Effects of systolic dysfunction on ventricular pressure-volume loop decreases the slope of the end-systolic pressure-volume relationship (ESPVR). If the left ventricle is involved, then left atrial and pulmonary venous pressures also rise. A plot of a system's pressure versus volume has long been used to measure the work done by To generate a PV loop for the left ventricle, the LV pressure is plotted against LV volume at multiple . Hence, the relationship between ventricular end-diastolic volume and dP/dt is a more accurate index of .. pulmonary artery. Left ventricular end-systolic pressure-volume relation in end-systolic pressure/ end-systolic volume, and no change in pulmonary arterial pressure with pacing.
Accordingly, fluid resuscitation, if associated with rapid increases in right atrial pressure, should be stopped until evidence of acute cor pulmonale is excluded [ 28 ]. Acute cor pulmonale is treated by improving LV systolic function, maintaining coronary perfusion pressure, or reducing pulmonary artery outflow impedance. Since more than half of RV systolic force is generated by LV contraction, through the free wall interconnection of fibers and not through stiffening or thickening of the intraventricular septum [ 24 ], efforts to increase LV contractility independent of maintaining coronary perfusion pressure are important.
Since RV coronary perfusion primarily occurs during systole, maintaining coronary perfusion pressure greater than pulmonary artery pressure by the use of systemic vasopressor therapy is also indicted [ 27 ]. Finally, since increased RV afterload is a major limitation to RV ejection, efforts to minimize pulmonary vascular resistance and increase pulmonary vascular compliance are also beneficial.
RV afterload The right ventricle, as opposed to the left ventricle, ejects blood into a low-pressure, high-compliance pulmonary circulation. Although the absolute compliance of the pulmonary circulation is one-seventh that of the systemic circulation, it stores much less blood and has the ability to collapse pulmonary vessels as well as have them distend.
Thus, the pulmonary circulation is capable of accommodating increased blood volumes without increasing pulmonary artery pressure as much as would occur on the systemic side if similar increases in flow were seen in the aorta.
This greatly benefits RV systolic function during exercise. Despite being compliant, this circuit does pose resistance to the ejecting right ventricle as quantified by pulmonary arterial pressure. RV afterload is conceptually similar to LV afterload and is determined by the wall tension of the RV.
Under normal conditions RV afterload is highly dependent on the distribution of blood flow in the lung, the degree of hyperinflation or increased alveolar pressure that may be present [ 29 ], and active increases in pulmonary vasomotor tone as may occur with inflammation and alveolar hypoxia. Increases in lung volume independent of changes in pulmonary vasomotor tone can also alter RV function [ 3031 ]. With inspiration, the expanding lungs compress the heart in the cardiac fossa [ 32 ], increasing juxtacardiac ITP.
Because the chest wall and diaphragm can move away from the expanding lungs, whereas the heart is trapped within this cardiac fossa, juxtacardiac ITP usually increases more than lateral chest wall ITP [ 3334 ].
The right ventricle: interaction with the pulmonary circulation
This selective cardiac compressive effect is due to increasing lung volume. It is not affected by the means whereby lung volume is increased. Thus, both spontaneous [ 35 ] and positive pressure-induced hyperinflation [ 36 — 38 ] cause similar compressive effects on cardiac filling. If one measured only intraluminal LV pressure, then it would appear as if LV diastolic compliance was reduced because the associated increase in pericardial pressure and ITP would not be seen.
When LV function is assessed as the relationship between end-diastolic volume and output, however, no evidence for impaired LV contractile function is seen [ 39 ] despite the continued application of PEEP [ 40 ]. These compressive can be considered as analogous to cardiac tamponade. This hyperinflation-induced impaired LV filling forms the basis for the recently completed clinical trial of pharmacologic lung reduction therapy using bronchodilator therapy [ 41 ]. By focusing on minimizing hyperinflation, the authors showed that exercise tolerance markedly improved and remained elevated over time.
In the aggregate, if RV failure occurs due to increased afterload or impaired contractility, then RV filling pressures rise and if mean systemic filling pressure does not rise proportionally, cardiac output falls because the pressure gradient for venous return decreases. Indirectly, this gives rise to the clinical observation that if fluid resuscitation causes right atrial pressure to rise, then the patient is probably not volume responsive because the normal response of a healthy individual to fluid resuscitation is to keep right atrial pressure constant as cardiac output increases owing to the increased pressure gradient for venous return to the heart.
Ventriculo-arterial coupling RV ejection of blood and input pulmonary arterial pressure and tone are tightly coupled. Clearly the cause of the pulmonary arterial pulse pressure is stroke volume. For the left side the mean arterial pressure and the magnitude of the pulse pressure rise for a given stroke volume are also a function of the input arterial resistance, compliance, and impedance [ 42 ].
As described above, RV Ees can be defined as the slope of the RV end-systolic pressure—volume relationship. RV end-systolic pressure is also a function of both RV stroke volume and a physical characteristic of the pulmonary arterial outflow tract. The greater the RV stroke volume for a given vascular tone and compliance, the greater the systolic pulmonary arterial pressure.
CV Physiology | Ventricular Systolic Dysfunction
However, systolic pulmonary arterial pressure is also a primary determinant of RV afterload. Thus, increases in systolic pulmonary arterial pressure for a constant preload and Ees will decrease RV stroke volume and increase RV end-systolic volume.
The slope of the relationship between RV stroke volume and systolic pulmonary arterial pressure is called pulmonary arterial elastance Ea.
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Thus, RV stroke volume not only is limited by but defines end-systolic pressure though arterio-ventricular coupling. Prior studies have identified that maximal LV myocardial efficiency, defined as the amount of external work performed for myocardial oxygen consumed, occurs when systemic Ea is approximately one-half LV Ees [ 44 ] and shows a stronger dependence on systemic Ea than LV Ees [ 45 ].
Uncoupling reflects a reduction of the LV ejection efficiency that can promote LV energetic failure. Presumably, this uncoupling occurs owing to a primary decrease in peripheral impedance and increase in peripheral arterial compliance [ 49 ].
Similar analysis can be done for the right ventricle. But many studies have shown that excess pulmonary Ea to RV Ees causes heart failure. RV contractility can be impaired by a variety of processes associated with increased pulmonary vascular resistance. For example, if RV dilation occurs, then systemic arterial hypotension can develop as LV end-diastolic volume is restricted.
This systemic arterial hypotension must decrease right coronary blood flow, causing ischemic RV dysfunction. Similarly, there are many causes of increased pulmonary artery resistance that are treated differently. For example, pulmonary vascular resistance can increase due to pulmonary vasoconstriction e.
Group I PH is most commonly due to abnormalities in the vascular wall of the pulmonary arterioles, although it also includes pulmonary veno-occlusive disease. The exact underlying pathologic changes reviewed in detail elsewhere 24,39 vary somewhat depending on the etiology, but in most cases there appears to be a mechanical obstruction to flow and a reduced responsiveness to vasodilators, accounting for the common term fixed PH although this is something of a misnomer since the disease process can be modified by various therapies.
Despite the comparative rarity of idiopathic PH a few thousand new cases per year worldwideit receives a disproportionate share of attention from PH specialists. Group II PH commonly referred to as pulmonary venous hypertension is defined as PH due to retrograde transmission of abnormally elevated pulmonary vein pressures from a variety of causes.
Group II PH is largely secondary to abnormalities of left sided heart anatomy or function, eg, LV systolic or diastolic dysfunction, mitral and aortic valve disease, and is essentially a passive process with respect to the pulmonary vasculature. Group II PH may theoretically be "reversed" by correction of the underlying pathologic process that led to elevated pulmonary vein pressure. However, in many conditions eg, mitral stenosis increases in pulmonary arteriole resistance may develop over time and become irreversible, presumably due to similar mechanisms as in some forms of Group I PH.
Although Group II PH is very common and indeed, some authors claim that the most common cause of right heart failure is left heart failureit is uncertain how much right heart failure in Group II actually contributes to mortality versus simply being a marker for more advanced left heart disease. Group III and Group IV PH are due to alterations in pre-capillary pulmonary arterioles, but in Group III these alterations are secondary to lung disease or hypoxemia and can to some extent be considered a normal, physiologic response to external stimuli.
Hypoxic pulmonary vasoconstriction, which normally matches pulmonary ventilation to pulmonary perfusion, may become pathologic when too many segments of lung become hypoxic and PVR rises too far. PH due to Group III processes may be "reversed" by vasodilators such as calcium channel blockers, direct pulmonary vasodilators such as nitroprusside, and inhaled agents such as nitric oxide, but over time abnormalities of the pulmonary vascular system may develop and become essentially permanent as in Group I PH.
Moreover, reversal of hypoxic pulmonary vasoconstriction through extrinsic means carries the potential to worsen hypoxemia through increased ventilation perfusion mismatch. Global statistics are not readily available for this group, but in the United States there are likely more than pulmonary embolism cases causing more than 60 deaths per year.
The RV free wall constitutes the anterior border of the RV and consists of a relatively thin crescent of muscle, lying anterior to the LV and interventricular septum. Spiral muscle bundles form a contiguous band-like structure functionally linking the RV and the LV, likely resulting in transmission of contractile force directly from the LV to the RV. This complex shape accounts for the difficulty in assessing RV size and function based on two dimensional imaging techniques,40 and also accounts for the dramatic changes in RV size and shape that occur with varying loading conditions.
In the LV, myocardial perfusion occurs predominantly in diastole when intramyocardial tissue pressure falls below aortic root pressure. Under normal loading conditions, RV intramyocardial tissue pressure remains below aortic root pressure throughout the cardiac cycle, permitting continuous coronary flow, but in severe RV pressure overload the RV coronary perfusion pattern begins to approximate that of the LV.
In contrast, ejection of blood by the RV proceeds with a sequential contraction beginning in the inflow tract, and moving in a wave toward the outflow tract. Since surface area of a cylinder is proportional to its radius, and volume is proportional to the square of the radius, ejection fraction in the LV is roughly proportional to the square of the change in endocardial surface area.
In contrast, because of the greater surface area to volume ratio of the RV, a greater ejection fraction is produced by a smaller change in surface area than would be required in the LV. The bellows-like arrangement of the RV not only allows large changes in RV volume with small changes in RV free wall surface area, but also helps buffer respiratory changes in RV output47 without necessitating altered contractile function on a breath-to-breath basis.
Illustration of shape changes in the heart during contraction. The circular cross section LV contracts by a uniform reduction in endocardial surface area, maintaining a nearly constant relationship between volume and surface area.
The crescentic RV flattens in systole, leading to a large volume change with minimal change in RV free wall area. During severe pressure overload, the interventricular septum shifts, increasing RV diastolic volume with little increase in RV free wall surface area.
Without an increase in surface area, the RV cannot recruit additional function via the Frank-Starling mechanism. At the same time, there is a reduction in LV end-diastolic volume and surface area, resulting in impaired LV pump function. Reproduced from Greyson CR. LV indicates left ventricle; RV, right ventricle. While the series configuration of the pulmonary and systemic circulation require average RV and LV stroke volume to be the same in the absence of intracardiac shuntsRV end-diastolic volume is normally somewhat greater than LV end-diastolic volume, while ejection fraction is smaller.
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.
Pressure–volume loop analysis in cardiology
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.19B. Left ventricular eccentricity index in end-systole
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. 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. Inotropic drugs include digitalis and drugs that stimulate the heart via beta-adrenoceptor activation or inhibition of cAMP-dependent phosphodiesterase. Afterload reducing drugs e. Venous dilators and diuretics are used to reduce ventricular preload and venous pressures pulmonary and systemic rather than augmenting systolic function directly.