The goal of this clinical practice guideline (CPG) is to provide patient care guidance and optimization of patients with hemodynamically significant dysrhythmias, such as symptomatic bradycardia, bundle branch blocks, and 2nd and 3rd degree (complete) heart block, in the aeromedical environment. This guideline reviews the physiology, indications, and algorithms for initiating and troubleshooting transcutaneous and transvenous cardiac pacing systems. A pre-flight checklist has been developed for patients that are to be transported. The algorithms to troubleshoot pacemaker malfunction also include the special conditions encountered by en route care personnel. Appendix A includes a basic transvenous pacemaker programming instruction set as reference; however, it is not intended to replace the device manual.
Temporary cardiac pacing, whether transcutaneous, transvenous, or epicardial, is a potentially lifesaving technique for patients with arrythmias which cause hemodynamic instability.
Etiology of malignant rhythms may be due to structural heart disease, most often and commonly associated with ischemia or infarction, but can also include adult congenital heart disease, infiltrative cardiomyopathies (amyloidosis, lymphoma), infection or inflammation (viral myocarditis, infectious endocarditis, Lyme disease, Chagas disease, diphtheria, toxoplasmosis, sarcoidosis, malaria, Dengue fever, viral hemorrhagic fevers, etc.), post-surgical (post coronary artery bypass grafting, valvular surgeries) or thoracic blunt force trauma. Nonstructural or extrinsic causes of arrythmias may include electrolyte and endocrine abnormalities, hypothermia, whether accidental or purposeful (targeted temperature management), drug or toxin effects (organophosphates, medication overdoses), and neurogenic shock.
When the cardiac conduction system suffers an insult, such as described above, the loci of cardiac impulse generation, in the sinoatrial (SA) node, and the pathway of electrical impulses downward through the intraatrial conduction pathways, atrioventricular (AV) node, bundle of His, bundle branches, and terminating with the Purkinje fibers, are all potential locations of dysfunction, resulting in a variety of dysrhythmias.
Of the resulting arrythmias and the associated hemodynamic compromise and end organ dysfunction that may present with those arrhythmias, those that benefit from cardiac pacing are bradycardia, symptomatic 2nd degree, type I (Wenckebach’s) block, 2nd degree, type II (Mobitz type II) block, 3rd degree (complete) block, sick sinus syndrome, and junctional (escape) rhythms. In some cases, tachyarrhythmias (such as Torsades de pointes and ventricular tachycardias) benefit from providing external electrical stimulus to overcome the native dysfunction (i.e. overdrive pacing). Most patients that require cardiac pacing suffer from symptomatic bradycardia or either 2nd - or 3rd -degree heart block.
Patients who present with the above arrythmias accompanied by hypotension and or signs of poor perfusion including syncope, altered mental status, signs of end organ ischemia such as angina warrant immediate intervention. If time and resources permit, a trial of pharmacological intervention is reasonable with a low threshold to progress to or add cardiac pacing. Drug therapies may include anticholinergic drugs such as atropine, or inotropes and chronotropes such as epinephrine or dobutamine, however do not delay initiation of cardiac pacing if medication is not readily available, or there is a lack of response to medication.
Cardiac pacing can be performed transcutaneous, through externally applied pacing pads, transvenous, via a central venous catheter serving as an introducer for a pacing wire that is floated through the venous system into the heart, or via epicardial leads that are placed surgically. Each application will be discussed below. Cardiac pacing is a temporary measure, designed to buy time for treatment and intervention, such as cardiac catheterization or electrophysiology studies, resolution of the underlying cause, or until definitive intervention, such as placement of a permanent pacemaker.
Pacing capabilities are depending on the echelon of care the patient is being retrieved from and can also be influenced by resource and conflict scale variables as well. CCATT and Aeromedical Evacuation (AE) teams do not have the capability to place transvenous pacers, however they should certainly be familiar with patient management, troubleshooting, and contingency plans, like transcutaneous pacing via appropriate flight approved equipment. Patients requiring cardiac pacing should be triaged as at urgent for patient movement as definitive care is usually not available until Role 3 facilities or higher. Besides familiarization with this CPG, augmenting the patient care team with a member who is familiar and comfortable with cardiac pacing and troubleshooting is advised if possible. If not, it is reasonable to call the ADVISOR hotline at 1-833-ADVSRLN (1-833-238-7756 or DSN 312-429-9089) to speak with a cardiologist for further guidance and support.
Both the right and left ventricles are stimulated with transcutaneous pacing. The atria are frequently stimulated in a retrograde fashion; this produces atrioventricular dyssynchrony which decreases cardiac output by about 20% from the loss of an atrial kick. Although a patient with symptomatic bradycardia will experience an increase in cardiac output and mean arterial pressure because of pacing, the cardiac output will not usually return to pre-bradycardia levels. This 20% cardiac output decrease, however, will usually be well tolerated unless left ventricular function is severely diminished.3
Steps for transcutaneous pacing
1. IF time and patient condition permits, provide IV analgesia (e.g. fentanyl) and/or IV anxiolysis (e.g. midazolam).
2. Apply pads in either anterior-lateral (AL) configuration (to the patients right upper chest wall and left lower chest wall, mid axillary line) or in an anterior-posterior (AP) fashion (anterior lower left chest wall and posteriorly under the left scapula).
a. The AL configuration is often used in emergent situation as you do not have to roll the patient, however the AP fashion supports a more appropriate vector for electrical conduction through the heart should defibrillation or cardioversion be required and has been found to produce mechanical capture (described below) at a lower energy output.4
b. Good skin-to-electrode lowers transthoracic impedance and improves electrical capture of the heart. Hair should be clipped or removed prior to pad placement and skin should be dry.
3.Turn device to “pacing mode” and notify the Aeromedical Evacuation (AE) MCD and/or other appropriate teams (e.g. Boom Operator, Load Master, Front End crew)
4. Apply ECG electrodes, if necessary, to evaluate underlying rhythm.
5. Appropriately set the desired heart rate, usually at least 30 beats above native rhythm, and typically between 60-80 bpm.
6. Starting at 70 milliamperes (mA) slowly increase the device’s current output in 10 mA increments until you see electrical capture, reflected on the devices ECG rhythm.
a. Some devices will recognize pacing spikes if toggled on.
7. Confirm mechanical capture by palpating a pulse.
8. Once pacing is captured and confirmed, set output to 5-10 mA over the capture threshold.
9. Re-evaluate patient’s circulation and overall condition
10. If analgesia and anxiolysis has not already been provided, administer if appropriate as transcutaneous pacing is considerably uncomfortable and usually not well tolerated in the awake patient.
Transcutaneous pacing points to consider
Trouble shooting transcutaneous pacing failure
Transvenous pacing utilizes a central venous catheter (CVC), usually placed into the right internal jugular or left subclavian vein, which serves as an introducer to “float” a pacing wire through the venous system utilizing a small balloon, terminating into the apex of right ventricle. Transvenous pacers (TVPs) typically have both atrial and ventricular electrodes which permit pacing in a physiological, dual chamber manner to promote AV synchrony, optimizing cardiac output. Transvenous pacing is very well tolerated and comfortable for the patient and does not require sedation, if secured well is less likely to fail or lose capture compared to transcutaneous pacing and has the added benefit of utilizing a pacer box to control pacing output.
TVP placement complications is not without risk. Complications may be related to venous access (e.g. arterial puncture, pneumothorax, etc.), right heart catheterization (e.g. dysrhythmias, atrial or ventricular perforation, misplacement of the wire into the coronary sinus, valvular damage, etc.), the pacing wire itself (e.g. wire fracture, displacement, fibrosis, infection), and the external generator.
Indications for prophylactic TVP placement
If a patient has required transcutaneous pacing and time and resources permit, a TVP should be placed urgently, ideally in the first 24 hours. Certain pathology also predisposes patients to arrythmias, and often a TVP should be place prophylactically prior to transport. Myocardial infarctions (MIs) affecting the inferior or posterior aspects of the myocardium can result in complete (3rd degree) heart block in up to 5% of patients. These patients may also have a high degree AV block (P wave to QRS complex ratio of ≥ 3:1), which is usually transient and less likely to be symptomatic. Right sided MIs often affect the SA node and conduction system, resulting in symptomatic bradycardia requiring pacing. An anterior-lateral MI may also result in high grade AV blocks, new bundle branch block, particularly the left bundle branch, or bi-fascicular blocks. Prior to transport a Cardiology consultation may be helpful to guide prophylactic TVP placement.
Epicardial wires are placed during cardiothoracic surgery and sutured directly into the epicardium and exit through the skin and are covered by a dressing. By surgical convention, atrial (A) wires emerge on the patient’s right, and ventricular (V) wire emerge on the patient’s left. These wires will connect to the pacemaker box using a special cable with a screw in connector that will accept the wires placed by the surgeon. Patients will always have V wires but will not uncommonly have A wires as well; a patient will never have only A wires. Pacer box usage is the same for both epicardial or transvenous pacing, with the exception being if the patient does not have atrial epicardial wires.
Transvenous Pacer Box nomenclature and modes
Ventricular demand pacing is the mode of choice during patient evacuations because attaining the correct electrode position when “floating” the transvenous pacemaker is relatively simple. Although the loss of AV synchrony can result in about a 20% decrease in cardiac output, it is generally tolerated by most patients, apart from those with significant myocardial depression. It is also the least sensitive to small changes in catheter positions.
Transvenous pacemaker modes to use for conduction pathologies are summarized in Table 1 below:
Troubleshooting transvenous pacing
1. Intermittent loss of capture must be addressed urgently, as sudden and complete loss of capture will likely result in hemodynamic instability or collapse. Consider in-flight diversion if possible or a communication patch to a Cardiologist.
2. Immediately prepare to transcutaneous pace while troubleshooting.
3. Check to ensure electrodes are properly inserted and attached to pacer box.
4. Ensure the pacer box has battery power.
5. Assess the patient for landmarks on the TVP catheter wire.
a. May also utilize point of care ultrasound to evaluate wire position.
6. Consider switching to asynchronous mode (e.g. DOO, VOO).
7. Evaluate systematically:
a. EMI from aircraft (pacemaker will be inhibited from firing and ECG will look like electrocautery or perhaps even VF)
i. Switch to asynchronous mode, but ensure rate is greater than the patient’s intrinsic rate to avoid R on T phenomenon.
1. DOO for 3rd degree heart block without atrial fibrillation
2. VOO for 3rd degree heart block with atrial fibrillation
b. Failure to pace due to output failure (pacing spikes absent or heart rate not reaching set value)
i. Increase mA (20mA atria and 25mA ventricle) and decrease sensitivity (if in VVI) while observing cardiac monitor to ensure there is electrical capture
ii. Switch to an asynchronous mode to prevent oversensing (DOO, VOO)
c. Failure to capture (visible pacing spikes on ECG but lack of mechanical capture – pulse, arterial line wave form pulsation)
i. Increase output
ii. Check connections, rule out mechanical issue
iii. May also be due to drug interaction (anti-arrhythmics) or post cardiac defibrillation
d. Failure to sense (producing pacing spikes inappropriately)
i. Decrease absolute value of sensing (therefore making it easier to inhibit)
e. Oversensing (inhibited pacing)
i. Large P or T waves may be sensed as intrinsic atrial activity
ii. Increase sensitivity (therefore making it hard to inhibit) or switch to asynchronous mode (DOO, VOO)
f. AV dyssynchrony – loss of atrial kick causing hypotension (SBP usually falls at least 20 points)
i. Ensure both leads are properly capturing and pacer is in dual chamber mode.
Transvenous pacing: Other points to consider
A schematic of the Medtronic 5388 is shown below (Figure A1); a few selected dials and buttons will be explained within this appendix. The Medtronic manual should be used for a comprehensive review of the device; the manual was used to construct this brief review in the event that the Medtronic manual would be unavailable in the deployed setting.
POWER ON/OFF: The ON button is marked in green (number 11, Figure A1) and the OFF button is number 12 above. Press the ON key once. The upper screen lights up and the pacers initiates a self-test. Once a successful self-test is completed the following occurs: A sufficiently charged battery will allow the device to begin sensing and pacing in both the atrium and ventricle at the following nominal parameter values. Press the “OFF” button twice within 5 seconds. After the first press, a message appears in the lower screen telling the user to press OFF a second time to turn the device off.
EMERGENCY/ASYNCHRONOUS BUTTON: Press this key (number 13, Fig A1) once to select high-output, dual- chamber asynchronous (DOO) pacing at any time, whether the device is off or locked. Use caution to avoid accidentally activating the Emergency key. This button should be used if electromagnetic interference causes over sensing inhibiting the pacemaker from firing causing hemodynamic instability. The device will pace at the following values:
Adjusting the rate, A output, and V output in emergency mode: These parameters can be adjusted using the three upper dials (numbers 4, 5, and 6) on the right side of device marked in yellow in Figure A1; these dials will be detailed below. To return the device to demand or synchronous pacing:
The device will begin synchronous pacing with the following values:
ADJUSTING RATE, A OUTPUT, AND V OUTPUT: the parameter settings are displayed numerically and graphically. The dials for adjustment are the numbers 4, 5, and 6 respectively (marked in yellow, Figure A1). The line next to each dial shows the range available for each parameter. The liner graph appears above the corresponding numerical value.
Rate dial (number 4 in Figure A1): The optimal RATE setting once the device turns on is 80 BPM. The pacing rate ranges from 30 to 200 beats per minute (BPM). Turning the RATE knob clockwise increases the rate, and counter-clockwise decreases the rate.
A (Atrial) OUTPUT dial (number 5 in Figure A1: The atrial output ranges from 0.1 to 20 mA. Turn the dial clockwise to increase A OUTPUT. Turn the dial counterclockwise to decrease or turn A OUTPUT OFF. When A OUTPUT is set to OFF, both the atrial output and the atrial sensitivity are turned off (i.e., there is no atrial pacing or sensing).
V (Ventricle) OUTPUT dial (number 6 in Figure A1): The ventricular output ranges from 0.1 to 25 mA. Turn the dial clockwise to increase V OUTPUT. Turn the dial counterclockwise to decrease or turn V OUTPUT to OFF. When V OUTPUT is set to OFF, both the ventricular output and the ventricular sensitivity are turned off (i.e. there is no ventricular pacing or sensing).
PACE LEDs
Adjusting Atrial and Ventricular Sensitivities