Intensive Care Med (1988) 14:77-79 Intensive Care ,Medicine © Springer-Ver!ag1988

Persistent ST-segment elevation following pericardiocentesis: caution with thrombolytic therapy

H.H. Hsia, N.H. Kander and M.J. Shea

Division of Cardiology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, Michigan, USA

Received: 15 January 1987; accepted: 17 January 1987

Abstract. We report a case of persistent electrocar- atrial was admitted to hospital for worsen- diographic ST-elevation following pericardiocentesis ing congestive . The patient's heart failure despite lack of evidence for transmural infarction or was felt to be related to verapamil used to control the vasospasm. The electrocardiographic pattern was felt . Previous echocardiographic evalua- to reflect subepicardial injury due to a small myocar- tion had demonstrated thickened anterior and post- dial laceration. The implications of this finding are erior leaflet echoes with parallel move- discussed. ment, a diminished E-F slope, left , and normal left ventricular function without pericar- Key words: Pericardiocentesis - Complications of dial effusion (Fig. 1). - Thrombolysis On the third hospital day, the patient suffered a witnessed . Cardiopulmonary resuscita- tion was started immediately. The initial rhythm was which subsequently converted Emergency pericardiocentesis for electromechanical to a pulseless idioventricular rhythm with cardiopul- dissociation is performed as a potential lifesaving monary resuscitation. The possibility of cardiac tam- maneuver for patients in whom pericardial tamponade ponade was entertained in view of the electromechan- or may be present. Frequently, ical dissociation. Therefore, two pericardiocenteses clinical proof of these conditions may be absent yet were attempted via the subxiphoid approach with a pericardiocentesis is performed empirically because 20-gauge spinal needle aimed toward the left shoulder. tamponade is a "reversible" cause of electromechan- The results were nonproductive for any fluid or blood ical dissociation. However, pericardiocentesis is not and the needle was quickly removed. No V-lead elec- without risk. Complications range from vasovagal trocardiographic monitoring was used and no rhythm reactions and transient to pulmonary disturbance was noted during the procedure. edema, pneumothorax and hemopericardium [1, 2]. Subsequently the patient converted to normal We report a case of a patient developing a new sinus rhythm with a blood pressure of 110/80 mmHg. focal injury pattern on the electrocardiogram follow- The immediate post-arrest electrocardiogram showed ing pericardiocentesis for electromechanical dissocia- new 1.5 mV ST-elevation in leads V4-5 (Fig. 2). tion. This was unrelated to infarction or vasospasm Because of post-arrest chest pain and in view of but was most likely due to a myocardial laceration. the electrocardiographic findings suggestive of The importance of this observation relates to the myocardial injury, it was felt that the patient could be rapidly changing treatment of acute myocardial infarc- suffering an acute myocardial infarction. An emergen- tion with the emphasis on venous lytic therapy and cy cardiac catheterization was performed which reveal- new interventional strategies. ed: mean right atrial pressure 8 mmHg; right ven- tricular pressure 39/6 mmHg; pulmonary artery Case report pressure 30/15, mean 22mmHg; mean pulmonary capillary wedge pressure 16 mmHg; estimated mitral A 66-year-old woman with longstanding rheumatoid valve area (Gorlin) 1.7cm 2, and cardiac index arthritis, rheumatic mitral stenosis and paroxysmal 2.91/min/m 2. Left ventriculography revealed normal 78 H.H. Hsia et al.: ST-elevation after pericardiocentesis

Fig. 1. The admission electrocar- diogram demonstrates sinus rhythm, poor R wave progression, prominent precordial voltage and atrial prema- ture contractions

segmental wall motion and overall normal left ven- The present case is unusual because following tricular contraction with mild mitral regurgitation and pericardiocentesis the injury pattern was observed to a calcified mitral valve. Coronary arteriography reveal- be localized to V 4 -V 5 and this persisted for over 24 h, ed a normal left dominant circulation without yet there was no complementary evidence for evidence of stenosis or vasospasm. Within 24 h the transmural injury. The electrocardiogram subsequent- creatine kinase rose to 2300 I.U. with 12% MB frac- ly returned to the baseline appearance with preserva- tion present. The electrocardiographic injury pattern tion of R-wave voltage without evidence of "Q" waves. persisted for 24 h but had completely resolved by 48 h. Ventriculography and echocardiography did not reveal A technetium pyrophosphate scan was obtained 72 h wall motion abnormalities and coronary arteriography post-arrest, no focal uptake was documented. A repeat during the ST-elevation revealed no evidence for echocardiogram showed no and vasospasm or significant coronary atherosclerosis. no wall motion abnormalities. The rise in creatine phosphokinase suggests myocar- dial damage occurred but the technetium scan did not Discussion reveal focal uptake nor was there evidence for a diffuse increased uptake. While post-cardioversion myone- In 1956, Bishop et al. [3] described the electrocar- crosis cannot be excluded, we feel that the relatively diographic changes during pericardiocentesis. The focal injury pattern with negative technetium scan and "current of injury" is detected as either ST-segment elevated enzymes are most consistent with a small area elevation or PR-segment elevation when the ven- of subepicardial injury and necrosis from the pericar- tricular or atrial epicardium is in contact with the nee- diocentesis needle. This is supported by the direction die. This observation has been used as a safeguard for of the pericardiocentesis attempts: from the subx- inadvertent myocardial injury; nevertheless, myocar- iphoid to left shoulder regions. While the persistence dial laceration without electrocardiographic changes of ST-segment elevation remained unexplained, it is have been well documented [4, 5]. doubtful that transmural injury occurred since there

Fig. 2. Electrocardiograph im- mediately after postresuscitation shows 1.5 mV ST-elevation in leads V4 5, which persisted during car- diac catheterization and did not resolve until 48 h later H.H. Hsia et al.: ST-elevation after pericardiocentesis 79 was normal regional wall motion at the time of repeat with the potential complication of myocardial lacera- echocardiography and the technetium scan was also tion could be catastrophic. normal. Persistent elevation of the ST-segments following Acknowledgement. We thank Lisa Hackbarth for excellent pericardiocentesis may have important implications secretarial assistance. for management. Such electrocardiographic changes are usually felt to reflect subepicardial injury as seen most commonly with acute coronary occlusion due to References thrombosis or vasospasm. Because myocardial salvage is clearly a time-dependent process, current thera- I. Miller JI (1986) Surgical management of pericardial disease. In: Hurst JW (ed) The Heart. McGraw-Hill, New York, p 2009 peutic strategies have increasingly centered on ad- 2. Wong B, Murphy J, Chang C J, Hassenein K, Dunn M (1979) The ministration of thrombolytic therapy via the in- risk of pericardiocentesis. Am J Cardiol 44:110 travenous route rather than the intracoronary route. 3. Bishop LH, Estes EH, Mclntosh HD (1956) The electrocar- This is in part related to timing and in part related to diogram as a safeguard in pericardiocentesis. JAMA 62:264 practicality and cost. While our patient had a relative 4. Sobel SM, Thomas HM, Evans RW (1975) Myocardial laceration not demonstrated by continuous electrocardiographic monitor- contraindication to lyric therapy, viz., cardiopulmon- ing occurring during pericardiocentesis. N Engl J Med 282:1222 ary resuscitation, many clinicians would be inclined to 5. Gueron M, Hirsch M, Wanderman K (1975) Myocardial lacera- pursue therapy in such a situation. In view of the case tion not shown by ECG during pericardiocentesis. N Engl J Med presented, a persistent focal electrocardiographic in- 293:938 jury pattern following pericardiocentesis should raise concerns about whether there is additional, concor- Dr. M. J. Shea dant evidence for myocardial injury. Independent con- Division of Cardiology firmation of ischemic injury should be established via University of Michigan Medical Center 1500 East Medical Center Drive echocardiography or, in some cases, coronary 3910 B Taubman Center arteriography and ventriculography. The risk of em- Ann Arbor, MI 48109-0366 piric lytic therapy in such a setting is unknown but USA