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--- beta_blocker_toxicity [2025/01/07 18:38] – Added emoji for drug dose jkohts
+++ beta_blocker_toxicity [2025/01/07 19:45] (current) – jkohts
@@ Line 219: / Line 219: @@
 **Glucagon**\\
-IV glucagon had been used as antidote for beta-blocker poisoning in the past but its use has been largely superseded by HIET. Glucagon increases cyclic AMP and activates myosin kinase independent of β-receptors.
+IV glucagon had been used as antidote for beta-blocker poisoning in the past but its use has been largely superseded by HIET. Glucagon increases intracellular cAMP and activates myosin kinase independent of β-receptors.
-💊 Glucagon IV 5-10 mg as a bolus, then an IV infusion titrated against heart rate and blood pressure (starting at 5-10 mg/hour).
+\\
+  * 💊 **Glucagon** IV 5-10 mg as a bolus, then an IV infusion titrated against heart rate and blood pressure (starting at 5-10 mg/hour, or the 'reponse dose' per hour).
-**Isoprenaline**  This is a non-selective competitive beta agonist. Doses should also be titrated against cardiac parameters and the dose required may be ten or twenty fold larger than normally used. As both the agonist and antagonist are competing for the same receptors, much larger doses are needed to reach the same level of receptor occupancy. Dose requirements will fall rapidly as the beta-blocking drug is metabolised.
+**Isoprenaline** \\
+Isoprenaline is a non-selective competitive β-agonist. Doses should also be titrated against cardiac parameters and the dose required may be ten or twenty fold larger than normally used. As both the agonist and antagonist are competing for the same receptors, much larger doses are needed to reach the same level of receptor occupancy. Dose requirements will fall rapidly as the β-blocking drug is metabolised.
-Patients who require inotropics support should be commenced on Dextrose & Insulin.
-This should be implemented in patients not responding to isoprenaline.
+**HIET**\\
+Patients who require inotropics support should be commenced on Dextrose & Insulin. This should be implemented in patients not responding to isoprenaline.
+<code>
+This section has been reworked 08/01. Goldfrank's has a discussion of calcium, general catecholamines (other than isoprenaline), and lipid emulsion.
+Do we want to include those in?
+Also, in what order should we include them?
+</code>
 ==== - Treatment of specific complications ====
-Seizures Glucose should be given regardless of a normal blood sugar. Otherwise, they should be treated conventionally with benzodiazepines(eg diazepam). If seizures are refractory-use phenobarbitone.
+**Seizures**\\
+Glucose should be given regardless of a normal blood sugar. Otherwise, they should be treated conventionally with benzodiazepines (eg diazepam). If seizures are refractory, use phenobarbitone.
+<code>Why phenobarb instead of usual status epilepticus protocol?</code>
-Arrhythmias Ventricular tachycardia (torsades de pointes) may occur with sotalol or occasionally propranolol. Conventional treatment is with magnesium, isoprenaline, or cardiac pacing. Magnesium has calcium channel blocking effects and is potentially hazardous as it may further impair cardiac conduction and contractility. It should be used with great caution if at all. Isoprenaline or cardiac pacing to achieve a heart rate of 120-140 bpm is the safest option.
+**Arrhythmias**\\
+Ventricular tachycardia (polymorphic VT, torsades de pointes) may occur with sotalol or occasionally propranolol. Conventional treatment is with magnesium, isoprenaline, or cardiac pacing. Magnesium has calcium channel blocking effects and is potentially hazardous as it may further impair cardiac conduction and contractility. It should be used with great caution if at all. Isoprenaline or cardiac pacing to achieve a heart rate of 120-140 bpm is the safest option.
+<code> Unsure about this due to very high target HR, and probably should caveat with needing invasive BP monitoring? </code>
 ==== - Observation/disposition ====
 ===== - Prognosis =====
+Occasional late complications/deterioration have been reported generally in patients who have had significant poisoning. It is likely that these relate to too rapid withdrawal of treatment. Long term sequelae have not been reported and no follow up is required after resolution of the clinical signs or ECG findings, unless the patient has been profoundly hypotensive.
-Occasional late complications/deterioration have been reported generally in patients who have had significant poisoning. It is likely that these relate to too rapid withdrawal of treatment. Long term sequelae have not been reported and no follow up is required after resolution of the clinical signs - ECG findings unless the patient has been profoundly hypotensive.
 ===== - References =====