Regulation of stroke volume & heart rate

• Measurement of cardiac output• Regulation of heart rate

– neural

• Regulation of stroke volume– Preload– Afterload– Neural

• Control of cardiac output

Measurement of cardiac output

• Fick indicator-dilution method– measures the time taken for an

injected dye to pass a sampling point

• Thermodilution• Echocardiography• Pulsed Doppler ultrasound

Regulation of heart rate

• Sympathetic nervous system– sympathetic nerves release norepinephrine– plus circulating epinephrine from adrenal medulla– both act on ß-receptors on sinoatrial node– increases slope of the pacemaker potential – increases heart rate = tachycardia

+25

0

-25

-50

-75

mV

Regulation of heart rate

• Parasympathetic nervous system– vagus releases ACh – acts on muscarinic receptors on sinoatrial node– hyperpolarises cells and decreases slope of pacemaker

potential– decreases heart rate = bradycardia

+25

0

-25

-50

-75

mV

Regulation of stroke volume - preload

Starlings Law states - the energy of contraction is proportional to the initial length of the cardiac muscle fibre

Length

Ten

sion

(= preload)

Regulation of stroke volume - preload

In vivo, preload is affected by the End Diastolic Volume

End Diastolic Volume

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oke

V

olu

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Increased venous return, increases EDV, and therefore increases stroke volume = self-regulation

Resting EDV

Regulation of stroke volume - afterload

• Afterload is the load against which the muscle tries to contract

• In vivo, afterload is set by the arterial pressure against which the blood is expelled (this in turn depends on the Total Peripheral Resistance)

• If TPR increases, stroke volume will go down

Regulation of stroke volume - neural

• Sympathetic nervous system– sympathetic nerves releasing norepinephrine– plus circulating epinephrine from adrenal medulla

– both act on ß1-receptors on the myocytes

– increases contractility (an inotropic effect)– gives stronger, but shorter contraction

• Parasympathetic– little effect

End Diastolic Volume

Str

oke

V

olu

me + sympathetic stimulation

Control of cardiac output• HR increases

– via decrease vagal tone– & increased sympathetic tone

• Contractility increases– via increased sympathetic tone– alters inotropic state & shortens systole

• Venous return increases– via venoconstriction– & skeletal/respiratory pumps– maintains preload

• Total peripheral resistance falls– due to arteriolar dilation in muscle, skin & heart– reduces afterload

• CO increase 4-6 times

HR x SV = CO

Summary• Heart rate

– sympathetic supply HR– parasympathetic supply HR

• Stroke volume– preload EDV, SV– afterload TPR, SV– neural sympathetic supply, SV

• Think integration– these work together to produce a co-ordinated

increase in CO, eg exercise