PY5.1-16 | Cardiovascular Physiology — Gate Quiz

Correct! CO = Heart Rate × Stroke Volume. Normal CO ≈ 72 beats/min × 70 mL/beat ≈ 5 L/min. Cardiac index normalises CO for body surface area (~3.2 L/min/m²).

Key concept: CO = HR × SV. Normal values: HR 72 bpm, SV 70 mL, CO ~5 L/min. Cardiac reserve: CO can increase to 20–25 L/min during exercise. Factors affecting SV: preload (Frank-Starling), afterload, contractility. Measured by Fick principle or thermodilution.

Incorrect. Cardiac output = Heart Rate (beats/min) × Stroke Volume (mL/beat). Normal ≈ 5 L/min at rest.

Correct! Frank-Starling law: increased preload (LVEDV) → optimal sarcomere stretch → enhanced actin-myosin overlap and Ca²⁺ sensitivity → greater force of contraction → increased stroke volume. This intrinsic mechanism matches cardiac output to venous return.

Key concept: Frank-Starling mechanism — the heart's intrinsic ability to match output to input. Increased LVEDV (preload) → sarcomere stretch to optimal 2.2 μm → max actin-myosin overlap → ↑Ca²⁺ sensitivity → ↑SV. Fails in severe heart failure (over-stretched sarcomeres). Heterometric autoregulation = Frank-Starling; Homeometric = Anrep effect.

Incorrect. Frank-Starling law states that increased preload → increased force of contraction (optimal sarcomere overlap) → increased stroke volume. The heart pumps what it receives.

Correct! Normal adult BP is 120/80 mmHg. JNC 8 / AHA 2017 classification: Normal <120/<80; Elevated 120–129/<80; Stage 1 HTN 130–139/80–89; Stage 2 HTN ≥140/≥90.

Key concept: BP classification — Normal: <120/<80; Elevated: 120–129/<80; HTN Stage 1: 130–139/80–89; HTN Stage 2: ≥140/≥90. Mean arterial pressure (MAP) = DBP + (1/3)(PP) = 80 + 13 ≈ 93 mmHg. Pulse pressure = SBP - DBP = 40 mmHg normally. Hypertension is the most common cardiovascular risk factor in India.

Incorrect. Normal adult blood pressure is 120/80 mmHg. Values ≥140/90 mmHg on two separate occasions define hypertension.

Correct! The plateau (Phase 2) of the ventricular AP lasts ~200–300 ms and is maintained by slow Ca²⁺ influx through L-type (long-lasting) voltage-gated Ca²⁺ channels balanced against K⁺ efflux. This Ca²⁺ influx triggers Ca²⁺-induced Ca²⁺ release (CICR) from the SR for contraction.

Key concept: Ventricular AP phases — Phase 0 (rapid depolarisation): fast Na⁺ channels; Phase 1 (early repolarisation): K⁺ efflux, Na⁺ channel inactivation; Phase 2 (plateau): L-type Ca²⁺ influx; Phase 3 (repolarisation): K⁺ efflux (IK channels); Phase 4 (resting): stable at -90 mV. Plateau prevents tetanus in cardiac muscle.

Incorrect. The plateau phase is maintained by slow Ca²⁺ influx (L-type Ca²⁺ channels) balanced against K⁺ efflux. Fast Na⁺ channels mediate Phase 0 (rapid depolarisation).

Correct! S1 ("lub") is produced by closure of the mitral (M1) and tricuspid (T1) valves at the beginning of ventricular systole (isovolumetric contraction phase). M1 precedes T1 slightly. S1 marks the onset of systole.

Key concept: Heart sounds — S1 (closure of AV valves, onset systole); S2 (closure of semilunar valves, end systole); S3 (rapid ventricular filling — normal in young, pathological in heart failure); S4 (atrial contraction against stiff ventricle — LVH, hypertension). Splitting of S2: physiological (inspiratory), paradoxical, fixed (ASD).

Incorrect. S1 = closure of AV valves (mitral + tricuspid) at start of systole. S2 = closure of semilunar valves (aortic + pulmonary) at end of systole.

Correct! In chronic hypertension, the autoregulatory curve shifts rightward — the kidney requires higher pressures to maintain normal flow. If BP is rapidly lowered (e.g., aggressive antihypertensive therapy), the kidney experiences ischaemia at pressures that would be normal for a normotensive person.

Key concept: Autoregulation maintains constant blood flow over a range of pressures (renal: 80–180 mmHg, cerebral: 60–150 mmHg). Chronic hypertension shifts these curves rightward — the organ adapts to higher pressures. This explains why: (1) aggressive BP lowering in chronic HTN can cause AKI or stroke, and (2) BP should be gradually normalised.

Incorrect. Chronic hypertension shifts the renal autoregulatory curve rightward. Rapid BP reduction to "normal" levels can cause acute kidney injury in chronically hypertensive patients.

Correct! At the arterial end of a capillary: hydrostatic pressure (~35 mmHg) > oncotic pressure (~25 mmHg) → net filtration pressure → fluid moves OUT. At the venular end: hydrostatic pressure falls to ~15 mmHg < oncotic pressure (~25 mmHg) → net absorption. Lymphatics drain the 10% excess.

Key concept: Starling forces — Net filtration = (Pc - Pi) - σ(πc - πi). Arterial end: Pc=35 > πc=25 → filtration. Venous end: Pc=15 < πc=25 → reabsorption. ~3 L/day filtered, 90% reabsorbed, 10% via lymphatics. Oedema = ↑Pc (HF) / ↓πc (hypoalbuminaemia) / ↑permeability (inflammation) / ↓lymph drainage.

Incorrect. At the arterial end of a capillary, hydrostatic pressure (~35 mmHg) exceeds plasma oncotic pressure (~25 mmHg), creating a net outward filtration force.

Correct! The PR interval (normal 0.12–0.20 sec) represents the time from the beginning of atrial depolarisation (P wave onset) to the beginning of ventricular depolarisation (QRS onset) — reflecting conduction through the AV node, bundle of His, and Purkinje fibres. Prolongation indicates AV block.

Key concept: ECG waves/intervals — P wave: atrial depolarisation; PR interval (0.12–0.20s): AV conduction; QRS complex (0.06–0.10s): ventricular depolarisation; ST segment: plateau phase; T wave: ventricular repolarisation; QT interval: ventricular depolarisation + repolarisation. Prolonged PR = 1st degree AV block; wide QRS = bundle branch block.

Incorrect. The PR interval represents AV conduction time (from atrial depolarisation through AV node to ventricular depolarisation onset). Normal: 0.12–0.20 sec.

Correct! Left coronary blood flow occurs predominantly during diastole. During systole, myocardial compression (intramyocardial pressure >100 mmHg) compresses coronary vessels, virtually stopping LCA flow. The right coronary artery (thin-walled RV) receives flow in both systole and diastole.

Key concept: Coronary perfusion — LCA: predominantly diastolic flow (systole compresses intramyocardial vessels). RCA: both phases. Coronary perfusion pressure = DBP - LVEDP. Tachycardia shortens diastole → reduces LCA filling time → risk of ischaemia. Subendocardium most vulnerable to ischaemia (highest intramural pressure, longest distance from epicardial vessels).

Incorrect. LCA flow occurs mainly during diastole because systolic myocardial contraction physically compresses intramyocardial coronary vessels. This is why tachycardia (shortened diastole) reduces coronary perfusion.

Correct! The fastest compensatory response to haemorrhage is the baroreceptor reflex. Reduced BP → reduced baroreceptor firing → ↑sympathetic tone → tachycardia (↑HR), vasoconstriction (↑SVR), increased contractility → partial BP restoration. This occurs within seconds.

Key concept: Compensatory responses in haemorrhage by timing — Immediate (seconds): baroreceptor reflex → ↑SNS → tachycardia + vasoconstriction; Minutes: ADH release, local autoregulation; 20–30 min: RAAS activation (↑angiotensin II, aldosterone); Hours: transcapillary fluid shift; Days: erythropoiesis. Class I shock (<15% blood loss) compensated; Class IV (>40%) life-threatening.

Incorrect. The immediate (within seconds) response is the baroreceptor reflex activating the sympathetic nervous system. RAAS takes 20–30 min; ADH takes minutes; transcapillary refill takes hours.