beta-blocker question

Dinith88 · Apr 14, 2009

Hi everyone, i just started nursing school and have some silly questions on the treatment modalities of CHF. How does Beta-blockers work? Yeah, seriously (i'm a newbie). I know when beta-1 receptors are blocked, it not only has negative chronotropic and dromotropic effects on the heart, but also has a negative inotropic result. In a patient with systolic heart failure (heart rate
I know coreg is proven to reduce mortality in CHF patients, but how? Is it because it reduces oxygen demand of the heart? And my last question (I promise): why are some CHF patients on digoxin (+ inotropic) while others are on beta-blockers (- inotropic)?
i'm a little bit confused, any insight would help!

Good Question!

OK my quick answer is:

Used to be everyone with a Dx of CHF got Dig. Not true anymore. Treatment of CHF with dig (these days) is individualized. This is mostly because there is evidence that dig has no long-term effect on mortality...BUT is useful in certain patients (mostly with Systolic heart-failure...patients with diastolic heart-failure arent afforded any benefit from dig) Probably best to look at the individual patient...do they have a Hx of a-fib/atrial-tachy-rhythm problems, systolic-vs-diastolic CHF, etc.?

And, you ask good questions about beta-blockers and their potential effect on reducing cardiac output...and the old-school cardiology thought was just that. They weren't prescribed for everyone with CHF but rather reserved for HTN, tachy-arrhythmias, etc.. BUT.. now, there is a wealth of evidence that beta-blockers do reduce mortality/morbidity in CHF (as you mentioned) and can help slow it's progression. This mechanism is mostly a matter of reducing/delaying myocardial remodeling, reducing myocardial O2 demand, etc.

So...your next assignment is to learn the difference between systolic and diastolic heart failure...

allnurses Guide · Apr 15, 2009

Beta blockers also act on B1 receptors in kidneys, which reduces renin release and avoids some of the cardio-renal syndrome - which is also be a contributor to CHF morbidity/mortality (vasoconstriction leads to increased afterload, more oxygen demand etc etc).

Agree re systolic -v- diastolic HF etiologies and choice of drugs. For example, HCM, the cardiac muscle is large and stiff and cannot fill - beta blockers reduce HR to permit more diastolic filling time, which in turn permits better stretch on the ventricle and better output (Frank-Starling's Law)