When a person is at rest, the heart pumps only 4 to 6 liters of blood each minute. During strenuous exercise, the heart may be required to pump four to seven times this amount. The basic means by which the volume pumped by the heart is regulated are (1) intrinsic cardiac regulation of pumping in response to changes in volume of blood flowing into the heart and (2) control of heart rate and strength of heart pumping by the autonomic nervous system.

INTRINSIC REGULATION OF HEART PUMPING—THE FRANK-STARLING MECHANISM

In Chapter 20, we will learn that under most conditions, the amount of blood pumped by the heart each minute is normally determined almost entirely by the rate of blood flow into the heart from the veins, which is called venous return. That is, each peripheral tissue of the body controls its own local blood flow, and all the local tissue flows combine and return by way of the veins to the right atrium. The heart, in turn, automatically pumps this incoming blood into the arteries so that it can flow around the circuit again.

This intrinsic ability of the heart to adapt to increasing volumes of inflowing blood is called the Frank-Starling mechanism of the heart, in honor of Otto Frank and Ernest Starling, two great physiologists of a century ago. Basically, the Frank-Starling mechanism means that the greater the heart muscle is stretched during filling, the greater is the force of contraction and the greater the quantity of blood pumped into the aorta. Or, stated another way: Within physiological limits, the heart pumps all the blood that returns to it by way of the veins.

What Is the Explanation of the Frank-Starling Mechanism? When an extra amount of blood flows into the ventricles, the cardiac muscle is stretched to a greater length. This stretching in turn causes the muscle to contract with increased force because the actin and myosin filaments are brought to a more nearly optimal degree of overlap for force generation. Therefore, the ventricle, because of its increased pumping, automatically pumps the extra blood into the arteries.

This ability of stretched muscle, up to an optimal length, to contract with increased work output is characteristic of all striated muscle, as explained in Chapter 6, and is not simply a characteristic of cardiac muscle.

In addition to the important effect of lengthening the heart muscle, still another factor increases heart pumping when its volume is increased. Stretch of the right atrial wall directly increases the heart rate by 10 to 20 percent, which also helps increase the amount of blood pumped each minute, although its contribution is much less than that of the Frank-Starling mechanism.

Ventricular Function Curves

One of the best ways to express the functional ability of the ventricles to pump blood is by ventricular function curves. Figure 1 shows a type of ventricular function curve called the stroke work output curve. Note that as the atrial pressure for each side of the heart increases, the stroke work output for that side increases until it reaches the limit of the ventricle’s pumping ability.

Fig1. Left and right ventricular function curves recorded from  dogs, depicting ventricular stroke work output as a function of left  and right mean atrial pressures. (Data from Sarnoff SJ: Myocardial contractility as described by ventricular function curves. Physiol Rev 35:107, 1955.)

Figure 2 shows another type of ventricular function curve called the ventricular volume output curve.

Fig2. Approximate normal right and left ventricular volume output curves for the normal resting human heart as extrapolated  from data obtained in dogs and data from human beings. 

The two curves of this figure represent function of the two ventricles of the human heart based on data extrapolated from experimental animal studies. As the right and left atrial pressures increase, the respective ventricular volume outputs per minute also increase.

Thus, ventricular function curves are another way of expressing the Frank-Starling mechanism of the heart. That is, as the ventricles fill in response to higher atrial pressures, each ventricular volume and strength of cardiac muscle contraction increase, causing the heart to pump increased quantities of blood into the arteries.

Control of the Heart by the Sympathetic and Parasympathetic Nerves

 The pumping effectiveness of the heart also is controlled by the sympathetic and parasympathetic (vagus) nerves, which abundantly supply the heart, as shown in Figure 3. For given levels of atrial pressure, the amount of blood pumped each minute (cardiac output) often can be increased more than 100 percent by sympathetic stimulation. By contrast, the output can be decreased to almost zero by vagal (parasympathetic) stimulation.

Fig3.  Cardiac sympathetic and parasympathetic nerves. (The  vagus nerves to the heart are parasympathetic nerves.) A-V, atrioventricular; S-A, sinoatrial. 

Mechanisms of Excitation of the Heart by the Sym pathetic Nerves. Strong sympathetic stimulation can increase the heart rate in young adult humans from the normal rate of 70 beats/min up to 180 to 200 and, rarely, even 250 beats/min. Also, sympathetic stimulation increases the force of heart contraction to as much as double the normal rate, thereby increasing the volume of blood pumped and increasing the ejection pressure. Thus, sympathetic stimulation often can increase the maximum cardiac output as much as twofold to threefold, in addition to the increased output caused by the Frank-Starling mechanism already discussed.

Conversely, inhibition of the sympathetic nerves to the heart can decrease cardiac pumping to a moderate extent. Under normal conditions, the sympathetic nerve fibers to the heart discharge continuously at a slow rate that maintains pumping at about 30 percent above that with no sympathetic stimulation. Therefore, when the activity of the sympathetic nervous system is depressed below normal, both the heart rate and strength of ventricular muscle contraction decrease, thereby decreasing the level of cardiac pumping as much as 30 percent below normal.

Parasympathetic (Vagal) Stimulation Reduces Heart Rate and Strength of Contraction. Strong stimulation of the parasympathetic nerve fibers in the vagus nerves to the heart can stop the heartbeat for a few seconds, but then the heart usually “escapes” and beats at a rate of 20 to 40 beats/min as long as the parasympathetic stimulation continues. In addition, strong vagal stimulation can decrease the strength of heart muscle contraction by 20 to 30 percent.

The vagal fibers are distributed mainly to the atria and not much to the ventricles, where the power contraction of the heart occurs. This distribution explains why the effect of vagal stimulation is mainly to decrease the heart rate rather than to decrease greatly the strength of heart contraction. Nevertheless, the great decrease in heart rate combined with a slight decrease in heart con traction strength can decrease ventricular pumping 50 percent or more.

Effect of Sympathetic or Parasympathetic Stimulation on the Cardiac Function Curve. Figure 4 shows four cardiac function curves. These curves are similar to the ventricular function curves of Figure 2. However, they represent function of the entire heart rather than of a single ventricle. They show the relation between right atrial pressure at the input of the right heart and cardiac output from the left ventricle into the aorta.

Fig4. Effect on the cardiac output curve of different degrees  of sympathetic or parasympathetic stimulation. 

The curves of Figure 4 demonstrate that at any given right atrial pressure, the cardiac output increases during increased sympathetic stimulation and decreases during increased parasympathetic stimulation. These changes in output caused by autonomic nervous system stimulation result both from changes in heart rate and from changes in contractile strength of the heart.

EFFECT OF POTASSIUM AND CALCIUM IONS ON HEART FUNCTION

 In the discussion of membrane potentials in Chapter 5, it was pointed out that potassium ions have a marked effect on membrane potentials, and in Chapter 6 it was noted that calcium ions play an especially important role in activating the muscle contractile process. Therefore, it is to be expected that the concentrations of each of these two ions in the extracellular fluids also have important effects on cardiac pumping.

Effect of Potassium Ions. Excess potassium in the extracellular fluids causes the heart to become dilated and flaccid and also slows the heart rate. Large quantities of potassium also can block conduction of the cardiac impulse from the atria to the ventricles through the A-V bundle. Elevation of potassium concentration to only 8 to 12 mEq/L—two to three times the normal value—can cause severe weakness of the heart, abnormal rhythm, and death.

These effects result partially from the fact that a high potassium concentration in the extracellular fluids decreases the resting membrane potential in the cardiac muscle fibers, as explained in Chapter 5. That is, high extracellular fluid potassium concentration partially depolarizes the cell membrane, causing the membrane potential to be less negative. As the membrane potential decreases, the intensity of the action potential also decreases, which makes contraction of the heart progressively weaker.

Effect of Calcium Ions. Excess calcium ions cause effects almost exactly opposite to those of potassium ions, causing the heart to move toward spastic contraction. This effect is caused by a direct effect of calcium ions to initiate the cardiac contractile process, as explained earlier in this chapter.

Conversely, deficiency of calcium ions causes cardiac weakness, similar to the effect of high potassium. Fortunately, calcium ion levels in the blood normally are regulated within a very narrow range. Therefore, cardiac effects of abnormal calcium concentrations are seldom of clinical concern.

EFFECT OF TEMPERATURE ON HEART FUNCTION

Increased body temperature, such as that which occurs when one has fever, greatly increases the heart rate, sometimes to double the normal rate. Decreased temperature greatly decreases heart rate, which may fall to as low as a few beats per minute when a person is near death from hypothermia in the body temperature range of 60° to 70°F. These effects presumably result from the fact that heat increases the permeability of the cardiac muscle mem brane to ions that control heart rate, resulting in acceleration of the self-excitation process.

Contractile strength of the heart often is enhanced temporarily by a moderate increase in temperature, such as that which occurs during body exercise, but prolonged elevation of temperature exhausts the metabolic systems of the heart and eventually causes weakness. Therefore, optimal function of the heart depends greatly on proper control of body temperature by the temperature control mechanisms explained in Chapter 74.

INCREASING THE ARTERIAL PRESSURE LOAD (UP TO A LIMIT) DOES NOT DECREASE THE CARDIAC OUTPUT

Note in Figure 5 that increasing the arterial pressure in the aorta does not decrease the cardiac output until the mean arterial pressure rises above about 160 mm Hg. In other words, during normal function of the heart at normal systolic arterial pressures (80 to 140 mm Hg), the cardiac output is determined almost entirely by the ease of blood flow through the body’s tissues, which in turn controls venous return of blood to the heart. This mechanism is the principal subject of Chapter 20.

Fig5. Constancy of cardiac output up to a pressure level of  160 mm Hg. Only when the arterial pressure rises above this normal  limit does the increasing pressure load cause the cardiac output to  fall significantly. 

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