60 Questions
Which β-adrenergic blocker is mentioned as having intrinsic sympathomimetic activity (ISA)?
Acebutolol
What is the cardiac effect of high doses of β-adrenergic blockers with intrinsic sympathomimetic activity (ISA)?
Tachycardia and hypertension
What contributes to the cardiac depressant effects of propranolol?
Membrane depressant effect
Which β-adrenergic blocker is mentioned as causing prolongation of the QT interval?
Sotalol
What is the most commonly reported sign of β-adrenergic blocker poisoning?
Bradycardia
What can worsen the prognosis in case of β-adrenergic blocker poisoning?
Chronic obstructive pulmonary disease (COPD)
What is a potential complication of therapeutic use of sotalol?
Torsades de pointes
Why is blood drug level determination alone unreliable for assessing possible overdose of β-adrenergic blockers?
Clinical symptoms persist beyond the drug’s half life
What electrographic changes are associated with β-adrenergic blocker poisoning?
Prolonged PR interval, absence of P waves
What effect does an overdose of β-adrenergic blockers have on myocardial contractility?
Diminished contractility
What is the primary reason for the toxicity of β-adrenergic antagonists?
Their ability to competitively antagonize the action of catecholamines at cardiac β-adrenergic receptors
What is the main purpose of using β-adrenergic blockers in medical treatment?
Treatment of hypertension, arrhythmia, angina, glaucoma, and migraine prophylaxis
How do the pharmacologic and pharmacokinetic differences among β-adrenergic blockers affect their use?
Influence their therapeutic applications, incidence of side effects, and type and severity of toxic reactions
What is the most common use of β-adrenergic blockers?
Treatment of hypertension
What is the main mechanism of action of β-adrenergic antagonists leading to toxicity?
Competitively antagonizing the action of catecholamines at cardiac β-adrenergic receptors
What is the impact of the pharmacologic and pharmacokinetic differences among β-adrenergic blockers on their side effects?
Influence the incidence of side effects
What role do β-adrenergic blockers play in the treatment of angina?
They are used for the treatment of angina
What is the most significant influence of the pharmacologic and pharmacokinetic differences among β-adrenergic blockers?
Their influence on therapeutic applications
What is the primary effect of β-adrenergic blockers on the incidence of side effects?
They influence the incidence of side effects
What is the primary reason for using β-adrenergic blockers in the treatment of arrhythmia?
Their ability to regulate heart rhythm
Which symptom is characteristic of propranolol poisoning?
Seizures
What is the recommended treatment for bradycardia in β-adrenergic blocker poisoning?
Atropine
What is the potential risk of orogastric lavage in β-adrenergic blocker poisoning?
Vagal stimulation
Which medication is preferred to be introduced first in β-adrenergic blocker overdose?
Glucagon
What is the potential effect of activated charcoal in β-adrenergic blocker poisoning?
Worsening bradycardia
What is the characteristic cardiac change in β-adrenergic blocker poisoning?
Prolonged QRS interval
Which medication may be considered in β-adrenergic antagonist overdose if other treatments fail?
Phosphodiesterase inhibitors
What is the potential effect of orogastric lavage in β-adrenergic blocker poisoning?
Vagal stimulation
What is the potential risk of giving glucose in β-adrenergic blocker poisoning?
Hyperglycemia
What is the potential risk of whole bowel irrigation with polyethylene glycol in β-adrenergic blocker poisoning?
Worsening bradycardia
What is the primary reason for the toxicity of β-adrenergic antagonists?
Competitive antagonism of catecholamines at cardiac β-adrenergic receptors
What is the most common use of β-adrenergic blockers?
Hypertension
What contributes to the cardiac depressant effects of propranolol?
Competitive antagonism of acetylcholine at cardiac muscarinic receptors
What electrographic changes are associated with β-adrenergic blocker poisoning?
Prolongation of the QT interval
What is the primary effect of β-adrenergic blockers on the incidence of side effects?
Reduction
What is the potential risk of giving glucose in β-adrenergic blocker poisoning?
Exacerbation of hypoglycemia
What is the potential effect of orogastric lavage in β-adrenergic blocker poisoning?
Reduction of drug absorption
What is the potential risk of whole bowel irrigation with polyethylene glycol in β-adrenergic blocker poisoning?
Exacerbation of drug absorption
What is the recommended treatment for bradycardia in β-adrenergic blocker poisoning?
Atropine
What is the potential effect of activated charcoal in β-adrenergic blocker poisoning?
Reduction of drug absorption
What electrographic changes are associated with β-adrenergic blocker poisoning?
Prolonged PR interval, widened QRS complex, absence of P waves, prolonged QT interval
What contributes to the cardiac depressant effects of propranolol?
Membrane depressant effect
What is the potential complication of therapeutic use of sotalol?
Torsades de pointes & ventricular dysrhythmias
What is the impact of the pharmacologic and pharmacokinetic differences among β-adrenergic blockers on their side effects?
It influences the incidence and severity of side effects
What is the most significant influence of the pharmacologic and pharmacokinetic differences among β-adrenergic blockers?
Their CNS effects
What is the primary reason for using β-adrenergic blockers in the treatment of arrhythmia?
To reduce heart rate and contractility
What is the potential risk of giving glucose in β-adrenergic blocker poisoning?
It may worsen hypoglycemia
What is the potential risk of whole bowel irrigation with polyethylene glycol in β-adrenergic blocker poisoning?
It may cause fluid overload
What is the potential risk of orogastric lavage in β-adrenergic blocker poisoning?
It may cause aspiration pneumonia
What is the most commonly reported sign of β-adrenergic blocker poisoning?
Bradycardia
Which of the following is a characteristic of propranolol poisoning?
Bradycardia and impaired AV conduction
What is the recommended management for sustained release β-adrenergic blocker poisoning?
Whole bowel irrigation with polyethylene glycol
What is the primary effect of glucagon in the treatment of β-adrenergic antagonist overdose?
Positive inotropic and chronotropic activity
In the management of bradycardia in β-adrenergic blocker poisoning, what is the next step if the patient fails to respond to atropine and fluids?
Use of inotropes
What is the potential complication of orogastric lavage in β-adrenergic blocker poisoning?
Vagal stimulation leading to bradycardia
Which medication may be considered if glucagon and inotropes fail in the management of β-adrenergic antagonist overdose?
Phosphodiesterase inhibitors
What is the cardiac effect of high doses of β-adrenergic blockers with intrinsic sympathomimetic activity (ISA)?
Prolonged QT interval
What is the potential risk of activated charcoal administration in β-adrenergic blocker poisoning?
Worsening of hypotension
What is the primary reason for giving glucose in the management of β-adrenergic blocker poisoning?
To counteract hypoglycemia
What is the potential effect of orogastric lavage in β-adrenergic blocker poisoning?
Worsening of bradycardia
Study Notes
Management of β-Adrenergic Blocker Poisoning
- Cardiac changes in β-adrenergic blocker poisonings are not uniformly reported and occur most frequently with drugs that have membrane stabilizing action.
- Propranolol possesses the most membrane stabilizing activity in its class and its poisoning is characterized by coma, seizures, hypotension, bradycardia, impaired AV conduction, and prolonged QRS interval.
- Ventricular tachydysrhythmias may also occur in β-adrenergic blocker poisoning.
- Management of poisoning includes maintaining airway ventilation, giving atropine before laryngoscopy, orogastric lavage, and activated charcoal administration.
- Orogastric lavage causes vagal stimulation and carries the risk of worsening bradycardia, so it is reasonable to pretreat patients with atropine.
- Activated charcoal can be given repeatedly during the first 24 hours and whole bowel irrigation with polyethylene glycol should be considered for sustained release preparations.
- Other areas of management include giving glucose for hypoglycemia, diazepam for convulsions, and monitoring potassium levels.
- In the treatment of bradycardia, atropine may be given if the patient is compromised hemodynamically and the hypotensive patient may respond to fluids in the absence of pulmonary edema.
- Patients who fail to respond to atropine and fluids require management with inotropes.
- When time permits, it is preferable to introduce medications sequentially, starting with glucagon followed by calcium, high dose insulin euglycemia therapy, a catecholamine, and if this fails, phosphodiesterase inhibitors.
- Glucagon produces positive inotropic and chronotropic activity and improves AV conduction.
- The phosphodiesterase inhibitors inamrinone and milrinone are theoretically beneficial in β-adrenergic antagonist overdose, and hemoperfusion and hemodialysis may be considered in cases involving nadolol and atenolol.
Management of β-Adrenergic Blocker Poisoning
- Cardiac changes in β-adrenergic blocker poisonings are not uniformly reported and occur most frequently with drugs that have membrane stabilizing action.
- Propranolol possesses the most membrane stabilizing activity in its class and its poisoning is characterized by coma, seizures, hypotension, bradycardia, impaired AV conduction, and prolonged QRS interval.
- Ventricular tachydysrhythmias may also occur in β-adrenergic blocker poisoning.
- Management of poisoning includes maintaining airway ventilation, giving atropine before laryngoscopy, orogastric lavage, and activated charcoal administration.
- Orogastric lavage causes vagal stimulation and carries the risk of worsening bradycardia, so it is reasonable to pretreat patients with atropine.
- Activated charcoal can be given repeatedly during the first 24 hours and whole bowel irrigation with polyethylene glycol should be considered for sustained release preparations.
- Other areas of management include giving glucose for hypoglycemia, diazepam for convulsions, and monitoring potassium levels.
- In the treatment of bradycardia, atropine may be given if the patient is compromised hemodynamically and the hypotensive patient may respond to fluids in the absence of pulmonary edema.
- Patients who fail to respond to atropine and fluids require management with inotropes.
- When time permits, it is preferable to introduce medications sequentially, starting with glucagon followed by calcium, high dose insulin euglycemia therapy, a catecholamine, and if this fails, phosphodiesterase inhibitors.
- Glucagon produces positive inotropic and chronotropic activity and improves AV conduction.
- The phosphodiesterase inhibitors inamrinone and milrinone are theoretically beneficial in β-adrenergic antagonist overdose, and hemoperfusion and hemodialysis may be considered in cases involving nadolol and atenolol.
Test your knowledge of the management of β-adrenergic blocker poisoning with this quiz. Explore the cardiac changes, treatment options, and key considerations for managing this type of poisoning.
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