Please write a lengthy paragraph that includes answers to this question(all part
ID: 3523656 • Letter: P
Question
Please write a lengthy paragraph that includes answers to this question(all parts answered please):
3. A patient with congestive heart failure is suffering from poor cardiac output. Her ejection fraction is 40%. As a result, her organs are poorly perfused with oxygenated blood and she tires easily.
a. What is ejection fraction, how is it calculated, and how does her ejection fraction compare to that of a normal, healthy heart?
b. Cardiac output may be improved by increasing the strength of ventricular contractility. Explain how contractility could be increased in cardiac muscle cells. Focus on how muscle fibers produce tension and how that tension can be increased during muscle contraction. (Hint: Ca2+ ions are important here).
Explanation / Answer
Ejection fraction is the percentage of blood that pumped out from ventricles by each contraction of the heart. It is generally calculated using echocardiography. By echocardiography end diastolic (EDV) and end systolic volume (ESV) of the heart is calculated then stroke volume(SV) is calculated by subtracting ESD from EDV( ie EVV - ESV = SV). The ejection fraction(%) is calculated as ( SV / EDV ) X 100.
Thus one patient has 60 ml SV and 120 ml EDV, his/her ejection fraction is 50%. The normal reference range of ejection fraction is from 55% to 75%. So her heart can pump out only 40% of her end diastolic volume which is insufficient to meet her total body oxygen demands.
To understand that cardiac contractility which can improve the cardiac output and thus the ejection fraction can be improved, we need to understand the mechanism of cardiac muscle contraction. Here we go. Pacemaker impulse activates the T tubule in the cardiac muscle. Ca++ enter the cells via T tubule activate ryanodine receptor 2 in the sarcoplasmic reticulum in the cardiac muscle. This activation of the ryanodine receptor cause release of Ca++ from the sarcoplasmic reticulum. There is increase int eh cytoplasmic Ca++ inside the cardiac muscle cells. This Ca++ activate myosin chain and thereby sliding of myosin on actin cause the contraction in cardiac muscle. Now, this mechanism is started when the concentration of cytoplasmic Ca++ is above the threshold. So any medicine which can maintain that concentration of Ca++ above the threshold, contractility of cardiac muscle could be increased. Like digoxin which blocks the Na+K+ pump of the heart muscle. As a result of this block, Na+ cannot go out of the cell. Increase in the Na inside the cell, this, in turn, increase the Ca++ entry into the cardiac cell by Na+ Ca++ exchanger channel of cardiac muscle cells. Ca++ enters cell and Na go out of the cell via Na Ca Exchanger. an increment in intracellular Ca++. Increased cardiac contractility.