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© WINFOCUS’ CRITICAL CARE ECHOCARDIOGRAPHY ACUTE COR PULMONALE: PULMONARY EMBOLISM AND ARDS Achikam Oren-Grinberg, MD, MS Assistant Professor in Anaesthesia Harvard Medical School Director of Critical Care Echocardiography Department of Anesthesia Critical Care and Pain Medicine Beth Israel Deaconess Medical Center Boston WINFOCUS’ BASIC ECHO (WBE)

ACUTE COR PULMONALE PULMONARY …€™**CRITICAL CARE ECHOCARDIOGRAPHY ACUTE COR PULMONALE: PULMONARY EMBOLISM AND ARDS Achikam Oren-Grinberg, MD, MS Assistant Professor in Anaesthesia

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© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

ACUTE COR PULMONALE: PULMONARY EMBOLISM AND

ARDSAchikam Oren-Grinberg, MD, MS

Assistant Professor in Anaesthesia Harvard Medical School

Director of Critical Care Echocardiography Department of Anesthesia

Critical Care and Pain Medicine Beth Israel Deaconess Medical Center

Boston

WINFOCUS’  BASIC  ECHO  (WBE)

!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!

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

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

blood flow in the pulmonary circulation, characterized by

augmented RV outflow impedance, RV ejection 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).

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!

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

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

blood flow in the pulmonary circulation, characterized by

augmented RV outflow impedance, RV ejection impairment, and RV size

enlargement.”

ACUTE COR PULMONALE

Pulmonary embolism

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).

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!

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

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

blood flow in the pulmonary circulation, characterized by

augmented RV outflow impedance, RV ejection impairment, and RV size

enlargement.”

ACUTE COR PULMONALE

Pulmonary embolism

ARDS

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).

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!GOALS

• To understand the role of echocardiography in the diagnosis of acute Cor Pulmonale due to - Pulmonary embolism - ARDS

• To understand the limitations of echocardiography in these settings

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!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)

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!

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

RV

LVVentricular P-V Loops:

Physiology

1. PV opening3. PV

closure

2. Relaxation Onset

ACP: PATHOPHYSIOLOGY

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).

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!ACP: PATHOPHYSIOLOGY

LVVentricular P-V Loops:

ACP

RV

1. PV opening3. PV

closure

2. Relaxation Onset

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 pressure decline. (for simplicity, the LV here is still represented as normal, as it was not 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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!ACP: PATHOPHYSIOLOGY

Piazza G.Goldhaber Z. CIRCULATION 2006;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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!ACUTE PE – DIAGNOSIS

The tool for PE diagnosis !

Multidetector CT

Echo is not the specific tool to diagnose pulmonary embolism, or at least it is rarely the tool....Multi-Slice Angio-CT is !!!In patients with a lowor intermediate clinical probability of PE as assessed by the Wells score, a negative CT had a high NPV for PE (96 and 89%, respectively),!whereas it was only 60% in those with a high pretest probability. Conversely, the PPV of a positive CT was high (92–96%) in patients with an intermediate or high clinical probability but much lower (58%) in patients with a low pretest likelihood of PE.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!PULMONARY EMBOLISM DIAGNOSIS

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!PULMONARY EMBOLISM DIAGNOSIS

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!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 undergo 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 to understand...)

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!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-scan !2) 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 bit 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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!ECHO FINDINGS IN PE

DIRECT VISUALIZATION OF EMBOLI

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-scan !2) 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 bit 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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!PE: DIRECT EVIDENCE

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!PE: DIRECT EVIDENCE

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!PE: DIRECT EVIDENCE

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!PE: DIRECT EVIDENCE

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

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

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

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

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!ECHO FINDINGS IN PE

DIRECT VISUALIZATION OF EMBOLI

2-D & DOPPLER SIGNS OF RV ACUTE OVERLOAD

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-scan !2) 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 bit 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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!ECHO FINDINGS IN PE

DIRECT VISUALIZATION OF EMBOLI

2-D & DOPPLER SIGNS OF RV ACUTE OVERLOAD

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-scan !2) 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 bit 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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!ACP: ECHO EVIDENCE

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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!ACP: ECHO EVIDENCE

1. RV DILATATION

2. RV DYSFUNCTION

3. SEPTAL DYSKINESIA

4. INCREASED RV AFTERLOAD (Doppler evidence)

RV strain

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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!ACP: ECHO EVIDENCE

1. RV DILATATION

2. RV DYSFUNCTION

3. SEPTAL DYSKINESIA

4. INCREASED RV AFTERLOAD (Doppler evidence)

RV strainPressure overload

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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!ACP: ECHO EVIDENCE

1. RV DILATATION

2. RV DYSFUNCTION

3. SEPTAL DYSKINESIA

4. INCREASED RV AFTERLOAD (Doppler evidence)

RV strainPressure overload

Help differentiate acute from chronic

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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!

2D EVIDENCE OF

COR PULMONALE

!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!ACP: ECHO EVIDENCE

Moderate: RVEDA/LVEDA 0.6-1.0

Severe: RVEDA / LVEDA > 1.0

1 RV DILATATIONNormal: RVEDA/LVEDA <0.6

Measurement: End diastole

!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!ACP: ECHO EVIDENCE

Moderate: RVEDA/LVEDA 0.6-1.0

Severe: RVEDA / LVEDA > 1.0

Jardin F. CHEST 1997;111:209–217

1 RV DILATATIONNormal: RVEDA/LVEDA <0.6

Measurement: End diastole

!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!ABSOLUTE RV SIZE

Reference range Mildly abnormal Moderately abnormal

Severely abnormal

Basal RV diameter (RVD 1), cm 2.0-2.8 2.9-3.3 3.4-3.8 > 3.9

Mid-RV diameter (RVD 2), cm 2.7-3.3 3.4-3.7 3.8-4.1 > 4.2

Base-to-apex length (RVD 3), cm 7.1-7.9 8.0-8.5 8.6-9.1 > 9.2 JA

SE 2

005;

18(1

2):1

440-

1463

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!ACP: ECHO EVIDENCE

12

2. RV DYSFUNCTION

!

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

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!ACP: ECHO EVIDENCE

12

2. RV DYSFUNCTION

!

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

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!ACP: ECHO EVIDENCE

3. SEPTAL DYSKINESIA

!

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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!ACP: ECHO EVIDENCE

3. SEPTAL DYSKINESIA

!

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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!PRESSURE OR VOLUME OVERLOAD?

!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!PRESSURE OR VOLUME OVERLOAD?

!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!PRESSURE OR VOLUME OVERLOAD?

!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!PRESSURE OR VOLUME OVERLOAD?

!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!PRESSURE OR VOLUME OVERLOAD?

!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!PRESSURE OR VOLUME OVERLOAD?

!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!McConnell Sign

!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!

Am J Cardiol 1996;78:468-473

McConnell Sign!

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!McConnell Sign

!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!McConnell Sign

!

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!

Sensitivity 77%

Specificity 94%

PPV 71%

NPP 96%

McConnell Sign!

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!!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!!

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!

Eur J Echocardiography 2005;6:11-14

!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!

Eur J Echocardiography 2005;6:11-14

!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!McConnell Sign

!

"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 of our “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.”

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!McConnell Sign

!

This finding should raise the level of clinical suspicion for the diagnosis of

acute pulmonary embolism

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!

DOPPLER EVIDENCE

(Doppler in PE 101)

!

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!RV OUTFLOW SYSTOLIC PATTERN

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!RV OUTFLOW SYSTOLIC PATTERN

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!RV OUTFLOW SYSTOLIC PATTERN

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!

INCREASED RV AFTERLOAD (Doppler on PA flow)

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

RVOT OUTFLOW PATTERN

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!

INCREASED RV AFTERLOAD (Doppler on PA flow)

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

ACP Normal

RVOT OUTFLOW PATTERN

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!

INCREASED RV AFTERLOAD (Doppler on PA flow)

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

ACP Normal

PA Acc Time

RVOT OUTFLOW PATTERN

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!

INCREASED RV AFTERLOAD (Doppler on PA flow)

Midsystolic deceleration

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

ACP Normal

RVOT OUTFLOW PATTERN

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!

INCREASED RV AFTERLOAD (Doppler on PA flow)

Midsystolic deceleration

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

ACP

M-Mode on PulmValve

RVOT OUTFLOW PATTERN

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!

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

Clinical Commentary 1313

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

Normal Volunteers ACP Complicating ARDS ACP Complicating MPE(n ! 24) (n ! 19) (n ! 18)

PAVTI, 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*

Definition of abbreviations: ACP ! acute cor pulmonale; ACT ! acceleration time; ARDS ! acute respiratory distress syndrome;FP ! flow period; MPE ! massive pulmonary embolism; PAVTI ! pulmonary artery velocity–time integral; peak velocity ! peakvelocity of pulmonary artery blood flow.

* p # 0.05, compared with normal volunteers.

acute respiratory distress syndrome and exhibiting acute cor By analogy with the left side, it is attractive to evaluate rightpulmonale, with an average value of 6.5 " 1.5 mm (mean " ventricular systolic function by measuring the fractional areaSD) (Figure 7). This finding suggests that, like other mammals, contraction in a long-axis view, which is easily obtained fromhumans may rapidly increase their right ventricular muscular an apical or a transesophageal approach. Right ventricular frac-mass in response to pressure overload. Katamaya and coworkers tional area contraction is calculated as right ventricular end-(11) inserted a balloon into the pulmonary artery of lambs, and diastolic area minus right ventricular end-systolic area, dividedthey inflated the balloon for 2 hours twice daily. After 4 days by right ventricular end-diastolic area. However, the large rangeof this procedure (i.e., a total of 16 hours of intermittent right of normal values (40 to 74% in our laboratory [13], 30 to 60%ventricular afterloading), they observed a significant increase in in Weyman’s laboratory [14]), and the lack of correlation withthe myocardial mass of the right ventricle. In patients with acute pulmonary artery systolic pressure or angiographic obstructionrespiratory distress syndrome, 48 hours of mechanical ventilation index in pathologic conditions (15, 16), make the fractional areawith an inspiratory/expiratory ratio of 1/2 also produce 16 hours contraction of little value in clinical practice.of intermittent right ventricular afterloading.

Severe right ventricular pressure overload causes a drop in ECHO–DOPPLER DEMONSTRATION OF RIGHTcardiac stroke output, which may be measured by both aortic VENTRICULAR DIASTOLIC OVERLOAD: RIGHTand pulmonary artery velocity–time integral. Whereas the nor- VENTRICULAR ENLARGEMENTmal value of pulmonary artery velocity–time integral by pulsed

A normal right ventricle has an end-diastolic volume similar toDoppler in a group of 24 normal volunteers was found to bethat of the left ventricle (17, 18). Because of its regular shape, left18 " 3 cm (mean " SD) (12), we found markedly reduced valuesventricular volume can easily be measured by two-dimensionalin acute cor pulmonale complicating both acute respiratory dis-

tress syndrome and massive pulmonary embolism (Table 2). echocardiography, even with a monoplane formula (19), and a

Figure 5. Continuous (A ) or pulsed (B )Doppler examination of pulmonary arteryflow at the level of the RV outflow tract.(A ) Acute cor pulmonale complicatingmassive pulmonary embolism; (B ) acutecor pulmonale complicating acute respi-ratory distress syndrome. Both patientshad a low cardiac output requiring vaso-active support. Note the premature peakvelocity with a reduced maximal velocity(0.5 to 0.7 m/second in [A], 0.4 m/secondin [B]) and the biphasic pattern of theDoppler profile (arrows).

Acc Time < 80 ms

INCREASED RV AFTERLOAD (Doppler on PA flow)

RVOT OUTFLOW PATTERN

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

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!CHRONIC PHT

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!DOPPLER TR JET

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.

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!DOPPLER TR JET

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.

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!DOPPLER TR JET

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.

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!RV OUTFLOW SYSTOLIC PATTERN

• Acute PE • Chronic PE • COPD • Primary pulmonary hypertension

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!

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IPH C4 BE6c5?i5 TB C^4

TRICUSPID REGURGITATION

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!THE “60/60” SIGN

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!

Specificity 98%Sensitivity 48%

Acute PE Acceleration time: < 60 ms

TVPG < 60 mmHg

THE “60/60” SIGN

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!HOW TO....

Parasternal short axis view

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!HOW TO....

Parasternal short axis view

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!HOW TO....

Parasternal short axis view

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!HOW TO....

Parasternal short axis view

Time 81 ms

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!HOW TO....

TV peak gradient

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!HOW TO....

TV peak gradient

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!HOW TO....

TV peak gradient

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!CLINICALLY

• High suspicion for acute PE - Hemodynamic collapse

• Unable to obtain CT

• Look for - Direct evidence of clot - Signs of RV strain - Sign of RV pressure overload - McConnell’s sign

• 60/60 sign

• Treatment...?

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!CLINICALLY

• High suspicion for acute PE - Hemodynamic collapse

• Unable to obtain CT

• Look for - Direct evidence of clot - Signs of RV strain - Sign of RV pressure overload - McConnell’s sign

• 60/60 sign

• Treatment...?

Indirect signs

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!TAKE HOME MESSAGE

ECHO IN PE1. Detection of emboli = Diagnosis of PE

Detection of ACP = presumptive diagnosis of massive PE !2. In High-risk PE (shock/hypotension): absence of echo

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

!3. In Non-high-risk PE (stable pts), a negative Echo

cannot exclude PE !4. A combination of 2-D and Doppler indirect signs is

advocated !5. 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.

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!ARDS-ASSOCIATED ACUTE COR PULMONALE

!

2. PRACTICAL APPLICATIONS • RV DYSFUNCTION:

RECOGNITION, SUPPORT

• VENTILATORY STRATEGY

• DIFFERENTIAL DIAGNOSIS ARDS vs. CARDIOGENIC

• INTRACARDIAC SHUNT DETECTION

1. WHY ECHO IN ARDS? RATIONALE FOR APPLICATION

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!ARDS-ASSOCIATED ACUTE COR PULMONALE

!

2. PRACTICAL APPLICATIONS • RV DYSFUNCTION:

RECOGNITION, SUPPORT

• VENTILATORY STRATEGY

• DIFFERENTIAL DIAGNOSIS ARDS vs. CARDIOGENIC

• INTRACARDIAC SHUNT DETECTION

1. WHY ECHO IN ARDS? RATIONALE FOR APPLICATION

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!CARDIOVASCULAR FAILURE IN ARDS

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

55

Table 2 Comparison of pa-tients with mild ALI or withARDS. Admission characteris-tics and underlying conditions,acute organ failures and out-come

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

Age (years) mean (SD) 49.9 (19.9) 55.4 (18.0)Male sex, n (%) 46 (74.2) 249 (62.1)

Admission category, n (%)

Surgical 29 (46.7) 134 (33.4)Medical 33 (53.2) 266 (66.3)Trauma, n (%) 18 (29.0) 84 (20.9)

Chest trauma 12 (19.4) 61 (15.2)

Chronic organ failure, n (%)

None 50 (80.6) 310 (77.3)One or more 12 (19.4) 91 (22.7)Immuno-incompetence 10 (16.1) 81 (20.2)

Aetiology of lung injury, n (%)b

Direct 42 (67.7) 219 (54.6)Indirect 9 (14.5) 82 (20.4)Mixed 9 (14.5) 86 (21.4)Unknown 2 (3.2) 14 (3.5)Pneumonia 25 (40.3) 186 (46.4)Inhalation 14 (22.6) 62 (15.5)Lung contusion 11 (17.7) 42 (10.5)Severe sepsis/shock 7 (11.3) 102 (25.4)Multiple blood transfusion 6 (9.7) 20 (5.0)

Acute organ dysfunction on ICU admission, n (%)

Number/type of organ dysfunction

0 1 (1.6) 7 (1.7)1 9 (14.5) 22 (5.5)

�2 52 (83.9) 372 (92.8)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)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)

Length of stay, mean (SD)

ICU 16.5 (19.1) 16.3 (15.2)Hospital 25.2 (19.6) 25.8 (28.7)

Mortality rate, n (%)

ICUc 14 (22.6) 196 (49.4)Hospitald 18 (32.7) 216 (57.9)

ICU intensive care unit, ALIacute lung injury, ARDS acuterespiratory distress syndrome,PCO2 partial pressure of car-bon dioxide, PaO2 /FiO2 ratioratio between arterial oxygentension and inspired oxygentension, SAPS II SimplifiedAcute Physiology Score II,LOD logistic organ dysfunctiona Mild ALI is defined as aPaO2/FiO2 ratio between 200and 300b The total amounts to morethan the number of cases, assome patients had multiplecauses recorded; Otheraetiologies were also reported,each representing less than 5%of recorded causes. They in-cluded: acute pancreatitis, near-drowning, non-thoracic trauma,burns, non-septic shock anddrug poisoningc 4 patients with ARDS werestill in ICU when the studyendedd 7 patients with ALI and 28with ARDS were still in hospi-tal when the study ended

(n=136). Of the latter 136 patients, 74 (54.4%) evolvedto ARDS, and 62 did not; therefore, 74 of 401 (18.4%)patients with ARDS had preceding mild ALI.

Table 1 shows the clinical characteristics of the prin-cipal study population (n=3,511) and of patients withALI/ARDS (n=463) and Table 2 compares patients with

ARDS (n=401) to those with mild ALI (n=62). Patientswith mild ALI had a lower mean age than patients withARDS, a higher proportion of surgical and trauma ad-mission, lower SAPS II and LOD scores, correspondingto a lower frequency of acute organ dysfunction. Theirmean PaO2/FiO2 ratio was 239±30 mmHg, compared

55

Table 2 Comparison of pa-tients with mild ALI or withARDS. Admission characteris-tics and underlying conditions,acute organ failures and out-come

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

Age (years) mean (SD) 49.9 (19.9) 55.4 (18.0)Male sex, n (%) 46 (74.2) 249 (62.1)

Admission category, n (%)

Surgical 29 (46.7) 134 (33.4)Medical 33 (53.2) 266 (66.3)Trauma, n (%) 18 (29.0) 84 (20.9)

Chest trauma 12 (19.4) 61 (15.2)

Chronic organ failure, n (%)

None 50 (80.6) 310 (77.3)One or more 12 (19.4) 91 (22.7)Immuno-incompetence 10 (16.1) 81 (20.2)

Aetiology of lung injury, n (%)b

Direct 42 (67.7) 219 (54.6)Indirect 9 (14.5) 82 (20.4)Mixed 9 (14.5) 86 (21.4)Unknown 2 (3.2) 14 (3.5)Pneumonia 25 (40.3) 186 (46.4)Inhalation 14 (22.6) 62 (15.5)Lung contusion 11 (17.7) 42 (10.5)Severe sepsis/shock 7 (11.3) 102 (25.4)Multiple blood transfusion 6 (9.7) 20 (5.0)

Acute organ dysfunction on ICU admission, n (%)

Number/type of organ dysfunction

0 1 (1.6) 7 (1.7)1 9 (14.5) 22 (5.5)

�2 52 (83.9) 372 (92.8)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)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)

Length of stay, mean (SD)

ICU 16.5 (19.1) 16.3 (15.2)Hospital 25.2 (19.6) 25.8 (28.7)

Mortality rate, n (%)

ICUc 14 (22.6) 196 (49.4)Hospitald 18 (32.7) 216 (57.9)

ICU intensive care unit, ALIacute lung injury, ARDS acuterespiratory distress syndrome,PCO2 partial pressure of car-bon dioxide, PaO2 /FiO2 ratioratio between arterial oxygentension and inspired oxygentension, SAPS II SimplifiedAcute Physiology Score II,LOD logistic organ dysfunctiona Mild ALI is defined as aPaO2/FiO2 ratio between 200and 300b The total amounts to morethan the number of cases, assome patients had multiplecauses recorded; Otheraetiologies were also reported,each representing less than 5%of recorded causes. They in-cluded: acute pancreatitis, near-drowning, non-thoracic trauma,burns, non-septic shock anddrug poisoningc 4 patients with ARDS werestill in ICU when the studyendedd 7 patients with ALI and 28with ARDS were still in hospi-tal when the study ended

(n=136). Of the latter 136 patients, 74 (54.4%) evolvedto ARDS, and 62 did not; therefore, 74 of 401 (18.4%)patients with ARDS had preceding mild ALI.

Table 1 shows the clinical characteristics of the prin-cipal study population (n=3,511) and of patients withALI/ARDS (n=463) and Table 2 compares patients with

ARDS (n=401) to those with mild ALI (n=62). Patientswith mild ALI had a lower mean age than patients withARDS, a higher proportion of surgical and trauma ad-mission, lower SAPS II and LOD scores, correspondingto a lower frequency of acute organ dysfunction. Theirmean PaO2/FiO2 ratio was 239±30 mmHg, compared

ACUTE ORGAN DYSFUNCTION ON ICU ADMISSION, n (%)

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

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.!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!CARDIOVASCULAR FAILURE IN ARDS

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

+

55

Table 2 Comparison of pa-tients with mild ALI or withARDS. Admission characteris-tics and underlying conditions,acute organ failures and out-come

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

Age (years) mean (SD) 49.9 (19.9) 55.4 (18.0)Male sex, n (%) 46 (74.2) 249 (62.1)

Admission category, n (%)

Surgical 29 (46.7) 134 (33.4)Medical 33 (53.2) 266 (66.3)Trauma, n (%) 18 (29.0) 84 (20.9)

Chest trauma 12 (19.4) 61 (15.2)

Chronic organ failure, n (%)

None 50 (80.6) 310 (77.3)One or more 12 (19.4) 91 (22.7)Immuno-incompetence 10 (16.1) 81 (20.2)

Aetiology of lung injury, n (%)b

Direct 42 (67.7) 219 (54.6)Indirect 9 (14.5) 82 (20.4)Mixed 9 (14.5) 86 (21.4)Unknown 2 (3.2) 14 (3.5)Pneumonia 25 (40.3) 186 (46.4)Inhalation 14 (22.6) 62 (15.5)Lung contusion 11 (17.7) 42 (10.5)Severe sepsis/shock 7 (11.3) 102 (25.4)Multiple blood transfusion 6 (9.7) 20 (5.0)

Acute organ dysfunction on ICU admission, n (%)

Number/type of organ dysfunction

0 1 (1.6) 7 (1.7)1 9 (14.5) 22 (5.5)

�2 52 (83.9) 372 (92.8)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)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)

Length of stay, mean (SD)

ICU 16.5 (19.1) 16.3 (15.2)Hospital 25.2 (19.6) 25.8 (28.7)

Mortality rate, n (%)

ICUc 14 (22.6) 196 (49.4)Hospitald 18 (32.7) 216 (57.9)

ICU intensive care unit, ALIacute lung injury, ARDS acuterespiratory distress syndrome,PCO2 partial pressure of car-bon dioxide, PaO2 /FiO2 ratioratio between arterial oxygentension and inspired oxygentension, SAPS II SimplifiedAcute Physiology Score II,LOD logistic organ dysfunctiona Mild ALI is defined as aPaO2/FiO2 ratio between 200and 300b The total amounts to morethan the number of cases, assome patients had multiplecauses recorded; Otheraetiologies were also reported,each representing less than 5%of recorded causes. They in-cluded: acute pancreatitis, near-drowning, non-thoracic trauma,burns, non-septic shock anddrug poisoningc 4 patients with ARDS werestill in ICU when the studyendedd 7 patients with ALI and 28with ARDS were still in hospi-tal when the study ended

(n=136). Of the latter 136 patients, 74 (54.4%) evolvedto ARDS, and 62 did not; therefore, 74 of 401 (18.4%)patients with ARDS had preceding mild ALI.

Table 1 shows the clinical characteristics of the prin-cipal study population (n=3,511) and of patients withALI/ARDS (n=463) and Table 2 compares patients with

ARDS (n=401) to those with mild ALI (n=62). Patientswith mild ALI had a lower mean age than patients withARDS, a higher proportion of surgical and trauma ad-mission, lower SAPS II and LOD scores, correspondingto a lower frequency of acute organ dysfunction. Theirmean PaO2/FiO2 ratio was 239±30 mmHg, compared

55

Table 2 Comparison of pa-tients with mild ALI or withARDS. Admission characteris-tics and underlying conditions,acute organ failures and out-come

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

Age (years) mean (SD) 49.9 (19.9) 55.4 (18.0)Male sex, n (%) 46 (74.2) 249 (62.1)

Admission category, n (%)

Surgical 29 (46.7) 134 (33.4)Medical 33 (53.2) 266 (66.3)Trauma, n (%) 18 (29.0) 84 (20.9)

Chest trauma 12 (19.4) 61 (15.2)

Chronic organ failure, n (%)

None 50 (80.6) 310 (77.3)One or more 12 (19.4) 91 (22.7)Immuno-incompetence 10 (16.1) 81 (20.2)

Aetiology of lung injury, n (%)b

Direct 42 (67.7) 219 (54.6)Indirect 9 (14.5) 82 (20.4)Mixed 9 (14.5) 86 (21.4)Unknown 2 (3.2) 14 (3.5)Pneumonia 25 (40.3) 186 (46.4)Inhalation 14 (22.6) 62 (15.5)Lung contusion 11 (17.7) 42 (10.5)Severe sepsis/shock 7 (11.3) 102 (25.4)Multiple blood transfusion 6 (9.7) 20 (5.0)

Acute organ dysfunction on ICU admission, n (%)

Number/type of organ dysfunction

0 1 (1.6) 7 (1.7)1 9 (14.5) 22 (5.5)

�2 52 (83.9) 372 (92.8)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)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)

Length of stay, mean (SD)

ICU 16.5 (19.1) 16.3 (15.2)Hospital 25.2 (19.6) 25.8 (28.7)

Mortality rate, n (%)

ICUc 14 (22.6) 196 (49.4)Hospitald 18 (32.7) 216 (57.9)

ICU intensive care unit, ALIacute lung injury, ARDS acuterespiratory distress syndrome,PCO2 partial pressure of car-bon dioxide, PaO2 /FiO2 ratioratio between arterial oxygentension and inspired oxygentension, SAPS II SimplifiedAcute Physiology Score II,LOD logistic organ dysfunctiona Mild ALI is defined as aPaO2/FiO2 ratio between 200and 300b The total amounts to morethan the number of cases, assome patients had multiplecauses recorded; Otheraetiologies were also reported,each representing less than 5%of recorded causes. They in-cluded: acute pancreatitis, near-drowning, non-thoracic trauma,burns, non-septic shock anddrug poisoningc 4 patients with ARDS werestill in ICU when the studyendedd 7 patients with ALI and 28with ARDS were still in hospi-tal when the study ended

(n=136). Of the latter 136 patients, 74 (54.4%) evolvedto ARDS, and 62 did not; therefore, 74 of 401 (18.4%)patients with ARDS had preceding mild ALI.

Table 1 shows the clinical characteristics of the prin-cipal study population (n=3,511) and of patients withALI/ARDS (n=463) and Table 2 compares patients with

ARDS (n=401) to those with mild ALI (n=62). Patientswith mild ALI had a lower mean age than patients withARDS, a higher proportion of surgical and trauma ad-mission, lower SAPS II and LOD scores, correspondingto a lower frequency of acute organ dysfunction. Theirmean PaO2/FiO2 ratio was 239±30 mmHg, compared

ACUTE ORGAN DYSFUNCTION ON ICU ADMISSION, n (%)

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

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.!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!CARDIOVASCULAR FAILURE IN ARDS

PREDICTORS OF DEATH & PROLONGED VENTILATION - N = 330

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

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.!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!CARDIOVASCULAR FAILURE IN ARDS

PREDICTORS OF DEATH & PROLONGED VENTILATION - N = 330

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

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.!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!

INCREASED TRANSPULMONARY

PRESSURE

INCREASED PULMONARY VASCULAR RESISTANCE

é  RV  AFTERLOAD

EFFECT OF VENTILATION ON RV

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)

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!

INCREASED TRANSPULMONARY

PRESSURE

INCREASED PULMONARY VASCULAR RESISTANCE

é  RV  AFTERLOAD

EFFECT OF VENTILATION ON RV

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)

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!ARDS-ASSOCIATED ACUTE COR PULMONALE

!

2. PRACTICAL APPLICATIONS • RV DYSFUNCTION:

RECOGNITION, SUPPORT

• VENTILATORY STRATEGY

• DIFFERENTIAL DIAGNOSIS ARDS vs. CARDIOGENIC

• INTRACARDIAC SHUNT DETECTION

1. WHY ECHO IN ARDS? RATIONALE FOR APPLICATION

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!HEMODYNAMIC SUPPORT

57Y    FEMALE  –      ARDS                                                              S.AUREUS  NOSOCOMIAL  PNEUMONIA

DAY 1

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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!HEMODYNAMIC SUPPORT

57Y    FEMALE  –      ARDS                                                              S.AUREUS  NOSOCOMIAL  PNEUMONIA

DAY 1

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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!HEMODYNAMIC SUPPORT

57Y    FEMALE  –      ARDS                                                              S.AUREUS  NOSOCOMIAL  PNEUMONIA

DAY 1 DAY 3PEEP 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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!HEMODYNAMIC SUPPORT

FLUID  OPTIMIZATION

VASOCONSTRICTOR

INOTROPE  

PULMONARY  VASODILATORS

57Y    FEMALE  –      ARDS                                                              S.AUREUS  NOSOCOMIAL  PNEUMONIA

DAY 1 DAY 3PEEP 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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!RV DYSFUNCTION IN ARDS

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

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

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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!RV DYSFUNCTION IN ARDS

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

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

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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!RV DYSFUNCTION IN ARDS

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

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

Pplat (cmH2O)

%

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

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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!RV DYSFUNCTION IN ARDS

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

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

Pplat (cmH2O)

%

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

• Highest mortality with ACP

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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!RV DYSFUNCTION IN ARDS

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

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

Pplat (cmH2O)

%

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

• Highest mortality with ACP

• Less severe ACP with lung protective ventilation

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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!ARDS-ASSOCIATED ACUTE COR PULMONALE

!

2. PRACTICAL APPLICATIONS • RV DYSFUNCTION:

RECOGNITION, SUPPORT

• VENTILATORY STRATEGY

• DIFFERENTIAL DIAGNOSIS ARDS vs. CARDIOGENIC

• INTRACARDIAC SHUNT DETECTION

1. WHY ECHO IN ARDS? RATIONALE FOR APPLICATION

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!

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

Received: 25 December 2006Accepted: 22 January 2007Published online: 1 February 2007© Springer-Verlag 2007

F. Jardin (✉) · A. Vieillard-BaronUniversity Hospital Ambroise Paré,Assistance Publique Hôpitaux de Paris,Medical Intensive Care Unit,9 avenue Charles de Gaulle,92104 Boulogne Cedex, Francee-mail: [email protected].: +33-1-49095604Fax: +33-1-49095892

Abstract Objective: Airway pressurelimitation is now a largely acceptedstrategy in adult respiratory distresssyndrome (ARDS) patients; however,some debate persists about the exactlevel of plateau pressure which canbe safely used. The objective of thepresent study was to examine if theechocardiographic evaluation of rightventricular function performed inARDS may help to answer to thisquestion. Design and patients: Formore than 20 years, we have reg-ularly monitored right ventricularfunction by echocardiography inARDS patients, during two differentperiods, a first (1980–1992) whereairway pressure was not limited, anda second (1993–2006) where airwaypressure was limited. By pooling ourdata, we can observe the effect ofa large range of plateau pressure uponmortality rate and incidence of acutecor pulmonale. Results: In this

whole group of 352 ARDS patients,mortality rate and incidence of corpulmonale were 80 and 56%, respec-tively, when plateau pressure was> 35 cmH2O; 42 and 32%, respec-tively, when plateau pressure wasbetween 27 and 35 cmH2O; and 30and 13%, respectively, when plateaupressure was < 27 cmH2O. Moreover,a clear interaction between plateaupressure and cor pulmonale wasevidenced: whereas the odd ratio ofdying for an increase in plateau pres-sure from 18–26 to 27–35 cm H2O inpatients without cor pulmonale was1.05 (p = 0.635), it was 3.32 in pa-tients with cor pulmonale (p < 0.034).Conclusion: We hypothesize thatmonitoring of right ventricular func-tion by echocardiography at bedsidemight help to control the safety ofplateau pressure used in ARDS.

Keywords ARDS · plateau pressure

Introduction

In 1970 Mead et al. emphasized the importance of uniformexpansion of air space as a protection against disten-sion, which is related to transpulmonary pressure [1].In mechanically ventilated patients, alveolar pressure isthe main determinant of transpulmonary pressure. Whenrecorded during a period of no flow, tracheal pressure ina mechanically ventilated patient can be used to measurealveolar pressure. Since 1975 experimental studies havefocused on the deleterious effects of mechanical venti-lation, such as pulmonary edema, and in 1985 Dreyfusset al. experimentally demonstrated in rats that high

inflation pressure, at a peak airway pressure currentlyused by clinicians in ARDS patients, may greatly altermicrovascular permeability [2, 3]. Despite these experi-mental evidence, airway pressure limitation was proposedas a respiratory strategy in adult respiratory distresssyndrome (ARDS) patients only in 1990 [4]. Whenused above functional residual capacity, application ofa positive pressure to the airways increases pulmonaryvascular resistance [5] and decreases pulmonary bloodflow [6], and these adverse effects can be considered asthe result of airway distension, because pulmonary cap-illaries, as intra-alveolar vessels, are stressed by alveolarpressure [7].

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

Received: 25 December 2006Accepted: 22 January 2007Published online: 1 February 2007© Springer-Verlag 2007

F. Jardin (✉) · A. Vieillard-BaronUniversity Hospital Ambroise Paré,Assistance Publique Hôpitaux de Paris,Medical Intensive Care Unit,9 avenue Charles de Gaulle,92104 Boulogne Cedex, Francee-mail: [email protected].: +33-1-49095604Fax: +33-1-49095892

Abstract Objective: Airway pressurelimitation is now a largely acceptedstrategy in adult respiratory distresssyndrome (ARDS) patients; however,some debate persists about the exactlevel of plateau pressure which canbe safely used. The objective of thepresent study was to examine if theechocardiographic evaluation of rightventricular function performed inARDS may help to answer to thisquestion. Design and patients: Formore than 20 years, we have reg-ularly monitored right ventricularfunction by echocardiography inARDS patients, during two differentperiods, a first (1980–1992) whereairway pressure was not limited, anda second (1993–2006) where airwaypressure was limited. By pooling ourdata, we can observe the effect ofa large range of plateau pressure uponmortality rate and incidence of acutecor pulmonale. Results: In this

whole group of 352 ARDS patients,mortality rate and incidence of corpulmonale were 80 and 56%, respec-tively, when plateau pressure was> 35 cmH2O; 42 and 32%, respec-tively, when plateau pressure wasbetween 27 and 35 cmH2O; and 30and 13%, respectively, when plateaupressure was < 27 cmH2O. Moreover,a clear interaction between plateaupressure and cor pulmonale wasevidenced: whereas the odd ratio ofdying for an increase in plateau pres-sure from 18–26 to 27–35 cm H2O inpatients without cor pulmonale was1.05 (p = 0.635), it was 3.32 in pa-tients with cor pulmonale (p < 0.034).Conclusion: We hypothesize thatmonitoring of right ventricular func-tion by echocardiography at bedsidemight help to control the safety ofplateau pressure used in ARDS.

Keywords ARDS · plateau pressure

Introduction

In 1970 Mead et al. emphasized the importance of uniformexpansion of air space as a protection against disten-sion, which is related to transpulmonary pressure [1].In mechanically ventilated patients, alveolar pressure isthe main determinant of transpulmonary pressure. Whenrecorded during a period of no flow, tracheal pressure ina mechanically ventilated patient can be used to measurealveolar pressure. Since 1975 experimental studies havefocused on the deleterious effects of mechanical venti-lation, such as pulmonary edema, and in 1985 Dreyfusset al. experimentally demonstrated in rats that high

inflation pressure, at a peak airway pressure currentlyused by clinicians in ARDS patients, may greatly altermicrovascular permeability [2, 3]. Despite these experi-mental evidence, airway pressure limitation was proposedas a respiratory strategy in adult respiratory distresssyndrome (ARDS) patients only in 1990 [4]. Whenused above functional residual capacity, application ofa positive pressure to the airways increases pulmonaryvascular resistance [5] and decreases pulmonary bloodflow [6], and these adverse effects can be considered asthe result of airway distension, because pulmonary cap-illaries, as intra-alveolar vessels, are stressed by alveolarpressure [7].

446

Also, whereas markedly harmful in patients exhibitingacute cor pulmonale, a plateau pressure between 27 and35 cm H2O appears less harmful in patients with normalechocardiographic findings, since mortality is similar thanfor a plateau pressure range of 18–26 cm H2O. In patientswithout acute cor pulmonale, the OR (95% CI) for anincrease in plateau pressure from 18–26 to 27–35 cm H2Ois 1.15 (range 0.64–2.08; p = 0.635). In patients with acutecor pulmonale, the OR (95% CI) for an increase in plateaupressure from 18–26 to 27–35 cm H2O is 3.32 (range1.09–10.12; p = 0.034), suggesting that the threshold fora safe plateau pressure depends on the presence or not ofacute cor pulmonale.

Finally, a plateau pressure above 35 cm H2O is asso-ciated with a high incidence of ACP and a high mortal-ity rate (Figs. 1, 2). In this group, an additive effect ofplateau pressure and acute cor pulmonale was observed.In patients without acute cor pulmonale, the OR (95% CI)for an increase in plateau pressure from 18–35 to more

Fig. 1 Mortality rate and incidence of acute cor pulmonale (ACP) areplotted against three ranges of plateau pressure (see text). Figures arethe exact number of patients concerned. ∗p < 0.05, when comparedwith the preceding range

Fig. 2 Mortality rate is plotted against three ranges of plateaupressure (see text), after separating patients with normal bedsideechocardiographic findings (normal), and patients exhibiting acutecor pulmonale (ACP) detected by echocardiography. Figures are theexact number of patients concerned. ∗p < 0.05, when compared withthe preceding range

than 35 cm H2O is 4.03 (range 1.94–8.36; p = 0.0002). Inpatients with acute cor pulmonale, the OR (95% CI) foran increase in plateau pressure from 18–35 to more than35 cm H2O is 10.97 (range 3.55–33.85; p < 0.0001).

DiscussionThis study has shown that mortality rate and incidence ofACP markedly increases in ARDS patients above a plateauof 26 cm H2O. With a plateau pressure between 27 and35 cm H2O, the mortality rate is markedly increased by thepresence of ACP.

There are several important limitations to this analysis.By pooling the data of these two periods, we were ableto observe the effect of a large range of plateau pres-sure, firstly upon mortality rate, and secondly upon theincidence of acute cor pulmonale. The value of plateaupressure, however, was not only a result of our therapeuticstrategy since, in both periods, it was also influenced bythe severity of ARDS. This, however, does not invalidateour comparison, especially on the influence of hemody-namic findings in each subgroup. The effect of airwaypressure limitation in the second period would tend toplace more severe patients in the low plateau pressuregroup, and, conversely, the absence of airway pressurelimitation in the first period would tend to place lesssevere patients in the high plateau pressure group. Botheffects would tend to mask the differences. No adjustmentcould be made on general severity since our database doesnot contain consistent information with the same severityscores over all these years.

Acute cor pulmonale is present in a minority of patients(13%) in the case of major airway pressure limitation, andcan probably be mainly attributed to the severity of under-lying lung disease; however, any responsibility of a pos-itive airway pressure, which is not physiological, cannotbe ruled out. In these patients, acute cor pulmonale, whennot worsened by aggressive respiratory support, does notinfluence mortality, as we have previously reported [20].

The current tendency in ARDS management is to re-duce tidal volume to a uniform value of 6 ml/kg predictedbody weight in all patients [21]. This strategy, whichproduced a marked reduction in plateau pressure, hasbeen shown to improve prognosis, when compared withthe traditional tidal volume of 12 ml/kg, used throughoutthe 1970s and 1980s [21]; however, because we totallyagree with Eichacker’s concept that “one size does not fitwith all” [22], we routinely used an alternative approach,which adapts tidal volume to the individual size of the“baby lung,” by adjusting tidal volume based on plateaupressure [23]. Because a direct reflection of this size isgiven by the value of the compliance of the respiratorysystem, monitoring of plateau pressure is fundamental inusing this strategy. An advantage of this approach is thatit allows adaptations to extreme conditions. In patients

Pplat (cmH2O)

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

ACP 13% for Pplat < 27 cmH2O

PROTECT THE RV IN ARDS!!

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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!

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

Received: 25 December 2006Accepted: 22 January 2007Published online: 1 February 2007© Springer-Verlag 2007

F. Jardin (✉) · A. Vieillard-BaronUniversity Hospital Ambroise Paré,Assistance Publique Hôpitaux de Paris,Medical Intensive Care Unit,9 avenue Charles de Gaulle,92104 Boulogne Cedex, Francee-mail: [email protected].: +33-1-49095604Fax: +33-1-49095892

Abstract Objective: Airway pressurelimitation is now a largely acceptedstrategy in adult respiratory distresssyndrome (ARDS) patients; however,some debate persists about the exactlevel of plateau pressure which canbe safely used. The objective of thepresent study was to examine if theechocardiographic evaluation of rightventricular function performed inARDS may help to answer to thisquestion. Design and patients: Formore than 20 years, we have reg-ularly monitored right ventricularfunction by echocardiography inARDS patients, during two differentperiods, a first (1980–1992) whereairway pressure was not limited, anda second (1993–2006) where airwaypressure was limited. By pooling ourdata, we can observe the effect ofa large range of plateau pressure uponmortality rate and incidence of acutecor pulmonale. Results: In this

whole group of 352 ARDS patients,mortality rate and incidence of corpulmonale were 80 and 56%, respec-tively, when plateau pressure was> 35 cmH2O; 42 and 32%, respec-tively, when plateau pressure wasbetween 27 and 35 cmH2O; and 30and 13%, respectively, when plateaupressure was < 27 cmH2O. Moreover,a clear interaction between plateaupressure and cor pulmonale wasevidenced: whereas the odd ratio ofdying for an increase in plateau pres-sure from 18–26 to 27–35 cm H2O inpatients without cor pulmonale was1.05 (p = 0.635), it was 3.32 in pa-tients with cor pulmonale (p < 0.034).Conclusion: We hypothesize thatmonitoring of right ventricular func-tion by echocardiography at bedsidemight help to control the safety ofplateau pressure used in ARDS.

Keywords ARDS · plateau pressure

Introduction

In 1970 Mead et al. emphasized the importance of uniformexpansion of air space as a protection against disten-sion, which is related to transpulmonary pressure [1].In mechanically ventilated patients, alveolar pressure isthe main determinant of transpulmonary pressure. Whenrecorded during a period of no flow, tracheal pressure ina mechanically ventilated patient can be used to measurealveolar pressure. Since 1975 experimental studies havefocused on the deleterious effects of mechanical venti-lation, such as pulmonary edema, and in 1985 Dreyfusset al. experimentally demonstrated in rats that high

inflation pressure, at a peak airway pressure currentlyused by clinicians in ARDS patients, may greatly altermicrovascular permeability [2, 3]. Despite these experi-mental evidence, airway pressure limitation was proposedas a respiratory strategy in adult respiratory distresssyndrome (ARDS) patients only in 1990 [4]. Whenused above functional residual capacity, application ofa positive pressure to the airways increases pulmonaryvascular resistance [5] and decreases pulmonary bloodflow [6], and these adverse effects can be considered asthe result of airway distension, because pulmonary cap-illaries, as intra-alveolar vessels, are stressed by alveolarpressure [7].

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

Received: 25 December 2006Accepted: 22 January 2007Published online: 1 February 2007© Springer-Verlag 2007

F. Jardin (✉) · A. Vieillard-BaronUniversity Hospital Ambroise Paré,Assistance Publique Hôpitaux de Paris,Medical Intensive Care Unit,9 avenue Charles de Gaulle,92104 Boulogne Cedex, Francee-mail: [email protected].: +33-1-49095604Fax: +33-1-49095892

Abstract Objective: Airway pressurelimitation is now a largely acceptedstrategy in adult respiratory distresssyndrome (ARDS) patients; however,some debate persists about the exactlevel of plateau pressure which canbe safely used. The objective of thepresent study was to examine if theechocardiographic evaluation of rightventricular function performed inARDS may help to answer to thisquestion. Design and patients: Formore than 20 years, we have reg-ularly monitored right ventricularfunction by echocardiography inARDS patients, during two differentperiods, a first (1980–1992) whereairway pressure was not limited, anda second (1993–2006) where airwaypressure was limited. By pooling ourdata, we can observe the effect ofa large range of plateau pressure uponmortality rate and incidence of acutecor pulmonale. Results: In this

whole group of 352 ARDS patients,mortality rate and incidence of corpulmonale were 80 and 56%, respec-tively, when plateau pressure was> 35 cmH2O; 42 and 32%, respec-tively, when plateau pressure wasbetween 27 and 35 cmH2O; and 30and 13%, respectively, when plateaupressure was < 27 cmH2O. Moreover,a clear interaction between plateaupressure and cor pulmonale wasevidenced: whereas the odd ratio ofdying for an increase in plateau pres-sure from 18–26 to 27–35 cm H2O inpatients without cor pulmonale was1.05 (p = 0.635), it was 3.32 in pa-tients with cor pulmonale (p < 0.034).Conclusion: We hypothesize thatmonitoring of right ventricular func-tion by echocardiography at bedsidemight help to control the safety ofplateau pressure used in ARDS.

Keywords ARDS · plateau pressure

Introduction

In 1970 Mead et al. emphasized the importance of uniformexpansion of air space as a protection against disten-sion, which is related to transpulmonary pressure [1].In mechanically ventilated patients, alveolar pressure isthe main determinant of transpulmonary pressure. Whenrecorded during a period of no flow, tracheal pressure ina mechanically ventilated patient can be used to measurealveolar pressure. Since 1975 experimental studies havefocused on the deleterious effects of mechanical venti-lation, such as pulmonary edema, and in 1985 Dreyfusset al. experimentally demonstrated in rats that high

inflation pressure, at a peak airway pressure currentlyused by clinicians in ARDS patients, may greatly altermicrovascular permeability [2, 3]. Despite these experi-mental evidence, airway pressure limitation was proposedas a respiratory strategy in adult respiratory distresssyndrome (ARDS) patients only in 1990 [4]. Whenused above functional residual capacity, application ofa positive pressure to the airways increases pulmonaryvascular resistance [5] and decreases pulmonary bloodflow [6], and these adverse effects can be considered asthe result of airway distension, because pulmonary cap-illaries, as intra-alveolar vessels, are stressed by alveolarpressure [7].

446

Also, whereas markedly harmful in patients exhibitingacute cor pulmonale, a plateau pressure between 27 and35 cm H2O appears less harmful in patients with normalechocardiographic findings, since mortality is similar thanfor a plateau pressure range of 18–26 cm H2O. In patientswithout acute cor pulmonale, the OR (95% CI) for anincrease in plateau pressure from 18–26 to 27–35 cm H2Ois 1.15 (range 0.64–2.08; p = 0.635). In patients with acutecor pulmonale, the OR (95% CI) for an increase in plateaupressure from 18–26 to 27–35 cm H2O is 3.32 (range1.09–10.12; p = 0.034), suggesting that the threshold fora safe plateau pressure depends on the presence or not ofacute cor pulmonale.

Finally, a plateau pressure above 35 cm H2O is asso-ciated with a high incidence of ACP and a high mortal-ity rate (Figs. 1, 2). In this group, an additive effect ofplateau pressure and acute cor pulmonale was observed.In patients without acute cor pulmonale, the OR (95% CI)for an increase in plateau pressure from 18–35 to more

Fig. 1 Mortality rate and incidence of acute cor pulmonale (ACP) areplotted against three ranges of plateau pressure (see text). Figures arethe exact number of patients concerned. ∗p < 0.05, when comparedwith the preceding range

Fig. 2 Mortality rate is plotted against three ranges of plateaupressure (see text), after separating patients with normal bedsideechocardiographic findings (normal), and patients exhibiting acutecor pulmonale (ACP) detected by echocardiography. Figures are theexact number of patients concerned. ∗p < 0.05, when compared withthe preceding range

than 35 cm H2O is 4.03 (range 1.94–8.36; p = 0.0002). Inpatients with acute cor pulmonale, the OR (95% CI) foran increase in plateau pressure from 18–35 to more than35 cm H2O is 10.97 (range 3.55–33.85; p < 0.0001).

DiscussionThis study has shown that mortality rate and incidence ofACP markedly increases in ARDS patients above a plateauof 26 cm H2O. With a plateau pressure between 27 and35 cm H2O, the mortality rate is markedly increased by thepresence of ACP.

There are several important limitations to this analysis.By pooling the data of these two periods, we were ableto observe the effect of a large range of plateau pres-sure, firstly upon mortality rate, and secondly upon theincidence of acute cor pulmonale. The value of plateaupressure, however, was not only a result of our therapeuticstrategy since, in both periods, it was also influenced bythe severity of ARDS. This, however, does not invalidateour comparison, especially on the influence of hemody-namic findings in each subgroup. The effect of airwaypressure limitation in the second period would tend toplace more severe patients in the low plateau pressuregroup, and, conversely, the absence of airway pressurelimitation in the first period would tend to place lesssevere patients in the high plateau pressure group. Botheffects would tend to mask the differences. No adjustmentcould be made on general severity since our database doesnot contain consistent information with the same severityscores over all these years.

Acute cor pulmonale is present in a minority of patients(13%) in the case of major airway pressure limitation, andcan probably be mainly attributed to the severity of under-lying lung disease; however, any responsibility of a pos-itive airway pressure, which is not physiological, cannotbe ruled out. In these patients, acute cor pulmonale, whennot worsened by aggressive respiratory support, does notinfluence mortality, as we have previously reported [20].

The current tendency in ARDS management is to re-duce tidal volume to a uniform value of 6 ml/kg predictedbody weight in all patients [21]. This strategy, whichproduced a marked reduction in plateau pressure, hasbeen shown to improve prognosis, when compared withthe traditional tidal volume of 12 ml/kg, used throughoutthe 1970s and 1980s [21]; however, because we totallyagree with Eichacker’s concept that “one size does not fitwith all” [22], we routinely used an alternative approach,which adapts tidal volume to the individual size of the“baby lung,” by adjusting tidal volume based on plateaupressure [23]. Because a direct reflection of this size isgiven by the value of the compliance of the respiratorysystem, monitoring of plateau pressure is fundamental inusing this strategy. An advantage of this approach is thatit allows adaptations to extreme conditions. In patients

Pplat (cmH2O)

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

ACP 13% for Pplat < 27 cmH2O

PROTECT THE RV IN ARDS!!

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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!

LIMIT  TRANSPULMONARY  PRESSURES    (Pplat  <  28CmH2O)

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

Received: 25 December 2006Accepted: 22 January 2007Published online: 1 February 2007© Springer-Verlag 2007

F. Jardin (✉) · A. Vieillard-BaronUniversity Hospital Ambroise Paré,Assistance Publique Hôpitaux de Paris,Medical Intensive Care Unit,9 avenue Charles de Gaulle,92104 Boulogne Cedex, Francee-mail: [email protected].: +33-1-49095604Fax: +33-1-49095892

Abstract Objective: Airway pressurelimitation is now a largely acceptedstrategy in adult respiratory distresssyndrome (ARDS) patients; however,some debate persists about the exactlevel of plateau pressure which canbe safely used. The objective of thepresent study was to examine if theechocardiographic evaluation of rightventricular function performed inARDS may help to answer to thisquestion. Design and patients: Formore than 20 years, we have reg-ularly monitored right ventricularfunction by echocardiography inARDS patients, during two differentperiods, a first (1980–1992) whereairway pressure was not limited, anda second (1993–2006) where airwaypressure was limited. By pooling ourdata, we can observe the effect ofa large range of plateau pressure uponmortality rate and incidence of acutecor pulmonale. Results: In this

whole group of 352 ARDS patients,mortality rate and incidence of corpulmonale were 80 and 56%, respec-tively, when plateau pressure was> 35 cmH2O; 42 and 32%, respec-tively, when plateau pressure wasbetween 27 and 35 cmH2O; and 30and 13%, respectively, when plateaupressure was < 27 cmH2O. Moreover,a clear interaction between plateaupressure and cor pulmonale wasevidenced: whereas the odd ratio ofdying for an increase in plateau pres-sure from 18–26 to 27–35 cm H2O inpatients without cor pulmonale was1.05 (p = 0.635), it was 3.32 in pa-tients with cor pulmonale (p < 0.034).Conclusion: We hypothesize thatmonitoring of right ventricular func-tion by echocardiography at bedsidemight help to control the safety ofplateau pressure used in ARDS.

Keywords ARDS · plateau pressure

Introduction

In 1970 Mead et al. emphasized the importance of uniformexpansion of air space as a protection against disten-sion, which is related to transpulmonary pressure [1].In mechanically ventilated patients, alveolar pressure isthe main determinant of transpulmonary pressure. Whenrecorded during a period of no flow, tracheal pressure ina mechanically ventilated patient can be used to measurealveolar pressure. Since 1975 experimental studies havefocused on the deleterious effects of mechanical venti-lation, such as pulmonary edema, and in 1985 Dreyfusset al. experimentally demonstrated in rats that high

inflation pressure, at a peak airway pressure currentlyused by clinicians in ARDS patients, may greatly altermicrovascular permeability [2, 3]. Despite these experi-mental evidence, airway pressure limitation was proposedas a respiratory strategy in adult respiratory distresssyndrome (ARDS) patients only in 1990 [4]. Whenused above functional residual capacity, application ofa positive pressure to the airways increases pulmonaryvascular resistance [5] and decreases pulmonary bloodflow [6], and these adverse effects can be considered asthe result of airway distension, because pulmonary cap-illaries, as intra-alveolar vessels, are stressed by alveolarpressure [7].

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

Received: 25 December 2006Accepted: 22 January 2007Published online: 1 February 2007© Springer-Verlag 2007

F. Jardin (✉) · A. Vieillard-BaronUniversity Hospital Ambroise Paré,Assistance Publique Hôpitaux de Paris,Medical Intensive Care Unit,9 avenue Charles de Gaulle,92104 Boulogne Cedex, Francee-mail: [email protected].: +33-1-49095604Fax: +33-1-49095892

Abstract Objective: Airway pressurelimitation is now a largely acceptedstrategy in adult respiratory distresssyndrome (ARDS) patients; however,some debate persists about the exactlevel of plateau pressure which canbe safely used. The objective of thepresent study was to examine if theechocardiographic evaluation of rightventricular function performed inARDS may help to answer to thisquestion. Design and patients: Formore than 20 years, we have reg-ularly monitored right ventricularfunction by echocardiography inARDS patients, during two differentperiods, a first (1980–1992) whereairway pressure was not limited, anda second (1993–2006) where airwaypressure was limited. By pooling ourdata, we can observe the effect ofa large range of plateau pressure uponmortality rate and incidence of acutecor pulmonale. Results: In this

whole group of 352 ARDS patients,mortality rate and incidence of corpulmonale were 80 and 56%, respec-tively, when plateau pressure was> 35 cmH2O; 42 and 32%, respec-tively, when plateau pressure wasbetween 27 and 35 cmH2O; and 30and 13%, respectively, when plateaupressure was < 27 cmH2O. Moreover,a clear interaction between plateaupressure and cor pulmonale wasevidenced: whereas the odd ratio ofdying for an increase in plateau pres-sure from 18–26 to 27–35 cm H2O inpatients without cor pulmonale was1.05 (p = 0.635), it was 3.32 in pa-tients with cor pulmonale (p < 0.034).Conclusion: We hypothesize thatmonitoring of right ventricular func-tion by echocardiography at bedsidemight help to control the safety ofplateau pressure used in ARDS.

Keywords ARDS · plateau pressure

Introduction

In 1970 Mead et al. emphasized the importance of uniformexpansion of air space as a protection against disten-sion, which is related to transpulmonary pressure [1].In mechanically ventilated patients, alveolar pressure isthe main determinant of transpulmonary pressure. Whenrecorded during a period of no flow, tracheal pressure ina mechanically ventilated patient can be used to measurealveolar pressure. Since 1975 experimental studies havefocused on the deleterious effects of mechanical venti-lation, such as pulmonary edema, and in 1985 Dreyfusset al. experimentally demonstrated in rats that high

inflation pressure, at a peak airway pressure currentlyused by clinicians in ARDS patients, may greatly altermicrovascular permeability [2, 3]. Despite these experi-mental evidence, airway pressure limitation was proposedas a respiratory strategy in adult respiratory distresssyndrome (ARDS) patients only in 1990 [4]. Whenused above functional residual capacity, application ofa positive pressure to the airways increases pulmonaryvascular resistance [5] and decreases pulmonary bloodflow [6], and these adverse effects can be considered asthe result of airway distension, because pulmonary cap-illaries, as intra-alveolar vessels, are stressed by alveolarpressure [7].

446

Also, whereas markedly harmful in patients exhibitingacute cor pulmonale, a plateau pressure between 27 and35 cm H2O appears less harmful in patients with normalechocardiographic findings, since mortality is similar thanfor a plateau pressure range of 18–26 cm H2O. In patientswithout acute cor pulmonale, the OR (95% CI) for anincrease in plateau pressure from 18–26 to 27–35 cm H2Ois 1.15 (range 0.64–2.08; p = 0.635). In patients with acutecor pulmonale, the OR (95% CI) for an increase in plateaupressure from 18–26 to 27–35 cm H2O is 3.32 (range1.09–10.12; p = 0.034), suggesting that the threshold fora safe plateau pressure depends on the presence or not ofacute cor pulmonale.

Finally, a plateau pressure above 35 cm H2O is asso-ciated with a high incidence of ACP and a high mortal-ity rate (Figs. 1, 2). In this group, an additive effect ofplateau pressure and acute cor pulmonale was observed.In patients without acute cor pulmonale, the OR (95% CI)for an increase in plateau pressure from 18–35 to more

Fig. 1 Mortality rate and incidence of acute cor pulmonale (ACP) areplotted against three ranges of plateau pressure (see text). Figures arethe exact number of patients concerned. ∗p < 0.05, when comparedwith the preceding range

Fig. 2 Mortality rate is plotted against three ranges of plateaupressure (see text), after separating patients with normal bedsideechocardiographic findings (normal), and patients exhibiting acutecor pulmonale (ACP) detected by echocardiography. Figures are theexact number of patients concerned. ∗p < 0.05, when compared withthe preceding range

than 35 cm H2O is 4.03 (range 1.94–8.36; p = 0.0002). Inpatients with acute cor pulmonale, the OR (95% CI) foran increase in plateau pressure from 18–35 to more than35 cm H2O is 10.97 (range 3.55–33.85; p < 0.0001).

DiscussionThis study has shown that mortality rate and incidence ofACP markedly increases in ARDS patients above a plateauof 26 cm H2O. With a plateau pressure between 27 and35 cm H2O, the mortality rate is markedly increased by thepresence of ACP.

There are several important limitations to this analysis.By pooling the data of these two periods, we were ableto observe the effect of a large range of plateau pres-sure, firstly upon mortality rate, and secondly upon theincidence of acute cor pulmonale. The value of plateaupressure, however, was not only a result of our therapeuticstrategy since, in both periods, it was also influenced bythe severity of ARDS. This, however, does not invalidateour comparison, especially on the influence of hemody-namic findings in each subgroup. The effect of airwaypressure limitation in the second period would tend toplace more severe patients in the low plateau pressuregroup, and, conversely, the absence of airway pressurelimitation in the first period would tend to place lesssevere patients in the high plateau pressure group. Botheffects would tend to mask the differences. No adjustmentcould be made on general severity since our database doesnot contain consistent information with the same severityscores over all these years.

Acute cor pulmonale is present in a minority of patients(13%) in the case of major airway pressure limitation, andcan probably be mainly attributed to the severity of under-lying lung disease; however, any responsibility of a pos-itive airway pressure, which is not physiological, cannotbe ruled out. In these patients, acute cor pulmonale, whennot worsened by aggressive respiratory support, does notinfluence mortality, as we have previously reported [20].

The current tendency in ARDS management is to re-duce tidal volume to a uniform value of 6 ml/kg predictedbody weight in all patients [21]. This strategy, whichproduced a marked reduction in plateau pressure, hasbeen shown to improve prognosis, when compared withthe traditional tidal volume of 12 ml/kg, used throughoutthe 1970s and 1980s [21]; however, because we totallyagree with Eichacker’s concept that “one size does not fitwith all” [22], we routinely used an alternative approach,which adapts tidal volume to the individual size of the“baby lung,” by adjusting tidal volume based on plateaupressure [23]. Because a direct reflection of this size isgiven by the value of the compliance of the respiratorysystem, monitoring of plateau pressure is fundamental inusing this strategy. An advantage of this approach is thatit allows adaptations to extreme conditions. In patients

Pplat (cmH2O)

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

ACP 13% for Pplat < 27 cmH2O

PROTECT THE RV IN ARDS!!

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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!

ALVEOLAR RECRUITMENT

Critical Care Vol 13 No 2 Gernoth et al.

Page 6 of 10(page number not for citation purposes)

tive airway pressure (CPAP) [28,29] and pressure control ven-tilation with high peak and end-expiratory pressure [30-33]. Asanimal models showed less cardiovascular compromise withthe latter approach [34], pressure control ventilation may beconsidered the optimal approach to lung recruitment [35].Accordingly, in this study we used the pressure control strat-egy, applying a stepwise increasing peak inspiratory pressureup to 50 cmH2O at a high level of PEEP, similar to theapproach used by Villagra and colleagues [33].

We observed a mean percentage increase in PaO2/FiO2 of22% following the RM and decremental PEEP trial. Further-more, the improvement in oxygenation was associated with anincrease in the dynamic respiratory compliance, suggestingthe presence of alveolar recruitment.

The oxygenation response in our study was in line with thatreported by Villagra and colleagues [33] but modest com-pared with the study by Grasso and colleagues [28]. This canbe explained by different types of patients, the ALI/ARDSonset time and ventilatory setting. In particular, it should beconsidered that our patients were on a lung protective strategywith low tidal volume and high PEEP (mean PEEP at baselineof 14 cmH2O), which is likely to result in a lesser improvementin respiratory function after RMs.

The primary complications possibly occurring during RMs arebarotrauma and haemodynamic compromise [16,17,36,37].RMs may impair haemodynamics, most commonly assessedby MAP or cardiac output, by two main mechanisms [8]. First,as the lung is recruited, high airway pressure can more readilybe transmitted across the lung parenchyma to the pleuralspace, impeding venous return and thus decreasing right ven-

Table 3

Haemodynamic data derived from PiCCO™-monitoring

T0 T20/30 TOLP

Heart rate (beats/min) 86 ± 20 89 ± 20 85 ± 18

Mean arterial pressure (mmHg) 79 ± 13 71 ± 17 79 ± 13

Central venous pressure (mmHg) 22 ± 6 26 ± 4 21 ± 5

Cardiac index (l/min/m2) 3.3 ± 0.7 3.1 ± 0.9 3.4 ± 0.6

Cardiac power index (W/m2) 0.58 ± 0.17 0.48 ± 0.19 0.66 ± 0.18b

Stroke volume index (ml/m2) 37 ± 9 34 ± 14 40 ± 10

Stroke volume variance (ml) 14 ± 7 17 ± 5 13 ± 4

Intrathoracic blood volume index (ml/m2) 883 ± 215 - 898 ± 241

Extravascular lung water index (ml/kg/m2) 16 ± 9 - 17 ± 10

aP < 0.05 compared with T0; bP < 0.05 compared with T20/30; Data are presented as mean ± standard deviation.PiCCO™ = Pulse Contour Cardiac Output Monitor; T0 = time at baseline; T20/30 = time when positive end-expiratory pressure at 20 cmH2O and driving pressure at 30 cmH2O; TOLP = time at open lung-positive end-expiratory pressure.

Figure 4

End-diastolic area changes of the left and right ventricle from T0 to T20/30 to TOLPEnd-diastolic area changes of the left and right ventricle from T0 to T20/30 to TOLP. *P < 0.05 compared with T0; †P < 0.05 compared with T20/30.

LVEDA = left ventricular end-diastolic area; RVEDA = right ventricular end-diastolic area; T0 = time at baseline; T20/30 = time when positive end-expir-atory pressure at 20 cmH2O and driving pressure at 30 cmH2O; TOLP = time at open lung-positive end-expiratory pressure.

BASAL FINAL PEEPRECRUITMENT

Available online http://ccforum.com/content/13/2/R59

Page 7 of 10(page number not for citation purposes)

tricular preload. Second, high alveolar pressure may increasepulmonary vascular resistance and right ventricular afterload.A recent systematic review [37] revealed hypotension (12%)and desaturation (9%) as the most frequent complications,although serious adverse events such as barotrauma wererare (1%). Given these side effects and the lack of informationon the influence on clinical outcome, the authors neither rec-ommend nor discourage RMs at this time. The latter point is

especially important, as the effect of RMs is relatively short-lived and RMs must be repeated several times a day in orderto maintain open lung ventilation.

The study presented here, albeit small, did not reveal majorcomplications. In particular, we did not observe any significantdecrease in MAP, stroke volume or CI during the RMs. Car-diac pumping capability, however, assessed by the cardiacpower index, which combines both pressure and flow domainsof the cardiovascular system, decreased. These findings of rel-ative haemodynamic stability during the RMs are in line withthose reported in the ARDS Network study [4,38] showing a10.6 ± 1.2 mmHg decrease in systolic blood pressure duringlung recruitment manoeuvre using CPAP over 5 to 10 sec-onds at 35 to 40 cmH2O and the study by Borges and col-leagues [30] using peak airway pressures up to 60 cmH2O,where none of the patients investigated experienced haemo-dynamic compromise during the RMs.

Despite maintained blood pressure and CI, the RMs inducedan acute cardiac stress test as evidenced by transoesopha-geal echocardiography. This implies that monitoring haemody-namics using arterial pressure and cardiac output in clinicalpractice is likely to miss specific changes in venous returnand/or right ventricular loading conditions. Echocardiographicassessment of vena cava diameters, which remainedunchanged during the RMs except for maximum IVC diameter,revealed maintained venous return in the present study. Thepatients in our study were at the lower limits of normovolaemia,as indicated by a mean intrathoracic blood volume index of883 ml/m2 and a stroke volume variation of 14%, suggestingthat RMs by pressure control ventilation can safely be per-formed at low normal volume status without the need to inducepotentially detrimental hypervolaemia. The importance of theintravascular volume status during the recruitment manoeuvrehas been specifically addressed by Nielsen and colleagues[15] in a porcine lung-lavage model: using transoesophagealechocardiography, they showed left ventricular compromiseresulting in a drop in cardiac output during lung recruitment bysustained inflation (40 cmH2O of CPAP for 30 seconds),which was accentuated by hypovolaemia and attenuated byhypervolaemia. Taken together, these findings underscore theneed to ensure an adequate intravascular volume statusbefore attempting RMs.

Although venous return was maintained, the RMs, by inducinglung inflation, most probably increased pulmonary vascularresistance [39], thus increasing right ventricular afterload. Thisincrease in right ventricular afterload could be assessedechocardiographically by the increase in right ventricular Teiindex and the increase in right ventricular end-diastolic diame-ter with a consecutive, acute leftward septal shift, reducing leftventricular size. These findings were not as severe as thoseseen in the study by Nielsen and colleagues [16], when 40cmH2O of CPAP for 10 to 20 seconds was applied to patients

Figure 5

(a) End-systolic transgastric midpapillary views obtained at baseline, (b) during the recruitment manoeuvre and (c) during open lung positive end-expiratory pressure(a) End-systolic transgastric midpapillary views obtained at baseline, (b) during the recruitment manoeuvre and (c) during open lung positive end-expiratory pressure. Note the massive dilation of the right ventricle (RV), causing acute leftward shift of the interventricular septum (IVC) and compression of the left ventricle (LV; d-shaped) during the recruit-ment manoeuvre.

BASAL

FINAL PEEP

RECRUITMENT

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Vol 13 No 2ResearchRespiratory and haemodynamic changes during decremental open lung positive end-expiratory pressure titration in patients with acute respiratory distress syndromeChristian Gernoth1, Gerhard Wagner2, Paolo Pelosi3 and Thomas Luecke1

1Department of Anesthesiology and Critical Care Medicine, University Hospital Mannheim, Faculty of Medicine, University of Heidelberg, Theodor-Kutzer Ufer, 68165 Mannheim, Germany2Department of Anesthesiology an Critical Care Medicine, Robert-Bosch Hospital, Auerbachstrasse 110, 70376 Stuttgart, Germany3Department of Ambient, Health and Safety, University of Insubria, c/o Villa Toeplitz Via G.B. Vico, 46 21100 Varese, Italy

Corresponding author: Thomas Luecke, [email protected]

Received: 7 Jan 2009 Revisions requested: 23 Feb 2009 Revisions received: 6 Mar 2009 Accepted: 17 Apr 2009 Published: 17 Apr 2009

Critical Care 2009, 13:R59 (doi:10.1186/cc7786)This article is online at: http://ccforum.com/content/13/2/R59© 2009 Gernoth et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Introduction To investigate haemodynamic and respiratorychanges during lung recruitment and decremental positive end-expiratory pressure (PEEP) titration for open lung ventilation inpatients with acute respiratory distress syndrome (ARDS) aprospective, clinical trial was performed involving 12 adultpatients with ARDS treated in the surgical intensive care unit ina university hospital.

Methods A software programme (Open Lung Tool™)incorporated into a standard ventilator controlled therecruitment (pressure-controlled ventilation with fixed PEEP at20 cmH2O and increased driving pressures at 20, 25 and 30cmH2O for two minutes each) and PEEP titration (PEEPlowered by 2 cmH2O every two minutes, with tidal volume set at6 ml/kg). The open lung PEEP (OL-PEEP) was defined as thePEEP level yielding maximum dynamic respiratory complianceplus 2 cmH2O. Gas exchange, respiratory mechanics andcentral haemodynamics using the Pulse Contour CardiacOutput Monitor (PiCCO™), as well as transoesophagealechocardiography were measured at the following steps: atbaseline (T0); during the final recruitment step with PEEP at 20cmH2O and driving pressure at 30 cmH2O, (T20/30); at OL-PEEP, following another recruitment manoeuvre (TOLP).

Results The ratio of partial pressure of arterial oxygen (PaO2) tofraction of inspired oxygen (FiO2) increased from T0 to TOLP (120

± 59 versus 146 ± 64 mmHg, P < 0.005), as did dynamicrespiratory compliance (23 ± 5 versus 27 ± 6 ml/cmH2O, P <0.005). At constant PEEP (14 ± 3 cmH2O) and tidal volumes,peak inspiratory pressure decreased (32 ± 3 versus 29 ± 3cmH2O, P < 0.005), although partial pressure of arterial carbondioxide (PaCO2) was unchanged (58 ± 22 versus 53 ± 18mmHg). No significant decrease in mean arterial pressure,stroke volume or cardiac output occurred during the recruitment(T20/30). However, left ventricular end-diastolic area decreasedat T20/30 due to a decrease in the left ventricular end-diastolicseptal-lateral diameter, while right ventricular end-diastolic areaincreased. Right ventricular function, estimated by the rightventricular Tei-index, deteriorated during the recruitmentmanoeuvre, but improved at TOLP.

Conclusions A standardised open lung strategy increasedoxygenation and improved respiratory system compliance. Nomajor haemodynamic compromise was observed, although theincrease in right ventricular Tei-index and right ventricular end-diastolic area and the decrease in left ventricular end-diastolicseptal-lateral diameter during the recruitment suggested anincreased right ventricular stress and strain. Right ventricularfunction was significantly improved at TOLP compared with T0,although left ventricular function was unchanged, indicatingeffective lung volume optimisation.

ALI: acute lung injury; ARDS: adult respiratory distress syndrome; Cdyn: dynamic compliance of the respiratory system; CI: cardiac index; CPAP: continuous positive airway pressure; EIP: end-inspiratory pressure; FiO2: fraction of inspired oxygen; FRC: functional residual capacity; IBW: ideal body weight; IVC: inferior vena cava; MAP: mean arterial pressure; OL-PEEP: open lung positive end-expiratory pressure; PaCO2: partial pressure of arterial carbon dioxide; PaO2: partial pressure of arterial oxygen; PEEP: positive end-expiratory pressure; PiCCO: Pulse Contour Cardiac Output Mon-itor; RM: recruitment manoeuvre; RR: respiratory rate; T0: time at baseline; T20/30: time when positive end-expiratory pressure at 20 cmH2O and driving pressure at 30 cmH2O; TOLP: time at open lung positive end-expiratory pressure; VILI: ventilator-induced lung injury; Vtinsp: inspiratory tidal volume.

CRIT CARE 2009

PROTECT THE RV IN ARDS!!

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., instead of 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 performed 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 open lung 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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!

ALVEOLAR RECRUITMENT

Critical Care Vol 13 No 2 Gernoth et al.

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tive airway pressure (CPAP) [28,29] and pressure control ven-tilation with high peak and end-expiratory pressure [30-33]. Asanimal models showed less cardiovascular compromise withthe latter approach [34], pressure control ventilation may beconsidered the optimal approach to lung recruitment [35].Accordingly, in this study we used the pressure control strat-egy, applying a stepwise increasing peak inspiratory pressureup to 50 cmH2O at a high level of PEEP, similar to theapproach used by Villagra and colleagues [33].

We observed a mean percentage increase in PaO2/FiO2 of22% following the RM and decremental PEEP trial. Further-more, the improvement in oxygenation was associated with anincrease in the dynamic respiratory compliance, suggestingthe presence of alveolar recruitment.

The oxygenation response in our study was in line with thatreported by Villagra and colleagues [33] but modest com-pared with the study by Grasso and colleagues [28]. This canbe explained by different types of patients, the ALI/ARDSonset time and ventilatory setting. In particular, it should beconsidered that our patients were on a lung protective strategywith low tidal volume and high PEEP (mean PEEP at baselineof 14 cmH2O), which is likely to result in a lesser improvementin respiratory function after RMs.

The primary complications possibly occurring during RMs arebarotrauma and haemodynamic compromise [16,17,36,37].RMs may impair haemodynamics, most commonly assessedby MAP or cardiac output, by two main mechanisms [8]. First,as the lung is recruited, high airway pressure can more readilybe transmitted across the lung parenchyma to the pleuralspace, impeding venous return and thus decreasing right ven-

Table 3

Haemodynamic data derived from PiCCO™-monitoring

T0 T20/30 TOLP

Heart rate (beats/min) 86 ± 20 89 ± 20 85 ± 18

Mean arterial pressure (mmHg) 79 ± 13 71 ± 17 79 ± 13

Central venous pressure (mmHg) 22 ± 6 26 ± 4 21 ± 5

Cardiac index (l/min/m2) 3.3 ± 0.7 3.1 ± 0.9 3.4 ± 0.6

Cardiac power index (W/m2) 0.58 ± 0.17 0.48 ± 0.19 0.66 ± 0.18b

Stroke volume index (ml/m2) 37 ± 9 34 ± 14 40 ± 10

Stroke volume variance (ml) 14 ± 7 17 ± 5 13 ± 4

Intrathoracic blood volume index (ml/m2) 883 ± 215 - 898 ± 241

Extravascular lung water index (ml/kg/m2) 16 ± 9 - 17 ± 10

aP < 0.05 compared with T0; bP < 0.05 compared with T20/30; Data are presented as mean ± standard deviation.PiCCO™ = Pulse Contour Cardiac Output Monitor; T0 = time at baseline; T20/30 = time when positive end-expiratory pressure at 20 cmH2O and driving pressure at 30 cmH2O; TOLP = time at open lung-positive end-expiratory pressure.

Figure 4

End-diastolic area changes of the left and right ventricle from T0 to T20/30 to TOLPEnd-diastolic area changes of the left and right ventricle from T0 to T20/30 to TOLP. *P < 0.05 compared with T0; †P < 0.05 compared with T20/30.

LVEDA = left ventricular end-diastolic area; RVEDA = right ventricular end-diastolic area; T0 = time at baseline; T20/30 = time when positive end-expir-atory pressure at 20 cmH2O and driving pressure at 30 cmH2O; TOLP = time at open lung-positive end-expiratory pressure.

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tricular preload. Second, high alveolar pressure may increasepulmonary vascular resistance and right ventricular afterload.A recent systematic review [37] revealed hypotension (12%)and desaturation (9%) as the most frequent complications,although serious adverse events such as barotrauma wererare (1%). Given these side effects and the lack of informationon the influence on clinical outcome, the authors neither rec-ommend nor discourage RMs at this time. The latter point is

especially important, as the effect of RMs is relatively short-lived and RMs must be repeated several times a day in orderto maintain open lung ventilation.

The study presented here, albeit small, did not reveal majorcomplications. In particular, we did not observe any significantdecrease in MAP, stroke volume or CI during the RMs. Car-diac pumping capability, however, assessed by the cardiacpower index, which combines both pressure and flow domainsof the cardiovascular system, decreased. These findings of rel-ative haemodynamic stability during the RMs are in line withthose reported in the ARDS Network study [4,38] showing a10.6 ± 1.2 mmHg decrease in systolic blood pressure duringlung recruitment manoeuvre using CPAP over 5 to 10 sec-onds at 35 to 40 cmH2O and the study by Borges and col-leagues [30] using peak airway pressures up to 60 cmH2O,where none of the patients investigated experienced haemo-dynamic compromise during the RMs.

Despite maintained blood pressure and CI, the RMs inducedan acute cardiac stress test as evidenced by transoesopha-geal echocardiography. This implies that monitoring haemody-namics using arterial pressure and cardiac output in clinicalpractice is likely to miss specific changes in venous returnand/or right ventricular loading conditions. Echocardiographicassessment of vena cava diameters, which remainedunchanged during the RMs except for maximum IVC diameter,revealed maintained venous return in the present study. Thepatients in our study were at the lower limits of normovolaemia,as indicated by a mean intrathoracic blood volume index of883 ml/m2 and a stroke volume variation of 14%, suggestingthat RMs by pressure control ventilation can safely be per-formed at low normal volume status without the need to inducepotentially detrimental hypervolaemia. The importance of theintravascular volume status during the recruitment manoeuvrehas been specifically addressed by Nielsen and colleagues[15] in a porcine lung-lavage model: using transoesophagealechocardiography, they showed left ventricular compromiseresulting in a drop in cardiac output during lung recruitment bysustained inflation (40 cmH2O of CPAP for 30 seconds),which was accentuated by hypovolaemia and attenuated byhypervolaemia. Taken together, these findings underscore theneed to ensure an adequate intravascular volume statusbefore attempting RMs.

Although venous return was maintained, the RMs, by inducinglung inflation, most probably increased pulmonary vascularresistance [39], thus increasing right ventricular afterload. Thisincrease in right ventricular afterload could be assessedechocardiographically by the increase in right ventricular Teiindex and the increase in right ventricular end-diastolic diame-ter with a consecutive, acute leftward septal shift, reducing leftventricular size. These findings were not as severe as thoseseen in the study by Nielsen and colleagues [16], when 40cmH2O of CPAP for 10 to 20 seconds was applied to patients

Figure 5

(a) End-systolic transgastric midpapillary views obtained at baseline, (b) during the recruitment manoeuvre and (c) during open lung positive end-expiratory pressure(a) End-systolic transgastric midpapillary views obtained at baseline, (b) during the recruitment manoeuvre and (c) during open lung positive end-expiratory pressure. Note the massive dilation of the right ventricle (RV), causing acute leftward shift of the interventricular septum (IVC) and compression of the left ventricle (LV; d-shaped) during the recruit-ment manoeuvre.

BASAL

FINAL PEEP

RECRUITMENT

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Available online http://ccforum.com/content/13/2/R59

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Vol 13 No 2ResearchRespiratory and haemodynamic changes during decremental open lung positive end-expiratory pressure titration in patients with acute respiratory distress syndromeChristian Gernoth1, Gerhard Wagner2, Paolo Pelosi3 and Thomas Luecke1

1Department of Anesthesiology and Critical Care Medicine, University Hospital Mannheim, Faculty of Medicine, University of Heidelberg, Theodor-Kutzer Ufer, 68165 Mannheim, Germany2Department of Anesthesiology an Critical Care Medicine, Robert-Bosch Hospital, Auerbachstrasse 110, 70376 Stuttgart, Germany3Department of Ambient, Health and Safety, University of Insubria, c/o Villa Toeplitz Via G.B. Vico, 46 21100 Varese, Italy

Corresponding author: Thomas Luecke, [email protected]

Received: 7 Jan 2009 Revisions requested: 23 Feb 2009 Revisions received: 6 Mar 2009 Accepted: 17 Apr 2009 Published: 17 Apr 2009

Critical Care 2009, 13:R59 (doi:10.1186/cc7786)This article is online at: http://ccforum.com/content/13/2/R59© 2009 Gernoth et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Introduction To investigate haemodynamic and respiratorychanges during lung recruitment and decremental positive end-expiratory pressure (PEEP) titration for open lung ventilation inpatients with acute respiratory distress syndrome (ARDS) aprospective, clinical trial was performed involving 12 adultpatients with ARDS treated in the surgical intensive care unit ina university hospital.

Methods A software programme (Open Lung Tool™)incorporated into a standard ventilator controlled therecruitment (pressure-controlled ventilation with fixed PEEP at20 cmH2O and increased driving pressures at 20, 25 and 30cmH2O for two minutes each) and PEEP titration (PEEPlowered by 2 cmH2O every two minutes, with tidal volume set at6 ml/kg). The open lung PEEP (OL-PEEP) was defined as thePEEP level yielding maximum dynamic respiratory complianceplus 2 cmH2O. Gas exchange, respiratory mechanics andcentral haemodynamics using the Pulse Contour CardiacOutput Monitor (PiCCO™), as well as transoesophagealechocardiography were measured at the following steps: atbaseline (T0); during the final recruitment step with PEEP at 20cmH2O and driving pressure at 30 cmH2O, (T20/30); at OL-PEEP, following another recruitment manoeuvre (TOLP).

Results The ratio of partial pressure of arterial oxygen (PaO2) tofraction of inspired oxygen (FiO2) increased from T0 to TOLP (120

± 59 versus 146 ± 64 mmHg, P < 0.005), as did dynamicrespiratory compliance (23 ± 5 versus 27 ± 6 ml/cmH2O, P <0.005). At constant PEEP (14 ± 3 cmH2O) and tidal volumes,peak inspiratory pressure decreased (32 ± 3 versus 29 ± 3cmH2O, P < 0.005), although partial pressure of arterial carbondioxide (PaCO2) was unchanged (58 ± 22 versus 53 ± 18mmHg). No significant decrease in mean arterial pressure,stroke volume or cardiac output occurred during the recruitment(T20/30). However, left ventricular end-diastolic area decreasedat T20/30 due to a decrease in the left ventricular end-diastolicseptal-lateral diameter, while right ventricular end-diastolic areaincreased. Right ventricular function, estimated by the rightventricular Tei-index, deteriorated during the recruitmentmanoeuvre, but improved at TOLP.

Conclusions A standardised open lung strategy increasedoxygenation and improved respiratory system compliance. Nomajor haemodynamic compromise was observed, although theincrease in right ventricular Tei-index and right ventricular end-diastolic area and the decrease in left ventricular end-diastolicseptal-lateral diameter during the recruitment suggested anincreased right ventricular stress and strain. Right ventricularfunction was significantly improved at TOLP compared with T0,although left ventricular function was unchanged, indicatingeffective lung volume optimisation.

ALI: acute lung injury; ARDS: adult respiratory distress syndrome; Cdyn: dynamic compliance of the respiratory system; CI: cardiac index; CPAP: continuous positive airway pressure; EIP: end-inspiratory pressure; FiO2: fraction of inspired oxygen; FRC: functional residual capacity; IBW: ideal body weight; IVC: inferior vena cava; MAP: mean arterial pressure; OL-PEEP: open lung positive end-expiratory pressure; PaCO2: partial pressure of arterial carbon dioxide; PaO2: partial pressure of arterial oxygen; PEEP: positive end-expiratory pressure; PiCCO: Pulse Contour Cardiac Output Mon-itor; RM: recruitment manoeuvre; RR: respiratory rate; T0: time at baseline; T20/30: time when positive end-expiratory pressure at 20 cmH2O and driving pressure at 30 cmH2O; TOLP: time at open lung positive end-expiratory pressure; VILI: ventilator-induced lung injury; Vtinsp: inspiratory tidal volume.

CRIT CARE 2009

PROTECT THE RV IN ARDS?

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., instead of 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 performed 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 open lung 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.

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!ISSUES:

• Retrospective approach

• ACP; Cause of worse outcome or sign of severity of disease?

• Is decreasing PEEP advantage or disadvantage?

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!DIFFERENT APPROACH

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

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© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

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© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

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© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

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© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!OUTCOME

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!OUTCOME

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!OUTCOME

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!

PROTECT THE RV IN ARDS

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!

PROTECT THE RV IN ARDS

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!ARDS-ASSOCIATED ACUTE COR PULMONALE

!

2. PRACTICAL APPLICATIONS • RV DYSFUNCTION:

RECOGNITION, SUPPORT

• VENTILATORY STRATEGY

• DIFFERENTIAL DIAGNOSIS ARDS vs. CARDIOGENIC

• INTRACARDIAC SHUNT DETECTION

1. WHY ECHO IN ARDS? RATIONALE FOR APPLICATION

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!CARDIOGENIC SHOCK

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!CARDIOGENIC SHOCK

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!ARDS-ASSOCIATED ACUTE COR PULMONALE

!

2. PRACTICAL APPLICATIONS • RV DYSFUNCTION:

RECOGNITION, SUPPORT

• VENTILATORY STRATEGY

• DIFFERENTIAL DIAGNOSIS ARDS vs. CARDIOGENIC

• INTRACARDIAC SHUNT DETECTION

1. WHY ECHO IN ARDS? RATIONALE FOR APPLICATION

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

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© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!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) - Optimize fluid status if possible - Prone position (unloads RV) - Limit Pplat, lower tidal volume - Avoid hypercapnia, acidosis - More careful recruitment maneuver

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!CONCLUSIONS

• Echo can help - Discriminate between cardiogenic and ARDS - Diagnose intracardiac shunts (hypoxia)

© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

!CONCLUSIONS

• Echo can help - Discriminate between cardiogenic and ARDS - Diagnose intracardiac shunts (hypoxia)

• Too soon to recommend adjusting ventilatory setting based echo finding of acute cor pulmonale

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!

THANK YOU!

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!57 Y.O. M POD # 1 FROM RETROPERITONEAL HEMATOMA EVACUATION

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!57 Y.O. M POD # 1 FROM RETROPERITONEAL HEMATOMA EVACUATION

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© WINFOCUS’    CRITICAL CARE ECHOCARDIOGRAPHY

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