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*….