The cardiac output is simply the amount of blood pumped by the heart per minute. Necessarily, the cardiac output is the product of the heart rate, which is the number of beats per minute, and the stroke volume, which is amount pumped per beat.
CO = HR X SV
The cardiac output is usually expressed in liters/minute. For someone weighing about 70 kg (154 lbs), the cardiac output at rest is about 5 liters/minute. In this case, if the heart rate is 70 beats/min, the stroke volume would be a little more than 70 ml/beat.
But of course this changes dramatically as a person begins to exercise. For a typical, fit young person, the cardiac output might go up to about 20 liters/min at the peak of exercise. However, for a world-class athlete in an endurance sport, the maximum cardiac output might be around 35 liters/min.
Let's first consider the regulation of the heart rate because this is the most straightforward of the two factors. The regulation boils down primarily to parasympathetic and sympathetic effects.
In a young person, an SA node without either parasympathetic or sympathetic effects will drive about 100 beats/min. This, of course, is substantially faster than the usual resting heart rate. Thus, at rest there is normally parasympathetic tone that keep the heart rate down to around 60-70 beats/min.
QUESTION: What is the most important type of ion channel that acetylcholine opens in the heart? (Recall that acetylcholine causes the pacemaker potential to move more slowly towards threshold. Answer
In order to increase the heart rate from the resting rate, the parasympathetic tone is withdrawn until the heart rate is about 100 beats/min. Then norepinephrine is released by sympathetic nerves. This increases the slope of the pacemaker potential by, for example, opening a Ca++ channel via a G protein. In this way, the pacemaker potential reaches threshold faster and the heart rate is increased.
Because the adrenergic receptors in the heart are all beta receptors, the hormone epinephrine has the same effect as norepinephrine released by sympathetic nerves. (But in various other organs, norepinephrine and epinephrine do not produce the same actions.)
Autonomic nerves not only innervate the SA node, but also are found elsewhere in the heart. Norepinephrine released by sympathetic nerves increases the force with which ventricular muscle fibers contract (by increasing the Ca++ effect). This tends to be significant mainly at the greatest levels of exercise.
For example, the ventricle of a 70 kg person at rest might hold about 100 ml of blood at the end of diastole. As noted above, a typical stroke volume is about 70 ml. Thus, the person's ejection fraction is 70%. This is the fraction of the blood in the ventricle that is ejected during systole. Norepinephrine, by increasing the force of contraction, would tend to increase the ejection fraction and thus the stroke volume.
The aortic pressure influences the stroke volume for a straightforward reason. If the aortic pressure increases, this pressure reduces the volume of blood that flows into the aorta during systole. The aortic pressure is called afterload because it is the "load" experienced by the ventricle after it begins contracting.
A drug might reduce the afterload, for example, by dilating arterioles. This allows blood to flow from the arteries more easily, thereby preventing the arterial pressure from increasing as blood is injected into it by the ventricle.
However, the factor we will be most concerned with is the Frank-Starling mechanism. Unfortunately, it is also the one most difficult to get your mind around. The Frank-Starling mechanism leads to changes in the stroke volume as a result of changes in the end-diastolic volume.
The end-diastolic volume is the volume of a ventricle at the very end of filling and just before systole begins. This can change because the ventricles are flexible and under different circumstances, the amount of blood flowing in during diastole varies. If less blood flows into the ventricle as it fills, the end-diastolic volume goes down. If more blood flows in, the end-diastolic volume goes up.
The Frank-Starling effect is due to the fact that heart muscle fibers respond to stretch by contracting more forcefully. This is not a passive, elastic effect, but rather due to an increased expenditure of ATP energy. (We are not going to try to explain the cellular basis of this effect. It is not as straightforward as you might think.)
Thus, if the end-diastolic volume increases, the muscle fibers are lengthened and the ventricle contracts more forcefully, ejecting a greater stroke volume. The figure to the right shows this Frank-Starling effect.
What factor alters the filling during diastole? For the right ventricle, this is the pressure in the right atrium, because this is the pressure that is experienced by the right ventricle as it fills. Since there is no valve at the entrance to the right atrium, the pressure in the right atrium is necessarily the same as the pressure in the veins at the entrance to the right atrium. This pressure in the large veins at the entrance to the right atrium is called the central venous pressure.
In other words, the central venous pressure is the same at the right atrial pressure, and this is the pressure that determines the filling of the right ventricle and thus its end-diastolic volume. The central venous pressure always is only a few mm Hg, but nonetheless it does change enough to significantly affect the stroke volume. In particular, posture changes this pressure and that is the factor with which we are here most concerned.
Recall how voluminous and thin-walled the superior and inferior vena cava are. You probably were able to put two fingers into the superior vena cava of the pig heart. When a person is lying down, the large veins in the chest are plump with blood. And because these veins are stretched, the pressure in them is higher than when they contain less blood. Consequently, when lying down, the central venous pressure is relatively high, the end-diastolic volume is relatively high and thus the stroke volume is comparatively high.
But this changes when we stand. The pressure in the large veins in the legs increases greatly. For example, one meter below the heart, the effect of gravity adds about 74 mm Hg of pressure. This causes the distensible, voluminous veins to expand, and blood pools in the leg veins. This reduces the blood in the central veins, and the central venous pressure drops. Because these central veins are very compliant structures, pressure cannot increase again in them until blood flows back into the thorax.
Lying down, of course, is one factor that would increase the amount of blood in the veins in the thorax and thus the central venous pressure. However, another important factor is muscle contraction. If the standing person begins walking, the contractions of the leg muscles squeeze on the leg veins, thereby forcing blood from those veins up into the thorax. This is called muscle pumping.
Thus, as a standing person begins walking, the end-diastolic volume and thus the stroke volume increase.
Muscle pumping works on the veins, but not the arteries, because veins are large, highly compliant and the larger ones have valves. In other words, contracting skeletal muscles serve as auxillary pumps, squeezing blood back into the central veins.
Given that the veins are so large and compliant, you might wonder why we are put together this way. It allows blood to move around substantially in the veins, altering central venous pressure and thus stroke volume.
The reason is that it allows us to function despite significant changes in extracellular fluid volume and thus blood volume. A person can lose a liter or more of blood or extracellular fluid through hemorrhage or diarrhea and still easily maintain arterial blood pressure. As volume is lost, the distensible veins simply contrict, compensating for the lost volume. Likewise, an increase in extracellular fluid volume is accommodated by distension of the veins. The central venous pressure is hardly affected.
Suppose your right ventricle began pumping just 1% more blood than your left ventricle. This would lead to a disaster fairly quickly if not corrected. Suppose your cardiac output is 5 liters/min. One percent of this is 50 ml/minute. If this continued for 20 minutes, one liter of blood would be transferred from your systemic circulation into you pulmonary circulation. Pressures throughout your pulmonary circulation would begin increasing and fairly soon you would "drown" from pulmonary edema.
Not good. Why doesn't this happen? As soon as a fairly small amount of blood is transferred from the systemic to pulmonary circulation, the pressure in the pulmonary veins and left atrium increases a little. This increases the filling of the left ventricle, and the resulting increase in its end-diastolic volume increases the stroke volume, correcting the problem. This is why even tiny differences in the pumping of the two ventricles are soon corrected.