Heart Study Guide

📖 Core Concepts Four‑chambered mammalian heart – two atria (receive) and two ventricles (pump). Unidirectional valves – atrioventricular (tricuspid, mitral) and semilunar (pulmonary, aortic) prevent backflow. Cardiac cycle – diastole (ventricles fill, AV valves open) → systole (ventricles contract, semilunar valves open). Cardiac output (CO) – volume pumped per minute; $CO = SV \times HR$. Frank‑Starling mechanism – greater end‑diastolic volume → stronger contraction → higher stroke volume. Conduction system – SA node → atria → AV node (delay) → His bundle → bundle branches → Purkinje fibers. Autonomic regulation – vagus (parasympathetic) ↓HR; sympathetic ↑HR & contractility via β₁ receptors. Coronary circulation – left main → LAD + circumflex; right coronary supplies AV node (≈90 %) and SA node (≈60 %). --- 📌 Must Remember Normal resting HR: 60‑100 bpm (athletes <60). Normal CO ≈ 5 L min⁻¹ (SV ≈ 70 mL, HR ≈ 72 bpm). AV valve closure → S1 (“lub”); Semilunar valve closure → S2 (“dub”). Systolic BP > Diastolic BP; afterload = arterial pressure the ventricle must overcome. Preload = ventricular filling pressure at end‑diastole (Frank‑Starling). Positive inotropes: adrenaline, noradrenaline, dopamine. Negative inotropes: calcium‑channel blockers. Major CAD risk factors: smoking, obesity, inactivity, hyperlipidemia, hypertension, diabetes. Heart failure classification: HFrEF (reduced EF) vs. HFpEF (preserved EF). --- 🔄 Key Processes Cardiac Cycle (one heartbeat) Diastole: AV valves open → passive ventricular filling. Atrial systole: atria contract → “atrial kick”. Ventricular systole: pressure ↑ → AV valves close (S1); semilunar valves open → ejection. Isovolumetric relaxation: semilunar valves close (S2) → ventricles relax → next cycle. Electrical Conduction SA node fires → depolarization spreads across atria → AV node delay (0.1 s) → His bundle → left/right bundle branches → Purkinje network → synchronized ventricular contraction. Frank‑Starling Adjustment ↑Venous return → ↑ end‑diastolic volume → stretch of myocardial fibers → ↑ Ca²⁺ sensitivity → ↑ SV. Baroreceptor Reflex (short‑term HR control) ↑ arterial pressure → baroreceptor ↑ firing → ↓ sympathetic, ↑ parasympathetic → ↓ HR & contractility. ↓ pressure → opposite effect → ↑ HR. --- 🔍 Key Comparisons Tricuspid vs. Mitral valve – 3 cusps vs. 2 cusps; right vs. left side. Pulmonary vs. Aortic semilunar valve – right ventricle → pulmonary trunk vs. left ventricle → aorta; both three‑cusp. Systolic vs. Diastolic murmur – systolic occurs after S1, before S2; diastolic occurs after S2, before next S1. Ischemic heart disease vs. Heart failure – CAD = supply problem (arterial narrowing); HF = pump problem (output insufficient). HFrEF vs. HFpEF – reduced EF (<40 %) vs. normal/preserved EF (≥50 %) with diastolic dysfunction. --- ⚠️ Common Misunderstandings “All heart sounds are normal” – S3 and S4 are pathologic in adults (S3 = volume overload; S4 = stiff ventricle). “Higher HR always means better cardiac output” – Extremely high HR reduces filling time → ↓ SV, may lower CO. “Aortic stenosis only causes a murmur” – It also raises afterload, can lead to LV hypertrophy and heart failure. “Right‑sided heart disease is always secondary to left‑sided disease” – Primary right‑sided pathology (e.g., pulmonary hypertension) exists. --- 🧠 Mental Models / Intuition Pump‑pipe analogy – Heart = pump, vessels = pipe network. Valves are “one‑way check valves” that keep flow forward. Electrical “train line” – SA node = station master, AV node = signal stop, bundle branches = tracks, Purkinje = high‑speed rail to all cars (myocytes). Pressure‑volume loop – Visualize a rectangle: bottom edge = diastolic filling, vertical rise = isovolumetric contraction, top edge = ejection, downstroke = isovolumetric relaxation. --- 🚩 Exceptions & Edge Cases Right coronary dominance – 90 % of people; in left‑dominant hearts the circumflex supplies AV node. Athlete’s heart – enlarged LV wall thickness & chamber size without pathology; distinguished by normal diastolic function and absence of symptoms. Fossa ovalis – remnant of foramen ovale; in 25 % of adults a small residual shunt (patent foramen ovale) may persist. Baroreceptor reset in chronic hypertension – set point shifts upward, blunting reflex. --- 📍 When to Use Which Assessing chest pain → Start with ECG + troponin (ischemia vs. non‑ischemic). Evaluating murmur → Use timing (systolic vs. diastolic) + radiation + maneuvers (standing, squatting) to differentiate stenosis vs. regurgitation. Choosing imaging – Transthoracic echo for routine valve/EF assessment; Transesophageal echo for prosthetic valves or posterior structures; Stress echo for ischemia. Treating tachyarrhythmia – Stable: beta‑blocker or calcium‑channel blocker; Unstable: synchronized cardioversion. Managing HF with reduced EF – First‑line: ACE‑I/ARB + beta‑blocker + MR antagonist; add SGLT2 inhibitor if tolerated. --- 👀 Patterns to Recognize Chest pain + ST‑segment depression → subendocardial ischemia (often due to demand‑supply mismatch). Palpitations + irregularly irregular rhythm → atrial fibrillation (absent P waves, variable R‑R). Elevated JVP + peripheral edema → right‑sided HF (especially if LV signs absent). Loud S2 with a split that widens on inspiration → pulmonary hypertension. --- 🗂️ Exam Traps “Aortic stenosis murmur heard best at the apex” – Wrong; best heard at the right upper sternal border radiating to carotids. “Increased preload always improves CO” – False in severe HF where the ventricle is already on the flat part of the Frank‑Starling curve. “Troponin rises only in myocardial infarction” – Incorrect; also rises in severe HF, myocarditis, pulmonary embolism. “All patients with a patent foramen ovale need closure” – Not true; most are asymptomatic. ---