Pacemaker nomenclature

The code for pacemaker is called NASPE/BPEG code. These stand for North American Society of Pacing and Electrophysiology and British Pacing and Electrophysiology Group. The first code was in 1974. Present code was made in 2002. Positions are in the order- chamber paced, chamber sensed, response to sensing, rate modulation and multisite pacing. For 1,2 and 5, codes may be OAVD- none, atrial, ventricular and dual. For 3, code may be OTID- none, triggered, inhibited or dual. For 4, OR- none or rate modulation present.

Indications for permanent pacing (PP)

Commonest indication for PP is sinus node disease, second commonest being AV node disease.

For complete heart block, PP is always indicated. There is some confusion about congenital CHB, with some experts of the opinion that PP is indicated here only if there is (CBSEE)

• Congestive heart failure
• Bradycardia of less than 50 when awake
• Syncope or presyncope
• Ectopy from ventricles or
• Exercise intolerance.

If second degree heart block is symptomatic, PP is indicated. If asymptomatic, PP is indicated if

• Asystole > 3 sec when awake
• Rate < 40 when awake

And may be indicated if

• Due to neuromuscular disorder
• Intra or infra Hisian block (not for supra Hisian).

For bi or tri fascicular block, PP is indicated if there is transient CHB and PP may be indicated if symptomatic.

For sinus node dysfunction, PP is indicated if symptomatic and is not indicated if asymptomatic. For reversible causes like Lyme disease, PP is naturally not indicated.

For neurocardiogenic syncope (VVS & carotid sinus hypersensitivity), if the predominant cause is cardioinhibitory rather than vasodepressor (this can be made more clear by tilt table testing), PP is indicated if drugs such as beta blockers are ineffective. Dual chamber pacing was found to be useful in this setting in some studies (VPS-I and VASIS) but not in others (VPS-II).

Pacing for the prevention of tachyarrhythmias- PP is indicated in pause-dependent VT and PP may be indicated for congenital long QT syndrome.

Pacing to prevent atrial fibrillation (AF)- Atrial pacing has been studied for prevention of AF. The concept is that it decreases the refractoriness of dispersion in the atrium. Various techniques are used. Usual single site atrial pacing, strial septal pacing and Bachmann’s bundle pacing are single site pacing techniques. Dual site pacing is with one lead in usual RA position and other lead in the coronary sinus. Many pacing algorithms have been developed too. Prevention of AF by pacing was shown in ADOPT trial, but was not shown in the ASPECT trial.

Cardiac resynchronization therapy- CRT is a technique to reestablish synchronous contraction between LV free wall and IVS. Usually, biventricular pacing is needed, but LV pacing alone can achieve this in some persons. Trials have shown that this improves functional status, but not longevity. The indication for CRT is if all of the following are met-

• NYHA III or IV
• Optimized medical therapy
• LVEF 0.35
• NSR
• QRS more than 120 msec

PP in HCM- Dual chamber PP for HCM has not been shown to improve symptoms, though it does decrease the LVOT gradient, presumably due to RV apical pacing causing altered septal activation leading to less LVOT narrowing and hence less Venturi effect causing less SAM. So, it is only a IIb indication.

Selection of appropriate pacing mode

For patients with sinus node dysfunction AAI is preferred to VVI due to definite morbidity benefit (thromboembolism, AF, HF) and controversial mortality benefit. (The main studies are MOST and Andersen et al.)

For heart blocks, DDD does not offer benefit over VVI (UKPACE study).

Along with an ICD, when antibradycardia pacing is not needed, VVI is better than DDD (DAVID study)!

Modes and timing cycles

VVI- after a ventricular event, the pacemaker delivers a ventricular spike only after waiting for a time interval called lower rate interval. If a ventricular activity occurs within this time, the LR timer is reset, but activity in an initial part of the LRI called the ventricular refractory period (VRP) will not reset the LR timer.

AAI- Like for VVI, there is a LR interval and an atrial refractory period. Before implanting an AAI for a sinus node disease, we have to be sure of good AV nodal conduction by demonstrating 1:1 conduction of atrial beats at a rate of 140/mt.

DDI- This is like a combination of AAI and VVI, but there is not VAT function, presence of which would have made it a DDD. VAT function (or tracking of P) refers to pacing of ventricle after a P wave if there is AV conduction (after waiting for an interval called the AVI or AV interval) to produce an intrinsic QRS. DDI is usually a programmable option in DDD pacemakers and is switched on if atrial tachyarrhythmias are causing problems.

VDD- This is used for heart blocks. Its advantage is use of a single lead only- the atrial sensor is at the atrial position of the ventricular lead. It essentially functions as a VVI, with the additional option of P tracking- that is, if an intrinsic P occurs, the ventricular lead will wait for AVI and will pace only if the P is not conducted to produe a QRS (if a P conducts in spite of the heart block, it is allowed to work!).

 DDD- In addition to the settings for VDD, there is a new setting to decide when atrial pacing should start if there is no atrial activity. After ventricular activity, if there is no atrial activity at the end of an interval called the VA interval, an atrial pacing spike is given. But, as for the VRP of VVI, there is an interval after the QRS when atrial activity is not sensed by the atrial sensor- this is called PVARP or post ventricular atrial refractory period. Since the atrial sensor is also not allowed to sense during the entire AVI, AVI + PVARP constitutes total atrial refractory period or TARP. The need for a PVARP is to avoid a retrograde P from being sensed and initiate an AVI, this again producing a retrograde P which is again sensed- thus causing an endless loop or pacemaker mediated tachycardia. If still this is occurring, just increase the PVARP so that the retrograde P would not be sensed.

 DDD is especially useful for AV block (even though, as told earlier, no benefit over VVI was shown in studies). DDD is not useful in SSS and AF.

DDD can manifest as

• NSR,
• atrial pacing if no atrial activity and normal AV conduction,
• P synchronous pacing if normal atrial activity and no AV conduction and
• AV sequential pacing if no atrial activity and no AV conduction.

 Rate adaptive pacing- The sensors usually measure activity, minute ventilation or QT. Activity sensors are most commonly used and may be accelerometers or piezoelectric crystals, the former being more physiological.

Nowadays DDDR is most commonly used. These can be reprogrammed to AAIR in cases of sinus node dysfunction only. VVIR is used instead of DDDR in patients with AF.

VVI is contraindicated if it causes hypotension or VA conduction.

Pacemakers are implanted epicardially if there is no access to the right ventricle or if there is an intracardiac shunt that could predispose to thromboembolism. A lateral subclavian approach is preferred to medial to avoid crush injury to lead and pneumothorax.

Pacemaker programming

Pulse width- usually triple the threshold is used.

Voltage- usually double the threshold is used.

Microjoules- not usually done- if done, usually triple the threshold is used.

Mode switching- If a rapid atrial rhythm occurs in a PP capable of P tracking (DDD or VDD), to avoid rapid ventricular rhythm the PP automatically switches off P tracking- that is, in effect it becomes DDI or VVI (note that if DDD/VDD – VAT = DDI/VVI).

AVI- is programmed in such a way as to support intrinsic AV conduction.

Pacemaker complications

During implantation, complications like pneumothorax, hemothorax, arterial puncture, AV fistula, thoracic duct injury and brachial plexus injury can occur.

For hematoma, aspiration is not advised. Evacuation is done only if absolutely necessary.

Lead entry into the LV, via a PFO, is recognized by posterior position on lateral view and by RBBB pacing pattern. It can cause embolization.

Lead perforation may manifest as cardiac tamponade, pericardial effusion, pericarditis, friction rub, increased threshold, RBBB pacing pattern or intercostal muscle or diaphragmatic contraction. Withdraw lead and reposition.

Subclavian vein thrombosis is usually asymptomatic.

Lead dislodgement may be macro or micro, former being visible radiographically.

Loose connector pin can cause loss of output.

Insulation break can cause sensing or pacing problems.

Lead fracture can occur, especially at the costoclavicular space.

VPCs can occur in the first two days of pacemaker implantation due to mechanical stimulation. They have the same configuration as the pacemaker induced complex. They resolve.

Diaphragmatic stimulation may be due to direct stimulation, when the left hemidiaphragm is paced, or due to phrenic nerve stimulation, when the right hemidiaphragm is paced. Try decreasing voltage or pulse width. If that does not work, reposition.

Pacemaker infection is usually local rather than septicemic. Early infection is caused by Staph aureus and is aggressive while late infection is caused by Staph epidermidis and is usually indolent. Local antibiotic irrigation helps to prevent infection. Treatment is removal of the entire system including leads.

Pacemaker erosion may be due to infection or a tight pocket. Treatment is removal of the system. The same system cannot be reimplanted at another site- a new one has to be used. So impending erosion is an emergency- revise the pocket and reimplant.

Troubleshooting

Failure to capture- Means a pacing artifact is present without depolarization. Causes are high threshold, lead fracture, insulation break, lead dislodgement, lead perforation, impending battery depletion, functional noncapture, and high threshold due to drugs or metabolic problems. Functional noncapture refers to failure to capture due to pacing spike falling in refractory period of a beat.

Failure to output- Means that there is no pacing artifact. Causes are oversensing, battery depletion, loose set screw, lead fracture, internal insulation failure in a bipolar lead and air in the pocket of a unipolar pacemaker.

True undersensing occurs due to lead dislodgement, lead fracture or battery depletion. Functional undersensing occurs when a cardiac activity falls within a programmed refractory period of the pacemaker.

Fusion beat is a hybrid of intrinsic and pacemaker induced activities. Pseudofusion beat is due to pacemaker spike falling on intrinsic activation, without pacemaker induced activation. It occurs in two situations- when pacing rate and intrinsic rate are similar and when there is an intraventricular conduction defect. In the former situation, it occurs because the initial part of the intrinsic activation is not sensed by the pacemaker and hence it discharges.