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Cardiac filling pressures are monitored to estimate cardiac filling volumes, which in turn determine the stroke output of the left and right ventricles. According to the Frank-Starling principle, the force of cardiac contraction is directly proportional to end-diastolic muscle fiber length at any given level of intrinsic contractility or inotropy. This muscle fiber length or preload is proportional to end-diastolic chamber volume. Even though it would be ideal to monitor cardiac chamber volumes continuously in critically ill patients, this goal remains elusive in clinical practice.
When a cardiac filling pressure is measured as a surrogate for estimating cardiac volume, one must not assume that these two variables always change in direct proportion or even in the same direction. In fact, the diastolic pressure-volume relationship in cardiac muscle is not linear, but rather curvilinear, with a progressively steeper slope at higher volumes ( Fig. 32-23 ).[292] [293] This diastolic
Figure 32-23
Ventricular diastolic pressure-volume relationship.
Along the flat portion of the curve, a 20-mL increase in ventricular volume causes
a small increase in ventricular pressure (A to B). In contrast, the same increase
in volume along the steep portion of the ventricular filling curve causes a marked
increase in filling pressure (C to D). Another problem associated with the use of
filling pressure as a surrogate for filling volume arises when shifts in the pressure-volume
relationship occur. At point C, ventricular volume is 100 mL and ventricular pressure
is 8 mm Hg. An increase in filling pressure to 15 mm Hg may accompany either increased
volume (D) or decreased volume (E). The latter occurs when ventricular compliance
changes and shifts the ventricular diastolic pressure-volume relationship up and
to the left. (Redrawn from Mark JB: Atlas of Cardiovascular Monitoring.
New York, Churchill Livingstone, 1998, Fig. 15-2.)
The relationship between ventricular volume and filling pressure depends on the portion of the pressure-volume curve over which the patient's heart is operating and the shape or slope of the curve. Commonly termed ventricular compliance, this change in pressure for a given change in volume (ΔP/ΔV) is actually the reciprocal of compliance and is more accurately termed ventricular elastance, distensibility, or stiffness.[297] [298] A patient with an abnormally stiff ventricle will have a greater change in end-diastolic pressure for any given change in end-diastolic volume, and the converse is true for a patient with an abnormally compliant ventricle. By definition, diastolic dysfunction is present when ventricular pressure is abnormally elevated for any given ventricular volume.
The ventricular diastolic pressure-volume relationship is influenced by the intrinsic properties of the ventricle, such as the passive mechanical characteristics of cardiac muscle, chamber geometry, and relaxation. In addition, external forces exerted by the pericardium, the adjacent ventricle, the coronary vasculature, and pleural pressure will further influence ventricular pressure-volume relationships. [299] [300] [301] [302] One should not equate cardiac filling pressures with filling volumes when patients are functioning over wide ranges of their diastolic pressure-volume curve or under conditions in which diastolic stiffness is abnormal or changing rapidly.
In general, all intravascular pressures measured in clinical practice are referenced to ambient atmospheric pressure. (Indeed, the first step in pressure transducer setup is to zero the transducer by exposing it to atmospheric pressure and assigning this pressure a value of zero by pressing the zero pressure button on the attached monitor. See "Technical Aspects of Direct Blood Pressure Monitoring.") Thus, a cardiac filling pressure of 10 mm Hg is 10 mm Hg higher than ambient atmospheric pressure. Does this pressure value accurately represent the distending force across the cardiac chamber wall at end-diastole?
To answer this question, one needs to consider transmural pressure. The cardiac chambers are all contained within the pericardium and thorax. Changes in pressure in the structures surrounding the heart will influence
Cardiac filling pressures are measured directly from a number of sites in the vascular system. CVP monitoring is the least invasive method, followed by PAP monitoring and left atrial pressure monitoring. Proper interpretation of all cardiac filling pressures requires knowledge of normal values for these pressures, as well as pressures in the cardiac chambers and great vessels and other measured and derived hemodynamic variables ( Table 32-7 ).
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