Cardiac pacemakers and their malfunctions are often daunting for the emergency physician to diagnose and manage. This is the first part of a series covering this area.
- Part 1. Pitfalls and pearls of temporary transvenous pacing.
- Part 2. Procedural instructions for placing a transvenous pacemaker and the use of the temporary pacer generator.
- Part 3. Introduction to permanent pacemakers and ICDs.
- Part 4. Diagnosing problems permanent pacemakers and ICDs.
On to a case for discussion.
A nursing patient was brought to the emergency department for evaluation of lethargy, “being floppy”, and hypotension (90/50 mmHg). He was known to have right-sided systolic dysfunction, medication controlled hypertension, insulin-controlled type 2 diabetes mellitus, and CKD Stage III.
On physical exam he was noted to be obtunded and bradycardic. IV access was established, and initial laboratory tests were sent. He was orotracheally intubated without difficulty and easily ventilated. Atropine was given without an increase in his heart rate. He was placed on transcutaneous pacing. We presumed the patient was suffering from hyperkalemia and he was given calcium gluconate, and shifted with insulin/glucose. It was difficult to establish good capture. Multiple different pad locations were attempted, and eventually we were able to get intermittent capture using a right-parasternal and apex pad location.
A 12-lead ECG was obtained as shown below. This was interpreted as sinus bradycardia, with a narrow QRS complex and significant T-waves abnormalities. There did not appear to be any ST-segment or T-wave changes concerning for ischemia. The large voltages recorded on the right-side of the strip occurred when the transcutaneous pacer was restarted.
A bedside cardiac ultrasound confirmed bradycardia. Contractility was adequate and there were no gross focal wall motion abnormalities.
The remainder of the FAST exam was was notable for free fluid in the abdomen. This included fluid in Morrison’s pouch, suprapubic region, splenorenal angle, as well as bilateral pleural effusions. This was presumed to be ascites. Evaluation of his IVC while being positively pressure ventilated showed a dilated vessel without significant respiratory variation. Images from the FAST exam and a video clip of the IVC ultrasound are shown below.