When to intubate in GCS?

GCS ≤ 8 requires intubation for airway protection. The patient cannot protect their own airway at this level of consciousness. Motor score is the most prognostically important component.

What is the best initial fluid for sepsis resuscitation?

Lactated Ringer's (LR) is the preferred resuscitation fluid. The SMART trial (2018) showed balanced crystalloids reduced death, new renal failure, and persistent renal dysfunction compared to normal saline.

When to start vasopressors in septic shock?

Start norepinephrine (first-line vasopressor) if MAP remains < 65 mmHg after initial 30 mL/kg crystalloid resuscitation, or earlier if patient is profoundly hypotensive. Do not delay pressors to complete full fluid resuscitation.

Why can serum uric acid be normal during acute gout?

During acute inflammation, IL-6 increases renal urate excretion and redistributes urate from plasma to tissues. Up to 40% of acute gout flares have normal serum uric acid. Joint aspiration with polarized microscopy is needed for definitive diagnosis.

How do you distinguish lupus flare from infection in SLE?

Key clues: CRP is low/normal in flare but elevated in infection. Complement (C3/C4) drops in flare but is normal/elevated in infection. Procalcitonin is elevated in bacterial infection but normal in flare. Anti-dsDNA rises in flare, stable in infection.

What is the difference between DKA and HHS?

DKA features acidosis (pH 600), hyperosmolality (> 320), and minimal ketosis -typically in Type 2 DM. DKA requires insulin drip; HHS requires aggressive fluid resuscitation first.

When to give tPA in acute ischemic stroke?

IV alteplase (tPA) can be given within 4.5 hours of last known well time in eligible patients. CT head must rule out hemorrhage first. For large vessel occlusion, mechanical thrombectomy can be performed up to 24 hours with favorable imaging.

What antibiotics for community-acquired pneumonia?

Inpatient non-ICU: ceftriaxone + azithromycin. ICU: ceftriaxone + azithromycin (add vancomycin if MRSA risk). Outpatient healthy: amoxicillin. Outpatient with comorbidities: augmentin + azithromycin or respiratory fluoroquinolone. Duration: 5 days if clinically stable for 48 hours.

How to interpret iron studies?

Iron deficiency: low ferritin (< 30), high TIBC, low iron, low transferrin saturation (< 20%). Anemia of chronic disease: normal/high ferritin (acute phase reactant), low TIBC, low iron. A ferritin of 50-100 in an inflamed patient may still represent iron deficiency.

What is the correction rate for hyponatremia?

Correct sodium no more than 8 mEq/L in 24 hours to avoid osmotic demyelination syndrome (ODS). For symptomatic severe hyponatremia with seizures, give 3% hypertonic saline 100-150 mL bolus over 10-20 minutes. If overcorrected, use D5W + DDAVP rescue protocol.

When to start antibiotics in meningitis?

Within 30-60 minutes. Do NOT delay antibiotics for LP or CT. Draw blood cultures, start empiric antibiotics (vancomycin + ceftriaxone ± ampicillin if > 50 or immunocompromised), then perform LP when possible. Dexamethasone should be given before or with the first antibiotic dose.

DOACs vs warfarin in antiphospholipid syndrome?

DOACs are contraindicated in APS. The TRAPS trial (2018) showed rivaroxaban was inferior to warfarin with more thrombotic events in triple-positive APS patients. Warfarin with INR target 2-3 is the standard for APS, indefinitely.

How to manage scleroderma renal crisis?

ACE inhibitors (captopril) are life-saving -start immediately and titrate aggressively. Do NOT hold for rising creatinine. Steroids > 15 mg prednisone per day precipitate scleroderma renal crisis. ARBs are NOT a substitute -evidence is only for ACEi.

What are the 4 pillars of heart failure treatment?

Guideline-directed medical therapy (GDMT) for HFrEF: (1) ARNI or ACEi/ARB, (2) beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) MRA (spironolactone or eplerenone), (4) SGLT2 inhibitor (dapagliflozin or empagliflozin). All four should be initiated and titrated to target doses.

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EMERGENTICU

Post-Cardiac Arrest Care (ROSC)

Return of spontaneous circulation is just the beginning. Post-cardiac arrest syndrome causes multi-organ dysfunction. Targeted temperature management, hemodynamic optimization, and finding the cause define survival and neurologic outcome.

🔍 Overview

Post-Cardiac Arrest Syndrome

After ROSC, four simultaneous processes occur:

Post-arrest brain injury -cerebral edema, impaired autoregulation, seizures (30–40% of arrests)
Post-arrest myocardial dysfunction -global systolic/diastolic dysfunction (peaks at 24–48 hrs, often reversible)
Systemic ischemia/reperfusion injury -cytokine storm, coagulopathy, multi-organ dysfunction
Precipitating cause -must identify and treat (ACS, PE, electrolytes, toxins)

Reversible Causes of Cardiac Arrest -The H's & T's

Mnemonic: 6 H's and 6 T's -Run through every H and T systematically during and after every arrest. If you don't find the cause, you can't fix it.

H's	Clue / How to Find	Fix
Hypovolemia	Flat IVC on echo, trauma, GI bleed	Volume resuscitation, blood products, source control
Hypoxia	SpO₂, cyanosis, airway obstruction	Secure airway, ventilate, confirm ETT placement
Hydrogen ion (acidosis)	ABG -pH < 7.1, severe DKA, renal failure, sepsis	Bicarb, treat underlying cause
Hypo/Hyperkalemia	ECG (peaked T's, wide QRS, sine wave), BMP	Calcium, insulin/glucose, dialysis (hyperK). IV KCl, Mg (hypoK).
Hypothermia	Core temp < 30°C, exposure history, near-drowning	Active rewarming. "Not dead until warm and dead."
Hypoglycemia	Fingerstick glucose, diabetic on insulin/sulfonylureas, altered mental status pre-arrest	D50W 25–50 mL IV push (1–2 amps). Recheck glucose q15min.

T's	Clue / How to Find	Fix
Tension pneumothorax	Absent breath sounds, tracheal deviation, hypotension, distended neck veins	Needle decompression (2nd ICS MCL) → chest tube
Tamponade (cardiac)	Distended neck veins, muffled heart sounds, hypotension (Beck's triad). Echo: effusion + RV collapse.	Pericardiocentesis (subxiphoid, echo-guided)
Toxins	Med hx, pill bottles, toxidrome. Common: TCA, digoxin, beta-blockers, CCBs, opioids.	Specific antidotes. Bicarb (TCA), digibind, glucagon (BB), high-dose insulin (CCB), naloxone.
Thrombosis -PE	RV dilation on echo, history of immobility/DVT, PEA arrest	tPA 50mg IV push (if massive PE during arrest), surgical/IR embolectomy
Thrombosis -MI	12-lead ECG: STEMI or new LBBB, regional wall motion abnormality on echo	Emergent cath lab -even during CPR (in select patients)
Trauma	Mechanism of injury, external signs of hemorrhage, unstable pelvis, distended abdomen	Massive transfusion protocol, surgical intervention, pelvic binder. Address hemorrhagic shock.

Immediately post-ROSC: ECG + echo. STEMI → cath lab immediately (even if neurologically devastated). Echo → wall motion, RV dilation (PE), tamponade, EF.

🚨 Management

Post-Arrest Bundle -ICU Protocol

Immediately Post-ROSC

12-lead ECG (STEMI → cath lab without delay), ABG, labs, portable CXR, bedside echo. Establish arterial line + central line. If still on scene -transport immediately. For OHCA without ST elevation, immediate angiography is NOT required -COACT, 2019 showed no benefit to immediate cath in non-STEMI arrest.

Airway & Ventilation

Confirm ETT position. Target SpO₂ 94–98% -do NOT hyperoxia (increases reperfusion injury). Target PaCO₂ 35–45 mmHg -avoid hypocapnia (causes cerebral vasoconstriction). Titrate FiO₂ to achieve SpO₂ target, not 100%.

Hemodynamics

Target MAP ≥ 65–70 mmHg. Norepinephrine first-line. Dobutamine if post-arrest myocardial dysfunction. Avoid hypotension (worsens brain injury). Avoid aggressive fluid loading in pulmonary edema.

Targeted Temperature Management (TTM)

Target core temperature 32–36°C for ≥ 24 hours in comatose survivors. TTM-2 2021: 33°C vs 37.5°C -no difference in survival. Current evidence: prevent fever (T > 37.7°C) is mandatory. Active cooling to 33°C still widely practiced and reasonable in deep coma. Use cooling blankets, Arctic Sun, or invasive methods.

Seizure Management

Continuous EEG monitoring -up to 30–40% have post-arrest seizures including NCSE. Treat seizures aggressively. Prophylactic AEDs not recommended routinely but use if clinical or EEG seizure.

Neurological Prognostication

Wait ≥ 72 hours after rewarming before prognostication (sedation/hypothermia confound exam). Use multimodal approach: neuro exam (pupillary reflex, corneal reflex, motor response), SSEP (bilateral absent N20 = poor prognosis), EEG, CT/MRI brain, NSE (serum marker). No single test is definitive.

Secondary Prevention ICD & Disposition

Every VT/VF survivor needs ICD evaluation before discharge unless the arrest was due to a completely reversible cause. Missing this step is a common disposition error and can be fatal, since recurrence risk is substantial.

Secondary prevention ICD is a Class I indication for any survivor of sudden cardiac arrest (VF or hemodynamically unstable sustained VT) NOT due to a transient or reversible cause. Trial basis: AVID 1997, CIDS 2000, CASH 2000, all showed ICD superior to amiodarone for secondary prevention.

When ICD IS indicated (Class I)

Survivor of VF or hemodynamically unstable VT NOT from a clearly reversible cause
Sustained VT with structural heart disease (ischemic or non-ischemic cardiomyopathy), whether or not hemodynamically tolerated
Syncope with inducible sustained VT on EP study in a patient with structural heart disease
Genetic arrhythmia syndromes with prior cardiac arrest: long QT, Brugada, ARVC, CPVT, HCM with prior arrest

When ICD is NOT indicated (reversible causes)

Acute MI with complete revascularization and no residual ischemia, VF within 24-48h of MI is often attributable to acute ischemia alone and doesn't by itself mandate secondary ICD
Electrolyte derangement (severe hypokalemia, hypomagnesemia), fully corrected, no structural substrate
Drug-induced QT prolongation, offending drug stopped and QTc normalized off the agent
Commotio cordis (blunt chest impact causing VF), structurally normal heart, no long-term risk
Severe acid-base or metabolic disturbance, cause identified and corrected
Illicit drug-induced arrest (cocaine, methamphetamine) with structurally normal heart and commitment to abstinence

Timing rules before implantation:

Post-MI primary prevention: wait ≥ 40 days if EF persistently ≤ 35% (DINAMIT 2004, IRIS 2009, no benefit from earlier ICD). But secondary prevention ICDs can go in sooner if the arrest was NOT attributable to the acute MI itself.
Post-revascularization (CABG/PCI): wait ≥ 90 days before primary prevention ICD assessment, EF often recovers with revascularization.
New cardiomyopathy (ischemic or non-ischemic): ≥ 3 months of maximally tolerated GDMT before primary prevention ICD assessment, 30-40% of patients recover EF above 35% on GDMT.
Neurologically devastated survivors: defer ICD, prognostication must first confirm meaningful neurologic recovery. Implanting in a patient who will not wake up is not appropriate.

Before-Discharge Checklist

EP consultation to decide ICD vs no ICD
Echocardiogram to document EF (primary vs secondary prevention logic differs)
Coronary angiography (if not already done) to rule out ischemic substrate
Cardiac MRI if etiology unclear, detects ARVC, infiltrative disease, myocarditis, scar burden
QTc measurement off all QT-prolonging drugs
Toxicology screen and medication review
Family history + genetic testing if channelopathy or ARVC suspected; family screening
GDMT initiation if structural heart disease (ARNI/ACEi/ARB, BB, MRA, SGLT2i)
Wearable cardioverter-defibrillator (LifeVest) bridge if ICD decision deferred (pending GDMT trial, revascularization recovery, neurologic prognostication), VEST 2018 evidence mixed; used pragmatically in many centers.
Return precautions and AED-at-home counseling for the family

💊 Medications & Doses

Medications

Drug	Dose	Role	Notes
Norepinephrine (Levophed)	0.1–1 mcg/kg/min	Vasopressor (first-line)	Maintain MAP ≥ 65–70 post-ROSC. Post-arrest myocardial dysfunction is common -monitor CO.
Dobutamine (Dobutrex)	2–15 mcg/kg/min	Post-arrest cardiogenic shock	Add if MAP adequate but echo shows severely reduced EF. Titrate to echo/clinical response.
Propofol (Diprivan)	5–50 mcg/kg/min	Sedation during TTM	Reduces shivering, facilitates temperature control. Monitor for propofol infusion syndrome.
Meperidine / Buspirone	Meperidine 25–50 mg IV PRN	Anti-shivering during TTM	Shivering increases metabolic demand and raises temperature. Treat aggressively. Magnesium also helps.
Aspirin + Heparin	Per ACS protocol	If ACS precipitant	Do not withhold antiplatelet/anticoagulation for neurologic concerns alone. Treat the cause.
Insulin infusion	Target BG 140–180 mg/dL	Glycemic control	Avoid both hypoglycemia and severe hyperglycemia. Tight control (< 110) increases hypoglycemia and worsens outcomes.

📋 On Rounds

On Rounds

Pimp Questions

Why do we avoid hyperoxia post-ROSC?

Hyperoxia (PaO₂ > 300 mmHg) worsens cerebral reperfusion injury through free radical generation. Multiple observational studies Kilgannon 2010 show increased mortality with hyperoxia post-ROSC. Target SpO₂ 94–98%, not 100%. Titrate FiO₂ down as soon as possible after ROSC.

When can you prognosticate neurological outcome after cardiac arrest?

Not before 72 hours after rewarming from hypothermia. Sedation, hypothermia, and metabolic derangements all suppress neurological function and mimic poor prognosis. Early withdrawal based on exam alone leads to self-fulfilling prophecy. Use multimodal assessment: neuro exam + SSEP + EEG + MRI brain + NSE levels.

What is targeted temperature management (TTM) and what does current evidence say?

TTM2, 2021: targeted hypothermia at 33°C did NOT improve survival or neurologic outcome compared to normothermia (targeting ≤ 37.5°C and actively preventing fever). This changed practice -the benefit is from preventing fever, not inducing hypothermia. Current approach: avoid fever aggressively (target ≤ 37.5°C × 72h). If using active cooling, 33°C × 24h is still acceptable. Rewarm slowly (0.25°C/hr).

When can you prognosticate neurologic outcome after cardiac arrest, and what tools do you use?

Wait ≥ 72 hours after rewarming (if TTM used) or ≥ 72h from ROSC. Earlier assessment is unreliable due to sedation, hypothermia, and metabolic derangements. Multimodal approach (no single test is sufficient): (1) Clinical exam: absent pupillary and corneal reflexes at 72h + bilaterally absent motor response = poor prognosis. (2) EEG: burst suppression or status epilepticus at 72h

Clinical Examples

Case 1: ROSC After VF Arrest with STEMI

Presentation: 58M found unresponsive at home. EMS: VF, defibrillated × 2, ROSC after 18 minutes of CPR. Arrives intubated. 12-lead ECG shows inferior STEMI.

Priorities: Cath lab activated immediately, PCI does not wait for neurologic prognostication. Post-PCI, initiate TTM: target ≤ 37.5°C × 72h with active fever prevention per TTM2, 2021. Titrate FiO₂ to SpO₂ 94–98%, avoid hyperoxia and hypoxia. MAP ≥ 65 with Norepinephrine; add Dobutamine if echo shows post-arrest low EF.

Teaching point: STEMI post-arrest goes to the cath lab regardless of coma. Post-arrest myocardial stunning is reversible, echo EF often normalizes by 48–72h. Rewarm slowly (0.25°C/hr) to avoid rebound hyperthermia.

Case 2: Neurologic Prognostication, Day 3 Post-Arrest

Presentation: 65F, out-of-hospital VF arrest, ROSC after 12 minutes. TTM completed (fever prevention protocol). Now day 3 post-normothermia, still comatose. GCS 5 (E1V1M3). Absent pupillary reflexes bilaterally. EEG shows burst suppression pattern. Family asking about prognosis.

Workup: SSEP, bilateral N20 waves absent (strongest predictor of poor neurologic outcome). MRI brain ordered. NSE level elevated. CT head: no hemorrhage, diffuse cerebral edema.

Management: Do not withdraw support yet, full 72h post-normothermia is mandatory. Convene multidisciplinary meeting (neurology, ICU, palliative). Absent bilateral N20 SSEPs + absent pupillary reflexes + burst suppression EEG = convergent poor prognosis. Family meeting with honest, compassionate goals-of-care discussion.

Teaching point: No single test predicts outcome, multimodal assessment required. Early withdrawal is a self-fulfilling prophecy.

Case 3: Hypoxic Cardiac Arrest from Opioid OD

Presentation: 45M found unresponsive, suspected fentanyl overdose. EMS: PEA, ROSC after 8 minutes of CPR and Naloxone administration. Non-shockable rhythm. Arrives intubated, GCS 6.

Priorities: No cardiac cause, PCI not indicated. ECG: no STEMI. Bedside echo: normal EF, no wall motion abnormality. CT head to rule out intracranial pathology. Target SpO₂ 94–98%, normocapnia (PaCO₂ 35–45). Fever prevention protocol initiated. Continuous EEG, treat seizures aggressively if present.

Goals of care: 8 minutes of CPR is relatively short, prognosis may be better than prolonged arrest. Defer prognostication ≥ 72h post-normothermia. If no meaningful neurologic recovery expected on reassessment, early goals-of-care conversation with family. Address substance use disorder, consider Buprenorphine initiation prior to discharge if recovery occurs.

Teaching point: Hypoxic arrests (OD, asphyxia) receive the same post-arrest bundle, TTM, avoid hyperoxia, EEG monitoring. The cause determines whether you go to the cath lab, not the post-arrest protocol itself.

📋 Sample Presentation

"Mr. Perez is a 55-year-old who suffered an out-of-hospital VF arrest with 18 minutes of CPR before ROSC. He was brought to our ICU intubated. Initial ECG showed STEMI -he underwent emergency PCI with drug-eluting stent to the RCA. He is on TTM protocol at 33°C, day 1. He is on NE 0.2 mcg/kg/min, MAP 68. Echo shows EF of 30% with inferior wall hypokinesis -on dobutamine 5 mcg/kg/min. SpO₂ 96% on FiO₂ 0.4, PaCO₂ 41. Continuous EEG shows no seizure activity. BG 152, on insulin drip. We will maintain cooling for 24 hours total, then rewarm at 0.5°C per hour. Neurological prognostication deferred for 72 hours post-rewarming."

Monitoring Parameters -Hypertensive Emergency

Parameter	Frequency	Target / Action
Vitals	q4h floor, q1–2h ICU	HR, BP, RR, SpO₂, Temp -notify for significant deviations
Labs (BMP, CBC)	Daily AM or as indicated	Trend Cr, K⁺, WBC, Hgb -adjust treatment based on trajectory
Disease-specific markers	Per clinical context	See Overview and Management tabs for condition-specific targets
I&Os	Strict if volume-sensitive	UOP ≥ 0.5 mL/kg/hr. Net fluid balance guides diuresis or resuscitation.
Telemetry	Continuous if indicated	Arrhythmia detection. Discontinue when no longer indicated (reduces alarm fatigue).
Clinical response	Each assessment	Symptom improvement, functional status, appetite, mental status -the exam matters more than labs

Don't just order labs -act on them. Every lab should have a clear clinical question. If you wouldn't change management based on the result, don't order it.

⚡ Summary

Summary

Immediate

ECG → STEMI → cath lab now. Echo → find reversible cause. Avoid hyperoxia, avoid hypocapnia.

Hemodynamics

MAP ≥ 65–70. NE first-line. Add dobutamine for low EF. Post-arrest myocardial dysfunction is often reversible at 48–72h.

TTM

Prevent fever (> 37.7°C) is mandatory. Cooling to 33°C reasonable in deep coma. 24 hours minimum. Rewarm slowly.

Seizures

30–40% have post-arrest seizures. Continuous EEG for comatose patients. Treat aggressively if detected.

Prognostication

Wait ≥ 72h post-rewarming. Multimodal: exam + SSEP + EEG + MRI + NSE. Never base on one test alone.

H's & T's

Always find the cause. Hypovolemia, Hypoxia, Hydrogen ion, Hypo/hyperK, Hypothermia, Hypoglycemia, Tension PTX, Tamponade, Toxins, Thrombosis (PE), Thrombosis (MI), Trauma.

📄 One Pager

ICU · One Pager

Post-Cardiac Arrest Care (ROSC)

ROSC is the beginning, not the end. ECG → echo → TTM → avoid hyperoxia → find the cause. Don't prognose for 72h post-rewarming.

❤️ Post-ROSC Bundle

12-lead ECG -STEMI → cath lab immediately (even if comatose)

Bedside echo -EF, wall motion, tamponade, RV dilation (PE)

Avoid hyperoxia -target SpO₂ 94–98%, NOT 100% (free radical injury) Kilgannon 2010

MAP ≥ 65–70 -NE first-line. Dobutamine if post-arrest low EF.

TTM: Prevent fever > 37.7°C mandatory. 33°C reasonable in deep coma TTM-2 2021

Continuous EEG -30–40% have post-arrest seizures (NCSE)

🔠 6 H's & 6 T's

Hypovolemia, Hypoxia
Hydrogen ion, Hypo/hyperK
Hypothermia, Hypoglycemia
Tension PTX, Tamponade
Toxins, Thrombosis (PE/MI)
Trauma

🧠 Prognostication

Wait ≥ 72h post-rewarming
Neuro exam + SSEP + EEG
MRI brain + NSE levels
No single test is definitive

⚠️ Pitfalls

Hyperoxia (FiO₂ 1.0 left on)
Early prognostication
Missing post-arrest NCSE
Delaying PCI for STEMI

🧪 Workup

Workup -Post-Cardiac Arrest Care (ROSC)

Topic-specific workup details are in the Overview and Management tabs.