50 year old male presents post heroin OD
Respiratory acidosis – pH 7.17 pCO2 84mmHg
Compensation – Expected HCO3 – use 10 to 1 rule, therefore expected HCO3 – 28.5mmol/l
Mildly raised lactate and BSL
The VBG shows a respiratory acidosis with adequate compensation with an expected HCO3 almost the same as the measure HCO3. In this clinical context the findings are secondary to hypoventilation from the opioid overdose. The HCO3 is almost >30 so one might consider a chronic component to the acidosis, if the patient has underlying COPD. The mildly elevated lactate is most likely secondary to poor oxygenation secondary to hypoventilation and the raised BSL from an acute stress response.
Naloxone pharmacodynamics -competitive opioid antagonist at mu, kappa and delta receptors, reversing opioid effects
Phamacokinetics – poor bioavailability with extensive first pass effect. Well absorbed after imi, SC or endotracheal administration, with rapid onset of action. It is metabolised by the liver. Duration of effect – depends on dose and the duration of effect of opioid, can range from 20 to 90 minutes.
Management of opioid OD
Use structured RRSIDEAD approach.
Antidote – naloxone. Dosage depends on if the patient is opioid dependant, as you do not want to cause acute withdrawal. 100mcg ivi or 400mcg imi or SC. One continues to give repeated doses until patient is rousable or RR >8. More than 400mcg is not usually necessary. If re sedation or drop in RR re occurs it may be necessary to start an infusion. If patients have taken longer acting opioids it will take some hours before they wear off.