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Dr. Ramon Joel Seastres wrote 09-11-2011 07:31:37 pm
How about combining Echo.in patient on PA catheter? Echocardiography (Tissue Doppler) correlating with CVP is a suitable objective assessment of RV preload and PA catheter for beat to beat evaluation of RV afterload and probably Echo.for assessment of RV contractility to correlate with PA cath variables extrapolating RV CO.Still depends on clinical setting and familiarity with monitoring devices.

Dr. Ramon Joel Seastres wrote 09-11-2011 07:34:09 pm
How about combining Echo.in patient on PA catheter? Echocardiography (Tissue Doppler) correlating with CVP is a suitable objective assessment of RV preload and PA catheter for beat to beat evaluation of RV afterload and probably Echo.for assessment of RV contractility to correlate with PA cath variables extrapolating RV CO.Still depends on clinical setting and familiarity with monitoring devices.

Haney Mallemat wrote 08-08-2011 09:55:11 am
The RV....the great mystery. Assessing the RV can be difficult, but trending the CVP may be helpful to assess how "hard" the RV is working. Furthermore, ECHO technologies like tissue Doppler may allow a more objective assessment of function.

Much more research is needed to evaluate the RV in critical illness.

Haney

AMIT KANSAL wrote 08-09-2011 09:42:12 pm
I consider left sided success as a surrogate marker for optimal Right heart Mx - CO measure from PICCO! (till I get comfortable with objective measurement of RV function).
The response in CO with Fluids/ inotropes/ PEEP alteration may serve the purpose.
Situation gets worse when dealing with RHF in ARDS - 20-25% of our ARDS patients are likely to get that! High PEEP/ permissive hypercapnia - not RV friendly.

Todd Fraser wrote 08-10-2011 11:03:46 am
I guess intuitively that makes sense. If the CO goes up, the right heart must be keeping up.

But what about when the CO is struggling - is it because the LV is not working well or is it because of ventricular interdependence and the RV is bringing the LV down? What signs are there that the RV is responsible for underfilling of the LV, or that septal deviation is preventing LV filling?

And when we do decide that, what are the best management options to assist the failing RV?

Izak Perold wrote 08-12-2011 08:53:44 am
Hi Guys!

I don't think vasopressors is that mean to the RV. Ischaemia is the final common pathway to failure, so decent RCA pressure is a must.

Vasopressors possibly restore the 3d configuration of the LV, giving the RV a nice firm septum to contract against.

Adrenegic receptors are probably sparser in the pulmonary vasculature than systemic.

Benjamin Moran wrote 08-12-2011 04:46:26 pm
Whilst I agree that if cardiac output is adequate, then the right side of the heart must be keeping up. However, it is more prone to fatigue than the left ventricle, and may tire if it is not looked after. Investigation of the RV usually consists of echo (I'm not good at quantitative measures such as TAPSE), with cardiac output monitoring (such as PiCCO). Investigation of end-organ effects are the usual urine output, lactate, ScvO2 along with clinical examination. I also investigate the aetiology of the RVF, which are many and varied, and treat accordingly.

While I'm treating the underlying cause, my approach to general management of RVF is always a simplistic (usually in this order):

1. Optimise preload- ensure adequate filling, using measures of fluid responsiveness to guide therapy (i.e. not CVP; using PLR, SVV, PPV/SPV- although these may be limited in pts with ARDS using low Vt ventilation)

2. Optimise contractility- dobutamine is my first choice (mostly because I use lactate levels which are increased with Adr, in combination with ScvO2, U/O and clinical examination to guide therapy). It results in decreased PVR(pulmonary vascular resistance), which is synergistic with iNO. It may result in systemic hypotension, and the use of vasoconstrictors may result in increased PVR. Adrenaline is my second choice. Even though it causes a rise in mPAP, results in a decrease in an increase in RV output, as contractility increases more. I'm not familiar enough with milrinone/levo

Chris Anstey wrote 08-15-2011 06:32:56 pm
Oddly, RV function is very difficult to assess.
Most of us rely of the fact that the pulmonary circulation is a capacitance system and that filling (and filling, and filling) the patient so that the LV works implies an optimally functioning right side of the circulation. Unfortunately this may not be so, particularly in the context of acute and/or chronic respiratory disease.
I tend to correct the things that I can (fluid status, oxygenation, acidosis etc.) and then reach for the drugs knowing full well that the pulmonary circulation vasoreceptors are different in type, number and sensitivity from those in the systemic, resistance circulation.
If I may paraphrase from the infamous St. Bartholomew's Day Massacre in 1572, 'put them all on levo(simendan) and let the Coroner sort it out' ;)

Alex McKenzie wrote 08-15-2011 07:04:39 pm
The RV is a whimpy little thing. There are studies that suggest that in the context of normal pulmonary resistance, a completely failed RV will not cause any distruption to cardiac output if there is a modest increase in CVP.

The issue becomes significant only when there are raised pulmonary resistances. It thus seems to make sense that we should focus on doing whatever we can to reduce the impact of what we do on pulmonary pressures and the rest will look after itself.

Jo Butler wrote 08-16-2011 04:26:15 pm
Levosimendan would have about as much evidence behind it as anything else in this area. How much do we really know about the effects of these drugs in clinical practice on pulmonary pressures and the ability of the right heart to cope? Not much, I'd suggest.

There are a couple of trials from 2006 (both in CCM) suggesting efficacy in right ventricular failure related to critical illness, one compared to dobutamine.

Large scale trials seem unlikely to occur until a universally accepted definition of right ventricular failure is developed. One review suggested "inadequate cardiac output with raised CVP, with abnormal RV contractility on imaging, and where LV function alone is insufficient to explain the clinical syndrome." Helpful.

Oliver Arkell wrote 08-23-2011 09:17:39 pm
Back to the initial question - how do you measure right heart function? If we're going to protect it, it might be worth monitoring how its going, otherwise we might be creating more trouble without any benefits.

What is the best marker of RV function? TAPSI? Other???