FAQ - cardiac output, high
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what isdifference between low and high cardiac output hypotensions?

The arterial pressure (or our blood pressure ) is determined by cardiac output, venous pressure and systemic vascular resistance ( the muscle tone of the peripheral blood vessels ). When any of the following is reduced, hypotension can occur. Cardiac output is just one of the factors here.

When the heart is diseased, the hypotension is most probably caused by low cardiac output. Meaning, the heart cannot pump out a good volume of blood to the other systems.

In other instances when there is a good cardiac output in a good functioning heart, but the blood vessels in the extremities are dilated, the blood pressure might still be low. This is a clear example of a high cardiac output hypotension.  (+ info)

High cardiac output?

I am only looking for the medical term to describe a symptom to an illness.
It is the word to describe cardiac force which is too high.

Palpitations is not a good word since it can describe arrythmias awareness, such as ectopic beats, tachycardia and so on.
Hypertension is not a good word since this usually is for describing artrial hypertension, it does not usually give reference to cardiac contraction force.
Cardiac output is no good because cardiac contraction force is one aspect of cardiac output, heart rate being the other.

If you excluding the names of conditions such as angina, cardiac hypertrophy and so on; I am trying to find the medical term to only describe the symptom of elevated cardiac contraction force.

Have any ideas?

There really isn't another name for it- Increased Cardiac Output is how it is referred to. Try the link below.

http://www.answers.com/topic/cardiac-output-2  (+ info)

does cardiac output and peripheral resistance increase or decrease when a person has chronic high blood ..?


confused. reference would be nice. explanation needed!

BLOOD PRESSURE = PVR multiplied by CARDIAC OUTPUT. So therefore when you have high blood pressure this means either your peripheral vascular resistance or your cardiac output has increased  (+ info)

Where can I find more information on cardiac output and pre-eclampsia?

I am trying to find any research that is available for public consumption on the relationship between high cardiac output and pre-eclampsia. We will be monitored for cardiac output when we conceive but I would like to know what it entails, what the possible outcomes could be, etc.

You will find everything you need at the following website:
http://www.preeclampsia.org/  (+ info)

How is blood flow and cardiac output in aortic aneurysm?

I think you have turbulent blood flow in aortic aneurymsms therefore high bp. But I don't get the blood pressure thing.
If they have high blood pressure, is blood flow to the body and organs good? Or do they have ischemia?

With high blood pressure this can be a sign of shock. The turbulent blood flow won't cause this. Shock being if this has ruptured. The high blood pressure could be the cause of the aneurysm secondary to an under lying cause.  (+ info)

Cardiac output?

Can anyone explains what is cardiac output and how cardiac output depends on factors.

This is a pretty complex question, but I'll try to keep the answer somewhat straightforward. Cardiac output is the volume of blood being pumped by the heart, in particular by a ventricle in a minute. The primary function of the heart is to impart energy to blood in order to generate and sustain an arterial blood pressure necessary to provide adequate perfusion of organs. The heart achieves this by contracting its muscular walls around a closed chamber to generate sufficient pressure to propel blood from the cardiac chamber (e.g., left ventricle), through the aortic valve and into the aorta.

Each time the heart beats, a volume of blood is ejected. This stroke volume (SV), times the number of beats per minute (heart rate, HR), equals the cardiac output (CO).

Some important terms to know in discussion of cardiac output:

Circulatory System: The circulatory system consists of the heart, the blood vessels, (arteries, arterioles, and blood) and its purpose is to carry oxygen and nutrients to tissues in the body, and to carry away the byproducts of metabolism.

Contractility: Contractility is the intrinsic ability of cardiac muscle to develop force for a given muscle length. It is also referred to as inotropism.

Preload: Preload is the muscle length prior to contractility, and it is dependent of ventricular filling (or end diastolic volume.) This value is related to right atrial pressure. The most important determining factor for preload is venous return.

Afterload: Afterload is the tension (or the arterial pressure) against which the ventricle must contract. If arterial pressure increases, afterload also increases. Afterload for the left ventricle is determined by aortic pressure, afterload for the right ventricle is determined by pulmonary artery pressure.

Determinants of Cardiac Performance:

When we discuss ventricular dysfunction, it is most often in reference to the left ventricle, however it is important to understand that the same basic principles apply to the right ventricle. The left and right sides of the heart exist in a series, and are therefore interdependent; in normal physiology, the right and left ventricle will have the same output. There are 2 main determinants in cardiac performance:

1. Heart Rate (HR)

Heart rate is directly proportional to cardiac output; an adult HR is normally 80-100 beats per minute (bpm.) Heart rate is an intrinsic factor if the SA (pacemaker) node in the heart, and it is modified by autonomic, humoral, and local factors. For example:

An increase in vagal activity via M2 cholinergic receptors in the heart will decrease the heart rate.
An increase in sympathetic activity via B1 and B2 adrenergic receptors throughout the heart will increase the heart rate.

2. Stroke Volume (SV)

Stroke Volume is determined by three factors: preload, afterload, and contractility. The preload gives the volume of blood that the ventricle has available to pump, as well as the end diastolic length of the muscle. The contractility is the force that the muscle can create at the given length, and the afterload is the arterial pressure against which the muscle will contract. These factors establish the volume of blood pumped with each heart beat. Valvular dysfunction and ventricular geometric form can also affect stroke volume, depending on the pathology of the valves or the ventricle.  (+ info)

What is the relation of hypertension and risk for decrease cardiac output?

I am doing my nursing care plan and I can't get the relation of hypertension and risk for cardiac output.

i'm not sure the exact form of the curve, but more hypertension there's more risk of low cardiac uotput.-
increasing the blood pressure increases the pressure the heart has to overpower to bomb the blood.-
there's a range where the compensatory mecanisms of the heart (frank-satrling and those) can mantain the output, but after they stop working the output start to decrease.-
hope you got this, i'm not very good with explanations.-
:)  (+ info)

How do you calculate this cardiac output equation?

Mrs. Jones has a heart rate of 85, a systolic pressure of 140 and diastolic pressure of 60, and an end diastolic volume of 110 and end systolic volume of 40. What is her cardiac output? Please help. Thanks

CO = Stroke volume x Heart rate
stroke volume = EDV - ESV
therefore 70 * 85
CO= 5950 ml/min  (+ info)

what is the connection between cardiac output and blood pressure?

If someone has decreased cardiac output, does that mean they have hypertension? Or hypoptension?

When your heart works hard, your blood pressure goes up. Your heart can be working hard because of exercise, clogged arteries, ageing, eating too much salt and lots of other things. When your heart doesn't have to work hard, your blood pressure is lower (but within a healthy range, never too low for a healthy heart). Things like dehydration, blood loss, tachycardia and other things can cause (too) low blood pressure.  (+ info)

How can decreased cardiac output be caused by increased fluid volume AND decreased fluid volume?

Why would a patient in renal failure have decreased cardiac output?

Check out starlings law.

Of course decreased fluid volume can decrease CO, but once fluid volume increases too much, the heart "stretches" too much and therefore contractility is affected. The heart muscle is sensitive to stretch- it's kinda like goldie locks and the three bears. Too little fluid= low CO, too much fluid= low CO (because the heart muscle is stretched so much that it can't squeeze effectively), just the right amount of fluid= perfect CO!  (+ info)

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