CASE REPORT
hemorrhage, intracerebral
Hypertensive Intracerebral Hemorrhage Simulating Acute Myocardial Infarction From the Departments of Internal Medicine* and
Sadasiva Rao Katta, MD* William A Berk, MD
Emergency Medicine,e Wayne State University Medical School, Detroit, Michigan. Received for publication August 9, 1991. Revision received February 24, 1992. Accepted for publication March 4, 1992.
The decision to administer thrombolytic therapy for acute myocardial infarction depends on clinical presentation and characteristic ECG findings of acute injury. Inappropriate initiation of thrombolysis may occur when other clinical entities mimic myocardial infarction both clinically and electrocardiographically. We present the case of a 49-year-old woman who presented with cardiovascular collapse and ECG findings strongly suggestive of myocardial infarction. Computed brain tomography eventually revealed right temporal lobe hemorrhage, the apparent cause of the observed ECG abnormalities. ST-segment elevation resolved rapidly, and serial creatine phosphokinase isoenzyme determinations were negative. Because closed-chest cardiac massage had been performed, a thrombolytic agent was not administered. Our experience emphasizes the importance of considering ECG findings in light of clinical presentation and of taking care to consider conditions other than myocardial infarction that may cause ST-segment elevation. [Katta SR, Berk WA: Hypertensive intracerebral hemorrhage simulating acute myocardial infarction. Ann EmergMeflAugust1992;21:1002-1005.] INTRODUCTION Until recently, management of myocardial infarction (MI) was primarily supportive. Thus it was reasonable to treat equivocal cases expectantly as MI, until and unless proven otherwise during a 24-hour period by isoenzyme determination. Although creatine phosphokinase isoenzyme elevation remains the standard for diagnosis of MI, 1 the advent of thrombolytic reconstitution of coronary perfusion has placed renewed emphasis on history-taking and the 12-lead ECG as diagnostic tools. Thus, most authorities recommend administration when a patient's history is suggestive, presentation is early, significant ST-segment elevation is observed, and the patient has no risk factors for life-threatening hemorrhage.~ Evaluating patients for thrombolysis requires careful consideration of the ECG in light of the patient's history and necessitates that clinicians be aware of alternative diagnoses compatible with an ECG suggestive of MI. Among a number of clinical entities that may inscribe characteristic changes on the ECG suggestive of acute infarction, intracerebral hemorrhage is an example of a condition for which thrombolysis could well prove catastrophic.
AUGUST 1992
21:8
ANNALS 0E EMERGENCY MEDICINE
! 002/
14 5
INTRACEREBRAL HEMORRHAGE Katta & Berk
We present a case in which presentation was consistent with and ECG changes were strongly suggestive of acute MI but that eventually proved secondary to hypertensive intracerebral hemorrhage. CASE
REPORT
A 49-year-old woman presented to the emergency department after suffering cardiac arrest. Her family stated she had awakened with a headache, shortness of breath, and a d r y cough. Shortly after relating these complaints, she collapsed. An emergency medical services unit was summoned and arrived within five minutes. They found the patient unresponsive b u t with intact circulation and respirations. However, while en route to the hospital, cardiac arrest occurred. CPR was initiated, but before medications could be administered, pulse and respirations resumed. No ECG was recorded during the episode. The patient's medical history included a 16-year history of hypertension and two previous MIs. On admission, the patient was unresponsive. Blood pressure was 130/110 mm Hg; pulse, 94; and respirations, 16. Pupils were midsized and nonreactive. Moderate jugular distension was present. Lung examination revealed bibasilar • tales, and h e a r t sounds were normal. P l a n t a r stimulation yielded upgoing toes bilaterally, and reflexes were symmetric. ECG revealed ST elevation and hyperacute T waves in the inferior leads with reciprocal ST depression and T-wave inversion in the anterior leads strongly suggestive of acute
'
..........
YFT. ].:.LR~
: ;
.... i . - +
DISCUSSION
The importance of ECG criteria for determining when to administer thrombolytic t h e r a p y for acute MI has increased the probability of administering these drugs to patients with problems that mimic MI electrocardiographically. Cerebrovascular accidents have long been appreciated for this potential, 2-a but the impact of misdiagnosis has become much greater with the routine use of thrombolytics to treat MI. Figure 2. Return of ST-segments to baseline two hours after admission. This tracing was unchanged f r o m one obtained shortly before admission
Figure 1. Admission ECG with ST-segment elevation in the inferior leads suggestive of acute inferior wall infarction ............
inferior wall MI (Figure 1). The patient was admitted to the coronary care unit, but because she had received closedchest cardiac message, no thrombolytic t h e r a p y was administered. An ECG performed on arrival in the coronary care unit revealed atrial fibrillation with a r a p i d ventricular response and a decrease in ST elevation. Tracings obtained beginning two hours later showed r e t u r n of the ST segment to baseline with Q waves in inferior leads (Figure 2), consistent with the patient's history of previous MI and unchanged from those obtained before the c u r r e n t episode. Serial creatine phosphokinase isoenzyme determination over the next 24 hours ruled out MI. Computed b r a i n tomography three hours after hospital admission revealed i n t r a c e r e b r a l hemorrhage involving the right temporal lobe with s u b d u r a l extension and midline shift. Neurosurgical consultation was requested, but before surgical intervention could be accomplished, the patient died.
x,
¢.
~:~!_
i::t :::]
~
j Figure 3. ST-segment elevation caused by several different underlying conditions. The lead shown is indicated f o r each tracing. A. Acute anterior wall MI in a 43~year-old man. B. Persistent ST-segment elevation in a 59-year-old man three months after MI, reflecting left ventricular aneurysm.
~r.
,tit. ' l , . ~ l iYl J .! l ~. . r!!lli!#j.it
C
C. A 30-year-old woman with viral pericarditis. D. Asymptomatic 34-year-old man with ST-segment elevation secondary to early repolarization. E. Hyperkalemia (potassium, 8.0 mEq/L) causing ST-segment elevation in a 34year-old man with renal failure.
tu, : &i/d:: ::i F:
:::.!:: !! i!il iii I!F
~
~
,
MIl~il!i~ti~iMi141~'4';{iil',iiiliii~l!mllt~l[I;I
VI
~Id,.i~:.l,d..ll..:l..:l,,l,~!l!dld~l~ V4
~',T', .l!l.l::d,:,l,~dh4!d,:,:l,IJ!.!t~hl~ ....... ....... :!"LI:2/./L:I:2&:,2,//:/,:
,,2,
V3
146/1003
ANNALS 0F EMERGENCY MEDICINE
21:8
AUGUST1992
INTRACEREBRAL HEMORRHAGE Katta & Berk
Several common entities, including early repolarization, s pericarditis, 6 hyperkalemia,7, 8 and either a left ventricular aaeurysms or previous large infarct, 1 also are associated with ST-segment elevation, which may be mistaken for acute MI. Less commonly, massive pulmonary embolism,9 pneumothotax, 1 and a n u m b e r of cardiac conditions 1° may mimic MI. In addition to history and examination, ECG characteristics to consider in determining the probability of MI include localized versus diffuse ST elevation, the presence or absence of reciprocal changes, and the contour of the ST segment. ST elevation is diffuse with early repolarization, pericarditis, and hyperkalemia, in contrast to the localized abnormalities associated with MI. Reciprocal changes suggest MI, whereas the characteristic initial upward slope of the current of acute i n j u r y seen with M[, sometimes referred to as "upward convexity," also may occur in association with other causes of ST elevation (Figure 3). Simulation of MI is perhaps the most dramatic but not the only ECG abnormality associated with cerebral hemorrhage. Other findings associated with cerebral hemorrhage include T-wave inversions suggestive of myocardial ischemia, atrial and ventricular arrhythmias, abnormal P and T waves, and prolongation of the QT interval. 11,12 Although the cause of these changes is debated, centrally mediated alterations in autonomic tone are the most likely cause. In animal experiments, direct stimulation of the cervical sympathetic nerve shortened the ventricular recovery period and ablation lengthened the refractory period. 13,14 The resulting changes in the canine ECG were similar to those observed in patients with cerebral hemorrhage. Further support for this hypothesis is found in studies of patients who manifested similar changes in their ECG after radical neck surgery that ablated the sympathetic trunk.iS We cannot rule out the possibility that the ECG abnormalities that both we and others have observed reflect transient coronary artery spasm as either a primary phenomenon in response to shock produced by cardiac arrest or from centrally mediated changes in vascular tone. Intracranial disorders other than hemorrhage also may be associated with significant ECG abnormalities. An age-indeterminate MI suggested by Q waves in the anterior leads resolving after several weeks has been reported in connection with metastatic malignancY involving the brain. 16 Cerebral infarction has been reported to cause T-wave changes that may mimic myocardial ischemia. 17 Meningitis has been associated with lengthening of the QT interval and abnormalities of the ST segment and T wave, 12 and serious head i n j u r y may cause abnormalities similar to those observed with acute episodes of cerebrovascular disease.18 Although thr0mbolytic therapy was fortuitously withheld from our patient because of the brief period of CPR she required, CPR is not necessarily a coutraindication to such therapy. For MI patients undergoing less than ten minutes of CPR, hemorrhagic complications were no more frequent than in those receiving no CPR. 19 A recent review suggests that
AUGUST1992
21:8
ANNALS OF EMERGENCY MEDtCINE
the decision to administer thrombolytics to patients who have undergone CPR should be based not on an absolute time limit but on a clinical assessment of the probability of significant thoracic trauma and the patient's neurologic status. 20
SUMMARY We describe the case of'a patient who presented with cardiovascular collapse and ECG changes strongly suggestive of acute MI. Our experience and that of others with patients who had sustained intracerebral hemorrhage6,17,18 indicate the potential for this entity to be misdiagnosed as acute MI early in a patient's clinical course. Reports of mistaken administration of thrombolytic therapy to patients with periearditis 21,22 or aortic dissection, 22 other conditions that may be electrocardiographically mimic MI, underscore the potential for error. Clinicians should consider the possibility of intracerebral hemorrhage before treatment of MI with thrombolytic agents.
REFERENCES 1. Pasternak RC, Braunwald E, Sobel BE: Acute myocardial infarction, in Braunwald E (ed): Heart Disease, ed 4. Philadelphia, WB Saunders, 1992, p 1290-1291. 2. Cropp 6J, Manning 6W: Electrocardiographic changes simulating myocardial ischemia and infarction associated with spontaneous intracranial hemorrhage. Circulation 1960;22:25-38. 3. Menon IS: Electrocardiographic changes simulating myocardial infarction in a cerebrovascular accident. Lancet1964;2:433-434. 4. Beard EF, Robertsen JW, Robertson RCL: Spontaneous subarachnoid hemorrhage simulating acute myocardial infarction. Am HeartJ 1959;58:755-759. 5. Chou TO: Electrocardiography in Clinical Practice, ed 3. Philadelphia, WB Saunders, 1991, p 119-194. 6. 6inzton LE, Laks MM: The differential diagnosis of acute pericarditis from the normal variant. Circulation 1982;65:1004-1009. 7. Simon BC: Pseudomyocardial infarction and hyperkalemia: A case report and subject review. J Emerg Mef11986;6:511-515. 8. Klein LW, Meller J: Hyperkalemia-induced pseudoinfarction pattern. MtSinaiMeflJ 1983;50:428-431. 9. Denton TA, Litavack F, Siegel RJ: Pseudoinfarction in patients with massive pulmonary embolism. West J Med 1986;145:98-101. 10. Proudfit WL, Heupler FA: Electrocardiographic evidence suggestive of myocardial infarction without significant organic heart disease. Am HeartJ 1985;110:448-452. 11. Yamour BJ, Sridharan MR, Rice JF, et al: Electrocardiographic changes in cerebrovascular hemorrhage. Am HeartJ 1980;99:294-300. 12. Hersch C: Electrocardiographic changes in subarachnoid haemorrhage, meningitis, and intracranial space-occupying lesions. BrHeartJ1964;26:785-792. 13. Abildskov JA, Millar K, Burgess M J, et al: The electrocardiogram and the central nervous system. Prob Carfliovasc Dis 1970;13:210-216. 14. Abildskov JSA: Electrocardiographic wave form and the central nervous system. Circulation 1970;41:371-373. 15. Hugenholtz PG: Electrocardiographic changes typical for central nervous system disease after right radical neck dissection. Am HeartJ 1967;74:438. 16. Conetta R, 6itler B: Electrocardiographic anterior wall pseudoinfarction pattern caused by a metastatic brain tumor. NYState J Med 1987;87:125-127. 17. Fentz V, 6ormsen J: Electrocardiographic patterns in patients with cerebrovascular accidents. Circulation 1962;25:22-28. 18. Hersch C: Electrocardiographic changes in head injuries. Circulation 1961;23:853-860.
1004/147
INTRACEREBRAL H E M O R R H A G E Katta & Berk
19. Califf RM, Topoi EJ, Kereaikes DJ, at al: Cardiac resuscitation should not be a contraindication to thrombolytic therapy for myocardial infarction (abstract). Circulation 1988;78(11):127.
Address for reprints: Sadasiva Rae Katta, MD, Department of Internal Medicine 5S-10, Detroit Receiving Hospital, 4201 St Antoine, Detroit, Michigan 48201.
20. Muller DWM, Topoi EJ: Selection of patients with acute myocardial infarction for thrembolytic therapy. Ann Intern Med 1990;113:949-960. 21. Tilley WS, Harston WE: Inadvertent administration of streptokinase to patients with pericarditis. Am J Med 1986;81:542-544. 22. Blankenship J C, Almquist AK: Cardiovascular complications of thrombolytic therapy in patients with a mistaken diagnosis of myocardial infarction. JAm Coil Cardiol 1989;14:1579-1582.
148/1005
ANNALS OF EMERGENCY MEDICINE
21:8
AUGUST1992
hemorrhage, intracerebral
Hypertensive Intracerebral Hemorrhage Simulating Acute Myocardial Infarction From the Departments of Internal Medicine* and
Sadasiva Rao Katta, MD* William A Berk, MD
Emergency Medicine,e Wayne State University Medical School, Detroit, Michigan. Received for publication August 9, 1991. Revision received February 24, 1992. Accepted for publication March 4, 1992.
The decision to administer thrombolytic therapy for acute myocardial infarction depends on clinical presentation and characteristic ECG findings of acute injury. Inappropriate initiation of thrombolysis may occur when other clinical entities mimic myocardial infarction both clinically and electrocardiographically. We present the case of a 49-year-old woman who presented with cardiovascular collapse and ECG findings strongly suggestive of myocardial infarction. Computed brain tomography eventually revealed right temporal lobe hemorrhage, the apparent cause of the observed ECG abnormalities. ST-segment elevation resolved rapidly, and serial creatine phosphokinase isoenzyme determinations were negative. Because closed-chest cardiac massage had been performed, a thrombolytic agent was not administered. Our experience emphasizes the importance of considering ECG findings in light of clinical presentation and of taking care to consider conditions other than myocardial infarction that may cause ST-segment elevation. [Katta SR, Berk WA: Hypertensive intracerebral hemorrhage simulating acute myocardial infarction. Ann EmergMeflAugust1992;21:1002-1005.] INTRODUCTION Until recently, management of myocardial infarction (MI) was primarily supportive. Thus it was reasonable to treat equivocal cases expectantly as MI, until and unless proven otherwise during a 24-hour period by isoenzyme determination. Although creatine phosphokinase isoenzyme elevation remains the standard for diagnosis of MI, 1 the advent of thrombolytic reconstitution of coronary perfusion has placed renewed emphasis on history-taking and the 12-lead ECG as diagnostic tools. Thus, most authorities recommend administration when a patient's history is suggestive, presentation is early, significant ST-segment elevation is observed, and the patient has no risk factors for life-threatening hemorrhage.~ Evaluating patients for thrombolysis requires careful consideration of the ECG in light of the patient's history and necessitates that clinicians be aware of alternative diagnoses compatible with an ECG suggestive of MI. Among a number of clinical entities that may inscribe characteristic changes on the ECG suggestive of acute infarction, intracerebral hemorrhage is an example of a condition for which thrombolysis could well prove catastrophic.
AUGUST 1992
21:8
ANNALS 0E EMERGENCY MEDICINE
! 002/
14 5
INTRACEREBRAL HEMORRHAGE Katta & Berk
We present a case in which presentation was consistent with and ECG changes were strongly suggestive of acute MI but that eventually proved secondary to hypertensive intracerebral hemorrhage. CASE
REPORT
A 49-year-old woman presented to the emergency department after suffering cardiac arrest. Her family stated she had awakened with a headache, shortness of breath, and a d r y cough. Shortly after relating these complaints, she collapsed. An emergency medical services unit was summoned and arrived within five minutes. They found the patient unresponsive b u t with intact circulation and respirations. However, while en route to the hospital, cardiac arrest occurred. CPR was initiated, but before medications could be administered, pulse and respirations resumed. No ECG was recorded during the episode. The patient's medical history included a 16-year history of hypertension and two previous MIs. On admission, the patient was unresponsive. Blood pressure was 130/110 mm Hg; pulse, 94; and respirations, 16. Pupils were midsized and nonreactive. Moderate jugular distension was present. Lung examination revealed bibasilar • tales, and h e a r t sounds were normal. P l a n t a r stimulation yielded upgoing toes bilaterally, and reflexes were symmetric. ECG revealed ST elevation and hyperacute T waves in the inferior leads with reciprocal ST depression and T-wave inversion in the anterior leads strongly suggestive of acute
'
..........
YFT. ].:.LR~
: ;
.... i . - +
DISCUSSION
The importance of ECG criteria for determining when to administer thrombolytic t h e r a p y for acute MI has increased the probability of administering these drugs to patients with problems that mimic MI electrocardiographically. Cerebrovascular accidents have long been appreciated for this potential, 2-a but the impact of misdiagnosis has become much greater with the routine use of thrombolytics to treat MI. Figure 2. Return of ST-segments to baseline two hours after admission. This tracing was unchanged f r o m one obtained shortly before admission
Figure 1. Admission ECG with ST-segment elevation in the inferior leads suggestive of acute inferior wall infarction ............
inferior wall MI (Figure 1). The patient was admitted to the coronary care unit, but because she had received closedchest cardiac message, no thrombolytic t h e r a p y was administered. An ECG performed on arrival in the coronary care unit revealed atrial fibrillation with a r a p i d ventricular response and a decrease in ST elevation. Tracings obtained beginning two hours later showed r e t u r n of the ST segment to baseline with Q waves in inferior leads (Figure 2), consistent with the patient's history of previous MI and unchanged from those obtained before the c u r r e n t episode. Serial creatine phosphokinase isoenzyme determination over the next 24 hours ruled out MI. Computed b r a i n tomography three hours after hospital admission revealed i n t r a c e r e b r a l hemorrhage involving the right temporal lobe with s u b d u r a l extension and midline shift. Neurosurgical consultation was requested, but before surgical intervention could be accomplished, the patient died.
x,
¢.
~:~!_
i::t :::]
~
j Figure 3. ST-segment elevation caused by several different underlying conditions. The lead shown is indicated f o r each tracing. A. Acute anterior wall MI in a 43~year-old man. B. Persistent ST-segment elevation in a 59-year-old man three months after MI, reflecting left ventricular aneurysm.
~r.
,tit. ' l , . ~ l iYl J .! l ~. . r!!lli!#j.it
C
C. A 30-year-old woman with viral pericarditis. D. Asymptomatic 34-year-old man with ST-segment elevation secondary to early repolarization. E. Hyperkalemia (potassium, 8.0 mEq/L) causing ST-segment elevation in a 34year-old man with renal failure.
tu, : &i/d:: ::i F:
:::.!:: !! i!il iii I!F
~
~
,
MIl~il!i~ti~iMi141~'4';{iil',iiiliii~l!mllt~l[I;I
VI
~Id,.i~:.l,d..ll..:l..:l,,l,~!l!dld~l~ V4
~',T', .l!l.l::d,:,l,~dh4!d,:,:l,IJ!.!t~hl~ ....... ....... :!"LI:2/./L:I:2&:,2,//:/,:
,,2,
V3
146/1003
ANNALS 0F EMERGENCY MEDICINE
21:8
AUGUST1992
INTRACEREBRAL HEMORRHAGE Katta & Berk
Several common entities, including early repolarization, s pericarditis, 6 hyperkalemia,7, 8 and either a left ventricular aaeurysms or previous large infarct, 1 also are associated with ST-segment elevation, which may be mistaken for acute MI. Less commonly, massive pulmonary embolism,9 pneumothotax, 1 and a n u m b e r of cardiac conditions 1° may mimic MI. In addition to history and examination, ECG characteristics to consider in determining the probability of MI include localized versus diffuse ST elevation, the presence or absence of reciprocal changes, and the contour of the ST segment. ST elevation is diffuse with early repolarization, pericarditis, and hyperkalemia, in contrast to the localized abnormalities associated with MI. Reciprocal changes suggest MI, whereas the characteristic initial upward slope of the current of acute i n j u r y seen with M[, sometimes referred to as "upward convexity," also may occur in association with other causes of ST elevation (Figure 3). Simulation of MI is perhaps the most dramatic but not the only ECG abnormality associated with cerebral hemorrhage. Other findings associated with cerebral hemorrhage include T-wave inversions suggestive of myocardial ischemia, atrial and ventricular arrhythmias, abnormal P and T waves, and prolongation of the QT interval. 11,12 Although the cause of these changes is debated, centrally mediated alterations in autonomic tone are the most likely cause. In animal experiments, direct stimulation of the cervical sympathetic nerve shortened the ventricular recovery period and ablation lengthened the refractory period. 13,14 The resulting changes in the canine ECG were similar to those observed in patients with cerebral hemorrhage. Further support for this hypothesis is found in studies of patients who manifested similar changes in their ECG after radical neck surgery that ablated the sympathetic trunk.iS We cannot rule out the possibility that the ECG abnormalities that both we and others have observed reflect transient coronary artery spasm as either a primary phenomenon in response to shock produced by cardiac arrest or from centrally mediated changes in vascular tone. Intracranial disorders other than hemorrhage also may be associated with significant ECG abnormalities. An age-indeterminate MI suggested by Q waves in the anterior leads resolving after several weeks has been reported in connection with metastatic malignancY involving the brain. 16 Cerebral infarction has been reported to cause T-wave changes that may mimic myocardial ischemia. 17 Meningitis has been associated with lengthening of the QT interval and abnormalities of the ST segment and T wave, 12 and serious head i n j u r y may cause abnormalities similar to those observed with acute episodes of cerebrovascular disease.18 Although thr0mbolytic therapy was fortuitously withheld from our patient because of the brief period of CPR she required, CPR is not necessarily a coutraindication to such therapy. For MI patients undergoing less than ten minutes of CPR, hemorrhagic complications were no more frequent than in those receiving no CPR. 19 A recent review suggests that
AUGUST1992
21:8
ANNALS OF EMERGENCY MEDtCINE
the decision to administer thrombolytics to patients who have undergone CPR should be based not on an absolute time limit but on a clinical assessment of the probability of significant thoracic trauma and the patient's neurologic status. 20
SUMMARY We describe the case of'a patient who presented with cardiovascular collapse and ECG changes strongly suggestive of acute MI. Our experience and that of others with patients who had sustained intracerebral hemorrhage6,17,18 indicate the potential for this entity to be misdiagnosed as acute MI early in a patient's clinical course. Reports of mistaken administration of thrombolytic therapy to patients with periearditis 21,22 or aortic dissection, 22 other conditions that may be electrocardiographically mimic MI, underscore the potential for error. Clinicians should consider the possibility of intracerebral hemorrhage before treatment of MI with thrombolytic agents.
REFERENCES 1. Pasternak RC, Braunwald E, Sobel BE: Acute myocardial infarction, in Braunwald E (ed): Heart Disease, ed 4. Philadelphia, WB Saunders, 1992, p 1290-1291. 2. Cropp 6J, Manning 6W: Electrocardiographic changes simulating myocardial ischemia and infarction associated with spontaneous intracranial hemorrhage. Circulation 1960;22:25-38. 3. Menon IS: Electrocardiographic changes simulating myocardial infarction in a cerebrovascular accident. Lancet1964;2:433-434. 4. Beard EF, Robertsen JW, Robertson RCL: Spontaneous subarachnoid hemorrhage simulating acute myocardial infarction. Am HeartJ 1959;58:755-759. 5. Chou TO: Electrocardiography in Clinical Practice, ed 3. Philadelphia, WB Saunders, 1991, p 119-194. 6. 6inzton LE, Laks MM: The differential diagnosis of acute pericarditis from the normal variant. Circulation 1982;65:1004-1009. 7. Simon BC: Pseudomyocardial infarction and hyperkalemia: A case report and subject review. J Emerg Mef11986;6:511-515. 8. Klein LW, Meller J: Hyperkalemia-induced pseudoinfarction pattern. MtSinaiMeflJ 1983;50:428-431. 9. Denton TA, Litavack F, Siegel RJ: Pseudoinfarction in patients with massive pulmonary embolism. West J Med 1986;145:98-101. 10. Proudfit WL, Heupler FA: Electrocardiographic evidence suggestive of myocardial infarction without significant organic heart disease. Am HeartJ 1985;110:448-452. 11. Yamour BJ, Sridharan MR, Rice JF, et al: Electrocardiographic changes in cerebrovascular hemorrhage. Am HeartJ 1980;99:294-300. 12. Hersch C: Electrocardiographic changes in subarachnoid haemorrhage, meningitis, and intracranial space-occupying lesions. BrHeartJ1964;26:785-792. 13. Abildskov JA, Millar K, Burgess M J, et al: The electrocardiogram and the central nervous system. Prob Carfliovasc Dis 1970;13:210-216. 14. Abildskov JSA: Electrocardiographic wave form and the central nervous system. Circulation 1970;41:371-373. 15. Hugenholtz PG: Electrocardiographic changes typical for central nervous system disease after right radical neck dissection. Am HeartJ 1967;74:438. 16. Conetta R, 6itler B: Electrocardiographic anterior wall pseudoinfarction pattern caused by a metastatic brain tumor. NYState J Med 1987;87:125-127. 17. Fentz V, 6ormsen J: Electrocardiographic patterns in patients with cerebrovascular accidents. Circulation 1962;25:22-28. 18. Hersch C: Electrocardiographic changes in head injuries. Circulation 1961;23:853-860.
1004/147
INTRACEREBRAL H E M O R R H A G E Katta & Berk
19. Califf RM, Topoi EJ, Kereaikes DJ, at al: Cardiac resuscitation should not be a contraindication to thrombolytic therapy for myocardial infarction (abstract). Circulation 1988;78(11):127.
Address for reprints: Sadasiva Rae Katta, MD, Department of Internal Medicine 5S-10, Detroit Receiving Hospital, 4201 St Antoine, Detroit, Michigan 48201.
20. Muller DWM, Topoi EJ: Selection of patients with acute myocardial infarction for thrembolytic therapy. Ann Intern Med 1990;113:949-960. 21. Tilley WS, Harston WE: Inadvertent administration of streptokinase to patients with pericarditis. Am J Med 1986;81:542-544. 22. Blankenship J C, Almquist AK: Cardiovascular complications of thrombolytic therapy in patients with a mistaken diagnosis of myocardial infarction. JAm Coil Cardiol 1989;14:1579-1582.
148/1005
ANNALS OF EMERGENCY MEDICINE
21:8
AUGUST1992
