Over the past 30 years, endocardial pacing has had a well proven history. In fact, the first human to ever undergo this procedure is still alive and well today. He does receive a more modern version as needed. Implanted, transveneous pacing is a method of stimulating the hearts contraction by means of brief pulses of electrical current passed through a portion of the heart wall. If the pulse is directly applied to the apex via a small (1 millimeter) electrode, a contraction is typically induced by pulses in the 1 volt / 1 milliampere / 1 millisecond range - a current level not perceivable by the patient. The impulse is graphed on the EKG as a near vertical line called a spike. When the heart responds to the electrical stimulus, as it normally would, it is recorded as a QRS immediately following the spike. The response of the myocardium (QRS) is called a ventricular capture. The key requirement for capture is that a sufficient current density be exceeded in a small region of the myocardium for a long enough time period to allow depolarization of the cells in contact with the electrode. Those cells then induce adjoining cells to depolarize, and the wave of depolarization propagates outward from the initial pacing site to involve the entire ventricular mass. This method of depolarization results in a wide and bizarre QRS complex on EKG, because ventricular activation occurs cell by cell rather than by simultaneous activation of the usual nerve pathway.
Today the use of sophisticated equipment allows physicians and paramedics to rapidly gain control of a slow heart by the application of a noninvasive external pacemaker. Using large electrodes on the surface of the thorax, (as opposed to being on the endocardium), a device creates a pulse of current that depolarizes a sufficient region of myocardium to become a self-propagating wave of depolarization. If the state of the myocardium is functional beyond this point, a contraction will ensue. However, since much of the externally applied current is diverted around the heart by nerves, blood vessels and the skeletal muscle of the chest wall, only a fraction of the current passing through the chest is actually delivered to the heart. This current is diffuse, rather than being concentrated in a small region. As a result much more energy is required for external pacing to achieve capture. The applied pulse of current is usually in the 200 volt / 90 milliampere / 20 millisecond range. Obviously, the much higher current creates cutaneous nerve stimulation, and the patient will feel an uncomfortable electrical jolt at a rate of 60 times a minute, for as long as the device is left in operation. Despite this one draw-back, there are many benefits. The external pacer can be applied in seconds, it does not require special skills, and it is noninvasive. Special circuits allow external pacers to operate in the VVI mode (ventricular demand), so as not to compete with the heart's own native beats. VVI operation also reduces the risk of a pacer spike landing on the T wave, producing the effect of a R on T, with the possible risk of inducing ventricular fibrillation. In special circumstances, VOO pacing (fixed rate) may be of use, such as when the patient is totally pacer dependent and artifact in the EKG inhibits life-saving pacer shocks. Examples of problems that can falsely inhibit the external pacer include seizures, road noise, electromagnetic interference, or an implanted pacemaker which is producing electrical spikes without capture of the myocardial tissue.
It is interesting to note that myocardial depolarization can be initiated with slightly less current if the apex of the heart is connected to the negative electrode of the pacing generator. This is usually true for both endocardial and external pacing, but is particularly important in external pacing because proper pad placement can achieve capture at a lower level of energy, which is more comfortable for the patient.
Although external pacing is uncomfortable, there are several techniques to minimize the discomfort. The first and most important is to explain to the patient that this will be uncomfortable and that it is absolutely necessary to help them. Pad placement is critical, apply as illustrated. Remember that if your placement is too low, you may have excessive diaphragmatic stimulation and could interfere with respirations. Placement that is too high or lateral will result in failure to capture or capture only at a very high current setting. The conductive part of the pad must not be on a break in the skin or on the nipple. Never under any circumstances shave the patient's chest! If chest hair is excessive, then clip the hair with scissors but do not nick the skin. Do not scrub or abrade the skin. Sometimes pressure on the anterior pad decreases the discomfort. Finally, if all else fails, and the patient is experiencing tremendous pain from the external pacemaker, the paramedic may have to medicate the patient with Morphine or Valium. Careful attention to respiration is mandatory.
Set the Pacer rate to 60 BPM and gradually increase the current until you see capture on the ECG. Most healthy hearts capture at about 70-120 mA however you may need more energy for your patient. Once you have capture on the ECG, verify that it is producing a pulse. Only the femoral pulse should be used as the sternocleidomastoid muscle can contract with pacing and you could mistake this as a pulse. See how MCC Students learn to pace!
Bradycardiac patient with signs of hypoperfusion
Pacer on and attached to patient. Note proper sensing as demonstrated by "flags" on the QRS
Pacer rate set and timing circuit activated. Current to the patient is raised until capture
Increasing the current to an effective level causes ventricular "capture". Assess vital signs
Although past ACLS recommendations encourage the use of external pacing for asystole, pulseless bradycardias and PEA, this recommendation was based on empiric information rather than sound scientific research. It has now been shown with well done studies, that only a few types of patients are likely to benefit from external pacing (with attainment of capture, a pulse, and clinical improvement) - primarily those patients who already have a palpable pulse, but with a rate too slow to maintain adequate perfusion. These patients are often conscious, and may be alert, but have hypotension, chest pain, or pulmonary edema as a result of extreme bradycardia. The offending bradyarrhythmias most often are sinus rhythm with 3rd degree AVHB, sinus rhythm with high grade AVHB, sinus bradycardia, junctional bradycardia, or occasionally idioventricular escape. The one common finding in patients who have these rhythms and who do respond to external pacing is that they have a palpable pulse with the bradycardic rhythm. In less common circumstances, patients who experience primary asystole resulting from the effects of anesthesia, or who develop sudden, profound hypoxia as in pulmonary edema, may benefit from external pacing and rapid attempts at oxygenation.
It is unfortunate that EMS medics try to pace pulseless rhythms because the time it takes to do so will be time wasted. You may even achieve capture but there will not be a femoral pulse. By tying up the medic with trying the pacemaker, the patient will be denied the timely treatment that could correct the cardiac arrest, namely, finding the cause of PEA or asystole and treating it.
It is best not to consider pacing in these instances but rather, give standard pharmacologic treatment:
1) patient is pulseless, unconscious, and clinically dead.
2) patient has QRS rate greater than 60 pulse or no pulse.
Consult with your medical director on these issues.
Updated: June 8, 1999