ARDS Flashcards
Respiratory failure & types
Failure of the respiratory system to do one or both of: oxygenation & CO2 elimination (hypoxemic or hypercapnic)
Hypoxemic/Type I respiratory failure
Most common, PaO2 < 60mmHg, associated with alveolar oedema & most acute resp diseases (pneumonia, COPD, pul oedema, pneumothorax, ARDS)
* Ventilation perfusion mismatch usually due to fluid or bronchospasms
* Shunt: persistance of hypoxemia despite 100% O2 due to deoxygenated blood bypassing alveoli & mixing with oxygenated blood, decreasing arterial O2 content
Hypercapnic/Type II respiratory failure
PaCO2 > 50mmHg (COPD, asthma, overdose, ARDS, muscle & neurological disorders)
* Ventilatory demands exceeds supply, which can be due to reduced respiratory drive, muscular/neurological/chest wall abnormalities, increased CO2 production
What is ARDS
- Acute respiratory distress syndrome
- Progressive respiratory failure whereby the alveolar-capillary interface is damaged, causing alvolar oedema & poor oxygenation
- PaO2/FiO2 (fraction of inspired air) ratio < 200
- High mortality rate
Aetiology
Develops from direct or indirect lung injury
* Sepsis (highest mortality rate) & SIRS
* Trauma
* Pneumonia, respiratory infections (flu)
* Burns
* Aspiration & inhalation injury
* Blood transfusions
Pathophysiology Phases
Phase 1: injury/exudative (1-7 days after injury)
Phase 2: repairative/proliferative (1-2 weeks after injury)
Phase 3: fibrotic/chronic (2-3 weeks after)
PP - Injury/exudative phase
- Lung injury or insult causes release of inflammatory mediators (neutrophils, histamine, serotonin, bradykinin)
- Adhere to vascular endothelium = damages & increases permeability
- Fluid passes into interstitial space, enlarges and pressure causes flow into alveoli
- Inflammatory mediators cause bronchospasms
- Damage also injurs type II alveolar cells, reducing surfactant production & causing alveolar collapse
- RESULT = impaired gas exchange, reduced lung compliance, pulmonary shunting (deoxygenated blood into L side of heart due to lack of oxygenation = hypoxaemia)
- Hypoxemia causes increased RR & CO, decreases TV to compensate BUT this fails due to increases atelectasis, pul oedema & shunt –> hypoventilation, decreased CO & tissue perfusion
PP - repairative/proliferative phase
- Increase in neutrophils, monocytes, lymphocyts and fibroblasts = dense & fibrous lung tissue
- Thickened alveolar membranes impairs diffusion = reduced oxygenation, lung compliance & shunting
- If treated = lesions resolve
- If left = widespread fibrosis (stiff lung)
PP - fibrotic/chronic phase
- Widespread remodelling with fibrous tissue = reduced compliance, gas exchange & pulmonary HTN
- May require long-term mechanical ventilation
Early manifestations
Initial presentation is often subtle and may not show for 1-2 days
* Dyspnoea, tachypnoea/hyperventilation, shallow breathing, coughing
* Inspiratory crackles
* Hypoxemia & respiratory alkalosis (due to hyperventilation causing reduced CO2)
* Minimal signs of oedema on CXR < 30%
Late manifestations
- Evident respiratory distress (tachypnoea, diaphoresis, tachycardia, cyanosis, pallor, altered LOC) = requires ETT if continued (NB: HTN, tachy will progress to HoTN & brady)
- Diffuse crackles & rhonchi (low tone wheezes due to oedema)
- Complete white lung on CXR from consolidation
- Hypoxemia despite increased oxygenation by mask etc = hallmark
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Diagnostic Criteria
- Symptoms
- Aetiology (direct or indirect)
- CXR (infiltration)
- Diminished compliance
- Gas exchange (PaO2/FiO2 < 200)
Patient Assessment
History: lung diseases, tobacco/toxins, recent trauma, obesity, previous intubation, O2/inhalers/immunosuppressants
Symptoms: (as previously), weight loss, chest pain, sleep changes, dizziness, headache, accessory muscles, change in mental state, ascites
Tests: CXR, TV/FVC, blood gasses (pCO2, pO2, SaO2, pH)
Treatment Goals
Goal:
* Maintain PaO2 > 60mmHg
* Normal pH through adequate ventilation
* Patent airway
* Sats > 90%
* Clear auscultation
Treatment
- High flow O2 (lowest effective dose to achieve PaO2 > 60mmHg) - necessary to treat refractory hypoxemia
- Intubation is often required to maintain these levels
- Higher levels of PEEP required to open collapsed alveoli but used with caution as it can compress capillary bed and lead to reduced L side return and reduce CO & BP
- If unresponsive to other therapies = place patient in prone position to reduce heart pressure on lungs and improve ventillation/perfusion ratio or use continuous lateral rotation therapy
- AB therapy if septic
- Fluid restriction in primary insult, fluid resuscitation in secondary (to treat circulatory shock from sepsis)
