Epinephrine and cardiac output
Common Questions and Answers about Epinephrine and cardiac output
epipen
The difference of normal cardiac output has a variation of about 34%. Therefore. just based on cardiac output variation the PAP can vary by 34%.
I have read your doctor's report (what you provide) to you, and there is not any opinion that is not in keeping with a good analysis and evaluation. I think you may be reading information that is confusing, however, if you don't trust your doctor's evaluation then see another doctor.
QUOTE:"by PikaPika88, 3 hours ago
A doctor works at the country side told me..... MI won't affect the blood pressure. Many MI patient remain in normal range of blood pressure. She didn't mention about the heart rate (pulse)."
How can it not effect vital signs? There has to be a misunderstanding!
The system compensates when there is low cardiac output. MI damages heart cells and impedes left ventricle contractions. Impeded left ventricle reduces cardiac output. ....
I was a patient with heart failure and hospitalized for several days. The discharge from the hospital provided written instruction saying weigh yourself every morning and if there is a few pounds gained over night to contact the doctor as that could indicate being in heart failure mode and fluids were backing up into the lungs and/or peripheral locations... the heart would not be strong enough to output the amount of blood received from the lungs. .
t ever heard of an increase of the EF when pulse rate increases. Cardiac output (CO) is increased and that metric is the total amount of blood pumped into circulation based on heart rate for one minute. A pacemaker would control the heart rate.
QUOTE: "My GP told me to cut the Atenolol in half and gave me an RX for Enalapril Maleate 5mg daily. He said hopefully the Enalapril would dilate the output artery(my words?) and increase EF and blood flow thus reducing fatigue".
If MVP is serious such as to reduce the cardiac output, the cardiac output is reduced, the heart will over compensate with an enlarged heart. An enlarged heart can effect the electrical pathways and that with RBBB can cause ventrical tachycardia.
"People who have a heart attack and develop a bundle branch block have a higher chance of complications and death than do people who have heart attacks and don't develop a bundle branch block.
The contribution of the heart to the regulation of blood pressure is through changes in cardiac output. Cardiac output is defined as the product of heart rate and stroke volume.
Either can be modified by climatic forces. The heart rate component is regulated by the autonomic nervous system, so its level of activity depends on the intensity of the stimulus at the time.
I recently had a right heart cath due to continuing symptoms of shortness of breath, chest pain on exertion, cold/tingly hands, swelling in ankles, fatigue (especially on stairs), "foggy" thinking episodes, pounding heartbeat at times. The results were a bit confusing to me and the doc didn't discuss much of it over the phone. All I have are a limited set of the test results as follows: PA Pressure - 88.9; Cardiac Output - 16.2; SBP - 150.
Extreme fatigue is a condition that exists. I have been told by my cardiologist and cardiac surgeon that these conditions should not exist related to my valve regurgitations. I also have been diagnosed with Fibromyalgia and a peripheal (sp?) sensory neuropathy.
Should I be seeking a second opinion?
Thank you.
My experience for heart failure was normal blood pressure and a heart rate sustained at 115 bpm. The higher heart rate is to increase the cardiac output (amount of blood pumped/per minute). The increase is due to a failure of the heart to meet the system's demand for oxygenated blood with normal heart rate, and the increase of the heart rate is compensation for a low volume per heartbeat.
Also the cardiac output may be inadequate, hence the breathlessness. For relief from your symptoms the blood flow and the cardiac output need to be improved. I would suggest to limit your walking, keep high risk factors like hypertension and diabetes under control and discuss the treatment options with your doctor.
Hope this helped and do keep us posted.
Eventually reduced cardiac output causes the left side of the heart to enlarge to compensate for the reduced cardiac output, and the left ventricle will begin to lose its contractility and as a consequence the systole EF will decrease.(Frank/Starling phenomonon).
By and large, diastolic dysfunction is chronic process. When this chronic condition is well tolerated by an individual, no specific treatment may be indicated.
almost always damaged left ventricle heart cells will impair left ventricle contractions and cardiac output will be reduced with each stroke. However, your 55% EF (55-75% normal) indicates very little if any impairment.
If cardiac output is reduced, you can have shortness of breath, muscle fatigue, and possibly angina (pain) due to ischemia (lack of blood low). Your doctor may want to rule pericarditis (inflamation of the area surrounding the heart) and that can cause pain.
Blood pressure = cardiac output x blood vessel resistance.
Blood vessel resistance depends (roughly) on constriction of the arteries, and muscle tone in the arteries. When your arteries contract / constrict (like you feel when you are anxious and your hands are ice cold) you increase your systolic and diastolic pressure. If the muscles in the blood vessels are tense, like during exercise, the blood vessels are behaving like pipes instead of soft hoses that bulge with the pulse.
If the heart size is reduced (reverse remodeling) contractions (stroke) would/could be stronger. A stronger heartbeat should/would increase the cardiac output and require fewer heartbeats given the same demand. It can be seen in an equation where cardiac output is stroke (amt of blood pumped with each heartbeat) times the number heartbeats in a 60 second interval...increased stroke fewer heartbeats, a decrease in stroke (weak heart) more heartbeats to meet the same demand.
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