DOCSLIB.ORG

Incessant Atrial Tachycardia Accelerated by Pregnancy

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Incessant Atrial Tachycardia Accelerated by Pregnancy 266 Br Heart J 1992;67:266-8 CASE REPORTS Br Heart J: first published as 10.1136/hrt.67.3.266 on 1 March 1992. Downloaded from Incessant atrial tachycardia accelerated by pregnancy J Colin Doig, Janet M McComb, Douglas S Reid Abstract sinus rhythm or affect the ventricular response A 24 year old patient presented with rate. Metoprolol and digoxin in combination incessant atrial tachycardia during the slowed the ventricular rate to 185 beats/min course of a twin pregnancy. Medical but the diurnal fluctuation in PP and RR treatment slowed the ventricular res- intervals continued. Flecainide was therefore ponse without restoring sinus rhythm. introduced in place of metoprolol and digoxin. During labour the tachycardia spontan- This slowed the atrial rate to 115 beats/min and eously reverted to sinus rhythm. Sub- allowed transient episodes of sinus rhythm at sequently the same arrhythmia was 75 beats/min to appear with a frontal P wave documented with a slower ventricular axis of + 10°. The PR interval was 200 ms with response than during pregnancy. no evidence of pre-excitation (fig 2). This was considered a satisfactory interim result and the patient was discharged on oral flecainide Case report 100 mg three times daily. During the next At 21 weeks' gestation of a twin pregnancy a 24 month the QRS duration increased from 80 ms year old patient was transferred for man- to 100 ms and the heart rate was never consis- agement of incessant supraventricular tently below 130 beats/min on Holter monitor- tachycardia because of concerns about the ing. Because of this inadequate rate control, effect on placental function. There was a three flecainide was stopped and amiodarone was http://heart.bmj.com/ month history ofpalpitation and chest discom- introduced at a dose of 800 mg a day for one fort, dizziness, and exertional dyspnoea that week and maintained at 400 mg daily. This had begun eight weeks into the pregnancy. slowed the heart rate to 110 beats/min. On this There was no history ofviral illness and she had treatment, she felt better, but was considerably been otherwise healthy with no previous his- restricted in her exercise capacity by palpita- tory of palpitation. At admission the heart rate tion, fatigue, and dyspnoea. There was no was 200 beats/min and systolic blood pressure clinical evidence of heart failure or com- was 90 mm Hg. Her electrocardiogram showed promised fetal development. on September 30, 2021 by guest. Protected copyright. a narrow QRS complex tachycardia with At 31 weeks' gestation two healthy infants upright P waves in the inferior limb leads and were delivered vaginally by forceps. Sinus VI, with a frontal P wave axis of + 900 (fig IA). rhythm returned spontaneously and the moth- The PR interval was 140 ms. Occasionally non- er's heart rate fell below 100 beats/min during conducted P waves of identical configuration the first stage of labour. After delivery she and timing were seen during the tachycardia reported that palpitation had ceased and she (fig 1B). The rate of the arrhythmia showed remained in sinus rhythm when seen in out- considerable diurnal variability ranging from patients two weeks after hospital discharge. 135 to 210 beats/min. Isolated ventricular Amiodarone was stopped at this time and her extrasystoles did not reset the tachycardia. electrocardiogram was similar to that in fig 2. There was QRS alternans at ventricular rates The diagnosis was therefore assumed to be faster than 190 beats/min. Haematological pregnancy related atrial tachycardia and this studies, urea and electrolytes, and liver func- was supported by the prominent left atrial tion tests were normal. A free thyroxine plasma component to the P wave in sinus rhythm. She Regional concentration of 164 nmol/l (normal range was re-referred, however, six months after Cardiothoracic with non-cardiac at which Centre, Freeman 60-140) and thyroid stimulating hormone con- delivery symptoms Hospital, Newcastle centration of 1-4 IU/I (normal range 0 15-3-2) time an electrocardiogram showed return of rate of 1 15 upon Tyne were consistent with pregnancy. Transthoracic atrial tachycardia with a ventricular J C Doig treat- x were normal. beats/min. She was on no antiarrhythmic J M McComb echocardiography and chest ray D S Reid Fetal echocardiography showed normal hearts ment. Correspondence to and rates. Dr J Colin Doig, University The arrhythmia did not respond to carotid Department of Cardiology, Valsalva manoeuvres or Discussion Regional Cardiothoracic sinus massage, sinus Centre, Freeman Hospital, intravenous verapamil. Digoxin was used with- Pregnancy is frequently associated with Newcastle upon Tyne, and increased has NE7 7DN. out benefit and cardioversion did not restore tachycardia ectopic activity Incessant atrial tachycardia accelerated by pregnancy 267 tachycardia such as was present in this patient is uncommon and has rarely been reported during pregnancy.89 It has not previously been seen reverting to sinus rhythm during labour. An automatic atrial tachycardia more typically Br Heart J: first published as 10.1136/hrt.67.3.266 on 1 March 1992. Downloaded from occurs in childhoodl'01 or complicating heart disease'2 or metabolic upset including digitalis toxicity.'3 In this case, recurrence of the same tachycardia some months later suggests that the patient had a potential for atrial tachycardia unrelated to pregnancy, but which first presen- ted at an accelerated rate during pregnancy. The mechanism of the tachycardia in this patient was probably enhanced sympathetic reactivity of an ectopic atrial focus. This !:: ..4 accords with the increased plasma cate- cholamine concentrations and the increased adrenergic receptor sensitivity during preg- nancy.4 " Increased atrial stretch due to plasma volume enlargement might also be implicated. The possible influence of the high concentra- '~~~.!..~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~..Fc tions of oestrogen and progesterone in preg- nancy is unknown. An enhanced response to S a. 5... I~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~.... prostaglandins has been reported in preg- nancy,'5 and in susceptible patients this could perhaps induce an atrial tachycardia. Thyrotoxicosis could also facilitate' atrial arrhythmias; but there was no clinical or biochemical evidence of thyroid overactivity. -e:;-:~~~~~~~ ~ ~~..~~~~~~~~~~~~~~~~~~_. Why the arrhythmia stopped during labour is ~ IK not clear. ~~~~~~~~~~~~~O' Because the persistent atrial tachycardia might have caused congestive cardiac failure in our patient'6'8 or have affected placental func- tion and subsequent fetal development'9 we tried to reduce the ventricular rate response when sinus rhythm could not be restored. The in pregnancy http://heart.bmj.com/ Figure I (A) Electrocardiogram showing narrow QRS tachycardia. (B) Rhythm management of such arrhythmias strip showing non-conducted P waves of identical configuration and timing during is difficult. Verapamil, digoxin, or cardio- tachycardia.I~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ selective f blockade are appropriate and usually well tolerated.202' Flecainide seems to in the atrium and the ventricle be safe and cardioversion is not contrain- been noted both as an throughout pregnancy.'2 Paroxysmal dicated.' Amiodarone is regarded agent supraventricular tachycardia has been seen' of last resort because of concerns about neon- in breast milk.2324 on September 30, 2021 by guest. Protected copyright. occurs in a patient with a history of atal goitre and its presence and usually to insert a tem- arrhythmias before preg- An alternative treatment is supraventricular to terminate the arr- nancy or in a patient with pre-existing porary pacing electrode rheumatic heart disease.5 Such arrhythmias hythmia or convert it to atrial fibrillation. but the Though appropriate radiation protection could usually occur in the third trimester6 to be is unknown.7 Persistent atrial be used, pacing was not thought likely true incidence successful in our patient and we thought that atrial fibrillation might further compromise placental function. This rare case highlights the risk that inpatients with the potential for atrial tachycar- dia the condition can be precipitated and accelerated by pregnancy. The arrhythmia was persistent and led to unrealised concerns about placental function but it reverted to sinus rhythm early during labour. Treatment of a persistent tachycardia in pregnancy may be potentially toxic to the mother or fetus or both. Despite a twin pregnancy and incessant supraventricular tachycardia our patient delivered two healthy infants. 1 Mendelson CL. Disorders of the heartbeat during preg- nancy. Am J Obstet Gynec 1956;72:1268-301. 2 Sullivan JM, Ramanathan KB. Management of medical problems in pregnancy-severe cardiac disease. N Engl J Figure 2 Electrocardiogram after return to sinus rhythm. Med 1985;313:304-9. 268 Doig, McComb, Reid 3 Oakley GDG. Pregnancy and heart disease. In: Julian DG, Camm AJ, Fox KM, Hall RJC, Poole-Wilson PA, eds. Camm AJ, Fox KM, Hall RJC, Poole-Wilson PA, eds. Diseases of the heart. London: Balliere Tindall, 1989: Diseases of the heart. London: Balliere Tindall, 1989: 1372-83. 1363-71. 15 Broughton Pipkin F, Morrison R, O'Brien PM. The effect of 4 Kay J, Priano LL. Paroxysmal atrial tachycardia during prostaglandin El upon the pressor and hormonal response pregnancy. Anesthesiol Rev to exogenous angiotensin II in human pregnancy. Clin Sci 1987;14:8-15. Br Heart J: first published as 10.1136/hrt.67.3.266 on 1 March 1992. Downloaded from 5 Szekely P, Snaith L. Heart disease and pregnancy. Edin- 1987;72:351-7. burgh: Churchill Livingstone, 1974:90-101. 16 Vitale P, de Stefano R, Vitale N, Pisacane C. Disfunzione 6 Perloff JK. Pregnancy and cardiovascular disease. In: miocardia conseguente a tachicardia sopraventricolare. G Braunwald E, ed. Heart disease. 3rd ed. Philadelphia: WB Ital Cardiol 1989;19:928-32. Saunders, 1988:1848-69. 17 Antonelli Incalzi R, Gemma A, Frustaci A, Rossi E, 7 Metcalfe J, McAnulty JH, Ueland K. Burwell andMetcalfe's Carbonin PU. Low atrial tachycardia as primary cause of Heart disease and pregnancy. 2nd ed. Boston: Little, the heart failure complicating congestive cardiomyopathy.
Load more

Recommended publications
  • Common Types of Supraventricular Tachycardia: Diagnosis and Management RANDALL A
    Common Types of Supraventricular Tachycardia: Diagnosis and Management RANDALL A. COLUCCI, DO, MPH, Ohio University College of Osteopathic Medicine, Athens, Ohio MITCHELL J. SILVER, DO, McConnell Heart Hospital, Columbus, Ohio JAY SHUBROOK, DO, Ohio University College of Osteopathic Medicine, Athens, Ohio The most common types of supraventricular tachycardia are caused by a reentry phenomenon producing acceler- ated heart rates. Symptoms may include palpitations (including possible pulsations in the neck), chest pain, fatigue, lightheadedness or dizziness, and dyspnea. It is unusual for supraventricular tachycardia to be caused by structurally abnormal hearts. Diagnosis is often delayed because of the misdiagnosis of anxiety or panic disorder. Patient history is important in uncovering the diagnosis, whereas the physical examination may or may not be helpful. A Holter moni- tor or an event recorder is usually needed to capture the arrhythmia and confirm a diagnosis. Treatment consists of short-term or as-needed pharmacotherapy using calcium channel or beta blockers when vagal maneuvers fail to halt or slow the rhythm. In those who require long-term pharmacotherapy, atrioventricular nodal blocking agents or class Ic or III antiarrhythmics can be used; however, these agents should generally be managed by a cardiologist. Catheter ablation is an option in patients with persistent or recurrent supraventricular tachycardia who are unable to tolerate long-term pharmacologic treatment. If Wolff-Parkinson-White syndrome is present, expedient referral
    [Show full text]
  • Original Article Reversibility of Both Sinus Node Dysfunction and Reduced HCN4 Mrna Expression Level in an Atrial Tachycardia
    Int J Clin Exp Pathol 2016;9(8):8526-8531 www.ijcep.com /ISSN:1936-2625/IJCEP0023042 Original Article Reversibility of both sinus node dysfunction and reduced HCN4 mRNA expression level in an atrial tachycardia pacing model of tachycardia-bradycardia syndrome in rabbit hearts Zhisong Chen1*, Bing Sun1*, Gary Tse2, Jinfa Jiang1, Wenjun Xu1 1Department of Cardiovascular Diseases, Tongji Hospital of Tongji University, Shanghai, P. R. China; 2School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, P. R. China. *Equal contributors. Received December 31, 2015; Accepted March 17, 2016; Epub August 1, 2016; Published August 15, 2016 Abstract: Objective: The aim of this study was to investigate potential reversible changes in sinus node function and mRNA expression levels of hyperpolarization-activated, cyclic nucleotide-gated ion channel subunit 4 (HCN4) in a tachycardia pacing model in rabbits. Methods: A total of 45 adult New Zealand white rabbits were randomized into the following three groups (n=15): pacing only, pacing-recovery and control. Following open thoracotomy, temporary pacing leads were attached to the right atrium. In the pacing only group, rapid atrial pacing was initiated at a rate of 350 stimuli per minute for 8 hours a day, continuing for 7 days. In the pacing-recovery group, the same pacing protocol was delivered, but pacing was then stopped for 7 days. In the control group, no tachycardia pacing was de- livered. The following parameters were measured before and after intervention, and compared between the groups: resting heart rate, intrinsic heart rate (measured after metoprolol and atropine administration) and corrected sinus node recovery time (CSNRT).
    [Show full text]
  • Aberrated Supraventricular Tachycardia Associated with Neonatal Fever and COVID-19 Infection Kali a Hopkins ‍ ‍ ,1 Gregory Webster2
    Case report BMJ Case Rep: first published as 10.1136/bcr-2021-241846 on 30 April 2021. Downloaded from Aberrated supraventricular tachycardia associated with neonatal fever and COVID-19 infection Kali A Hopkins ,1 Gregory Webster2 1Department of Paediatrics, SUMMARY Her blood pressure was 87/63 mm Hg and her Northwestern University A 9-day- old girl presented during the 2020 SARS- peripheral oxygen saturation was 97%. Her lungs Feinberg School of Medicine, CoV-2 pandemic in wide-complex tachycardia with were clear to auscultation. She had no murmur or Chicago, Illinois, USA acute, symptomatic COVID-19 infection. Because the hepatosplenomegaly, and her capillary refill was 2 s. 2Division of Cardiology, Ann potential cardiac complications of COVID-19 were Three- lead telemetry revealed a regular, WCT. Her and Robert H Lurie Children’s mother, the primary caregiver, was acutely symp- Hospital of Chicago, Chicago, unknown at the time of her presentation, we chose Illinois, USA to avoid the potential risks of haemodynamic collapse tomatic with suspected COVID-19 illness (later associated with afterload reduction from adenosine. verified by PCR) and other household contacts Correspondence to Instead, a transoesophageal pacing catheter was placed. were COVID-19 positive. The infant had no family Dr Kali A Hopkins; Supraventricular tachycardia (SVT) with an aberrated history of sudden death or rhythm disorders. kahopkins@ luriechildrens. org QRS morphology was diagnosed and the catheter was used to pace-terminate tachycardia. This presentation INVESTIGATIONS Accepted 18 April 2021 illustrates that the haemodynamic consequences of a The initial 12- lead ECG recorded regular tachy- concurrent infection with largely unknown neonatal cardia at 215 beats per minute (figure 1).
    [Show full text]
  • ACLS Rhythms for the ACLS Algorithms
    A p p e n d i x 3 ACLS Rhythms for the ACLS Algorithms The Basics 1. Anatomy of the cardiac conduction system: relationship to the ECG cardiac cycle. A, Heart: anatomy of conduction system. B, P-QRS-T complex: lines to conduction system. C, Normal sinus rhythm. Relative Refractory A B Period Bachmann’s bundle Absolute Sinus node Refractory Period R Internodal pathways Left bundle AVN branch AV node PR T Posterior division P Bundle of His Anterior division Q Ventricular Purkinje fibers S Repolarization Right bundle branch QT Interval Ventricular P Depolarization PR C Normal sinus rhythm 253 A p p e n d i x 3 The Cardiac Arrest Rhythms 2. Ventricular Fibrillation/Pulseless Ventricular Tachycardia Pathophysiology ■ Ventricles consist of areas of normal myocardium alternating with areas of ischemic, injured, or infarcted myocardium, leading to chaotic pattern of ventricular depolarization Defining Criteria per ECG ■ Rate/QRS complex: unable to determine; no recognizable P, QRS, or T waves ■ Rhythm: indeterminate; pattern of sharp up (peak) and down (trough) deflections ■ Amplitude: measured from peak-to-trough; often used subjectively to describe VF as fine (peak-to- trough 2 to <5 mm), medium-moderate (5 to <10 mm), coarse (10 to <15 mm), very coarse (>15 mm) Clinical Manifestations ■ Pulse disappears with onset of VF ■ Collapse, unconsciousness ■ Agonal breaths ➔ apnea in <5 min ■ Onset of reversible death Common Etiologies ■ Acute coronary syndromes leading to ischemic areas of myocardium ■ Stable-to-unstable VT, untreated ■ PVCs with
    [Show full text]
  • Dysrhythmias
    CARDIOVASCULAR DISORDERS DYSRHYTHMIAS I. BASIC PRINCIPLES OF CARDIAC CONDUCTION DISTURBANCES A. Standard ECG and rhythm strips 1. Recordings are obtained at a paper speed of 25 mm/sec. 2. The vertical axis measures distance; the smallest divisions are 1 mm ×1 mm. 3. The horizontal axis measures time; each small division is 0.04 sec/mm. B. Normal morphology Courtesy of Dr. Michael McCrea 1. P wave = atrial depolarization a. Upright in leads I, II, III, aVL, and aVF; inverted in lead aVR b. Measures <0.10 seconds wide and <3 mm high c. Normal PR interval is 0.12–0.20 seconds. 2. QRS complex = ventricular depolarization a. Measures 0.06-0.10 seconds wide b. Q wave (1) <0.04 seconds wide and <3 mm deep (2) Abnormal if it is >3 mm deep or >1/3 of the QRS complex. c. R wave ≤7.5 mm high 3. QT interval varies with rate and sex but is usually 0.33–0.42 seconds; at normal heart rates, it is normally <1/2 the preceding RR interval. 4. T wave = ventricular repolarization a. Upright in leads I, II, V3–V6; inverted in aVR b. Slightly rounded and asymmetric in configuration c. Measures ≤5 mm high in limb leads and ≤10 mm high in the chest leads 5. U wave = a ventricular afterpotential a. Any deflection after the T wave (usually low voltage) b. Same polarity as the T wave c. Most easily detected in lead V3 d. Can be a normal component of the ECG e. Prominent U waves may indicate one of the following: (1) Hypokalemia (<3 mEq/L) (2) Hypercalcemia (3) Therapy with digitalis, phenothiazines, quinidine, epinephrine, inotropic agents, or amiodarone (4) Thyrotoxicosis f.
    [Show full text]
  • The Bradycardia-Tachycardia Syndrome Treatment with Cardiac Drugs and Adrenal Corticosteroid Junichi FUJII, M.D., Nobumitsu TAKA
    The Bradycardia-Tachycardia Syndrome Treatment with Cardiac Drugs and Adrenal Corticosteroid Junichi FUJII, M.D., Nobumitsu TAKAHASHI,M.D., and Kazuzo KATO, M.D. Seven patients of S-A block complicated by tachycardic paroxysms of atrial fibrillation or flutter were described and the medical treatment in this syndrome was reappraised. Damage to S-A node and adjacent atrial tissue was assumed in all patients. All the patients had syncopal attacks associated with cardiac arrest occurring especially at the termina- tion of tachycardia. Overdrive suppression of diseased S-A node and lower automatic pacemakers was demonstrated by ECG recordings. The term "bradycardia-tachycardia syndrome" or "syndrome of alternating bradycardia and tachycardia" seemed appropriate. In spite of difficulty of medical treatment reiterated by previous de- scriptions, 6 of 7 patients were improved with drug therapy, including adrenal corticosteroid. Adrenal corticosteroid in combination with or- ciprenaline or belladonna alkaloids was most helpful among the drugs used. Obviously, pacemaker implantation should be performed without delay in patients with frequent and prolonged attacks of syncope. But not all patients have need of pacemaker implantation. A trial of drug therapy may be permitted in many patients of this syndrome before in- troduction of pacemaker. Additional Indexing Words: Sick sinus syndrome S-A block Atrial tachyarrhythmias Syn- cope Overdrive suppression ECENTLY there have been some reports concerning the patients with S-A block or sinus bradycardia accompanied by paroxysmal atrial tachy- arrhythmias such as fibrillation, flutter and paroxysmal tachycardia. As pointed out by several authors, these patients repeatedly exhibited syncopal attacks associated with asystole following termination of the tachycardia.
    [Show full text]
  • 90 Correlation of Cardiac Hemodynamics and Bioenergetics Using Phosphorus Nmrspectroscopy
    CARDIOLOGY 125A DETECTION OF ATRIOVENTRICULAR VALVE ABNORMALITIES FUNCTIONAL THYROTOXIC CARDIOMYOPATHY IN CHILDREN. BY ECHOCARDIOGRAPHY IN CHROMOSOMAL ANOMALIES Anita Cavallo, Alfonso Casta, H. Daniel Fawcett, 85 Alfonso Casta, Karen Haslund, Kirk Aleck, Janet Martin L. Nusynowitz, and Wendy J. Wolf (Spon. by Williams, Chalermlarp Mongkalsmai, Amarjit Singh, Walter J. Meyer), Departments of Pediatrics and Radiology, uni­ (Span. by Ben Brouhard) U.ni v. of Texas, Ga 1 veston, Southern versity of Texas Medical Branch, Galveston, Texas. Illinois Univ., Springfield, Minneapolis Children's Health Myocardial performance during thyrotoxicosis (T) was evalu­ Center tted by multigated radionuc lide angiocardiography during graded Cardiac malformations are not uncommon in chromosomal anoma­ =xercise in 8 children (8-17 ys) with Graves' disease. With lies and may contribute to early death. In this study, two­ exercise, heart rate (HR) and systolic blood pressure (SBP) in­ dimensional echocardiography demonstrated unusual atrioventric­ creased in all patients; left ventricular ejection fraction ular valve abnormalities in 4 neonates without overt structural (LVEF) increased normally by 7 to 10% in 4 (2 male, 2 female), heart defects (except for 1) and chromosomal anomalies. Three but did not increase significantly in 1 (male) and decreased by of 4 presented with signs of congestive heart failure: one had 3 to 8% in 3 (female) . There was no s ignificant difference in partial trisomy llp, redundant mitral and tricuspid valves the duration of T, resting and exercise HR and SBP, or resting and an aneurysm of the interatrial septum; one had Teschler/ LVEF, between patients with normal and abnormal responses . The Nicola-Killian syndrome, a redundant mitral valve and a small change in LVEF was inversely correlated with serum T4 (r= -.82, atrial septal defect; and one had trisomy 18, a large ventric­ p<.02) and T3 (r= -.88, p<.OS).
    [Show full text]
  • 2017 HRS/EHRA/ECAS/APHRS/SOLAECE Expert Consensus Statement on Catheter and Surgical Ablation of Atrial fibrillation
    2017 HRS/EHRA/ECAS/APHRS/SOLAECE expert consensus statement on catheter and surgical ablation of atrial fibrillation Hugh Calkins, MD (Chair),1 Gerhard Hindricks, MD (Vice-Chair),2,* Riccardo Cappato, MD (Vice-Chair),3,{ Young-Hoon Kim, MD, PhD (Vice-Chair),4,x Eduardo B. Saad, MD, PhD (Vice-Chair),5,z Luis Aguinaga, MD, PhD,6,z Joseph G. Akar, MD, PhD,7 Vinay Badhwar, MD,8,# Josep Brugada, MD, PhD,9,* John Camm, MD,10,* Peng-Sheng Chen, MD,11 Shih-Ann Chen, MD,12,x Mina K. Chung, MD,13 Jens Cosedis Nielsen, DMSc, PhD,14,* Anne B. Curtis, MD,15,k D. Wyn Davies, MD,16,{ John D. Day, MD,17 André d’Avila, MD, PhD,18,zz N.M.S. (Natasja) de Groot, MD, PhD,19,* Luigi Di Biase, MD, PhD,20,* Mattias Duytschaever, MD, PhD,21,* James R. Edgerton, MD,22,# Kenneth A. Ellenbogen, MD,23 Patrick T. Ellinor, MD, PhD,24 Sabine Ernst, MD, PhD,25,* Guilherme Fenelon, MD, PhD,26,z Edward P. Gerstenfeld, MS, MD,27 David E. Haines, MD,28 Michel Haissaguerre, MD,29,* Robert H. Helm, MD,30 Elaine Hylek, MD, MPH,31 Warren M. Jackman, MD,32 Jose Jalife, MD,33 Jonathan M. Kalman, MBBS, PhD,34,x Josef Kautzner, MD, PhD,35,* Hans Kottkamp, MD,36,* Karl Heinz Kuck, MD, PhD,37,* Koichiro Kumagai, MD, PhD,38,x Richard Lee, MD, MBA,39,# Thorsten Lewalter, MD, PhD,40,{ Bruce D. Lindsay, MD,41 Laurent Macle, MD,42,** Moussa Mansour, MD,43 Francis E. Marchlinski, MD,44 Gregory F.
    [Show full text]
  • Banner Staff Service ECG Study Guide
    Banner Staff Service ECG Study Guide Edited by Larry H. Lybbert, MS, RN Table of Contents ECG STUDY GUIDE ................................................................................................................................................... 3 ECG INTERPRETATION BASICS........................................................................................................................... 4 EKG GRAPH PAPER ..................................................................................................................................................4 RATE MEASUREMENT...............................................................................................................................................9 The Six Second Method........................................................................................................................................9 Large Box Method................................................................................................................................................9 Small Box Method ................................................................................................................................................9 BASIC EKG RHYTHM ANALYSIS GUIDE ................................................................................................................11 Rhythm Interpretation........................................................................................................................................13 Six Basic Steps for Rhythm Interpretation
    [Show full text]
  • Tachycardia Related Cardiomyopathy: Response to Control of the Arrhythmia
    Tachycardia Related Cardiomyopathy: Response to Control of the Arrhythmia BURT I. BROMBERG, M.D., MACDONALD DICK 11, M.D., A. REBECCA SNIDER, M.D., WILLIAM A. SCOTT, M.D., GERALD A. SERWER, M.D., EDWARD L. BOVE, M.D., and KATHLEEN P. HEIDELBERGER, M.D. From the Division of Pediatric Cardiology, C. S. Mott Children S Hospital, and the Departments of Pediatrics, Surgery, and Pathology, University of Michigan, Ann Arbor, Michigan To evaluate the clinical response of five children ingfraction (20% pre vs 34% post; P = 0.006), with automatic atrial tachycardia (AA T) and as- mean ejection fraction (36% pre vs 50% post; P sociated cardiomyopathy to arrhythmia control, < 0.01), mean velocity of’ circumferential fiber we compared pretreatment and posttreatment 24- shortening (0.62 pre vs 1.20 post; P = 0.003). hour ECG heart rates, cardiothoracic ratio by Mean E-point septa1 separation corrected for end- chest radiograph, and echocardiographic mea- diastolic dimension also showed a trend toward sures of ventricular ,function. Two children were improvement (0.25 pre vs 0.16 post; P = 0.11). treated with amiodarone, two with surgical exci- Right ventricular endocardial biopsies in four were sion and cryoablation of the ectopicfocus, and one nonspecific; an atrial biopsy from surgery showed with digoxin alone. Signijicantly slower mean a Purkinje fiber-like tissue in one patient, but was heart rates were achieved, along with a dominant nonspecijic in another. We conclude that cardio- sinus rhythm and improvement in symptoms. myopathy can be causally linked to automatic Control of the AAT resulted in improved mean atrial tachycardia and that aggressive medical cardiothoracic ratio (0.53 pre vs 0.49 post; P and/or surgical management is warranted in those = 0.021, as well as improvement in a number of patients with signs and symptoms of impaired ven- echocardiographic measurements: mean shorten- tricular function.
    [Show full text]
  • Management of Atrial Tachycardia in the Newborn with Enterovirus Myocarditis
    The Ochsner Journal 12:163–166, 2012 Ó Academic Division of Ochsner Clinic Foundation Management of Atrial Tachycardia in the Newborn With Enterovirus Myocarditis Daniel H. Petroni, MS,* Song G. Yang, MD, PhD,* Mudar M. Kattash, MD,* Christopher S. Snyder, MD* *Department of Pediatric Cardiology, Tulane University School of Medicine, New Orleans, LA Department of Pediatric Cardiology, Ochsner Clinic Foundation, New Orleans, LA meningoencephalitis, myocarditis, and hepatitis.2 In ABSTRACT addition, infants younger than 10 days are unable to Neonatal enterovirus myocarditis is a rare but serious infection mount a significant immune response and are at a that is often an underrecognized cause of cardiovascular higher risk of a serious infection from these nonpolio collapse. Enterovirus myocarditis in patients with such EVs.2 collapse should be suspected when signs of congestive heart Clinical manifestations of EV myocarditis in neo- failure and tachyarrhythmia are present. The majority of nates may include signs of congestive heart failure reported electrical disturbances associated with enterovirus and tachycardia. The mechanism of EV-induced myocarditis are ventricular in origin, but the infection can damage to cardiac myocytes is unknown, but it has present as atrial tachyarrhythmia. Atrial tachyarrhythmias been suggested that the mechanism is through a associated with enterovirus myocarditis are difficult to manage direct viral-mediated cytotoxicity as well as damage because of their resistance to conventional antiarrhythmic from the body’s own immune response.3 Abnormal- therapy. We present 2 cases of neonates with atrial ities most commonly seen on electrocardiogram tachycardia associated with enterovirus myocarditis who (EKG) in patients with EV myocarditis include sinus responded to a combination of amiodarone and flecainide.
    [Show full text]
  • Supraventricular Arrhythmias.Pdf
    general: - SVTs are any tachycardia that require atrial - sometimes called ectopic atrial tachycardia or AV nodal tissue for their initiation & maintenance - SVTs are usually narrow complexes but may be wide complex in ecg: the setting of bundle branch block or pre-excitation - p wave morphology is often abnormal but monomorphic atrial rate is often 130-160bpm and may exceed 200bpm - in critical illness the continuing arrhythmogenic and chronotropic factors make - AV block is common rate control of SVTs difficult general - digoxin often results in poor rate control in critical illness (although it may have clinical: unifocal minor inotropic and vasopressor effects that are beneficial) - digoxin toxicity is the most common cause especially when AV block is present atrial - magnesium provides effective rate control and may revert SVT - other causes include myocardial infarction, chronic lung disease & metabolic disturbance tachycardia - amiodarone may be useful for rate control treatment: - cardioversion is indicated in unstable patients but is more likely to maintain SR - if applicable digoxin is stopped and toxicity is treated; if loading with an anti-arrhythmic such as amiodarone has been performed prior otherwise it may be used to control ventricular rate - blockers or amiodarone are alternatives - overdrive pacing may be ineffective but may slow ventricular rate by increasing AV block AV node dependent (junctional tachycardias): - synchronised cardioversion may be required but should be avoided with digoxin toxicity (i) AV nodal re-entrant
    [Show full text]