Published Dec 9, 2014
mooshgigila
39 Posts
This is more pharmacology than anything, and may not impact my patient care. But I'm curious and hoping that finding the answer will help me understand meds more.
I understand that Digoxin is used for heart failure because it increases contractility. It also causes anorexia as a side effects because it stimulates the sympathetic nervous system.
I also understand that Carvedilol and other beta-blockers improve the mortality and morbidity for patients with HF because they block the effects that the sympathetic and catecholamine release have on the body.
How does this work? Why does one med that stimulates the sympathetic nervous system work, and the other that blocks it works as well?
Esme12, ASN, BSN, RN
20,908 Posts
HI!
Thread moved for best response
icuRNmaggie, BSN, RN
1,970 Posts
HR X SV=CO
heartrate X stroke volume = cardiac output
Dig is a parasympathetic drug which lowers the heartrate by lowering the sinoatrial firing rate. Dig increases filling time, and improves coronary perfusion and contractility and CO. With the improvement in Cardiac output, the compensatory sympathetic stimulation actually decreases.
In CHF, cardioselective beta blockers decrease circulating vasoconstrictors such as norepi, renin and endothelin snd may reduce the production of inflammatory cytokines that worsen HF.
Beta blockers decrease left ventricular remodeling, improve oxygen supply, decrease PVCs, decrease the risk of sudden cardiac death and afib and have been shown to decrease mortality, improve excercise tolerance and slow the progrssion of heart failure and can improve the EF over several months time.
These meds are givne in conjuction with a diuretic to reduce preload. Does that make sense?