Cardiac Output (CO)
Definition
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Cardiac Output (CO) = Heart Rate (HR) × Stroke Volume (SV)
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Units: milliliters per minute (mL/min)
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Normal value: ~ 5 L/min (70 bpm × 70 mL/beat)
Heart Rate (HR)
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Normal: 60–100 bpm
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Intrinsic pacemaker: SA node → sets sinus rhythm (60–80 bpm at rest)
Regulators of Heart Rate
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Autonomic Nervous System
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Sympathetic (NE, Epi on β1 receptors) → ↑ HR (positive chronotropy)
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Parasympathetic (ACh on M2 receptors) → ↓ HR (negative chronotropy)
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Hormones
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Thyroid hormones (T3, T4) → ↑ HR, ↑ basal metabolic rate
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Other stimulators: epinephrine, norepinephrine
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Body Temperature
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↑ Temp → ↑ HR
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↓ Temp → ↓ HR
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Electrolytes
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Calcium (Ca²⁺)
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↑ Ca²⁺ → ↑ HR (positive chronotropy)
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↓ Ca²⁺ → ↓ HR
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Potassium (K⁺)
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↑ K⁺ (hyperkalemia) → dangerous ↓ HR, may cause arrest
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↓ K⁺ (hypokalemia) → arrhythmias
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Chemoreceptors
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Located in carotid and aortic bodies
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Stimulated by:
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↓ O₂ (hypoxia)
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↑ CO₂ (hypercapnia)
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↓ pH (acidosis)
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Effect: ↑ HR (secondary to ↑ sympathetic drive; stronger effect on respiration than HR)
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Age & Sex
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Fetus/infant: very high HR (~120–140 bpm)
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Adults: 60–100 bpm
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Males: ~64–72 bpm
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Females: ~72–80 bpm
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Elderly: HR may increase again
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Clinical Conditions
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Bradycardia (<60 bpm): causes → ↑ parasympathetic tone, drugs, endurance athletes (↑ SV compensates for ↓ HR)
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Tachycardia (>100 bpm): causes → sympathetic activation, thyroid hormone excess, anxiety, drugs
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Stroke Volume (SV)
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Formula: SV = End-Diastolic Volume (EDV) – End-Systolic Volume (ESV)
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Normal: 120 mL – 50 mL = ~70 mL/beat
Determinants of Stroke Volume
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Preload
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Definition: degree of stretch of myocardium before contraction (≈ EDV)
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Factors increasing preload:
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↑ Venous return via:
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Muscular pump (skeletal muscle contraction)
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Respiratory pump (↓ thoracic pressure, ↑ abdominal pressure)
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Venoconstriction (↑ venous tone via sympathetic activity)
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Adequate filling time (↓ HR allows more filling)
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Frank-Starling Law: greater stretch (EDV) → stronger contraction (↑ SV)
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Limiting factor: infarcted/fibrotic myocardium (↓ compliance)
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Contractility
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Definition: strength of contraction at a given preload
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Increased by:
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Sympathetic stimulation (NE/Epi on β1 → ↑ Ca²⁺)
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Thyroid hormone (↑ β1 receptor expression)
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Glucagon
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Drugs: digitalis, dopamine, dobutamine, isoproterenol, atropine
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Decreased by:
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β-blockers (e.g., propranolol, metoprolol)
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Ca²⁺ channel blockers (e.g., verapamil, diltiazem)
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Ions:
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↑ Ca²⁺ → ↑ contractility
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Severe ↑ K⁺ → ↓ contractility
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Afterload
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Definition: resistance the ventricles must overcome to eject blood
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Determined by: arterial pressure & vascular resistance
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↑ Afterload → ↓ SV (e.g., hypertension, aortic stenosis)
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Summary
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CO = HR × SV (~5 L/min at rest)
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HR regulators: ANS, hormones, temperature, electrolytes, chemoreceptors, age, clinical states
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SV regulators: preload (EDV & venous return), contractility (Ca²⁺, sympathetic drive, hormones, drugs), afterload (vascular resistance)
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Exercise → ↑ CO (by ↑ HR and ↑ SV)
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Endurance training → ↑ SV, resting bradycardia.
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