In HF patients , SV is lesser compared to normal individuals.
In HF patients , EF is much more compared to normal individuals.
Anemia is not related to HF.
None of the mentioned is correct
None of the mentioned.
Increase the preload & decrease the afterload
Decrease the preload & increase the afterload.
Increase the preload & afterload
Decrease the preload & the afterload
Ca+2\due to excessive beta activation
Ca+2\due to excessive beta inhibition
K+\due to excessive beta activation
K+\due to excessive beta inhibition
Prolonged beta activation decreases caspases
Down regulation takes place after increased sympathetic stimulation
Vagal activity is increased in order to compensate HF
All of the mentioned .
Most of Digoxin is metabolized and excreted by the kidneys
Glycosides are widely distributed to tissues.
Digoxin has a narrow therapeutic window
By decreasing cardiac remodelling
By increasing Heart rate
By increasing renin release
By activating NE
Decreases intracellular Ca+2
Increases cardiac contractility
Digoxin works by blocking voltage-sensitive calcium channels
Digoxin is used for rhythm control in patients with atrial fibrillation
Digoxin increases conduction velocity through the AV node
Digoxin levels of 1 to 2ng\ml are desirable in the treatment of atrial fibrillation
عشان ماتنسوها :P
Here's an interesting quiz for you.