CO Poisoning

PGY1 PGY2 PGY3 PGY4 Toxicology

I had a patient with Carbon Monoxide poisoning. Patient had mental status changes and was unresponsive.We transferred patient to a hyperbaric center and this is the review that I did with my resident and student for Carbon Monoxide poisoning, mainly from Tintinalli’s:

CO is a colorless, tasteless, odorless, and a product of incomplete combustion. The most challenge in CO poisoning is diagnosis due to unspecific presentation such as headaches, confusion, lightheadedness, vertigo, and flu-like symptoms. CNS complication, cardiac complication and death could be result of severe intoxication.

1. Normal physiologic blood carbon monoxide levels is  ~1% in healthy nonsmokers but can be higher in other conditions such as hemolysis or sepsis. Baseline blood levels in smokers is up to 10% . (Tintinalli’s)

2. The binding affinity of hemoglobin in adult person for carbon monoxide is about 200 to 250 times stronger than the affinity between hemoglobin and oxygen.

3. Pulse Ox. 101: Probe is placed over a vascular bed (finger, earlobe). Light-emitting diodes (LEDs) emit light of two different wavelengths:
Red = 660 nm  Infrared = 940 nm, HbO2 absorbs more infrared light than Hb. Hb absorbs more red light than HbO2. Difference in absorption is measured.

4. Some light is absorbed by: Arterial blood, Venous blood, Tissues. Light that passes through the tissues is detected by a photodetector.

3. Half-lives of COHb on room air at normal atmospheric pressure range from 249 to 320 minutes. On 100% oxygen at atmospheric pressure, this is reduced to an average of 74 to 80 minutes. (Tintinalli’s)

4. Routine arterial blood gas (ABG) analyzers without co-oximetry calculate, rather than measure, saturation, and will not differentiate or identify the contribution of dyshemoglobinemias to total saturation. As a result, the oxygen saturation may appear artificially high in routine blood gas analysis. Because the correlation between arterial and venous COHb levels is excellent, a venous blood gas sample analyzed with co-oximetry is usually sufficient. (Tintinalli’s)

5. Standard pulse oximetry is unreliable in the diagnosis of carbon monoxide poisoning. The wavelengths for COHb fall into the same range of those for oxyhemoglobin, which makes it difficult for standard pulse oximetry to differentiate the two. As a result, in the patient with carbon monoxide poisoning, the oxyhemoglobin saturation by pulse oximetry reading will be artificially high. The pulse oximetry gap is a measure of this discordance. When the pulse oximetry values are compared with the oxygen saturation on an ABG, the oxygen saturation on the pulse oximeter will be higher than the saturation on the ABG. (Tintinalli’s)

6. Initial resuscitation steps are the same as initial resuscitation of any critically ill patient. If carbon monoxide poisoning is strongly suspected based on history, supplemental oxygen in the highest concentrations available should be initiated immediately.(Tintinalli’s)

The decision to initiate hyperbaric oxygen (HBO) treatment requires careful assessment of many factors, including the blood COHb level, comorbid conditions (including pregnancy), stability of the patient, and location of the nearest center with emergency hyperbaric capabilities. Despite several clinical trials and decades of experience, the question of who will benefit most from HBO, and when to refer patients, remains controversial. (Tintinalli’s)

7. Fetal hemoglobin has a much greater affinity for CO than adult hemoglobin. Pregnant mothers may exhibit mild to moderate symptoms, yet the fetus may have devastating outcomes.


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