9F 2014 Utah Acute Cor Pulmonale Grinberg

8/18/2019 9F 2014 Utah Acute Cor Pulmonale Grinberg

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© !"#$%&'() CRITICAL CARE ECHOCARDIOGRAPHY

ACUTE COR PULMONALE:PULMONARY EMBOLISM AND

ARDS Achikam Oren-Grinberg, MD, MS

Assistant Professor in AnaesthesiaHarvard Medical School

Director of Critical Care EchocardiographyDepartment of Anesthesia

Critical Care and Pain Medicine

Beth Israel Deaconess Medical CenterBoston

!"#$%&'() +,("& -&.% /!+-0


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Jardin F. CURR OPIN CRIT CARE 2009;15(1):67-70

“ A form of acute right heart failureproduced by increase in resistance to

blood flow in the pulmonarycirculation, characterized by

augmented RV outflow impedance, RVejection impairment, and RV size

enlargement.”

ACUTE COR PULMONALE

The term “Acute Cor Pulmonale” defines the common pathophysiology of the acute RV failure encountered in different clinical syndromes.

The core of this process is the increase in PVR, which can be absolute (a major increase, hardly bore by a previously normal RV, example PE) or relative (minor, but jeopardizing an already failing RV: example mech vent on RV with CAD or sepsis-related dysfunction).

Of the common critical care scenarios associated with this clinical picture we will deal only with the non-perioperative ones (PE, ARDS).


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enlargement.”

ACUTE COR PULMONALE

Pulmonaryembolism





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enlargement.”

ACUTE COR PULMONALE

Pulmonaryembolism

ARDS





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ACP: PATHOPHYSIOLOGY

RV

LV

LARA

“PRELOAD TOLERANT”

“AFTERLOAD VULNERABLE”

RVLV

From its anatomical and physiological properties (low wall thickness, ejection on a low-resistance circulation) the RV derives its:

PRELOAD TOLERANCE (it can widely adapt to increases in venous return)

AFTERLOAD VULNERABILITY (it can stand only mild increases in afterload)


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Adapted from: Redington AN. BR HEART J 1990; 63:45– 49

RV

LV

Ventricular P-V Loops:Physiology

1. PVopening3. PV

closure

2. RelaxationOnset


Looking at the P-V curve of a normal RV, in comparison the one of the LV, it has:

1) smaller peak systolic pressures

2) smaller end-diastolic pressure

3) the pressure-volume loop is more triangular than that of the left ventricle: ejection from the right ventricle starts early during the pressure increase and the isovolaemic contraction phase is consequently not well defined. The ejection continues after the peak

pressure during pressure decline (between points 2 and 3).


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LV

Ventricular P-V Loops:ACP

RV

1. PVopening3. PV

closure

2. RelaxationOnset

RV O2 Consumption

RV Myocardial Perfusion

Adapted from: Redington AN. BR HEART J 1990; 63:45– 49

With increased RV afterload the pressure-volume loop resembles that of the left ventricle (no more triangular): there is a well defined systolic shoulder (significant isovolumic contraction) and there is no ejection during the p ressure decline. (for simplicity, the LV here is still represented as normal, as it wasnot influenced by the RV failure)

Appearance of isovolumic contraction + disappearance of ejection during relaxation determine markedly increased energy expenditure

This, coupled with increased end-diastolic pressure (= reduction in the coronary perfusion gradient to RV subendocardial layers) makes RV perfusion at risk:A) no more systo-diastolic perfusion but rather purely diastolic, as it is for the LV

B) High dependence from the Systemic diastolic pressure


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Piazza G.Goldhaber Z. CIRCULATION 2 006;114: e28-e32

RV

LV

RV dysfunction interferes with LV filling and contractility, leading to decrease in CO and hence, further reduction in RV perfusion (reduced coronary pressure gradient and flow). The RV is thus at risk of ischemia, which in the natural history of ACP represents the terminal event.

This is the vicious circle of ACP


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PULMONARY EMBOLISM DIAGNOSIS


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PULMONARY EMBOLISM DIAGNOSIS

ACUTE PE DIAGNOSIS


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ACUTE PE – DIAGNOSIS

This lack of enthusiasm from echocardiography in the diagnosis of PE is seen in recent guidelines describing the appropriate use of echocardiography. These guidelines found insufficient evidence (I in the chart) for the use of echocardiography in the diagnosis of PE.

The problem that we, clinicians, are dealing with is the patient in shock, sometime with a very suggestive story where an acute event is identified (“the patient stood up and then collapsed...”) and inability to send the patient to the CT scan to make the diagnosis (too unstable hemodynamically, renal failure, etc.).Then, we try to get information that may prove us right/wrong with our suspicion of significant PE.

ACUTE PE DIAGNOSIS


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ACUTE PE DIAGNOSIS


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ACUTE PE DIAGNOSIS

Torbicki A. et al. ESC Guidelines on the diagnosis and management of acute pulmonary embolism -EUR H J 2008

The European guidelines, however, take a different approach. They differentiate between suspected PE with hemodynamic compromise and without. If there is hemodynamic compromise and the patient is unstable/unable to underg o CT scan, the Europeans value the input of echocardiography.

This is the scenario where most of us will use echocardiography with the hope for further understanding our individual patient’s physiology.

Based on these guidelines, in the setting of suspected PE presenting with cardiovascular failure, an echo can be used to exclude acute PE leading to hemodynamic compromise, or it can be used to decide to initiate therapy if no contradiction exist (not to make the diagnosis, though, which is important tounderstand...)

ECHO FINDINGS IN PE


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ECHO FINDINGS IN PE

DIRECT VISUALIZATION

OF EMBOLI

2-D & DOPPLER SIGNS

OF RV ACUTE OVERLOAD

TTE ACCURACY (patients with a clinical suspicion of PE):

sensitivity 60-70%

specificity of 80-90%.

TEE ACCURACY (patients with a clinical suspicion of PE and RV overload):

sensitivity 80%

specificity of 97%.

The diagnostic role of Echo in PE lies on 2 different types of finding:

1) the direct visualization of emboli, and this practically abolishes the need for a CT-scan2) When these are not detected, Echo is only able to diagnose ACP, i.e. indirect signs of a severe acute pulmonary embolism

The overall accuracy of Echo in the diagnosis of PE is weak on the side of sensitivity: i.e. PE not associated with ACP are missed. TEE does a little b it better, especially in the detection of intracavitary thrombi.

KEY MESSAGE: A NEGATIVE ECHO CANNOT IN A STABLE PATIENT CANNOT EXCLUDE PE

Perrier A, Tamm C, Unger PF, Lerch R, Sztajzel J. Diagnostic accuracy of

Doppler-echocardiography in unselected patients with suspected pulmonary

embolism. Int J Cardiol 1998;65:101–10

Pruszczyk P, Torbicki A, Pacho R, Chlebus M, Kuch-Wocial A, Pruszynski B et al.

Noninvasive diagnosis of suspected severe pulmonary embolism: transesophageal

echocardiography vs spiral CT. Chest 1997;112:722–728.

ECHO FINDINGS IN PE


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ECHO FINDINGS IN PE


OF EMBOLI











PE: DIRECT EVIDENCE


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PE: DIRECT EVIDENCE


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PE: DIRECT EVIDENCE


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PE: DIRECT EVIDENCE


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63 Y.O. M POD # 3 FROM TOE AMPUTATION


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63 Y.O. M POD # 3 FROM TOE AMPUTATION


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ECHO FINDINGS IN PE


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OF EMBOLI

2-D & DOPPLER SIGNS












ECHO FINDINGS IN PE


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OF EMBOLI

2-D & DOPPLER SIGNS












ACP: ECHO EVIDENCE


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1. RV DILATATION

2. RV DYSFUNCTION

3. SEPTAL DYSKINESIA

4. INCREASED RV AFTERLOAD(Doppler evidence)

The Echo evidence of ACP is based on identification of 1., and of 2., (and the first is a diastolic finding, i.e. expression of Volume overload while the second mainly of Pressure overload, occurring in systole).

But not only, as the formers are signs that can be found in other situations than ACP (ex. RV AMI for 1, or LBB for 2.).

The diagnosis of ACP requires demonstration of the hemodynamic cause of these 2 signs, i.e of the increase in pulmonary vascular resistance.

ACP: ECHO EVIDENCE


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1. RV DILATATION

2. RV DYSFUNCTION



RV strain




ACP: ECHO EVIDENCE


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1. RV DILATATION

2. RV DYSFUNCTION



RV strain

Pressure overload




ACP: ECHO EVIDENCE


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1. RV DILATATION

2. RV DYSFUNCTION



RV strain

Pressure overload

Help differentiate acutefrom chronic





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2D EVIDENCE

OFCOR PULMONALE

ACP: ECHO EVIDENCE

Normal: RVEDA/LVEDA


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Moderate: RVEDA/LVEDA 0.6-1.0

Severe: RVEDA / LVEDA > 1.0

1 RV DILATATION

Normal: RVEDA/LVEDA 0.6

Measurement:End diastole

ACP: ECHO EVIDENCE

Normal: RVEDA/LVEDA


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Moderate: RVEDA/LVEDA 0.6-1.0

Severe: RVEDA / LVEDA > 1.0

Jardin F. CHEST 1997;111:209–21 7

1 RV DILATATION

Measurement:End diastole

ABSOLUTE RV SIZE


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J A S E 2 0 0 5 ; 1 8 ( 1 2 ) : 1 4 4 0 - 1

4 6 3

ACP: ECHO EVIDENCE


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!"

2. RV DYSFUNCTION

Progression of dysfunction is expressed by the appearance of hypokinesia. Marked in the 2nd clip. TAPSE helps us in quantification.

ACP: ECHO EVIDENCE


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!"

2. RV DYSFUNCTION

Progression of dysfunction is expressed by the appearance of hypokinesia. Marked in the 2nd clip. TAPSE helps us in quantification.

ACP: ECHO EVIDENCE


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The second hallmark of ACP is septal dyskinesia, a pathological motion of the septum, that instead of moving opposite to its front LV wall (the postero-lateral wall) moves in the same direction.

ACP: ECHO EVIDENCE


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© !"#$%&'()

CRITICAL CARE ECHOCARDIOGRAPHY


The second hallmark of ACP is septal dyskinesia, a pathological motion of the septum, that instead of moving opposite to its front LV wall (the postero-lateral wall) moves in the same direction.


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PRESSURE OR VOLUME OVERLOAD?


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CRITICAL CARE ECHOCARDIOGRAPHY



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!"#$%&'() CRITICAL CARE ECHOCARDIOGRAPHY



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©

!"#$%&'() CRITICAL CARE ECHOCARDIOGRAPHY

McConnell Sign


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McConnell Sign


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McConnell Sign


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McConnell Sign


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Eur J Echocardiography 2005;6:11-14

McConnell Sign


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"Although this regional pattern of RV dysfunction was relatively sensitive and specific for

acute pulmonary embolism when tested in the larger patient cohort, patients with other

causes of an acute increase in RV afterload may have similar findings. For example, one ofour “false positive” cases had acute respiratory distress syndrome."

“This study focused on the utility of identifying a regional RV wall motion pattern in

patients in whom abnormal RV function had already been identified. This study was not

designed to establish the overall utility of echocardiography in the diagnosis of acute

pulmonary embolism, and these data do not provide justification for performing

echocardiography routinely to establish the diagnosis of pulmonary embolism.”

McConnell Sign


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DOPPLER

EVIDENCE

(Doppler in PE 101)

RV OUTFLOW SYSTOLIC PATTERN


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INCREASED RV AFTERLOAD (Doppler on PA flow)

RVOT OUTFLOW PATTERN


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Matsuda M. Br Heart J 1986, 56:158-16 . - Torbicki A. Eur Respir J 1999; 13: 616-621




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ACP Normal




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ACP Normal

PA Acc Time




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Midsystolic deceleration


ACP Normal




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Midsystolic deceleration


ACP

M-Mode on PulmValve

l l

TABLE 2. PULSED DOPPLER ANALYSIS OF PULMONARY BLOOD FLOW IN NORMAL VOLUNTEERSAND IN SUBJECTS WITH ACUTE COR PULMONALE




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Vieillard-Baron A. Am J Respir Crit Care Med 2002 ;166:1310–1319

Nor ma l V ol un te er s A CP C om pl ic at in g A RD S A CP C om pl ic at in g MPE

(n 24) (n 19) (n 18)

PA VTI, cm 18 3 11 4* 9 3*

Peak velocity, m/s 0.80 0.20 0.82 0.21 0.64 0.17*

ACT, ms 125 23 76 27* 68 36*

FP, ms 304 23 244 32* 252 32*

ACT/FP, % 41

7 32

13* 25

8*

:

.

. .

ll l

l l l ll l l

l l

l l l

Acc Time < 80 ms

And this is found both in pts with ACP due to PE and to ARDS in this study of patients in the medical ICUs

CHRONIC PHT


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DOPPLER TR JET


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Because previously normal RV cannot acutely handle the increased load associated with a marked increase in pulmonary resistance, pressure in the pulmonary artery, does not rise excessively despite acute increase in pulmonary resistance. This is a good validated

cutoff.

DOPPLER TR JET


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cutoff.

DOPPLER TR JET


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cutoff.



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• Acute PE

• Chronic PE

• COPD

• Primary pulmonary hypertension

TRICUSPID REGURGITATION


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THE “60/60” SIGN


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Acute PE

Acceleration time: < 60 ms

THE “60/60” SIGN


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TVPG < 60 mmHg

HOW TO....

Parasternal short axis view


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HOW TO....



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HOW TO....



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HOW TO....Parasternal short axis view


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Time 81 ms

HOW TO....TV peak gradient


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CLINICALLY

• High suspicion for acute PE- Hemodynamic collapse

• Unable to obtain CT


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• Look for- Direct evidence of clot

- Signs of RV strain- Sign of RV pressure overload- McConnell’s sign

• 60/60 sign

• Treatment...?

CLINICALLY

• High suspicion for acute PE- Hemodynamic collapse

• Unable to obtain CT


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• Look for- Direct evidence of clot

- Signs of RV strain- Sign of RV pressure overload- McConnell’s sign

• 60/60 sign

• Treatment...?

TAKE HOME MESSAGE

ECHO IN PE

+, Detection of emboli = Diagnosis of PEDetection of ACP = presumptive diagnosis of massive PE

-, In High-risk PE (shock/hypotension): absence of echosigns of RV strain practicall e cl des PE (Echo = “


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signs of RV strain practically excludes PE (Echo = “theD-Dimer of High risk PE”)

., In Non-high-risk PE (stable pts), a negative Echocannot exclude PE

/, A combination of 2-D and Doppler indirect signs isadvocated

0, Challenge with chronic PHT, ARDS

Altogether, Echo allows you to diagnose PE with certainity only when intracavitary tromboemboly are detected. Detection of ACP may or may not be associated with PE and from a practical point of view the absence of this finding is a useful exclusion criteria only in patients with severe hemodynamic derangement.Highest accuracy in the Echo diagnosis is reached with the combination of multiple indices. And it is important not to misdiagnose a chronic cor pulmonale as a PE.

ARDS-ASSOCIATED

ACUTE COR PULMONALE

-, PRACTICALAPPLICATIONS

+, WHY ECHO IN ARDS? RATIONALE FOR

APPLICATION


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APPLICATIONS • RV DYSFUNCTION:

RECOGNITION, SUPPORT

• VENTILATORY STRATEGY

• DIFFERENTIAL DIAGNOSIS ARDS vs. CARDIOGENIC

• INTRACARDIAC SHUNTDETECTION

ARDS-ASSOCIATED

ACUTE COR PULMONALE

-, PRACTICALAPPLICATIONS


APPLICATION


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APPLICATIONS • RV DYSFUNCTION:





CARDIOVASCULAR FAILURE IN ARDS

. . . .

. .

. .

. . . . . .

Respiratory 60 (96.8) 382 (95.3)Cardiovascular 24 (38.7) 222 (55.4)Neurological 28 (45.2) 142 (35.4)Renal 41 (66.1) 300 (74.8)Li er 7 (11 3) 67 (16 7)

.,

Mild ALI (n=62)a ARDS (n=401)

. . . . , . .

,

. . . .

ACUTE ORGAN DYSFUNCTION ON ICU ADMISSION, n (%)

Mild ALI (n=62) ARDS (n=401)


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Brun-Buissson C, et al. ALIVE Study. INT CARE MED 2003

Liver 7 (11.3) 67 (16.7)Haematological 5 (8.1) 75 (18.7)Severe sepsis/shock 6 (9.7) 91 (22.7)Arterial blood pH, mean (SD) 7.40 (0.10) 7.34 (0.14)PCO2, mean (SD) 39.7 (9.5) 44.9 (12.7)PaO2 /FiO2 ratio (day 0), mean (SD) 239 (30) 119 (43)SAPS II on admission, median (IQR) 34 (24–45) 41 (32–52)LOD score at inclusion, mean (SD) 4.9 (2.5) 7.1 (3.5)

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First of all there’s an EPIDEMIOLOGICAL REASON. ARDS is not just a matter of lung but also of circulation. Considering altogether ARDS/ALI patients, roughly 9 ALI/ARDS patients out of 10 show cardiovascular failure on admission, regardless of the aetiology of lung injury.

Secondly, the target of echocardiographic investigation, cardiovascular failure, has a great impact on PROGNOSIS of ARDS pts.Amongst predictive factors of death and prolonged ventilation, the greatest difference in the group of ARDS pts with good and bad outcome is made by a higher oxygenation index and by the presence of shock on day 3.


+

. . . .

. .

. .

. . . . . .

Respiratory 60 (96.8) 382 (95.3)Cardiovascular 24 (38.7) 222 (55.4)Neurological 28 (45.2) 142 (35.4)Renal 41 (66.1) 300 (74.8)Liver 7 (11 3) 67 (16 7)

.,

Mild ALI (n=62)a ARDS (n=401)

. . . . , . .

,

. . . .

ACUTE ORGAN DYSFUNCTION ON ICU ADMISSION, n (%)

Mild ALI (n=62) ARDS (n=401)


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Brun-Buissson C, et al. ALIVE Study. INT CARE MED 2003

Liver 7 (11.3) 67 (16.7)Haematological 5 (8.1) 75 (18.7)Severe sepsis/shock 6 (9.7) 91 (22.7)Arterial blood pH, mean (SD) 7.40 (0.10) 7.34 (0.14)PCO2, mean (SD) 39.7 (9.5) 44.9 (12.7)

PaO2 /FiO2 ratio (day 0), mean (SD) 239 (30) 119 (43)SAPS II on admission, median (IQR) 34 (24–45) 41 (32–52)LOD score at inclusion, mean (SD) 4.9 (2.5) 7.1 (3.5)

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PREDICTORS OF DEATH & PROLONGED VENTILATION - N = 330


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2nd International Study of Mech Ventilation and ARDS-net Investigators. CRIT CARE 2007



INCREASEDTRANSPULMONARY

PRESSURE

EFFECT OF VENTILATION ON RV


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INCREASED PULMONARY

VASCULAR RESISTANCE

! 12 ,$3-14%,5

That’s why Mech Vent increases RV afterload with a variable magnitude, cyclically shifting from PEEP to Pplat.

This has been very well demonstrated by Prof. Jardin and his group, by Doppler study of pulmonary artery flow. As you can see in this clip from his original work (you can find it as ESM of this publication), each mech inspiration is capable of inducing a reduction of RV ejection.

The fact that this is not merely the consequence of cyclic reduction in venous return to the right section of the heart is well demonstrated by the fact that the size of the RV increases with inspiration (this can be dramatic when RV function is particulary compromised: videoclip)

INCREASEDTRANSPULMONARY

PRESSURE

EFFECT OF VENTILATION ON RV


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INCREASED PULMONARY

VASCULAR RESISTANCE

! 12 ,$3-14%,5

That’s why Mech Vent increases RV afterload with a variable magnitude, cyclically shifting from PEEP to Pplat.

This has been very well demonstrated by Prof. Jardin and his group, by Doppler study of pulmonary artery flow. As you can see in this clip from his original work (you can find it as ESM of this publication), each mech inspiration is capable of inducing a reduction of RV ejection.

The fact that this is not merely the consequence of cyclic reduction in venous return to the right section of the heart is well demonstrated by the fact that the size of the RV increases with inspiration (this can be dramatic when RV function is particulary compromised: videoclip)

ARDS-ASSOCIATED

ACUTE COR PULMONALE

-, PRACTICAL APPLICATIONS


APPLICATION


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• RV DYSFUNCTION:RECOGNITION, SUPPORT





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HEMODYNAMIC SUPPORT

!" # %&'()& * (+,-

-.(/+&/- 0 1-121'3() 4 0&/'103(

DAY 1


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DAY 1

And Echo is here extremely useful in careful titration of volume loading after the first stage of volume resuscitation (note appearance of RV dysfunction with ARDS development in this patient, and loss of volume responsiveness).

Fluid therapy of course must be balanced between treatment of volume responsiveness and overall excess of fluid administration, as we all know that fluid accumulation is strictly correlated to outcome of ARDS patients.

Accurate and prompt recognition of a shift to absence of volume responsiveness, such as in this patient, thus avoids potentially harmful administration of fluids.


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HEMODYNAMIC SUPPORT

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DAY 1 DAY 3PEEP 14,


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PEEP 14,

Vt 430,

Pplat 30

DAY 1 DAY 3

And Echo is here extremely useful in careful titration of volume loading after the first stage of volume resuscitation (note appearance of RV dysfunction with ARDS development in this patient, and loss of volume responsiveness).

Fluid therapy of course must be balanced between treatment of volume responsiveness and overall excess of fluid administration, as we all know that fluid accumulation is strictly correlated to outcome of ARDS patients.

Accurate and prompt recognition of a shift to absence of volume responsiveness, such as in this patient, thus avoids potentially harmful administration of fluids.

RV DYSFUNCTION IN ARDS

N = 352 ARDS patient (1980-2006), 101 ACP cases%


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Jardin F, Vieillard-Baron A. INT CARE MED 2007

Pplat (cmH2O)

RV dysfunction (indicated as Acute Cor Pulmonale) is not rare in ARDS. This case series describes a very high prevalence in the period of “aggressive ventilation” (up to the 90s), and a sharp reduction with the recent lung protective strategies.

ARDS pts. with ACP still have higher mortality. Less severe RV dysfunction is nowadays more frequent.


N = 352 ARDS patient (1980-2006), 101 ACP cases

P l t ( H2O)

%


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Pplat (cmH2O)





Pplat (cmH2O)

%


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Pplat (cmH2O)

• ! 1/3 ARDS patients develop Acute Core Pulmonale (ACP)





Pplat (cmH2O)

%


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Pplat (cmH2O)


• Highest mortality with ACP





Pplat (cmH2O)

%


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Pplat (cmH2O)


• Highest mortality with ACP

• Less severe ACP with lung protective ventilation



ARDS-ASSOCIATED ACUTE COR PULMONALE

-, PRACTICAL APPLICATIONS • RV DYSFUNCTION:


APPLICATION


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Intensive Care Med (2007) 33:444–447DOI 10.1007/s00134-007-0552-z O R I G I N A L

François JardinAntoine Vieillard-Baron

Is there a safe plateau pressure in ARDS?

The right heart only knows

PROTECT THE RV IN ARDS!!


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;;

;

:

;;

;

:

Pplat (cmH2O)

%N = 352 ARDS patient(1980-2006),

101 ACP cases

ACP 13%for Pplat < 27 cmH2O

These are the same data shown about epidemiology of ACP in ARDS: they clearly indicate that an overall ventilatory strategy based on low plateau pressures markedly reduces the incidence of ACP. Low plateau pressures (even smaller than those indicated by recent international guidelines) are thus advocated.







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;;

;

:

;;

;

:

Pplat (cmH2O)

%N = 352 ARDS patient(1980-2006),

101 ACP cases



4"6"3 31,#(7'46%#,18 71-(('1-( /79:;< = >?&@.>%0







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;;

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Pplat (cmH2O)

%N = 352 ARDS patient(1980-2006),

101 ACP cases



ALVEOLAR RECRUITMENT

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BASAL

Open Access

.

Vol 13 No 2

ResearchRespiratory and haemodynamic changes during decrementalopen lung positive end-expiratory pressure titration in patients

with acute respiratory distress syndromeChristianGernoth1, Gerhard Wagner2, PaoloPelosi3 and ThomasLuecke1

. .

. . . .

CRIT CARE 2009



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;

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BASAL FINAL PEEPRECRUITMENT

[

[ :

[

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.

;.

FINAL PEEP

RECRUITMENT

.

. . .

. ..

.

Another issue is to check the state of RV function before performing aggressive alveolar recruitment maneuvers . Optimize volume status, and in patients with ACP vasoactive support may need to be temporarily increased before the maneuver + more gentle recruitment may be the best choice (i.e., insteadof prolonged end-inspiratory occlusion at 40-45 cmH2O, PEEP set at 20 cmH2O and incremental support for a couple o minutes, for example)

(In this study, recruitment was per formed at pressure-controlled ventilation with fixed PEEP at 20 cmH2O and increased driving pressures at 20, 25 and 30 cmH2O for two minutes each. PEEP was then titrated downward (PEEP lowered by 2 cmH2O every two minutes, with tidal volume set at 6 ml/kg). The openlung PEEP (FINAL PEEP) was defined as the PEEP level yielding maximum dynamic respiratory compliance plus 2 cmH2O). TEE monitoring shows a significant RV dilatation and displacement of the IVS towards the LV.

ALVEOLAR RECRUITMENT

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Vol 13 No 2

ResearchRespiratory and haemodynamic changes during decrementalopen lung positive end-expiratory pressure titration in patients

with acute respiratory distress syndromeChristianGernoth1, Gerhard Wagner2, PaoloPelosi3 and ThomasLuecke1

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CRIT CARE 2009

PROTECT THE RV IN ARDS?


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BASAL FINAL PEEPRECRUITMENT

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FINAL PEEP

RECRUITMENT

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Another issue is to check the state of RV function before performing aggressive alveolar recruitment maneuvers . Optimize volume status, and in patients with ACP vasoactive support may need to be temporarily increased before the maneuver + more gentle recruitment may be the best choice (i.e., insteadof prolonged end-inspiratory occlusion at 40-45 cmH2O, PEEP set at 20 cmH2O and incremental support for a couple o minutes, for example)

(In this study, recruitment was per formed at pressure-controlled ventilation with fixed PEEP at 20 cmH2O and increased driving pressures at 20, 25 and 30 cmH2O for two minutes each. PEEP was then titrated downward (PEEP lowered by 2 cmH2O every two minutes, with tidal volume set at 6 ml/kg). The openlung PEEP (FINAL PEEP) was defined as the PEEP level yielding maximum dynamic respiratory compliance plus 2 cmH2O). TEE monitoring shows a significant RV dilatation and displacement of the IVS towards the LV.


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DIFFERENT APPROACH


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OUTCOME


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OUTCOME


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OUTCOME


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PROTECT THERV IN ARDS


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APPLICATION


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CARDIOGENIC SHOCK


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CARDIOGENIC SHOCK


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VENTILATORY STRATEGY


APPLICATION


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CONCLUSIONS

• Heart-lung interaction in ARDS is very complex

• Echocardiography can help diagnose ACP in ARDS

• If diagnosis of ACP is made, consider- Pulmonary vasodilators

- Inotropic support (dobutamine, milrinone,

epinephrine)


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epinephrine)- Optimize fluid status if possible

- Prone position (unloads RV)

- Limit Pplat, lower tidal volume

- Avoid hypercapnia, acidosis

- More careful recruitment maneuver

CONCLUSIONS

• Echo can help- Discriminate between cardiogenic and ARDS

- Diagnose intracardiac shunts (hypoxia)


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THANK

YOU!


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YOU!

57 Y.O. M POD # 1 FROM RETROPERITONEALHEMATOMA EVACUATION


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57 Y.O. M POD # 1 FROM RETROPERITONEALHEMATOMA EVACUATION


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9F 2014 Utah Acute Cor Pulmonale Grinberg

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