Echocardiography

2nd Edition-2010

on Handbook eports eR ECG Cas l

ggarwa

A Dr KK

IJCP Daryacha, 39, Hauz Khas Village New Delhi - 110 016 Bangalore, Chennai, Hyderabad, Kolkata, Mumbai

Not for Sale (For Private Circulation Only)

IJCP Š Copyright 2010 IJCP Publications Ltd. All rights reserved.

The copyright for all the editorial material contained in Handbook on ECG Case Reports Volume 2, in the form of layout, content including images and design, is held by IJCP Publications Ltd. No part of this publication may be published in any form whatsoever without the prior written permission of the publisher.

Published, Printed and Edited by Dr KK Aggarwal, on behalf of IJCP Academy of CME as a part of their social commitment towards upgrading the knowledge of Indian doctors.

Published at Daryacha, 39, Hauz Khas Village, New Delhi - 110 016 E-mail: editorial@ijcp.com, emedinews@gmail.com Website: www.ijcpgroup.com HIP/IN/Bangalore/1127

Disclaimer: Although great care has been taken in compiling and checking the information given in the book to ensure that it is accurate, the publisher/ its agents and sponsors shall not be responsible for any error omissions or inaccuracy in this publication whether arising from negligence or otherwise.

Inclusion or exclusion of any product does not mean that the publisher advocates or rejects its use either in general or particular.

From the Desk of Group Editor-in-chief

Treadmill High Risk Stratification

A

number of adverse predictors have been identified during exercise treadmill testing. These include:



Poor exercise capacity (<5 METs)

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Abnormally low peak systolic blood pressure (<130 mmHg)

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A fall in systolic blood pressure during exercise

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Exercise-induced chest pain or angina

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≥2 mm of ischemic ST depression at a low workload (stage 2 or less, or ≤130 beats/min)

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Early onset (stage 1) or prolonged duration (>5 min) of ST depression

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Multiple leads (>5) with ST depression

The most popular validated treadmill score is Duke score. It uses three exercise parameters: Duke prognostic treadmill score = exercise time (minutes based on the Bruce protocol) - (5 × maximum ST segment deviation in mm) - (4 × exercise angina [0 = none, 1 = nonlimiting and 2 = exercise limiting]).

Patients are classified as low, moderate or high risk according to the score:   

Low-risk: Score ≥+5 Moderate-risk: Score from –10 to +4 High-risk: Score ≤–11

The scores correlate with both the severity of coronary disease and prognosis in men but may be less effective for risk stratification in women.

And much more in this issue ...

Suggested reading 1. Shaw LJ, Peterson ED, Shaw LK, et al. Use of a prognostic treadmill score in identifying diagnostic coronary disease subgroups. Circulation 1998;98(16):1622-30.

2. Alexander KP, Shaw LJ, Shaw LK, et al. Value of exercise treadmill testing in women. J Am Coll Cardiol 1998;32(6):1657-64.

Dr KK Aggarwal Padma Shri and Dr BC Roy National Awardee Sr Physician and Cardiologist, Moolchand Medcity President, Heart Care Foundation of India Group Editor-in-Chief, IJCP Group of Publications Editor-in-Chief, eMedinewS emedinews@gmail.com

VI

Preface

ECG Abnormalities During Recovery

I

n addition to the changes that are induced by ischemia during exercise, certain changes that occur during recovery also have diagnostic and prognostic significance. ď&#x201A;&#x;

About 8% patients develop ST segment depression during recovery rather than during exercise; this change is a predictor of a greater likelihood of coronary heart disease (CHD)1 and may have a prognostic significance similar to similar changes occurring during exercise, even in apparently healthy individuals.2 Inclusion of ST depression during recovery significantly increases the sensitivity of the exercise test (from 50% to 59%) without change in predictive value.

ď&#x201A;&#x;

The progressive rise in heart rate with exercise is mediated by an increase in sympathetic activity and a decline in parasympathetic activity. These changes are reversed and the heart rate slows during recovery.3 A slower rate of heart rate recovery is associated with impaired reactivation of parasympathetic tone and an adverse prognosis. In the study failure of the heart rate to fall rapidly (defined as 12 beats/min or less) VII

during the one minute ‘cool down phase’ after exercise cessation, while the patient was still standing, was associated with an increase in overall mortality at six year follow-up. In a study of 5,713 asymptomatic men cited above, subjects in the lowest quintile of heart rate recovery (<25 beats/min reduction in the first minute after exercise) had a significantly higher incidence of sudden death (adjusted relative risk 2.1) compared to those in the highest quintile (>40 beats/min reduction).4 

There is an association between exercise-induced ventricular arrhythmia and increased mortality risk. In a review of almost 30,000 patients referred to symptom-limited exercise testing who did not have a history of heart failure, arrhythmia or valve disease, frequent ventricular ectopy occurred only during exercise in 3%, only during recovery in 2% and in both time periods in 2%.5 At a mean 5.3 year follow-up, only frequent ventricular ectopy occurring during recovery was associated with an increased risk of mortality after adjusting for confounding variables.

This compilation from IJCP is a real good academic feast for the readers.

References 1. Lachterman B, Lehmann KG, Abrahamson D, et al. “Recovery only” ST segment depression and the predictive accuracy of the exercise test. Ann Intern Med 1990;112(1):11-6.

2. Rywik TM, Znk RC, Gittings NS, et al. Independent prognostic VIII

significance of ischemic ST segment response limited to recovery from treadmill exercise in asymptomatic subjects. Circulation 1998;97(27):2117-22.

3. Imai K, Sato H, Hori M, et al. Vagally mediated heart rate recovery after exercise is accelerated in athletes but blunted in patients with chronic heart failure. J Am Coll Cardiol 1994;24(6):1529-35.

4. Jouven X, Empana JP, Schwartz PJ, et al. Heart-rate profile during exercise as a predictor of sudden death. N Engl J Med 2005;352(19):1951-8.

Dr Praveen Chandra Chairman Division of Interventional Cardiology Medanta â&#x20AC;&#x201C; The Medicity Gurgaon

IX

Contents 1.

Atrioventricular Re-entrant Tachycardia: Clues to Underlying Accessory Pathway and Its Location ............................................................... 1

2.

Pseudoinfarction Pattern in a Patient with Hyperkalemia, Diabetic Ketoacidosis and Normal Coronary Vessels: A Case Report ............ 7

3.

Door to ECG Time is 40 Minutes: Is the Doctor Negligent?....................... 16

4.

Electrocardiographic Changes in Hiatal Hernia: A Case Report .................. 19

5.

ST-T Changes in ECG ................................................................................. 24

6.

Pneumopericardium should be Considered with Electrocardiogram Changes after Blunt Chest Trauma: A Case Report ..................................... 26

7.

Persistent ST-T Changes in Inferior Leads ................................................... 37

8.

QT Interval Prolongation after Sertraline Overdose: A Case Report . .......... 39

9.

Complete Heart Block in Pregnancy ............................................................ 46

10. Differential Diagnosis of Complete Heart Block .......................................... 53 11. A Case of COPD with Cor Pulmonale ........................................................ 55 12. Electrocardiographic Changes in a Rare Case of Flecainide

Poisoning: A Case Report . ........................................................................... 57 13. Atrial Fibrillation with Multiple Infarcts ...................................................... 66 14. Aortic Regurgitation with LVH Pattern ....................................................... 72 15. Hypertrophic Obstructives Cardiomyopathy ................................................ 74 16. Hypertensive Crisis-induced Electrocardiographic Changes:

A Case Series ................................................................................................ 76 17. Acute Dyspnea and Tachycardia in a Cigarette Smoker ............................... 92 18. A Faulty Recording of the ECG ................................................................... 96 19. Diabetic Congestive Cardiomyopathy in Congestive Heart Failure . ............ 99 20. Silent Myocardial Ischemia ......................................................................... 101 21. RSR Pattern in I, aVL and V6 Leads .......................................................... 103 22. Inferior Wall Myocardial Infarction ............................................................ 105 23. Ventricular Tachycardia with Slow Irregular Pattern ................................... 107

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Atrioventricular Re-entrant Tachycardia: Clues to Underlying Accessory Pathway and Its Location Avinash Talele, Sagar Kabde Naresh Kumar, MK Jain Rewa, MP

Introduction The term Wolff-Parkinson-White syndrome (WPW) designates a condition comprising both pre-excitation and tachyarrhythmias.

The term paroxysmal supraventricular tachycardia (PSVT) refers to a clinical syndrome characterized by a rapid, regular tachycardia with abrupt onset and termination. Supraventricular tachycardias (SVTs) include all tachyarrhythmias that either originate from or incorporate supraventricular tissue in a re-entrant circuit.

Pre-excitation occurs in the general population at a frequency of around 0.15-0.25%.1 Of these, 50-60% of patients become symptomatic. Approximately one-third of all patients with PSVT are diagnosed as having an accessory pathway (AP)-mediated tachycardia. Patients with AP-mediated tachycardias most commonly present with the syndrome of PSVT.2 Localization of the site of AP is possible with 90% sensitivity and 99% specificity by observing delta-wave and QRS morphology in sinus rhythm.3 Detection of associated AP and its location is also possible, albeit difficult, during SVT, if attention is given to certain

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findings like QRS alternans, ST segment depression and T-wave changes.4,5

Case report A 28-year-old male patient presented to ICU with complaint of palpitation for two hours. The episode had started suddenly during rest. He remembered having similar palpitations on and off for few years which used to subside on its own.

At presentation, he was uncomfortable, anxious but hemodynamically stable. His pulse rate was 232/minute, blood pressure was 110/86 mmHg. His 12-lead ECG (Fig. 1) was recorded, which revealed SVT (AVRT) at the rate of 236/minute. RP interval was 0.08 seconds.

Figure 1. Shows AVRT with QRS alternans in lead V1 and V4 indicating underlying AP. ST segment depression in V3 to V6 is suggestive of left lateral pathway.

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QRS morphology shows QRS alternans (beat-to-beat oscillations in QRS) best seen in V1 and V4. ST segment depression in V3 to V6 and T-wave inversion in lead I and aVL was also observed. This finding indicates presence of left lateral pathway.5 Vagal maneuvers (carotid sinus massage and valsalva maneuver) were carried out. The patient did not respond to it. Intravenous adenosine terminated the SVT. Transthoracic echocardiography was normal.

Discussion The beat-to-beat oscillation of the QRS complex (QRS alternans) in lead V1 and V4 (Fig. 2) is the clue for tachycardia mediated with AP. QRS voltage and cycle length alternation can be seen during supraventricular re-entrant tachycardias, especially in atrioventricular re-entrant tachycardia (AVRT).6 QRS alternans may be present in nearly 38% of patients with circus-movement tachycardia involving AP.7 Green and co-workers reported a series of 161 patients with SVT out of which 36 had QRS alternans. Of these 36 patients, 33 had AVRT (92%), two had AVNRT and one had atrial tachycardia. Their findings indicated that the presence of QRS alternans during narrow QRS tachycardia has a specificity of 96% and a predictive accuracy of 92% for the incorporation of an accessory AV pathway in the tachycardia circuit.8 QRS alternans has been considered to be strongly suggestive of AV re-entrant tachycardia.

However, it may also occur during AV nodal re-entrant tachycardia.4 The mechanism for this is unclear. Morady and colleagues proposed that QRS alternans is largely a

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rate-related phenomenon, being observed more commonly when the rate of tachycardia exceeds 200bpm.4 It could also be caused by oscillations in the relative refractory period of the His-Purkinje system.9 Another noteworthy observation during SVT was ST segment depression in leads V3-V6 (Fig. 1). This change of ST segment in patients with PSVT with accessory pathway provides a clue to the location of accessory pathway. The location of the ST segment depression may vary with location of the AP. ST segment depression in V3-V6 is almost invariably seen with a left lateral pathway.5 This patient too had left lateral pathway as is seen in Figure 2. Other findings which suggest the location of accessory pathway include, a negative T-wave in the

Figure 2. Reveals sinus rhythm (80/minute) with short PR interval of 0.10 seconds. There is evidence of pre-excitation with left lateral accessory pathway (positive delta-wave and positive QRS in V1, isoelectric delta-wave in lead I and aVL). No ST segment changes seen.

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inferior leads which is associated with a posteroseptal or posterior pathway; and a negative or notched T-wave in V2 or V3 with a positive retrograde P-wave in at least two inferior leads suggests an anteroseptal pathway. ST segment depression may also occur during orthodromic AVRT. It may occur even in the young, who are unlikely to have coronary artery disease.

Transthoracic echocardiography revealed normal study.

Deal et al reported that it is less likely to have organic heart disease in patients with left-sided accessory pathways than in those with right-sided pathways (5% vs 45%).10

Summary Presence of QRS alternation during sustained narrow QRS tachycardia is indicative of an accessory AV pathway.

The ST segment and T-wave changes helped in locating the site of the AP. Left-sided APs are less likely to be associated with organic heart disease.

References 1. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias-executive summary. Eur Heart J 2003;24:1857-97.

2. Munger TM, Packer DL, Hammill SC, et al. A population study of the natural history of Wolff-Parkinson-White syndrome in Olmsted Country, Minnesota, 1953-1989. Circulation 1993;87(3):866-73.

3. Arruda MS, McClelland JH, Wang X, et al. Development and validation of an ECG algorithm for identifying accessory pathway ablation site in Wolff-Parkinson-White syndrome. J Cardiovasc Electrophysiol 1998;9(1):2-12.

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4. Morady F, DiCarlo LA Jr, Baerman JM, et al. Determinants of QRS alternans during narrow QRS tachycardia. J Am Coll Cardiol 1987;9(3):489-499.

5. Riva SI, Della Bella P, Fassini G, et al. Value of analysis of ST segment changes during tachycardia in determining type of narrow QRS complex tachycardia. J Am Coll Cardiol 1996;27(6): 1480-5.

6. Maury P, Raczka F, Piot C, et al. QRS and cycle length alternans during paroxysmal supraventricular tachycardia: what is the mechanism? J Cardiovasc Electrophysiol 2002;13(1):92-3.

7. Kappenberger LJ, Fromer MA, Steinbrunn W, et al. Efficacy of amiodarone in the Wolff-Parkinson-White syndrome with rapid ventricular response via accessory pathway during atrial fibrillation.

Am J Cardiol 1984;54(3):330-5.

8. Green M, Heddle B, Dassen W, et al. Value of QRS alternation in determining the site of origin of narrow QRS supraventricular tachycardia. Circulation 1983;68(2):368-73.

9. Lai WT, Voon WT, Yen HW, et al. Comparison of the electrophysiologic effects of oral sustained-release and intravenous verapamil in patients with paroxysmal supraventricular tachycardia.

Am J Cardiol 1993;71(5):405-8.

10. Deal BJ, Keana JF, Gillette PC, et al. Wolff-Parkinson-White syndrome and supraventricular tachycardia during infancy: management and follow-up. J Am Coll Cardiol 1985;5(1):130-5. ď&#x201A;&#x2014;ď&#x201A;&#x2013;

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Pseudoinfarction Pattern in a Patient with Hyperkalemia, Diabetic Ketoacidosis and Normal Coronary Vessels: A Case Report Antonios Ziakas, Christos Basagiannis, Ioannis Stiliadis Greece

Abstract

Introduction: A rare electrocardiographic finding of hyperkalemia is ST segment elevation or the so called ‘pseudoinfarction’ pattern. It has been suggested that hyperkalemia causes the ‘pseudoinfarction’ pattern not only through its direct myocardial effects, but also through other mechanisms, such as anoxia, acidosis, and coronary artery spasm. Case presentation: A 33-year-old Caucasian woman with insulin-treated diabetes presented with continuous epigastric pain of four hours duration. Her coronary heart disease risk factors apart from diabetes included hypercholesterolemia and smoking. Her initial electrocardiogram revealed ST segment elevation in the anteroseptal leads consistent with anterior myocardial infarction. Blood tests revealed hyperglycemia, hyperkalemia, metabolic acidosis and urine ketones, while a bed-side cardiac echocardiogram showed no segmental wall motion abnormality. We provisionally diagnosed diabetic ketoacidosis that was possibly precipitated by acute myocardial infarction, as there were findings in favor of (epigastric pain, electrocardiogram pattern, presence of 3 coronary heart disease risk factors) and against (young age, normal echocardiogram) the diagnosis of acute myocardial infarction. We performed cardiac angiography in order to exclude an anterior acute myocardial infarction, which could lead to myocardial damage and possible severe complications should there be a delay in treatment. Angiography revealed normal coronary arteries.

During the procedure, ST segment elevation in the anteroseptal leads was still present in our patient’s electrocardiogram results. Conclusion: ST segment elevation is a rare manifestation of hyperkalemia. In our patient, coronary spasm did not contribute to such an electrocardiography finding.

Introduction It has been reported that hyperkalemia can rarely produce abnormal ST segment elevation simulating an acute

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myocardial infarction.1-7 This electrolyte abnormality influences the electrocardiogram (ECG) not only through its direct myocardial effects, but also through other yet vaguely understood mechanisms, such as anoxia, acidosis, and perhaps impaired contractility.1,2 We present the case of a patient with diabetic ketoacidosis and hyperkalemia whose initial ECG showed a pseudoinfarction pattern, but an urgent coronary angiogram revealed normal coronary arteries.

Case presentation A 33-year-old Caucasian Greek woman presented to the emergency department of the Hospital with a continuous epigastric pain of four hours duration and intermittent vomiting. Her medical history included hypercholesterolemia and type 1 diabetes for 16 years treated with insulin injections twice daily. Our patient had omitted all insulin injections since 36 hours prior to presentation. Regarding coronary risk factors, apart from diabetes and hypercholesterolemia, she was a smoker of more than two packs of cigarettes daily.

On initial assessment she was drowsy with tachycardia (112 pulses/minute), tachypnoea (28 breaths/minute) and hypotension (85/44 mmHg). A physical examination of her abdomen had normal results. Her initial ECG revealed sinus tachycardia, ST segment elevation in the anteroseptal leads consistent with anterior myocardial infarction, and intraventricular conduction delay (Fig. 1A). A urine dipstick test detected ketones, bedside capillary testing using a glucometer showed high

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glucose concentrations, and arterial blood gas analysis indicated metabolic acidosis (pH = 7.16, carbon dioxide partial pressure = 13 mmHg, oxygen partial pressure = 123 mmHg, bicarbonate concentration = 4 mmol/L, base excess = â&#x20AC;&#x201C;24 mmol/L). We provisionally diagnosed diabetic ketoacidosis, possibly precipitated by an acute myocardial infarction.

We initially treated our patient with fluid replacement with normal saline, intravenous insulin at seven units/ hour, sodium bicarbonate, aspirin, clopidogrel, and low molecular weight heparin. Biochemical results showed the following serum concentrations: potassium = 7.2 mEq/L, sodium = 127 mEq/L, urea = 97 mg/dl, creatinine = 2.26 mg/dl, and glucose = 676 mg/dl. A bed-side cardiac ECG showed no segmental wall motion abnormality and a normal ejection fraction. As there were findings both for (epigastric pain, ECG pattern, presence of three coronary heart disease risk factors) and against the diagnosis of acute myocardial infarction (young age, normal ECG), we performed coronary angiography in order to exclude anterior acute myocardial infarction, which could lead to severe myocardial damage and possible severe complications (heart failure, among others) if treatment was delayed. During angiography, which revealed normal coronary arteries, ST segment elevation in the anteroseptal leads was still present in her ECG findings.

A repeat biochemical test after three hours showed the following values: sodium = 130 mEq/L, potassium =

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A

B

Figure 1(A) 12-lead electrocardiogram of our patient on admission showing ST segment elevation in the anteroseptal leads and intraventricular conduction delay. (B) 12-lead electrocardiogram of our patient showing a complete resolution of the anteroseptal ST segment elevation and the intraventricular conduction delay.

4.9 mEq/L, and glucose = 255 mg/dl. A repeat ECG showed a complete resolution of the anteroseptal ST segment elevation and intraventricular conduction delay (Fig. 1B). Her troponin I concentration 12 hours after admission was normal (0.1 Îźg/L). Our patient subsequently made an uneventful recovery. When she was discharged 10

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seven days after, both her ECG and biochemical results were normal.

Discussion Our patient, who had known diabetic ketoacidosis and hyperkalemia, had initial ECG findings suggestive of a myocardial infarction, but urgent coronary angiography revealed normal coronary arteries.

Although total body potassium concentrations may be considerably depleted in cases of diabetic ketoacidosis, plasma potassium concentrations at the time of presentation are usually normal or high. Acidosis, which causes potassium ions to leave the cells, as well as insulin deficiency and renal impairment, all contribute to hyperkalemia.8 Potassium concentrations above 6.0 mmol/L have been reported in 22% to 32% cases at the time of presentation.9,10 Hyperkalemia has profound effects on myocardial conduction and repolarization and hence on surface ECG. There is a peaking of the T waves and sometimes shortening of the QT interval. The ST segment may virtually disappear and become incorporated into the proximal limb of the T wave. P wave amplitude progressively diminishes and eventually disappears when serum potassium concentrations are above 7.5 mmol/L. This may lead to sinoventricular rhythm. Intraventricular conduction defect is manifested as widening of the QRS, which often resembles right bundle branch block with either a left anterior or a left posterior hemiblock.

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A sine wave pattern may occur in patients with end-stage hyperkalemia.11 A rare manifestation of hyperkalemia is ST segment elevation or ‘pseudoinfarction’.1-7 Because this pattern disappears after treatment, the term ‘dialyzable current of injury’ has been considered appropriate. It is debatable whether ST elevation is a primary repolarization abnormality or an artifact caused by the merging of the terminal R portion of the QRS with the T wave. It is possible that this electrolyte abnormality influences the ECG not only through its direct myocardial effects, but also through other yet vaguely understood mechanisms, such as anoxia, acidosis, and perhaps impaired contractility.1,2 It has also been suggested that in cases with hyperkalemia due to diabetic ketoacidosis, changes in ECG are also due to other metabolic abnormalities specific to diabetic ketoacidosis.7 It is interesting to note that severe diabetic ketoacidosis might be associated with myocardial necrosis, which might be due to an atherothrombotic process superimposed on a pre-existing coronary artery disease or coronary artery spasm.12 Furthermore, coronary spasm triggered by hyperkalemia has been suggested as a contributor to these ECG changes.13 In our case, our patient underwent urgent cardiac angiography as the diagnosis of acute myocardial infarction was not definite. This was in order to absolutely exclude an anterior acute myocardial infarction, which could lead to myocardial damage and possible severe complications. It is interesting to note 12

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that angiography showed normal coronary vessels, while the ECG had changes suggestive of anterior myocardial infarction. To the best of our knowledge, this is the first case in the literature involving pseudoinfarction pattern due to hyperkalemia, in which cardiac angiography was performed during the transient ECG changes.

Conclusions We conclude that ST segment elevation is a rare manifestation of hyperkalemia, and in our case coronary spasm did not contribute to this electrocardiography finding. However, as we only report one specific case, conclusions on the relationship between coronary spasm and hyperkalemiaâ&#x20AC;&#x2122;s pseudoinfarction pattern should not be made until further studies are done. With the current emphasis on reducing door-to-needle times for thrombolysis or primary Percutaneous Coronary Intervention (PCI) to curtail morbidity and mortality from coronary artery disease, it is worth remembering that metabolic abnormalities can sometimes alter electrocardiographic appearances. Starting thrombolysis or proceeding to urgent cardiac catheterization before metabolic abnormalities are corrected may thus expose our patient to unnecessary treatment, along with its attendant risks.

Consent Written informed consent was obtained from our patient for publication of this case report and any accompanying images.

A copy of the written consent is available for review by the Editor-in-Chief of this journal.

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Competing interests The authors declare that they have no competing interests.

References 1. Levine HD, Wanzer SH, Merrill JP: Dialyzable currents of injury in potassium intoxication resembling acute myocardial infarction or pericarditis. Circulation 1956, 13:29-36.

2. Levine HD, Merrill JP, Somerville W: Advanced disturbances of the cardiac mechanism in potassium intoxication in man. Circulation 1951, 3:889-905.

3. Cohen A, Utarnachitt RV: Electrocardiographic changes in a patient with hyperkalemia and diabetic acidosis associated with acute anteroseptal pseudomyocardial infarction and bifascicular block. Angiology 1981, 32:361-364.

4. Johnson CD: Electrocardiogram of the month: pseudo-acute myocardial infarction. Boletin Asociaciòn MÊdica de Puerto Rico 1983, 75:288-289.

5. Kamimura M, Hancock EW: Acute MI pattern in diabetic ketoacidosis. Hosp Pract 1992, 27:28-30.

6. Lim YH, Anantharaman V: Pseudomyocardial infarct electrocardiographic pattern in a patient with diabetic ketoacidosis.

Singapore Med J 1998, 39:504-506.

7. Sweterlitsch EM, Murphy GW: Acute electrocardiographic pseudoinfarction pattern in the setting of diabetic ketoacidosis and severe hyperkalemia. Am Heart J 1996, 132: 1086-1089.

8. Krentz AJ, Natrass M: Acute metabolic complications of diabetes mellitus: diabetic ketoacidosis, hyperosmolar non-ketotic syndrome and lactic acidosis. In Textbook of Diabetes Volume 39.

2nd edition. Edited by Pickup JC, Williams G. Oxford: Blackwell Sciences; 1997:1-23.

9. Van Gaal L, de Leeuw I: Hyperkalemia in diabetic ketoacidosis.

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Diabetes Care 1981, 4:576-577.

10. Beigelman PM: Severe diabetic ketoacidosis (diabetic “coma”).

482 episodes in 257 patients: experience of three years. Diabetes 1971, 20:490-500.

11. Schafroth L: An Introduction to Electrocardiography. 7th edition, London: Oxford University Press; 1990.

12. Tretjak M, Verovnik F, Vujkovac B, Slemenik-Pusnik C, Noc M: Severe diabetic ketoacidosis associated with acute myocardial necrosis. Diabetes Care 2003, 26:2959-296.

13. Pastor J, Castellanos A, Moleiro F, Myerburg R: Patterns of acute inferior wall myocardial infarction caused by hyperkalemia.

J Electrocardiology 2001, 34:53-58.

Citation: Ziakas et al., Pseudoinfarction pattern in a patient with hyperkalemia, diabetic ketoacidosis and normal coronary vessels: a case report. Journal of Medical Case Reports; 2010, 4:115.

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Door to ECG Time is 40 Minutes: Is the Doctor Negligent?

Rajiv Garg Noida

A

50-year male reported to the casualty room with chest pain. ECG was done after 40 minutes, which showed acute myocardial infarction (MI). The patient later died.

Was the doctor negligent?

Lacs of people are treated for acute heart attack in the emergency room. A growing number of patients, who have been discharged without proper diagnosis, could suffer permanent damage and even death. Studies have shown that anywhere between 2-5% of patients are being allowed to go home with undiagnosed heart attacks.

Careful evaluation of patientâ&#x20AC;&#x2122;s symptoms should be the first step to ensure an accurate diagnosis.

According to New England Journal of Medicine, patients whose symptoms are overlooked or ignored usually include young women and nonwhite patients (Indians). Women have higher rates of atypical symptom presentations and nonwhites typically have more risk factors for coronary artery disease (CAD) than whites. However, these considerations do not seem to have impacted physician practice. Patients who believed they were experiencing a heart attack would typically present a range of symptoms. Their general complaints included chest pain or discomfort, pain radiating to the jaw or arm, nausea, sweating and shortness of breath. However, many may report with only atypical symptoms including fatigue, 16

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dizziness, fainting and various gastrointestinal complaints such as indigestion, gas and abdominal pain. According to the American College of Emergency Physicians (ACEP), in the emergency department the evaluation and treatment of adults with nontraumatic chest pain begins with a thorough survey of the patient’s medical history, symptoms and a lengthy, physical exam.

At the completion of the exam, if the physician suspects a heart attack, further diagnostic and treatment interventions must be immediate: 

It is generally recommended upon the patient’s arrival to the emergency department that oxygen be administered to improve shortness of breath, which increases the oxygen delivery to the heart muscle.



Also, the standard of care mandates that an electrocardiogram or ECG be done within 10 (or no more than 20 minutes) minutes after the patient’s arrival, and medications such as nitroglycerin and morphine should be administered to help dilate heart blood vessels and decrease pain and anxiety.



Once the patient’s treatment begins, a physician must evaluate diagnostic test results to determine whether a heart attack is occurring. The most widely interpreted test to rule out MI is an ECG.



Unfortunately, emergency room physicians can easily misinterpret ECG readings. There have been independent reviews of ECG interpretations that have shown nearly half of all misdiagnosed patients could have been properly diagnosed if doctors had improved ECG reading skills.



Despite patient presentation and history differences, a 17

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leading factor in the rising rates of missed diagnosed heart attacks in emergency departments is physician’s inexperience. In cases where this has occurred, patients were typically seen by a physician with an average 2-3 years experience, versus five or more years experience where patients were correctly diagnosed.

Most of the physicians who missed the correct diagnosis were not board-certified in any specialty area of practice. The less experienced physician may be making crucial mistakes by not performing thorough history notations or down playing atypical symptom clusters associated with heart attacks.



Summary

When evaluating a suspected heart attack patient in the emergency room, the physician with good ECG reading skills, who carefully considers symptoms and pays extra attention to higher risk populations would less likely have premature discharges and would have the patient admitted for further observation. This would allow more time for an accurate diagnosis and treatment, preventing any possible tragic outcome.

Take home message

 

 

18

Emergency room doctor: Should have knowledge how to read ECGs. Emergency room should be manned by either senior resident or junior residents with 2-3 years experience.

Door to ECG time should be <20 minutes (ideal 10 minutes) Door to needle time should be <30 minutes.

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Electrocardiographic Changes in Hiatal Hernia: A Case Report Gregoriana Zanini, Giuseppe Seresini, Marco Racheli, Monica Bortolotti, Adriana Virgillo, Adriana Novali, Claudia Benetello and Gian Franco Pasini

Abstract

Italy

We describe the case of a 78-year-old woman admitted to our department for suspected silent myocardial ischemia with the evidence of T wave inversion in anterior lead. All the instrumental exams excluded inducible myocardial ischemia. A gastroscopy showed a moderate hiatal hernia. We postulate that electrocardiogram modification could be attributed to hiatal hernia.

Case presentation A 78-year-old Caucasian Italian woman was admitted to our department for suspected silent myocardial ischemia in a recent electrocardiogram (ECG) showing T wave inversion in precordial leads V1-V3 (Fig. 1). The patient had an history of hypertension in treatment with ACEinhibitors and hypercholesterolemia and she performed an ECG as a screening for hypertension; she had no history of myocardial infarction or angina pectoris, and there was no family history of ischemic heart disease.

She had exertional dyspnea for the past 1 year. On admission the patient was asymptomatic with a blood pressure of 130/85 mmHg, normal pulse heart rate in regular rhythm.

There was not significant alteration at the physical examination. Hematological exam did not show significant alteration in particular no evidence of anemia, kidney or hepatic disease. Electrolytes were normal and there wasnâ&#x20AC;&#x2122;t evidence of thyroid dysmetabolism.

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Figure 1. Electrocardiogram (ECG) showing T wave inversion in precordial leads V1-V3.

The chest X-ray showed a normal heart shadow and the ECG demonstrated sinus rhythm with T wave inversion in leads V1-V3 (Fig. 1).

Transthoracic echocardiography (TTE) revealed normal wall motion of all the left ventricle, no pulmonary hypertension and there wasn’t pericardial effusion. In addition way TTE revealed an apparent left atrial “mass” in a dilated left atrium, with its maximal size when the left atrium was imaged in a posterior plane, but smaller or absent in more anterior planes (Figs. 2 and 3).

In the doubt of a giant hiatal hernia the patient was submitted to a gastroscopy that confirmed our suspicions.

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Figure 2. Transthoracic echocardiography (TTE) apical four chamber view shows an apparent left atrial â&#x20AC;&#x153;massâ&#x20AC;? in a dilated left atrium.

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Figure 3. Transthoracic echocardiography (TTE) apical two chamber view.

Then the patient performed an exercise test that was maximal and negative for myocardial ischemia.

To confirm the diagnosis the patient was submitted to another inducible myocardial ischemia test (Dipyridamole Myocardial Perfusion Scintigraphy) also negative.

We discharged the patient with hypotensive therapy (ACE-inhibitor) and gastro protection. We re-evaluated the patient after one month and she told us a sensible reduction in exert ional dyspnea.

Discussion ECG specific abnormality in healthy women is frequent especially localized in lateral size but T wave inversion in precordial leads V1-V3 are very suspicious of ischemia also in asymptomatic women. We describe the case of a middle age women with poorly cardiovascular risk factors, asymptomatic for angina but symptomatic for dyspnea. Her ECG abnormalities was suspicious of silent ischemia but all tests made to detect inducible ischemia were negative.

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Transthoracic Echocardiography revealed a presence of a hiatal hernia like a left atrial mass that maybe the cause for these ECG abnormalities.

It was realized about 20 years ago that the sonographic appearance of a diaphragmatic hernia could simulate a left atrial mass.1 Over the last 10 years, many reports of single cases of hiatal hernia have been appeared in the cardiac echocardiography literature,2 and only few instances of cardiac compression causing serious symptoms (like syncope or dyspnea with recurrent heart failure or arrhythmia) have been reported.3-6 Hokamaki et al. described the case of a women with the same age of our women admitted for chest pain and with dynamic ST-T wave changes due to a giant hiatal hernia.

Surgical correction of the hiatal hernia restore ECG to normal.7 Sonoda et al. reported ST segment alteration during an oesophageal reconstruction surgery.8 Siu et al.,5 demonstrated how a hiatal hernia could bring recurrent heart failure.

In conclusion, there are very few cases in the literature about these ST segment alteration related to hiatal hernia but all are described in women and all in middle age women.

So we could postulate that in our case ST segment alteration and exertional dyspnea may be due to the hiatal hernia. The misdiagnosis of these pathology could make the physician to a round of complex and reiterated exams that due a sensible increase in healthy cost and sometimes to a uncorrected treatment.

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Consent

Written informed consent was obtained from the patient for publication of this case report and accompanying images.

A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors declare that they have no competing interests.

References

1. Nishimura RA, Tajik AJ, Schattenberg TT, Seward JB: Diaphragmatic hernia mimicking an atrial mass: a two-dimensional echocardiographic pitfall. J Am Coll Cardiol 1985, 5:992.

2. Khouzam RN, Akhtar A, Minderman D, Kaiser J, Dâ&#x20AC;&#x2122;Cruz IA: Echocardiographic aspects of hiatal hernia. A review. J Clin Ultrasound 2007, 35:196-203.

3. Akdemir I, Davutoglu V, Aktaran S: Giant hiatal hernia presenting with stable angina pectoris and syncope - a case report. Angiology 2001, 52:863-865.

4. Kounis NG, Zavras GM, Kitrou MP, Soufras GD, Constantinidis K: Unusual electrocardiographic manifestation in condition with increased intrathoracic pressure. Acta Cardiol 1988, 43:653-661.

5. Siu CW, Jim MH, Ho HH, Chu F, Chan HW, Lau CP, Tse HF: Recurrent acute heart failure caused by sliding hiatus hernia.

Postgrad Med J 2005, 81:268.

6. Ueda T, Mizushige K: Large hiatus hernia compressing the heart and impairing the respiratory function. J Cardiol 2003, 41:211.

7. Hokamaki J, Kawano H, Miyamoto S: Dynamic electrocardiographic changes due to cardiac compression by a giant hiatal hernia. Intern Med 2005, 44:136-140.

8. Sonoda K, Ikeda S, Seki M, Koga S, Futagawa K, Yoshitake T, Miyahara Y, Kohno S: Chest pain and ST segment Depression caused by expansion of gastric tube used for esophageal reconstruction. Intern Med 2005, 44:217-221.

Citation: Zanini et al., Electrocardiographic changes in Hiatal hernia: a case report. Cases Journal 2009, 2:8278.

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ST-T Changes in ECG AP Jain Wardha

Case history A 55-year-old male patient was operated upon for a brain tumor. The tumor was malignant in nature and had spread to various parts of the brain. A routine preoperative ECG was done as shown in Figure. He gave a history of some â&#x20AC;&#x2DC;heart diseaseâ&#x20AC;&#x2122; for more than 18 years.

He had mild palpitation and exertional dyspnea and not other symptoms.

The ECG showed very tall R waves in left ventricular leads (I, aVL and V5-V6) and deep S waves in V1-V2 with tall positive T waves. Of particular note are deep

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T inversions seen in I, II aVL and V3-V6. The QRS axis is around –10°. The other features are all normal.

These features are suggestive of severe left Ventricular hypertrophy (LVH) with systolic overload pattern or strain pattern.

The ST-T changes as seen in this ECG may be a sign of cardiomyopathy, subendocardial myocardial infarction (MI), cerebrovascular accident or increased intracranial tension, electrolyte imbalance (such as hypokalemia), etc.

Take home message This patient had proven hypertrophic obstructive cardiomyopathy (HOCM) for the past 18 years, a diagnosis that had been confirmed on echocardiography.

Hence, the pattern seen in the ECG agrees with the diagnosis except for the absence of big Q waves, which are usually seen in HOCM. The long duration of his known ‘heart problem’ for the last 18 years rules out other conditions as mentioned above as the causative condition. This case well-illustrates the significance of correlation between the clinical diagnosis and the findings on ECG. If the patient had had an acute episode suggestive of MI and previous history of a condition like hypertension, then the ECG finding may have been in agreement with LVH complicated by subendocardial MI. 

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Pneumopericardium should be Considered with Electrocardiogram Changes after Blunt Chest Trauma: A Case Report Arjan JM Konijn, Peter HM Egbers, MichaĂŤl A Kuiper

Abstract

Amsterdam, The Netherlands

Introduction: Electrocardiogram (ECG) abnormalities in patients with blunt chest trauma are diverse and non-specific, but may be indicative of potentially life-threatening conditions. Case presentation: We report a rare case of pneumopericardium with extreme ECG abnormalities after blunt chest trauma in a 22-year-old male. The diagnosis was confirmed using computed tomography (CT) scanning. The case is discussed, together with its differential diagnosis and the etiology of pneumopericardium and tension pneumopericardium.

Conclusion: Pneumopericardium should be distinguished from other pathologies such as myocardial contusion and myocardial infarction because of the possible development of tension pneumopericardium. Early CT scanning is important in the evaluation of blunt chest trauma.

Introduction When an electrocardiogram (ECG) is obtained during the diagnostic processing and evaluation of a trauma patient (as in the present case), it is important to realize that ECG findings in patients with cardiac trauma are diverse and non-specific. These findings may be non-specific ST segment or T-wave changes, axis deviation and dysrhythmias, such as premature atrial contractions, bundle branch blocks and ventricular fibrillation.1 Diagnostic considerations in a patient with blunt chest trauma and ECG abnormalities include, amongst others, myocardial contusion and myocardial ischemia. Other causes involve the presence of air in thoracic structures that do not normally contain air, for example pneumothorax, pneumomediastinum and 26

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pneumopericardium. These options are discussed in a stepwise manner and related to the patient in this case report.

Case presentation A 22-year-old male, with no previous medical history, was admitted to the intensive care unit (ICU) at our hospital with blunt thoracic trauma and near-drowning after a high-energy trauma. The man had been driving a car when, for no apparent reason, he lost control and drove into a ditch filled with water.

The patient consequently aspirated water, but managed to reach solid ground. He was transported by ambulance to the hospital emergency unit, where he was found to be in respiratory failure, probably as a result of severe lung contusion. He was subsequently intubated and mechanically ventilated. During the first few days of admission, pressure-controlled ventilation was used with relatively high ventilator settings. During the first hours after admission these settings were a positive end-expiratory pressure level of 18 cm H2O, inspiratory pressure level of 13 cm H2O, a fractional inspired oxygen level of 60% and a respiration frequency of 30 cycles per minute. No recruitment maneuver was performed. A central venous line was inserted into the right femoral vein. Other than fractures of the left clavicle and superficial hematomas, there were no abnormalities on physical examination of the thorax. In particular, no asymmetrical pulmonary auscultation, subcutaneous emphysema or abnormal heart sounds were present. Chest radiography and a 12-lead ECG were performed on admission (Fig. 1).

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No significant abnormalities were observed at the time, but shortly thereafter, the ECG showed ST-depression in leads II, III, aVF and V3 and V4. No major hemodynamic problems occurred, and the creatine phosphokinase and accessory MB-fraction indicated only a loss of skeletal muscle. However, extreme ECG abnormalities developed during the following hours (Figs. 2 and 3). CT scanning of the thorax, performed approximately 12 hours after admission, showed a pneumopericardium, as well as pneumomediastinum and bilateral pneumothorax (Fig. 4). Severe lung contusion and hematothorax were also apparent on these images.

Transesophageal echocardiography (TEE) was performed after transthoracic echocardiography had failed to deliver the required image quality. TEE did not identify any wall motion abnormalities, and the accident appeared to have had no abdominal or cerebral repercussions.

Both the pneumothorax and pneumopericardium resolved after the insertion of a left-sided chest tube. The right-

Figure 1. ECG performed on admission.

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Figure 2. ECG showing the most striking abnormalities. Interestingly, there is no change in QRS amplitude, frequently seen in pericardial tamponade.

Owing to technical problems, lead V2 is absent.

Figure 3. ECG performed shortly after drainage. The remaining abnormalities resolved completely in approximately 12 h. Owing to technical problems, lead V2 is absent.

sided pneumothorax resolved spontaneously, after which the patient made a rapid recovery and was discharged from the ICU on day 5. He was discharged from hospital five days later, having made a complete recovery.

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Discussion In this case, a likely differential diagnosis was myocardial contusion, which has a broad variety of presenting symptoms, the most frequent being precordial pain which is not relieved by analgesia. In addition to ECG changes, other Figure 4. CT scan, transversal view, showing pneumothorax, findings include dyspnea, pneumomediastinum and pneumopericardium. Hematothorax is present at peri cardial friction rub, the time of scanning. pulmonary rales and an elevated central venous pressure. This complex of symptoms may mimic those of acute coronary syndrome, although symptoms may also be completely absent. Myocardial contusion can be diagnosed using echocardiography, as this imaging modality visualizes the actual contusion as well as changes in cardiac chamber size, wall motion abnormalities and the presence of cardiac tamponade.2 Echocardiography was performed on this patient after pneumopericardium had been diagnosed. Although cardiac contusion might easily have coexisted, none of the aforementioned abnormalities were seen. In such a situation it is important to recognize the inferior diagnostic quality of transthoracic echocardiography compared with TEE. Acute coronary syndrome was unlikely to occur in this patient because he was young and had no predisposing medical history, such as angina.1 However, even in 30

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young people traumatic myocardial infarctions have been reported that can result from acute thrombotic coronary occlusion, intimal tears and vessel rupture.3 As mentioned above, the cardiac enzyme profile indicated a loss of skeletal muscle, with serial measurements of CK and accessory MB-fraction showing peak levels of 2,600 and 29 U/l, respectively. Unfortunately, the level of troponins, which has been shown to be more useful in detecting myocardial injury than CK and CKMB over the past decade, was not measured.4 Nonetheless, it was concluded that significant myocardial contusion or infarction was highly unlikely.

The presence of extraluminal air is a frequent complication in cases of blunt thoracic trauma, because the differing electrophysiological behavior of air can cause the ECG to change frequently. The incidence of pneumothorax in this population is approximately 40%, while that of pneumomediastinum may be as high as 10%.5,6 Pneumopericardium, however, is rare and, to the best of the authorsâ&#x20AC;&#x2122; knowledge, no incidence rates have been recorded. Neither have any clinical trials been conducted on trauma patients in which this pathological entity is described.

Traumatic rupture or penetration of the alveoli, pleurae and/or thoracic wall by fractured ribs may result in pneumothorax. In addition, tracheobronchial tears may cause pneumothorax, as well as pneumomediastinum, although this depends on the localization of the lesion with respect to the position of the pulmonary ligament.

Pneumothorax or pneumomediastinum occurs when the lesion lies distal or medial, respectively, to the 31

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pulmonary ligament. Other conditions that may lead to pneumomediastinum include esophageal disruption and direct communication of the mediastinum with the pneumothorax. However, in the majority of cases pneumomediastinum results from alveolar rupture and/or positive-pressure mechanical ventilation. Initially, air leaks from the lumen of the lung and then travels along the peribronchovascular sheaths, dissecting in a medial direction and resulting in mediastinal air. This mechanism, which is known as the Macklin effect, was first described more than 65 years ago.6,7 In the event of pneumopericardium, the Macklin effect is once again the major cause, although higher intrathoracic pressures are required; however, as these conditions share etiology, it is not surprising that high intrathoracic pressures are often accompanied by pneumomediastinum. It is most likely that air enters the pericardial sac along the venous sheaths, where the collagenous support of the pericardial reflections is weaker.8 Understandably, it may take some time for a clinically relevant pneumopericardium or pneumomediastinum to be revealed. The pericardial space may also be connected directly to pleural or tracheobronchial gases as a consequence of pericardial tear.

Brander et al.9 reviewed previous reports on pneumopericardium which described symptoms such as chest pain, dyspnea, palpitations, distant heart sounds, shifting precordial tympani, mill wheel murmur and different ECG findings such as ST depression/elevation, T-wave inversion and low voltages. However, as these authors stated, none of these was specific.9 32

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Options for the diagnosis of pneumopericardium, pneumothorax and pneumomediastinum include plain chest radiography, ultrasound and CT scanning. In trauma patients (such as the case reported here), CT scanning is the most appropriate imaging modality.

Previous reports have described pneumopericardium in very diverse circumstances such as laparoscopy, in fistula formation between the esophagus or bronchus owing to cancer or ulceration, in barotrauma in women who are in labor or during delivery, and in purulent pericarditis.9 Imaging modalities other than CT scanning may be more appropriate, depending on the individual case.

Pneumopericardium is usually self-limiting and resolves spontaneously, but may require intervention such as drainage of the accompanying pneumothorax. Notably, complications such as tension pneumopericardium are described in up to 37% of reported cases. In this situation a pressurized compartment is created by the one-way valve principle, and possibly worsened by mechanical ventilation. This in turn may lead to a lifethreatening cardiac tamponade, requiring emergency pericardiocentesis or surgery.10 In the reported patient, the ECG changes occurred after emergency department evaluation and ICU admittance. No abnormalities were seen on plain chest radiography taken on admission, while CT scanning revealed pneumothorax, pneumomediastinum and pneumopericardium. These three entities, but predominantly pneumopericardium, are the most likely explanation for the extreme ECG changes. Pneumopericardium and pneumomediastinum most likely occurred at the trauma and worsened 33

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during mechanical ventilation, as the ECG abnormalities became more impressive as time progressed, and highpressure mechanical ventilation was used. There was no indication for the presence of tension pneumopericardium, as no major hemodynamic problems had occurred.

Drainage of the pneumothorax led to a resolution of the pneumopericardium and pneumomediastinum, which in turn resulted in a rapid normalization of the ECG. High-energy blunt chest trauma with bone fractures should heighten the suspicion of intrathoracic organ lesions. CT scanning is the preferred imaging modality in trauma patients, and should be performed at an early stage to exclude pneumothorax, pneumomediastinum, pneumopericardium, hematothorax and lesions of any intrathoracic structures such as aortic dissection.

However, as many of these entities may develop and become clinically relevant within a few hours of the initial trauma, it is important to perform regular reassessments.

ECG is a primary aid in this process as it not only assists in indicating ischemic and traumatic myocardial damage but also identifies potentially life-threatening conditions such as pneumothorax, pneumomediastinum and pneumopericardium.

Conclusion This report describes a rare case of pneumopericardium with extreme ECG abnormalities after blunt chest trauma. This condition should be distinguished from other pathologies such as myocardial contusion and myocardial infarction because of the possible development of tension pneumopericardium. Early CT scanning and frequent 34

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clinical reassessments are important in the evaluation of blunt chest trauma.

Competing interests The author(s) declare that they have no competing interests.

Consent Written informed consent was obtained from the patient for publication of this case report and any accompanying images.

A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Acknowledgements The authors wish to thank Jeanine Mysliwiec for revising the manuscript to correct imperfections in the written English.

References 1. Plautz CU, Perron AD, Brady WJ: Electrocardiographic ST segment elevation in the trauma patient: acute myocardial infarction vs. myocardial contusion. Am J Emerg Med 2005, 23:510-516.

2. Bansal MK, Maraj S, Chewaproug D, Amanullah A. Myocardial contusion injury: redefining the diagnostic algorithm. Emerg Med J 2004, 22(7):465-469.

3. Zajarias A, Thanigaraj S, Taniuchi M: Acute coronary occlusion and myocardial infarction secondary to blunt chest trauma from an automobile airbag deployment. J Invasive Cardiol 2006;18: E71-E73.

4. Collins JN, Cole FJ, Weireter LJ, Riblet JL, Britt LD: The usefulness of serum troponin levels in evaluating cardiac injury.

Am Surg 2001, 67:821-825.

5. Rowan KR, Kirkpatrick AW, Liu D, Forkheim KE, Mayo JR, Nicolaou S: Traumatic pneumothorax detection with thoracic US: correlation with chest radiography and CT-initial experience.

Radiology 2002, 225:210-214.

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6. Wicky S, Wintermark M, Schnyder P, Capasso P, Denys A: Imaging of blunt chest trauma. Eur Radiol 2000, 10:1524-1538.

7. Macklin CC: Transport of air along sheaths of pulmonic blood vessels from alveoli to mediastinum. Clinical implications. Arch Intern Med 1939, 64:913-926.

8. Mansfield PB, Graham CB, Beckwith JB, Hall DG, Sauvage LR. Pneumopericardium and pneumomediastinum in infants and children. J Pediatr Surg 1973, 8:691-999.

9. Brander L, Ramsay D, Dreier D, Peter M, Graeni R: Continuous left hemidiaphragm sign revisited: a case of spontaneous pneumopericardium and literature review. Heart 2002, 88:5.

10. Haan JM, Scalea TM: Tension pneumopericardium: a case report and a review of the literature. Am Surg 2006, 72:330-331.

Citation: Konijn et al.; Pneumopericardium should be considered with electrocardiogram changes after blunt chest trauma: a case report. Journal of Medical Case Reports, 2008, 2:100.

ď&#x201A;&#x2014;ď&#x201A;&#x2013;

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Persistent ST-T Changes in Inferior Leads Amit Rai New Delhi

Case history

A 49-year-old male was referred for a coronary angiogram.

He had irregular pulse, dyspnea on exertion and angina.

He had a past history of a myocardial infarction (MI) about three years back. Angiography showed 3-vessel disease with poor LV function with ejection fraction = 30%. The patient was discharged on medications as he was considered not fit for surgery. The ECG taken on the day of angiography is shown in Figure.

Inverted P, QRS and T waves in lead I are findings that are immediately noticeable. All these waves are upright in lead aVR. The waves are all negative in aVL lead.

These changes, in particular, inverted â&#x20AC;&#x2DC;Pâ&#x20AC;&#x2122; waves in lead

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I suggest dextrocardia. But the normal progression of the ‘R’ waves from VI-V5 rules out this diagnosis. This technical dextrocardia occurred due to the common technical fault - accidental switching of leads between the right arm and the left arm. However, one should not miss the changes of pathological ‘Q’ with a small ‘R’ and inverted ‘T’ waves in leads II, III, aVF that indicate a probable recent inferior wall MI of undetermined age (probably recent). Inverted ‘T’ waves in V6 indicate lateral wall ischemia. Upright ‘T’ waves in VI-V3 may signify reciprocal changes to ‘T’ inversions in II, III and aVF.

Take home message The patient had severe coronary artery disease as confirmed by coronary angiography. The LV function was also poor. Due to akinesia of inferior, apical and anterior walls of the LV, surgery was advised against.

The persistent ST-T changes several years after MI in inferior leads suggest an aneurysm or akinesia, but angiography showed no aneurysms. In ‘technical dextrocardia’, there is usually switching of right and left arm leads; nevertheless, aVF is not affected. The ECG herein shows changes of MI, which should not be missed, in aVF and therefore II (aVF-aVR) and II (aVF-aVL). The lateral wall ischemia is manifested by ‘T inversions in V6. 

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QT Interval Prolongation after Sertraline Overdose: A Case Report Rudolf A de Boer, Tonnis H van Dijk, Nicole D Holman, Joost P van Melle Groningen, The Netherlands

Abstract

Background: Selective serotonin reuptake inhibitors (SSRIs) are the most common antidepressants used in first-world countries and are generally well tolerated. Specifically, less cardiovascular toxicity has been reported in comparison with tricyclic antidepressants. Here we report QT interval prolongation after an overdose of the SSRI sertraline. Case presentation: A previously healthy female patient presented with an attempted suicide with overdoses sertraline (2250 mg), diazepam (200 mg), and temazepam (400 mg). Routine laboratory studies were normal and her ECG upon admission showed a normal QT interval. The next day, her ECG showed prolongation of the QTC interval up to 525 ms. After discontinuation of sertraline the QT interval normalized. Echocardiography and exercise electrocardiography were normal. After hospitalization, the patient resumed sertraline in the normally recommended dose and QT interval remained within normal ranges. Conclusion: It seems that the SSRI sertraline in overdose may cause QT interval prolongation.

Background Since their introduction in 1987, the use of Selective Serotonin Reuptake Inhibitors (SSRIs) has increased dramatically.1 They clearly have a more favorable safety profile compared to tricyclic antidepressants,2 although prolongation of the QT interval has been reported as a side effect.3 This is an important side effect since prolongation of the QT interval is strongly associated with life-threatening arrhythmias, most notably torsades de pointes. Although sertraline belongs to the same class of antidepressants, controversy persists whether this holds true for the SSRI sertraline.4 Here we here present 39

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a patient with prolonged QT interval after sertraline overdose.

Case presentation A 40-year-old female patient was referred to our emergency department because of an intended overdose with 200 mg diazepam, 400 mg temazepam, and 2250 mg sertraline.

Her main complaints were fatigue and drowsiness. Blood pressure, pulse rate, and auscultation of the heart and lungs were normal. The patient was treated with sodiumsulfate and charcoal and was admitted to the intensive care unit for continuous control of vital signs. Routine laboratory studies (hematology, chemistry) were normal.

Plasma levels of diazepam and temazepam were elevated, 1155 ugr/l (normal: 125-750 ugr/l) and 1710 ugr/l (normal: 300-900 ugr/l, respectively). Plasma levels of sertraline and desmethylsertraline were 174 ug/l (normal 20-55 ug/l5) and 276 ng/l, respectively.

Her ECG upon admission (upper panel of the figure) shows a sinus rhythm (77 b.p.m.) without conduction disturbances. QT interval in lead V2 was 370 ms. We used the Bazett method (QT time divided by the square root of the RR interval) to calculate the corrected QT (QTC) QTC at admission was 420 ms and negative T waves were found in leads V1-V3. A second ECG, taken one day after admission (lower panel of the figure), showed a markedly prolonged QT interval with deepened negative T waves in leads V140

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Figure 1. ECGs of the patient. ECG of the patient upon admission (upper panel) shows a normal sinus rhythm with a QT interval in lead V2 of 370 ms (QTC 420 ms). There were negative T-waves in leads V1-V3. A second ECG was obtained one day after admission (lower panel) shows a markedly prolonged QT interval of 520 ms in V2 (QTC 525 ms).

V3. QT interval was 520 ms in V2, at a heart rate (HR) of 63 b.p.m. (QTC 525 ms). An old ECG (August 2002) showed a sinus rhythm with a HR of 63 b.p.m. and a QT interval in lead V2 of 370 ms (QTc 373 ms; ECG not shown).

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After 4 days the patient was discharged to a psychiatric hospital because the risk for another suicide attempt was deemed high by the psychiatric consultant. After discharge, the patient underwent further out-patient cardiac evaluation. Echocardiography revealed no structural heart disease. On exercise electrocardiography, patient reached 88% of her maximum HR - no abnormal ST segment changes were observed. Hereafter, the use of sertraline was resumed in a dose of 50 mg twice daily under guidance of her psychiatrist. Control ECG revealed a normal QT interval (not shown).

Discussion We here present a patient with prolonged QT interval associated with sertraline overdose. An acquired cause of QT prolongation was suspected since QT intervals had been normal on admission, about 3 hours after ingestion of 2250 mg of sertraline (11 times the maximum recommended dose of 200 mg/day), and were markedly prolonged after one day in hospital. The QT interval normalized after sertraline withdrawal. Therefore, a temporal relation existed between the overdose of sertraline and the development of QT prolongation. However, other causes for QT prolongation, both acquired and inherited, must be considered. For example, combinations of psychoactive drugs have been shown to cause prolongation of the QT interval,6 and our patient ingested temazepam as well as nitrazepam in overdose.

Whereas previous clinical studies7-10 did not reveal 42

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any QT prolongation as a side-effect of sertraline, this case report suggests it may have this potential. We

are aware of 1 additional report by Amin et al11 who described â&#x20AC;&#x2DC;a clinically significantâ&#x20AC;&#x2122; increase in QT interval after treatment with 200 mg of sertraline, however

the magnitude of QT prolongation was not specified.

Naturally, implications of this finding are limited because it is only a single case. Two other limitations deserve

comment. First, we did not perform a rechallenge with

high dosage of sertraline, since this would be unethical.

Second, only one blood sample was taken to assess plasma concentration of sertraline - the sertraline plasma level

was found clearly increased according to other reports.5,12

It was therefore not possible to investigate the relation between the course of QT interval prolongation and their paralleled serum levels of sertraline

Conclusion Our observation suggests that the SSRI sertraline may have the potential to prolong QT interval in rare cases.

This case underscores the need for continuous post marketing surveillance.

List of abbreviations HR heart rate LV left ventricular QTc Corrected QT interval SSRI selective serotonin reuptake inhibitor

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References 1. Meijer WE, Heerdink ER, Leufkens HG, Herings RMC, Egberts ACG, Nolen WA: Incidence and determinants of long-term use of antidepressants. Eur J Clin Pharmacol 2004, 60:57-61.

2. Kelsey JE, Nemeroff CB: Selective serotonin reuptake inhibitors: introduction and overview. In Kaplan and Sadockâ&#x20AC;&#x2122;s Comprehensive Textbook of Psychiatry 7th edition. Edited by: Sadock BJ, Sadock VA. Philadelphia: Lippincott Williams & Wilkins; 2000: 2432-2435.

3. Al-Khatib SM, LaPointe NM, Kramer JM, Califf RM: What clinicians should know about the QT interval. JAMA 2003, 289:2120-2127.

4. Gillespie JA, Clary CM: Medications that prolong the QT interval.

JAMA 2003, 290:1025. (letter) 5. [ h t t p : / / w w w. m d b r o w s e . c o m / D r u g i n f / S / s e r t r a l i n e . htm#Sertraline].

6. Sala M, Vicentini A, Brambilla P, Montomoli C, Jogia JR, Caverzasi E, Bonzano A, Piccinelli M, Barale F, De Ferrari GM: QT interval prolongation related to psychoactive drug treatment: a comparison of monotherapy versus polytherapy. Ann Gen Psychiatry 2005, 4:1.

7. Isbister GK, Bowe SJ, Dawson A, Whyte IM: Relative toxicity of selective serotonin reuptake inhibitors (SSRIs) in overdose.

J Toxicol Clin Toxicol 2004, 42:277-285.

8. Fisch C, Knoebel SB: Electrocardiographic findings in sertraline depression trials. Drug Invest 1992, 4:305-312.

9. Fabre LF, Abuzzahab FS, Amin M, Claghorn JL, Mendels J, Petrie WM, Dube S, Small JG: Sertraline safety and efficacy in major depression: a double-blind fixed-dose comparison with placebo.

Biol Psychiatry 1995, 38:592-602.

10. Glassman AH, Oâ&#x20AC;&#x2122;Connor CM, Califf RM, Swedberg K, Schwartz P, Bigger JT Jr, Krishnan KR, van Zyl LT, Swenson 44

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JR, Finkel MS, Landau C, Shapiro PA, Pepine CJ, Mardekian J, Harrison WM, Barton D, Mclvor M, Sertraline Antidepressant Heart Attack Randomized Trial (SADHEART) Group: Sertraline treatment of major depression in patients with acute MI or unstable angina. JAMA 2002, 288:701-709.

11. Amin M, Lehmann H, Mirmiran J: A double-blind, placebocontrolled dose-finding study with sertraline. Psychopharmacol Bull 1989, 25:164-167.

12. Preskorn SH: A tale of two patients. J Pract Psych Behav Health 1999:160-164 [http://www.preskorn.com/columns/9905.html.].

Citation: de Boer et al.; QT interval prolongation after sertraline overdose: a case report. BMC Emergency Medicine 2005, 5:5.

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Complete Heart Block in Pregnancy MB Bellad, JC Shravage, HA Dhumale, PC Halkati, Mamatha K Belgaum

Abstract

Heart block during pregnancy is usually congenital. Patients with complete heart block may remain asymptomatic during pregnancy and have an uncomplicated labor and delivery without treatment.

Introduction Complete heart block in pregnancy is a relatively rare and potentially serious problem.1 The first case was reported in 1914 by Nanta and to date more than 100 cases have been documented.2 Heart block may be congenital or acquired secondary to cardiac surgery, rheumatic heart disease or infective disorder.3 Heart block, whether congenital or acquired, rarely causes any special obstetric problems.4 This report describes a case of congenital complete heart block in pregnancy and its successful outcome after cesarean section and cardiac pacemaker insertion.

Case report A 20-year-old, primigravida married for one and a half years was referred to the outpatient department of obstetrics and gynecology with history of eight months amenorrhea and complete heart block which was recognized at 7th month of pregnancy. There was no history suggestive of heart disease, no history of taking any drugs and no family 46

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Echocardiogram and 2D Doppler report. history of heart disease. Her pulse rate was 38/min and regular; blood pressure 120/80 mmHg; there was no pallor, edema or cyanosis. Cardiovascular system revealed no abnormality, respiratory system was clear. On abdominal examination there was a singleton pregnancy, with cephalic presentation, with the uterus corresponding to 32 weeks, relaxed and fetal heart rate 130/min. Her hemoglobin was 10.8 g/dl, blood group â&#x20AC;&#x2DC;Aâ&#x20AC;&#x2122; positive, FBS 77 mg/dl, urine routine normal, electrocardiogram showed escape rhythm with ventricular rate 30-40/min with narrow 47

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Echocardiogram and 2D Doppler Report 2D measurements M-mode

Others

M-mode

LV study

M-mode

LV study

AVCS

1.76 cm

IVSd

0.75 cm

LVVd Teich

81.51 cm3

AoRoot

2.66 cm

IVSs

1.00 cm

LVVs Teich

24.83 cm3

LA D

3.61 cm

LVIDd

4.27 cm

SV Teich

56.68 cm3

LA/Ao

1.36

% FS

38.82%

LVd MassASE

104.4 g

EF Teich

69.54%

LVs MassASE

70.39 g

LVIDs

2.61 cm

LVPWd

0.85 cm

LVPWs

1.05 cm

Mitral valve Doppler

Aortic valve Doppler

MVpeakV

1.32 m/s

AVpeakV

1.92 m/s

MVmeanV

0.67m/s

AVpeakPG

14.74 mmHg

MVpeakPG

6.96 mmHg

MVmeanPG

2.49 mmHg

Tricuspid valve Doppler TVpeakV

Pulmonic valve Doppler 1.02 m/s

PVpeakPG

9.60 mmHg Contâ&#x20AC;&#x2122;d...

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... Contâ&#x20AC;&#x2122;d

TVmeanV

0.54 m/s

TVpeakPG

4.17 mmHg

TVmeanPG

1.60 mmHg

PVpeakV

1.55 m/s

Comments Impression: Normal resting LV function No regional wall motion abnormality IAS and IVS intact Trivial MR Normal PA pressure

Electrocardiogram

QRS complexes. 2D echo and color Doppler showed normal resting left ventricular function, no regional wall motion abnormalities, trivial mitral regurgitation and normal pulmonary artery pressure. Ultrasound showed a single, live, intrauterine gestation corresponding to her dates with adequate liquor, placenta fundoposterior and no fetal anomalies were seen. Patient was advised for temporary pacemaker at the time of delivery and permanent pacemaker after delivery.

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Patient came for regular follow-up visits and was admitted in active phase of labor at 39 weeks of gestation.

She had no other symptoms at the time of admission.

A temporary pacemaker insertion was done under local anesthesia with an antibiotic cover. Patient was taken for emergency lower segment cesarean section for failure to progress under spinal anesthesia and delivered a male baby weighing 3.25 kg. Her postpartum period was uneventful. A permanent pacemaker was inserted five days after surgery with pulse rate of 82/min and was discharged on 5th day.

Discussion Heart block during pregnancy is usually congenital.

Patients with complete heart block may remain asymptomatic during pregnancy and have an uncomplicated labor and delivery without treatment.4 Symptoms may be as following: Fatigue, dizziness, lightheadedness and syncope. Signs are profound bradycardia which may be seen during pregnancy for a number of other reasons like hyperkalemia, hypothyroidism or medications such as β-blockers, calcium channel blockers or digitalis.3 Cannon â&#x20AC;&#x2DC;aâ&#x20AC;&#x2122; waves may be observed intermittently in the jugular venous pulsations when the right atrium contracts against a closed tricuspid valve due to atrioventricular dissociation.4

Effect of complete heart block on pregnancy and management Women with congenital complete heart block may tolerate pregnancy well. Labor can be complicated by syncope and 50

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6D

Fetal measurements BPD

67.1 mm

27 w

0

D

CI

89%

HC

245 mm

26 w

4

D

FL/BPD

74%

OFD

82.5 mm

—

—

D

FL/AC

24%

AC

208 mm

25 w

3

D

FL/HC

20%

FL

49.6 mm

26 w

5

D

HC/AC

1.18%

26 W

8D

Average size (AVA) EDD (AVA) 02/03/04

EFW 888 ± 133 g

EDD (LMP) 28/02/04

FHR (BPM) 140

Gestation

Seegle

Presentation

Vertex

Placenta

Anteria

PL Grade

0

Amniotic fluid

Adeglate

Anatomy survey Kidneys

Left

N

Extremities

Right N N

Spinf

N

4-Chamber heart

N

Lat. Ventricle

N

Anomalies: Nil Comments: Nil IMP: Low side fetus 26 w 3D

convulsions due to slowing of the heart rate during the Valsalva maneuver, which may occur during forceful uterine contractions in the second stage of labor.5 It is preferable to deliver these women in a lateral decubitus position and minimize the bearing down by prophylactic forceps. As volume shifts and blood loss are greater in those undergoing cesarean section these procedures should be performed only for the obstetric indications.1 Complete heart block in patients with Ultrasonography 51

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prolonged QT interval or left atrial enlargement on electrocardiogram, has a higher incidence of sudden death and therefore insertion of prophylactic pacemaker is recommended.1,5 For symptomatic patients in the first and second trimester, permanent pacemaker implantation is the therapy of choice and it can be performed under echocardiographic control. In symptomatic patients who present at or near term, temporary pacing followed by the induction of labor at the earliest possible time is suggested to prevent complications of prolonged temporary pacing.1,5 Improvement of atrioventricular nodal conduction during two successive uncomplicated pregnancies in a patient with congenital heart block has been reported.

Symptomatic patients with complete heart block have been treated during pregnancy, with either temporary or permanent pacemaker and numerous pregnancies have been reported in patients after pacemaker implants.1

References 1. Avasthi K, Gupta S, Avasthi G. An unusual case of complete heart block with triplet pregnancy. Indian Heart J 2003;55:641-2.

2. Jaffe R, Gruber A, Fejgin M, et al. Pregnancy with an artificial pacemaker. Obstet Gynecol Surv 1987;42:137-9.

3. Josephson ME, Marchlinski FE, Buxton AE. In: Harrisonâ&#x20AC;&#x2122;s Principles of Internal Medicine. 12th edition 1991:907­â&#x20AC;&#x2018;8.

4. Perloff JK, Braunwald MD. In: Heart Disease. 6th edition, Zipes, Libby (Eds.) Philadelphia: WB Saunders Company, 2001.

5. Dalvi BV, Chaudhuri A, Kulkarni HL, et al. Therapeutic guidelines for congenital complete heart block presenting in pregnancy.

Obstet Gynecol 1992;79:802-4.

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Differential Diagnosis of Complete Heart Block HK Chopra New Delhi

Case history A 38-year-old man presented to his family physician with fever. Examination of the patient revealed a slow heart rate. An ECG was taken which is shown in Figure. The patient gave no history of any illness earlier. He also had no symptoms related to the cardiovascular system. He did not complain of giddiness or syncope at anytime.

The ECG findings of a slow ventricular rate of around 45/min; comparatively faster but variable atrial rate of around 95/min and variable P-R intervals confirm the diagnosis of complete heart block. The narrow QRS complexes also support this diagnosis. Variable height of R waves in the same lead (clearly visible in the rhythm

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strip shown in Figure) is another interesting finding on the ECG. The rather taller R waves usually may be due to the superimposition of the independent P waves.

Plotting the P waves, starting with any two consecutive clearly visible P waves can easily show this.

Take home message The complete heart block in this patient is likely to be congenital in nature. But, the ventricular rate is slower than the usual rate for congenital complete heart block.

The heart rate increased to around 60/min after administration of 1.2 mg atropine intravenously suggesting congenital complete heart block. Keeping in view the fact that the patient was asymptomatic as regards the complete heart block and resided in a city, a close follow-up was recommended; a permanent pacemaker was not advised. A pacemaker needs to be implanted if the patient develops symptoms like giddiness or syncope. This approach is in contrast to that adopted in acquired complete heart block which requires implantation of permanent pacemaker even if the patient is asymptomatic because sudden death is not uncommon in these patients. Sinus arrhythmia explains the variability of P-P interval. ď&#x201A;&#x2014;ď&#x201A;&#x2013;

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A Case of COPD with Cor Pulmonale V Anand New Delhi

Case history A 44-year-old male, a nonsmoker presented to the hospital with severe dyspnea and orthopnea. Examination showed the patient to be acutely, ill with signs of peripheral cyanosis and chronic obstructive pulmonary disease (COPD) with bilateral wheeze over the chest. The rest of the history, including past history, was not significant.

His ECG is shown in Figure.

Abnormal right axis deviation (QRS axis = +16(J) as depicted by dominant ‘S’ in lead I and II and dominant ‘R’ in aVR. There is a right atrial enlargement as seen by peaked ‘P’ waves especially in lead II measuring 3.5 55

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mm, as QR pattern in V1 with ST-T depression from V1-V4 which indicates severe RVH of systolic overload type. There are deep S waves (in fact S > R) in all chest leads except V1.

Take home message The major signs and symptoms were severe dyspnea with peripheral cyanosis. A past history was negative for heart disease. The patient was a proven case of COPD with cor pulmonale.

Presence of abnormal right axis deviation, RAE and severe RVH fits in with the diagnosis of cor pulmonale.

The clockwise rotation seen by deep ‘S’ waves upto V6 is also in accord with the diagnosis of RVH in cor pulmonale. As there is no LAE, this excludes any left heart disease with pulmonary hypertension.

A clockwise rotation and continuation of the QR pattern (or dominant ‘R’ pattern) from V1 to left-sided leads is usually seen in isolated pulmonary valve stenosis or primary pulmonary hypertension, which is not evident in this case. Deep ‘S’ waves in all chest leads except V1 provide the most vital clue to the diagnosis of COPD and cor pulmonale. The deep ‘S’ waves are due to the downward displacement of the heart in emphysema and cor pulmonale. The result is dominant negative complexes as the depolarization of the ventricles will tend to go away from the normally placed chest leads all of which are above the downwardly displaced heart.

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Electrocardiographic Changes in a Rare Case of Flecainide Poisoning: A Case Report Andrea Rognoni, Marzia Bertolazzi, Marzia Peron, Sergio Macciò, Gemma Ternavasio Cameroni, Angelo Gratarola, Giorgio Rognoni Verceli, Italy

Abstract

Flecainide is a class IC antiarrhythmic drug with sodium channel blocking activities. We report a case of a 57 year-old woman who attempted a suicide by ingesting approximately 1.8 g of flecainide. On the surface electrocardiogram this results in a large QRS complex and in prolongation of the QTc interval.

Overdose with a class IC drug is very uncommon, its management is difficult and the mortality high. Because of a hemodynamic instability and in addition to supportive care and antidysrhythmics, she was treated with a high dose of sodium bicarbonate in hypertonic solution; after this infusion the patientâ&#x20AC;&#x2122;s QRS progressive narrowed. In conclusion, sodium bicarbonate may be useful in the treatment of widened QRS and to stabilize a overdose of class IC anti-arrhythmic drugs.

Introduction Flecainide is a Vaughn-Williams class IC antiarryhthmic agent used for the treatment of supraventricular and, also, ventricular arrhythmias.

In some countries, such as United states, its use is limited because of known proarrhythmic effects.1 Chemically, it causes a rate-dependent slowing of a rapid sodium channels slowing phase of depolarization.2 Flecainide, also, slows conduction in all cardiac fibers, increasing conduction times in the atria, ventricles, atrioventricular node and His-Purkinje system and can cause myocardial depression. Flecainide is cleared mainly by the liver at a relatively high rate (5.6 ml/kg per minute) but its large value of distribution (4.9 ml(kg)) yields a large half-life 57

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of 11 hours.3 Oral loading-dose 50 of flecainide is 50-498 mg/kg in rat; it is extensively metabolized mainly to m-Odealkylated flecainide and the m-O-dealkylated lactam of flecainide; the first makes up to 20% of the drugâ&#x20AC;&#x2122;s antiarrhythmic activity. Furthermore flecainide is excreted mainly in urine (about 10 to 50% as the unchanged drug and the remainder as metabolites, depending on type of administration; about 5% is excreted in feces).

Flecainide is a rare cause of suicide attempt by drug overdose; furthermore there are not specific antidote and no way of rapidly eliminating the drug from the body.4 Commonly recommended therapies, including hemodialysis (in this case we can remove only 1% of unchanged flecainide), treatment with hypertonic saline solution and pacing, have not been shown to improve survival. In the literature we find also some anecdotal case report of particularly therapy used to treat flecainide overdose. Timperly et al,5 in 2005, reported a case complicated by cardiogenic shock and treated with pharmacological inotropic support and intra-aortic balloon pump; in 48 hours both QRS and ventricular function had returned to normality.

Yasui et al,6 described, in a young woman, another possible approach such as peripheral cardiopulmonary bypass support (CBS) to maintain perfusion of the liver; this CBS successfully supported the patient until flecainide level decreased as a result of redistribution and normal clearance mechanisms. We report a case of flecainide poisoning which was successfully treated with high dose of sodium bicarbonate in hypertonic solution.

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Case report A 57 year-old women with a history of previous supraventricular tachyarrhythmia and chronic therapy with flecainide acetate (100 mg every day) without any cardiovascular risk factors, was admitted to our Emergency-Department having ingested 18 tablets of flecainide acetate (equivalent to approx 1.8 g) for a suicide attempt.

On admission she was responsive and conscious; pulse was 90 bpm and blood pressure 110/70 mmHg. The first electrocardiogram (EKG) showed a sinusal rhythm with a large QRS complex (similar to a right bundle branch block) and a very long QT tract (about 500 msec.) (Fig. 1).

The patient was carried into our Intensive Care Unit (ICU) and initially treated with oxygen and intravenous crystalloids. The results of the first arterial blood analysis were PH 7,472, PCO2 41.2 mmHg, PO2 130 mmHg (oxygen 41/minutes non invasive), HCO 29.8 ng/l.

The hematochemical parameters were: K+ 3.5 mmol/l, Na+ 143 mmol/l, Cl– 103 mmol/l. Flecainide serum levels after 30 minutes from admission were 1940 μg/ml (therapeutic range are 200-1000 μg/ml).

Furthermore a therapy with instillation of 40 mg of activated charcoal and 40 mg of MgSO4 was started.

Approximately 45 minutes after admission to our ICU the poison Centre of “San Matteo Hospital” at Pavia (far off 60 Km) was contacted; they suggested bolus of sodium bicarbonate (NaCO3) 150 mEq and NaCO3 59

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Figure 1. The first electrocardiogram with a large QRS complex and a very long QTC interval.

Figure 2. The pre-discharge electrocardiogram.

130 mEq in slow infusion (1-2 mEq/h) for 24 hours.

Flecainide serum levels 6 hours after the beginning of this infusion were 990 Îźg/ml.

Good progress were made over the next 72 hours and no signs of organ dysfunction were evident. None were apparent and the EKG had returned to normality and a psychiatric referral was made (Fig. 2). The serum concentration of flecainide progressively returned to normal (Fig. 3) and four days after the overdose the patient was transferred to medical ward and after other three days she was discharged to home.

Discussion

As far as we are aware, there are no previously reported cases of high dose of sodium bicarbonate being used to treat acute flecainide overdose. This drug is a class IC antiarrhythmic agent which acts by blocking sodium channels involved in cardiac depolarization; this results in marked suppression of the cardiac conduction 60

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Figure 3. Flecainide levels during hospitalization.

system in addition to a moderate negative inotropic effect.7 All these actions are manifest on the EKC by increased length of PR, QRS and QTC intervals.

The pharmacokinetics qualities of flecainide are high oral bioavailability of 95% elimination, half-life seems variable with a quarter of the drug undergoing renal excretion unchanged8 the remainder undergoes hepatic metabolism to inactive derivatives.

The therapeutic range of flecainide is considered to be 200-1000 Îźg/ml. In a toxic flecainide overdose, adverse cardiac effects including bradycardia, atrioventricular block, pulse less electrical activity and asystole can occur within 30 to 120 minutes of ingestion.9 Treatment should be direct at decreasing gastrointestinal absorption through gastric emptying and administration of activate charcoal;9 furthermore serum flecainide levels should be 61

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reduced through maintenance of organs perfusion which allows drug clearance and distribution.

In the literature many proarrhythmic effects of flecainide are described; they may be related to its promoting re-entry in ventricular issue.9 Worsening of existing ventricular arrhythmias or the onset of ones can occur in up to 30% of patients10 Because type IC drugs such as flecainide produce both therapeutic and toxic effects due to extensive rate-dependent sodium channel - blockade in the myocardium, attempt to treat toxicity with hypertonic sodium bicarbonate or molar lactate have been attempted in animals11 and in humans8,9,12 with mixed success.

Keyler et al11 showed, in rats treated with 6 mEq/kg of hypertonic sodium bicarbonate, reduced to 26% flecainide induced QRS prolongation. Like-wise, 5 mEq/kg of hypertonic sodium bicarbonate in dogs resulted in significant shortening of the QRS and his ventricular intervals within 10 minutes.13 Furthermore the same authors reported that of in dogs with pacing induced dysarrhythmias after flecainide administration, 6 of 7 responded to hypertonic sodium bicarbonate, with only 1 of 7 responding to placebo.13 Hypertonic sodium bicarbonate and sodium clorate work by increasing the extra cellular concentration of sodium displacing flecainide from its receptors sites either inside the selectivity filter of the fast sodium channels or at on external anesthetic receptors site.14 Because flecainide is a weak acid with a high pKa, alkalinization may also decrease the active-ionized fraction of flecainide necessary for sodium channels blockade.

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Chouty et al15 used doses of 500 mL of 1 M sodium lactate endovenous for more than 30 minutes to treat three cases of flecainide poisoning with rapid narrowing of the QRS interval and correction of hypotension, and another flecainide overdose responded to combination to a combination of 250 mmol of hypertonic sodium bicarbonate, 136 mmol NaCl and physostigmine 2 mg endovenous in the report of Wilkelman.9 Our patient’s dysarrhythmia did not resolve until sodium bicarbonate was administered. All our observations suggest that sodium bicarbonate may be useful for the treatment of widened QRS and ventricular ectopy resulting from flecainide toxicity.

Consent Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editorin-Chief of this journal.

Competing interests The authors declare that they have no competing interests.

References 1. Roden DM, Woosley RL: Drug therapy: Flecainide. N Engl J Med 1986, 315:36-41.

2. Wang Z, Fermini B, Nattel S: Mechanism of flecainide’s rate dependent actions on action potential duration in canine atrial tissue. J Pharmacol Exp Ther 1992, 267(2):575-581.

3. Funck-Brentano C, Becquemont L, Kroemer HK, Bühl K, Knebel NG, Eichelbaum M, Jaillon P: Variable disposition kinetics and electrocardiographic effects of flecainide during repeated dosing 63

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in humans: contribution of genetic factors, dose-dependent clearance, and interaction with amiodarone. Clin Pharmacol Ther 1994, 55:256-269.

4. Siegers A, Board PN: Amiodarone used in successful resuscitation after near-fatal flecainide overdose. Resuscitation 2002, 53: 105-108.

5. Timperly J, Mitchell ARJ, Brown PD, West NEJ: Flecainide overdose - support using an intra-aortic balloon pump. BMC Emergency Medicine 2005, 5:10.

6. Yasui RK, Culclasure TF, Kaufman D, Freed CR: Flecainide Overdose: Is Cardiopulmonary Support the treatment? Annals of Emergency Medicine 1997, 29:680-682.

7. Bourke JP, Cowan JC, Tansuphaswadikul S, Campbell RWF: Antiarrhythmic drug effects on left ventricular performance. Eur Heart J 1987, 8(Suppl A):105-111.

8. Koppel C, Oberdisse U, Heinemeyer G: Clinical course and outcome in class 1C antiarrhythmic overdose. Clin Toxicol 1990, 28:433-444.

9. Winkelmann BR, Leinberger H: Life-threatening toxicity: A pharmacodynamic approach. Ann Intern Med 1987, 106: 807-814.

10. Gotz D, Pohle S, Freed CR: Extracorporeal pump assistance: novel treatment for acute lidocaine poisoning. Eur J Clin Pharmacol 1982, 22:129-135.

11. Keyler DE, Pentel PR: Hypertonic sodium bicarbonate partially reverses QRS prolongation due to flecainide in rats. Life Sci 1989, 264:1575-1580.

12. Pentel PR, Goldsmith SR, Salerno DM, Nasraway SA, Plummer DW: Effect of hypertonic sodium bicarbonate on encainamide overdose. Am J Cardiol 1986, 57:878-880.

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13. Bajaj AK, Woosley RL, Roden DM: Acute electrophysiologic effects of sodium bicarbonate administration in dogs treated with O - desmethyl encainide. Circulation 1989, 80:994-1002.

14. Ranger S, Sheldon R, Femrini B, Natttel S: Modulation of flecainide’s cardiac sodium channel blockade actions by extra cellular sodium: a possible cellular mechanism for the action of sodium salts in flecainide cardiotoxicity. J Pharmacol Exp Ther 1993, 264:1160-1167.

15. Chouty F, Funck-Brentano C, Landau JM, Lardoux H: Effectiveness of intravenous high dose molar lactate in flecainide poisoning. Presse Med 1987, 16:808-810.

Citation: Rognoni et al.; Electrocardiographic changes in a rare case of flecanide poisoning: a case report. Cases Journal 2009, 2:9137.

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Atrial Fibrillation with Multiple Infarcts SM Rajendran, N Faizal Ahamed, Arun R, B Vinod Kumar, V Lakshmipriya

Abstract

We report the case of a patient of atrial fibrillation who presented with atypical manifestations of cardioembolism.

Introduction Atrial fibrillation was first described by Arthur Cushing and Charles Edmunds in 1906. It is the most common sustained arrhythmia marked by disorganized, repaid and irregular atrial activation. The loss of atrial appendage contractility and emptying lead to the risk of clot formation and subsequent thromboembolic events. Emboli from the heart most often lodge in the MCA, the PCA or one of their branches; infrequently the anterior cerebral artery (ACA) territory is involved. The location and size of an infarct within a vascular territory depends on the extent of the collateral circulation.

Case report A 65-year-old male laundry worker came with one day history of weakness of left upper and lower limbs. On examination, patient had pulse rate of 96/min, irregularly irregular and pulse deficit of 16. Blood pressure was 130/70 mmHg. Auscultation revealed Grade II pan systolic murmur in mitral area, bilateral rhonchi and basal crepts. Patient had been treated for an unknown cardiac disease seven years ago. Patient gave a history 66

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exertional breathlessness and palpitation since six years.

He is not on any medications currently. He is a chronic smoker and alcoholic.

During the first day of hospitalization, the patient recovered completely from the neurological deficit. He was given warfarin and amiodarone on the second day, he developed wide-based gait (ataxia) swaying to the right side. There were no other cerebellar signs. By the third day, there was no ataxia and the patient was able to walk normally.

Investigations ECG

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ECG on the first day revealed atrial fibrillation.

Subsequent ECG, taken on the second day, showed anteroseptal MI and lateral wall ischemia in sinus rhythm.

CT brain CT brain showed large hypodense lesion measuring 4.4. Ă&#x2014; 4 cm in the right cerebellar hemisphere with significant mass effect on brain stem. There was also a wedgeshaped hypondense lesion involving the left occipital region suspected to be a infarct. Calcific lesions were noted in the left parietal and occipital regions.

MRI MRI revealed a wedge-shaped lesion appearing hyperintense on T2 and DWI in the superior half or right cerebellar hemisphere that was probably a subacute nonhemorrhagic infarct. Chronic infarct with gliosis was noted in the left occipital and frontal regions.

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Small hypodense lesion measuring 5.5 mm noted in the parietal region suggesting calcified granuloma.

Echo Findings on Echo were: Hypokinesia of basal, mid, apical septa and anterior segment of left ventricle; moderateto-severe LV systolic dysfunction; moderate-to-severe MR (Grade III), Grade II AR, mild TR. Dilatation of LA and RA. No clots or vegetations visualized. LVEF was 38%.

USG abdomen showed Grade I fatty liver.

Discussion Atrial fibrillation is characterized by disorganized atrial electrical activation and uncoordinated atrial contraction.

The surface electrogram characteristically demonstrates rapid fibrillatory waves with changing morphology and a ventricular rhythm that is irregularly irregular.

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The clinical importance of atrial fibrillation is related to: 1) The loss of atrial contractility, 2) the inappropriate fast ventricular response and 3) the loss of atrial appendage contractility and emptying leading to the risk of clot formation and subsequent thromboembolic events.2 Stroke is the most feared consequence of atrial fibrillation.

Most thrombus-associated with atrial fibrillation arise within the left atrial appendage.3 Embolic strokes tend to be sudden in onset, with maximum neurologic deficit at once. With reperfusion following more prolonged ischemia, petechial hemorrhage can occur.

The most significant causes of cardioembolic stroke in most parts of the world include atrial fibrillation, MI, prosthetic valves, rheumatic disease and ischemic cardiomyopathy.

Nonrheumatic atrial fibrillation is the most common cause of cerebral embolism overall.

Treatment of atrial fibrillation must take into account the clinical situation in which the arrhythmia is encountered, the chronicity of atrial fibrillation, the status of the patientâ&#x20AC;&#x2122;s level of anticoagulation/risk factors for stroke, the patientâ&#x20AC;&#x2122;s symptoms, the hemodynamic impact of the atrial fibrillation, and the ventricular rate.

Conclusion Atrial fibrillation may present with multiple infarcts with atypical features.

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Suggested reading 1. Fye WB. Tracing atrial fibrillation - 100 years. N Engl J Med 2006;355(14):1412-4.

2. Marchlinski F. The Tachyarrhythmias. 17th ed. Chapter 226. In: Harrison’s Principles of Internal Medicine. Braunwald F, Kasper, Hauser Longo, Jameson Loscalzo, McGraw-Hill Philadelphia PA 2008;2:1428.

3. Stoddard MF, Dawkins PR, Prince CR, et al. Left atrial appendage thrombus is not uncommon in patients with acute atrial fibrillation and a recent embolic event: a transesophageal echocardiographic study. J Am Coll Cardiol 1995;25(2):452-9. 

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Aortic Regurgitation with LVH Pattern Prachi Garg New Delhi

Case history A 28-year-old diagnosed case of rheumatic heart disease with aortic regurgitation (AR) presented with complaints of chest pain and palpitation with exertional dyspnea for six years. Clinical examination showed typical clinical signs of cardiomegaly with left ventricular hypertrophy (LVH) but no positive signs of heart failure. His ECG is shown in Figure.

The ECG shows that the P-R interval is at the upper limit of the normal range i.e. 0.20 second (5 mm) and the QRS axis is about +20째. Deep S waves in V1 and V2 (>35 mm) and tall R waves in V5 and V6 (>38 mm) are the most major findings on the ECG, which indicate LVH.

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ST-T changes are also seen in V5, V6 where T waves are inverted, which point to LVH of systolic overload type.

Inverted T waves are also seen in leads II, III and aVF. U waves are prominent in V1-V5. Bifid P waves in leads V1 to V4 are due to U waves merging with the P waves.

Take home message The ECG with LVH pattern reflects moderately severe AR in this patient. But, the pattern of ST-T depression in V5,V6 may in place of a diastolic overload pattern as should occur in AR (tall R waves with raised ST segment and upright T waves) indicates systolic overload pattern or the so called ‘strain’ pattern. But, the voltage of the complex is usually not very high as is customary in the usual systolic overload pattern.

For this reason, the LVH in the ECG shown herein does not fit in with either systolic or diastolic overload pattern. Such an observation is also not unusual as the true findings of systolic or diastolic overload correlates in real life with only 40-50% cases.

Digitalis, which this patient was taking, may also cause these ST-T changes. This is further supported by the long P-R interval (even though at upper limit of normal range) of 0.20 second. But, these indicate only digitalis effect and not toxicity, which manifests as an arrhythmia or 2° or 3° heart block. The U waves in the chest leads may not be of much significance as they are quite common and are present in about 20-30% of normal adults especially in the chest leads.

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Hypertrophic Obstructives Cardiomyopathy Rajiv Garg New Delhi

Case history A 49-year-old male had symptom of high fever. On examination, a soft ejection systolic murmur along the left sternal border was found. There was no past history of any major illness like hypertension or diabetes. There were no symptoms or signs indicative of congenital or rheumatic heart disease. The ECG taken is shown in Figure.

Deep T inversions in leads I, II, aVL and V4-V6 with deep S in V2 (30 mm) and tall R in V5 (20 mm) are the most remarkable findings on ECG. This is in accord

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with LVH of systolic overload type. However, it may also be due to nonischemic causes of T-wave abnormality or subendocardial infarction.

Take home message This patient was a diagnosed case of hypertrophic obstructive cardiomyopathy (HOCM) by 2D Echo. The fever was due to an unrelated viral infection. He was managed with propranolol administered in doses of 120 mg/day. Presence of ‘T’ inversions in anterolateral leads in association with deep Q waves may indicate HOCM. But often, ‘T’ inversions may the only finding.

So, HOCM should be suspected when other known causes of T-wave inversions (ischemic and nonischemic) are not suggested by history or clinical examination. Mitral valve prolapse syndrome can be a differential diagnosis in this patient, but it does not explain the LVH unless associated with severe mitral regurgitation. 

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Hypertensive Crisis-induced Electrocardiographic Changes: A Case Series Khalid Abou Farha, AndrĂŠ van Vliet, Sjoerd van Marle, Patrick Vrijlandt, Daan Westenbrink Groningen and Zuidlaren, The Netherland

Abstract

Introduction: Myocardial injury is one of the most notorious complications of a hypertensive crisis. Key electrocardiograph signs used to detect cardiac injury such as ST segment changes and cardiac arrhythmias usually indicate acute ongoing end-organ damage. Lack of early signs to predict end-organ damage might lead to a delay in the initiation of therapy and selection of the incorrect therapeutic strategy. Case presentation: We describe five cases of tall, hyper acute symmetrical T-waves alone or accompanied by other electrocardiograph abnormalities in five healthy participants: three women aged 52, 60 and 62-years and two men aged 49 and 66-years, during a tyramine-monoamine oxidase inhibitor interaction, phase I clinical trial. T-wave changes appeared early during the course of the hypertensive crisis and were attributed to subendocardial ischemia. The changes were transient and reverted to baseline in parallel with a fall in blood pressure. Conclusion: Recognition of tall symmetrical T-waves in early phases of hypertensive crisis heralds commencement of myocardial damage. This calls for prompt medical intervention to avoid an impending irreversible myocardial injury. It is our belief that these findings will add new insight into the management of hypertensive crisis and will open avenues of further investigation.

Introduction A hypertensive crisis (HC), defined as a rapid and inappropriate intense elevation of blood pressure with or without a risk of rapid damage to target organs such as the heart,1-3 is a common presentation to the emergency department and appears without history of hypertensive diseases in 23% of cases.4,5 Although HC is uncommonly encountered in clinical trial settings, some investigational drug interaction studies, such as tyramine combined with 76

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monoamine oxidase inhibitors, might trigger HC.1,3,6 In this regard, rapid blood pressure (BP) elevation above 180/100 to 110 mmHg.3,5,7 or a sudden increase in systolic BP by more than 60 mmHg above baseline in otherwise cardiovascular healthy patients might be an alarming sign.6 There are two main subtypes of HC: hypertensive emergency and hypertensive urgency. Clinical distinction between both subtypes is important for risk stratification and initiation of therapy. On the one hand, hypertensive emergency, characterized by life-threatening end-organ damage, requires immediate reduction in BP with parenteral medications. On the other hand, hypertensive urgency, a less aggressive form without evidence of acute target organ damage, requires more conservative therapy aiming to lower BP over a period of hours to days most commonly using oral medications.1,3,5 One of the tools used in the diagnostic workup of hypertensive crisis is the electrocardiogram (ECG). This might reveal evidence of myocardial ischemia or infarction, typically T-wave inversion and in more severe cases, ST segment displacement.1,7-9 These changes mirror cardiac injury and indicate a hypertensive emergency situation and therefore necessitate prompt medical intervention.

The design of the clinical trial was recommended by the division of Neurology product of the U.S. Food and Drug administration (FDA). The clinical study protocol, amendments and informed consent including statement of willingness (English and Dutch) were reviewed (from legal, ethical and medical points of view) and approved 77

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by the independent Ethics Committee, of the foundation â&#x20AC;&#x153;evaluation of Ethics in biomedical researchâ&#x20AC;?, BEBO Foundation, Assen, the Netherlands. The Committee is accredited by the central committee on research involving human subjects and by the Dutch association of Ethics Committees. The committee is constituted according to the Dutch national act on medical-scientific research in human being, the regulations of the U.S. FDA as laid down in the code of Federal regulations, 21 GFR, part 56 (Institutional Review Board) and the ICH Harmonized Tripartite Guideline E6 on Good Clinical Practice (ICHGCP). During the review process and prior to approval of the clinical study documents, the members of the committee have taken into consideration the contents of the above mentioned regulations and the declaration of Helsinki (1964) as amended by the 52nd General Assembly, of the World Medical Association (Edinburgh 2000) and the EU Clinical Trial Directive 2001/20/EC. All subjects enrolled in this trial provided written informed consent before participating in any study-related activity.

They were informed about the nature and purpose of the trial, participation and termination conditions, risk and benefits. The study was conducted in our Clinical facility centre located in the campus of the University Medical Centre, Groningen, the Netherlands.

Case presentation The aim of this trial was to evaluate the interaction between tyramine and both selective and non-selective MAO inhibitors. Tyramine was administered in an escalating dose level design of 25 mg ascending up 78

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to and including 800 mg during a period of 10 days.

This tyramine dose escalation design was, however, discontinued on achieving an increase of more than 30 mmHg in systolic BP (compared with baseline values) on three successive measurements with a period of five minutes between measurements.

As previously mentioned, Prior to study initiation written informed consent was obtained from all participated subjects, 179 healthy male and female volunteers, aged 40-70 year (inclusive). This was followed by their medical history being established; complete physical examination, thorough laboratory investigations and electrocardiograph assessments including exercise electrocardiography.

These parameters indicated the healthy non-pathologic status of all participants. At pre-dose time points, baseline assessments of the participantsâ&#x20AC;&#x2122; BP values were determined. After dosing, a regular BP evaluation was performed at five-minute intervals for a period of two hours and thereafter four times hourly for a subsequent period of two hours. Continuous telemetric recording was performed pre-dose to provide baseline reference values, and until at least four hours post-dose.

The trial protocol specified that during the course of the trial, a hypertensive episode of more than 60 mmHg above predetermined baseline values would imply the use of intravenous labetalol, an alpha and beta blocking agent.

This was the case in 35 male and female participants.

ECGs and/or telemetric recordings during the hypertensive episodes were available from 21 out of 35 participants.

In the electrocardiograph records from all 21 patients, clinically important T-wave changes were observed.

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The material used for this report was obtained from five participants: three women aged 52-years-old to 62-years-old and two men aged 49 years-old and 66-years-old. A hypertensive episode with a rapid increase in systolic BP >60 mmHg above the baseline value has been observed after an oral tyramine dose, as low as 100 mg in the three female participants and as high as 500 mg in the two male participants.

Parallel with the peak BP, four participants, Patients 1 to 4, reported rapid onset of an array of angina symptoms.

These were severe headache and neck pain in Patient 1, skipped beats, warm sensation, abdominal palpitation and anxiety in Patient 3, severe headache and chest compression in Patient 2, and throat tightness, palpitation and severe occipital pain in Patient 4. The other male participant, Patient 5, reported no complaints during the paroxysm of BP elevation.

Synchronous with the peak BP levels, telemetric recordings of all five participants showed obvious T-wave changes.

The T-waves clearly lost their peculiar asymmetry and became hyper acute, pointed and high amplitude reaching values of ca. 0.7 mV, 0.65 mV, 0.7 mV and 0.9 mV in leads II of, respectively, Patients 2, 1, 3 and 4. These values were 2 to 4 times the values obtained at baseline.

In the remaining male patient, Patient 5, where timematched 12-lead ECG rhythm traces were available, the T-wave amplitudes were 0.5 mV, 1.2 mV, 1.3 mV and 1 mV, respectively, in leads II and V3-V5. Again these values were approximately two times the values seen in the corresponding leads at the baseline time point. All ECG recording electrodes were remounted at identical 80

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locations. This avoided inconsistency in voltage tracings obtained at different time points.

In Patient 2, T-wave changes were an isolated event without any associated abnormal telemetric findings (Fig. 1). In the remaining four participants T-wave changes were accompanied by other electrocardiograph abnormalities.

Patient 1 demonstrated a 2:1 atrioventricular second degree heart block (A-V block) with a heart rate of 60 bpm and narrow QRS complexes but with constant PR and RR intervals between conducted beats (Fig. 2). Patient 3 demonstrated ventricular bigeminy (Fig. 3), while Patient 5 demonstrated a few sudden cardiac cycles with prolonged PR interval reaching 360 ms, greater than two times the baseline value, with a heart rate of 54 bpm (Fig. 4).

Patient 4 showed an accelerated idioventricular rhythm (AIVR). This was followed later by evident inferior lead a

b

c

Figure 1. Telemetric recording obtained (at double standardization, 10 mm = 0.5 mV) from a female patient depicting tall symmetric T-wave during a paroxysm of hypertensive crisis compared to baseline (a) and after normalization of blood pressure (c).

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a

b

c

Figure 2. Telemetric recording obtained (at double standardization, 10 mm = 0.5 mV) from a female patient, depicting A-V second degree heart block (b) during an episode of hypertensive crisis. Notice the tall symmetric T-wave compared to baseline (a) and after normalization of blood pressure (c). a

b

c

d

Figure 3. Telemetric recording obtained (at normal standardization, 10 mm = 1 mV) from a female patient, depicting tall symmetric T-wave seen early in the course of a hypertensive crisis episode (b) and in parallel with ventricular bigeminy (c). Recordings a and d demonstrate normal electrical cardiac activities at pre-dose (before tyramine administration) and post blood pressure normalization time points, respectively.

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a

b

c

Figure 4. (a) Electrocardiogram recordings obtained (at normal standardization, 10 mm = 1 mV) from a male patient, depicting tall symmetric T-wave (seen in V3 to V5) associated with prolonged PR interval as seen in leads II, III and aVF (arrows), during a hypertensive crisis episode. (b) Tracings a and c demonstrate normal electrical cardiac activities at predose (before tyramine administration) and post blood pressure normalization time points, respectively.

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a

b

c

d

e

Figure 5. Telemetric recordings obtained (at normal standardization, 10 mm = 1 mV) from a male patient, depicting tall symmetric T-wave seen in the course of hypertensive crisis (b) and in parallel with accelerated idioventricular rhythm (c) ST segment depression (d) is also noted. Figure a and e demonstrate telemetric recordings obtained at pre-dose (before tyramine administration) and post blood pressure normalization time points, respectively.

ST segment depression (Fig. 5). All five participants were promptly treated with labetalol, given intravenously as an infusion in doses ranging from 6 to 16.5 mg.

Subsequent normalization of BP was followed by clearing of symptoms in the four symptomatic participants and gradual disappearance of associated electrocardiograph abnormalities including the A-V block. In the patient with prolonged PR interval, the PR duration returned 84

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to baseline value directly after labetalol treatment. Given the severe ischemic changes observed in the telemetric recording of Patient 4, he was referred to the cardiology care unit of the University Hospital Groningen. Assessment of serum cardiac enzymes revealed a Troponin T level of 0.20 mcg/L, i.e. 20 fold the reference value (<0.01 mcg/L).

The patient was subsequently admitted to the cardiology care unit with suspected acute coronary syndrome. Full cardiological investigations were performed including coronary angiography and the patient was discharged three days later after confirmation of a normal cardiac structural and functional profile.

It is noteworthy that inspection of the telemetric recordings of two participants, a female patient with A-V block and the male patient with AIVR, revealed the start of T-wave changes as BP increased by values more than 25 mmHg above baseline.

Discussion The extent of clinical and electrocardiographic findings encountered during the trial were unforeseen. However, given the known pharmacological effects of the study medication and the risk of blood pressure changes, the trial was conducted under close and continuous medical observation and monitoring conditions.

An adequate and prompt treatment protocol for cases exceeding pre specified safety margin was set up in close collaboration with the intensive care unit of the University Medical Centre Groningen.

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We have illustrated the appearance of symmetrical pointed tall T-waves with values of 0.65 mV or higher in lead II of four participants and at least 1mV in precordial leads of one male participant, early during the course of hypertensive crisis, with an emerging onset at >25 mmHg elevation of systolic BP in two participants, i.e. before reaching values that would normally be denoted as hypertensive crisis. This was associated with angina symptoms in four participants, and followed by characteristic electrocardiograph changes that resolved after labetalol-induced normalization of BP. Typically, T-waves in healthy patients have non-pointed smooth asymmetric profiles with amplitudes that are age, sex and ECG lead dependent. In healthy male and female patients aged 40 to 60-years, average T-wave amplitudes of 0.23 mV and 0.21 mV, respectively, have been described in lead II of the ECG recording.10 In leads V3 through V5 of male patients aged 40 to 60years, reference average T-wave amplitudes of 0.6 mV, 0.54 mV and 0.39 mV have been described.10 Loss of asymmetrical T-wave profile with increased amplitude is suspicious, especially for patients older than 40 years.11 In this regard, hyperkalemia, myocardial ischemia and cerebrovascular accidents have all been implicated in the etiology.10 Our findings can be clarified by the fact that HC causes a sudden increase in the afterload on the heart. This leads to an increase in the myocardial workload and myocardial oxygen demand thereby causing myocardial ischemia.12 86

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In the very early phases of myocardial ischemia, the first area to be affected is the subendocardium, being farthest from the blood supply.10,12,13 This leads to a delay in the subendocardial recovery time probably due to activation of the ATP-sensitive K channels13 that appears electrocardiographically as tall hyper acute T-waves. At the same time, prolonged ventricular subendocardial recovery explains the associated cardiac arrhythmias observed in two participants.

This point is crucial in planning a therapeutic strategy for HC cases, since tall T-waves appear in the early reversible ischemic phase before myocardial injury occurs. In this context, the clinical significance of Twave changes is underlined in the HC situation seen in patients with diabetes mellitus who suffer cardiac autonomic neuropathy and lack typical angina symptoms.

An appropriate treatment with parenteral first line medications such as labetalol in this early reversible phase might be an end-organ salvage measure.

Interestingly, one male patient demonstrated a prolonged PR interval while, in one female patient, a 2:1 second degree A-V block was observed during the hypertensive episode. The association of the A-V block with HC, symmetrical tall T-waves and the absence of bradycardia indicates ischemic rather than vagally induced heart block as an underlying mechanism.

Treating both participants with labetalol led to normalization of BP and was followed by resolution of the A-V block profile and reduction in the associated symptoms in the female patient. The relationship between 87

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myocardial ischemia and A-V block including a 2:1 second degree heart block has been previously reported.14 The central role of myocardial ischemia in the pathogenesis of A-V block seen during HC should, therefore, be considered in the therapeutic approach to non-vagally induced A-V block.

Finally, three points are worth mentioning. First, most of our findings were noted in telemetric records. This facilitates detailed tracing of cardiac electrical activity changes occurring during the hypertensive episodes.

Compared to the routine 12-lead ECG tracing, telemetric recordings appear technically a more time sparing procedure, requiring less frequent electrode mounting.

In addition, it is a more informative tool, in detecting early cardiac electrical changes associated with HC, given the fact that cardiac electric activity can be displayed on a continuous basis. Therefore, we believe that, in the HC situation, the use of a telemetric recording or bedside monitoring is superior to ECG tracing in risk stratification and thence, offers a timely targeting of a successful treatment strategy. Second, this study is based on incidental observations during a phase I clinical trial.

Accordingly, verification of these unforeseen findings with other supplemental investigational tests such as cardiac markers was not scheduled and was not done on any participant except for Patient 4. Further investigations to explore the clinical significance of T-wave changes in HC are, therefore, still warranted. Lastly, the trial gives a sound signal and a clear warning sign to the serious 88

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risk of cardiac damage during hypertensive crises. Still worthy of notice, the observed untoward cardiovascular effect resulting from Tyramine administration in supra physiologic escalating doses. This should raise the question whether Tyramine administration in ascending doses could be justified in future clinical trials.

Conclusions

An asymmetric tall T-wave is an important early ECG myocardial ischemic sign which should not be overlooked in clinical evaluation of patients suffering from drugor non-drug-related hypertensive crisis. Recognition of T-wave abnormalities should facilitate rapid and appropriate interventions that might abort the cascade of progressive cardiac damage. In the setting of hypertensive crisis, an A-V block associated with an asymmetric tall Twave, particularly in the absence of bradycardia, should draw attention to the ischemic nature of the disorder which usually requires controlling of BP by parenteral first line medication.

Consent Written informed consent was obtained from all participants for publication of this case series. Copies of the written informed consent are available for review by the Editor-in-Chief of this journal.

Competing interests The authors declare that they have no competing interests.

Acknowledgements

The authors wish to express their appreciation to Mrs Helen Pruim-Tait, MSc, Project Manager at the PRA International

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Institute, for manuscript.

revising

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this

References 1. Bhalla H: Hypertensive crisis. In Manual of Cardiovascular Medicine. Edited by Marso SP, Griffin BP. Topol EJ. USA: Lippincott, Williams & Wilkins; 2000;434-445.

2. Bales A: Hypertensive crisis. Postgrad Med 1999, 105:1-18.

3. Vaidyya CK, Ouellette JR: Hypertensive urgency and emergency.

Hosp Physician March 2007:43-50.

4. Zampaglione B, Pascale C, Marchisio M, Cavallo-Perin: Hypertensive urgencies and emergencies, prevalence and clinical presentation. Hypertension 1996, 27:144-147.

5. Rehman SU, Basile JN, Vidt DG: Hypertensive emergencies and urgencies. In Hypertension. A Companion to Braunwald’s Heart Disease. Edited by Black HR, Elliott WJ. 1st edition. Canada: Saunders; 2007:517-524.

6. Seiler B, Levitt EB: University of Maryland researchers find heart disease in marathon runner: Is too much exercise a bad thing? [http://www.umm.edu/news/releases/marathon_runner.htm] 7. Tisdale JE, Huang MB, Borzak S: Risk factors for hypertensive crisis: importance of outpatient blood pressure control. Fam Pract 2004, 21:420-424.

8. Choudry FA, Magee K, Green R: She’s gonna blow! Can J Diagn 2004:1-4.

9. Goldberger AL: Electrocardiography. In Harrison’s Principles of Internal Medicine Volume 1. 15th edition. Edited by Brauwnwald E, Fauci AS, Kasper DL, Hauser SL, Longo DL, Jameson JL. New York: McGraw-Hill; 2001:1262-1271.

10. Surawicz B, Knilans TK: Normal electrocardiogram: origin and description. In Chou’s Electrocardiography in Clinical Practice, 90

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Adult and Paediatric. 5th edition. Edited by Surawicz B, Knilans TK. Philadelphia, PA: WB Saunders; 2000:3-27.

11. Hoon RS, Durairi M, Balasubramanian V, Shadaven MG: Significance of tall precordial T-waves: an electrocardiographic study in Indians. Chest 1973, 64:327-330.

12. Panacek EA: Hypertensive emergencies and urgencies. In Emergency Cardiac Care. Edited by Gilber WB, Aufderheide TP. St Louis, MO: Mosby Yearbook, Inc; 1994:528-548.

13. Tsunehiro K, Kubota I, Tachibana H, Yamaki M, Tomoike H: Glibenclamide attenuates peaked T-wave in early phase of myocardial ischemia. Cardiovasc Res 1996, 31:683-687.

14. El-Sharif, Scherlag BJ, Lazzara R, Hope R, Williams DO, Samet P: The pathophysiology of tachycardia-dependent paroxysmal atrioventricular block after acute myocardial ischemia. Circulation 1974, 50:515-528.

Citation: Farha et al.; Hypertensive Crisis-induced Electrocardiographic Changes: A Case Series.

Journal of Medical Case Reports 2009, 3:7283.

ď&#x201A;&#x2014;ď&#x201A;&#x2013;

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Acute Dyspnea and Tachycardia in a Cigarette Smoker E William Hancock USA

A

75-year-old woman presented to the emergency department with exacerbation of dyspnea, wheezing and swelling of the legs that had begun 24 hours earlier.

The patient had been treated for lung disease for many years and her usual symptoms were dyspnea on very little exertion, a chronic nonproductive cough and episodic wheezing. She had smoked cigarettes for 55 years but had stopped 5 years ago. Her medications included meprobamate, chlorothiazide, triamterene, loratadine, clonazepam, oxaprozin, montelukast, ipratropium and home oxygen.

On examination, the patient appeared thin and dyspneic. Her temperature was 37.2째C; radial pulse 125 bpm; respiratory rate, 36/min; blood pressure, 105/55 mmHg; and oxygen saturation, 98% while receiving oxygen 3l/min by nasal canula. Jugular venous pressure was slightly elevated. Breath sounds were diffusely faint, with prolonged expiration but no crackles or wheezes. Cardiac rhythm was irregular at 135 bpm with normal heart sounds. Mild edema of the ankles was present.

Serum electrolyte, blood urea nitrogen, creatinine and glucose levels were normal. White blood cell count was 15,000/mm3; hematocrit was 44%. An arterial blood 92

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sample taken while the patient was on nasal oxygen had a pH of 7.46; pO2 80 mmHg; pCO2 31 mmHg. The chest X-ray showed over-inflated lungs and normal heart size.

The ECG is given in the previous page.

What is the rhythm mechanism?

What is the likely cause of the arrhythmia?

What is the most appropriate immediate therapy for the arrhythmia?

Analysis of the ECG

The rhythm is erratically irregular at 135 bpm. P waves precede each QRS complex, with approximately constant PR intervals. The irregular cardiac rhythm is therefore caused by an irregular atrial rhythm. The P waves are not only irregular but also markedly varied in morphology from beat-to-beat. At least three morphologies are seen in lead II; no single type predominates.

I-II-III

aVR-aVL-aVF

V1-V2-V3

V4-V5-V6

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The QRS complexes are within the normal range, but show a rightward axis of +80째 and a late precordial transition.

The atrial rhythm mechanism is typical of multifocal atrial tachycardia (MAT), also known as chaotic atrial rhythm or rapid wandering atrial pacemaker.

Principal consideration in the differential diagnosis is sinus tachycardia with frequent atrial premature complexes. This distinction is sometimes difficult to make and perhaps arbitrary when a few P waves appear to have a normal morphology and a constant cycle length.

In this case, however, a subpopulation of normal P waves is not apparent; all P waves are most likely ectopic.

MAT is seen most frequently in patients with severe chronic obstructive pulmonary disease (COPD), usually when respiratory failure occurs during treatment in the intensive care unit (ICU). In this case, respiratory failure occurred before admission to the ICU. Probable factors in the genesis of MAT include hypoxemia, hypercarbia, respiratory acidosis, atrial stretch from right-sided congestive heart failure, enhanced neural and hormonal sympathetic activity, and various drugs (especially bronchodilator and digoxin). High blood levels of theophylline often used to be a cause, although this is less common now because the drug is used less aggressively in critical care medicine. The inhaled bronchodilators and right-sided congestive heart failure appear to be the most prominent causes in this case.

MAT that occurs during respiratory failure does not respond predictably to specific antiarrhythmic treatment.

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β-blockers may be effective but are often avoided because they can aggravate obstructive airway disease.

Unless pulmonary vascular congestion or systemic hypotension is present, one might consider withholding specific antiarrhythmic measures and simply treating the pulmonary disease. This patient was treated with intravenous diltiazem for four days, during which the MAT rate gradually slowed until it reverted to sinus rhythm with only occasional atrial premature complexes.

Her respiratory status also improved markedly during the 7-day hospitalization. Exacerbations of COPD are one of the most frequent reasons for hospitalization.

MAT is sometimes a factor in precipitating such crises and also a frequent complication during the patient’s hospital stay. Correct differentiation from other atrial arrhythmias, such as fibrillation, flutter or the re-entrant supraventricular tachycardias is important in planning the appropriate management.

Source: Hospital Practice 1999;34(3):33-4.

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A Faulty Recording of the ECG Rajiv Garg Noida

Case history A 42-year-old male presented with complaint of nonspecific chest pain. A routine ECG was taken (Fig. 1a). There was no previous history of any illness or of cardiovascular problems. The clinical examination was not significant.

ECG showed negative P waves in Lead I and aVL and all negative waves in AVL. The negative P-wave in lead I points to dextrocardia (Note: P waves are usually not negative in lead I even in nodal rhythm. The precordial

Figure 1a.

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leads nevertheless appear normal with the height of R waves increasing progressively from V1-V4. This is not in favor of a diagnosis of dextrocardia where the R waves reduce in height as we proceed towards the left chest leads. Hence, the ECG shows an incongruity between the precordial and limb leads. Closer inspection reveals that the lead aVR appears like aVL and vice-versa.

This establishes the diagnosis of a â&#x20AC;&#x2DC;technical dextrocardiaâ&#x20AC;&#x2122; that occurred as a result of the ECG technician connecting the left arm electrode to the right arm and vice-versa.

Such a situation is not infrequent. But the diagnosis can be made if chest leads are examined.

The leads were correctly placed and a second ECG was taken Figure 1b.

Figure 1b.

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Take home message No correlation between the clinical presentation and the ECG can be made in this case as it is entirely a technical problem in recording of the ECG. There is no dextrocardia and the patient is a normal person. ď&#x201A;&#x2014;ď&#x201A;&#x2013;

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Diabetic Congestive Cardiomyopathy in Congestive Heart Failure Prachi Garg New Delhi

Case history A 34-year-old male presented with signs of heart failure.

The patient was a known diabetic. He also gave a history of some heart trouble in his family, which he could not clarify further. The ECG is shown in Figure.

ECG showed a left bundle branch block (LBBB) pattern in leads I, V5 and V6 (RSR pattern). Unifocal ventricular ectopics were recorded in leads I, II, III, V1-V3 including the rhythm strip. A severe LVH is suggested by the presence of PR interval at the upper limit of normal [0.20 sec], S-wave in V2 >25 mm and R in V6 >30 mm.

The ST-T changes seen in leads I, II, aVF and V6 are

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either indicative of LVH or digitalis effect. The QR pattern in aVL lead is in fact deceptive as there no Q-wave is seen in the corresponding leads like I, V5 and V6 (all left ventricular leads). This pattern is likely to be rSR pattern with initial ‘r’ not seen clearly.

Take home message The patient was an established case of diabetic/congestive cardiomyopathy in severe congestive heart failure. His two brothers had similar conditions and one had died of sudden cardiac death. Presence of LBBB, LVH, VPCs in the ECG, in a patient of this young age are strongly suggestive of a diagnosis of cardiomyopathy. The family history of ‘cardiac condition’ further supports the diagnosis. The ST-T changes could have been either due to LVH or digitalis which the patient was taking. 

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Silent Myocardial Ischemia AK Gaur New Delhi

Case history A 71-year-old diabetic patient underwent kidney transplant for renal problems. Post-transplant, he was doing quite-well except for occasional atypical discomfort in the chest. Holter monitoring was done for the same (Figure).

On examination of the records from the Holter monitor, the upper panel showed marked ST depression of >3 mm with downward or horizontal slope. Such changes in STT indicate significant ischemic heart disease.

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Take home message The patient did not have the classic chest pain suggestive of angina pectoris. He had infrequent discomfort in the chest with or without exertion. The patient did not have any pain or discomfort at the time of the Holter monitoring showing the above characteristic changes of myocardial ischemia (MI). This is termed as silent myocardial ischemia.

Silent MI is more prevalent than what has been assumed to be. About 70-80% of all ischemic episodes in patients with ischemic heart disease (IHD) as recorded

by Holter monitoring or stress test are usually silent.

The remaining 20-30% present with chest pain. The condition is more common in patients with diabetes as was the case with this patient. ď&#x201A;&#x2014;ď&#x201A;&#x2013;

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RSR Pattern in I, aVL and V6 Leads OP Gupta Wardha

Case history A 58-year-old male had been diagnosed with ischemic heart disease (IHD) for several years. He had no history of myocardial infarction. On examination, pulse and BP were within normal limits. Cardiovascular examination also revealed no abnormality. A routine check ECG was taken (Figure).

ECG showed a normal PR interval of 0.16 second. The QRS axis is about –35° (lead II showing somewhat more negative QRS complex). The most remarkable finding on ECG was a slurred QRS in all the leads, in particular the chest leads, with a duration of 0.14 second (3.5 mm). Deep S waves follow ‘r’ waves in V1-V5 with a vertical but slurred QRS complex in V6. RSR pattern

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is suggested in I, aVL and V6 points to the diagnosis of a left bundle branch block (LBBB). Depending on the duration of the slurred QRS in left ventricular leads, the LBBB can be defined as incomplete (>0.10 but <0.12 sec) or complete (QRS >0.12 sec). ECG also shows ST-T changes, which are sagging and depressed in I, aVL and V6 leads. These ST-T changes are secondary to the LBBB and do not inevitably indicated myocardial ischemia (MI).

The QS pattern in V1-V5, in the presence of LBBB, may not signify any anteroseptal MI. The RSR pattern of LBBB would have been more evident, if V7, V8 leads had been taken, as there is a clockwise rotation with right ventricular pattern (QS) continuing upto V5.

Take home message The diagnosis of LBBB is consistent with the clinical diagnosis of IHD, one of the commonest etiologies. The additional diagnosis of MI should not be considered because the patient only had angina pectoris and there was no history of MI. Because the axis is around –35° and the P-R interval is normal, the diagnosis of bifascicular or trifascicular block need not be contemplated. 

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Inferior Wall Myocardial Infarction OP Gupta New Delhi

Case history A 49-year-old male, a nonsmoker, nonhypertensive, nondiabetic patient was hospitalized with severe chest pain.

He was managed as a case of acute myocardial infarction (MI). The ECG is shown in Figure. The recovery of the patient was uneventful.

The heart rate was around 60/minute. The ECG shows a recent inferior wall MI with pathological ‘Q’ waves, symmetrical ‘T’ inversion and coved ST segment

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(convexity upward) in leads II, III and aVF. T waves are also slightly flattened in V6. QRS axis is around –30°.

There are tall ‘R’ waves, with R/S ratio >1 in V2, V3.

Take home message The ECG of this patient showed clear features of a recent MI (ST has come down to isoelectric level but ‘T’ waves are still inverted in the inferior leads). The patient had no other risk factors other than a strong family history of coronary artery disease. The relatively slow heart rate may probably due to the fact that the patient was possibly on b-blockers.

The reciprocal changes in anterior leads - V2, V3 showing tall ‘R’s and tall ‘T’s in presence of a pathological ‘Q’ and inverted ‘T’ in inferior leads may lead to a suspicion of an infero-posterior wall MI. The flattening of ‘T’ waves in V6 may indicate lateral wall ischemia though leads I and aVL do not show these changes. 

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Ventricular Tachycardia with Slow Irregular Pattern MJ Khan New Delhi

Case history This case illustrates the ECG of a patient with diabetes, who had episodes of silent myocardial ischemia a few months before. He also had undergone a kidney transplant. The patient developed heart attack and did not survive the attack. The ECG strips shown here are available from the monitor (Fig.).

Very wide and bizarre QRS patterns at a rate of about 100/min are seen in the ECG strips (top 2 panels). This

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feature is characteristic of a ventricular tachycardia with slow irregular pattern as shown in the second rhythm strip. The ventricular rate reduced to about 50/min even though the wide bizarre pattern persisted as is evident from the third strip. These beats are also abnormal (from the ectopic ventricular focus) and may be called idioventricular rhythm because of the slow rate.

The patient may have developed a 2:1 exit block at the site of ventricular ectopic focus. This means that every second ectopic beat could not come out of the area and so could not form the QRS complex. Such a scenario can occur in a myocardial infarction with edema around the zone of the ectopic focus leading to conduction disturbances. The last strip shows a straight-line confirming ventricular arrest since no electrical activity is recorded. The last bizarre complex with arrows is suggestive of the cardiac massage that was carried out on this patient with the mechanical movement caused by the cardiac massage.

Take home message The patient was unconscious at the time of recording of the ECG which shows ventricular tachycardia and asystole. The patient had a heart attack a few hours earlier and this episode occurred during sleep. Such an occurrence is not unusual and is seen in about 10-15% cases of all heart attacks. The patient died and could not be revived despite all possible measures including CPR carried out from the time of the arrhythmia presented in the ECG. 108