Critical Care Medicine: Specific Critical Care Topics
Pulmonary and Critical Care Medicine · Critical Care Medicine 🎯 Practice these cards
The initial treatment of anaphylaxis is ____, given intramuscularly or intravenously; biphasic reactions can recur ____ to 72 hours after resolution, so high-risk patients warrant extended observation of up to ____ hours.
The initial treatment of anaphylaxis is epinephrine, given intramuscularly or intravenously — never delay it in favor of adjuncts like antihistamines or glucocorticoids. Biphasic anaphylaxis (recurrence of symptoms 1 to 72 hours after the initial episode resolves) is more likely after a severe initial episode or when more than one dose of epinephrine was required; when biphasic risk is present, extended observation of up to 6 hours or longer is warranted.
Organ-system involvement in anaphylaxis: skin and mucosa in about ____%, respiratory in about ____%, cardiovascular and gastrointestinal each in about ____%, and neurologic in about 15%.
Organ involvement in anaphylaxis: skin and mucosa (pruritus, flushing, urticaria, angioedema) in about 85% of patients; respiratory (dyspnea, stridor, wheeze) in about 70%; cardiovascular (hypotension, tachycardia) and gastrointestinal (abdominal pain, vomiting, diarrhea) each in about 45%; and neurologic (anxiety, encephalopathy) in about 15%. The distributive shock of anaphylaxis closely mimics septic shock; airway-compromising angioedema is the most feared complication.
Approved by the FDA in August 2024, neffy is a 2 mg ____ epinephrine spray for anaphylaxis in patients weighing ≥____ kg; a second dose may be given after ____ minutes in the same nostril.
In August 2024 the FDA approved neffy, a 2 mg intranasal epinephrine spray for emergency treatment of type I allergic reactions including anaphylaxis in adults and children weighing ≥30 kg — the first non-injectable epinephrine product. A second dose may be given after 5 minutes in the same nostril. IM epinephrine remains first-line in clinical settings; neffy is primarily a community option, particularly for needle-averse patients.
Heat stroke is defined by core temperature above ____ °C (104 °F) plus ____; untreated mortality reaches ____%, and centrally acting antipyretics are ineffective.
Heat stroke is defined by core temperature above 40 °C (104 °F) plus encephalopathy. Classic (nonexertional) heat stroke strikes elderly patients with comorbidities and predisposing medications (often with hot, dry skin); exertional heat stroke strikes young, healthy individuals when heat, activity, and humidity coincide, commonly with rhabdomyolysis and AKI. Untreated mortality reaches 60%. Above 42 °C direct cellular injury ensues, so cooling is a race. Centrally acting antipyretics (NSAIDs, acetaminophen) are not effective.
The 2025 SCCM heat stroke guideline prioritizes cold- or ice-water immersion, targeting core temperature below ____ °C within ____ minutes of recognition, and issues strong recommendations against ____ and antipyretics.
The first dedicated SCCM GRADE guideline on heat stroke (February 2025) recommends active over passive cooling and now prioritizes cold- or ice-water immersion (1–5 °C or 9–12 °C), which achieves the fastest cooling rates (≥0.155 °C/min), for both classic and exertional heat stroke — a shift from MKSAP's 2022 position that immersion was not first-line. The target is core temperature below 39 °C within 30 minutes of recognition. The guideline issues strong recommendations AGAINST dantrolene and against antipyretics (acetaminophen, NSAIDs, salicylates).
Malignant hyperthermia is triggered by volatile anesthetics and ____; early perioperative clues are ____ muscle rigidity and an unexplained rise in end-tidal/arterial PCO2; treatment is stop the trigger, active cooling, and ____.
Malignant hyperthermia occurs in people with a rare autosomal dominant derangement of intracellular calcium metabolism exposed to volatile anesthetics (halothane, isoflurane) or the depolarizing paralytic succinylcholine. Masseter muscle rigidity and an unexplained rise in end-tidal/arterial PCO2 are early perioperative clues; the response includes rhabdomyolysis, arrhythmias, and core temperatures of 45 °C or higher with mortality up to 10%. Treatment is immediate discontinuation of the triggering agent, active cooling, and dantrolene every 5 to 10 minutes until rigidity and hyperthermia resolve, monitoring for hyperkalemia.
NMS evolves over days to weeks with lead-pipe rigidity and hyporeflexia, whereas serotonin syndrome develops within ____ hours of a serotonergic drug change and features ____ and ____.
Neuroleptic malignant syndrome develops over days to weeks after antipsychotic exposure or dopamine-withdrawal, with the tetrad of fever, mental status change, severe 'lead-pipe' rigidity, and dysautonomia, plus hyporeflexia and no clonus; treatment is stopping the trigger, active cooling, and rehydration (dantrolene/bromocriptine anecdotal). Serotonin syndrome evolves within 24 hours of starting or increasing a serotonergic drug, features myoclonus and hyperreflexia, and resolves within about 24 hours of drug removal; benzodiazepines first, cyproheptadine if they fail. Time course and reflex findings are the bedside discriminators.
Accidental hypothermia staging: mild = 32–35 °C with shivering; moderate = ____–32 °C, at which shivering ____; severe = below ____ °C with coma, absent reflexes, and ventricular arrhythmias.
Accidental hypothermia (core temperature <35 °C) is staged: mild 32–35 °C with shivering, tachycardia, and poor judgment; moderate 28–32 °C, at which shivering ceases and hypotension, bradycardia, somnolence, and Osborne (J) waves appear; severe <28 °C with coma, absent reflexes, ventricular arrhythmias, and asystole. Once core temperature falls below 32 °C and shivering stops, active rewarming is required. Medications are generally withheld below 30 °C, and 'no one is dead until they are warm and dead.'
For hypothermic cardiac arrest, the recommended rewarming is ECLS, preferably ____; per the HOPE score, proceed when estimated survival probability is ≥____% — a threshold that prevented 37% of futile attempts while missing no ____.
Extracorporeal life support is recommended for hypothermic patients in cardiac arrest because it maximizes rewarming rate and provides hemodynamic support; venoarterial ECMO is increasingly favored over cardiopulmonary bypass. The 2021 ERC guidance favors the HOPE score (age, sex, mechanism, CPR duration, serum potassium, core temperature) over the historical potassium cutoff for selecting patients for ECLS: a 2025 validation showed that using a HOPE <10% threshold to withhold ECLS would have prevented 37% of futile rewarming attempts while missing no survivors. Proceed when estimated survival probability is ≥10%.
In CO poisoning, standard pulse oximetry is ____ because it cannot distinguish carboxyhemoglobin; diagnosis requires blood gas with ____; hyperbaric oxygen is indicated when carboxyhemoglobin is ≥____% with evidence of organ ischemia.
Standard pulse oximetry cannot differentiate oxyhemoglobin from carboxyhemoglobin, so readings are falsely reassuring in CO poisoning; diagnosis requires blood gas analysis with CO-oximetry (COHb <3% in normal individuals, up to 10–15% in smokers). Because oxygen and CO compete for hemoglobin, treatment is supplemental oxygen: the carboxyhemoglobin half-life is 300 minutes on ambient air, 90 minutes on 100% oxygen, and about 30 minutes with hyperbaric oxygen. Patients with COHb ≥25% plus evidence of organ ischemia should receive hyperbaric oxygen if possible. Roughly 40% of severe poisonings develop delayed neurologic sequelae, typically within 20 days.
The preferred cyanide antidote is ____ (usual adult dose 5 g), which converts cyanide to nontoxic cyanocobalamin; ____ should be avoided in smoke-inhalation victims because inducing ____ is unsafe when carboxyhemoglobin is already elevated.
Cyanide inhibits cellular respiration by binding cytochrome oxidase c, producing clinical hypoxia despite a normal oxyhemoglobin saturation; suspect it in fire victims with profound acidosis or collapse (CO co-exposure is common) and in patients on prolonged nitroprusside infusions. Hydroxocobalamin (usual adult dose 5 g) avidly binds cyanide to form soluble, nontoxic cyanocobalamin and is the most commonly recommended antidote. Nitrites induce methemoglobin to bind cyanide but should be avoided in smoke-inhalation victims, who may already carry high carboxyhemoglobin levels; sodium thiosulfate donates sulfur to convert cyanide to thiocyanate. A normal serum lactate effectively rules out significant exposure.
Ethylene glycol and methanol cause both an increased ____ gap metabolic acidosis and an increased ____ gap; treatment is IV ____ plus early hemodialysis, while isopropyl alcohol (osmolal gap + ketosis, no anion gap) needs only supportive care.
Ethylene glycol (metabolized to oxalic acid → renal tubule crystallization and kidney injury) and methanol (metabolized to formic acid → retinal toxicity and blindness) both cause an increased anion gap metabolic acidosis plus an increased osmolal gap. Management is competitive inhibition of alcohol dehydrogenase with IV fomepizole (IV ethanol only if unavailable), plus hemodialysis as soon as possible in confirmed poisoning or suspected cases with high anion gap acidosis or end-organ damage. Isopropyl alcohol is the exception: osmolal gap and ketones without anion gap acidosis, needing only supportive care.
Sympathomimetic toxicity (cocaine, amphetamines) presents with tachycardia, hypertension, diaphoresis, and ____; first-line treatment of agitation is ____, while ____ should be avoided because of unopposed alpha-stimulation.
The sympathomimetic toxidrome (cocaine, amphetamines, ephedrine) causes tachycardia, hypertension, diaphoresis, agitation, seizures, and mydriasis. Benzodiazepines are the cornerstone of agitation management, and beta-blockers should be avoided — blocking beta receptors leaves activated alpha receptors unopposed, theoretically precipitating severe hypertension. Opioid toxidrome: miosis, respiratory depression, hypothermia, bradycardia. Anticholinergic: dry skin/mucosae, mydriasis, hyperthermia, urinary retention. Flumazenil for benzodiazepine overdose can precipitate life-threatening seizures in chronic users — support ventilation instead.
Xylazine is a veterinary ____-agonist sedative adulterating illicit fentanyl; it causes characteristic necrotic ____ and is NOT reversed by ____.
Xylazine, a veterinary alpha-2-agonist sedative, has become a widespread adulterant in illicit fentanyl (designated an emerging drug threat by the U.S. ONDCP in April 2023). It causes hypotension, CNS and respiratory depression, and characteristic necrotic skin ulcers; it is NOT reversed by naloxone, is not detected on routine toxicology screens, and has no approved antidote — management is supportive (airway, blood pressure). Naloxone should still be administered because opioid co-toxicity is usually present. Naloxone 4 mg nasal spray became the first over-the-counter naloxone product in March 2023.
After anoxic brain injury, prognosis should not be declared irreversible until after ____ to ____ days of supportive care; coma on the Glasgow Coma Scale is defined as a total score of 3 to ____.
Anoxic brain injury is CNS damage from prolonged, profound tissue hypoxia (cardiac arrest, asphyxiation, near-drowning); imaging shows edema and loss of gray-white matter demarcation. Prognosis is often not immediately apparent: patients require supportive care for 3 to 5 days or longer before the extent of injury can be declared irreversible — premature pessimism is the classic error. Coma severity is graded with the Glasgow Coma Scale (eye + verbal + motor; total 3–15), with a score of 3–8 defining coma, 9–12 moderate brain injury, and 13–15 mild.
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