Afterload

Afterload

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.

It decreases preload and afterload as a result of the dilation in the venous and arterial vasculature from the nitric oxide.

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.

Yes

Back pressure exterted by arterial blood

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.

ACE inhibitors primarily affect afterload by causing vasodilation, which reduces systemic vascular resistance. This action can lower blood pressure and decrease the workload on the heart. While they may have some indirect effects on preload by reducing fluid retention, their main impact is on afterload reduction.

it decreases blood volume and preload

afterload

Afterload.

If afterload increases, cardiac output may decrease, assuming other factors remain constant. This is because the heart has to work harder to eject blood against the higher resistance, potentially leading to reduced stroke volume. Over time, the heart may compensate through hypertrophy, but acute increases in afterload typically result in diminished cardiac performance.

The proper term for the resistance against which the heart must pump is "afterload." Afterload refers to the pressure in the arteries that the heart must overcome to eject blood during systole. It is influenced by factors such as arterial stiffness and systemic vascular resistance. High afterload can make it more difficult for the heart to pump effectively, potentially leading to heart failure.

vasodilation, anemia, cirrhosis, shock states (results in massive vasodilation)

The resistance against which the ventricle contracts is know as afterload.

I looked it up in Wikipedia and I think you're looking for afterload.

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.

Left-sided afterload is primarily measured using the systemic vascular resistance (SVR), which reflects the resistance the left ventricle must overcome to eject blood into the aorta. This can be calculated using the formula: SVR = (MAP - CVP) / CO, where MAP is the mean arterial pressure, CVP is the central venous pressure, and CO is the cardiac output. Additionally, techniques like echocardiography can assess left ventricular wall stress and other parameters related to afterload indirectly.

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.

Phenylephrine is an alpha agonist, which produces peripheral arteriolar constriction, thereby increasing afterload and causing reflex bradycardia in most cases.

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.

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.

Decreasing afterload refers to the reduction of the resistance that the heart must overcome to pump blood during systole. This can occur due to vasodilation or decreased vascular resistance, which makes it easier for the heart to eject blood. A lower afterload can improve cardiac output and reduce the workload on the heart, making it particularly beneficial in conditions like heart failure. This physiological change can enhance overall cardiovascular efficiency and support better perfusion of tissues.

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.

Cardiac contractility is the force of contraction possible for any given length of the cardiac muscle. It is related to the intracellular calcium levels.

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.

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.

Decreasing preload may be indicated in conditions like heart failure, where fluid overload is present, leading to symptoms like pulmonary congestion. In contrast, reducing afterload is often necessary in cases of hypertension or aortic stenosis, where high systemic vascular resistance can strain the heart. Clinical assessment, including blood pressure readings, heart function, and patient symptoms, guides these decisions. Ultimately, the goal is to optimize cardiac output and alleviate symptoms while considering the underlying condition.

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.

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

The pressure in the aorta that the left ventricle must pump blood against is called systemic arterial pressure. This pressure is necessary to ensure adequate blood flow to the tissues and organs of the body.

Dopamine vasoconstricts, so it increases the blood pressure in cardiogenic shock. Nitroprusside is a vasodilator, it decreases preload (left ventricular stretch) and afterload (resistance). They are used in combination in cardiogenic shock to achieve a good hemodynamic effect or "good balance" or adequate blood flow.

Yes, an increase in afterload (pressure the heart must pump against to eject blood) typically causes the heart to work harder to overcome this resistance, leading to increased cardiac workload. This can result in the heart needing to pump with more force to maintain adequate blood flow to the body.

1. Administer Oxygen

2. Decrease preload by getting patient to sit upright and dangle legs over side of bed, this decreased blood return to heart

3. Relieve anxiety, decreasing sympathetic drive.

4. Administer medication safely to reduce preload, afterload and contractility of the heart

5. Reduce movements of the patient, to decrease oxygen demands.

An increase in stroke volume can be due to factors such as increased cardiac contractility (force of heart contractions), decreased afterload (pressure the heart must overcome to eject blood), or increased preload (volume of blood returned to the heart). These factors can result in more blood being pumped out by the heart with each contraction, leading to an increased stroke volume.

The intra-aortic balloon pump (IABP) is timed to deflate just before systole, specifically at the onset of the R-wave on the ECG. This timing allows for optimal coronary perfusion by promoting diastolic blood flow during the heart's relaxation phase. The balloon inflates during diastole to increase blood flow to the coronary arteries and deflates before the heart contracts to reduce afterload. Proper timing is crucial for maximizing hemodynamic support.

A decrease in stroke volume can be caused by several factors, including reduced preload, which is the volume of blood returning to the heart; increased afterload, which is the resistance the heart must work against to pump blood; and impaired contractility, often due to conditions like heart disease or myocardial infarction. Additionally, factors such as dehydration, severe blood loss, or arrhythmias can also contribute to a diminished stroke volume. These changes can lead to inadequate blood flow and oxygen delivery to the body's tissues.

The intra-aortic balloon pump (IABP) should be deflated just before the onset of ventricular systole, specifically during the diastolic phase of the cardiac cycle. This timing allows for optimal augmentation of coronary artery perfusion and reduces afterload when the heart contracts. Proper timing enhances cardiac output and myocardial oxygen supply while minimizing the workload on the heart. Continuous monitoring of the patient's hemodynamic status is essential to ensure appropriate timing of balloon inflation and deflation.

Stroke volume is defined as the amount of blood ejected by the heart's left ventricle during each contraction. It is a key component of cardiac output, which is the total volume of blood pumped by the heart per minute. Stroke volume is influenced by factors such as heart muscle contractility, preload (the volume of blood in the ventricles at the end of diastole), and afterload (the resistance the heart must overcome to eject blood). Understanding stroke volume is essential for assessing heart function and overall cardiovascular health.

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.

Increasing end-diastolic volume (EDV) enhances stroke volume due to the Frank-Starling mechanism, where greater ventricular filling leads to stronger contractions. Higher end-systolic volume (ESV) can also increase stroke volume when it results from reduced afterload or increased contractility, allowing the heart to eject more blood with each beat. Thus, both EDV and ESV can influence stroke volume, primarily through changes in the heart's filling and pumping efficiency.

Intrinsic factors of cardiac output primarily include heart rate and stroke volume. Heart rate is influenced by the autonomic nervous system and hormonal regulation, while stroke volume is determined by factors such as preload (the degree of stretch of the heart muscle), afterload (the resistance the heart must work against), and contractility (the strength of heart muscle contractions). Together, these factors dictate the volume of blood the heart pumps per minute, which is crucial for maintaining adequate circulation and meeting the body's metabolic demands.

Cardiac output is regulated by several factors, primarily heart rate and stroke volume. The autonomic nervous system adjusts heart rate through sympathetic and parasympathetic influences, while stroke volume is influenced by factors such as preload (the volume of blood in the ventricles before contraction), afterload (the resistance the heart must overcome to eject blood), and contractility (the strength of heart muscle contractions). Hormones like adrenaline and factors such as blood volume and venous return also play critical roles in modulating cardiac output to meet the body's varying demands for oxygen and nutrients.

Cardiac output (CO) is determined by the heart rate (HR) and the volume of blood pumped by each beat (stroke volume - SV). Mathematically, cardiac output can be represented by the equation:

CO = HR x SV

As such, if total cardiac output falls as a result of decreased stroke volume, the heart rate can increase to keep the total cardiac output normal, to a certain extent.

Stroke volume is more complicated; it is determined by many different factors, including preload, afterload, competence of the atrioventricular valves, ventricular cavity size, and the strength of the squeeze of the cardiac muscle, amongst others. Any change in one of these factors requires a compensation in one or more of the others to maintain cardiac output.

Does blood pressure affect your heart rate?

Regular heart rate is 60-100.

Increase in heart rate within this normal range increases cardiac output and blood flow/volume; therefore, increases blood pressure. In healthy people, even with heart rate increase, there is not an important spike in blood pressure, because healthy vessels will dilate to accommodate more blood flow. The increase in blood pressure is usually small and doesn't pose risks.

Increased heart rate and cardiac output decreases blood pressure if heart rate is extremely high. When heart rate is high (out of normal range 60-100 beats per minute), there is no time for the heart to fill with blood (preload) resulting in low stroke volume; therefore, reduced blood pressure.

Remember, the heart spends more time in diastolic (preload time) than systolic (contraction of the heart). When heart rate is too high, this normal diastolic time is reduced which contribute to low stroke volume and low blood pressure.

stroke volume is affected by Preload, Afterload, and Contractility