Cardiac output is the amount of blood ejected by a ventricle in a given unit of time, for example the amount of blood ejected by the left ventricle into the aortic arch per minute. The cardiac output can be changed by variations in its controlling factors. Changes in cardiac output are vital to the functioning of the body and as such can be caused to increase or decrease to aid said function. Alternatively illness or disease can cause adverse, unwanted effects on cardiac output. Anxiety and excitement, eating, exercise, high environmental temperatures, and pregnancy will all increase cardiac output. Sitting or standing from a lying position, heart disease, and rapid arrhythmias will all cause cardiac output to decrease.
[...] This causes potassium to leak out of the cells and accumulate in the tight extra cellular space of the myocardium. The high potassium levels leads to depolarization and spontaneous firing of the action potential. This spontaneous firing is also seen in hyperkaleamia. A high sympathetic drive will stimulate the pacemaker cells leading to spontaneous depolarization. Abnormal depolarization circuits, cause abnormal propagation i.e. re-entry of the depolarization, where a wave of depolarization chases itself in a circuit throughout the myocardium causing repeated depolarisations. [...]
[...] These actions are important as adrenaline can cause dysrythmias by its effects on the pacemaker potential and on the slow inward calcium current. This drug class includes atenolol, esmolol, propranolol, and metoprolol. Class III act mainly by blocking potassium channels, and thus prolonging depolarization. These drugs do not affect the sodium channel, and therefore conduction velocity is not decreased. This prolongation of the action potential duration and refractory period, combined with the maintenance of normal conduction velocity, prevent re-entrant dysrythmias, i.e. [...]
[...] They can also be used in ventricular dysrhythmias, and the prevention of recurrent paroxysmal atrial fibrillation triggered by vagal over activity. Class Ib drugs have fast onset and offset kinetics, meaning they have little or no effect at slower heart rates, and more effects at faster heart rates. These drugs shorten the action potential duration and reduce refractoriness. They will decrease the depolarization slope in partially depolarized cells with fast response action potentials. Class Ib drugs tend to be much more specific for voltage gated sodium channels than Ia drugs. [...]
[...] Yet, if the membrane potential is less negative, some of the fast sodium channels will be in an inactivated state, thus causing a lesser response to excitation of the cell membrane, and a less steep depolarization slope, thus conduction through the heart may be delayed increasing the risk of dysrhythmia. Phase 1 of the action potential occurs with inactivation of the fast sodium channels. The transient net outward current, causing the small deflect, is caused by the movement of potassium and chloride ions. [...]
[...] During the activation of a cell by an action potential in the presence of adrenaline or nor-adrenaline, systolic calcium ion inward current increases, thus giving increased tension to the cardiac muscles due to the calcium ions allowing a greater number of cross bridges to form between acting and myosin filaments via acting on troponin C. Vagul stimulation will release acetylcholine from nerve endings. This acts on muscarinic receptors in SA nodal membranes, having 2 effects. Firstly it will decrease the pacemaker current, thus decreasing the slope of the pacemaker depolarization. [...]
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