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Brugada Electrocardiographic Pattern in Carbon Monoxide Poisoning
October 2011, Vol 140, No. 4_MeetingAbstracts
Case Reports: Sunday, October 23, 2011 | October 2011
Brugada Electrocardiographic Pattern in Carbon Monoxide Poisoning Jaya Prakash Sugunaraj, MD; Jung Julie Kang, MD; Wilbert Aronow, MD; Kausik Kar, MD; Chandrasekar Palaniswamy, MD; Jessica Most, MD Chest. 2011;140(4_MeetingAbstracts):35A. doi:10.1378/chest.1119956
Abstract INTRODUCTION: Cardiovascular complications of carbon monoxide (CO) poisoning include myocardial ischemia, left ventricular dysfunction, or arrhythmias. We report the first case of Brugada pattern in CO poisoning in the English literature. CASE PRESENTATION: : A 56-year-old Asian male was found unconscious in his home by his son who called emergency medical services. Patient regained consciousness while receiving 100% oxygen by means of nonrebreather reservoir face mask in the ambulance. Upon arrival to the emergency room (ER), the patient was awake, but complained of mild headache and dizziness. He denied any chest pain, palpitation or shortness of breath. Past medical history was significant for dyslipidemia treated with simvastatin. Family history was negative for sudden cardiac death. Vital signs on admission showed a temperature of 100.4 F, heart rate of 110 beats/minute, blood pressure of 129/89 mmHg, respiratory rate of 24 per minute, with oxygen saturation of 100% on non-rebreather mask delivering 100% oxygen. Arterial blood gas analysis by co-oximetry showed pH-7.48, pCO2-33 mmHg, pO2-250 mmHg, HCO3-24.6 mmol/L, and oxygen saturation of 99%. Carboxyhemoglobin level on admission was 25.2%. Creatine kinase, creatine kinase-MB isoenzyme, and troponin I was within normal limits. Electrocardiogram done in ER showed sinus tachycardia at 104 beats per minute, left axis deviation, and ST-segment elevation of 3.5 mm in V1-V2 with a saddleback appearance, characteristic of type 2 brugada electrocardiographic pattern (BEP). Portable chest radiograph was within normal limits. The patient was admitted to telemetry unit and administered 3 hyperbaric-oxygen treatments (HBOT) within a 24-hour period. Transthoracic 2-dimensional echocardiogram was within normal limits. Repeat electrocardiogram after HBOT showed resolution of the brugada pattern. DISCUSSION: The Brugada syndrome is a clinical and electrocardiographic entity consisting of right bundle-branch block and unusual ST-segment elevation in the right precordial leads (V1 to V3) and responsible for at least 4% of all sudden deaths and at least 20% of sudden deaths in patients with structurally normal hearts. Mutations in SCN5A, a cardiac sodium channel gene, transmitted in an autosomal dominant pattern are implicated as a cause. BEP in absence of clinical symptoms can occur in variety of other conditions. This is the first report in the English literature of BEP due to CO poisoning. Myocardial injury occurs frequently in patients with CO poisoning and is a significant predictor of long term mortality. In a prospective study 1of 230 patients, mean age 47.2 years, 72% men, with moderate to severe CO poisoning, myocardial injury was reported in 37% of patients. Ischemic electrocardiographic changes were seen in 30%, and positive biomarkers in 35%. The current indications for HBOT in CO poisoning from cardiovascular standpoint are cardiac ischemia, arrhythmias, or carboxyhemoglobin level >20% with underlying coronary artery disease. Recent data demonstrate that a type I BEP pattern alone, even when other clinical criteria are not fulfilled, can be associated with sudden cardiac death during follow up. Thus, all patients who present as BEP pattern, in the setting of CO poisoning should be considered at risk, and timely HBOT may help in recovery.
CONCLUSIONS: CO poisoning should be considered one of the differentials of BEP. Even in the absence of arrhythmias or myocardial ischemia, BEP in a patient with CO poisoning may be considered for hyperbaric oxygen therapy. Reference #1 Henry CR, Satran D, Lindgren B, Adkinson C, Nicholson CI, Henry TD. Myocardial injury and long-term mortality following moderate to severe carbon monoxide poisoning. JAMA. 2006 Jan 25; 295(4):398-402. Reference #2 Probst V, Veltmann C, Eckardt L, et al. Long-term prognosis of patients diagnosed with Brugada syndrome: Results from the FINGER Brugada Syndrome Registry. Circulation. 2010 Feb 9; 121(5):635-43. DISCLOSURE: The following authors have nothing to disclose: Jaya Prakash Sugunaraj, Jung Julie Kang, Wilbert Aronow, Kausik Kar, Chandrasekar Palaniswamy, Jessica Most No Product/Research Disclosure Information 01:30 PM - 02:45 PM
Case Reports: Sunday, October 23, 2011 | October 2011
Brugada Electrocardiographic Pattern in Carbon Monoxide Poisoning Jaya Prakash Sugunaraj, MD; Jung Julie Kang, MD; Wilbert Aronow, MD; Kausik Kar, MD; Chandrasekar Palaniswamy, MD; Jessica Most, MD Chest. 2011;140(4_MeetingAbstracts):35A. doi:10.1378/chest.1119956
Abstract INTRODUCTION: Cardiovascular complications of carbon monoxide (CO) poisoning include myocardial ischemia, left ventricular dysfunction, or arrhythmias. We report the first case of Brugada pattern in CO poisoning in the English literature. CASE PRESENTATION: : A 56-year-old Asian male was found unconscious in his home by his son who called emergency medical services. Patient regained consciousness while receiving 100% oxygen by means of nonrebreather reservoir face mask in the ambulance. Upon arrival to the emergency room (ER), the patient was awake, but complained of mild headache and dizziness. He denied any chest pain, palpitation or shortness of breath. Past medical history was significant for dyslipidemia treated with simvastatin. Family history was negative for sudden cardiac death. Vital signs on admission showed a temperature of 100.4 F, heart rate of 110 beats/minute, blood pressure of 129/89 mmHg, respiratory rate of 24 per minute, with oxygen saturation of 100% on non-rebreather mask delivering 100% oxygen. Arterial blood gas analysis by co-oximetry showed pH-7.48, pCO2-33 mmHg, pO2-250 mmHg, HCO3-24.6 mmol/L, and oxygen saturation of 99%. Carboxyhemoglobin level on admission was 25.2%. Creatine kinase, creatine kinase-MB isoenzyme, and troponin I was within normal limits. Electrocardiogram done in ER showed sinus tachycardia at 104 beats per minute, left axis deviation, and ST-segment elevation of 3.5 mm in V1-V2 with a saddleback appearance, characteristic of type 2 brugada electrocardiographic pattern (BEP). Portable chest radiograph was within normal limits. The patient was admitted to telemetry unit and administered 3 hyperbaric-oxygen treatments (HBOT) within a 24-hour period. Transthoracic 2-dimensional echocardiogram was within normal limits. Repeat electrocardiogram after HBOT showed resolution of the brugada pattern. DISCUSSION: The Brugada syndrome is a clinical and electrocardiographic entity consisting of right bundle-branch block and unusual ST-segment elevation in the right precordial leads (V1 to V3) and responsible for at least 4% of all sudden deaths and at least 20% of sudden deaths in patients with structurally normal hearts. Mutations in SCN5A, a cardiac sodium channel gene, transmitted in an autosomal dominant pattern are implicated as a cause. BEP in absence of clinical symptoms can occur in variety of other conditions. This is the first report in the English literature of BEP due to CO poisoning. Myocardial injury occurs frequently in patients with CO poisoning and is a significant predictor of long term mortality. In a prospective study 1of 230 patients, mean age 47.2 years, 72% men, with moderate to severe CO poisoning, myocardial injury was reported in 37% of patients. Ischemic electrocardiographic changes were seen in 30%, and positive biomarkers in 35%. The current indications for HBOT in CO poisoning from cardiovascular standpoint are cardiac ischemia, arrhythmias, or carboxyhemoglobin level >20% with underlying coronary artery disease. Recent data demonstrate that a type I BEP pattern alone, even when other clinical criteria are not fulfilled, can be associated with sudden cardiac death during follow up. Thus, all patients who present as BEP pattern, in the setting of CO poisoning should be considered at risk, and timely HBOT may help in recovery.
CONCLUSIONS: CO poisoning should be considered one of the differentials of BEP. Even in the absence of arrhythmias or myocardial ischemia, BEP in a patient with CO poisoning may be considered for hyperbaric oxygen therapy. Reference #1 Henry CR, Satran D, Lindgren B, Adkinson C, Nicholson CI, Henry TD. Myocardial injury and long-term mortality following moderate to severe carbon monoxide poisoning. JAMA. 2006 Jan 25; 295(4):398-402. Reference #2 Probst V, Veltmann C, Eckardt L, et al. Long-term prognosis of patients diagnosed with Brugada syndrome: Results from the FINGER Brugada Syndrome Registry. Circulation. 2010 Feb 9; 121(5):635-43. DISCLOSURE: The following authors have nothing to disclose: Jaya Prakash Sugunaraj, Jung Julie Kang, Wilbert Aronow, Kausik Kar, Chandrasekar Palaniswamy, Jessica Most No Product/Research Disclosure Information 01:30 PM - 02:45 PM