Bradycardia & Conduction Defects

 

• Sinus bradycardia

  Definition

  Sinus rhythm <60 bpm.

  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).

  Presentation

  Often asymptomatic. Otherwise:

  • Syncope
  • Fatigue
  • Palpitations

  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.

• 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.

  1st degree AV block

  • Prolonged PR interval (>0.2 seconds, 5 small squares).
  • No treatment required.

  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.

  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.

  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.

  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.

• 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.

  Left bundle branch block (LBBB)

  Causes:

  • Anterior MI (LAD). May be the initial ECG sign.
  • HTN
  • Myocarditis
  • Cardiomyopathy
  • Aortic valve disease.

  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}.

  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.

  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}.

  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.

  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.

  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.

  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.

• 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.

  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.

• 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.

  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.

• 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.

• Pacemakers and ICDs

  Implantable devices used to control cardiac rhythm, collectively known as cardiac conduction devices.

  Devices and indications

  Implantable cardioverter-defibrillators (ICDs) are used to prevent sudden cardiac death (SCD) in:

  • {LVSD with EF <35%} 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 <35%} plus {very wide QRS [>150 ms] or LBBB}.
  • Can be pacer only (CRT-P) or include an ICD function (CRT-D).

  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.

  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).

  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.

  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.

  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).

• 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.

  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.

  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.

  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.