Cardiac Function Disorders, Heart Failure & Circulatory Shock – Exam Study Notes

Pericardium and Pericardial Disorders

  • Pericardium – Structure & Role

    • Double-layered serous membrane (visceral + parietal layers)

    • Functions

    • Isolates heart from adjacent thoracic structures

    • Anchors/maintains anatomic position

    • Prevents acute over-filling

    • Couples ventricular distensibility during diastole ➜ both ventricles fill equally (prevents left/right volume mismatch)

  • Pericardial Effusion

    • Any abnormal fluid accumulation in pericardial cavity (transudate, exudate, blood, chyle)

    • Small slow-growing effusions may be asymptomatic; rapid accumulations (≥150–200 mL) raise intrapericardial pressure → compromise cardiac filling

  • Cardiac Tamponade

    • Pathologic rise in pericardial pressure causing diastolic compression of all four chambers

    • Etiologies: trauma, post-MI rupture, iatrogenic, malignancy, pericarditis, aortic dissection

    • Beck triad: ↓ arterial BP, jugular venous distention, muffled heart sounds

    • Pulsus paradoxus (\Delta SBP > 10\,\text{mmHg during inspiration}) is classic

  • Pericarditis

    • Acute, chronic, or constrictive inflammatory process

    • Acute: sharp, pleuritic chest pain, relieved by leaning forward; pericardial friction rub; diffuse ST-segment elevation on ECG

    • Chronic: often autoimmune; no pathogen isolated

    • Constrictive: calcified scar between visceral/parietal layers ➜ fixed CO/reserve, ascites, pedal edema, Kussmaul sign (↑ JVP with inspiration)

  • Diagnostics

    • ECG, CXR, echocardiogram; pericardial rub on auscultation

Coronary Circulation & Ischemic Heart Disease

  • Major Coronary Arteries

    • Left Main (LM) ➜ Left Anterior Descending (LAD) & Circumflex (LCx)

    • Right Coronary Artery (RCA) ➜ Posterior Descending (PDA)

  • Coronary Heart Disease (CHD)

    • Impaired flow → angina, myocardial infarction (MI), arrhythmias, conduction blocks, heart failure, sudden death

  • Types of Angina

    • Chronic Stable Angina: fixed atherosclerotic obstruction, predictable with exertion/stress, relieved by rest/nitrates

    • Variant/Prinzmetal (vasospastic) Angina: coronary spasm, often at rest, transient ST elevation

    • Silent Ischemia: objective evidence without pain

    • Unstable Angina (UA): part of Acute Coronary Syndrome (ACS)

  • Unstable Angina – Diagnostic Basis

    • Pain severity/pattern, hemodynamic stability, ECG changes, serum cardiac markers (negative troponin/CK-MB)

    • Pain criteria:

    • At rest ≥20 min

    • New severe onset

    • Crescendo pattern (more severe/prolonged/frequent than before)

  • Acute Myocardial Infarction (AMI – STEMI)

    • Abrupt severe, crushing substernal pain → arm/neck/jaw; nausea/vomiting; anxiety, doom; diaphoresis, cool–clammy skin

    • ST-segment elevation STEMI vs non-STEMI (subendocardial)

    • Determinants of infarct size: site & extent of occlusion, duration, collateral supply, metabolic demand, HR/BP/rhythm

  • Transmural vs Subendocardial Infarcts

    • Transmural: full-thickness wall, single artery occlusion

    • Subendocardial: inner 1/3–1/2 wall, severe narrowing but patent lumen

  • Silent Ischemia – Who’s Affected?

    • Asymptomatic individuals

    • Post-MI patients

    • Known angina patients who also have painless episodes

  • Post-MI Medical Management

    • Reperfusion: Thrombolytics, Percutaneous Coronary Intervention (PCI), Coronary Artery Bypass Grafting (CABG), atherectomy

    • Cardiac Rehabilitation: exercise, risk-factor modification, psychosocial support

  • Lifestyle (Non-Pharmacologic) Angina Therapy

    • Smoking cessation, stress reduction, regular aerobic exercise

    • Diet ↓ cholesterol & saturated fat, weight control

    • Avoid cold/exertion triggering vasoconstriction

  • Antiplatelet/Anticoagulant Drugs

    • Aspirin: irreversibly blocks TXA₂ synthesis

    • Clopidogrel/Ticlopidine: inhibit ADP receptor

    • GP IIb/IIIa receptor antagonists: final common pathway blockade; used in ACS

    • Goal: prevent platelet aggregation & thrombosis progression

Myocardial & Endocardial Diseases

  • Myocarditis

    • Inflammation of myocardium + conduction system without MI evidence

    • Viral > bacterial/toxic/autoimmune causes; may produce arrhythmias/heart failure

  • Cardiomyopathies – Overview

    • Heterogeneous myocardial diseases with mechanical/electrical dysfunction ± inappropriate hypertrophy/dilation, often genetic

    • Primary vs Secondary

  • Primary Cardiomyopathy Classification

    • Genetic: Hypertrophic (HCM), Arrhythmogenic RV (ARVC), Left-ventricular non-compaction, conduction disorders, ion-channelopathies

    • Mixed: Dilated (DCM), Restrictive

    • Acquired: Myocarditis, Peripartum, Stress (Takotsubo), Alcoholic

  • Key Types

    • Dilated: ventricular dilation + systolic failure

    • Hypertrophic: asymmetric septal hypertrophy, diastolic dysfunction, sudden death in athletes

    • Restrictive: stiff ventricle, impaired filling

    • ARVC: fibrofatty replacement of RV, arrhythmias

    • Peripartum: last trimester–5 mo postpartum

  • Management Options

    • Pharmacology (β-blockers, ACE-I, diuretics)

    • Device: ICD, pacemaker, ventricular assist

    • Ablation, transplant for end-stage

    • Goal = symptom relief, survival prolongation

  • Infective Endocarditis (IE)

    • Damaged endocardial surface + pathogen entry ➜ vegetations (fibrin, platelets, microbes) on valves

    • Common microbes: Viridans streptococci, S. aureus, Enterococci, HACEK group, fungi

    • Risk: prosthetic valves, congenital heart disease, IV-drug use, gum manipulation

  • Rheumatic Fever / Rheumatic Heart Disease

    • Post-Group-A β-hemolytic streptococcal pharyngitis

    • Acute: pancarditis, migratory polyarthritis, skin & CNS involvement

    • Recurrent: progressive valve damage

    • Chronic: permanent deformity (esp. mitral stenosis)

Valvular Heart Disorders

  • Basic Valve Physics

    • Purpose: unidirectional flow

    • Pathology

    • Stenosis: narrowed orifice → pressure overload

    • Regurgitation (incompetence): incomplete closure → volume overload

  • Common Lesions

    • Mitral Stenosis, Mitral Regurgitation, Mitral Valve Prolapse

    • Aortic Stenosis, Aortic Regurgitation

  • Diagnostics

    • Cardiac auscultation ➜ murmurs, clicks

    • Echocardiography (M-mode, 2-D, Doppler, TEE) is gold standard for structure/function assessment

Heart Failure (HF)

  • Compensatory/Adaptive Mechanisms

    • Frank-Starling SV↑when  EDV↑SV \uparrow \text{when} \; EDV \uparrow (eventually plateaus)

    • Sympathetic activation (↑HR, contractility, vasoconstriction)

    • RAAS: Ang II⇒vasoconstriction;  Aldosterone⇒Na+/H2O retentionAng\ II \Rightarrow vasoconstriction; \; Aldosterone \Rightarrow Na^+ /H_2O\, retention

    • Natriuretic peptides (ANP, BNP), Endothelins

    • Myocardial hypertrophy & remodeling (initially adaptive ➜ maladaptive)

  • Hemodynamic Categories

    • High-Output: increased demand (e.g., anemia, thyrotoxicosis)

    • Low-Output: impaired pump (ischemia, cardiomyopathy)

  • Functional Types

    • Systolic HF: impaired ejection, ↓EF (<40%)

    • Diastolic HF: impaired filling, preserved EF

  • Side-Specific Manifestations

    • Left-sided: pulmonary congestion/edema, ↓CO → fatigue, cyanosis

    • Right-sided: systemic venous congestion, hepatosplenomegaly, ascites, JVD, peripheral edema (often secondary to LHF or cor pulmonale)

  • Acute vs Chronic

    • Chronic: persistent low output, volume overload, venous congestion

    • Acute Decompensated: rapid symptom escalation → pulmonary edema, hypotension, urgent therapy needed

Pediatric & Congenital Cardiology

  • Fetal Circulation Highlights

    • Parallel circuits; RV output to placenta via ductus arteriosus, LV to upper body

    • Foramen ovale + ductus arteriosus close post-natally

  • Shunts & Cyanosis

    • ↑ systemic resistance → Left→Right shunt (acyanotic)

    • ↑ pulmonary resistance/obstruction → Right→Left shunt (cyanotic)

    • Stress/crying feedings raise PVR → transient cyanosis

  • Major Defects

    • PDA, ASD, VSD, Endocardial cushion, Pulmonary stenosis, Tetralogy of Fallot, Transposition of great vessels, Coarctation, Kawasaki disease

  • Kawasaki Disease

    • Acute, immune-mediated vasculitis of medium vessels (coronary arteries at risk)

    • Phases:

    • Acute: fever, conjunctivitis, mucositis, rash, edema of hands/feet, cervical lymphadenopathy

    • Subacute: defervescence, desquamation

    • Convalescent: resolution ~8 wks

  • Heart Failure in Children

    • Causes: congenital structural lesions, post-surgical, cardiomyopathies

    • Manifestations: tachypnea, feeding difficulty, FTT, hepatomegaly

Aging & the Heart

  • ↑ Vascular stiffness (arteriosclerosis)

  • ↓ β-adrenergic responsiveness → limited max HR/contractility

  • Left-ventricular hypertrophy & ↓ compliance

  • Contributes to HFpEF, isolated systolic hypertension

Circulatory Failure (Shock)

  • General Definition

    • Acute failure of circulatory system to provide adequate tissue perfusion/oxygenation

  • Compensatory Systems

    • Sympathetic (↑HR, vasoconstriction)

    • Renal (RAAS, ADH)

  • Major Types & Core Pathophysiology

    • Cardiogenic: pump failure after MI, arrhythmia, cardiomyopathy

    • Hypovolemic: ↓ preload (hemorrhage, dehydration, burns)

    • Distributive: massive vasodilation → relative hypovolemia

    • Septic: infection-triggered cytokine storm

    • Anaphylactic: IgE-mediated histamine release

    • Neurogenic: loss of SNS tone (spinal cord injury)

    • Obstructive: mechanical block of central circulation (cardiac tamponade, tension pneumothorax, massive PE, dissecting aneurysm)

  • Sepsis & Septic Shock

    • Dysregulated host response to infection → life-threatening organ dysfunction

    • Vasodilation, ↑ capillary permeability, coagulopathy, mitochondrial dysfunction

    • Treatment: early antibiotics, source control, fluid resuscitation, vasopressors (norepinephrine)

  • Complications of Shock

    • Acute Lung Injury / ARDS: non-cardiogenic pulmonary edema ⇒ severe hypoxemia

    • Acute Renal Failure: ischemic tubular necrosis

    • GI ischemia/ulcers, bacterial translocation

    • Disseminated Intravascular Coagulation (DIC): systemic microthrombi, consumption coagulopathy

    • Multiple Organ Dysfunction Syndrome (MODS): progressive failure ≥2 organ systems; high mortality

  • Global Management Principles

    • Rapid recognition & reversal of underlying cause

    • Fluid resuscitation (crystalloid/colloid), maintain MAP≥65 mmHgMAP \ge 65\,\text{mmHg}

    • Restore oxygen delivery: supplemental O₂, mechanical ventilation if needed

    • Hemodynamic monitoring & support (inotropes, vasopressors)

    • Correct coagulopathy, renal replacement therapy when indicated

Key Equations & Physiologic Relationships

  • Cardiac Output: CO=HR×SVCO = HR \times SV

  • Mean Arterial Pressure: MAP=13(SBP−DBP)+DBPMAP = \tfrac{1}{3}(SBP - DBP) + DBP

  • Laplace Law (ventricular wall stress): σ=P×r2h\sigma = \dfrac{P \times r}{2h} (P=pressure, r=radius, h=wall thickness)

  • Fick Principle for Coronary Flow Reserve: MVO2∝HR×SBPMVO_2 \propto HR \times SBP

Cross-Links & Clinical Pearls

  • Pericardial effusion → cardiac tamponade is a form of obstructive shock (mechanical barrier to preload)

  • Chronic systemic hypertension & aortic stenosis share pathophysiology of pressure overload → concentric LV hypertrophy and eventual diastolic HF

  • Beta-blockers improve survival in HF by slowing HR (↓MVO₂) & blunting SNS-mediated remodeling

  • BNP is elevated in HF; useful for differentiating dyspnea from cardiac vs pulmonary cause

  • Pulsus paradoxus in tamponade mirrors mechanics in severe asthma/COPD exacerbations (exaggerated negative intrathoracic pressure)

  • Kawasaki disease is leading cause of acquired heart disease in children in developed countries; IVIG + aspirin given to prevent coronary aneurysms

Sample Exam-Style Questions (Self-Check)

  1. Which shock type shares pathophysiology with acute pericardial tamponade? ➜ Obstructive shock.

  2. A loud S₁ opening snap & diastolic rumble at apex suggest which valve lesion? ➜ Mitral stenosis.

  3. Explain why nitrates relieve angina: venodilation ↓ preload → ↓ LV wall stress & O₂ demand (Laplace law).

  4. Name three criteria that make chest pain "unstable".

  5. Why are β-blockers contraindicated in cardiogenic shock? (Negative inotropy worsens pump failure.)