Carbon monoxide pathophysiology and treatment

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Carbon Monoxide Pathophysiology and Treatment
Stephen R. Thom, M.D., Ph.D.
Dr. Thom is Professor of Emergency Medicine and Chief, Hyperbaric Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA.
Within the past 12 months, Dr. Thom reports no commercial conflicts of interest.

Release Date: 07/31/2007
Termination Date: 07/31/2010

Estimated time to complete: 1hour(s).

Albert Einstein College of Medicine designates this enduring material for a maximum of 1 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Albert Einstein College of Medicine is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education forphysicians.

Learning Objectives
Upon completion of this Cyberounds®, you should be able to:
• Discuss the overlapping elements associated with CO pathology
• Discuss the latest information on clinical evaluation and health risks for CO poisoning
• List the CO poisoning treatment options, including evidence related to hyperbaric oxygen therapy (HBOT).


Though emergency physicians areaware of the general risks posed by carbon monoxide (CO), new research findings are beginning to influence clinical management. With this new information about the cardiac and nervous system risks from CO and the underlying mechanisms for injury, it is hoped that the high incidence of morbidity from CO can one day be reduced and that the clinical management of CO poisoning will become lesschallenging.
Environmental CO contamination from incomplete combustion of carbon-containing substances is a major public health threat.
Environmental CO contamination from incomplete combustion of carbon-containing substances is a major public health threat. Many poisonings could be avoided simply by improved communication about its dangers. This is an international problem and CO may be responsible forover half of all fatal poisonings.(1),(2),(3) It is estimated that CO poisoning is the third leading cause of unintentional deaths in the United States and that the incidence of nonfatal poisonings varies from 15,000 to 40,000 cases per year.(1),(2),(3),(4),(5),(6),(7) Because misdiagnosis of CO poisoning is common, however, the true incidence is likely much higher.(8),(9)
Pathophysiology
Theaffinity of CO for heme-containing proteins is well-established -- five processes occur simultaneously and contribute to CO poisoning (Table 1). Below is a brief discussion of each process.

Table 1. Mechanisms of CO Pathology.
• Impaired O2 delivery and utilization
• O2-CO-nitric oxide (•NO) competition
• Perivascular oxidative changes
• Excitotoxicity
• Immunological responses

ImpairedO2 Delivery and Utilization
CO has a high affinity for binding to hemoproteins and deleterious effects can occur as the result of impaired O2 delivery. The affinity of CO for hemoglobin is more than 200-fold greater than that of O2 and formation of carboxyhemoglobin (COHb) is well-recognized as an effect of CO exposure.(10) When CO occupies hemoglobin binding sites for O2, the arterial O2 contentis reduced. CO binding also influences the sigmoidal shape of the oxyhemoglobin dissociation curve, interfering with the release of O2 to the tissues. The 'left' shift of the oxyhemoglobin dissociation curve results in an exaggerated lowering of venous O2 partial pressure (Figure 1).(11)

Figure 1. Oxygen-hemoglobin Curve.

Three curves are shown: One (solid line) depicts the normaldissociation curve, the dashed line shows the impact of reducing the hemoglobin content by half (anemia) and one (small dotted line) the impact of 50% COHb. The left shift associated with COHb demonstrates the extra adverse effect of CO versus merely loss of hemoglobin O2 carrying capacity. The partial pressure of O2 when hemoglobin gives up 50% of its available O2 is at ~16 mm Hg when COHb is 50%,...
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