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

Pulmonary Embolism

Clot in the pulmonary vasculature. Severity ranges from subclinical (Category A) to cardiopulmonary failure (Category E). The AHA/ACC 2026 guideline introduces a new A–E classification system, classify immediately to determine disposition and therapy.

🔍 Overview

Pathophysiology

PE kills via acute right ventricular failure, not hypoxemia. Clot lodges in pulmonary vasculature → acute ↑ PVR → RV pressure overload → RV dilation → interventricular septum bows into LV → ↓ LV preload → ↓ cardiac output → obstructive shock → PEA arrest. Understanding this mechanism drives every management decision: why you avoid fluids, why intubation is dangerous, why thrombolysis saves lives in massive PE.

Risk Stratification,2026 AHA/ACC Clinical Categories (A–E)

🚨 NEW 2026 PARADIGM: The AHA/ACC 2026 guideline replaces "massive / submassive / low-risk" with an integrative Category A–E system. This incorporates clinical severity scores, biomarkers, RV imaging, hemodynamics, and respiratory status, shifting focus from anatomical clot burden to pathophysiological impact. Patients may transition between categories with reassessment.

Category	Description	Criteria	Disposition	Treatment
A SUBCLINICAL Old: incidental (not previously classified)	Asymptomatic, incidental PE (found on CT for another reason)	No symptoms attributable to PE. Incidental finding (e.g., cancer staging CT).	ED discharge with DOAC	Anticoagulation. Segmental or larger → treat. Isolated subsegmental → shared decision-making (treat vs surveillance).
B LOW SEVERITY Old: Low-risk PE	Symptomatic, low clinical severity	PESI* (Pulmonary Embolism Severity Index) ≤ 85 (class I–II), sPESI* (simplified PESI) = 0, Hestia < 1. Normal hemodynamics. B1 = subsegmental, B2 = non-subsegmental.	Early discharge (24–48h or directly from ED)	DOAC (apixaban or rivaroxaban). No heparin bridge. Close follow-up in 48–72h HESTIA, 2011.
C ELEVATED SEVERITY Old: Intermediate-low (C1–C2) / Submassive (C3)	Elevated clinical severity score ± RV dysfunction ± biomarkers	PESI III–V, sPESI ≥ 1, or Hestia ≥ 1. C1 = normal RV + normal biomarkers C2 = abnormal RV OR elevated biomarker C3 = abnormal RV AND elevated biomarker	Hospitalize. C3 → monitored bed (ICU/stepdown)	Anticoagulation. PERT* (Pulmonary Embolism Response Team) assessment for C2–C3 (Class 1). Close monitoring first 24–72h. Advanced therapy only if clinical deterioration.
D INCIPIENT FAILURE Old: Submassive PE (high-risk subset)	Incipient cardiopulmonary failure	D1 = transient hypotension (SBP < 90 that responds to fluids/single pressor) D2 = normotensive shock (AKI, lactate ↑, oliguria, altered MS, ↑ O2 requirement, worsening RV strain)	Hospitalize, ICU/monitored bed	Anticoagulation + PERT (Class 1). CDT* (Catheter-Directed Thrombolysis) or mechanical thrombectomy may be considered (Class 2b). Systemic tPA if rapidly deteriorating.
E CARDIOPULMONARY FAILURE Old: Massive PE	Persistent hypotension / cardiac arrest	E1 = SBP < 90 for ≥ 15 min despite resuscitation, requiring vasopressors, or cardiac arrest	ICU. Emergent intervention.	Systemic thrombolysis (Class 1). CDT / mechanical thrombectomy (Class 2a). Surgical embolectomy if others unavailable. VA-ECMO* (Veno-Arterial Extracorporeal Membrane Oxygenation) as bridge.

🔄 Old → New mapping: "Massive PE" ≈ Category E. "Submassive PE" ≈ Category C3–D (depending on hemodynamics). "Low-risk PE" ≈ Category A–B. The 2026 system adds granularity, C1 vs C2 vs C3 determines monitoring intensity, and D captures the "pre-arrest" patients who were previously lumped into submassive.

How to Categorize at the Bedside,4-Step Algorithm

Work top-down. Stop at the first category that fits. You need 4 pieces of data: (1) vitals & pressor status, (2) PESI/sPESI or Hestia score, (3) RV assessment (bedside echo or CT-PA RV:LV ratio ≥ 1.0), (4) biomarkers (troponin, BNP/NT-proBNP).

Step	Ask	If YES →
1	Hemodynamic collapse? Cardiac arrest, or SBP < 90 for ≥ 15 min despite fluids, requiring vasopressors.	E Activate PERT, prepare systemic tPA / thrombectomy / ECMO.
2	Incipient failure? Transient hypotension responding to fluids or single pressor (D1), OR normotensive shock: lactate ↑, AKI, oliguria, altered MS, rising O2 needs, worsening RV strain (D2).	D ICU, PERT consult, anticoag + consider CDT/thrombectomy (Class 2b).
3	Symptomatic with elevated severity? PESI III–V, sPESI ≥ 1, or Hestia ≥ 1, but hemodynamically stable. Then sub-classify using RV + biomarkers: • Both normal → C1 (ward) • One abnormal (RV OR biomarker) → C2 (monitored bed + PERT) • Both abnormal (RV AND biomarker) → C3 (ICU/stepdown + PERT)	C Hospitalize. Monitoring intensity matches the subcategory.
4	Symptomatic but low severity? sPESI = 0, PESI class I–II, Hestia 0, normal vitals, no RV strain, no biomarker elevation. B1 = subsegmental, B2 = non-subsegmental.	B DOAC, early discharge or directly from ED, 48–72h follow-up.
0	Asymptomatic incidental finding (e.g., PE seen on cancer staging CT, no PE-attributable symptoms).	A Outpatient DOAC if segmental or larger; shared decision-making if isolated subsegmental.

⚡ Bedside shortcut: Check vitals first (rules in/out D & E in 10 seconds). If stable, calculate sPESI: if 0, patient is B. If ≥ 1, get bedside echo + troponin + BNP to separate C1 / C2 / C3. The only categories requiring advanced imaging and biomarkers before categorization are C and its subtypes.

🔴 Re-categorize q6–12h in the first 24–72h. Patients transition. A C2 can decompensate to D or E. A D1 resolving with fluids may re-stratify to C3. Don't lock in the ED category: serial lactate, troponin trend, and RV reassessment drive escalation and de-escalation.

Risk Factors (Virchow's Triad), "SHE"

Mechanism	Examples
Stasis	Immobilization, post-op (especially ortho), long flights, paralysis, obesity, heart failure
Hypercoagulability	Cancer (especially pancreatic, lung, GI), OCPs/HRT, pregnancy/postpartum, Factor V Leiden, prothrombin mutation, antiphospholipid syndrome, nephrotic syndrome
Endothelial injury	Surgery, trauma, central venous catheters, prior DVT/PE, smoking

Presentation

Dyspnea -most common symptom (~80%), often acute onset
Pleuritic chest pain -sharp, worse with inspiration (~50%)
Tachycardia -often out of proportion to clinical picture
Hypoxia -but ~20% have normal SpO2 (A-a gradient usually elevated)
Syncope -suggests massive PE (transient loss of CO). Present in ~10%. In patients hospitalized for first-episode syncope, ~17% had PE on systematic workup PESIT, 2016, consider PE workup in unexplained syncope with risk factors.
Hemoptysis (~7%), leg swelling (concurrent DVT in ~50%)
New-onset atrial fibrillation -RV dilation stretches the RA → Afib

Classic triad (dyspnea + pleuritic pain + hemoptysis) is present in < 20% of cases. PE is a great mimicker -always on your differential for unexplained tachycardia, new Afib, syncope, or hypoxia out of proportion. Post-op patients with sudden desaturation = PE until proven otherwise.

Wells Score for PE

Criterion	Points
Clinical signs/symptoms of DVT	3.0
PE is #1 diagnosis or equally likely	3.0
Heart rate > 100	1.5
Immobilization (≥ 3 days) or surgery in past 4 weeks	1.5
Previous DVT/PE	1.5
Hemoptysis	1.0
Active cancer (treatment within 6 months or palliative)	1.0

Score ≤ 4 (PE unlikely): Check D-dimer. If negative → PE ruled out. If positive → CTPA.
Score > 4 (PE likely): Go directly to CTPA. Skip D-dimer (too many false positives).

🧪 Workup

Diagnostic Algorithm

Step-by-step: Clinical suspicion → PERC (if low risk) → Wells score → D-dimer (if Wells ≤ 4) → CTPA (if D-dimer positive or Wells > 4). Unstable patient → bedside echo → treat empirically.

Step 1

Assess clinical suspicion. Is PE on the differential? If clinical gestalt is very low → apply PERC rule. If all 8 negative → stop. No further testing needed.

Step 2

Calculate Wells score. ≤ 4 (PE unlikely) → proceed to D-dimer. > 4 (PE likely) → skip D-dimer, go directly to CTPA.

Step 3

D-dimer (if Wells ≤ 4). Use age-adjusted cutoff for patients > 50: age × 10 ng/mL (e.g., 65-year-old → cutoff 650). Negative → PE ruled out. Positive → CTPA.

Step 4

CTPA -gold standard imaging. Sensitivity > 95%, specificity > 97%. Also provides RV/LV ratio for risk stratification. If PE confirmed → risk stratify (massive vs submassive vs low-risk).

Unstable

Patient too unstable for CT? Bedside echo → if RV strain + clinical picture → treat empirically with systemic tPA. Do not delay for imaging.

YEARS Algorithm (Simplified Approach)

Alternative to traditional Wells pathway. Check 3 items: (1) clinical signs of DVT, (2) hemoptysis, (3) PE is most likely diagnosis. If none present AND D-dimer < 1000 → PE excluded. If any present AND D-dimer < 500 → PE excluded. Otherwise → CTPA. Reduces unnecessary CT scans by ~14% YEARS, 2017.

Diagnostic Tests

Test	When	Key Points
CTPA	Gold standard -test of choice	Sensitivity > 95%. Shows clot location, RV/LV ratio (> 0.9 = submassive), saddle PE. Avoid if contrast allergy or severe CKD → V/Q scan. Look for RV enlargement, septal bowing, reflux of contrast into IVC/hepatic veins.
D-dimer	Low/intermediate pretest (Wells ≤ 4)	High sensitivity (~95%), low specificity (~50%). Negative = rules out PE (NPV > 99%). Age-adjusted cutoff: age × 10 for > 50yo. Elevated in: cancer, pregnancy, post-op, DIC, infection -many false positives. Never order if high pretest probability.
V/Q Scan	Contrast allergy, severe CKD, pregnancy (controversial)	Reports as normal, low, intermediate, or high probability. Most useful if result is normal (rules out) or high probability (rules in). Intermediate = non-diagnostic → need CTPA or further workup. Best in patients with normal baseline CXR.
Bedside Echo	Unstable patient -cannot go to CT	Does NOT confirm PE but supports empiric treatment if: RV dilation (RVEDD > LVEDD), septal bowing (D-sign), McConnell's sign (RV free wall akinesis with apical sparing, ~95% specific), 60/60 sign (RVSP < 60 + PA acceleration time < 60 ms), TAPSE < 16 mm.
Troponin	All confirmed PE	Elevated = myocardial injury from RV strain = submassive PE. Prognostic -higher mortality, increased risk of hemodynamic deterioration. Serial trending useful.
BNP / NT-proBNP	All confirmed PE	Elevated = RV pressure overload. BNP > 100 or NT-proBNP > 600 = higher risk. Combined with troponin for risk stratification.
Lower Extremity US	DVT suspected, or CTPA unavailable	Concurrent DVT found in ~50% of PE. Positive DVT + symptoms = treat for PE even without CTPA. Also useful in pregnancy to avoid radiation.
ECG	All suspected PE	Most common: sinus tachycardia. Classic findings (often absent): S1Q3T3, RBBB, RV strain pattern (T-wave inversions V1-V4), right axis deviation. New Afib in ~10%. Normal ECG does NOT rule out PE.

Imaging & Diagnostic Findings

Specific signs to look for on each modality. Most individual findings are insensitive (absent in many true PEs) but specific (strongly suggest PE when present). Use them to support diagnosis and risk stratification, not to rule PE out.

Modality	Key Findings	Clinical Significance
ECG	Sinus tachycardia (most common, ~40%). S1Q3T3 (deep S wave in lead I, Q wave in lead III, and T-wave inversion in lead III, reflects acute right-heart strain rotating the heart's electrical axis; classic but only ~20% of PEs). New RBBB, incomplete or complete (acute RV pressure overload slows right-sided conduction). TWI V1–V4 (RV strain pattern, repolarization abnormality across the right precordial leads). Right axis deviation. New atrial fibrillation (~10%, RV dilation stretches the right atrium). Low-voltage QRS or ST-depression in inferior leads.	None are sensitive or specific. Normal ECG does NOT rule out PE. Main value: rule out STEMI and pericarditis. S1Q3T3 + TWI V1–V4 together suggest larger clot burden / RV strain, associated with Categories C2–D.
Chest X-Ray	Normal CXR is the single most common finding (24–40%). Overall sensitivity ~33%, specificity ~59%, so CXR cannot rule PE in or out. Most common abnormal findings: linear/plate-like atelectasis (~70% of abnormal CXRs; splinting from pleuritic pain and surfactant dysfunction), small unilateral pleural effusion (30–50%, usually on the PE side), elevated hemidiaphragm (~20%, splinting on the PE side). Eponymous signs (high specificity, low sensitivity, mostly boards / pattern recognition): Westermark sign (focal oligemia, a wedge-shaped region of decreased pulmonary vascular markings distal to the clot, because the embolus blocks arterial flow and downstream vessels collapse). Sens ~14%, Spec ~92%. Hampton's hump (wedge-shaped, pleural-based opacity with apex pointing toward the hilum, representing pulmonary infarction; late finding, > 12–24h after embolism, often near costophrenic angle). Sens ~22%, Spec ~82%. Infarction occurs in only ~10% of PEs because the lung has dual blood supply (pulmonary + bronchial); when it does, usually with concurrent CHF or shock impairing bronchial collateral. Fleischner sign (enlarged central pulmonary artery, from acute pulmonary hypertension distending the PA, or a proximal clot directly bulging the vessel). Sens ~20%, Spec ~80%. Palla sign (enlarged right descending pulmonary artery, specific to right-sided massive PE). Knuckle sign (abrupt tapering or "cut-off" of an occluded pulmonary artery branch on CXR).	Primary role: rule out mimics (pneumonia, pneumothorax, large effusion, pulmonary edema, widened mediastinum suggesting aortic dissection). Never exclude PE based on CXR, since 24–40% of confirmed PEs have a normal film. Essential baseline before V/Q scan, since V/Q is most reliable when the baseline CXR is clear; abnormal CXR pushes you to CTPA. Pearl: sudden hypoxia + tachycardia + a clear chest is a classic PE clue. When the CXR cannot explain the patient's oxygen requirement, PE moves up the differential.
Lower-Extremity Doppler Ultrasound	Non-compressible common femoral or popliteal vein = acute DVT (primary finding). Loss of respiratory phasicity in the vein. Absent color Doppler flow within the lumen. Directly visible intraluminal echogenic thrombus. Concurrent DVT found in ~50% of confirmed PE.	Positive DVT + PE-compatible symptoms = treat as PE even without CTPA (same anticoagulation). Especially useful in pregnancy (avoids fetal radiation), contrast allergy, severe CKD. Negative scan does NOT rule out PE, proximal calf-vein DVTs can still embolize.
Spiral CT (CTPA)	Intraluminal filling defect in pulmonary artery (dark clot surrounded by bright contrast within the vessel, the direct diagnostic sign). Saddle PE (large clot straddling the main PA bifurcation like a saddle over a horse's back, occludes both left and right pulmonary arteries). RV/LV ratio > 1.0 (measured on axial reconstructions, the RV is bigger than the LV, indicating acute pressure overload; prognostic for Category C2–C3). Septal bowing into LV (same mechanism as echo D-sign). Reflux of contrast into IVC / hepatic veins (contrast injected into an arm vein normally flows forward through the right heart, but with failing RV the tricuspid valve leaks and contrast washes backward down the IVC, sign of severe RV dysfunction). Pulmonary infarct (wedge-shaped peripheral opacity, same finding as Hampton's hump on CXR, seen earlier on CT). Enlarged main PA (> 29 mm, upstream dilation from proximal clot).	Gold standard. Sensitivity > 95%, specificity > 97%. Also drives risk stratification (RV/LV ratio separates C1 from C2–C3). Avoid if contrast allergy or severe CKD (CrCl < 30), use V/Q scan. Look explicitly at the RV in the report; don't just read "PE positive/negative."
V/Q Scan	Mismatched segmental perfusion defects (a lung segment ventilates normally on the radiolabeled gas scan but shows no perfusion on the radiolabeled-albumin scan, because the clot blocks blood flow while the airway is still open; this is the hallmark of PE). Reported by PIOPED criteria (from the Prospective Investigation of Pulmonary Embolism Diagnosis, 1990 landmark study, established the four-tier probabilistic reporting): normal, low, intermediate, or high probability.	Normal scan rules out PE (NPV > 95%). High-probability scan rules in PE (PPV ~85%). Intermediate / low probability = non-diagnostic in ~70% of cases, need CTPA or lower-extremity US. Preferred in pregnancy (lower breast radiation than CTPA by some protocols), contrast allergy, and severe CKD. Requires clear baseline CXR.
Echocardiography (Bedside / TTE)	Six bedside findings, in order of how often you'll see them: RV dilation. RVEDD > LVEDD, or RV/LV ratio > 1 in the apical four-chamber view. What you're seeing: the normally smaller RV is now bigger than the LV. Why: acute clot burden raises RV afterload, the thin-walled RV dilates rather than hypertrophies acutely. Septal flattening / D-sign. Best seen on parasternal short-axis. What you're seeing: the LV cavity, normally circular, is squashed into a "D" shape. Why: high RV pressure bows the interventricular septum leftward into the LV. McConnell's sign. RV free-wall akinesis with preserved apical contraction. What you're seeing: the RV mid-wall barely moves but the RV apex still squeezes. Why: the apex is tethered to and tugged along by the still-contracting LV, masking the stunned RV mid-wall. ~95% specific for acute PE. 60/60 sign. Two cutoffs both under 60: RVSP < 60 mmHg AND pulmonary acceleration time < 60 ms. Why: reflects acute PA obstruction without the chronic adaptation of established pulmonary hypertension (in chronic PH the RV can generate much higher pressures). Distinguishes acute PE from chronic PH. TAPSE < 16 mm. Tricuspid Annular Plane Systolic Excursion. What you're measuring: how far the tricuspid annulus descends toward the apex during systole, in M-mode. Why: the RV contracts mostly longitudinally; reduced annular descent is a quick proxy for RV systolic function. Lower TAPSE = worse RV. Clot in transit (rare). Mobile thrombus directly visualized in RA, RV, or main PA. Why it matters: very high mortality, often triggers immediate systemic thrombolysis or surgical embolectomy without waiting for CTPA.	Does not definitively diagnose PE. In an unstable patient with compatible clinical picture, RV strain findings support empiric systemic thrombolysis without CTPA. Also central to risk stratification: RV dysfunction defines the transition from C1 to C2–C3. Serial echo tracks RV recovery after treatment.
Pulmonary Angiography	Direct catheter-based contrast injection into the pulmonary arteries. Intraluminal filling defect or abrupt vessel cutoff. Allows measurement of PA pressures.	Historical gold standard, replaced by CTPA for diagnosis (CTPA is non-invasive, faster, as accurate). Still clinically relevant as the access route during catheter-directed therapy (EKOS, FlowTriever, Penumbra Indigo), diagnostic angiography and intervention occur together. Invasive, risk of contrast load and catheter-induced arrhythmia. Rarely indicated for diagnosis alone.

Combining signs: No single finding diagnoses PE. Clinical gestalt + Wells / YEARS + D-dimer + CTPA is the diagnostic pathway. Imaging findings above are for pattern recognition on exam, read-outs, and risk stratification, not stand-alone rule-in or rule-out tools.

PE in Special Populations

Pregnancy

PE is a leading cause of maternal mortality. D-dimer is physiologically elevated in pregnancy -less useful. Start with lower extremity US → if positive DVT, treat without CTPA. If US negative → CTPA (preferred over V/Q in most guidelines -lower fetal radiation, more definitive). Anticoagulation: LMWH (enoxaparin) -DOACs are contraindicated in pregnancy. Continue through postpartum (minimum 3 months total, at least 6 weeks postpartum).

Cancer-Associated PE

LMWH was traditional standard. Now DOACs (edoxaban, rivaroxaban) are options for non-GI cancers Hokusai-VTE Cancer, 2018 SELECT-D, 2018. Avoid DOACs in GI/GU cancers (higher mucosal bleeding risk). Duration: indefinite while cancer is active.

Renal Failure (CrCl < 30)

Use UFH (renally cleared, titratable, reversible). Avoid LMWH (accumulates → bleeding). Avoid DOACs if CrCl < 25-30. V/Q scan instead of CTPA if concerned about contrast nephropathy.

🚨 Management

Category E, Cardiopulmonary Failure (formerly "Massive PE")

This is a time-critical emergency. Do NOT wait for CTPA if echo shows RV strain + clinical picture fits. Mortality without treatment: 25–65%. Systemic thrombolysis is Class 1 per AHA/ACC 2026.

0–5 min

Recognize & stabilize. IV access × 2 large-bore. Supplemental O2 (high-flow NC or NRB). Avoid intubation if possible -positive pressure ventilation drops preload → hemodynamic collapse. If must intubate: ketamine induction (maintains hemodynamics), low tidal volume, lowest PEEP tolerated. Have vasopressors running BEFORE induction.

0–15 min

Hemodynamic support. Cautious IV fluids (250-500 mL max -RV is volume-sensitive, overloading worsens septal bowing and drops CO). Norepinephrine first-line pressor (supports MAP without increasing PVR). Consider vasopressin as adjunct. Avoid phenylephrine (pure alpha = increases PVR).

0–30 min

Systemic thrombolysis. Alteplase (tPA) 100 mg IV over 2 hours -standard protocol. In cardiac arrest: 50 mg IV bolus (push dose), may repeat × 1. Start heparin drip after tPA infusion (no bolus). Continue CPR for at least 60-90 min after tPA in arrest -it takes time to work. Jerjes-Sanchez, 1995

If tPA contraindicated

Catheter-directed therapy (CDT) or mechanical thrombectomy, Class 2a for Category E1 per AHA/ACC 2026. Options: catheter-directed lysis (low-dose tPA 12-24 mg over 12-24h directly into PA via EKOS), mechanical thrombectomy (FlowTriever, Penumbra Indigo), or hybrid. Surgical embolectomy if CDT unavailable and patient deteriorating.

Refractory

VA-ECMO as bridge to intervention or recovery in centers with capability. Consider if: cardiac arrest refractory to tPA, contraindication to lysis with ongoing hemodynamic collapse.

Category C3–D, Elevated Severity / Incipient Failure (formerly "Submassive PE")

The gray zone. These patients are stable NOW but can decompensate rapidly. Close ICU/step-down monitoring is essential. PERT activation is Class 1 for Categories C–E per AHA/ACC 2026.

Immediate

Anticoagulation with heparin drip (UFH 80 units/kg bolus → 18 units/kg/hr, target aPTT 60-80). Heparin preferred initially because it's titratable and reversible if escalation needed. LMWH is recommended over UFH (Class 1) when parenteral therapy is needed and escalation is not anticipated AHA/ACC 2026. Use UFH if: high bleeding risk, considering thrombolysis, anticipating procedures, renal failure, or potential ECMO.

Risk assess

Check all prognostic markers: troponin (RV injury), BNP/NT-proBNP (RV strain), RV/LV ratio on CT (> 0.9), bedside echo (RV function, McConnell's sign, TAPSE). Calculate sPESI. Higher burden = closer monitoring.

Activate PERT

Pulmonary Embolism Response Team -multidisciplinary team (pulm, IR, CT surgery, heme, critical care). If available, activate early for submassive PE. They guide decisions about escalation to CDT or lysis.

Escalation triggers

Worsening tachycardia, rising troponin/BNP, new hypotension (SBP < 90), increasing O2 requirement, worsening RV on repeat echo → patient is transitioning from Category C to D. Escalate to catheter-directed therapy (Class 2b for D1–D2) or mechanical thrombectomy (Class 2b for D1–D2) per AHA/ACC 2026. Half-dose tPA (50 mg over 2h) remains an option MOPETT, 2013. HI-PEITHO, 2026 showed 61% reduction in decompensation with CDT in intermediate-high-risk PE.

PEITHO → HI-PEITHO evolution: PEITHO (2014) showed routine systemic tPA for submassive PE increased major bleeding (6.3%) and hemorrhagic stroke (2%) PEITHO, 2014. HI-PEITHO (2026) showed catheter-directed low-dose thrombolysis reduced decompensation by 61% in intermediate-high-risk PE (Category C3) without increased major bleeding HI-PEITHO, 2026. CDT is now the preferred escalation pathway over systemic tPA for Category C3–D patients. AHA/ACC 2026: mechanical thrombectomy is NOT recommended (Class 3: No Benefit) in low-risk PE (Categories A–C1).

Category A–B, Subclinical / Low Severity (formerly "Low-Risk PE")

DOACs are recommended over VKAs (Class 1) per AHA/ACC 2026: Apixaban 10 mg BID × 7 days → 5 mg BID or Rivaroxaban 15 mg BID × 21 days → 20 mg daily. No heparin bridging needed AMPLIFY, 2013 EINSTEIN-PE, 2012. Apixaban preferred over rivaroxaban based on COBRRA, 2026 (54% less bleeding, equal efficacy).
If using warfarin: bridge with LMWH/UFH until INR 2-3 × 2 consecutive days. Monitor INR weekly then monthly.
Category A: Asymptomatic/incidental PE → can discharge from ED with DOAC.
Category B: Symptomatic low-severity → early discharge (24–48h or directly from ED) if sPESI = 0 AND Hestia criteria negative (see below).

Hestia Criteria -Outpatient PE Treatment

If ALL of the following are absent, patient may be safe for outpatient management:

Hemodynamically unstable (SBP < 100, requiring pressors)
Thrombolysis or embolectomy needed
Active bleeding or high bleeding risk
Need > 24h O2 to maintain SpO2 > 90%
PE diagnosed while on anticoagulation
Severe pain requiring IV analgesia > 24h
Medical or social reason for admission (> 24h)
CrCl < 30 mL/min
Severe liver disease
Pregnancy
History of HIT

sPESI = 0 + all Hestia criteria absent → candidate for discharge with DOAC and close follow-up (48-72h). Saves bed-days with no difference in outcomes HESTIA, 2011.

Catheter-Directed Therapy (CDT)

Modality	Mechanism	When to Consider
EKOS (EkoSonic)	Ultrasound-assisted catheter-directed lysis. Low-dose tPA (9–17 mg over 12–24h) delivered directly into PA with ultrasound waves to enhance clot penetration.	Category D–E (Class 2a for E1, Class 2b for D1–D2) per AHA/ACC 2026. Validated in HI-PEITHO, 2026 (61% reduction in decompensation, no increased bleeding) ULTIMA, 2014.
FlowTriever	Mechanical aspiration thrombectomy. No lytic agent needed, purely mechanical clot removal.	Class 2a for Category E1, Class 2b for D1–D2, Class 3 (No Benefit) for A–C1 per AHA/ACC 2026. Preferred over systemic tPA when bleeding risk is high FLARE, 2020.
Penumbra Indigo	Continuous aspiration mechanical thrombectomy (CAT).	Similar indications to FlowTriever. Lytic-free option. Same class recommendations per AHA/ACC 2026.
Surgical Embolectomy	Open cardiothoracic surgery to remove clot from PA.	Last resort. Category E when CDT unavailable and patient failing. Requires cardiothoracic surgery and cardiopulmonary bypass.

Anticoagulation Duration

Scenario	Duration	Notes
Provoked PE (major reversible risk factor: surgery, immobilization, trauma, OCPs)	3 months then stop	Transient risk factor removed. Low recurrence after stopping (~3%/year). AHA/ACC 2026: stopping at end of initial treatment phase is recommended when a major reversible risk factor is identified.
Unprovoked PE (no identifiable trigger) or persistent risk factors	≥ 3–6 months, then extend indefinitely	AHA/ACC 2026: extended anticoagulation beyond 3–6 months is recommended for first acute PE without a major reversible risk factor. Extended-dose DOAC (apixaban 2.5 mg BID or rivaroxaban 10 mg daily) reduces recurrence with lower bleeding AMPLIFY-EXT, 2013.
Recurrent VTE (2nd unprovoked event)	Indefinite	Lifelong anticoagulation. Use extended-dose DOAC for lower bleeding risk.
Cancer-associated PE	Indefinite (while cancer active)	LMWH historically preferred CLOT, 2003. DOACs (edoxaban, rivaroxaban, apixaban) now acceptable alternatives, but avoid DOACs in GI/GU cancers (higher mucosal bleeding) Hokusai-VTE Cancer, 2018.
PE with thrombophilia	Consider indefinite	Antiphospholipid syndrome = indefinite warfarin (avoid DOACs,TRAPS, 2018). Factor V Leiden homozygous = consider indefinite. Heterozygous = treat like unprovoked.

IVC Filter Indications

Absolute contraindication to anticoagulation (active life-threatening bleed) + acute proximal DVT/PE
Recurrent PE despite therapeutic anticoagulation
Always use retrievable filters -remove within 30-90 days once anticoagulation can be started. Permanent filters cause long-term complications (IVC thrombosis, filter migration, fracture).
IVC filter is NOT a substitute for anticoagulation. Start anticoag as soon as safe and retrieve the filter.

Evidence base: Adding an IVC filter to anticoagulation does NOT improve outcomes in patients who can be anticoagulated. PREPIC, 1998 showed a retrievable filter reduced early PE but doubled DVT recurrence, with no mortality benefit. PREPIC 2, 2015 confirmed no benefit in high-risk PE when anticoagulation is feasible. Reserve filters strictly for patients who genuinely cannot be anticoagulated.

tPA Contraindications

Absolute	Relative
Active internal bleeding (excluding menses) Hemorrhagic stroke (any time) Ischemic stroke within 3 months Intracranial neoplasm, AVM, or aneurysm Known bleeding diathesis Significant head trauma or facial trauma within 3 months Intracranial/spinal surgery within 3 months Suspected aortic dissection	Recent surgery/procedure within 10 days Recent internal bleeding (2-4 weeks) Uncontrolled HTN (SBP > 180) Current anticoagulation (INR > 1.7) Pregnancy Active peptic ulcer disease CPR > 10 min (relative, not absolute) Diabetic retinopathy

In cardiac arrest from massive PE, relative contraindications may be overridden. The risk of death from PE outweighs the bleeding risk. Discuss with your attending.

📋 Case 1, Submassive PE (Post-Surgical)

Patient: 45M, post-op day 3 from knee surgery, sudden-onset dyspnea, HR 110, SpO2 92%, BP 128/82.

Pre-test probability: Wells score = 4.5 (HR > 100 = 1.5, immobilization/surgery = 1.5, PE most likely dx = 1.5) → PE likely → CTPA directly (skip D-dimer).

CT-PA: Saddle PE with RV dilation, RV/LV ratio 1.2.

Risk stratification:

Hemodynamically stable (BP > 90) → NOT massive
RV dilation on CT + troponin 0.08 (elevated) + BNP 450 → Submassive PE
sPESI score: age > 45 (+1), HR > 110 (+1) = 2 → high risk for decompensation

Treatment:

Anticoagulation: Heparin drip (80 units/kg bolus → 18 units/kg/hr). Target aPTT 60-80.
Disposition: ICU admission. Activate PERT if available.
Monitor: Serial troponin q6h, repeat echo in 24h, continuous telemetry.
Escalation plan: If SBP drops < 90, increasing O2, or worsening RV → catheter-directed therapy or half-dose tPA.
Transition: Once stable × 24-48h → apixaban 10 mg BID × 7 days → 5 mg BID.
Duration: Provoked (surgery) → 3 months. OCPs stopped.

📋 Case 2, Massive PE with Cardiac Arrest

Patient: 62F with metastatic ovarian cancer, found unresponsive. PEA arrest. No pulse. CPR initiated.

Bedside echo during CPR: Severely dilated RV, septal bowing into LV, no pericardial effusion.

Clinical reasoning: PEA arrest + cancer + massively dilated RV → massive PE until proven otherwise.

Treatment:

Push-dose tPA: Alteplase 50 mg IV bolus during CPR. Continue CPR for 60–90 min (tPA needs time).
Second bolus: If no ROSC after 15 min → repeat alteplase 50 mg IV.
ROSC achieved: Start heparin drip (no bolus after tPA). ICU admission. Post-ROSC care.
Imaging: CTPA once stable confirms bilateral PE with large clot burden.
Long-term: Cancer-associated PE → indefinite anticoagulation with LMWH (GU cancer, avoid DOACs).

Key lesson: In cardiac arrest with suspected PE, do NOT wait for imaging. Empiric tPA saves lives. Relative contraindications are overridden when the patient is coding.

📋 Case 3, Low-Risk PE Sent Home

Patient: 28F on OCPs, presents with 2 days of pleuritic chest pain and mild dyspnea. HR 88, BP 124/76, SpO2 98%.

Wells score: 4.5 (HR < 100 = 0, PE most likely dx = 3, OCPs = 1.5) → PE likely → CTPA.

CT-PA: Subsegmental PE in right lower lobe. RV/LV ratio 0.7 (normal). No RV strain.

Risk stratification:

Hemodynamically stable, no RV dysfunction, troponin negative, BNP normal → Low-risk PE
sPESI = 0 (age < 80, no cancer, no cardiopulm disease, HR < 110, SBP > 100, SpO2 > 90%)
Hestia criteria, all absent

Treatment:

Outpatient management: sPESI = 0 + Hestia negative → safe for discharge.
Rivaroxaban 15 mg BID × 21 days → 20 mg daily. No heparin bridge needed.
Stop OCPs. Discuss alternative contraception.
Follow-up: PCP in 48–72 hours. Repeat imaging NOT routinely needed.
Duration: 3 months (provoked, OCP-related). No thrombophilia workup unless recurrent.

Key lesson: Not every PE needs admission. Low-risk PE with sPESI = 0 and Hestia-negative can go home safely on a DOAC.

📋 Case 4, PE in Pregnancy

Patient: 31F, 28 weeks pregnant, acute dyspnea and tachycardia (HR 115). SpO2 94%. Left leg swelling for 3 days.

D-dimer: Elevated, but D-dimer is physiologically elevated in pregnancy → not reliable.

Diagnostic approach:

Step 1: Lower extremity compression US → positive for left popliteal DVT.
Step 2: DVT confirmed + symptoms → treat for PE without CTPA (avoid radiation if DVT already found).

Treatment:

Enoxaparin 1 mg/kg BID (weight-based, use pre-pregnancy or actual weight). DOACs are contraindicated in pregnancy.
Monitor anti-Xa levels (target 0.6–1.0 at peak, 4h post-dose). Dose adjustments needed as pregnancy progresses.
Delivery plan: Switch to UFH at 36 weeks (shorter half-life, reversible with protamine). Hold LMWH 24h before planned delivery.
Postpartum: Resume LMWH → transition to DOAC or warfarin after delivery. Continue for minimum 3 months total AND at least 6 weeks postpartum.

Key lesson: In pregnancy, start with leg US, if DVT is found, treat without CT. LMWH is the anticoagulant of choice. Plan the delivery switch to UFH early.

📋 Case 5, Incidental PE Found on Staging CT

Patient: 58M with newly diagnosed lung adenocarcinoma. Staging CT chest/abdomen/pelvis incidentally finds a segmental PE in the right pulmonary artery. Asymptomatic. HR 78, BP 132/80, SpO2 97%.

Clinical question: Does an incidental PE need treatment?

Answer: Yes.

Incidental PE in cancer patients carries same mortality and recurrence risk as symptomatic PE.
ISTH and ASCO guidelines: Treat incidental PE the same as symptomatic PE.
Exception: isolated subsegmental PE, discuss with hematology, may consider surveillance.

Treatment:

LMWH or DOAC (this is lung cancer, not GI, DOACs are acceptable).
Apixaban 10 mg BID × 7 days → 5 mg BID.
Duration: Indefinite while cancer is active. Reassess if cancer enters remission.
Check for RV strain: Echo + troponin + BNP to rule out submassive component despite being asymptomatic.

Key lesson: Incidental PE in cancer patients is NOT benign. Treat it. Always check RV function even in asymptomatic patients.

📋 Case 6, Recurrent PE While on Anticoagulation

Patient: 54M with unprovoked PE 4 months ago, currently on apixaban 5 mg BID. Presents with new pleuritic chest pain and dyspnea. HR 105, SpO2 93%.

CTPA: New segmental PE in left lower lobe. RV/LV ratio 0.8. Old clot in right PA partially resolved.

Key questions:

Is the patient actually taking the medication? Check adherence, missed doses are the #1 cause of "failure."
Is there an occult malignancy? Unprovoked recurrent VTE has up to 10% cancer detection rate within 1 year.

Workup:

Age-appropriate cancer screening (CT chest/abdomen/pelvis, CBC, CMP, LDH, UA)
Thrombophilia workup: antiphospholipid antibodies (lupus anticoagulant, anticardiolipin, beta-2 glycoprotein)
Consider anti-Xa level to confirm adequate drug levels

Treatment:

Switch to LMWH (enoxaparin 1 mg/kg BID), more reliable in cancer/malabsorption.
Consider IVC filter if recurrent PE despite therapeutic anticoagulation.
Lifelong anticoagulation, second unprovoked event = indefinite treatment.

Key lesson: Recurrent PE on a DOAC, check adherence first, then hunt for cancer and antiphospholipid syndrome. Switch drug class and plan for lifelong anticoagulation.

📋 Case 7, The PE That Wasn't (Aortic Dissection)

Patient: 67M with HTN, acute tearing chest pain radiating to back. Diaphoretic. HR 108, BP 185/110 right arm, 142/88 left arm. SpO2 95%.

Initial concern: Tachycardia + chest pain + dyspnea → PE was on the differential.

Red flags that point AWAY from PE:

Tearing/ripping quality radiating to back, classic dissection.
> 20 mmHg BP differential between arms, highly specific for type A dissection.
Severe hypertension, PE typically causes hypotension, not hypertension.
No VTE risk factors, no immobilization, surgery, or cancer history.

CTA chest: Stanford Type B aortic dissection. No PE.

Why this matters:

If you gave heparin for presumed PE → catastrophic bleeding into false lumen.
Always consider the differential before anticoagulating. PE, dissection, STEMI, and tamponade can all present with chest pain + tachycardia.

Key lesson: Not every tachycardic chest pain is PE. Check BP in both arms. Tearing pain to back + BP differential = dissection until proven otherwise. Anticoagulating a dissection can be fatal.

📋 Case 8, Saddle PE with Thrombus-in-Transit

Patient: 48F, 1 week post-cesarean section, sudden collapse. HR 130, BP 78/50, SpO2 82% on NRB. Altered mental status.

Bedside echo: Massively dilated RV. Mobile thrombus seen in the right atrium straddling the tricuspid valve (thrombus-in-transit). McConnell's sign positive.

This is a surgical emergency:

Thrombus-in-transit = clot trapped between venous system and pulmonary arteries. Mortality > 40% without intervention.
Risk of complete PA occlusion if thrombus embolizes further.

Treatment:

Systemic tPA 100 mg over 2 hours, despite being 1 week post-cesarean (relative contraindication overridden by life-threatening PE).
Norepinephrine for hemodynamic support. Avoid aggressive fluids.
If tPA fails or contraindicated: Emergent surgical embolectomy or catheter-directed therapy.
VA-ECMO as bridge if available and patient continues to deteriorate.
Post-stabilization: Heparin drip → transition to LMWH (postpartum, can use DOAC if not breastfeeding).

Key lesson: Thrombus-in-transit on echo is a surgical emergency. Don't wait for CT. Lyse immediately or call CT surgery. Post-surgical status is a relative, not absolute, contraindication when the patient is dying.

Monitoring by Category (2026 AHA/ACC)

Monitoring intensity tracks the A–E category. Re-categorize q6–12h in the first 24–72h, patients transition. Column headers below refer to the 2026 categories (old "massive" ≈ E, "submassive" ≈ C3–D, "low-risk" ≈ A–B).

Parameter	D – E (ICU)	C1 – C3 (Ward / Monitored bed)	A – B (Home / ED discharge)
Vitals	Continuous telemetry + q1–2h. Arterial line if on pressors.	Continuous telemetry + q2–4h. (C1 may step down to q4h once stable.)	q8h inpatient; home pulse ox optional after discharge.
Re-categorize	q6h first 24–48h, watch for drift toward/from C.	q12h first 24–48h, C2/C3 can decompensate to D.	At 48–72h follow-up visit.
Troponin	q6h × 24h then daily. Rising = decompensation. Falling = RV recovery.	q6–12h × 24h for C2–C3. Baseline only for C1.	Baseline if not already done.
BNP / NT-proBNP	Baseline + q24h. Falling = RV recovery.	Baseline for all C. Repeat at 24h for C2–C3.	Baseline only if category unclear.
Lactate	q4–6h until clearing. Rising lactate = normotensive shock (D2) → escalate.	Baseline for C3. Recheck if clinically worsening.	Not routine.
Echocardiography	Repeat at 24–48h. Track TAPSE, RV/LV ratio, septal position.	Repeat at 24–48h for C2–C3. Not routine for C1.	Not routine. Only if symptoms persist at follow-up.
aPTT (if heparin drip)	q6h until therapeutic (60–80), then q12–24h.	q6h until therapeutic, then q12–24h if still on heparin.	N/A (on DOAC).
Platelet count	Baseline then q2–3 days. HIT screen if on heparin > 4 days.	Baseline. q2–3 days if on heparin > 4 days.	Baseline.
Hemoglobin	Daily. Watch for bleeding, especially post-tPA.	Daily × 48h then as clinically indicated.	Baseline. Repeat if bleeding signs.
Renal function	Daily BMP. Contrast nephropathy (post-CTPA) + drug dosing.	Baseline + q24–48h.	Baseline. Confirm CrCl for DOAC dosing.
Bleeding assessment	q shift: gums, GI (stool guaiac), hematuria, ecchymoses, access sites.	Daily exam + patient-reported.	Educate patient on bleeding signs.
SpO2 / O2 requirement	Continuous. Increasing O2 = deterioration → escalate.	Continuous or q2–4h. Wean as tolerated.	Wean to SpO2 ≥ 92% before discharge.

Escalation Triggers

Activate PERT / escalate care if any of the following develop:

SBP drops < 90 mmHg or new vasopressor requirement
Rising troponin or BNP despite anticoagulation
Worsening RV function on repeat echo
Increasing O2 requirement or new intubation need
New arrhythmia (Afib, VT)
Altered mental status (low CO to brain)

Transition to Oral Anticoagulation

When stable × 24-48h (vitals normalized, O2 weaned, troponin trending down): transition from heparin drip to oral DOAC.

Apixaban: Stop heparin → start apixaban 10 mg BID × 7 days → 5 mg BID. No overlap needed.
Rivaroxaban: Stop heparin → start rivaroxaban 15 mg BID × 21 days → 20 mg daily. No overlap needed.
Edoxaban: Requires 5-10 days of parenteral anticoag first → then edoxaban 60 mg daily.
Warfarin: Start warfarin while on heparin. Continue heparin until INR 2-3 × 2 consecutive days (typically 5-7 days overlap).

Follow-Up After Discharge,2026 AHA/ACC Structured Framework

AHA/ACC 2026 mandates structured post-PE follow-up, this is now a formal guideline recommendation, not just good practice.

Within 1 week of discharge: Communication or clinic evaluation to assess symptoms, bleeding, medication adherence, and early complications AHA/ACC 2026.
At or before 3 months: Clinical visit to determine anticoagulation duration (stop vs extend). Reassess risk factors, provoked vs unprovoked status, bleeding risk. This is the key decision point AHA/ACC 2026.
CTEPH screening at every visit for ≥ 1 year: If persistent dyspnea → echo → V/Q scan if elevated RVSP. CTEPH develops in 2–4% of PE survivors.
Thrombophilia workup: Consider if unprovoked PE in patient < 50 (Factor V Leiden, prothrombin mutation, antiphospholipid antibodies). Test AFTER completing anticoagulation (DOACs and warfarin affect results).
Cancer screening: If unprovoked PE in patient > 50 → age-appropriate cancer screening (colonoscopy, mammogram, CT chest, PSA if male).

📋 On Rounds

Pimp Questions

Why does PE cause RV failure? Walk me through the pathophysiology.

Clot in PA → acute ↑ pulmonary vascular resistance (PVR) → RV pressure overload → RV dilation → interventricular septum bows into LV (D-sign) → ↓ LV preload → ↓ cardiac output → obstructive shock. Simultaneously, RV wall tension increases → RV myocardial O2 demand rises while coronary perfusion falls → RV ischemia. Death is from acute cor pulmonale and cardiogenic shock, not hypoxemia.

What are the 8 PERC criteria and when do you apply them?

PERC (Pulmonary Embolism Rule-out Criteria): Apply ONLY when clinical gestalt is LOW (< 15% pretest). All 8 must be negative: (1) Age < 50, (2) HR < 100, (3) SpO2 ≥ 95%, (4) No hemoptysis, (5) No estrogen use, (6) No prior DVT/PE, (7) No unilateral leg swelling, (8) No recent surgery/trauma requiring hospitalization in past 4 weeks. All negative → PE ruled out without D-dimer. If ANY positive → proceed with Wells + D-dimer pathway.

What are the components of the Wells score for PE?

7 criteria: Clinical DVT signs (3.0), PE is #1 or equally likely diagnosis (3.0), HR > 100 (1.5), immobilization ≥ 3 days or surgery within 4 weeks (1.5), prior DVT/PE (1.5), hemoptysis (1.0), active cancer (1.0). ≤ 4 = PE unlikely → D-dimer. > 4 = PE likely → CTPA directly. The "PE most likely" criterion is subjective -this is the main limitation of Wells vs Geneva.

What is subsegmental PE and do you treat it?

Subsegmental PE: clot in subsegmental arteries (small, distal). Increasingly detected with better CT resolution. If no DVT on LE US and low risk for recurrence → may not need anticoagulation. Shared decision-making with the patient. If DVT present, prior VTE, cancer, or inpatient/immobilized → treat with standard anticoagulation. This is a gray zone -discuss with hematology or your attending.

How do you manage PE in pregnancy?

PE is a leading cause of maternal mortality. Workup: D-dimer unreliable (physiologically elevated). Start with LE US → if positive DVT, treat without CTPA. If negative → CTPA (preferred for definitive diagnosis). Treatment: LMWH (enoxaparin 1 mg/kg q12h) -DOACs are contraindicated (cross placenta). Continue through pregnancy + at least 6 weeks postpartum (minimum 3 months total). Hold LMWH 24h before planned delivery.

What is CTEPH and when should you suspect it?

CTEPH (Chronic Thromboembolic Pulmonary Hypertension): Occurs in ~4% of PE survivors. Organized thrombus persists → chronic PVR elevation → progressive RV failure. Suspect if: persistent dyspnea/exercise intolerance 3-6 months after PE despite anticoagulation. Screen with echo (elevated RVSP). Confirm with V/Q scan (more sensitive than CTPA for chronic disease). Treatment: pulmonary endarterectomy (PEA) is potentially curative.

📣 Sample Presentation

One-Liner

"Ms. Park is a 42-year-old on OCPs presenting with acute pleuritic chest pain and dyspnea × 1 day. HR 112, SpO2 93%. Wells score 7.5 (high). CTPA shows bilateral segmental PE with RV/LV ratio 1.2. Troponin 0.08. Classified as submassive PE."

Key Points to Cover on Rounds

Submassive PE (hemodynamically stable but RV strain). RV/LV ratio 1.2 on CTPA. Troponin mildly elevated 0.08, BNP 380. sPESI score 1. Anticoagulation: heparin drip started, aPTT 72 (therapeutic). Plan to transition to apixaban 10 mg BID × 7 days then 5 mg BID once stable. OCPs stopped. LE US: DVT left popliteal vein. Monitoring: serial troponin q6h (trending down 0.08 → 0.05), repeat echo tomorrow. Escalation plan: if SBP drops < 90 or worsening RV → PERT activation for CDT. Duration: 3 months (provoked by OCP + immobility).

Daily Rounds Checklist

Anticoagulation therapeutic? → aPTT in range (60-80) if on heparin drip. Anti-Xa if using LMWH. Confirm DOAC dosing correct.
Hemodynamics stable? → HR trending down? BP stable? O2 requirement decreasing? Any signs of deterioration?
Troponin/BNP trend? → Falling = good. Rising = RV strain worsening → consider escalation.
RV function reassessment? → Repeat echo in 24-48h for submassive PE. TAPSE, RV/LV ratio improving?
Bleeding assessment? → Any signs of bleeding (GI, gums, hematuria, bruising)? Hgb stable?
DVT prophylaxis bilateral? → Concurrent DVT? Lower extremity US result? SCDs on non-affected leg.
Transition plan? → When to switch from heparin to oral DOAC? Which DOAC? Duration decision documented?
IVC filter needed? → Only if anticoag contraindicated. If placed, document retrieval plan (30-90 days).
Etiology workup? → Provoked vs unprovoked? If unprovoked and < 50yo: consider thrombophilia workup (after acute treatment). If > 50 + unprovoked: age-appropriate cancer screening.
Disposition planning? → If low-risk (sPESI 0, Hestia negative): outpatient with 48-72h follow-up. Submassive: when safe to step down from ICU?

💊 Medications & Doses

Anticoagulation

Drug (Brand)	Dose	Monitoring	Reversal	Notes
Apixaban (Eliquis) 1ST LINE	10 mg BID × 7 days → 5 mg BID Extended: 2.5 mg BID	No routine monitoring. Anti-Xa if needed (rare).	Andexanet alfa (Andexxa). PCC 50 units/kg if unavailable.	Lowest bleeding risk of all DOACs. No bridging. Preferred in CKD (less renal clearance). Avoid if CrCl < 25. AMPLIFY, 2013
Rivaroxaban (Xarelto) 1ST LINE	15 mg BID × 21 days → 20 mg daily Extended: 10 mg daily	No routine monitoring.	Andexanet alfa. PCC if unavailable.	No bridging. Must take with food (bioavailability drops 40% without). Caution if CrCl < 30. EINSTEIN-PE, 2012
Heparin (UFH) MASSIVE/SUBMASSIVE	80 units/kg bolus → 18 units/kg/hr drip	aPTT q6h until therapeutic (60-80 sec), then q12-24h.	Protamine sulfate (1 mg per 100 units heparin given in past 2-3h).	Short half-life (60-90 min). Use when intervention likely or high bleed risk. Reversible. Monitor for HIT (platelet count q2-3 days).
Enoxaparin (Lovenox) BRIDGE / PREGNANCY	1 mg/kg SC q12h Or 1.5 mg/kg SC daily	Anti-Xa level (target 0.6-1.0 for q12h dosing). Check in obesity, renal impairment, pregnancy.	Protamine (partial reversal only ~60%).	Bridge to warfarin or primary therapy in pregnancy. Avoid if CrCl < 30 → use UFH. Weight-based, no cap needed in obesity (check anti-Xa).
Edoxaban (Savaysa)	60 mg daily (after 5-10 days of parenteral anticoag)	No routine monitoring.	PCC. No specific reversal agent.	Requires heparin/LMWH lead-in (unlike apixaban/rivaroxaban). Avoid if CrCl > 95 (paradoxically less effective). Good option for cancer-associated PE (non-GI) Hokusai-VTE Cancer, 2018.
Dabigatran (Pradaxa)	150 mg BID (after 5-10 days of parenteral anticoag)	No routine monitoring. Renal function q6–12mo.	Idarucizumab (Praxbind) 5 g IV, specific monoclonal reversal.	Direct thrombin inhibitor. Requires heparin/LMWH lead-in. Avoid if CrCl < 30. GI upset common. Noninferior to warfarin for VTE RE-COVER, 2009.
Warfarin (Coumadin)	Start 5 mg daily, adjust to INR 2-3	INR daily until stable, then weekly, then monthly. Target 2.0-3.0.	Vitamin K (oral/IV) + 4-factor PCC (KCentra) for life-threatening bleed. FFP if PCC unavailable.	Requires 5-7 day heparin/LMWH bridge. INR 2-3 × 2 consecutive days before stopping bridge. Many drug/food interactions. Last-line behind DOACs except in APS.

Thrombolytics

Drug	Dose	Route	Notes
Alteplase (tPA, Activase) MASSIVE PE	100 mg IV over 2 hours Cardiac arrest: 50 mg IV bolus	Systemic IV	Standard of care for massive PE. Major bleeding ~10%, ICH ~2%. Start heparin drip after infusion (no bolus). Continue CPR 60-90 min post-tPA if in arrest.
Alteplase (low-dose, CDT)	12-24 mg over 12-24 hours via catheter directly into PA	Catheter-directed (EKOS)	Used with ultrasound-assisted catheter. Significantly lower systemic bleeding than full-dose IV. Requires IR/interventional cardiology ULTIMA, 2014.
Half-dose tPA	50 mg IV over 2 hours	Systemic IV	For submassive PE with deterioration. Lower bleeding risk than full dose. Improved pulmonary artery pressures in MOPETT trial MOPETT, 2013. Not universally accepted -discuss with attending.
Tenecteplase	Weight-based single bolus	Systemic IV	Single-bolus administration (easier than 2h alteplase infusion). Studied in PEITHO for submassive PE -reduced decompensation but increased bleeding/stroke. Not first-line for submassive.

Vasopressors for PE-Related Shock

Agent	Dose	Why in PE	Avoid
Norepinephrine 1ST LINE	0.01-3 mcg/kg/min	↑ SVR + mild inotropy. Supports MAP without significantly increasing PVR.	-
Vasopressin ADJUNCT	0.03 units/min (fixed)	V1-mediated vasoconstriction. Does not increase PVR. NE-sparing.	-
Dobutamine	2-20 mcg/kg/min	If evidence of RV failure with low CO. Adds inotropy to support RV contractility.	Can worsen hypotension (beta-2 vasodilation). Only use with concurrent vasopressor.
Phenylephrine AVOID	-	-	Avoid in PE. Pure alpha agonist → increases PVR → worsens RV afterload → further RV failure.

Key principle: In PE-related shock, the RV is failing against high PVR. You want to: (1) support SVR (norepinephrine), (2) avoid increasing PVR further (no phenylephrine), (3) consider RV inotropy if CO is low (dobutamine). Fluids are usually harmful -limit to 250-500 mL.

⚡ Summary

Summary

Diagnose

Low gestalt → PERC (if all 8 negative → stop). Otherwise → Wells ≤ 4 → D-dimer (age-adjusted). Wells > 4 → CTPA directly. Unstable → bedside echo → treat empirically.

Massive PE

SBP < 90 or cardiac arrest → systemic tPA 100 mg/2h (50 mg bolus in arrest). Cautious fluids (250-500 mL max). Norepi for MAP. Avoid intubation. CDT if tPA contraindicated. ECMO as bridge.

Submassive PE

Stable + RV strain (troponin, RV/LV > 0.9). Heparin drip. Activate PERT. Serial troponin + repeat echo. Escalate to CDT or half-dose tPA if deteriorating. PEITHO: no routine lysis.

Anticoagulation

DOAC first-line (apixaban 10→5 or rivaroxaban 15→20). No bridging. Duration: provoked = 3 months. Unprovoked = indefinite. Cancer = indefinite (avoid DOAC in GI cancers). APS = warfarin.

Outpatient PE

sPESI = 0 + Hestia criteria all negative → safe for home with DOAC + 48-72h follow-up. 30-day mortality ~1%. Same outcomes as inpatient.

Catheter-Directed

EKOS (low-dose tPA into PA), FlowTriever / Penumbra (mechanical, lytic-free). Lower bleeding than systemic tPA. For submassive deterioration or massive with tPA contraindication.

Special Populations

Pregnancy: LMWH (DOACs contraindicated). CKD: UFH if CrCl < 30. Cancer: LMWH or DOAC indefinitely. IVC filter: only if anticoag absolutely contraindicated. Always retrieve.

Don't Miss

CTEPH (4% of PE survivors -persistent dyspnea at 3-6 months → echo + V/Q). Paradoxical embolism (PFO + DVT → stroke). Subsegmental PE -may not need treatment if no DVT. HIT on heparin.

📄 One Pager

Pulmonology / Hematology · One Pager

Pulmonary Embolism

PE kills via RV failure, not hypoxia. PERC → Wells → D-dimer → CTPA. Massive = tPA. Submassive = heparin + watch for deterioration. Low-risk = outpatient DOAC.

🧪 Diagnostic Algorithm

Low gestalt → PERC (all 8 negative → stop). Wells ≤ 4 → D-dimer (age-adjusted: age × 10 if > 50). Wells > 4 → CTPA directly. Unstable → bedside echo → treat empirically. V/Q if contrast allergy/CKD.

🚨 Treatment by Severity

Massive (SBP < 90): tPA 100 mg/2h. Norepi. Cautious fluids (250-500 mL). Avoid intubation. CDT if tPA contraindicated.
Submassive (stable + RV strain): heparin drip. PERT. Serial troponin. Escalate if deteriorating.
Low-risk (sPESI 0 + Hestia negative): outpatient DOAC.

💊 Key Drugs

Apixaban10 mg BID × 7d → 5 BID (1st line)

Rivaroxaban15 mg BID × 21d → 20 daily (with food)

Heparin (UFH)80 U/kg bolus → 18 U/kg/hr (aPTT 60-80)

Enoxaparin1 mg/kg SC q12h (pregnancy, bridge)

Alteplase (tPA)100 mg/2h systemic, 50 mg bolus in arrest

CDT (EKOS)12-24 mg tPA over 12-24h into PA

⏱️ Duration

Provoked: 3 months
Unprovoked: ≥ 6 months, consider indefinite
Recurrent: Indefinite (reduced-dose DOAC)
Cancer: Indefinite (LMWH or DOAC, avoid DOAC in GI cancers)
APS: Warfarin (DOACs inferior)

🫀 RV Failure Principles

Fluids: 250-500 mL MAX (RV volume-sensitive). Pressors: norepi 1st line (avoid phenylephrine → ↑ PVR). Intubation: avoid if possible (PPV ↓ preload → PEA). If must: ketamine, low PEEP, pressors running first.

⚠️ Pitfalls

D-dimer without Wells/PERC (ordering reflexively)
Aggressive fluids in massive PE (worsens RV failure)
Intubation without hemodynamic preparation
Missing submassive PE (not checking troponin/BNP)
Routine tPA for submassive (PEITHO: ↑ bleeding)
Not considering outpatient treatment for sPESI 0
Forgetting CTEPH screening at 3-6 months
DOACs in pregnancy or APS