ACUTE RESPIRATORY DISTRESS SYNDROME

DEFINITION AND DIAGNOSIS ETIOLOGY PATHOGENESIS TREATMENT CONCLUSIONS

ARDS VS ACUTE LUNG INJURY

A LI i th e te rm u se d fo r p a ti n ts w i s e th

si n i ca n t h yp oxe m i ( Pa O 2 / Fi 2 ra ti o f g fi a O o < 300 )

A R D S i th e te rm u se d fo r a su b se t o f A LI s

p a ti n ts w i se ve re h yp oxe m i ( Pa O 2 / Fi 2 e th a O ra ti o f < 2 0 0 ) o

DEFINITION syndrome: A clinical

Severe dyspnea of rapid onset. Diffuse pulmonary infiltrate /Rx Pulmonary-artery wedge pressure <18mmHg or the absence of clinical evidence of left atrial hypertension PaO2/ FiO2 < 300 ALI PaO2/ FiO2 < 200 ARDS

ETIOLOGY

PATHOGENESIS
EXUDATIVE PROLIFERATIVE FIBROTIC

0-7

14

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Loss of type 1 pneumocytes Loss of tight alveolar barrier IL1,TNF, IL8,Leukotrines Accumulation of WBCs and plasma proteins in

air spaces Dysfunctional pulmonary surfactant leading to hyaline membrane formation

Pathology of ARDS
ARDS is a diffuse inflammatory process

involving both lungs, in which the overall lung volume increases secondary to inflammatory and proteinaceousmaterials 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.

Alveolar edema in dependent portions of lung Atelectsis Intrapulmonary shunting Hypoxemia Increased work of breathing Dyspnoea Microvascular obstruction Decreased pulmonary blood flow to ventilated

parts Increased dead space and pulmonary HTN

RADIOGRAPHIC FINDINGS
Chest x-ray-Alveolar and interstitial opacities

involving at least 3/4of lung fields Patchy or homogenous b/l infiltrates Findings of barotrauma-Pneumothrax CT-extensive heterogeneity of lung involvment Needs to be differentiated cardiogenic vs non cardiogenic edema.

Cardiogenic vs. NonCardiogenic Edema

CARDIOGENIC

Patchy infiltrates appear in lung bases first Effusion may be present Clinical signs and symptoms lag behind radiographic Evidence. NONCARDIOGENIC Infiltrates are more homogenous. Neither pleural effusion nor curley B lines Radiographic evidence lag behind clinical

Cardiogenic vs. Non-Cardiogenic Edema via CXR

Bilateral infiltrates predominately in lung bases. Kerley Bs. Cardiomegaly.

Diffuse Bilateral patchy infiltrates homogenously distributed throughout the lungs. Positive tube sign. No Kerley Bs.

Cardiogenic vs. Non-Cardiogenic Edema via CT

Septalthickening. lung bases.

More severe in

No septalthickening. Diffuse alveolar infiltrates. Atelectasis of dependent lobes usually seen (not well shown here)

PROLIFERATIVE PHASE
Neutrophils Gradully replaced by lymphocytes Type 2 pneumocyte proliferation Alveolar type 3 procollagen peptide which is a

marker of pul.fibrosis

FIBROTIC PHASE
Extensive alveolar duct and alveolar fibrosis Leads to increased dead space Deceased lung compliance pneumothorax

AnloInteresting nNote a re th e A l f th e p re d i o si g co d i o n s sh sp n ti
c b i i to tri g e r a syste m i i fl m m a to ry a l ty g c n a

re sp o n se . H u m .
T h e m a j ri o f A R D S d e a th s a re N O T d u e to o ty

re sp i to ry fa i u re , b u t m u l p l o rg a n fa i u re ra l ti e l se co n d a ry to syste m i i fl m m a to ry c n a p ro ce sse s.

DIFFERENTIAL DIAGNISIS
Cardigenic pulmonary edema Diffuse pneumonia Alveolar hemorrhage Acute interstitial lung disease Acute interstitial pnumonitis Acute immonological lung injury Hypersensitivity pneumonitis Toxin injury Neurogenic pulmonary edema

TREATMENT GOAL
Adequate oxygenation with avoidance of complications and adequate nutrition. Recognition and treatment of underlying medical and surgical disorder Prophylaxis against DVT,GIT bleed and central venous catheter infection prevention. Prompt recognition of nosocomial infections

MECHANICAL VENTILATION
Repeated alveolar collapse and overdistention Lead to hypothesis low TV protect against

ventilation induced lung injury.

TIDAL VOLUME
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 acidemiacan 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 overinflationof alveoli that are already maintaining aeration. Setting PEEP too high also increases intrathoracicpressure leading to decreased venous return.

Start patients at a PEEP trial of 5 12 cm H2O and increase if needed.

DiureticsA Good or Bad Therapy in ARDS?

Yes Diuretics have been shown to decrease any pulmonary edema that is present, increase lung compliance, and improve gas exchange. However they have shown no survival benefit.

DIURETICS
No Diuretics are not anti-inflammatory agents: lung infiltrates in ARDS are neutrophils and proteins, NOT edema Hemodynamic compromise: tissue oxygenation = #1 concern. Aggressive diuretics decrease venous pressures leading to decrease CO and increased tissue ischemia

Use of Pulmonary Arterial Catheters in ARDS

S w a n - G a n z C a th e te r

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

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 criteriaas set by the AmericanEuropean Consensusthe 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 left-atrium.

In ARDS, PCWP is used to estimate pulmonary

capillary pressure. PCWP CANNOT be equal to pulmonary capillary pressure and left atrialpressure. 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 diagnosticcriterion for ARDS.