ABSTRACT
Attempted atrial transseptal puncture in a 63-year-old man undergoing an ablative procedure for atrial fibrillation was complicated by inadvertent delivery of an 8 Fr sheath across the aorta. Due to obesity-related perioperative risks, we opted for percutaneous repair rather than open-heart corrective surgery. Our case is unique for the novel percutaneous delivery of an Amplatzer atrial septal defect (ASD) closure device to the defect in the non-coronary aortic cusp through an 8 Fr left atrial multipurpose sheath not designed for this purpose. At 9-month follow-up, he had a mild residual internuclear ophthalmoplegia.
Subject(s)
Aortic Rupture/etiology , Cardiac Catheterization/instrumentation , Heart Septal Defects, Atrial/therapy , Medical Errors/adverse effects , Septal Occluder Device/adverse effects , Angioplasty, Balloon, Coronary , Aortic Rupture/diagnostic imaging , Atrial Fibrillation/therapy , Cardiac Catheterization/methods , Heart Septal Defects, Atrial/diagnostic imaging , Humans , Male , Middle Aged , Tomography, X-Ray Computed , Treatment OutcomeABSTRACT
INTRODUCTION: Shocks from implantable cardioverter-defibrillators (ICDs) have been shown to reduce sudden cardiac death but are also associated with adverse events. Although the association with psychological harm and impaired quality of life is widely acknowledged, cardiac injuries as a direct consequence of transvenous ICD shocks are less well known. CASE PRESENTATION: We report a case of atrioventricular block and ventricular pacing-dependency following repeated ICD shocks. CONCLUSION: Multiple ICD shocks may result in AV block and pacing-dependency. This has important ramifications for those with a depleted pulse generator following repeated shock therapy.
Subject(s)
Atrioventricular Block/diagnosis , Atrioventricular Block/etiology , Defibrillators, Implantable/adverse effects , Electric Injuries/diagnosis , Electric Injuries/etiology , Atrioventricular Block/prevention & control , Diagnosis, Differential , Electric Injuries/prevention & control , Equipment Failure , HumansABSTRACT
AIM: Our manuscript proposes recommendations to standardise implantable cardioverter-defibrillator (ICD) programming practice in New Zealand (NZ) and provides a review of the literature behind such an initiative. BACKGROUND: Shocks have traditionally been the mainstay of ICD therapy for ventricular tachyarrhythmia. There is substantial evidence to suggest shocks may cause psychological harm, are often painful and may increase hospitalisation for heart failure. Shock therapy may be reduced by avoiding unnecessary therapy of non-sustained arrhythmia, utilising anti-tachycardia pacing to terminate ventricular tachycardia and by using algorithms to identify non-ventricular rhythms with rates overlapping therapy zones. This manuscript outlines evidence-based strategies to safely reduce unnecessary shocks from ICDs and includes manufacturer-specific parameters for ease of practical use. CONCLUSION: These recommendations aim to optimise programming of ICD devices in NZ. Developed from a substantial evidence base they are intended to align national programming practice in the hope that we achieve fewer hospitalisations, improved quality of life and possibly achieve greater survival for our ICD-treated patients.
Subject(s)
Defibrillators, Implantable , Software , Tachycardia, Ventricular/diagnosis , Tachycardia, Ventricular/therapy , Algorithms , Cardiac Pacing, Artificial , Electric Countershock/adverse effects , Humans , New ZealandABSTRACT
The respiratory component of heart rate variability (respiratory sinus arrhythmia, RSA) has been associated with improved pulmonary gas exchange efficiency in humans via the apparent clustering and scattering of heart beats in time with the inspiratory and expiratory phases of alveolar ventilation, respectively. However, since human RSA causes only marginal redistribution of heart beats to inspiration, we tested the hypothesis that any association between RSA amplitude and pulmonary gas exchange efficiency may be indirect. In 11 patients with fixed-rate cardiac pacemakers and 10 healthy control subjects, we recorded R-R intervals, respiratory flow, end-tidal gas tension and the ventilatory equivalents for carbon dioxide and oxygen during 'fast' (0.25 Hz) and 'slow' paced breathing (0.10 Hz). Mean heart rate, mean arterial blood pressure, mean arterial pressure fluctuations, tidal volume, end-tidal CO(2), and were similar between pacemaker and control groups in both the fast and slow breathing conditions. Although pacemaker patients had no RSA and slow breathing was associated with a 2.5-fold RSA amplitude increase in control subjects (39 +/- 21 versus 97 +/- 45 ms, P < 0.001), comparable (main effect for breathing frequency, F(1,19) = 76.54, P < 0.001) and reductions (main effect for breathing frequency, F(1,19) = 23.90, P < 0.001) were observed for both cohorts during slow breathing. In addition, the degree of (r = 0.36, P = 0.32) and reductions (r = 0.29, P = 0.43) from fast to slow breathing were not correlated to the degree of associated RSA amplitude enhancements in control subjects. These findings suggest that the association between RSA amplitude and pulmonary gas exchange efficiency during variable-frequency paced breathing observed in prior human work is not contingent on RSA being present. Therefore, whether RSA serves an intrinsic physiological function in optimizing pulmonary gas exchange efficiency in humans requires further experimental validation.
