vasodilation, anemia, cirrhosis, shock states (results in massive vasodilation)
A change in cardiac output without any change in the heart rate, pulmonary artery wedge pressure (PAWP = equated to preload) or systemic vascular resistance (SVR = afterload) would have to be due to a change in the contractility of the heart. Cardiac output (CO) is roughly equal to stroke volume x heart rate. Stroke volume is related to preload, contractility, and afterload. As you can see, the only variables you have not controlled for is cardiac contractility.
Cardiac contractility is the force of contraction possible for any given length of the cardiac muscle. It is related to the intracellular calcium levels.
Afterload
Phenylephrine is an alpha agonist, which produces peripheral arteriolar constriction, thereby increasing afterload and causing reflex bradycardia in most cases.
afterload
The aorta and the pulmonary arteries provide right and left ventricular afterload. Afterload is the resistance the blood loaded into the heart when it tries to leave.
Morphine decrease cathecolamines therefore decreases afterload.
Reduces the work load and increases cardiac output
It decreases preload and afterload as a result of the dilation in the venous and arterial vasculature from the nitric oxide.
Venous return controls EDV (end diastolic volume) and thus stroke volume and cardiac output. Venous return is dependent on: - blood volume and venous pressure - vasoconstriction caused by the sympathetic nervous system - skeletal muscle pumps - pressure drop during inhalation
Afterload is the tension or stress developed in the wall of theleft ventricleduring ejection. In other words, it is the endLoadagainst which the heart contracts to eject blood.
Afterload