Paroxysmal Supraventricular Tachycardia in an Octogenarian

The Journal of Emergency Medicine, Vol. 43, No. 3, pp. 457–460, 2012 Published by Elsevier Inc. Printed in the USA. 0736-4679/$ - see front matter doi:10.1016/j.jemermed.2011.06.033 Clinical Communications: Adults PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA IN AN OCTOGENARIAN Nancy Lutwak, MD* and Curt Dill, MD*† *VA New York Harbor Healthcare Center, New York, New York and †Department of Emergency Medicine, NYU School of Medicine, New York, New York Reprint Address: Nancy Lutwak, MD, VA New York Harbor Healthcare Center, 423 East 23rd Street, New York, NY 10010 may have new onset of this dysrhythmia as a result of catecholamine surges caused by stress, infection, or pain. Our patient had cholecystitis, choledocholithiasis, and pancreatitis. , Abstract—Background: Paroxysmal supraventricular tachycardia is a common dysrhythmia that occurs at all ages. Its management is determined by presenting symptoms and previous history of the patient. Patients present with a continuum of symptoms ranging from palpitations to syncope. The incidence of supraventricular tachycardia increases with age. Objectives: To discuss the etiology, precipitating factors, and acute management of supraventricular tachycardia; and to discuss nodal reentry circuits and representative electrocardiographic findings. Case Report: We present the case of an 84-year-old man with gallstone pancreatitis, choledolcholithiasis, and cholecystitis complicated by paroxysmal supraventricular tachycardia. We review this dysrhythmia, emphasizing its significance in elderly patients. Conclusion: Supraventricular tachycardia is a common dysrhythmia that can result in syncope or myocardial infarction. We present a case of an elderly man with new-onset atrioventricular (AV) nodal reentry tachycardia, possibly precipitated by overdrive of his autonomic nervous system due to pain and infection. As the percentage of the elderly in our population is growing rapidly and the incidence of AV nodal reentry tachycardia increases with age, emergency physicians should be familiar with this dysrhythmia—its etiology, precipitating factors, presentations, and treatment. It will present more frequently in the future. Published by Elsevier Inc. CASE REPORT The patient was an 84-year-old man presenting to the Emergency Department (ED) with abdominal pain and poor appetite for 1 week. He denied shortness of breath, chest pain, dizziness, palpitations, and lightheadedness. Past medical history was positive for dermatological carcinoma, left inguinal hernia repair, obstructive uropathy, hypertension, and dementia. He denied having angina, cardiac dysrhythmias, or congestive heart failure in the past and was taking no medication. Family history was positive for breast carcinoma (mother). He denied smoking cigarettes, drinking alcohol, and using illicit drugs. He lived with his wife. On physical examination, the patient had a temperature of 35.9  C (96.6 F), respiratory rate of 26 breaths/min, and blood pressure of 153/95 mm Hg. The heart rate was 186 beats/min. He was not diaphoretic and was not in distress. He was awake and alert. Abdomen was tender in the supraumbilical area, although he had no rebound or guarding. There was no thyromegaly. The remainder of the examination was negative. Electrocardiogram (ECG) revealed supraventricular tachycardia at a rate of 180 beats/min, without evidence of ischemia (Figure 1). The patient was given adenosine , Keywords—dysrhythmia; supraventricular tachycardia; PSVT INTRODUCTION The incidence of supraventricular tachycardia increases with age. Elderly patients, like the one in our case report, RECEIVED: 6 December 2010; FINAL SUBMISSION RECEIVED: 23 February 2011; ACCEPTED: 2 June 2011 457 458 N. Lutwak and C. Dill Figure 1. Electrocardiogram of patient in the Emergency Department. 6 mg intravenous push (IVP), which converted the rhythm to normal sinus at 70 beats/min, again without evidence of ischemia. Laboratory studies were positive for creatinine of 1.6 mg/ dL, total bilirubin of 3.3 mg/dL (normal .1–1.2), direct bilirubin of 1.5 mg/dL, alkaline phosphatase of 184 U/L, serum glutamic-oxaloacetic transaminase of 296 IU/L and serum glutamic-pyruvic transaminase of 260 U/L. Glucose was 148 mg/dL. Amylase was 4790 U/L (normal 25–125), lipase was 3132.1 U/L (normal 7–60), and white blood cell count was 15.0, 80% neutrophils with 10% bands. Point-of-care troponin-Biosite (Biosite Incorporated, San Diego, CA) was < 0.05 Ng/mL (negative). Ultrasound of the abdomen was positive for gallstones and biliary sludge. Computed tomography scan of the abdomen and pelvis revealed a dilatated common bile duct (1.5 cm) with a possible calculus and a 4.5-cm complex fluid collection at the inferior margin of the pancreatic body, probably a complex pseudocyst. The gallbladder was distended without wall thickening. In the ED, the patient had another episode of supraventricular tachycardia at a rate of 180 beats/min, which again converted to normal sinus rhythm after administration of 6 mg of intravenous adenosine. The man was admitted to the intensive care unit and was started on amoxicillin-clavulanic acid 1.5 mg every 6 h. He had short runs of supraventricular tachycardia and was started on metoprolol. An echocardiogram revealed a left ventricle with normal wall motion, ejection fraction of 65%, normal valves, and a slightly dilatated left atrium. The following day an endoscopic retrograde cholangiopancreatography was performed and 27-mm stones were removed from the common bile duct. One week later, the patient was discharged on metoprolol after computed tomography scan of the abdomen and pelvis showed improved pancreatitis and a smaller fluid collection. He was to return for laparoscopic cholecystectomy. In 4 weeks, the patient was brought to the operating room. On induction of anesthesia, before intubation, the patient developed a short run of supraventricular tachycardia refractory to esmolol, but responsive to metoprolol. He was not hypotensive; however, the surgery was postponed. He later had placement of a cholecystostomy tube resulting in multiple complications and hospitalizations. DISCUSSION Paroxysmal supraventricular tachycardia occurs frequently and is a recurrent condition that accounts for many visits to EDs (1,2). In addition, palpitations are a common symptom leading patients to seek medical attention from their family physicians (3). Elderly patients often have tachycardias, and atrioventricular nodal reentrant tachycardia is the most common regular supraventricular tachycardia in the elderly Paroxysmal Supraventricular Tachycardia (4,5). The incidence of supraventricular tachycardia (SVT) is estimated to be 35 per 100,000 people per year (6). Some studies, however, have shown the rate to be 12% in a normal disease-free population aged 16–65 years, whereas others report an incidence of 18%. The incidence increases with age and cardiac disease but is difficult to quantify because many episodes are asymptomatic (7). The incidence of this dysrhythmia increases with age even among people without coronary artery disease, whether at rest, routine activity, or with exercise. Incidence of isolated SVT beats in healthy people aged 80–89 years during exercise is 76% (8). In older patients with no evidence of cardiac disease, the incidence of brief asymptomatic runs of paroxysmal supraventricular tachycardia (PSVT) is 13% (8). Some patients with PSVT report palpitations on arrival to the ED or in their physician’s office. The palpitations start and stop abruptly and their duration is highly variable (7). Palpitations may be initially misdiagnosed by family physicians as panic, anxiety, or stress, particularly in women (3). Other common symptoms of SVT are lightheadedness, chest pain, dyspnea, anxiety, and pounding in the chest and neck (6). Pre-syncope may occur and if the PSVT is extremely rapid, syncope may result from compromise in cardiac output (7). Syncope is uncommon, as is myocardial infarction or heart failure. The symptoms may be quite subtle, however, and many will not seek medical attention. The more symptomatic patients may have underlying heart disease (9). Usually, PSVT starts and stops abruptly but may be more prolonged secondary to the cardiac adrenergic drive resulting from anxiety or hypotension produced by the dysrhythmia itself. There may also be an urge to urinate due to the release of atrionatriuretic peptide (7). By contrast, sinus tachycardias usually accelerate and decelerate more gradually (6). Sudden cardiac arrest due to SVT is quite rare (9). In healthy elderly people, SVT seems to be benign and does not increase the risk of cardiac mortality. Even if the beats are frequent or complex, there is no increased risk of cardiac-related death. Of note, regardless of patient age, the presence and severity of underlying cardiac disease is much more important prognostically than having this dysrhythmia. Patients with ectopic beats from SVT are usually asymptomatic even if the beats are frequent, and consequently, no treatment is necessary. The risk of cardiac events is not increased in patients with no underlying cardiac illness (8). Rarely, patients with SVT present with cardiomegaly or chronic cardiac failure (7). SVT is uncommonly associated with structural heart disease, but rarely can occur in hypertrophic cardiomyopathy with accessory pathways or Ebstein anomaly. The dysrhythmia is usually induced by premature ectopic beats from the atria or ventricle. Precipitating factors include excessive alcohol, caffeine, illicit drugs, and hyperthyroidism (6). SVT can be triggered by catechol- 459 amine release during times of intense exercise, emotional difficulties, or in illness like pheochromocytoma (3). New onset of atrioventricular (AV) nodal reentrant tachycardia in older adults may be influenced by the autonomic nervous system rather than by changes in AV nodal conduction (10). ECGs of patients with PSVT usually have narrow QRS complexes at a rate of 150–200 beats/min. PSVT is most commonly a result of AV reentry. In AV nodal reentry tachycardia (AVNRT), the reentry circuit is in or close to the AV node and is small. The larger reentry circuit associated with AV reentry tachycardia (AVRT) involves the atria, AV node, and the ventricles. AVNRT can occur in young and older patients, is uncommonly incessant, and is not associated with a poor prognosis. The QRS on the ECG is narrow unless there is a bundle branch block, and usually there is no visible P wave. AVNRT, the most common form of PSVT, is caused by an antegrade limb that is a slow AV nodal pathway and a retrograde limb that is a fast AV nodal pathway. Generally, the atria and ventricle are simultaneously activated so the P wave is very close, obscured by or buried within the QRS complex. In contrast, patients with AVRT usually present at younger ages, and the P wave on ECG is in the ST segment, T wave, or visible between successive R waves. This occurs because the ventricle and the atria are sequentially activated (7). Because the tachycardia of AVNRT and AVRT is dependent on conduction in the AV node, an interruption of this conduction will terminate the tachycardia (7). PSVT may be terminated by vagal maneuvers, but carotid sinus massage should be performed cautiously in older patients (8). Intravenous adenosine or verapamil will cause termination of AVNRT by slowing conduction in the antegrade AV nodal pathway (11). Verapamil should not be used in patients with hypotension. Adenosine has a rapid onset of action and there is a low risk of causing hypotension. There is a low risk of adverse effects in patients who are young as well as in patients older than 70 years when using intravenous adenosine (8). When given adenosine 6 mg IVP, SVT is terminated in 60–80% of patients, and a dose of 12 mg IVP results in 90–95% termination. If adenosine is not effective or is contraindicated, intravenous b-blocker may be used (6). Adenosine is usually effective within 15–30 s and may cause facial flushing, dyspnea, or chest pain. The half-life of adenosine is extremely short. It is an A1 receptor agonist that may cause bronchospasm in patients with asthma. Dipyridamole potentiates its effects, and heart transplant patients have supersensitivity to it, requiring special care (9). Flecainide or propafenone should be used in patients with WolffParkinson-White syndrome (7). Any patient with PSVT with resultant heart failure, cardiac ischemia, hypotension, or cerebral ischemia must 460 have immediate cardioversion beginning at 25–50 joules (8). Recurrences can be prevented with b-blockers or calcium channel blockers given once a day. Long-term medical treatment of patients with recurrent SVT may not be necessary (6). The severity and frequency of the symptoms must be considered in directing the best ongoing care (6,9). Patients with Wolff-Parkinson-White syndrome, syncope or dyspnea with palpitations, tachycardia with wide QRS complexes of unknown origin, or tachycardia with narrow QRS complexes that is refractory to medication should be evaluated by a specialist (11). Electrophysiological transesophageal studies reveal clinical and electrophysiological differences in patients with PSVT who have AVRT and AVNRT. If slow pathway ablation is deemed necessary in elderly patients, it is as effective and safe as in younger patients (5). AVNRT increases with age and is an acquired disease. An episode may be triggered by a ventricular premature contraction and ECG may reveal negative P waves in the inferior leads. Patients usually report feeling a rapid heart rate (7). The real incidence of AVNRT in older patients may be underestimated. There is a female predominance for AVNRT greater than two to one. There is also a 10-year gap in clinical presentation between AVRT and AVNRT due to the increased incidence of AVNRT in elderly patients. There is a link between AVNRT and outflow tract ventricular dysrhythmias that may be caused by an inflammatory process of the epicardium/myocardium. Clinical clues to correct electrocardiographic diagnosis of AVNRT include older age, female gender, and the patient feeling neck palpitations (12). The spectrum of dysrhythmias is significantly different among patients without and with structural heart disease. AVNRT occurs less frequently than atrial flutter in patients with structural heart disease (13). In the aging population, anti-dysrhythmic medications, such as b-blockers or amiodarone, may not be well tolerated. Radiofrequency catheter ablation is now being used safely and more frequently in elderly patients for AVNRT, atrial fibrillation, and atrial flutter (13,14). The incidence of sick sinus syndrome, which is thought to be caused by fibrotic changes in sinus nodal tissue, also increases with age. This leads to episodes of alternating atrial brady-tachy dysrhythmias, sinus pauses, and chronic atrial dysrhythmias. This syndrome is the cause for half of the implantation of pacemakers in the United States. Sinus node function declines as age increases; older patients have decreased heart rates and lengthened conduction times in the sinus node. This may result from degenerative changes as well as problems with gap junctions and ion channels (15). Elderly patients with atrial fibrillation stemming from the brady-tachy syndrome may present with dizziness, N. Lutwak and C. Dill dyspnea, heart failure, or syncope. The long-term use of medications to control the atrial fibrillation may not be well tolerated in this population. Rapid atrial pacing recently has been shown to prevent recurrence of this dysrhythmia in elderly patients with the brady-tachy syndrome (16). CONCLUSION Our elderly patient had AV nodal reentry tachycardia, a dysrhythmia that increases with age. It was controlled with b-blockers and adenosine. The onset of this dysrhythmia may have been precipitated by catecholamine surges secondary to his acute infection, pain, and later, by induction of anesthesia. REFERENCES 1. Amitrano D, Ammendola E, Cavallaro C, Santangelo L. Retrospective analysis of 300 cases of paroxysmal supraventricular tachycardia by electrophysiological transesophageal study. Minerva Cardioangiol 2006;54:363–8. 2. Murman DH, McDonald AJ, Pelletier AJ, Camargo CA Jr. U.S. emergency Department visits for supraventricular tachycardia, 1993–2003. Acad Emerg Med 2007;14:578–81. 3. Abbott AV. Diagnostic approach to palpitations. Am Fam Physician 2005;71:743–50. 4. Yangni N’Da O, Brembilla-Perrot B. 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