Acute Respiratory Distress Syndrome (ARDS)

Mrs. Roberta Schembri is admitted to a Medical Ward with a diagnosis of ARDS. She was receiving treatment at home for viral pneumonia and had appeared to be improving until yesterday.

• The nurse is assessing Mrs. Schembri for associated clinical manifestations with ARDS. Which symptoms identified by the nurse positively correlate with ARDS?
• The nurse is performing a neurological assessment. Which clinical signs observed by the nurse suggest that Mrs. Schembri may be developing cerebral hypoxia, and what is the pathophysiological basis for these signs?
• Schembri is receiving oxygen via nasal cannula at 6 L/min. Estimate her FiO₂. Also, interpret the following ABG results: pH 7.32, PaCO₂ 50 mmHg, PaO₂ 62 mmHg, HCO₃⁻ 26 mEq/L.
• Schembri’s oxygen saturation levels continue to decline despite supplemental oxygen. What advanced interventions might the healthcare team consider to improve oxygenation in a patient with ARDS?

Part 1: Acute Respiratory Distress Syndrome (ARDS).

a)    Clinical Manifestations Positively Correlating with ARDS.

The nurse should look for the following key symptoms and signs that align with ARDS (Chen et al., 2005).

• Severe dyspnea (shortness of breath) and increased work of breathing caused by difficulty in oxygen exchange due to impaired alveolar function.
• Tachypnea (rapid breathing) due compensate low oxygen levels and increased carbon dioxide in blood.
• Refractory hypoxemia (low oxygen that does not improve with oxygen therapy) as fluids in alveoli prevent oxygen absorption despite supplement oxygen.
• Cyanosis (bluish discoloration of lips or fingers) due to inadequate oxygenation of blood leading to hypoxia.
• Crackles on auscultation (due to alveolar fluid) result due to fluid accumulation in the lungs due to inflammation & increased capillary permeability.
• Restlessness, confusion, or anxiety (due to hypoxia).
• Use of accessory muscles during breathing as body struggles to take enough oxygen
• Decreased oxygen saturation despite supplemental oxygen due to less ability of lungs to oxygenate the blood is severely impaired.
• Diffuse pulmonary infiltrates on chest X-ray (ground-glass appearance) due to fluid in the alveoli and inflammation in the lungs causing obstructs normal lung function.

These symptoms arise due to alveolar-capillary membrane damage causing fluid leakage and impaired gas exchange.

b)    Neurological Signs Suggesting Cerebral Hypoxia and Pathophysiology.

Observed signs of cerebral hypoxia.

• Confusion.
• Agitation.
• Restlessness.
• Drowsiness or lethargy.
• Headache.
• Poor concentration or unresponsiveness.

Pathophysiological explanation.

Hypoxia leads to inadequate oxygen delivery to brain tissue. Since neurons are susceptible to oxygen deprivation, even mild hypoxemia can impair cognitive function and consciousness. Accumulation of CO₂ (hypercapnia) can also cause vasodilation in cerebral vessels, increasing intracranial pressure and worsening neurological symptoms (Busl & Greer, 2010).

c)     FiO₂ Estimation and ABG Interpretation.

FiO₂ Estimation:

A nasal cannula at 6 L/min provides an estimated FiO₂ of ~44%.

ABG Analysis:

• pH: 7.32 (↓ slightly acidic).
• PaCO₂: 50 mmHg (↑ hypercapnia).
• PaO₂: 62 mmHg (↓ hypoxemia).
• HCO₃⁻: 26 mEq/L (normal).

Interpretation:

• This indicates respiratory acidosis with hypoxemia.
• The elevated PaCO₂ and low pH suggest hypoventilation.
• PaO₂ is below normal despite 44% FiO₂, indicating refractory hypoxemia, a hallmark of ARDS.

d)    Advanced Interventions for Worsening Oxygenation

If oxygen saturation continues to decline, the healthcare team may consider (Simonte et al., 2024):

1. High-Flow Nasal Cannula (HFNC) or Non-Invasive Ventilation (NIV) (e.g., BiPAP).
2. Endotracheal Intubation and Mechanical Ventilation with.
   • Low tidal volume ventilation (6 mL/kg ideal body weight).
   • PEEP (Positive End-Expiratory Pressure) to prevent alveolar collapse.
3. Prone positioning (shown to improve oxygenation by enhancing ventilation-perfusion matching).
4. Sedation and neuromuscular blockade to improve ventilator synchrony.
5. Fluid management (conservative strategy to reduce pulmonary edema).
6. ECMO (Extracorporeal Membrane Oxygenation) in severe refractory cases.
7. Treating the underlying cause (e.g., antiviral treatment if viral pneumonia is still active).