Pacemaker Function and Failure

Last Updated on by frcemuser

Implantable devices in cardiology is a term covering a variety of diagnostic and therapeutic modalities. This article will cover:

  • Device therapy for brady-arrhythmias (conventional pacemakers)
  • Device therapy for tachy-arrhythmias (automatic implantable cardioverter defibrillators, or ICDs)
  • Device therapy for heart failure (cardiac resynchronisation therapy [CRT], or biventricular pacing)

Conventional pacemaker function

  • Device anatomy
    • Various forms of conventional pacing are available, and the choice depends predominantly upon the electro-anatomical site and nature of the conduction problem. These devices are delivered transvenously, so pacing activity originates from the right heart. Right atrial leads are usually positioned with the tip in the RA appendage. Traditionally, the RV lead is positioned at the RV apex.
  • Pacemaker nomenclature
    • Pacing: delivery of a programmed electrical stimulus from the pacemaker to the myocardium via the implanted lead.
    • Capture: successful depolarisation of the myocardium from a pacemaker stimulus. Failure to capture leads to a pacing spike on the ECG, but no depolarisation.
    • Threshold: the lowest output voltage from the device that will reliably capture.
    • Oversensing and undersensing: the pacemaker will see an enormous amount of electrical activity across a wide range of frequencies. Some will of course be generated by the heart’s own electrical cycle, but much of the rest will come from non-cardiac sources such as skeletal muscle activity. If the device is too sensitive, it will see depolarisations that are not really there, and if it is not sensitive enough it will miss normal intrinsic depolarisations. Undersensing leads to overpacing and oversensing leads to underpacing.
    • Lower Rate Limit (LRL): the slowest rate, or longest cycle length, that the device will allow the heart to drop to.
    • Upper Rate Limit (URL): the fastest heart rate, or shortest cycle length, that the device will pace at.
    • Battery End Of Life (EoL): As the battery is depleted, replacement needs to be planned. With follow-up in specialised pacing clinics, it is rare for a battery to become completely exhausted and the unit to fail.
    • Hysteresis: This can be a difficult concept to understand, but can lead to a misdiagnosis of pacemaker failure. In the simplest set-up, a pacemaker with an LRL of 50/min would start pacing as soon as the intrinsic rate fell to 49/min. This is undesirable, partly due to the unnecessary drain on battery life, but also because intrinsic activity is now known to be preferable to paced activity wherever possible. Hysteresis is the separation of the lower pacing rate from the lower sensing rate. In practical terms, this means that the device will pace at 50/min, but only when the intrinsic rate drops to, for example, 40/min. It is easy to see why this might give the impression that the device has malfunctioned, if the patient’s own rate is perhaps 42/min, but the pacemaker has not stepped in.
  • Pacemaker classification (NBG Codes)
    • In simple terms, the pacemaker may have leads to either, or both, of the right atrium (RA), or right ventricle (RV). This is the origin of the terms single-chamber and dual chamber systems. A standardised nomenclature for pacemaker modes explains, using a three-letter code, which chambers of the right heart are involved, as well as the way in which the device interprets electrical signals:
      • 1st letter: the chamber paced: A(trium), V(entricle), or D(ual)
      • 2nd letter: the chamber sensed: again, A,V, D, or very occasionally, neither (O)
      • 3rd letter: the way in which the signals determine the activity of the pacemaker itself: I(nhibited), T(riggered), or D(ual). The differences between these are not relevant here.
    • Common modes of pacing are:
      • VVI: a single lead to the RV provides both sensing information and pacing
      • DDD: leads are positioned in both the RA and RV, and can both sense and pace
  • Pacing leads
    • The major distinction is between passive and active fixation.
    • Passive fixation leads use small tines at the tip to hook into the trabeculations of the right heart, and provide resistance to displacement.
    • Active fixation uses a corkscrew mechanism to drive into the myocardium itself. Active leads are much less likely to displace. They are often used in the ventricular leads of ICDs.
    • Both types develop a fibrotic reaction at the tip over time, which increases stability.

Conventional pacemaker failure

Pacemakers are amongst the most reliable of medical devices, but problems do occur. These can be broken down in a number of ways, but it is probably most convenient to consider them in the following fashion.

  • Device failure: failure to sense and/or pace appropriately. This may happen at any stage after implant. In some situations problems can be overcome with adjustments to programming, but in other cases the device may need replacement.
  • Lead failure: in the immediate post-implant period the leads may displace. This may be fairly subtle, and manifest with a change in the parameters detected at device interrogation. In some cases the displacement can be much more obvious, with a marked shift in position within the desired chamber, or displacement into another chamber. It is relatively unusual for displacement to occur later, unless there has been significant chest trauma or cardiac surgery.
  • Pocket problems: The pacemaker itself is implanted in a pocket created within the deep tissues of the anterior chest wall, and is conducted as an aseptic procedure; infection does still occur however. This may be related to the incision, the pocket, or the device/leads. Although it may be reasonable to try and treat these infections conservatively with antibiotics, the system often has to be revised or extracted. Patients with convincing signs of infection should be admitted for treatment and expert evaluation. The pacemaker box may also cause problems with its site. Patients may find it uncomfortable, or occasionally it may erode towards the surface, threatening the viability of the overlying tissue. This usually requires operative revision. Certainly any patient with tissue breakdown over the site of the box should be admitted for specialist evaluation.

Pacemaker problems may be implicated in a wide variety of patient presentations to the ED. It is best to approach these in a systematic way, and try to answer the following points if at all possible:

  • What device is implanted, and when?
  • How is the device set up, in terms of mode and rate etc.?
  • What is the patient’s own intrinsic rhythm and rate?
  • Is there evidence of appropriate pacing activity on the surface ECG?
  • Is there evidence of appropriate sensing on the surface ECG?
  • If no to 4 and 5, is there evidence of inappropriate pacing/sensing?
  • Is there any evidence of a mechanical complication, i.e. lead displacement, fracture etc.?
  • Is there evidence of a local complication such as infection or erosion?

Answering these questions may be difficult at first presentation in the ED, but useful information can be gathered from the history, clinical examination, surface ECG, chest x-ray and blood tests.

Implantable cardioverter defibrillator (ICD) function

  • Components of the ICD
    • ICDs are superficially similar to conventional pacemakers. The simplest system consists of a single lead to the RV, and a hermetically sealed titanium can containing the computer, battery, and circuitry. The battery is generally larger than that for a conventional unit. The defibrillation shock is generated by a system of capacitors which store charge until it is sufficient to deliver.
    • The lead or leads are implanted in the same fashion as those for conventional pacing. The RV lead is required to deliver the high-energy shock, but can also be used for pacing and sensing. An ICD lead can be readily recognised on the plain chest x-ray by the appearance of a coil wrapped around the inner core.
  • Functions of the ICD
    • Current advanced ICDs can offer treatment in three different ways:
      • Conventional anti-bradycardia pacing (already discussed)
      • Anti-tachycardia (ATP) pacing
      • Defibrillation shocks
    • ICDs are extremely sensitive and effective medical devices, but come with a significant cost burden, and issues around implantation. For those reasons, there are some very clear directions to clarify who should be considered for an implant.
    • Because VT is potentially amenable to termination by pacing, unlike VF, the device will often be programmed to try several repeated bursts of ATP for tachycardia recognised as VT. It is estimated that greater than 95% of VT is successfully pace-terminated in this fashion. It will only deliver shock therapy if the tachycardia persists (i.e. ATP has been unsuccessful), or if VF is recognised.
    • If defibrillation is unsuccessful, further shocks will be delivered. Many devices now have a limit to the shocks delivered for any one tachycardia episode. Most shocks are delivered at an energy level in the range of 26-36J. Shocks at this level cannot be mistaken by the patient, as it is a violent event. In general terms, if a conscious patient is unsure whether a shock has been delivered, it probably has not. If a patient has lost consciousness, only formal device interrogation will reveal what therapy has occurred.

Implantable cardioverter defibrillator (ICD) failure

Any of the problems associated with conventional pacing may also be an issue with ICDs. In addition, however, there are more specific potential problems. ICD patients are likely to attend the ED for one of the following reasons.

  • Delivered shock therapy whilst conscious
    • To a large extent this is why the device is implanted, but further evaluation is always needed. Even a single shock may be extremely disturbing for the patient, and at the far end of the scale is ICD storm, where repeated defibrillation occurs again and again. The first step is to determine whether the therapy was appropriate (for VF/untreated VT), or inappropriate (usually due to misidentification of the rhythm, or noise artifact secondary to lead fracture).
    • Clinical assessment within the ED will include the following:
      • Identification and management of pro-arrhythmic electrolyte abnormalities: esp. K+ and Mg++
      • Identification and management of acute myocardial ischaemia: approximately 5% of sustained monomorphic VT occurs as a result of acute ischaemia. This can be evaluated through the clinical history, the ECG and biomarkers of myocardial necrosis. A small troponin leak is well recognised in association with cardioversion, either external or internal, and is not necessarily indicative of high risk ACS. The resting ECG may be helpful but may be obscured by pre-existing abnormalities such as LBBB. If an ACS is suspected, the patient should be managed in conventional fashion.
      • Identification of lead fracture: a plain chest x-ray is helpful, but by no means definitive
      • Identification of decompensated left ventricular failure: this can result in ventricular arrhythmias due to LV wall stretch, and should be treated conventionally. Once again, the history, physical examination and CXR are the major diagnostic tools.
    • A patient who is well, with a stable rhythm, and who has had a very limited number of shocks, does not necessarily require admission. These patients can be discharged if the investigations listed above are normal, and follow-up arranged for the next working day by the pacing clinic where device interrogation can occur. If abnormalities are detected on investigation in the ED, then further evaluation as an inpatient is indicated.
  • Syncope
    • It should be remembered that syncope may not necessarily be secondary to a cardiac cause, even in patients with ICDs.
    • In the context of a patient with an ICD it is important to consider the following issues:
      • Sustained bradycardia is unlikely if the ICD has pacing functions, but is possible if there is any evidence suggestive of pacemaker failure (as covered above).
      • VF will rapidly lead to loss of consciousness. A shock would obviously pass unnoticed by the patient.
      • Patients who have had sustained VT may or may not be aware of palpitations immediately beforehand, and there is often a degree of retrograde amnesia following a shock / collapse; a normal ECG at presentation does not exclude this as a cause.
    • Once again, device interrogation will reveal the nature of any delivered therapy; proper assessment and evaluation of the syncopal patient will take more time than is available in the ED, and admission is usually appropriate.
  • Associated cardiac symptoms
    • Chest pain, palpitations and dyspnoea may all be seen in ICD patients attending the ED, whether related to the underlying cardiac condition, or as a manifestation of issues around therapy from the device. In general, these should be approached as they would for any other patient. The possibility of pneumothorax following recent implantation should not be forgotten, nor the possibility of device infection/endocarditis if a non-specific infective picture is apparent.
  • Unrelated issues
    • Clearly ICD patients may present with other intercurrent problems. This does not usually present difficulties, but a few specific points should be borne in mind:
      • MRI scanning should not be undertaken without appropriate cardiology consultation since damage can be caused to the device and the patient.
      • Emergency surgery: it is rare for the ICD itself to present problems at surgery. There is a theoretical risk that electrical noise from the diathermy current may be interpreted as ventricular fibrillation and lead to a shock. This is rare with modern equipment, particularly if the surgical field and diathermy pads are distant to the heart. Even if a shock is delivered, it poses no risk to the surgeon or staff. Ideally though, the defibrillation therapy can be programmed off for the duration of the surgery.
      • Patients who are dead or dying: if ICD patients have reached the stage where, for whatever reason, it is accepted that they are for palliation rather than active treatment, the ICD should be electively reprogrammed with the tachyarrhythmia therapy disabled. This may not be possible if the deterioration is very sudden. In these situations, an external magnet should be taped in place above the device.

Cardiac resynchronisation therapy (CRT)

Indications for implantation of these devices are continuously evolving. The response rate to CRT is somewhere in the region of 60-70% of patients selected by current guidelines, with perhaps a further 10% of non-responders improving once their device parameters have been reprogrammed in conjunction with various echo measurements.

CRT troubleshooting:

  • Many of the problems associated with CRT devices are those of conventional pacemakers and ICDs (if that function is also present). These have previously been covered.
  • The major extra problem to consider is that the epicardial LV lead is much more vulnerable to displacement than the intra-cardiac leads.
  • For the huge majority of patients with CRT, LV pacing is achieved through epicardial stimulation. Of these, the majority have a highly mobile thin lead delivered through the venous system to the right atrium. From there, it is manipulated out through the coronary sinus, and into a branch of one of the epicardial cardiac veins.
  • Although displacement is generally a problem soon after implant, it can be delayed for weeks or months. Even a minor shift in the lead tip can lead to failed LV sensing or pacing, and should be considered if patients present with decompensated heart failure after an initial improvement from CRT.
  • A CXR and ECG performed in the ED will be appropriate in patients in whom failed CRT is suspected; these investigations will be difficult to interpret and expert advice should be sought.

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