Post-Cardiac Arrest Care Flashcards
7 cards from real ACLS practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.
Read the first 7 Post-Cardiac Arrest Care flashcards as text
What is the recommended mean arterial pressure (MAP) target during post-cardiac arrest care to ensure adequate organ perfusion?
Answer: Greater than 65 mmHg
A MAP greater than 65 mmHg is the minimum recommended to ensure adequate perfusion of vital organs after ROSC.
A post-cardiac arrest patient's arterial blood gas shows PaO2 of 200 mmHg on 100% FiO2. What is the most appropriate next action?
Answer: Wean FiO2 to achieve SpO2 94–98%
Hyperoxia is harmful post-arrest; FiO2 should be titrated to maintain SpO2 94–98% and PaO2 within normal range.
Which electrolyte abnormality is most commonly associated with recurrent ventricular fibrillation after ROSC?
Answer: Hypomagnesemia
Hypomagnesemia lowers the threshold for ventricular fibrillation and should be corrected in post-arrest patients.
Targeted temperature management (TTM) at 36°C versus 33°C has been shown to result in:
Answer: Similar neurological outcomes between the two targets
The TTM trial demonstrated no significant difference in outcomes between 33°C and 36°C, supporting either target as acceptable.
Which finding on a 12-lead ECG post-ROSC is the strongest indication for emergent coronary angiography?
Answer: ST-segment elevation in two or more contiguous leads
ST-elevation post-ROSC indicates acute coronary occlusion and warrants immediate catheterization lab activation regardless of patient responsiveness.
When should neurological prognostication be performed after targeted temperature management in a post-cardiac arrest patient?
Answer: At least 72 hours after return to normothermia
Prognostication should be deferred until at least 72 hours after normothermia to allow sedation and TTM effects to clear.
A post-arrest patient is mechanically ventilated with PaCO2 of 30 mmHg. Why is this problematic?
Answer: Hypocapnia causes cerebral vasoconstriction and reduces cerebral blood flow
Hypocapnia causes cerebral vasoconstriction, reducing perfusion to an already-vulnerable post-ischemic brain.