ARDS University of Washington Department of Respiratory Care Services Skills Day May, 2006

ARDS

University of Washington

Department of Respiratory Care Services

Skills Day May, 2006

CASE PRESENTATION

• A 62 year old woman with a history of coronary artery disease comes to the ER with shortness of breath over the past 8 hours. A CXR reveals a bilateral alveolar filling process and her arterial blood gas shows marked hypoxemia despite a 70 % high flow mask.

• A PA catheter is placed to assess the cause of the bilateral infiltrates.

CASE PRESENTATION

• SVR - 500 dynes/sec/cm2

• PA - 21/ 13 mm Hg

• PAOP - 11 mm Hg

• CO - 9 LPM You should:

1) Consider a inotrope such as dobutamine as she is in CHF.

2) Administer dopamine IV, evaluate carefully for a source of infection and cover with broad spectrum antibiotics

3) Consider volume infusion with normal saline to treat her volume depletion.

CASET PRESENTATION• She develops progressive hypoxemia

despite 100 % non-rebreather mask and is intubated.

• The most appropriate ventilator management would include the following settings:

A) VT = 600ml, PEEP = 15cmH2OB) VT = 600 ml, PEEP = 5 cmH2OC) VT = 400 ml, PEEP = 10 cmH2OD) VT = 400 ml, PEEP = 17.5 cmH2O

ARDS Definition

• American-European Consensus Conference-1994– Acute onset of respiratory symptoms (with associated

predisposing factor)

– Bilateral infiltrates on CXR

– PCWP ≤18 or the absence of clinical evidence of LA hypertension

– PaO2/FiO2 ratio:· ≤ 200 = ARDS

· ≤ 300 = ALI (acute lung injury)

ARDSPredisposing Factors

–Direct Lung Injury

· Pneumonia

· Aspiration

· Lung contusion

· Near-drowning

· Inhalation injury

· Fat emboli

–Indirect lung injury

·Sepsis

·Severe trauma

·Acute pancreatitis

·Blood transfusions

·Cardiopulmonary bypass

PATHOGENESIS• Target organ injury from host’s inflammatory response and

uncontrolled liberation of inflammatory mediators

• Localized manifestation of SIRS

• Neutrophils and macrophages play major roles

• Complement activation

• Cytokines: TNF-, IL-1, IL-6

• Platelet activation factor

• Eicosanoids: prostacyclin, leukotrienes, thromboxane

• Free radicals

• Nitric oxide

PATHOPHYSIOLOGY

• Abnormalities of gas exchange

• Oxygen delivery and consumption

• Cardiopulmonary interactions

• Multiple organ involvement

ABNORMALITIES OF GAS EXCHANGE

• Hypoxemia: HALLMARK of ARDS– Increased capillary permeability

– Interstitial and alveolar exudate

– Surfactant damage

– Decreased FRC

– Diffusion defect and right to left shunt

ARDS STAGES

• Acute or Exudative Phase

• Proliferative or Subacute Phase

• Chronic Phase

–Scarring

–Recovery

ARDS STAGES

• Acute, exudative phase– rapid onset of respiratory failure after trigger

– diffuse alveolar damage with inflammatory cell infiltration

– hyaline membrane formation

– capillary injury

– protein-rich edema fluid in alveoli

– disruption of alveolar epithelium

NORMAL ALVEOLUS

Type I cell

EndothelialCell

RBC’s

Capillary

Alveolarmacrophage

Type IIcell

ACUTE PHASE OF ARDS

Type I cell

EndothelialCell

RBC’s

Capillary

Alveolarmacrophage

Type IIcell

Neutrophils

Proliferative Phase

• Subacute, Proliferative phase:

– persistent hypoxemia

– development of hypercarbia

– fibrosing alveolitis

– further decrease in pulmonary compliance

– pulmonary hypertension

Chronic Phase

• Chronic phase

– obliteration of alveolar and bronchiolar spaces and pulmonary capillaries

• Recovery phase

– gradual resolution of hypoxemia

– improved lung compliance

– resolution of radiographic abnormalities

ARDS Treatments

• Decades of Ineffective Treatments– Steroids

– NSAIDs

– Pentoxyphlline

– Nitric oxide

– surfactant

– ……….

Low Tidal Volume Strategies in ARDSLow Tidal Volume Strategies in ARDS

• High lung inflation volumes over distend more compliant portions of the lung.

• In the past our high tidal volume strategies may have actually caused lung injury (“ventilator lung”).

• Using lower lung volumes may prevent over distension and reduce ventilator induced lung injury.

ARDS NETWORK

• Clinical Trials Network > 20 centers nationwide• Multiple Trials• Initial Study “ARMA”• Randomized to 6 ml/kg (IBW) vs. 12 ml/kg and

plateau pressure <30 cm• Study was halted early due to significant survival

improvement in one group

New England Journal of Medicine 2000;342:1301-8

Mortality Prior to Hospital DischargeMortality Prior to Hospital Discharge

0

10

20

30

40

50

Mortality (Percent)

6 ml/kg 12 ml/kg

P=0.0054

What about PEEP ?

• 549 ARDS Patients

• Randomized to high or low PEEP levels– 5 versus 12 cm PEEP

– ? Differences in mortality, ventilator, ICU and hospital days

High vs. Low PEEP Protocol

High vs. Low PEEP

Where do I set PEEP ?

Recruitment Maneuvers

• Hyperinflation maneuvers to open collapse lung

• Some parts of lung are open, some are collapsed

• Detrimental effects:– “Baby lungs” can be overdistended

– Collapsed portions can put traction on normal portions causing injury

– Opening and closing of collapsed or atelectatic areas could cause “shear stress injury”

Baby Lung Effect Shear Force Effect

NEJM 1998;347

• CT Scan and outcome study of patients with ARDS who had recruitable lung looked at

• Percentage of recruitable lung looked at as a predictor of outcomes

• 13% of lung was recruitable

• Higher percentage of recruitable lung correlted with:

– Higher oxygenation requirments

– Heavier lungs

– Worse outcome

• BOTTOM LINE: THE JURY IS STILL OUT ON RECRUITMENT MANEUVERS

• KCLIP DATA

• Survey of ALI and ARDS in King County

NEJM 2005;353:1685

• KCLIP Cohort

NEJM 2005;353:1685

NEJM 2005;353:1685

ARDS

• Big Problem

• Small tidal volumes

• Small pressures

• PEEP around 10

• No recruitment maneuvers at this time.