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.
The cardiac cycle is influenced by several factors, including heart rate, preload, afterload, and contractility. Heart rate determines the frequency of cycles, while preload refers to the volume of blood in the ventricles at the end of diastole, affecting stroke volume. Afterload is the resistance the heart must overcome to eject blood, and contractility reflects the strength of the heart's contractions. Additionally, autonomic nervous system activity and hormonal influences can also modulate these factors, impacting the overall efficiency of the cardiac cycle.
The strength of force of each heartbeat is referred to as cardiac contractility. It is a measure of the heart's ability to contract and pump blood efficiently. Factors such as heart rate, volume of blood, and hormones can influence cardiac contractility.
afterload
Stroke volume is primarily regulated by three factors: preload, afterload, and contractility. Preload refers to the degree of stretch of the cardiac muscle fibers before contraction, influenced by venous return. Afterload is the resistance the heart must overcome to eject blood, primarily determined by arterial pressure and vascular resistance. Contractility refers to the intrinsic strength of the heart muscle's contraction, which can be affected by factors such as sympathetic stimulation and the availability of calcium.
Norepinephrine
Stroke volume is determined by three factors, altering any of them can change the stroke volume. These factors are preload, afterload, and contractility. The relationship is: SV = P*C/A What this means is that preload and contractility are directly proportional to the stroke volume and afterload is inversely proportional to stroke volume. If you increase preload (within certain limits), stroke volume will increase according to the Starling curve. Increasing contractility (many things can increase this), makes the heart pump harder and increases stroke volume. Increasing afterload decreases stroke volume. All of these can be reversed (decreasing preload and contractility = decreased stroke volume, etc). Get a good physiology book and it will explain all of this very well.
cardiac output
Yes - an increase in contractility would lead to an increase in stroke volume. An increased stroke volume would cause an increased cardiac output.
it is the amount of blood available for the heart to pump when the ventricles contract
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