senior talk- ards

7/31/2019 Senior Talk- ARDS

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ByDr. Mohsin Riaz

PG Anesthesia Allied Hospital, FSD.


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ARDS Severe, acute lung injury, involving diffuse alveolar

damage, increased microvascular permeability andnon-cardiogenic pulmonary edema.

Acute refractory hypoxemia

High mortality 40-60%

Annual incidence in US is 75/ 100.000

First described in 1967


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Diagnostic criteria:Acute onset of respiratory failure

Bilateral infiltrates on CXR

PCWP


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Mechanism ;Activation of inflammatory mediators and cellular

components, resulting in damage to capillaryendothelium and alveolar epithelial cells.

Increased permeability of alveolar -capillarymembrane.

Influx of protein rich edema fluid and inflammatory

cells into air spaces Dysfunction of surfactant


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Causes

DIRECT LUNG INJURYCOMMON

Pneumonia

Aspiration

LESS COMMON

Pulm contusion

Fat emboli Near-drowning

Inhalation injury

Reperfusion injury (transplantetc)

INDIRECT LUNG INJURYCOMMON

Sepsis*

Severe trauma with shock andmultiple transfusions

LESS COMMON

Cardiopulm bypass Acute pancreatitis

Transfusions

Drug overdose


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Pathophysiology

Occurs in stages:

1. Exudative ( Acute Phase) 0-4 days

2. Proliferative ( 4-8 day)

3. Fibrotic ( >8 days)

4. Recovery


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Exudative Phase In ALI/ARDS damage to either one occurs

resulting in increased permeability of the barrier

influx of protein-rich edema fluid into the alveolarspace

Injury of Type I cells results loss of epithelialintegrity and fluid extravasation (edema)

Injury of Type II cells then impairs the removal ofthe edema fluid


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Exudative Phase

Dysfunction of Type II cells also leads to reducedproduction and turnover of surfactant which leadsto alveolar collapse

If severe injury to epithelium occurs disorganized/insufficient epithelial repair occurs

resulting in fibrosis In addition to inflammatory process, there is

evidence that the coagulation system is alsoinvolved


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2.Fibrotic PhaseAfter acute phase some pts. will have rapid

resolution some progress to fibrotic phase

Alveolar space is filled with mesenchymal cells

and their products Reepithelialization and new blood vessel

formation occurs in disorganized manner

Fibroblasts also proliferate, collagen is depositedresulting in thickening of interstitium

Fibrosing alveolitis and cyst formation


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3.Proliferative PhaseWith intervention (mechanical ventilation) there is

clearance of alveolar fluid

Soluble proteins are removed by diffusion betweenalveolar epithelial cells

Insoluble proteins are removed by endocytosis andtranscytosis through epithelial cells and phagocytosis

through macrophages


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Proliferative Phase Type II cells begin to differentiate into Type I cells and

reepithelialize denuded alveolar epithelium

Further epithelialization leads to increased alveolarclearance


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Consequences Impaired gas exchangeleading to severe

hypoxemia , ventilation-perfusion mismatch,

increase in physiologic dead space Decreased lung compliance due to the

stiffness of poorly or non-aerated lung

Pulm. HTN 25% of pts, due to hypoxic

vasoconstriction, Vascular compression by positiveairway compression, airway collapse and lungparenchymal destruction


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Clinical FeaturesPts are critically ill

develop rapidly worsening tachypnea, dyspnea,hypoxia requiring high conc of O2

Occurs within hours to days ( usually12-48 hours)of inciting event

Early clinical features reflects precipitants of

ARDS Physical exam shows cyanosis, tachycardia,

tachypnea and diffuse rales and other signs ofinciting event


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Work UpARDS is a clinical diagnosis

No specific lab abnormality beyond disturbance in gas

exchange is evident Radiologic findings may be consistent but not

diagnostic

w/u therefore is useful in identifying inciting event or

excluding other causes of lung injury


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Work Up

- CBC, Renal panel, Coags, LFTs, pancreatitic enzymes,

- Blood cx, urine cx

- CXR

- CT

- Bronchoscopy/BAL

- CVP, PCWP


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CXR


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Treatment No specific therapy for ARDS exists

Mainstay of treatment is supportive care

Treat underlying/inciting conditions


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Protocol for low vol. ventilation in

ARDSOPTIMAL GOALS;

VT=6ml/kg, Ppl


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5. Adjust Fio2 to achieve Spo2>90

SECOND STAGE;

1. When VT=6ml/kg, measure Ppl.

2. If Ppl >30cmH2O, decrease VT in 1ml/kgincrements until Ppl


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THIRD STAGE;

1. Monitor arterial blood gases for respiratory acidosis.

2. If pH=7.15-7.30,increase respiratory rate until pH>7.30or RR=35bpm.

3. If pH


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other ventilation strategies Recruitment maneuvers

Prone

Inhaled nitric oxide

High frequency oscillation


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Shortcut to imagesCAIYXVFR.lnk


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