Right Ventricular Failure

Reviewed and revised 26 June 2014


  • mortality as high as LV failure
  • RV is better suited to volume overload than left due to compliance and thin wall but when PVR increases for whatever reason -> RV dilates
  • when the dilation maximised -> reversal of the ventricular septal gradient with abnormal septal movement, rising atrial pressures and TR
  • this eventually produces a global reduction in left sided preload -> systemic coronary perfusion and systemic hypotension.
  • this process is termed ‘auto-aggravation’



  • volume/pressure overload: LVF, PE, ARDS, amniotic fluid embolism
  • mechanical: MV
  • sepsis
  • cardiac: cardiomyopathies, ARVD, TV rupture, tricuspid or pulmonary regurgitation


  • respiratory: cor pulmonale, OSA, COPD
  • muscular disease
  • neuromuscular; poliomyelitis, amyotrophic lateral sclerosis, muscular dystrophy
  • connective tissue: SLE, CREST, RA, hepatic porto-pulmonary syndrome
  • cardiac: LVF, intra-cardiac shunt, cardiomyopathies


  • low cardiac output
  • hypotension
  • hepatic enlargement
  • raised JVP (often difficult to assess in MV patients, large habitus, COPD)
  • peripheral oedema (may or may not have this)


  • CXR: dilation of RV on lateral, helps with assessment of pulmonary cause of PHTN
  • ECHO: TR, long axis cavity size, short axis septal kinetics, apex loses triangular shape, RVED area/LVED area (> 0.6 or > 1), inferior hypokinesis, RV size compared to LV size, loss of inspiratory collapse of IVC, dilation of PA
  • right heart catheterisation: elevated pressures
  • BNP: correlates with degree of heart failure and monitors response to treatment (difficult to interpret in the critically ill due to co-existing heart and lung disease)



  • disrupt the cycle of auto-aggravation
  • reduce afterload (increases EF)
  • preload optimization (difficult to judge c/o elevated atrial pressures) -> use volume changes
  • avoid hypoxia and hypercarbia
  • titrate PEEP appropriately
  • avoid high TV

Volume optimization

  • sequential monitored fluid challengers
  • once not volume response stop
  • if volume overloaded reduce preload (e.g. fluid and salt restriction, diuretics, renal replacement therapy)
  • sequential ECHO, a right heart catheter or PAC can be helpful in fluid titration

Mechanical Ventilation and PEEP

  • distending alveolar pressure transmitted through pulmonary capillary bed -> determines the opening pressure of pulmonary valve
  • also PEEP determines preload because of transmitted pressure to RV
  • low TV
  • PEEP to limit gas trapping

Inotropes and Vasopressors

  • no selective right heart inotrope exists
  • beta-agonists, calcium sensitisers and phosphodiesterase inhibitors
  • must decrease afterload or else increased contractility and myocardial O2 consumption will take place
  • levosimendan: shown to reduce PVR and improve RV function
  • noradrenaline, phenylephrine and vasopressin: improve afterload and thus coronary perfusion but if not appropriately used will increase myocardial O2 consumption
  • milrinone and amrinone: increased contractility via a non-beta-adrenergic mechanisim -> does not increase myocardial oxygen demand, can be nebulised with prostaglandin I2 -> decreases PVR

Afterload Reduction

  • prostaglandins (INH, IV, SC): increased NO release
  • NO: pulmonary vasodilator, oxygenation and PVR improve but no mortality benefit, rebound pulmonary hypertension observed
  • sildenafil: oral medication, phosphodiesterase enzyme
  • milrinone (PDE-III inhibitor): decreases PVR, can be given IV or nebulised
  • systemic vasodilators: SNP, GTN, hydralazine -> cost = reduced coronary perfusion
  • recombinant BNP: neseritide, reduces preload and afterload -> improved Q without inotropy (increased mortality + renal failure)

Surgical Intervention and RV support

  • biventricular pacing
  • RVAD (LVAD if LVF is the cause of RVF)
  • ECMO
  • Transplant


  • O2
  • mechanical ventilation – aggressively treat hypercarbia, acidosis, (all increase PVR)
  • avoidance of hypothermia (increased PVR)
  • bronchodilators
  • fluid/volume
  • vasodilators + inotropes
  • sildenafil 50-100mg PO preoperatively
  • inhaled nitric oxide 20-40ppm (good in bypass, doesn’t cause systemic hypotension as inactivated when bound to Hb)
  • milrinone (50mcg/kg bolus -> 0.2-0.8mcg/kg/min)
  • dipiridamole (0.2-0.6mg/kg IV over 15min bd)
  • inhaled prostacyclin (increases cAMP) – 50mcg in saline nebulised every hour OR 50ng/kg/min nebulised into inspiratory limb
  • IV prostacyclin (if inhaled not available) – 4-10ng/kg/min
  • bosentan
  • pacing to improve A-V synchrony
  • RV assist device

References and Links

Journal articles

  • Lahm T, McCaslin CA, Wozniak TC, Ghumman W, Fadl YY, Obeidat OS, Schwab K, Meldrum DR. Medical and surgical treatment of acute right ventricular failure. J Am Coll Cardiol. 2010 Oct 26;56(18):1435-46. doi: 10.1016/j.jacc.2010.05.046. Review. PubMed PMID: 20951319. [Free Full Text]
  • Walker LA, Buttrick PM. The right ventricle: biologic insights and response to disease: updated. Curr Cardiol Rev. 2013 Feb 1;9(1):73-81. Review. PubMed PMID: 23092273; PubMed Central PMCID: PMC3584309.

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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