Cardiovascular System Pathophysiology

Heart Structure

• Four chambers: right atrium (RA), right ventricle (RV), left atrium (LA), left ventricle (LV)
• Wall layers: epicardium, myocardium, endocardium
• Pericardium: protective sac surrounding heart
• Valves: tricuspid, pulmonary, mitral (bicuspid), aortic

Blood Flow Through the Heart

Deoxygenated blood → Superior/Inferior vena cava → RA → Tricuspid valve → RV → Pulmonary valve → Pulmonary artery → Lungs (oxygenation) → Pulmonary vein → LA → Mitral valve → LV → Aortic valve → Aorta → Systemic circulation

Cardiac Output

• Formula: Cardiac Output (CO) = Heart Rate (HR) × Stroke Volume (SV)
• Normal CO: 4-8 L/min at rest
• Stroke Volume: 60-100 mL per beat
• Determined by: preload, afterload, and contractility

Coronary Circulation

• Right Coronary Artery (RCA): supplies RA, RV, inferior wall LV, SA node
• Left Coronary Artery (LCA): splits into LAD and circumflex
  • LAD: anterior wall LV, interventricular septum
  • Circumflex: LA, lateral wall LV
• Autoregulation: maintains constant blood flow despite pressure changes

Systole (Contraction - 0.3 seconds)

• Atrial systole: atria contract, push blood into ventricles (atrial kick = 20% of CO)
• Isovolumetric contraction: all valves closed, pressure increases
• Ventricular ejection: aortic and pulmonary valves open, blood ejected

Diastole (Relaxation - 0.5 seconds)

• Isovolumetric relaxation: all valves closed, pressure decreases
• Ventricular filling: AV valves open, ventricles fill passively (70% of filling)
• Atrial contraction: final 30% of ventricular filling

Key Hemodynamic Parameters

• Preload: ventricular filling pressure (right = CVP 2-8 mmHg, left = PCWP 8-12 mmHg)
• Afterload: resistance ventricle must overcome (SVR 800-1200 mmHg·min/L)
• Contractility: force of myocardial contraction (affected by catecholamines, calcium)
• Blood Pressure: Systolic 90-120 mmHg, Diastolic 60-80 mmHg, MAP 70-100 mmHg

Coronary Artery Disease (CAD)

Atherosclerotic narrowing of coronary arteries reduces blood flow, especially with increased demand.

• Stable Angina: predictable chest pain with exertion, caused by fixed stenosis, relieved by rest/nitrates
• Unstable Angina: unpredictable pain, indicates plaque rupture, precursor to MI
• Acute MI: complete coronary occlusion → myocardial necrosis, can be STEMI or NSTEMI

Heart Failure

Hypertension

• Primary (90-95%): multifactorial etiology, sympathetic overactivity, RAAS abnormalities
• Secondary: due to identifiable cause (renal disease, endocrine disorders)
• Consequences: LV hypertrophy, vascular remodeling, endothelial dysfunction, target organ damage

Arrhythmias

• Mechanisms: enhanced automaticity, triggered activity, reentry
• Atrial Fibrillation: loss of coordinated atrial contraction → irregular ventricular response, thrombus formation risk
• Ventricular Fibrillation: chaotic electrical activity → cardiac arrest, requires immediate defibrillation

Valvular Disease

• Stenosis: narrowed valve opening → ↑ resistance to flow, ↑ pressure gradient
• Regurgitation: valve doesn't close completely → backflow, ↑ volume load
• Mitral Stenosis: ↑ LA pressure → pulmonary congestion, A-fib risk
• Aortic Stenosis: LV hypertrophy, classic triad: syncope, angina, dyspnea

Chest Pain Characteristics

• Anginal Pain: pressure/heaviness/squeezing, substernal, radiates to shoulder/arm/jaw, provoked by exertion, relieved by rest/nitrates (5-15 min)
• MI Pain: severe, crushing, unrelenting, starts abruptly, lasts >30 min, associated with dyspnea/diaphoresis/nausea

Diagnostic Tests

• EKG: ST elevation (STEMI), ST depression, T wave inversion, Q waves, shows rate/rhythm
• Cardiac Biomarkers: Troponin (most specific), CK-MB, myoglobin, BNP (heart failure)
• Echocardiography: visualizes structure, measures ejection fraction, assesses valve function
• Cardiac Catheterization: gold standard for CAD diagnosis, measures pressures, coronary anatomy
• Stress Testing: reproduces ischemia if coronary stenosis

Stable Angina

• Nitrates: vasodilation, reduce preload, ↓ oxygen demand
• Beta-blockers: ↓ HR, contractility, BP
• ACE inhibitors/ARBs: vasodilation, remodeling prevention
• Statins: plaque stabilization, LDL lowering
• Aspirin: antiplatelet, ↓ thrombosis risk
• PCI/CABG: revascularization for significant stenosis

Acute Coronary Syndrome (STEMI/NSTEMI)

Immediate: Aspirin, P2Y12 inhibitor, anticoagulation, beta-blocker, ACE-I/ARB

Reperfusion (STEMI): Primary PCI (preferred), thrombolytics if PCI unavailable, CABG if anatomy unsuitable

Post-MI Prevention: DAPT (12 months), beta-blocker, ACE-I, statin, cardiac rehabilitation

Heart Failure Management

• Systolic: ACE-I/ARB (cornerstone), beta-blockers, aldosterone antagonists, ARNI, loop diuretics, devices (ICD, CRT)
• Diastolic: blood pressure control, avoid tachycardia, diuretics, manage underlying cause

Hypertension Management

• Lifestyle: DASH diet, weight loss, sodium restriction, exercise, stress reduction
• Pharmacotherapy: ACE-I/ARB, thiazide diuretics, CCBs (first-line), target BP <130/80

1. A 65-year-old man presents with substernal chest pressure radiating to his jaw during yard work, relieved after 10 minutes of rest and sublingual nitroglycerin. What pathophysiological process is occurring during this anginal episode?

2. Compare and contrast the pathophysiology of STEMI versus NSTEMI, including the extent of myocardial damage and expected biomarker patterns.

3. Explain the Frank-Starling mechanism and how it becomes maladaptive in chronic heart failure.

4. A patient with a history of MI develops acute pulmonary edema. Explain the sequence of events from the initial MI to pulmonary edema development.

5. How does hypertensive vascular remodeling contribute to diastolic dysfunction?