Geert Kleinnibbelink

General Introduction and Outline of Thesis 17 1 Afterload is defined as ventricular wall stress during ventricular ejection which is proportional to the mean pressure that the ventricle must develop to eject blood during systole. The LV and RV need to generate the pressure to overcome the vascular resistance in the respective circulations. For the systemic circulation this is the mean arterial pressure (MAP) and for the pulmonary circulation the mean pulmonary arterial pressure (mPAP). Both are proportionate with vascular resistance and cardiac output. In general, any decrease (e.g. vasodilation) or increase (e.g. vasoconstriction) in vascular resistance will lead to a lower or higher afterload, respectively. A higher afterload will lead to a lower SV (due to an increase in ESV) and a lower afterload will lead to a higher SV (due to a decrease in ESV). Contractility refers to the ability of the myocardium to contract. The more forceful the contraction, the smaller ESV and the greater the SV. Less forceful contractions result in smaller SVs and larger ESVs. Where the pulmonary circulation is a low-pressure system, the systemic circulation is a high-pressure system. As these circumstances (i.e. afterload) differ in both circulations, it’s understandable that the RV and LV behave functionally different as is outlined in Figure 3B . As is demonstrated, during the cardiac cycle the pressure variation in the RV is much lower, whereas both ventricles have the same SV. The above described haemodynamic differences results in different function between both ventricles to generate the same CO. During exercise, CO can increase 4- to 5-fold up to 20-30 L/min. When exercise performed under demanding conditions, a temporary reduction in cardiac function post-exercise lasting for hours to days has been observed. 13-19 This transient decline in cardiac function is typically referred to as exercise-induced cardiac fatigue (EICF). Several hypotheses = =