Cardiology

ACUTE CORONARY SYNDROME
Dr. T N Gupta
MD
Introduction
• Group of heart conditions related to
obstruction of coronary arteries including
myocardial infarction and unstable angina
• These conditions are due to decreased blood
flow in the coronary arteries such that part of
heart muscle is unable to function or dies.
• Reduction in blood flow in coronary arteries
occurs due to atherosclerosis and occlusion
of an artery by an embolus or thrombus
Types
• Based on ECG and cardiac enzymes, ACS is
classified into
1.STEMI
2.NSTEMI
3.Unstable Angina
1.Myocardial Infarction
(STEMI)
Introduction
Myocardial infarction refers to the process by
which myocardial tissue is destroyed in
regions of the heart that are deprived of an
adequate blood supply because of a reduced
coronary blood flow.
Incidence
• Every 40 seconds, someone in the United
States has a heart attack.
• Every year, about 790,000 Americans have a
heart attack. Of these cases
 580,000 are a first heart attack.
 210,000 happen to people who have already
had a first heart attack.
• One of 5 heart attacks is silent—the damage
is done, but the person is not aware of it.
• Globally 80% mortality from ACS.
Etiology
CAD is commonly caused by damage to the heart or
blood vessels(Coronary Artery)
• Atherosclerosis or a buildup of fatty plaques in the
arteries.
•Vasospasm(sudden constriction or narrowing ) of
coronary artery ( from acute blood loss, anemia etc) it is
a rare cause
•Increased demand for oxygen e.g. tachycardia,
thyrotoxicosis, ingestion of cocaine -
Study on modifiable Risk Factors
A study showed high prevalence of
–hypertension,
–smoking,
–diabetes and
–Dyslipidemia
(Nepal, Bista, Khaliq, Manoj, Choudhary,&
Bhattarai, 2017)
Novel Risk Factors
• C-reactive protein (CRP)
• Lipoprotein
• Homocysteine
• Small, dense LDL-C particles
• Fibrinogen
• Serum amyloid
• Coronary calcium
(Boudi,2016)
PATHOPHYSIOLOGY
PATHOPHYSIOLOGY
Risk factors/ the Etiological
Decreased blood supply to the heart/ decreased cardiac

output

Decreased oxygenation

Tissue damage
Necrosis
Presence of Clinical manifestations

Cause of death from MI
• Ventricular fibrillation – Heart beats more than
300 times per min
• Heart block – Blockage of conduction system.

Needs pacemaker
• Heart failurer – Failure to pump . Needs medicines

or biventricular pacemaker
• Cardiogenic Shock
Diagnostic Evaluation
•
DIAGNOSIS
At least two of the followings
1. Patient history & type of pain/ complains of client
Signs & symptoms of client (angina or angina
equivalent )
2. Cardiac Biomarker
• Troponin is primarily used for diagnosing MI because it
has good sensitivity and specificity (after 6 hrs of pain).
• The increasing Troponin trend is the important thing to
look for in diagnosing MI ( normal range troponin I <1.0
ug /ml ).
• CPK-MB (normal range < 25 IU / lt )
3. Acute ischemia ECG changes
Diagnostic evaluation cont..
• Stress Test
• Tread mill test
• Angiogram
• CBC, RFT, Lipid profile, Sugar, urine r/e
• CXR
ST Elevation -Infarction
The ECG changes seen with a ST elevation infarction are:
Before injury Normal ECG
Ischemia ST depression, peaked T-waves, then T-

wave inversion
Injury ST elevation
ST elevation along with Appearance of Q
Infraction waves
ST segments and T-waves return to
Fibrosis normal, but Q-waves persist
ECG in MI
ECG in MI
Variable Shapes Of ST Segment
Elevations in AMI
Goldberger AL. Goldberger: Clinical Electrocardiography: A

Simplified Approach. 7th ed: Mosby Elsevier; 2006.
ECG Changes
ST elevation &
depression
T-waves
peaked flattened
Appearance inverted
of pathologic
Q-waves
II, III and aVF looks at the inferior surface of the heart
I, aVL, V5 and V6 look at the lateral surface of the heart
V1 and V2 look at the anterior surface of the heart
V3 and V4 look at the interventricular septum of the heart
Summary table of ECG in MI
Location ST elevation Coronary Artery
Anterior MI V1-V6 LAD
Septal MI V1-V4 LAD septal branches
Lateral MI I, aVL, V5, V6 LCX
Inferior M I II, III, aVF RCA
V7, V8, V9 RCA

Posterior MI
RCA
Right Ventricle MI V1, V4R
ST Elevation
DRUG THERAPY
Medical Management
Major treatment
1.Emergency angioplasty
2. Thrombolytic agent: clot buster medicine
• Cardiac monitor
• Supplemental oxygen
• Aspirin
• Establish iv line
• Morphine
• Nitrate
• Anticoagulant
SURGICAL MANAGEMENT
CABG
Nursing Management
• Relieving pain and other s/s of ischemia

• Improving respiratory function
• Promoting adequate tissue perfusion
• Reducing anxiety
• Monitor and manage complication
• Health education
2. NSTEMI
• Both Non STEMI and STEMI both are

commonly known as heart attack. But they
are different from each other in some extent.
STEMI accounts 70% and NSTEMI 30% of all
myocardial infarction. Some differences are
Differences in STEMI and
NSTEMI
Differences in Pathophysiology
STEMI NSTEMI
•Complete occlusion of •Complete occlusion of

major artery minor artery or partial
• full thickness damage occlusion of major
of heart muscle artery
•Partial thickness
damage of heart
muscle
Differences in Pathophysiology
cont..
Differences in clinical Presentation
STEMI NSTEMI
Similar
Differences in ECG
STEMI NSTEMI
ST segment elevation No ST segment

due to full thickness elevation
injury of heart muscle
Differences in ECG cont..
Differences in ECG cont..
Differences in cardiac markers
STEMI NSTEMI
All cardiac markers elevation in both

Differences in Complications
STEMI NSTEMI
More common and more severe in STEMI.

•Arrhythmia
•Cardiogenic shock
•Left ventricular failure
•Ventricle wall rupture
•Cardiac tamponade
•Severe mitral regurgitation due to papillary
muscle rupture
•VSD
Differences in Treatment
STEMI NSTEMI
•All medicines •All medicines

•PCI is choice of • angiography and
treatment revascularization by PCI
•If PCI is not possible or CABG is treatment of
thrombolytic therapy is choice in medium to
second option high risk
•Drug treatment is
appropriate for low risk
patients
Differences in prognosis
STEMI NSTEMI
•Short term(in hospital •Short term mortality is

or one month) mortality lower (3.5%)
is higher (10-15%)
• after hospital discharge •Re infarction 15-25%
Re infarction 5-8%
•Long term(two year •Long term(two year
mortality) 30% mortality) 30%
Some issues
Work Issues
• Start with alternate half days, and build up to

your normal routine over 2-3 weeks.
• Start with light or less challenging duties at first.
• Include additional rest periods if tiredness is a
problem.
• There are few jobs that are not possible to do ,
like heavy weight lifting etc.
• Sexual activity can be regained after 4-6 wks.
Driving and flying issues
• Can resume car driving
after four wks.
• Patient should not drive
during angina.
 Pt. can usually

resume air travel
after six weeks.
Key ways to help prevent heart
disease:
• Don’t smoke or use tobacco products
– Tobacco smoke contains more than 4,800
chemicals; many of which can damage heart
and blood vessels
• Get active
– Exercise
– Gardening
– Taking the stairs
• Eat a heart-healthy diet
– Research shows that fruits, vegetables, whole
grains and low-fat dairy products that can help
protect your heart
Key ways to help prevent heart
disease cont..:
• Maintain a healthy weight
– excess weight can lead to conditions that
increase your chances of heart
• Get regular health screenings
– Blood Pressure
– Cholesterol Levels
• Stress-free
– Relax
– Smile
Cardiac Rehabilitation
• Discharge teaching and counseling
• 8 weeks counseling cession
8 weeks structured education
program
1. First week before discharge (patient or his/
her family member) – prevention and
control measures for heart disease
2. Second week information regarding heart
attack
3. Information regarding diabetes
4. Ways of finding CAD
(every Tuesday at 1 pm in conference hall)
8 weeks structured education
program cont..
5. Information regarding medication
6. Healthy diet for healthy heart
7. Regular exercise for healthy heart
8. Life style after heart attack
3.UNSTABLE ANGINA
Angina pectoris commonly known
as angina – is chest pain often due
to ischemia of the heart muscle, due to
obstruction or spasm of the coronary
arteries.
Classification of angina
1. Exertional angina, Stable, Atherosclerotic,
Classic,
Due to obstruction of coronaries by atheroma.
2. Variant, Vasospastic angina
due to Spasm of coronaries.
3- Unstable angina.
Due to spasm and partial obstruction of
coronaries.
Etiology and risk factor
Similar to MI
Clinical manifestations
• Chest pain or discomfort
• Pain in arms, neck, jaw, shoulder or back
accompanying chest pain
• Nausea
• Fatigue
• Shortness of breath
• Sweating
• Dizziness
Characteristics of unstable angina
• Occurs even at rest

• Is a change in usual pattern of angina
• Is unexpected
• Is usually more severe and lasts longer than
stable angina, maybe as long as 30 minutes
• May not disappear with rest or use of angina
medication
• Might signal a heart attack
Management
Goal: The main goals of treatment in angina
pectoris are to relieve the symptoms ,slow
the progression of disease and reduce the
possibility of future event especially MI and
premature death
Management
• Rest
• Nitroglycerin
• Aspirin
• Oxygen
• BB
• Calcium channel blocker
• Statin
• Clot preventing drug such as clopidogrel
TIMI Score
• TIMI (Thrombolysis in Myocardial Infarction)
score is used in patients with NSTEMI (Non ST-
segment elevation myocardial infarction), STEMI
(ST-segment elevation myocardial infarction) and
unstable angina to define risk. TIMI Study Group
established this risk score. TIMI Study Group is
an Academic Research Organization affiliated
with Harvard Medical School, and Brigham and
Women’s Hospital in Boston
TIMI variables
1. Age ≥ 65
2. Aspirin use in the last 7 days (patient experiences
chest pain despite ASA use in past 7 days)
3. At least 2 angina episodes within the last 24hrs
4. ST changes of at least 0.5mm in contiguous leads
5. Elevated serum cardiac biomarkers
6. Known Coronary Artery Disease (CAD) (coronary
stenosis ≥ 50%)
7. At least 3 risk factors for CAD, such as:
TIMI variables cont..
– Hypertension -> 140/90 or on anti-
hypertensives
– Current cigarette smoker
– Low HDL cholesterol (< 40 mg/dL)
– Diabetes mellitus
– Family history of premature CAD
• Male first-degree relative or father younger
than 55
• Female first-degree relative or mother
younger than 65
Score Interpretation:
% risk at 14 days of: all-cause mortality, new or
recurrent MI, or severe recurrent ischemia
requiring urgent revascularization.
• Score of 0-1 = 4.7% risk
• Score of 2 = 8.3% risk
• Score of 6-7 = at least 40.9% risk
Risk Stratification
Risk stratification Score
Low risk patients 0–2
Medium risk patients 3–4
High risk patients 5-7

Management strategies according to
TIMI score
• In low risk patients with NSTEMI or unstable
angina, drug therapy is appropriate and
surgical intervention is reserved for those
who fail to settle with drug therapy. By
contrast, medium to high risk patients with
NSTEMI or unstable angina should be treated
with multiple drugs and considered for early
coronary angiography and revascularization.
1 Fibrinolytic Therapy
STK
•Widely available and beneficial
•Where there is no access of primary PCI
•It should be chosen as soon as possible
•Door to needle time 30 min
•Chest pain duration < 12hours(preferably < 3 hours)
•It is preferred where PCI Centre is far from > 120min
•There should not be contraindication
Contraindications
(absolute)
• Hypersensitivity
• Any prior ICH
• Cerebral neoplasm
• Known structural cerebral vascular lesions
• Severe uncontrolled hypertension
( unresponsive to emergency therapy)
• Suspected aortic dissection
Contraindications
(absolute)
• Ischemic stroke within 3 month(except acute
ischemic stroke within 4.5 hours)
• Active bleeding or bleeding diathesis
( excluding menses)
• Significant closed head or facial trauma
within 3 month.
• Prior treatment within 6 month
Contraindications
(relative )
• Recent surgery( major < 3 weeks)
• Chronic Hypertension
• Pregnancy .
• Active peptic ulcer
• Recent internal bleeding(2 to 4 week)
• traumatic or prolonged CPR(> 10 min)
Contraindications cont..
(relative )
•Recent internal bleeding

• Active GI Bleeding
•Oral anticoagulant therapy
•Dementia
Preparation of Medicine
Dissolve 5ml NS+ STK

95ml NS Micro drip set
Total 100ml STK
Points to be considered
• Store STK in refrigerator but do not fridge.
• After dissolving in normal saline it can be
stored up to 24 hours without losing its
potency.
Tenecteplase
Dose
Patient weight TNKase Volume to be
administered
(kg) (mg) (ml)
< 60 30 6
< 60 to < 70 35 7
>70 to < 80 40 8
> 80 to < 90 45 9
> 90 50 10
Tenecteplase cont…
• Should not exceed 50 mg and is based upon

patient weight
• A single bolus dose should be administered
over 5 seconds
• Inject the entire contents of the syringe (6ml)
into the 30mg TNKase (VELIX-30) vial
directing the diluents stream into the
powder.
Tenecteplase cont…
• TNKase may be administered as
reconstituted at 5mg/ml
• Intravenous UFH; intravenous UFH is to be
administered as soon as possible:
• Followed by clexane BD
2.Primary PCI
• It is a preferred method
• Better outcome than thrombolytic therapy
• Less chance of ICH and other complications
• It is preferred
- Chest pain of duration < 12 hours
- Door to balloon time< 90 min
- Contraindication to Thrombolysis
- transfer to PCI capable Centre time < 120 min
PTCA
3. Other medical management
(low molecular weight heparin)
• Chest pain of duration > 12 hours with no
chest pain
• Hemodynamically stable
• Asymptomatic
• Contraindication to Thrombolysis
• Patients with successful fibrinolysis but are
not treated at PCI capable centre should be
encouraged to be transferred for
angiography and eventually PCI or CABG
Conclusion
• ACS includes UA,NSTEMI and STEMI
• Management guideline focus
 immediate assessment and intervention
(MONA+BAH)
 Risk stratification
Rapid reperfusion therapy for STEMI(PCI Vs
thrombolytic)
 conservative vs. invasive therapy for UA&
NSTEMI)
Aggressive attention to secondary prevention
add aspirin, statin, beta blocker,
ACE inhibitor ,patient education
HYPERTENSION
Dr. Triloki Nath Gupta

MD
Overview
• Introduction
• Epidemiology and genetic considerations
• Goals of therapy
• Compelling indications
• Lifestyle modifications
• Treatment
• Hypertensive emergencies
Introduction
• Persistent elevation of arterial blood pressure (BP)
• Clinically defined as that level of blood pressure at
which institution of therapy reduces BP related
morbidity and mortality.
• Approx. 7.6 million deaths (13-15 % of total) and 92
million disability-adjusted life years worldwide
attributed to high BP in 2001
• Nepal (18 to 39%)
• Most patients asymptomatic
• Increasing prevalence with aging of population and
epidemic of overweight/obesity
• Control of BP leads to a reduction in events: approx.
– 50% reduction in heart failure
– 40% reduction in stroke
– 20-25% reduction in MI
• Cardiovascular disease risk doubles for every
20-mmHg increase in systolic and 10-mmHg
increase in diastolic pressure.
• Among older individuals, systolic blood pressure
and pulse pressure are more powerful
predictors of cardiovascular disease than is
diastolic blood pressure.
Epidemiology and Genetic
Considerations
• Prevalence of hypertension vary among countries and
among subpopulations within a country
• The probability that a middle-aged or elderly individual
will develop hypertension in his or her lifetime is 90%.
• Both environmental and genetic factors may contribute to
regional and racial variations in blood pressure and
hypertension prevalence
• Obesity and weight gain are strong, independent risk
factors for hypertension (~60% of hypertensives are >20%
overweight)
• Hypertension prevalence is related to dietary NaCl intake,
and the age-related increase in blood pressure may be
augmented by a high NaCl intake.
• Low dietary intakes of calcium and potassium also may

contribute to the risk of hypertension.
•
• The urine sodium-to-potassium ratio is a stronger correlate
of blood pressure than is either sodium or potassium alone.
• Alcohol consumption, psychosocial stress, and low levels of

physical activity also may contribute to hypertension.
• BP heritabilities are 15–35%. In twin studies, heritability
estimates are ~60% for males and 30–40% for females.
• High blood pressure before age 55 occurs 3.8 times more
frequently among persons with a positive family history of
hypertension
• Hypertension represents a polygenic disorder in which a
combination of genes acts in concert with environmental
exposures to make only a modest contribution to blood
pressure.
• Further, different subsets of genes may lead to different
phenotypes associated with hypertension, e.g., obesity,
dyslipidemia, insulin resistance.
Guidelines in measuring BP
• Condition:
-Posture (sitting,supine,standing)
-Circumstances (no caffeine.no smoking)
• Equipment:
-Cuff size(40%W,80%L)
-Manometer
• Technique:
-Number of readings ( average of 2 or more sitting BP)
-Performance
-Recordings
In children and adolescents, hypertension generally is
defined as systolic and/or diastolic blood pressure consistently
>95th percentile for age, sex, and height. Blood pressures between
the 90th and 95th percentiles are considered prehypertensive and
are an indication for lifestyle interventions.
• Home blood pressures, including 24-h blood pressure
recordings, more reliably predict target organ damage than do
office BP.
• BP tends to be higher in the early morning hours, soon after
waking, than at other times of day.
• Myocardial infarction and stroke are more common in the
early morning hours.
• Nighttime BP are generally 10–20% lower than daytime blood
pressures, and an attenuated nighttime BP "dip" is associated
with increased cardiovascular disease risk.
• Recommended criteria for a diagnosis of hypertension are
average awake BP 135/85 mmHg and asleep BP 120/75
mmHg. These levels approximate a clinic blood pressure of
140/90 mmHg.
Systemic HTN - Pathophysiology
Desmukh, et al. Pathophysiology of Heart Disease, Ch 13. 1997

Types
 Essential hypertension:(primary or idiopathic)
– ~80-95% of cases
– hereditary component
 Secondary hypertension:
– 5-20% of cases
– Common causes: CKD, Renovascular disease
– Other causes: Rx drugs, street drugs, natural products, food,
industrial chemicals
Secondary Causes of Systolic and Diastolic Hypertension
Renal Parenchymal diseases, renal cysts (including polycystic kidney disease),

renal tumors (including renin-secreting tumors), obstructive uropathy
Renovascular Arteriosclerotic, fibromuscular dysplasia
Adrenal Primary aldosteronism, Cushing's syndrome, 17 -hydroxylase deficiency,
11 -hydroxylase deficiency, 11-hydroxysteroid dehydrogenase deficiency
(licorice), pheochromocytoma
Aortic coarctation
Obstructive sleep apnea
Preeclampsia/eclampsia
Neurogenic Psychogenic, diencephalic syndrome, familial dysautonomia, polyneuritis
(acute porphyria, lead poisoning), acute increased intracranial pressure,
acute spinal cord section
Miscellaneous endocrine Hypothyroidism, hyperthyroidism, hypercalcemia, acromegaly
Medications High-dose estrogens, adrenal steroids, decongestants, appetite
suppressants, cyclosporine, tricyclic antidepressants, monamine oxidase
inhibitors, erythropoietin, nonsteroidal anti-inflammatory agents, cocaine
Mendelian forms of
hypertension
Rare Mendelian Forms of Hypertension
Disease
 Glucocorticoid-remediable hyperaldosteronism
 17 -hydroxylase deficiency
 11 -hydroxylase deficiency
 11 -hydroxysteroid dehydrogenase deficiency (apparent
mineralocorticoid excess syndrome)
 Liddle's syndrome
 Pseudohypoaldosteronism type II (Gordon's syndrome)
 Hypertension exacerbated in pregnancy
 Polycystic kidney disease
Systolic Hypertension with Wide Pulse Pressure
1. Decreased vascular compliance (arteriosclerosis)
2. Increased cardiac output.
a. Aortic regurgitation
b. Thyrotoxicosis.
c. Hyperkinetic heart syndrome.
d. Fever.
e. Arteriovenous fistula
f. Patent ductus arteriosus
Causes of 2˚ Hypertension
Prescription drugs: • Situations:
– β-blocker or centrally acting
– NSAIDs, COX-2 inhibitors α-agonists
– venlafaxine • When abruptly discontinued
– bupropion – β-blocker without α-
– bromocriptine blocker first when treating
– buspirone pheochromocytoma
– carbamazepine • Food substances:
– clozapine – Sodium
– ketamine – Ethanol
– metoclopramide – Licorice
– Energy drinks
Causes of 2˚ Hypertension
Target-Organ Damage
• Brain: Stroke, Transient ischemic attack, dementia
• Eyes: Retinopathy
• Heart: Left ventricular hypertrophy, angina
• Kidney: Chronic kidney disease
• Peripheral Vasculature: Peripheral arterial disease

Hypertensive retinopathy
• Grade 1 Arteriolar thickening, tortuosity and increased reflectiveness
('silver wiring')
• Grade 2 Grade 1 plus constriction of veins at arterial crossings
('arteriovenous nipping')
• Grade 3 Grade 2 plus evidence of retinal ischaemia (flame-shaped or
blot haemorrhages and 'cotton wool' exudates)
• Grade 4 Grade 3 plus papilloedema
Hypertension consequences:
Approach to patient with
Hypertension:
Patient's Relevant History
Duration of hypertension
Previous therapies: responses and side effects
Family history of hypertension and cardiovascular disease
Dietary and psychosocial history
Other risk factors: weight change, dyslipidemia, smoking, diabetes, physical inactivity
Evidence of secondary hypertension: history of renal disease; change in appearance; muscle
weakness; spells of sweating, palpitations, tremor; erratic sleep, snoring, daytime
somnolence; symptoms of hypo- or hyperthyroidism; use of agents that may increase blood
pressure
Evidence of target organ damage: history of TIA, stroke, transient blindness; angina,
myocardial infarction, congestive heart failure; sexual function Other comorbidities
Approach to patient with Hypertension cond..
Physical Examination:
•Body habitus, weight
•BP- both arms, preferably in supine, sitting and standing position to
evaluate for postural drop.
•Lower limb BP in hypertensives <30 years
•Heart rate
•Neck- enlarged thyroids (signs of hypo- or hyperthyroidism)
•Examination of blood vessels: funduscopic examination, auscultation
for bruits over the carotid and femoral arteries, and palpation of
femoral and pedal pulses.
•Heart: loud S2 due to closure of the aortic valve and S4 gallop
attributed to atrial contraction against a noncompliant left ventricle.
LVH may be detected by an enlarged, sustained, and laterally displaced
apical impulse
•Abdomen: Kidney palpation
•Signs of CHF and a neurologic examination.
Hypertension: investigation of all patients

Urinalysis for blood, protein and glucose

Blood urea, electrolytes and creatinine

N.B. Hypokalaemic alkalosis may indicate primary
hyperaldosteronism but is usually due to diuretic
therapy

Blood glucose

Serum total and HDL cholesterol

12-lead ECG (left ventricular hypertrophy, coronary
artery disease)
Hypertension: investigation of selected patients
 Chest X-ray: to detect cardiomegaly, heart failure, coarctation of the aorta

 Ambulatory BP recording: to assess borderline or 'white coat' hypertension
 Echocardiogram: to detect or quantify left ventricular hypertrophy
 Renal ultrasound: to detect possible renal disease
 Renal angiography: to detect or confirm presence of renal artery stenosis
 Urinary catecholamines: to detect possible phaeochromocytoma (p. 779)
 Urinary cortisol and dexamethasone suppression test: to detect possible
Cushing's syndrome (p. 770)
 Plasma renin activity and aldosterone: to detect possible primary
aldosteronism
Clinical Controversy
• White coat hypertension: elevated BP in clinic followed by
normal BP reading at home
• Aggressive treatment of white coat hypertension is
controversial
• Patients with white coat hypertension may have increased
CV risk compared to those without such BP changes
• Classification based on average of > 2 properly measured
seated BP measurements from > 2 clinical encounters
• If systolic & diastolic blood pressure values give different
classifications, classify by highest category
• Prehypertension: patients likely to develop hypertension
• Ambulatory BP measurements may be more accurate &
better predict target-organ damage than manual BP
measurements using a sphygmomanometer in a clinic
setting (gold standard)
• Many patients may be misdiagnosed, misclassified poor
technique, daily BP variability, white coat HTN
• Validated ambulatory BP monitoring: role in the routine
HTN management unclear
• Prehypertension: patients do not have HTN but at risk for
developing it.
• Trial of Preventing Hypertension (TROPHY) showed
treating prehypertension with candesartan decreased
progression to stage 1 hypertension
RISK FACTORS FOR ADVERSE
PROGNOSIS IN HTN
• BLACK RACE
• YOUTH
• MALE GENDER
• SMOKING
• DM
• OBESITY
• ALCOHOL INTAKE
• HYPERCHOLESTROLEMIA
• EVIDENCE OF END ORGAN DAMAGE(LVH,LVSTRAIN,MI,CHF)
• RETINAL HEMORRHAGE & EXUDATE
• PAPILLEDEMA
• RENAL: IMP REN FUN
• CVA
Treatment Goals
1. Reduce morbidity & mortality
2. Select drug therapy based on

evidence
3. Demonstrating risk reduction

Hypertension and Diabetes
• Hypertension co-exists with type II in about 40% at age 45
rising to 60% at age 75
• 70% type2 DM die of cardiovascular disease
• At least 60% of patients will require 2 or 3 antihypertensive

agents to achieve tight control.
Compelling Indications
• Heart Failure
• Post Myocardial Infarction
• High Coronary Disease Risk
• Diabetes Mellitus
• Chronic Kidney Disease
• Recurrent Stroke Prevention

Compelling Possible
Class of drug indications indications Caution Compelling CI
β-blockers MI, angina Heart failure5 Asthma or chronic
Heart failure5 Peripheral vascular obstructive
disease pulmonary disease
Diabetes (except with Heart block
coronary heart disease)
Calcium channel Older patients, Angina - -

blockers isolated systolic
(dihydropyridine) hypertension
Calcium channel Angina Older patients Combination with β- Atrioventricular

blockers (rate- blockade block, heart failure
limiting)
Thiazides or Older patients, - - Gout6
thiazide-like isolated systolic
diuretics hypertension, heart
failure, secondary
stroke prevention
The influence of comorbidity on the choice of antihypertensive drug therapy
Class of Compelling
drug Compelling indications Possible indications Caution CI
α-blockers Benign prostatic hypertrophy - Postural Urinary
hypotension, incontinence
heart failure1
ACE Heart failure Chronic renal disease2 Renal Pregnancy
inhibitors Left ventricular dysfunction, post-MI Type 2 diabetic impairment2 Renovascular
or established coronary heart disease nephropathy Peripheral disease2
Type 1 diabetic nephropathy vascular disease3
Secondary stroke prevention4
Angiotensi ACE inhibitor intolerance Left ventricular Renal Pregnancy

n II Type 2 diabetic nephropathy dysfunction after MI impairment2
receptor Hypertension with left ventricular Intolerance of other Peripheral
blockers hypertrophy antihypertensive drugs vascular disease3
Heart failure in ACE-intolerant Proteinuric renal
patients, after MI disease, chronic renal
disease2
Heart failure
Logical Combinations
- ACE -
Diuretic CCB
blocker inhibitor blocker
Diuretic -  -  
-blocker  - * - 
CCB - * -  
ACE inhibitor  -  - 
-blocker     -

* Verapamil + beta-blocker = absolute contra-indication

Kieran McGlade Nov 2001
Hypertensive emergencies
• Hypertensive crisis includes Hypertensive emergency and urgency
• Usually develops in patients with a previous history of elevated BP
• but may arise in normotensive
• The severity correlates not only to absolute level but also with
rapidity of development because of failure of autoregulatory
mechanism.
Hypertensive urgency
• Defined by substantial increase in BP usually with
DBP>120mmhg
• Occur in approx 1% of hypertensive
 Hypertension with optic disc edema
 Progressive end organ complications rather than damage
 Severe perioperative hypertension
• Warrants BP reduction over hours

Hypertensive emergencies
• Include accelerated HTN defined by SBP>210 and
DBP>130mmhg presenting with
 Headache
 Blurrred vision
 Focal neurological symptoms
 Malignant HTN
• Immediate BP reduction over mins.

• Pathologically, the syndrome is associated with diffuse
necrotizing vasculitis, arteriolar thrombi, and fibrin
deposition in arteriolar walls.
• Fibrinoid necrosis has been observed in arterioles of kidney,
brain, retina, and other organs.
• Clinically, the syndrome is recognized by progressive
retinopathy (arteriolar spasm, hemorrhages, exudates, and
papilledema), deteriorating renal function with proteinuria,
microangiopathic hemolytic anemia, and encephalopathy

• Although blood pressure should be lowered rapidly in
patients with hypertensive encephalopathy, there are
inherent risks of overly aggressive therapy.
• In hypertensive individuals, the upper and lower limits of
autoregulation of cerebral blood flow are shifted to higher
levels of arterial pressure, and rapid lowering of blood
pressure to below the lower limit of autoregulation may
precipitate cerebral ischemia or infarction as a consequence
of decreased cerebral blood flow.
• Renal and coronary blood flows also may decrease with overly
aggressive acute therapy.
• The initial goal of therapy is to reduce mean arterial blood

pressure by no more than 25% within minutes to 2 h or to a
blood pressure in the range of 160/100–110 mmHg. This may
be accomplished with IV nitroprusside, a short-acting
vasodilator with a rapid onset of action that allows for minute-
to-minute control of blood pressure.
• Parenteral labetalol and nicardipine are also effective agents

for the treatment of hypertensive encephalopathy.
• In patients with hypertensive emergency without
encephalopathy or another catastrophic event, it is preferable
to reduce blood pressure over hours or longer rather than
minutes.
• This goal may effectively be achieved initially with frequent

dosing of short-acting oral agents such as captopril, clonidine,
and labetalol.
• Currently, in the absence of other indications for
acute therapy, for patients with cerebral infarction
who are not candidates for thrombolytic therapy
 institute antihypertensive therapy only for patients
with a systolic blood pressure >220 mmHg or a
diastolic blood pressure >130 mmHg.
 If thrombolytic therapy is to be used, the
recommended goal blood pressure is <185 mmHg
systolic pressure and <110 mmHg diastolic pressure.
 In patients with hemorrhagic stroke, suggested guidelines
for initiating antihypertensive therapy are systolic >180

mmHg or diastolic pressure >130 mmHg.
 The management of hypertension after subarachnoid

hemorrhage is controversial. Cautious reduction of blood
pressure is indicated if mean arterial pressure is >130 mmHg.
• In addition to pheochromocytoma, an adrenergic crisis due
to catecholamine excess may be related to
 cocaine or amphetamine overdose,
 clonidine withdrawal,
 acute spinal cord injuries, and
 an interaction of tyramine-containing compounds with

monamine oxidase inhibitors.
• These patients may be treated with phentolamine or
nitroprusside.
Hypertensive Emergencies
Do not use short-acting nifedipine (lowers BP fast enough to
provoke ischemia).
Thank you…
DISEASES OF THE PERICARDIUM
Dr. T. N. gupta
 Heart – covered by Pericardium

 Visceral & parietal ( pain fibers)
 15-50 ml fluid –lubricates the heart
 Pericardium
- prevents sudden dilatation of the cardiac chambers during
exercise & with hypervolemia (limits distension of the heart)
- restricts the anatomic position of the heart ,minimizes friction
between the heart & surrounding structures
- prevents displacement of the heart & kinking of the great
vessels
- retards the spread of the infections from the lungs & pleural
cavities to the heart (acts as a barrier to infection)
 Total absence – does not produce obvious clinical disease
 Pericarditis :Inflammation of the Pericardium
 Pericarditis – Acute < 6wks

Sub acute 6 wks-6 months
Chronic > 6 months
ACUTE PERICARDITIS
Acute Pericarditis – When inflammation develops suddenly
Etiology
1.Infection- Viral, Tuberculosis ,Pyogenic
2.Acute Rheumatic Fever
3.Collagen Vascular Diseases – SLE, RA
4. Post- Myocardial Infarction ( Dressler`s Syndrome)
4. Neoplasm –CA Lung
5. Metabolic – Uremia
6. Trauma
7. Radiation
8. Myxoedema
9. Idiopathic
10. Drugs
ACUTE PERICARDITIS
Clinical Features
 Pain in the chest – main symptoms.
Pain occurs when parietal layer is inflamed.
Sharp & stabbing ,retrosternal,
 associated pleuritis –
Pain increases –
- deep breathing & coughing, swallowing, lifting
hands, change of posture
ACUTE PERICARDITIS
 Low grade fever

 Difficulty in breathing
 Pericardial friction rub
- high pitch, scratchy & leathery, systolic &
diastolic components
- best heard with diaphragm of the stethoscope,
left lower sternum with light pressure, patient
sitting up, stooping forward & breath held at the
end of full expiration
ACUTE PERICARDITIS
ACUTE PERICARDITIS
Investigations
1.Blood:Leucocytosis & raised ESR
2.EKG: ST segment elevation in most of the leads with
concavity upwards & T waves are upright
3.X-ray chest:- if pericardial effusion >200ml –
enlarged cardiac silhouette
- Pul.TB, Pneumonia, neoplasm
4.Echocardiography: Pericardial effusion
5.Other Investigations: Etiology of Pericarditis
ACUTE PERICARDITIS
ACUTE PERICARDITIS
Differential Diagnosis
i. Unstable angina
ii.Pulmonary Infarction
iii.Pneumonia iv. Pneumothorax v. Dissecting aneurysm of the
aorta
Treatment
- Pain chest – Analgesic i.e.
Aspirin or Endomethacin
- Cause of Pericarditis
- Steroid
CHRONIC CONSTRICTIVE PERICARDITIS
Chronic Pericarditis
- Pericardium becomes thickened, fibrosed &
calcified
- does not permit the ventricles to expand fully
& its filling during diastole & pressure in
ventricles increases
- pressure in both the atria, pulmonary veins &
systemic veins also increases
- Cardiac output begins to fall & heart rate
increases ( Compensatory Tachycardia)
- may lead to constrictive pericarditis
Etiology
a. Tuberculosis
b. Chronic bacterial, Viral or Fungal
infection
c. Neoplasm
d. Connective tissue disorder
e. Idiopathic
Clinical Features
1. Gradual onset – SOB exertion, pedal edema, ascites &
fatigability
2. Pulsus Paradoxus, Tachycardia, AF
3. Right Ventricular Failure – Raised JVP with
prominent Y descent, Kussmaul`s sign, ascites,
edema, enlarged Liver
4. Pericardial Knock: rapidly expanding ventricles
strike against the thickened & calcified pericardium ,
early diastole(0.06-0.12sec), high pitched, louder
during deep inspiration
Investigations
1. EKG: low voltage QRS, flat or inverted T
waves & AF
2. X-ray Chest: Cardiac size Normal.
Calcification ( lateral oblique)
3. CT/MRI
4. Catheterization – Equalization of pressure
in ventricles (square root)
 D/D:
i. Restrictive Cardiomyopathy
ii. Cirrhosis of liver
iii. Right sided heart failure due to other causes
 Treatment:
1. Pericardiectomy
2. Drug treatment – depending upon etiology i.e.. TB
PERICARDIAL EFFUSION
&
CARDIAC TAMPONADE
Pericardial Effusion
-Fluid in the Pericardium
Cardiac Tamponade
The accumulation of fluids in the pericardium in a quantity
sufficient to cause serious obstruction to the inflow of blood
to the ventricles or impairs diastolic filling of the Ventricles –
Circulatory embarrassment result in CardiacTamponade.
- 200ml fluid rapidly
> 2litres in slowly developing effusion
&
CARDIAC TAMPONADE
Etiology
 Neoplastic Diseases
 Tuberculosis
 Hemopericardium
 Trauma
 Cardiac Surgery
 Uremia
 Idiopathic
&
CARDIAC TAMPONADE
Clinical Features
1. Dry cough, hoarse voice, difficulty in swallowing chest pain,
SOB. Patient prefers to sit up in bed ,stooping a little forward
2. Large effusion-
compression collapse of Lt. lower lobe of the lung – dull percussion
note below inferior angle of scapula & bronchial breathing – Ewart`s
sign
left border of heart does not coincides with apex beat
3. Apical impulse cannot be felt & heart sound's becomes muffled
4. Sinus tachycardia, raised JVP( with prominent X descent & absent Y
descent), Hypotension, Pulsus paradoxus & distant heart sounds
5. Positive Kussmaul`s sign, pericardial Knock –rare in Cardiac
Tamponade
&
CARDIAC TAMPONADE
Investigations
1. EKG: Low voltage complexes with or without electrical alternans
2. X-ray Chest: Enlarged cardiac silhouette ,symmetrical &
pear shaped. Lungs appear clear ,no
congestion
3.Echocardiography: Most sensitive -15 ml ( 2D)
Echo free space between heart walls & the Pericardium
Diastolic Collapse of RA & RV – Temponade
4. Diagnostic aspiration: analyzed in order to find out the
etiology of the effusion
D/D: Cardiomyopathy
Rt.sided heart failure i.e. Corpulmonale
&
CARDIAC TEMPONADE
X-ray Chest
&
CARDIAC TAMPONADE
&
CARDIAC TAMPONADE
Treatment:
1. Small effusion – treat depending upon etiology (TB)
2. Cardiac Tamponade – Pericardiocentesis & etiological
treatment
3. Surgical Pericardiotomy
4. Ionotrophic support & aggressive I/V saline to maintain
adequate ventricular filling
Diuretics, Nitrates or any other preload –reducing agents
are absolutely contraindicated
Infective Endocarditis
Dr. T. N. Gupta
MD
Outlines
• Introduction
• Epidemiology
• Types
• Pathophysiology
• Clinical features
• Investigation
Outlines cont.
• Diagnosis
• Complications
• Treatment
• Nursing management
• Prognosis
• Prevention strategies
• Conclusion
Endocarditis
• Inflammation of the endocardium layer of
the heart
Types of Endocarditis
(Bacterial Endocarditis )
• is an infection of the heart valves or the
heart’s inner lining (endocardium).
• occur if certain types of bacteria enter the
bloodstream.
• but occasionally fungi and other microbes
attack the lining of the heart or the heart
valves.
• It generally occurs in patients with altered and
abnormal heart architecture(septal defect)in
combination with exposure to bacteria
(Bacterial Endocarditis ) Cont..
• Bacterial endocarditis- causes growths
or holes on the valves or scarring of the
valve tissue, most often resulting in a
leaky heart valve.
• Before the age of modern antibiotics it was
almost universally fatal.
Causative organisms
The three most commons
1.Staphylococcus aureus
2. Streptococci of the Viridans group
3. Coagulase negative Staphylococci are the three
most common organisms responsible for infective
endocarditis.
4. Others
other types of Streptococci and
Enterococci are also a frequent cause of infective
endocarditis
Where these bacteria found ?
• can be found in the mouth,

• on the skin,
• in the intestines
• respiratory system
• in the urinary tract.
Epidemiology of IE
• Case rates
• 7-25% of cases involve prosthetic valves
• 25-45% of cases predisposing condition
can not be identified
Epidemiology of IE
• Pediatric population
• The vast majority (75-90%) of cases after the
neonatal period are associated with an
underlying congenital abnormality
• Bicuspid Aortic valve,VSD,Tetralogy of Fallot
• Risk of post-op infection in children with IE is
50%
Epidemiology
In U.S and Western Europe
• incidence of community acquired
endocarditis 1.7-6.2 cases/ 100,000
person/years.
• M:F ratio 1.7:1
Prosthetic Valves
7-25% of cases involve prosthetic valves
• mechanical and bio prostheses after 5 years Infection
rates same on both,
• but higher for mechanical in first 3 months
Onset:
• Early onset within 2 months of surgery and usually
hospital acquired
• late onset 12 months post surgery and usually
community acquired
Nosocomial Infective Endocarditis
• 7-29% of all cases seen in tertiary referral
hospitals->48 hours of hospitalization to
within 2-3months of discharge
• half of them due to intravascular devices
• Other sources: GU and GIT procedures or
Surgical-wound infection
Type of IE
Acute:
• usually occurs when heart valves are
colonized by virulent bacteria in the course
of microbemia.
Sub acute
usually have underlying valvular heart
disease and are infected by less virulent
organisms
Acute endocarditis most often occurs when an
aggressive species of especially a staphylococcus
(staph), enters the bloodstream and attacks a normal,
undamaged heart valve.
Once staph bacteria begin to multiply inside the heart,
they may send small clumps of bacteria called septic
emboli into the bloodstream to spread the infection to
other organs, especially to the kidneys, lungs and brain.
Intravenous (IV) drug users are at very high risk of acute
endocarditis, because numerous needle punctures give
aggressive staph bacteria many opportunities to enter
the blood. If untreated, this form of endocarditis can be
fatal in less than six weeks.
Subacute endocarditis :
Caused by one of the viridans group of streptococci

(Streptococcus sanguis, mutans, mitis or milleri) that
normally live in the mouth and throat.
Streptococcus bovis or Streptococcus equinus also can

cause subacute endocarditis, typically in patients who have
some form of gastrointestinal cancer, usually colon cancer.
Subacute endocarditis tends to involve heart valves that
already are damaged in some way, and it usually is less
likely to cause septic emboli than acute endocarditis.
If untreated, subacute bacterial endocarditis can worsen for
as long as one year before it is fatal.
Pathophysiology
 an intravascular catheter or other device may
directly abrade the endocardium. In injection drug
users, direct injection of contaminating debris may
damage the tricuspid valve surface.
 The endothelial damage triggers sterile thrombus
formation, which occurs by deposition of fibrin
and platelets.
 Physiologic stresses such as hypersensitivity
states, hormonal changes, and high altitude can
also induce sterile endocardial thrombosis
• Routine daily activities such as chewing food and
tooth brushing lead to frequent low-level, transient
bacteremias in healthy adults
• Bloodborne bacteria may adhere to the damaged
endocardial surface.
• Amount of dextran present in the streptococcal cell
wall, as well as specific surface proteins responsible
for adhere
• Once bacteria have attached to the endocardium,
the vegetation “matures” through additional
deposition of fibrin and bacterial proliferation.
• Fever occurs in 97% of people
• Malaise and endurance fatigue in 90% of people.
• A new or changing heart murmur
• Weight loss, and coughing occurs in 35% of people.
• Vascular phenomena: septic embolism (causing
thromboembolic problems such as stroke
or gangrene of fingers),
• Janeway lesions (painless hemorrhagic cutaneous
lesions on the palms and soles), intracranial
hemorrhage, conjunctiva hemorrhage, splinter
hemorrhages, kidney infarcts, and splenic infarcts.
• Immunologic phenomena: Glomerulonephritis
which allows for blood and albumin to enter the
urine,
• Osler's nodes (painful subcutaneous lesions in the
distal fingers), Roth's spots on the retina, positive
serum rheumatoid factor
• Other signs may include; night sweats, rigors,
anemia, spleen enlargement
Subacute IE Acute IE
bacterial weak strong
virulence
valve Have lesions normal
Dry, crisp A larger, soft
vegetation Bacteria are less, little  Many bacteria,
or no necrosis much necrosis
final result the vast majority of 50% died in days or
people heal weeks.
Bacteria ichorrhemia Sepsis
into the
blood
embolism Non-infectious Multiple embolic
infarction microabscesses
Common Peripheral
Manifestations.
(A)Splinter hemorrhages under the

fingernails, red for the first-two to
three days and brownish thereafter.
(B)Panel shows conjunctival

petechiae.
(C) Osler's nodes are tender,

subcutaneous nodules
(D)Janeway's lesions - nontender,

erythematous, hemorrhagic, or
pustular lesions often on the palms
or soles. 25
Vasculitis /Clubbing
27
28
Infective endocarditis:
metastatic infections due to
emboli.
Investigations
• Blood culture three –1/2 hour interval

from three different sites.
• Blood culture negative or may be
positive
• Investigations continued…
• ESR
• CRP
• CXR –PAV
• ECG
• Echocardiography Transthoracic -3-5mm of
vegetation sensitivity(65%)
• TEE –1-1.5mm of vegetation sensitivity
(90%)
Laboratory manifestations:%
• Anemia 70-90 %
• Leukocytosis 20-30 %
• Microscopic hematuria 30-50 %
• Elevated erythrocyte sedimentation rate>90 %
• Rheumatoid factor 50 %
• Circulating immune complexes 65-100 %
• Decreased serum complement 5-40 %
Definitive diagnosis with 80%
accuracy
2 major criteria
: 1 major and 3 minor criteria
: 5 minor criteria
: pathology/histology findings
• Possible : 1 major and 1 minor criteria
: 3 minor criteria
COMPLICATIONS
 Damage to valves & heart
 congestive cardiac failure, aortic valve
endocarditis, pericarditis, infection beyond valve→
CCF, tamponade or fistulae
 Embolic episodes
 Regurgitations
 Extension of infection to myocardium
 Abscess
 Conduction disorders(A-V, fascicular or bundle
branch block),
 Pulmonary abscesses.
• Treatment organism specific
• Inj Cetriazone 100 mg /kg per day IV for 6
weeks
• Inj. Gentamycin 5mg per kg /day two
weeks if no renal impairment for two
weeks
Prevention
Procedure recommended for prophylaxis
Nursing Management
Monitor
•Vital sign • CVP
•Pulse pressure • Arrhythmia
•Saturation • ABG
•Weight • Lungs sound
•s/s of embolization • Renal status
•BUN
Nursing Management
• Administer oxygen
• Rest and comfort
• Semi fowler position
• Measure i/o
• Record daily weight
• Administer iv antibiotic
• Administer antipyretic
• Evaluate jugular vein distension
Prognosis
• Despite the use of antibiotic agents,
mortality is at 20-25%.
• Serious morbidity occurs in 50-60% of
children with documented infective
endocarditis
• Comorbidity index, recurrence of
endocarditis, and history of an aortic valve
endocarditis in women were independent
predictors of excess mortality.
Conclusions
• Serious microbial infection
• Usually bacterial may be caused by other
microbes
• Majority cases in alter heart structure
• Prevention is the key concept
• Oral hygiene is very crucial
• Need longer antibiotic, debridement or valve
replacement
• Without treatment it may be fatal
Dr. T. N. Gupta
MD
Acute Rheumatic fever
 ARF is a sequlae of streptococcal infection— 2 to 3
weeks after group A streptococcal (GAS)pharyngitis
 Most commonly in children and has rheumatologic,

cardiac, and neurologic manifestations
 declined in most developed countries.
 Diagnosis rests on a combination of clinical

manifestations that can develop in relation to GAS
pharyngitis
 Rheumatic fever begins with a strep
throat (also called strep pharyngitis).
Strep throat is caused by Group A
hemolytic Streptococcus bacteria. It is
the most common bacterial infection of
the throat.
 Rheumatic heart disease is a condition in
which the heart valves are damaged by
rheumatic fever.
Rheumatic fever
 Rheumatic fever is an
inflammatory disease. It can
affect many of the body's
connective tissues — especially
those of the heart, joints, brain
or skin.
 Anyone can get acute rheumatic
fever, but it usually occurs in
children 5 to 15 years old. The
rheumatic heart disease that
results can last for life.
Rheumatic Fever (RF)
Definition:
 Rheumatic fever (RF) is an autoimmune disease
affecting the heart and extracardiac sites (joints,
brain, skin and others)
Three Basic Stages
Epidemiology
 Ages 5-15 yrs are most susceptible
 Rare <3 yrs
 Girls>boys
 Common in 3rd world countries
 Environmental /predisposing factors-- over crowding,
poor sanitation, poverty,
 Incidence more during fall ,winter & early spring
 In Developed countries , the prevalence is sporadic.
 Prevalence of acute rheumatic fever and RHD in Indian
population varies from 0.5 /1000 to 11/1000
 Prevalence in Nepal is 1.3 per 1000 school Children.
Nepal
 Nepal is a developing nation in South Asia with a
population of 2 crore 66 lakhs million people.
 Nepal Heart Foundation (NHF) has made an expert
estimate of prevalence of RHD at 2 per 1,000
schoolchildren.(2013)
 On this basis, the NHF estimates approximately
75,000 RHD patients live throughout the country
 The incidence of RF is estimated to be 15,000 per year
(Dr. PR Regmi)
ETIOLOGY
 Unknown
 Rheumatic fever(Group A beta hemolytic
streptococcus)
Theories of Pathogenesis:
 Toxic products of streptococci

 Immunologic cross-reactivity between Streptococcal
substances and heart muscle (heart reactive antibodies)
 Sensitized T-lymphocytes may lead to cardiac injury
PATHOPHYSIOLOGY
 Due to etiological factors and predisposing factors
 Erosion occurs at the valves of the heart specially mitral and

aortic valves
 Leading to inflammatory process
 Gradual development of the stenosis/regurgitation of the valves
 If not managed on timely, may develop Heart failure

Theories of Pathogenesis:
 Toxic products of streptococci

 Immunologic cross-reactivity between Streptococcal
substances and heart muscle (heart reactive antibodies)
 Sensitized T-lymphocytes may lead to cardiac injury
SIGN & SYMPTOMS(1944-1992
2015 Revised Johns criteria
Essential Criteria: Recent h/o sore throat or positive
throat swab culture or ASO titer or recent h/o scarlet
fever.
As revised John’s criteria

Initial RFA: 2major or 1 Major+2minor + Essential
Criteria
Recurrent ARF: 2major or 1 Major+2minor or 3 minor
CLINICAL FEATURES
 ARTHRITIS (35-66%)
 CARDITIS (50-70% OF CASES)
 CHOREA (10-30% OF CASES) female
 ERYTHEMIA MARGINATUM ( < 6%)
 SUBCUTANEOUS NODULES(10%)
Laboratory Findings
 High ESR>60mm
 Anemia, leucocytosis
 Elevated C-reactive protein
 ASO titre >200 Todd units.(Peak
value attained at 3 weeks, then
comes down to normal by 6 weeks)
 Throat culture-GABH
streptococci+ve fidgety
Laboratory Findings (Contd)
 ECG- prolonged PR interval, 2nd or 3rd
degree blocks,ST depression, T inversion
 2D Echo cardiography- valve edema,mitral
regurgitation, LA & LV dilatation,pericardial
effusion, decreased contractility.(Mitral valve is
attacked in 75-80%, the Aortic valve attacked in
30% and pulmonary and tricuspid valve in 5%) .
 Subclinical-pathological valvular regurgitation detected on

echocardiography that is not evident clinically repeat 14-
21days
RHEUMATIC HEART DISEASE
 Rheumatic heart disease: all the heart layers are
affected (pancarditis)
1. Rheumatic myocarditis
2. Rheumatic pericarditis
3. Rheumatic endocarditis
Aschoff’s body
Blood
fibrinoid degeneration
vessel
Aschoff cells
Rheumatic Mitral Valve
Small vegetations are

formed at injured parts
Rheumatic Mitral Stenosis
Fusion of commisures
Thick valve leaflet

CHRONIC RHEUMATIC VALVULAR DISEASE
 Mitral & Aortic Valves Pathology:
 Thickening of valve leaflet, especially along the lines of
closure
 Fusion of commissures
 Result is mitral or aortic stenosis, insufficiency, or both
Hemopericardium
EXTRACARDIAC LESIONS OF RHEUMATIC FEVER
Joints: Rheumatic arthritis affect the large joints in a fleeting way
i.e joint inflammation is followed by joint resolution, then
another joint become inflamed followed by resolution and so
on. The affected joint is painful, tender, hot & swollen.
Brain: Rheumatic chorea (rapid involuntary purposeless

movements); it is due to inflammation of the basal ganglia.
The condition is reversible
Skin: Rheumatic subcutaneous nodules occur over bony

prominences and their structure is similar to the Aschoff
bodies.
Rheumatic arteritis: affecting the coronaries, renal, mesenteric

and cerebral arteries
Pleurisy and peritonitis: serofibrinous type

Complication of ARF
 Arterial fibrillation to stroke
 Heart failure
 infective Endocarditis
 PAH
Treatment
 Step I - primary prevention
(eradication of streptococci)
 Step II - anti inflammatory treatment
(aspirin,steroids)
 Step III- supportive management &
management of complications
 Step IV- secondary prevention
(prevention of recurrent attacks)
Management of the acute attack.
Management of the current infection.
Prevention of further infection and attacks.
Acute Attack:
Eradicate streptococcal organisms & bacterial
antigens from the pharyngeal region.( Penicillin.
benzathine benzylpenicillin , cephalosporins,
erythromycin)
High doses of salicylates.
Corticosteroids : the treatment of severe carditis
Treatment for Heart failure: Digoxin, Diuretics,

vasodilators.
Chorea:
Haloperidol
Complete physical and mental rest.
STEP I: Primary Prevention of Rheumatic Fever
(Treatment of Streptococcal Tonsillopharyngitis)
Agent Dose Mode Duration
Benzathine penicillin G 600 000 U for patients Intramuscular Once
< 27 kg (60 lb)

1 200 000 U for patients >27 kg
or
Penicillin V Children: 250 mg 2-3 times daily Oral 10 d
(phenoxymethyl penicillin) Adolescents and adults:
500 mg 2-3 times daily
For individuals allergic to penicillin
Erythromycin: 20-40 mg/kg/d 2-4 times daily Oral 10 d
Estolate (maximum 1 g/d)
or
Ethylsuccinate 40 mg/kg/d 2-4 times daily Oral 10 d
(maximum
Recommendations 1 g/d) Heart Association
of American
What to do?
 Regular medicine
 PTMC
 Valve repair
 Valve replacement
INJECTION PENCILLINE
(PENCOM/PENIDURE
 Penicillin gets widely distributed through out
the body and reaches high concentration in
the urine. It also reaches significant level in
bile, liver, skeletal muscle, brain and plasma.
Its level gets raised in the present of
inflammation.
INDICATION & CONTRAINODICATION
OF INJ. B.PENICILLINE
INDICATION
 Rheumatic Heart Disease
 Rheumatic fever
CONTRAINDICATION
 Hypersensitivity
 Renal failure
 Lactation
PRECAUTATION
 Patient with a history of general
allergic
 Renal disease
 Intestinal disease
ROUTE OF ADMINISTRATION AND DOSES
DRUG WEIGHT IN DOSES DURATION

KGS
PENCILLINE <27 KG 6 LAKHs 3 WEEKLY

OR
1 MONTH
PENCILLINE >27 KG 12 ,,
LAKHs
Time Frame for Penicillin
Injection
 Category – 1
 Rheumatic fever but no
carditis
For the five years or
till the age of 21 ,
longer period should
be followed.
 Category – 2
 Rheumatic fever and carditis
but no residual effect to heart
valves
For the 10 years or till the age of 25 , longer
period should be followed.
Category – 3
 Rheumatic heart disease
Till the age of 40 or life long.
COMPLICATIONS OF INJECTION:
 Anaphylactic shock
 Vasovegal reaction
 Pain
 Haematoma
 Bleeding
 Infection
 Gangrene
SKIN TEST
 This is a test done on the skin to identify the
allergy substance( the allergen) that is the trigger
for an allergic
 Dose 0.1 ml of solution
 Route – Intra dermal
 Site forearms
PROCEDURE OF SKIN TEST
In this test a small needle is used to

prick the skin through 0.1ml of
Injection Penidura. It is usually done
on the forearm. The test is not painful
and results are immediately available.
SKIN TEST
PROCEDURE OF INJECTION
PENICILLIN:
Route: Intra muscular (Dorso-gluteal site)
Upper outer quarter
PROCEDURE OF INJECTION PENICILLIN:
Route: Intra muscular (Dorso-gluteal site)
 Same procedure of intra muscular injection.
 Special precaution such as:
 Patient accompanied by visitor.
 Patient shouldn’t be empty stomach.
 New patient should be explained about indication and
contra-indication of this injection.
 Consent should be taken.
 This injection should not be given to weak patient like
patient having fever, diarrhea, immediate after surgery,
dizziness, shortness of breath etc.
Cont…..
 Keep the patient in comfortable position.
 Give the Injection Penicillin.
 Immediate after inject watch the patient
condition.
 Watch the symptoms of anaphylactic shock.
ANAPHYLACTIC SHOCK
 Anaphylactic shock is a sudden catastrophic

allergic reaction that involves the whole body.
 Prompt medical treatment is essential otherwise
heart and circulation may fail and patient could
die
SIGN AND SYMPTOMS:
 Itchy skin and rashes

 Sneezing or runny nose with blockage.
 Coughing, wheezing and shortness of breath.
 Itchy red eyes and nose.
 Swelling of the mouth, vomiting and diarrhea.
 A generalized reaction then rapidly follows with an itchy
rash that spread over the whole body. The face and soft
tissues begin to swell and breathing becomes difficult.
 The pressure begins to drop. At this point the victim
collapse and loss consciousness.
 These symptoms develop very rapidly with in few minutes.
MANAGEMENT:
 First Aid.
 If the patient is conscious and having
breathing difficulties, help them to sit up. If
patient have low BP they are better off
lying flat with their legs raised.
 If the patient is unconscious, check their
airways and breathing and put them in
comfortable position.
 If you know that the person is susceptible
to anaphylactic, ask if they carry a Pre-
loaded adrenaline syringe.
 IV access
 Oxygen inhalation
 Intra-venous fluids
 Anti-histamine (Injection. Avil )
 Injection Adrenaline
 Injection Hydrocortisone
 If needed CPR should be established
immediately and transfer the patient
to critical care unit.
Valve replacement
 Manufactured Mechanical Valve
 Patients who receive a manufactured valve will nearly always require a
blood thinning medication throughout the remainder of their
lives. The blood thinner will keep clots from forming, which is critical
for the person with a mechanical valve because clots can lodge in the
valve flaps or hinges and cause a malfunction. Clots can also break off
and form into an embolism (traveling clot), which may move through
the bloodstream and lodge into a vessel where it may eventually lead
to problems like heart attack or stroke.
Tissue Valve (sometimes called ‘bioprosthetic’
valves)
 Tissue valves are created from animal donors’ valves
or other animal tissue that's strong and flexible.
Tissue valves can last 10-20 years, and usually don't
require the long-term use of medication. For a young
person with a tissue valve replacement, the need for
additional surgery or another valve replacement later
in life is highly likely.
Percutaneous Trans-Mitral
Commissurotomy
 is a procedure done for a cardiac pathology called
MITRAL STENOSIS. Mitral stenosis is a pathology of
one of the valves in the heart called the Mitral valve,
where-by it undergoes progressive thickening resulting
from child hood throat infection by a bacteria called
Beta Hemolytic Streptococci. This thickening of the
valve results in progressive obstruction to blood flow
across the valve thereby causing back pressure to build
inside the chambers behind the valve thereby resulting
in breathing difficulty, abnormal heart beats and even
clot formation leading to stroke or paralysis.
 The treatment for this condition may be open heart
surgery and replacement of the valve with a metal
valve or tissue valve or without open heart surgery by
means of a balloon passed into the heart and across
the valve via the leg usually, by means of a small tube
inserted under mere local anaesthesia, with the
patient being discharged usually with-in 2 days
following the procedure called Percutaneous Trans-
Mitral Commissurotomy or PTMC
THANK YOU
HEART FAILURE
Dr. T. N. Gupta
MD
Outlines
• Definition
• Introduction
• Epidemiology
• Major risk factors
• Etiology
• Pathophysiology
• Remodeling of the heart
• Types of heart failure
• Functional classifications of heart failure
• Compensatory mechanisms of heart failure
Outlines cont..
• Diagnosis
• Medical management
• Nursing management
• Complication
Definition
• Heart failure describes the clinical syndrome
that can results from any structural or
functional cardiac disorders that impairs the
ability of ventricles of the heart to fill with
blood or to eject blood.
Definitions
Heart failure is a clinical syndrome characterized by
decreased systemic perfusion, inadequate to meet
the body's metabolic demands as a result of impaired
cardiac pump function - Cleveland Clinic
A pathophysiologic state in which an abnormality of

cardiac function is responsible for failure of the heart
to pump blood at a rate commensurate with
metabolic requirements of the tissues -E Braunwald
Introduction
Heart failure may affect either side of
the heart but since both sides of the
heart are part of one circuit, when one
half of the pump begins to fail it
frequently leads to increase strain on
and eventual failure of the other side.
Introduction cont..
The heart pumps blood inadequately,
leading to reduced blood flow, back-up
(congestion) of blood in the veins and
lungs, and other changes that may
further weaken the heart.
Introduction cont..
• Heart failure does not mean
the heart has stopped working. Rather,
it means that the heart's pumping
power is weaker than normal.
• In heart failure, blood moves through
the heart and body at a slower rate, so
that pressure in the heart increases.
Epidemiology
• It affects 6 million Americans
• Roughly 670,000 people are diagnosed each
year
• Affects 10% of people over 65 years
• Affects over 50% of people with 85+ years
• Approx 10% of patients with HF die each yr.
• It is the most common condition for which
patients 65 + require admission to hospital
Major Risk Factors
Etiology
A. Mechanical abnormalities
1. Increased pressure load
– Central (aortic stenosis, aortic coarctation...)
– Peripheral (systemic hypertension)
2. Increased volume load
– valvular regurgitation
– hypervolemia
3. Obstruction to ventricular filling
– valvular stenosis
– pericardial restriction
B. Myocardial Damage
1. Primary
• Cardiomyopathy
• Myocarditis
2. Secondary
• Toxicity
• Hypothyroidism/hypothyroidism
• MI
• Lungs disease
• Kidney diseases
C. Altered Cardiac Rhythm
1. Ventricular flutter and fibrilation
2. Extreme tachycardia
3. Extreme bradycardias
Compensatory Mechanisms
1. Renin-angiotensin-aldosterone system
2. Sympathetic nervous system
• Release of epinephrine and norepinephirne
3. Structural changes:
 Enlargement of ventricles
 Enlargement of the muscular walls of the
ventricles (ventricular hypertrophy).
4. Frank - Starling mechanism
Pathophysiology
• Due to above mentioned causes
• Pump fails → decreased stroke volume /CO.
• Compensatory mechanisms kick in to increase
CO
– SNS stimulation → release of
epinephrine/nor-epinephrine
• Increase HR
• Increase contractility
Pathophysiology cont..
• Peripheral vasoconstriction (increases
after load)
– Myocardial hypertrophy: walls of heart thicken
to provide more muscle mass → stronger
contractions
– Hormonal response: ↓ renal perfusion
interpreted by juxtaglomerular apparatus
as hypovolemia. Thus:
• Kidneys release rennin, which stimulates
conversion of antiotensin I →
angiotensin II, which causes:
Pathophysiology cont..
–Aldosterone release → Na retention

and water retention (via ADH
secretion)
–Peripheral vasoconstriction
• Compensatory mechanisms may restore CO
to near-normal.
• But, if excessive the compensatory
mechanisms can worsen heart failure
Remodeling of the heart
To compensate for increased input due to
high blood pressure, the heart can grow in
size or enlarge. Because of elongation of the
heart muscle cells, which result in thinner
and weaker cell walls. The cell muscle itself
becomes thinner and weaker.
To compensate for weakened pumping
action, the nervous system can signal the
heart to beat faster. In the long run, this
actually create more damage.
Remodeling of the Heart cont..
• The body's blood vessel can also
change: to compensate for lower blood
flow, they constrict and become more
narrow. In turn, this cause the heart to
work harder and beat faster thus
increasing blood pressure and
compounding the vicious cycle that will
ultimately lead to heart failure.
Types
• Acute and chronic heart failure
• Left sided and Right sided heart failure
Types of heart failure cont..
Acute heart failure:
when the heart muscle suddenly and
often totally fails in its functions as a
pump the results of sudden failure are
shock, cardiac arrest, syncope and
sudden death.
Causes of acute heart failure
Acute Heart failure is caused by many condition
that damage the heart muscle including:
Etiology
• Myocardial infarction
• Pulmonary embolism, blocking blood flow through
the pulmonary circulation- the heart fails if it can not
pump hard enough to overcome the obstruction
• Severe cardiac arrhythmia
• Rupture of heart chambers or valve cusp
Chronic heart failure:
when heart failure that develops slowly and
has milder symptoms called chronic heart
failure.
Etiology
• Degenerative heart changes with advancing age
• Anemia
• Lung disease
• Hypertension
Types cont..
1. Left-sided heart failure
• Systolic dysfunction
• Diastolic dysfunction
2. Right-sided heart failure
Left Sided Heart Failure
• Systolic dysfunction (or systolic heart failure)
occurs when the heart muscle doesn't
contract with enough force, so there is less
oxygen-rich blood that is pumped
throughout the body.
• Diastolic dysfunction (or diastolic heart
failure) occurs when the heart contracts
normally, but the ventricles do not relax
properly or are stiff, and less blood enters
the heart during normal filling.
Common Symptoms of heart failure
29
Right sided
• The right ventricle fails when the
pressure developed within it by the
contracting myocardium is not enough
to push blood through the lungs.
31
Symptoms
Think FACES...
• Fatigue
• Activities limited
• Chest congestion
• Edema or ankle swelling
• Shortness of breath
The Vicious Cycle of Congestive Heart
Failure
Functional Classification of Heart Failure
New York Heart Association (NYHA)
Class of patients % Symptoms
No symptoms or
I 35% limitations in ordinary
physical activity
II 35% Mild symptoms and

slight limitation during
ordinary activity
III 25% Marked limitation in

activity even during
minimal activity.
Comfortable only at rest
IV 5% Severe limitation.
Experiences symptoms
even at rest
1.Patient history
2.Physical examination
3.Diagnostic studies
• Chest x-ray: whether the heart is
enlarged, whether there is congestion
in the lungs.
• ECG: low voltage, evidence of chamber
enlargement, ST, T changes and
arrhythmias
• Echo: LV ejection fraction, valvular lesions,
wall motion abnormalities
• cardiac catheterization with angiography:
indicated for severe cases of congestive heart
failure in an attempt to assess and evaluate
the progression and prognosis of the
syndrome.
• A biopsy of heart muscle is needed
Complications
• Pleural effusion
• Atrial fibrillation (most common
dysrhythmia)
– Loss of atrial contraction (kick) -reduce
CO by 10% to 20%
– Promotes thrombus/embolus formation
inc. risk for stroke
– Treatment may include cardioversion,
antidysrhythmics, and/or anticoagulants
Complications cont..
• High risk of fatal dysrhythmias (e.g., sudden
cardiac death, ventricular tachycardia) with HF
and an EF <35%
– HF lead to severe hepatomegaly, especially

with RV failure
• Fibrosis and cirrhosis - develop over time
– Renal insufficiency or failure
Mortality in HF
• Absolute mortality is approximately 50% within 5
years of diagnosis.
• In the ARIC study, mortality rates after hospitalization
30-day 10.4%
1-year 22%
5-year 42.3%
40
Management cont..
• Potassium supplements to prevent
digitalis toxicity and hypokalemia
• Diet: low sodium (small frequent ) to
limit fluid retention and promote fluid
excretion
• Paracentesis if ascites exist and causing
respiratory distress
Management cont..
• Cardiac resynchronization therapy: use of
right and left ventricular pace makers to
synchronize contraction and improve
cardiac output (Biventricular pacemaker )
• Heart transplantation
• Left ventricular assist device (LVAD)
Treatment Summary
1. Emergency management
• Position
• Oxygen
• Diuretics
• Morphine
2. Control with (Maintenance )
• Medication
• Diet
• Fluid restrictions
• CRT
• LVAD
Nursing management
• Keep the patient in comfortable position
preferably in semi/high fowler’s
position(propped up orthopnic position ).
• Administer oxygen and check oxygen
saturation.
• Monitor vital signs, neurostatus ,changes in
heart rate and respiratory rate/patterns as
well as changes in LOC.
• Elevate extremities except when the client is
in acute distress
Nursing management cont..
• Change position slowly and frequently
• Monitor intake and output
• Daily electrolyte
• Restrict fluid as ordered
• Collaborate with client to establish balance
schedule of rest and activities.
• Administer medications and assess the
patient’s response to them
• Weight the patient daily at the same time in
the same scale, usually in the morning after
the patient urinates.
• Evaluate electrolyte levels(Na, K and
creatinine)
• Assess the level of pain
• Assess degree of discomfort associated with
activity.
• Monitor for restless, anxious behavior and
promote self care participation.
• Provide high nutritional diet with low salt
and animal protein.
• Give passive exercise for prevention of
venous thrombosis in leg, chest infection and
bedsore.
• Maintain calm and quite environment.
• Monitor for increased crackles, Ronchi or
pulmonary congestion.
• Identify and evaluate the severity of edema
(assessing for pitting edema)
• Determine the degree of jugular vein
distension.
• Provide high nutritional diet with low salt
and animal protein
• Monitor the presence of ascites.
• Reassure the patient and the relatives to
reduce emotional stress .
Conclusion
• HF is common.
• HF has worse prognosis.
• Treatment should be focused on β-blocker,
ACEI and aldosterone antagonist .
THANK YOU
CARDIOMYOPATHY
AND
MYOCARDITIS
Dr. T. N. Gupta
CARDIOMYOPATHIES
INTRODUCTION
 Brigden -1956
 Heart Muscle Disease
 Primary disorders or disease of the heart

muscle
 Involves myocardium directly
 Are not the result of hypertension or
congenital, valvular, coronary, arterial or
pericardial abnormalities
CARDIOMYOPATHIES
CLASSIFICATIONS
1. Etiologic basis:
A. Primary Cardiomyopathy – No cause is found

heart muscle disease of unknown cause
i.e. Idiopathic DCM, Endomyocardial fibrosis,
Eosinophilic endomyocardial disease,
B. Secondary Cardiomyopathy –Myocardial disease of known

cause or associated with a disease involving other organ
system.
If the etiology is known.
CARDIOMYOPATHIES
2. Pathophysiology & Clinical
Classification:
a. Dilated Cardiomyopathy (DCM)
b. Hypertrophy Cardiomyopathy
c. Restrictive Cardiomyopathy
Dilated Cardiomyopathy (DCM)
- Left ventricles dilates and

- there is impaired ventricular contraction
- leading to progressive left sided and later on right sided heart failure.
Functional MR or TR
Etiology
1.Infection: Viral, Protozoal, Fungal, bacterial
2.Toxins: Alcohol
3.Drugs: Doxorubicin
3.Peripartum Cardiomyopathy,
4.Muscular dystrophy ( Friedrich ataxia)
5. Connective tissue disorders: SLE,PAN
6.Beriberi
7.Endocrine disorders: Thyrotoxicosis, DM, Myxedema
8.Reversible DCM : Pregnancy, Selenium def., Hypophosphatemia,
Hypocalcaemia, Cocaine abuse, Chr.uncontrolled tachycardia, alcohol abuse
Clinical Features
 Symptoms of left or right sided heart failure
 Exertional dyspnoea, fatigue, orthopnea, PND,
palpitation,
 Systemic embolization – Stroke & syncope
On examination
 Sinus tachycardia, Pulses alternans, AF, raised JVP,
edema, Hepatomegaly,Crepitation,3rd & 4th heart
sound,
 Murmur of MR & TR – LV dilated – AV ring dilate
Investigations
 EKG:
- AF, Ventricular arrhythmias, LBBB, low voltage QRS
complexes ,Non-specific ST –T wave changes
 X-ray chest:
- Cardiomegaly & lung congestion( Pulmonary edema)
 Echocardiography:
- Dilatation of all chambers & Global hypokinesia (LV)
- Color Doppler – MR & TR
 Cardiac Catheterization:
- LV dilatation & dysfunction, decreased cardiac output, increased
Lt. & Rt. sided filling pressure
 Transvenous endomyocardial biopsy:
- Amyloid, Acute Myocarditis
Differential Diagnosis
 IHD
 Alcoholic heart disease
Treatment
1.Anti- failure Treatment:
- Limited Physical activity
- S/R diet ,Ace – inhibitor,
- Diuretics ( Spironolactone),
- Digitalis,
- Angiotension II receptor blocker,
- B-blocker (Carvidilol),
- Anticoagulant – If AF or evidence of thromboembolism
2. Cardiac Transplant
3. Immunosuppressive therapy
5. ICD & Pump
4. Avoid proarrythmic drugs
 Death is due to CHF or Ventricular

arrhythmias
 Sudden death is constant threat
HYPERTROPHIC CARDIOMYOPATHY
 Left ventricular hypertrophy of unknown
cause.
 Familial (50%) or Sporadic
 Characterized by left ventricular
hypertrophy, typically of a non-dilated
chamber
 without any obvious cause such as
hypertension & AS
 Disproportionate LV hypertrophy typically
involving IVS more than LV free wall.
 Mid-systolic apposition of the AML against
hypertrophied IVS, i.e. SAM( systolic
anterior motion) of MV.
 Diastolic dysfunction –characterized by
increased stiffness – this results in elevated
diastolic filling pressure and is present
despite a hyperdynamic LV
Clinical Feature
 Variables, asymptomatic
 Dyspnoea, angina on effort, syncope, palpitation, Sudden death
 Pulse brisk & Jerky, rapidly raising carotid pulse
 Double or triple apical precordial impulse (Lt. atrial gallop & double systolic
impulse), 4th heart sound,
 Late onset Mid systolic diamond shape murmur in between LLSB & apex
 Murmur louder –Valsalva, & standing & decrease on Squatting
 Pansystolic murmur of MR – papillary muscle dysfunction
 Reverse splitting of S2 – severe obstruction
Investigations
1. EKG:
- LVH & LAE, Lt axis deviation
- Q wave in lead II,III, aVF
- Arrhythmias - AF/PSVT/VT
2. X-ray: Mild to Mod. Cardiac enlargement
3.Echo: Asymmetrical Septal hypertrophy (IVS:
Left ventricular free wall is 1.3 or more)
- Systolic anterior motion (SAM) of the
anterior mitral valve leaflet in mid systole in M-
mode.
Treatment
Progression of diseases cannot be checked
by any medicines.
Aim is to control the symptoms and prevent
sudden death.
1. Beta blockers – improves diastolic filling
2. Calcium channel blockers – Verapamil
3. Amiodarone – for arrhythmias
4. ICD ( Implantable cardioverter defibrillator)
5. Surgery – Myotomy / Myectomy
6. Infraction of the IV septum – induced by ethanol in septal artery
1st degree relatives should be screened
AOVID : Digitalis, Diuretics, Nitrates , B-agonist.
Predictors of sudden Death are:

 Age <30 yrs
 Ventricular tachycardia
 Syncope
 Family history
 Marked ventricular hypertrophy
 Previous history of resuscitation
RESTRICTIVE CARDIOMYOPATHY
 Hallmark is
- the ventricular wall are excessively rigid &
impede ventricular filling
- is abnormal diastolic function in the presence
of normal ventricular systolic function
- Right sided failure
Etiology : Two types

A. Myocardial
B. Endocardil
Myocardial Types:
Infiltrative – Amyloid, Sarcoid
Non-infiltrative – Idiopathic or Scleroderma
Storage disease – Hemochromatosis
Endocardial Types: Endomyocardial fibrosis, Carcinoid,
Metastatic malignancy
Clinical Features
 Similar to constrictive pericarditis
 Right sided heart failure – raised JVP, edema,
ascites,enlarged tender liver, heart sound distant, 3rd & 4th
heart sound present ,
Investigations
EKG: Low voltage complexes,
arrhythmias, non-specific ST-T changes
X-ray chest: Mild cardiomegaly
Echo: Symmetrical LVH, Diastolic dysfunction
Diagnosis is confirmed by cardiac catheterization &
endomyocardial biopsy
 D/D – Constrictive pericarditis, Primary
Amyloidosis, Sarcoidosis, Hemochromatosis,
Carcinoid Syndrome
Treatment
1.According to underlying cause /etiology
2.Steroids or cytotoxic drugs are used for the
treatment of endomyocardial fibrosis
3.Dysferamine in Hemochromatosis
MYOCARDITIS
Introduction
 Cardiac Inflammation
 Inflammation of Myocardium
Etiology
 Infection: cause myocardial damage by three basic
mechanism
-Invasion of the myocardium
-Production of a myocardial toxin
-Immunologically mediated damage
MYOCARDITIS
A. Infection
Viral – Coxsackie B, Polio, influenza, adeno, echo, rubella
 Bacterial – Diphtheria -25%. Liberation of toxin that inhibits protein
synthesis –leads to dilated ,flabby, hypocontractile heart and conducting
abnormalities. 1st wk Cardiomegaly – CHF,DCM – antitoxin/antibiotics
 Spirochetal –Leptospirosis, Lyme disease 10 %
 Parasites – Cystecercosis,Toxoplamosis
 Fungal – Aspergillosis
 Ricketssial – Q fever
 HIV – 10% of HIV
B. Hypersensitivity state – drugs, Ac. Rheumatic fever
C. Chemicals
D. Physical agents
E. Radiation
MYOCARDITIS
Clinical Features
Focal inflammation – asymptomatic
Diffuse myocarditis – Fulminant fatal heart
failure
Mild cases – Self limiting & often
unrecognized
Viral myocarditis initial episodes
unrecognized –idiopathic DCM
MYOCARDITIS
More overt cases-
 Acute congestive heart failure
 Arrhythmias – in structurally normal heart
 Non –specific symptoms – fatigue, dyspnoea, palpitation, precordial
discomfort
On examination:
Mild cases – no findings at all
In more severe cases
- tachycardia, muffled 1st heart sound, third heart
sound or ventricular gallop
- Transient apical systolic murmur (MR) , diastolic murmur are rare
- Precordial rub may be present
- Arrhythmias – tachy & brady
- Evidence of CHF ( crepitations, raised JVP, edema, hepatomegaly)
- Pulmonary & Systemic emboli
MYOCARDITIS
Natural History of Human myocarditis
Cardiotrophic viral infection –
1. Asymptomatic – complete recovery or DCM after long latency period
2. Symptomatic –
a. Fulminant presentation –
i. Death due to either Fulminant HF or Intractable arrhythmias
ii. Complete recovery
b. Non-Fulminant presentation
i. Progressive downhill course over months
- Death or Transplantation
ii. Spontaneous recovery
- asymptomatic for life
- recurrence of DCM after long latency period
iii. Recovery after immunosuppressive therapy
- recurrence after immunosuppressive therapy is stopped
- Asymptomatic for life
MYOCARDITIS
Investigations
1.EKG: Atrial & ventricular arrhythmias
Conduction defect, transient ST & wave changes
2.X-ray chest: Normal or markedly enlarged heart &
Pulmonary congestion
3.Echocardiography: LV systolic dysfunction, Global
Hypokinesia
4.Diagnosis: Viral myocarditis- detection of virus in stool,
throat washing, blood, myocardium, pericardial
fluid
5.Endomycardial biopsy: confirms the diagnosis of Myocarditis
MYOCARDITIS
Management
i. Bed rest ( restricted activity)
ii. Treat underlying cause of myocarditis
iii. Symptomatic arrhythmias – anti-arrhythmic agents
iv. CHF – S/R diet, diuretics, ace-inhibitors,
digoxin( low dose) sensitive to it
v. Steroids & immunosuppressive therapy –
role is controversial. No beneficial effect. Prognosis
Develops DCM
Death – Fulminant heart failure
ventricular arrhythmias
 Peripartum cardiomyopathy is DCM.
 Diuretics (spironolactone) in t/t of DCM.
 Avoid digiatlis,diuretics,nitrates,b-agonists in HCM.
 CAUSES of myocarditis :
cosxackie virus
bacterial- diptheria
spirochetes- leptospirosis
In 10% of HIV Patients
Conduction Disorders: Heart
Block
Dr. T. N. Gupta
MD
ANATOMY OF THE CONDUCTING
SYSTEM
• Pacemaker function of the heart resides in the
sinoatrial (SA)node
• Location At the junction of the right atrium and
superior vena cava.
• Approximately 1.5 cm long and 2 to 3 mm wide
• BLOOD SUPPLY OF SA NODE:

-Sinus node artery, which arises from either the
right coronary artery (60%)or the left circumflex
coronary artery (40%).
NERVE SUPPLY
• The SA node, atrium, and AV node are significantly
influenced by autonomic tone.
• Vagal influences :
- Depress automaticity of the SA node
- Depress conduction
- Prolong refractoriness in the tissue
surrounding SA node
- Prolong AV nodal conduction and refractoriness.
• Sympathetic influences exert the opposite effect.
Normal Heart Function
Sinoatrial Node
Atrioventricular Node
Bundle of HIS
Left Bundle Branch (LBB)
Posterior Fascicle of LBB
Anterior Fascicle of LBB
Right Bundle Branch (RBB)

Purkinje Fibers
Sinus Node Dysfunction
1.Sinus bradycardia
2.Sinus arrest
3.SA block
4.Brady-tachy syndrome
5.Chronotropic incompetence
Causes of sinus node dysfunction
• Idiopathic
- Degenerative process
- Normal aging
• Acute myocardial ischemia or infarction
- Right or left circumflex artery occlussion
- Jarisch-bezold reflex
• Medications
- Beta blockers
- Diltiazem, Verapamil
- Digitalis
-Class I antiarrhythmic agents
- Class III antiarrhythmic agents ( Amiodarone, Sotalol)
- Clonidine
SINUS NODE DYSFUNCTION
• Miscellaneous
-Senile amyloidosis
-Hypothyroidism
-Advanced liver disease
-Hypothermia
- Typhoid fever
- Brucellosis
-Hypervagotonia(vasovagal syncope),severe
hypoxia, hypercapnia, acidemia, and acute
hypertension
MANIFESTATIONS
• Fatigue
• Paroxysmal dizziness
• Presyncope or syncope.
Sick sinus syndrome
• Combination of symptoms
-Dizziness
-Confusion
-Fatigue
-Syncope
- Congestive heart failure
• Caused by SA node dysfunction
• Manifested by marked sinus bradycardia,
sinoatrial block, or sinus arrest.
Conditions associated with vagally
mediated bradyarrhythmias
• Sleep
• Vomiting, retching
• Suctioning
• Nasal intubation
• Gastric intubation
• Urination
• Defecation
• Coughing
• Swallowing
• CNS trauma with high intracranial pressure
Sinus Bradycardia
Persistent slow rate from the SA node.

 Theparameters from this waveform include:
Rate <60 bpm
PR interval = 180 ms (.18 seconds)
Sinus Arrest
Failure of sinus node discharge resulting in the absence of

atrial depolarization and periods of ventricular asystole
PR interval = 180 ms (.18 seconds)

SA Exit Block
Transient blockage of impulses from the SA node

Rate = 52 bpm
PR interval = 180 ms (.18 seconds)
Bradycardia-Tachycardia (Brady-Tachy)
Syndrome
Intermittent episodes of slow and fast rates from the SA node or

atria
Rate during bradycardia = 43 bpm
Rate during tachycardia = 130 bpm
Bradycardia-tachycardia
syndrome
Rhythm strip of ECG lead II showing spontaneous cessation of supraventricular

tachycardia followed by a 6-s pause prior to resumption of sinus activity.
Patient was asymptomatic during supraventricular tachycardia, but the sinus

pause caused severe light-headedness.
TREATMENT
• Permanent pacemakers are the mainstay of therapy for
patients with symptomatic SA node dysfunction.
• Patients with symptomatic chronic sinus bradycardia or

frequent prolonged episodes of sinus node dysfunction do
better with dual-chamber pacemakers that preserve the
normal AV activation sequence.
• Recent studies suggest that AV sequential pacing may

also be useful in preventing atrial fibrillation, an important
component of the bradycardiatachycardia syndrome, and
stroke, a known complication of atrial fibrillation.
AV Block
First-degree AV block
Second-degree AV block
Mobitz types I and II
Third-degree AV block
Bifascicular and
Trifascicular block
Causes of Acquired AV Block
• Idiopathic AV Block
• Coronary artery disease
• Calcific valvular disease
• Postoperative or traumatic
• AV node ablation
• Therapeutic irradiation of chest
• Infectious:
- syphilis
-Diptheria
-Chagas’disease
-Tuberculosis
-Toxoplasmosis
-lyme disease, viral myocarditis, infective endocarditis
• Collagen vascular disease
-RA, Scleroderma, Dermatomyositis,
Ankylosing spondylitis, PAN, SLE, Marfan syndrome
• Infiltrative
-Sarcoidosis, Amyloidosis,haemochromatosis,malignancy
• Neuromuscular
-Kearns –sayre syndrome
-Myotonic muscular dystrophy
-Peroneal muscular atrophy(Charcot-Marie-Tooth disease)
-Scapuloperoneal syndrome
- Limb gridle dystrophy
• Drug effect :
- Digoxin, Beta blockers, Ca-blocking agents,
Amiodarone,Class I C agents
Types of heart block:
• First-degree AV block
-In the presence of a QRS complex of normal
duration, a PR interval 0.24 s almost invariably
is due to a delay within the AV node.
• Second-degree heart block
1. Mobitz type I second-degree AV block (AV
Wenckebach block)
2. Mobitz type II second-degree AV block
• Third-degree heart block or Complete heart
block
First-Degree AV Block
AV conduction is delayed, and the PR interval

is prolonged (> 200 ms or .2 seconds)
Mobitz type I second-degree AV
block
• Progressive PR interval prolongation prior to
block of an atrial impulse
• Pause that follows is less than fully compensatory
(i.e., is less than two normal sinus intervals)
• PR interval of the first conducted impulse is
shorter than the last conducted atrial impulse
prior to the blocked P wave.
• Difference between the longest and shortest PR
intervals exceeds 100 ms.
Second-Degree AV Block
Mobitz I (Wenckebach)
Progressive prolongation of the PR interval until a ventricular beat is dropped

Ventricular rate = irregular
Atrial rate = 90 bpm
PR interval = progressively longer until a P-wave fails to conduct
NoQRS
Second Degree AV Block Mobitz II
• Conduction fails suddenly and unexpectedly

without a preceding change in PR intervals
• Due to disease of the His-Purkinje system
and is most often associated with a prolonged
QRS duration.
• Important to recognize this type of block
because it has a high incidence of
progression to complete heart block with an
unstable, slow, lower escape pacemaker.
Second-Degree AV
Block Mobitz II
Regularly dropped ventricular beats

2:1 block (2 P waves to 1 QRS complex)
Ventricular rate = 60 bpm
Atrial rate = 110 bpm
Third-degree AV block
 P waves are completely dissociated from the QRS complexes.
 QRS complexes are narrow, indicating a junctional escape rhythm.
 The atrial and ventricular rates are stable

Bifascicular Block
Right bundle branch block

and left posterior hemiblock
Bifascicular Block
Bifascicular block refers to
conduction disturbances below
the atrioventricular (AV) node in
which the right bundle branch
and one of the fascicles of the
left bundle branch are involved.
Right bundle branch block

and left anterior hemiblock
Trifascicular Block
• Complete block in
the right bundle
branch and complete
or incomplete block
in both divisions of
the left bundle
branch
• Prolongation of PR
interval
TREATMENT
• Pharmacologic Therapy
-Atropine (0.5 to 2.0 mg intravenously)
-Isoproterenol (1 to 4 mcg/min intravenously)
-Pacemakers
-TEMPORARY PACING
-PERMANENT PACING
TACHYARRHYTHMIAS
Tachyarrhythmias
• Commonly encountered entities in
practice
• Defined as cardiac rhythms whose
ventricular rate exceeds 100 bpm.
• Based on the QRS duration:
Narrow complex (QRS < 120 ms)
Broad complex (QRS > 120 ms)
Atrial Fibrillation
• Irregular rhythm
• Absence of definite p waves
• Narrow QRS
• Can be accompanied by rapid ventricular response
MAT
PAC
• P wave from another atrial focus

• Occurs earlier in cycle
• Different morphology of p wave
Atrial Flutter
Classic
II inverted
“sawtooth”
flutter waves
4:1 2:1 at 300 min-1
(best seen in
V1 II, III and AVF)
Note variable
ventricular
response
A three-lead ECG rhythm strip during sinus rhythm and the abrupt onset of
orthodromic AV-bypass tachycardia. Arrows indicate the retrograde P waves
visible in lead II.
WIDE - COMPLEX
TACHYCARDIA
Monomorphic
VT
Polymorphic
VT
V1
Torsades de Pointes
Ventricular Fibrillation (VF)
• Totally chaotic rapid ventricular rhythm

• Often precipitated by VT
• Fatal unless promptly terminated (DC shock)
TREATMENT
Hemodynamically unstable!
• Don’t Panic.
• It doesn’t matter whether it is wide-

complex or narrow – DC shock is the
easiest, fastest and most efficient solution.
Treatment of SVT
• ACUTE TREATMENT: vagal maneuvers,
short acting a-v nodal blocking agents-
adenosine, verapamil, dilitiazem,
metoprolol.
• CHRONIC PHARMACOLOGIC
TREATMENT: CCB, BRB
• RADIOFREQUENCY ABLATION: high
success rate, definitive cure.
Carotid Sinus Massage
Stimulation of
carotid sinus
triggers
baroreceptor
reflex and
increased vagal
tone, affecting
SA and AV
nodes
RATE CONTROL IN AF
• Rationale
– Control of symptoms
– Tachycardia-related cardiomyopathy
• Drugs
– Digoxin
 -blockers
– Calcium channel blockers
• Invasive
– AV node ablation / permanent pacemaker
RESTORATION OF SINUS
RHYTHM
• DC cardioversion or pharmacologic
conversion if less than 48 hours duration
or following TEE on Heparin without
evidence of left atrial thrombus.
• Following cardioversion : anticoagulation
for 4 weeks with goal INR of 2 to 3 until
atrial function normalizes.
• DRUGS: Ibutilide is the only approved
drug.
Chronic Management of Atrial
Fibrillation
• Patients with atrial fibrillation, paroxysmal or
sustained should be anticoagulated if any of
the following risk factors for stroke are
present:
– diabetes – hypertension
– valvular disease – congestive heart failure
– hyperthyroidism – age greater than 65
– Prior CVA
Chronic management of Atrial
Fibrillation
• Class III agents may • Class IC agents safe
have improved in absence of
efficacy structural heart
– Amiodarone disease.
• pulmonary toxicity • Few side effects
• thyroid • Need stress testing
• liver
• Can lead to 1 to 1
– Dofetilide ventricular
• Torsades des Pointes conduction of atrial
– Safe in CHF and flutter
CAD • Use with beta blocker
– Limited due to side
effect profile
Treatment of ATRIAL FLUTTER
• ANTICOAGULATION : Same guidelines
as in AF
• RATE CONTROL: Same agents as used
in AF ( agents those reduce a-v nodal
conduction)
• OVERDRIVE ATRIAL PACING
• CATHER ABLATION
TREATMENT OF VT & VF
• UNSYNCHRONISED DC
CARDIOVERSION: primary therapy for
pulseless VT & VF
• DRUGS:
LIDOCAINE, MEXILITINE, BRB, SOTALOL,
AMIODARONE, PHENYTOIN
• ICD.
• RADIOFREQUENCY CATHETER
ABLATION
Implantable Cardiodefibrillator
• Superior to Drug therapy in patients with
sudden death and coronary disease
• Reduced risk of death in patients with
sudden death coronary disease and EF
<35% over drugs
• Reduces risk of death in patients with
inducible VT and reduced L.V. fxn and
CAD by nearly 50%
Treatment of Torsades de
Pointes
• DC Cardioversion
• Remove Offending Agent
• Replete Potassium
• Treat with Magnesium even if normal
• Consider increasing heart rate
– isoproterenol
– Pacing
• Treat Congenital with Beta blockers and Pacing
or ICD
• ?Cervicothoracic sympathectomy
all cases accompanied
with hypoxia
extracardiac
Causes of cardiac
arrest
cardiac
Primary lesion of cardiac muscle leading to the
progressive decline of contractility, conductivity
disorders, mechanical factors
Causes of circulation
arrest
Cardiac Extracardiac
• Ischemic heart disease • airway obstruction
(myocardial infarction,
stenocardia) • acute respiratory failure
• Arrhythmias of different • shock
origin and character
• Electrolytic disorders • reflector cardiac arrest
• Valvular disease • embolisms of different origin
• Cardiac tamponade • drug overdose
• Pulmonary artery
thromboembolism • electrocution
• Ruptured aneurysm of aorta • poisoning
arrest
Blood pressure measurement

Taking the pulse on peripheral
arteries

Loss of time !!!
Auscultation of cardiac tones
Symptoms of cardiac
 arrest
absence of pulse on carotid arteries – a
pathognomonic symptom
 respiration arrest – may be in 30 seconds after
cardiac arrest
 enlargement of pupils – may be in 90 seconds after
cardiac arrest
VENTRICULAR FIBRILLATION OR PULSELESS TACHYCARDIA
Witnessed Unwitnessed
Precordial thump
Check pulse, if none:
Begin CPR
Defibrillate with 200 joules
Defibrillate with 200-300 joules
Establish IV access, intubate
Adrenaline 1 mg push
Lidocaine 1 mg/kg IV, ET
Operations in case of asystole
Asystole
•Start CPR
• IV line
• Adrenaline:IV 1 mg, each 3-5 min.
-or
- intratracheal 2 - 2.5 mg
- in the absence of effect increase
the dose
-Atropine 1 mg push (repeated once
in 5 min)
•Na Bicarbonate 1 Eq/kg IV

•Consider pacing
OBJECTIVE
1. Define defibrillation.
2. State the purpose of defibrillation.
3. Describe the mechanism of defibrillation.
4. Identify the equipment used in defibrillation and
its preparation
5. Demonstrates the procedure of defibrillation
6. Identify the precautions to be observe in
defibrillation.
7. Describe the complications associated with
defibrillation.
8. Describe the care after defibrillation
2
NORMAL CONDUCTION SYSTEM OF
THE HEART
3
CARDIOVERTER/DEFIBRILLATOR
Definition of Cardioversion
• Cardioversion is a method to restore a
rapid heart beat back to normal –Mayo
clinic.
• Cardioversion is used in persons who

have heart rhythm problems
(arrhythmias), which can cause the heart
to beat too fast. ----Wikipedia
Cardioversion is a process that aims to
convert an arrhythmia back to sinus rhythm.
Electrical cardioversion is used when the
patient has a pulse but is either unstable, or
chemical cardioversion has failed or is unlikely
to be successful.
Cardioversion
PURPOSES:
• To treat atrial fibrillation or atrial flutter to

regain heart rhythm.
• To treat disturbances originating in the upper

Chambers (atria) of the heart.
Indications for electrical cardioversion include
the following:
• Supraventricular tachycardia (atrioventricular
nodal reentrant tachycardia [AVNRT] and
atrioventricular reentrant tachycardia [AVRT])
• Atrial fibrillation
• Atrial flutter
• Ventricular tachycardia with pulse
INDICATION
Any patient with reentrant tachycardia with
narrow or wide QRS complex (ventricular rate
>150 bpm) who is unstable (eg, ischemic chest
pain, acute Pulmonary edema, hypotension,
acute altered mental status, signs of shock)
CARDIOVERSION
Types Of Cardioversion
Cardioversion can be "chemical" or

"electrical".
• Chemical cardioversion: refers to the use of

antiarrhythmia medications
to restore the heart's normal rhythm.
Types Of Cardioversion
Electrical cardioversion : (also known

as " direct-current" or DC cardioversion);
is a procedure whereby a synchronized
electrical shock is delivered through the chest
wall to the heart through special electrodes
or paddles that are applied to the skin
of the chest and back.
PREPARATION
• Nil per os (NPO) for 8 hours prior to the
procedure
• Stop digoxin 48 hours prior to the procedure
• Continue medications on the morning of the
procedure under the direction of the physician
• After the procedure, do not drive, operate
machinery, or sign important documents for 24
hours and/or until sedation has worn off
Defibrillation
Defibrillation is a process in which an

electronic device sends an electric
shock to the heart to stop an
extremely rapid, irregular heartbeat,
and restore the normal heart rhythm.
---- Medical dictionary.
15
Defibrillation
It is an immediate treatment for the life-
threatening arrhythmias in which the patient
does not have a pulse, ie ventricular fibrillation
(VF) or pulseless ventricular tachycardia (VT). ---
Wikipedia
INDICATION
Indications for defibrillation include the
following:
• Pulseless ventricular tachycardia (VT)
• Ventricular fibrillation (VF)
• Cardiac arrest due to or resulting in VF
CONTRA- INDICATION
• Dysrhythmias due to enhanced
automaticity, such as in digitalis
toxicity and catecholamine-
induced arrhythmia
• Multifocal atrial tachycardia

EQUIPMENT
• Defibrillators (automated external
defibrillators [AEDs], semiautomated AEDs,
standard defibrillators with monitors)
• Paddle or adhesive patch
• Conductive gel or paste
• ECG monitor with recorder
• Oxygen equipment
• Intubation tray
EQUIPMENT
• Emergency pacing equipment
• Blood pressure cuff (automatic or manual)
• Pulse recorder
• Oxygen saturation monitor
• Intravenous access
• Suction device
• Code Cart with ACLS (Advanced
Energy selection for defibrillation or
cardioversion
• In 2015, the American Heart Association
issued guidelines for initial energy
requirements for monophasic and biphasic
waveforms. [9]
• Energy requirements are as follows:
• 50-150 Joules for monophasic and biphasic
devices
• 100 joules for Common devices
• Ventricular tachycardia with pulse energy
requirements are as follows:
• 200 Joules for monophasic devices
• 100 Joules for biphasic devices
• Ventricular fibrillation or pulseless ventricular
tachycardia energy requirements are as follows:
• 360 Joules for monomorphic devices
• 270 Joules for biphasic devices
PREPARATION
• Nil per os (NPO) for 8 hours prior to the
procedure
• Stop digoxin 48 hours prior to the procedure
• Continue medications on the morning of the
procedure under the direction of the physician
• After the procedure, do not drive, operate
machinery, or sign important documents for 24
hours and/or until sedation has worn off
Defibrillation
Purpose:
Defibrillation is performed to correct life-
threatening fibrillations of the heart, which
could result in cardiac arrest. It should be
performed immediately after identifying
that the patient is experiencing a cardiac
emergency, has no pulse, and is
unresponsive.
26
Defibrillation
Precautions:
1. Defibrillation should not be performed on a
patient who has a pulse or is alert, as this
could cause a lethal heart rhythm disturbance
or cardiac arrest.
2. The paddles used in the procedure should
not be placed on a woman's breasts or over
a pacemaker
27
Defibrillation
Mechanism:
Fibrillations cause the heart to stop pumping
blood, leading to brain damage.
Defibrillators deliver a brief electric shock to the
heart, which enables the heart's natural
pacemaker to regain control and establish a
normal heart rhythm.
28
Defibrillation
Preparation:
• After help is called for, cardiopulmonary
resuscitation (CPR) is begun and continued until the
caregivers arrive and set up the defibrillator.
• Electrocardiogram leads are attached to the patient's
chest.
• Gel or paste is applied to the defibrillator paddles, or
two gel pads are placed on the patient's chest.
• The caregivers verify lack of a pulse.
29
DURING DEFIBRILLATION
• Place the paddles on the sternum and another
one at the apex of the heart.
• Press the charge button
• Announce I CLEAR, YOU CLEAR AND ALL CLEAR
Deliver the shock.
Care after cardioversion and
defibrillation
The patient's cardiac status, breathing, and vital
signs are monitored until he or she is stable.
An electrocardiogram and chest x ray are taken.
The patient's skin is cleansed to remove gel or
paste, and, if necessary, ointment is applied to
burns.
An intravenous line provides additional medication,
as needed.
31
Complications:
• Skin burns from the defibrillator

paddles are the most common.
• Other risks include injury to the
heart muscle,
• abnormal heart rhythms,
• and blood clots.
32
Points to be remember while
Defibrillating.
• Provided by nursing staff that are certified to
perform defibrillation.
• The success of resuscitation of patients with
ventricular fibrillation relates to how fast
electrical defibrillation can be applied.
• The longer the duration of fibrillation, the
greater the deterioration of the myocardium,
because a fibrillating heart consumes a very
large amount of oxygen.
33
THANK YOU
AORTIC REGURGITATION AND
AORTIC STENOSIS
Dr. T. N. Gupta
MD
Aortic Regurgitation
 Aortic regurgitation is the flow of blood back into the left

ventricle from the aorta during diastole.
 Causes include:
 Inflammatory lesions that deform the leaflets of the aortic
valve
 Endocarditis
 Congenital abnormalities, diseases such as syphilis
 A dissecting aneurysm that causes dilation or tearing of the
ascending aorta
 Deterioration of an aortic valve replacement
Pathophysiology
 Blood from the aorta returns to the left ventricle during

diastole
 Left ventricle dilates, trying to accommodate the increased
volume of blood
 Left ventricle hypertrophies, trying to increase muscle
strength to expel more blood
 Arteries attempt to compensate for the higher pressures
by reflex vasodilation
 Peripheral arterioles relax, reducing peripheral resistance
and diastolic blood pressure
Clinical Manifestations
 Sudden manifestations of cardiovascular collapse

 Severe dyspnea, chest pain and hypotension
indicating Left ventricular failure
 Cardiogenic shock, life threatening emergency
 Exertional dyspnea, orthopnoea and paroxysmal
nocturnal dyspnea develop after considerable
dysfunction of heart
Diagnostic Investigations
 Diastolic murmur is heard as a high-pitched, blowing

sound at the third or fourth intercostal space at the
left sternal border
 Pulse pressure (difference between systolic and
diastolic pressures) is considerably widened
 Water-hammer pulse, in which the pulse strikes the
palpating finger with a quick, sharp stroke and then
suddenly collapses
 Diagnosis may be confirmed by

 Echocardiogram
 Radionuclide imaging
 ECG
 Magnetic resonance imaging
 Cardiac catheterization
Medical Management
 Antibiotic prophylaxis is needed to prevent

endocarditis before the patient undergoes invasive or
dental procedures
 Aortic valvuloplasty or valve replacement
 Surgery is recommended for any patient with left
ventricular hypertrophy, regardless of the presence
or absence of symptoms
Aortic Stenosis
 Aortic valve stenosis is narrowing of the orifice

between the left ventricle and the aorta.
 Causes include:
 Congenital leaflet malformations
 Rheumatic endocarditis
 Cusp calcification of unknown cause
 Fused leaflets of aortic valve
Pathophysiology
 Progressively narrowing of valve orifice

 Left ventricle contract slowly but with greater energy
 Obstruction to left ventricular outflow increases
pressure on the left ventricle
 Heart muscle hypertrophies
 When these compensatory mechanisms of the heart
begin to fail, clinical signs and symptoms develop
Pathophysiology of Aortic Stenosis
 Exertional dyspnea, caused by left ventricular failure.

 Dizziness and syncope because of reduced blood flow
to the brain.
 Angina pectoris that results from the decreased blood
flow into the coronary arteries.
 May be a low pulse pressure (30 mm hg or less)
because of diminished blood flow.
 Systolic crescendo-decrescendo murmur which is low-

pitched, rough, rasping, and vibrating may be heard
over the aortic area
 If the examiner rests a hand over the base of the
heart, a vibration may be felt.
 Evidence of left ventricular hypertrophy may be seen
on a 12-lead ECG and echocardiogram.
 Left-sided heart catheterization is necessary to
measure the severity of the valvular abnormality
Medical Management
 Antibiotic prophylaxis to prevent endocarditis

 After left ventricular failure or dysrhythmias occur,
medications are prescribed
 Definitive treatment is surgical replacement of the
aortic valve
 Patients who are not surgical candidates may benefit
from one- or two-balloon percutaneous valvuloplasty
procedures
Medical Management
 Drug alert: Nitroglycerine

 Use cautiously in patient with Aortic Stenosis, since
significant hypotension may occur
 Chest pain can worsen due to decrease in preload and
drop in BP.
Nursing Management
 Health education on valvular heart disease

 Emphasizes the need for prophylactic antibiotic
therapy before any invasive procedure
 Patient’s heart rate, blood pressure, and respiratory
rate are measured
 Heart and lung sounds are auscultated and peripheral
pulses palpated
 Assess for signs and symptoms of heart failure
Nursing Management
 Assesses for dysrhythmias by palpating the patient’s pulse

for strength and rhythm
 Assesses for dizziness, syncope, increased weakness, or
angina pectoris
 Collaborates with the patient to develop a medication
schedule and teaches about the name, dosage, actions,
side effects
 Assist the patient with planning activity and rest periods to
achieve a lifestyle acceptable to the patient
Mitral Regurgitation
Mitral Stenosis
Dr. T. N. Gupta
MD
Mitral Regurgitation
 Mitral regurgitation (MR) involves blood
flowing back from left ventricle into left
atrium during systole.
 Often the margin of mitral valve cannot
close during systole.
 The leaflets cannot close because of
thickening and fibrosis of leaflets and
chordae tendinae resulting in their
contraction.
Etiology
 Degenerative changes of mitral valve
(e.g.mitral valve prolapse)
 Ischemia of left ventricle
 Rheumatic heart disease
 Myxomatous changes which enlarges left
atrium and ventricle
 Infective endocarditis may cause
perforation of leaflet
 Collagen vascular diseases (e.g. systemic
lupus erythematous)
 Cardiomyopathy
Pathophysiology
Clinical Features
Symptoms :
 Chronic mitral regurgitation is often
asymptomatic
 Acute mitral regurgitation usually
manifests as severe congestive
heart failure
 Fatigue
 Dyspnea on Exertion
 Palpitation
 Cough
Clinical Features
Signs
 Pulse: Brisk carotid upstroke, Atrial
Fibrillation
 Blood Pressure: Usually normal
 Apex: Laterally displaced, diffuse, ill
sustained
 S1 - Normal
 S3 - Present (severe MR, and increases
with expiration)
 Murmur - Loud holosystolic murmur at the
apex radiating to the left axilla
Investigations
E.C.G.
 Atrial fibrillation in 60 – 75 %, and 50 % in surgically
corrected cases.
 Left Ventricular Hypertrophy
Chest X – Ray
 Cardiomegaly
 Dilated Left Atrium
Echocardiography:
 Loss of function of leaflets
 Dilated Left Atrium, Left Ventricle and Left
Ventricular Hypertrophy
 Rheumatic MR – thickened leaflets
 Ischaemic MR - ruptured chordae, regional wall
motion abnormalities, flail leaflets
Investigations
 Doppler echocardiography is used to
diagnose and monitor the
progression of mitral regurgitation.
 Transesophageal echocardiography
provides the best images of the
mitral valve.
Medical Management
 Management is similar to congestive heart
failure.
 Patients with MR benefit from after load

reduction (arterial dilation) by treatment with,
Angiotensin converting enzyme (ACE) inhibitors
Hydralazine
 Rheumatic fever and Infective endocarditis

prophylaxis.
 Atrial fibrillation rate is control by use of digoxin

and beta blockers, amiodarone.
Surgical Management
 Mitral valve reconstruction

 Mitral valve replacement
MVR should be performed before

LV function deteriorates
irreversibly.
Mitral Stenosis
 Mitral stenosis is an obstruction of
blood flowing from the left atrium into
the left ventricle.
 Often caused by rheumatic

endocarditis, which progressively
thickens the mitral valve leaflets and
chordae tendineae.
 The leaflets often fuse together.

Mitral Stenosis
Etiology
Rheumatic Fever
Congenital
Infective Endocarditis
Connective Tissue Disorders
Massive Annular Calcification
Endocardial Fibroelastosis
Prosthetic Valve
Pathophysiology
Pathophysiology
Clinical Features
 Dyspnea on exertion
 Hoarseness (from atrial
enlargement pressing on the
laryngeal nerve)
 Hemoptysis (from pulmonary
hypertension)
 Fatigue (from atrial fibrillation)
 Chest pain (from decreased CO
and coronary perfusion)
Clinical Features
 Atrial fibrillation on ECG
 Palpitations
 Stroke (from emboli)
 Loud, accentuated S1
 Low pitched, diastolic murmur
(best heard at apex with the
stethoscope)
Complications of Mitral
Stenosis
 Atrial Fibrillation
 Embolism
 Acute Pulmonary oedema
 Pulmonary HTN
 Right Ventricular Hypertrophy / Dilatation
 Left Ventricular Dysfunction
 Tricuspid Regurgitation
 Heart Failure
 Infective Endocarditis
Investigations
 ECG and cardiac catheterization with
angiography may be used to determine the
severity of mitral stenosis.
 Chest X- Ray:
 Heart shadow normal in size
 Evidence of LA enlargement:
Straightening of left heart border
 Central radio density
 Elevation of left main bronchus
Investigations
ECHOCARDIOGRAPHY
 Thickened / Calcified Leaflets

 Thickening / Shortening / Fusion of chordae
 Fusion of the commissures
 Calcification of the annulus
 Decreased EF slope (Normal 70 to 150 cm/
sec)
 LA enlargement / thrombus
 LV size: normal or small
 RV: enlarged
Treatment
A) Medical
 Rheumatic fever prophylaxis

 Infective endocarditis prophylaxis
 Restriction of physical activity within one’s
cardiac reserve
 Arrhythmias – restore sinus rhythm if
possible
 Emboli – anticoagulants
 Elevated pulmonary venous pressure –
diuretics
 Heart failure – digitalis, diuretics, ACE
inhibitors
Treatment
B) Interventional
Indications of PTCA
 Pulmonary arterial hypertension
 Pulmonary oedema
 Persistent or recurrent atrial fibrillation
 Thromboembolism
 Pregnancy
C) Surgical
 Closed mitral commissurotomy (CMC)
 Open mitral commissurotomy (OMC)
 Mitral valve replacement (MVR)
Management of MS in
Pregnancy
 Ist Trimester: Assess the patient. If
symptomatic do echo, if MS is not critical
close follow up and use diuretics. If stenosis
is critical, plan for PTMC (preferred) in the IInd
Trimester.
 IIIrd Trimester: Hospital delivery, supervised

jointly by cardiologist and obstetrician.
Second stage of labour must be short and
assisted delivery is preferred. Because
increased valsalva effort may precipitate
pulmonary oedema.
Any Query ????
Atherosclerosis
Dr. T. N. Gupta
Introduction
 An abnormal accumulation of lipid, or fatty,
substances and fibrous tissue in the vessel
wall is known as Atherosclerosis.
 These substances create blockages or narrow

the vessel in a way that reduces blood flow to
the myocardium.
 Atherosclerosis is a progressive disease that

can be curtailed and, in some cases, reversed.
Introduction
Pathophysiology
Pathophysiology
Pathophysiology
Pathophysiology
 Produces symptoms and complications
according to the location and degree of
narrowing of the arterial lumen, thrombus
formation, and obstruction of blood flow to the
myocardium.
 Impediment to blood flow is usually

progressive, causing an inadequate blood
supply that deprives the muscle cells of
oxygen needed for their survival the condition
is known as ischemia.
 Acute onset of chest pain
 Women have been found to have more
atypical symptoms of myocardial ischemia
(e.g., shortness of breath, nausea, unusual
fatigue) than men.
 Changes on the electrocardiogram (ECG)

 High levels of cardiac enzymes
 Dysrhythmias
 Sudden death
Risk Factors of Coronary Atherosclerosis
Non-modifiable Risk Factors
Family history of coronary heart disease
Increasing age
Gender (heart disease occurs three times more often in men than in
premenopausal women)
Race (higher incidence of heart disease in African Americans than in
Caucasians)
Modifiable Risk Factors

High blood cholesterol level
Cigarette smoking, tobacco use
Hypertension
Diabetes mellitus
Lack of estrogen in women
Physical inactivity
Obesity
Preventive Measures
Controlling Cholesterol Abnormalities
Four elements of fat metabolism: total
cholesterol, LDL, HDL, and triglycerides are
primary factors affecting the development of
heart disease.
LDL exerts a harmful effect on the arterial wall
and accelerates atherosclerosis.
In contrast, HDL transports cholesterol to the
liver, where it is biodegraded and then excreted.
The desired goal is to have low LDL values and
high HDL values.
Preventive Measures
Dietary Measures
Soluble dietary fiber may also help lower
cholesterol levels.
Soluble fibers, which are found in fresh fruit, cereal
grains, vegetables, and legumes, enhance the
excretion of metabolized cholesterol.
The label information of interest to a person

attempting to eat a heart-healthy diet is as follows:
• Serving size, expressed in household measures
• Amount of total fat per serving
• Amount of saturated fat per serving
• Amount of cholesterol per serving
• Amount of fibre per serving
Preventive Measures
Physical Activity
Regular, moderate physical activity increases

HDL levels and reduces triglyceride levels. The
goal for the average person is a total of 30
minutes of exercise, three to four times per week.
Nurse should inform patients to stop any activity

if they develop chest pain, unusual shortness of
breath, dizziness, light headedness, or nausea.
Preventive Measures
Medications
Medications are used in some instances to
control cholesterol levels.
If diet alone cannot normalize serum

cholesterol levels, several medications have a
synergistic effect with the prescribed diet.
Lipid-lowering medications can reduce CAD

mortality in patients with elevated lipid levels
and in those with normal lipid levels.
Preventive Measures
Promoting Cessation of Tobacco Uses
Cigarette smoking contributes to the
development and severity of CAD in three ways.
First,
the inhalation of smoke increases the blood
carbon monoxide level, causing haemoglobin, the
oxygen carrying component of blood, to combine
more readily with carbon monoxide than with
oxygen.
Second, the nicotinic acid in tobacco triggers the
release of catecholamines, which raise the heart
rate and blood pressure. Nicotinic acid can also
cause the coronary arteries to constrict.
Preventive Measures
Promoting Cessation of Tobacco Uses
Third, use of tobacco causes a detrimental
vascular response and increases platelet
adhesion, leading to a higher probability of
thrombus formation.
A person with increased risk for heart disease

is encouraged to stop tobacco use through any
means possible: counselling, consistent
motivation and reinforcement messages,
support groups, and medications.
Thank you !!!!!
Aneurysm
Dr. T. N. Gupta
MD
Aortic Aneurysm
 An aneurysm is a localized sac or dilation formed at a weak
point in the wall of the aorta
It may be classified by its shape or form.

 A saccular aneurysm projects from one side of the vessel
only.
 If an entire arterial segment becomes dilated, a fusiform
aneurysm develops.
 Very small aneurysms due to localized infection are called
mycotic aneurysms.
 Aneurysms are serious because they can rupture, leading to

hemorrhage and death.
Etiologic Classification of
Arterial Aneurysms
 Congenital: Primary connective tissue disorders (Marfan’s
syndrome, Ehlers-Danlos syndrome) and other diseases (focal
medial agenesis, tuberous sclerosis, Turner’s syndrome,
Menkes’ syndrome)
 Mechanical (hemodynamic): Poststenotic and
arteriovenous fistula and amputation-related
 Traumatic (pseudoaneurysms): Penetrating arterial
injuries, blunt arterial injuries, pseudoaneurysms
 Infectious (mycotic): Bacterial, fungal, spirochetal
infections
Etiologic Classification of
Arterial Aneurysms
 Inflammatory (noninfectious): Associated with
arteritis (Takayasu’s disease, giant cell arteritis, systemic
lupus erythematosus, Behçet’s syndrome, Kawasaki’s
disease) and periarterial inflammation (ie, pancreatitis)
 Pregnancy-related degenerative: Nonspecific,
inflammatory variant
 Anastomotic (postarteriotomy) and graft
aneurysms: Infection, arterial wall failure, suture
failure, graft failure
Adapted with permission from Rutherford, R. B. (1999).

Vascular surgery (Vols. 1 and 2, 5th ed.). Philadelphia: W.
B. Saunders.
Thoracic Aortic Aneurysm
 Approximately 85% of all cases of thoracic aortic

aneurysm are caused by atherosclerosis.
 Occur most frequently in men between the ages 40

and 70 years.
 Thoracic area is the most common site for a

dissecting aneurysm.
 About one third of patients with thoracic aneurysms

die of rupture of the aneurysm (Rutherford, 1999).
 Pain is the most prominent symptom (pain is usually
constant and boring but may occur only when the
person is supine)
 Dyspnea, the result of pressure of the sac against the
trachea, a main bronchus, or the lung itself
 Cough, frequently paroxysmal and with a brassy quality
 Hoarseness, stridor, or weakness or complete loss of
the voice (aphonia), resulting from pressure against the
left recurrent laryngeal nerve
 Dysphagia (difficulty in swallowing) due to
impingement on the esophagus by the aneurysm
 When large veins in the chest are compressed by the

aneurysm, the superficial veins of the chest, neck, or
arms become dilated, and edematous areas on the
chest wall and cyanosis are often evident.
 Chest x-ray
 Transesophageal echocardiography
 CT
Medical Management
 Controlling blood pressure and correcting risk factors may

be helpful
 Systolic pressure is maintained at about 100 to 120 mm

Hg with antihypertensive medications (eg, hydralazine
hydrochloride [Hydralazine])
 Pulsatile flow is reduced by medications that reduce

cardiac contractility (eg, propranolol)
Surgical Management
 Goal of surgery is to repair the aneurysm and restore

vascular continuity with a vascular graft
 Intensive monitoring is usually required after this

type of surgery
 Repair of thoracic aneurysms using endovascular

grafts implanted (deployed) percutaneously in an
interventional laboratory (eg, cardiac catheterization
laboratory) may decrease postoperative recovery
time and decrease complications
Abdominal Aortic Aneurysm
 The most common cause of abdominal aortic

aneurysm is atherosclerosis.
 Most of these aneurysms occur below the renal

arteries (infrarenal aneurysms).
 Untreated, the eventual outcome may be rupture

and death.
Risk Factors
 Congenital weakness, trauma, or disease

 Genetic predisposition, smoking (or other tobacco
use), and hypertension
 All aneurysms involve a damaged media layer of the
vessel
 After an aneurysm develops, it tends to enlarge
 More than one half of patients with aneurysms have
hypertension
 Feel their heart beating in their abdomen when lying

down
 Feel an abdominal mass or abdominal throbbing
 If the abdominal aortic aneurysm is associated with

thrombus, a major vessel may be occluded or
smaller distal occlusions may result
 A small cholesterol, platelet, or fibrin emboli may

lodge in the digital arteries, causing blue toes
 Pulsatile mass in the middle and upper abdomen.

 A systolic bruit may be heard over the mass.
 Duplex ultrasonography or CT is used to determine

the size, length, and location of the aneurysm.
 Ultrasonography is conducted at 6-month intervals

until the aneurysm reaches a size at which surgery to
prevent rupture is of more benefit than the possible
complications of a surgical procedure.
Surgical Management
 Open surgical repair of the aneurysm by resecting the

vessel and sewing a bypass graft in place.
 An infrarenal abdominal aortic aneurysm can be
treated by endovascular grafting
 Endovascular grafting involves the transluminal
placement and attachment of a sutureless aortic graft
prosthesis across an aneurysm
 Potential complications include bleeding, hematoma, or
wound infection at the femoral insertion site; distal
ischemia or embolization; dissection or perforation of
the aorta; graft thrombosis; graft infection; break of
the attachment system; graft migration; proximal or
distal graft leaks; delayed rupture; and bowel ischemia.
Nursing Management
 Nursing assessment is guided by anticipating that the

patient may have cardiovascular, cerebral, pulmonary,
and renal impairment from atherosclerosis.
 Signs of impending rupture include severe back pain

or abdominal pain, which may be persistent or
intermittent and is often localized in the middle or
lower abdomen to the left of the midline.
 Indications of a rupturing abdominal aortic aneurysm

include constant, intense back pain; falling blood
pressure; and decreasing hematocrit.
Nursing Management
 The overall surgical mortality rate associated with a

ruptured aneurysm is 50% to 75%.
 Postoperative care requires intense monitoring of

pulmonary, cardiovascular, renal, and neurologic
status.
 Possible complications of surgery include arterial

occlusion, hemorrhage, infection, ischemic bowel,
renal failure, and impotence.
Have Nice Day !!!!!!
ANEMIA
Dr. T. N.
Gupta
INTRODUCTION
Anemia, a condition in which the hemoglobin

concentration is lower than normal, reflects the
presence of fewer than normal RBCs within the
circulation.
As a result, the amount of oxygen delivered to

body tissues is also diminished.
The most common hematologic condition which

is sign of an underlying disorders.
CLASSIFICATION ON THE BASIS OF
ETIOLOGY
Loss of RBCs: Occurs with bleeding, potentially from any

major source, such as the gastrointestinal tract, the uterus,
the nose, or a wound.
Decreased production of RBCs: Can be caused by a
deficiency in cofactors (including folic acid, vitamin B12, and
iron) required for erythropoiesis; RBC production may also
be reduced if the bone marrow is suppressed (eg, by tumor,
medications, toxins) or is inadequately stimulated because
of a lack of erythropoietin (as occurs in chronic renal
disease).
Increased destruction of RBCs: May occur because of an
overactive RES (Reticuloendothelial system) including
hypersplenism) or because the bone marrow produces
abnormal RBCs that are then destroyed by the RES (eg,
sickle cell anemia).
TYPES OF ANEMIA
Hypoproliferative (Resulting From Defective

RBC Production)
Iron deficiency
Vitamin B12 deficiency (megaloblastic)
Folate deficiency
Decreased erythropoietin production (eg, from
renal dysfunction)
Cancer /inflammation
TYPES OF ANEMIA
Bleeding (Resulting From RBC Loss)

Bleeding from gastrointestinal tract, menorrhagia
(excessive menstrual flow), epistaxis (nosebleed),
trauma
Hemolytic (Resulting From RBC Destruction)
Altered erythropoiesis (sickle cell anemia,
thalassemia, other hemoglobinopathies)
Hypersplenism (hemolysis)
Drug-induced anemia
Autoimmune anemia
Mechanical heart valve related anemia
CLINICAL MANIFESTATIONS
Aside from the severity of the anemia itself,

several factors influence the development of
anemia-associated symptoms:
Speed with which the anemia has developed
Duration of the anemia (ie, its chronicity)
Metabolic requirements of the individual
Other concurrent disorders or disabilities (eg,
cardiopulmonary disease)
Special complications or concomitant features of
the condition that produced the anemia
A person who has been anemic for a very long

time, with hemoglobin levels between 9 and 11 g/
dl, usually has few or no symptoms other than
slight tachycardia on exertion and fatigue.
Patients who customarily are very active or who
have significant demands on their lives are more
likely to have symptoms
Patients with coexistent cardiac, vascular, or
pulmonary disease may develop more pronounced
symptoms of anemia (eg, dyspnea, chest pain,
muscle pain or cramping) at a higher hemoglobin
level
DIAGNOSTIC INVESTIGATIONS
The hemoglobin, hematocrit, reticulocyte count,

and RBC indices, particularly the mean corpuscular
volume (MCV), peripheral blood smear.
Iron studies (serum iron level, total iron-binding

capacity [TIBC], percent saturation, and ferritin),
as well as serum vitamin B12 and folate levels
Erythropoietin levels
Bone marrow aspiration
NURSING DIAGNOSIS
Activity intolerance related to weakness, fatigue,

and general malaise
Imbalanced nutrition, less than body
requirements, related to inadequate intake of
essential nutrients
Ineffective tissue perfusion related to inadequate
blood volume or hematocrit
Noncompliance with prescribed therapy
IRON DEFICIENCY ANEMIA
Iron deficiency anemia typically results when the

intake of dietary iron is inadequate for
hemoglobin synthesis.
More commonly in underdeveloped countries,

where inadequate iron stores can result from
inadequate intake of iron (seen with vegetarian
diets) or from blood loss (eg, from intestinal
hookworm).
ETIOLOGY
Men and postmenopausal women is bleeding (from
ulcers, gastritis, inflammatory bowel disease, or
gastrointestinal tumors)
Premenopausal women is menorrhagia (excessive

menstrual bleeding) and pregnancy with inadequate
iron supplementation
Patients with chronic alcoholism often have chronic

blood loss from the gastrointestinal tract which leads to
anemia iron malabsorption, as is seen after
gastrectomy or with celiac disease
Smooth, sore tongue, brittle and ridged nails,

and angular cheilosis (an ulceration of the corner
of the mouth)
Signs subside after iron-replacement therapy
Health history may be significant for multiple

pregnancies, gastrointestinal bleeding, and pica (a
craving for unusual substances, such as ice, clay,
or laundry starch)
Peripheral blood smear

Bone marrow aspiration
Serum ferritin levels
Hemoglobin level
MCV (mean corpuscular volume) which measures
the size of the RBC
Hematocrit and RBC levels
MEDICAL MANAGEMENT
Stool specimens should be tested for occult
blood.
People 50 years of age or older should have a
colonoscopy, endoscopy, or other examination of
the gastrointestinal tract to detect ulcerations,
gastritis, polyps, or cancer.
Several oral iron preparations: ferrous sulfate,
ferrous gluconate, and ferrous fumarate are
available.
Intravenous or intramuscular administration of
iron dextran may be needed.
NURSING MANAGEMENT
Food sources high in iron include organ meats
(beef or calf’s liver, chicken liver), other meats,
beans (black, pinto, and garbanzo), leafy green
vegetables, raisins, and molasses.
Taking iron-rich foods with a source of vitamin C

enhances the absorption of iron.
Encourages patients to continue iron therapy as

long as it is prescribed, although they may no
longer feel fatigued.
HEALTH EDUCATION
Take iron on an empty stomach (1 hour before or

2 hours after a meal). Iron absorption is reduced
with food, especially dairy products.
To prevent gastrointestinal distress, the following

schedule may work better if more than one tablet
a day is prescribed: Start with only one tablet per
day for a few days, then increase to two tablets
per day, then three tablets per day. This method
permits the body to adjust gradually to the iron.
HEALTH EDUCATION
Increase the intake of vitamin C (citrus fruits and juices,

strawberries, tomatoes, broccoli), to enhance iron
absorption.
Eat foods high in fiber to minimize problems with
constipation.
Remember that stools will become dark in color.
Liquid forms of iron supplementation may be better

tolerated than solid forms, although they are more
expensive. The liquid forms can discolor teeth. Use a
straw or place the spoon at the back of the mouth to
take the supplement; rinse mouth thoroughly afterward.
MEGALOBLASTIC ANEMIA
Megaloblastic anemia is caused by deficiencies of
vitamin B12 or folic acid, identical bone marrow and
peripheral blood changes occur, because both
vitamins are essential for normal DNA synthesis.
RBCs that are produced are abnormally large and

are called megaloblastic RBCs.
A bone marrow analysis reveals hyperplasia

(abnormal increase in the number of cells), and the
precursor erythroid and myeloid cells are large and
bizarre in appearance.
MEGALOBLASTIC ANEMIA
Pancytopenia (a decrease
in all myeloid-derived cells)
can develop. In an advanced
situation, the hemoglobin
value may be as low as 4 to
5 g/dL, the WBC count 2,000
to 3,000/mm3, and the
platelet count less than
50,000/mm3.
RBCs are abnormally

shaped, and the shapes may
vary widely (poikilocytosis).
PATHOPHYSIOLOGY
Folic Acid Deficiency

Folic acid, a vitamin that is necessary for normal
RBC production, is stored as compounds referred
to as folates.
Quickly depleted when the dietary intake of
folate is deficient (within 4 months).
Folate is found in green vegetables and liver.
Folate deficiency occurs in people who rarely eat
uncooked vegetables.
PATHOPHYSIOLOGY
Vitamin B12 Deficiency

Deficiency of vitamin B12 can develop in strict
vegetarians who consume no meat or dairy
products
Occurs in Crohn’s disease, ileal resection,
gastrectomy, absence of intrinsic factor; as in
pernicious anemia.
Intrinsic factor is normally secreted by cells
within the gastric mucosa; normally it binds with
the dietary vitamin B12 and travels with it to the
ileum, where the vitamin is absorbed.
In the case of folic acid deficiency, even small

amounts of folate will increase the serum folate
level, sometimes to normal. Measuring the
amount of folate within the RBC itself (red cell
folate) is therefore a more sensitive test in
determining true folate deficiency.
Patients with pernicious anemia develop a
smooth, sore, red tongue and mild diarrhea.
Extremely pale, particularly in the mucous
membranes.
Paresthesias in the extremities.
Schilling test
Patient receives a small oral dose of radioactive
vitamin B12, followed in a few hours by a large,
nonradioactive parenteral dose of vitamin B12
(this aids in renal excretion of the radioactive
dose).
If no radioactivity is present in the urine (ie, the

radioactive vitamin b12 stays within the
gastrointestinal tract), the cause is
gastrointestinal malabsorption of the vitamin b12.
Schilling test
If the urine is radioactive, the cause of the
deficiency is not ileal disease or pernicious anemia
Same procedure is repeated, but this time intrinsic
factor is added to the oral radioactive vitamin B12.
If radioactivity is now detected in the urine (ie, the
B12 was absorbed from the gastrointestinal tract in
the presence of intrinsic factor), the diagnosis of
pernicious anemia can be made.
Schilling test is useful only if the urine collections
are complete.
MEDICAL MANAGEMENT
Folate deficiency is treated by increasing the
amount of folic acid in the diet and administering 1
mg of folic acid daily.
Folic acid is administered intramuscularly only for
people with malabsorption problems.
Vegetarians can prevent or treat vitamin B12
deficiency with oral supplements through vitamins or
fortified soy milk.
If deficiency is due to defective absorption or
absence of intrinsic factor, replacement is by monthly
intramuscular injections of vitamin B12, usually at a
dose of 1000 μg.
HAVE A NICE DAY !!!!
LEUKEMIA
DR. T. N. GUPTA
INTRODUCTION
• Leukemia, literally “white blood,” is a neoplastic

proliferation of one particular cell type
(granulocytes, monocytes, lymphocytes, or
megakaryocytes).
• The defect originates in the hematopoietic stem
cell, the myeloid, or the lymphoid stem cell.
• Leukemias is an unregulated proliferation of
WBCs in the bone marrow.
• In acute forms (or late stages of chronic forms),
the proliferation of leukemic cells leaves little
room for normal cell production.
CAUSES
• Genetic influence
• Viral pathogenesis
• Bone marrow damage from radiation

exposure or from chemicals such as
benzene and alkylating agents
CLASSIFICATION
According to the stem cell line involved;

•Lymphoid
•Myeloid
Based on the time it takes for symptoms to evolve;

•Acute
•Chronic
ACUTE MYELOID LEUKEMIA (AML)
• AML results from a defect in the hematopoietic

stem cell that differentiates into all myeloid cells:
monocytes, granulocytes (neutrophils, basophils,
eosinophils), erythrocytes, and platelets.
• Patients with AML have a potentially curable

disease.
• Patients who are older or have a more
undifferentiated form of AML tend to have a
worse prognosis.
• Fever and infection result from neutropenia
• Weakness and fatigue from anemia
• Bleeding tendencies from thrombocytopenia
• Proliferation of leukemic cells within organs leads

to a variety of additional symptoms: pain from an
enlarged liver or spleen, hyperplasia of the gums,
and bone pain from expansion of marrow
• CBC results show a decrease in both erythrocytes

and platelets.
• Although the total leukocyte count can be low,
normal, or high, the percentage of normal cells is
usually vastly decreased.
• Bone marrow analysis shows an excess of
immature blast cells (more than 30%).
• In acute promyelocytic leukemia patients have
problem with bleeding, in that they have
underlying coagulopathy and a higher incidence
of disseminated intravascular coagulation (DIC).
COMPLICATIONS
• Bleeding and infection (bleeding correlates with

the level of platelet deficiency (thrombocytopenia)
• Ecchymoses (bruises) and petechiae (pinpoint

red or purple hemorrhagic spots on the skin)
• Common sites of bleeding are gastrointestinal,

pulmonary, and intracranial
• Likelihood of infection increases with the degree

and duration of neutropenia
MEDICAL MANAGEMENT
• Overall objective of treatment is to achieve

complete remission, in which there is no
detectable evidence of residual leukemia
remaining in the bone marrow.
• Aggressive administration of chemotherapy,
called induction therapy, which usually requires
hospitalization for several weeks.
• Induction therapy typically involves high doses of
cytarabine (cytosar, ara-c) and daunorubicin
(daunoxome) or mitoxantrone (novantrone) or
idarubicin (idamycin).
MEDICAL MANAGEMENT
• Aim of induction therapy is to eradicate the

leukemic cells, but this is often accompanied by
the eradication of normal types of myeloid cells.
• Patient is typically very ill, with bacterial, fungal,
and occasionally viral infections, bleeding, and
severe mucositis, which causes diarrhea and a
marked decline in the ability to maintain
adequate nutrition.
• Supportive care includes administering blood
products (RBCs and platelets) and promptly
treating infections.
MEDICAL MANAGEMENT
• When the patient has recovered from the

induction therapy (ie, the WBC and platelet
counts have returned to normal and any infection
has resolved), the patient typically receives
consolidation therapy (post-remission therapy).
• Goal of consolidation therapy is to eliminate any

residual leukemia cells that are not clinically
detectable, thereby diminishing the chance for
recurrence.
MEDICAL MANAGEMENT
• A recent study of long-term survival of patients with
AML found that only 11% survived 10 years or longer
(Micallef et al., 2001).
• Bone marrow transplantation (BMT) or peripheral blood

stem cell transplantation(PBSCT). When a suitable
tissue match can be obtained, the patient embarks on
an even more aggressive regimen of chemotherapy
(sometimes in combination with radiation therapy), with
the treatment goal of destroying the hematopoietic
function of the patient’s bone marrow.
• Patients’ are supported with antimicrobial therapy and

transfusions as needed.
COMPLICATIONS OF TREATMENT
• Massive leukemic cell destruction from

chemotherapy results in release of electrolytes and
fluids within the cell into the systemic circulation
• Increased uric acid and phosphorus levels make
patients vulnerable to renal stone formation and
renal colic
• Hyperkalemia and hypocalcemia can lead to
cardiac dysrhythmias, hypotension
• Neuromuscular effects such as muscle cramps,
weakness, spasm/tetany, confusion, and seizure
may occur
STUDY ON
• Chronic Myeloid Leukemia
• Acute Lymphocytic Leukemia
• Chronic Lymphocytic Leukemia

Dr. T. N. Gupta
MD
 Hemophilia A is caused by a genetic defect
that results in deficient or defective factor
VIII.
 Hemophilia B (also called Christmas disease)

stems from a genetic defect that causes
deficient or defective factor IX.
 Bothtypes of hemophilia are inherited as X-
linked traits, so almost all affected people
are males; females can be carriers but are
almost always asymptomatic.
 Disease is recognized in early childhood,

usually in the toddler age group.
 Hemorrhages (involve various parts of the
body, occur even after minimal trauma,
severity of the bleeding depend on the
degree of factor deficiency)
 Hemarthroses and hematomas, can
frequently occur in patients with severe
factor VIII deficiency (ie, less than 1% of
normal levels)
 Most commonly affected joints by bleeding
are the knees, elbows, ankles, shoulders,
wrists, and hips
 Note pain in a joint before they are aware of
swelling and limitation of motion.
 Chronic pain or ankylosis (fixation) of the
joint occurs.
 When the hematomas occur within muscle
peripheral nerves can be compressed that
results in decreased sensation, weakness,
and atrophy of the area involved.
 Spontaneous hematuria and gastrointestinal
bleeding.
 Infusion of fresh frozen plasma
 Factor VIII and factor IX concentrates are

available to all blood banks
 Concentrates are given when they are

actively bleeding or as a preventive measure
before traumatic procedures (eg, lumbar
puncture, dental extraction, surgery)
 Aminocaproic acid is a fibrinolytic enzyme
inhibitor that can slow the dissolution of
blood clots that do form
 Desmopressin induces a transient rise in

factor VIII levels, the mechanism for this
response is unknown.
 However, desmopressin is not effective in

patients with severe factor VIII deficiency.
 From childhood, patients are helped to
accept themselves and the disease
 Encourage to maintain independence by

preventing unnecessary trauma that can
cause acute bleeding episodes
 Patientswith mild factor deficiency may not

be diagnosed until adulthood, they need
extensive teaching about activity restrictions
and self-care measures
 Avoid any medications that interfere with
platelet aggregation, such as aspirin, NSAIDs,
herbs, nutritional supplements, and alcohol.
 Splints and other orthopedic devices may be
useful in patients with joint or muscle
hemorrhages.
 Splints and other orthopedic devices may be
useful in patients with joint or muscle
hemorrhages.
 Encouraged to carry or wear medical
identification.
 Analgesicsare commonly required to

alleviate the pain associated with
hematomas and hemorrhage into joints.
 Warm baths promote relaxation, improve

mobility, and lessen pain
 Between 15% and 50% of patients with
hemophilia A and between 1% and 3% of
patients with hemophilia B develop
antibodies (inhibitors) to factor
concentrates, complicating factor
replacement management
 These patients may require plasmapheresis

or concurrent immunosuppressive therapy
Buerger’s Disease
Raynaud’s Disease
Dr. T. N. Gupta
MD
Buerger’s Disease/
Thromboangitis Obleterans
 Buerger’s disease is characterized by recurring
inflammation of the intermediate and small arteries and
veins of the lower and (in rare cases) upper extremities.
 Buerger’s disease is believed to be an autoimmune disease

that results in occlusion of distal vessels.
 Heavy smoking or chewing of tobacco is a causative or an

aggravating factor.
 Buerger’s disease is generally bilateral and symmetric
with focal lesions.
 Foot cramps after exercise

 Burning pain aggravated by emotional disturbances,
nicotine, or chilling
 Cold sensitivity confined to hands
 Intense rubor (reddish blue discoloration) of the foot
 Absence of the pedal pulse but with normal femoral and
popliteal pulses
 Radial and ulnar artery pulses are absent or diminished
 Definite redness or cyanosis of the part appears when
the extremity is in a dependent position
Buerger’s Disease & Gangrene
 Segmental limb blood pressures: Identify distal location

of the lesions or occlusions
 Duplex ultrasonography: Document patency of the

proximal vessels and to visualize the extent of distal
disease
 Contrast angiography: Demonstrate anatomy of the

diseased portion
Management
Main objectives of treatment are:

 Improve circulation to the extremities.
 Prevent the progression of the disease.
 Protect the extremities from trauma and infection.
 Treatment of ulceration and gangrene is directed toward

minimizing infection and conservative débridement of
necrotic tissue.
 Patients are strongly advised to stop using tobacco
completely.
Surgical Management
 A regional sympathetic block or ganglionectomy may be

useful to produce vasodilation and increase blood flow.
 Indications for amputation are worsening gangrene,

especially if the infected area is moist, severe rest pain,
or fulminating sepsis.
 Toe amputation, transmetatarsal amputation, below-

knee amputation or an above-knee amputation may be
required.
Nursing Management
 If an amputation is performed, immediate postoperative
care includes elevating the stump for the first 24 hours to
promote venous return and minimize edema.
 Incision is monitored for signs of hematoma

(unapproximated suture line, discoloration or ruddy color
changes of the skin along the suture line, tenderness with
palpation, or oozing of dark blood from the suture line).
 Elastic bandages are removed and reapplied as prescribed

by the surgeon.
Nursing Management
 Consultation with spiritual advisors.
 Patient may decide to be fitted for and learn to use a
prosthetic device.
 Rehabilitation facilities, home care, and outpatient
therapy can assist the patient to adapt to the changes in
lifestyle.
 Assisted in developing a plan to stop using tobacco and to
manage pain.
 Encouraged to make the lifestyle changes necessary with a
chronic disease, including modifications in diet, activity,
and hygiene (skin care).
Raynaud’s Disease
 Raynaud’s disease is a form of intermittent
arteriolar vasoconstriction that results in coldness,
pain, and pallor of the fingertips or toes.
 Patients with the disease seem to have immunologic
disorders.
 Raynaud’s phenomenon is used to refer to
localized, intermittent episodes of vasoconstriction
of small arteries of the feet and hands that cause
color and temperature changes.
 Generally unilateral and affecting only one or two
digits.
Risk Factors
 Emotional factors
 Unusual sensitivity to cold
 Common in women between 16 and 40 years of age
 Occurs more frequently in cold climates and during the
winter
 May occur with scleroderma, systemic lupus
erythematosus, rheumatoid arthritis, obstructive arterial
disease, or trauma
 Prognosis for raynaud’s disease varies; some patients
slowly improve, some become progressively worse, and
others show no change
 Pallor by sudden vasoconstriction

 Cyanotic due to pooling of deoxygenated blood during
vasospasm
 Exaggerated reflow (hyperemia) due to vasodilation, a
red color is produced (rubor) when oxygenated blood
returns to the digits after the vasospasm stops
 Characteristic sequence of color change of raynaud’s
phenomenon is described as white, blue, and red
 Numbness, tingling, and burning pain
Medical Management
 Avoiding stimuli (eg, cold, tobacco) that provoke

vasoconstriction.
 Calcium channel blockers: nifedipine is effective for

treating an acute episode of vasospasm.
 Sympathectomy (interrupting the sympathetic nerves by

removing the sympathetic ganglia or dividing their
branches) may help.
Nursing Management
 Exposure to cold must be minimized, and in areas where

the fall and winter months are cold, the patient should
remain indoors as much as possible and wear layers of
clothing when outdoors.
 Hats and mittens or gloves should be worn at all times

when outside.
 Patients should avoid all forms of nicotine; the nicotine

gum or patches used to help people quit smoking may
induce attacks.
Nursing Management
 Sharp objects should be handled carefully to avoid

injuring the fingers.
 Patients should be informed about the postural

hypotension that may result from medications, such as
calcium channel blockers, used to treat Raynaud’s
disease.
 Discuss regarding safety precautions related to alcohol,

exercise, and hot weather.
Any Questions?

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ACUTE CORONARY SYNDROME

Risk factors/ the Etiological

Decreased blood supply to the heart/ decreased cardiac

Presence of Clinical manifestations

• Heart block – Blockage of conduction system.

• Heart failurer – Failure to pump . Needs medicines

Before injury Normal ECG

Ischemia ST depression, peaked T-waves, then T-

Goldberger AL. Goldberger: Clinical Electrocardiography: A

Anterior MI V1-V6 LAD

Septal MI V1-V4 LAD septal branches

Lateral MI I, aVL, V5, V6 LCX

Inferior M I II, III, aVF RCA

V7, V8, V9 RCA

• Relieving pain and other s/s of ischemia

• Both Non STEMI and STEMI both are

•Complete occlusion of •Complete occlusion of

ST segment elevation No ST segment

All cardiac markers elevation in both

More common and more severe in STEMI.

•All medicines •All medicines

•Short term(in hospital •Short term mortality is

• Start with alternate half days, and build up to

 Pt. can usually

• Occurs even at rest

Low risk patients 0–2

Medium risk patients 3–4

High risk patients 5-7

•Recent internal bleeding

Dissolve 5ml NS+ STK

• Should not exceed 50 mg and is based upon

Dr. Triloki Nath Gupta

• Epidemiology and genetic considerations

• Low dietary intakes of calcium and potassium also may

• Alcohol consumption, psychosocial stress, and low levels of

Desmukh, et al. Pathophysiology of Heart Disease, Ch 13. 1997

Renal Parenchymal diseases, renal cysts (including polycystic kidney disease),

• Heart: Left ventricular hypertrophy, angina

• Kidney: Chronic kidney disease

• Peripheral Vasculature: Peripheral arterial disease

 Chest X-ray: to detect cardiomegaly, heart failure, coarctation of the aorta

2. Select drug therapy based on

3. Demonstrating risk reduction

• 70% type2 DM die of cardiovascular disease

• At least 60% of patients will require 2 or 3 antihypertensive

• Post Myocardial Infarction

• High Coronary Disease Risk

• Chronic Kidney Disease

• Recurrent Stroke Prevention

Calcium channel Older patients, Angina - -

Calcium channel Angina Older patients Combination with β- Atrioventricular

Angiotensi ACE inhibitor intolerance Left ventricular Renal Pregnancy

-blocker  - * - 

CCB - * -  

ACE inhibitor  -  - 

-blocker     -

• Usually develops in patients with a previous history of elevated BP

• but may arise in normotensive

 Hypertension with optic disc edema