Problem
A. How safe is it to stop giving carvedilol to a heart failure patient? Might the medication at any point be eased off? When you suddenly stop taking carvedilol, what are the effects and dangers? In heart failure patients, what, if any, causes the discontinuation of carvedilol?
B. When it comes to treating cardiac failure, what are the benefits and drawbacks of furosemide?
C. Can furosemide be administered once daily in heart failure?
D. What are the clinical signs and symptoms of a Valsalva's sinus rupture?
E. Does a dose of 2.5-10 g/kg/min of dobutamine cause significant tachycardia?
F. Are beta-blockers recommended for heart failure? If so, in all cases or just a few?
G. For what reason does long haul treatment by digitalis cause gynaecomastia?
H. Why are arrhythmias caused by toxic doses of digoxin, which decrease cardiac tissue's excitability, but not by therapeutic doses, which increase cardiac tissue's excitability?
I. One of the side effects of digitalis is hypokalemia. In treatment we give K . How does the hyperkalaemia improve the digitalis harmfulness?
J. Why should serum potassium be measured before digoxin treatment?
K. Loop diuretics like furosemide can be given intravenously to quickly reduce pulmonary oedema. Is this because arteriolar vasodilatation, which reduces afterload independently of its diuretic effect, is to blame? I ask this because I have been informed that this medication has a venodilatatory effect rather than an effect on arterioles (with the exception of efferent arterioles in the kidney). What might have led to such divergent opinions?