The effects of acute afterload change on systolic ventricular function in conscious dogs with normal vs. failing hearts

Abstract

Background: To date, no data exist on the linearity and, therefore, the usefulness of the preload recruitable stroke work (PRSW) and end-systolic pressure-volume (ESPVR) relationships during acute afterload changes in heart failure. Aims: Our aim was, therefore, to characterize both relationships in a model of ventricular pacing induced heart failure at baseline and during acute changes in afterload. Methods: Dynamic left ventricular volume and transmural pressure were measured in 10 conscious dogs using sonomicrometry and micromanometry under control conditions and during heart failure produced by 3 weeks of rapid right ventricular pacing. Afterload was varied from baseline with intravenous infusions of nitroprusside and phenylephrine. Left ventricular function was assessed using the PRSW and ESPVR relationships. Results: Cardiac output demonstrated a linear inverse relationship with afterload in both normal and failing hearts (r )0.5, P-0.001) with failure producing a parallel, downward 2 shift of the afterload (x) vs. cardiac output (y) relationship (P-0.01). Yet, afterload variation did not affect PRSW or ESPVR relationships in either normal or failing hearts (r -0.12, P)0.05). Conclusion: Thus, the PRSW and ESPVR relationships are 2 insensitive to acute afterload changes in both failing and normal hearts, and the failing left ventricle is no more afterload-sensitive than the normal heart.

Quantitative assessment of cardiac output and left ventricular function by noninvasive phase‐contrast and cine MRI: Validation study with invasive pressure‐volume loop analysis in a swine model

“…Previous work has shown that analysis of the time‐varying ratio of instantaneous pressure (P) to volume (V) obtained from an indwelling conductance catheter yields accurate assessment of intrinsic ventricular diastolic and systolic properties independently of loading conditions (7, 8). Therefore, dynamic PV loop analysis has been considered the gold standard in assessment of cardiac conditions (9, 10). Several load‐independent indices obtained from PV measurements are commonly used to evaluate contractility of the left ventricle (LV), including slope of the end‐systolic PV relationship, slope of the maximum first derivative of LV pressure (dP/d t max ), and preload‐recruitable stroke work (11–13).…”

The Effectiveness of Inodilators in Reducing Short Term Mortality among Patient with Severe Cardiogenic Shock: A Propensity-Based Analysis

“…Moreover, a recent cardiogenic shock paradigm suggested that severe impairments in cardiac function may be associated with systemic inflammation and thus with a certain degree of vasodilatation [6]. Inopressors might, in turn, alter peripheral microcirculation [3], increase left ventricular afterload [4] and thus alter organ perfusion. We used the data from 3 different observational cohorts (ALARM-HF [8], EFICA [7] and AHEAD [12]) and compared inopressors alone to a combination of inopressors plus inodilators.…”

“…Excessive vasoconstriction may, in turn, impair macro-hemodynamics by increasing left ventricular afterload [4], [20] and promoting myocardial oxygen delivery/oxygen consumption imbalance [21]. Catecholamines have been advocated to affect the restoration of cardiac function and increase short- and long-term mortalities [22].…”

“…Because blood pressure occasionally fails to increase, vasopressors are often considered as the next-step therapy [2]. However, vasopressors might alter peripheral microcirculation [3] and increase left ventricular afterload [4]. Hence, two theories are encountered: 1) treatment should focus on inotropic support and limitation of left ventricular afterload to avoid any type of vasoconstriction [5]; and 2) similar to sepsis, cardiogenic shock is rapidly associated with a systemic inflammatory state that may require additional vasopressors to restore organ perfusion [6].…”

The Pressure-Volume Loop Revisited

“…E es revealed by an afterload increment in stunned hearts can be an unmasking of cardiac failure with concomitant excessive afterload dependence. Whether the failing myocardium in fact is excessively afterload dependent or not is somewhat controversial (10), but most studies will indicate such an afterload sensitivity (32,33).…”