Right Ventricular Failure

The right ventricle is fragile and right ventricular failure can be challenging to manage.

Epidemiology and Risk Factors

Pathophysiology

RV failure results from interplay of several mechanisms:

  • Myocyte hypertrophy
    Occurs due to chronic ↑ afterload. This mirrors the response seen in LV disease, and occurs in phases:
    • Homeometric adaptation
      Adaptive hypertrophy that leads to ↑ contractility and preservation of SV.
    • Heterometric adaptation
      Transition to maladaptive changes, with:
      • ↓ β-receptor density
      • Failure of cAMP stimulation
      • Vasodilation
        Fall in EF requires ventricular enlargement to maintain stroke volume. As in LV disease, this indicates decompensation.
    • Dysoxia
      Progressive hypertrophy ↑ O2 demand; when this exceeds supply contractility furhter declines and ventriculoarterial uncoupling occurs.
  • Neurohormonal activation
  • Fibrosis
    Collagen proliferation occurs due to mechanical stress, ischaemia, and neuromormonal activation. This results in impaired luisotropy and diastolic dysfunction.
  • Ischaemia

Key haemodynamic principles include:

With (particularly acute) RV failure, RVEDP rises and RV perfusion pressure is reduced due to a higher downstream pressure. Similar physiology is seen during pulmonary hypertension, as the high RVSP reduces RV perfusion during ventricular systole.

Coronary perfusion pressure of <30mmHG is associated with severe reduction in myocardial blood flow, leading to ischaemia and significant RV dysfunction. This leads to the “Right Ventricular Spiral of Death”, where RV dysfunction leads to ↓ LV preload, which in turn causes a ↓ LV SV, a ↓ MAP, and further RV impairment.

  • Preload
    The RV is thin-walled and compliant, and in normal circumstances is able to tolerate significant variability in preload. However:
    • Excessive ↑ preload displaces the interventricular septum leftwards, and so impair LV function
      • This further impairs the RV by ↓ perfusion
      • This effect is more pronounced with pre-existing RV dysfunction
    • Chronic ↑ in preload results in:
      • RV dilation and loss of contractile reserve
      • Venous congestion of the whole body capillary bed
        ↓ Perfusion to all organ systems.
  • Afterload
    The RV is thin walled and weak, and is highly sensitive to changes in afterload.
    • Changes in symptomatology therefore usually mirror changes in afterload
    • Acute ↑ afterload can rapidly lead to circulatory collapse
    • The prime determinant of RV afterload is pulmonary vascular impedance, and all determinants are intra-thoracic
  • Perfusion pressure
    The RV usually perfuses throughout the cardiac cycle, although in disease (with an ↑ in RVEDP) this may fall, ↑ the sensitivity of the RF to hypotension.

\(RV \ Coronary \ Perfusion \ Pressure = P_{Aortic Root} - P_{RV}\)

Aetiology

Assessment

Features are typically non-specific:

  • ↓ Exercise tolerance
  • Dyspnoea
  • Early satiety
  • Abdominal fullness

History

  • Coronary artery disease
  • Left heart failure
  • Valvular heart disease
  • Chronic lung disease
  • VTE
  • Connective tissue diseases
  • HIV
  • Smoking
  • Weight loss therapy

Examination

  • ↑ JVP
  • RV heave
  • Prominent S2
    Secondary to pulmonary hypertension.
  • TR
  • Hepatomegaly
  • Pulsatile liver

Investigations

Bedside:

  • TTE
    • TAPSE
    • Dilation
  • ECG
    Identification of RV ischaemia and RVH.

Laboratory:

Imaging:

  • Cardiac MRI
    Particular for congenital disease.

Other:

  • Right heart catheterisation
    A full study consists of:
    • Invasive pressure measurement
      • RA
      • RV
      • PA
      • CO by thermodilution and/or Fick
    • Pressure-volume loop generation
      Requires conductance catheterisation.

Diagnostic Approach and DDx

Management

  • Defend coronary perfusion
  • Determine cause
  • Optimise determinants of cardiac output
    Preload, afterload, contractility, rate, and rhythm.

Resuscitation:

  • C
    • Defend coronary perfusion
      The RV is sensitive to changes in perfusion pressure, and therefore aggressive defence of the systemic perfusion pressure is essential. Noradrenaline is excellent for this.
    • Preload
      Volume overload is exceedingly detrimental to RV function, as excessive distension of the RV will impair LV filling and further worsen the haemodynamic state.
      • Volume state is often difficult to determine
      • Volume reduction is typically most beneficial with:
        • Chronic RV failure
        • Presence of TR
          Generally indicates ventricular dilation.
      • Volume loading is typically most beneficial with:
        • Acute RV afterload
          e.g. PE.
        • Acute ↓ RV contractility
          e.g. RV infarction.
    • Afterload
      Reduction in RV afterload is almost always beneficial, although must be balanced against ↓ SVR and worsening RV perfusion. Approaches include:
      • Correcting physiology
        • Normoxia
        • Normocapnoea
        • Normal pH
        • Treating pain
      • Rapid onset pulmonary vasodilators
        • Nitric oxide
        • Prostacyclins
          • Iloprost
          • Epoprostenol
    • Contractility
      Indicated for RV failure complicated by cardiogenic shock. Options include:
      • Inotropes
        • Adrenaline
        • Milrinone
        • Dobutamine
      • Vasopressors
        To improve (or defend) perfusion and therefore ↑ RV contractility.
        • Noradrenaline
        • Phenylephrine
        • Vasopressin
      • Mechanical support
        For cardiogenic shock unreponsive to pharmacological therapy. Options include:
        • ECMO
        • Temporary RVAD
          If RV afterload not prolonged.
    • Rhythm

RV afterload reduction is less effective when afterload is not raised, and may be detrimental in outflow tract obstruction (e.g. ToF).

Specific therapy:

  • Pharmacological
    • Pulmonary vasodilators
      Combination therapy is typically standard, and may involve:
      • Calcium-channel blockers
        For idiopathic, drug associated, or vasoreactive disease.
        • Amlodipine
        • Diltiazem
      • Endothelin antagonists
        For PAH.
        • Bosentan
        • Ambrisentan
        • Macitentan
      • Direct pulmonary vasodilators
        • Sildenafil
          PO. Slow onset, takes 2-3 days to achieve maximal effect.
    • Inotropes
      • Digoxin
  • Procedural
    • Atrial septostomy
      Palliative procedure for severe PAH, creating a right-to-left shunt.
    • Pulmonary thromboendarterectomy
      In CTEPH.
    • Lung transplant
    • Heart-lung transplant
  • Physical

Supportive care:

Disposition:

Preventative:

Marginal and Ineffective Therapies

Anaesthetic Considerations

Complications

Prognosis

Key Studies

Rate/Rhythm

References

  1. Houston BA, Brittain EL, Tedford RJ. Right Ventricular Failure. New England Journal of Medicine. 2023 Mar 23;388(12):1111–25.