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Haemodynamic monitoring using echocardiography: a trial 1

added by Emmel

Haemodynamic monitoring using echocardiography: a trial 1
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Posted By: diego (929 days ago)

WHAT IS DOING THE ADMINISTRATOR OF THIS
WEBSITE ? IT'S
UNACCEPTABLE SUCH A SPAMMING
ACTION IN HERE . I THINK I ' M
GONNA SHUT DOWN
MY MEMBERSHIP . THIS WEBSITE IS GONNA DIE/>WHO IS SUPPOSED TO BE THE SDMINISTRATOR?

Posted By: ohtusabes (951 days ago)

Hello my friends.
Looking in literature I find an interesting CI
measure formula that seems to correlate very well with PA cath CO. />
CI= 172 x (mean velocity LVOT) -172

In appareance
it could be used safely in patients without LVOT abnormalities and
don´t include LVOT diameter (a clear factor of error calculate
CO).

The work is old but...is interestingly:
/>Evangelista et al: Cardiac Index Quantification by Doppler
Ultrasound in Patients Without Left Ventricular Outflow Tract
Abnormalities. J Am Col Cardiol 1995;25:710-6.

PD: Diego
if you tell me your e-mail I send you.

Best for all!

Posted By: diego (953 days ago)

Hi Pablo I think I got your doubts . I will try to give to you my
point of view . 1) If you measure aortic flow too close to the valve
for sure you are not estimating the flow thru the region you measured
in M mode orB mode ( I mean aortic root diameter ) . So it's important
that if you see a clear click closure echoe....you move slightly
upward . 2) About CW , I 've read a lot about it . Some authors
suggest to use CW either PW for aortic flow measurement . In my
opinion CW ( except in the case of valvular stenosis ) doesn't offer
any additional accuracy . CW does sample a number of vectors loosing
in this way the spatial accuracy of the measurement itself .
I
hope I gave you my opinion clearly .
ciao
Diego

Posted By: ohtusabes (953 days ago)

Hi, its me again. I have a questions about CO measurement.
/>If I use (LVOT d)2 x 0.785 and use PW sample closely to valve I
assume I am using the same region and this accurates the
measurement.

If I use aortic root and put the PW sample in
LVOT I am not using the same region and this I think is not the
ideal...What happens if I use CW doppler in this case? It will be more
representative?

Sorry for questions but it is
important.

Best
Pablo

Posted By: ohtusabes (953 days ago)

Very interesting comments. Really helps a lot.

Jörg: we
are waiting the second part!

Best

Posted By: diego (953 days ago)

the same as you do Pablo , Actually I use the click closure only as a
landmark so to speak . Actually measuring the VTI too close to the
valve ( CLICK CLOSURE ECHOES ) does not offer the correct site of
measurement . I was just asking because some cardiologists perform the
VTI estimation to close to the valve . The attempt to freeze the LVOT
it's a good idea in order to minimize inaccuracy of measurements ./>To Jorg : You really go Jorg and you're doing a great and valuable
job . I hope that many other users in here join our discussions . I
appreciate the comments of Pablo a lot . he does give to use THE REAL
POINT OF VIEW of the intensivist . The heart as a pump is only a small
part of a larger and greater hidrodynamic circuit . We must try to
understand the way the heart and the circulatory sistem shake their
hands each other.......that's all
thanks again for this
interesting discussion Jorg and Pablo

Posted By: ohtusabes (953 days ago)

And Diego, yes, I put PW sample close to aortic click (but of course
not inside the valve). And you?

Best
Pablo

Posted By: ohtusabes (953 days ago)

Hi Diego and Jörg.

To Diego: I don´t use miorelaxant
(unless patient are not fully adapted, without ventilatory efforts)and
not put end-expiratory pause to measure VTI but, seems a good way to
"freeze" aortic root... I will probe the next time and I will probe
aortic root diameter x 0.785...Thanks a lot for data!

Best
regards my friends
Pablo

Posted By: Emmel (953 days ago)

Thanks a lot for comments!! That helps me very much to improve my
"anaesthesiological" point of view for critical ill patients on icu,
because I still have a too "cardiological" way of looking on
haemodynamic in ICU. In your comments I learn a lot to improve my
skills. I know that somethings in that vid doesn´t fit, but it was a
trial to train and exercise that kind of "echodynamic".
/>...by the way: I used your LVOT-area-formula (aorta-root-diameter x
0,785) in an echocardiographical measurement on icu today, diego! />

Thank you very much! I´ll post another "haemodynamic
trial" in a few days! I hope for your comments again!

Posted By: diego (953 days ago)

Hola pablo thanks again for writing me back so soon . I must say that
the measurement
Of the aortic root using M MODE does offer the
theorical advantage
Of a greater spatial resolution thanks to the
precise detection of the M echoes
Of the anterior and posterior
aortic wall . I agree with you ... I don't know
How more accurate
it is .
The formula you reported it's not part of my baggage so
to speak .
I would like to know if in your clinical practice you
are used to paralyze
The patient via miorelaxant and if you put
the ventillator in end expiratiry
Pause before measuring the VTI
. In this way you can basically reduce
The phisiologic anterior
motion of the aorti. Root during cardiac cycle .
And what do you
think about the PW in proximity of aortic valve closure
Click
?????
Best regards
Diego

Posted By: ohtusabes (954 days ago)

I was reading your estimation of LVOT area with aortic root
measurement. I really don´t see this formula... Is more accurate than
LVOT diameter measure?
Do you measure in M-mode with leading edge
technique? I think it is a more easy technique and with less error
between operators...but I really don´t know how accurate is.../>
Suppose we can´t measure well LVOT and aortic root... what do
we do now?

what do you think about using LVOT diameter with
Nidorf formula? (this formula is used by USCOM CO measurement
technology to calculate automatically LVOT diameter)

Nidorf
formula: LVOT (cm)= 0.01× body height+ 0.25

Best/>Pablo

Posted By: ohtusabes (954 days ago)

Thanks for your comments Diego. In fact, are not confusing.
I
think all of us try to make it easy...I prefer echohemodynamic to PA
cat and in reality, in my ICU, we don´t use PA catheter so much (1-2
times/year?).
Is true like you say about central venous oxygen
saturation and lactate and the gradients about lactate... the
discreancy between ScVO2 and lactate are a lot of times because of
territory drained by SVC (respiratory muscles)and great VO2 of this
musculature. A work by Hernandez et. at measure scVO2 before and after
simply intubating and ventilating patients and see that scVO2 was
better after intubating...and simply because the work of respiratory
muscles was reduced (Critical Care 2009, 13:R63.)
With respect to
arterial lactate and scVO2 like a paired mix of goals of reanimation,
Jansen et al (Am J Respir Crit Care Med 2010; 182: 752–761.) studied
this and seems to be a good tool.

And if you sum echo all
is better...

I use dp/Dt for contractility estimation,
eyeballing, Simpson (I look if are congruent with eyeballin)...and in
several times I am wrong when I ask the cardio eyeballing)... I know
that the important thing for us is SV and CO/CI (the net result of
all) but I think that it is important to know where the problem
is...

Best regards,
Pablo

Posted By: diego (954 days ago)

HI JORG AND HI PABLO I HAVE BEEN LOOKING TO YOUR ENTHUSIASTIC COMMENTS
ABOUT THIS APPROACH . I DO THINK THAT ECHODYNAMICS EVALUATION THRU
ECHOCARDIOGRAPHY IS A REALLY CHALLENGING AND FEASIBLE WAY TO HANDLE
THE COMPLEX SCENARIO OF HEMODYNAMIC INSTABILITY IN ICU CRITICALLY SICK
PATIENTS .
FIRST OF ALL THE COMPARISON BETWEEN THE cARDIAC
OUTPUT OBTAINED VIA A PA CATH AMD CARDIAC OUTPUT OBTAINED VIA TTE
STUDY IS NOT THE PIVOTAL POINT . INFACT YOU KNOW THAT IN ACTUAL FACT
THE VOLUME OF BLOOD EJECTED IN THE SMALL AND IN THE SYSTEMIC
CIRCULATION IS NOT THE SAME AT ALL . IN ACTUAL FACT THIS DISCREPANCY
IS STRONGLY AUGMENTED IN CO EXISTEMCE OF TV RIGURGITATION ( YOU TALK
ABOUT 3,4 M/SEC TV VELOCITY) AND RV SYSTOLIC FUNCTION IMPAIRMENT ( RV
INFARCTION?? YES ?? )
EVEN IN THE EVALUATION OF PAP MOST OF
RECENT STUDIES DO SHOW A GOOD CORRELATION BETWEEN PA MEASUREMENT AND
TTE EVALUATION .
ABOUT THE AKI YOPU TALKED ABOUT I WOULD SAY THAT
IN PRESENCE OF RV IMPAIRMENT ONE OF THE MOST SIGNIFICANT DETERMINANTS
IS THE SPLANCHINC CONGESTION AND VENOUS STASIS . I DIDN'T REALIZED IF
THE AKI YOU TALKED ABOUT CAME OUT IN THE CONTEXT OF CLEAR LV
DYSFUNCTION SECONDARY TO RV IMPAIRMENT ( LOW OUTPIT STATUS ) OR IN THE
CONTEXT OF ISOLATED ELEVATED CVP ( VENOUS STASIS )
ABOUT THE VTI
EVALUATION I AM USED TO PARALIZED THE PATIENT VIA MIORELAXANT DRUGS
AND I PUT A EXPIRATORY PAUSE BEFORE MEASURING THE VTI IN ORDER TO
REDUCE THE PHISIOLOGIC MOTION OF THE AORTIC BOX . THEN I AM USED TO
APPLY AORTIC ROOT DIAMETER X 0,785 IN ORDER TO GET THE AREA .
I
RARELY USE DP/DT EVALUATION IN THE EVALUATION OF LV CONTRACTILITY AND
IN MY HUMBLE OPINION IT'S NOT THE POINT .
TO PABLO....I OFTEN SAW
A CLEAR DISCREPANCY BETWEEN LACTATE LEVELS AND SVCO2 AND THIS
DISCREPANCY NEVER SURPRISED ME . IN ACTUAL FACT THE GRADIENT BETWEEN
LACTATE LEVEL IN PERIPHERAL VENOUS BLOOD AND IN THE MIXED VENOUS BLOOD
IS MUCH MORE RELIABLE .
MAYBE MY COMMENT IS A LITTLE BIT
CONFUSING ....I TRIED TO DO MY BEST......HEY JORG BY THE WAY YOU DID A
GOOD JOB AND JUST FOR YOUR CURIOSITY ...TRY TO EVALUATE SV USING THE
DIAMETER AND THEN USING THE AREA :) YOU WILL FIND AN INTERESTING
RESULT
CIAO JORG AND CIAO PABLO

Posted By: ohtusabes (964 days ago)

This is a very instructive case Jörg and all measurements and
calculations must be put in the complete patient movie, if not,
doesn´t work.

Best
Pablo

Posted By: Emmel (964 days ago)

Hello Pablo!

Thank once more for comment!
/>You´re right! I also think that patient got a acute kidney injury
in context of preexisting chronical renal failure (diabetical and/ or
hypertensive nephropathy; diabetes mellitus type 2 and arterial
hypertension is known as preexisting illness). In my opinion it is a
combination of cardiorenal origin and contrast-agent induced renal
failure (about 230 ml contrast-agent in cardiac catheter).
CVP 19
mmHg and you´re also right that patient was a fluid responder. CVP >
22 mmHg showed a better haemodynamic and clinical picture.
/>One part of the therapeutical treatment in that case was:
dobutamine, levosimendane, over the course of time milrinone for
inotropic support.

Damn! Should I´ve done a mathematical
mistake in calculation of LVOT? I´m embarrassed!
Thank you very
much for hints, tipps and positive criticism!

Best
wishes,

Jörg.

Posted By: ohtusabes (964 days ago)

LVOT area are well calculated.?

LVOTd: 1.53 cm;
LVOTa:
pi (3.14) x r2
LVOTa: 3.14 x (0.76)2
LVOTa: 1.81
/>SV: 1.81 x VTI(23.5)
SV: 42.5 ml

CO: 42.5 x 110= 4.6
L/min

I think this CO is not bad but it is a compensated
state ligated to elevated heart rate.
If SV are higher maybe
heart rate slows... and with this catecholamine release and SVR slows
and perfussion to renal and splachnic tissues is better.
/>Best
Pablo

Posted By: ohtusabes (964 days ago)

Lactate are elevated and ScVO2 are low and hemodynamics (SV and CO)
don´t correlate and patient is in AKI, so, cardiorenal type 1
syndrome is the logical view and in context of RV infarction and low
RV output...so LV output... fluid challenges, dobutamine (or other
inotropic)and reduced RV afterload is the standard treatment. If CVP
is 10, 19 or 25 don´t mean patient are not fluid responder and If you
think in RV infarction problem the RV transforms in a passive conduit
and elevation of right circuit pressures with fluid challenges allows
a better RV output to pulmonary veins, in conjunction with optimized
afterload of RV and inotropic support.

Best
Pablo

Posted By: Emmel (964 days ago)

Sorry, I forgot some information!

central-venous O2 was
initally 61%; mixed-venous O2 was initially 55% (measured via
PA-cath).

Regards,

Jörg

Posted By: Emmel (965 days ago)

Hello Pablo!

Thanks a lot for comment! That is very
helpful!
That case was a trial to compare PA-cath with
echocardiographic measurement of haemodynamic. I´m an internist in my
medical education for cardiologist and intensivist. Most internists
alternatively internal-intensivists don´t commonly use
echocardiographic-haemodynamic evaluation. So I try to learn that in
an "anaestesiological" way.
I´m going to give you some more
information about that patient.

Lactate about 5 mmol/l and
anuria, so we started CVVH.
Invasive measured CVP was 19 mmHg./>That patients got a severe infarction of right ventricle and
ischemia of posterior and inferior wall of LV. (severe thrombotic
occlusion of RCA > in cardiac catheter we implantated 3 stents, but
there was still a coronary low flow with thrombotic residuals despite
of thrombus aspiration via catehter: so we started application of
tirofiban in addition to dual antiaggregatorical therapy (clopidogrel
and acetylsalicyl-acid).
tissue measurement of LV: E/E` 12,7
(E-velocity: =,53 m/s, E`0,04 m/s)
You´re very right with
LVOT-diameter: I´m not sure, whether my measurement is correct. The
possibility of inaccuracy of measurement of LVOT-diameter in TTE is
not small in my opinion.
TAPSE was about 8 mm/ tricuspid annular
systolic velocitiy in tissue doppler was < 10 cm/s

And
you´re also right: the echocardiographic picture in apical 4 chamber
view doesn´t fit to the measured dp/dt of 320 mmHg/s.
/>Thanks a lot for your very helpful comment. I will post some more
"echodynamic trials" in future and I´m looking for your´s, diego´s
and some more of communities comments, hints and tipps.
That will
help me to improve my basal skills in echodynamic!

Best
wishes and regards,

Jörg.

Posted By: ohtusabes (965 days ago)

Other thing about dp/dt measurement that alerts about a wrong number
is that don´t correlate with eyeballing of LV contractility...that
seems acceptable.

Best

Posted By: ohtusabes (965 days ago)

Very good approach. In my ICU I use echo for hemodinamic measurement
and a few are important.

I look dp/dt and the 3m
measurement I think is not properly placed, but in reality I don´t
see very well the slope. 320 mmHG of dp/Dt (altough is preload
sensitive) is a very bad contractility...

LVOT diameter is
very small...In males approximate 2 cm...in woman 1.75 cm. But if you
measure well is it. (this is the real problem with LVOT because small
variation in LVOT diameter impacts a lot in LVOT area and SV)./>
In reality, I think you need less things:

1- SV
with VTI LVOT, LVOT area. CO. Cardiac index.
2- TV regurgitation
and estimation of sPAP (mPAP, dPAP are not very important). If jet is
not available you measure PV aceleration time and roughly estimate if
PAP are high or not.
3- How is IVC? all correlation of IVC and
CVP are in patients in spontaneous ventilation not in fully adapted
MV...so CVP is important? for calculate sPAP yes...for fluid
responsiveness assessment? really not.
4- How is RV? function?
TAPSE? Dp/DT of RV? dilated? is ventricular interdependence a problem?

5- How is LV diastole? This patient have a condition that
predispose to stiff LV? (hypertrophy? ischemia) is LA enlarged? (a
sign of chronically elevated LVEDP); how is mitral inflow pattern?
finally if you have tissue doppler how is medial or lateral E/e´?/>
And with this I think is all...You don´t need to calculate
(because in fact we don´t direct measure hemodinamic variables like
PVR...SVR...and because are not very important).

And with
echo measurements you correlate with arterial lactate and if you want
ScVO2 and the picture is complete.

What do you think?/>
Best
Pablo


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This is a trial: haemodynamic measurements/ results by echocardiography in comparison with PA-cath-results. about 75 y old patient with cardiogenic shock by occlusion of RCA. Echocardiographic results: 1. contractility by mv-insufficiency: dp/dt about 320 mmHg/s (this shows a distinct impairment of left ventricle). 2. an approach to LVEDP by E/E`: about 12,7 mmHg 3. approach to CVP alternatively RAP: collapsibility of IVC: one can see, that there is no undulation/ collapsibility of IVC, diameter of IVC > 2 cm: RAP about 15-20 mmHg 4. approach to cardiac output: LVOT-VTI about 23,5 cm, LVOT-area 1,53 cm^2 (radius 0,7 cm) > stroke volume about 36 ml; heart rate: 110/min > cardiac aoutout about 3,9 l/min 5. tricupid valve (TV): Vmax: 3,4 m/sec, PAPs 35 mmHg + CVP; ATC of PV-flow 89 msec, PV-VTI 12,3 cm, one can calculates the PVR with two methods: > a. PVR= TV-flow velocity/ VTI of RVOT x 10 + 0,16; in this case you can calculate: PVR= 3,4 m/s / 0,125 m x 10 + 0,16 = 276 dyn*s*cm^-5 > b. PVR= (PAPm-PCWP)/CO x 79,9; in this case I couldn´t measure the PAPm and PAPd because I couldn´t depict a PV-insufficiency-signal by echocardiography. In comparison: the PA-cath-results: PCWP (LVEDP) 13-14 mmHg, CVP 19 mmHg, CO 4,3-4,5 l/min, PVR 285 dyn*s*cm^-5, SVR 890 dyn*s*cm^-5, cardiac power 0,71 W In my opinion is echocardiographic measurements of a few parameters a good option to approach haemodynamic in patient and to make a fast decision of therapeutical treatment in ER or ICU. I´m lookinf forward to any comment, hints, tipps and critic. That could help me to improve my skills in that kind of echocardiographic technique.


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