic vascular resistance leading to
elevations in blood pressure.
 Seizure Syncope
Preceding Aura (eg, smell, visual disturbance) Prodrome (eg, nausea, diaphoresis) or
symptoms or none none
Patient position Any position Often standing (vasovagal), but can
occur in any position (cardiogenic)
Tongue biting Common, often lateral Rare, frontal if present
Convulsive Common, typically start before or Less common but can occur after
movements simultaneous with LOC LOC*
Urinary Common Less common but can occur after
incontinence LOC*
Post-episode Variable (minutes to hours or days), Rapid (1-2 minutes), no residual
recovery residual confusion is common deficit
LOC = loss of consciousness.

*Due to transient cerebral hypoperfusion and hypoxia.

Clues to etiology of syncope

Vasovagal  Trigger (eg, emotional stress, prolonged standing)
 Prodrome (eg, nausea, sweating, warmth)

Carotid  Tactile stimulation of carotid sinus while standing

hypersensitivit
y
Autonomic  Orthostasis
dysfunction  Predisposing disease (eg, DM, Parkinson)

Hypovolemia  Orthostasis

 History consistent with volume loss

LV outflow  Syncope with exertion

obstruction  Systolic murmur

Ventricular  No warning symptoms

tachycardia  Cardiomyopathy or ischemic HD (monomorphic)
 QT interval prolongation (polymorphic)

Conduction  Preceding fatigue or lightheadedness

impairment*  ECG abnormalities (eg, sinus pauses, dropped QRS)

*Sick sinus syndrome or advanced atrioventricular block.

 Vasovagal syncope
Clinical  Pathogenesis: Vagal cause sinus bradycardia with sinus arrest
presentation  Inciting event (eg, stress, prolonged standing)
 Prodrome (eg, pallor, nausea, diaphoresis)
 Consciousness regained rapidly (eg, <1 minute)
 Situational syncope is a form of vasovagal (neurally mediated) syncope
associated with specific triggers (eg, micturition, defecation, cough).
These triggers cause an alteration in the autonomic response and can
precipitate a predominant cardioinhibitory, vasodepressor, or mixed
response.

Diagnosis  Mainly clinical diagnosis

 Upright tilt table testing in uncertain cases

Treatment  Reassurance
 Avoidance of triggers
 Counterpressure techniques for recurrent episodes

Cardiogenic syncope
Etiology Clues to diagnosis
Aortic stenosis or HCM  Exertional syncope
 Systolic murmur on examination

Ventricular tachycardia  No preceding symptoms

 Cardiomyopathy or previous MI

Sick sinus syndrome  Preceding fatigue or dizziness

 Sinus pauses on ECG

Advanced AV block  Bifascicular block or ↑ PR interval on ECG

 Dropped QRS complexes on ECG

Torsades de pointes  No preceding symptoms

 Medications that prolong QT interval
 Hypokalemia or hypomagnesemia

Exertional syncope: HCM/AS or arrhythmia

 Cardiac myxoma
Tumor characteristics  Benign neoplasm, 80% located in left atrium

Clinical features  Position-dependent mitral valve obstruction

o Middiastolic murmur
o Dyspnea, lightheadedness, syncope
 Embolization of tumor fragments (eg, stroke)
 Constitutional symptoms (eg, fever, weight loss)

Diagnosis &  Echocardiography & prompt surgical resection

management

Reverberation of the walls of the dilated LV during the passive filling phase of diastole. The
S3 is present prior to the development of decompensated heart failure, and the absence of an S3
helps exclude severe chronic MR. An S3 is also commonly heard with decompensated heart
failure of any etiology.

Seizure Vasovagal syncope

Triggers  Lack of sleep  Prolonged standing
 Flashing light  Physical/emotional stress
 Emotional stress  Heat
 Alcohol
withdrawal
 Idiopathic

Clinical clues  Preceding aura  Preceding lightheadedness (ie,

(eg, olfactory presyncope)
hallucinations)  Unlikely to occur while sleeping/sitting
 Can occur with  Uncommon to have clonic jerks (can
sleeping/sitting occur with prolonged cerebral
 Tonic/clonic hypoperfusion)
movements
 Rapid, strong  Weak, slow pulses
pulses  Pallor & diaphoresis
 Tongue biting
 Incontinence

Sequelae  Delayed return to  Immediate return to baseline

baseline (postictal
drowsiness or
 confusion)

Seizure vs syncope
Generalized seizure Vasovagal syncope Cardiogenic syncope
Triggers  Lack of sleep  Prolonged standing  Exertion
 Flashing light  Physical/emotional  Dehydration
 Emotional stress
stress

Event  ± Preceding  Presyncope (eg,  Sudden LOC

features aura lightheadedness, pallor, without
diaphoresis) prodrome
 LOC & loss of
postural tone
 Tonic-clonic
convulsions

Postevent  Delayed return  Immediate return to  Immediate

features to baseline (ie, baseline return to
postictal state) baseline

LOC = loss of consciousness.

Clues to etiology of syncope

Reflex Vasovagal  Trigger (eg, emotional stress, prolonged standing)
syncope  Prodrome (eg, nausea, sweating, warmth)

Situational  Occurs with micturition, defecation, swallow, or cough

Carotid  Tactile stimulation of carotid sinus while standing

hypersensitivit  Advanced age, carotid atherosclerosis
y
Orthostatic Medications  Vasodilators (eg, alpha-1 blockers, antihypertensives)
syncope  Inotropic/chronotropic blockade (eg, beta blockers)

Hypovolemia  History consistent with volume loss

Autonomic  Advanced aged

dysfunction  Predisposing disease (eg, DM, Parkinson)

Cardiac LV outflow  Syncope with exertion

syncope obstruction  Systolic ejection murmur
 Ventricular  No warning symptoms
tachycardia  Cardiomyopathy or ischemic HD (monomorphic)
 QT-interval prolongation (polymorphic)

Conduction  Preceding fatigue or light-headedness

impairment*  ECG abnormalities (eg, sinus pauses, dropped QRS)

*Sick sinus syndrome or advanced atrioventricular block.

DM = diabetes mellitus; HD = heart disease; LV = left ventricular.

Vasovagal & situational syncope

Triggers  Pain,* anxiety,* emotional stress, heat, prolonged standing
 Situational: cough,* micturition,* defecation, eating, hair-combing*,
swallowing

Clinical  Prodrome (eg, light-headedness, warmth, pallor, nausea, diaphoresis)

presentatio  Rapid recovery of consciousness (eg, <1-2 min)
n 
o Vasodepressor response: Arterial and venous vasodilation
o Cardioinhibitory response: Decreased heart rate and
contractility result in decreased CO

Together, these effects can result in global cerebral hypoperfusion and

syncope.
Diagnosis  Mainly based on clinical history of event
 Upright tilt table testing sometimes indicated in uncertain cases

Treatment  Reassurance & avoidance of triggers

 Counterpressure techniques for recurrent episodes

*Particularly common triggers in the pediatric population.

Breath-holding spells occur in children age 6 months to 5 years and present with either cyanosis
or pallor (ie, pallid breath-holding spell) following physical or emotional distress. Although a
period of confusion can follow a pallid breath-holding spell, this patient's age makes the
diagnosis unlikely.

Autonomic dysfunction is common with Parkinson disease and can lead to neurogenic orthostatic
hypotension, with patients experiencing lightheadedness or syncope on standing. The disorder is
typically recognized by a ≥20 mm Hg drop in systolic blood pressure with standing and an
absence of the expected increase in heart rate. Degenerative process of CNS nuclei or autonomic
ganglia.
 Postural tachycardia syndrome generally affects young women and typically causes excessive
tachycardia without associated hypotension on standing.

JVP:

Due to AV dissociation (Vtach, AV complete block and frequent PVCs)

Patients may sometimes report symptoms associated with cannon A waves, including headache,
jaw pain, and sensation of neck pulsation.
Preventive medicine:
 Screening: abdominal aortic aneurysm
Patient  Men
population  Age 65-75

Risk factor  Any smoking history

indication
Test  One-time abdominal duplex ultrasound

Patients with Turner syndrome are at increased risk for cardiovascular abnormalities and should
undergo cardiac evaluation (eg, echocardiography, 4-extremity blood pressures) to evaluate
for bicuspid aortic valve, coarctation of the aorta, and aortic root dilation.

Screening for intracranial aneurysms is recommended by some experts for Patients with
autosomal dominant polycystic kidney disease or with a family history of aneurysms in ≥2 first-
degree relatives.

Patients with hypertension should be screened for diabetes mellitus with either fasting blood
glucose, which can be obtained as part of a serum chemistry panel, or hemoglobin A1c. Even in
the absence of hypertension, screening is advised for patients age 40-70 with a BMI ≥25 kg/m2
(ie, overweight or obese).

Drugs:
Prior to begin Amidrone, baseline CX-ray and PFT and TSH and following up with PFT is
guided by development of symptoms like cough, fever and dyspnea. Amiodarone can cause a
variety of endocrinopathies, including both hypo- and hyperthyroidism (for which periodic
thyroid function monitoring is recommended).

Major side effects of amiodarone

Cardiac  Sinus bradycardia, heart
block
 Risk of proarrhythmias: QT
prolongation & risk of
torsade de pointes

Pulmonary  Pulmonary toxicity is dose

accumulative
 Chronic interstitial
pneumonitis (cough, fever,
dyspnea, pulmonary
infiltrates) most common
  chronic interstitial
pneumonitis (usually within
months of therapy),
organizing pneumonia,
acute respiratory distress
syndrome, diffuse alveolar
hemorrhage, pulmonary
nodules, and solitary
masses.

Endocrine  Hypothyroidism
 Hyperthyroidism

Gastrointestinal  Elevated transaminases,

/ hepatitis
hepatic
Ocular  Corneal microdeposits
 Optic neuropathy

Dermatologic  Blue-gray skin

discoloration

Neurologic  Peripheral neuropathy

Verapamil and Diltiazem also display use dependence, with an increase in calcium channel
blockade with increasing ventricular activation. They cause a prolongation of the refractory
period of the AV node, leading to an increased PR interval

Class IC cause use dependance prolongation of QRS on ECG, less commonly is IB

Indications for statin therapy in prevention of ASCVD

Secondary prevention  Established ASCVD
o Acute coronary syndrome
o Stable angina
o Arterial revascularization (eg, CABG)
o Stroke, TIA, PAD

Primary prevention  LDL ≥190 mg/dL

 Age ≥40 with diabetes mellitus
 Estimated 10-year risk of ASCVD >7.5%-10%

BBs should be started as soon as hyperthyrodisim is diagnosed and continued until cure of hyperthyrodisim is
 acheived.

Sodium bicarbonate is useful in the management of patients with TdP due to quinidine use. It is also beneficial
in patients with cardiac arrest due to metabolic acidosis, hyperkalemia, or tricyclic antidepressant overdose.

Cutaneous flushing and intense generalized pruritus are well-known side effects of high-dose niacin therapy
(high dosage is required to treat lipid abnormalities). These effects are explained by niacin-induced peripheral
vasodilation,

The mechanism involved in this reaction is believed to be drug-induced release of histamine and
prostaglandins, not a true hypersensitivity reaction

Symptoms of digoxin toxicity

Cardiac  Life-threatening arrhythmias

Gastrointestinal  Anorexia
 Nausea & vomiting
 Abdominal pain

Neurologic  Fatigue
 Confusion
 Weakness
 Color vision alterations (yellow)

Because digoxin is renally cleared, elderly patients who are susceptible to dehydration and acute kidney injury
are particularly prone to toxicity. Blood Digoxin level is diagnostic but normal sometimes.

Amiodarone (or verapamil, quinidine, and propafenone) increases the serum levels of digoxin (by interfering
with digoxin metabolism) and can lead to toxicity in a patient who has previously been on a stable digoxin
regimen. It is recommended that the digoxin dose be decreased by 25%-50% when initiating amiodarone
therapy, with close monitoring of digoxin levels once weekly for the next several weeks.

Vasopressor-induced vasoconstriction can negatively impact the intestines (causing mesenteric ischemia)
and/or kidneys (causing renal failure), bilateral and symmetrical dry gangrene

New-onset type 2 diabetes mellitus, hepatic dysfunction, and myalgia are known side effects of HMG-CoA
reductase inhibitors (ie, statins).

Medication-induced orthostasis
Mechanism Examples
α-1 blockade–mediated vasodilation  Terazosin, prazosin, doxazosin
 Antipsychotics (eg, risperidone)
 Antihistamines, TCAs

Other vasodilation  ACE inhibitors & ARBs

 Dihydropyridine CCBs
 Hydralazine, nitrates
  Phosphodiesterase inhibitors

Volume depletion  Diuretics

 SGLT-2 inhibitors

Sympathetic blockade  Beta blockers

 Clonidine

ARBs = angiotensin II receptor blockers; CCBs = calcium channel blockers; SGLT = sodium-
glucose cotransporter; TCAs = tricyclic antidepressants.

ECG effects of antiarrhythmic drugs

PR interval QRS duration QT interval
(prolonged via Ca2+ (prolonged via Na+ (prolonged via K+
channel inhibition or channel inhibition) channel inhibition)
sympathetic blockade)
Class IA − ↑ ↑
(eg,
procainamide)
Class IB − − −
(eg, lidocaine)
Class IC − ↑
(eg, flecainide)
Class II ↑ − −
(eg, metoprolol)
Amiodarone ↑ ↑ ↑
Sotalol ↑ − ↑
Other class III − − ↑
(eg, dofetilide)
Class IV ↑ − −
(eg, verapamil)
ARBs provide the greatest reduction in LVH of all first-line antihypertensive agents