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BCA Neuroanesthesia & Neurosurgical Procedures Flashcards

6 cards from real BCA practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.

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  1. Which medication is the FIRST-LINE treatment for intraoperative cerebral vasospasm following subarachnoid hemorrhage (SAH)?

    Answer: Nimodipine

    Nimodipine, a calcium channel blocker with cerebrovascular selectivity, is the only agent proven to reduce neurological deficits from cerebral vasospasm after SAH.

  2. In the prone position for spine surgery, the MOST important padding consideration to prevent perioperative vision loss is:

    Answer: Avoiding direct pressure on the eyes and orbits

    Direct orbital pressure compresses the central retinal artery, leading to ischemic optic neuropathy or central retinal artery occlusion and permanent vision loss.

  3. Which parameter most directly determines cerebral perfusion pressure (CPP)?

    Answer: Mean arterial pressure minus intracranial pressure

    CPP = MAP − ICP; mean arterial pressure is used (not systolic or diastolic) because it reflects average driving pressure throughout the cardiac cycle.

  4. Postoperative nausea and vomiting (PONV) is particularly dangerous after neurosurgery because:

    Answer: Vomiting and retching significantly increase intracranial pressure

    Forceful vomiting and retching dramatically elevate intracranial pressure, risking cerebral herniation in patients with already compromised intracranial compliance.

  5. Which intravenous induction agent INCREASES intracranial pressure and is therefore CONTRAINDICATED in patients with elevated ICP?

    Answer: Ketamine

    Ketamine causes cerebral vasodilation and increases CMRO2 and CBF, elevating ICP; it is generally avoided in patients with intracranial hypertension.

  6. Intraoperative EEG burst suppression is MOST commonly targeted during:

    Answer: Carotid endarterectomy with cerebral protection

    During carotid endarterectomy, burst suppression is deliberately induced with barbiturates or propofol to maximize cerebral metabolic protection during periods of carotid clamping.