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Regulation of Stroke Volume


degree of stretch of cardiac muscle cells before they contract (Frank-Starling law of the heart)

•Cardiac muscle exhibits a length-tension relationship
•At rest, cardiac muscle cells are shorter than optimal length
•Slow heartbeat and exercise increase venous return
•Increased venous return distends (stretches) the ventricles and increases contraction force


Contractile strength at a given muscle length, independent of muscle stretch and EDV

Increase Contractility

Increased Ca2+ influx due to sympathetic stimulation

Hormones (thyroxine, glucagon, and epinephrine)

Decrease contractility


Increased extracellular K+

Calcium channel blockers


Pressure that must be overcome for ventricles to eject blood

increases afterload


resulting in increased ESV and reduced SV

Sympathetic nervous system

activated by emotional or physical stressors

Norepinephrine causes the pacemaker to fire more rapidly (and at the same time increases contractility)

Parasympathetic nervous system

opposes sympathetic effects

Acetylcholine hyperpolarizes pacemaker cells by opening K+ channels

The heart at rest exhibits vagal tone (parasympathetic)

Atrial (Bainbridge) reflex

a sympathetic reflex initiated by increased venous return

Stretch of the atrial walls stimulates the SA node

Also stimulates atrial stretch receptors activating sympathetic reflexes

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