Indications for pacemakers (PPM)
- Symptomatic bradycardia
-
- Assuming no reversible cause
- Could be due to sinus bradycardia, 1st degree heart block, type 1 2nd degree heart block, or sinus node disease
-
- Acquired type 2 second degree HB, or Complete Heart Block
-
- Even if asymptomatic
- And assuming not reversible – although if a drug is suspected, the heart block will probably come back on stopping the drug, so often not considered reversible
-
- Tachy-brady syndrome – for example if bradycardia is caused by rate control drugs for fast AF
- Syncope with bi/tri-fascicular block or pauses >6s (without correlation with symptoms)
-
- Often missed
- Tri-fascicular = RBBB, LAD, prolonged PR.
- Bifasicular = RBBB / LBBB (but usually RBBB), and axis deviation (either left or right).
- Axis reminders!
-
- LAD deviation = I pos, II and III neg
- RAD deviation = I, II and III all negative
- Normal axis = I pos, II more pos, III either pos or neg (but smaller than II)
-
-
- Alternating LBBB and RBBB
- Some special cases – neuromuscular disease, long QT, mitochondrial disease, congenital AV block, very long PR interval (>300ms) in the absence of symptoms
- When not to pace
-
- Asymptomatic sinus node disease
- Sinus node disease or AV block, regardless of symptoms, if cause is reversible (eg patient on rate-limiting drugs, ischaemia)
- Asymptomatic BBB or bifascicular block
- Unexplained syncope, but without evidence of conduction disease/ arrythmia
-
Notes on the pathologies
- Bradycardia
-
- If bradycardic, always assess for symptoms as this can have a bearing on whether or not a PPM is required. Ask about syncope, dizziness, ‘seizures’, drowsiness, unexplained falls, fatigue, SOB/HF
- There are lots of reversible causes of bradycardia – more here
- No drugs are effective for chronic bradycardia. So once reversible causes addressed, only question is PPM or no PPM
- Pacemaker more likely to be indicated if HR <30 at night or <40 during the day
- AF and Complete Hart Block together is frequently missed – can look like a regular slow narrow complex escape rhythm, but no P waves visible and irregular baseline. They need anticoagulation and a PPM
-
- Sinus node disease
-
- Pauses – no magic number as to what’s significant. Symptom-rhythm correlation is key. >3s may be enough if convincing symptoms, whereas >6s enough if asymptomatic or syncope occurs but doesn’t correlate
- Can also cause sinus bradycardia, chronotropic incompetence, sick sinus syndrome – sinus arrest, no P wave/QRS
- Can occur post AVN ablation
- PPM indicated when symptoms are due to/likely due to bradycardia, but not if asymptomatic or due to reversible cause
- Won’t kill you (even if you’re syncopal)! But can make you feel ill. If asymptomatic – quite hard to justify a PPM, even if quite long pauses
-
- AV block
-
- Can kill you
- PPM may be indicated if not due to a reversible cause
- Always indicated for 3rd or 2nd degree type 2 (irrespective of symptoms)
- Consider in type 1 second degree heart block, after EPS (usually doesn’t need pacing, but consider if very symptomatic)
- 2:1 block would usually require a PPM
- Consider causes – MI, aortic valve disease, infiltration, inflammation, drugs (eg digoxin, verapamil, betablocker, timolol eye drops)
-
Types of device
- Can usually identify a device from the CxR and ECG
-
- Look for number and position of the leads, presence of a shocking coil (ICD).
- CRT devices have 3 leads.
- Should have a LBBB pattern to paced beats if pacing the RV (eg dual chamber), and mainly upward deflection in V1 in dual chamber PPMs.
- Some leads are fixed in position in the heart (screwed in, aka active fixation), some not (passive fixation)
-
- The code
-
- First letter A/V/D/O (atria, ventricular, duel, none) – what it paces
- Second letter A/V/D/O – what it senses
- Third letter – I/T/D (inhibits, triggers, duel) – response to sensing (so if someone has intermittent CHB, the PPM will inhibit (I) itself when they have a normal HR. Alternatively a PPM might trigger (T) ventricular pacing once activity is sensed in the atria
- Fourth letter – R – rate response to exercise
-
- Indications for different pacemaker types
-
- Heart block / AV block – usually DDDR
- Carotid sinus hypersensitivity – DDDR
- SA node disease – usually needs AAIR PPM unless abnormal AV conduction (so should have normal PR interval and normal QRS)
- Slow AF – use VVIR PPM
- Resynchronisation in HF (wide QRS, EF < 35%, symptomatic CCF) – biventricular PPM
-
- Dual chamber PPMs are common
-
- RA and RV leads (atrial leads have a J-shape, ventricular leads vary in orientation). Might be better to have CRT if they have heart failure however
- Probably only pacing when required to (eg too bradycardic)
-
- Single chamber PPM
-
- Have a lead in the RV and are used for tachy-brady syndrome, slow AF or permanent AF (VVI typical pacemaker used here)
- Single lead RA devices are now very rare
-
- Conduction system pacing
-
- Hopefully QRS looks normal (or a bit right bundle) – more physiological than older devices, but minimal RCT data as yet.
- Consider if expecting a high ventricular pacing burden, instead of CRT if LV systolic dysfunction and AV block, if RV pacing has induced LV dysfunction, failed CRT, CRT-non-responders. May in the future be used in everyone (evidence pending)
-
- Leadless PPM
-
- New
- Inserted via groin. Like a small pellet which sits in the ventricle.
- Aveir (can be dual chamber), empower, micra (both single) – manufacturers.
- Not first line
- Useful if previous device infections or IE, or at risk of device erosion, high infection risk, upper body vascular issues, dialysis patients, anyone with planned radiotherapy over pectoral area.
-
- Redundant leads can be seen if unable to retrieve them and patient has been upgraded
- Left bundle area pacing – more physiological compared to RV apical pacing. Reduces risk of pacing-induced cardiomyopathy
Cardiac Resynchronization Therapy (CRT) / Biventricular Pacemaker
- Indicated if severe LV dysfunction (EF <35% despite optimum medical treatment – re-echo after a few months of treatment) and…
-
- If in SR (tend to respond better)
-
- LBBB with QRS >130ms
- Non-LBBB QRS >150ms
-
- If in AF – QRS >130ms with tight rate control (either with drugs or AV node ablation and PPM control)
- If already RV paced, or planning RV pacing, and they have some LV dysfunction
- If in SR (tend to respond better)
-
- 3 leads: RA, RV and LV leads (actually goes into a vein / coronary sinus near LV) for bad HF (with or without ability to shock). Defib leads go into RV. The atrial leads can look close together on a CxR
- 1/3 don’t respond (difficult to predict responders – tell patients this)
- Can reduce MR
- If coronary disease – it will be an ICD as well (ie CRT-D). If not, might just be a CRT-P
- Should pace all of the time unlike some other PPMs (if not – that might be what’s wrong!)
Implantable Cardioverter-defibrillator (ICD)
- Can deliver shocks, anti-tachy pacing or pacing
- They are also pacemakers… often with a base rate of 40 bpm (pacing RV routinely not good for your heart, as it gives you LBBB, so only triggered if HR very low). They don’t prevent VF or VT – just treat it
- You can’t get a shock from touching a patient when they get shocked
- Indications
-
- For sustained VT with syncope or haemodynamic compromise (as long as >48 hours post-MI)
- For sustained tolerated VT if EF > 40% and not for ablation or amiodarone
- Cardiac arrest due to VF/VT with no treatable cause
- Inherited cardiomyopathy or channelopathy or sarcoid
- Primary prevention – symptomatic HF and EF <35% despite optimum medical tx (ischaemic HD or not), or asymptomatic and EF <30%. Coronary disease causes scarring and puts people at higher risk. Only > 40 days after MI
-
- Must have life expectancy (with good quality of life) of >1 year
- Patients must understand consequences – shocks can be upsetting, can impact driving etc
- Types
-
- Transvenous (typical)
- Subcutaneous-ICD (new)
-
- Subcutaneous ICD
-
- No venous leads and no vascular access required, only a tunnelled shocking lead to sternum.
- Increasingly MRI compatible.
- Less risk of lead failure and infection, so better in young people reduces risk of lead infection/breaking.
- Easy to remove.
- However… no bradycardia pacing function, higher risk of inappropriate shocks, challenging at extremes of BMI
-
- Shocks
-
- These feel like being punched in the chest, not a tingle on the chest wall. You know about it! Often people will collapse
- Can get inappropriate shocks, for instance an ICD that shocks fast AF (it shouldn’t do)
-
- Consider deactivation in deteriorating / very frail patients / when doing a DNA-CPR
General tips on managing patients with pacemakers
- If PPM in situ, a magnet can make it pace a standard HR (eg 80) without sensing (tape magnet to chest). In ICDs they turn off the shock function, but in PPMs they revert device to VOO mode at a set rate
- Ischemia very hard/impossible to diagnose with paced ECGs
- If needs defibrillation, place pads 10-15cm from the device
- If syncope, falls, palpitations or chest pain – get a PPM interogated (it could be malfunctioning device, but could also be a tachyarrhythmia like VT)
- Be sure you need one if dealing with a young person (having a PPM shortens your life)
- PPMs don’t usually stop tachycardia (except in cases of ICDs which can sometimes overdrive pace for VT) – so fast AF and no pacing spikes does not mean PPM has malfunctioned
- Patients must be fully informed – ie if device can shock, if they are MRI compatible, if they should avoid magnet scanners at airports
- If using diathermy in surgery near to PPM site, patient might need their PPM mode changing (often to VOO) as cautery will mess with the ECG and might cause the PPM to inhibit itself. Check with technicians, and check if patient pacing dependent
- At end of life – leave PPM alone (it won’t stop them from dying). If CRT/ICD – turn off with magnet. Strap it over the PPM – leave it on
- Hardware and techniques are rapidly evolving – so keep up to date
Pacemaker insertion and complications
- A single chamber PPM takes about 30 minutes to insert
- A dual chamber takes 45-60 minutes
- Usually done under sedation with LA
- Often go home same day
- 1:1000 chance of fatal complication
- Complications (around 4% risk of acute complication)
-
- Tracking – when a PPM paces too fast in response to an atrial arrythmia. Drugs won’t help slow them down. Find a magnet
- Infected PPMs
-
- Biggest risk
- Also risk of IE and PPM failure.
- Extraction required
- Usually occurs soon after insertion (or if late, consider IE)
-
- Haematoma
-
- Common
- Rarely requires holding anticoagulation and evacuation (or maybe better to let the patient’s body disperse the clot rather than re-operating)
-
- Pneumothorax
-
- Only if subclavian access was required
- Do CxR post procedure
-
- Pericardial effusion / tamponade
- Lead damage / fracture
-
- Do CxR and pacing check
- Can occur after fall/trauma
-
- ‘Active leads’ can perforate myocardium
-
- If lead breaks often just detach lead from box and attach new lead, don’t try to remove the broken lead
-
- ICD can sometimes misdiagnose an arrhythmia
-
- A magnet can turn off the shock function of an ICD but will not stop it pacing if required
-
- Twitching of chest/hiccupping – PPM voltage too high
- Lead displacement
-
- 4-5% risk
- Rare after 6 weeks.
- Not a big problem if atrial lead displaces
- If ventricular lead displaces may represent in old bradyarrhythmia
-
- Pacemaker induced cardiomyopathy – these patients could benefit from a left sided wire to resynchronise their ventricles
- Low battery – A clue might be a paced rhythm of exactly 65 (elective replacement mode). Especially if patient has missed all follow up
- Under or over-sensing – can pace inappropriately, or fail to pace when required
- Failure to capture – output could be set below the threshold, could be lead issues, or issues with the myocardium/electrolytes
- Programming issues
-
The ECG in paced patients
- No pacing spikes can be normal if waiting to kick in (doesn’t necessarily mean it’s not working)
- Atrial and ventricular pacing spikes = dual chambered PPM. LBBB pattern
- If just ventricular spikes = still probably a dual chamber PPM but atrial lead not being needed right now
- For patients with CRTs – QRS complexes are narrower than those of above. More often RBBB pattern
- RBBB pattern might be a concern after PPM insertion especially if there are spikes too – could be that the lead went into the artery and the LV, or there is a perforated septum and the lead went into the LV from the RV (although it could be that the patient has RBBB at baseline and the PPM is not pacing)
- STEMI in paced rhythm – Can check The Sgarbossa Criteria. Treat as a STEMI until proven otherwise ie refer early on primary pathway