Search results
Results from the WOW.Com Content Network
To sum up, cardiac preload is related to the heart’s volume of blood returns from the venous returns; afterload is related heart’s pressure that needs to eject the blood out of the heart into the rest of the body, and the contractility is related to heart’s ability to squeeze blood out of ventricles.
Nitroglycerin and Morphine are often given to bring down the preload and afterload; these two drugs, having a direct effect on the preload and afterload, are commonly given to clients with acute myocardial infarction.
Preload, in addition to afterload and contractility, is one of the 3 main factors that directly influence stroke volume (SV), the amount of blood pumped out of the heart in 1 cardiac cycle.
As such afterload can be related to the amount of systemic resistance the ventricles must overcome to eject blood into the vasculature. Afterload is proportionate to systemic blood pressures and is inversely related to stroke volume, unlike preload and contractility.
Contractile function describes the ability of the myocardium, in a given hemodynamic state (at certain preload and afterload conditions). This is synonymous with systolic function and can be estimated by echocardiography.
The systolic performance of the heart is determined by 3 factors: preload, afterload, and contractility. The direct relationship between preload and cardiac output was formulated in the early 1900s based on the work of Otto Frank and Ernest Starling. It led to the well-known Frank-Starling curves.
The three primary factors to consider are preload, or the stretch on the ventricles prior to contraction; the contractility, or the force or strength of the contraction itself; and afterload, the force the ventricles must generate to pump blood against the resistance in the vessels.
As preload increases, contractility increases and, therefore, stroke volume (SV) increases. If more blood fills the LV during diastole, the LV will pump harder because it has more blood to eject during systole.
Contractility is the change in peak isometric force (isovolumic pressure) at a given initial fibre length (end diastolic volume). Physiological determinants of contractility include: Preload: Increasing preload increases the force of contraction
Afterload = left ventricular wall tension required to overcome resistance to ejection (impedance to ejection of blood from the heart into the arterial circulation). Contractility = the change in force generated independent of preload; synonymous with inotropy