Control of cardiac output

CO = HR x SV

End diastole volume - end systole volume

Increasing the Ca2+ sensitivity of the contractile apparatus Increasing the cellular concentration of Ca2+

“Force of ventricular contraction is dependent on the length of ventricular muscle fibres in diastole” Intrinsic property of cardiac muscle Isolated muscle cells stretching the sarcomere increase force of contraction Length dependent increase in Ca2+ sensitivity results in greater number of cross bridges

Venous return Central venous pressure

Blood volume Skeletal muscle pump Respiratory pump Venous tone Gravity

Increased blood volume due to renal failure increases venous return Decreased blood volume due to dehydration or haemorrhage leads to reduced venous return

Skeletal muscle contraction increases venous return

Inspiration decreases thoracic pressure and increases abdominal pressure

Increase in sympathetic activity will evoke venoconstriction Venoconstriction reduces the volume of blood in the veins at a given pressure Venoconstriction increases venous return

Supine Uniform distribution of blood across the body Standing Redistribution of blood due to gravity Venous pooling in lower extremities Reduction in thoracic blood volume Venous return is reduced

Any factor which influences the stretch of cardiac muscle cells before contraction

Atrial contraction Heart rates over 180 beats/min

Increased contractility

Increased sympathetic nerve activity Increased Ca2+ influx Increased no. of cross bridge formation

The load against which the heart must contract to eject the stroke volume

Aortic/pulmonary artery pressure is the most important factor in determining after load Increased resistance in the pulmonary/peripheral circulation increases after load