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Right heart failure by Hergen Buscher
This document discusses treatment of right heart failure. It begins by explaining how the right heart is both similar and different to the left heart in its structure and function. It notes that right heart failure can be difficult to diagnose and monitor due to its complex geometry. The document then discusses why right heart failure sometimes requires treatment, focusing on conditions like pulmonary hypertension. It concludes by outlining approaches to treating right heart failure, such as treating the underlying cause, optimizing preload and contractility, reducing afterload, and considering mechanical support in severe cases.
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Right heart failure by Hergen Buscher
- 1. Kingscliff Treating the Right Heart Hergen Buscher St. Vincent’s Hospital, Sydney
- 2. Objectives I want to confuse you I want to show you some photos – not all of them are nice
- 3. Objectives • Why isthe right heart not that different • Why is the right heart different • Why is it such a pain to treat it • Why we don't have to care • Why we sometimes have to care • How we should treat if we have to
- 4. Why is theright heart not that different • Right ventricular preload • Right ventricular contractility • Right ventricular afterload • Inflammation, sepsis can cause RV dysfunction • Decreased coronary perfusion from hypotension • Prone to coronary disease (RCA) • Arrhythmia
- 5. Why is theright heart different • Highly compliant • Active pumping for optimal function • Complex structure • RV volume larger than LV volume • Higher RV end-diastolic volume • RV muscle mass 1/6 that of LV • Right coronary perfusion occurs in systole too • Increase pulmonary vascular resistance • Hypoxia • Acidosis • Hypercapnia • Increased airway pressure
- 6. RV RV LV LV
- 11. Under Pressure • Achronically hypertrophied RV usually tolerates a significantly elevated PAP • RV without pre-existing hypertrophy will not be able to generate a systolic PAP > 50 to 60 mm Hg
- 12. Why is RHFailure such a pain to look after ..... Because it is harder to diagnose and monitor Complex three-dimensional geometry Complex left ventricular/septum interactions
- 13. Diagnostic Tools Preload Contractility Afterload Clinical √ Echocardiography √ ? √ PAC √ √ MRI √
- 14. Echocardiographic Indicators ofRight Heart Function • Tricuspid annular plane systolic excursion index • Tissue Doppler • Tei index • Right ventricular peak strain index • Right ventricular volume • Right ventricular mass • RV stroke index • Pulsatility • Compliance • Capacitance • Distensibility • Elastic modulus • Pressure-independent stiffness index
- 15. Why we don'thave to care
- 16. LV dysfunction inducesRV dysfunction • Afterload increase • Displacement of the interventricular septum • Impairment of RV filling (ventricular inter- dependence) Pulmonary disease induces RV dysfunction via Increase in pulmonary resistance
- 17. Why we sometimeshave to care
- 18. Pulmonary Hypertension • PAHis a severe disease with poor outcomes • Median survival without treatment is 2.8 years • 1-year, 3-year, and 5-year survival rates is 68, 48, and 34%, respectively
- 19. Right ventricle toleft ventricle interdependence Anatomical shared • Ventricular septum • Pericardium • Myocardial fibres One ventricle affects • Size • Shape • Pressure-volume relationship
- 20. ICU relevant conditionsand treatments can worsen RVF • Hypoxia • Hypercapnia • Acidosis • Mechanical ventilation • increases intrathoracic pressures • decreases RV preload Opposite effect to LV • increases RV afterload • results in diminished CO if RV function was compromised before intubation
- 22. How we shouldtreat (if we have to)?
- 23. Treat the underlying disease • LV failure • Lung Disease • RV Infarct • Endocarditis • ARDS, Sepsis • PE
- 24. Treat confounding factors • Hypoxia • Acidosis • Hypercarbia • Avoid high ventilatory pressures • Arrhythmia • Repair TV
- 25. Optimise Preload CVP is Crap Many studies suggest that both central venous pressure and RV end-diastolic volume may not reflect RV preload. Keep them dry In general, patients with RV failure and marked volume overload benefit from progressive diuresis. Give Volume if you have to and considered () in the absence not to high Acute volume loading is sometimes if your crap indicator is of marked elevation of central venous pressure (12 to 15 mm Hg). Stop doing it if it doesn’t work! If no hemodynamic improvement is observed with an initial fluid challenge of (Give the worst type of fluid only) 500 mL normal saline, volume loading should not be continued as it may lead to further hemodynamic compromise. Although volume loading is commonly used () most studies addressing volume Everybody does it but we don’t really know loading () have not demonstrated significant hemodynamic improvement AHA Guidelines
- 26. Increase Contractility Dobutamine •Decreases PVR Noradrenaline •Increased HR •Increases Systemic BP/MAP •Systemic hypotension •Increases PVR •May be needed to improve Milirone coronary perfusion •phosphodiesterase III inhibitor •cAMP dependent vasodilatation Vasopressin •Prolonged half-life - 2.5 hours •May be more selective to SVR •Side effect - ventricular tachyarrthymias •Systemic hypotension Levosimendan •Vasodilatory effect, by opening ATP channels •Positive inotropic effect (increasing calcium sensitivity) •May have more specific pulmonary vasodilatory properties
- 27. Reduce Inhaled Nitric oxide (iNO) •Endothelium derived vasodilator Afterload •Activates guanylate cyclase •Increases intracellular cGMP •Decreases PVR •Rapid inactivation by haemoglobin Glyceryl Trinitrate •Prodrug •Denitrated to produce the active metabolite NO •Cave: Sildenafil Nebulised Iloprost Abrupt •Synthetic analogue of prostacyclin PGI2 •Dilates pulmonary (and systemic) arterial vascular beds discontinuation Sildenafil may lead to •Selective inhibitor of cGMP (via phosphodiesterase type 5) •I.v. formulation coming soon rebound PH Bosentan • Endo-thelin receptor antagonist •Increasing CO and decreasing PAP in PH •Long half lives (5 h) •Hepatotoxicity
- 28. Mechanical Support • LVAD •BiVAD • TAH • ECMO • Transplant
- 29. Thanks*…. *To Mark and Pierre