Control of Cardiac Output - Additional Information

Contractility
Contractility is the force of contraction. The contractility of cardiac muscle is increased by sympathetic nerve stimulation, adrenaline and drugs such as digoxin. It is decreased by prolonged ischaemia.

Sympathetic Nerves
The sympathetic nerves controlling the heart arise in the cardiac centre (cardioaccelerator centre) of the medulla oblongata and pass down the spinal cord. They then leave the spinal cord chiefly from the thoracic segments (T1-T5), synapse in the cervical ganglia and innervate the sino-atrial and atrioventricular nodes and atrial and ventricular muscle cells.

Their effects are mediated via release of noradrenaline from the nerve terminals which then acts on β₁-adrenoceptors on heart cells. The effects of sympathetic nerve stimulation are to increase heart rate, decrease AV - node delay and increase both atrial and ventricular contractility.

Parasympathetic Nerve
The parasympathetic nerves arise in the cardioinhibitory centre of the cardiac centre and leave in cranial nerve X (the vagus) to innervate the sinoatrial node, the AV - node and atrial muscle.

These nerves release acetylcholine form their nerve endings which acts on muscarinic cholinoceptors on heart cells. The effects of parasympathetic nerve stimulation are to decrease heart rate, increase the AV - node delay and decrease atrial contractility. Significantly there is little parasympathetic innervation of ventricular muscle and hence little effect on stroke volume.