CARBON MONOXIDE
- Derives from combustion (fire, cigarettes, domestic heaters, paint remover that is metabolized in liver into CO). City residents and smokers may have CO level of 5-10%.
- CO has high affinity to Hgb that causes Left shift of OxHgb curve. Also CO inhibits cytochrome A3 and binds to myocardial cells that causes cardiac toxicity.
- Pt c/o flu-like symptoms when in subacute stage and diagnosis is easily missed if not suspected. Pts report HA, dizziness, N/V. Other pts may present with more acute picture and manifest with: Cyanosis, Neuro (HA>Dizziness>AMS>SZ>Coma),Cardiac toxicity (mainly manifested from lack of O2 such as angina, ST/T changes, ventricular arrhythmia), Pulmonary (ARDS, dyspnea, tachypnea), GI upset, Metabolic acidosis 2ry to hypoxia, ATN 2ry to myoglobinuria.
- To diagnose
pt with toxicity we must perform COHb measurement. VBG is accurate for diagnosis. Performing O2SAT with pulsOx, is not reliable method to reveal if pt is CO intoxicated. Normal levels are considered 0-5%, yet smokers and pts suffering from hemolytic anemia due to by-product of hemolysis may have higher levels. There is no level that can accurately predict which of the pts have toxic level and how severe the manifestations can be. Due to "wash out" phenomena and "normalization" of pt's CO by the time he/she comes to ER, it is important to find out if pt suffered LOC or / and SZ since these could be the clue that CO was very high at scene and pt may require HBO even if CO on arrival to ER is normal.
- Treatment c/w administration of 100% O2 when pts CO level is . In this way CO T1/2 is 1.5 hrs . O2 is administered until CO level is <10%. Pts that have acute symptoms of CO toxicity will benefit from HBO and indications are AMS, SZ, Syncope, Pregnancy, Level >25%, signs of cardiac toxicity.