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

Hypertensive Emergency

BP usually > 180/120 with acute end-organ damage. The organ being damaged determines the drug and the target. Do NOT drop BP too fast -cerebral autoregulation cannot keep up.

🔍 Overview

Hypertensive Emergency vs Urgency

Emergency: Severely elevated BP + acute end-organ damage. Requires IV therapy, ICU admission, controlled BP reduction.

Urgency: Severely elevated BP without end-organ damage. Can be managed with oral agents and close outpatient follow-up. NOT an emergency. Outpatient target: SBP <130 for high-risk patients SPRINT, 2015. First-line: thiazide-type diuretic ALLHAT, 2002.

End-Organ Damage to Look For

Neurologic: Hypertensive encephalopathy (AMS, headache, vision changes), hemorrhagic stroke, ischemic stroke
Cardiac: Aortic dissection, ACS, acute pulmonary edema
Renal: AKI, hematuria, proteinuria (hypertensive nephrosclerosis)
Ophthalmologic: Papilledema, retinal hemorrhages (fundoscopy)
Hematologic: Microangiopathic hemolytic anemia (MAHA), TTP-like picture
OB: Eclampsia, HELLP syndrome

Aortic Dissection must be excluded first if BP very high + chest/back pain. Different drugs, different targets. CTA chest/abdomen/pelvis immediately. Do NOT give nitroprusside until dissection excluded.

🚨 Management

BP Reduction Targets -By Syndrome

General Rule: Reduce MAP by no more than 25% in the first hour, then to 160/100 over the next 2–6 hours. Exception: aortic dissection (aggressive), ischemic stroke (conservative).

Syndrome	Target	First-Line Drug
Hypertensive encephalopathy	MAP reduction 20–25% in 1h	Nicardipine or labetalol IV
Aortic dissection (Type A/B)	SBP < 120, HR < 60 ASAP	Esmolol + nitroprusside or nicardipine
Acute pulmonary edema	Rapid reduction	Nicardipine + nitroglycerin IV + diuresis
ACS with hypertension	SBP < 140	Nitroglycerin IV + beta-blocker
Ischemic stroke	Only treat if BP > 220/120 (no tPA) or > 185/110 (if tPA candidate) AHA/ASA, 2019	Labetalol or nicardipine IV -go slow
Hemorrhagic stroke	SBP < 140 ATACH-2, 2016 INTERACT2, 2013	Nicardipine or labetalol IV
Eclampsia	SBP < 160, DBP < 110	Labetalol IV or hydralazine IV + MgSO₄ MAGPIE, 2002
Pheochromocytoma crisis	MAP reduction 20–25%	Phentolamine IV -α-blockade first, then add beta-blocker

Never use beta-blockers alone in pheochromocytoma. Unopposed α stimulation → paradoxical hypertensive crisis. Always α-block first.

Swipe for more examples

📋 Case 1, Hypertensive Emergency Management

Patient: 52M presents with BP 228/134, headache, blurred vision, chest pain. Cr 2.4 (baseline 1.0). Troponin 0.08. UA: 2+ protein, RBC casts.
This is a hypertensive EMERGENCY (not urgency) -end-organ damage present: AKI, proteinuria with active sediment (renal), troponin elevation (cardiac), visual changes (retinal/CNS).
Step 1 -Choose IV agent based on end-organ damage:
- Renal damage → Nicardipine (Cardene) 5mg/hr IV, titrate by 2.5mg/hr q5-15min (max 15mg/hr). Smooth, titratable, no renal dosing needed.
- Aortic dissection → Esmolol (Brevibloc) drip first (target HR <60), THEN add nicardipine. Must reduce HR before afterload reduction.
- Acute pulmonary edema → Nitroglycerin (Nitrostat) drip + furosemide (Lasix).
- Eclampsia → Magnesium sulfate + hydralazine (Apresoline) or labetalol (Trandate).
- Stroke → see specific stroke BP targets (different for ischemic vs hemorrhagic, tPA vs no tPA).
Step 2 -BP target:
- Reduce MAP by no more than 25% in the first hour. Then toward 160/100 over next 2-6 hours.
- Do NOT normalize BP rapidly → risk of watershed infarction (brain, kidneys).
- Exception: Aortic dissection → SBP <120 within 20 minutes.
Step 3 -Transition to oral:
- Once stable on IV × 12-24h → start oral antihypertensive (amlodipine 5-10mg, lisinopril, etc.).
- Overlap IV + PO for 2-4 hours before weaning drip.
Hypertensive URGENCY (BP >180/120 WITHOUT end-organ damage): Do NOT use IV meds. Restart/uptitrate oral meds. Discharge with close follow-up. The BP did not get this high overnight and does not need to come down overnight.

📋 Case 2, Hypertensive Emergency with Acute Aortic Dissection

Patient: 58M with sudden tearing chest pain radiating to back. BP 210/120. CT angiography: Stanford Type B dissection.
Step 1 -IV esmolol drip FIRST: Target HR <60 BEFORE lowering BP. Beta-blocker first to reduce aortic shear stress. Do NOT lower BP without HR control first, dropping BP alone causes reflex tachycardia → increased aortic shear → propagation of dissection.
Step 2 -Add vasodilator AFTER HR controlled: Nicardipine or nitroprusside for BP target <120 systolic within 20 minutes. Never nitroprusside alone, must have beta-blocker on board first.
Step 3 -Pain control: IV morphine. Pain drives catecholamine release → higher BP. Adequate analgesia is part of BP management.
Type A (ascending) → emergent surgery. Type B (descending) → medical management unless complicated (malperfusion, rupture, refractory pain).
Key Lesson: In dissection, HR control comes BEFORE BP control. Esmolol first, then vasodilator. Target SBP <120 and HR <60. Never nitroprusside alone.

📋 Case 3, Hypertensive Emergency with Acute Pulmonary Edema

Patient: 72F with flash pulmonary edema, BP 230/130, SpO2 82%, severe respiratory distress.
Step 1 -Position + BiPAP immediately: Sit upright. BiPAP reduces preload + afterload + improves oxygenation. Start before anything else.
Step 2 -IV nitroglycerin drip: Start 5 mcg/min, titrate rapidly up to 200 mcg/min if needed. Potent vasodilator that reduces both preload AND afterload. Nitroglycerin is MORE important than diuresis in the first 30 minutes.
Step 3 -IV furosemide 80-120mg: Important but secondary to nitroglycerin. The acute crisis is afterload-driven, not volume-driven (though volume contributes).
Do NOT give labetalol, negative inotropy worsens acute decompensated heart failure. Avoid beta-blockers in this setting.
BP target: Reduce by 25% in the first hour. Reassess with repeat CXR, SpO2 trending, work of breathing.
Key Lesson: Flash pulmonary edema = BiPAP + nitroglycerin drip. Nitroglycerin is the hero, not lasix. Avoid beta-blockers in acute decompensated HF.

💊 Medications & Doses

IV Antihypertensive Agents

Drug	Dose	Onset	Best For	Avoid In
Nicardipine (Cardene)	5–15 mg/hr IV drip	5–10 min	Most hypertensive emergencies. Excellent titratable agent.	Advanced aortic stenosis
Labetalol (Trandate)	20–80 mg IV bolus q10min, or 0.5–2 mg/min drip	5 min	Aortic dissection, stroke, eclampsia	Asthma, severe bradycardia, acute HF
Esmolol (Brevibloc)	500 mcg/kg bolus, then 50–200 mcg/kg/min	1–2 min	Aortic dissection (HR control)	Bronchospasm, bradycardia
Sodium Nitroprusside	0.3–10 mcg/kg/min	Seconds	Hypertensive emergency when other agents fail	Renal failure (cyanide toxicity), elevated ICP, pregnancy
Nitroglycerin (Nitrostat)	5–200 mcg/min IV	1–2 min	Pulmonary edema, ACS	Aortic dissection (reflex tachycardia), PDE5 inhibitor use
Hydralazine (Apresoline)	10–20 mg IV q4–6h	10–20 min	Eclampsia (if labetalol not available)	Aortic dissection, aortic aneurysm (reflex tachycardia worsens shear stress), CAD (unpredictable response, reflex tachycardia), elevated ICP

Related Topics

Acute Decompensated Heart FailureAcute Exacerbation of COPD (AECOPD)Acute Ischemic StrokeAcute Mesenteric IschemiaAcute PancreatitisAirway & Ventilator Management

🧪 Workup

Workup -Hypertensive Emergency

The workup answers ONE question: Is there end-organ damage? YES → hypertensive emergency (IV meds, ICU). NO → hypertensive urgency (oral meds, outpatient). The BP number alone does NOT define the emergency.

Test	Looking For	End-Organ Damage
BMP + Cr	Cr above baseline	Renal: AKI from malignant nephrosclerosis
UA + microscopy	Proteinuria, hematuria, RBC casts	Renal: Active sediment = hypertensive nephropathy
Troponin	Elevated, rise-fall	Cardiac: Demand ischemia or ACS from afterload
ECG	LVH, ST/T changes, new arrhythmia	Cardiac: Acute ischemia, atrial strain
CXR	Pulmonary edema, wide mediastinum	Cardiac: Flash pulmonary edema. Wide mediastinum → CTA for dissection
Fundoscopy	Flame hemorrhages, papilledema	Retinal/CNS: Grade III-IV = malignant HTN
CT head	Hemorrhage, PRES, ischemia	CNS: Order if headache, AMS, focal deficits, seizures, visual changes
Peripheral smear	Schistocytes, low platelets	Hematologic: MAHA from shear stress. Check LDH ↑, haptoglobin ↓
BNP	Elevated	Cardiac: Flash pulmonary edema from afterload crisis
Urine drug screen	Cocaine, amphetamines	Etiology: Avoid beta-blockers with cocaine (unopposed alpha)
Pregnancy test	Positive β-hCG	Etiology: Pre-eclampsia/eclampsia → magnesium + delivery

Emergency vs Urgency: Emergency = elevated BP + end-organ damage → IV meds, ICU, reduce MAP 25% in first hour. Urgency = elevated BP WITHOUT damage → oral meds, discharge with follow-up 24-72h. Do NOT use IV meds for urgency.

📋 On Rounds

On Rounds

Pimp Questions

Why should you not lower BP too fast in hypertensive emergency?

Chronic hypertension shifts the cerebral autoregulation curve rightward. These patients need higher perfusion pressures to maintain cerebral blood flow. Rapid BP reduction causes cerebral ischemia -watershed infarcts, blindness (anterior ischemic optic neuropathy), renal infarction. Max 25% MAP reduction in first hour.

What is the BP target for ischemic stroke and why is it different?

Only treat if BP > 220/120 (no tPA) because elevated BP in ischemic stroke maintains perfusion to the ischemic penumbra. Lowering BP aggressively expands the infarct. Exception: if patient is a tPA candidate, reduce to < 185/110 first to reduce hemorrhage risk.

Why do you target only 25% MAP reduction in the first hour instead of normalizing BP?

Cerebral autoregulation is shifted right in chronic hypertension. The brain has adapted to higher pressures -the autoregulatory curve (which maintains constant cerebral blood flow across a range of MAPs) shifts upward. If you drop BP too quickly to "normal" levels, you fall below the lower limit of autoregulation → cerebral hypoperfusion → watershed stroke.

What IV antihypertensive do you choose for different end-organ emergencies?

Match the drug to the complication: Nicardipine (DHP CCB drip): best all-purpose -works for most emergencies. Smooth, titratable, no CNS depression. Clevidipine: ultra-short acting CCB -good when minute-to-minute control needed. Labetalol: combined α/β blocker -good for aortic dissection (reduces HR + BP), preeclampsia (safe in pregnancy). Esmolol: ultra-short BB -best for dissection when you need rapid HR < 60.

Clinical Examples

📋 Case 1, Hypertensive Emergency with Acute Kidney Injury

Patient: 54M, non-adherent to amlodipine and lisinopril, presents with headache, blurred vision, and nausea. No chest pain or focal neurologic deficits.

Key findings: BP 238/142, HR 92. Fundoscopy: flame hemorrhages + papilledema. Cr 3.4 (baseline 1.2), proteinuria 3+, hematuria. CT head negative. TTE: LVH, EF 55%.

Management:

IV nicardipine drip starting at 5 mg/hr, titrate q5-15 min (max 15 mg/hr)
Target: reduce MAP by 25% in first hour, then to 160/100 over next 2-6h
Arterial line for continuous BP monitoring
Trending Cr q12h, expect improvement with controlled BP reduction
Transition to oral amlodipine 10 mg + lisinopril 20 mg when stable on drip x 24h

Teaching point: Hypertensive nephrosclerosis with acute end-organ damage (AKI + papilledema) defines hypertensive emergency. Nicardipine is first-line for most hypertensive emergencies: smooth, titratable, no CNS depression. Renal function often improves with controlled BP reduction.

📋 Case 2, Hypertensive Emergency in Acute Ischemic Stroke

Patient: 72F, HTN and AF (not on anticoagulation), presents with acute right-sided weakness and aphasia. Symptom onset 2 hours ago. NIHSS 14.

Key findings: BP 204/118, HR 88 irregular. CT head: no hemorrhage. CTA: left MCA occlusion. tPA candidate (within window, no contraindications).

Management:

BP must be < 185/110 BEFORE tPA administration
IV labetalol 10-20 mg bolus; repeat if needed. Alternatively, nicardipine drip
Once tPA given: maintain BP < 180/105 for 24 hours
If NOT a tPA candidate: only treat BP if > 220/120 (permissive hypertension protects the penumbra)
Thrombectomy evaluation given large vessel occlusion

Teaching point: BP management in stroke differs from other hypertensive emergencies. Aggressive BP lowering in ischemic stroke expands the infarct by reducing perfusion to the penumbra. The only reason to lower BP acutely is to safely give tPA. AHA/ASA Stroke Guidelines, 2019

📋 Case 3, Pheochromocytoma Crisis

Patient: 42F, no prior medical history, presents with episodic severe headaches, palpitations, and diaphoresis. In the ED, BP spikes to 260/150 with HR 132 during a paroxysm.

Key findings: Between episodes: BP 145/90. 24h urine metanephrines: 4x upper normal. CT abdomen: 4.2 cm right adrenal mass. Plasma-free metanephrines markedly elevated.

Management:

Phentolamine 5 mg IV bolus for acute crisis (alpha-blocker)
Start phenoxybenzamine 10 mg BID, titrate up over 10-14 days pre-operatively
Add beta-blocker (propranolol) ONLY AFTER adequate alpha blockade (typically 3-5 days later)
NEVER give beta-blocker first, causes unopposed alpha stimulation and hypertensive crisis
High-sodium diet + liberal fluids to restore intravascular volume before surgery

Teaching point: Pheochromocytoma hypertensive crisis requires alpha-blockade FIRST. Beta-blockers before alpha-blockade removes the beta-2 vasodilatory counterbalance, leaving unopposed alpha vasoconstriction. This is one of the most testable concepts in medicine.

📋 Sample Presentation

"Mrs. Okafor is a 58-year-old with poorly controlled hypertension who presented with BP 210/130, severe headache, and confusion. She was found to have papilledema on fundoscopy and elevated creatinine of 2.8 from a baseline of 1.0, consistent with hypertensive emergency with end-organ damage involving the CNS and kidneys. CT head showed no hemorrhage. She was started on nicardipine drip and MAP was reduced by 22% over the first hour to 147. She is now alert, BP 158/96 on nicardipine 8 mg/hr. Plan is to continue gradual reduction to target BP 150/90 over the next 24–48 hours, then transition to oral agents."

Monitoring Parameters -Hypertensive Emergency

Parameter	Frequency	Target / Action
Arterial line BP	Continuous (art line mandatory in ICU)	Reduce MAP no more than 25% in the first hour. Cuff pressures are insufficient for IV drip titration -art line is standard of care.
MAP during titration	q5–15 min while adjusting IV drip	First hour: ≤ 25% MAP reduction. Next 2–6h: target ~160/100. Next 24–48h: gradual normalization. Too fast → watershed stroke.
Neuro checks	q1–2h during active titration	GCS, pupil reactivity, focal deficits, level of consciousness. New deficit during BP lowering → stop titration, allow BP to rise, urgent imaging (stroke?).
Urine output	q1h (Foley)	UOP ≥ 0.5 mL/kg/hr. Declining UOP during BP reduction = renal hypoperfusion -may need to allow higher BP target.
Creatinine	q12–24h	Trend from baseline. Rising Cr suggests renal end-organ injury or overly aggressive BP lowering. Adjust target accordingly.
Troponin	On admission, repeat at 6h if elevated or ongoing chest pain	Hypertensive emergency can cause demand ischemia (type 2 MI). Elevated troponin changes management -cardiology consult.
Fundoscopic exam	On admission, repeat if worsening	Papilledema, flame hemorrhages, cotton-wool spots, AV nicking. Presence confirms end-organ damage and classifies as true emergency vs urgency.
Transition to oral agents	After 12–24h stable on IV drip	Start long-acting oral antihypertensives (amlodipine, lisinopril, etc.) with IV drip overlap. Wean drip gradually as oral agents take effect (24–48h). Do not abruptly stop IV.

BP reduction timeline: 25% MAP reduction in first hour → 160/100 over next 2–6h → gradual normalization over 24–48h. Exception: aortic dissection -target SBP < 120 + HR < 60 within minutes (esmolol + nicardipine). Exception: ischemic stroke -do NOT lower BP unless > 220/120 (or > 185/110 if tPA candidate).

⚡ Summary

Summary

Emergency vs Urgency

Emergency = high BP + end-organ damage (CNS, cardiac, renal, eyes). Urgency = high BP alone -restart oral meds, outpatient f/u. Outpatient target SBP <120 SPRINT, 2015.

Exclude First

Aortic dissection -if chest/back pain + high BP. CTA immediately. Requires aggressive reduction and beta-blockade.

BP Reduction Rule

Reduce MAP by ≤ 25% in first hour. Then to 160/100 over next 6 hrs. Except dissection (aggressive) and ischemic stroke (conservative).

Go-To Drug

Nicardipine IV -titratable, reliable, works for most emergencies. Labetalol for dissection/stroke/eclampsia.

Pheo Rule

Alpha-block FIRST (phentolamine), THEN add beta-blocker. Never beta-block first -causes unopposed alpha hypertensive crisis.

Nitroprusside Warning

Risk of cyanide toxicity in renal failure and prolonged use. Also causes elevated ICP. Use only when other agents fail.

📄 One Pager

ICU · One Pager

Hypertensive Emergency

End-organ damage defines the emergency. The organ being damaged determines the drug and the target. Never drop BP > 25% in first hour.

🚨 Exclude First -Aortic Dissection

Chest/back pain + very high BP → CTA chest/abdomen NOW
Target SBP < 120, HR < 60 ASAP
Esmolol + nicardipine or nitroprusside
Never nitrates alone (reflex tachycardia)

📐 BP Reduction Rule

Reduce MAP ≤ 25% in first hour
Then to 160/100 over 2–6h
Exception: Dissection (aggressive) and ischemic stroke (conservative)
Ischemic stroke: only treat if BP > 220/120

💊 Drug by Syndrome

Most emergenciesNicardipine 5–15 mg/hr IV

Aortic dissectionEsmolol + nicardipine

ACS / pulmonary edemaNitroglycerin IV + labetalol

Stroke (hemorrhagic)Nicardipine → SBP < 140

EclampsiaLabetalol IV + MgSO₄

PheochromocytomaPhentolamine (α first!) then β-blocker

⚠️ Pheo Rule

α-block FIRST with phentolamine
THEN add beta-blocker
Beta-block first → unopposed α → crisis

🧠 Why Not Too Fast?

Chronic HT shifts autoregulation rightward
Rapid drop → cerebral ischemia
Watershed infarcts, blindness, renal infarction

🩺 Health Check