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Old 11-17-2011
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Heart Query regarding use of beta betablocker in CHF

In first aid its mentioned that beta blocker is used in CHF, in CHF the cardiac output is inadequate to meet the perfusion of tissue, but if administer beta blocker the cardiac out will further decrease as it will block beta 1 receptors 2, beta 1 receptor increase renin, contractility, heart rate, , giving beta blocker means heart rate will decrease in turn it will decrease the stroke volume thus in nut shell cardiac output ...........then why the hell beta blocker in CHF?
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Old 11-17-2011
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Hey Chakram! I think one important point is that u should never use Beta blockers in decompensated HF. But when the patient has adequate medications and is an compensated stage, u can benefit from Betablocker cause the reduce the activation of RAAS and as well reduce oxygen deman in Myocard. So i guess all your assumptions are right but they count more for a decompensated state, where it is contraindicated to use them. Hope it helps!
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Old 11-17-2011
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Just wanted to add something else: Even if a RAAS activation is good for the short term condition, it is contraproductive for CHF. It causes fluid overload, and thus increases the effort for the Myocard. And aldosteron causes remodeling which is also negative for the heart... etc etc
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Old 11-17-2011
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Default thnx,but stll baffld buddy

Quote:
Originally Posted by Glomerulus View Post
Hey Chakram! I think one important point is that u should never use Beta blockers in decompensated HF. But when the patient has adequate medications and is an compensated stage, u can benefit from Betablocker cause the reduce the activation of RAAS and as well reduce oxygen deman in Myocard. So i guess all your assumptions are right but they count more for a decompensated state, where it is contraindicated to use them. Hope it helps!
thnx buddy but ,when the oxygen demnd of heart will decrease , but howz that supposed to improve cardiac output???????????
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Old 11-17-2011
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Default cant get it ,

Quote:
Originally Posted by Glomerulus View Post
Just wanted to add something else: Even if a RAAS activation is good for the short term condition, it is contraproductive for CHF. It causes fluid overload, and thus increases the effort for the Myocard. And aldosteron causes remodeling which is also negative for the heart... etc etc
stll baffled , further what does "remodelling " imply 2 nd howz it negatv fr the heart
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Old 11-17-2011
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It doesnt improve cardiac output. They have conducted several studies with different substances and the drugs used in CHF are ACE-inh. or AT 1 Blockers, Beta blockers and diuretics when indicated. Positive inotropic substances (as digoxin) might improve life quality in acute HF but has no effect on mortality. Other inotropic substance are not used anymore since studies showed the actually increase mortality. So main goal for CHF is lower oxygen demand, deactivate RAAS which is bad cause remodeling and fluid overload, beta blocker . Thats what I learnt... Hope it helps!
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Old 11-17-2011
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Quote:
Originally Posted by CHAKRAM View Post
stll baffled , further what does "remodelling " imply 2 nd howz it negatv fr the heart
The thing is our RAAS system helps us on a short term when we dont have enough volume (eg hypovolemic shock). So it helps the body increasing sympathicus tone thus causing vasoconstriciton and centralisation. Additionally aldosteron and angiotensin are augmented meaning there is water and salt retention. Now in CHF the heart doesnt supply the body with enough blood/oxygen. The reaction is the same as in hypovolemic shock, our body activates RAAS which is good so tissue is supplied with O2 and whatever in needs. Problem is on a long term it is negative for a patient with CHF:
1.) Patient is overload with fluid. Causes edema in the periphery and in the lungs (due to increase hydrostatic pressure). This again activates the RAAS cause even if there is too much water in the body, the plasma volume is decreased.
2.) Studies have shown that aldosteron causes negative remodeling to the heart. With fibrosis etc. This furthermore decreases cardiac capacity and make the heart more fragile for exemple to arrhythmias.

Does this answer your question? I am not sure if I am really helping you.. maybe I dont understand what u exactly mean. Hope it helps!
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