Abstract
Afterload of the left ventricle (LV) is defined as ventricular wall stress while ejecting LV stroke volume (SV). When the afterload increases at a given level of myocardial contractility or preload, SV decreases, reaching zero level (afterload mismatch). Then the treatment of afterload mismatch is an important framework during cardiovascular anesthesia. Normally, an effective arterial elastance (Ea) to end-systolic elastance (Ees) ratio (Ea/Ees) is maintained at an optimal level of 0.5 to 1. Relief of afterload mismatch by vasodilator is the mainstay during hemodynamic management of patients with severely depressed myocardial systolic function, such as in dilated cardiomyopathy.
In the current understanding of the pathophysiology of chronic heart failure (HF), HF with LV diastolic dysfunction is increasingly compared to HF with systolic dysfunction. Vasodilator therapy for HF will still be controversial. In patients with diastolic dysfunction, myocardial contractility could be preserved, and ino-dilator (e.g. phosphodiesterase III inhibitor) possibly worsens myocardial function.
Afterload mismatch is a conceptual framework for the assessment of LV function ; however, in our clinical understanding, the increase in afterload will be sure to cause hemodynamic instability or myocardial dysfunction. Mismatch between afterload and myocardial contractility, and between preload should be modulated within this framework.
