Carbon monoxide poisoning: Too easily overlooked

Nursing, May 2004 by Balch, Coleen

In a moderately to heavily exposed patient, arterial blood gas analysis may reveal metabolic acidosis with a markedly decreased pH, but PaO^sub 2^ will be normal and PaCO^sub 2^ values will vary. For accuracy, measure oxygen saturation by co-oximetry.

Obtain a COHb level for any patient with headache or dizziness of nontraumatic origin whose family members are similarly affected or who uses gas for heating and cooking. But remember that the correlation between COHb levels and toxicity can be skewed by delays in measuring COHb and the effect of oxygen therapy. (For a rough guide, see As Carboxyhemoglobin Levels Rise....) Some otherwise-healthy people remain asymptomatic with a COHb level of 10%, but someone with cardiac disease might develop angina with a COHb level of 3%.

For a more reliable reflection of tissue poisoning, obtain a serum lactate level to show the extent of acidosis. Also obtain a 12-lead electrocardiogram. Although results may be within normal limits, they may also reveal arrhythmias, conduction defects, or ST-segment abnormalities. A chest X-ray can detect or rule out pneumonia, aspiration, atelectasis, and pulmonary edema, and a computed tomography scan of the brain can reveal cerebral edema or mass effect (a tumor or blood clot causing pressure on the brain). Obtain a chemistry panel to assess for dehydration. Obtain serum creatine kinase, lactate dehydrogenase, and urine for myoglobin to detect hypoxia-induced muscle necrosis, which may result in renal failure.

Treating your patient

First and foremost: Remove the patient from the source of CO and begin 100% oxygen therapy immediately via a tight-fitting non-rebreather mask or an endotracheal tube, depending on her condition. Some experts consider oxygen mandatory for any exposure, with or without symptoms.

If it's available and the patient's condition permits, hyperbaric oxygen therapy, although costly, is recommended for patients who have severe neuropsychiatric symptoms, cardiac ischemia, or hemodynamic instability or are in a coma or pregnant. Some experts advocate using hyperbaric oxygen for patients with COHb levels greater than 25%, patients whose clinical status is worsening despite regular oxygen therapy, and patients with persistent symptoms (no matter what their COHb level).

Hyperbaric oxygen therapy dissolves enough oxygen in the plasma to satisfy the body's needs despite nonfunctioning hemoglobin and reduces the half-life of CO. Patients treated with hyperbaric oxygen therapy appear to have fewer delayed neurologic syndromes, although patients who've lost consciousness during CO exposure are at higher risk for persistent neurologic deficit regardless of the type of oxygen therapy.

Hyperbaric oxygen therapy is most effective when initiated 2 to 6 hours after exposure. Potential hazards include promotion of oxygen toxicity, leading to neurologic dysfunction; barotrauma, especially of the middle ear; free radical production; tension pneumothorax; and nitrogen embolus.

Very unstable patients, who theoretically need hyperbaric oxygen therapy the most, may not be able to receive it if they're likely to need emergency treatment for cardiopulmonary collapse.