They are not inherently either. They can be good if they are used properly. For example, because diuretics increase urine output and decrease blood volume, if someone with high blood pressure takes some prescribed diuretics they can decrease their blood volume and thus their blood pressure. This can be very beneficial. However, if someone already has a blood pressure that is too low, possibly after they have been bleeding out, then taking diuretics would further decrease their BP and this could result in insufficient blood flow to the brain resulting in syncope, brain damage, or death
loop diuretics loop diuretics The Potassium sparing kind. IE. Hydrochlorothiazide with triamterene or "Dyazide."
The connection between diuretics and hyperglycemia involves intracellular K+ levels. Intracellular K+ is involved in the secretion of a lot of hormones...including insulin. Some diuretics cause hypokalemia, (decrease in K+). This inhibits insulin secretion and can lead to hyperglycemia. It's not really a problem unless the patient is pre-diabetic. In that case, it is significant enough to push them over to diabetes. Hope this helped!
Yes they do! Diuretics are an antihypertensive drug and they cause xerostomia, diuretics increase urine output not increase saliva production.
Loop diuretics work by restraining the sodium-potassium-chloride cotransporter. Thiazide diuretics restrain the sodium-chloride transporter. Carbonic anhydrase inhibiting diuretics work by restraining bicarbonate transport.
Afterload
It decreases preload and afterload as a result of the dilation in the venous and arterial vasculature from the nitric oxide.
afterload
Morphine decrease cathecolamines therefore decreases afterload.
the strength of the contraction. The ability of the heart to contract independtely of preload and afterload.
Preload, afterload, and cardiac contractility or inotropy.
increase preload
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.
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.
When a person has hypertension, the ventricles will hypertrophy, which makes the chambers larger. Afterload is directly related to the chamber size, and contraction velocity is inversely related to afterload. Contraction velocity is a measure of contractility. So, as chambers hypertrophy, contactility decreases.
Severe dehydration will decrease preload because there won't be as much volume coming into the heart.
Afterload refers to the pressure that the ventricles must overcome in order to eject blood. Hypertension increases the afterload, causing the end systolic volume to increase. The stroke volume will hence decrease.