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Qt2g74c8n4.Pdf UCLA UCLA Previously Published Works Title Digitalis toxicity: a fading but crucial complication to recognize. Permalink https://escholarship.org/uc/item/2g74c8n4 Journal The American journal of medicine, 125(4) ISSN 1555-7162 Authors Yang, Eric H Shah, Sonia Criley, John M Publication Date 2012-04-01 Peer reviewed eScholarship.org Powered by the California Digital Library University of California REVIEW Digitalis Toxicity: A Fading but Crucial Complication to Recognize Eric H. Yang, MD,a Sonia Shah, MD,b John M. Criley, MDb aDivision of Cardiology, Department of Medicine, University of California at Los Angeles; bDivision of Cardiology, Department of Medicine, Harbor-UCLA Medical Center, Torrance, Calif. ABSTRACT Digoxin usage has decreased in the treatment of congestive heart failure and atrial fibrillation as a result of its inferiority to beta-adrenergic inhibitors and agents that interfere with the deleterious effects of the activated renin-angiotensin-aldosterone system. As a result of reduction of usage and dosage, glycoside toxicity has become an uncommon occurrence but may be overlooked when it does occur. Older age, female sex, low lean body mass, and renal insufficiency contribute to higher serum levels and enhanced risk for toxicity. Arrhythmias suggesting digoxin toxicity led to its recognition in the case presented here. © 2012 Elsevier Inc. All rights reserved. • The American Journal of Medicine (2012) 125, 337-343 KEYWORDS: Arrhythmia; Digitalis; Digoxin; Heart failure; Toxicity Cardiac glycosides have been used for the treatment of history of chronic renal insufficiency with an admission congestive heart failure for over 2 centuries, and in the creatinine of 3.78 mg/dL, or glomerular filtration rate of treatment of arrhythmias for over 100 years, and were for 16.8 mL/min/1.73 m2; the serum level ranged from 2.7 to many years a leading agent responsible for iatrogenic 4.1 mg/dL for the past 2 years before admission. He was morbidity and mortality. The development of more ef- diagnosed with nonischemic cardiomyopathy by cardiac fective cardiac drugs in the last half of the 20th century catheterization a decade prior, with normal coronary arte- has led to diminished utilization, but not abandonment of riography and a left ventricular ejection fraction of 10%- glycosides. The incidence of toxicity has subsequently de- 15% on ventriculography. A transthoracic echocardiogram creased, as has the level of suspicion of more recently a year before admission demonstrated an improved left trained physicians. ventricular ejection fraction of 50% on medical therapy. He had no known allergies, and denied any tobacco, alcohol, or CASE PRESENTATION illicit drug use. His outpatient regimen had consisted of digoxin 0.125 A 73-year-old African-American male with multiple medi- mg daily, carvedilol 25 mg twice a day, diltiazem extended- cal problems was admitted for recurrent episodes of syn- release 120 mg daily, simvastatin 20 mg daily, furosemide cope associated with coughing, and increasing weakness 40 mg twice a day, valsartan 160 mg daily, spironolactone and dyspnea on exertion at 10 feet. He denied any history of 25 mg daily, amlodipine 10 mg twice a day, calcium acetate palpitations, chest pain, or paroxysmal nocturnal dyspnea. 667 mg with meals, isosorbide dinitrate 10 mg 3 times daily, The patient’s comorbidities included obesity, hyperten- hydralazine 10 mg 3 times daily, and subcutaneous insulin. sion, diabetes mellitus, and dyslipidemia. He also had a He had been taking this regimen consistently for approxi- mately 2 years. Funding: None. Conflict of Interest: None. An electrocardiogram on admission demonstrated sinus Authorship: All authors had a significant role in writing the manu- rhythm, first-degree atrioventricular block with a PR inter- script. val of 236 ms, and a left bundle branch block pattern with Requests for reprints should be addressed to Eric H. Yang, MD, a QRS width of 176 ms, which had been present on previous Division of Cardiology, Department of Medicine, University of California at Los Angeles, 100 UCLA Medical Plaza, Suite 630, Los Angeles, CA electrocardiograms. A corrected QT interval was increased 90095. at 529 ms. Premature ventricular complexes also were noted E-mail address: [email protected]. (Figure 1). 0002-9343/$ -see front matter © 2012 Elsevier Inc. All rights reserved. doi:10.1016/j.amjmed.2011.09.019 338 The American Journal of Medicine, Vol 125, No 4, April 2012 The patient subsequently developed altered mental sta- tricular block with return of the left bundle branch block tus, associated with hypercarbic hypoxemic respiratory fail- pattern and a prolonged PR interval of 276 ms. When seen by ure that required endotracheal intubation. A repeat transtho- the cardiology consultation service, the patient was resting racic echocardiogram performed on hospital day #3 showed comfortably and denied any nausea, vomiting, vision changes, a depressed left ventricular ejection fraction of 25%-30%, seeing green or yellow, chest pain, or palpitations. On exam- with global left ventricular hypo- ination the patient was afebrile, with kinesis, but no significant valvar a heart rate of 83 beats per minute, disease. His clinical state was CLINICAL SIGNIFICANCE blood pressure of 115/59 mm Hg, further complicated by worsen- respiratory rate of 20 breaths per ing renal failure, necessitating he- ● Digoxin toxicity, although an infrequent minute, and oxygen saturation of modialysis on hospital day #18. occurrence, may be present in older pa- 100% on tracheostomy collar. His He also required emergent trache- tients (women more than men) with renal jugular venous pressure was esti- otomy due to traumatic self-extu- insufficiency or other drugs that interfere mated at 10 cm H20. Auscultation bation, causing vocal cord paraly- revealed regular rhythm with no mur- with glycoside pharmacokinetics. sis and tracheal trauma. murs, rubs, or gallops. He had de- During this time, digoxin was ● Arrhythmias caused by digitalis glyco- creased breath sounds in his posterior administered along with his conges- sides include blockage of sinoatrial and lung bases. No peripheral edema was tive heart failure medications. The atrioventricular conduction and en- present. patient had a prolonged hospital hanced automaticity of atrial, junc- Serum potassium was 3.9 course due to renal failure and re- tional, and ventricular cells. mmol/L, bicarbonate 24 mmol/L, spiratory issues, including pneumo- and a digoxin level was 1.6 ng/mL, nia. On hospital day #32, 2 hours ● Anti-digoxin antibody administration is previously obtained approximately after receiving his daily digoxin indicated for patients with refractory, 30 hours before the patient’s pre- dose, the patient was noted to be life-threatening arrhythmias and hemo- sentation of heart block. Digoxin nonresponsive, and bradycardia was dynamic instability. levels were obtained 2 hours before noted on the telemetry monitor. An the daily administration of digoxin. electrocardiogram revealed com- Because of a high clinical suspi- plete atrioventricular heart block cion for digoxin toxicity, digoxin with a sinus rhythm of 90 beats per minute, and a fascicular and atrioventricular nodal blocking agents (carvedilol and dil- escape rhythm of 50 beats per minute with multiple premature tiazem) were discontinued. ventricular complexes (Figure 2). A repeat electrocardiogram Approximately 3 hours after the return of sinus rhythm, 10 minutes later demonstrated resolution of complete atrioven- the patient developed bradycardia, became unresponsive, Figure 1 Electrocardiogram on admission. Sinus rhythm rate 73 beats per minute, with 3 ventricular premature complexes (*), first-degree atrioventricular block (PR interval of 236 ms), and left bundle branch block. Ladder indicates delayed atrioventricular conduc- tion and premature ventricular complexes (*upward arrows) followed by compensatory pauses. Yang et al Digitalis Toxicity 339 Figure 2 Complete heart block. Sinus rhythm, rate 87 beats per minute, ventricular rate 50 beats per minute, with 3 premature ventricular complexes (PVCs). The prevalent QRS complexes exhibit a superior axis and are positive in lead V1, suggesting an escape focus in the left posterior fascicle (downward arrows). The PVCs (upward arrows) reset the fascicular pacemaker. and progressed to pulseless electrical activity. Precordial confirmed by a 4.3-ng/mL serum digoxin level, 7 vials of chest compressions were initiated while epinephrine and 38-mg digoxin-specific antibody fragments were adminis- atropine were administered. Ventricular fibrillation ensued, tered as an intravenous bolus. A temporary transvenous which required 3 200-joules countershocks to convert to a pacemaker electrode was placed in the right ventricle. hemodynamically stable wide complex tachycardia (Figure The patient gradually regained atrioventricular node 3). Intravenous amiodarone and sodium bicarbonate were conduction with first-degree atrioventricular block (PR administered, but the patient was noted to develop third- interval of 350 ms) with left bundle branch block (Figure degree atrioventricular block with sinus rhythm of 64 beats 4), which he maintained throughout the remainder of his per minute, and an escape rhythm suggestive of an origin hospitalization. The right ventricular pacemaker elec- from the left posterior fascicle with a rate of 47 beats per trode was removed 2 days later. The patient remained minute. Because of mounting suspicion of digoxin toxicity, neurologically intact, with
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