Looking Back, Going Forward: Understanding Cardiac Pathophysiology from Pressure–Volume Loops

Figures

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  Figure 1. (A) Normal pressure–volume loop of the left ventricle. Ventricular volumes are on the x-axis, and ventricular pressures are on the y-axis. Each segment of the loop represents a phase of the cardiac cycle: a–b, ventricular filling; b–c, isovolumic contraction; c–d, ejection; and d–a, isovolumic relaxation. See text for details. (B) Changes in ventricular contractility. Under constant preload (EDV) and afterload (Ea) conditions, a rise in contractility (red) results in a leftward shift of the ESPVR or V120, accompanied by an increase in both ESP and SV; on the contrary, a depression in myocardial contractility (blue) results in a rightward shift of the ESPVR or V120, with a consequent reduction in both ESP and SV. (C) Changes in diastolic properties. The curvilinear shape of the EDPVR suggests that the ventricle becomes increasingly stiffer at higher volumes (green). A stiff ventricle (red) shows a leftward shift of the EDPVR or V30, while a compliant ventricle shows (blue) a rightward shift of the EDPVR or V30. (D) Time-varying elastance. Pressure–volume curve of multiple points of the cardiac cycle which progressively increases the elastance from diastole to the end of systole…

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  Figure 2. (A) Changes in preload. Under constant afterload (Ea) and contractility (Emax) conditions, a volume depletion (blue) results in a smaller and leftward-shifted PVL, with smaller EDV, ESP, and SV; on the contrary, a volume overload (red) results in a bigger and rightward-shifted PVL, with higher EDV, ESP, and SV. (B) Changes in afterload. Under constant preload (EDV) and contractility (Ees) conditions, an increased afterload (rightward shift of Ea—red) determines an increased ESP accompanied by a lower SV; on the contrary, a reduced afterload (leftward shift of Ea—blue) determines a reduced ESP accompanied by a higher SV.

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  Figure 3. (A) Ventricular energetics. SW, stroke work, expressed by the following formula: SW=∫EDVESVPVdV−∫EDVESVEDPVRVdV. PE, potential energy, expressed by the following formula: PE=∫V0V1ESPVRdV−∫V0V1EDPVRVdV. (B) Myocardial oxygen consumption. The x-axis is the PVA. The y-axis is the MVO2. The association between MVO2 and PVA is highly linear and does not change in terms of slope and y-axis intercept under conditions of constant contractility. Conversely, an enhanced contractility increased the MVO2 intercept without any change in the slope, reflecting a higher oxygen consumption due to an additional cross-bridge cycling (revised from Bastos et al. [3]).

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  Figure 4. Ventriculo-arterial coupling and the corresponding ventricular energetics. Under resting conditions, the optimal VAC of < 1 (red) maximizes mechanical efficiency of the heart. Under pathological or stressful conditions, the ventricle maximizes the SW at the expense of mechanical efficiency, thus equalizing ventricular and arterial elastances (VAC = 1 − black). When VAC > 1 (blue), the extremely high PE makes ventricular contraction totally inefficient, causing hemodynamic derangements.

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  Figure 5. Normal and pathological RV PVL. Physiological RV PVL shows a triangular shape due to a shortened isovolumic contraction, an early peak chamber pressure, and a lower ESP point (closed to the diastolic pressure). An acute pressure overload alters the RV PVL shape into a trapezoid or notched one, with a late peak chamber pressure and an increased ESP.