TCP is a temporizing measure until transvenous pacing is initiated in patients with unstable bradycardias who do not improve with atropine. TCP can also be used in patients with acute MI who have signs of conduction pathway abnormalities such as new bundle branch or bifascicular blocks. For these patients, the team should obtain cardiac consultation as they will need complex management. Additional information can be obtained by reviewing the ACC/AHA Guidelines for treating STEMI at https://www.ahajournals.org/doi/10.1161/circ.110.9.e82.
Cardiac pacing has been utilized since the 1800s and has gone through considerable evolution. Pacing uses electrical impulses originating from electrodes to cause depolarization of the cardiac myocytes and subsequent contractions. TCP is performed via skin electrodes, while transvenous pacing is performed via electrodes passed intravenously into the right heart or (less commonly) the heart surface.
Pacemaker Illustration
A pulse generator is used to initiate pacemaker activity and can be external or implanted surgically as a permanent pacemaker. Temporary transvenous pacing utilizes an external pacemaker. Typically, this is used until the bradycardia resolves or the patient undergoes surgical implantation of a permanent pacemaker. Responders should be aware that permanent pacemakers can cause ECG artifacts that can be mistaken for arrhythmias.
The increasing availability of transcutaneous pacers over the past three decades ensures they are more available when needed for emergency treatment.
In an emergency, TCP is used for managing symptomatic bradycardia. It is painful and less reliable than transvenous pacing and should be used only until transvenous pacing is available.
TCP may also be utilized for stable patients with significant conduction pathway abnormalities that are at risk for deteriorating (e.g., asymptomatic Mobitz II 2nd-degree block or narrow QRS 3rd-degree block). It is a temporary measure and should not be used for long-term management.
In patients managed with TCP, close monitoring for response is necessary. The goal heart rate should be the lowest possible required for adequate perfusion and resolution of symptoms as increasing the heart rate leads to increased oxygen use. For most patients, a rate between 60 and 70 bpm is reasonable. It is vital to understand that pacing will only improve symptoms due to bradycardia.
Alert patients may have significant pain from TCP due to the contraction of skeletal muscle with each beat. Patients will also need to be prepared for transvenous pacing, regardless of the efficacy of TCP. Cardiac consultation is indicated in these patients.
As TCP may be painful, adequate analgesia or sedation is required. Specific sedatives can negatively affect the cardiac rhythm by further slowing it. When considering analgesics and sedation, the following pathway may be a beneficial approach:
Standby pacers are used for those patients at high risk for needing pacing in the future. Often these patients have stable vital signs, but they have significant conduction pathway abnormalities that are likely to deteriorate. Their ECG findings suggest a block at locations associated with a poor prognosis and an extensive acute MI that may lead to significant cardiac dysfunction. Reperfusion of the coronary vessels is vital in indicated patients as well as TCP or transvenous pacing.
Typically, TCP is the best option for patients in this category who are at risk for advanced heart block. It may also be used in patients with conduction pathway abnormalities (such as left bundle branch or bifascicular block in association with 1st-degree heart block) who require surgical intervention but who are not candidates for transvenous pacing because the likelihood of deterioration into unstable bradycardia is not enough to warrant the risks of placement. Instead, TCP can be used on standby in case a heart block develops during a surgical intervention. When using TCP in these situations, it serves as temporary management until transvenous pacing is available.
Research has evaluated the role of pacers in bradycardic and asystolic patients with no pulse. Some research indicates a benefit in those patients who receive pacing within 10 minutes of cardiac arrest, while others show no short- (survival to admission) or long-term (survival to discharge) benefits.
Research does not indicate that TCP improves outcomes in patients with symptomatic bradycardia compared to adrenergic medications. Additionally, there does not seem to be a benefit for out-of-hospital TCP in patients with cardiac arrest due to asystole or new-onset asystole following defibrillation. Randomized controlled trials of CPR in combination with pacing do not improve outcomes in post-defibrillator asystole.
On the other hand, patients with cardiac arrest associated with a drug overdose may benefit from pacing as it can be temporizing management for unstable bradycardia or pulseless electrical activity (PEA). Similarly, pacing may benefit patients with acid-base or electrolyte abnormalities. The similarities are that these patients usually have a normal heart that has been temporarily affected by the condition.
Since pacing can provide adequate myocyte contractions, it is life-preserving until the electrolyte or acid-base imbalance or drug overdose has been managed and the conduction pathway returns to its normal function.
Patients who have profound hypothermia are usually not candidates for pacing. In this case, bradycardia is physiologic as the metabolic rate responds by slowing to match the hypothermic state. Additionally, hypothermic myocytes are at risk for pacing-associated ventricular fibrillation that may be refractory to defibrillation. In such patients, pacing may not be appropriate.
Pacing does not improve survival for adults or children with witnessed OHCA. However, it may still be indicated in the case of bradycardia associated with congenital heart conditions, 3rd-degree block, sinus node abnormities, post-cardiac surgery dysfunction, and drug overdoses.
TCP allows cardiac stimulation via the administration of an electrical impulse through the chest wall into the cardiac muscle. It is also referred to as external or non-invasive pacing. TCP is not benign and does have some adverse effects. The skeletal muscle contractions can be uncomfortable for patients, and it may instigate ventricular arrhythmias.
TCP is useful in the emergency setting as it is easy to initiate and often readily available on external defibrillators. These devices have multipurpose electrodes that administer defibrillation, pacing, and monitor the ECG. It is important to note that the placement of a right and anterior subclavicular with a left apex chest electrode may not be effective for TCP. In this situation, the electrode placed on the right side should be moved to the back. TCP is also useful in patients receiving or who will need to receive fibrinolytics because no venipuncture is necessary.
Transcutaneous Pacing Pad Placements
As noted above, TCP devices are readily available both inside and outside of the hospital with standard defibrillators. These modern devices allow several output options. The features of TCPs include:
When using TCP, it is vital to ensure that capture is achievable and the patient can tolerate it. If there is too much pain, the clinician can administer benzodiazepines to decrease anxiety and relax the musculature along with narcotics for pain control.
Initial Bradycardia Before TCP
TCP Attempted at Too Low a Threshold
There can be complications associated with TCP:
Electrical activity (myocyte depolarization) must be coupled with mechanical activity (myocyte contraction) to be effective. This requires complex interactions of the myocytes, extracellular space, electrolyte gradient as well as effective actin and myosin interactions. As noted above, electrical-mechanical disassociation can occur in which the cell depolarizes with no adequate muscular contraction. This is a failure of electrical-mechanical association.
With pacing, each pacing spike has a subsequent myocyte depolarization. In temporary transvenous pacemakers, the pacer electrode is most often in the right ventricle. However, in permanent or implanted pacemakers, it may be placed in the atrium, the ventricle, or both. The placement of a permanent pacer leads to a difference in the observed ECG strip. As with temporary pacers, the associated QRS indicates electrical capture only and must be combined with an evaluation of the patient’s hemodynamic state to ensure good electrical-mechanical association.
Dual-Chamber Pacemaker ECG