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.

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.

it decreases blood volume and preload

afterload

Afterload.

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.

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.

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 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.

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.

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

The clinical term for loss of blood (also known as low blood volume) is hopovolemia. Hypovolemia is a dangerous condition and can result in hypovolemic shock and eventually, death. From a first aid standpoint, it is vital that any external bleeding is controlled, and the patient treated for hypovolemic shock.

Possible signs and symptoms of blood loss include the following:

- Obvious signs of open trauma

- Weakness, dizziness and lethargy

- Signs of hypovolemic shock

- Pain

- Fainting

- Nausea and vomiting

- Patient may know that he/she is bleeding

- Visual detection by first aider

- Detection through the Primary Haemorrhage Check (primary survey/blood check)

It is important any serious bleeding be evaluated by a medical professional urgently. If in doubt about the severity of the condition, call an ambulance or seek urgent medical aid.

Cardiac ischemia occurs when there is reduced blood flow to the coronary arteries This usually occurs due to the formation of a plaque in the coronary artery resulting in the interior of the artery become narrowing and hence reduced blood flow to the heart. The blood contains oxygen so the heart receives less oxygen. Angina or chest pain will occur as a symptom of myocardial ischemia.

Coronary blood flow is determined by the heart's oxygen demand. Nitric oxide can be released from healthy endothelium cells to result in vasodilation and increased blood flow. However, endothelium cells which are damaged by plagues will release fewer nitric oxide. The presence of plagues in blood vessels hence results in less vasodilation in its area.

Nifedipine is a dihydropyridine. It can treat cardiac ischemia by acting as a vasodilator through the inhibition L-type voltage-sensitive calcium channels of smooth muscles. More blood will hence flow to the heart and meet its oxygen demands. It doesn't slow down cardiac conduction so it has no anti-arrthymic action. Although nifedipine has a negative inotropic effect, it is overshadowed by a reflex increase in heart rate and decreased afterload so it can ultimately improve blood flow to the heart.

Factors that can increase stroke volume include increased preload (end diastolic volume), increased contractility of the heart muscle, decreased afterload (resistance to ejection of blood), and a higher heart rate. Adequate hydration, regular exercise, and a healthy diet can also support optimal stroke volume.

Two liter blood loss would be close to half the volume of an adult human. It'd be a life-threatening situation and the victim would be severely anemic, probably unconscious. If not you can expect paleness, weak pulse, and very low blood pressure.

Heart rate and blood pressure are intimately related. Nerves and hormones constantly monitor and balance the heart rate and blood pressure.