Acute Respiratory Distress Syndrome Hol y Starks, MS4 March 2007
Outline Definitions and Diagnosis Pathophysiology Cardiogenic vs Noncardiogenic Edema Management of ARDS Pulmonary Artery Catheters
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.
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. 288996.
ARDS Diagnostic Criteria From the AmericanEuropean 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).
Predisposing Conditions Sepsis (#1 cause) Severe Trauma Severe PNA DIC Aspiration Drug overdose: Heroin, Near Drowning methamphetamine, cocaine Smoke inhalation Acute pancreatitis Multiple blood product transfusions Severe Burn Look for the + Tube Sign!!!!
Positive Tube Sign The majority of patients with ARDS require intubation and mechanical ventilation www.fhs.mcmaster.ca/…/photos.htm
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.
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.
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 overal lung volume increases, but the there is a decreased volume of lung available for gas exchange.
Histologic Findings Hyaline Protein in air spacesCellular 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.
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.
Cardiogenic vs. NonCardiogenic Edema Cardiogenic NonCardiogenic 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)
Cardiogenic vs. NonCardiogenic Edema Cardiogenic NonCardiogenic Excess fluid in alveoli Protein, inflammatory Due to high pulmonary cel s, and fluid capil ary pressure accumulation in the (estimated by alveoli measuring pulmonary Due to “other” artery wedge pressure) systemic factors NOT elevated pulmonary capil ary pressure
Cardiogenic vs. NonCardiogenic Edema via CXR Cardiogenic NonCardiogenic Bilateral infiltrates predominately in lung bases. Kerley B’s. Diffuse Bilateral patchy infiltrates Cardiomegaly. homogenously distributed throughout the lungs. Positive tube sign. No Kerley B’s.
Cardiogenic vs. NonCardiogenic Edema via CT m h o t Cardiogenic t d p e :/ = /r NonCardiogenic q a u d i . z u & su im hs i . d e = d 1 u/ 6 m 07 ed 8 p & ix q / u m iz e = d n p o ix & _ c i o m m ag eb e. a h c t k m to l? =mode=caption_list No septal thickening. Diffuse alveolar infiltrates. Atelectasis of Septal thickening. More severe in lung dependent lobes usually seen (not bases. well shown here)
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
NonCardiogenic 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
Management for ARDS There is no definitive treatment for ARDS
Management: Reducing Ventilator Induced Lung Injury Low tidal volume mechanical ventilation In ARDS there is a large amount of poorly compliant (i.e. nonventilating) lung and a small amount of healthy, compliant lung tissue. Large tidal volume ventilation can lead to overinflation of the healthy lung tissue resulting in ventilatorinduced lung injury of that healthy tissue. PEEP Setting a PEEP prevents further lung injury due to shear forces by keeping airways patent during expiration
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 lungprotective TVs. Absolute limits is unclear, but a pH of 7.27.25 and a PCO2 of 6070 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. Set ing 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.
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 present, infiltrates in ARDS are increase lung compliance, neutrophils and proteins, NOT edema and improve gas exchange. However they have shown Hemodynamic compromise: tissue oxygenation = #1 no survival benefit. concern. Aggressive diuretics decrease venous pressures leading to decrease CO and increased tissue ischemia
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 60day 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 FluidManagement Strategies in Acute Lung Injury. N Engl J Med. 354 (24). pp 256475.
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.
Use of Pulmonary Arterial Catheters in ARDS SwanGanz Catheter
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 smal bal oon at the end of the catheter he was able to float the tip of the catheter through the right heart into the pulmonary arteries.
Uses of the PAC Guide therapy, aid in determining diagnoses, help determine prognosis Measures Central venous and pulmonary artery pressures Pulmonary capil ary wedge pressure (PCWP) → leftarterial pressure Mixed venous blood gases Cardiac output Can also determine systemic and pulmonary vascular resistances from the above measurements
Uses of the PAC in ARDS Used to aid in diagnosis Traditional y placed to confirm noncardiogenic edema verses cardiogenic edema in cases of uncertainty If PCWP is elevated > 18 mm Hg then by diagnostic criteria—as set by the AmericanEuropean Consensus —the edema is NOT noncardiogenic. Used to guide treatment
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 leftatrium. In ARDS, PCWP is used to estimate pulmonary capil ary pressure. PCWP CANNOT be equal to pulmonary capil ary 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 capil ary pressure. Suggests wedge pressure should not be part of the diagnostic criterion for ARDS.
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 arterialvenous circuit within the lung. But wait; don’t we need a complete circuit to measure the left atrium pressure from a catheter sit ing in the pulmonary artery? It is conceivable that a PAC may in fact be measuring VENTILATORY PRESSURES not left atrial pressure.
Should PCWP Be Used to Dictate the Treatment of ARDS? The Fluid and Catheter Treatment Trial (FACTT) A randomized, multicenter trial comparing outcomes of ARDS patients with use of PACs vs. CVCs (central venous catheters).
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 catheterrelated complications (mainly arrhythmias). ARDS Clinical Trial Network. 2006. PulmonaryArtery versus Central Venous Catheter to Guide Treatment of Acute Lung Injury. N Engl J Med. 354 (21). pp 221324.
FACTT Conclusions in Regards to PACs PACguided therapy for ARDS does not improve survival or organfunction, reduce ventilator time or decrease ICUstays. Although associated with more complications, major harm did not occur from PAC use. The evidence does not favor the routine use of the PAC.
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 set ings, but their use should be pursued with though towards how the information gathered wil aid patient management.
References • ARDS Clinical Trial Network. 2006. Comparison of Two FluidManagement Strategies in Acute Lung Injury. N Engl J Med. 354 (24). pp 256475. • ARDS Clinical Trial Network. 2006. PulmonaryArtery versus Central Venous Catheter to Guide Treatment of Acute Lung Injury. N Engl J Med. 354 (21). pp 221324. • Fan, E., Needham, D.M., Stewart, T.E. Ventilatory Management of Acute Lung Injury and Acute Respiratory Distress Syndrome. 2005. JAMA. 294 (22). pp. 288996. • HansenFlaschen, 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., Mat hay, M.A. 2006. Pulmonary Artery Catheter and Fluid Management in Acute Lung Injury and the Acute Respiratory Distress Syndrome. Clin Chest Med. 27. pp 627628. • Marino, P.L. The ICU Book. 3rd Ed. Lippincot Wil iams & Wilkins. Philadelphia. pp. 419 35. • Pet y, T.L. Acute Respiratory Distress Syndrome: Consensus, Definitions, and Future Directions. 1996. Crit Care Med. 24(4). pp 555556. • Rouby, JJ., 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. S28595. • Weinhouse, G.L., Manaker, S. SwanGanz Catheterization: Indications and Complications. 2006. www.utdol.com.