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.

RoundsRx

Dashboard

Overview

Recent

Rotations

Quick Reference

Antibiotic Guide Analgesia Guide Sedation Guide Bowel Regimen Electrolyte Replacement Pain Management & Conversions Drug Interactions Anticoag Reversal IV Fluid Guide Inotropes Guide Vasopressors Insulin Guide Code Blue & Rapid Response Procedures Guide ECG Interpretation Lab Interpretation Radiology Quick Ref GCS Pocket Card Admission Orders & I-PASS Landmark Trials

Tools

💎 Clinical Pearls 🧠 Pimp Me Quiz 🧮 Clinical Calculators 📰 What's New 🎓 Intern Survival Guide ✅ Rounding Checklists 🩺 Procedure Guides ⚡ Electrolyte Replacement 💧 IV Fluids Guide 🩸 Transfusion Guide 💓 ECG Pattern Guide 🧪 Lab Interpretation Guide 📱 QR Poster 🔗 Resources 🎙️ Channels & Podcasts 🎮 Medical Games 🏛️ Famous Cases 🎬 Media Library

ℹ️ About

Available offline

EmergentCardiology

Myocarditis

Inflammation of the myocardium. Classic presentation: young patient with recent viral illness → chest pain + troponin elevation + new HF. Ranges from mild (self-limited) to fulminant (cardiogenic shock). Cardiac MRI is the key diagnostic tool.

🔍 Overview

Presentation Spectrum

Type	Presentation	Hemodynamics	Prognosis
Acute (non-fulminant)	Chest pain, dyspnea, palpitations. Preceded by viral URI 1–4 weeks prior. Mild-moderate LV dysfunction.	Stable. Mild EF reduction.	~50% recover fully. ~25% develop chronic DCM. ~25% stable but reduced EF.
Fulminant	Rapid-onset cardiogenic shock within days. Severe biventricular failure. Arrhythmias.	Hemodynamic collapse. May need MCS (Impella, ECMO).	Paradoxically better long-term prognosis if they survive the acute phase -~90% recover LV function (robust immune response clears the virus).
Chronic active	Persistent HF symptoms > 3 months. Ongoing inflammation on biopsy.	Progressive LV dilation and dysfunction.	May progress to DCM. May need transplant evaluation.
Giant cell	Rapidly progressive HF + VT. Young-middle age.	Severe. Refractory arrhythmias.	Worst prognosis. Median survival ~5 months without transplant. Immunosuppression is indicated.

Etiology

Viral (most common) -Coxsackievirus B, parvovirus B19, HHV-6, adenovirus, SARS-CoV-2, influenza
Autoimmune -SLE, sarcoidosis, eosinophilic myocarditis (hypersensitivity)
Drug/toxin -immune checkpoint inhibitors (PD-1/PD-L1 -pembrolizumab, nivolumab), doxorubicin, cocaine, amphetamines
Giant cell myocarditis -idiopathic, associated with autoimmune diseases (IBD, thymoma)

Checkpoint inhibitor myocarditis: rare (~1%) but mortality > 40%. Presents 1–3 months after starting therapy. Stop the drug immediately. High-dose IV methylprednisolone. Cardiology + oncology co-management.

Diagnosis

Test	Findings
Troponin	Elevated (may mimic MI). Often with recent viral prodrome.
ECG	Diffuse ST changes (may mimic pericarditis or STEMI), sinus tachycardia, arrhythmias (VT, heart block), low voltage.
Echo	New wall motion abnormalities (often non-territorial -unlike MI). Reduced EF. May see pericardial effusion.
Cardiac MRI KEY DIAGNOSTIC TOOL	Lake Louise criteria: (1) T2 hyperintensity (edema), (2) late gadolinium enhancement -mid-wall or epicardial pattern (unlike MI which is subendocardial/transmural). (3) T1 mapping abnormalities. Sensitivity ~80%, specificity ~90%.
Endomyocardial biopsy	Gold standard but rarely done (low sensitivity due to sampling error). Indicated in: fulminant myocarditis, suspected giant cell, no improvement despite treatment, need to guide immunosuppression.

🚨 Management

Treatment

Supportive care -standard HF therapy if reduced EF (ACEi/ARB, beta-blocker, diuretics as needed). Avoid NSAIDs in acute phase (may impair healing).
Activity restriction -no competitive sports for 3–6 months minimum. Risk of fatal arrhythmias with exertion. Repeat echo and MRI before return to play.
Arrhythmia management -telemetry monitoring. Life vest (wearable defibrillator) if EF < 35% acutely. Avoid permanent ICD in acute phase -EF may recover. Reassess at 3–6 months.
Fulminant → ICU. Inotropes, vasopressors. Early MCS (Impella/ECMO) if deteriorating -these patients often recover if supported through the acute phase.
Giant cell myocarditis → immunosuppression (cyclosporine + steroids ± azathioprine). Early transplant evaluation. Giant Cell Myocarditis Registry, 1997: immunosuppression improved survival from 3 months to 12 months.
Checkpoint inhibitor myocarditis → stop drug + high-dose IV methylprednisolone 1g/day × 3–5 days, then oral taper.

Monitoring, Myocarditis

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.

🧪 Workup

Workup

Troponin -elevated, trend q6-8h
ECG -diffuse ST changes, arrhythmias
Echo -EF, wall motion, pericardial effusion
Cardiac MRI (gold standard) -T2 edema, mid-myocardial LGE
ESR, CRP
Endomyocardial biopsy -only if giant cell suspected

💊 Medications

Medications

Drug	Dose	Route	Notes
Lisinopril (Zestril)	2.5-20 mg daily	PO	ACEi for LV remodeling. Start low, uptitrate. ARB if ACEi-intolerant.
Carvedilol (Coreg)	3.125-25 mg BID	PO	Low-dose BB -titrate cautiously. Hold if cardiogenic shock or decompensated HF.
Furosemide (Lasix)	20-80 mg PRN	IV/PO	Diuresis for fluid overload/congestion. Titrate to euvolemia.
Avoid NSAIDs	-	-	Worsen myocardial inflammation and necrosis. Contraindicated even though chest pain is prominent.
Immunosuppression	Per biopsy/pathology	IV/PO	ONLY for giant cell myocarditis (cyclosporine + steroids) or eosinophilic myocarditis (high-dose steroids). NOT for viral myocarditis.
IVIG	2 g/kg over 2-5 days	IV	Consider in select cases (pediatric, fulminant). Evidence mixed. Not routine.
Inotropes / MCS	Per hemodynamics	IV	Milrinone or dobutamine for cardiogenic shock. Impella/ECMO for fulminant myocarditis with refractory shock.

📋 On Rounds

How does cardiac MRI distinguish myocarditis from MI?

Late gadolinium enhancement (LGE) pattern. In MI, LGE follows a coronary distribution and is subendocardial or transmural (starts from the endocardium and extends outward). In myocarditis, LGE is typically mid-wall or epicardial (spares the subendocardium) and is non-territorial (doesn't match a coronary artery distribution).

Why does fulminant myocarditis have a paradoxically better long-term prognosis?

Fulminant myocarditis represents an overwhelming but robust immune response -the immune system aggressively attacks the virus (and unfortunately, the myocardium). If the patient survives the acute phase (with MCS if needed), the strong immune response effectively clears the virus, and the myocardium recovers -~90% regain normal LV function.

Why do you avoid NSAIDs in acute myocarditis even though they're first-line for pericarditis?

In pericarditis, inflammation is limited to the pericardium -NSAIDs reduce inflammation and improve symptoms. In myocarditis, the inflammation involves the myocardium itself. Animal studies showed NSAIDs increased myocardial necrosis and mortality in viral myocarditis by impairing the immune response needed to clear the virus and by increasing viral replication. NSAIDs also reduce renal blood flow which is detrimental in patients with reduced EF.

A 28-year-old recovered from myocarditis with EF 35%. When can they return to exercise?

No competitive sports or intense exercise for minimum 3-6 months after acute myocarditis regardless of EF recovery. This is because active myocardial inflammation creates a substrate for fatal ventricular arrhythmias during exercise (catecholamine surge + inflamed myocardium = VT/VF). Before returning: (1) ≥ 3 months from onset, (2) EF normalized on repeat echo, (3) No LGE on cardiac MRI (or stable/reduced)

Clinical Examples

📋 Case 1, Viral Myocarditis with Acute HF

Patient: 26M with chest pain and dyspnea 10 days after a flu-like illness. Troponin 6.8, BNP 2400. ECG: diffuse ST elevation without reciprocal changes. Echo: EF 30%, global hypokinesis. No coronary disease on angiography.

Key findings: Acute viral myocarditis with new-onset HFrEF. Clean coronaries exclude ACS. Diffuse ST changes (not territorial) + recent viral prodrome + young patient = classic presentation.

Management:

Cardiac MRI, Lake Louise criteria: T2 edema + LGE in non-coronary distribution (mid-wall/epicardial) confirms myocarditis
GDMT for HFrEF: ACEi/ARB, beta-blocker (once stable), MRA if EF ≤ 35%
Telemetry monitoring, arrhythmia risk highest in acute phase (VT/VF)
NO NSAIDs (worsen inflammation and remodeling in myocarditis)
Repeat echo at 3-6 months, most viral myocarditis recovers EF (60-70% normalize)

Teaching point: Do NOT place an ICD during acute myocarditis even if EF ≤ 35%. Most patients recover EF, wait ≥ 3-6 months and reassess. LifeVest (wearable defibrillator) is a bridge if high arrhythmia risk.

📋 Case 2, Fulminant Myocarditis

Patient: 32F with 2 days of progressive dyspnea, now in cardiogenic shock. HR 120, BP 72/48, cool extremities, lactate 6.2. Echo: EF 10%, global severe hypokinesis. Troponin 42. No prior cardiac history.

Key findings: Fulminant myocarditis, rapid-onset cardiogenic shock in a previously healthy patient. Paradoxically, fulminant myocarditis has BETTER long-term prognosis than acute myocarditis if the patient survives the acute phase (stronger immune response → better viral clearance).

Management:

ICU, vasopressors/inotropes (dobutamine 5 mcg/kg/min + norepinephrine for MAP ≥ 65)
Early mechanical circulatory support: Impella or VA-ECMO if refractory to inotropes
Endomyocardial biopsy, rule out giant cell myocarditis (requires immunosuppression) or eosinophilic myocarditis
Avoid beta-blockers acutely in cardiogenic shock (can worsen hemodynamics)
If giant cell myocarditis on biopsy: high-dose steroids + cyclosporine (without immunosuppression, mortality > 80%)

Teaching point: Fulminant myocarditis is a "bridge to recovery" disease, patients who survive the acute phase often recover near-normal EF. Aggressive mechanical support (ECMO/Impella) saves lives. Biopsy is critical to exclude giant cell myocarditis.

📋 Case 3, Immune Checkpoint Inhibitor Myocarditis

Patient: 58M on pembrolizumab for melanoma × 3 cycles. New fatigue, dyspnea, palpitations. Troponin 2.4 (was normal at baseline). ECG: new conduction delay, PR prolongation. Echo: EF 45% (was 60%).

Key findings: Immune checkpoint inhibitor (ICI) myocarditis, occurs in 1-2% of ICI-treated patients but mortality is 25-50%. Can present with conduction abnormalities, arrhythmias, or HF. Often coexists with myositis and myasthenia gravis.

Management:

Hold pembrolizumab immediately (permanently discontinue, do not rechallenge)
High-dose methylprednisolone 1g IV daily × 3-5 days → prednisone 1 mg/kg with slow taper
If steroid-refractory: add mycophenolate, infliximab, or abatacept
Continuous telemetry, high-grade AV block and VT are common and often fatal
Check CK (concurrent myositis), anti-AChR antibodies (concurrent MG), and cardiac MRI

Teaching point: ICI myocarditis is the most lethal irAE, early troponin monitoring and a low threshold for holding therapy saves lives. Conduction abnormalities (PR prolongation, BBB) may be the first sign before EF drops.

📣 Sample Presentation

One-Liner

"Mr. Reyes is a 28-year-old presenting with chest pain and dyspnea 10 days after a viral illness. Troponin 8.2, BNP 1,400. ECG shows diffuse ST changes. Echo EF 35% with global hypokinesis. Cardiac MRI shows late gadolinium enhancement consistent with myocarditis."

Don't Miss

Giant cell myocarditis: rapid HF + VT + young. Needs biopsy. Treatment: immunosuppression. Consider transplant early.

📄 One Pager

Cardiology · One Pager

Myocarditis

Young + chest pain + troponin + new HF after viral illness. Cardiac MRI = gold standard. No NSAIDs. No exercise × 3-6 months.

🧪 Diagnosis

Suspect: young patient + chest pain + troponin ↑ + new HF + recent viral illness
ECG: diffuse ST changes, low voltage, arrhythmias
Echo: reduced EF, regional or global wall motion abnormality
Gold standard: Cardiac MRI -mid-myocardial LGE (not subendocardial like MI)

🚨 Management

Standard HF therapy: ACEi + low-dose BB + diuretics PRN
Avoid NSAIDs (worsen myocardial necrosis in animal models)
Activity restriction: no exercise × 3-6 months minimum
Arrhythmia monitoring: telemetry (VT/VF risk during active inflammation)
Follow-up echo at 3-6 months (EF should recover in most viral cases)

⚠️ Return to Activity Criteria

≥ 3 months from symptom onset
EF normalized on echo
No LGE on cardiac MRI (or stable/reduced)
No arrhythmias on Holter + exercise stress test
Normal inflammatory markers (CRP, troponin)
Gradual return, individualized [ESC Sports Cardiology 2020]

💊 Key Drugs

ACEi/ARBStandard HF dosing

Low-dose BBCarvedilol or metoprolol

DiureticsFurosemide PRN for congestion

AvoidNSAIDs, intense exercise

⚠️ Pitfalls

NSAIDs in acute myocarditis
Early return to exercise (arrhythmia risk)
Missing giant cell myocarditis (rapid HF + VT → biopsy)
Confusing with STEMI (check MRI pattern)