chapter 12 pt3 Flashcards
clinical presentation of opioid poisonings ?
pinpoint pupils
resp depression
antagonist for opioid poisonings
naloxone
non iv routes quicker as time saved in not finding IV access which can be extremely difficult in IV drug user - IM , IN , SC
initial dose 400mcg IV
800mcg IM
800mcg SC
2mg IN
large opioid overdoses needs a naloxone titration to total 10mg
give increments of naloxone till patient is breathing properly and breathing reflexes are illicit
why can giving naloxone still can give persistent resp depression
duration of action of naloxone is 45-70min
respiratory depression in opioid over dose persist for 4-7hrs
complication of acute withdrawal of opioids ?
sympathetic excess = pulmonary edema , ventriloquist’s arrythmia , severe agitation
cause of cardiac arrest in opioid intoxication ?
respiratory depression and arrest leading to severe brain hypoxia = prognosis poor
clinical manifestation of benzodiazepine overdose
loss of consciousness , respiratory depression and hypotension
antidote for benzodiazepine
FLUMANZIL - can b used if NO history of seizures risk of seizure
CONTRAINDICATED - benzodiazepine independence and co-ingestion of pro cnvulasant medications scubas tricyclic antidepressants
not routinely used in comatose
complication of flumanzil ?
reversing benzodiazepine toxicity with flumanzil can cause significant toxicity - leading to seizure , arrhythmia , hypotension , and withdraws symptom
what are the tricyclic antidepressants and cyclic drugs ?
amitriptyline
desipramine
imipramine
nortriptyline
doxepin
clomipramine
ECG of tricyclic antidepressants ?
cardiac toxicity due to anti cholinergic and sodium channel blocking effects produce broad complex tachycardia
clinical presentation of cyclic drugs?
alpha 1 receptor blockers - hypotension
anticholinergic drugs - dilated pupils, fever , dry skin
delirium
tachycardia
ileus
urinary retention
treatment for cyclic drugs?
consider sodium bicarbonate for tricyclic induced ventricular contraction abnormalities
ph of 7.45-7.55 accepted
local anaesthesia clinical manifestations ?
severe agitation
loss of consciousness
tonic clonic seizures
ECG changes of local anaesthesia ?
bradycardia
conduction block
a-systole
v-tach
local anaesthesia cardiac arrest management ?
ALS
with
IV 20 percent lipid emulsions of 1.5ml /kg
follow by 15ml/kg/hr
give up to 3 boluses of lipid at 5 mins interval - until max of 12ml/kg lipid emulsion reached
what are examples of stimulants ?
cocaine and amphetamines
clinical manifestation of stimulants ?
hypertension
agitation
tachycardia
hyperthermia
myocardial ischemia
treatment for stimulants
sell doses of IV benzodiazepines - first line
glyceryl trinitrate and phentolamine can reverse cocain induced coronary vasoconstriction
Nitrates only second line therapy
treatment for drug induced bradycardia
severe bradycardia from poisoning to drug overdose may be refectory from ALS protocol due to prolonged receptor binding
= atropine
atropine most beneficial in which toxins ?
organophosphate
carbamate
nerve agent
acetylcholinervse inhibiting substance
what is used in refractory bradycardia caused by beta blockers
isoprenaline
if isoprenaline does nit work what do we do ?
transcutaneous pacing
