Right heart failure by Hergen Buscher

Hergen Buscher's presentation on right heart failure.

1. Treating the Right
Heart
Hergen Buscher
St. Vincent’s Hospital, Sydney
Kingscliff

2. I want to confuse you
I want to show you some photos –
not all of them are nice
Objectives

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. .
. LVLV
RVRV

11. • 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
Under Pressure

12. Why is RH Failure such a pain
to look after
Complex three-dimensional geometry
Complex left ventricular/septum interactions
..... Because it is harder to diagnose and monitor

13. Diagnostic Tools
Preload ContractilityAfterload
Clinical √
Echocardiography√ ? √
PAC √ √
MRI √

14. •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
Echocardiographic Indicators of Right Heart Function

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
of the other

20. •Hypoxia
•Hypercapnia
•Acidosis
•Mechanical ventilation
•increases intrathoracic pressures
•decreases RV preload
•increases RV afterload
•results in diminished CO if RV function was compromised
before intubation
ICU relevant conditions and treatments can worsen RVF
Opposite
effect to LV

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. Many studies suggest that both central venous pressure and RV end-diastolic
volume may not reflect RV preload.
In general, patients with RV failure and marked volume overload benefit from
progressive diuresis.
Acute volume loading is sometimes considered () in the absence of marked
elevation of central venous pressure (12 to 15 mm Hg).
If no hemodynamic improvement is observed with an initial fluid challenge of
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
loading () have not demonstrated significant hemodynamic improvement
Optimise Preload
AHA Guidelines
CVP is Crap
Keep them dry
Give Volume if you have to and if your crap indicator is not to high
Stop doing it if it doesn’t work!
(Give the worst type of fluid only)
Everybody does it but we don’t really know

26. Increase Contractility
Dobutamine
•Decreases PVR
•Increased HR
•Systemic hypotension
Milirone
•phosphodiesterase III inhibitor
•cAMP dependent vasodilatation
•Prolonged half-life - 2.5 hours
•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
Noradrenaline
•Increases Systemic BP/MAP
•Increases PVR
•May be needed to improve
coronary perfusion
Vasopressin
•May be more selective to SVR

27. Reduce
Afterload
Abrupt
discontinuation
may lead to
rebound PH
Inhaled Nitric oxide (iNO)
•Endothelium derived vasodilator
•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
•Synthetic analogue of prostacyclin PGI2
•Dilates pulmonary (and systemic) arterial vascular beds
Sildenafil
•Selective inhibitor of cGMP (via phosphodiesterase type 5)
•I.v. formulation coming soon
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. *To Mark and Pierre
Thanks*….