All are true about staing of b-Blocker therapy in a case of CHF except aEUR'
They should be staed with optimal dose Beta blocker therapy represents a major advance in the treatment of patients with depressed ejection fraction. - Although the negative inotropic effect of beta blocker resulted in their contraindication in left ventricular dysfunction until very recently, there is now evidence that, not only are they tolerated, but they greatly improves prognosis. How does blockade of fi receptors help in hea failure?? Left ventricular dysfunction results in neurohormonal activation (renin angiotensin aldosterone system, sympathetic system, cytokine release) which, although beneficial in acute cases is reponsible for gradual deterioration in myocardial function. For instance , in response to decrease in cardiac output, an increase in circulating norepinephrine (NE) can be seen which acts on the sympathetic myocardial receptors paicularly beta-1 thus increasing tnyocardial contractility. In addition, by stimulating peripheral alpha receptor, NE induces peripheral vasoconstriction, which helps to maintain blood pressure - This effect is counter balanced by peripheral *to-2 stimulation and consequent vasodilation. Prolonged exposure of hea to alpha and beta receptor stimulation unfounately, promotes left ventricular modelling, cell death due to necrosis or apoptosis and water/ salt retention. 8 blockers interfere with the harmful effect of sustained activation of the adrenergic nervous system by competitively antagonizing one or more adrenergic receptors. When given along with ACE inhibitors beta blockers reverse the process of RV remodelling, improve patient symptoms, prevents hospitalisation and prolongs life. Therefore II blockers are indicated for patients with symptomatic or asymptomatic HF and depressed Ejection Fraction < 40%. There are three beta blockers that have been shown to be effective in reducing the risk of death in patients with chronic HE : - Bisoprolol - Metoprolol - Carvedilol Current recommendation are to consider the addition of fl blockers in the case of patients presenting with functional class II or Ill congestive hea failure if caused by systolic function. Dose of 13eta blockers First of all, treatment should be staed at extremely low doses:? - This dosage should be maintained for at least two to .four weeks and is increased only if the patient has tolerated it well. - if the patient does not tolerate the increased dosage the medication should not be considered a failure and treatment should be maintained at the tolerated dose. - The dose of beta blocker should he increased, until, the dose, used are similar to those that have been repoed to be effective in clinical trials. Administering ,8 blockers may lead to worsening fluid retention consequent to the withdrawl of adrenergic suppo to the hea and the circulation. - Thus it is impoant to optimize the dose of diuretic before staing therapy with beta blockers. - The increased, fluid retention can usually be managed by increasing the dose of diuretics. Beta blockers in NYHA class IV :? Since most of the clinical trials of Beta blocking agents have been conducted in patients with hea failure NYHA .functional class 11/ HI, until recently, there was limited information regarding safety and efficacy of Beta blockers in patients with hea failure NYHA functional class IV. Carvedilol prospective Randomized cumulative survival (COPER- NICUS) - The COPERNICUS TRIAL was designed as multicentric multinational trial in patients with severe hea failure randomized to Carvedilol vs Placebo. -The result of COPERNICUS demonstrates that even in patients with advanced hea .failure, Carvedilol exes a beneficial effect.
They should be staed with optimal doses
They should be gradually increased over weeks
Special precautions should be taken in cases of NYHA class III and IV
Carvedilol and Metoprolol are the preferred drugs