Cardiovascular Physiology

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Rapid summary for last-minute revision before your exam.

Cardiovascular Physiology — Key Facts for NEET PG

• Cardiac output (CO): HR × SV = 5 L/min; normal HR 60–100 bpm
• Frank-Starling mechanism: Increased venous return → increased stroke volume (length-tension)
• SA node: Primary pacemaker (60–100 bpm); AV node: 40–60 bpm; Purkinje: 20–40 bpm
• ECG: P wave (atrial depolarization), QRS (ventricular depolarization), T wave (ventricular repolarization)
• ⚡ Exam tip: PR interval >0.2 sec = first-degree AV block; Absent P wave + irregular baseline = atrial fibrillation

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🟡 Standard — Regular Study (2d–2mo)

Standard content for students with a few days to months.

Cardiovascular Physiology — NEET PG Study Guide

Cardiac Cycle

Phases:

Phase	Duration	Key Events
Atrial systole	~0.1 sec	Atrial contraction → atrial pressure > ventricular pressure
Isovolumetric contraction	~0.05 sec	Ventricles contract, all valves closed, pressure rises
Ventricular ejection	~0.25 sec	Semilunar valves open; ejection phase
Isovolumetric relaxation	~0.08 sec	All valves closed; pressure falls
Ventricular filling	~0.4 sec	AV valves open; passive filling

⚡ Exam tip: S4 occurs during atrial systole (late diastole) — stiff, non-compliant ventricle (e.g., LVH, hypertrophic cardiomyopathy); S3 occurs during rapid ventricular filling — volume overload

Cardiac Action Potential

Ventricular Myocyte AP:

Phase	Key Events
Phase 0	Rapid depolarization — Na⁺ influx via fast voltage-gated Na⁺ channels
Phase 1	Initial repolarization — transient K⁺ efflux
Phase 2	Plateau — Ca²⁺ influx (L-type Ca²⁺ channels) balances K⁺ efflux
Phase 3	Rapid repolarization — Ca²⁺ channels close, K⁺ efflux increases
Phase 4	Resting membrane potential — K⁺ leak channels

Pacemaker Cells (SA Node):

• No stable resting potential
• Spontaneous diastolic depolarization (funny current, If)
• Threshold reached → AP
• Calcium channels (L-type) mediate upstroke (slow response)

⚡ Exam tip: Phase 4 slope determines heart rate — sympathetic ↑ slope → faster HR; parasympathetic ↓ slope → slower HR

Cardiac Conduction System

Sequence: SA node → Atrial muscle → AV node → Bundle of His → Left and right bundle branches → Purkinje fibers → Ventricular myocardium

Key Features:

• SA node: Intrinsic rate 60–100/min — primary pacemaker
• AV node: Intrinsic rate 40–60/min — delay allows atrial contraction before ventricular contraction
• Bundle of His: Only electrical connection between atria and ventricles
• Purkinje fibers: Intrinsic rate 20–40/min — fastest conduction for coordinated ventricular contraction

⚡ Exam tip: Wenckebach (Mobitz Type I) = progressive PR prolongation → dropped beat; Mobitz Type II = sudden AV block without preceding PR prolongation

ECG Interpretation

Leads:

• Limb leads: I, II, III, aVR, aVL, aVF
• Precordial leads: V1–V6

Waveforms:

Wave	Represents	Duration
P wave	Atrial depolarization	<0.08 sec
PR interval	AV nodal conduction	0.12–0.20 sec
QRS complex	Ventricular depolarization	<0.12 sec
ST segment	Ventricular plateau	—
T wave	Ventricular repolarization	—
QT interval	Total ventricular activity	<0.44 sec

Mean Electrical Axis:

• Normal: −30° to +90°
• Left axis deviation: <−30° (e.g., left anterior fascicular block, LVH)
• Right axis deviation: >+90° (e.g., RVH, pulmonary embolism)

⚡ Exam tip: ST elevation in contiguous leads = myocardial infarction; ST depression = ischemia; T wave inversion = ischemia/infarction

Cardiac Output and Hemodynamics

Cardiac Output Formula:

CO = HR × SV

Stroke Volume determinants:

Factor	Effect
Preload	Venous return → Frank-Starling
Afterload	↑ afterload → ↓ SV
Contractility	Sympathetic stimulation → ↑ contractility → ↑ SV

Blood Pressure:

BP = CO × Peripheral Resistance (SVR)

Resistance (Poiseuille’s Law):

R = 8ηL / πr⁴

• Resistance inversely proportional to radius⁴
• Small changes in radius → large changes in resistance

⚡ Exam tip: Sympathetic vasoconstriction in skin → ↓ blood flow → thermoregulation; Active skeletal muscle → vasodilation (metabolic regulation)

Coronary Circulation

Left Coronary Artery:

• LAD: Supplies anterior LV, anterior 2/3 of interventricular septum
• LCx: Supplies lateral LV, left atrium

Right Coronary Artery:

• Supplies RV, inferior LV (in right-dominant circulation, 70%)
• SA nodal artery (60%), AV nodal artery (90%)

Coronary Blood Flow:

• Left coronary flow: Greatest during diastole (subendocardial compression during systole)
• Right coronary flow: Relatively maintained during systole
• Autoregulation: Maintains flow despite BP changes
• Metabolic regulation: Adenosine, NO → vasodilation during increased oxygen demand

⚡ Exam tip: Aortic regurgitation → ↑ diastolic pressure gradient → increased coronary flow; Aortic stenosis → decreased coronary flow

Blood Volume Distribution

Region	Percentage of Total Blood Volume
Venous system (veins)	~64%
Heart and pulmonary circulation	~14%
Arterial system	~13%
Capillaries	~6%
Arterioles, metarterioles, etc.	~3%

⚡ Exam tip: Veins act as blood reservoirs — venoconstriction mobilizes stored blood (e.g., during hemorrhage)

Microcirculation

Starling Forces:

Force	Normal Value	Direction
Capillary hydrostatic pressure (Pc)	~25 mmHg (arterial end)	Outward
Interstitial hydrostatic pressure	~0 mmHg	Variable
Plasma oncotic pressure (πc)	~25 mmHg	Inward
Interstitial oncotic pressure	~2 mmHg	Variable

Net Filtration:

• At arterial end: Net outward pressure → filtration
• At venous end: Net inward pressure → reabsorption

⚡ Exam tip: Heart failure → ↑ central venous pressure → ↑ capillary hydrostatic pressure → edema

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🔴 Extended — Deep Study (3mo+)

Comprehensive coverage for students on a longer study timeline.

Cardiovascular Physiology — Comprehensive NEET PG Notes

Detailed Cardiac Cycle Analysis

Left Ventricle Pressure-Volume Loop:

Phase	Loop Movement
Diastasis	Bottom left (low pressure, moderate volume)
Atrial systole	Up left side (↑ pressure, ↑ volume)
Isovolumetric contraction	Vertical up (↑ pressure, constant volume)
Ejection	Right to top (↓ volume, ↓ pressure)
Isovolumetric relaxation	Vertical down (↓ pressure, constant volume)

Sounds During Cardiac Cycle:

• S1: AV valve closure (mitral first, then tricuspid) — “lub”
• S2: Semilunar valve closure (aortic first, then pulmonary) — “dub”
• S3: Rapid ventricular filling (during early diastole) — physiologic in children, pathological in adults
• S4: Atrial contraction (late diastole) — always pathological in adults

Jugular Venous Pulse (JVP):

Wave	Origin
a wave	Atrial contraction
c wave	Bulging of AV valves during isovolumetric contraction
x descent	Atrial relaxation
v wave	Venous filling against closed tricuspid
y descent	Tricuspid opening

⚡ Exam tip: Cannon a waves = forceful atrial contraction against closed tricuspid (AV dissociation, complete heart block); Absent a waves + regular “a” waves in neck = atrial fibrillation

Detailed Cardiac Electrophysiology

Ion Channels in Ventricular Myocyte:

Phase	Primary Current	Channel
0	INa (Na⁺ influx)	Nav1.5
1	Ito (K⁺ efflux)	Kv4.x
2	ICa-L (Ca²⁺ influx) + IKr (K⁺ efflux)	Cav1.2, hERG
3	IKr (K⁺ efflux)	hERG (IKr)
4	IK1 (K⁺ leak)	Kir2.x

SA Node Cell Electrophysiology:

• Phase 0: Ca²⁺ influx via L-type channels (slow response)
• Phase 3: K⁺ efflux via delayed rectifier
• Phase 4: Funny current (If) + decay of Ca²⁺ current → diastolic depolarization

Autonomic Regulation of Heart Rate:

Parameter	Sympathetic	Parasympathetic
Receptor	β1-adrenergic	Muscarinic (M2)
Effect on HR	↑ HR	↓ HR
AV nodal delay	↓	↑
Contractility	↑	↓ (minimal)
Mechanism	↑ cAMP → ↑ If, ↑ ICa	↓ cAMP → ↓ If

⚡ Exam tip: Vagal escape = prolonged vagal stimulation → heart rate recovers despite continued stimulation (acetylcholine breakdown)

Detailed ECG Analysis

ECG Lead Placement:

• Limb leads: Form Einthoven triangle
  • Lead I: RA (−) to LA (+)
  • Lead II: RA (−) to LL (+)
  • Lead III: LA (−) to LL (+)
• Augmented leads: aVR (right arm), aVL (left arm), aVF (left foot)

Heart Rate from ECG:

• Regular rhythm: 1500 / (# of large squares between R-R)
• Irregular rhythm: 1500 / (average R-R interval)

Myocardial Infarction ECG Changes:

Time	ECG Changes
0–30 min	Hyperacute T waves
Hours–days	ST elevation (transmural)
1–3 days	Q waves appear
Days–weeks	ST returns to baseline
Weeks–months	Persistent Q waves (scar)

⚡ Exam tip: ST depression in V1–V4 with tall R waves = posterior MI (look at posterior leads V7–V9)

Arrhythmias:

Arrhythmia	Key Feature
Sinus tachycardia	HR >100, normal P wave, regular
Sinus bradycardia	HR <60, normal P wave, regular
Atrial flutter	”Sawtooth” pattern (atrial rate ~300, ventricular rate lower)
Atrial fibrillation	Irregularly irregular rhythm, absent P waves
Ventricular tachycardia	Wide QRS (>0.12 sec), AV dissociation
Ventricular fibrillation	Chaotic baseline, no identifiable waves

Detailed Hemodynamics

Vascular Anatomy:

Segment	Function
Arteries	Pressure reservoir, smooth muscle for regulation
Arterioles	Major resistance vessels (SVR), vasoconstriction/dilation
Capillaries	Site of exchange (nutrients, gases, water)
Venules	Begin exchange
Veins	Return blood, capacitance vessels

Laplace’s Law (for spherical structures):

Wall stress = (Pressure × Radius) / (2 × Wall thickness)

• In heart: ↑ wall thickness normalizes wall stress (concentric hypertrophy)
• In aneurysm: ↑ radius → ↑ wall stress → risk of rupture

⚡ Exam tip: Windkessel effect = elastic arteries store energy during systole and release during diastole → maintains diastolic pressure

Cardiac Output Regulation

Factors Affecting Cardiac Output:

Variable	Increased CO	Decreased CO
Heart rate	↑ HR	↓ HR
Preload	↑ Venous return	↓ Venous return
Afterload	↓ Systemic resistance	↑ Systemic resistance
Contractility	↑ Sympathetic tone	↓ Contractility

Frank-Starling Mechanism:

• Increased venous return → increased end-diastolic volume → increased preload → increased stroke volume
• Ejection fraction (EF) = SV/EDV × 100 (normal >55%)
• Preload measured clinically as PCWP (pulmonary capillary wedge pressure)

Baroreceptor Reflex:

• Receptors: Carotid sinus (CN IX), Aortic arch (CN X)
• ↑ BP → baroreceptors fire → ↑ parasympathetic (↓ HR) + ↓ sympathetic → ↓ BP
• Rapid regulation (seconds)

Chemoreceptor Reflex:

• Detects: ↓ PaO₂, ↑ PaCO₂, ↓ pH in arterial blood
• Carotid bodies (main), aortic bodies
• Stimulates vasomotor center → ↑ BP, ↑ HR

⚡ Exam tip: Valsalva maneuver = ↑ intrathoracic pressure → ↓ venous return → ↓ CO → ↓ BP → compensation → release → ↑ BP overshoot; used to diagnose different conditions

Renal and Hormonal Regulation

Renin-Angiotensin-Aldosterone System (RAAS):

1. ↓ renal perfusion → juxtaglomerular cells release renin
2. Renin converts angiotensinogen → angiotensin I
3. ACE (lung) converts Ang I → Angiotensin II
4. Ang II: Vasoconstriction + stimulates aldosterone + ADH + thirst
5. Aldosterone: ↑ Na⁺ reabsorption, ↑ K⁺ excretion (principal cells of collecting duct)

Atrial Natriuretic Peptide (ANP):

• Released from atrial myocytes in response to stretch (volume overload)
• ↑ Na⁺ excretion (natriuresis)
• Vasodilation
• Inhibits renin and aldosterone

⚡ Exam tip: ACE inhibitors (captopril, enalapril) block conversion of Ang I → Ang II → ↓ efferent arteriolar pressure → beneficial in diabetic nephropathy; ** Cough is a common side effect (bradykinin accumulation)

Cardiovascular Adjustments

Exercise:

• Sympathetic activation → ↑ HR, ↑ contractility, ↑ BP, vasodilation in active muscle
• Venous return increases (muscle pump, respiratory pump)
• Parasympathetic withdrawal contributes to initial HR increase
• Maximum CO can reach 25–30 L/min in trained athletes

Postural Changes (supine → standing):

• ↓ venous return → ↓ preload → ↓ SV → ↓ BP
• Baroreceptor reflex → ↑ HR, ↑ SVR
• After few seconds, compensatory mechanisms stabilize BP

Hemorrhage:

• ↓ circulating volume → ↓ venous return → ↓ CO
• Compensatory: ↑ HR, ↑ SVR, ↑ ADH, ↑ aldosterone, thirst
• If >30% blood loss → decompensated shock

Practice Questions for NEET PG

1. Draw and label the cardiac cycle (left ventricular pressure-volume loop).
2. Compare the action potential of a ventricular myocyte with that of a SA node cell.
3. Describe the conduction system of the heart and explain the importance of AV nodal delay.
4. A patient has a prolonged QT interval. Which channels could be affected?
5. Calculate cardiac output given HR and stroke volume. What factors determine stroke volume?
6. Explain the baroreceptor reflex response to acute hemorrhage.
7. Describe the RAAS and its role in blood pressure regulation.

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