Carbon monoxide cardiotoxicity

Cardiac dysfunction including arrhythmias and myocardial ischemia have often been reported in carbon monoxide poisoning; scattered punctiform hemorrhages throughout the heart have been documented in autopsy samples. An appropriate diagnostic approach is crucial to assess carbon monoxide cardiac damage. This evaluation may be confounded by several factors, including the absence of overt symptoms and of specific ischemic changes in the electrocardiogram. In experimental studies, laboratory animals can develop cardiac changes similar to those seen in humans and therefore proved to be useful models to study the effects and the mechanisms of cardiac damage due to carbon monoxide. These investigations, as well as others performed in vitro, provide support for a direct action of carbon monoxide on the heart, in addition to systemic hypoxia produced by carboxyhemoglobin formation. This review focuses on the diagnostic aspects of carbon monoxide cardiotoxicity. Experimental results obtained in animals and in vitro models are also discussed.     

急性一氧化碳中毒心肌损害的探讨

目的探讨急性一氧化碳（CO）中毒对心肌的损害,使急性CO中毒患者得到更全面的治疗。方法分析急性CO中毒153例患者的临床表现、心电图及心肌酶改变。结果153例急性CO中毒患者中86.3%出现昏迷,13.7%出现心力衰竭,随机将其中65例中毒患者作心电图及心肌酶检查,发现86.2%出现心电图改变,67.7%出现心肌酶改变。结论急性CO中毒不仅对神经系统造成损害,对心肌的损害也很严重,需要给予相应的治疗。     

The evaluation of myocardial damage in 83 young adults with carbon monoxide poisoning in the East Anatolia region in Turkey

Carbon monoxide (CO) poisoning is the leading cause of death from intoxication. In CO poisoning, it is important to know if there are any symptoms regarding myocardial damage, which are usually unobserved as a result of hypoxia. This study was planned to assess myocardial damage in young healthy patients with CO poisoning. Eighty-three young healthy cases who had been exposed to CO were included in this study. The demographic and clinical characteristics, the origin of CO gas and smoking habits of the patients were recorded. The evaluation of ECG, peripheral ABG, complete blood count and serial cardiac biomarkers (creatine kinase, creatine kinase-myocardial band and troponin I) measurements were performed in all cases. Additionally, echocardiogram (ECHO) and myocardial perfusion single-photon emission computed tomography (SPECT) were performed at the appropriate times in all cases. The mean age of the patients was 27.3 +/- 10.9 years. The main complaint of the patients was loss of consciousness with a 62.7% rate. The average carboxyhaemoglobin level of the patients was 34.4 +/- 15.9%. Sinus tachycardia was present in 26.5% of patients. Diagnostic ischaemic ECG changes were present in 14.4% of patients. In myocardial SPECT, myocardial ischaemic damage was observed in 9 cases, in 6 of whom ECHO findings were also confirmed. Myocardial damage due to CO poisoning should not be ignored. If patients are at risk in terms of myocardial damage, further studies, such as ECHO and scintigraphy are needed to determine myocardial damage resulting from CO poisoning. However, in the young adults of the risk group, if the baseline ECG and serial cardiac biomarkers are normal, further studies such as ECHO and scintigraphy, considering the length of exposure and the severity of poisoning, may not be necessary for the evaluation of myocardial damage due to CO poisoning.     

H-FABP in cases of carbon monoxide intoxication admitted to the emergency room

Introduction: Carbon monoxide (CO) intoxication causes cardiovascular problems as a result of diffuse tissue hypoxia. Cardiac biochemical markers and electrocardiographic changes have been reported in CO intoxications. Human fatty acid-binding protein (H-FABP) has been recently used as a reliable marker in identifying early cardiac damage. In this prospective study, we aimed to investigate the advantages of the use of H-FABP, in evaluating the findings of myocardial ischemia in patients with CO intoxication in our region. Methods: Twenty four successive patients admitted to the emergency department with acute CO intoxication were included in our study. Serum traditional markers and H-FABP were also taken in the earliest period for evaluation of cardiac damage. Results: The creatinine kinase MB (CKMB) levels were positive in 11 of the patients; however, H-FABP and troponin T levels were positive in only 3 of them. One of these subjects had elevated level of H-FABP in the short-term and increasing troponin T level increasing level of troponin T during the follow-up period. Conclusion: The obtained data supports the use of H-FABP, a specific indicator in identifying the cardiotoxicity of CO intoxications at an early phase.     

A case of carbon monoxide poisoning with thrombus in the heart: a case report

Carbon monoxide is a nonirritant, odorless, colorless gas, and is lighter than air. It is an end product of the incomplete combustion of hydrocarbons. Its effects are most prominent in organs sensitive to oxygen deprivation, such as the heart, brain, and kidney. Carbon monoxide poisoning becomes more abundant in winter and at cold places. In Turkey, every year we see several deaths due to poisonous gas leaks from coal or wood stoves. Deaths particularly due to hypoxia-related central nervous system damage and ventricular dysrhythmias are observed. On the other hand, an association between thromboembolic accidents and carbon monoxide poisoning has been shown in literature. Thromboembolic accidents in the mesenteric, central nervous system, and extremities are reported. However, no atrial thrombus has been mentioned. In this study, a case of an atrial thrombus associated with carbon monoxide poisoning following a diagnosis of carbon monoxide poisoning and treatment in the emergency room is reported and the literature is revisited.     

Carbon monoxide poisoning--a public health perspective

Carbon monoxide (CO) may be the cause of more than one-half of the fatal poisonings reported in many countries; fatal cases also are grossly under-reported or misdiagnosed by medical professionals. Therefore, the precise number of individuals who have suffered from CO intoxication is not known. The health effects associated with exposure to CO range from the more subtle cardiovascular and neurobehavioral effects at low concentrations to unconsciousness and death after acute or chronic exposure to higher concentrations of CO. The morbidity and mortality resulting from the latter exposures are described briefly to complete the picture of CO exposure in present-day society. The symptoms, signs, and prognosis of acute CO poisoning correlate poorly with the level of carboxyhemoglobin (COHb) measured at the time of hospital admission; however, because CO poisoning is a diagnosis frequently overlooked, the importance of measuring COHb in suspicious settings cannot be overstated. The early symptoms (headache, dizziness, weakness, nausea, confusion, disorientation, and visual disturbances) also have to be emphasized, especially if they recur with a regular periodicity or in the same environment. Complications occur frequently in CO poisoning. Immediate death is most likely cardiac in origin because myocardial tissues are most sensitive to the hypoxic effects of CO. Severe poisoning results in marked hypotension, lethal arrhythmias, and electrocardiographic changes. Pulmonary edema may occur. Neurological manifestation of acute CO poisoning includes disorientation, confusion, and coma. Perhaps the most insidious effect of CO poisoning is the development of delayed neuropsychiatric impairment within 2-28 days after poisoning and the slow resolution of neurobehavioral consequences. Carbon monoxide poisoning during pregnancy results in high risk for the mother by increasing the short-term complication rate and for the fetus by causing fetal death, developmental disorders, and chronic cerebral lesions. In conclusion, CO poisoning occurs frequently; has severe consequences, including immediate death; involves complications and late sequelae; and often is overlooked. Efforts in prevention and in public and medical education should be encouraged.     

A Case of Carbon Monoxide Poisoning with Thrombus in the Heart: A Case Report

Carbon monoxide is a nonirritant, odorless, colorless gas, and is lighter than air. It is an end product of the incomplete combustion of hydrocarbons. Its effects are most prominent in organs sensitive to oxygen deprivation, such as the heart, brain, and kidney. Carbon monoxide poisoning becomes more abundant in winter and at cold places. In Turkey, every year we see several deaths due to poisonous gas leaks from coal or wood stoves. Deaths particularly due to hypoxia-related central nervous system damage and ventricular dysrhythmias are observed. On the other hand, an association between thromboembolic accidents and carbon monoxide poisoning has been shown in literature. Thromboembolic accidents in the mesenteric, central nervous system, and extremities are reported. However, no atrial thrombus has been mentioned. In this study, a case of an atrial thrombus associated with carbon monoxide poisoning following a diagnosis of carbon monoxide poisoning and treatment in the emergency room is reported and the literature is revisited.     

Anthracycline-induced cardiotoxicity in children with cancer: strategies for prevention and management

The fact that anthracyclines are cardiotoxic seriously narrows their therapeutic index in cancer therapy. The cardiotoxic risk increases with the cumulative dose and may lead to congestive heart failure (CHF) and dilated cardiomyopathy in adults and in children. The prevention of anthracycline-induced cardiotoxicity is particularly important in children who can be expected to survive for decades after being cured of their malignancy. Attempts to reduce anthracycline cardiotoxicity have been directed towards: (i) decreasing myocardial concentrations of anthracyclines and their metabolites by dose limitation and schedule modification; (ii) developing less cardio-toxic analogs; and (iii) concurrently administering cardioprotective agents to attenuate the effects of anthracyclines on the heart. As regards schedule modification, avoidance of anthracycline peak levels may reduce the pathologic and clinical cardiotoxicity, although this has not always been observed. The analogs of doxorubicin, such as idarubicin and epirubicin, have similar cardiotoxicity to that of doxorubicin when given in amounts of equivalent myelotoxicity. Liposomal anthracyclines are a new class of agents that may permit more specific organ targeting, thereby producing less systemic and cardiac toxicity, but more studies are required to assess the advantages, if any, of these preparations over classical anthracyclines. The cardioprotective agent, dexrazoxane, an iron chelator, is highly effective and provides short-term cardioprotection to most patients receiving even the most intensive doxorubicin-containing regimens. Its long-term benefits remain to be determined. In addition, data remain insufficient to make specific recommendations regarding current use of dexrazoxane in children. It is thought that subtle abnormalities, related to anthracycline treatment in childhood, can develop into more permanent myocardial disease resulting in cardiomyopathy, which may progress to CHF. As regards the therapy of patients with anthracycline cardiotoxicity, two different situations have, therefore, to be considered: (i) if the patient presents with cardiac abnormalities, such as a reduction in fractional shortening at echocardiogram, without cardiac symptoms; and (ii) if the patient has CHF. In the presence of CHF, recovery with digitalis-diuretic therapy alone seldom occurs, and in patients who have refractory hemodynamic decompensation, heart transplantation is indicated. In patients with CHF, therapy with ACE inhibitors induces improvement in left ventricular structure and function, but this improvement is transient. Randomized clinical trials are, therefore, necessary to determine the effects of ACE inhibitors in mild-to-moderate left ventricular dysfunction. The beneficial effects of beta-adrenoceptor antagonists (beta-blockers) on cardiac function in heart failure due to anthracyclines seem comparable with those observed in other forms of heart failure with systolic dysfunction. Many drugs are available to treat children with CHF due to anthracycline treatment, but they are only palliative.     

Serum levels of NT-ProBNP as an early cardiac marker of carbon monoxide poisoning

Acute carbon monoxide (CO) poisoning may cause cardiotoxicity. The natriuretic peptides, including atrial natriuretic peptide, brain natriuretic peptide (BNP), N-BNP, and NT-proBNP (N-terminal pro brain natriuretic peptide), are endogenous cardiac hormones that may be secreted upon myocardial stress. The aim of this study was to assess the plasma NT-proBNP level in acute CO poisoning and to compare it with healthy control. After approval by the ethical committee, 15 healthy controls and 15 patients admitted to the Gaziantep University Hospital (Gaziantep, Turkey) between January 2005 and July 2005 with the diagnosis of carbon monoxide poisoning were studied. Echocardiography was performed to all patients. Serum NT-proBNP, creatine kinase (CK), creatine kinase-MB (CK-MB), and troponin-T were also analyzed, along with the carboxyhemoglobin (COHb) level. The correlation between serum NT-proBNP and COHb level was investigated. Electrocardiography (ECG) was performed to all patients and healthy controls, and the results were compared. Differences in troponin, CK, and CK-MB levels were not statistically significant between groups (p > 0.05). The level of NT-proBNP and COHb were found to be increased in the study group. There was a positive correlation between the COHb and the NT-proBNP (r = 0.829, p < 0.01), and between the COHb and the CK (r = 0.394, p < 0.01). There was no difference between groups in other parameters, all of which were within normal range. Thus, in this study we showed that the plasma NT-proBNP level may contribute to the early diagnosis of cardiotoxicity in patients with carbon monoxide poisoning.     

Serum Levels of NT-ProBNP as an Early Cardiac Marker of Carbon Monoxide Poisoning

Acute carbon monoxide (CO) poisoning may cause cardiotoxicity. The natriuretic peptides, including atrial natriuretic peptide, brain natriuretic peptide (BNP), N-BNP, and NT-proBNP (N-terminal pro brain natriuretic peptide), are endogenous cardiac hormones that may be secreted upon myocardial stress. The aim of this study was to assess the plasma NT-proBNP level in acute CO poisoning and to compare it with healthy control. After approval by the ethical committee, 15 healthy controls and 15 patients admitted to the Gaziantep University Hospital (Gaziantep, Turkey) between January 2005 and July 2005 with the diagnosis of carbon monoxide poisoning were studied. Echocardiography was performed to all patients. Serum NT-proBNP, creatine kinase (CK), creatine kinase-MB (CK-MB), and troponin-T were also analyzed, along with the carboxyhemoglobin (COHb) level. The correlation between serum NT-proBNP and COHb level was investigated. Electrocardiography (ECG) was performed to all patients and healthy controls, and the results were compared. Differences in troponin, CK, and CK-MB levels were not statistically significant between groups (p > 0.05). The level of NT-proBNP and COHb were found to be increased in the study group. There was a positive correlation between the COHb and the NT-proBNP (r = 0.829, p < 0.01), and between the COHb and the CK (r = 0.394, p < 0.01). There was no difference between groups in other parameters, all of which were within normal range. Thus, in this sudy we showed that the plasma NT-proBNP level may contribute to the early diagnosis of cardiotoxicity in patients with carbon monoxide poisoning.     

A review of carboxymyoglobin formation: a major mechanism of carbon monoxide toxicity

Clinical data suggest, and experimental studies indicate direct cardiotoxic effects of carbon monoxide, apart from carboxyhemoglobin formation. Carbon monoxide interactions with cytochrome oxidase and myoglobin are suspect. Of these, myoglobin is the favored tissue target for carbon monoxide binding. On what evidence? Examination of the literature reveals the following: A 16% greater "volume of distribution" (Vd) for carbon monoxide, versus other blood volume indicators, concentrating in skeletal and cardiac muscle; A high myoglobin content in these tissues corresponding to this "excess" Vd for carbon monoxide; Evidence from animals of significant carboxymyoglobin concentrations; Hemeprotein independent changes produced by carbon monoxide which promote carbon monoxide-myoglobin interactions; A high ratio of deoxymyoglobin (carbon monoxide binding form) to oxymyoglobin intracellularly; Direct intercellular measurements of oxymyoglobin saturations and "cycling" in vivo illustrating favorable conditions for carbon monoxide binding; Data indicating decrements in cardiac performance with loss of functional myoglobin; Evidence that myoglobin is important to the proper functioning of cardio-adaptive mechanisms in stress. The total picture of carbon monoxide poisoning must take into account pathogenic effects due to carboxymyoglobin formation.     

Recent advances in the prevention of anthracycline cardiotoxicity in childhood

The prevention of anthracycline cardiotoxicity is particularly important in children who can be expected to survive for decades after cancer chemotherapy with these agents. The rapid increase in clinical toxicity at doses greater than 550 mg/m(2) of doxorubicin (DOX) has made this dose the limiting one in order to avoid DOX-induced cardiac failure. However, arbitrary dose limitation is inadequate because of variability of individual tolerance. Decreasing myocardial concentrations of anthracyclines (ANT) and their metabolites and schedule modification of administration can reduce anthracycline cardiotoxicity. Anthracycline structural analogues such as epirubicin, idarubicin and mitoxantrone have been used in clinical practice. In addition, the liposomal ANT, which can be incorporated into a variety of liposomal preparations, are a new class of agents that may permit more specific organ targeting of ANT, thereby producing less cardiac toxicity. Much interest has focused on the administration of ANT in conjunction with another agent that will selectively attenuate the cardiotoxicity. As is known, the ANT chelate iron and the DOX-iron complex catalyzes the formation of extremely reactive hydroxyl radicals. Many agents, such as dexrazoxane (DEX), able to remove iron from DOX, have been investigated as anthracycline cardioprotectors. Clinical trials of DEX have been conducted in children and significant short-term cardioprotection with no evidence of interference with antitumor activity has been demonstrated. Whether long-term cardiac toxicity will also be avoided in surviving patients has not yet been determined.     

一氧化碳中毒迟发型神经损伤临床特点及预后分析

目的探讨一氧化碳中毒迟发型神经损害临床特点及预后。方法对本院收治的23例一氧化碳中毒迟发型神经损害患者的临床特点及资料进行系统分析,并对预后进行评定。结果在药物对症治疗基础上行高压氧治疗,有效率为95.7%。一氧化碳中毒迟发型神经损害患者预后情况与年龄、昏迷时间、高压氧开始时间、治疗次数,以及并发症等密切相关。结论临床需加强对一氧化碳中毒迟发性神经损伤的认识,高压氧开始时间早及治疗持续时间长,预后越好。     

儿童意外中毒141例的分析与预防

目的分析儿童意外中毒的常见原因、种类、症状、治疗及预防。方法对广东省汕头市澄海区人民医院2006年1月至2010年12月收治的141例儿童急性中毒病例进行回顾性分析。结果儿童意外中毒的常见原因为:误服药物或化工用品122例(86.52%),医源性5例(3.55%),其他(投毒、自杀、一氧化碳中毒等)14例(9.93%)。结论儿童意外中毒以儿童误服中毒为主。预防儿童意外中毒的发生,需要个人、家庭、医务人员、甚至全社会的共同努力。     

Drug-induced myocardial dysfunction – recommendations for assessment in clinical and pre-clinical studies

ABSTRACT

Introduction: Drug-induced myocardial dysfunction is an important safety concern during drug development. Oncology compounds can cause myocardial dysfunction, leading to decreased left ventricular ejection fraction and heart failure via several mechanisms. Cardiovascular imaging has a major role in the early detection and monitoring of cardiotoxicity. Echocardiography is the method of choice because of its widespread availability, low cost, and absence of radiation exposure. Cardiac magnetic resonance imaging can provide better reliability, reproducibility, and accuracy in the detection of drug-induced myocardial dysfunction. In addition, it enables assessment of myocardial edema, fibrosis, and necrosis. Cardiac serologic biomarkers such as troponins and B-type natriuretic peptides are used in combination with imaging during drug development. This article provides a general overview of each imaging modality and practical guidance for early detection and monitoring of cardiotoxicity.

Areas covered: Cardiovascular imaging modalities and cardiac biomarkers for monitoring of cardiac function and early detection of drug-induced myocardial dysfunction in drug development.

Expert opinion: Some new drugs especially in the oncology field, can cause myocardial dysfunction. Depending on the strength of pre-clinical or clinical data, CV imaging modalities and cardiac biomarkers play an important role in the early detection and mitigation plans for such drugs during their development.     

Rhabdomyolysis and acute renal failure following carbon monoxide poisoning: two case reports with muscle histopathology and enzyme activities.

Two patients with carbon monoxide poisoning are presented, both of whom suffered rhabdomyolysis complicated by acute renal failure. One patient, an attempted suicide, developed a compartment syndrome of the right thigh that required fasciotomy and recovered after a period of hemofiltration and hemodialysis. Muscle biopsy appearances were consistent with partial muscle infarction. The other patient, rescued from a smoke filled room, exhibited raised creatine kinase but no evidence of muscle swelling. He developed anuric renal failure and adult respiratory distress syndrome and died despite maximum intensive care. Muscle biopsy showed early evidence of muscle necrosis. In both cases there was a marked reduction of enzyme activities in the muscle biopsy consistent with metabolic derangement. Although there was a clinical compartment syndrome in the first case, there was no muscle swelling at the time of biopsy or subsequently in the second case. A direct toxic effect of carbon monoxide may thus have been an important mechanism contributing to the muscle necrosis in the second case, although local ischemia may have been an exacerbating factor in the first case.     

Occult carbon monoxide poisoning in patients with neurologic illness

To investigate occult carbon monoxide poisoning in patients with neurologic illness, we prospectively studied 168 patients who presented to the emergency department between December 1987 and February 1988 with neurologic symptoms for evidence of carbon monoxide exposure. Patients with known carbon monoxide poisoning were excluded. The mean carboxyhemoglobin level was 3.1 percent; there were no significant differences in carboxyhemoglobin between categories of neurologic illness (F(5,162) = 1.35; p less than 0.25). Five patients (3 percent) had a carboxyhemoglobin greater than 10 percent, with levels ranging from 11.7 percent to 29.5 percent. After controlling for the effects of active and passive exposure to cigarette smoke, problems with the home heating system (odds ratio 9.6; p less than 0.03) and the presence of cohabitants with concurrent headache or dizziness (odds ratio 21.6; p less than 0.0001) were associated with an increased risk of a carboxyhemoglobin greater than 10 percent. A rule for obtaining carboxyhemoglobin tests only on patients who used gas stoves for heat or who had symptomatic cohabitants would have correctly identified all patients with carboxyhemoglobins greater than 10 percent, correctly excluded 77 percent of patients with lower levels, and eliminated the need for testing in 75 percent of cases. We conclude that unrecognized carbon monoxide poisoning occurs in a small but important fraction of patients with wintertime neurologic illness and can be identified by a characteristic risk factor profile.     

Biological plausibility for carbon monoxide as a copollutant in PM epidemiologic studies

Several recent epidemiologic studies investigating the short-term effects of particulate matter (PM) concentrations have shown carbon monoxide (CO) to have the strongest and most consistent statistical relationship with hospital admissions for cardiac diseases. This article suggests a potential hypothesis for these epidemiologic observations. Oxygen (O2) is transported, in reversible combination with hemoglobin, from the lungs to the tissues, where it diffuses into cardiac myocytes. Within the myocyte a portion of the O2 diffuses directly to the mitochondria, while the remaining O2 is transported by facilitated diffusion bound to myoglobin, a heme protein found in muscle. Within the mitochondria, O2 reacts to produce adenosine triphosphate (ATP), a high-energy phosphate compound that provides energy for all cell functions. Accordingly, the sustained production of ATP depends on the continuous delivery of O2 to the mitochondria, and failure at any point in the O2 transport system will compromise ATP production and myocardial function. Myoglobin, a fundamental constituent of cardiac muscle is essential for delivering O2 to the mitochondria. Myoglobin concentrations in cardiac tissue were 50% lower in patients with heart failure than in patients dying from noncardiac causes. Myoglobin concentrations are also severely depressed in animal models of congestive heart failure. Consequently, the role of myoglobin as a cellular transporter of O2 is seriously impaired by heart disease. Carbon monoxide reduces O2 transport to the tissues and, within the tissues, binds with myoglobin to form carboxymyoglobin (COMb). Thus, in cardiac patients CO further exacerbates the disease-related loss of myoglobin function. This further disrupts O2 transport and promotes adverse consequences for the compromised heart. Moreover, during hypoxia CO has the propensity of leaving the blood and binding with myoglobin in the intracellular compartment. Elderly persons with preexisting cardiopulmonary disorders appear to be at maximum risk of harmful health effects due to ambient air pollution exposure. Many of these disorders result in generalized or regional hypoxia. It is reasonable to hypothesize that CO also moves out of the blood of these patients and into the heart tissue whenever they are under hypoxic stress, such as exercise. Accordingly, CO binds with the marginal myoglobin concentrations present in the hearts of cardiac patients and further compromises cardiac function, resulting in poor tolerance of activity. Therefore, reduced cardiac myoglobin in people with heart disease, further exacerbated by CO moving into the cardiac tissue during episodes of hypoxia, may account for the positive association between ambient CO concentrations and hospitalization for heart disease.     

Effects of granulocyte colony-stimulating factor on electrocardiogram changes after carbon monoxide poisoning in rats

Carbon monoxide (CO), which is produced by the incomplete combustion of hydrocarbons, has many toxic effects on different organs, especially the brain and heart. CO-induced cardiotoxicity leads to several deleterious effects, including electrocardiogram (ECG) abnormalities. The present study aimed to evaluate the protective effect of recombinant human granulocyte colony-stimulation factor (G-CSF) on ECG after CO poisoning in rats. Single and multiple doses of G-CSF (10, 50, and 100 μg/kg) were administered to groups, each containing 5 male Wistar rats (16 groups for ECG analysis and 16 groups for pathological analysis). Rats were already exposed to CO at either 1,500 or 3,000 ppm concentrations for 60 minutes. ECG findings (e.g., ST-segment and T-wave changes), cardiac arrhythmias (e.g., heart blocks and ventricular and supraventricular arrhythmias), and histological changes were determined after G-CSF administration. At 3,000 ppm, frequencies of ST elevation, depression, and T inversion in ECG were significantly reduced after G-CSF treatment. Also, some of the cardiac arrhythmias (e.g., atrioventricular block type 1 and 2) after CO poisoning were suppressed after G-CSF treatment. However, G-CSF did not show protective effects on cardiomyocyte pathological consequences in CO-poisoned rats. Therefore, G-CSF could protect against ECG changes after CO-induced cardiac ischemia, but did not affect pathological changes.     

Epidemiology of acute carbon monoxide poisoning in a Spanish region

BACKGROUND: In Spain, as in most of the world, the incidence of acute carbon monoxide poisoning is probably underestimated. METHODS: During an eighteen-month period we studied, by means of a standardized data collection form, all the cases of acute carbon monoxide poisoning that were diagnosed in 2 university hospitals. RESULTS: During the study, 154 patients were diagnosed with carbon monoxide poisoning. The mean age was 32.2+/-15.5 years. The two principal exposure sites were the kitchen (43%) and bathroom (23%). The majority of the cases related to malfunction of the water heater (30%) and of the central heating (23%) and 68% occurred in the home. Improper combustion of butane (31%), propane (13%), and natural gas (12%) were most frequent. The most prevalent clinical manifestations were headache (94%), dizziness (56%), nausea (45%), loss of consciousness (38%), and weakness (34%). Five patients died. In 14.4%, symptoms suggested delayed neurological syndrome. The largest number of cases of poisoning occurred during the months of December and January. CONCLUSIONS: Compared with previous Spanish series or with the antecedent year, acute carbon monoxide poisoning has a high prevalence in our region. Two factors appear to be essential to the accurate diagnosis of acute carbon monoxide poisoning: 1) the ability of emergency room physicians to recognize the clinical symptoms of carbon monoxide poisoning and 2) access to a carbon monoxide-oximeter.