1.4.3 Control of cardiac output
1.4.3 Control of cardiac output

Cardiac output depends on stroke volume and heart rate. Stroke volume is dependent on three important factors: preload, afterload and contractility. All of these factors are inextricably linked (Figure 1.7). It is important that each of these is understood because they are important concepts in cardiology. However, any discussion of these factors invariably includes a substantial amount of over


Preload is the force distending the ventricles. It can be assessed by measuring end-diastolic pressure, or estimated from measurement of end-diastolic dimenof the ventricles. An intrinsic property of myocardial cells, within normal limits, is that the force of their contraction depends on the length to which they are stretched. The greater the stretch (within certain limits), the greater the force of contraction. This property is known as the Frank-Starling phenomenon. It occurs because stretching of the myofibrils results in more efficient creation of cross-bridges between the contractile proteins. Thus, an increase in the distenof the ventricle will result in an increase in the force of contraction sufficient to pump the extra volume. An increase in preload will result in a concomitant increase in cardiac output.

An ability to increase preload is required for animals to be able to maintain a suitable cardiac output in the face of the demands of exercise, systemic vaso(increased afterload) or cardiac disease. A fixed, low preload restricts cardiac output. This occurs in a number of situations, for example in animals with hypovolaemic or septic shock, or in animals with pericardial effusions which have resulted in cardiac tamponade. Preload may also be too high in certain situations. For example, if there is marked volume overload of the ventricle or poor myocardial contractility which results in a high end diastolic filling pressure, this will lead to blood ‘damming back’ into the atria and veins, i.e. congestive heart failure. Diuretics are used to reduce preload and remove the fluid build-up which results from congestive failure (section 6.9.1). Over-diuresis can reduce preload sufficiently that cardiac output is limited and may worsen some of the clinical features of heart failure. Factors which affect preload are summarised in Table 1.1.


Afterload is the force against which the ventricles must act in order to eject blood. This is largely dependent on aortic blood pressure, which in turn depends on vascular resistance; however, it also contains a component of myocardial stiffIncreasing afterload increases myocardial oxygen consumption and may decrease stroke volume. Homeostatic mechanisms usually prevent a fall in blood pressure, which might result from reductions in afterload, by causing vasoconand therefore restoring blood pressure. However, reductions in after-load may also result in an increase in stroke volume and this will maintain blood pressure, within limits. In animals with AV valve regurgitation, there is a reduction in afterload because blood can leak back into the low pressure atria. Thus the total stroke volume will increase, but the forward stroke volume will not change (or may even fall in severe cases). Vasodilators reduce afterload and result in an improved forward stroke volume. Factors which affect afterload are summarised in Table 1.1.


The strength of the force of myocardial contraction is dependent on direct autonomic control affecting preload and afterload but also on the contractility of the myocardium. Contractility is a measure’ of the intrinsic ability of the myoto contract to produce a peak tension from a given resting fibre length. This property is independent of loading conditions. It should not be confused with the force of contraction, which is directly affected by preload and afterload. The degree of contractility is also known as the inotropic state. A positive inoresponse is an increase in contractility. Myocardial contractility can be increased directly by sympathetic stimulation, to some extent by a decrease in parasympathetic tone and indirectly by an increase in heart rate.

When contractility is reduced, for example as a result of myocardial disease, stroke volume will fall. This will result in a reflex increase in heart rate and an adjustment in the tone of the peripheral cardiovascular system to ensure that blood pressure is maintained. In the long-term, changes in sodium and water retention will occur, and a high level of catecholamines will be present until an equilibrium is met. To some extent, this will improve contractility via beta receptor mechanisms. Factors which affect contractility are summarised in Table 1.1.

Stroke volume

Stroke volume is the amount of blood ejected by the ventricles per beat. The ejection fraction is the proportion of the stroke volume which is ejected (Figure 1.8). Usually this is equal to the forward stroke volume, which is the amount ejected into the great arteries. However, when the AV valves leak, some of theblood will flow in a retrograde direction into the atria. The regurgitant fraction is the proportion of the end-diastolic volume which flows back into the atria (in the case of AV regurgitation) and makes no contribution to the forward stroke volume. Stroke volume is determined by the volume and pressure of blood filling the ventricles (i.e. preload), the resistance to ejection (i.e. afterload), and myocell shortening (i.e. contractility). Long4erm changes in stroke volume are mediated by the load imposed on the heart. For example, volume overload as a result of valvular incompetence, or isotonic exercise training, will result in an increase in stroke volume.

Heart rate

Cardiac output is dependent on stroke volume and heart rate. In fact, changes in cardiac output in the horse are usually mediated by changes in heart rate. Preafterload and contractility alter so that stroke volume can be maintained. The horse has a remarkable capacity to increase cardiac output, by a factor of approximately six-fold from resting values This is almost entirely due to an increase in heart rate from approximately 24-40 bpm, to a maximal heart rate of the order of 220-240 bpm. Heart rate is controlled by the balance of paraand sympathetic innervation The high vagal tone which is present in normal horses at rest is mediated by the release of the neurotransmitter acetylcholine from parasympathetic synapses. This maintains a slow rate of discharge of the sinoatrial (SA) node and may result in slow or intermittently blocked conduction through the atrioventricular node. It also maintains a relalow inotropic state. The almost instantaneous increase in heart rate to increased demand for cardiac output results from a fall in vagal tone and from the release of noradrenaline from sympathetic fibres, mediated by BI receptors. The humoral component (adrenaline) takes some minutes to operate, but may have altered in anticipation of an increase in demand for heart rate due to behavioural responses. Catecholamine release also causes an increase in inotropic state. A change in autonomic tone which results in an increase in heart rate is known as a positive chronotropic response. A drug with the same action is known as a positive chronotrope, one with the opposite effect as a negative chronotrope. Factors which affect heart rate are summarised in Table 1.1.