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.

🔍 Overview

Aortic Stenosis

Severity

Parameter	Mild	Moderate	Severe
Aortic valve area (AVA)	> 1.5 cm²	1.0–1.5 cm²	< 1.0 cm²
Mean gradient	< 20 mmHg	20–40 mmHg	> 40 mmHg
Peak velocity	< 3 m/s	3–4 m/s	> 4 m/s

When to Intervene

Symptomatic severe AS: any symptom from the classic triad → immediate referral for AVR
Classic triad (SAD): S yncope (3-year survival without AVR) · A ngina (5-year) · D yspnea/HF (2-year). Once symptoms develop, mortality is 50% at 2 years without surgery.
Asymptomatic severe AS with EF < 50% → AVR
TAVR (transcatheter) now approved for all surgical risk categories PARTNER 3, 2019

⚠️ Avoid vasodilators in severe AS. Afterload reduction (nitrates, ACEi, hydralazine) can cause severe hypotension -the fixed obstruction prevents compensatory increase in CO. Also avoid rapid fluid depletion -AS patients are preload-dependent.

Mitral Regurgitation

Feature	Acute MR	Chronic MR
Cause	Papillary muscle rupture (post-MI), chordae rupture, endocarditis	Mitral valve prolapse (#1), rheumatic disease, annular dilation from LV dilation
LV size	Normal (no time to dilate)	Dilated (volume overload compensated)
LA size	Normal → pulmonary edema (no compliance)	Dilated (accommodates regurgitant volume)
Murmur	May be soft or absent (equalization of pressures)	Holosystolic at apex, radiates to axilla
Treatment	Emergent surgery. Afterload reduction (nitroprusside, IABP) as bridge.	Surgery when: symptomatic, or asymptomatic with EF ≤ 60% or LVESD ≥ 40 mm. MitraClip for high surgical risk.

Aortic Regurgitation

Feature	Acute AR	Chronic AR
Cause	Endocarditis (valve destruction), aortic dissection, trauma	Bicuspid aortic valve, rheumatic disease, aortic root dilation (Marfan, HTN)
LV response	Normal size → cannot accommodate volume → pulmonary edema	Eccentric hypertrophy (LV dilation -"cor bovinum")
Pulse pressure	May be narrow (LV can't compensate)	Wide (bounding "water-hammer" pulse, Corrigan pulse, de Musset sign)
Murmur	Short early diastolic (equalization)	Blowing early diastolic at LUSB, best heard sitting up and leaning forward
Treatment	Emergent surgery. Nitroprusside bridge. IABP is CONTRAINDICATED in AR.	Surgery when symptomatic, or asymptomatic with EF < 55% or LVESD > 50 mm or LVIDd > 65 mm.

⚠️ IABP is contraindicated in aortic regurgitation. The balloon inflates in diastole -this increases aortic diastolic pressure and worsens regurgitant flow back into the LV.

Mitral Stenosis

Feature	Details
#1 Cause	Rheumatic heart disease (virtually always). Rare in developed countries now.
Pathophysiology	Stenotic MV → ↑ LA pressure → LA dilation → atrial fibrillation → pulmonary HTN → RV failure
Murmur	Low-pitched diastolic rumble at apex with opening snap. Best heard in left lateral decubitus. Shorter snap-to-rumble interval = more severe.
Key complication	Afib (from LA dilation) → high stroke risk → anticoagulate with warfarin (DOACs inferior in mechanical/rheumatic valvular disease)
Severity	Normal MVA ~4–6 cm². Severe MS: MVA < 1.5 cm², mean gradient > 10 mmHg
Treatment	Rate control (BB/CCB) + anticoagulation if Afib. Intervention: percutaneous mitral balloon commissurotomy (PMBC) if pliable valve, no significant MR, no LA thrombus. Otherwise → surgical MV replacement.

Tricuspid Regurgitation

Feature	Details
#1 Cause	Functional/secondary -RV dilation from pulmonary HTN, LV failure, or COPD stretches the tricuspid annulus
Primary causes	Endocarditis (IVDU -right-sided), Ebstein anomaly, carcinoid, rheumatic, pacemaker leads
Murmur	Holosystolic at LLSB. ↑ with inspiration (Carvallo sign) -increased RV venous return augments regurgitant flow
Exam findings	Elevated JVP with prominent CV waves, pulsatile liver, peripheral edema, ascites
Treatment	Treat the underlying cause (pulmonary HTN, LV failure). Diuretics for volume overload. Surgery rarely needed unless primary TR with severe symptoms.

Murmur Quick Reference

Lesion	Murmur	Timing	Best Heard	Key Maneuver
Aortic Stenosis	Crescendo-decrescendo (ejection)	Systolic	RUSB → carotids	↓ with Valsalva (except HCM)
Mitral Regurgitation	Holosystolic (blowing)	Systolic	Apex → axilla	↑ with handgrip (↑ afterload)
Aortic Regurgitation	Early diastolic (blowing, decrescendo)	Diastolic	LUSB, sitting up/leaning forward	Wide pulse pressure, water-hammer pulse
Mitral Stenosis	Low-pitched rumble with opening snap	Diastolic	Apex, left lateral decubitus	Louder with exercise (↑ flow)
Tricuspid Regurgitation	Holosystolic (blowing)	Systolic	LLSB	↑ with inspiration (Carvallo sign)

When to Get an Echo

New murmur with symptoms (dyspnea, syncope, chest pain)
Any diastolic murmur (always pathologic)
Any holosystolic murmur (MR or TR)
Grade ≥ 3/6 systolic murmur
Systolic murmur + abnormal symptoms/exam findings
Known valve disease with change in symptoms

Benign flow murmurs (grade 1–2/6 systolic at LUSB, no radiation, no symptoms, young patient) do NOT need echo. But when in doubt -echo.

📋 On Rounds

What is the classic triad of symptomatic aortic stenosis?

SAD: Syncope, Angina, Dyspnea (HF). They appear in that order as the disease progresses. Once any symptom develops, average survival without AVR: syncope = 3 years, angina = 5 years, heart failure = 2 years. This is why symptomatic severe AS is an indication for urgent valve replacement -delay costs lives.

Why is IABP contraindicated in aortic regurgitation?

The IABP inflates during diastole to augment coronary perfusion and deflates during systole to reduce afterload. In AR, blood regurgitates from aorta into LV during diastole. IABP inflation during diastole increases aortic diastolic pressure → drives MORE blood backward through the incompetent valve → worsens regurgitation and LV volume overload. Use nitroprusside or Impella instead for hemodynamic support in acute AR.

A patient with severe aortic stenosis needs non-cardiac surgery. How do you manage this?

Severe AS + non-cardiac surgery = high perioperative risk (hypotension, HF, death). Key principles: (1) Symptomatic severe AS → defer elective surgery until valve intervention (TAVR or SAVR). (2) If surgery is urgent/emergent: proceed with invasive hemodynamic monitoring, maintain preload (avoid dehydration), avoid vasodilators and rapid HR changes, goal-directed fluid management

What is the most important echo measurement in aortic stenosis and what values define severe?

Aortic valve area (AVA) is the gold standard. Severe AS: AVA < 1.0 cm², mean gradient > 40 mmHg, peak velocity > 4 m/s. BUT these can be discordant in low-flow, low-gradient AS (low EF → low gradient despite severe stenosis). In this case, do a dobutamine stress echo: if AVA remains < 1.0 cm² as flow increases → truly severe ("fixed" stenosis → valve intervention). If AVA improves → pseudosevere (improve EF medically).

Clinical Examples

📋 Case 1, Symptomatic Severe Aortic Stenosis

Patient: 76M with progressive dyspnea on exertion and an episode of exertional syncope. Crescendo-decrescendo systolic murmur at RUSB radiating to carotids. Echo: AVA 0.6 cm², mean gradient 48 mmHg, peak velocity 4.5 m/s, EF 55%.

Key findings: Symptomatic severe AS (SAD triad: Syncope, Angina, Dyspnea). Once symptoms develop, mortality without intervention: syncope = 3-year, angina = 5-year, HF = 2-year median survival.

Management:

Immediate referral for aortic valve replacement, do NOT delay
Heart team discussion: TAVR vs SAVR. TAVR now approved for all surgical risk categories PARTNER 3, 2019
TAVR preferred if: age > 65, high surgical risk, no bicuspid valve. SAVR preferred if: age < 50, bicuspid, concomitant CABG needed
AVOID vasodilators (ACEi/nitrates) and excessive diuresis, fixed obstruction means preload-dependent
No balloon valvuloplasty as definitive therapy (restenosis in weeks), only as bridge to TAVR/SAVR

Teaching point: Symptomatic severe AS is a surgical emergency, median survival without intervention is 2-5 years depending on symptoms. There is no effective medical therapy for AS. The only treatment is valve replacement.

📋 Case 2, Acute Severe Mitral Regurgitation

Patient: 62M, 3 days post-inferior STEMI. Sudden dyspnea, new holosystolic murmur radiating to axilla, flash pulmonary edema. BP 85/50. Echo: EF 50%, flail posterior MV leaflet, severe eccentric MR jet. BNP 4200.

Key findings: Acute severe MR from papillary muscle rupture post-MI. The posteromedial papillary muscle (single blood supply from PDA) is vulnerable in inferior MI. This is a surgical emergency, mortality without surgery approaches 75% at 24h.

Management:

Emergent cardiac surgery consult for MV repair or replacement
Afterload reduction: nitroprusside or IV nitroglycerin (reduces regurgitant fraction by lowering SVR)
IABP for hemodynamic stabilization as bridge to OR (reduces afterload during systole → reduces MR)
Inotropes (dobutamine) if cardiogenic shock
Avoid increasing afterload (phenylephrine, vasopressin), worsens regurgitation

Teaching point: Acute severe MR is a volume + pressure emergency. The LV has not had time to dilate and compensate. Unlike chronic MR (where EF can be preserved for years), acute MR → immediate pulmonary edema and shock. Surgery is the only definitive treatment.

📋 Case 3, Mitral Stenosis with New Atrial Fibrillation

Patient: 42F immigrant from South Asia with progressive dyspnea, now palpitations. HR 142 irregularly irregular, bilateral rales. Echo: MVA 1.1 cm² (moderate-severe MS), LA diameter 5.8 cm, RV pressure 55 mmHg. No MV thrombus on TEE.

Key findings: Rheumatic mitral stenosis with new Afib. MS increases LA pressure → LA dilation → Afib. Afib causes loss of atrial kick + rapid rate → dramatically worsened hemodynamics. MS + Afib = high stroke risk (warfarin required, not DOACs).

Management:

Rate control with IV diltiazem or beta-blocker, slower HR = longer diastolic filling time through stenotic valve
IV furosemide for pulmonary congestion (MS causes pulmonary venous HTN)
Anticoagulation with warfarin (NOT DOACs, valvular AF from MS requires warfarin, INR 2-3)
Once stable: percutaneous mitral balloon commissurotomy (PMBC) if valve morphology favorable (Wilkins score ≤ 8)
If PMBC not feasible: surgical MV repair or replacement

Teaching point: Mitral stenosis with Afib is the ONE scenario where warfarin is mandatory over DOACs. DOACs have not been studied in rheumatic MS. Rate control is more important than rhythm control, slow rates improve diastolic filling through the stenotic valve.

📣 Sample Presentation

One-Liner

"Mr. Morris is a 78-year-old presenting with exertional syncope and progressive dyspnea. Echo shows severe aortic stenosis with AVA 0.7 cm², mean gradient 52 mmHg, EF 55%. Symptomatic severe AS."

Key Points to Cover on Rounds

Symptomatic severe AS (syncope + dyspnea). AVA 0.7, mean gradient 52, EF preserved. STS score 4.2% (intermediate risk). CT surgery and structural heart consulted -candidate for TAVR vs SAVR discussion. Medical optimization: gentle diuresis for volume overload. Avoiding vasodilators and aggressive diuresis. Plan: outpatient TAVR evaluation, cardiac cath to assess coronary anatomy.

🧪 Workup

Diagnostic Evaluation -Valvular Heart Disease

Echo is the cornerstone. Every suspected valvular lesion needs echocardiography for severity grading. Additional testing depends on the clinical context and surgical candidacy.

Test	Purpose	When to Order
TTE (transthoracic echo)	Valve area, gradients, regurgitation severity, EF, chamber dimensions	All suspected valvular disease. First-line imaging.
TEE (transesophageal echo)	Superior visualization of mitral valve, prosthetic valves, endocarditis vegetations, LA thrombus	Prosthetic valve evaluation, pre-surgical planning, suspected endocarditis with negative TTE, pre-cardioversion in AF with valvular disease
ECG	LVH (voltage criteria in AS), atrial fibrillation (common in MS, MR), conduction abnormalities	All patients -baseline and with any symptom change
BNP / NT-proBNP	Assess hemodynamic burden, detect subclinical decompensation	Baseline and trending with symptom changes. Helps time intervention in asymptomatic severe disease.
Exercise stress test	Unmask symptoms in "asymptomatic" severe AS or MR. Assess functional capacity and hemodynamic response.	Asymptomatic severe valve disease when surgery timing is uncertain. Contraindicated in symptomatic severe AS.
Cardiac catheterization	Coronary anatomy pre-operatively, hemodynamic assessment when echo is discordant	Pre-surgical evaluation (assess CAD), discrepant echo findings

Monitoring and Follow-Up

Setting	Monitoring	Purpose
Inpatient (high risk)	Continuous telemetry	Detect arrhythmias (VT, pauses, heart block). Minimum 24-48h
Holter monitor	24-48h outpatient	Frequent symptoms (> 1/week). Captures rhythm during symptoms
Event monitor	2-4 weeks outpatient	Less frequent symptoms. Patient-activated during episodes
Implantable loop recorder	Up to 3 years	Recurrent unexplained syncope. Gold standard for infrequent events. ISSUE-3
Orthostatic vitals	At follow-up visits	Confirm response to treatment. SBP drop > 20 or DBP > 10 within 3 min of standing
Driving restrictions	Counsel at discharge	Varies by state/country. Generally no driving for weeks to months after cardiac syncope

💊 Medications

Key Medications -Valvular Heart Disease

Mechanical valves require warfarin ONLY. DOACs are contraindicated -dabigatran caused increased thromboembolic events and bleeding in mechanical valves RE-ALIGN, 2013.

Indication	Drug	Dose / Target	Notes
Mechanical valve anticoagulation	Warfarin (Coumadin)	Target INR 2.5–3.5 (mitral) or 2.0–3.0 (aortic bileaflet)	Warfarin ONLY. DOACs contraindicated [RE-ALIGN]. Lifelong therapy. Add ASA 81mg for additional protection.
AF with valvular disease (MS or mechanical valve)	Warfarin (Coumadin)	Target INR 2.0–3.0	Warfarin, NOT DOACs. "Valvular AF" = moderate-severe MS or mechanical valve. All other AF with valve disease can use DOACs.
Volume overload / congestion	Furosemide (Lasix)	20–80 mg PO/IV daily, titrate to symptoms	Diuretics for symptom relief in any valve lesion with congestion. Caution in severe AS -avoid excessive preload reduction.
Afterload reduction (regurgitant lesions)	ACEi/ARB (e.g., lisinopril, losartan)	Standard dosing, titrate to BP	Beneficial in chronic MR and AR with LV dysfunction or HTN. Reduces regurgitant volume. Avoid vasodilators in severe AS.
Rate control (MS with AF)	Beta-blockers or CCBs	Metoprolol 25–100mg BID or diltiazem 30–60mg TID	Slowing HR increases diastolic filling time -critical in MS. Avoid tachycardia.

Endocarditis Prophylaxis

Prophylaxis indications (dental procedures involving gingival manipulation or perforation):

Prosthetic heart valve (mechanical or bioprosthetic)
Prior infective endocarditis
Unrepaired cyanotic CHD (including palliative shunts/conduits)
Cardiac transplant with valvulopathy
Drug: Amoxicillin 2g PO 30–60 min before procedure. If PCN allergy: clindamycin 600mg PO or azithromycin 500mg PO.

⚡ Summary

Summary

Severe AS

AVA < 1.0 cm², mean gradient > 40, Vmax > 4 m/s. Symptoms = exertional dyspnea, syncope, angina.

AS Treatment

Symptomatic severe AS → TAVR or SAVR. No medical therapy stops progression. Avoid vasodilators, cautious diuresis.

Severe MR

Acute (papillary rupture): emergent surgery. Chronic: surgery when EF ≤ 60% or LVESD ≥ 40mm, or symptomatic.

Low-Flow AS

Low EF → low gradient despite severe AS. Dobutamine stress echo: AVA stays < 1.0 = truly severe. AVA improves = pseudo-severe.

Anticoag

Mechanical valve = warfarin (lifelong, INR 2.5-3.5 for mitral, 2.0-3.0 for aortic). DOACs contraindicated [RE-ALIGN].

Murmur Tip

Crescendo-decrescendo at RUSB radiating to carotids = AS. Holosystolic at apex radiating to axilla = MR.

📄 One Pager

Valvular Heart Disease -Quick Reference Card

Print this page (Ctrl/Cmd + P) for a condensed reference card. All tabs will print on the same page for a complete topic summary.

VALVULAR HEART DISEASE -AT A GLANCE

📋 Diagnose: See Overview tab for criteria
🧪 Workup: Focused labs + imaging → see Workup tab
⚡ Treat: Evidence-based algorithm → see Management tab
💊 Drugs: Key medications with dosing → see Medications tab
📣 Present: One-liner + key points → see Rounds tab

📄 One Pager

Cardiology · One Pager

Valvular Heart Disease

Severe AS = AVA < 1.0 + symptoms → TAVR/SAVR. Severe MR = surgery when EF ≤ 60% or LVESD ≥ 40mm. Don't delay intervention.

🧪 Severe Aortic Stenosis

AVA < 1.0 cm², mean gradient > 40 mmHg, Vmax > 4 m/s
Symptoms: exertional dyspnea, syncope, angina
Once symptomatic → 2-year survival ~50% without intervention
Low-flow low-gradient: dobutamine stress echo to differentiate true vs pseudo-severe

🚨 When to Intervene

Symptomatic severe AS → TAVR or SAVR (no medical therapy works)
Asymptomatic severe AS + EF < 50% → surgery
Severe MR → surgery when EF ≤ 60% or LVESD ≥ 40mm
Acute severe MR (papillary rupture) → emergent surgery

💊 Anticoagulation

Mechanical valve = warfarin lifelong (DOACs contraindicated [RE-ALIGN])
INR target: 2.5-3.5 (mitral), 2.0-3.0 (aortic)
Bioprosthetic: warfarin × 3-6 months → then ASA only
TAVR: DAPT × 3-6 months → then ASA

💊 Key Drugs

No medical Rx for ASValve replacement is the only treatment

Avoid in ASVasodilators, aggressive diuresis

MR afterload reductionACEi for chronic MR

WarfarinMechanical valves only

⚠️ Pitfalls

Vasodilators in severe AS (fixed obstruction → hypotension)
DOACs with mechanical valve [RE-ALIGN increased events]
Missing low-flow low-gradient AS (gradient looks mild)
Delaying surgery in asymptomatic severe with declining EF

CommonCardiology

Syncope

Transient loss of consciousness with spontaneous recovery due to global cerebral hypoperfusion. The #1 question: is this cardiac or benign? Risk-stratify to determine who goes home vs who gets telemetry.

🔍 Overview

Etiology

Category	% of Syncope	Examples	Risk
Reflex / vasovagal	~50–60%	Emotional trigger, prolonged standing, pain, micturition, carotid sinus hypersensitivity	Benign. Prodrome (lightheadedness, warmth, diaphoresis, nausea).
Orthostatic hypotension	~15%	Volume depletion, medications (antihypertensives, diuretics), autonomic neuropathy (diabetes, Parkinson)	Low. SBP drop ≥ 20 or DBP ≥ 10 within 3 min of standing.
Cardiac -arrhythmic	~10–15%	Bradycardia (sick sinus, heart block), VT, SVT, long QT, Brugada, channelopathies	HIGH. Sudden onset without prodrome. Exertional syncope. Family history of SCD.
Cardiac -structural	~5%	Severe AS, HCM (LVOT obstruction), massive PE, cardiac tamponade, aortic dissection	HIGH. Exertional syncope, new murmur, dyspnea.
Neurologic	Rare (< 5%)	Vertebrobasilar TIA, subclavian steal. Seizure is NOT syncope (different mechanism).	Variable. True neurologic syncope is rare -most "neurologic" syncope is actually cardiac.

High-Risk Features -Admit These Patients

If ANY of these are present → admit for telemetry + further workup:

Exertional syncope -cardiac until proven otherwise (AS, HCM, arrhythmia)
Syncope while supine or seated -eliminates orthostatic/vasovagal
No prodrome -sudden LOC without warning suggests arrhythmia
Abnormal ECG: long QT, Brugada pattern, heart block, new LBBB, delta wave (WPW)
Family history of sudden cardiac death (especially < 50 yo)
Known structural heart disease (HF, prior MI, EF < 35%)
Associated chest pain, dyspnea, or palpitations
Significant injury from the fall

🧪 Workup

Initial Workup -All Syncope

Test	Why
ECG MANDATORY	EVERY syncope patient gets an ECG. Look for: long QT, short QT, Brugada, WPW (delta wave), heart block, prior MI (Q waves), HCM (LVH + septal Q waves), arrhythmia.
Orthostatic vitals	Lying → sitting → standing. SBP drop ≥ 20 or DBP ≥ 10 or HR rise > 30 = positive.
BMP, CBC, glucose	Dehydration, anemia, hypoglycemia (not true syncope but a mimic).
Troponin	If ACS suspected or exertional syncope.
Echo	If structural heart disease suspected (new murmur, exertional syncope, abnormal ECG). Identifies AS, HCM, RV strain (PE), effusion.
Telemetry / Holter / Loop recorder	If arrhythmic cause suspected. Telemetry inpatient. Holter for 24–48h. Implantable loop recorder (ILR) for recurrent unexplained syncope. ISSUE-3, Brignole 2012

Routine head CT, EEG, and carotid US are NOT indicated for syncope unless focal neurologic signs are present. Syncope ≠ seizure. Syncope ≠ stroke. Over-ordering these wastes resources.

Canadian Syncope Risk Score -30-day serious adverse event risk after ED syncope (guides admission vs discharge)

Validated score for ED risk stratification. Predicts 30-day serious adverse events. Canadian Syncope Risk Score, Thiruganasambandamoorthy 2016

Predictor	Points
ED diagnosis: vasovagal	−2
Heart disease history (HF, CAD, VHD)	+1
Any ED SBP < 90 or > 180	+2
Troponin elevated (> 99th percentile)	+2
Abnormal QRS axis (< −30° or > 100°)	+1
QRS > 130 ms	+1
Corrected QT > 480 ms	+2
ED diagnosis: cardiac syncope	+2

Score ≤ −1: very low risk (~1%) → safe for discharge. Score ≥ 3: high risk (~20%+) → admit. San Francisco Syncope Rule, Quinn 2004

📋 On Rounds

Why is exertional syncope a red flag?

Exercise increases myocardial oxygen demand and cardiac output requirements. If there's a fixed obstruction (severe AS, HCM with LVOT obstruction), the heart cannot increase CO to match demand → BP drops → cerebral hypoperfusion → syncope. In arrhythmic causes, exercise triggers catecholamine-mediated arrhythmias (VT in ARVC, polymorphic VT in CPVT, long QT).

When is head CT indicated in syncope?

Almost never for syncope itself. Syncope is caused by transient global cerebral hypoperfusion -not a structural brain lesion. Head CT is indicated if: (1) significant head trauma from the fall (especially on anticoagulation), (2) focal neurologic deficits suggesting stroke (but stroke rarely presents as pure syncope), (3) concern for SAH (thunderclap headache). Routine head CT in simple syncope has an extremely low diagnostic yield (< 2%)

What high-risk features on ECG should make you admit a syncope patient?

Admit and monitor if any of: (1) Brugada pattern (coved ST elevation V1-V3), (2) Long QT (QTc > 500), (3) Short QT (QTc < 340), (4) Epsilon waves or TWI V1-V3 (ARVC), (5) WPW (delta wave + short PR), (6) New bundle branch block, (7) Mobitz II or 3rd degree AV block, (8) ST elevation (STEMI), (9) Non-sustained VT on telemetry.

A 22-year-old collapses during basketball and is resuscitated. What do you screen for?

Sudden cardiac arrest in a young athlete = mandatory structural/electrical workup: (1) Echo: HCM (septal thickness ≥ 15 mm), ARVC (RV dilation/dysfunction), dilated cardiomyopathy, anomalous coronary arteries. (2) ECG: WPW, long QT, Brugada, ARVC (epsilon waves, TWI V1-V3). (3) Cardiac MRI: definitive for ARVC (fatty infiltration, fibrosis), myocarditis, scar. (4) Genetic testing if channelopathy suspected

Clinical Examples

📋 Case 1, Vasovagal Syncope in a Young Patient

Patient: 22F, no PMH, witnessed syncopal episode while standing in church. Felt warm, lightheaded, and nauseated before losing consciousness for ~10 seconds. No seizure activity, no tongue biting.

Key findings: Exam normal. ECG: normal sinus rhythm, PR 160 ms, QTc 410 ms, no Brugada pattern. Orthostatic vitals: supine 118/72 HR 68 → standing 92/58 HR 102 (positive). Troponin negative. CBC, BMP normal.

Management:

Low-risk by Canadian Syncope Risk Score, safe for discharge
Classic vasovagal: prodrome (warmth, nausea), upright posture trigger, brief LOC with rapid recovery
Counseling: increase fluid intake (2-3 L/day), increase salt (≥ 6g/day), counter-pressure maneuvers (leg crossing, hand grip)
Avoid prolonged standing, dehydration, and known triggers
No medications needed for first-episode vasovagal syncope

Teaching point: Vasovagal syncope is the most common cause of syncope (~40%). The classic prodrome (warmth, diaphoresis, nausea, tunnel vision) followed by brief LOC with rapid recovery is diagnostic. ECG is the only mandatory test, routine head CT has < 2% yield and is not indicated without head trauma or focal deficits.

📋 Case 2, Cardiac Syncope from Complete Heart Block

Patient: 78M, HTN and prior MI, presents after sudden LOC without warning while sitting in his chair. Wife witnessed 15-second LOC with pallor. No prodrome, no postictal state.

Key findings: HR 34, BP 98/60. ECG: complete (3rd degree) AV block with ventricular escape rhythm at 32 bpm. Wide QRS escape complexes. No P-wave/QRS relationship (AV dissociation). Troponin mildly elevated.

Management:

Admit to telemetry/ICU, transcutaneous pacer pads on standby
Atropine 0.5-1 mg IV (may not work in infranodal block with wide escape)
Isoproterenol drip or temporary transvenous pacemaker if hemodynamically unstable
Permanent pacemaker (dual-chamber DDD), Class I indication for symptomatic CHB
Echo to assess structural heart disease; hold AV-nodal blocking agents

Teaching point: Syncope without prodrome ("no warning") while sitting or supine is cardiac until proven otherwise. Red flags: exertional syncope, syncope while supine/seated, family history of sudden cardiac death < 50, structural heart disease. Complete heart block requires a pacemaker regardless of symptoms.

📋 Case 3, Exertional Syncope in a Young Athlete

Patient: 17M, previously healthy, collapses during basketball practice. Brief LOC with rapid recovery. Teammate says he "just dropped" mid-sprint. No prodrome.

Key findings: Grade III/VI harsh crescendo-decrescendo systolic murmur at LLSB that increases with Valsalva and standing. ECG: LVH with deep Q waves in lateral leads, T-wave inversions. Echo: septal thickness 22 mm, LVOT gradient 45 mmHg at rest (increases to 80 mmHg with Valsalva).

Management:

Immediate disqualification from competitive sports
Hypertrophic cardiomyopathy (HCM) with dynamic LVOT obstruction confirmed
ICD evaluation, exertional syncope in HCM is a major risk factor for sudden cardiac death
Start beta-blocker (metoprolol) or verapamil for symptom control
Screen all first-degree relatives (autosomal dominant inheritance)
Avoid dehydration, vasodilators, and high-intensity exertion

Teaching point: HCM is the most common cause of sudden cardiac death in young athletes in the US. The murmur of HCM is unique: it increases with maneuvers that decrease preload (Valsalva, standing) because reduced LV volume worsens LVOT obstruction. All other murmurs decrease with these maneuvers. Exertional syncope in a young person mandates full structural and electrical cardiac workup.

📣 Sample Presentation

One-Liner

"Ms. Nguyen is a 22-year-old presenting after witnessed syncope at church. She felt lightheaded and warm before losing consciousness for ~10 seconds with no seizure activity. ECG normal sinus, no Brugada, no long QT. Orthostatic positive."

Key Points to Cover on Rounds

Classic vasovagal prodrome (warmth, lightheadedness, standing). Witnessed brief LOC, no seizure activity, rapid return to baseline. ECG: normal sinus, PR normal, QTc 420. Troponin negative. Orthostatic: supine 112/70→standing 88/58 with symptoms. No high-risk features (no exertional, no supine, no FH SCD, no structural heart disease). Plan: discharge with reassurance, hydration, leg crossing techniques, return precautions.

Monitoring and Follow-Up

Setting	Monitoring	Purpose
Inpatient (high risk)	Continuous telemetry	Detect arrhythmias (VT, pauses, heart block). Minimum 24-48h
Holter monitor	24-48h outpatient	Frequent symptoms (> 1/week). Captures rhythm during symptoms
Event monitor	2-4 weeks outpatient	Less frequent symptoms. Patient-activated during episodes
Implantable loop recorder	Up to 3 years	Recurrent unexplained syncope. Gold standard for infrequent events. ISSUE-3
Orthostatic vitals	At follow-up visits	Confirm response to treatment. SBP drop > 20 or DBP > 10 within 3 min of standing
Driving restrictions	Counsel at discharge	Varies by state/country. Generally no driving for weeks to months after cardiac syncope

⚡ Management

Management by Etiology

Type	Management
Vasovagal	Reassurance and education. Counter-pressure maneuvers (leg crossing, hand grip, squatting). Increase fluid/salt intake (2-3 L/day, 6-10 g salt). Avoid triggers. Tilt training for recurrent episodes
Orthostatic	Review and stop offending meds (diuretics, alpha-blockers, vasodilators). Compression stockings. Increase fluids/salt. Rise slowly. Midodrine 2.5-10 mg TID if refractory. Fludrocortisone 0.1-0.2 mg daily
Cardiac arrhythmia	Bradycardia (SSS, CHB, Mobitz II) → pacemaker. VT → ICD. WPW → ablation. Long QT → avoid QT-prolonging drugs, beta-blocker, consider ICD
Structural cardiac	Aortic stenosis → valve replacement. HCM → avoid dehydration/vasodilators, beta-blocker, ICD if high risk. PE → anticoagulation
Carotid sinus	Avoid tight collars/neck manipulation. Pacemaker if cardioinhibitory type with recurrent syncope
Situational	Avoid triggers (cough, micturition, defecation). Sit to urinate. Treat underlying cough. Counter-pressure maneuvers

Disposition

Admit if: Abnormal ECG, exertional syncope, syncope while supine, significant injury, known structural heart disease, family history of sudden cardiac death, new murmur, older age with no clear cause
Discharge if: Young patient, classic vasovagal prodrome, situational trigger, orthostatic (correctable), normal ECG, no structural heart disease, normal exam

💊 Medications

Medications for Recurrent Syncope

Drug	Indication	Dose	Notes
Midodrine	Orthostatic hypotension	2.5-10 mg PO TID	Alpha-1 agonist. Give morning/noon/afternoon. Avoid evening dose (supine HTN)
Fludrocortisone	Orthostatic hypotension	0.1-0.2 mg PO daily	Volume expansion. Monitor K+ and edema. Avoid in HF
Droxidopa	Neurogenic orthostatic hypotension	100-600 mg PO TID	For autonomic failure (Parkinson's, MSA). Norepinephrine prodrug
Beta-blockers	Long QT syndrome	Nadolol 40-80 mg daily preferred	Reduces risk of cardiac events in LQTS. Non-selective preferred
SSRI (paroxetine)	Refractory vasovagal	20 mg PO daily	Limited evidence. Consider in severely recurrent vasovagal only

Most syncope does not need medications. Vasovagal is treated with counter-pressure maneuvers, hydration, and trigger avoidance. Medication review (stopping offending agents) is often the most important intervention.

⚡ Summary

Summary

Most Common

Vasovagal (~50%). Prodrome: warmth, nausea, diaphoresis, tunnel vision → brief LOC → rapid recovery.

High-Risk ECG

Brugada, long QT, WPW, CHB, Mobitz II, new BBB, epsilon waves (ARVC), ST elevation.

Admit If

Exertional syncope, supine syncope, FH sudden death, structural heart disease, abnormal ECG, older patient.

Workup

ECG (everyone). Echo if cardiac suspected. Orthostatics. Labs: glucose, Hgb, troponin if cardiac concern.

Low Risk

Young, vasovagal prodrome, situational (cough/micturition), orthostatic, normal ECG → discharge with follow-up.

Young Athlete SCA

Mandatory workup: echo (HCM), ECG (WPW/QT), cardiac MRI (ARVC), genetic testing. Survivors get ICD.