Beta Blockers Case Study

Beta adrenergic receptor antagonists (Beta Blockers)
For several years, CHF treatment involved drugs with sympathomimetic properties. This was based on the belief that heart failure is fundamentally a disorder of reduced stroke volume and cardiac output. Long-term use of sympathomimetics was expected to improve clinical outcomes based on relief obtained from short term use of dopamine and dobutamine. Under this model, the use of beta adrenergic receptor antagonists was believed to be counterintuitive; however, the reverse appears to be the case in the clinical settings. Chronic sympathomimetic use is associated with increased mortality rates and there is considerable evidence from several placebo controlled randomized clinical trials that beta-blockers
Initiation of a beta-blockers at usual doses in patients with heart failure patients can potentially lead to symptomatic worsening or acute decompensation due to theirits negative inotropic effects. Therefore beta-blockers should be initiated at very low doses followed by gradual increments in dose. Patients should be carefully monitored for changes in vital signs and symptoms during this increment period. Planned upward titration in the dose of a beta blocker should be delayed until any untoward effects observed with lower doses have disappeared in these patients. Even when symptoms do not improve with beta blockers, long-term treatment needs to be maintained to minimize the risk of major clinical events. The initial and maximum doses of these agents are mentioned in the table below (1ACC). Efforts should be made to reach the target dose shown to be effective in major clinical trials with these
Patients presenting with fluid retention or worsening symptoms generally respond favourably to intensification of conventional therapy and once treated they remain excellent candidates for long term treatment with beta blockers. Bradycardia produced by beta blockers is generally asymptomatic and requires no intervention; however, if it is accompanied by dizziness or light headedness or if second- or third-degree heart block occurs, reduction in the dose of beta blocker is warranted. Risk of hypotension may be minimized by taking beta blocker and ACE inhibitor at different times during the day. Hypotensive symptoms may also respond to a decrease in the dose of diuretics in volume depleted patients. The symptom of fatigue is multifactorial and may be related to other causes such as sleepas sleep apnea, excessive diuresis, or