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Cause: Rapid accumulation of fluid (blood, pus, or effusion) in the pericardial cavity.
Effect: Compression of the heart → prevents full ventricular filling → decreased cardiac output.
Clinical Signs:
Distended neck veins (↑ venous pressure)
Hypotension
Muffled heart sounds (Beck’s triad)
Treatment: Emergency pericardiocentesis (needle inserted at left 5th intercostal space near sternum).
Definition: Inflammation of the pericardium (viral, bacterial, or post-MI).
Symptoms: Sharp, substernal pain relieved by leaning forward.
Finding: Pericardial friction rub on auscultation due to roughened pericardial layers.
Cause: Complete blockage of a coronary artery (most often LAD).
Pathophysiology: Ischemia → necrosis of myocardial tissue.
ECG Changes: ST elevation, pathological Q wave, inverted T wave.
Clinical Feature: Severe crushing chest pain radiating to left arm, neck, or jaw.
Cause: Transient myocardial ischemia without necrosis due to coronary artery narrowing.
Symptoms: Tightness or heaviness in chest on exertion, relieved by rest or nitrates.
Right dominance: RCA supplies posterior septum → occlusion causes inferior wall infarction.
Left dominance: LCX supplies posterior septum → infarction may involve most of left ventricle.
Co-dominance: Lesser extent of infarction due to collateral flow.
Cause: Incomplete closure of foramen ovale due to failure of septum primum and secundum fusion.
Effect: Left-to-right shunt → right atrial and ventricular dilation.
Clinical Sign: Fixed splitting of second heart sound (S₂).
Cause: Defective membranous part of interventricular septum (commonest congenital cardiac defect).
Effect: Left-to-right shunt → pulmonary hypertension → right ventricular hypertrophy.
Complication: Eisenmenger’s syndrome (reversal of shunt → cyanosis).
Cause: Persistence of ductus arteriosus after birth.
Effect: Blood flows from aorta → pulmonary artery (left-to-right shunt).
Clinical Feature: Continuous “machinery” murmur at left 2nd intercostal space.
Treatment: Indomethacin (to close PDA) or surgical ligation.
Components (PROV):
P – Pulmonary stenosis
R – Right ventricular hypertrophy
O – Overriding aorta
V – Ventricular septal defect
Effect: Right-to-left shunt → cyanosis and clubbing.
Clinical Sign: Squatting improves symptoms by increasing systemic resistance.
Cause: Failure of spiral rotation of aorticopulmonary septum.
Effect: Aorta arises from right ventricle; pulmonary trunk from left ventricle.
Consequence: Parallel circulation incompatible with life unless shunts (ASD, PDA) persist.
Cause: Constriction of aortic lumen near ductus arteriosus.
Types:
Pre-ductal: Ductus arteriosus remains patent (in infancy).
Post-ductal: Collateral circulation via intercostal arteries (adult type).
Clinical Sign:
Weak femoral pulses
Radio-femoral delay
Rib notching on X-ray (due to enlarged intercostal arteries).
Mechanism: Visceral pain from myocardium transmitted via T1–T5 spinal nerves.
Perception: Left chest, shoulder, medial arm, and neck — same dermatomes as cardiac afferents.
Cause: Disturbances in conduction pathway (SA, AV, or Purkinje system).
Types:
Tachycardia (↑ rate)
Bradycardia (↓ rate)
Heart block (AV conduction failure)
Treatment: Pacemaker for complete block.
Cyanotic: Right-to-left shunt → decreased oxygenation (e.g., Tetralogy, Transposition).
Acyanotic: Left-to-right shunt → pulmonary overload (e.g., ASD, VSD, PDA).
Mechanism: Post-infarction inflammation (Dressler’s syndrome) → pericarditis → fluid accumulation.
Symptoms: Low-grade fever, chest pain, friction rub, pericardial thickening.
Cause: Chronic inflammation leading to fibrosis and calcification of pericardium (e.g., post-tubercular).
Effect: Rigid pericardium restricts diastolic filling → right-sided heart failure.
Clinical Features:
Elevated jugular venous pressure (JVP)
Ascites and pedal edema
Kussmaul’s sign (rise of JVP during inspiration)
Treatment: Pericardiectomy (surgical removal of pericardium).
Cause: Infection of endocardial surface (commonly valves) by bacteria like Streptococcus viridans.
Types:
Acute: Rapid and destructive (Staph. aureus).
Subacute: Slow and less aggressive.
Clinical Features:
Fever, murmur, splinter hemorrhages, Osler’s nodes.
Commonly affects mitral valve.
Complication: Embolic infarcts in brain, spleen, or kidneys.
Cause: Autoimmune reaction to Streptococcus pyogenes throat infection.
Result: Chronic inflammation and scarring of heart valves (especially mitral valve).
Clinical Features:
Mitral stenosis or regurgitation
Opening snap and diastolic murmur
“Fish-mouth” deformity of mitral orifice.
Cause: Redundant valve leaflets bulge into left atrium during systole.
Clinical Features:
Mid-systolic click followed by late systolic murmur.
May cause palpitations or endocarditis.
Common in: Young women with connective tissue disorders (e.g., Marfan syndrome).
Cause: Calcification of aortic valve cusps in elderly or congenital bicuspid valve.
Effect: Left ventricular hypertrophy due to pressure overload.
Symptoms: Dyspnea, angina, syncope on exertion.
Murmur: Harsh systolic murmur radiating to carotids.
Cause: Incomplete closure of aortic valve (post-rheumatic, infective endocarditis).
Effect: Backflow of blood into left ventricle → dilatation and hypertrophy.
Clinical Signs:
“Water hammer” pulse (Corrigan’s pulse).
Early diastolic murmur.
Cause: Post-rheumatic fibrosis causing narrowing of mitral orifice.
Effect: Left atrial pressure ↑ → pulmonary congestion → right heart failure.
Symptoms: Dyspnea, hemoptysis, orthopnea.
Murmur: Diastolic, low-pitched “rumbling” murmur at apex.
Cause: Viral infection (e.g., Coxsackie B virus).
Effect: Inflammation of myocardium → reduced contractility → heart failure.
Clinical Features: Fever, palpitations, arrhythmias, chest pain.
Left-sided failure: Pulmonary congestion, dyspnea, orthopnea.
Right-sided failure: Systemic venous congestion, ascites, ankle edema.
Common Causes:
Hypertension
Ischemic heart disease
Valvular disorders
Mechanism: Fatal arrhythmia (ventricular fibrillation) often following acute myocardial ischemia.
Common Cause: Coronary artery thrombosis or severe atherosclerosis.
Prevention: Early reperfusion therapy and defibrillation.
Mechanism: Constriction distal to origin of left subclavian artery.
Features:
Hypertension in upper limbs
Weak pulses in lower limbs
“Rib notching” on X-ray (collateral flow via intercostal arteries).
Definition: Heart positioned on right side due to reverse rotation during embryogenesis.
Variants:
Isolated: Only heart is reversed.
With situs inversus: All organs reversed.
Clinical Relevance: Often asymptomatic unless associated with other defects (Kartagener syndrome).
Pathogenesis: Long-standing left-to-right shunt (ASD, VSD, PDA) → pulmonary hypertension → reversal to right-to-left shunt.
Result: Cyanosis, clubbing, and polycythemia.
Cause: Failure of aorticopulmonary septum to form.
Result: Common arterial trunk supplying both systemic and pulmonary circulations → cyanosis.
Anomaly: Both aorta and pulmonary trunk arise from right ventricle.
Effect: Severe cyanosis; survival depends on VSD allowing mixing of blood.
Cause: Abnormal communication between right pulmonary vein and right atrium.
Result: Oxygenated blood enters right atrium → mild cyanosis and dyspnea.
Cause: Failure of left cardinal vein to regress.
Drainage: Opens into coronary sinus instead of right atrium.
Clinical Importance: Important during central venous catheterization or pacemaker insertion.
Rare anomaly due to faulty pleuropericardial membrane fusion.
Clinical Presentation: Asymptomatic or with displaced heart shadow on X-ray.
Risk: Cardiac herniation in partial defects.
Cause: Pressure or volume overload (hypertension, valvular disease).
Types:
Concentric: Due to pressure overload (e.g., aortic stenosis).
Eccentric: Due to volume overload (e.g., aortic regurgitation).
Complication: Decreased compliance and arrhythmia risk.
Mechanism: Transient vasospasm of coronary artery → ischemia without atherosclerosis.
Feature: Chest pain at rest with ST elevation on ECG, relieved by nitrates.
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