Toxic Alcohols Exam 3 Flashcards
1
Q
Toxic effects of TCA’s
A
- QRS widening
- dysrhythmias
- seizures (can be controlled)
- CNS effects
- myocardium effects
2
Q
Toxicity of TCA’s in relation to QRS widening
A
- QRS > 100 msec, 1/3 of patients had seizures
- QRS > 160 msec, 1/2 of patients had ventricular dysrhythmias
- QRS < 100 msec, no significant toxicity
3
Q
Toxic effects of TCA’s: CNS effects
A
Anticholinergic effects
- Hot as a hare (hyperthermia)
- Dry as a bone (dry skin)
- Red as a beet (flushed)
- Blind as bat (mydriasis)
- Mad as a hatter (delirium)
Central anticholinergic effects include
- Agitation, excitability
- Lethargy
- Hallucinations
- Hyperthermia
- Ataxia
- Choreoathetoid movements
- Seizures
- Coma
Other anticholinergic effects
- Tachycardia
- Dilated pupils
- Dry flushed skin
- Decreased GI motility
- Urinary retention
4
Q
Toxic effects of TCA’s: seizures
A
- happens shortly after duration
- brief and resolves itself
- If persistent must be controlled to prevent hypoxia and lactic acidosis, both of which may predispose to life-threatening ventricular dysrhythmias
- Patients with protracted seizures are also at risk for developing rhabdomyolysis and acute renal failure
5
Q
Toxic effects of TCA’s: myocardium effects
A
- TCAs block myocardial sodium channels, resulting in a membrane depressant effect on the heart; increased threshold for excitability.
- Also block potassium channels which further prolongs action potential duration in most cardiac cells
- Classic sign of TCA toxicity is prolongation of the QRS complex
- Hypertension ( caused by release of NE) or hypotension
6
Q
Toxic effects of TCA’s: hypotension
A
Caused by
- Negative inotropic effects of TCAs
- Potent alpha-adrenergic antagonist effects, which results in decreased peripheral vascular resistance
7
Q
Treatment of TCA toxicity
A
- ABCs
- Decontamination: activated charcoal (1-2g/kg body weight)
- BZDs for seizures; if doesn’t work -> consider barbiturates or propofol; if doesn’t work -> NMB and general anesthesia; DO NOT USE PHENYTOIN
- Hypotension: IV fluids; 10-30mL/kg of LR or NS; if doesn’t work -> vasopressors (NE); DO NOT USE DOPAMINE
- Dysrhythmias: bicarb, hyperventilation (can lead to resp. alkalosis), hypertonic saline (if pt also have hypotension but rarely used)
8
Q
Treatment of TCA toxicity: dysrhythmias
A
- Sodium bicarbonate
- Start bicarb immediately if QRS widening to 100 msec or greater is noted
- Hypotension is also an indication for alkalization, as it has responded to bicarb administration in experimental models
- No evidence to support a role for bicarb in TCA poisoning in patients who present with altered mental status without QRS widening or hypotension
- Sodium bicarbonate reverses the quinidine-like effects that produce the major, life-threatening CV manifestations of TCA overdose
- 1-2 mEq/kg administered IV as a bolus over 1-2 minutes. Larger doses may be required for unstable ventricular dysrhythmias
- Repeat PRN to achieve pH of 7.45-7.55
- Continuous infusion – add 1-3 50 mL ampules to liter of IVF and run at maintenance or more than maintenance, depending on fluid requirements and BP of patient
- Administer over 4-6 hours, maintaining pH at target level.
- infusion may be DCd if width of QRS complex remains less than 100 msec without administration of sodium bicarbonate
9
Q
What should you avoid when treataing TCA toxicity: dysrhythmias
A
AVOID all IA and IC antidysrhythmics -> worsen hypotension and cardiotoxicity
- quinidine
- procainamide
- disopyramide
- flecainide
- encainide
- propafenone
Beta blockers and calcium channel blockers are dangerous for patients with wide-complex dysrhythmias, as they slow conduction velocity, decrease heart rate, and lower blood pressure
10
Q
Patient disposition: TCA toxicity
A
- Admit any patient with QRS interval of >100 msec
- Admit any patient who has experienced a seizure
- Admit any patient in need of psychiatric or medical support
- Most patients with ECG abnormalities should be placed in the ICU for minimum of 12-24 hours
- Patients who have been decontaminated, who never seize or develop abnormal ECGs (other than sinus tachycardia) can be safely discharged after six hours of observation if otherwise stable
11
Q
SSRI overdose effects
A
- nausea
- vomiting
- lethargy
- sedation
- possible serotonin syndrome
- QTc prolongation and seizures with Celexa
12
Q
Hunter serotonin toxicity criteria
A
Any ‘yes’ decision to any of the following decision rules suggests definite or significant serotonin toxicity:
- If the patient has spontaneous clonus.
- If the patient has inducible clonus AND agitation OR diaphoresis.
- If the patient has ocular clonus AND agitation OR diaphoresis.
- If the patient has tremor AND hyperreflexia.
- If the patient is hypertonic AND has a temperature greater 38 degrees C AND ocular clonus OR inducible clonus.
13
Q
serotonin syndrome
A
- mental status changes
- agitation
- myoclonus
- hyperreflexia
- diaphoresis
- shivering
- tremor
14
Q
Treatment of SSRI overdose
A
- Administration of activated charcoal
- Rule out co-ingestants (ECG, drug screen, APAP level)
- Treatment is primarily symptomatic and supportive care
15
Q
Treatment of serotonin syndrome
A
- For mild cases, consider use of cyproheptadine (Periactin)
- Adult dose: 12 milligrams orally initially, followed by 2 milligrams every 2 hours if symptoms persist. Max of 32 milligrams may be administered in 24 hours
- Pediatric dose: 0.25 milligrams/kilogram/day divided every 6 hours, maximum dose 12 milligrams/day
- Benzodiazepines for sedation, hydration, and external cooling are important to help prevent progression to severe toxicity
- For severe toxicity elective intubation, neuromuscular paralysis, mechanical ventilation, and aggressive cooling measures are indicated
- Benzodiazepines for sedation, hydration, and external cooling are important to help prevent progression to severe toxicity
- For severe toxicity elective intubation, neuromuscular paralysis, mechanical ventilation, and aggressive cooling measures are indicated
