Medical Physiology, 3rd Edition

Cardiac Dynamics

The heart is a system of two pumps linked in series. The muscular wall of the left ventricle is thicker and more powerful than that of the right. The interventricular septum welding the two pumps together is even thicker. The thick muscular walls of the ventricles are responsible for exerting the heart's pumping action.

The heart does not depend on a rhythm generator in the brain, like the central pattern generators (see p. 390) that drive other rhythmic behaviors such as respiration, locomotion, chewing, and shivering. Instead, pacemaker cells within the heart itself initiate cardiac excitation. When the heart is in a normal sinus rhythm, the pacemaker cells setting the rate are located in the sinoatrial (SA) node of the right atrium (see p. 489). The action potential then spreads through atrial myocytes and specialized tracts or bundles. The impulse cannot cross from the atria to the ventricles except through the AV node. The AV node inserts a time delay into the conduction that is essential to allow the ventricles to finish filling with blood before contraction and ejection occur. From the AV node, the impulse spreads through the bundle of His and then the right and the left bundle branches, the latter of which divides in an anterior and posterior fascicle. Finally, the system of Purkinje fibers excites the ventricular myocytes, where the impulse propagates from cell to cell through gap junctions.

The right ventricle contracts like a bellows, whereas the left ventricle contracts like a hand squeezing a tube of toothpaste

The two ventricles share a common envelope of spiral and circular muscle layers. The arrangement of the spiral bundles ensures that ventricular contraction virtually wrings the blood out of the heart, although incompletely. The apex contracts before some of the basal portions of the ventricle, a sequence that propels blood upward to the aortic and pulmonary valves.

The mechanical action of the right ventricle resembles that of a bellows used to fan a fire (Fig. 22-8A). Although the distance between the free wall and the septum is small, the free wall has such a large surface area that a small movement of the free wall toward the septum ejects a large volume.


FIGURE 22-8 Comparison of the dynamics of the left and right ventricles.

The mechanism of emptying of the right ventricle involves three motions. First, the longitudinal axis of the right ventricle shortens when spiral muscles pull the tricuspid valve ring toward the apex. Second, the free wall of the right ventricle moves toward the septum in a bellows-like motion. Third, the contraction of the deep circular fibers of the left ventricle forces the septum into a convex shape, so that the septum bulges into the right ventricle. This bulging of the septum stretches the free wall of the right ventricle over the septum. These three motions are well suited for ejection of a large volume, but not for development of a high pressure. The right ventricle ejects the same blood volume as the left ventricle does, but it does so at much lower intraventricular pressures.

The mechanical action of the left ventricle occurs by a dual motion (see Fig. 22-8B): First, constriction of the circular muscle layers reduces the diameter of the chamber, progressing from apex to base, akin to squeezing a tube of toothpaste. Second, contraction of the spiral muscles pulls the mitral valve ring toward the apex, thereby shortening the long axis. The first mechanism is the more powerful and is responsible for the high pressures developed by the left ventricle. The conical shape of the lumen gives the left ventricle a smaller surface-to-volume ratio than the right ventricle and contributes to the ability of the left ventricle to generate high pressures.

The contraction of the atria normally makes only a minor contribution to the filling of the two ventricles when the subject is at rest (see Box 22-1). However, the contraction of the atria is a useful safety factor in at least two circumstances. During tachycardia, when the diastolic interval—and thus the time for passive filling—is short, the atrial contraction can provide a much-needed boost. Atrial contraction is also useful in certain pathological conditions. For example, when a narrowed (i.e., stenotic) AV valve offers substantial resistance to the flow of blood from atrium to ventricle, the atrial pump can make an important contribution to ventricular filling.

The right atrium contracts before the left, but the left ventricle contracts before the right

When the cardiac cycle was introduced above in the chapter, we assumed that the events on the right and left sides of the heart happen simultaneously. However, as we have already noted in our discussion of the splitting of heart sounds, the timing of the two sides of the heart is slightly different (see Fig. 22-8C).

Atrial Contraction

Because the SA node is located in the right atrium, atrial contraction begins and ends earlier in the right atrium than in the left (see Fig. 22-8C, “Contraction” panel).

Initiation of Ventricular Contraction

Ventricular contraction starts slightly earlier on the left side, and the mitral valve closes before the tricuspid valve. However, this timing difference in the closure of the AV valves (see Fig. 22-8C, “Valve movements” panel) is so small that it is unusual to hear a split S1. On the other hand, the right ventricle has a briefer period of isovolumetric contraction because it does not need to build up as much pressure to open its semilunar (i.e., outflow) valve and to initiate ejection. Thus, the pulmonary valve opens slightly ahead of the aortic valve.

Ventricular Ejection

Ejection from the right ventricle lasts longer than that from the left. The semilunar valves do not close simultaneously. The aortic valve, with its higher downstream pressure, closes before the pulmonary valve. Therefore, the pulmonary valve—with its lower downstream pressure—opens first and closes last. This timing difference in the closure of the semilunar valves explains the normal physiological splitting of S2(see Fig. 22-8C, “Sounds” panel). During inspiration, the relatively negative intrathoracic pressure enhances filling of the right heart, causing it to have a larger end-diastolic volume and therefore more blood to eject. The additional time required for right ventricular ejection postpones the closure of the pulmonary valve (P2), broadening the physiological splitting of S2 (see p. 511).

Ventricular Relaxation

Isovolumetric relaxation is briefer in the right heart than in the left. The pulmonary valve closes after the aortic valve, and the tricuspid valve opens before the mitral valve. Therefore, the right ventricle begins filling before the left.

Measurements of ventricular volumes, pressures, and flows allow clinicians to judge cardiac performance

Definitions of Cardiac Volumes

The cardiac output is the product of heart rate and stroke volume (see p. 414). The stroke volume (SV) is the difference between ventricular end-diastolic volume (EDV) and ventricular end-systolic volume (ESV); that is, the difference between the maximal and minimal ventricular volumes. EDV is typically 120 mL, and ESV is 50 mL, so that



The ejection fraction (EF) is a dimensionless value, defined as the SV normalized to the EDV:



In our example, the EF is (70 mL)/(120 mL) or ~0.6. The value should exceed 55% in a healthy person. Whereas the ejection fractions of the left and right ventricles as a rule are equal, clinicians normally measure left ventricular ejection fraction (LVEF).

Measurements of Cardiac Volumes

Clinicians routinely measure the volumes of the cardiac chambers by means of angiography or echocardiography (see pp. 426–428). One-dimensional (or M-mode) echocardiography allows one to assess left ventricular performance in terms of linear dimensions and velocities by providing measurements of (1) velocity of the posterior left ventricular wall, (2) fractional shortening of the left ventricular circumference, and (3) rate of fractional circumferential shortening. Two-dimensional echocardiography makes it possible to determine several ventricular volumes:

• Left ventricular end-diastolic volume (LVEDV)

• Left ventricular end-systolic volume (LVESV)

• Stroke volume (SV = LVEDV − LVESV)

• Left ventricular ejection fraction (LVEF = SV/LVEDV)

Measurement of Ventricular Pressures

For right-sided heart catheterizations, clinicians use a Swan-Ganz catheter, which consists of three parallel tubes of different lengths. The longest is an end-hole catheter with a balloon flotation device that directs the tip in the direction of the blood flow. The other two tubes are side-hole catheters that terminate at two points proximal to the tip. The physician advances the catheter percutaneously through a large systemic vein, into the right heart, and then into the pulmonary circulation, where the tip of the longest tube literally wedges in a small pulmonary artery. Because a continuous and presumably closed column of blood connects the probe's end and the left atrium, the wedge pressure is taken as an index of left atrial pressure. For left-sided heart catheterizations, clinicians insert a simple catheter percutaneously into an artery and then advance the catheter tip upstream to the left heart. Table 22-3 lists some of the most important pressure values for the right and left sides of the heart.

TABLE 22-3

Comparison of Pressures in the Right and Left Circulations











a wave



c wave



v wave





Peak systolic



Peak systolic



End diastolic



End diastolic











Peak systolic



Peak systolic



End diastolic



End diastolic











Measurement of Flows

The cardiologist can calculate flow from changes in ventricular volume, as measured by echocardiography and the Doppler ultrasound technique (see pp. 427–428), both of which measure the flow of blood in the outflow tract (i.e., aorta). Figure 22-8D and E illustrate the profiles of outflow pressure and velocity for the two ventricles. Although the two ventricles expel on average the same amount of blood in a single cardiac cycle, the peak velocity is much higher in the left ventricle. In addition, the velocity rises far more rapidly in the left ventricle, which indicates greater acceleration of the blood during ejection. The pressure wave is about five times larger in the left ventricle than in the right, and the rate at which the pressure rises (ΔPt) is more rapid in the left ventricle.

The pressure-volume loop of a ventricle illustrates the ejection work of the ventricle

In Figure 22-1, we saw separate plots of ventricular pressure against time and volume against time. If, at each point in time, we now plot pressure against volume, the result is a pressure-volume loop, as is shown in Figure 22-9 for the left ventricle. This loop is a “phase plot” that describes the relationship between left ventricular pressure and left ventricular volume during the cardiac cycle. Notice that, although time does not explicitly appear in this plot, as we make one complete counterclockwise cycle around the loop, we sequentially plot pressure and volume at all time points of the cardiac cycle. However, the distance between two points on the loop is not proportional to elapsed time.


FIGURE 22-9 Pressure-volume loop of the left ventricle.

In examining this pressure-volume loop, we will arbitrarily start at point A in Figure 22-9, and then consider each of the segments of the loop (e.g., AB, BC, and so on) before again returning to point A. Although we use the left ventricle as an example, a similar analysis applies to the right ventricle.

Segment AB

Point A in Figure 22-9 represents the instant at which the mitral valve opens. At this point, left ventricular volume is at its minimal value of ~50 mL, and left ventricular pressure is at the fairly low value of ~7 mm Hg. As the mitral valve opens, the ventricle begins to fill passively, because atrial pressure is higher than ventricular pressure. During interval AB, ventricular pressure falls slightly to ~5 mm Hg because the ventricular muscle is continuing to relax during diastole. Thus, despite the rapid entry of blood, ventricular pressure falls to its lowest value in the cardiac cycle.

Segment BC

During a second phase of ventricular filling, volume rises markedly from ~70 to ~120 mL, accompanied by a rather modest increase in pressure from ~5 to ~10 mm Hg. The modest rise in pressure, despite a doubling of ventricular volume ΔV, reflects the high compliance (C = ΔVP) of the ventricular wall during late diastole. The relationship between pressure and volume during segment BC is similar to that in blood vessels (see p. 454).

Segment CD

Point C in Figure 22-9 represents the closure of the mitral valve. At this point, ventricular filling has ended and isovolumetric contraction—represented by the vertical line CD—is about to begin. Thus, by the definition of isovolumetric, ventricular volume remains at 120 mL while left ventricular pressure rises to ~80 mm Hg, about equal to the aortic end-diastolic pressure.

Segment DE

Point D in Figure 22-9 represents the opening of the aortic valve. With the outlet to the aorta now open, the ventricular muscle can begin to shorten and to eject blood. During this period of rapid ejection, ventricular volume decreases from ~120 to ~75 mL. Notice that as contraction continues during interval DE, the ventricular pressure rises even farther, reaching a peak systolic value of ~130 mm Hg at point E.

Segment EF

Point E in Figure 22-9 represents the instant at which the ventricular muscle starts to relax. During this period of decreased ejection, ventricular pressure falls from ~130 to ~100 mm Hg. Nevertheless, blood continues to leave the ventricle, and ventricular volume falls from ~75 mL at point E to ~50 mL at point F. Point F represents end-systolic volume and pressure. Notice that the ventricle does not shrink to zero volume at the end of systole. In total, 120 − 50 = 70 mL of blood has left the ventricle during systole (i.e., between points D and F). Therefore, the stroke volume is substantially less than the maximum ventricular volume (i.e., EDV). The ejection fraction in this example is ~60%, which is in the normal range. Ejection occurs against aortic pressures ranging between 80 and 130 mm Hg. Therefore, ejection is not “isotonic” (see pp. 237–238).

Segment FA

Point F in Figure 22-9 represents the closing of the aortic valve. At this point, ejection has ended and isovolumetric relaxation is about to begin. The ventricular volume remains at 50 mL, while left ventricular pressure falls from ~100 mm Hg at point F to ~7 mm Hg at point A. At the end of isovolumetric relaxation, the mitral valve opens and the cardiac cycle starts all over again with ventricular filling.

The six segments of the pressure-volume loop in Figure 22-9 correspond to different phases of the cardiac cycle:

• Phase 1, the inflow phase, includes segments AB and BC.

• Phase 2, isovolumetric contraction, includes segment CD.

• Phase 3, the outflow phase, includes segments DE and EF.

• Phase 4, isovolumetric relaxation, includes segment FA.

Segments CDEF represent systole, whereas segments FABC represent diastole.

The “pumping work” done by the heart accounts for a small fraction of the total energy the heart consumes

The heart does its useful work as a pump by imparting momentum to the blood and propelling it against the resistance of the periphery.

Work, in its simplest definition, is the product of the force applied to an object and the distance the object moves (W = force × distance). In considering pressure-volume work, we must revise this definition. Imagine that we have a volume of blood in a syringe. If we apply a constant force to the plunger—that is, if we apply a constant pressure to the blood—the plunger moves a certain distance as we eject the blood through the needle, thereby reducing blood volume by an amount ΔV. How much work have we done? For pressure moving a fluid, the external work is



If the aortic pressure were constant, the work done with each heartbeat would be simply the product of the aortic pressure (P) and the stroke volume (ΔV = SV = EDV − ESV).

The pressure-volume relationships in Figure 22-10 illustrate the pressure-volume work of the left ventricle. The surface below the segment ABC (i.e., filling phase) is the work done by the blood (previously contained in the venous reservoirs and atria at a low pressure) on the ventricle (see Fig. 22-10A). The surface below DEF (i.e., ejection phase) is the work done by the heart on the blood during the ejection (see Fig. 22-10B). The difference between the areas in Figure 22-10A and B—that is, the area within the single-cycle loop—is the net external work done by the heart (see Fig. 22-10C). imageN22-5


FIGURE 22-10 External work of the left ventricle.


“Pumping Work” Done by the Heart

Contributed by Emile Boulpaep

In applying Equation 22-4,


to the external work done by the heart, we assumed that the left ventricle pumps against a constant aortic pressure. In reality, of course, the aortic pressure is not constant. Thus, in Equation 22-4 we also should have included a V · ΔP term to take into account the changing aortic pressure, so that Equation 22-4 becomes

image (NE 22-2)

Nevertheless, our calculation of work using the area of the loop in Figure 22-10C does take this extra term into account.

The pressure-volume diagram for the right ventricle has the same general shape. However, the area (i.e., net external work) is only about one fifth as large because the pressures are so much lower.

The area of the loop in Figure 22-10C—that is, the pressure-volume work (P · V)—ignores the speed at which the ventricle pumps the blood (i.e., the acceleration that the heart imparts to the blood, or the time it takes to complete one cardiac cycle). Thus, the work per beat should also include the kinetic energy (imagemv2) that the heart imparts to the ejected blood:



Of its total external work, the heart delivers only a relatively small fraction as kinetic energy. Moreover, the total external work is itself only a small portion of the total energy that the heart actually expends. Like other muscles, the heart not only shortens and performs classical work (e.g., isotonic contraction), but it also maintains active tension without shortening (i.e., isometric contraction; see pp. 237–238). During the isovolumetric contraction, the ventricle develops and maintains a high pressure without performing any total external work—just as we perform no useful work when we hold a weight without lifting it. However, in both isometric exercises, the muscle breaks down ATP as long as it maintains isometric tension; the energy ends up as heat. This type of energy cost in heart muscle is called tension heat,imageN22-6 which is proportional to the product of the tension of the ventricular wall (T) and the length of time (Δt) that the ventricle maintains this tension (i.e., tension-time integral). In the case of the heart, the pressure against which the ventricle must pump is a major determinant of the wall tension.


Tension Heat

Contributed by Emile Boulpaep

From the physical sciences, we know that we can define external mechanical work as the product of force and displacement. In the case of the heart, the external mechanical work is the product of the changes in pressure (i.e., force per unit area) and volume (i.e., displacement in three dimensions):

image (NE 22-3)

This is the equation we introduced in imageN22-5. The first term is particularly important during isovolumetric contraction, and the second term is particularly important during the ejection phase. However, as we noted on page 521, the heart consumes more energy than we can account for by the external mechanical work in the above equation.

Imagine that the left ventrical had to maintain itself for some time at point D in Figure 22-9. Here there is neither a change in pressure nor a change in volume, so that the above equation would tell us that the heart is performing no external mechanical work. Maintaining this isometric tension is like extending an arm holding a weight without lifting it—we do no external mechanical work, yet we burn ATP—tension heat. Moreover, this tension heat is proportional not only to the mass of the weight but also to how long we hold it! In contrast, if we transferred the weight from our arm to a nail in the wall, that nail could hold that weight for an indefinite period without consuming any energy.

If the path DEF in Figure 22-9 (i.e., ejection) were perfectly horizontal (a volume decrease at constant pressure), the external mechanical work would be P · ΔV (i.e., the second term in the above equation). However, merely maintaining this constant pressure during the period of ejection requires energy—tension heat. Moreover, just as in our analogy with the extended arm holding the weight, the tension heat of the heart is proportional to the pressure (i.e., the tension) and the time the pressure is maintained, as described by the third term in Equation 22-6. Returning to Figure 22-9, we can increase the tension heat either by elevating the path DEF (i.e., raising the pressure) or increasing the time interval (Δt) between D and F (i.e., slowing the ejection of the same volume). In practice, the Δt for each ejection might increase with aortic stenosis, which increases the ejection time. Alternatively, cumulative Δt (i.e., the aggregate Δt over a minute's time) will increase with a high heart rate. Thus, performing the same external work at a high heart rate requires more total energy consumption than performing the same work at a low heart rate.

The total energy transformed in one cardiac cycle is the sum of the total external work done on the blood and the tension heat:



where k is a proportionality constant that converts T · Δt into units of energy. The tension heat is the major determinant of the total energy requirements of the heart. Total external work represents a relatively small fraction (3%) of the total energy needs of the heart at rest, rising to as much as 10% during exercise. The heat developed as part of the tension-time integral remains the major component of the total energy consumption, even during exercise.

The tension heat is not only far more costly for the heart than the pressure-volume work but is also of considerable practical interest for the patient with coronary artery disease who wishes to step up cardiac output during increased physical activity. The major burden for such an individual may be not so much the total external work expended in driving additional blood through the circulation (i.e., increasing the cardiac output), but rather an increase in tension heat (k · T · Δt). Thus, it is advantageous to the patient to have a low wall tension (T)—that is, a low blood pressure. It is also advantageous for the patient not to spend too much time (Δt) in systole. The heart spends a greater fraction of its time in systole when the heart rate is high. Thus, the cardiac patient is better off to increase cardiac output at low pressure and low heart rate (i.e., a low T · Δt product). The only option left is to increase stroke volume.

The ratio of the ventricle's total external work (P · V + imagemv2) to the total energy cost (i.e., W/E) is the heart's mechanical efficiency. Note that the mechanical efficiency has nothing to do with how effective the ventricle is at expelling blood (i.e., ejection fraction).