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Sudden Cardiac Arrest and Cardiopulmonary Resuscitation (CPR)

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  1. Introduction to sudden cardiac arrest and resuscitation
    4 Chapters
    1 Quiz
  2. Resuscitation physiology and mechanisms
    2 Chapters
  3. Causes of sudden cardiac arrest and death
    2 Chapters
  4. ECG atlas of ventricular tachyarrhythmias in cardiac arrest
    8 Chapters
  5. Cardiopulmonary Resuscitation
    10 Chapters
  6. Special Circumstances
    11 Chapters
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Poisoning and drug toxicity

In adolescents and young adults, intoxication events leading to cardiac arrest are notably prevalent, primarily due to the misuse of prescription medications and illicit substances. Currently, opioid overdose stands as a predominant etiological factor for cardiac arrest within this demographic on a global scale. Numerous substances possess the potential to induce cardiac arrest or cause profound cardiopulmonary depression. Table 1 delineates substances for which specific antidotes are available. The detrimental effects of these substances can potentially be reversed if interventions are promptly instituted. In scenarios where an antidote is not available, it is essential to provide supportive care and maintain vital functions artificially until the substance undergoes renal elimination, hepatic elimination or is removed by means of dialysis.

Paracetamol (Acetaminophen)N-Acetylcysteine
Anticoagulants (apixaban)Andexanet alpha
The Black Widow, Spider BettLactrodectus antivenom
Botulism (botulinum toxin)Botulism Ininum antitoxin
Beta-blockerGlucagon IV
Calcium flow inhibitor (calcium blocker)Calcium iv
High dose insulin with glucose IV
Pralidoxime chloride
Cyanide antidote kit (includes amyl nitrate, sodium nitrite, and sodium thiosulfate)
Digitalis glycosides (digoxin, digitoxin, oleander)Digoxin-specific Fab fragments
Ethylene glycolFomepizo|121:Ethylene Glycol||122:leethanol
Heavy metalsChelating substances
Ionizing radiationPotassium iodide
IsoniazidPyridoxine (Vitamin B6)
Methemoglobin-forming substancesMethylene blue
MethotrexateLeucovorin (folinic acid) Glucarpidase (carboxypeptidase-G2)
ThalliumPrussian blue
Tricyclic AntidepressantsSodium Bicarbonate
Unfractionated HeparinProtamine
Valproic acidL-carnitine (limited evidence) |
WarfarinVitamin K
Fresh frozen plasma
Prothrombin complex concentrate

Actions in suspected poisoning and cardiac arrest

Promptly contact the closest intensive care unit (ICU) possessing expertise in toxicological management. Severe poisoning mandates intricate care, often encompassing hemodialysis, intubation, and prolonged ICU admissions. Pending the correct level of care, the following actions can be performed.

  • CPR
    • Initiate CPR in adherence to standard guidelines. However, refrain from rescue breaths to mitigate the risk of potential contaminants endangering the rescuer.
  • Contact expertise
    • Contact the nearest poison center (or call 911 US, 112 EU).
    • Contact the nearest intensive care unit with expertise in toxicological emergencies.
  • Antidote
    • Administer the specific antidote promptly upon suspicion of poisoning.
  • Decontamination
    • Disrobe the patient of any attire possibly contaminated with the toxicant.
    • Irrigate skin and eyes using saline solution (NaCl) if suspected of toxin exposure.
    • Gastrointestinal lavage is infrequently employed due to aspiration risks and inconclusive evidence. However, in cases of iron, lithium, or potassium intoxication where lavage might prove beneficial, the procedure should be conducted post-intubation. Avoid lavage if gastrointestinal perforation or obstruction is suspected.
    • If the patient is intubated, administer activated charcoal through a gastric tube at a dose of 0.5 g/kg. Refrain from using activated charcoal if more than one hour has elapsed post-ingestion unless the ingested substance has the propensity to form bezoars or is a sustained-release formulation. Note: activated charcoal is ineffective against alcohols, lithium, and heavy metals.
  • Enhance elimination
    • Induce diuresis through urine alkalinization, contingent upon renal elimination of the toxicant. This can be accomplished using an infusion of sodium bicarbonate combined with furosemide at a dose of 1 mg/kg.
  • Advanced elimination
    • Hemodialysis
    • Hemofiltration
    • Plasmapheresis


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