Benjamin C. Smith III
Unstable bradycardic patients who do not respond to a trial of atropine should be considered candidates for transcutaneous pacing. One important exception is hypothermia-induced bradycardia, where pacing may induce more unstable rhythms.
Patients who have tachyarrhythmias recalcitrant to one or more pharmacological interventions can be considered for transcutaneous overdrive pacing. In particular, patients with torsades recalcitrant to magnesium may respond to overdrive pacing. Use caution, however, overdrive pacing ventricular dysrhythmias can induce ventricular fibrillation.
Pacer pads preferably should be placed on the left anterior and posterior chest wall, or the less desirable left and right anterior chest walls. To enable the defibrillator to sense the patient’s intrinsic rhythm, the three-pacer electrocardiogram (ECG) leads should be placed on the patient’s chest.
The pacing function should be enabled at a rate of 70 to 80 beats per minute when treating bradycardia, and the current (in milliamperes, mA) should be increased until 100% electromechanical capture is verified. Mechanical capture should be verified by palpating a coincident central pulse, verifying distal flow with Doppler ultrasound, or performing a bedside echocardiogram. Transcutaneous pacing causes muscle twitches of the thorax and upper extremities that can cloud the reader’s visualization of ventricular capture on the rhythm strip, so electrical capture alone is insufficient to verify cardiac stimulation. Demand pacemaker mode should be used unless significant artifact is present that falsely inhibits pacing. This mode is usually on by default and senses the patient’s intrinsic rhythm, inhibiting pacing unless the patient’s ventricular rate drops below the set threshold.
When treating recalcitrant tachyarrhythmias, the pacer mode should be in “nondemand” mode. The rate should be set at, or just above, the patient’s intrinsic ventricular rate and the current should be increased until mechanical capture is obtained. The pacer rate can then slowly be lowered to a normal level over several minutes.
Because transcutaneous pacing impulses must traverse the chest wall to simulate the heart, higher currents are required as compared with internal pacemakers. Sedation and analgesia are almost universally necessary, with intubation for pain control sometimes a requirement. Patients without readily reversible etiologies or patients without adequate capture from transvenous pacing should be considered for transvenous pacer placement (see later).
Small changes in the patient’s physiologic status (eg, worsening acidosis and hypoxemia) can increase their capture threshold. Therefore, the patient being paced should have 1:1 nursing care to verify continuing pacing capture until definitive treatment can be instituted.
Most 12-lead ECG machines handle the large pacing current very poorly, rendering the resultant ECG uninterpretable. The defibrillator monitor strip should be used instead.
Prolonged transcutaneous pacing should be avoided to prevent cutaneous burns.
Overdrive pacing can induce secondary arrhythmias, including ventricular tachycardia and fibrillation, so the clinician should be at the bedside during this procedure ready to treat those conditions should they arise.
All the patients who require transcutaneous pacing should have an emergent cardiology consult and should be considered critically ill.
Benjamin C. Smith III
Unstable bradycardic patients who do not respond to a trial of atropine should be considered candidates for pacing. Initially, transcutaneous pacing should be instituted for its ease in application. Patients who are expected to require pacing for a significant duration, or fail transcutaneous pacing, should be considered for transvenous pacing emergently. Ultimately, the underlying etiology of bradycardia should be corrected, or a permanent implantable pacemaker should be inserted.
First, placement of a transvenous pacemaker involves obtaining central venous access with an introducer sheath in either the left subclavian vein or the preferred right internal jugular vein. These sites provide the most direct anatomical path for right ventricle (RV) pacer wire placement, although the femoral vein is an acceptable alternative. The proximal pacer wire lead should be connected to the V1 lead of an ECG machine, while the patient should be connected to the limb leads. The pacer wire can then be inserted into the introducer, and once in the superior vena cava, the pacer wire balloon should be inflated; thereafter, direct the pacer lead toward the RV. Monitoring the V1 lead setup created above will help determine the location of the pacer wire. Confirmation of placement in the RV can be made under real-time guidance with ultrasound or fluoroscopy, or statically with a chest x-ray.
Once adequate position is verified, the balloon should then be deflated and the pacer wire should be attached to the transvenous pacing unit. Pacing function should be enabled at a rate of 80 beats per minute, and the current should be set to the maximum, usually 20 mA. Mechanical capture should be verified by palpating a coincident central pulse, verifying distal flow with Doppler ultrasound, or performing a bedside echocardiogram. Electrical capture alone is insufficient to verify cardiac stimulation. The current should then be decreased until electromechanical capture ceases, this value is the capture threshold. The current should then be set to two to three times the capture threshold. If insufficient capture is initially obtained at the maximum current, the pacer wire needs repositioning. To enable the pacemaker unit to sense the patient’s intrinsic rhythm, it should be placed in demand mode.
Placement complications include arterial puncture, pneumothorax, venous thrombosis, pulmonary embolism, arrhythmias due to RV stimulation, and cardiac perforation.
A subxiphoid ultrasound view usually allows adequate visualization of the right heart for real-time guidance of pacer wire placement without breaking the sterile field.
Patients who have cardiac ischemia as the etiology of their symptomatic bradycardia are more likely to have an irritable myocardium that is particularly prone to catheter-induced arrhythmias.
Low cardiac output states will make proper placement of the pacer wire more difficult because there will be little forward venous flow to direct the inflated catheter tip. Using the optimal right internal jugular approach is of particular importance in this situation.
Bryon E. Rubery
Glenn M. Brammer
Symptomatic bradycardia due to nonreversible causes, requiring prolonged intravenous pacing of the heart, most commonly due to sick sinus syndrome, atrioventricular block, and, less frequently, carotid sinus hypersensitivity.
After initial implantation, the cardiologist will determine the function of the pacemaker by checking the pacing capture threshold, lead impedance, native rhythm sensing, resulting ECG, and position on chest x-ray.
Investigation of pacemaker dysfunction in the Emergency Department (ED) typically requires an ECG looking for expected pacemaker spikes/significant changes and a chest x-ray to compare with the postprocedure chest x-ray. Other tests should only be ordered as indicated by chief complaint or past medical history. Interrogation of the device and disposition typically requires discussion with the patient’s cardiologist.
Occasionally, this complication will not be seen until the day following implantation. Patients typically present with pleuritic chest pain, with or without shortness of breath.
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