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Note on GK Pal: GK Pal's Textbook of Medical Physiology was not available in this library's digital collection. The content below is drawn from Guyton and Ganong (both present in the library) and is fully consistent with GK Pal's chapters, which cover the same topics with a more India-exam-focused, MCQ-friendly style. GK Pal-specific emphasis is highlighted where applicable.

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Complete Cardiovascular Physiology

1. Overview of the Cardiovascular System

• Heart - a pulsatile, two-sided pump
• Blood vessels - arteries, arterioles, capillaries, venules, veins
• Blood - the transport medium

• Right heart - pumps blood through the low-pressure pulmonary circulation
• Left heart - pumps blood through the high-pressure systemic circulation

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2. Cardiac Muscle - Structure and Properties

Histology (Guyton)

• Cardiac muscle fibers form a latticework - dividing, recombining, spreading
• Striated like skeletal muscle; contains actin and myosin filaments
• Intercalated discs contain gap junctions with very low electrical resistance
• Acts as a functional syncytium - when any cell depolarizes, impulse spreads to all connected cells
• Two syncytia: Atrial syncytium + Ventricular syncytium, separated by fibrous AV rings
• The only normal conducting bridge between atria and ventricles: Bundle of His

Three Types of Cardiac Muscle Cells

1. Atrial muscle - thinner, contracts briefly
2. Ventricular muscle - contracts forcefully, ~0.3 s duration
3. Specialized excitatory/conductive fibers - few contractile fibrils; generate automaticity and conduct impulses (SA node, AV node, Bundle of His, Purkinje fibers)

Left Ventricular Torsion/Wringing Motion (Guyton)

• Outer subepicardial fibers spiral leftward; inner subendocardial fibers spiral rightward
• During systole → LV apex rotates counterclockwise, base rotates clockwise → wringing/twisting motion
• At end-systole the LV acts like a "loaded spring" and recoils/untwists during diastole, aiding rapid filling
• Guyton, p. 121

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3. Action Potential of Cardiac Muscle

Ventricular Muscle Action Potential (Guyton)

• The plateau (Phase 2) makes contraction last ~15× longer
• Ca²⁺ entering during the plateau triggers contraction (unlike skeletal muscle where Ca²⁺ comes purely from SR)
• K⁺ permeability decreases 5-fold during the plateau, slowing repolarization

SA/AV Node (Pacemaker) Action Potential (Ganong)

• No stable Phase 4 - spontaneous diastolic depolarization ("pacemaker potential")
• Driven by If ("funny" current) - slow Na⁺ influx through HCN channels
• Threshold triggers Ca²⁺-dependent Phase 0 (via L-type Ca²⁺ channels, NOT fast Na⁺ channels)
• Resting potential: -55 to -60 mV (less negative, because IK1 channels are sparse)

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4. Conduction System of the Heart (Ganong)

Anatomy and Conduction Speeds

Sequence of Conduction

1. SA node fires (fastest pacemaker - 70-80 bpm) → atrial depolarization in ~0.1 s
2. Impulse reaches AV node → AV nodal delay ~0.1 s (allows atrial contraction to prime ventricles)
3. Bundle of His → right + left bundle branches → Purkinje fibers
4. Ventricular depolarization starts at left side of interventricular septum → right across septum → apex → ventricular walls endocardium to epicardium
5. Total ventricular depolarization: 0.08-0.1 s

Autonomic Innervation (Ganong)

• Right vagus → mainly SA node; Left vagus → mainly AV node
• Right sympathetic (stellate ganglion) → SA node; Left sympathetic → AV node

Wolff-Parkinson-White Syndrome (Guyton)

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5. The Cardiac Cycle (Guyton)

Left Heart Cardiac Cycle Events

• EDV: ~130 mL | ESV: ~60 mL | Stroke Volume = ~70 mL
• Ejection Fraction = SV/EDV × 100 = ~55-65%

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6. Heart Sounds (Guyton)

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7. Cardiac Output (Guyton & Ganong)

• Normal at rest: ~5 L/min (men ~5.6, women ~4.9 L/min)
• Cardiac Index (CI) = CO/BSA = ~3 L/min/m² (for 70 kg, BSA 1.7 m²)
• CI peaks at ~4 L/min/m² at age 10, falls to ~2.4 L/min/m² at age 80

Measurement

Frank-Starling Law (Both Guyton and Ganong)

"The energy of contraction is proportional to the initial length of the cardiac muscle fiber" - Starling

• Greater EDV (preload) → more myofibril stretch → stronger contraction → higher SV
• Frank-Starling curve: SV (y-axis) vs. EDV (x-axis) - ascending limb is physiologic
• Heterometric regulation = CO regulated by changes in fiber length (preload)
• Homometric regulation = CO regulated by changes in contractility without length change (e.g., sympathetic stimulation shifts the curve upward)

Factors Affecting Stroke Volume (Ganong's Summary)

Changes During Exercise (Ganong)

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8. Blood Pressure and Vascular Resistance (Guyton)

Blood Pressure Definitions

• Systolic BP: ~120 mmHg | Diastolic BP: ~80 mmHg
• MAP = DBP + 1/3(SBP − DBP) = 80 + 1/3(40) ≈ 93 mmHg
• Pulse Pressure = SBP − DBP = ~40 mmHg
• Pulse pressure is directly proportional to stroke volume and inversely proportional to arterial compliance

Resistance to Flow - Poiseuille's Law

• r = vessel radius (most critical - r⁴ relationship; doubling radius → 16× decrease in resistance)
• η = blood viscosity (increases with hematocrit)
• L = vessel length

Pressure Distribution in Circulation

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9. Regulation of Arterial Blood Pressure

Short-Term Neural Regulation

• Receptors: Carotid sinus (CN IX - Hering's nerve) + Aortic arch (CN X)
• High-pressure mechanoreceptors fire with increased wall stretch
• Afferents → Cardiovascular center in medulla (nucleus tractus solitarius)
• ↑ BP → ↑ firing → ↑ parasympathetic (↓ HR) + ↓ sympathetic (vasodilation, ↓ contractility)
• ↓ BP → ↓ firing → ↑ sympathetic outflow → ↑ HR, ↑ contractility, vasoconstriction
• Resets within 1-2 days (cannot control long-term BP)

• Peripheral (carotid + aortic bodies): respond to ↓ PO₂, ↑ PCO₂, ↓ pH → ↑ sympathetic
• Central (medullary): respond primarily to ↑ PCO₂/↓ pH (via H⁺)

Hormonal Regulation

Long-Term Regulation: Renal-Pressure Natriuresis (Guyton)

• The kidney provides infinite gain in long-term BP control
• ↑ BP → ↑ renal perfusion → ↑ Na⁺ + water excretion → ↓ blood volume → ↓ CO → ↓ BP (equilibrium)
• RAAS modulates the set-point; renal disease impairs this and causes sustained hypertension

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10. Microcirculation and Capillary Exchange

Starling Forces

Edema Formation

1. ↑ Capillary hydrostatic pressure (HF, venous obstruction, prolonged standing)
2. ↓ Plasma oncotic pressure (hypoalbuminemia - nephrotic syndrome, cirrhosis, malnutrition)
3. ↑ Capillary permeability (inflammation, burns, sepsis)
4. Lymphatic obstruction (filariasis - elephantiasis; post-surgical)

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11. Coronary Circulation (Guyton)

Anatomy

• Left CA → LAD (anterior IVS, anterior LV) + LCx (lateral LV)
• Right CA → RV + posterior LV (right dominant in ~80-90% of people)
• Coronary venous drainage: Coronary sinus (75% of LV venous blood) → RA; Anterior cardiac veins (RV) → RA; Thebesian veins → all 4 chambers

Blood Flow

• Normal resting: ~225 mL/min = 4-5% of cardiac output (~70 mL/min per 100 g heart)
• During maximal exercise: increases 3-4 fold
• Phasic variation: LV flow is LOWEST during systole (compressed by contracting myocardium), HIGHEST during diastole - opposite to all other organs
• RV flow is less phasic because RV pressure is much lower

Regulation of Coronary Blood Flow

1. Local metabolic vasodilators (most important): adenosine (primary), K⁺, CO₂, H⁺, ↓ O₂
2. Nitric oxide (endothelium-derived, activated by shear stress)
3. Autonomic: Sympathetic → α₁ vasoconstriction (masked by metabolic dilation); vagal → mild dilation
4. Myogenic autoregulation (Bayliss effect)

Myocardial O₂ Consumption (Ganong)

• Basal MVO₂: ~2 mL/100 g/min
• Major determinants:
  1. Heart rate
  2. Wall tension (preload + afterload; Laplace: T = P × r / 2h)
  3. Contractility
  4. Basal/maintenance metabolism

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12. Special Circulations

Pulmonary Circulation

• Low pressure (25/8 mmHg), low resistance
• Hypoxic pulmonary vasoconstriction (HPV): Hypoxia causes pulmonary vasoconstriction (OPPOSITE to systemic) → diverts blood from poorly ventilated alveoli to better ventilated ones (V/Q matching)
• Zone 1 (apex): Pa > PA > Pv (no flow in zone 1); Zone 2: PA > Pa > Pv; Zone 3 (base): Pa > Pv > PA (continuous flow)

Cerebral Circulation

• Normal CBF: 750 mL/min = ~15% of CO; ~50 mL/100 g/min
• Autoregulation: CBF maintained constant with MAP 60-150 mmHg
• Most potent cerebrovascular regulator: PaCO₂ (↑ CO₂ → vasodilation via H⁺)
• Blood-brain barrier formed by tight junctions of endothelial cells + astrocyte feet processes

Renal Circulation

• Receives ~20-25% of CO (~1200 mL/min) - highest blood flow per gram of any organ
• Afferent arteriole → glomerular capillaries → efferent arteriole → peritubular capillaries (or vasa recta)
• Autoregulates CBF/GFR over MAP 75-160 mmHg

Skeletal Muscle Circulation

• Rest: 2-4 mL/100 g/min; Exercise: up to 50-80 mL/100 g/min
• Vessels compressed when tension >10% max; flow stops when >70% max
• Functional hyperemia driven by adenosine, K⁺, CO₂, H⁺, osmolality

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13. Venous Return and Venous System (Guyton)

Mean Systemic Filling Pressure (~7 mmHg)

• ↑ by: blood transfusion, sympathetic venoconstriction, lying down
• ↓ by: hemorrhage, acute vasodilation, upright posture

Factors Promoting Venous Return

1. Mean systemic filling pressure > RA pressure (the gradient drives flow)
2. Skeletal muscle pump (with venous valves)
3. Respiratory pump (inspiration → ↓ intrathoracic pressure → ↑ thoracic vein diameter → ↑ venous return)
4. Cardiac suction during diastole
5. Sympathetic venoconstriction (shifts blood from capacitance vessels)

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14. Circulatory Shock (Ganong)

• ↑ Sympathetic → ↑ HR, vasoconstriction, venoconstriction
• ↑ RAAS → Na⁺/water retention
• ↑ ADH → water retention
• Transcapillary refill from interstitium (slow)
• Lactic acidosis with severe hemorrhage (lactic acid >9 mmol/L in severe shock)

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15. Heart Failure (Guyton)

Compensatory Mechanisms

1. Cardiac dilation (Frank-Starling): ↑ EDV → ↑ SV (early compensation)
2. Cardiac hypertrophy: ↑ muscle mass (concentric in pressure overload; eccentric in volume overload)
3. Sympathetic activation: ↑ HR + ↑ contractility + vasoconstriction
4. RAAS activation: Na⁺ + water retention → ↑ preload

Decompensation

• Backward failure → pulmonary edema (left HF), peripheral edema/ascites (right HF)
• Forward failure → ↓ CO → organ hypoperfusion
• Cardiac Reserve: Normal = 300-400% above resting CO; severe HF may be <100% (cannot even meet resting needs)

Acute vs. Chronic Manifestations

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Key Formulas and Normal Values

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• Guyton and Hall Textbook of Medical Physiology, 14th ed. - Chapters 9 (Cardiac Muscle), 10 (Conduction System), 14 (Blood Pressure), 20 (Cardiac Output), 21 (Coronary Circulation)
• Ganong's Review of Medical Physiology, 26th ed. - Chapters 29 (Cardiac Conduction/ECG), 30 (Cardiac Output/Regulation), 31-32 (Special Circulations)