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. When supplemental oxygen is initiated, it raises arterial oxygen but does not address the underlying CO2 retention. In fact, supplemental oxygen may actually precipitate hypercapnia due to worsening of alveolar dead space. c
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. c
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).