8.3

Cardiac Output (CO)

Definition: The rate at which a ventricle pumps blood.

Typical Value: Approximately 5 liters per minute.

Formula:

C

O

=

H

R

×

S

V

HR (Heart Rate): Number of heart contractions per minute.

SV (Stroke Volume): Volume of blood pumped per beat.

Control of Cardiac Output

Extrinsic Control:

Origin: Outside of the heart, such as neural and hormonal control.

Intrinsic Control (Autoregulation):

Autonomic Input:

Sympathetic Fibers: Innervate the SA node, AV node, and ventricular myocardium.

Parasympathetic Fibers: Innervate the SA node and AV node.

Heart Rate Control

SA Node: The heart rate is primarily determined by the SA node's firing frequency.

Intrinsic Rate: Without external influence, the SA node fires at 100 beats per minute.

Parasympathetic Dominance: At rest, the parasympathetic system slows the heart rate to around 75 beats per minute.

Sympathetic Dominance: During excitement, the sympathetic system increases the heart rate.

Factors Affecting Heart Rate (HR):

Neural Control:

Sympathetic Neurons: Increase action potential (AP) firing, speeding up the heart rate.

Release norepinephrine (NE).

NE binds to beta-1 (β1) adrenergic receptors.

Activates cAMP 2nd messenger system.

Opens Na+ funny channels and Ca2+ channels, increasing the rate of spontaneous depolarization.

Increases the rate of APs at the AV node, decreasing delay, and shortening systole.

Parasympathetic Neurons: Decrease AP firing, slowing down the heart rate.

Release acetylcholine (ACh).

ACh binds to muscarinic cholinergic receptors.

Opens K+ channels, preventing the opening of funny channels and Ca2+ channels.

Slows spontaneous depolarization and hyperpolarizes the pacemaker cells.

Decreases the rate of APs at the AV node, increasing delay, and lengthening systole.

Hormonal Control:

Epinephrine (Adrenaline): From the adrenal medulla, mimics sympathetic neural control, increasing heart rate.

Integration:

Sympathetic and parasympathetic systems are always active, but one usually predominates.

Because

C

O

=

H

R

×

S

V

, when HR increases, CO usually increases as well.

Factors Affecting Stroke Volume (SV)

Ventricular Contractility:

Definition: Capacity of a muscle for generating force.

More forceful contraction expels more blood, increasing CO.

Sympathetic Control:

Sympathetic activity causes both atria and ventricles to contract with more force.

NE binds to β1 adrenergic receptors on contractile cells, activating cAMP and protein kinases.

Protein kinases open Ca2+ channels, enhance release of Ca2+ from the sarcoplasmic reticulum, increase myosin ATPase activity, and speed up Ca2+ reuptake.

Results: Cells contract more forcefully and quickly.

End-Diastolic Volume (EDV) and Starling’s Law:

Starling’s Law: The ventricle contracts with greater or lesser force so that the stroke volume matches the venous return.

If EDV increases, SV increases; if EDV decreases, SV decreases.

Factors Affecting EDV:

Preload: Tension on the myocardium before it begins to contract.

Filling Time & Atrial Pressure:

Lower HR: Increases filling time, increasing preload and EDV.

Higher HR: Decreases filling time, decreasing preload and EDV.

Central Venous Pressure:

Increased venous pressure increases EDV and SV.

Decreased venous pressure decreases EDV and SV.

Afterload:

Definition: The pressure the ventricles must work against to pump blood.

Impact: Increases in arterial pressure increase afterload, causing SV to decrease.

Resistance in Vasculature: Higher resistance increases afterload, making the heart work harder.