Cardiac Activation.

Control of cardiac performance and output

Cardiac Performance

The interrelations among influences on ventricular end-diastolic volume (EDV)

through stretching of the myocardium and the contractile state of the myocardium. Levels of ventricular EDV associated with filling pressures that result in dyspnea and pulmonary edema are shown on the abscissa. Levels of ventricular performance required when the subject is at rest, while walking, and during maximal activity are designated on the ordinate. The broken lines are the descending limbs of the ventricular-performance curves, which are rarely seen during life but show the level of ventricular performance if end-diastolic volume could be elevated to very high levels. For further explanation, see text.

Ventricular Afterload

Interactions in the intact circulation of preload, contractility, and afterload in producing SV.

Stroke volume combined with heart rate determines cardiac output, which, when combined with peripheral vascular resistance, determines arterial pressure for tissue perfusion. The characteristics of the arterial system also contribute to afterload, an increase of which reduces stroke volume. The interaction of these components with carotid and aortic arch baroreceptors provides a feedback mechanism to higher medullary and vasomotor cardiac centers and to higher levels in the central nervous system to affect a modulating influence on heart rate, peripheral vascular resistance, venous return, and contractility.

Assessment of Cardiac Function

The responses of the left ventricle to increased afterload, increased preload, and increased and reduced contractility are shown in the pressure-volume plane.

Left. Effects of increases in preload and afterload on the pressure-volume loop. Since there has been no change in contractility, ESPVR (the end-systolic pressure volume relation) is unchanged. With an increase in afterload, stroke volume falls (1 -> 2); with an increase in preload, stroke volume rises (1-> 3).

Right. With increased myocardial contractility and constant LV end-diastolic volume, the ESPVR moves to the left of the normal line (lower end-systolic volume at any end-systolic pressure) and stroke volume rises (1 -> 3). With reduced myocardial contractility, the ESPVR moves to the right; end-systolic volume is increased and stroke volume falls (1 -> 2).

Mechanisms that cause diastolic dysfunction reflected in the pressure-volume relation.

The bottom half of the pressure-volume loop is depicted. Solid lines represent normal subjects; broken lines represent patients with diastolic dysfunction.