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Outpatient Management of Stable Heart Failure with Reduced Ejection Fraction
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Leah Reid, Jonathan Murrow, Kent Nilsson, Catherine Marti
Digoxin poisoning can be a life-threatening event. Among patients with HF, significant toxicity most commonly emerges at serum concentrations greater than 2.0 ng/mL. Frequently, neurological or gastrointestinal symptoms are the first symptoms. Disturbances in cardiac conduction are also commonly seen with toxicity, including ectopic beats of atrioventricular, junctional, or ventricular origin; atrioventricular block; a slow ventricular rate response to atrial fibrillation; or an accelerated atrioventricular junctional rhythm.38 Life-threatening digoxin toxicity can be reversed with anti-digoxin immunotherapy.39
Ablation of SVT (AVNRT and AVRT)
Published in Andrea Natale, Oussama M. Wazni, Kalyanam Shivkumar, Francis E. Marchlinski, Handbook of Cardiac Electrophysiology, 2020
Kushwin Rajamani, Patrick Tchou
In unusual cases, the slow pathway may be located along the mitral annulus or the AV node may have slow pathway extensions along both the tricuspid and mitral annuli. The mitral annular extensions can sometimes be targeted via the anterior wall of the proximal coronary sinus. When ablation along the tricuspid annulus and the proximal coronary sinus fails, the slow pathway may be located along the mitral annulus. Ablating this pathway may require access to the left atrium via a transeptal approach. Locating the site of ablation is similar to the right side approach. The annulus is mapped anatomically. The sites of ablation typically have a smaller A than V electrogram. The compact node near the His bundle should be avoided. The inferior end of the septal mitral annulus should be targeted first with gradual migration of the ablation site superiorly as needed to achieve slow pathway ablation. Junctional rhythm should be monitored during RF application to assure persistence of retrograde conduction, just as during ablation on the right side.
Cardiology
Published in Paul Bentley, Ben Lovell, Memorizing Medicine, 2019
Escape beats: When another area of the heart generates the impulseUsually occurs when sinus node not working/going too slowTypes: AtrialAV nodal: Ongoing AV escape beats = nodal or ‘junctional’ rhythmVentricular: Fast ventricular rhythm = ventricular tachycardia (VT)Slow rhythm = idioventricular rhythms (occurs in complete HB)
Electrocardiographic changes after breast reduction surgery
Published in Journal of Plastic Surgery and Hand Surgery, 2023
Ayca Ergan Sahin, Tugce Yasak, Burak Yılmaz, Ahmet Anil Sahin, Ali Rıza Demir, Ozlem Colak
We have reviewed the database of hospital records and retrieved the patients who had undergone BRS due to macromastia and who have ECG in the records pre- and post-operatively, retrospectively. Study population included 33 female patients who had undergone BRS between the time period of January 2011 to January 2021 at a tertiary training and research hospital. The patients, who did not have ECG for the time period of pre-operatively and post-operatively in their records, were not included in the study. All patients were over 18 years old. Exclusion criteria were: patients with diagnosis of hypertension, coronary artery disease, history of coronary intervention or coronary artery bypass surgery, known moderate to severe valvular heart disease, pulmonary hypertension, heart failure with reduced or preserved ejection. Patients who had diagnosis those might cause changes in ECG were excluded from the study such as patients who had chronic kidney disease or with electrolyte imbalance or were on dialysis. Patients with atrial dysrhythmia such as patients who had atrial fibrillation or flutter, pre-excitation syndrome, and patients with junctional rhythm or patients with history of pacemaker implantation were not included in the study. Patients who were under treatment of type I and III antiarrhythmic drugs those might interfere with ECG recording were also excluded from the study. Additionally, patients who had unsuitable ECG for evaluation were not included to the study group.
Atypical tachycardia mimicking typical reentry: what is the mechanism?
Published in Acta Cardiologica, 2022
Hussam Ali, Guido De Ambroggi, Pierpaolo Lupo, Sara Foresti, Carmine De Lucia, Riccardo Cappato
Conventional radiofrequency ablation of the slow pathway at the inferior portion of Koch triangle produced prolonged junctional rhythm and rendered the tachycardia not inducible anymore. The patient remained asymptomatic and arrhythmia-free during the next 10-months follow-up period. This case highlights that atypical AVNRT, particularly at fast rates, may mimic common atrial flutter. The fast atrial rate can produce physiological AV block while focal atrial activation propagating from the slow pathway region is extremely slow, or functionally blocked, at the CTI mimicking counterclockwise atrial flutter activation pattern and producing flutter-like P waves on the surface ECG. Pacing manoeuvres, particularly from the ventricle by applying multiple extrastimuli to penetrate the circuit, are essential to elucidate the tachycardia mechanism and to guide successful catheter ablation.
Flecainide toxicity late after liver transplantation
Published in Baylor University Medical Center Proceedings, 2021
Ossama Elsaid, Kristen M. Tecson, Hafiza Khan, Manish D. Assar
A 50-year-old woman with a history of liver cirrhosis post-liver transplant and a history of supraventricular tachycardia, managed with flecainide 50 mg twice daily for 7 years, presented with syncope. She had dizziness, malaise, fever, nausea, vomiting, and sudden visual disturbance. On presentation, her blood pressure was 90/50 mm Hg and her heart rate was 35 beats/min. The electrocardiogram showed junctional rhythm with a QRS duration of 150 msec with a 3-second sinus pause on telemetry (Figure 1). The sodium level was 125 mEq/L; serum creatinine, 8.79 mg/dL (baseline 1.5); aspartate transaminase, 951 U/L; alanine transaminase, 846 U/L; alkaline phosphatase, 469 U/L; and total bilirubin, 1.4 mg/dL. The flecainide level was 2.2 μg/mL (therapeutic 0.2–1.0 μg/mL; toxic >1.5 μg/mL).