**14. Beta-blockers poisoning**

Beta adrenergic antagonists (beta blockers) are groups of medications which have been used in treatment of different cardiovascular, neurological and ophthalmological diseases more than 30 years, Bête blockers toxicity has significant morbidity and mortality [17].

#### **14.1. Mechanism of action**

Beta receptors are divided by location and action to beta 1, beta 2, and beta 3 (see the **Table 3**).

There are two groups of beta-blockers: selective and non-selective.

Competitive antagonism of the beta receptor decreases cellular levels of cyclic adenosine monophosphate (cAMP). Beta-1 selective blocker causing in depressed myocardial contractility,


**Table 3.** Beta receptor: Locations and actions.

decreased automaticity in pacemaker cells, and decreased conduction through the AV node. Non- selective beta blockade results in systemic effects including bronchoconstriction, impaired gluconeogenesis and decreased insulin release. Same Beta blockers (e.g., propranolol) have high lipid solubility leading to rapid cross of the blood brain barrier into the central nervous system, causing a neurological manifestation such as seizures and delirium [45, 47].

#### **14.2. Clinical features**

The major system affected by β-blocker toxicity is the cardiovascular system; patients present with bradycardia and hypotensive. The cause of bradycardia is sinus node suppression or conduction abnormalities but ingestion of β-blockers with partial agonist activity may cause hypertension and tachycardia as early presentation. The β-blockers with sodium channel block affect may cause a wide-complex bradycardia.

Sotalol causes potassium channels block leading to prolonging the QT interval.

Β-Blockers also have effect on CNS and pulmonary system. Neurologic features include delirium, coma and seizures with more lipophilic. Β-blockers (propranolol) have more neurological manifestations. Bronchospasm and hypoglycaemia can be in β-blockers toxicity [47, 48].

### **14.3. Treatment**

**Location Action Antagonism**

General supportive care is an Initial step in treatment of digoxin toxicity; it includes securing airway and adequate ventilation and boluses of fluid IV in case of hypotension. Activated charcoal helps in early acute ingestion [42], Atropine can be given in case of Symptomatic bradycardia). Digoxin-specific antibody fragments (digoxin-Fab) are antidotes for digoxin. The indication to use (digoxin- Fab) includes Life-threatening dysrhythmias unresponsive to standard therapy and hyperkalaemia excess 6 mEq/L. [43] Digoxin-Fab doses are based on the total-body load of digoxin, which can be calculated from either the estimated dose ingested or the serum digoxin level, each vial of Digoxin-Fab reverses approximately 0.5 mg of ingested digoxin. If the amount of ingested digitalis is unknown, digoxin Fab 10 vials for adults empirically can be given. Hyperkalaemia is treated with insulin, dextrose, sodium bicarbonate. The use of calcium salts in digoxin induced hyperkalaemia is controversial because old literature

> Decreases inotropy Decreases chronotropy Inhibits renin release

Causes bronchospasm Inhibits glycogenolysis and

Minimal vasoconstriction

gluconeogenesis

Inhibits lipolysis Inhibits thermogenesis

Increases inotropy Increases chronotropy Stimulates renin release

shows increase incidence of ventricular dysrhythmias and increase mortality [44].

than 30 years, Bête blockers toxicity has significant morbidity and mortality [17].

There are two groups of beta-blockers: selective and non-selective.

Beta adrenergic antagonists (beta blockers) are groups of medications which have been used in treatment of different cardiovascular, neurological and ophthalmological diseases more

Beta receptors are divided by location and action to beta 1, beta 2, and beta 3 (see the **Table 3**).

Competitive antagonism of the beta receptor decreases cellular levels of cyclic adenosine monophosphate (cAMP). Beta-1 selective blocker causing in depressed myocardial contractility,

> bronchodilation Relaxes uterus

gluconeogenesis Vasodilation

Stimulates lipolysis Stimulates thermogenesis

Increases force of contraction Stimulates glycogenolysis and

B1 Myocardium Kidney Eye

**13.5. Treatment**

262 Essentials of Accident and Emergency Medicine

B2 Bronchial smooth muscle Skeletal muscle

**14. Beta-blockers poisoning**

**14.1. Mechanism of action**

Skeletal muscle

**Table 3.** Beta receptor: Locations and actions.

Liver Vascular

B3 Adipose tissue

GI decontamination can be done by giving Activated charcoal within 1 h of ingestion and air way is the main aim treatment in beta-blocker toxicity focusing on restore perfusion to critical organ systems by increasing cardiac output by: fluid resuscitation and glucagon (3–10 mg), vasopressor (e.g., epinephrine) and high dose Insulin- glucose (insulin 1 unit/kg IV bolus). Intravenous lipid emulsion therapy may be used in case of sever toxicity and refractory to treatment. In case of refractory to pharmacologic therapy, haemodialysis, haemoperfusion, cardiac pacing, placement of intra-aortic balloon pumps can be used. Wide QRS-interval dysrhythmias due to sodium channel blockade treated with sodium bicarbonate 2–3 mEq/kg over 1–2 min [49, 50].
