A 59-year-old man with a history of chronic obstructive pulmonary disease presented to the emergency room with severe sinus bradycardia and hypotension. Due to his history of recurrent dizziness and presyncope, prior work up with Holter cardiac event monitor showed predominant sinus bradycardia with no evidence of chronic incompetence and no clear correlation of his symptoms to the bradycardia episodes. His most recent echocardiogram showed normal left ventricular systolic function and wall motion. Myocardial perfusion study done for recurrent chest pain showed normal myocardial perfusion and normal ejection fraction on Gated SPECT. Tilt table test was markedly abnormal consistent with severe dysautonomia. His baseline blood pressure was 113/70 mmHg, and his HR was 49 beats per minute. Only two minutes into the test, his blood pressure dropped to 60/29 mmHg while his heart rate remained at 47 bpm. The patient was offered pacemaker therapy after his abnormal tilt table test but he refused.\nA few weeks later, the patient presented to the emergency room with syncope. Initial ECG showed severe sinus bradycardia, heart rate in the low 40 s with normal PR interval, and left anterior fascicular block. He was hypotensive and diaphoretic. He denied any chest pain, pressure, or tightness. There were no significant signs of cerebral hypoperfusion. The patient was not on any bradycardia-inducing medications, and initial blood work showed no reversible cause of his severe sinus bradycardia.\nThe patient was started on intravenous fluid hydration, and a bedside echocardiogram was obtained. Echocardiogram showed normal biventricular systolic function and no significant valvular abnormalities. Atropine was given but resulted in minimal, transient improvement in his heart rate to the low 50 s. The systolic blood pressure remained below 80 mmHg. Dopamine followed by norepinephrine drips were administered, and the patient was sent to the electrophysiology laboratory for dual-chamber permanent pacemaker therapy.\nDuring implantation of a permanent pacemaker, the right atrial lead was appropriately placed via the left subclavian vein into the right atrial appendage. However, the ventricular lead was placed via the subclavian artery into the left ventricular cavity. He was admitted to the hospital overnight and a chest X-ray was obtained the next day, showing no evidence of pneumothorax (Figure ). Surprisingly, his ECG showed atrial pacing with long AV delay and intermittent ventricular pacing with the paced ventricular beats showing right bundle branch block morphology contrary to the expected left bundle branch block morphology seen when the lead is inside the right ventricular cavity (Figure ). A limited bedside Echo was obtained that showed the ventricular lead clearly crossing the aortic valve to the left ventricular cavity and fixed into the inferolateral wall of the left ventricle (Figure ). Early recognition of this serious pacemaker implantation complication led to pacemaker revision the same day with extraction of the arterial lead and reinsertion of the ventricular lead via the left subclavian vein into the right ventricular cavity (Figure ). The pacemaker revision went uncomplicated.
A 23-year-old female with Ebstein's anomaly of tricuspid valve underwent one and half ventricular repair with tricuspid valve annuloplasty, atrial septal defect closure and cavopulmonary anastamosis of right superior venacava to the right pulmonary artery. She also needed dual chamber pacing for symptomatic bradycardia secondary to sinus nodal and atrioventricular nodal disease. There was no pre-excitation or tachyarrhythmias. Left atrial and left ventricular epicardial leads were connected to a pulse generator that was implanted in epigastric subcutaneous pocket. There was synchronous atrioventricular pacing with acceptable pacing thresholds during the time of implantation. Three months later, new onset symptomatic diaphragmatic pacing was observed from atrial lead. So the pacemaker was reprogrammed to pace ventricle alone. After another two months, diaphragmatic pacing was observed from ventricular lead too. The threshold voltage for ventricular capture was more than that of the diaphragm. The reasons for delayed onset diaphragmatic pacing through both leads almost five months after the epicardial lead placement and pacemaker implantation was not understood. Her symptoms related to bradycardia warranted permanent dual chamber pacing. Since extensive dissections will be needed through the previous surgical scars and adhesions in midline sternotomy and left thoracotomy, a second epicardial lead repositioning was not considered. A minimal incision right anterolateral thoracotomy was made and two introducer sheaths were inserted through two pursestring sutures placed on the right atrial free wall.() Two screw-in endocardial leads were inserted through the sheaths under transesophageal echocardiographic guidance into the right atrial appendage tip and right ventricular apex to achieve atrioventricular pacing. On a follow up of nine months, the patient was asymptomatic, pacing was synchronous and chest X-ray showed both the new and old leads. ()