Acute Respiratory Distress Syndrome Flashcards
(28 cards)
Definition of ARDS: clinical syndrome of
- Severe dyspnea of rapid onset
- Hypoxemia
- Diffuse pulmonary infiltrates leading to respiratory failure
Medical illness associated with development of ARDS
MC: penumonia (80%)
2nd: sepsis (40-60%)
Surgical conditions associated with ARDS
Pulmonary contusion
Multiple bone fractures
Chest wall trauma/flail chest
Clinical variables associated with development of ARDS
Older age
Chronic alcohol abuse
Pancreatitis
Pneumonia
Sepsis (40-60%)
Severity of critical illness
Three phases of ARDS
Exudative phase
Proliferative phase
Fibrotic phase
Exudative phase
Injured cells: alveolar capillary endothelial cells & Type I pneumocytes (alveolar epithelial cells)
Edema fluid rich in protein
(+) Inflam cytokines (IL1,IL8, TNF) and leukotriene B4
Plasma protein+dysfunctional pulmonary surfactant=hyaline membrane whorl
Alveolar edema: in dependent portion (diminished aeration)->collapse of dependent lung-> decreased lung compliance ->intrapulmonary shunting and hypoxemia ->dyspnea
Microvascular occlusion-> dec pulmonary arterial blood flow ->inc dead space ->pulmonary hypertension
Prominent findings in early ARDS (Exudative phase)
Severe hypoxemia
Hypercapnia
**Secondary to increase in pulmonary dead space
Differential diagnosis of ARDS
Cardiogenic pulmonary edema
Bilateral pneumonia
Alveolar hemorrhage
Proliferative phase
Occur in day 7 to 21
Patients liberated from MV
Fate of patients
1. Develop progressive lung injury
2. Resolution of symptoms
First signs of Resolution in ARDS (Seen in proliferative phase)
Initiation of lung repair
Organization of alveolar exudates
Shift from neutophil to lymphocyte-predominant pulmonary infiltrates (type II pneumocytes)
Fibrotic phase
After 3-4 weeks
Alveolar edema and inflammatory exudates convert to alveolar duct and interstitial fibrosis
Hallmarks: disruption of acinar architecture ->emphysema like changes with large bullae
Marker associated with increased mortality risk
Lung biopsy evidence for pulmonary fibrosis in ANY phase of ARDS
General principles in the treatment of ARDS
- recognition and treatment of underlying medical disorders (pneumonia, sepsis, aspiration, trauma)
- Minimization of uneccesary procedures
- Bundled care for ICU patients (prophy for DVT, GI bleeding, aspiration, excerssive sedation, prolonged MV, central venous catheter infections)
- Prompt recognition of nosocomial infections
- Adequate nutrition vua enteral route
2 Principal mechanisms for lung injury
- Volutrauma (overdistention from excess tital volume) and barotrauma (increased alveolar pressures)
- Atelectrauma (from recurrent alevolar collapse)
Chest CT findings of ARDS
Principally involving dependent portions of the lung with relative sparing of other regions
**Compliance differs in affected vs normal areas->attempts to fully inflate consolidated lungs–>overdistention and injury to the more normal areas
Ventilator induced injury: seen particularly with high tidal volume ventilation
High tidal volume ventilation
Strategies to prevent ARDS during ventilation
low VT ventilation (6 ml/kg of PBW)
Plateau pressue at <=30 cm H20
PEEP adjusted to minimize FIo2
Mortality rate is lower by 31%
Causes for reduced lung compliance
1.Presence of alveolar and interstitial fluid
2. Loss of surfactant
Best PEEP
- Able to promote alveolar recruitment
- Minimize alveolar overdistentionand hemodynamic instability
- Provide adequate PaO2 while minimizing Fio2
Prone positioning
Reduction in 28 day mortality for patients with severe ARDS PAO2/Fio2 <150 mmg HG
Recruitment maneuvers
- Increase PEEP to high levels to recruit atelectatic lung
- Alternate modes of MV (airway pressure release ventilation and high frequency oscillatory ventilation)
- Lung-replacement therapy with extracorporeal membrane oxygenation (ECMO)
Fluid management
Increased pulmonary vascular permeability ->leading to intersitial and alveolar edema fluid rich in protein
***CENTRAL FEATURE IN ARDS
Agressive attempts to reduce left atrial filing pressures with fluid restriction and diuresis
this is limited by hypotension and hypoperfusion
True or false
current evidence does not support the routine use of glucocorticoids in the care of ARDS patients
True
Mortality in ARDS is attributable to
Non pulmonary causes
Sepsis and nonpulmonary organ failure >80% of deaths