Unformatted text preview: It’s just Darvocet…
It’s just Darvocet… William Deaton, D.O. Metro Health Hospital Grand Rapids, MI • Case: 47 y/o W female presenting to Spectrum ED after husband found her down in the bathroom. EMS states patient had vomited in the bathroom and was minimally responsive when they arrived, but maintaining her airway by herself. Vitals were stable, but she had a wide QRS on the rhythm strip. Upon our assessment, patient was alert, but mildly confused. She states she takes Darvocet and Soma for chronic pain. She was outside working in the garden today and felt like she “was over doing it”, so she has been taking extra Darvocet throughout the day. She does not remember how many she has taken, but thinks it may be around 10 over the course of 46 hours. Other than chronic pain, past history is negative. Surgical and family history are noncontributory. • PE: Other than a fine tremor in upper extremities, was completely normal. But in ED, patient had a GCS of 13.
• Labs: CBC, Chem 12 WNL. UDA positive for opiates, APAP level elevated, comp drug screen showed propoxyphene, APAP, nicotine, and soma metabolites. Propoxyphene
Comes in 3 different compounds, Darvocet, Darvon, and Darvon Compound.
1/24 the strength of morphine. (Vicodin is 1:1 and Dilaudid 13:1)
Analgesic duration of 46 hours.
T 1/2 of 612 hours
Hepatic metabolism with renal excretion.
First breakdown results in norproxyphene which is not active for pain, but is a Na+ blocker. Darvocet
• 3 different toxicities can occur:
1) APAP toxicity. (Will not go over today)
2) Opoid toxicity but…since 1/24 the strength of morphine, highly unlikely to cause a significant effect.
• 3) Sodium channel blockade. Sodium Channels
Sodium Channels Sodium Channels
Classified on the stimulus that opens them.
Ligand Gated, opens on a receptor basis. (Nicotinic receptor for Ach).
Voltage Gated, needs to reach a threshold level on the cell membrane in order to open. These are affected by the Na+ blockade. Voltage Gated Sodium Voltage Gated Sodium Channels
• Role in the cell is to generate and conduct action • •
Depolarization of the cell membrane producing a action potential produces a conformational change in the sodium channel causing it to become open, and an influx of sodium into the cell. This is responsible for phase 0 of the action potential.
Additional conformational change occurs, and causes the cell to go into a inactivated state, stopping the influx of Na+ into the cell.
During repolarization of the cell, the channel then undergoes another change into the resting state. Voltage Gated Sodium Voltage Gated Sodium Channels
• Most Na+ blockers bind • only to the inactivated and activated channels.
If tachycardia is present, there are more channels in the activated and inactivated states, making the channel blockade more profound. Sodium Channel Blockade
Sodium Channel Blockade
• The toxic effects of sodium channel blockade • are varied, with the cardiotoxicity being the most lethal.
Intraventricular conduction defects, ventricular arrhythmias, negative inotropic effects, bradyrhythmias or tachyrhythmias (only if the drug is also anticholinergic, which most are), and seizures are the most common findings. QRS Prolongation
• QRS complex is widened by the Vmax of phase 0 of the AP being depressed. This may look wide on the EKG, or take appearance of a known bundle branch block. Near complete Na+ Blockade may take appearance of a sine wave rhythm. QRS Prolongation
• Sodium Bicarb in BOLUS form •
• only has been proven to narrow the QRS within 12 minutes on most occasions. This is done by increasing the Vmax of phase 0 on the AP from the increased availability of Na+.
12 mEq/kg or until the serum pH is 7.55.
Close attention to the electrolytes, acid/base and fluid balance is needed. Hypotension
• This is due to the negative inotropic effects of • • the sodium channel blockade. Possibly due to the decrease in the Na+/Ca++ exchange and fall in intracellular Ca++.
Usually responds well to fluid boluses. If this does not respond, and bicarb has been given, norepinephrine is the medication of choice. This provides both positive inotropy and vasoconstriction. Most Na+ blockers are also alpha blockers, and dopamine may lower blood pressure. Bradyrhythmias
• Characteristic of SEVERE Na+ blockade. • Usually have accompanying wide QRS and •
• severe hypotension.
Bicarb is the first line therapy with 12mEq/kg bolus. If this does not correct, isoproterenol or epinephrine infusion may help.
Try to determine if other bradycausing drug may be a coingestant and treat appropriately. Tachyarrhythmias
• All class Ia drugs (quinidine, procanamide) and •
• class Ic drugs (flecanide, propafenone) also depress phase 0 of the AP, so they should not be given.
Sinus tachycardia rarely requires treatment.
Physostigmine in the anticholinergic Na+ blockade patients could lessen the Na+ blockade, but the risk/benefit ratio is not favorable. Hypertonic Saline
• Hypertonic Saline may be used in the event that ventricular arrhythmias, QRS widening, or hypotension is refractory to the bicarb therapy. If the pH is >7.55, then a hypertonic saline infusion may be used. This may help overcome the Na+ blockade by raising the serum Na+ concentration. Dispo
• If the patient has any of the above signs/symptoms, they need to be admitted to at least a tele floor, if not the ICU.
• If the patient remains asymptomatic and has NO ECG changes after 6 hours, they may be safely discharged. If a suicide attempt, involve psych and MSW. References
• Kolecki P, Curry S, Poisoning by Sodium Chanel Blocking Agents. •
• J Medical Toxicology, Oct 97, Vol 13, Num 4.
Tintinalli, Sixth Edition.
Ling et al. Toxicology Secrets. 2001.
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- Fall '11
- Eli Lilly and Company, Darvocet, sodium channel blockade, Dextropropoxyphene