2. Outline
Definitions and Diagnosis
Pathophysiology
Cardiogenic vs Non-cardiogenic Edema
Management of ARDS
Pulmonary Artery Catheters
3. Definition
A diffuse inflammatory injury of the lungs which
is an EXPRESSION of a host of various
diseases and is not a specific disease entity in
and of itself. It is often—but not always—
accompanied by inflammatory injury of other
organ systems.
Inflammatory cells and proteinaceous fluid
accumulate in the alveolar spaces leading to a
decrease in diffusing capacity and hypoxemia.
4. Acute Lung Injury (ALI) vs. ARDS
ALI is the term used for patients with significant
hypoxemia (PaO2/FiO2 ratio of <300)
ARDS is the term used for a subset of ALI
patients with severe hypoxemia (PaO2/FiO2
ratio of <200)
Fan, E. et al. Ventilatory Management of Acute Lung Injury and Acute Respiratory Distress
Syndrome. 2005. JAMA. 294 (22). pp. 2889-96.
5. ARDS Diagnostic Criteria
From the American-European Consensus Conference on ARDS
1. Acute Onset
2. Predisposing Condition
3. Bilateral Infiltrates
4. PaO2/FiO2 < 200 mm Hg
5. Wedge Pressure ≤ 18 mm Hg or no clinical
evidence of LA HTN.
Note: According to The ICU Book, wedge pressure should be excluded
from the diagnostic criteria because it underestimates capillary
hydrostatic pressure (p 435).
6. Predisposing Conditions
Sepsis (#1 cause) Severe Trauma
Severe PNA DIC
Aspiration Drug overdose:
Near Drowning Heroin, methamphetami
Smoke inhalation ne, cocaine
Multiple blood product Acute pancreatitis
transfusions Severe Burn
Look for the + Tube Sign!!!!
7. Positive Tube Sign
The majority of patients with ARDS
require intubation and mechanical
ventilation
www.fhs.mcmaster.ca/.../photos.htm
8.
9. An Interesting Note
All of the predisposing conditions share the
ability to trigger a systemic inflammatory
response. Hum….
The majority of ARDS deaths are NOT due to
respiratory failure, but multiple organ failure
secondary to systemic inflammatory processes.
10. Pathology of ARDS
A diffuse inflammatory process
Circulating neutrophils are activated and become ―sticky.‖
They adhere to the vascular endothelium and spill their
cytoplasmic granules which then damage the endothelium
leading to leaky capillaries. The result: An exudative fluid
accumulates in the lung parenchyma, which leads to further
damage locally (i.e. alveolar cell damage) decreasing
oxygenation and lung compliance.
Fibrin Deposition. Fibrin release is triggered by tissue factor.
Over time the fibrin can later remodel to form fibrosis.
Marino, P.L. The ICU Book. 3rd Ed. Lippincott Williams & Wilkins. Philadelphia. 2007.
12. Again…
ARDS is a diffuse inflammatory process
involving both lungs, in which the overall lung
volume increases secondary to inflammatory and
proteinaceous materials accumulating in the lung
parenchyma. This results in a loss of
compliance and severe loss of gas exchange.
The overall lung volume increases, but the
there is a decreased volume of lung available
for gas exchange.
13. Histologic Findings
Hyaline Protein in air spaces
Cellular Congestion
Typical histological
findings in ARDS
www.burnsurgery.com/.../pulmonary/part3/sec4.htm
alveolar
inflammation, thickened
septal from protein leak
(pink), congestion and
decreased alveolar volume
←Normal Lung Histology—large alveolar volumes,
septal spaces very thin, no cellular congestion.
14. Determining ARDS Radiographically
Can be difficult to do. Should always try to
make the diagnosis in light of the clinical picture.
Need to determine Cardiogenic vs. Non-
cardiogenic edema.
15. Cardiogenic vs. Non-Cardiogenic
Edema
Cardiogenic Non-Cardiogenic
Patchy infiltrates Infiltrates are more
appearing in the lung homogeneous
bases first No pleural effusions
Effusions may be present No Kerley B’s
Clinical signs and Radiographic evidence
symptoms lag behind lags behind clinical signs
radiographic evidence (i.e. and symptoms (i.e. the
CXR is more impressive CXR is unimpressive given
than the degree of the degree of hypoxemia)
hypoxemia)
16. Cardiogenic vs. Non-Cardiogenic
Edema
Cardiogenic Non-Cardiogenic
Excess fluid in alveoli Protein, inflammatory
Due to high cells, and fluid
pulmonary capillary accumulation in the
pressure (estimated by alveoli
measuring pulmonary Due to “other”
artery wedge pressure) systemic factors NOT
elevated pulmonary
capillary pressure
17. Cardiogenic vs. Non-Cardiogenic
Edema via CXR
Cardiogenic Non-Cardiogenic
Bilateral infiltrates predominately in
Diffuse Bilateral patchy infiltrates
lung bases. Kerley B’s. Cardiomegaly.
homogenously distributed throughout the
lungs. Positive tube sign. No Kerley B’s.
18. Cardiogenic vs. Non-Cardiogenic
Edema via CT
Cardiogenic
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Non-Cardiogenic
No septal thickening. Diffuse alveolar
infiltrates. Atelectasis of dependent
Septal thickening. More severe in lung lobes usually seen (not well shown
bases. here)
19. Cardiogenic Edema:
Weenie Man ENDOthelium
Vascular Endothelium
breaks under stress
easily, however it also
repairs itself quickly
Cardiogenic edema often
develops quickly and can
resolve quickly because
vascular endothelium is
able to repair itself
quickly
20. Non-Cardiogenic Edema:
Muscle Man EPIthelium
Alveolar epithelium is quite
resistant to damage. It
withstands greater force before
becoming damaged.
However, once ―broken‖ it takes
much longer to heal than weenie
man endothelium.
Cellular damage in Non-
Cardiogenic edema runs along a
spectrum from predominately
vascular endothelial damage to
predominately alveolar epithelial
damage
22. Management: Reducing Ventilator-
Induced Lung Injury
Low tidal volume mechanical ventilation
In ARDS there is a large amount of poorly compliant (i.e.
non-ventilating) lung and a small amount of
healthy, compliant lung tissue. Large tidal volume ventilation
can lead to over-inflation of the healthy lung tissue resulting
in ventilator-induced lung injury of that healthy tissue.
PEEP
Setting a PEEP prevents further lung injury due to shear
forces by keeping airways patent during expiration
23. The Flip Side
Is there such thing as too low a TV?
Tidal Volume must be sufficient for gas exchange to take place.
Permissive hypercapnia is the term used to state that a certain degree of
hypercapnia and its resulting acidemia can be allowed in order to maintain
lung-protective TVs.
Absolute limits is unclear, but a pH of 7.2-7.25 and a PCO2 of 60-70 mm Hg
is a good cut off range.
Is there such thing as too much PEEP?
PEEP serves to help open less compliant alveoli and keep alveolar open
during expiration, but it too can lead to overinflation of alveoli that are
already maintaining aeration.
Setting PEEP too high also increases intrathoracic pressure leading to
decreased venous return.
Start patients at a PEEP trial of 5 – 12 cm H2O and increase if needed.
24. Diuretics—A Good or Bad Therapy
in ARDS?
Yes No
Diuretics have been shown Diuretics are not anti-
to decrease any pulmonary inflammatory agents: lung
edema that is infiltrates in ARDS are
neutrophils and
present, increase lung proteins, NOT edema
compliance, and improve gas
Hemodynamic compromise:
exchange. However they tissue oxygenation = #1
have shown no survival concern. Aggressive diuretics
benefit. decrease venous pressures
leading to decrease CO and
increased tissue ischemia
25. FACTT Study: New Evidence for
the Benefits of Diuretic Use in ARDS
Large prospective trial addressed the use of
conservative (higher, more frequent lasix doses) verse
liberal fluid management (more frequent fluid boluses).
Outcomes: NO significant difference in 60-day
mortality between the two groups, however the
conservative fluid group had improved lung
function, shorter durations of mechanical
ventilation, and shorter ICU stays, SUPPORTING
THE USE OF DIURETICS.
ARDS Clinical Trial Network. 2006. Comparison of Two Fluid-Management Strategies in
Acute Lung Injury. N Engl J Med. 354 (24). pp 2564-75.
26. Management: Fluid Status
Remember, the #1 goal in therapy is to decrease
tissue ischemia. We must maintain ARDS
patient’s CO to insure tissue profusion.
In the FACTT study, conservative fluid
therapy was not followed if a patient
was deemed to be in shock, in the
presence of oliguria, or if a patient’s
circulation was deemed inadequate.
28. History of Pulmonary Arterial
Catheters
1945: Dexter used PAC
under fluoro to diagnose
congenital heart
disease, mitral valve
disease, and left ventricular
failure.
1975: Swan developed a
technique that enabled the
use of PAC at the bedside.
Initially used to guide therapy
following acute MI.
By inflating a small balloon at the end
of the catheter he was able to float the
tip of the catheter through the right
heart into the pulmonary arteries.
29. Uses of the PAC
Guide therapy, aid in determining
diagnoses, help determine prognosis
Measures
Central venous and pulmonary artery pressures
Pulmonary capillary wedge pressure (PCWP) → left-
arterial pressure
Mixed venous blood gases
Cardiac output
Can also determine systemic and pulmonary vascular
resistances from the above measurements
30. Uses of the PAC in ARDS
Used to aid in diagnosis
Traditionally placed to confirm non-cardiogenic
edema verses cardiogenic edema in cases of
uncertainty
If PCWP is elevated > 18 mm Hg then by diagnostic
criteria—as set by the American-European Consensus—
the edema is NOT noncardiogenic.
Used to guide treatment
31. Should PCWP Be Used to Confirm
the Diagnosis of ARDS?
PCWP is an estimate of left atrium pressure
When the PAC balloon is inflated it occludes blood flow
through the lungs. The pressure measured in this closed
circuit is equal to the pressure in the left-atrium.
In ARDS, PCWP is used to estimate pulmonary
capillary pressure. PCWP CANNOT be equal to
pulmonary capillary pressure and left atrial pressure. If
this were true there would be no pressure gradient
making forward blood flow through the pulmonary
arteries possible. Therefore PCWP underestimates
pulmonary capillary pressure.
Suggests wedge pressure should not be part of the
diagnostic criterion for ARDS.
32. Further Reason Why PCWP Should
Not Be Used to Diagnose ARDS
In ARDS, arterial and venous thrombosis in the
pulmonary vasculature is very common (i.e. destruction
of the weenie man endothelium). This means there is a
disruption in the arterial-venous circuit within the lung.
But wait; don’t we need a complete circuit to measure
the left atrium pressure from a catheter sitting in the
pulmonary artery?
It is conceivable that a PAC may in fact be measuring
VENTILATORY PRESSURES not left atrial
pressure.
33. Should PCWP Be Used to Dictate
the Treatment of ARDS?
The Fluid and Catheter Treatment Trial
(FACTT)
A randomized, multi-center trial comparing
outcomes of ARDS patients with use of PACs vs.
CVCs (central venous catheters).
34. FACTT
Result: No difference in mortality, number of
days on the ventilator or in the ICU, lung or
kidney function, rates of hypotension, ventilator
settings or use of dialysis between two groups.
The PAC group had ≈ twice as many catheter-
related complications (mainly arrhythmias).
ARDS Clinical Trial Network. 2006. Pulmonary-Artery versus Central Venous Catheter to Guide
Treatment of Acute Lung Injury. N Engl J Med. 354 (21). pp 2213-24.
35. FACTT Conclusions in Regards to
PACs
PAC-guided therapy for ARDS does not
improve survival or organ-function, reduce
ventilator time or decrease ICU-stays. Although
associated with more complications, major harm
did not occur from PAC use. The evidence
does not favor the routine use of the PAC.
36. Other Evidence For or Against PAC
There have been multiple studies designed to
determine the effect of mortality and morbidity
of PAC use in ICU patients.
No randomized trials that I could find suggested that
PAC use either increased or decreased mortality.
Their use may provide useful information in limited
settings, but their use should be pursued with
though towards how the information gathered will
aid patient management.
37. References
• ARDS Clinical Trial Network. 2006. Comparison of Two Fluid-Management Strategies in Acute Lung
Injury. N Engl J Med. 354 (24). pp 2564-75.
• ARDS Clinical Trial Network. 2006. Pulmonary-Artery versus Central Venous Catheter to Guide
Treatment of Acute Lung Injury. N Engl J Med. 354 (21). pp 2213-24.
• Fan, E., Needham, D.M., Stewart, T.E. Ventilatory Management of Acute Lung Injury and Acute
Respiratory Distress Syndrome. 2005. JAMA. 294 (22). pp. 2889-96.
• Hansen-Flaschen, J., Siegel, M.D. Acute Respiratory Distress Syndrome: Definition; Epidemiology;
Diagnosis; and Etiology. 2006. www.utdol.com.
• Heresi, G.A., Arroligo, A.C., Weidemann, H.P., Matthay, M.A. 2006. Pulmonary Artery Catheter
and Fluid Management in Acute Lung Injury and the Acute Respiratory Distress Syndrome. Clin Chest Med.
27. pp 627-628.
• Marino, P.L. The ICU Book. 3rd Ed. Lippincott Williams & Wilkins. Philadelphia. pp. 419-35.
• Petty, T.L. Acute Respiratory Distress Syndrome: Consensus, Definitions, and Future Directions. 1996.
Crit Care Med. 24(4). pp 555-556.
• Rouby, J-J., Puybasset, L., Nieszkowska, A., Lu, Q. Acute Respiratory Distress Syndrome: Lessons form
Computed Tomography of the Whole Lung. 2003. Crit Care Med. 31(4S). pp. S285-95.
• Weinhouse, G.L., Manaker, S. Swan-Ganz Catheterization: Indications and Complications. 2006.
www.utdol.com.
