Respiratory failure and arrest

Clinical features

• Hypoxemia: Dyspnea, tachypnea, cyanosis, tachycardia, restlessness, confusion/agitation.
• Hypercapnia
  • Somnolence/Lethargy (CO2 Narcosis): CO2 rapidly crosses BBB → severe CNS acidosis. ↓ neuronal excitability and suppressed RAS.
    • HY: Suspect in COPD pt given 100% O2 who becomes suddenly lethargic.
  • Morning Headache: PaCO2 is a potent cerebral vasodilator. Baseline hypoventilation worsens during sleep (e.g., OSA, severe COPD) → overnight ↑ CO2 → cerebral vasodilation → mild ↑ ICP → stretche the meninges c
  • Asterixis: Metabolic encephalopathy disrupts diencephalon motor centers → intermittent loss of extensor tone.
    • HY Causes: ↑ CO2 (Hypercapnia), ↑ NH3 (Hepatic), ↑ BUN (Uremia).
  • Bounding Pulse: Acidosis causes direct peripheral vasodilation + compensatory sympathetic surge (↑ HR, ↑ SV). High SV pumped into dilated vessels = widened pulse pressure.
  • Diminished RR: This is the cause, not the effect. CNS insult (opioid OD, brainstem stroke) blunts medullary respiratory center → hypoventilation → failure to blow off CO2.
• Respiratory Arrest: Apnea, agonal gasps, unresponsiveness, loss of airway reflexes (often rapidly precedes cardiac arrest).

Diagnosis

• Initial/Screening: Pulse oximetry (SpO2 < 90%), continuous cardiac monitoring.
• Confirmatory/Gold Standard: Arterial Blood Gas (ABG).
  • Type 1: PaO2 < 60 mmHg with normal/low PaCO2.
  • Type 2: PaCO2 > 50 mmHg with pH < 7.30 (acidemia).
• Key Labs:
  • CBC (anemia, infection), BMP (electrolyte-induced weakness, bicarb levels for chronicity).
  • Tox screen (suspected OD).
  • BNP/Troponin (cardiogenic etiology).
• Imaging: CXR (initial structural eval for PNA, pneumothorax, pulmonary edema, ARDS).
• Advanced: CT Pulmonary Angiography (CTPA) if PE suspected. Echocardiogram for heart failure.