It is helpful in myocardial ischemia. It decreases mortality rate by reducing ventricular arrhythmia.
Mechanism of action:
It acts on both β1 and β2 adrenoceptors i.e. cause their blockage.
It has both negative inotropic and chronotropic effect resulting in the decrease of cardiac output.
It also decreases SA and AV nodal activity.
It shows promising effects in angina by decreasing cardiac output, work load on the heart and oxygen consumption of the heart muscles at rest and in physical activity.
In the first instance, it produces anti-hypertensive effects by reduced cardiac output associated with bradycardia. And its long term use inhibits renin secretion, which results in reduced peripheral resistance leading to anti-hypertensive effects.
Due to β2-blockade, it causes an elevated airway resistance.
It causes an increased sodium retention.
Its effects are due to β-adrenoceptor blockade but also due to a direct membrane effect. It
1. Suppresses SA nodal firing
2. Reduces automaticity in purkinje fibers
3. A substantial promotion in effective refractory period of AV node
1. Chronic form of angina pectoris
2. prophylaxis of myocardial infarction and migraine
It is used for:
1. Atrial flutter or fibrillation
2. Sudden outburst of supraventricular tachycardia
3. Ventricular arrhythmias due to:
a. increased adrenergic activation
b. Toxicity caused by digitalis
Sedation, depression, cardiac failure, nausea, vomiting, bronchconstriction, diarrhea, rashes, fever, impaired metabolism (Due to reduced glycogenolysis and glucagon secretion caused by β-blockade)