right heart failure by hergen buscher
DESCRIPTION
Hergen Buscher's presentation on right heart failure.TRANSCRIPT
Treating the Right Heart
Hergen BuscherSt. Vincent’s Hospital, Sydney
Kingscliff
I want to confuse you
I want to show you some photos –
not all of them are nice
Objectives
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
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
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
LVLVLVLVRVRVRVRV
• 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
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
Diagnostic Tools
Preload Contractility Afterload
Clinical √
Echocardiography √ ? √
PAC √ √
MRI √
• 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
Why we don't have to care
LV dysfunction induces RV dysfunction
• Afterload increase
• Displacement of the interventricular septum
• Impairment of RV filling (ventricular inter- dependence)
Pulmonary disease induces RV dysfunction viaIncrease in pulmonary resistance
Why we sometimes have to care
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
Right ventricle to left ventricle
interdependenceAnatomical shared
• Ventricular septum• Pericardium• Myocardial fibres
One ventricle affects
• Size• Shape• Pressure-volume relationship
of the other
• 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
Oppositeeffect to LV
How we should treat
(if we have to)?
Treat the underlying disease
• LV failure
• Lung Disease
• RV Infarct
• Endocarditis
• ARDS, Sepsis
• PE
Treat confounding factors
• Hypoxia
• Acidosis
• Hypercarbia
• Avoid high ventilatory pressures
• Arrhythmia
• Repair TV
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 dryGive 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
Increase ContractilityDobutamine
•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
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
Mechanical Support
• LVAD
• BiVAD
• TAH
• ECMO
• Transplant
*To Mark and Pierre
Thanks*….