Article, Cardiology

Importance of bedside echocardiography for detection of unsuspected isolated right ventricular infarction as a cause of cardiovascular collapse

after a 41-day of hospitalization. Electrocardiogram after discharge revealed normal sinus rhythm.

Cardiac tamponade is caused by fluid accumulation around the cardiac chambers that influence cardiac output significantly [1]. It is also an important differential diagnosis in patients of pulseless electrical activity. There are many causes of acute cardiac tamponade, including trauma, post- myocardial infarct rupture, and aortic dissection. The incidence of acute Pericardial tamponade is approximately 2% of penetrating trauma [2]. Malignancy, tuberculosis, and idiopathic pericarditis are common etiologies of subacute tamponade [3].

atrial flutter is a rare manifestation of cardiac tamponade [4,5]. It is usually associated with organic heart disease, such as ischemic heart disease, acute myocardial infarction, caridomyopathy, myocarditis, and, less common, pulmonary embolism. The most common ECG sign of large pericardial effusion is low voltage of the QRS complexes [6]. Sinus tachycardia with combination of low voltage may imply Bedside echocardiography f”>pericardial effusion with tamponade. Chronic obstructive pulmonary disease, cardiomyopathy, pleural effusion, and condition after open heart surgery, however, could also have similar patterns. Electrical alternans with sinus tachycardia is a more specific sign in cardiac tamponade, but the absence of it does not exclude cardiac tamponade.

Echocardiography now is a standard diagnostic tool for pericardial effusion and cardiac tamponade [7-9]. Diastolic compression of right atrium and right ventricle on 2-dimen- sional and Doppler echocardiography suggests cardiac tamponade. Elective treatment may be done earlier if there is no sign of shock but echocardiographic findings of tamponade present. Fluid resuscitation is still the first step of treatment in hemodynamic unstable patients with cardiac tamponade, and next is removal of pericardial effusion, whether by catheter pericardiocentesis or immediate surgery [7,10]. Catheter pericardiocentesis now is a favorable therapy in most clinical physicians because of its accessi- bility and low complication rate under cardiac echocardi- ography guidance.

Our case emphasis that, although very rare, atrial flutter can be the ECG sign of cardiac tamponade. Thus, urgent further survey, especially cardiac echocardiography, is important for patients with new onset of atrial flutter. Atrial flutter should be considered as a possible ECG finding in patients with cardiac tamponade.

I-Chuan Chen MD Te-Fa Chiu MD

Jih-Chang Chen MD Department of Emergency Medicine Chang Gung Memorial Hospital

Chang Gung University College of Medicine

Taoyuan, Taiwan, ROC E-mail address: [email protected]

doi:10.1016/j.ajem.2006.05.023

References

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  2. Naclerio EA. Penetrating wounds of the heart. Experience with 249 patients. Dis Chest 1964;46:1 – 22.
  3. Merce J, Sagrista Sauleda J, Permanyer Miralda G, Carballo J, Olona J, Soler Soler J. Pericardial effusion in the elderly: a different disease? Rev Esp Cardiol 2000;53(11):1432 – 6.
  4. Pousset F, Le Heuzey JY, Pialoux G, et al. Cardiac lymphoma presenting as atrial flutter in an AIDS patient. Eur Heart J 1994; 15(6):862 – 4.
  5. Ogimoto A, Hamada M, Shigematsu Y, et al. Cardiac tamponade with paroxysmal atrial flutter controlled by antituberculous therapy. Nippon Ronen Igakkai Zasshi 2004;41(1):112 – 6.
  6. Bruch C, Schmermund A, Dagres N, et al. Changes in QRS voltage in cardiac tamponade and pericardial effusion: reversibility after peri- cardiocentesis and after anti-inflammatory drug treatment. J Am Coll Cardiol 2001;38(1):219 – 26.
  7. Maisch B, Seferovic PM, Ristic AD, et al. Guidelines on the diagnosis and management of pericardial diseases executive summary; the task force on the diagnosis and management of pericardial diseases of the European society of cardiology. Eur Heart J 2004;25(7):587 – 610.
  8. Cheitlin MD, Armstrong WF, Aurigemma GP, et al. ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiogra- phy: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASE Committee to Update the 1997 Guide- lines for the Clinical Application of Echocardiography). Circulation 2003;108(9):1146 – 62.
  9. Cheitlin MD, Alpert JS, Armstrong WF, et al. ACC/AHA Guidelines for the Clinical Application of Echocardiography. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Clinical Application of Echocardiography). Developed in collaboration with the American Society of Echocardiography. Circulation 1997;95(6):1686 – 744.
  10. Salem K, Mulji A, Lonn E. Echocardiographically guided pericardiocentesis–the gold standard for the management of peri- cardial effusion and cardiac tamponade. Can J Cardiol 1999;15(11): 1251 – 5.

Importance of bedside echocardiography for detection of unsuspected isolated Right ventricular infarction as a cause of Cardiovascular collapse

Isolated right ventricular infarction is a rare and commonly overlooked condition, because of scarce electro- cardiographic changes. We present 2 cases of isolated right ventricular infarction that went unrecognized in the ED. Both patients presented with signs of circulatory collapse, third-degree atrioventricular block, and without prominent Ischemic changes in the electrocardiogram. Diagnosis was further obfuscated by the absence of chest pain and Atypical clinical presentation with left-hand paresis in one patient and hypothermia in the second. Echocardiography was performed as part of the evaluation of unexplained hypotension. In both cases, it revealed right ventricular dysfunction, which suggested possible acute right ventric- ular infarction. Diagnosis was confirmed by the finding of subtotal ostial thrombotic occlusions of the right coronary

Fig. 1 Standard electrocardiogram recorded at the time of admission to the emergency department showing complete atrioventricular block and very subtle ST-segment elevations in inferior leads.

artery in both cases. Echocardiography played a decisive role in the Diagnostic procedure, enabling prompt therapeu- tic intervention and subsequent resolution of shock.

Isolated right ventricular infarction is a rare event present in less than 5% of autopsies [1]. History and clinical presentation are unremarkable in one third of cases [2]. Electrocardiogram (ECG) usually shows ischemic changes in inferior wall and typical changes in V4R lead. However, ECG may also lack evident signs of myocardial ischemia, which often obscures the diagnosis [3,4]. Echocardiography represents an easily accessible and noninvasive diagnostic option which often resolves clinical dilemma. We present 2 cases of acute isolated right ventricular infarction associated with circulatory collapse that were unrecognized until echocardiographically dem- onstrated severe right ventricular failure directed suspicion toward the correct underlying cause.

A 78-year-old man without any chronic disease presented to the emergency department because of weakness. He reported paleness and sweating, while denying chest pain, palpitations, or dyspnea. In addition, his main complaint was paraesthesia and decreased strength in his left hand. On admission, his blood pressure was 70/35 mm Hg and pulse was weak with a rate of 35 per minute. Lung fields were clear on auscultation and heart sounds were normal. The emergency physician documented a slightly decreased strength in the patient’s left hand and flexion of the elbow. Electrocardiogram demonstrated complete atrioventricular block and rather subtle ST-segment elevations in inferior leads and minimal ST-segment depression in lateral leads (Fig. 1). Because of suspected Adams-Stokes syndrome and

unexplained neurologic deficit, he was admitted to the intensive care unit. Cardiac necrosis markers on admission were negative, and chest x-ray was normal. arterial blood gases were normal. We could not confirm any paresis in the left upper extremity. To clarify the patient’s hemodynamic condition, we performed echocardiography and found normal left chambers without any regional wall motion defects, but dilated and hypokinetic right ventricle (Fig. 2). Acute isolated right ventricular infarction was suspected as a

Fig. 2 Echocardiogram recording from the first patient. Record- ing during systole shows dilated right ventricle with absent contraction of the lateral wall. The right ventricle is larger than the left ventricle. RV indicates right ventricle; LV, left ventricle; RA, right atrium.

Fig. 3 Standard electrocardiogram from the second patient. It demonstrates junctional rhythm and unspecific widespread changes in ST segment and T waves in inferior and anterior leads. Note fine artefacts due to patient’s tremor associated with hypothermia.

possible cause and confirmed with a Right-sided ECG leads recording. Patient received isotonic saline and was referred to the catheterization laboratory. We found Single-vessel disease with an ostial subtotal thrombotic lesion of the right coronary artery . After direct stenting, TIMI 3 flow resorted and right-sided ECG changes resolved. The remaining course was uneventful and the patient was discharged without any sequelae.

The second patient was a 74-year-old man who was admitted because of hypothermia, hypotension, and som- nolence. On the day of admission, he went to work in the forest and was found lying in the stream several hours later. On admission, he was somnolent, hypothermic at 318C, and his blood pressure was 70/50 mm Hg; his pulse was weak with a rate of 32 per minute. Neck veins were engorged, lung fields were clear on auscultation, and heart sounds were normal without any murmurs. Besides obtundation, there were no neurologic deficits. During the laboratory examination, we registered increased urea and creatinine; Troponin I levels were normal at the time of admission. Arterial blood gas analysis demonstrated metabolic lactic acidosis (pH 7, 21; pCO2, 4.0 kPa; HCO3, 12.1 mmol/L; pO2, 10.6 kPa) and increased lactate to 9.7 mmol/L. Electrocardiogram showed junctional rhythm, with a ven- tricular rate of 25 per minute, slight ST-segment elevation, and inverted T waves in D III and aVF, as well as concave type ST-segment elevation in anterior leads (Fig. 3). Electrocardiographic changes were judged to be nonspecif- ic, especially in the context of hypothermia and hypoten- sion, and the patient was transferred to the intensive care

unit. Echocardiography was performed as part of the evaluation of circulatory shock of uncertain etiology. It demonstrated decreased left ventricular systolic function with hypokinesia of the left ventricular posterior wall and, most notably, dilated and hypokinetic right ventricle (Fig. 4). Subsequent ECG recording of right-sided leads showed ST- segment elevations. Urgent coronarography demonstrated ostial occlusion of the RCA and chronic occlusion of the left circumflex artery with autocollaterals (Fig. 5). After intra- aortic balloon pump insertion, target lesion was successfully

Fig. 4 Echocardiogram recording from the second patient demonstrating similar characteristics as in the first patient.

Fig. 5 Coronary arteriogram of the RCA from the second patient. On the left panel, ostial occlusion of the RCA is evident. Right panel shows large RCA after successful Balloon angioplasty and stent implantation.

resolved by percutaneous balloon angioplasty and stent implantation. After the procedure, the patient’s status slowly improved; he was weaned from intra-aortic balloon counter- pulsation on day 3. Subsequent course was uneventful.

Determining the etiology of cardiovascular collapse in critically ill patients is crucial to a rapid and appropriate therapeutic response. Besides other possible mechanisms, such as left ventricular dysfunction, or inadequate preload, severe right ventricular dysfunction due to isolated myo- cardial infarction of the right ventricle is a rare but potentially reversible cause of hypotension. Usually, isolat- ed right ventricular infarction does not present a Diagnostic dilemma because of ischemic changes in standard 12-lead ECG. In the first patient, ECG did show subtle ischemic changes in inferior leads, suggesting inferior wall ischemia. In the second patient, ECG was even less conclusive owing to more widespread ST-segment and T-wave changes. However, in both patients, the complexity of clinical presentation and confusing findings at admission blurred the underlying pathologic event. Echocardiography was used as part of the diagnostic workup of a hemodynamically compromised patient with no evident underlying cause of his status. Although we cannot exclude the possibility of coincident involvement of the left ventricular inferior wall, absence of any segmental left ventricular contractility defects by echocardiography indicates that, even if such did exist, it was not clinically significant. Finding of severely compromised right ventricular function with preserved left ventricular contractility in hypotensive patients generally suggests pulmonary embolism or right ventricular infarction as possible causes. In our case, right ventricular dysfunction in combination with bradycardia and absence of hypoxemia made diagnosis of pulmonary embolism much less likely and pointed toward a correct underlying cause. In the second patient, hypothermia could,

at least partially, account for bradycardia and decreased systolic function of the left ventricle. Nevertheless, exceed- ingly compromised left and right ventricular function with respect to the Severity of hypothermia indicated an additional cause of compromise in myocardial contractility. In this patient, more widespread ischemic ECG changes and additional posterior wall hypokinesia were a consequence of double-vessel coronary occlusion. However, acute deterio- ration with shock was caused by acute right ventricular infarction due to ostial RCA occlusion, as left circumflex artery occlusion was old and was autocollateralized.

Echocardiography has been previously shown to provide valuable information on a hypotensive patient with regard to volume status, contractility, and valvular function [5-7]. Evaluation of right ventricular function and dimensions provides information with regard to preload status, as well as a potential cause of hypotension, such as pulmonary embolism and right ventricular dysfunction. As such, echocardiography was also endorsed by emergency medi- cine physicians who use it to perform and interpret goal- oriented examinations and reduce time to diagnosis [8]. right ventricular myocardial infarction is a known deter- minant of short- and long-term prognosis which is amenable to treatment [3,9,10]. In one study, clinical signs of right ventricular dysfunction were present in only one tenth of patients admitted with diagnosis of acute Inferior wall myocardial infarction. However, subsequent echocardiogra- phy and ECG demonstrated associated right ventricular infarction in 37% of these patients [9]. The acute in-hospital mortality rate of patients with right ventricular infarction is 3 times higher than in those with inferior infarction [3,9]. Rapid determination of correct diagnosis with timely treatment is therefore crucial. Echocardiographic detection of isolated or predominant right ventricular dysfunction in hypotensive patients is an important marker of possible

infarction of the right ventricle and should lead to further attempts to exclude or confirm this diagnosis.

These cases illustrate the diversity of clinical presentation in acute isolated right ventricular infarction. We emphasize the decisive role of echocardiography in reducing the time to diagnosis and expedite patient care. It should represent a standard investigation in patients with unexplained cardio- vascular presentation.

Mitja Lainscak MD, MSc General Hospital Murska Sobota Murska Sobota, Slovenia

Andrej Pernat MD, PhD Department of Cardiology University Medical Centre Ljubljana SI-1000 Ljubljana, Slovenia

E-mail address: [email protected] doi:10.1016/j.ajem.2006.05.022

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  2. Kinch JW, Ryan TJ. Right ventricular infarction. N Engl J Med 1994; 330:1211 – 7.
  3. Zehender M, Kasper W, Kauder E, et al. Right ventricular infarction as an independent predictor of prognosis after acute Inferior myocardial infarction. N Engl J Med 1993;328:981 – 8.
  4. Antonelli D, Schiller D, Kaufman N, Barzilay J. Isolated right ventricular infarction: a diagnostic challenge. Cardiology 1984;71: 273 – 6.
  5. Sanfilippo A, Weyman A. The role of echocardiography in managing critically ill patients. J Crit Illn 1988;3:27 – 44.
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  7. Heidenreich PA, Stainback RF, Redberg RF, et al. Transesophageal echocardiography predicts mortality in critically ill patients with unexplained hypotension. J Am Coll Cardiol 1995;26:152 – 8.
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  10. Skali H, Zornoff LA, Pfeffer MA, et al. Prognostic use of echocardi- ography 1 year after a myocardial infarction. Am Heart J 2005;150: 743 – 9.

Acute myocardial infarction diagnosed early by Multidetector computed tomography

The development of multidector computed tomography (MDCT) has allowed assessment of not only coronary artery stenoses and occlusion, but also coronary artery plaques and myocardial perfusion [1]. Previous literature has empha- sized its usefulness for detecting obstructive coronary artery

disease [2,3]. Recent publications also confirm that myo- cardial infarctions (MIs) can be seen on MDCT scan, but enrolled patients in these studies were in the subacute or chronic stage of MI [4 – 6]. The clinical utility of MDCT to demonstrate acute MI has been reported in some cases with non-ST-elevation MI [1,7 – 9]. Herein, we present a case of hyperAcute stage of ST-elevation MI incidentally diagnosed early by this imaging modality before the electrocardiogram (ECG) or cardiac biomarkers became positive.

A 52-year-old man presented to our emergency depart- ment (ED) with 20-minute symptoms of persistent anterior chest pain radiating to back associated with diaphoresis. He had a history of malignant melanoma of the right big toe postoperation. Physical examination was unremarkable. The initial ECG showed normal sinus rhythm with no evidence of ischemic changes, and cardiac enzyme analysis was within normal limits, with a creatine kinase (CK) of 34 U/L, CK-MB of 1 U/L, and troponin I of 0.04 ng/mL. Initial treatment included oxygen, aspirin, nitroglycerin, and morphine. A cardiologist was consulted because of unresolved symptoms, and bedside echocardiogram was interpreted as normal left ventricular function with an ejection fraction of 67%. A 40-slice, non-ECG-gated MDCT angiography (Philips, Cleveland, OH; 40 x 0.625-mm collimation, 500-millisec- ond rotation, 120 kV) was ordered to evaluate for potential aortic dissection, which demonstrated normal aorta but an area of transmural hypodensity with normal wall thickening along the anterior wall of the left ventricular and poor contrast-perfused left anterior descending coronary artery suggesting an occlusion (Fig. 1). The repeated ECG 10 minutes after MDCT scan showed ST-segment elevation in leads V2 through V5. Primary coronary angiography was performed immediately and revealed a total occlusion of the middle LAD (Fig. 2). The patient underwent successful percutaneous transluminal coronary angioplasty with stent placement. Serial cardiac enzyme analysis confirmed a MI with an early peaking CK value of 2224 U/L (7% MB form) at 6 hours after onset of symptoms. The rest of the hospitali- zation course was uneventful.

Evaluating patients who present with symptoms sugges- tive of acute coronary syndrome (ACS) remains a clinical challenge in the ED. Acute coronary syndrome constitutes a variety of clinical presentations, and other differential diagnosis such as abnormalities of the great vessels, pericardial disease, or gastrointestinal disorders may mimic it. Early diagnosis of ST-elevation MI is essential goal because it indicates the potential for a substantial irrevers- ible infarction and is the primary indication for Emergent reperfusion therapy to salvage the myocardium.

The 12-lead ECG and cardiac enzyme levels are used to screen a suspected patient for ACS. It is known that a normal initial ECG does not preclude the diagnosis of acute MI [10], and cardiac enzymes may require 4 to 8 hours to have elapsed after the onset of coronary artery occlusion. The subsidiary noninvasive echocardiography is highly dependent on the operator and reader, and may be less

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