• Normal RV function: governed by systemic venous return, PA pressure, pericardial compliance, and native contractility of the RV free wall and interventricular septum (where RV and LV are “tethered”).

  • The RV is coupled to the high-compliance, low-resistance pulm circulation -> RV ejects blood at lower pressure compared to LV -> RV is more afterload sensitive than LV. RV can adapt to changes in volume > pressure.

• Acute RV Failure: RV & LV interdependent -> failure of RV -> failure of LV via: 

  • (1) decreased LV preload, as RV output = LV preload 

  • (2) septal bowing into LV, causing diastolic impairment (“Diastolic Ventricular Interaction”)

  • Increased RV afterload (e.g. PE, hypoxia, acidemia), Increased RV preload (e.g. L->R shunt or TV disease), or Decreased RV contractility (e.g. MI, myocarditis) all lead to increased RV wall stress & resultant ischemia

• Chronic RV Failure: gradual increase in RV afterload (from Pulmonary Hypertension/Pulmonic Stenosis/Tricuspid Regurgitation) RV -> “death spiral”

Eur Heart J 2020;41:543

Circ 2018;137:e578-e622

• Exam: Increased JVP, peripheral edema, RV heave, pulsatile liver, split S2, new TR (holosystolic murmur at LLSB with radiation to RLSB)

• Imaging: PA/lateral CXR; CT -> RV/LV ratio >0.9 suggests RV strain

• Echo: measure RV size/function to elucidate underlying etiology. RVEF based on displacement of base towards apex; TAPSE =tricuspid annular plane systolic excursion (normal ≥ 17 mm; reflects RV apex-to-base shortening, correlates with RVEF)

  • RVSP: correlates w/ RHC but can vary up to 10mmHg (esp w/ chronic lung disease, PPV)

• RHC w/ placement of PA line: gold standard for measurement of ventricular filling pressures, CO, PA pressures

  • RV function: CVP/PCWP ratio: normal = 0.5; Increase beyond this is sign of RV failure; PAPi: (PAs – PAd)/CVP <0.9 = RV failure, for pts w/ VAD <1.85 = RV failure; RV stroke work index: (mPAP – CVP) x (CI/HR) x 0.0136 (normal 8-12 g/m/beat/m2)

• Labs: NT-proBNP, troponin, also Cr and LFTs secondary to venous congestion

AHA: Circ 2018;137:e578 

• Treat reversible causes (pericardial disease, RVMI, PE, hypoxemia, infections)

• Preload (CVP goal 8-12mmHg): both hypo- and hypervolemia can decrease CO

  • Volume Depletion (PE, Tamponade, RVMI): judicious IVF (0.5-1L) in absence of CVP elevation (goal CVP 10-14 in RVMI)

  • Volume Overload: IV diuresis to decrease RV filling pressures, decrease functional TR, and improve LV CO

• Afterload:

  • Systemic: if pt hypotensive, start pressors – do not tolerate HoTN as propagates RV death spiral (CPP = Aortic DiastolicPressure - LVEDP); no clinical data regarding pressor of choice, but often choose vasopressin or norepinephrine (vaso affects PVR less than norepi)

  • Pulmonary: remove factors that increase pulm vasc tone (e.g. hypoxemia, acidemia). Consider pulm vasodilators if evidence of PAH(inhaled > oral to deliver vasodilators to ventilated vascular beds)

    • Types: iNO, prostacyclin agonists (epoprostenol, inhaled or IV), endothelin antagonists (e.g. bosentan, ambrisentan), nitricoxide enhancers (e.g. PDE-5 inhibitors: sildenafil, tadalafil)

• Contractility: dobutamine or milrinone; milrinone: decreases RV afterload by pulmonary vasodilation but increases risk of hypotension

• Devices: if refractory RVF, consider RV MCS and/or pulmonary support (Impella RP, VA-ECMO)

Curr Heart Fail Rep 2012;9:228

• RV preload is “extra thoracic” and afterload is “intrathoracic” -> intubation & positive pressure ventilation increases pulmonary vascular resistance (PVR) and increases RV afterload -> decreased RV dilation -> “death spiral”

• Intubation/NIPPV in RV failure precipitate risk for hemodynamic collapse & cardiac arrest

  • Drugs commonly used in intubation (BZDs, propofol, muscle relaxants) -> tendency towards vasodilation and negative inotropy -> decreased venous return -> decreased LV preload -> systemic hypoTN -> propagates “death spiral”

  • Consider RSI (etomidate >> propofol for induction) & push dose epinephrine (10-20mcg), vasopressin (1-2U), or phenylephrine if emergent intubation anticipating hypotension

• Vent management: prevent hypoxemia & hypercarbia (Increased PVR), consider moderate TV (~8cc/kg), low PEEP (<12 cm H2O), and moderate plateau pressure goal (<30 mmHg) to help minimize RV afterload

ACC/AHA: Circ 2013;127:e362

• EKG: check R-sided ECG leads in pts with inferior STEMI (10-15% have RV involvement)

  • 1mm STE in V4R -> 88% Sn, 78% Sp in inferior STEMI; STE III>II suggests RCA > LCx and RVMI

  • High-grade AV block seen in ~50% of pts with RVMI

• Management: pts with RVMI may initially benefit from fluid bolus; caution w/ TNG (decreases preload) & BB