ARDS Flashcards
Define ARDS
Acute respiratory distress syndrome
o Clinical syndrome of acute respiratory failure
o Characterized by flooding of the alveoli with protein-rich edema fluid
• “Diffuse Alveolar Damage”
o Result in severe hypoxemia and reduced lung compliance
Diagnosis of ARDS
Berlin Definition:
o Acute = respiratory symptoms begin within 1 week of known insult
o Bilateral = opacities on chest imaging (must not be fully explained by pleural effusions, lobar collapse, lung collapse, or pulmonary nodules)
o Non-cardiac = symptoms and imaging not fully explained by CHF or fluid overload (requires clinical judgment and sometimes echo)
o Moderate to severe hypoxemia = defined by ratio of arterial oxygen tension to concentration of inspired O2 as a fraction of 1 (PaO2/FiO2)
Severity of ARDS
(defined by hypoxemia)
o Mild ARDS:
• PaO2/FiO2 >220 mmHg but ≤ 300 mmHg
• On ventilator settings that include PEEP or CPAP ≥ 5 cm H2O
o Moderate:
• PaO2/FiO2 > 100 mmHg but ≤ 200 mmHg
• With PEEP ≥ 5 cm H2O
o Severe:
• PaO2/FiO2 ≤ 100 mmHg
• With PEEP ≥ 5 cm H2O
Major causes of ARDS
o Majority: pneumonia (34%) o Extrapulmonary sepsis (27%) o Aspiration of gastric contents (15%) o Trauma (11% • Pulmonary contusion • Multiple long bone fractures
Outcomes with ARDS
- High mortality: 30-40%
- Death usually due to multiple organ failure not unsupportable respiratory failure
Lung function in survivors:
• Most = return to normal or near normal
• Minority = restriction, obstruction, and diffusion impairments
Long term effects:
• Reduced health-related quality of life
• Persistent physical functional limitations due to muscle weakness and fatigue
• Long-term cognitive dysfunction
• Persistent psychological symptoms including depression and PTSD symptoms
Describe the basis of changes in pulmonary physiology produced by acute lung injury
• Intense inflammatory reaction
Causes injury to:
o Capillary endothelium
o Alveolar epithelium
Results:
“Leaky” alveolar-capillary units = water and protein leak into interstitial and alveolar spaces
• Loss of “sieve” capacity by endothelium
High permeability pulmonary edema
• Forms without elevated capillary hydrostatic pressure if lymphatic system is overwhelmed
• Distributed heterogeneously (More edema collecting in dependent portions of lung)
Describe changes in pathology and radiography in ARDS
Rapid changes in Chest radiograph
• Normal → interstitial edema → alveolar edema (diffuse bilateral infiltrates)
• Physical exam = heavy, boggy lungs; would be able to express proteinaceous fluid
o Pathology: alveoli filled with proteinaceous fluid and neutrophils
• Fibrin, fibrinogen, other debris → pink-staining coagulum lining alveoli
• “Hyaline membranes”
• Necrosis of Type I pneumocytes and endothelial cells
• Increased procoagulant activity in alveoli and capillaries (clots and neutrophils obliterate small vessels)
List the physiologic changes in ARDS
- Decreased static lung compliance
- Intrapulmonary shunting (principle cause of hypoxemia)
- Increased dead space (contributes to hypercarbia)
- Pulmonary HT
Describe the physiologic changes in ARDS
Decreased static lung compliance
• Higher pressure needed to achieve change in lung volume
• Increased elastic work of breathing and respiratory muscle fatigue
• Breathing at lower tidal volume and lower FRC
Intrapulmonary shunting (principle cause of hypoxemia)
• Due to alveoli filled with fluid = unventilated
• Also caused by surfactant depletion and dysfunction → alveolar collapse
o Due to injury to Type II pneumocytes → decreased surfactant production
o Plasma protein leak (albumin and fibrin)
• Get hyaline membranes
• Inactivates surfactant
• Distinguishes ARDS from cardiogenic pulmonary edema (low V/Q, treated better with supplemental O2)
Increased dead space (contributes to hypercarbia)
• Obliteration of small vessels
• Breathing at low Vt → increased Vd/Vt
• Overdistension of more compliant alveoli if on ventilator
Pulmonary HT
• Result of physical obstruction of pulmonary capillary bed
o Endothelial damage
o In situ thrombosis
o Interstitial edema and scar
• Many vasoconstrictive mediators in pulmonary vasculature
o Alveolar hypoxia → widespread hypoxic pulmonary vasoconstriction
o Mediators (thromboxane A2)
ARDS symptoms
- Dyspnea
* Tachypnea
ARDS treatment
• No specific therapy
• Treat underlying cause (ex: infection)
• Supportive care:
• Minimize edema formation (fluid management)
• Use ventilatory strategies with elevated PEEP
o “Open lung approach, minimize cyclic atelectasis, improve oxygenation
• Positive pressure ventilation with low Vt (reduces mortality in ARDS)
o Recruits atelectatic alveoli
Iatrogenic factors that can exacerbate initial lung injury response
Nosocomial infection Ventilator induced lung injury o Barotraumas (tendency towards alveolar over-distension in face of high inspiratory pressures) o Atelectrauma (cyclic atelectasis) Oxygen toxicity (controversial)
Describe the pathologic changes associated with ARDS as it evolves from acute to more chronic stages.
Fibroproliferative stage (within a few days) o Intense proliferation reaction (endothelial cells, Type II pneumocytes, fibroblasts) o Reparative value o Remodels lung →can result in severely fibrotic lung
Patients who survive ARDS
o Have pulmonary fibrosis and vascular remodeling
o Occurs over time
o Near-complete normalization of pulmonary function is common
Identify other etiologies of non-cardiogenic pulmonary edema
Neurogenic pulmonary edeam
o Cause: transient (but profound) increase in sympathetic tone
o Associated with increased intracranial pressure → increased pulmonary vascular and systemic pressures
o Seen within minutes to hours of severe CNS insult (ex: seizures, head injury, cerebral hemorrhages)
o Turbulent flow → shearing and impact forces → high pressure edema and endothelial damage
o Resolves after stimulus withdrawn
o Not associated with acute and chronic inflammatory changes seen in ARDS
High altitude pulmonary edema
o Generally occurs over 9,000 feet
o Associated with exercise
o Caused by combination of high pressure and shearing and impact damage
o Resolves after stimulus withdrawn
o Not associated with acute and chronic inflammatory changes seen in ARDS
Fat embolism syndrome
o Self-limited but severe edema
o Occurs within 72 hours of long bone fractures
o Marrow releases neutral fats = aggregate in pulmonary capillary bed
o Lipase → toxic fatty acids
o Symptoms:
• Pathognomonic petechial rash of head, chest, axilla, and sub-conjunctiva (lasts several days)
• Neurologic signs: delirium, occasionally focal neurological deficits and seizures
• Hypoxemia
• Dyspnea
• Tachycardia
Describe how the factors governing movement of fluid and solutes across membranes are perturbed in different kinds of pulmonary edema
- Four major physiologic compensation mechanisms
- Protect the lung against formation of pulmonary edema:
Include:
Increased hydrostatic pressure gradient → decreased interstitial oncotic pressure
• Due to sieving effect of semi-permeable endothelial membrane
• Produces counterbalancing increase in oncotic pressure gradient
Increased plasma oncotic pressure
• Due to sieving effect
• Increases oncotic pressure gradient
• Counterbalances hydrostatic effect
Increased interstitial hydrostatic pressure from interstitial edema formation
• Reduces hydrostatic pressure gradient
Lymphatic system
• In response to increased fluid filtration = can increase its capacity up to 15-fold
