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.
Decreased afterload occurs when the resistance the heart must overcome to eject blood is reduced. This can be caused by factors such as vasodilation, which decreases systemic vascular resistance, or conditions like sepsis that lead to widespread blood vessel dilation. Additionally, medications such as ACE inhibitors or nitrates can also lower afterload by relaxing blood vessels. Ultimately, decreased afterload facilitates easier ventricular ejection, improving cardiac output.
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
Afterload
Phenylephrine is an alpha agonist, which produces peripheral arteriolar constriction, thereby increasing afterload and causing reflex bradycardia in most cases.
The systemic arteries provide afterload for the left ventricle, while the pulmonary arteries provide afterload for the right ventricle. Afterload refers to the resistance that the ventricles must overcome to eject blood during systole.
afterload
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.
The intra-aortic balloon pump inflates during diastole to increase coronary artery perfusion and cardiac output, and deflates during systole to reduce afterload on the heart.