68 Questions
Propranolol has a membrane depressant effect which contributes to its cardiac depressant effects
True
Most poisonings involve propranolol
False
High doses of β-adrenergic blockers with intrinsic sympathomimetic activity can cause tachycardia & hypertension
True
The high lipid solubility of certain β-adrenergic blockers, especially propranolol, accounts for the CNS effects
True
In overdose, pharmacokinetic parameters may change drastically due to decreased cardiac output with subsequently reduced hepatic & renal blood flow
True
Blood drug level determination alone is reliable for assessing possible overdose
False
The most commonly reported signs & symptoms of β adrenergic blocker poisoning are listed in (Table 2)
True
Certain disease states like chronic obstructive pulmonary disease (COPD) & congestive heart failure (CHF) can improve the prognosis of poisoning
False
An overdose of β-adrenergic blockers causes an increase in myocardial contractility
False
Electrographic changes consist of first degree AV block, widening of the QRS complex, absence of P waves, prolongation of the QT interval
True
Sotalol & acebutolol prolong the QT interval
True
The prolonged QT interval by sotalol predisposes to torsades de pointes & ventricular dysrhythmias
True
β-adrenergic blockers are used for the treatment of hypertension, arrhythmia, angina, glaucoma, and migraine prophylaxis.
True
β-adrenergic blockers have significant pharmacologic and pharmacokinetic differences.
True
The toxicity of β-adrenergic antagonists is primarily due to their ability to enhance the action of catecholamines at cardiac β-adrenergic receptors.
False
Pharmacokinetic differences do not influence the therapeutic applications, incidence of side effects, and type & severity of toxic reactions when β-adrenergic blockers are taken in overdose.
False
Bradycardia is not a symptom of propranolol poisoning.
False
Ventricular tachydysrhythmias may occur in β-adrenergic blocker poisoning.
True
Orogastric lavage carries the risk of worsening bradycardia.
True
Activated charcoal can only be given once within the first 24 hours of poisoning.
False
Whole bowel irrigation with polyethylene glycol is not recommended for sustained release preparations.
False
Glucagon may be given if the patient is compromised hemodynamically.
True
Phosphodiesterase inhibitors inamrinone and milrinone are not beneficial in β-adrenergic antagonist overdose.
False
Hemoperfusion and hemodialysis are not considered in cases involving nadolol and atenolol.
False
Management of poisoning includes giving atropine after laryngoscopy.
False
Inotropes are not required for patients who fail to respond to atropine and fluids.
False
It is preferable to introduce medications sequentially, starting with insulin euglycemia therapy followed by glucagon.
False
Phosphodiesterase inhibitors improve AV conduction in β-adrenergic antagonist overdose.
False
______ poisoning is characterized by coma, seizures, hypotension, bradycardia, impaired AV conduction, and prolonged QRS interval.
Propranolol
Ventricular tachydysrhythmias may also occur in β-adrenergic blocker ______.
poisoning
Activated ______ can be given repeatedly during the first 24 hours and whole bowel irrigation with polyethylene glycol should be considered for sustained release preparations.
charcoal
In the treatment of bradycardia, ______ may be given if the patient is compromised hemodynamically and the hypotensive patient may respond to fluids in the absence of pulmonary edema.
atropine
Patients who fail to respond to atropine and fluids require management with ______.
inotropes
______ produces positive inotropic and chronotropic activity and improves AV conduction.
Glucagon
The phosphodiesterase inhibitors inamrinone and milrinone are ______oretically beneficial in β-adrenergic antagonist overdose, and hemoperfusion and hemodialysis may be considered in cases involving nadolol and atenolol.
the
______ of β-Adrenergic Blocker Poisoning includes maintaining airway ventilation, giving atropine before laryngoscopy, orogastric lavage, and activated charcoal administration.
Management
______ areas of management include giving glucose for hypoglycemia, diazepam for convulsions, and monitoring potassium levels.
Other
When ______ 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.
time
الكاتيكوالمينات في المستقبالت األدرينالية بيتا القلبية A ______ depressant effect likely contributes to the cardiac depressant effects of propranolol.من المحتمل أن يساهم التأثير المثبط للغشاء في التأثيرات المثبطة للقلب للبروبرانولول
membrane
Most poisonings involve ______ معظم حاالت التسمم تنطوي على بروبرانولول
propranolol
High doses of β-adrenergic blockers with intrinsic sympathomimetic activity (ISA) (e.g., acebutolol & pindolol can cause ______ & hypertension ) (على سبيلISA( الجرعات العالية من حاصرات بيتا األدرينالية ذات النشاط الودي الداخلي
tachycardia
The high ______ solubility of certain β-adrenergic blockers, especially propranolol accounts for the CNS effects ، وخاصة البروبرانولول،إن القابلية العالية للذوبان في الدهون لبعض حاصرات بيتا األدرينالية.مسؤولة عن تأثيرات الجهاز العصبي المركزي
lipid
In overdose, pharmacokinetic parameters may change drastically due to decreased ______ output with subsequently reduced hepatic & renal blood flow قد تتغير معلمات الحركية الدوائية بشكل كبير بسبب،في حالة تناول جرعة زائدة انخفاض النتاج القلبي مع انخفاض تدفق الدم الكبدي والكلوي الح ًقا
cardiac
Blood drug level ______ alone is unreliable for assessing possible overdose because clinical symptoms might persist beyond the drug’s half life تحديد مستوى الدواء في الدم وحده ال يمكن االعتماد عليه لتقييم الجرعة الزائدة المحتملة ألن األعراض السريرية قد تستمر بعد نصف عمر الدواء
determination
Characteristics of poisoning The most commonly reported signs & symptoms of β adrenergic blocker poisoning are listed in (______) Certain disease states can worsen the prognosis. For example, in case of chronic obstructive pulmonary disease (COPD) & congestive heart failure (CHF) في، على سبيل المثال.بعض الحاالت المرضية يمكن أن تؤدي إلى تفاقم التشخيص )CHF( ) وقصور القلب االحتقانيCOPD( حالة مرض االنسداد الرئوي المزمن
Table 2
An overdose causes a ______ of myocardial contractility, producing bradycardia & severe hypotension leading to cardiogenic shock مما يؤدي إلى بطء القلب،تؤدي الجرعة الزائدة إلى انخفاض انقباض عضلة القلب وانخفاض ضغط الدم الشديد مما يؤدي إلى صدمة قلبية
diminution
Electrographic changes consist of first degree ______ block (prolonged PR interval), widening of the QRS complex, absence of P waves, prolongation of the QT interval ،) طويلPR من الدرجة األولى (فاصل______ تتكون التغييرات الكهربية من إحصار QT وإطالة فترة،P وغياب موجات،QRS واتساع مجمع
AV
______, & acebutolol prolong the QT interval The prolonged QT interval by sotalol predisposes to torsades de pointes & ventricular dysrhythmias may complicate the therapeutic use of sotalol قد تؤدي النقاط واضطراب النظم.
Sotalol
Certain disease states like chronic obstructive pulmonary disease (COPD) & congestive heart failure (CHF) can ______ the prognosis of poisoning
improve
Most poisonings involve ______
propranolol
______ produces positive inotropic and chronotropic activity and improves AV conduction
glucagon
The most commonly reported signs & symptoms of β adrenergic blocker poisoning are listed in (______)
Table 2
The high ______ solubility of certain β-adrenergic blockers, especially propranolol accounts for the CNS effects
lipid
β-adrenergic blockers are used for the treatment of hypertension, arrhythmia, angina, glaucoma, and migraine prophylaxis
In overdose, pharmacokinetic parameters may change drastically due to decreased ______ output with subsequently reduced hepatic & renal blood flow
cardiac
Toxicity of β adrenergic blockers Most of the toxicity of β adrenergic antagonists is because of their ability to competitively antagonize the action of catecholamines at cardiac β-adrenergic receptors
Activated ______ can be given repeatedly during the first 24 hours and whole bowel irrigation with polyethylene glycol should be considered for sustained release preparations
charcoal
______ areas of management include giving glucose for hypoglycemia, diazepam for convulsions, and monitoring potassium levels
Critical
Certain disease states like chronic obstructive pulmonary disease (COPD) & congestive heart failure (CHF) can ______ the prognosis of poisoning
worsen
Most of the toxicity of β adrenergic ______ is because of their ability to competitively antagonize the action of catecholamines at cardiac β-adrenergic receptors.
antagonists
Toxicity of β adrenergic ______ Most of the toxicity of β adrenergic antagonists is because of their ability to competitively antagonize the action of catecholamines at cardiac β-adrenergic receptors.
blockers
______ blockers are widely used for treatment of many disease states, including hypertension, arrhythmia, angina, glaucoma, & migraine prophylaxis.
Β-adrenergic
Applications
These differences influence their therapeutic applications, incidence of side effects, & type & severity of toxic reactions when taken in overdose.
Adrenergic
Β-adrenergic blockers are widely used for treatment of many disease states, including hypertension, arrhythmia, angina, glaucoma, & migraine prophylaxis.
Treatment
Β-adrenergic blockers are widely used for treatment of many disease states, including hypertension, arrhythmia, angina, glaucoma, & migraine prophylaxis.
Reactions
These differences influence their therapeutic applications, incidence of side effects, & type & severity of toxic reactions when taken in overdose.
Side
These differences influence their therapeutic applications, incidence of side effects, & type & severity of toxic reactions when taken in overdose.
Toxicity
Toxicity of β adrenergic blockers Most of the toxicity of β adrenergic antagonists is because of their ability to competitively antagonize the action of catecholamines at cardiac β-adrenergic receptors.
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.
Make Your Own Quizzes and Flashcards
Convert your notes into interactive study material.
Get started for free
