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What decreases cardiac output without change in heart rate PAWP or SVR Is it preload afterload or 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.
What else can I help you with?
In a healthy individual which of the following would be low Contractility Preload Stroke volume or Afterload.?
afterload
What is myocardial 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.
Does diuretics decrease preload or afterload?
it decreases blood volume and preload
What effect does Sodium Nitroprusside have on afterload and preload?
It decreases preload and afterload as a result of the dilation in the venous and arterial vasculature from the nitric oxide.
How can stroke volume can be altered?
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.
What are the factors that affects the cardiac cycle?
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.
Does preload influence cardiac contractility?
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.
Dose morphine increase or decrease afterload?
Morphine decrease cathecolamines therefore decreases afterload.
What factors regulat stroke volume?
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.
What are 3 important factors affecting stroke volume?
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
Do angiotensin II blockers affect preload or afterload?
Afterload
Does decreased peripheral resistance increase cardiac output?
Decreased peripheral resistance can increase cardiac output, yes, but it is not necessarily a 1 to 1 relationship. Cardiac output is a complex mechanism - cardiac output depends on stroke volume and heart rate. Heart rate is easy to understand, but stroke volume is a little trickier. Stroke volume depends on three things: contractility of the cardiac muscle, preload - or the filling of the heart, and afterload. Contractility is partially determined by preload, how healthy the cardiac muscle is, and the effects of circulating bioamines, such as epinephrine, norepinephrine, dopamine, as well a any medications being taken that may affect contractility, such as beta blockers. Increased contractility causes a harder "squeeze," increasing the stroke volume on a beat by beat basis. Infarction of a portion of the wall decreases the amount of cardiac muscle present, decreasing the ability to contract, but also decreasing the ability to fill the ventricle, since scar tissue does not stretch like healthy muscle. Excessive hypertrophy (such as that caused by prolonged hypertension or hypertrophic cardiomyopathy), while helpful to a point in increasing contractility, will eventually impede filling of the ventricle by preventing the "stretch" before contraction and decrease the cardiac output. Preload is basically how filled the ventricle is before it contracts. Decreased filling, obviously, decreases the stroke volume, thereby decreasing the cardiac output. The cardiac myocyte works best when slightly overstretched. This optimally apposes the actin and myosin myofilaments and produces the best power for contraction, which is the purpose of the atrial contraction - it provides just that little bit of extra fill before the AV valves close and optimizes the preload on the heart. Too much preload, however, is bad, as the myofibrils can be overstretched and then are less effective. This is all nicely explained by the Starling curve. Afterload is basically what you asked about. It is partially determined by peripheral vascular resistance, but other factors interact as well. You have to remember that the vascular system is not a rigid tube, it is a living thing. As such, other obstacles can, and do, occur. For instance, aortic sclerosis is the most common cause of heart murmur in adults. The narrowing of the aortic valve and its impedence to blood flow increases the afterload on the heart, thereby decreasing the stroke volume. Septal hypertrophy, as seen in hypertrophic cardiomyopathy, can cause an intermittent occlusion or partial occlusion of the aortic outflow tract, increasing afterload, especially during high flow states and high heart rates.
