Another Critical Care deep dive into pacemaker nomenclature, complications and ICD use

1. Cardiac pacemakers and
implanted defibrillators
Dr Andrew Crofton
Emergency Registrar
Disclaimer: https://criticalcarecollaborative.com/disclaimer/

2. 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

3. 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)

4. 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

5. 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

6. Nomenclature
Letter position I II III IV V
Category Chamber(s) paced Chamber(s) sensed Response to sensing Programmability, rate Antiarrhythmic
functions
O, none
A, atria
V, ventricle
D, dual (A+V)
S, single chamber
O, none
A, atria
V, ventricle
D, dual (A+V)
S, single chamber
O, none
T, triggered
I, inhibited
D, dual (D + I)
O, none
P, simple program
M, multiprogram
C, communicating
(telemetry)
R, rate modulation
O, none
P, pacing
S, shock
D, dual (P+S)
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

7. 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

8. 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

9. 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

10. 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

11. 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

12. 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

13. Complete AV block in acute MI
Feature Inferior Anterior
Onset Slow Sudden
Type Mobitz I Mobitz 2
Ventricular rate >45 <45
Escape pacemaker Stable unstable
Response to atropine Yes No
Haemodynamic effects No Yes
Permanent pacing No Yes (if high-degree AV
block)
Prognosis Good Terrible

14. Indications for permanent pacing
 Class I
 Chronic symptomatic 2nd or 3rd 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)
 1st degree block with depressed LV function and symptoms of LV failure
 Class III (not indicated)
 Asymptomatic 1st degree block or reversible AV block due to drugs

15. 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

16. 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

17. 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

18. 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

19. 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)

20. 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

21. 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

22. Pacemaker evaluation
 Evaluation
 Examination of pocket
 CXR to confirm lead placement and device itself
 Electrolytes
 Cardiac enzymes
 ECG
 Interrogation
 Magnet fixed-rate testing

23. 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

24. 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

25. 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

26. Pneumothorax
 Seen in 1% of patients after insertion
 More common with subclavian insertion technique

27. 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

28. 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

29. 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

30. 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

31. 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

32. 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

33. 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

34. 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

35. 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

36. 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

37. 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

38. 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