acute respiratory distress syndrome acnp boot camp 2014 stephanie davidson, acnp-bc

Acute Respiratory Distress Syndrome

ACNP Boot Camp 2014Stephanie Davidson, ACNP-BC

Objectives• Review the causes and differentials for ARDS• Briefly discuss the pathophysiology • Discuss the clinical manifestations of ARDS• Understand evidence based treatment

options

Statistics• Epidemiology

– Annual incidence: 60/100,000– 20% ICU patients meet criteria for ARDS

• Morbidity / Mortality– 26-44%, most (80%) deaths attributed to non-pulmonary

organ failure or sepsis• Risk Factors

– Advanced age, pre-existing organ dysfunction or chronic medical illness

– Patient with ARDS from direct lung injury has higher incidence of death than those from non-pulmonary injury

Levy BD, & Choi AM, Harrison’s Principles of Internal Medicine, 2012

Bernard et al. AJRCCM 1994; 149:818Rice et al. Chest 2007: 132: 410

June 20, 2012, Vol 307, No. 23

et al. JAMA 2012; 307:2530

-European Society of Intensive Care Medicine with endorsement from American Thoracic Society and Society of Critical Care Medicine-Devised three mutually exclusive severity categories: Mild, Moderate and Severe-Took into account: timing, chest imaging, origin of edema, oxygenation

et al. JAMA 2012; 307:2530

ARDS network N Engl J Med 2000; 342:1301

Pneumonia 35%

Differentials• Left ventricular failure/volume overload• Mitral stenosis• Pulmonary veno-occlusive disease• Lymphangitic spread of malignancy• Interstitial and/or airway disease

– Hypersensitivity pneumonia– Acute eosinophilic pneumonia– Acute interstitial pneumonitis

Pathophysiology

1. Direct or indirect injury to the alveolus causes alveolar macrophages to release pro-inflammatory cytokines

Ware et al. NEJM 2000; 342:1334

Pathophysiology

2. Cytokines attract neutrophils into the alveolus and interstitum, where they damage the alveolar-capillary membrane (ACM).

Ware et al. NEJM 2000; 342:1334

Pathophysiology

3. ACM integrity is lost, interstitial and alveolus fills with proteinaceous fluid, surfactant can no longer support alveolus

Ware et al. NEJM 2000; 342:1334

Pathophysiology• Consequences of lung injury include:

– Impaired gas exchange– Decreased compliance– Increased pulmonary arterial pressure

Impaired Gas Exchange• V/Q mismatch

– Related to filling of alveoli– Shunting causes hypoxemia

• Increased dead space– Related to capillary dead space and V/Q mismatch– Impairs carbon dioxide elimination– Results in high minute ventilation

Decreased Compliance• Hallmark of ARDS• Consequence of the stiffness of poorly or

nonaerated lung• Fluid filled lung becomes stiff/boggy• Requires increased pressure to deliver Vt

Increased Pulmonary Arterial Pressure• Occurs in up to 25% of ARDS patients• Results from hypoxic vasoconstriction• Positive airway pressure causing vascular

compression• Can result in right ventricular failure• Not a practice we routinely measure

• Treat the underlying cause• Low tidal volume ventilation• Use PEEP• Monitor Airway pressures• Conservative fluid management• Reduce potential complications

Evidence based management of ARDS

Hypothesis:In patients with ALI, ventilation with smaller tidal volumes (6 mL/kg)

will result in better clinical outcomes than traditional tidal volumes (12 mL/kg) ventilation.

ARDS Network N Engl J Med 2000; 342:1301

Low Tidal Volume Ventilation• When compared to larger tidal volumes, Vt of 6ml/kg of ideal

body weight:• Decreased mortality• Increased number of ventilator free days• Decreased extrapulmonary organ failure

• Mortality is decreased in the low tidal volume group despite these patients having:• Worse oxygenation• Increased pCO2 (permissive hypercapnia)• Lower pH

ARDSnet. NEJM 2000; 342: 1301

Low Tidal Volume VentilationARDS affects the lung in a

heterogeneous fashion• Normal alveoli• Injured alveoli can

potentially participate in gas exchange, susceptible to damage from opening and closing

• Damaged alveoli filled with fluid, do not participate in gas exchange

Low Tidal Volume Ventilation• Protective measure to avoid over distention of

normal alveoli• Uses low (normal) tidal volumes• Minimizes airway pressures• Uses Positive end-expiratory pressure (PEEP)

Hypothesis:

In patients with ALI ventilated with 6 mL/kg, higher levels of

PEEP will result in better clinical outcomes than lower levels of

PEEP.

N Engl J Med 2004; 351:327

PEEP• Higher levels of PEEP/FiO2 does not improve

outcomes – may negatively impact outcomes:

• Causing increased airway pressure• Increase dead space• Decreased venous return• Barotrauma

PEEP• Positive End Expiratory Pressure• Every ARDS patient needs it• Goal is to maximize alveolar recruitment and

prevent cycles of recruitment/derecruitment

Meade, M et al, JAMA. 2008; 299(6):637-645

-983 patients, randomized into control group with ALI protocol, low Vt and PEEP vs. Open lung group with low Vt, higher PEEP and recruitment maneuvers-No statistically significant difference in mortality outcomes

Mercatt, M, et al. JAMA. 2008; 299(6):646-655.

-Multicenter randomized trial, 767 patients. Set a PEEP aimed to increase alveolar recruitment while limiting hyperinflation-Randomly assigned two groups: moderate PEEP (5-9cm H2O) vs. level of PEEP to reach a plateau pressure of 28-30cm H2O-Found that it didn’t significantly reduce mortality; however, it did improve lung function and decreased days on vent and organ failure duration

PEEP• As FiO2 increases, PEEP should also increase

ARDSnet. NEJM 2004; 351, 327

Auto Peep

Airway Pressures in ARDS• Plateau pressure is most predictive of lung injury• Goal plateau pressure < 30, the lower the better

• Decreases alveolar over-distention and reduces risk of lung strain

• Adjust tidal volume to ensure plateau pressure at goal• It may be permissible to have plateau pressure > 30 in

some cases• Obesity• Pregnancy• Ascites

Terragni et al. Am J Resp Crit Care Med. 2007; 175(2):160

Permissible Plateau Pressures• Assess cause of high Plateau Pressures• Always represents some pathology:

– Stiff, non-compliant lung: ARDS, heart failure– Pneumothorax– Auto-peeping– Mucus Plug– Right main stem intubation– Compartment syndrome– Chest wall fat / Obesity

Airway Pressures

Peak Inspiratory Pressure

Plateau Pressure

PEEP

Airway Pressures

Time

N Engl J Med 2006; 354: 2213

Fluid and Catheter Treatment Trial--No need for routine PAC use is ALI patients--Support use of conservative strategy fluid management in patients with ALI

Results• Using the data from a PAC compared to that from a CVC in

an explicit protocol:– Did not alter survival.– Did not improve organ function.– Did not change outcomes for patients entering in shock

compared to those without shock.• PAC use resulted in more non-fatal complications, mostly

arrhythmias.

N Engl J Med 2006; 354: 2213

N Engl J Med. 2006;354:2564

~Hypothesis: Diuresis or fluid restriction may improve lung function but could jeopardize extrapulmonary organ perfusion

~Conclusion: Conservative fluid management improved lung function and shortened mechanical ventilation times and ICU days without increasing nonpulmonary organ failures

Fluid Management• Increased lung water is the

underlying cause of many of the clinical abnormalities in ARDS (decreased compliance, poor gas exchange, atelectasis)

• After resolution of shock, effort should be made to attempt diuresis

• CVP used as guide, goal <4• Shortens time on vent and ICU

length of stay (13 days vs 11 days)

ARDSnet. NEJM 2006; 354: 2564

Hypothesis: Early application of prone positioning would improve survival in patients with severe ARDS.

Conclusion: Early application of prolonged prone positioning significantly decreased 28 day and 90 mortality in patients with severe ARDS.

Guerin et al. NEJM. 2013; 368:2159

Weaning• Daily CPAP breathing trial

– FiO2 <.40 and PEEP <8– Patient has acceptable spontaneous breathing efforts– No vasopressor requirements, use judgement

• Pressure support weaning– PEEP 5, PS at 5cm H2O if RR <25– If not tolerated, ↑RR, ↓Vt – return to A/C

• Unassisted breathing– T-piece, trach collar– Assess for 30minutes-2 hours

Weaning• Tolerating Breathing Trial?

– SpO2 ≥90– Spontaneous Vt ≥4ml/kg PBW– RR ≤35– pH ≥7.3– Pass Spontaneous Awakening Trial (SAT)– No Respiratory Distress ( 2 or more)

• HR > 120% baseline• Accessory muscle use• Abdominal Paradox• Diaphoresis• Marked Dyspnea

– If tolerated, consider extubation

Putting it all together1) Calculate patient’s predicted body weight:

• Men (kg) = 50 + 2.3(height in inches – 60)• Females (kg) = 45.5 + 2.3(height in inches – 60)

2) Set Vt = predicted body weight x 6cc3) Set initial rate to approximate baseline minute

ventilation (RR x Vt)4) Set FiO2 and PEEP to obtain SaO2 goal of >=88%5) Diurese after resolution of shock 6) Refer to ARDSnet guidelines

Troubleshooting Common Problems

Refractory Hypoxia• Mechanical Trouble (tubing, ventilator, ptx, plugging)• Neuromuscular blockade• Recruitment maneuvers – positioning, “good lung down”

optimizes V/Q mismatch• Increase PEEP• Inhaled epoprostenol sodium (Flolan)

– When inhaled, the vasodilator reaches the normal lung, is concentrated in normal lung segments and recruits blood flow to functional alveoli where it is oxygenated. This decreases shunting and hypoxemia

• High frequency ventilation

Ferguson, N, et al, NEJM 2013; 368: 795-805.

-Randomized control trial, stopped with 548 of 1200 patients-Found early initiation of HFOV does not reduce and may increase hospital mortality

Young, D, et al,NEJM. 2013; 368:806-813

-Multicenter randomized trial with 795 patients enrolled-found there is no significant effect of 30 day survival between patients who received HFOV and conventional mechanical ventilation

Papazian, L, et al. NEJM 2010; 363: 1107-1116.

-Neuromuscular blocking agents may increase oxygenation and decrease ventilator associated lung injury in severe ARDS patients-Multicenter double blind trial with 340 patients; received 48hrs of cisatracurium (Nimbex) or placebo-Found that early administration of NBA improved 90 day survival and increased time off vent without increase in muscle weakness

Supportive Therapies• Treat underlying infection• DVT prophylaxis / stress ulcer prevention• HOB 30°• Hand washing• Use full barriers with chlorhexadine• Sedation / analgesia• Feeding protocol• Avoid contrast nephropathy• Pressure ulcer prevention, turning Q2h• Avoid steroid use

~No benefit of corticosteroids on survival

~When initiated 2 weeks after onset of ARDS, associated with significant increase in mortality rate compared to placebo group

N Engl J Med. 2006; 354:1671

Conclusion• Recovery dependent on health prior to onset• Within 6 months, will have reached max recovery• At 1 year post-extubation, >1/3 have normal spirometry• Significant burden of emotional and depressive symptoms

with increased depression and PTSD in ARDS survivors• Survivor clinic catches symptoms early by screening patients

• New treatment modalities, lung protective ventilation

Levy BD, & Choi AM, Harrison’s Principles of Internal Medicine, 2012

Questions ?

ReferencesAcute Respiratory Distress Syndrome Network: Ventilation with Tidal Volumes as

compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. New Engl J Med. 2000; 342: 1302-1308.

ARDSNet: Higher versus lower Positive End-Expiratory Pressures in patients with the acute respiratory distress syndrome. New Engl J Med. 2004; 351: 327-336.

ARDSNet: Efficacy and Safety of Corticosteroids for persistent acute respiratory distress syndrome. New Engl J Med. 2006; 354: 1671-1684.

ARDSNet: Comparison of Two fluid management strategies in acute lung injury. New Engl J Med. 2006; 354: 2564-75.

ARDSNet: Pumonary Artery versus Central Venous catheter to guide treatment of acute lung injury. New Eng J Med. 2006; 354: 2213-2224.

Et al: Acute respiratory distress syndrome: The Berlin Definition. JAMA. 2012; 307(23): 2526-2533.

Ferguson N, et al: High frequency oscillation in early acute respiratory distress syndrome. New Engl J Med. 2013; 368: 795-805.

Guerin C et al: Prone positioning in severe acute respiratory distress syndrome. New Engl J Med. 2013; 368: 2159-2168.

ReferencesLevy B.D., Choi A.M. (2012). Chapter 268. Acute Respiratory Distress Syndrome. In A.S.

Fauci, D.L. Kasper, J.L. Jameson, D.L. Longo, S.L. Hauser (Eds), Harrison's Principles of Internal Medicine, 18e. Retrieved August 17, 2013 from http://www.accesspharmacy.com.proxy.library.vanderbilt.edu/content.aspx?aID=9105737.

Meade M, et al: Ventilation Strategy Using low tidal volumes, recruitment maneuvers and high post end expiratory pressure for acute lung injury and acute

respiratory distress syndrome. JAMA. 2008; 299(6):637-645.Mercatt M, et al: Post end-expiratory pressure settings in adults with acute lung injury

and acute respiratory distress syndrome. JAMA. 2008; 299(6): 645-655.Papazian L, et al: Neuromuscular blockers in early acute respiratory distress syndrome.

New Engl J Med. 2010; 363:1107-1116.RiceTW et al: Comparison of the SpO2/FiO2 Ration and the PaO2/FiO2 Ratio in

patients with acute lung injury or acute respiratory distress syndrome. Chest. 2007; 132: 410-417.

Terragan PP et al: Tidal hyperinflation during low tidal volume ventilation in Acute respiratory distress syndrome. J Resp Crit Care Med. 2007; 175: 160-166Ware LB, Matthay MA: The Acute Respiratory Distress Syndrome. New Engl J Med.

2000; 342: 1334-1349.Young D, et al: High frequency oscillation for acute respiratory distress syndrome. New Engl J Med. 2013; 368:806-813.

References