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

Cardiogenic Shock

Cardiac pump failure causing inadequate tissue perfusion. Cold, clammy, hypotensive with elevated filling pressures. In-hospital mortality 40–50%. Identify and reverse the cause -fast.

🔍 Overview

Definition & Criteria

Cardiogenic shock = cardiac pump failure resulting in tissue hypoperfusion. Classic hemodynamic criteria: SBP < 90 mmHg for > 30 min (or vasopressor requirement), CI < 2.2 L/min/m², PCWP > 15 mmHg.

Causes

Cause	Key Features
Acute MI / ACS (~70–80%)	Most common cause. Large anterior STEMI, RV infarct. Emergent PCI/cath lab. SHOCK trial: early revascularization ↓ 6-month mortality SHOCK, 1999.
Acute decompensated HFrEF (~10–15%)	End-stage HF on maximal GDMT. Progressive pump failure. Bridge to LVAD/transplant or palliative.
Acute valvular emergency (~5–8%)	Acute severe MR (papillary muscle rupture post-MI), acute AR (endocarditis, aortic dissection), critical AS. Emergent surgical consult.
Fulminant myocarditis (~2–5%)	Viral (Coxsackie, parvovirus B19), giant cell, eosinophilic. Young patient, rapid-onset HF. MRI if stable, biopsy if refractory. May need mechanical circulatory support (MCS) bridge to recovery.
Massive PE (~2–3%)	RV failure from acute pressure overload. Not true "pump" failure -it's obstructive. tPA, catheter-directed therapy, or surgical embolectomy.
Cardiac tamponade (~1–2%)	Beck's triad: hypotension, JVD, muffled heart sounds. Pulsus paradoxus > 10 mmHg. Emergent pericardiocentesis.
Arrhythmia-induced (~1–2%)	Refractory VT/VF, complete heart block, tachycardia-mediated cardiomyopathy. Treat the rhythm -cardioversion, pacing, amiodarone.
Takotsubo (~1–2%)	Apical ballooning, post-emotional/physical stress. Often mimics STEMI. Usually recovers in days to weeks. Supportive care.
Post-cardiotomy (~2–6%)	Low CO syndrome post-cardiac surgery (CPB-related stunning). Milrinone or dobutamine. IABP/Impella if refractory.

Recognition -Cold & Wet Profile

Hypotension (SBP < 90) + cool, clammy extremities
Mottled skin, cyanosis of peripheries
Altered mental status (cerebral hypoperfusion)
Oliguria / anuria (renal hypoperfusion)
Elevated JVP, S3, pulmonary crackles (elevated filling pressures)
Lactate > 2 (tissue hypoperfusion)

Do NOT give aggressive fluids -will worsen pulmonary edema without improving CO
Do NOT use beta-blockers, calcium channel blockers, or nitrates in acute CS

🧪 Workup & Diagnosis

Immediate Workup

ECHO is the most important early test. Get it immediately -confirms diagnosis, identifies cause, guides management.

ECG immediately -rule out STEMI (immediate cath lab activation), complete heart block, arrhythmia
Bedside echo -EF, wall motion abnormalities, tamponade, valvular emergency, RV failure
Troponin, BNP -confirm myocardial injury, severity of HF
ABG -lactate, acid-base (metabolic acidosis = bad sign)
BMP -creatinine, K⁺, glucose
CXR -pulmonary edema, cardiomegaly
Invasive monitoring (PA catheter / arterial line) -if diagnosis uncertain or refractory to treatment

Hemodynamic Profiles by PA Catheter

Shock Type	CO	SVR	PCWP
Cardiogenic	↓↓	↑↑	↑↑
Distributive (Septic)	↑ or normal	↓↓	Low/normal
Hypovolemic	↓	↑	↓↓
Obstructive (PE/Tamponade)	↓	↑	Variable

🚨 Management

Management

Immediate

ABCs, ICU transfer, arterial line, central line. Cardiac monitoring. Call cardiology immediately. If STEMI -activate cath lab NOW (door-to-balloon < 90 min). Do NOT delay revascularization for hemodynamic stabilization.

Vasopressors (MAP target ≥ 65)

Norepinephrine first-line for vasopressor support. Do NOT use dopamine (increased arrhythmias in SHOCK trial). Add vasopressin or epinephrine for refractory hypotension.

Inotropes (for low CO)

Dobutamine 2–20 mcg/kg/min -increases CO, reduces afterload. Use when MAP is adequate but CO is still low (cold, not adequately responding to pressors alone). Can cause hypotension and tachyarrhythmias.

Revascularization (if ACS)

Emergency PCI SHOCK 1999: early revascularization reduces 1-year mortality in cardiogenic shock from MI. Do not delay for stabilization. Surgical revascularization if anatomy unsuitable for PCI.

Mechanical Circulatory Support

IABP (intra-aortic balloon pump) -no mortality benefit IABP-SHOCK II 2012. Impella or ECMO for refractory CS. Consider early in rapidly deteriorating patients -get mechanical circulatory support (MCS) team involved before the patient is "too sick."

Treat the Cause

Tamponade → pericardiocentesis. Acute severe MR/VSD → surgery. Fulminant myocarditis → steroids + mechanical circulatory support (MCS) bridge. Complete heart block → temporary pacing. Identify and reverse.

💊 Medications & Doses

Medications

Drug	Dose	Role	Notes
Norepinephrine (Levophed) 1ST LINE	0.1–1 mcg/kg/min	First-line vasopressor	Preferred over dopamine in CS. Increases MAP without excessive tachycardia.
Dobutamine (Dobutrex)	2–20 mcg/kg/min	Inotrope	↑CO, ↓SVR. Use when MAP adequate but CO still low. Titrate to clinical response. Can cause arrhythmias.
Milrinone (Primacor)	0.375–0.75 mcg/kg/min	Inotrope/vasodilator	PDE3 inhibitor. Good in chronic HF (not beta-blocked). Avoid if hypotensive (vasodilatory). Renally cleared.
Vasopressin (Pitressin)	0.03–0.04 units/min	Vasopressor add-on	Nonadrenergic -useful adjunct to reduce catecholamine dose. Fixed dose.
Aspirin + Heparin	325 mg PO + UFH per ACS protocol	ACS-associated CS	Antiplatelet + anticoagulation for PCI. Do not hold for hemodynamic instability.

📋 On Rounds

On Rounds

Pimp Questions

Why is dopamine avoided in cardiogenic shock?

SOAP II, 2010 and SHOCK trial subgroup: dopamine causes significantly more arrhythmias (especially atrial fibrillation) compared to norepinephrine in cardiogenic and other shock states, without mortality benefit. Norepinephrine is safer and equally effective.

What did the IABP-SHOCK II trial show?

IABP-SHOCK II 2012: Intra-aortic balloon pump did NOT reduce 30-day mortality in cardiogenic shock complicating MI compared to medical therapy alone. This changed practice -IABP is no longer routinely recommended for CS despite being widely used before this trial.

How do you differentiate cardiogenic shock from septic shock at the bedside?

Cardiogenic: cold extremities, mottled, elevated JVP, pulmonary edema (crackles), narrow pulse pressure, low-output state. Echo: poor EF, dilated LV. PA catheter: CI < 2.2, PCWP > 15, elevated SVR. Septic: warm extremities (early), bounding pulses, wide pulse pressure, dry lungs, high-output state. Echo: hyperdynamic LV. PA catheter: CI > 2.5, PCWP low/normal, low SVR.

A patient with cardiogenic shock has MAP 62 on norepinephrine but cardiac index is 1.4. What do you add?

Add an inotrope -dobutamine or milrinone. The MAP is adequate (≥65) but cardiac output is critically low (CI < 2.2). Norepinephrine raises MAP via vasoconstriction but doesn't improve forward flow. Dobutamine (β₁ > β₂): increases contractility and CO, first-line inotrope. Start 2.5 mcg/kg/min, titrate to CI > 2.2. Risk: tachycardia, hypotension from β₂ vasodilation.

What is an Impella and how does it differ from IABP and ECMO?

Impella: percutaneous axial flow pump placed across the aortic valve (femoral artery → LV). Actively pumps blood from LV into aorta. Provides 2.5-5.5 L/min support depending on device. Unloads the LV (reduces wall stress, O₂ demand). IABP: inflates in diastole (augments coronary perfusion), deflates in systole (reduces afterload). Only provides ~0.5 L/min augmentation -modest hemodynamic support. No mortality benefit IABP-SHOCK II, 2012.

Why does VA-ECMO increase LV afterload, and why is that dangerous?

VA-ECMO returns oxygenated blood into the femoral artery → flows retrograde into the aorta → increases aortic pressure against which the LV must eject. If the LV is too weak to open the aortic valve against this increased pressure, the LV becomes a stagnant, distended chamber → LV distension → increased wall stress → increased O₂ demand → worsening ischemia → pulmonary edema (blood backs up into lungs).

What is the SCAI classification of cardiogenic shock and why does it matter?

SCAI shock classification (Society for Cardiovascular Angiography and Interventions) stages A through E: A = At risk (large MI, no shock), B = Beginning (hypotension or tachycardia, but adequate perfusion), C = Classic (hypoperfusion requiring intervention -pressors or MCS), D = Deteriorating (failing initial therapy, escalating support), E = Extremis (refractory shock, CPR, multiple pressors at max).

A patient has an acute massive MI with cardiogenic shock. Should you stabilize hemodynamics before taking them to the cath lab?

NO -do NOT delay revascularization to "stabilize" the patient. The SHOCK, 1999 trial showed that early revascularization (PCI or CABG within 6h) reduced 6-month mortality from 63% to 50% compared to initial medical stabilization. The myocardium is dying -every minute of delay = more infarct → worse pump function → deeper shock. Start pressors and inotropes while preparing for cath, not instead of cath.

What are the mechanical complications of MI that cause cardiogenic shock, and how do you diagnose them?

Three mechanical complications (typically 3-7 days post-MI): (1) Ventricular septal rupture (VSR): new harsh holosystolic murmur + step-up in O₂ sat from RA to PA on PA catheter. Echo: VSD with L→R shunt. Treatment: surgical repair (emergent). (2) Papillary muscle rupture: new severe MR (holosystolic murmur at apex, but may be soft if severe). PA catheter: large V waves on PCWP tracing. Echo: flail mitral leaflet.

How do you use a PA catheter to guide management in cardiogenic shock?

PA catheter (Swan-Ganz) gives 4 key hemodynamic parameters: (1) CI (cardiac index): < 2.2 = cardiogenic shock. Target > 2.2 with inotropes. (2) PCWP: > 15 = volume overloaded / high filling pressures. Guide diuresis or vasodilator therapy. (3) SVR: elevated in cardiogenic shock (compensatory vasoconstriction). If very high (> 1,800) → afterload reduction may improve forward flow

Clinical Examples

📋 Case 1, Anterior STEMI with Cardiogenic Shock

Patient: 59M, PMH HTN, smoking. Crushing chest pain x2h. ECG: ST elevation V1-V5. BP 78/50, HR 110, cold/clammy, JVP elevated.

Key findings: Lactate 5.8, troponin > 50, BNP 1200. Echo: anterior wall akinesis, EF ~15%. Cardiogenic shock from anterior STEMI.

Management:

Emergent cardiac cath, do NOT delay for stabilization SHOCK, 1999
Norepinephrine first-line, NOT dopamine SOAP II, 2010
Dobutamine 2-20 mcg/kg/min if MAP adequate but CI < 2.2
Activate MCS team early for Impella consideration
Aspirin 325 mg + heparin per ACS protocol

Teaching point: The cath lab IS the treatment for MI-related CS. Every minute of delay = more infarct = deeper shock. Start pressors while preparing for PCI, not instead of PCI.

📋 Case 2, Mechanical Complication Post-MI

Patient: 72F, POD 5 from inferior STEMI. Sudden hypotension (BP 65/40), new loud holosystolic murmur at LLSB, acute respiratory distress.

Key findings: Echo: VSD with L-to-R shunt. PA catheter: O2 sat step-up from RA to RV. CI 1.6, PCWP 24.

Management:

Norepinephrine for MAP support
IABP for temporary support (reduces afterload, decreases L-to-R shunt)
Emergent cardiac surgery, surgical VSD repair is definitive
Nitroprusside if MAP tolerates (reduces shunt fraction)

Teaching point: Mechanical complications (VSD, papillary muscle rupture, free wall rupture) occur 3-7 days post-MI. Any acute deterioration in this window requires immediate echo. New murmur post-MI = VSD or acute MR until proven otherwise.

📋 Case 3, Refractory CS Requiring VA-ECMO

Patient: 45M with fulminant myocarditis. EF 5%, SCAI stage D. On max NE + dobutamine + vasopressin. Lactate rising 6 to 12.

Key findings: Refractory CS despite maximal medical therapy. Worsening multiorgan failure.

Management:

VA-ECMO as bridge to recovery or transplant
Add Impella for LV venting (ECPELLA), ECMO increases LV afterload
Monitor for LV distension (aortic valve not opening = inadequate venting)
Endomyocardial biopsy; empiric steroids if giant cell myocarditis suspected
Transplant evaluation

Teaching point: VA-ECMO provides support but increases LV afterload. Without LV venting, the LV distends, worsening ischemia and pulmonary edema. IABP provides insufficient support IABP-SHOCK II, 2012.

📋 Sample Presentation

"Mr. Kim is a 61-year-old with no known cardiac history who presented with anterior STEMI complicated by cardiogenic shock. He underwent emergency PCI with stenting of the LAD. Echo post-cath shows EF of 20% with anterior wall akinesis. He was started on norepinephrine and dobutamine in the cath lab. He is on NE 0.3 mcg/kg/min and dobutamine 10 mcg/kg/min. This morning his MAP is 67, lactate trending down from 6.2 to 3.1, UO 40 mL/hr. He remains intubated. We are in contact with our mechanical circulatory support (MCS) team regarding Impella consideration given refractory shock. Cardiology and cardiac surgery are both following."

⚡ Summary

Summary

Definition

SBP < 90 + CI < 2.2 + PCWP > 15. Cold, clammy, low output despite adequate filling pressures.

Most Common Cause

Acute MI (large anterior STEMI). Always get ECG immediately and activate cath lab if STEMI.

Vasopressors

Norepinephrine first. NOT dopamine (arrhythmias). Add vasopressin or epinephrine if refractory.

Inotropes

Dobutamine when MAP adequate but CO still low. Milrinone alternative (avoid if hypotensive).

Key Intervention

Treat the cause. PCI for ACS. Pericardiocentesis for tamponade. Early mechanical circulatory support (MCS) if refractory.

Mortality

40–50%. Early revascularization + mechanical circulatory support (MCS) = best chance. Do not delay PCI for "stabilization."

📄 One Pager

ICU · Cardiology · One Pager

Cardiogenic Shock

Cold, clammy, low output with elevated filling pressures. Mortality 40–50%. Treat the cause fast. NE first, NOT dopamine. Early mechanical circulatory support (MCS) if refractory.

❤️ Definition & Causes

SBP < 90 + CI < 2.2 + PCWP > 15
Acute MI (large anterior STEMI)
Acute valvular emergency
Fulminant myocarditis
Massive PE / tamponade

🔍 Key Workup

ECG immediately -activate cath lab if STEMI
Echo -EF, wall motion, tamponade, RV
Troponin, BNP, ABG, lactate
PA catheter if diagnosis unclear

🚨 Management

ICU, art line + central line. Call cardiology immediately. Do NOT delay PCI for "stabilisation."

Norepinephrine (NOT dopamine SOAP II, 2010) for MAP ≥ 65. Add vasopressin if refractory.

Dobutamine 2–20 mcg/kg/min if MAP adequate but CO still low.

Emergency PCI if STEMI SHOCK 1999 -early revascularisation reduces 1-year mortality.

Mechanical circulatory support -Impella/ECMO if refractory. IABP no longer routine IABP-SHOCK II 2012.

Treat the cause: Drain tamponade, pace if heart block, repair valve, treat myocarditis.

💊 Drugs

Norepinephrine (Levophed)0.1–1 mcg/kg/min

Dobutamine (Dobutrex)2–20 mcg/kg/min

Vasopressin (Vasostrict)0.03 u/min

Milrinone (Primacor)0.375–0.75 mcg/kg/min

🚫 Do NOT Use

Dopamine (↑ arrhythmias)
Beta-blockers
CCBs
Aggressive fluids
IABP routinely

📊 Differentiating Shock

CO↓↓ (vs ↑ in sepsis)

SVR↑↑ (vs ↓ in sepsis)

PCWP↑↑ (vs low in sepsis)