Pacemakers and ICD

Indications for emergency pacing

• Symptomatic bradycardia
• Symptomatic high-grade AV block (Mobitz II or complete)
• Severe sick sinus syndrome with asystole >3s and syncope
• Overdrive pacing for torsades de pointes
• Overdrive pacing for recurrent monomorphic VT
  • Risk of inducing VF and limited by machine pacing limit of 180
• Overdrive pacing of unstable SVT
  • Only once pharmacological and electrical cardioversion have failed

Emergency pacing

• Transcutaneous pacing for severe hypotension with bradycardia
  • 70% survive with good neurological outcome vs. 15% with non-pacing modalities
  • May be able to pace RV infarct when transvenous pacing fails (as can directly pace LV)

Technique for transcutaneous pacing

• External pads and electrodes for monitoring required
• If bradyasystolic peri-arrest, ramp up current to 100mA and titrate down once stabilised
• If less severe compromise, can titrate up from 10mA to usually 50-100mA and then maintain at 1.25x the threshold
• Set rate to 80bpm and increase by 10bpm until perfusing (up to 100/min)
• May be fixed or demand (synchronous)
  • Fixed (asynchronous) pacing carries risk of R on T, however, there is little outcome data to support a preference for either
• Need electrical and mechanical capture
  • US can be helpful for ensuring mechanical capture if poorly perfused
• Reasons for failed capture may include
  • Inadequate current
  • Faulty electrical contact
  • Electrode placement
  • Patient size
  • Underlying pathology
  • PTX, severe ischaemia, pericardial effusion or metabolic derangement

Resuscitation in patients with permanent pacemakers

• If countershock required, place pads at least 8cm from the pulse generator
• After countershock, interrogate the pacemaker to ensure still functioning as can suffer from:
  • Pacemaker inhibition due to reversion to noise mode
  • Deletion (reprogramming)
  • Circuit damage
  • Myocardial damage near lead tip caused by current transmission via the electrode to the myocardial interface
• Defibrillation can lead to global myocardial ischaemia which in turn also increases the pacing threshold thus causing capture failure
  • If this occurs, try transcutaneous pacing at a higher current

Nomenclature

Most commonly VVI and DDD

The fifth letter is rarely used

Third position D indicates both triggered and inhibition responses can occur

i.e. If atrial activity sensed, atrial pacing is inhibited but triggers ventricular pacing

Programmability

• Activity sensors: Vibration detectors (accelerometers or piezoelectric crystal)
  • May respond to certain activities e.g. using a drill
• Minute ventilation sensors
  • Measures impedence between pacemaker unit and electrode

Magnet inhibition

• Placing magnet over permanent pacemaker causes sensing to be inhibited and results in asynchronous mode (AOO, VOO, DOO)
  • Usually at rate of 100
  • Risk of R on T

Pacing modes for bradycardia

• Single-chamber pacing
  • AOO and VOO
    • Asynchronous and virtually obsolete except in a few emergency situations
  • AAI
    • Atrial demand pacing
    • Indicated in sinus bradycardia providing AV conduction is intact
    • Only paces if does not sense atrial activity
  • VVI
    • Ventricular demand pacing
    • Most commonly used mode in life-threatening bradycardias
    • Spontaneous ventricular activity is sensed and low risk of R on T
    • AV synchrony is lost

Pacing modes for bradycardia

• Dual chamber pacing
  • DVI (AV sequential pacing)
    • Will pace atria, wait and then pace ventricle if no ventricular activity sensed
    • To maintain AV synchrony in the absence of atrial sensing, pacing rate must be higher than intrinsic spontaneous atrial rate
    • Indicated if impaired AV conduction and atrial bradycardia
    • Not useful if atrial tachyarrhythmias exist as cannot pace faster than them
  • VDD (Atrial synchronous ventricular inhibited)
    • Paces only the ventricle but senses both
    • Sensed P-wave triggers ventricular pacing

Pacing modes for bradycardia

• Dual chamber pacing
  • DDD (Dual pacing and sensing)
    • Atrial impulse triggers ventricular pacing unless senses autonomous ventricular activity
    • Upper rate limiters prevent ventricular pacing of atrial tachyarrhythmias
    • If atrial bradycardia with intact AV conduction – Atrial pacing
    • If sinus rhythm with AV block – synchronised ventricular pacing of intrinsic P waves
    • If sinus bradycardia with AV block – Sequential atrial then ventricular pacing
    • Normal sinus rhythm and AV conduction – Inhibition of both atrial and ventricular pacing
    • Can suffer re-entry loops where PVC is transmitted retrogradely to atria, where it is sensed and results in ventricular pacing with endless loop

Pacing modes for bradycardia

• Dual chamber pacing
  • DDI (AV sequential, non-P-wave synchronous)
    • Sensing of both but sensed atrial events do not trigger ventricular pacing
    • Prevents endless loop phenomenon or tracking of SVTs
    • Useful for SA node dysfunction with episodic atrial tachyarrhythmias
    • Will simply pace ventricle at backup rate in the setting of atrial tachyarrhythmia

Complete AV block in acute MI

Indications for permanent pacing

• Class I
  • Chronic symptomatic 2^nd or 3^rd degree AV block
  • SA node dysfunction with documented sinus bradycardia
  • Recurrent syncope associated with carotid sinus hypersensitivity
• Class II-IIa
  • Asymptomatic complete AV block with average ventricular rate >40 in awake patient
• Class IIb (weak supportive evidence)
  • 1^st degree block with depressed LV function and symptoms of LV failure
• Class III (not indicated)
  • Asymptomatic 1^st degree block or reversible AV block due to drugs

Indications for permanent pacing

• Other
  • HOCM (Class IIb)
    • Usually for symptomatic patients with high gradient in LVOT
    • DDD pacing with short AV interval caused RV apical activation with altered septal activation to reduce LVOT gradient and systolic anterior motion of mitral valve
  • Heart failure
    • Class IIa for NYHA III/IV patients with dilated or ischaemic cardiomyopathy, QRS >130ms
    • Cardiac resynchronisation therapy (CRT) is indicated in these patients via biventricular pacing to improve survival and symptoms

Fixed-rate vs. demand

• Fixed-rate pulse generators produce an electrical signal regardless of patients own intrinsic electrical rhythm
  • Can result in serious arrhythmias if discharges during vulnerable period (T wave)
• Demand pacing
  • Typically discharges if no sensed electrical activity after certain time period 
  • May be inhibited by intrinsic sensed electrical activity or triggered to discharge during absolute refractory period

Pacing in tachyarrhythmias

• May be useful for:
  • SVT: AVNRT, AVRT (rarely required)
  • Atrial flutter (rapid atrial overdrive pacing)
  • Unifocal atrial tachycardia (rapid atrial overdrive pacing helpful if re-entry pathway driven but less so if autonomous focus firing at rapid rate)
  • Ventricular tachycardia
    • Should not be used if very rapid ventricular rates >300 or significant haemodynamic instability exists
• No value in sinus tachycardia, AF or VF

Pacing in tachyarrhythmias

• Torsades
  • Pace atria or ventricle at 110-120/min
• SVT
  • Atrial pacing at 60-80 and slowly increase to 10-20% faster than spontaneous atrial rate
  • Atria then paced for around 30 seconds then switched off with ensuing sinus rhythm
  • If fails, try different atrial pacing site and faster rate

Pacing in tachyarrhythmias

• VT
  • Ventricular burst pacing
    • Pace ventricle at 120% of spontaneous VT rate for 5-10 beats then stop
    • Can precipitate faster VT and VF
  • Underdrive ventricular pacing at rate <50% of VT rate is sometimes successful
  • Overdrive atrial pacing may be useful if 1:1 AV conduction and ventricular rate relatively slow (120-180/min)

Features

• Lithium batteries have lifespan of 8-12 years
• Most units preset for rates near 70, with pacing interval of 0.84 seconds
• Demand pacemakers have built-in refractory period of 0.2 to 0.4 seconds during which it will not sense, to prevent it being inhibited by its own stimulus
• Magnets held over most units will convert them from demand to fixed-rate mode
  • Can quickly ascertain paced rate, however, should only be performed for short periods due to risk of arrhythmia in fixed-rate mode (due to stimulus in vulnerable period)
• More sophisticated units can be interrogated 

Pacemaker malfunctions

• 1) Problems with the pocket
• 2) Problems with the leads
• 3) Failure to pace
• 4) Failure to sense – Leads to fixed rate pacing and risk of arrhythmia
• 5) Malfunction causing overpacing or runaway pacing

Pacemaker evaluation

• Evaluation
  • Examination of pocket
  • CXR to confirm lead placement and device itself
  • Electrolytes
  • Cardiac enzymes
  • ECG
  • Interrogation
  • Magnet fixed-rate testing

Pacemaker syndrome

• Seen in 20% of patients in early phase with symptoms of syncope, near-syncope, orthostatic dizziness, exercise intolerance, dizziness, uncomfortable pulsations over neck/abdomen and RUQ pain
• AV synchrony and presence of ventriculoatrial conduction are most common in VVI but can be seen with DDI mode
• In VVI
  • If the sinus node is intact, an atrial impulse can occur when the tricuspid and mitral valves are closed with increased jugular and pulmonary venous pressure leading to symptoms of CCF
  • Atrial distension can lead to reflex vasodepressor effects mediated by the CNS
  • If contribution of atrial contraction to late diastolic ventricular filling is important, then orthostatic hypotension can occur
• In DDI with AV block
  • If sinus node discharge rate exceeds the programmed rate of the pacemaker, can get atrial contraction against closed valves with subsequent pacemaker syndrome
• Typically symptoms are mild and patients adapt to them over time
• Unfortunately, symptoms are severe in 1/3 and may warrant upgrade from VVI to dual-chamber pacing or lowering the rate of VVI pacing 
• If symptoms occur in DDI, then optimising the timing of atrial and ventricular pacing is often required

Pacemaker infection

• Seen in <1% soon after placement
• Mostly S. aureus or S. epidermidis early on
• Presents as local inflammation or abscess at site
• Skin adherence to the device with discolouration is highly suggestive
• If only superficial infection suspected, antibiotics and analgesics with early review is indicated
• If erosion of skin occurs, requires surgical replacement
• Cardiac device-related IE can occur presenting with sepsis and positive BC without local inflammation at pocket

Thrombophlebitis and venous obstruction

• Extensive venous collaterals exist making this quite rare (0.3-3% of patients)
• Site of insertion makes no difference
• Symptoms include oedema, pain or venous engorgement ipsilaterally
• Treatment is IV heparin then oral NOAC/warfarin

Pneumothorax

• Seen in 1% of patients after insertion
• More common with subclavian insertion technique

Undersensing

• Failure to sense intrinsic cardiac activity with subsequent asynchronous, fixed-rate pacing
• Causes include increased threshold (exit block), poor lead contact, new BBB, inferior MI or programming issues
• Pacing spikes within QRS complexes is highly suggestive of this
• Lead dislodgement usually occurs within 2 days of insertion

Oversensing

• Pacemaker senses electrical activity not from atria or ventricles; it is thus inhibited, and generation of pacemaker impulse suppressed leading to bradycardia
• Unipolar electrodes are more prone to environmental sensing than bipolar leads
• Suxamethonium-induced depolarisation fasciculations
• Crosstalk (atrial output sensed by ventricular lead)
• Why might tachyarrhythmia arise?
  • Intrinsic depolarisation occurring during pacemaker refractory period, this not being sensed, and pacemaker firing soon after in the vulnerable period to initiate a re-entrant tachycardia
  • Maintenance of the tachyarrhythmia does then not involve the pacemaker at all
  • Emergency therapy can involve re-programming, or more commonly, magnet conversion to asynchronous, fixed-rate mode

Output failure

• Paced stimulus not generated when expected
• Results in decreased or absent pacemaker activity on ECG
• Causes include oversensing, wire fracture, lead displacement
• Steps:
  • Make sure pacemaker box is on and connected
  • Increase pacemaker current (up to 200mA for transcutaneous or 20mA for transvenous)
  • Asynchronous DOO/VOO mode selected to avoid oversensing
  • Convert to transcutaneous pacing  while new pacing system inserted

Failure to capture

• Paced stimulation does not cause myocardial depolarisation
• Electrode displacement, wire fracture, electrolyte disturbance, MI at lead tip or exit block
• Seen with amiodarone, flecainide, hyperkalaemia, acidosis, alkalosis, cardiac perforation and improper settings also
• If patients native heart rate is higher than the paced rate, no pacemaker activity is expected and output failure/capture failure cannot be recognised on ECG
• Suxamethonium causes depolarisation fasciculations that can lead to oversensing and subsequent failure to capture

Failure to capture

• Rx
  • Place in left lateral position (maximises electrode contact with endocardium)
  • Maximise pacemaker output
  • Use asynchronous mode
  • Transcutaneous if failing transvenous (as can directly pace LV)
  • Isoprenaline/adrenaline infusion to increase intrinsic HR

Pacemaker-associated dysrhythmias

• Pacemaker-mediated tachycardia (PMT)
  • Re-entry tachycardia with antegrade pathway via pacemaker and retrograde via AV node
  • Caused by retrograde P waves being sensed as native atrial activity by dual chamber pacemaker
  • Get paced tachycardia at rate determined by pacemaker
  • Can be terminated by AV block e.g. adenosine OR magnet application
• Sensor-induced tachycardia
  • Modern sensors respond to exercise, tachypnoea.etc.
  • Sensors may misfire in the presence of vibrations, loud noise, fever, limb movement or electrocautery with subsequent inappropriately fast rate
  • Ventricular rate cannot exceed programmed max of 160-180
  • Terminated by magnet application

Pacemaker-associated dysrhythmias

• Runaway pacemaker
  • Low battery voltage in older units results in pacing spikes at 2000bpm with risk of subsequent VF
  • Paradoxically, may be failure to capture due to low amplitude pacing spikes and subsequent bradycardia
  • Application of magnet may be lifesaving
• Lead displacement arrhythmia
  • If dislodged, lead may float in RV causing tickling of myocardium causing ventricular ectopics, possible VT and failure to capture
  • CXR helps confirm diagnosis
  • If changes from typical LBBB pattern (indicating RV placement) to RBBB pattern, suggests erosion through interventricular septum

Pacemaker-associated dysrhythmias

• Twiddler’s syndrome
  • Pulse generator rotation in pocket with dislodgement of leads and subsequent diaphragmatic or brachial plexus pacing
• RV perforation
  • RBBB instead of LBBB
  • Pacing of diaphragm
  • Haemopericardium rarely

ICD

• Reduce mortality from 30-45% to <2% per year in those at risk of sudden cardiac death
• Mostly follow a tiered approach to ventricular arrhythmias
  • Antitachycardia pacing
  • Low-energy cardioversion
  • Defibrillation
• Projected lifespan of 6-9 years
• Most common cause of death is CCF and this should be managed as usual

ED evaluation of ICD

• Causes of inappropriate shock delivery
  • False sensing
  • SVT with RVR
  • Muscular activity (shivering, diaphragm contraction)
  • Extraneous source (tapping of chest wall, vibrations)
  • Sensing T waves as QRS (double counting)
  • Sensing lead fracture or migration
  • Unsustained tachyarrhythmia
  • ICD-pacemaker interactions
  • Component failure

ED evaluation

• Ask about symptoms around event, number of shocks, activity at the time and any recent anti-arrhythmic drug changes
• Look for signs of trauma
• 12-lead
  • Any shock-related ST changes should resolve within 15 minutes and if not suggests new ischaemia
• CXR
  • Electrode migration, displacement or fracture
• Anti-arrhythmic drug levels and serum electrolytes
• If patient is receiving repeated inappropriate shocks, temporarily deactive with a magnet over the device (can simply remove magnet if want to shock again)
  • All ICD’s should then be evaluated by a cardiologist if been magnetised
• If in cardiac arrest:
  • Follow normal protocols
  • Place pads at least 8cm from generator

Disposition

• Need to discuss with treating cardiologist
• Admission generally warranted if:
  • Cardiovascular instability
  • 2 or more shocks in a 1-week period
  • Correctable causes of dysrhythmia
  • Any sign of infection or mechanical disruption of the system

Last Updated on October 28, 2020 by Andrew Crofton