All inotropes are designed for left ventricular failure.
I think that no selective right heart inotrope exists for today. In patients with severe, hemodynamically compromising RV failure, inotropic therapy is administered, using dobutamine (2-5 mcg/kg/min), dobutamine and inhaled nitric oxide, or dopamine alone. Milrinone is preferred if the patient is tachycardic or on beta-lockers (milrinone and amrinone increased contractility via a non-beta-adrenergic mechanisim -> does not increase myocardial oxygen demand, can be nebulised with prostaglandin I2 -> decreases PVR), Levosimendan shown the ability to reduce PVR and improve RV function.Use of digoxin in RV failure associated with chronic obstructive pulmonary disease (COPD) not associated with LV dysfunction appears not to improve exercise tolerance or RV ejection fraction.
Trials should be performed comparing percutaneous RVADs with inotropes (dobutamine/milrinone).
In the Pediatric field, there is a lot of experience but no clear evidence based on trials.
Evidence of epinephrine's influence on Emax can be found in this paper
Instantaneous Pressure-Volume Relationship of the Canine Right Ventricle
Maughan et al : Circulation Research
Very tricky.
Contrary to the left ventricle, the muscle bulk of the RV is smaller and the RV output is more influenced by the afterload than what can be seen on the left side. As such, I think we should more importantly focus if it will be more beneficial for a failing RV in critical care settings to introduce an inotropic agent or a pulmonary vasodilator.
By experience and as correctly noted above, the most beneficial inotropes are the ino-pulmonary-dilators (Right sided inodilators) - Should we benefit from the progress in the field of pulmonary arterial hypertension in the critical care field and use more pulmonary vasodilators?
RVAD/ECLS are they a further solution? I don't know!
What is the role of inhalational agents through the ventilator circuit? Theoretically, we can benefit from the pulmonary vasodilatation and subsequent increase in CO without inducing more systemic hypotension.
Anyway, a profound understanding of the difference between the right and left circulation and real time "accurate and precise" monitoring tools (which can assess both independently and together right and left circulation) are fundamental for any successful management.
Is the PAC our best tool now for quantifying PA resistance and pressures? No answer!
More questions than answers !!!
May Prof. Tulloh has more answers than us....
thank you all.
I find this a really important and interesting question. We really need proper prospective studies, both clinical and translational to determine :- whether the PDE5i or other PDEi have a role in RV contractility, role of sympathomimetics and PDE3i, understanding how RV-PA coupling helps, ensuring maximum RV efficiency - which might not be just contractile force but strain etc as well. We know there is no role for ACEi and I cant believe that epinephrine is really good for longer term support by the time we have depleted the ATP stores..
Agree with these answers.
Unfortunately clinically it is difficult to separate out RV performance improvements from pulmonary vascular resistance. Some vasodilators (e.g. inhaled nitric oxide) cause pulmonary vasodilation, and thus a drop in RV afterload hence RV performance may be improved.
iNO up to 20ppm has some effect.
Alternatively, inhaled milrinone (PDE5 inhibitor) can cause a similar effect as well as theoretically lead to improved lusitropy thus improving RV performance.
As suggested earlier, sildenafil can lead to a drop in pulmonary pressures, so when a swan ganz is in situ, once can see a rise in cardiac output of the RV due to a lowering of the RV afterload.
As all inotropes act by increasing intracellular calcium, we have no specific way of targeting the RV vs the LV as myocytes are the same in both chambers. What differs is their contractile pattern and organisation. Thus it is unlikely there would ever be a "true" RV inotrope alone.
To date, best results have been achieved with mechanical RV support and inotropes in the face of a failing RV.
I am a physicist modeling the cardiac ejection process and developing new measures to assess RV ejection efficiency. -As perhaps is well known I am finding RV ejection efficiency correlates inversely with PA impedance load. Perhaps on track to non-invasive load assessment methods- in any case looking forward to presenting results in a publication or at conference.