Cardiac Output & its regulation- Physiology

Cardiac output (CO)

Volume of blood pumped by each ventricle per minute

Formula for CO

CO = SV x HR

Normal resting CO in adult

~5 L/min

CO during exercise

20–25 L/min, up to 35–40 L/min in trained athletes

Cardiac reserve

Difference between resting CO and maximum CO during exercise

Cardiac index

CO adjusted for body surface area (L/min/m²)

Venous return (VR)

Volume of blood entering each atrium per minute

Relationship of CO and VR

CO must equal VR to maintain balance

Effect of increased metabolic rate

↑ CO and ↑ VR

Determinants of CO

Heart rate (HR) and Stroke volume (SV)

Effect of HR on CO

↑ HR → ↑ CO (up to a limit)

Effect of SV on CO

↑ SV → ↑ CO (if HR constant)

Regulation of HR

Autonomic nervous system, hormones, temperature, electrolytes

Sympathetic effect on HR

NE/Epi via β₁ receptors → ↑ HR

Parasympathetic effect on HR

Ach via vagus nerve (M2 receptors) → ↓ HR

Hormonal regulation of HR

Epinephrine and thyroid hormones ↑ HR; Bradykinin and Ach ↓ HR

Temperature effect on HR

Fever ↑ HR

Electrolyte effect on HR

High potassium ↓ HR (risk of cardiac arrest)

Mechanism of sympathetic effect on HR

↑ Na⁺ & Ca²⁺ channel opening, ↓ K⁺ permeability → faster depolarization → ↑ HR

Mechanism of parasympathetic effect on HR

Closure of Na⁺ & Ca²⁺ channels, opening of K⁺ channels → hyperpolarization → ↓ HR

Cardio‑acceleratory centre (CAC)

Stimulates SNS → ↑ HR and ↑ RR

Chemoreceptor stimulation

↓ PO₂, ↑ PCO₂, ↓ pH → activate CAC → ↑ HR

Bradycardia

HR < 60 bpm (PSNS, drugs, endurance activity)

Tachycardia

HR > 100 bpm (SNS, high thyroid hormone, drugs, anxiety)

Stroke volume (SV)

Volume of blood ejected per ventricle per beat

Formula for SV

SV = EDV - ESV

Normal SV

120 − 50

EDV (End‑diastolic volume)

Volume in ventricle before contraction

ESV (End‑systolic volume)

Volume remaining after contraction

Factors affecting SV

Preload, Afterload, Contractility (Inotropy)

Preload definition

Initial stretch of cardiac myocytes before contraction (EDV)

Factors influencing preload

Venous return, blood volume, atrial contraction, filling time

Effect of preload on SV

↑ preload → ↑ SV (Frank‑Starling law); ↓ preload → ↓ SV (e.g., hemorrhage, dehydration)

Effect of ↑ HR on preload

Excessively high HR reduces filling time → ↓ preload → ↓ SV

Frank‑Starling law

↑ VR → ↑ EDV → stronger contraction → ↑ SV (within physiological limits)

Physiological significance of Frank‑Starling law

Balances right and left ventricular output, prevents blood accumulation

Frank‑Starling curve upward shift

↑ contractility (e.g., sympathetic stimulation)

Frank‑Starling curve downward shift

↓ contractility (e.g., heart failure)

Flattened Frank‑Starling curve

Severe dysfunction (e.g., cardiomyopathy)

Afterload definition

Resistance heart must pump against (mainly aortic pressure)

Factors influencing afterload

Hypertension, ↑ SVR, aortic stenosis

Effect of afterload on SV

↑ afterload → ↓ SV; ↓ afterload → ↑ SV

Contractility definition

Strength of myocardial contraction independent of preload

Effect of contractility on SV

↑ contractility → ↑ SV; ↓ contractility → ↓ SV

Positive inotropic factors

Sympathetic stimulation (β₁), Epinephrine, Norepinephrine, Thyroid hormone, Glucagon, Digitalis, Dopamine, Epinephrine

Negative inotropic factors

β‑blockers, Ca²⁺ channel blockers, Acidosis, Heart failure, ↑ K⁺, ↑ Na⁺, ↑ H⁺

Inotropy definition

Myocardial contractility

Positive inotropes

↑ contractility → ↑ SV (catecholamines, digitalis)

Negative inotropes

↓ contractility → ↓ SV (β‑blockers, acidosis, heart failure)

Effect of decreased inotropy on PV loop

↓ contractility → ↓ SV, ↑ ESV, clinical: heart failure, MI

Effect of decreased ventricular compliance on PV loop

Stiff ventricles → ↓ EDV, ↑ EDP, clinical: hypertrophy, fibrosis, restrictive cardiomyopathy

Factors affecting EDV

Venous return, atrial contraction, ventricular compliance, heart rate

Effect of venous return on EDV

↑ VR → ↑ EDV → ↑ SV

Effect of atrial contraction on EDV

Enhanced contraction → ↑ EDV

Effect of ventricular compliance on EDV

↓ compliance → ↓ EDV

Effect of HR on EDV

Excessively high HR → ↓ filling time → ↓ EDV

Clinical example of ↓ compliance

Congestive heart failure → ↓ EDV

Ejection fraction (EF)

EF = (SV/EDV) x 100

Normal EF

50–70%

Borderline EF

41–49% (slightly reduced pumping, SOB during activity)

Reduced EF

≤40% (symptoms at rest, poor daily activity tolerance)

Clinical use of EF

Index of contractility

Factors influencing venous return

Pressure gradient, skeletal muscle pump, venous valves, respiratory pump, sympathetic stimulation, blood volume

Pressure gradient

Higher venous pressure vs. right atrium → drives VR

Skeletal muscle pump

Muscle contraction compresses veins → pushes blood to heart

Venous valves

Ensure one‑way blood flow, prevent pooling

Respiratory pump

Inhalation ↓ thoracic pressure → draws blood to heart; exhalation ↑ abdominal pressure → aids blood movement

Sympathetic stimulation

Venoconstriction → ↑ VR → ↑ preload → ↑ SV

Blood volume

↑ volume (IV fluids, salt retention) → ↑ VR; ↓ volume (dehydration, hemorrhage) → ↓ VR

Clinical relevance of CO regulation

Heart failure → ↓ contractility → ↓ CO; Hypertension → ↑ afterload → ↓ SV → ↓ CO; Exercise → ↑ SNS → ↑ CO

Knowledge check: Preload definition

Volume of blood in ventricle at end of diastole

Knowledge check: Afterload definition

Pressure ventricle must overcome to eject blood

Knowledge check: Inotropy definition

Ability of heart muscle to contract forcefully

Knowledge check: Frank‑Starling law definition

Relationship between preload and stroke volume

Knowledge check: Effect of increased afterload

↓ stroke volume

Knowledge check: Upward shift of Frank‑Starling curve

↑ contractility (e.g., sympathetic stimulation)

Knowledge check: Effect of β₁ receptor stimulation

↑ HR and ↑ contractility → ↑ CO

Knowledge check: Which does NOT increase SV?

Increased afterload