Back pressure exterted by arterial blood
Afterload.
When a person has hypertension, the ventricles will hypertrophy, which makes the chambers larger. Afterload is directly related to the chamber size, and contraction velocity is inversely related to afterload. Contraction velocity is a measure of contractility. So, as chambers hypertrophy, contactility decreases.
Preload refers to the degree of stretch of cardiac muscle cells before contraction. These muscles exhibit a length-tension relationship. When the cardiac muscle cells are at rest, they are shorter than their optimal length. The most important factor affecting the stretching of cardiac muscles is the venous return, that is, the amount of blood returning back to the heart. Slow heartbeat and exercise can increase the venous return. This will lead to the stretching of the ventricles and it will hence increase the contraction force.As reflected by the Frank-Starling Law, the stroke volume increases with the end diastolic volume. The greater filling volume will lead to the heart to stretch more and this will increase its force of contraction.
Heart rate and blood pressure are intimately related. Nerves and hormones constantly monitor and balance the heart rate and blood pressure.
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Yes
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.
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
The resistance against which the ventricle contracts is know as afterload.
Yes, stroke volume is inversely proportional to afterload. An increase in afterload, such as from increased vascular resistance, can lead to a decrease in stroke volume due to the additional pressure the heart has to work against to eject blood. Conversely, decreasing afterload can help increase stroke volume.
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.
Afterload
Increased vasoconstriction leads to an increase in afterload, which is the resistance the heart must overcome to eject blood from the left ventricle. As a result, the heart has to work harder to pump blood against the increased resistance, which can lead to increased myocardial oxygen demand and potentially contribute to the development of heart failure over time.
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.
Afterload of the heart is when there is tension or stress that is placed on the wall of the left ventricle when blood is being pushed out of the heart. This can cause too much blood to build up in the heart at any given time. Preload of the heart is when there is tension or stress placed on the right ventricle of the heart when blood is taken into the heart. This can mean that not enough blood is being pumped into the heart as needed. The effects of preload of the heart can lead to poor circulation and lower blood pressure.
afterload