Preload does not directly influence cardiac contractility, as they are distinct concepts. Preload refers to the degree of stretch of the cardiac muscle fibers at the end of diastole, which affects the volume of blood in the ventricles. While increased preload can enhance the force of contraction through the Frank-Starling mechanism, contractility itself is primarily influenced by factors such as sympathetic nervous system stimulation and circulating hormones. Thus, while preload can affect the overall cardiac output, it does so indirectly through its interaction with contractility.
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
Inotropes are medications that alter the force or energy of cardiac muscle contractions. Positive inotropes, such as dopamine and dobutamine, increase cardiac output by enhancing myocardial contractility, which can be beneficial in conditions like heart failure. Conversely, negative inotropes decrease contractility, potentially reducing cardiac output. The choice of inotrope depends on the clinical scenario and the underlying cardiac function.