Cardiovascular Physiology - WBUHS 1st Professional MBBS Exam Guide

• Group A - Long Answer Questions (LAQ): 12 marks each
• Group B - Short Answer Questions (SAQ): 7 marks each
• Group C - Short Notes: 4 marks each
• Group D - Explain Why / Application: 2-3 marks each

GROUP A - LONG ANSWER QUESTIONS (12 Marks)

1. Cardiac Cycle [Most Repeated - 2+6+4]

• All valves closed
• LV pressure rises rapidly from ~5 mmHg to 80 mmHg
• Volume remains constant at End Diastolic Volume (EDV) = ~130 mL
• Starts when LV pressure exceeds LA pressure (mitral valve closes)
• Ends when LV pressure exceeds aortic pressure (80 mmHg)

• Aortic valve opens
• LV pressure peaks at ~120 mmHg
• Volume falls from 130 mL to ~60 mL (Stroke Volume = 70 mL)
• T-wave of ECG occurs; aortic pressure peaks
• Divided into rapid ejection (first 1/3) and reduced ejection (last 2/3)

• All valves again closed
• LV pressure falls rapidly from 80 mmHg to ~5 mmHg
• Volume remains constant at End Systolic Volume (ESV) = ~60 mL

• Mitral valve opens when LV pressure falls below LA pressure
• Volume increases from 60 mL to 130 mL
• Three sub-phases: Rapid filling → Slow filling (Diastasis) → Atrial systole (contributes ~25 mL)

• LV pressure curve (rises during contraction, peaks ~120 mmHg)
• Aortic pressure curve (dicrotic notch marks aortic valve closure)
• LV volume curve (falls during ejection, lowest at ESV)
• ECG: P wave → Atrial systole; QRS → Ventricular systole; T wave → Repolarization
• Phonocardiogram: S1 (MV closure) and S2 (AV closure)

2. Regulation of Blood Pressure [Repeated - 8+2+2]

• Receptors: High-pressure baroreceptors in carotid sinus (CN IX) and aortic arch (CN X)
• Afferents: Hering's nerve → CN IX → NTS in medulla; Aortic depressor nerve → CN X → NTS
• Integration: Nucleus Tractus Solitarius (NTS) → Cardiovascular centre (vasomotor + cardioinhibitory)
• Response to raised BP: ↑ baroreceptor firing → ↓ sympathetic output + ↑ vagal tone → ↓ HR, ↓ contractility, vasodilation → BP falls
• Response to fall in BP: Opposite - ↑ sympathetic, ↓ vagal → ↑ HR, vasoconstriction → BP rises
• Operates within seconds; resets in chronic hypertension

• Peripheral chemoreceptors (carotid + aortic bodies): respond to ↓PO2, ↑PCO2, ↓pH → vasoconstriction + ↑BP
• Central chemoreceptors (medulla): respond to ↑PCO2 → vasomotor centre stimulated

• Triggered when cerebral blood flow falls severely
• Massive sympathetic discharge → severe hypertension + bradycardia
• Last-ditch mechanism; indicates brain herniation

• ↓BP/↓Na+ → Renin from JG cells → Angiotensin I → (ACE in lung) → Angiotensin II
• Ang II: potent vasoconstrictor + stimulates aldosterone → Na+/water retention → ↑BP

• ↓BP → ↓capillary hydrostatic pressure → fluid moves from interstitium into capillaries → ↑blood volume → ↑BP

• Most powerful long-term regulator
• ↑BP → pressure natriuresis/diuresis → ↓blood volume → BP returns to normal
• Operates over hours to days

• Regulate Na+ and water balance → long-term blood volume control

3. ECG - Waves, Segments and Heart Block [Repeated - 6+2+4]

• P wave absent: atrial fibrillation; tall + broad P: atrial enlargement
• Prolonged PR: 1st degree heart block
• Widened QRS: bundle branch block or ventricular arrhythmia
• ST elevation: myocardial infarction (injury current); ST depression: ischemia/digitalis
• Prolonged QT: risk of torsades de pointes (dangerous arrhythmia)
• Tall T: hyperkalemia; inverted T: ischemia, LBBB, ventricular hypertrophy

• PR interval >0.20 sec (>5 small squares)
• All P waves followed by QRS
• Benign; no treatment needed
• ECG: Prolonged PR interval

• Type I (Mobitz I / Wenckebach): Progressive PR lengthening until a P wave is not conducted (dropped QRS). Benign.
• Type II (Mobitz II): Constant PR interval but sudden non-conducted P waves. More serious - can progress to complete block. Needs pacemaker.

• No relationship between P waves and QRS complexes (AV dissociation)
• Atria and ventricles beat independently
• Escape rhythm: junctional (rate 40-60 bpm) or ventricular (rate 20-40 bpm)
• Symptoms: syncope (Stokes-Adams attacks), heart failure
• Requires permanent pacemaker

4. Cardiac Output [Repeated - 2+6+4]

• CO = Heart Rate × Stroke Volume
• Normal: 5 L/min (at rest, 70 kg male)
• Cardiac Index = CO / Body Surface Area = 3.2 L/min/m²

• Normal: 60-100 bpm (SA node sets the pace at ~70 bpm)
• ↑HR by: Sympathetic (beta-1), catecholamines, thyroid hormones, fever, exercise, ↓vagal tone
• ↓HR by: Parasympathetic (vagus), ↑ICP (Cushing reflex), athletes (vagal dominance)
• Note: Too fast HR (>180) is counterproductive as it reduces diastolic filling time → ↓SV → ↓CO

• = End-diastolic volume (EDV); the stretch on ventricular muscle before contraction
• Frank-Starling Law: "The strength of ventricular contraction is proportional to initial length of muscle fiber (within physiological limits)"
• ↑Venous return → ↑EDV → ↑stretch → ↑crossbridge formation → ↑SV
• Physiological importance: Ensures both ventricles eject equal stroke volumes; automatically compensates for increased venous return (exercise, lying down)
• Increased by: ↑venous return, bradycardia, ↑blood volume
• Decreased by: hemorrhage, dehydration, tachycardia

• = Resistance against which ventricle must eject blood = Aortic pressure (systemic vascular resistance)
• ↑Afterload → ↑wall tension needed → ↑O2 consumption → ↓SV (if not compensated)
• Increased in: hypertension, aortic stenosis
• Decreased by: vasodilator drugs

• = Intrinsic ability of heart to contract at a given preload and afterload
• ↑Contractility: Sympathetic stimulation, catecholamines, cardiac glycosides (digoxin), ↑Ca²+, Bowditch effect (↑HR)
• ↓Contractility: Heart failure, beta-blockers, calcium channel blockers, hypoxia, acidosis

• Determined by: mean systemic filling pressure - right atrial pressure
• Factors promoting venous return: skeletal muscle pump, respiratory pump (inspiration ↓intrathoracic pressure → ↑venous return), venous tone, body position

• Cause: During systole, high stroke volume (LV pumps normal + regurgitated blood) → very high systolic BP. During diastole, blood flows back into LV → aortic diastolic pressure falls very low.
• Result: Pulse pressure (systolic - diastolic) greatly increased (normal 40 mmHg; in AR can be 80-100 mmHg)
• Clinical signs: "Water hammer pulse" (Corrigan's pulse) - abrupt rise and rapid collapse; Pistol shot sound over femoral artery; Duroziez sign; head bobbing (de Musset's sign); capillary pulsations (Quincke's sign)

• Cause: During diastole, blood jets back from aorta through incompetent valve into LV, creating turbulent flow
• Character: High-pitched, blowing, early diastolic murmur at left sternal border (3rd-4th ICS); best heard leaning forward in expiration
• Austin Flint murmur: Functional mid-diastolic murmur at apex due to regurgitant jet partially closing mitral valve

GROUP B - SHORT ANSWER QUESTIONS (7 Marks)

1. Baroreceptor Reflex [2+5]

• Carotid sinus baroreceptors: Located at bifurcation of common carotid artery; innervated by CN IX (Hering's nerve); most sensitive, respond to pressures of 60-180 mmHg
• Aortic arch baroreceptors: Innervated by CN X (vagus); less sensitive, higher threshold

• These are mechanoreceptors (stretch receptors) in vessel walls
• Normal firing rate at MAP ~100 mmHg
• ↑BP → ↑wall stretch → ↑receptor firing → afferents to NTS in medulla → NTS activates cardioinhibitory centre (↑vagal tone) + inhibits vasomotor centre (↓sympathetic)
• Net effect: ↓HR + ↓contractility + vasodilation → CO falls → TPR falls → BP returns to normal

• ↓BP → ↓stretch → ↓receptor firing → ↓NTS activity → ↑sympathetic + ↓vagal → ↑HR + ↑contractility + vasoconstriction → BP rises

• Resets over 1-2 days in chronic hypertension (baroreceptors adapt to new level)
• Cannot maintain long-term BP control (renal mechanism is superior for long-term)

2. Marey's Law [2+4+1]

• ↑BP → ↑stretch on carotid sinus/aortic arch baroreceptors → ↑firing in CN IX/X → NTS in medulla → ↑vagal (cardioinhibitory) activity + ↓sympathetic → ↓HR
• Reverse: ↓BP → ↓baroreceptor firing → ↓vagal + ↑sympathetic → ↑HR

1. Bainbridge Reflex: ↑venous return → ↑right atrial stretch → ↑HR (despite ↑BP) - tachycardia with ↑BP
2. Cushing Reflex: ↑ICP → ↑BP + bradycardia (Marey's law here) but primary cause is ischemic CNS, not arterial baroreceptors
3. Exercise: ↑HR despite ↑BP (cortical override of baroreceptors)
4. Thyrotoxicosis / Fever: ↑HR regardless of BP
5. Emotional stress/anxiety: ↑HR despite ↑BP

3. Cardiac Output - Fick's Method [2+5]

1. Measure O₂ consumption: Patient breathes into a spirometer for 1 minute → O₂ consumed = ~250 mL/min at rest
2. Collect arterial blood: From any systemic artery (e.g., brachial artery) → measure O₂ content (~200 mL O₂/L blood)
3. Collect mixed venous blood: Via cardiac catheter from pulmonary artery (right heart) → O₂ content (~150 mL O₂/L blood)
4. Calculate: CO = 250 mL/min ÷ (200 - 150) mL/L = 250/50 = 5 L/min

GROUP C - SHORT NOTES (4 Marks Each)

1. Augmented Limb Leads in ECG

• aVR, aVL, aVF are unipolar leads derived from Goldberger's modification of Wilson's central terminal
• aVR = Right arm; views heart from right shoulder; normally all complexes negative (QRS mainly negative, T negative)
• aVL = Left arm; views heart from left shoulder
• aVF = Left foot; views inferior surface of heart (diaphragmatic surface)
• "Augmented" because signal is amplified by 50% by disconnecting the limb being recorded from the central terminal
• Clinical uses: aVF shows inferior MI (with II, III); aVL shows lateral MI; aVR - ST elevation suggests left main/proximal LAD disease

2. CVS Adjustments During Exercise

• ↑HR (up to 180-200 bpm) - sympathetic + withdrawal of vagal tone + circulating catecholamines
• ↑Contractility (↑SV up to 110 mL from 70 mL)
• ↑CO (up to 20-25 L/min; trained athletes may reach 35 L/min)

• ↑Blood flow to working muscles (arterioles dilate due to local metabolites: CO₂, lactic acid, adenosine, ↓pH, ↓O₂)
• ↑Coronary blood flow (up to 5x resting)
• ↓Flow to gut, kidneys, skin (initially)
• ↑Skin blood flow later (thermoregulation)

3. Standard Limb Leads in ECG

• Bipolar leads (I, II, III) based on Einthoven's triangle
• Lead I: Left arm (+) - Right arm (-); records lateral heart activity
• Lead II: Left leg (+) - Right arm (-); greatest voltage normally (R wave tallest); detects inferior MI
• Lead III: Left leg (+) - Left arm (-); inferior heart
• Einthoven's Law: Voltage in Lead II = Lead I + Lead III
• Standard recording: Paper speed 25 mm/sec; 1 mV = 10 mm; each small square = 0.04 sec; large square = 0.20 sec

4. PR Interval

• Measured from beginning of P wave to beginning of QRS complex
• Normal: 0.12-0.20 seconds (3-5 small squares)
• Represents: Atrial depolarization + AV nodal delay (AV node slows conduction to allow atrial contraction before ventricular systole)
• Short PR (<0.12 sec): Pre-excitation syndromes (WPW syndrome - accessory pathway bypasses AV node); LGL syndrome; junctional rhythms
• Long PR (>0.20 sec): 1st degree AV block (seen in rheumatic fever, digoxin toxicity, myocarditis, elderly)
• AV node delay is normally 0.07-0.10 sec; acts as a "gatekeeper"

5. 2nd Degree AV Nodal Block

• Progressive PR interval lengthening with each beat until one P wave fails to conduct (dropped QRS)
• Then cycle repeats (grouped beating)
• Site: AV node (supranodal)
• Cause: Inferior MI, increased vagal tone, digoxin toxicity
• Usually benign; may not need pacemaker

• Constant PR interval but sudden, unexpected dropped QRS (non-conducted P wave)
• Site: Below AV node (His-Purkinje); more dangerous
• Cause: Anterior MI, fibrosis, cardiomyopathy
• May progress to complete heart block → requires permanent pacemaker

6. Subendocardial Region of LV is Specially Vulnerable to Ischemia

1. Highest wall tension: Subendocardial region experiences maximum compressive force during systole (Laplace's law: T = P × r/2h); this compresses intramyocardial vessels
2. Perfusion only during diastole: Coronary perfusion of LV occurs mainly in diastole; LV subendocardium is compressed during systole. If diastolic time shortens (tachycardia) or diastolic aortic pressure falls, subendocardium is underperfused
3. Longest distance from epicardial coronary arteries: Blood must travel from epicardial vessels through the wall to reach subendocardium - highest resistance path
4. Higher oxygen demand: Innermost fibers do more work due to greater shortening needed
5. End-artery territory: No anastomotic protection

7. Normal ECG Waves (Brief)

• P, QRS, T wave significance
• Normal values
• Represent sequential depolarization and repolarization
• U wave: Purkinje/papillary muscle repolarization

8. Sinoaortic Reflex

• Another name for the baroreceptor reflex (see Group B Q1 above, in 4-mark condensed form)
• "Sino" = carotid sinus; "Aortic" = aortic arch
• Rapid neural reflex maintaining BP homeostasis via stretch receptors in carotid sinus and aortic arch

GROUP D - EXPLAIN WHY (2-3 Marks Each)

1. Why does tachycardia occur in cardiovascular shock?

• Shock → ↓BP → ↓baroreceptor firing → reflex ↑sympathetic + ↓vagal → ↑HR (tachycardia); attempts to maintain CO

1. Why does inspiration cause physiological splitting of S2?

• Inspiration → ↓intrathoracic pressure → ↑venous return to right heart → ↑RV stroke volume → pulmonary valve closes later (P2 delayed); simultaneously, ↑pulmonary vascular capacitance → ↓venous return to LV → ↓LV stroke volume → aortic valve closes earlier (A2 earlier) → A2-P2 gap widens → audible split

1. Why is aortic valve closed at rest longer than open?

• Diastole (0.5 sec) > systole (0.3 sec) at normal heart rate; valve open only during ejection phase

1. Why does lying down increase cardiac output?

• ↑venous return (gravity assists pooled blood in legs to return to heart) → Frank-Starling mechanism → ↑SV → ↑CO

1. Why does the left ventricle have a thicker wall than the right?

• LV pumps against systemic circulation (pressure ~120/80 mmHg); RV against pulmonary circulation (~25/10 mmHg); LV wall is 3x thicker (8-12 mm vs 3-5 mm)

QUICK SUMMARY: HIGH-FREQUENCY TOPICS BY YEAR

Exam tip: WBUHS Paper 1 physiology always has one long question from CVS. The cardiac cycle, BP regulation, and ECG rotate as the most common 12-mark questions. Learn your Wiggers diagram, ECG intervals, and the baroreceptor arc diagram - they appear in virtually every exam.