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.
Afterload
It decreases preload and afterload as a result of the dilation in the venous and arterial vasculature from the nitric oxide.
it decreases blood volume and preload
afterload
Morphine decrease cathecolamines therefore decreases 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.
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.
Cardiac contractility is the force of contraction possible for any given length of the cardiac muscle. It is related to the intracellular calcium levels.
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.
John is about to preload his truck with logs.
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.
Preload is caused by decreased blood volume in ventricles. Therefore, decreased preload directly caused by bleeding, polyuria, dehydration.