Acute Right Ventricular (RV) Failure & Massive Pulmonary Embolism (PE) – Study Notes

Case Example

• 42 y/o female: acute pleuritic chest pain + SOB x2 hrs

• History: HTN, tobacco use, recent right leg fracture & surgery → leg swelling

• Presentation: tachycardic, hypotensive, tachypneic, hypoxic, afebrile

• POCUS: dilated RV, septal flattening, RV > LV → concerning for massive PE

Pathophysiology of Acute RV Failure

1. DVT → PE → acute rise in pulmonary vascular resistance (PVR).

2. RV poorly tolerates acute ↑ afterload → dilation & impaired contractility.

3. RV dilation → ↓ RV output → ↓ LV preload.

4. LV compression (septal shift + pericardial constraint) → ↓ LV filling → ↓ cardiac output.

5. Hypotension → ↓ coronary perfusion (esp. RCA) → worsening RV ischemia.

6. Vicious cycle (“death spiral”): RV dilation → ↓ CO → hypotension → ischemia → worsening RV failure → cardiogenic shock → death.

Key Management Principles

Oxygenation & Ventilation

• Oxygen = pulmonary vasodilator.

• Avoid hypoxia & hypercapnia (both ↑ PVR).

• Use HFNC, BiPAP, CPAP as first-line.

• Avoid intubation if possible:

  • Positive pressure ↑ intrathoracic pressure → ↓ preload & BP.

  • Sedatives & induction agents cause hypotension.

  • Intubation may worsen RV failure.

• If unavoidable:

  • Hemodynamically neutral strategy (e.g., ketamine).

  • Preemptively optimize BP with vasopressors.

  • Have push-dose pressors at bedside.

  • Avoid high tidal volumes & over-bagging.

Fluids & Preload

• RV is preload dependent, but…

• Excess fluids worsen RV dilation → ↓ contractility → ↓ CO.

• Give only 250–500 mL trial, reassess.

• Avoid aggressive fluid resuscitation unless clear hypovolemia.

Vasopressors & Inotropes

• First-line: norepinephrine (reasonable) or epinephrine (possibly superior).

• Second-line: vasopressin (low dose 0.03 units/min) → causes systemic vasoconstriction without ↑ PVR.

• Inotropes (dobutamine, milrinone) → consider in refractory cardiogenic shock (consult ICU/cardiology).

Pulmonary Vasodilators

• Inhaled nitric oxide or epoprostenol: ↓ PVR, improve V/Q mismatch.

• Useful in hypoxic patients not improving on HFNC/BiPAP.

• May bridge to avoid intubation or during peri-intubation.

Definitive Therapy for Massive PE

1. Anticoagulation

   • Start heparin (bolus + infusion) as soon as PE suspected.

   • If giving TPA → hold heparin infusion for 2–3 hrs post-dose.

2. Systemic Thrombolysis (TPA)

   • Full-dose TPA = standard of care for massive PE.

   • Half-dose TPA (50 mg) studied (Wang 2014, etc.):

     • Less bleeding risk, but higher risk of treatment failure.

     • Consider in low body weight (<65 kg) or very high bleeding risk.

     • Not guideline standard yet.

3. Catheter-directed Thrombolysis

   • Lower systemic bleeding risk.

   • More often used in submassive PE.

   • Requires stable patient + specialized center.

4. Surgical Embolectomy

   • Option for patients not candidates for TPA or failed TPA.

   • Specialized centers only.

5. ECMO

   • Bridge for unstable/dying patients with massive PE.

   • Early consult is critical (before TPA if possible).

6. During Cardiac Arrest

   • If massive PE suspected/confirmed:

     • 50 mg TPA IV push during arrest (may repeat once).

     • Shown to improve ROSC.

Case Outcome

• Patient stabilized on BiPAP + norepinephrine.

• CTA confirmed saddle PE.

• Received full-dose TPA → admitted to ICU → recovery.

Final Take-Home Points

• Avoid hypoxia, hypercapnia, and intubation when possible.

• Fluids: small bolus only (250–500 mL), avoid overload.

• Pressors early (NE or epi → add vasopressin if needed).

• Consider inotropes if progressing to cardiogenic shock.

• Inhaled pulmonary vasodilators for refractory hypoxemia.

• Systemic TPA = gold standard for massive PE (half-dose only in select high-risk patients).

• Early ECMO/advanced therapy consult in deteriorating patients.

• During arrest with suspected PE → TPA push 50 mg IV.