End systolic pressure volume relationship of the lungs

Single-beat estimation of right ventricular end-systolic pressure-volume relationship.

technique could define the right ventricular end-systolic pressure-volume relation pulmonary artery-dicrotic notch pressure: end-ejection volume ratio and was. This study assessed whether the end-systolic pressure-volume relationship pulmonary arterial pressure, left atrial pressure, ejection fraction, and cardiac. Effective arterial elastance is defined as the ratio of end systolic pressure to stroke volume, although classically the term "elastance" is simply the reciprocal of .

As afterload increases, RV end diastolic volume rises while ejection fraction falls. Suga and Sagawa developed the methodology for describing left ventricular function in terms of a "time varying elastance", where elastance is equal to the slope of the pressure volume relation at specific "isochronal" times in the cardiac cycle.

In contrast, ejection of blood through the pulmonary valve may continue even when RV pressure is falling due to momentum of the blood into the low input impedance pulmonary circuit. This late ejection, or "hangout period",51 makes identification of "end-systole" problematic in the RV, and contributes to the more triangular shape of the RV pressure-volume loop. The result is that pressure-volume loops are more difficult to interpret in the RV than in the LV,49,52 and the endsystolic pressure volume relation is not necessarily the preferred method for assessing RV contractile function.

Comparison of pressure volume loops obtained in humans with micromanometer catheters and ventriculography in the LV left and RV right. LV pressure volume loops are nearly square, simplifying identification of isovolumic contraction and relaxation phases. In contrast, the RV loop is more triangular, with poorly defined end-systole. Reproduced from Redington AN. As described previously, elastance is related to impedance, so maximal power transfer from the ventricle to the vascular system is achieved if ventricular Emax and vascular Ea elastance are equal.

The RV has a less clearly defined end-systole, and Emax is consequently more difficult to define. Nevertheless, several investigators have found that RV-pulmonary vascular coupling can be analyzed in a similar way, and that, if end-systole is suitably defined, coupling is also nearly optimal under normal conditions ie, the ratio of RV Emax to pulmonary artery elastance Ea is close to 2.

They speculated that the RV free wall served no other purpose than to provide capacitance to the pulmonary circulation. However, RV pressure development is a combination of interactions among the RV free wall, the interventricular septum, and the LV free wall,58,59 and the importance of RV free wall contractile function depends in large part on pulmonary vascular resistance and RV pressure.

For example, while right coronary artery RCA occlusion and RV free wall contractile dysfunction may have little effect on RV pressure development or systemic hemodynamics under normal conditions, RV ischemia results in systemic hypotension when pulmonary vascular resistance increases. Each loop represents a single cardiac cycle. Example of RV pressure-volume loops obtained in an isolated working dog heart under baseline conditions red lines and following inotropic stimulation with epinephrine salmon lines.

The series of loops in each case is obtained by varying the outflow resistance. Note that a nearly straight line can be drawn that is tangent to each loop under a particular condition; although end-systole is difficult to identify, this line is essentially equivalent to the end-systolic pressure volume relation as obtained in isolated left ventricles, where the slope is a reflection of underlying contractile state.

Reproduced from Maughan WL. Copyrightwith permission from Wolters Kluwer Health. RV indicates right ventricle. However, in comparison with the LV, the adult RV has very limited capacity to produce elevated pressure. Those limits are illustrated in Figure 4, which shows that stroke volume as a fraction of control declines much more quickly in the RV than in the LV as mean ejection pressure increases. First, the thinner RV free wall experiences a greater rise in wall tension with increments in RV pressure.

Second, the radius of curvature of the RV increases during contraction rather than decreasing as happens in the LV, which means that shape dependent reduction of stress during contraction due to declining radius of curvature does not occur in the RV as it does in the LV. Comparison of the effect of ejection pressure on ejection fraction in the RV and the LV. Note that for any increment in ejection pressure, the decrement in ejection fraction is much greater in the RV than in the LV.

Reproduced from Heart Disease, Braunwald E. Copyrightwith permission from Elsevier. Several mechanisms potentially contribute to increased contractile function in the setting of increased demand.

These include the Anrep effect homeometric auto regulationthe Frank-Starling mechanism sometimes referred to as heterometric auto regulationand catecholamine induced inotropy. The Anrep effect is an intrinsic increase in contractile function that occurs in response to increased afterload in the absence of external regulatory changes such as catecholamine stimulation.

Pressure–volume loop analysis in cardiology - Wikipedia

Anrep effect can be demonstrated in isolated muscle strips,69 but its presence in vivo has been controversial. Some evidence suggests that Anrep effect is the primary mechanism for initial adaptation to pressure overload in the RV,70,71 although this may be more important in neonatal than in adult RVs. The Frank-Starling mechanism is often viewed as the primary means by which the heart adapts to an increase in demand, but shape differences between the RV and the LV alter how the Frank-Starling mechanism operates.

In both RV and LV, an increase in end-systolic pressure is normally accompanied by an increase in both end -systolic and end- diastolic volume. However, in the RV under normal loading conditions, much of the increase in volume is due to an increase in RV free wall septal dimension, with much less increment in RV free wall surface area. Because the increment in RV free wall area for a given increment in central venous pressure is small, recruitment via the Frank-Starling mechanism is reduced.

At increased afterload, as the RV becomes more cylindrical and other compensatory mechanisms are exhausted, the Frank-Starling mechanism becomes more important. However, neonatal RVs can tolerate ongoing PH, and congenital heart disease patients tolerate supersystemic pulmonary pressures for years with little disability eg, Eisenmenger syndrome. The reason for this difference is unknown. RV hypertrophy may develop in chronic pressure overload,73 although whether this helps to normalize stress or results in contractile dysfunction is uncertain.

Numerous biochemical alterations have been reported in various models of chronic RV pressure overload: Experimentally, chronic RV volume overload does not appear to impair RV contractile function,81 and clinically, patients with volume overload due to congenital heart disease appear to do well for many years.

This is seen most clearly in pulmonary embolism, where volume loading may adversely affect LV function. Experimental data obtained more than 50 years ago showed that the RV has a very limited capacity to compensate for such loads.

Figure 5 shows the result of progressively occluding the pulmonary artery in open chest dogs. At point A, central venous pressure begins to rise, recruiting function via the Frank-Starling relation; when RV pressure reaches a threshold level at point B, systemic pressure drops abruptly and catastrophically.

Result of progressively occluding the pulmonary artery in an open chest dog. Initially, a progressive rise in pulmonary artery pressure is well tolerated, with essentially unchanged systemic pressure.

At point A, central venous pressure begins to rise, permitting recruitment of function via the Frank-Starling relation, until RV pressure reaches a threshold level at point B, at which point systemic pressure drops abruptly and catastrophically. Reproduced from Guyton AC. The mechanism of RV failure and hemodynamic collapse at this point is due to the interaction of several factors.

Just prior to hemodynamic collapse, reduced cardiac output may occur consequent to interventricular interaction. As the RV dilates in response to pressure overload, restraint from the pericardium and from shared muscle fiber bundles of the RV and LV constrain further RV dilation and shift the RV diastolic pressure-volume relation to a steeper portion of the curve, so that further increases in RV pressure result in less RV free wall stretch and hence less recruitment of function via the Frank-Starling relation.

At the same time, interventricular septal shift impairs LV ejection. This combination results in a net decrease in cardiac output.

Single-beat estimation of right ventricular end-systolic pressure-volume relationship.

Figure 6 shows short axis views of dog hearts subjected to experimental pulmonary embolism: Short axis images from the ventricle of a dog obtained using magnetic resonance imaging in diastole and systole under baseline conditions A and following experimental pulmonary embolization B. Reproduced from Dell'Italia LJ. Copyrightwith permission from The American Physiological Society Once cardiac output begins to fall, hemodynamic collapse progresses rapidly. Figure schematizes the likely mechanism of hemodynamic collapse: Proposed schema for the mechanism of abrupt hemodynamic decompensation in the setting of a severe increase in pulmonary inflow impedance.

Once pulmonary resistance reaches level B in figure 5, RV output falls below a critical level, resulting in systemic hypotension, precipitation of RV ischemia, a decline in intrinsic RV contractile function, further decrease in RV output, and a progressive downward spiral to hemodynamic collapse and death.

In the absence of some intervention to reduce pulmonary impedance or increase cardiac output, this process is irreversible. Because hemodynamic collapse in this scenario is abrupt and frequently irreversibleand right heart failure does not become manifest by elevated central venous pressure until RV compensation is nearly exhausted, many if not most patients who present with signs and symptoms of right heart failure are likely found within a very narrow hemodynamic range, where central venous pressure has begun to rise but systemic pressure has not yet begun to fall between points A and B in fig.

Recent experimental evidence suggests that progressive RV contractile dysfunction unrelated to ischemia develops in acute RV pressure overload25, within this range, and potentially contributes to sudden hemodynamic deterioration in patients who otherwise appear hemodynamically stable.

Several mechanisms may contribute to progressive RV dysfunction in this setting. Abnormalities of ventricular-vascular coupling can reduce the efficiency of power transmission from the RV to the pulmonary circulation. Calpain inhibition appear to attenuate dysfunction92 and reduce RV apoptosis94 from pressure overload. Calpain may cause contractile dysfunction via degradation of intercellular adhesion proteins such as talin that coordinate cardiac contraction.

Perhaps this could explain why patients with apparently stable pulmonary hemodynamics can abruptly decompensate. Alternatively, RV contractile dysfunction might render a patient more susceptible to hemodynamic collapse following a subsequent event that further compromises RV contractile function. Improved understanding of the mechanism of RV failure in the setting of PH is likely to increase interest in this neglected disorder, and may facilitate development of new therapeutic approaches that go beyond merely reducing pulmonary vascular impedance and begin to address the underlying mechanisms of RV failure.

Therefore, the net effect is a decrease in stroke volume shown as a decrease in the width of the pressure-volume loop. Because stroke volume decreases and end-diastolic volume increases, there is a substantial reduction in ejection fraction EF. Heart failure caused by systolic dysfunction is commonly refered to as heart failure with reduced ejection fraction HFrEF. Note that with acute systolic dysfunction, there is no change in the end-diastolic pressure-volume relationship EDPVR.

The force-velocity relationship provides insight as to why a loss of contractility causes a reduction in stroke volume see figure. Briefly, at any given preload and afterloada loss of inotropy results in a decrease in the shortening velocity of cardiac fibers. Because there is only a finite period of time available for ejection, reduced ejection velocity results in less blood ejected per stroke. The residual volume of blood within the ventricle is increased increased end-systolic volume because less blood is ejected.

The reason preload increases as inotropy declines acutely is that the increased end-systolic volume is added to the venous return filling the ventricle. An important and deleterious consequence of systolic dysfunction is the rise in end-diastolic pressure.

If the left ventricle is involved, then left atrial and pulmonary venous pressures also rise. This can lead to pulmonary congestion and edema. If the right ventricle is in systolic failure, the increase in end-diastolic pressure will be reflected back into the right atrium and systemic venous vasculature.

This can lead to peripheral edema and ascites. Treatment for systolic dysfunction involves the use of inotropic drugs, afterload reducing drugs, venous dilators, and diuretics.