acute respiratory distress syndrome(ards)

7/31/2019 ACUTE RESPIRATORY DISTRESS SYNDROME(ARDS)

1/45

ACUTE RESPIRATORY

DISTRESS SYNDROME

(ARDS)

Timothy G. Janz, MD

Department of Emergency Medicine

Pulmonary/Critical Care Division

Department of Internal Medicine


2/45

ARDSDefinitions

Acute Lung Injury

150200 mmHg < PaO2/FIO2 < 250300 mmHg

ARDS

PaO2/FIO2 < 150200 mmHg


3/45

ARDSEpidemiology

Incidence:

571 per 100,000

Financial cost:

$5,000,000,000 per annum


4/45

ARDSPathophysiology

Profound inflammatory response

Diffuse alveolar damage acute exudative phase (1-7days)

proliferative phase (3-10 days)

chronic/fibrotic phase (> 1-2 weeks)


5/45

ARDSAcute Exudative Phase

Basement membrane disruption Type I pneumocytes destroyed

Type II pneumocytes preserved

Surfactant deficiency inhibited by fibrin

decreased type II production

Microatelectasis/alveolar collapse


6/45



7/45



8/45



9/45

ARDSProliferative Phase

Type II pneumocyte

proliferate

differentiate into Type I cells

reline alveolar walls

Fibroblast proliferation

interstitial/alveolar fibrosis


10/45

ARDSProliferative Phase


11/45

ARDSFibrotic Phase

Characterized by:

local fibrosis

vascular obliteration

Repair process:

resolution vs fibrosis


12/45

ARDSPathophysiology

Interstitial/alveolar edema

Severe hypoxemia

due to intra-pulmonary shunt (V/Q = 0)

shunt ~ 25% - 50%

Increased airway resistance


13/45

ARDSPathophysiology

High ventilatory demands

high metabolic state

increased VD

/VT

decreased lung compliance

Pulmonary HTN

neurohumoral factors, hypoxia, edema


14/45

ARDSEtiology


15/45

ARDSEtiology

Hospital-acquired

infection/sepsis

massive blood transfusions

gastric aspiration

Community-acquired

trauma

pneumonia drugs/aspiration/inhalations


16/45

ARDSClinical Phases

I. Injury Phase

II. Latent/Lag Phase

III. ARF Phase

IV. Recuperative/Terminal Phase


17/45

ARDSClinical Features

Acute dyspnea/tachypnea rales/rhonchi/wheezing

Resistant hypoxemia PaO2/FIO2 < 150200 mmHg

CXR diffuse, bilateral infiltrates

No evidence of LV failure (PAWP < 18 mmHg)


18/45

ARDSClinical Features: CXR


19/45

ARDSClinical Features: CXR


20/45

ARDSDifferential Diagnosis

CARDIOGENIC PULMONARY EDEMA

Bronchopneumonia

Hypersensitivity pneumonitis

Pulmonary hemorrhage

Acute interstitial pneumonia (Hamman-Rich Syndrome)


21/45

ARDSDiagnosis

Resistant hypoxemia PaO2/FIO2 < 150200 mmHg

CXR diffuse, bilateral infiltrates

No evidence of LV failure (PAWP < 18 mmHg)


22/45

ARDSDiagnosis


23/45

ARDSDiagnosis

Based on clinical criteria

no diagnostic tests

Confirmatory tests:

PA catheter

PAWP = normal/reduced

[bronchial secretion protein]:[serum protein] ratio > 70% - 80%


24/45

ARDSTreatment: Standard

Rx underlying cause

Adequate oxygenation/ventilation PaO2 > 60 mmHg; SaO2 > 90%

PEEP usually needed to meet O2 goals

Prevents/corrects alveolar collapse converts: (V/Q = 0) to V/Q mismatch

ARDS


25/45

ARDSOpen-Lung Approach to PEEP

Amato,Am J Respir Crit Care Med1995; 152:183

ARDS


26/45

ARDSTreatment: PEEP

Open-lung approach

Not practical

Does not improve outcomes

Optimal PEEP

???

Most cases: PEEP ~ 1520 cmH2O

ARDS


27/45

ARDSOptimal PEEP

Maximize lung compliance

Crs = Vt/(PplateauPEEP)

Maximize O2

delivery

DO2 = 10 x CO x (1.34 x Hgb x SaO2)

Lowest PEEP to oxygenate @ FIO2 < .60

Empiric approach:

PEEP = 16 cmH2O and Vt = 6 ml/kg

ARDS


28/45

ARDSOptimal PEEP

ARDS Network protocol

FIO2 - 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0PEEP - 5 5-8 8-10 10 10-14 14 14-18 18-22

ARDS Network,N Engl J Med2000; 342:1www.ardsnet.org

ARDS


29/45

ARDSVentilator-Induced Lung Injury

ARDS


30/45

ARDSTreatment:Lung-Protective Ventilation

ARDS Network,N Engl J Med2000; 342:1301ardsnet.org

ARDS


31/45

ARDSTreatment: Lung-Protective Ventilation

VT = 6 mL/kg

Limit plateau pressures < 30 cmH2O Volume controlled ventilation

Limit peak airway pressures < 40 cmH2O

Pressure controlled ventilation

ARDS


32/45


VT = 6 mL/kg

Limit peak airway pressures < 40 cmH2O

Limit plateau pressures < 30 cmH2O

ARDS


33/45


Complications: (derecruitement)

Elevated PaCO2

Limit: pH > 7.207.25

Worsening hypoxemia Correction:

Recruitement maneuver

increasing PEEP

ARDS


34/45

ARDSTreatment: Mechanical Ventilation (MV)

Pressure controlled ventilation

Controlled airway pressures

Controlled inspiratory times

Patient comfort

Effectiveness:

PCV = VCV

ARDS


35/45

ARDSTreatment: Alternate Modes of MV

Inverse-ratio ventilation

Airway pressure-release ventilation

Bilevel airway pressure ventilation

Proportional-assist ventilation

High-frequency ventilation

ECMO

Tracheal gas insufflation

ARDS


36/45

ARDSTreatment: Prone Positioning

Chatte,Am J Respir Crit Care Med 1997; 25:153

ARDS


37/45


ARDS


38/45


65% responders

Multiple proposed mechanisms Improved oxygenation

Difficult to implement

No improvement in outcomes

ARDS


39/45

ARDSTreatment: Partial Liquid Ventilation

Lungs filled to FRC with perflubron 17 times more O2 dissolved than water

Low surface tension

Gravitates to dependent areas of lungs

Nontoxic Minimally absorbed

Eliminated by evaporation

ARDS


40/45

ARDSTreatment: Partial Liquid Ventilation

Used as lavage + conventional MV

Multiple proposed mechanisms

Improves oxygenation

No improvement in outcomes

ARDS


41/45

ARDSTreatment: Vasodilators

Gerlach,Eur J Clin Invest 1993; 23:499


42/45

ARDS


43/45

ARDSTreatment: Other Modalities

Antiinflammatory agents

Steroids may have a role

Antioxidants

Surfactant replacement

Increased alveolar fluid removal

Effect sodium channels

Activate Na+-K+-ATPase pump

ARDS


44/45

ARDSPrognosis

Mortality 30% - 50%

Death from respiratory failure = 15% - 18%

Most common cause of death - sepsis/infection

Outcomes Majority have near-normal lung function

Small % develop pulmonary fibrosis Neuropsychiatric sequelaemay be high

The End


45/45

The End

acute respiratory distress syndrome(ards)

Documents