Bradycardias and conduction defects Sinus bradycardia Sinus rhythm Causes Myocardial: inferior MI, myocarditis. CV drugs: β-blockers, α2-agonists (clonidine), rate-limiting CCBs, digoxin, amiodarone. CNS drugs: opioids, BZD. Sick sinus syndrome Metabolic: ↑K+, hypothyroidism, hypothermia. Physiological states: high levels of fitness, pain. Anorexia nervosa. Cushing reflex: response to ↑ICP. Sick sinus syndrome Aka sinus node dysfunction. Usually due to idiopathic SA node fibrosis. May also be secondary to cardiomyopathy, infiltrative disease (amyloidosis, sarcoidosis, haemochromatosis), drugs (digoxin, β-blockers), or metabolic problems (↑K+, ↓Ca2+, ↓thyroid). Causes sinus bradycardia, sinus arrest, or exit block. May also cause episodes of tachycardia (tachy-brady syndrome, brady-tachy syndrome). Keywords: what is bradyarrhythmias, bradyarrhythmia vs bradycardia, types of bradyarrhythmias, sinus bradycardia, wide qrs complex bradycardia causes, bradyarrhythmia ppt, sinus bradycardia left axis deviation, wide complex bradycardia treatment, what is bradyarrhythmias, bradyarrhythmia vs bradycardia, types of bradyarrhythmias, sinus bradycardia, wide qrs complex bradycardia causes, bradyarrhythmia ppt, bradycardias and conduction defects

1. Bradycardias and
conduction defects
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2. Sinus bradycardia
Definition
Sinus rhythm
Causes
Myocardial: inferior MI, myocarditis.
CV drugs: β-blockers, α2-agonists (clonidine), rate-limiting CCBs, digoxin, amiodarone.
CNS drugs: opioids, BZD.
Sick sinus syndrome
Metabolic: ↑K+, hypothyroidism, hypothermia.
Physiological states: high levels of fitness, pain.
Anorexia nervosa.
Cushing reflex: response to ↑ICP.

3. Sick sinus syndrome
Aka sinus node dysfunction.
Usually due to idiopathic SA node fibrosis. May also be secondary to cardiomyopathy, infiltrative
disease (amyloidosis, sarcoidosis, haemochromatosis), drugs (digoxin, β-blockers), or metabolic
problems (↑K+, ↓Ca2+, ↓thyroid).
Causes sinus bradycardia, sinus arrest, or exit block. May also cause episodes of tachycardia
(tachy-brady syndrome, brady-tachy syndrome).

4. Presentation
Often asymptomatic. Otherwise:
Syncope
Fatigue
Palpitations

5. Sinoatrial exit block and sinus arrest
Failure of impulse formation (arrest) or conduction from (exit block) the SA node.
Absent P waves on ECG.
Escape rhythm may take over: junctional — narrow QRS 45–60bpm — or ventricular — wide
QRS 30–45 bpm.
Its causes overlap with those of sinus bradycardia, including sick sinus, ↑K+, inferior MI, and CV
drugs.

6. Atrioventricular (AV) block
Aka heart block.
Causes
Idiopathic
RCA infarct (inferior MI), as this supplies the AV node.
Myocarditis
Drugs: β-blockers, calcium channel blockers, adenosine, digoxin, cholinesterase inhibitors.

7. 1st degree AV block
Prolonged PR interval (>0.2 seconds, 5 small squares).
No treatment required.

8. 2nd degree AV block
Intermittent conduction of the P wave to the ventricles.
The conduction ratio is the number of P waves to QRS complexes e.g. 4:3.
A conduction ratio of 2:1 is untypable as it is hard to determine if there is progressive PR
prolongation.
High grade 2nd degree block is when 2 consecutive P waves fail to conduct to the ventricles.
The P waves are regular, distinguishing it from ectopic atrial contractions.

9. 2nd degree AV block type 1
Aka Mobitz type 1, or Wenckebach.
Progressively prolonged PR interval until a P wave fails to transmit to the ventricles.
No treatment required.
Can sometimes be hard to distinguish from Mobitz type 2 when increases in PR are small. Look
for the biggest increase, which is between the 1st and 2nd PR after the missed QRS.

10. 2nd degree AV block type 2
Aka Mobitz type 2.
Constant PR interval but intermittent failure to transmit to the ventricles.
High risk of progression to 3rd degree block so often requires pacemaker treatment.

11. 3rd degree AV block
Aka complete heart block.
No transmission of P waves into ventricles, with a ventricular escape rhythm taking over.
QRS is usually wide, but occasionally the bundle of His provides the pacemaker and thus the QRS
is narrow.
HR 20–40.
This is one cause of AV dissociation. Others include accelerated idioventricular rhythm (ectopic
focus in ventricles with HR 50–110) and VT.
Requires pacemaker.

12. Bundle branch blocks
General features
Blockage in the bundle branches, which lie between the bundle of His and the Purkinje fibres.
Depolarisation instead spreads via the (slower) myocardium, causing broad QRS complexes.
The altered depolarisation sequence also leads to altered repolarisation, and hence ST-T
changes.

13. Left bundle branch block (LBBB)
Causes:
Anterior MI (LAD). May be the initial ECG sign.
HTN
Myocarditis
Cardiomyopathy
Aortic valve disease.

14. ECG:
Deep, wide S in V1 and RSR’ (M-shaped) in V6: SLaM (LBBB).
V1: delayed LV depolarisation results in a deep, wide S wave.
V6: right to left septal depolarisation, instead of the usual left to right, leads to initial R wave in
V6 followed by a dip during RV depolarisation, then 2nd R wave as depolarisation reaches the LV.
Same pattern seen in lead I. Often the middle notch of the M is very small, such that it simply
looks like a broad R wave.
Discordant T waves in V1 and V6.
Criteria: {broad QRS} + {broad R in V6} + {broad S in V1 or 2}.

15. Right bundle branch block (RBBB)
Causes:
Increased RV pressure: primary pulmonary HTN, cor pulmonale, PE.
Acquired heart disease: anterior MI (LAD), myocarditis, cardiomyopathy.
Congenital
Iatrogenic e.g. cardiac catheterisation.
Can also be a normal ECG variant in healthy individuals.

16. ECG:
rSR in V1 (M-shaped) and QRS (W-shaped) in V6: MaRroW (RBBB).
Electrophysiology: the initial rS (V1) and QR (V6) reflect a normal left to right septal
depolarisation and LV depolarisation. The delayed RV depolarisation leads to a 2nd broad R
wave in V1 and a late ‘slurred’ S wave in V6.
Instead of rSR, sometimes V1 simply has one large R ± a small notch as it rises.
Criteria: {broad QRS} + {slurred S V6 and/or rSR V1} + {overall +ve QRS in V1}.

17. Left anterior and posterior fascicular
block
Blockage in one of the two branches of the left bundle branch.
LAFB is much commoner, and in isolation may simply be a benign feature of aging. Other causes
include anterior MI, IHD, aortic valve disease, HTN, or cardiomyopathy.
LPFB is associated with inferior MI or cardiomyopathy.
Aka left anterior and posterior hemiblocks.

18. ECG
QRS normal or slightly prolonged (80–120 ms).
LAFB:
Left axis deviation.
Small Q and tall R (qR pattern) in lateral leads (I and aVL) with prolonged R peak time (>45 ms) in
aVL.
Small R and deep S (rS pattern) in inferior leads.
LPFB is the opposite:
Right axis deviation.
Small R and deep S in lateral leads.
Small Q and tall R in inferior leads, with prolonged R peak time in aVF.

19. Bifasciular and trifascicular block
Bifascicular block:
RBBB plus {LAFB or LPFB}. Conduction is via the single remaining fascicle.
ECG: RBBB plus left or right axis deviation.
Causes: IHD (50%), HTN (25%), aortic stenosis, anterior MI, congenital, ↑K+.
Clinical significance uncertain, but carries a 1% annual risk of progression to complete heart
block.

20. Trifascicular block:
May not be a clinically useful term. It implies blockage in right bundle plus both fascicles, which
is essentially just 3rd degree AV block.
In practice, it may be used to describe an incomplete trifascicular block where there is still
partial/intermittent transmission in one of the fascicles, plus associated 1st/2nd degree AV
block. Resulting ECG shows RBBB, LAFB or LPFB, and prolonged PR.

21. Escape rhythms and ectopic beats
Definitions
Escape rhythm: a non-sinus pacemaker takes over from a non-functioning SA node. Beat
occurs after the next expected sinus beat. HR is <60, except in ‘accelerated’ escape rhythm,
which is 60–100.
Ectopic beat: a non-sinus beat occurs before the next expected sinus beat. Often irregular
ventricular ectopics, which are non-pathological; can also be regular e.g. ventricular bigeminy.

22. ECG findings in escape rhythms
Atrial escape rhythms: HR 40–60, P wave may be inverted.
Junctional escape rhythms: HR 40–60, P wave hidden in QRS complex
Ventricular escape rhythms: HR 20–40, broad QRS.

23. Cardiac axis deviation
Cardiac axis which is less than -30° (left axis deviation, LAD) or greater than +90°
(right axis deviation, RAD).
ECG
Look at the QRS complexes in the limb leads:
In LAD, they’re Leaving (QRS pointing away from each other): +ve QRS (dominant R) in I and aVL,
-ve QRS (dominant S) in II and aVF.
In RAD, they’re Romantic (QRS pointing towards each other): -ve QRS (dominant S) in I and aVL,
+ve QRS (dominant R) in III and aVF.

24. Causes
LAD:
Left anterior fascicular block.
LBBB
LVH
Inferior MI
RAD:
Left posterior fascicular block.
RVH
Lateral MI
Lung disease: PE, COPD.
↑K+
May be a normal variant.
WPW syndrome and ventricular ectopics can cause either.

25. Acute management of bradycardia
1. Atropine 500 mcg IV if there is cardiac ischaemia, syncope, SBP <90, or HF.
2. Further measures if there is inadequate response or risk of asystole: further atropine (up to
3 mg), transcutaenous pacing, adrenaline infusion, or isoprenaline infusion (β1 agonist). Risk
of asystole is defined as severe AV block (3rd degree or 2nd degree type 2), recent asystole,
or ventricular pauses (> 3 s).
3. Definitive management with transvenous and/or permanent pacemaker.

26. Pacemakers and ICDs
Implantable devices used to control cardiac rhythm, collectively known as cardiac conduction
devices.

27. Devices and indications
Implantable cardioverter-defibrillators (ICDs) are used to prevent sudden cardiac
death (SCD) in:
{LVSD with EF ❤5%} plus {wide QRS [120–149 ms] or high SCD risk}.
Sustained VT causing syncope or haemodynamic instability.
Congenital high risk conditions e.g. long QT, Brugada, HCM.
Secondary prevention: post VF or VT cardiac arrest.
Permanent pacemakers (PPMs) are used to maintain an adequate heart rate in:
AV block: 3rd degree or 2nd degree type 2.
Sinus node dysfunction with symptomatic bradycardia.
Carotid sinus syndrome.
Cardiac resynchronization therapy (CRT, aka biventricular pacemaker):
Indication: {LVSD NYHA class 2–4 with EF ❤5%} plus {very wide QRS [>150 ms] or LBBB}.
Can be pacer only (CRT-P) or include an ICD function (CRT-D).

28. Structure and mechanism
Pulse generator — comprising a battery, control circuits, and transmitter/receiver — is placed in
the infraclavicular area (subcutaneously or submuscularly). Requires reimplantation every 5–10
years due to battery lifespan.
Pacing leads (one or two) extend from the generator, transvenously, into the right atrium and/or
ventricle (plus left ventricle in CRT), with the tips implanted in the myocardium. These leads
both sense cardiac depolarization and deliver cardiac stimulation.
PPMs can provide either a fixed impulse rate (‘asynchronous’), or an impulse in response to
absent depolarization (‘synchronous’).
ICDs respond to ventricular tachycardias with a defibrillation shock. Many devices also have a
pacer function, both to treat co-morbid arrhythmias and to deliver antitachycardia pacing before
shocking.

29. Pacemaker codes and modes
Standard 5 letter code to describe PPMs, with often just the first 3 used:
1. Where it’s pacing: Atria, Ventricles, or Dual (A+V).
2. Where it’s sensing: Atria, Ventricles, or Dual (A+V).
3. Response to sensing depolarization: Triggers pacing, Inhibits pacing (i.e. doesn’t pace), Dual
(triggers and inhibits).
4. Rate modulation: ability to adjust HR in response to physiological need.
5. Anti-tachycardia function: Pacing, Shock, or Dual (P+S).

30. Common modes:
VVI: no pacing if ventricular depolarization detected, otherwise it paces. AAI is the same for the
atria.
DDD: senses both A and V, and takes over if either don’t work.
VDD: used in AV block, as it senses both A and V but only paces V.
VOO: asynchronous pacing, which should be used during surgery as diathermy may affect
device.

31. Interpreting pacemaker ECGs
Most pacemaker leads sit in RV causing LBBB pattern, though a minority are LV and RBBB.
If patient’s heart rate is above PPM threshold, pacing spikes will be appropriately absent.
See pacemaker and ICD complications for abnormal ECG findings in presence of PPM.

32. Device interrogation and manipulation
Investigate cardiac symptoms in PPM/ICD patients as usual, including with an ECG, but specific device
interrogation may also be needed:
Should be done by specialists using specialist devices. Even in asymptomatic patients it is done
regularly e.g. 3-monthly.
Pacemaker/ICD magnets allow basic device manipulation. When placed over a PPM, it will revert
to asynchronous mode (good if device is undersensing or overpacing), and when placed over an
ICD, it will prevent shocks (but not pacing).

33. Pacemaker and ICD complications
General
Acute (post-placement): pneumothorax, infection, bleeding (including pocket haematoma).
Device-related pain.
ICD malfunctions
Inappropriate ICD shocks: may be triggered by atrial arrhythmias (AF, SVT) or device
malfunction.
Failure to shock. If this occurs, treat ventricular dysrhythmias as usual e.g. external defibrillation,
anti-arrhythmic drugs.

34. PPM malfunctions
Bradycardia
Failure to output/pace: no impulse (e.g. due to device malfunction, battery failure) and hence
no pacing artefact on ECG.
Failure to capture i.e. no response from heart (e.g. due to poor lead contact, cardiac problem).
ECG shows pacing spikes not followed by atrial or ventricular activity.
Oversensing: noise (e.g. movement artefacts) misinterpreted as cardiac activity and hence PPM
fails to pace.

35. Tachycardia
Pacemaker-mediated tachycardia: PPM forms re-entrant loop. Less common with new devices.
Sensor-induced tachycardia: noise (e.g. movement artefacts) misinterpreted as physiologically
increased heart rate and PPM increases rate. Occurs in newer devices which allow
physiologically-varied heart rate in response to need.
Can also be due to all the usual causes of tachycardia e.g. physiological response, SVT.

36. Other dysrhythmias
Undersensing (e.g. due to poor lead contact), leading to asynchronous pacing. Suggested by
pacing spikes within or just after QRS.
Pacemaker syndrome: AV dyssyncrhony due to PPM failing to perfectly replicate normal cardiac
contraction. Causes reduced cardiac output, fatigue, dizziness, and palpitations.

37. Thank You
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