Cardiogenic Shock Research Paper

mediators, causing increasing capillary permeability and widespread fluid shift into the interstitial space, which was no longer functioning to maintain vascular volume (known as third spacing) in addition, causing further vasodilation to occur.

Systolic heart failure is characterized by enlarged ventricles that are unable to fully contract to pump enough blood into circulation to adequately perfuse tissues. The enlargement in ventricles is due to an increased end-systolic volume. If the heart is not able to sufficiently pump the expected volume of blood with each contraction, which in a normal healthy heart is 50-60%, there will be a residual volume left in the heart after every pump (Heart Healthy Women, 2012). With the next period of filling, the heart will receive the same amount of blood volume from the atria combined with that residual volume from the previous contraction. This causes the ventricles to have to dilate to accommodate this increase in volume. The dilation causes the walls of the ventricles to stretch and become thin and weak. Also the myocardium, the muscle layer of the heart, will stretch and not be able to adequately make a full and forceful enough contraction to push blood from the ventricles (Lehne, 2010).

* Vaso-constriction – the blood vessels narrow, taking blood away from areas of the body, ie skin

Deacreased vascular resistance and increased arterial pressure causes an increase in blood flow. This is important to supply organs with oxygen. 4. Restate your predictions that were correct and give data from your experiment that support them. Restate your predictions that were not correct and correct them with supporting data from your experiment. MAP would increase due to increase in activity, SVR would decrease due to decrease in resistance, CO would increase due to more force of blood being expelled.

flow changes, and even a condition called cardiomyopathy. The pancreas can also be effected by

This causes the ventricles to dilate in order to maintain adequate stroke volume. Usually, this will improve over the next 7-10 days.

In systolic ventricular dysfunction or systolic heart failure the heart is not able to produce enough output for adequate tissue perfusion. Heart rate and stroke volume produce cardiac output. Contractility, preload, and afterload influence the heart’s stroke volume. These factors are important in understanding the pathophysiologic consequences of this syndrome and possible treatments. Patients with systolic heart failure usually have dilated, large ventricles and impaired systolic function.

Stroke volume is the amount of blood pumped out of the heart during each contraction measured in mL/beat. A long term effect of exercise on stroke volume is that it will increase. As the left ventricle grows in size, more blood can be filtered in and out.

*Both sides of the heart are doing this at the same exact time and contracting/relaxing is what pumps the blood from one place to the other.

The increased resistance of blood flow through the pulmonary semilunar valve from the right ventricle backs up the pressure of blood

Stroke volume is the amount of blood pumped out of the heart and into the body from the left ventricle during each contraction and is measured in millilitres per beat. When the heart is resting stroke volume is at a normal pace. When the heart rate starts to increase stroke volume has to become faster and pump more blood out of the heart

When the ventricles are contracting at a rate greater than one hundred beats per minute, the heart becomes inefficient. Blood cannot properly fill the ventricular chambers before it is forced out. This decreases the amount of oxygenated blood circulating through the body.

In a sweeping fashion, the right atrium contracts and forces the final volume of blood into the right ventricle. The left atrium contracts and contributes the final 20% of volume to the left ventricle.

Arteriolar vascular constriction, heart rate increases, and renal retention of sodium and water all help to regulate cardial output. Ventricular dilatation is commonly seen. A large amount of ventricular myocardium is lost, contractility may be greatly compromised, and cardiogenic shock may ensue.

reports the amount of force exerted by the blood into the arteries during ventricular contraction.