Regulation of stroke volume & heart rate

1. 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

2. 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

3. +25 0 mV -25 -50 -75 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

4. +25 0 mV -25 -50 -75 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

6. Tension Length Regulation of stroke volume - preload Starlings Law states - the energy of contraction is proportional to the initial length of the cardiac muscle fibre (= preload)

7. Stroke Volume Resting EDV End Diastolic Volume Regulation of stroke volume - preload In vivo, preload is affected by the End Diastolic Volume Increased venous return, increases EDV, and therefore increases stroke volume = self-regulation

8. 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

9. + sympathetic stimulation Stroke Volume End Diastolic Volume Regulation of stroke volume - neural • Sympatheticnervous 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

10. Control of cardiac output HR x SV = CO • 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

11. 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