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Pathophysiology of heart failure: Left ventricular pressure-volume and other hemodynamic relationships

INTRODUCTION

Heart failure may be due to either systolic or diastolic dysfunction of the left ventricle. While both are characterized by elevated left ventricular filling pressures, the underlying hemodynamic processes differ considerably. These differences can be best understood when described in terms of the left ventricular pressure-volume and other hemodynamic relationships that provide patient-specific insight regarding the basis of cardiac dysfunction. Understanding these principles has practical implications for the treatment of patients with heart failure, first by defining the predominant type of hemodynamic abnormality (eg, systolic versus diastolic dysfunction) and second, by clarifying filling pressures, loading conditions, and vascular resistances that can be important in determining the most effective therapeutic approach. (See "Overview of the therapy of heart failure due to systolic dysfunction".)

NORMAL LEFT VENTRICULAR PRESSURE-VOLUME RELATIONSHIP

As a pump, the ventricle generates pressure (to eject blood) and displaces a volume of blood. The normal relationship between left ventricular pressure generation and ejection can be expressed as a plot of left ventricular pressure versus left ventricular volume (figure 1). At end–diastole, the fibers have a particular stretch or length, which is determined by the resting force, myocardial compliance, and the degree of filling from the left atrium. This distending force is the preload of the muscle.

After depolarization, the ventricle generates pressure isovolumically (without any change in volume), which leads to the opening of the aortic valve and the ejection of blood. Up to this point, the course of systolic pressure is related to the force created by the myocardium. The magnitude of this force is a function of both chamber pressure and volume. During ejection, the myocardium must also sustain a particular force, which is a function of the resistance and capacitance of the circulatory vasculature and is called the afterload.

The volume of ejected blood represents the forward effective stroke volume of systolic contraction. At end–ejection, the aortic valve closes followed by isovolumic relaxation, as left ventricular pressure falls while volume remains constant. When pressure falls sufficiently, the mitral valve opens and left ventricular diastolic filling begins (figure 1).

Thus, the three major determinants of the left ventricular forward stroke volume/performance are the preload (venous return and end–diastolic volume), myocardial contractility (the force generated at any given end–diastolic volume), and the afterload (aortic impedance and wall stress) [1].

       

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Literature review current through: Aug 2014. | This topic last updated: Aug 19, 2014.
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