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Cardiovascular Physiology

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Cardiovascular Physiology — Key Facts for FMGE Core concept: The heart functions as a dual pump; cardiac output is determined by heart rate and stroke volume; blood flows through vasculature driven by pressure gradients High-yield point: Starling’s law of the heart explains how preload affects stroke volume; understanding pressure-volume loops is key ⚡ Exam tip: Cardiac output = HR × SV; normal CO is ~5 L/min; be clear about the phases of the cardiac cycle and what happens to pressures, volumes, and heart sounds

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Cardiovascular Physiology — FMGE Study Guide

Cardiac Cycle

Phases

Systole:

  1. Isovolumetric contraction: AV valves close, semilunar valves closed, pressure rises rapidly
  2. Rapid ejection: Semilunar valves open, blood ejected rapidly; ventricular pressure peaks
  3. Reduced ejection: Slower ejection, pressure begins to fall; systole ends

Diastole: 4. Isovolumetric relaxation: Semilunar valves close, AV valves still closed, pressure falls; ventricular volume unchanged 5. Rapid filling: AV valves open, blood rushes into ventricles; 70% of filling occurs 6. Reduced filling (diastasis): Slower filling; atrial contraction contributes final filling 7. Atrial systole (atrial kick): Atrial contraction adds final 15-25% of ventricular filling

Heart Sounds

S1 (lub): AV valve closure (mitral first, then tricuspid); marks beginning of systole S2 (dub): Semilunar valve closure (aortic first, then pulmonic); marks end of systole S3: Rapid ventricular filling (in children/young adults, pathological in adults - dilated ventricle) S4: Atrial contraction against stiff ventricle (hypertrophied ventricle - HTN, hypertrophy)

Pressure-Volume Loop

  • Bottom right: End-diastolic volume (EDV) - filled, starting contraction
  • Right side: Isovolumetric contraction (vertical up - pressure ↑, volume same)
  • Top: End-systolic volume (ESV) - maximal pressure, minimal volume
  • Left side: Isovolumetric relaxation (vertical down - pressure ↓, volume same)
  • Bottom left: End-diastolic volume (EDV) - starting filling
  • Loop area: Stroke work (external work done by heart)

Cardiac Output

Equation

CO = HR × SV

  • Normal CO: 5 L/min (at rest)
  • CO = SV × HR; SV = EDV - ESV

Heart Rate

  • Normal: 60-100 bpm
  • Chronotropic: HR control (+ or -)
  • Dromotropic: Conduction velocity (+ or -)
  • Inotropic: Contractility (+ or -)

Stroke Volume Determinants

Preload (venous return/end-diastolic volume):

  • Stretch of cardiac muscle before contraction
  • Starling’s law: Increased preload → increased SV (within physiological limits)
  • Dependent on: Venous return, atrial contraction, ventricular compliance

Afterload (arterial pressure ventricle must overcome):

  • Aortic pressure during systole
  • Increased afterload → decreased SV (heart works harder)
  • Dependent on: Systemic vascular resistance (SVR), arterial pressure, ventricular radius

Contractility (inotropic state):

  • Intrinsic strength of cardiac muscle independent of preload/afterload
  • Increased by: Sympathetic stimulation, catecholamines, increased Ca²⁺
  • Decreased by: Beta-blockade, HF, hypoxia, acidosis

Regulation of Cardiac Output

Starling mechanism: Adjusts SV based on EDV to match venous return Autonomic nervous system: Sympathetic (↑HR, ↑contractility) vs parasympathetic (↓HR) Afterload: Peripheral resistance affects how much work heart must do Heart rate changes: Account for most immediate CO changes

Cardiac Electrical Activity

Pacemaker Cells

SA node (primary pacemaker):

  • Intrinsic rate: 60-100 bpm
  • Slow response fibers (no fast Na channels; Ca-dependent action potential)
  • Located in right atrium near SVC opening

AV node:

  • Intrinsic rate: 40-60 bpm
  • Delays impulse transmission (allows atrial contraction before ventricular contraction)
  • Located at base of interatrial septum

Purkinje fibers:

  • Intrinsic rate: 20-40 bpm
  • Fast conduction (fast Na channels)
  • Distribute impulse throughout ventricles

Cardiac Action Potential

Non-pacemaker (ventricular myocyte):

  • Phase 0: Rapid depolarization (fast Na channels - similar to neurons)
  • Phase 1: Early repolarization (K efflux)
  • Phase 2: Plateau (Ca²⁺ influx via L-type Ca channels balanced by K efflux) - unique to cardiac muscle
  • Phase 3: Repolarization (K efflux > Ca²⁺ influx)
  • Phase 4: Resting membrane potential (K leak channels, Na/K ATPase)

Pacemaker cells (SA node):

  • Slow response AP: No phase 0 (no fast Na); upstroke via L-type Ca channels
  • Phase 4 diastolic depolarization: Funny current (If) causes slow depolarization
  • Phases 0-3: Similar but more gradual than ventricular myocytes

Conduction Velocity

  • Atrial pathways: 1 m/s
  • AV node: 0.05 m/s (slow - allows time for atrial contraction)
  • Bundle of His: 1 m/s
  • Purkinje fibers: 2-4 m/s (fastest)
  • Ventricular muscle: 0.3-0.5 m/s

Hemodynamics

Blood Flow (Q)

Q = ΔP / R (Ohm’s law analog)

  • Blood flow is proportional to pressure gradient and inversely proportional to resistance

Resistance

R = 8ηL / πr⁴ (Poiseuille’s law)

  • Most important factor: Radius (4th power!)
  • Small changes in radius cause large changes in resistance
  • η (viscosity): Affected by hematocrit; polycythemia increases viscosity

Blood Pressure

  • Systolic: Peak pressure during ventricular contraction
  • Diastolic: Lowest pressure during ventricular relaxation
  • Pulse pressure: Systolic - Diastolic (normal ~40 mmHg)
  • Mean arterial pressure (MAP): Diastolic + 1/3 pulse pressure
  • MAP = CO × SVR (approximately)

Resistance in Series vs Parallel

  • Series: Total = R1 + R2 + … (each resistance adds)
  • Parallel: 1/Rtotal = 1/R1 + 1/R2 + … (total resistance is less than any individual)
  • Systemic circulation: SVR (TPR) = arterioles + capillaries + venules
  • Most resistance in arterioles (functional vasoconstriction/dilation)

Coronary Circulation

  • Left coronary artery: Supplies LV, most of septum; feeds left anterior descending (LAD) and left circumflex
  • Right coronary artery: Supplies RA, RV, SA node (in 60%), AV node (in 90%)
  • During systole: Coronary flow almost stops (high intramural pressure compresses vessels)
  • During diastole: Major coronary fill occurs
  • LV subendocardium: Most vulnerable to ischemia (highest pressure, longest systolic compression)
  • Exercise: ↑CO, ↓diastolic time → can limit coronary flow if stenosis present

Blood Volume Distribution

  • Veins (~64%): Largest reservoir; capacitance vessels; most blood at rest
  • Heart and lungs (~13%): Smaller reservoirs
  • Arteries (~8%): High-pressure system
  • Capillaries (~5%): Site of exchange
  • Venules and small veins (~10%): Blood storage

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