Brain Resuscitation Questions PDF

\-\-- \#\#\# \*\*Neuronal Injury & Pathophysiology\*\* 1\. \*\*What is the timeline for neuronal injury progression after ischemic insult?\*\* Neuronal injury is dynamic and continues for hours to days after the initial ischemic insult. 2\. \*\*What percentage of the body's cardiac output and ox...

\-\-- \#\#\# \*\*Neuronal Injury & Pathophysiology\*\* 1\. \*\*What is the timeline for neuronal injury progression after ischemic insult?\*\* Neuronal injury is dynamic and continues for hours to days after the initial ischemic insult. 2\. \*\*What percentage of the body's cardiac output and oxygen consumption does the brain account for?\*\* The brain receives 15% of cardiac output and uses 20% of the body's oxygen, despite being only 2% of body weight. 3\. \*\*What causes cytotoxic edema after cerebral ischemia?\*\* ATP depletion disrupts osmotic gradients, leading to water influx into cells. Cytotoxic edema peaks 48--72 hours post-injury. 4\. \*\*What is the Monro-Kellie doctrine?\*\* The skull is a fixed-volume container; increases in brain, blood, or CSF volume must be offset by reductions in other components, or ICP will rise. 5\. \*\*How does elevated ICP exacerbate ischemic injury?\*\* Increased ICP reduces cerebral perfusion pressure (CPP = MAP -- ICP), lowering blood flow and worsening ischemia. \-\-- \#\#\# \*\*Hemodynamic & Oxygenation Targets\*\* 6\. \*\*What are the hemodynamic targets for mean arterial pressure (MAP) and cerebral perfusion pressure (CPP)?\*\* Maintain MAP \>65 mmHg and CPP \>60 mmHg to ensure adequate cerebral blood flow. 7\. \*\*What PaO₂ range is recommended to avoid hypoxemia and hyperoxemia?\*\* Target PaO₂ of 80--120 mmHg and oxyhemoglobin saturation in the high 90s. 8\. \*\*Why is hyperoxemia harmful in brain resuscitation?\*\* Excess oxygen generates reactive oxygen species, worsening neuronal injury. \-\-- \#\#\# \*\*ICP Management Strategies\*\* 9\. \*\*List the stepwise approach to managing elevated ICP.\*\* 1\. Optimize positioning (e.g., 30° head elevation). 2\. Provide analgesia/sedation. 3\. Use hypertonic therapy (mannitol or hypertonic saline). 4\. Administer barbiturates. 5\. Initiate hypothermia (TTM). 6\. Consider surgical decompression. 10\. \*\*When is therapeutic hyperventilation appropriate?\*\* Only for life-threatening cerebral herniation or severe ICP elevation as a short-term bridge to definitive therapy (e.g., surgery). Target PaCO₂ 35--40 mmHg. \-\-- \#\#\# \*\*Seizures & Temperature Control\*\* 11\. \*\*How should acute seizures be managed?\*\* Treat with IV lorazepam. Avoid prophylactic antiepileptics; use continuous EEG if seizures are suspected. 12\. \*\*Why is fever control critical in brain injury?\*\* Fever increases metabolic demand and inflammation, exacerbating secondary injury. Treat temperatures \>38°C with acetaminophen. 13\. \*\*What is targeted temperature management (TTM), and how is it applied?\*\* Maintain comatose cardiac arrest survivors at 33--36°C for 24 hours in the ICU to reduce metabolic demand and improve outcomes. \-\-- \#\#\# \*\*Prognostication & Family Communication\*\* 14\. \*\*Why is neurological prognostication unreliable before 72 hours post-normothermia?\*\* Early exams lack accuracy; delayed neuronal injury and recovery timelines require prolonged observation. 15\. \*\*What is the most common cause of death in cardiac arrest survivors?\*\* Withdrawal of life-sustaining treatment due to perceived poor neurological prognosis. 16\. \*\*What role do emergency physicians play in family communication?\*\* They must set realistic expectations, emphasize uncertainty in early prognosis, and advocate against premature care withdrawal. \-\-- \#\#\# \*\*Guidelines & Outcomes\*\* 17\. \*\*What organizations provide post-cardiac arrest care guidelines?\*\* AHA, ERC, and ESICM, based on ILCOR's CoSTR recommendations. 18\. \*\*What survival rates are reported for out-of-hospital vs. in-hospital cardiac arrest?\*\* Out-of-hospital: 12% survival (75% with favorable neurology). In-hospital: 25% survival. 19\. \*\*How do standardized post-resuscitation protocols impact outcomes?\*\* They improve survival and neurological recovery by addressing multisystem insults (e.g., hemodynamics, temperature, seizures). \-\-- \#\#\# \*\*Miscellaneous Key Points\*\* 20\. \*\*What are the three components of intracranial volume?\*\* Brain (\~80%), blood (\~10%), and CSF (\~10%). 21\. \*\*What is the final consequence of uncontrolled intracranial hypertension?\*\* Cerebellar tonsillar herniation through the foramen magnum, compressing medullary cardiorespiratory centers. 22\. \*\*Why has no neuroprotectant therapy succeeded in clinical trials?\*\* Despite targeting molecular pathways in ischemic injury, none have shown reproducible clinical benefit. 23\. \*\*How does cerebral arteriolar vasodilation worsen ICP?\*\* Vasodilation increases cerebral blood volume, raising ICP and further reducing CPP (vicious cycle). 24\. \*\*What conditions share overlapping pathophysiology with hypoxic-ischemic brain injury?\*\* Stroke and traumatic brain injury (TBI). 25\. \*\*What compensatory mechanisms delay ICP elevation initially?\*\* Shifting CSF to the spinal subarachnoid space and reducing venous blood volume. \-\--