Resources

1. Ventetuolo CE, Klinger JR. Management of Acute Right Ventricular Failure in the Intensive Care Unit. Annals ATS. 2014;11(5):811-822. doi:10.1513/AnnalsATS.201312-446FR
2. Konstam MA, Kiernan MS, Bernstein D, et al. Evaluation and Management of Right-Sided Heart Failure: A Scientific Statement From the American Heart Association. Circulation. 2018;137(20):e578-e622. doi:10.1161/CIR.0000000000000560

Background

Right ventricular (RV) failure occurs when the RV fails to maintain enough blood flow through the pulmonary circulation to achieve adequate left ventricular filling.

Normal Pulmonary Circulation and RV

Pulmonary Circuit

• the pulmonary circuit is normally a low pressure circuit. Even with exertion, pulmonary pressures increase minimally and PVR falls despite rises in cardiac output. This difference is due to the ability of the lungs to recruit underutilized vessels as CO increases
• in the pulmonary circuit, the arterial/venous mean pressure gradient is typically less than 10 mmHg (small)
• the pulmonary circuit has LOW vascular tone, making it resistant to alterations from systemically-active vasoactive medications (vasodilators, catecholamines)

RV

• thin walled (2-3 mm), able to produce less contractile force. Has a greated EDV and SA per unit of blood, and the RV achieves a similar SV as the LV with lower energy expenditure
• muscle fibers are arranged longitudinally: the apex will contract towards the TV
• does not handle increases in afterload well: this sharply decreases contractility as compared to the LV
• process of interventricular dependence (with RV enlargement) leads to reduced LV filling which is typically refractory/paradoxically responsive to volume expansion

Causes

• Acute RHF
  • Pulmonary embolism
  • Right-sided myocardial infarction
  • Acute on chronic RHF
• Chronic RHF
  • Cor pulmonale (Pulmonary hypertension)

Evaluation of RV Function in Critical Illness

• physical examination
  • RV filling pressure elevation: JVD, peripheral edema
  • S2 splitting
  • TR murmur
  • RV heave
• Echocardiogram
  • RV systolic function
    • tricuspid annular plane systolic excursion (TAPSE) measures the longitudinal systolic displacement of the RV base toward the RV apex
      • Correlates well with RV ejection fraction
      • Normal TAPSE = 2.4 to 2.7 cm. Less than 1.8 cm has an 87% accuracy at predicting SVI < 29 ml/m2
      • Associated with poorer prognosis in RHF and PAH
    • Estimates of RV systolic pressure obtained by echocardiogram correlate well with measurements made by right heart catheterization, but the variance between measures can be greater than 10 mm Hg in up to 50% of cases. Particularly poor in patients with chronic lung disease as well as those with positive pressure ventilation.
  • LV dysfunction
  • Valvular disease
• RHC
  • When reliable measurement of pulmonary hemodynamics is needed, pulmonary artery catheterization provides valuable information on RV and LV filling pressures, cardiac output, and pulmonary artery pressure
  • ESCAPE: routine use of Swan-Ganz catheter in decompensated heart failure did not improve mortality or LOS. Patients had a transient improvement in symptoms but experienced a higher rate of complications.

Management

Causes of RV failure in critical illness can be divided into three main categories: (1) excessive preload; (2) excessive afterload; and (3) insufficient myocardial contractility. Management is directed at addressing these three factors.

RV Preload

• fluid management is critical:
  • fluid volume - hypovolemic, bleeding, third-spacing, insensible losses
  • venous return - systemic vascular tone, vasodilatation vs vasoconstriction states, positive pressure ventilation
• the goal preload should be to keep RV transmural filling pressures in a moderately elevated range (8-12 mmHg) and adjust from there to optimize CO. The RV has a flatter Starling curve, meaning that greater changes in volume are required to impact contractility than the LV.
• RV preload may need to be increased or decreased, generally depending on the afterload:
  • high afterload (pulmonary hypertension etc): volume loading can lead to interventricular dependence and impaired LV diastolic filling, increased RV myocardial demands. --> decrease RV volume (diuresis, ultrafiltration)
  • low afterload (RV infarction etc): RV EDP needs to be increased above normal to maintain CO --> increase RV volume (fluids)
• It may be useful to monitor SvO2 (normal 70-80%) and CVP to guide management, and even consider Swan-Ganz placement for better hemodynamic assessment

RV Afterload

• excessive afterload is implicated in almost all acute RHF, and addressing this is usually the most effective management strategy.
• focus on reversible factors (i.e. not chronic cardiopulmonary conditions that are irreversible):
  • hypoxic vasoconstriction
    • alveolar hypoxia
    • pulmonary arterial hypoxemia
  • hypercapnea
  • acidemia
  • excessive high or low lung volumes
  • sepsis and endothelial dysfunction
  • pulmonary thrombosis
• if needed, consider pulmonary vasodilators:
  • inhaled NO
  • inhaled epoprostenol
  • PDE-5 inhibitors: sildenafil, tadalafil

RV Contractility

• decreased contractility in acute RHF is due to (1) overstretch of myocytes (2) cellular metabolic derangement (3) perfusion-demand mismatch. Address these issues first
  • (1) overstretch - optimize preload
  • (2) metabolic derangement - fix reversible systemic issues
  • (3) RV perfusion - fix systemic hypotension (to optimize coronary perfusion pressure) particularly diastolic hypotension, reduce RV wall tension
• if that fails, then consider:
  • vasopressors: NE often the vasopressor of choice due to limited B1 inotropy and positive effects on RV oxygen delivery. Low-dose vasopressin reasonable as well due to pulmonary vasodilatory effect (0.01 to 0.03 U/min)
  • inotropes: low-dose dopamine, milrinone (less chronotropic effect), or dobutamine are all reasonable choices
• if that fails then consider:
  • mechanical support - ECLS has been used in RV failure as a bridge to endarterectomy, lung transplant. Venoarterial makes sense over venovenous.