Login | Sign Up | Help

Post-CPR

added by Emmel

Post-CPR
Comments
Posted By: ohtusabes (963 days ago)

Hello Emmel. The case is very interesting and with very points of
discussion:
First, in our ICU rarely we use actually PA catheter,
so, estimated EDP is made by echo...with multimodal approach.
We
use dinamic predictors of fluid responsiveness like delta pulse
pressure, delta SV, delta IVC diameter and not static index like CVP
or Wedge Pressure.
We use thoracic echo to look if patients have
US B lines, expression (not always) of elevated evLW and indicative of
lung edema.
Yes we use diuretics in case when ventricular
interdependence occurs or likely occurs, US B lines are present or
biventricular disfunction appear and always when is clear that
patients are not fluid responsive. The point here is a titrated use
because risk of hipovolemia and if this happens, yes, cardiac output
drops.
If PH have a postcapillary component restoration of LV
function and maybe diuretics still may be considered.
Thinking in
this patient the RV maybe improve with supportive care and treating
the infection. Miocardial stunning postCPR is another possibility. So,
dobutamine is the inotropic of choice, simple because the afterload of
RV drops with it.

Best my friend and we have in contact./>Pablo

Posted By: Emmel (963 days ago)

Hello Pablo!
Thanks a lot for comment!
This case was a
"desaster".
That patient had a severe COPD and actually an acute
infection- exacerbation (gram-negative rod-cells). mechanical
ventilation was very hard, but we could avoid hypoxaemia.
You´re
definitely right: volume is the wrong way. Using echocardiography we
tried a short volume-challenge with 250ml cristaloid-infusion: no
effect on haemodynamic (blood-pressure, estimated stoke-volume). But I
don´t agree with loop-diuretics in that situation: CVP was 17 mmHg
and echocardiographic estimated LVEDP was 19 mmHg and I think that
patient needs that preload for the left ventricle in this case (high
dose catecholamines, about 75ml/h spontaneous diuresis). Do you have
another experience in cases like this especially with diuretics?
Definitely no lung oedema! So please let me know, I´m very interested
in your experiences! Maybe glyteroltrinitrate could help if one wants
to lower LVEDP and PVR.
The patient had definitely no pulmonary
embolism (ct-scan, TEE). But he had two components of PH:
post-capillary PH and a remodeling of pulmonary arteries (TPG > 15
mmHg; PVR > 250 dyn+sec+cm^-5 in echocardiographic estimation). After
all it is a severe seconary PH in context of severe COPD in
combination with ischemic component (condition after cardiac
infarction of inferior wall caused by occlusion of RCA for years)./>Last cardiac catheter was 2 weeks before admission to our icu: there
is no possibility to improve the coronary status. We decided against
cardiac catheter.
We started application of
phosphodiesterase-inhibitor type 5 (revatio 3 x 20 mg/d). No iloprost
in that situation because in bronchoscopy we found in all bronchia a
lot of pus and I think in that situation there won´t be no
benefit.
Best wishes and thanks a lot for your opinion!
I´m
glad that you join EchoJournal.
Jörg.

Posted By: ohtusabes (963 days ago)

Hi. Very interesting.
It seems like two situations are here:/>
Pulmonary hypertension and ischemic right ventricle.
/>Treatment in this context must appoint to:

1- optimize RV
afterload (so, don´t allow hipoxemia and if possible, allow
spontaneous ventilation and reduce PPV.)
2- With RV dilatation
and RV/LV ratio > 0.7 I think this patient is not fluid responsive.
Thinking in ventricular interdependence and limited LV filling I could
trial a loop diuretic. (judicious and titrated)
3- Look for
causes (distinct for PE) of PH.
4- Cardiac catheterization and
PCI if available.

Best,
Pablo


Video Information
From:

Emmel

Send PM
(105) | (12) | (3)
Added: 17-01-2012
Runtime: 0m 12s
Views: 3011
Comments: 3

Login to Rate Video

Current Rating:
     
(2 Votes)


Description

about 85 y old patient with severe acute RV-failure in context of chronic ischemic RV-failure. No sign of pulmonary embolism in initial TEE and ct-scan. First TTE we found a distinct RV-wall movement disorder. haemodynamic deteriorated rapidly, so we had to start cardiac resusciation for 3 minutes. in TTE we could see a distinct rv-pressure-overload with systolic d-sign. Actually vasopressor and inotropics save the situation. Any other hints in treatment of acute RV-Failure except inotropics and/ or vasopressor?


Video URL: