Myocardial Toxicity from Carbon Monoxide Poisoning

Anderson, Robert

doi:10.7326/0003-4819-67-6-1172

Cited by 85 publications

(29 citation statements)

References 13 publications

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“…At least one study suggests that CO-related increases in coronary perfusion pressure are related to both endothelium-dependent and -independent mechanisms, suggesting more than one mechanism of action for CO. 20 The trend toward decreased pO 2 during the basal phase in the CO and nitrogen control groups cannot be explained. However, statistically the difference in pO 2 was not significant and the pO 2 decreased during the experimental phase and returned to baseline levels in the recovery in these groups ( Figure 5). …”

Section: Discussionmentioning

confidence: 82%

“…1 In addition to its well-described neurological toxicity, clinically, CO poisoning may lead to myocardial ischemia, manifested by chest pain, electrocardiogram changes (ST-segment depression and T-wave depression), and myocardial infarction, and is associated with long-term morbidity and mortality. 2,3 Previous animal studies have suggested that CO may produce direct toxicity to the myocardium rather than indirect hypoxic damage. 4 Experimentally, CO has been shown to decrease regional myocardial segment work and increase coronary flow with increasing concentrations; however, the site and mechanism of CO myocardial toxicity has not been elucidated.…”

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confidence: 99%

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Carbon Monoxide Has Direct Toxicity on the Myocardium Distinct from Effects of Hypoxia in an Ex Vivo Rat Heart Model

Suner

Jay

2008

Academic Emergency Medicine

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Objectives: Carbon monoxide (CO) toxicity causes significant central nervous system and cardiac injury. Although the neurological damage caused by CO toxicity is extensively described, the mechanisms underlying myocardial insult are unclear. The authors used an externally perfused isolated rat heart model to examine the effects of a physiological saline solution (Krebs Henseleit HEPES, KHH) aerated with CO on cardiac function.Methods: Fifteen rats were equally divided into three groups: the control group (KHH + 100% O 2 ), the nitrogen control group (KHH + 70% O 2 , 30% N 2 ), and the CO group (KHH + 70% oxygen, 30% CO). Left ventricular peak systolic pressure (LVPsP), end diastolic pressure (LVEdP), and coronary perfusion pressure were measured while the isolated heart was paced and perfused on a modified Langendorf apparatus.Results: Left ventricular generated pressure (LVGP = LVPsP ) LVEdP) decreased in the nitrogen control and CO groups compared to the control group. There was higher LVGP in the recovery phase between the nitrogen control group compared to the CO group. Both groups had increased lactic acid levels in the experimental phase.Conclusions: Carbon monoxide with hypoxia and hypoxemic hypoxia both result in similar depression of cardiac function. Hearts poisoned with CO with hypoxia do not recover function to the extent that hearts rendered hypoxic with nitrogen do when perfused with 100% oxygen after the insult. This suggests that CO causes direct myocardial toxicity distinct from the effects of hypoxia.ACADEMIC EMERGENCY MEDICINE 2008; 15:59-65 ª

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Section: Discussionmentioning

confidence: 82%

mentioning

confidence: 99%

Carbon Monoxide Has Direct Toxicity on the Myocardium Distinct from Effects of Hypoxia in an Ex Vivo Rat Heart Model

Suner

Jay

2008

Academic Emergency Medicine

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“…Since the first report about CO-induced cardiac damage by Klebs in 1865, heart failure and myocardial ischemia have been described in the patients after acute exposure to the CO. 1)6) After exposure to CO, several clinical manifestations have been reported, including arrhythmias and electrocardiographic alterations, 1) acute myocardial infarction, 7) pulmonary edema, and cardiogenic shock. 8) Moreover, acute circulatory collapse and myocardial damage have been frequently observed in lethal cases.…”

Section: D a Bmentioning

confidence: 99%

Transient Left Ventricular Systolic Dysfunction Associated with Carbon Monoxide Toxicity

Jang

Park

2010

J Cardiovasc Ultrasound

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I In nt tr ro od du uc ct ti io on nCarbon monoxide (CO) can cause functional and morphological alternations of the heart mainly due to myocardial hypoxemia and direct action of CO on the heart. 1)2) CO has about 250-fold higher affinity for hemoglobin as compared to oxygen and forms carboxyhemoglobin (CO-Hb). In the presence of CO-Hb, a leftward shift of the oxygenated hemoglobin dissociation curve observed and leads to impairment of tissue oxygen delivery and makes cellular hypoxia. 1)CO induced cardiotoxicity has many clinical manifestations including arrhythmias, pulmonary edema and heart failure, and myocardial infarction. Echocardiography is known as the most useful method in the detection the presence of cardiac toxicity and assessment of its severity. We report a case with transient severe left ventricular dysfunction after intentional exposure to CO. The patient was early detected with an echocardiographic exam and treated with conventional treatment including high concentration of oxygen. C Ca as se eA 28-year-old man was admitted to our emergency room for altered mentality due to intentional exposure to CO. On his arrival, blood pressure was 104/80 mmHg, the pulse 126 beat per minute, axillary temperature 37.7°£C and the respirations were 32 breaths per minute. On blood analysis, AST/ALT 37/29 IU/L, CK 412 U/L, CK-MB 6.9 ng/mL, troponin I 0.96 ng/mL, N-terminal pro B-type natriuretic peptide 451.5 pg/mL, and CO-Hb 27.7%. The patient was intubated and treated with high concentration of oxygen therapy. A radiograph of the chest showed pulmonary edema and mild cardiomegaly (Fig. 1A). An electrocardiogram revealed sinus tachycardia of heart rate 120 per minute. Transthoracic echocardiogram showed global hypokinesia of left ventricle with severe systolic dysfunction ( Fig. 2A and B). He was treated with diuretics, angiotensin converting enzyme inhibitor and urine alkalinization. Cardiac enzymes were elevated to CK 5,994 U/L, CK-MB 38.6 ng/mL, and troponin I 11.7 ng/mL on the third admission day. CK level was elevated to 15,951 U/L due to rhabdomyolysis and normalized with urine alkalinization. The follow-up chest radiograph showed normalized cardiac size and disappearance of pulmonary edema (Fig. 1B). The echocardiography Carbon monoxide (CO) is one of well known chemical asphyxiants which cause tissue hypoxia with prominent neurologic and cardiovascular injury. Cardiac dysfunction after CO poisoning can be presented as two clinical patterns. One is transient global left ventricular (LV) dysfunction and the other is LV dysfunction with regional wall motion abnormalities. In this case report, we present a case with transient LV systolic dysfunction caused by intentional exposure to CO. After conservative treatment including high concentration of oxygen, the patient recovered completely without any complication.

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“…The explanations that have been proposed for this form of pulmonary edema are [1] a direct toxic effect of CO on the lungs, [2] an acute left heart failure, and [3] a neurogenic mechanism. Earlier investigations, especially on non-mammalian forms of life, had suggested that CO could directly affect certain intracellular processes by mechanisms other than the anoxia consecutive to COHb formation [5].…”

Section: Discussionmentioning

confidence: 99%

Acute pulmonary edema following carbon monoxide poisoning

1980

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This report describes a patient who presented with coma and acute pulmonary edema after severe carbon monoxide poisoning. Hemodynamic evaluation revealed elevated systemic and pulmonary arterial, pulmonary wedge and right atrial pressures, together with an increased cardiac output. These findings are compatible with the hypothesis that a neurogenic mechanism plays a role in the pulmonary edema of carbon monoxide poisoning.

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Myocardial Toxicity from Carbon Monoxide Poisoning

Cited by 85 publications

References 13 publications

Carbon Monoxide Has Direct Toxicity on the Myocardium Distinct from Effects of Hypoxia in an Ex Vivo Rat Heart Model

Carbon Monoxide Has Direct Toxicity on the Myocardium Distinct from Effects of Hypoxia in an Ex Vivo Rat Heart Model

Transient Left Ventricular Systolic Dysfunction Associated with Carbon Monoxide Toxicity

Acute pulmonary edema following carbon monoxide poisoning

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