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. 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

4. 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

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

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

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. Regulation of stroke volume - neural Sympathetic nervous system –sympathetic nerves releasing norepinephrine –plus circulating epinephrine from adrenal medulla –both act on ß 1 -receptors on the myocytes –increases contractility (an inotropic effect) –gives stronger, but shorter contraction Parasympathetic –little effect End Diastolic Volume Stroke Volume + sympathetic stimulation

10. 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

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