1/6
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai |
|---|
No analytics yet
Send a link to your students to track their progress
What are the symptoms of cocaine toxicity?
Tachycardia
HTN
Anxiety
Seizure
Tachypnoea
Dilated pupils
Sweaty / pale
Euphoria / energetic
Agitated
How do you treat cocaine toxicity?
O2 – if sats are low, 15l high flow
IM midazolam - for severe HTN / chest pain
GTN - for chest pain w BP over 90
Fluids – if hypotensive, 250ml bolus over 60 secs grey cannula
What are the benefits for GTN in cocaine toxicity?
Vasodilator = reduced BP = reduces preload
Relief of coronary spasm from vasodilation
Reduces pain through improved coronary blood flow + reduced preload = less strain
What are the risks of using GTN in cocaine toxicity?
Hypotension - vasodilator
Reflex tachycardia - drop in BP creates auto response to increase HR
Inferior stemi = severe drops in BP due to right ventricular infarct - worsened by GTN
What are the benefits of midazolam in cocaine toxicity?
Reduces agitation / anxiety - inhibits CNS stimulation
Reduces HTN / tachycardia - inhibits CNS stimulation
Rapid onset
What are the risks of midazolam for cocaine toxicity?
CNS depressant - enhances GABA in CNS = respiratory depression as brains drive to breathe is reduced = airway obstruction
Hypotension - CNS depressant + vasodilation
Paradoxical reaction - from genetics - increasing agitation
thermoregulation impaired - redistribution of heat to peripheral tissues, dropping core temp
What is the pathophysiology behind cocaine toxicity?
Binds to dopamine, catecholamine and serotonin transport proteins = inhibits re-uptake.
Accumulation of dopamine binds to opioid receptors in brain = euphoria.
Accumulation of catecholamines = overactivity of sympathetic NS = vasoconstriction = tachycardia + HTN.
Accumulation of serotonin in CNS = excessive stimulation of 5-HT receptors = agitation, mood alterations, hyperthermia.
Cocaine blocks sodium channels, prolonging depolarisation, causing prolonged QT interval and ventricular abnormalities e.g. Brugada Syndrome.
Increased myocardial oxygen demand + coronary artery spasm = chest pain+ increased platelet adhesiveness and aggregation causes occlusion and thus myocardial infaction.