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Carbon Monoxide Poisoning

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Carbon Monoxide Poisoning CARBON MONOXIDE POISONING DANA BARTLETT, BSN, MSN, MA, CSPI Dana Bartlett is a professional nurse and author. His clinical experience includes 16 years of ICU and ER experience and over 20 years of as a poison control center information specialist. Dana has published numerous CE and journal articles, written NCLEX material, written textbook chapters, and done editing and reviewing for publishers such as Elsevire, Lippincott, and Thieme. He has written widely on the subject of toxicology and was recently named a contributing editor, toxicology section, for Critical Care Nurse journal. He is currently employed at the Connecticut Poison Control Center and is actively involved in lecturing and mentoring nurses, emergency medical residents and pharmacy students. ABSTRACT Known as the silent killer, carbon monoxide poisoning in individuals can present in various ways and the medical literature continues to contain areas of uncertainty and controversy. Symptoms of carbon monoxide poisoning tend to be non-specific in mild and severe cases. Delayed neuropsychiatric effects can occur, which are considered a serious complication. Diagnosis of carbon monoxide poisoning is based upon the patient history and physical examination as well as an elevated carboxyhemoglobin level. The etiology, clinical presentation and treatment are discussed, including those for children and special cases such as pregnancy. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 1 Policy Statement This activity has been planned and implemented in accordance with the policies of NurseCe4Less.com and the continuing nursing education requirements of the American Nurses Credentialing Center's Commission on Accreditation for registered nurses. It is the policy of NurseCe4Less.com to ensure objectivity, transparency, and best practice in clinical education for all continuing nursing education (CNE) activities. Continuing Education Credit Designation This educational activity is credited for 2 hours. Nurses may only claim credit commensurate with the credit awarded for completion of this course activity. Statement of Learning Need Carbon monoxide poisoning is a common and potentially fatal event with nonspecific clinical findings. Clinicians knowledgeable in the identification and treatment of carbon monoxide poisoning can help to initiate neuroprotective interventions and improve patient outcomes. Course Purpose This course will help clinicians identify carbon monoxide (CO) exposures and the standard treatments for CO poisoning. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 2 Target Audience Advanced Practice Registered Nurses and Registered Nurses (Interdisciplinary Health Team Members, including Vocational Nurses and Medical Assistants may obtain a Certificate of Completion) Course Author & Planning Team Conflict of Interest Disclosures Dana Bartlett, RN, MA, MSN, CSPI, William S. Cook, PhD, Douglas Lawrence, MA, Susan DePasquale, MSN, FPMHNP-BC – all have no disclosures Acknowledgement of Commercial Support There is no commercial support for this course. Please take time to complete a self-assessment of knowledge, on page 4, sample questions before reading the article. Opportunity to complete a self-assessment of knowledge learned will be provided at the end of the course. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 3 1. Carbon monoxide is produced by: a. incomplete combustion of carbon-containing fuel b. combustion of nitrogen-containing materials c. vapors emitted from carbon-containing fuel d. combustion of in organic acids 2. Carbon monoxide can also be produced by: a. toluene b. methylene chloride c. cyanide d. cadmium 3. One of the basic ways by which CO causes harm is: a. decreased production of hemoglobin b. production of abnormal hemoglobin c. tissue hypoxia d. pulmonary and coronary vasoconstriction 4. One of the basic ways by which CO causes harm is: a. damage to pulmonary capillaries b. production of methemoglobin c. hemolysis d. direct cellular toxicity 5. Two organs particularly vulnerable to CO poisoning are: a. the brain and the heart b. the kidneys and the pancreas c. the thyroid gland and the small bowel d. the lungs and the liver nursece4less.com nursece4less.com nursece4less.com nursece4less.com 4 Introduction Carbon monoxide (CO) is sometimes called the silent killer, and aptly so. It is a gas that is produced by incomplete combustion of carbon- containing material, it is colorless, odorless, and tasteless, and CO can be lethal. Despite large-scale public education and prevention programs, CO exposure is still a serious public health problem. The pathophysiology, clinical effects, and the best methods for treating CO poisoning have been intensively studied, but there are still areas of uncertainty and controversy. Epidemiology As mentioned in the introduction, despite increased public awareness of the dangers of CO and widespread public education and prevention measures, CO poisoning is still very common. Many sources consider CO poisoning to be among the leading causes of poisoning deaths in the United States, and CO poisoning is perhaps the number one worldwide cause of death by poisoning.1,2,3 Carbon monoxide is produced by the incomplete combustion of carbon-containing material. Automobile exhaust and home heating and/or cooking systems that use oil, gas, coal, or wood are the most common causes of CO poisoning, excluding exposures to fires. Carbon monoxide is also produced when tobacco is burned. Exposures to carbon monoxide and cases of CO poisoning can happen at any time of the year but are more common during the winter months. If temperatures are particularly cold and/or there is a power outage, people may attempt to heat their homes in ways that are nursece4less.com nursece4less.com nursece4less.com nursece4less.com 5 unsafe. In 2011, in Connecticut, a heavy snowstorm caused a widespread power outage and ambient temperatures at the time were quite cold. Emergency rooms in the state were inundated with cases of carbon monoxide poisoning as people were using gasoline generators and charcoal burning grills inside their homes to try and stay warm.4 Two other sources of carbon monoxide are methylene chloride and methylene iodide. Methylene chloride is a chemical that is often used as a component of commercially available paint strippers. Inhaled methylene chloride vapors or methylene chloride that is ingested or dermally absorbed is converted in vivo to CO. Because it is stored in fat tissues and the metabolizing enzymes are quickly saturated, peak CO levels produced by methylene chloride inhalation, ingestion, or dermal absorption are seen 8 hours or longer after an exposure.5 Methylene iodide is used by jewelers to examine gems and, like methylene chloride, it is converted in vivo to CO.6 Carbon monoxide poisoning caused by either of these is very uncommon. Carbon Monoxide: Pathophysiology The traditional and commonly understood mechanism of CO poisoning is that CO preferentially binds to hemoglobin, displacing oxygen from hemoglobin binding sites and causing cellular and tissue hypoxia. The binding of CO to hemoglobin and the reduced oxygen delivery to tissues and organs is certainly one of the primary ways that CO acts a poison. But research has shown that CO poisoning is much more complex and there are multiple, dynamic processes by which CO causes harm. 7-13 Some of these are known to affect humans and some have only been found in animal models. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 6 Hemoglobin Binding Carbon monoxide binds avidly to hemoglobin: it has an affinity for hemoglobin that is 200-250 times greater than that of oxygen. When CO displaces oxygen from hemoglobin and CO occupies the binding sites for oxygen on hemoglobin, this results in CO and hemoglobin combining to form carboxyhemoglobin (COHb). Carboxyhemoglobin does not bind with oxygen, so most of the hemoglobin is rendered functionally useless. Oxygen Transfer and the Oxyhemoglobin Dissociation Curve The oxyhemoglobin dissociation indicates how saturated hemoglobin is at any particular level of oxygen tension of the blood. It also indicates how tightly hemoglobin holds on to oxygen and how easily it releases oxygen for transfer to the tissues. Carbon monoxide shifts the oxyhemoglobin dissociation curve to the left so for any particular level of oxygen saturation less oxygen will be transferred to the tissues. This happens for two reasons. First, CO greatly increases the attachment of oxygen to hemoglobin. Second, because there is very little oxygen bound to hemoglobin, the difference between the oxygen level in tissues and the oxygen level of hemoglobin is greatly decreased. This difference is usually a strong driving force for the transfer of oxygen from hemoglobin to the tissues, but it is significantly diminished by the presence of CO. In CO poisoning the oxyhemoglobin dissociation curve shifts to the left and less oxygen reaches the tissues. nursece4less.com nursece4less.com nursece4less.com nursece4less.com 7 Binding to Myoglobin Myoglobin is an oxygen-transporting and storage pigment that is found inside cells. Carbon monoxide binds to myoglobin - particularly in the myocardium - thus preventing oxygen utilization. Interference with Oxidative Phosphorylation Carbon monoxide binds with mitochondrial cytochrome oxidase, an important enzyme that is needed for proper functioning of the electron transport chain in cellular respiration that produces the bulk of the adenosine
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