Nursing home staff became concerned about a patient because he was “floppy.” He was a 59-year-old man with stage 3 chronic kidney disease, right ventricular heart failure, hypertension, cirrhosis, and insulin-dependent type 2 diabetes mellitus. He had been sleeping all day, according to his nurse, but he was not responding when she checked on him in the evening, and she could “drop his arm and it would just hit his face.”

He was hypotensive (90/50 mm Hg) and bradycardic (about 30 beats/min) in the ED. Respirations were slow and shallow. He was protecting his airway, but was hypoxic (SpO 2 82%). IV access was established, and initial laboratory tests were sent. He was orotracheally intubated without difficulty and easily ventilated. Atropine was given, but did not increase his heart rate. The symptomatic bradycardia meant starting transcutaneous pacing. Fingerstick glucose was 174 mg/dL. Given his history of kidney disease and diabetes mellitus, there was a high suspicion for hyperkalemia so he was empirically treated with calcium gluconate and shifted with insulin/glucose. It was difficult to get good electrical capture with the transcutaneous pacing. Multiple different pad locations were attempted, and eventually we were able to achieve intermittent capture using pads in the right-parasternal and apex position.

A 12-lead ECG was obtained that demonstrated sinus bradycardia with a narrow QRS complex and no T-wave abnormalities. ( Figure 1.) There was no ST-segment changes concerning for ischemia.

Figure 1. Presenting ECG with initiation of transcutaneous pacing. The large voltages recorded on the right side of the ECG occurred when the transcutaneous pacing was started.

A limited transthoracic echocardiogram showed severe bradycardia in action, but the actual contractility was normal, and no focal wall motion abnormalities were identified. ( Figure 2 .)

Figure 2. Click here to see a limited transthoracic echocardiogram using the subcostal window.

A small pericardial effusion could be seen as the thin hypoechoic line starting anteriorly and wrapping around the apex to the posterior aspect. No echocardiographic evidence for tamponade was present based on the lack of right ventricle collapse during diastole.

Abdominal ultrasound was notable for a small amount of intraperitoneal free fluid, pleural effusions, and a dilated IVC with no respiratory variation. ( Figures 3, 4, and 5 .)

Figure 3 (left). Abdominal ultrasound in the hepatorenal (Morrison) window. A small amount of free fluid is visible in the potential space between the liver and kidney. Figure 4 (center). Right thoracic ultrasound showing pleural effusion. Lung parenchyma is usually anechoic, preventing visualization of the posterior lung bases. The lung base is clearly seen in this situation, however, and is hypoechoic, indicating a fluid-filled area consistent with pleural effusion. Figure 5 (right). Ultrasound view of the IVC. It is dilated, and there was no respiration variation. Click here to watch an ultrasound of this finding .

This was presumed to be volume overload from a combination of ascites given the patient’s history of cirrhosis and renal failure.

Initial laboratory tests showed normal blood counts and a chemistry panel that was notable for a potassium of 7.4 mEq/dl. Given the difficulty of achieving adequate transcutaneous pacing, a right internal jugular introducer sheath was inserted, and a transvenous pacing wire was placed with successful mechanical and electrical capture. (See Table 1 for how to place a transvenous pacemaker. Figure 6 shows the pacing wire within the right ventricle.)

Table 1. Abbreviated Procedural Steps for Transvenous Cardiac Pacing

1. The entire procedure should be done under sterile conditions with full barrier drapes.

2. The sterile sleeve should be placed on the pacer wire once the sheath introducer is placed.

3. Inflation of the floating balloon should be verified.

4. The proximal (+) lead should be on the positive terminal on the connector adaptor.

5. The distal (-) lead should be attached to lead V1 on the cardiac monitor using an alligator clip.

6. The balloon should be inflated after the pacing wire is threaded 15-20 cm to exit the end of the sheath.

7. Advance the pacing wire in a smooth fashion while monitoring the ECG. Marked ST-segment elevation will occur when the lead tip contacts the endocardium.

8. Secure the protective sleeve.

9. Detach the negative lead from the ECG, and connect it to the connector adaptor of the pulse generator.

10. Initial generator settings should be 80 beats/min, output 5mA, and sensitivity of 3 mV.

11. You should be able to note mechanical capture by noting cardiac contractility at the rate set on the pulse generator. This can be done by palpating a pulse or contractions over the anterior chest wall or by visualization using ultrasound.

12. Test electrical capture by challenging the required output threshold and sensitivity.

A. With sensitivity set to maximum, gradually reduce your output threshold until electrical capture is lost. Set the output threshold at 2-2.5 times the value at which capture was lost.

B. Set the rate at 10 beats/min above the intrinsic rhythm. Place the pacemaker in asynchronous mode and ensure complete capture.

C. Then with the sensitivity set at about 3 mA, decrease the rate until pacing ceases. Verify that the generator is indicating that a native beat is sensed on every cycle. If not, increase the sensitivity. Reduce the sensitivity if the pacer oversenses and is being triggered by p or T waves. Set the sensing level at half of the value once the sensing level is determined (i.e., reduce the sensitivity by half.)



Figure 6. Click here to see a cardiac ultrasound in subcostal window. Transvenous pacer wire can be visualized as the hyperechoic structure within the right ventricle.

A chest radiograph and ECG was not obtained in ED following placement of the transvenous pacemaker. The patient was admitted to the medical ICU and cardiology consultation was requested. Emergent hemodialysis was arranged with the nephrology service. Unfortunately, intermittent loss of capture started occurring during transport from the ED to the ICU and from the trolley to the bed. Within a short time, the transvenous pacemaker failed capture completely despite increasing the output and sensitivity settings on the pacemaker, and the patient returned to his native bradycardic rhythm. The admitting team obtained a chest radiograph. ( Figure 7 .)

Figure 7. AP chest radiograph after arrival in the ICU.

The endotracheal tube is in good position, and external pacer pads are over the left hemithorax. The pacer wire takes a crazy course, however. It can be seen entering from the top of the film through the right internal jugular vein and descending the SVC (right of midline) to the heart. It is coiled in the right ventricle, however, and part of the wire is likely looping through the tricuspid valve. The electrode tip appears to be abutting the high septal wall. A schematic is shown to help visualize the misplaced pacer wire. ( Figure 8 . )

Figure 8. Schematic of misplaced pacing wire.

A 12-lead ECG was obtained immediately after the pacer was placed. ( Figure 9 .) Pacer spikes appear prior to each QRS complex. The emergency physician interpreted this ECG as an indication of successful placement, which is why a chest x-ray was not immediately obtained. This is an abnormal ECG for a patient undergoing transvenous pacing, however. The QRS complex is narrow with an axis downward and to the left, indicating that the lead contact is atrial or high on the septal wall. A properly placed right ventricular lead placement in the apex should result in a LBBB and an upwards QRS complex. Capture was likely lost when the pacing tip was pushed out of the ventricle and was not in contact with the right atrium wall.

Figure 9. ECG after transvenous pacer placed.

The patient was taken to the cardiac catheterization lab to reposition the pacing wire under fluoroscopy. The wire was confirmed to be coiled and almost tied in a knot. The tip was in the atria, and the floating balloon was partially inflated. It was repositioned without difficulty and achieved excellent capture. The patient was returned to the MICU, and ultimately underwent emergent dialysis to correct the underlying hyperkalemia.