Cardiology
Human Heart
Four chambers, four valves, two circulations — anatomy of the cardiovascular pump
The heart is a four-chambered muscular pump roughly the size of a fist (300 g adult), located in the middle mediastinum. Right atrium receives systemic venous blood via SVC and IVC; right ventricle pumps it through the pulmonary valve to the pulmonary artery and lungs. Left atrium receives oxygenated blood via four pulmonary veins; left ventricle pumps it through the aortic valve to the aorta and systemic circulation. Four valves prevent backflow — tricuspid and mitral (atrioventricular), pulmonary and aortic (semilunar). Coronary arteries supply the myocardium — left main divides into LAD and circumflex; right coronary supplies the inferior wall, SA node (60%), AV node (90%). Cardiac output = stroke volume × heart rate, ~5 L/min at rest. The conducting system (SA node → AV node → His bundle → Purkinje fibers) coordinates electrical activation.
- Weight~300 g adult; size of a fist
- Chambers4 (RA, RV, LA, LV)
- Valves4 (tricuspid, pulmonary, mitral, aortic)
- Cardiac output~5 L/min rest; up to 25 L/min exercise
- PacemakerSA node 60-100/min
- Coronary supplyLAD, circumflex, RCA
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Why heart anatomy matters
- Chest pain workup. Localize ischemia by ECG lead group.
- Heart failure management. Tailor therapy to systolic vs diastolic dysfunction.
- Valvular disease. Murmur location predicts the affected valve.
- Cardiac surgery planning. Coronary anatomy determines bypass strategy.
- Congenital disease. Tetralogy of Fallot, transposition, VSD, ASD.
- Pacemaker indications. Conduction system disease — SA node dysfunction, AV block.
- Athletic screening. HCM, anomalous coronary artery cause sudden cardiac death.
Common errors
- Calling all chest pain cardiac. PE, dissection, pericarditis, esophageal, MSK overlap.
- Ignoring right ventricular MI. Inferior MI with V4R ST elevation; preload-dependent — avoid nitrates.
- Treating HFpEF like HFrEF. ACE inhibitors and beta blockers don't reduce mortality in HFpEF.
- Missing aortic dissection. Sudden tearing chest/back pain, BP differential between arms.
- Beta blocker in cardiogenic shock. Worsens hemodynamics; address underlying cause.
- Forgetting SGLT2 inhibitors in HF. Reduce HF hospitalization and mortality regardless of diabetes status.
Frequently asked questions
How does the cardiac cycle work?
Diastole — ventricles relax and fill (~0.5 sec); atrial kick adds final 20-30%. Systole — ventricular contraction (~0.3 sec). Pressure rises in LV until it exceeds aortic pressure (~80 mmHg) — aortic valve opens, ejection. Mitral valve closed during systole. End-systolic volume ~50 mL; end-diastolic ~120 mL; stroke volume ~70 mL; ejection fraction normal 55-70%. Heart sounds — S1 (mitral and tricuspid closure, start of systole), S2 (aortic and pulmonary closure, end of systole), S3 (early diastolic, rapid filling, normal in young or HF), S4 (atrial kick into stiff ventricle).
What's the conducting system?
SA node in right atrium near SVC junction — pacemaker, rate 60-100. Impulse spreads through atria, reaches AV node at base of right atrium near tricuspid valve. AV node delays conduction (~100 ms) to allow atrial contraction. Bundle of His travels into interventricular septum, splits into right bundle and left bundle (further into anterior and posterior fascicles). Purkinje fibers spread to ventricular myocardium, depolarize endocardium-to-epicardium and apex-to-base in <100 ms.
What are heart murmurs?
Turbulent flow audible on auscultation. Systolic — aortic stenosis (crescendo-decrescendo at right upper sternal border, radiates to carotids), mitral regurgitation (holosystolic at apex, radiates to axilla), tricuspid regurgitation, mitral valve prolapse (mid-systolic click), VSD (harsh holosystolic at left lower sternal border). Diastolic — aortic regurgitation (decrescendo at left sternal border, leaning forward), mitral stenosis (low-pitched rumble at apex with opening snap). Innocent murmurs are common in children — short, soft, systolic, no symptoms.
How does coronary circulation work?
Left main coronary divides into left anterior descending (LAD — anterior wall, septum) and left circumflex (lateral wall). Right coronary artery supplies inferior wall, right ventricle, SA node in 60%, AV node in 90% (right-dominant circulation in 85% of people). Posterior descending artery from RCA in right-dominant, from circumflex in left-dominant. Coronary perfusion occurs mostly in diastole because systolic pressure compresses intramural vessels. Heart rate-dependent — tachycardia shortens diastole, can ischemize.
What is heart failure?
Inability of heart to meet metabolic demand. HFrEF (reduced EF <40%) — systolic dysfunction; ischemic, dilated, valvular causes. HFpEF (preserved EF >50%) — diastolic dysfunction, stiff ventricle; hypertension, aging, restrictive cardiomyopathy. Symptoms — dyspnea, orthopnea, paroxysmal nocturnal dyspnea, fatigue, edema. NYHA class I-IV by symptom severity. Treat HFrEF with quadruple therapy — ACEi/ARB/ARNI (sacubitril-valsartan), beta blocker (carvedilol, metoprolol succinate, bisoprolol), MRA (spironolactone), SGLT2 inhibitor (dapagliflozin, empagliflozin).
What's myocardial infarction?
Cell death from prolonged ischemia, usually atherosclerotic plaque rupture with thrombosis. STEMI — full-thickness, ST elevation, urgent reperfusion within 90 minutes (PCI) or 12 hours (fibrinolytic). NSTEMI — subendocardial, troponin rises without ST elevation; risk-stratify and revascularize within 24-72 hours. Universal treatment — dual antiplatelet (aspirin + clopidogrel/ticagrelor/prasugrel), high-intensity statin, beta blocker, ACEi if EF reduced, anticoagulation per protocol. Cardiac rehab post-discharge.
How do you assess pumping function?
Echocardiogram measures ejection fraction, chamber sizes, wall motion, valves. Cardiac MRI for tissue characterization (fibrosis, infiltrative). Stress testing — exercise or pharmacologic (dobutamine, regadenoson) with ECG, echo, or nuclear imaging detects ischemia. Catheterization — gold standard for coronary anatomy and pressures. BNP and NT-proBNP elevated in heart failure (volume overload stretches ventricle, releases peptide). Troponin rises with myocardial injury. Right heart cath for pulmonary hypertension or shock states.