Hergen Buscher's presentation on right heart failure.

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 is the 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 the right 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 the right 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
• A chronically 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 RH Failure 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 of Right 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't have to care

16. LV dysfunction induces RV
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 sometimes have to care

18. Pulmonary Hypertension
• PAH is 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 to left
ventricle interdependence
Anatomical shared
• Ventricular septum
• Pericardium
• Myocardial fibres
One ventricle affects
• Size
• Shape
• Pressure-volume
relationship

20. ICU relevant conditions and 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 should treat
(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