A case of appropriate inappropriate device therapy: Hyperkalemia-induced ventricular oversensing

Abstract

A 56-year-old woman with a history of congenital heart disease, type 2 diabetes mellitus and heart failure received inappropriate, but potentially life-saving, therapy from her implantable cardioverter defibrillator (ICD). At five years of age, she underwent surgical repair of a sinus venosus atrial septal defect with redirection of the pulmonary veins. As an adult, an ICD was subsequently implanted for a history of syncope and sustained ventricular tachycardia in the setting of left ventricular dysfunction. A coronary angiogram during her index admission revealed normal coronary artery anatomy. Her clinical course was also complicated by the development of atrial flutter with poorly controlled ventricular response rates, requiring atrioventricular nodal ablation. Thereafter, she was pacemaker-dependent, with no evident escape rhythm. In February 2005, she received seven appropriate device therapies for polymorphic ventricular tachycardia in the setting of hypokalemia (plasma potassium concentration ([K + ])=2.1 mM) and a prolonged QT interval. Given this history of hypokalemia and torsade de pointes requiring therapy, she was maintained on oral potassium supplementation.She was readmitted to hospital in April 2006 with pleuritic chest pain, hypotension and leukocytosis. Her baseline 12-lead electrocardiogram (ECG) confirmed a ventricular paced rhythm of 80 beats/min ( Figure 1A). Her baseline plasma [K + ] was 4.1 mM and magnesium concentration was 0.89 mM on admission. Her medications on admission included furosemide, metolazone, acetylsalicylic acid, warfarin, candesartan, spironolactone, amiodarone, metformin, pantoprazole, and magnesium and potassium supplementation. Over the ensuing 24 h, it became apparent that she was septic. In association with this, she became progressively hypotensive, and her serum creatinine increased from a baseline value of 134 μM to 265 μM, in association with oliguria. Telemetry analysis revealed gradual widening of the paced QRS complex, T wave changes, delay in the pacing artifact to ventricular activation time ( Figure 1B) and, ultimately, intermittent loss of ventricular capture (Figure 2A). This was followed by the development of a slow sinusoidal ventricular tachycardia, at a rate of 100 beats/min to 125 beats/min (610 ms to 480 ms) ( Figure 2B), which was terminated by the delivery of device therapy. This tachycardia was below the programmed detection rate of the device, which was programmed to deliver defibrillation therapy for rates of or greater than 176 beats/min (340 ms). Interrogation of the ICD logs revealed fractionation of the intracardiac electrogram ( Figure 3A), coupled with T wave oversensing ( Figure 3B) during the slow ventricular tachycardia, resulting in ventricular oversensing and the delivery of inappropriate, but life-saving, therapy. Interrogation of the ICD revealed a total of six episodes of ventricular arrhythmia detected by the device, which occurred over a 13 min period (Table 1). Three of the detected tachyarrhythmias that resulted in delivered ...

Correlation between Surface and Intracardiac Electrocardiogram in a Patient with Inappropriate Defibrillation Shocks Due to Hyperkalemia

“…While the intracardiac R and T waves remained stable during follow-up, the peak-topeak T wave amplitude at the time of admission had increased to 4.5 mV, and its slope was steeper (Fig. 3) (3,4). In the present patient, hyperkalemia was apparently induced by the combined effects of medications and dehydration during a minor illness.…”

A case of inappropriate implantable cardioverter defibrillator therapy induced by T‐wave oversensing due to hyperkalemia

“…T-wave oversensing is caused by alternations or variations in intracardiac electrograms for reasons such as hyperglycemia, drugs, sympathetic tones, ventricular pacing, and hyperkalemia. Several similar cases of hyperkalemia-induced T-wave oversensing with inappropriate ICD therapies have been reported [1] , [2] . However, the relationship between 12-lead surface electrograms and internal ICD electrograms during hyperkalemia was not fully elucidated.…”

Intraprocedural Assessment of Stimulation, Sensing, Detection, and Defibrillation

“…[97][98][99][100] Prominent T waves are also seen with acute myocardial infarction, subarachnoid hemorrhage, ventricular hypertrophy, and early repolarization (Fig. [97][98][99][100] Prominent T waves are also seen with acute myocardial infarction, subarachnoid hemorrhage, ventricular hypertrophy, and early repolarization (Fig.…”