Acute Respiratory Distress Syndrome

 https://docs.google.com/presentation/d/1QYq-IFQ3zOBc_TG1Dp1hXGYihy9idOEV/edit?usp=sharing&ouid=118367072448693089465&rtpof=true&sd=true

https://docs.google.com/document/d/15PF6cLXq4SJMZaTBX-_9LP_kZt_-CfRW/edit?usp=sharing&ouid=118367072448693089465&rtpof=true&sd=true

- cont lung protective ventilation: pH > 7.25, Pplat < 30, PaO2 > 65 

ARDS:

Sepsis, Pancreatitis / Pneumonia, Aspiration, Uremia, Trali / Trauma,

Dysregulated inflammatory response of cytokines neutrophils proteases that disrupt the surfactant production, cause endothelial injury andlead to endothelial and alveolar epithelial cell injury, excess fluid and protein extravasation causing increased V/Q mismatch decreased lung compliance and increases shunt and dead space.

 

 

Acute respiratory Distress syndrome

Abnormal CXR, respiratory failure within 1 week, Decreased P/F Ratio, symptoms of distress not related to overload or heart failure

 

Mild ARDS > 150 Hemodynamically stable

NIPPV, bipap CPAP

 

Unstable – Ventilator

ARMA trial 4 to 8 cc/kg 11% reduction in mortality with LTVV

 Plateau pressures less than 30 cm H2O

Driving Pressure P plat – PEEP < 15 cm H2O

Plateau pressure – alveoli hurting barotrauma, Vt increase plateau pressure

Vt ~ 6ml/kg

Rationale

~6ml/kg of the ideal body weight

1)   Prevents atelectrauma (injury from opening and closing of the distal airways and alveoli

2)   Improves homogeneity of lung parenchyma reducing gross differences in regional lung compliance

3)   Improves V/Q mismatch and shunt maintaining alveolar recruitment

Hypercapnea good

FiO2 < 60%, SpO2 88%- 92%

 

 

nonventilator

Proning Proseva

Prone positioning supine: most dependent areas is the posterior lung fields, heart compresses on consolidated areas of tissues. Heart sitting back and pushing back. Areas have decreased aeration, less aeration. Not ventilating alveoli appropriately, no O2 in blood.

Anterior, superior,

 

P/F ratio < 150 early proning 12 hours a day 18:6, 16:8

CESAR trial: improved mortality in ARDS in centers capable of administering ECMO, improved mortality simply being at tertiary referral center itself

 

High PEEP strategy

ECMO

Paralysis

Recruitment maneuvers: high CPAP to open alveoli pressure 35 – 40

Caution of recruitment maneuvers in those with hypovolemia or shock for propensity of hemodynamic deterioration during maneuver

 

FACCT trial excessive fluid resuscitation harmful to ARDS patients, liberal based off of CVP and pulmonary artery occlusion pressure, mortality did not differ between groups

Conservative fluid management improved oxygenation and decreased time on the ventilator

 

Paralytics controversial

 

 

Inhaled nitric oxide

PGI2, prostaglandins

PEEP increases plateau pressure P plat – barotrauma > 30cm H2O

 

Inhale go through alveoli and blood, go through blood of well aerated alveoli. Less moving out of pulmonary capillary blood. Nitric oxide

Dilate the pulmonary capillary. Dilated pulmonary capillary, increase blood flow to alveoli

Nitric oxide well aerate alveoli increased the blood blood flow. May increase oxygenation

Low tidal volumes, 320 ccs, take in more breath over the ventilator

 

Paralytics Sedation, propofol, midazolam -> sedation propofol midazolam decrease respiratory drive

Paralyze them to get out of asynchronous state time to rest and be dependent on the ventilator. Cisatracurium, paralyzed not try to breathe over, propofol, midazolam.

Continuously hypoxemic extracorporeal membrane oxygenation.

 

Take blood from IVC, deoxygenated blood oxymizer.

 

 

 

 

Diagnosis

Ventilator and non ventilator management

 

Phase 1 - Exudative phase - leakage of protein-rich fluid 

Phase 2 - Proliferative phase - endothelial cells, pneumocytes, fibroblasts proliferate

Phase 3 - Fibrotic phase - fibrosis and irreversible reduction in diffusion capacity with severe dyspnea

 

Acute respiratory distress syndrome (ARDS) refers to inflammatory lung damage triggered by alveolar injury (eg, aspiration of water) or intense systemic inflammation (eg, sepsis, pancreatitis).  ARDS has a mortality rate of approximately 40%; those who survive often have reduced lung function that persists for months or years and is sometimes permanent.

The pathogenesis of ARDS can progress through 3 phases, although most patients move through only the first 2.  The exudative phase (phase 1) involves inflammatory disruption of the alveolar-capillary membrane with leakage of protein-rich fluid from the alveolar capillaries into the alveoli and surrounding interstitium.  Gas exchange is acutely impaired by alveolar edema and by hyaline membranes that develop on the alveolar surface.  After 1-2 weeks, ARDS progresses to the proliferative phase (phase 2), during which endothelial cells, pneumocytes, and fibroblasts proliferate in an attempt to repair damage.  Collagen is deposited in the interstitium and may lead to scarring.

The majority of ARDS survivors have a persistent reduction in diffusion capacity that eventually normalizes after several years (Choice B).  These patients may remain in a prolonged proliferative phase in which interstitial collagen deposition and remodeling impair gas diffusion across the alveolar-capillary membrane, causing an increased alveolar-arterial oxygen gradient that manifests clinically with mild dyspnea.  A small percentage of surviving patients likely enter and remain in the fibrotic phase (phase 3) of ARDS, during which severe interstitial fibrosis develops and manifests as an irreversible reduction in diffusion capacity with marked clinical symptoms (eg, severe dyspnea).

 

 

 

 

Ninja Nerd Science

https://www.youtube.com/watch?v=X4C68KNYk2o

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