Hospital Practice
ISSN: 2154-8331 (Print) 2377-1003 (Online) Journal homepage: http://www.tandfonline.com/loi/ihop20
Acute Myocardial Infarction or Pericarditis? E. William Hancock To cite this article: E. William Hancock (1992) Acute Myocardial Infarction or Pericarditis?, Hospital Practice, 27:11, 25-26, DOI: 10.1080/21548331.1992.11705518 To link to this article: http://dx.doi.org/10.1080/21548331.1992.11705518
Published online: 17 May 2016.
Submit your article to this journal
View related articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ihop20 Download by: [University of Saskatchewan Library]
Date: 15 June 2016, At: 02:05
ECG Casebook E. WILLIAM HANCOCK, Editor
Downloaded by [University of Saskatchewan Library] at 02:05 15 June 2016
Acute Myocardial Infarction or Pericarditis? A 74-year-old woman was transferred from a small community hospital because of sudden hypotension and pertcardial effusion. She had been hospitalized two days earlier after the sudden onset of chest pain. The ECG was initially normal; serial ECGs showed only slight depression of the ST segments in the anterolateral leads. The creatine kinase levels rose from a normal level initially to a peak of 450 units. No thrombolytic or anticoagulant therapy was given, but she was considered to have had a small non-Q-wave myocardial infarction. On the third day she complained of recurrent chest pain and weakness and was found to have a pulse of 110 and blood pressure of 70/40. The ECG showed no new changes. Echocardiography showed a moderate pertcardial effusion, mostly anterior to the right atrium and ventricle; there was hypokinesis of the anterolateral wall. An obese woman, she appeared to be in moderate distress from chest discomfort; her pulse was 111, blood pressure 80/60, respiratory rate 22, and temperature 37.8°. Her hands and feet were cool and moist. The arterial pulse was barely palpable, without detectable paradox. The jugular venous pressure was indeterminate because of poor visualization of the neck veins. The heart sounds were faint. with no murmur, S 3 , or S 4 . The ECG is shown.
Is the ECG pattern one of acute myocardial infarction or pericarditis? Has the non-Q-wave infarct extended, expanded, or ruptured? What is the most appropriate management plan?
1-11-111
aVR-aVL-aVF
Hospital Practice November 15. 1992
25
Downloaded by [University of Saskatchewan Library] at 02:05 15 June 2016
Analysis ofthe ECG The ECG shows sinus tachycardia, normal P-R interval, and a normal QRS complex. The ST segments are elevated in the inferolateralleads and depressed in leads VI to v3. Leads I and aVL show slightly downsloping ST segments without J-point depression. The elevation of the ST segment in leads II and aVF is more apparent than real. because there is depression of the PQ segment in these leads. PQ depression is a useful diagnostic sign of acute pericarditis, showing sensitivity and specificity that is virtually as high as that of the better-known ST-segment elevation. This ECG could be regarded as showing definite signs of acute pericarditis. However, the entire 12-lead pattern is hardly consistent with pericarditis alone because of the ST depression in leads VI to v3. In acute pericarditis, there is often ST depression in lead V1 , but V2 and V3 are expected to show ST elevation. Furthermore. there is a presumptive clinical diagnosis of acute myocardial infarction in this patient. Therefore, the ECG is best interpreted as showing both acute pericarditis and ischemic ST-segment abnormality consistent with recent non-Qwave infarction. Pericardia! effusion in patients with recent myocardial infarction may result from complicating pericarditis, or it may represent hemopericardium. Extension or expansion of a recent infarction may be associated with either, but the association is not a necessary or particularly common one. Myocardial rupture must be considered as a cause of pericardia! effusion, particularly when chest pain and hypotension develop suddenly. Myocardial rupture is usually thought of as occurring very suddenly, with the onset of shock 26
(electromechanical dissociation), ending fatally before surgical therapy can be carried out. However, there are cases of myocardial rupture that are not so quickly fatal and are better termed subacute rupture. In these cases the rupture does not perforate the epicardium, and the resulting hemopericardium is prevented or is limited to a local area. Adhesions in the pericardia! space may also produce this effect. The contained hemopericardium may be amenable to surgical therapy. The patient was managed by placement of an intra-aortic balloon pump, followed by cardiac catheterization, which showed total occlusion of the left circumflex artery, diffuse disease of the left anterior descending branch, and a normal right coronary artery. Cardiopulmonary bypass was then established with peripheral cannulation, followed by sternotomy, which revealed a tense hemopericardium with a large amount of clotted blood. Hemorrhage occurred freely from a small site on the lateral free wall of the left ventricle when the clot was removed. The bleeding site was oversewn, and the patient made a good recovery. The ECG is not specifically diagnostic, but the findings correlate well with the pathology that was present: a small non-Q-wave lateral infarct complicated by subacute rupture and hemopericardium. The ECG cannot differentiate pericarditis of the usual type complicating myocardial infarction from that caused by hemopericardium. The entity of subacute rupture of the heart in acute myocardial infarction is a subtle one that deserves greater recognition. D Dr. Hancock is Professor of Medicine, Division of Cardiovascular MedIcine, Stanford University School of Medicine.
ISSN: 2154-8331 (Print) 2377-1003 (Online) Journal homepage: http://www.tandfonline.com/loi/ihop20
Acute Myocardial Infarction or Pericarditis? E. William Hancock To cite this article: E. William Hancock (1992) Acute Myocardial Infarction or Pericarditis?, Hospital Practice, 27:11, 25-26, DOI: 10.1080/21548331.1992.11705518 To link to this article: http://dx.doi.org/10.1080/21548331.1992.11705518
Published online: 17 May 2016.
Submit your article to this journal
View related articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ihop20 Download by: [University of Saskatchewan Library]
Date: 15 June 2016, At: 02:05
ECG Casebook E. WILLIAM HANCOCK, Editor
Downloaded by [University of Saskatchewan Library] at 02:05 15 June 2016
Acute Myocardial Infarction or Pericarditis? A 74-year-old woman was transferred from a small community hospital because of sudden hypotension and pertcardial effusion. She had been hospitalized two days earlier after the sudden onset of chest pain. The ECG was initially normal; serial ECGs showed only slight depression of the ST segments in the anterolateral leads. The creatine kinase levels rose from a normal level initially to a peak of 450 units. No thrombolytic or anticoagulant therapy was given, but she was considered to have had a small non-Q-wave myocardial infarction. On the third day she complained of recurrent chest pain and weakness and was found to have a pulse of 110 and blood pressure of 70/40. The ECG showed no new changes. Echocardiography showed a moderate pertcardial effusion, mostly anterior to the right atrium and ventricle; there was hypokinesis of the anterolateral wall. An obese woman, she appeared to be in moderate distress from chest discomfort; her pulse was 111, blood pressure 80/60, respiratory rate 22, and temperature 37.8°. Her hands and feet were cool and moist. The arterial pulse was barely palpable, without detectable paradox. The jugular venous pressure was indeterminate because of poor visualization of the neck veins. The heart sounds were faint. with no murmur, S 3 , or S 4 . The ECG is shown.
Is the ECG pattern one of acute myocardial infarction or pericarditis? Has the non-Q-wave infarct extended, expanded, or ruptured? What is the most appropriate management plan?
1-11-111
aVR-aVL-aVF
Hospital Practice November 15. 1992
25
Downloaded by [University of Saskatchewan Library] at 02:05 15 June 2016
Analysis ofthe ECG The ECG shows sinus tachycardia, normal P-R interval, and a normal QRS complex. The ST segments are elevated in the inferolateralleads and depressed in leads VI to v3. Leads I and aVL show slightly downsloping ST segments without J-point depression. The elevation of the ST segment in leads II and aVF is more apparent than real. because there is depression of the PQ segment in these leads. PQ depression is a useful diagnostic sign of acute pericarditis, showing sensitivity and specificity that is virtually as high as that of the better-known ST-segment elevation. This ECG could be regarded as showing definite signs of acute pericarditis. However, the entire 12-lead pattern is hardly consistent with pericarditis alone because of the ST depression in leads VI to v3. In acute pericarditis, there is often ST depression in lead V1 , but V2 and V3 are expected to show ST elevation. Furthermore. there is a presumptive clinical diagnosis of acute myocardial infarction in this patient. Therefore, the ECG is best interpreted as showing both acute pericarditis and ischemic ST-segment abnormality consistent with recent non-Qwave infarction. Pericardia! effusion in patients with recent myocardial infarction may result from complicating pericarditis, or it may represent hemopericardium. Extension or expansion of a recent infarction may be associated with either, but the association is not a necessary or particularly common one. Myocardial rupture must be considered as a cause of pericardia! effusion, particularly when chest pain and hypotension develop suddenly. Myocardial rupture is usually thought of as occurring very suddenly, with the onset of shock 26
(electromechanical dissociation), ending fatally before surgical therapy can be carried out. However, there are cases of myocardial rupture that are not so quickly fatal and are better termed subacute rupture. In these cases the rupture does not perforate the epicardium, and the resulting hemopericardium is prevented or is limited to a local area. Adhesions in the pericardia! space may also produce this effect. The contained hemopericardium may be amenable to surgical therapy. The patient was managed by placement of an intra-aortic balloon pump, followed by cardiac catheterization, which showed total occlusion of the left circumflex artery, diffuse disease of the left anterior descending branch, and a normal right coronary artery. Cardiopulmonary bypass was then established with peripheral cannulation, followed by sternotomy, which revealed a tense hemopericardium with a large amount of clotted blood. Hemorrhage occurred freely from a small site on the lateral free wall of the left ventricle when the clot was removed. The bleeding site was oversewn, and the patient made a good recovery. The ECG is not specifically diagnostic, but the findings correlate well with the pathology that was present: a small non-Q-wave lateral infarct complicated by subacute rupture and hemopericardium. The ECG cannot differentiate pericarditis of the usual type complicating myocardial infarction from that caused by hemopericardium. The entity of subacute rupture of the heart in acute myocardial infarction is a subtle one that deserves greater recognition. D Dr. Hancock is Professor of Medicine, Division of Cardiovascular MedIcine, Stanford University School of Medicine.
