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232 PART 3: Cardiovascular Disorders

■ THE END-SYSTOLIC V-P CURVE AND CONTRACTILITY systemic pressure (Pms; see below). These actions in turn decrease

The normal diastolic V-P relation is demonstrated by the continuous LVEDV and LVEDP. The reduction in end-diastolic volume tends to
line in the lower right-hand portion of Figure 31-5. Consider the effects decrease LVEDP along the steep diastolic V-P curve so that there is a large
when the ventricle contracts during systole without ejecting any blood, reduction in LVEDP for a small reduction in LVEDV and SV. Further,
as if the aortic valve could not open. A very large pressure is generated the potential adverse effect of reduced SV is often offset by increased
during this isovolumic contraction from a normal LVEDV, but when contractility and reduced afterload when myocardial wall stress is decre-
the LVEDV is reduced, the pressure generated during a similar iso- ased by the reduction in LVEDV and LVEDP (see Chaps. 35 and 37).
volumic contraction is much less, as a manifestation of the force-length Reduced afterload and reduced myocardial O consumption improve
2
characteristics of the myocardium. 2,3,12,13 That is, the less the muscle is ventricular pumping function by shifting the end-systolic V-P relation
stretched, the less force it can generate, a manifestation of the length- up and to the left, so LVESV decreases and SV increases. Further, the
dependent activation of actin-myosin cross-bridges. The units of force decreased end-DP reduces the complication of cardiogenic pulmo-
in the hollow sphere of myocardium are the units of pressure, or force nary edema.
per unit area. A line connecting the end-systolic V-P points is linear and Positive inotropic agents such as dopamine and dobutamine act
extrapolates toward the origin (see the continuous end-systolic V-P line directly on the myocardium to reduce end-systolic volume at a given
in Fig. 31-5, upper left). end-SP, thereby increasing SV (see Chaps. 35 and 37). Dopamine also
Of course, the aortic valve does open in early systole when the iso- causes venoconstriction by increasing Pms and VR, so the increase in SV
volumic pressure exceeds the aortic DP; then LV volume decreases as the is often associated with increased LVEDV, whereas dobutamine tends to
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SV is ejected (see Fig. 31-5). The contracting ventricle shortens against increase SV and decrease LVEDV. Afterload-reducing agents such as
the aortic afterload pressure until its volume reaches the end-systolic vol- nitroprusside dilate peripheral arteries to decrease end-SP and afterload;
ume; at that lower volume, the maximum pressure that can be generated in turn, end-systolic volume decreases along the depressed end-systolic
V-P relation to increase SV. Nitroprusside and other arteriolar vaso-
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is equal to the afterload pressure, so the aortic valve closes and ejection
is over. If the afterload pressure were decreased, the ventricle could eject dilating agents also decrease end-DP without changing end-diastolic
volume; this effect appears to enhance ventricular function viewed on the
further to a lower end-systolic volume, where the maximum generated 17
pressure equals the reduced afterload; hence, SV would increase. Starling relation, as discussed above. The decrease in LVEDP decreases
pulmonary edema and may decrease myocardial oxygen demands by
The line connecting all end-systolic V-P points is an indicator of the
pumping function or contractility of the heart because this line defines decreasing ventricular wall stress. To the extent that it decreases ven-
tricular wall stress, end-systolic V-P relations may shift to the left due to
the volume to which the ventricle can shorten against each afterload for
a given contractile state. 12-15 Agents that enhance contractility (eg, epi- enhanced contractility. In some patients with cardiogenic shock, vasodi-
lator therapy appears to increase SV and Q ˙ t without decreasing or even
nephrine, calcium, dobutamine, and dopamine) shift the end-systolic V-P
relation up and to the left; then the ventricle can shorten to a smaller end- increasing arterial BP, that is, arterial dilation appears to reduce end-
16,17
systolic volume for each afterload, thereby increasing SV at a given LVEDV/ systolic volume at a given end-SP as if contractility were enhanced.
LVEDP. 12,13 Conversely, negative inotropic agents such as metoprolol, myo- Noninvasive bilevel mechanical ventilation (or continuous positive
cardial ischemia, hypoxia, and acidemia depress the end-systolic V-P airway pressure, CPAP) lowers both preload and afterload, in addition
18
relation down and to the right, as indicated by the interrupted end-systolic to beneficial effects on gas exchange and work of breathing. Q ˙ t is not
V-P line shown in Figure 31-5. 14,15 Then end-systolic volume is increased reduced despite decreased transmural pressures, indicating improved
for a given pressure afterload, thereby reducing the SV at a given filling pump function.
pressure. Such a reduction in contractility is a common cause for the Other concomitant effects of critical illness cause ventricular dys-
depressed Starling curve AB shown in in Figure 31-4. function characterized by reduced SV at increased Pla (see Table 31-1).
Arterial hypoxemia and acidemia depress the end-systolic V-P curve
15
14
■ AN APPROACH TO ACUTE VENTRICULAR DYSFUNCTION and increase diastolic stiffness, as shown by the interrupted curve in
Figure 31-5. Acute arterial hypertension raises the pressure afterload,
These concepts provide a framework for understanding the patho- so SV decreases as end-systolic volume increases along the continu-
physiology and therapy of acute myocardial infarction (see Chap. 37). ous end-systolic V-P curve in Figure 31-5. Then LVEDV increases to
Figure 31-5 depicts normal diastolic and systolic V-P relations and indi- accommodate VR, so LVEDP increases, often more than expected, due
cates a normal systolic ejection (continuous lines). From an LVEDV of to diastolic stiffness, in turn due to LV hypertrophy in the hypertensive
120 mL and an LVEDP of 10 mm Hg, the ventricle contracts isovolumi- patient. Accordingly, pulmonary edema is a common complication, and
cally until the aortic valve opens at a DP of 80 mm Hg. Blood is then ejected it responds to vasodilator therapy when BP is decreased. In some or all
as SP increases to 110 mm Hg and decreased toward an LVESP of 90 mm of these conditions, diastolic dysfunction merits special management.
7
Hg and an LVESV of 50 mL, when the aortic valve closes to generate the When acute or acute-on-chronic congestive heart failure is present,
dicrotic notch on the arterial pressure trace. Accordingly, SV is 70 mL decreasing LVEDP and LVEDV, maintaining atrial contraction, increas-
at a Pla of 10 mm Hg and Q ˙ t is 5.6 L/min when HR is 80 beats/min. ing the duration of diastole, and minimizing myocardial ischemia are
Acute myocardial infarction depresses the end-systolic V-P relation so helpful. Each of these therapeutic measures is also helpful in managing
that the end-systolic volume is increased to 90 mL at a reduced LVESP hypoperfusion states associated with diastolic dysfunction. 7
of 75 mm Hg (interrupted lines). At the same time, the end-diastolic Valvular dysfunction mimics systolic and diastolic dysfunctions such
volume is increased to 130 mL to accommodate the VR, and end-DP that LVEDV is much increased and the forward SV is reduced (see
is increased even more than expected (LVEDP = 30 mm Hg) due to Chap. 41). With aortic regurgitation, after a vigorous systolic ejection,
the shift up and to the left of the end-diastolic V-P relation (inter- aortic blood runs off forward and backward in diastole such that LVEDP
rupted line). Thus SV (40 mL) and Q ˙ t (4.4 L/min) are reduced despite increases and arterial DP decreases toward equal values at 40 mm Hg.
reflex tachycardia (HR = 110 beats/min) at an increased LV filling The large LVEDV then ejects a large SV to increase SP to 120 mm Hg,
pressure, and BP is decreased (SP/DP = 90/70 mm Hg) despite the reflex causing a bounding PP of 80 mm Hg, but the aortic regurgitation reduces
increase in SVR. forward SV and Q ˙ t to a low value. Consider also mitral valve incom-
Conventional therapy consists of preload reduction, inotropic agents, petence. During systole, a large fraction of the blood ejected from the
and afterload reduction, in addition to measures to reestablish and ventricle regurgitates to the left atrium, thereby reducing forward SV
maintain coronary blood flow (see Chap. 37). Interventions such as and Q ˙ t but increasing LVEDV and LVEDP when the left atrium fills the
morphine, furosemide, and nitrates decrease VR by dilating venous ventricle in diastole. In this circumstance, PP and BP are decreased. In
capacitance beds to increase the unstressed volume and decrease mean both cases, the ventricular mechanics resemble the interrupted curves

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