Less commonly, the cardiac, pulmonary and renal systems are injured. Also, a leftward shift in the oxyhemoglobin dissociation curve occurs resulting in an impaired ability of oxyhemoglobin to release oxygen at the tissue level. Further poisoning of cells occurs due to binding of CO to myoglobin, reduced cytochromes, and cellular enzymes. The result is impaired oxidative phosphorylation and release of free radicals. These radicals can also inactivate mitochondrial enzymes, impair electron transport and accelerate production of reduced oxygen.
Acute mortality is attributed to dysrhythmias caused by hypoxia.
Patients with cardiovascular disease are more at risk. The delayed toxicity, referred to here as DNS, occurs in the perivascular area of the CNS and may be due to secondary hemorrhagic necrosis. This is exacerbated by hypoxia and hypotension as well as oxidative injury, due to leukocyte proteases. Most of the neuronal injury appears to be in the hippocampus and globus pallidus, resulting in a Parkinsonian syndrome and dementia, clinically. Patients most at risk are those over 60 with cardiovascular disease.