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• W2062933172 abstract "Myocardial stunning is defined as a prolonged myocardial dysfunction with gradual return of contractile activity after a brief episode of severe ischemia. Usually it is seen in patients with myocardial infarction following treatment with thrombolytic agents, in patients with angina, and in patients recovering from cardiopulmonary bypass surgery. We report an interesting case of myocardial stunning following respiratory arrest. Myocardial stunning is defined as a prolonged myocardial dysfunction with gradual return of contractile activity after a brief episode of severe ischemia. Usually it is seen in patients with myocardial infarction following treatment with thrombolytic agents, in patients with angina, and in patients recovering from cardiopulmonary bypass surgery. We report an interesting case of myocardial stunning following respiratory arrest. Herein is the report of a case of myocardial stunning after respiratory arrest.Case ReportSudden respiratory arrest following intravenous injection of diazepam and methohexatal developed in a 24-year-old previously healthy white woman during a dental procedure. She became cyanotic and was successfully intubated within 3 to 4 min. The cardiac monitoring at that time revealed a normal sinus rhythm, and she was transferred to Nassau County Medical Center. At the time of arrival in the emergency department, findings of the physical examination were as follows: pulse, 90 beats per minute; BP, 80/50 mm Hg; temperature, 35.5°C; and spontaneous respiratory rate, 20 breaths per minute. The remainder of the physical examination disclosed no abnormalities. At the time of admission, laboratory values, including complete and differential WBC counts and renal and hepatic profiles, were normal. The arterial blood gas level with an FIo2 of 1.0 revealed a pH value of 7.52, a Po2 value of 554 mm Hg, and a PCO2 level of 32 mm Hg. A 12-lead ECG was normal except for sinus tachycardia. For hypotension, she required temporary inotropic support. She was extubated 4 h after admission to the hospital, and the postextubation arterial blood gas values were normal.Ten hours later, she developed precordial chest pain and shortness of breath. The pain was localized and reproducible in nature. Results of physical examination disclosed a pulse of 110 beats per minute, BP of 100/70 mm Hg, and a respiratory rate of 30 breaths per minute. She had bibasilar crackles and an S3 gallop. An ECG revealed T-wave inversions in leads 1, aVL, V3–6. A transthoracic two-dimensional echocardiogram revealed diffuse hypokinesis of the left ventricle with an approximate ejection fraction of 25%. Left ventricular size was normal, and there was no evidence of pericardial effusion. A chest roentgenogram showed pulmonary edema. Serial tests for creatine kinase-MB isoenzyme were negative.The patient was treated with bed rest, analgesic agents, and diuretics, and her symptoms improved. Subsequent ECGs showed diffuse and deep T-wave inversions and QT interval prolongation. These changes were most pronounced on day 3 of hospitalization, after which they started receding gradually (Fig 1). A repeat echocardiogram 2 weeks later showed complete restoration of left ventricular function (ejection fraction of 55%). The electrocardiographic abnormalities returned to normal after 3 months. A MUGA scan and stress echocardiogram showed an ejection fraction of 65% and an excellent augmentation with exercise. The patient has returned to full-time work and has remained asymptomatic 6 months after the respiratory arrest.DiscussionMyocardial stunning is defined as a prolonged myocardial dysfunction with gradual return of contractile activity after a brief episode of severe ischemia. This phenomenon was first described as a distinct clinical entity by Braunwald and Kloner1Braunwald E Kloner RA The stunned myocardium, prolonged post-ischemic ventricular dysfunction.Circulation. 1982; 66: 1146Crossref PubMed Scopus (2373) Google Scholar in 1982. It has been described in patients with coronary artery disease following successful thrombolytic therapy, after percutaneous transluminal coronary angioplasty, demand induced ischemia,1Braunwald E Kloner RA The stunned myocardium, prolonged post-ischemic ventricular dysfunction.Circulation. 1982; 66: 1146Crossref PubMed Scopus (2373) Google Scholar and coronary vasospasm.2Fournier C et al.Stunned myocardium following coronary spasm.Am Heart J. 1991; 121: 593-595Abstract Full Text PDF PubMed Scopus (40) Google Scholar It also has been described as an uncommon feature of conditions like toxic shock syndrome,3Crews JR Harrison JK Corey GR et al.Stunned myocardium in toxic shock syndrome.Ann Intern Med. 1992; 117: 912-913Crossref PubMed Scopus (9) Google Scholar Legionnaires' disease,4Rajan RT Freeman I Khan FA et al.Myocardial stunning with Legionnaires' disease.Cardiovasc Rev Rep. 1994; 15: 65-71Google Scholar and following electroconvulsive therapy.5Zhu W Olson DE Karon BL et al.Myocardial stunning after electro-convulsive therapy.Ann Intern Med. 1992; 117: 914-915Crossref PubMed Scopus (30) Google ScholarThe exact mechanism of myocardial stunning is not clear. Jennings et al6Jennings RB Murry CE Steenbergen C Jr et al.Development of cell injury in sustained acute ischemia.Circulation. 1990; 82: II-2-II-12Google Scholar proposed that myocardial ischemia leads to reduction in both creatine phosphate and adenosine triphosphate. With reperfusion, there is immediate restoration of creatine phosphate levels to normal or slightly above normal, while adenosine triphosphate takes several days to return to normal. This depletion of the total adenine nucleotide pool leads to prolonged depression of myocardial contractility. The other possible mechanisms include alterations in sarcoplasmic calcium adenosine triphosphatase and calcium metabolism, upregulation of the gene for heat shock protein, and generation of oxygen-free radicals.Our patient, who was a healthy young female with no risk factors for coronary artery disease, developed prolonged myocardial depression following a brief episode of severe hypoxemia. The global nature of ventricular hypokinesis, the absence of cardiac enzymes, and the complete restoration of electrical and mechanical function of the heart strongly support the diagnosis of myocardial stunning in this patient. The chest pain was most likely musculoskeletal in origin even though pericarditis could not be excluded with certainty. Coronary spasm due to stress-related catecholamine surge is unlikely because of its rare occurrence and the absence of ST segment elevations.A careful search of the English-language medical literature did not reveal any previous reports of myocardial stunning following respiratory arrest. This case illustrates that myocardial stunning may occur as a sequela following successful resuscitation from respiratory arrest. This condition can occur in young subjects without any preexisting coronary artery disease, and because it is reversible, it does not necessarily indicate a grim prognosis. Hence, we recommend that such patients should be closely observed for any signs of cardiac decompensation. Herein is the report of a case of myocardial stunning after respiratory arrest. Case ReportSudden respiratory arrest following intravenous injection of diazepam and methohexatal developed in a 24-year-old previously healthy white woman during a dental procedure. She became cyanotic and was successfully intubated within 3 to 4 min. The cardiac monitoring at that time revealed a normal sinus rhythm, and she was transferred to Nassau County Medical Center. At the time of arrival in the emergency department, findings of the physical examination were as follows: pulse, 90 beats per minute; BP, 80/50 mm Hg; temperature, 35.5°C; and spontaneous respiratory rate, 20 breaths per minute. The remainder of the physical examination disclosed no abnormalities. At the time of admission, laboratory values, including complete and differential WBC counts and renal and hepatic profiles, were normal. The arterial blood gas level with an FIo2 of 1.0 revealed a pH value of 7.52, a Po2 value of 554 mm Hg, and a PCO2 level of 32 mm Hg. A 12-lead ECG was normal except for sinus tachycardia. For hypotension, she required temporary inotropic support. She was extubated 4 h after admission to the hospital, and the postextubation arterial blood gas values were normal.Ten hours later, she developed precordial chest pain and shortness of breath. The pain was localized and reproducible in nature. Results of physical examination disclosed a pulse of 110 beats per minute, BP of 100/70 mm Hg, and a respiratory rate of 30 breaths per minute. She had bibasilar crackles and an S3 gallop. An ECG revealed T-wave inversions in leads 1, aVL, V3–6. A transthoracic two-dimensional echocardiogram revealed diffuse hypokinesis of the left ventricle with an approximate ejection fraction of 25%. Left ventricular size was normal, and there was no evidence of pericardial effusion. A chest roentgenogram showed pulmonary edema. Serial tests for creatine kinase-MB isoenzyme were negative.The patient was treated with bed rest, analgesic agents, and diuretics, and her symptoms improved. Subsequent ECGs showed diffuse and deep T-wave inversions and QT interval prolongation. These changes were most pronounced on day 3 of hospitalization, after which they started receding gradually (Fig 1). A repeat echocardiogram 2 weeks later showed complete restoration of left ventricular function (ejection fraction of 55%). The electrocardiographic abnormalities returned to normal after 3 months. A MUGA scan and stress echocardiogram showed an ejection fraction of 65% and an excellent augmentation with exercise. The patient has returned to full-time work and has remained asymptomatic 6 months after the respiratory arrest. Sudden respiratory arrest following intravenous injection of diazepam and methohexatal developed in a 24-year-old previously healthy white woman during a dental procedure. She became cyanotic and was successfully intubated within 3 to 4 min. The cardiac monitoring at that time revealed a normal sinus rhythm, and she was transferred to Nassau County Medical Center. At the time of arrival in the emergency department, findings of the physical examination were as follows: pulse, 90 beats per minute; BP, 80/50 mm Hg; temperature, 35.5°C; and spontaneous respiratory rate, 20 breaths per minute. The remainder of the physical examination disclosed no abnormalities. At the time of admission, laboratory values, including complete and differential WBC counts and renal and hepatic profiles, were normal. The arterial blood gas level with an FIo2 of 1.0 revealed a pH value of 7.52, a Po2 value of 554 mm Hg, and a PCO2 level of 32 mm Hg. A 12-lead ECG was normal except for sinus tachycardia. For hypotension, she required temporary inotropic support. She was extubated 4 h after admission to the hospital, and the postextubation arterial blood gas values were normal. Ten hours later, she developed precordial chest pain and shortness of breath. The pain was localized and reproducible in nature. Results of physical examination disclosed a pulse of 110 beats per minute, BP of 100/70 mm Hg, and a respiratory rate of 30 breaths per minute. She had bibasilar crackles and an S3 gallop. An ECG revealed T-wave inversions in leads 1, aVL, V3–6. A transthoracic two-dimensional echocardiogram revealed diffuse hypokinesis of the left ventricle with an approximate ejection fraction of 25%. Left ventricular size was normal, and there was no evidence of pericardial effusion. A chest roentgenogram showed pulmonary edema. Serial tests for creatine kinase-MB isoenzyme were negative. The patient was treated with bed rest, analgesic agents, and diuretics, and her symptoms improved. Subsequent ECGs showed diffuse and deep T-wave inversions and QT interval prolongation. These changes were most pronounced on day 3 of hospitalization, after which they started receding gradually (Fig 1). A repeat echocardiogram 2 weeks later showed complete restoration of left ventricular function (ejection fraction of 55%). The electrocardiographic abnormalities returned to normal after 3 months. A MUGA scan and stress echocardiogram showed an ejection fraction of 65% and an excellent augmentation with exercise. The patient has returned to full-time work and has remained asymptomatic 6 months after the respiratory arrest. DiscussionMyocardial stunning is defined as a prolonged myocardial dysfunction with gradual return of contractile activity after a brief episode of severe ischemia. This phenomenon was first described as a distinct clinical entity by Braunwald and Kloner1Braunwald E Kloner RA The stunned myocardium, prolonged post-ischemic ventricular dysfunction.Circulation. 1982; 66: 1146Crossref PubMed Scopus (2373) Google Scholar in 1982. It has been described in patients with coronary artery disease following successful thrombolytic therapy, after percutaneous transluminal coronary angioplasty, demand induced ischemia,1Braunwald E Kloner RA The stunned myocardium, prolonged post-ischemic ventricular dysfunction.Circulation. 1982; 66: 1146Crossref PubMed Scopus (2373) Google Scholar and coronary vasospasm.2Fournier C et al.Stunned myocardium following coronary spasm.Am Heart J. 1991; 121: 593-595Abstract Full Text PDF PubMed Scopus (40) Google Scholar It also has been described as an uncommon feature of conditions like toxic shock syndrome,3Crews JR Harrison JK Corey GR et al.Stunned myocardium in toxic shock syndrome.Ann Intern Med. 1992; 117: 912-913Crossref PubMed Scopus (9) Google Scholar Legionnaires' disease,4Rajan RT Freeman I Khan FA et al.Myocardial stunning with Legionnaires' disease.Cardiovasc Rev Rep. 1994; 15: 65-71Google Scholar and following electroconvulsive therapy.5Zhu W Olson DE Karon BL et al.Myocardial stunning after electro-convulsive therapy.Ann Intern Med. 1992; 117: 914-915Crossref PubMed Scopus (30) Google ScholarThe exact mechanism of myocardial stunning is not clear. Jennings et al6Jennings RB Murry CE Steenbergen C Jr et al.Development of cell injury in sustained acute ischemia.Circulation. 1990; 82: II-2-II-12Google Scholar proposed that myocardial ischemia leads to reduction in both creatine phosphate and adenosine triphosphate. With reperfusion, there is immediate restoration of creatine phosphate levels to normal or slightly above normal, while adenosine triphosphate takes several days to return to normal. This depletion of the total adenine nucleotide pool leads to prolonged depression of myocardial contractility. The other possible mechanisms include alterations in sarcoplasmic calcium adenosine triphosphatase and calcium metabolism, upregulation of the gene for heat shock protein, and generation of oxygen-free radicals.Our patient, who was a healthy young female with no risk factors for coronary artery disease, developed prolonged myocardial depression following a brief episode of severe hypoxemia. The global nature of ventricular hypokinesis, the absence of cardiac enzymes, and the complete restoration of electrical and mechanical function of the heart strongly support the diagnosis of myocardial stunning in this patient. The chest pain was most likely musculoskeletal in origin even though pericarditis could not be excluded with certainty. Coronary spasm due to stress-related catecholamine surge is unlikely because of its rare occurrence and the absence of ST segment elevations.A careful search of the English-language medical literature did not reveal any previous reports of myocardial stunning following respiratory arrest. This case illustrates that myocardial stunning may occur as a sequela following successful resuscitation from respiratory arrest. This condition can occur in young subjects without any preexisting coronary artery disease, and because it is reversible, it does not necessarily indicate a grim prognosis. Hence, we recommend that such patients should be closely observed for any signs of cardiac decompensation. Myocardial stunning is defined as a prolonged myocardial dysfunction with gradual return of contractile activity after a brief episode of severe ischemia. This phenomenon was first described as a distinct clinical entity by Braunwald and Kloner1Braunwald E Kloner RA The stunned myocardium, prolonged post-ischemic ventricular dysfunction.Circulation. 1982; 66: 1146Crossref PubMed Scopus (2373) Google Scholar in 1982. It has been described in patients with coronary artery disease following successful thrombolytic therapy, after percutaneous transluminal coronary angioplasty, demand induced ischemia,1Braunwald E Kloner RA The stunned myocardium, prolonged post-ischemic ventricular dysfunction.Circulation. 1982; 66: 1146Crossref PubMed Scopus (2373) Google Scholar and coronary vasospasm.2Fournier C et al.Stunned myocardium following coronary spasm.Am Heart J. 1991; 121: 593-595Abstract Full Text PDF PubMed Scopus (40) Google Scholar It also has been described as an uncommon feature of conditions like toxic shock syndrome,3Crews JR Harrison JK Corey GR et al.Stunned myocardium in toxic shock syndrome.Ann Intern Med. 1992; 117: 912-913Crossref PubMed Scopus (9) Google Scholar Legionnaires' disease,4Rajan RT Freeman I Khan FA et al.Myocardial stunning with Legionnaires' disease.Cardiovasc Rev Rep. 1994; 15: 65-71Google Scholar and following electroconvulsive therapy.5Zhu W Olson DE Karon BL et al.Myocardial stunning after electro-convulsive therapy.Ann Intern Med. 1992; 117: 914-915Crossref PubMed Scopus (30) Google Scholar The exact mechanism of myocardial stunning is not clear. Jennings et al6Jennings RB Murry CE Steenbergen C Jr et al.Development of cell injury in sustained acute ischemia.Circulation. 1990; 82: II-2-II-12Google Scholar proposed that myocardial ischemia leads to reduction in both creatine phosphate and adenosine triphosphate. With reperfusion, there is immediate restoration of creatine phosphate levels to normal or slightly above normal, while adenosine triphosphate takes several days to return to normal. This depletion of the total adenine nucleotide pool leads to prolonged depression of myocardial contractility. The other possible mechanisms include alterations in sarcoplasmic calcium adenosine triphosphatase and calcium metabolism, upregulation of the gene for heat shock protein, and generation of oxygen-free radicals. Our patient, who was a healthy young female with no risk factors for coronary artery disease, developed prolonged myocardial depression following a brief episode of severe hypoxemia. The global nature of ventricular hypokinesis, the absence of cardiac enzymes, and the complete restoration of electrical and mechanical function of the heart strongly support the diagnosis of myocardial stunning in this patient. The chest pain was most likely musculoskeletal in origin even though pericarditis could not be excluded with certainty. Coronary spasm due to stress-related catecholamine surge is unlikely because of its rare occurrence and the absence of ST segment elevations. A careful search of the English-language medical literature did not reveal any previous reports of myocardial stunning following respiratory arrest. This case illustrates that myocardial stunning may occur as a sequela following successful resuscitation from respiratory arrest. This condition can occur in young subjects without any preexisting coronary artery disease, and because it is reversible, it does not necessarily indicate a grim prognosis. 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