Acute Respiratory Distress Syndrome Flashcards
What is ARDS?
- First described in 1967, but in retrospect it was not new entity
- Estimated incidence in the U.S. is over 150,000 cases per year
- 40 to 75 cases per 100,00 pop. annually
- Mortality rate approaching 25-30%
- The hallmark of ARDS is a proteinaceous pulmonary edema that results from increased capillary permeability
- Major public health problem and cause of death
What are the stresses of ARDS?
- Timing
- Chest imaging
- Origin of edema
- Severity of hypoxia
Explain the berlin definition of ARDS?
Timing: Within 1 week of a known clinical insult or new or worsening respiratory symptoms
Chest imaging: Bilateral opacities – not fully explained by effusions, lobar/lung collapse, or nodules
Origin of edema: Respiratory failure not fully explained by cardiac failure or fluid overload. Need objective assessment (e.g., echocardiography) to exclude hydrostatic edema if no risk factor present
Oxygenation:
Mild – 200 mm Hg < PaO2/FiO2 ≤ 300 mm Hg with PEEP or CPAP ≥ 5 cm H2O
Moderate – 100 mm Hg < PaO2/FiO2 ≤ 200 mm Hg with PEEP ≥ 5 cm H2O
Severe – PaO2/FiO2 ≤ 100 mm Hg with PEEP ≥ 5 cm H2O
ARDS is what?
an inflammatory syndrome characterized by increase alveolar capillary permeability leading to acute lung injury and diffuse alveolar damage.
Pathogenesis of ARDS?
Insult leading to
Structural changes in the alveolocapillary unit (diffuse alveolar damage) which
Affects gas exchange and/or vascular permeabilit
Direct Conidtions associated with ARDS development?
Direct Pulmonary injury affecting lung epithelium
- Common – Pneumonia (viral and bacterial) – Aspiration of gastric contents – Mechanical ventilation
- Less Common – Inhalation injury (toxic gas) – Reperfusion injury – Pulmonary contusion – Near drowning – Re-expansion injury
Indirect conditions associated with ARDS?
Indirect Lung injury affecting the vascular endothelium
- Common – Sepsis – Severe non-thoracic trauma with shock and multiple transfusion
- Less Common – Acute pancreatitis – Medication and drug overdose – Anaphylaxis – Neurogenic
Subphenotypes of ARDS? What characterizes them?
Two Subphenotypes
A. Hyperinflammatory: Characterized by high levels of inflammatory biomarkers, shock, metabolic acidosis, and mortality: Responsive to high PEEP, Fluid conservative management, low mortality.
B. Noninflammatory: More responsive to low PEEP, fluid conservative management, high mortality.
Why does fluid accumulate in ARDS? results in?
In ARDS, fluid accumulates because the permeability of the capillary endothelial and alveolar epithelial barrier is increased as a result of damage to one or both of these cell populations whereas hydrostatic pressures are normal.
ARDS results in a noncardiogenic pulmonary edema
What are the phases and the diffuse alveolar damage that happens?
- Exudative phase, <7-10 days
- Proliferative phase, > 7-14 days (approximately)
- Fibrotic phase, after 2 weeks
What is the acute exudative phase?
- Release of inflammatory mediators, proteases, and oxidants
- Injury to alveolar epithelium and alveolar capillary endothelium
- Increase permeability edema (proteinaceous) leads to stiff lung
- Decreased surfactant production and function leads to alveoli collapse resulting in shunt-like gas exchange
- Hyaline membrane formation
What is the proliferative phase?
- Hypertrophic type II alveolar epithelial cells replicate to replace lost type I cells
- Inflammation and fibroblast proliferation in the interstitium
- Fibroblasts invade the alveolar space • Hyaline membranes disappear
- Intra-alveolar plugs of proliferative fibroblast
What is the chronic Fibrotic phase?
- Regions of intense fibrosis
- Obstruction and/or destruction of the pulmonary vascular bed
Pathologic features of ARDS?
- Inflammatory cell infiltrate
- Loss of alveolar type I epithelial cells
- Proteinaceous fluid accumulation in the interstitium and alveoli
- Areas of alveolar collapse
- Hyperplasia of alveolar type II epithelial cells
- Fibrosis
ARDS pathophysiology?
Evolves Around Gas Exchange
- Shunting and V/Q mismatch leads to Hypoxemia
- Alterations to surfactant production and effectiveness
- Lung mechanics reflect heterogeneous disease involvement
- Decreased pulmonary compliance
- Decreased FRC (Functional Residual Capacity)
- Increased pulmonary vascular resistance
- VO2 (oxygen consumption) to DO2 (delivery) markedly abnormal
Clinical presentation of ARDS?
- Inciting event respiratory distress
- CXR lags behind clinical picture
- Respiratory symptoms other than dyspnea uncommon
- PE: increased HR, increased RR, increased WO
Clinical Features of ARDS?
- Dyspnea, tachypnea
- Rales / crackles
- ↓P02, normal or ↓PC02, ↑ Aa gradient
- Radiography- Bilateral interstitial and alveolar edema
- Diminished compliance (<40 mL/cmH20)
- Severe hypoxemia refractory to oxygen therapy (Pa02/FI02 < 300)
- Normal pulmonary vascular pressure PCW<18mmHg
Diagnostic Criteria of ARDS?
- Respiratory failure not fully explained by cardiac failure or fluid overload
- Identifiable cause or associated condition
- Dyspnea (usually severe)
- Hypoxemia (usually refractory to supplemental O2)
- Bilateral CXR infiltrates (interstitial alveolar)
- Reduced respiratory system compliance
Management of ARDS?
- Address precipitating cause
- Primary supportive measures – Oxygen support – Mechanical ventilation/low tidal volume – Antibiotics for infection as indicated – Nutritional support – trophic enteral preferred – Conservative fluid management – Cardiovascular support – DVT/PE prophylaxis – GI prophylaxis to prevent stress ulcers
O2 use in ARDS?
- Lowest possible FiO2 that maintains O2 sat ≥ 88%-95% 2. O2 sat ≤ 97%may confer a reduced ICU mortality 3. Target FiO2 of < 0.6
Explain ARDS Oxygenation Options Based on PaO2/FIO2
Mild: 200 mmHg < PaO2/FiO2 ≤ 300 mmHg with PEEP > 5 cm H2O or CPAP Noninvasive Positive Pressure Ventilation (NPPV) ± High-Flow Nasal Cannula (HFNC) Helmet ventilation
Moderate: 100 mmHg < PaO2/FiO2 ≤ 200 with PEEP ≥ 5 cm H2O) ? High-Flow Nasal Cannula (HFNC) or helmet ventilation Mechanical Ventilation (MV)
Severe: PaO2/FiO2 ≤ 100 mmHg with PEEP > 5cm H2O Mechanical Ventilation + prone positioning ExtraCorporeal Membrane Oxygenation (ECMO) consider neuromuscular blockade early on (< 48 hours for 48 hours
At all levels of PaO2/FiO2 mechanical ventilation is always an option
What are some aspects of mechanical ventilation?
- Prevent/reduce ventilator induced lung injury – Barotrauma: excessive airway pressure – Volutrauma: over distension of lung units – Atelectotrauma: Repetitive openings and closings of terminal lung units – Biotrauma: Local and systemic inflammatory response to mechanical ventilation
- Mechanical Ventilation – Pressure and volume limitation – Plateau pressure ≤ 30mm H2O – Low tidal volume – Driving pressure <15 (plateau pressure – PEEP)
- PEEP and recruitment maneuvers
- Consider neuromuscular blockade early on (< 48 hours) for 48 hour
- Permissive hypercapnia initially felt to be relatively benign. Now a realization that elevated CO2 levels have significant physiologic effects
- Use of prone position for patient with PaO2/FiO2 ≤ 150 Hg
- Lowest possible FiO2 that maintains O2 sat ≥ 88% target FiO2 of < 0.6 (60%)
Problems to address with O2 using mechanical ventilation in ARDS?
- Barotrauma: Excessive airway pressure Try to keep plateau pressure < 30 mm H2O Try to keep driving pressure (Plat-total PEEP) < 15
- Volutrauma: over distension of lung units Use low tidal volume (LTV) based on ideal body weight May need to accept a degree of CO2 retention: permissive hypercapnia
- Atelectotrauma Repetitive openings and closings of terminal lung units Treatment: Positive End Expiratory Pressure to prevent alveolar collapse
- Biotrauma Local and systemic inflammatory response to mechanical ventilation
What does mechanical ventilation require? Associated with?
Requires endotracheal intubation or tracheostomy
Associated with numerous complications:
Infections: Ventilator Associated Pneumonia (VAP) from bypassing host defense mechanism Neurologic: Cognitive Decline, Delirium Respiratory: Ventilator Induced Lung Injury (VILI) Musculoskeletal: Critical Care Myopathy
What does ECMO stand for?
ExtraCorporeal Membrane Oxygenation
Predictors of mortality in ARDS?
Outcome of ARDS?
- For survivors the prognosis for return of lung function over time is good
- Unfortunately many suffer neuropsychological sequelae
- Reduced quality of life from muscle wasting and weakness
Mortality of ARDS?
Decreased over the last 10 to 15 years 60% 25-30%
Due to advances in critical care especially the ARDS net trials
What improves outcome in ARDS?
Lung protective ventilation strategy improves outcome in ARDS
ARDS recommendations for treating?
Based on F/U ARDS Network Investigation current recommendations include:
- Tidal volume goal 4-6mL/Kgm IBW • Plateau pressure < 30 cm H2O
- Adjustment of FIO2 and PEEP to achieve PaO2 of 55-80 mmHg or SpO2 of 88-95%
- Adjustment of respiratory rate to reach a goal pH of 7.3-7.45 with a maximum of 35 breaths/minute
- Conservative fluid management
In ARDS patients 6ml/kg IBW tidal volume was associated with?
In ARDS patients, 6 ml/kg IBW tidal volume ventilation strategy was associated with: –Reduced mortality prior to hospital discharge –Increased ventilator-free days –Increased organ failure-free days –Lower IL-6 levels
What three variables accurately identify ARDS phenotypes?
Interleukin 8
Serum bicarbonate
Tumor Necrosis Factor receptor 1 (TNFR1)
