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Cardiology

Right ventricular failure

RV is coupled to a high-compliance, low-resistance circuit and is more afterload-sensitive than the LV. It tolerates volume better than pressure.

Frederick Lang5 min6 questions2 trials

Why the RV fails differently

Normal RV output is set by systemic venous return, PA pressure, pericardial constraint, and the contractility of the free wall plus the interventricular septum — where the two ventricles are tethered (). The RV is coupled to a high-compliance, low-resistance pulmonary circuit, so it ejects at much lower pressure than the LV and is far more afterload-sensitive. It tolerates volume better than pressure.

The RV death spiral
  1. 1

    RV fails

    Acute afterload (PE, hypoxia, acidemia), preload overload, lost contractility (RVMI, myocarditis), or lost compliance (tamponade).

  2. 2

    LV is starved and crushed

    ↓ LV preload, plus ventricular interdependence: the septum bows left, LV compliance falls, LV filling pressure rises.

  3. 3

    Cardiac output falls

    Systemic MAP drops. Functional TR worsens. Hypoxemia feeds back as still more pulmonary afterload.

  4. 4

    Coronaries empty

    ↓ coronary perfusion pressure ischemicizes an already failing RV free wall.

  5. 5

    The spiral tightens

    Worse RV output, worse LV filling, worse MAP. Arrest is sudden. ().

Do not tolerate hypotension. Goal MAP >65 and MAP > mPAP (EHJ Acute Cardiovasc Care 2022;11:77).

Acute

  • ↑ afterload: PE, hypoxemia, acidemia
  • ↑ preload: tricuspid lesion, post-LVAD
  • ↓ contractility: MI, myocarditis
  • ↓ compliance: tamponade

Chronic

  • ↑ afterload: pulmonary hypertension, pulmonic stenosis
  • ↑ preload: tricuspid regurgitation
  • ↓ contractility: intrinsic cardiomyopathy
  • ↓ compliance: constrictive pericarditis

Bedside and workup

  • Exam: ↑ JVP, Kussmaul (JVP rises with inspiration), edema, RV heave, pulsatile liver, split S2, new TR ().
  • ECG: RAD, R/S >1 in V1, P pulmonale (>2.5 mm inferiorly), S1Q3T3, atrial arrhythmias.
  • Labs: NT-proBNP, troponin; ↑ Cr and LFTs from venous congestion (LFTs may be normal in chronic RV failure).
  • CXR; chest CT RV/LV >0.9 suggests strain.
  • Echo: aortic root : LA : RV ≈ 1:1:1 in the parasternal long axis; RV should be smaller than LV in apical 4-chamber. TAPSE ≥17 mm is normal apex-to-base shortening. RVSP from the TR jet tracks RHC within ~10 mmHg (worse with lung disease or PPV).

RHC is the gold standard for filling pressures, CO, and PA pressures.

PA catheter numberHow to read it
CVP / PCWPNormal ~0.5. Rising ratio = RV dysfunction.
PAPi(PAs − PAd) / CVP. <0.9 = RV failure. On a VAD, <1.85.
RV stroke work index(mPAP − CVP) × (CI / HR) × 0.0136. Normal 8–12 g·m/beat/m².
PVR(mPAP − PCWP) / CO, Wood units. Afterload of the RV.

Management

Fix the reversible cause first: pericardium, RVMI, PE, hypoxemia, infection (). Then preload, then afterload, then contractility, then a device.

Preload — CVP goal 8–12 mmHg

Both empty and overfilled RV cut cardiac output.

Volume-responsive (PE, RVMI)

  • Judicious 0.5–1 L if CVP is not already high.
  • RVMI CVP goal 10–14 mmHg.
  • Stop fluids the moment JVP is climbing and the septum is bowing.

Volume-overloaded

  • IV diuresis to drop RV pressure, shrink functional TR, and let the LV fill.
  • CRRT if loops fail.
  • Chronic PH-RV failure is rarely a 2 L bolus.

Afterload — systemic and pulmonary

  • Systemic: if hypotensive, start a pressor immediately. Hypotension is the spiral. No trial has crowned a first pressor; vasopressin or norepinephrine is the usual choice — vasopressin raises SVR with less PVR rise than norepinephrine ().
  • Pulmonary: strip out hypoxia and acidemia. If PVR is >2.0–2.5, add a pulmonary vasodilator, inhaled > oral so it hits ventilated lung: iNO, prostacyclin (epoprostenol inhaled or IV), endothelin antagonists (bosentan, ambrisentan), PDE-5 inhibitors (sildenafil, tadalafil).

Contractility and devices

  • Milrinone drops RV afterload via pulmonary vasodilation and costs MAP. Epinephrine raises RV contractility and MAP.
  • RVMI: revascularize urgently. Inotropes can worsen ischemia.
  • Refractory: RV MCS and/or biventricular support — ProtekDuo, Impella RP, VA-ECMO.

Intubation is a procedure, not a reflex

Positive-pressure ventilation hurts the RV twice: ↑ intrathoracic pressure cuts venous return (preload), and ↑ transpulmonary pressure raises PVR (afterload) (Curr Heart Fail Rep 2012;9:228). Induction drugs (benzodiazepines, propofol, paralytics) vasodilate and negatively inotrope — venous return falls, MAP falls, the spiral accelerates.

  • Prefer a trial of HFNC for hypoxemic failure; it barely touches RV afterload compared with NIV / the ventilator.
  • If you must intubate: RSI with ketamine or etomidate ≫ propofol. Push-dose epinephrine 5–20 mcg (or phenylephrine) ready. Norepinephrine already running.
  • Vent: prevent hypoxemia and hypercarbia (both ↑ PVR). Moderate TV (~8 mL/kg), PEEP <8 cm H2O, plateau <30 mmHg.

Right-ventricular myocardial infarction

Check right-sided leads in every inferior STEMI — 10–15% involve the RV (ACC/AHA, ).

  • 1 mm STE in V4R: ~88% sensitive, 78% specific in inferior STEMI.
  • STE III > II points to RCA rather than LCx, and to RVMI.
  • High-grade AV block in ~50%.
  • A fluid bolus may help if CVP is not already high. Caution with nitroglycerin (↓ preload) and β-blockers.