Arrhythmia and Cardiopulmonary Resuscitation

1.0 Introduction

Continuous monitoring of rate and rhythm is usually performed in ICU using a 5 lead ECG set‐ up. For diagnostic interpretations, 12 lead ECG are performed.

ECG measures the electrical activity associated with depolarisation of myocardial tissues.

 The sinoatrial node (SA ‐ see diagram below) is a specialised group of cells in the top corner of the right generates an electrical impulse.  Depolarisation then spreads through the right atrium to the atrioventricular (AV) node.  There is usually a slight delay at the AV node, which allows time for the atria to contract and fill the ventricles.  The depolarisation wave then moves quickly into the atrioventricular bundle and into the Bundle of His. The Bundle of His continues to the base of the ventricles, and then divides into many smaller pathways called the Purkinje fibres. Transmission to the Purkinje fibres results in ventricular contraction.

The contraction of myocardial cells relies on the regulation of movement of Na+, K+ and Ca+ ions. Variations in and rhythm can be reflective of electrolyte disturbances. Alternatively it may be indicative of cardiac ischaemia, infarction, electrolyte and endocrine disturbances.

2.0 The 'Normal' ECG (recorded at 25mm/sec)

Key Features of Normal :

 the rate is > 60 and < 100  regular atrial & ventricular contractions (R‐R interval remains constant)  a P wave (representing atrial depolarisation) precedes every QRS complex  the PR interval is < 210 msec  the width of the QRS complex is < 120msec  a T wave is evident after every QRS (ventricular repolarisation)  the QTc (corrected QT interval ) is < 440msec

3.0 Classification

The three basic components of any arrhythmia include: rate (fast /slow), width of the QRS complex (wide /narrow), and rhythm (regular/irregular). The following table classifies commonly encountered in the ICU.

Wide (QRS > 120msec) Narrow (< 120msec) Slow (HR < 60) Regular Regular ‐ ventricular escape (complete heart ‐ sinus bradycardia block) ‐ second degree AV block (Mobitz I and ‐ sinus bradycardia with aberrancy (L II) or R BBB) ‐ third degree AV block with junctional ‐ idioventricular rhythm escape rhythm ‐ pacemaker rhythm Irregular Irregular ‐ slow atrial ‐ ventricular ectopy ‐ atrial ectopy Fast (HR > 100) Regular Regular ‐ monomorphic ventricular ‐ sinus tachycardia ‐ uni‐focal atrial tachycardia ‐ SVT with aberrancy (L or R BBB) ‐ atrio‐ventricular re‐entry tachycardia ‐ accelerated idioventricular rhythm (AVRT) ‐ atrio‐ventriuclar nodal re‐entry Irregular tachycardia (AVNRT) ‐ ‐ polymrophic Irregular ‐ ‐ ‐ multi‐focal atrial tachycardia

4.0 Bradycardia and Conduction Blocks

4.1 Sinus Bradycardia

Requires the presence of a p‐wave preceding each narrow QRS complex and rate < 60 beats / min. The common causes encountered in the ICU, and appropriate treatment options are summarised in the following table:

Causes of Sinus Bradycardia: Acute myocardial infarction / ischaemia (particular inferior territory infarcts) Sick sinus syndrome Trauma ‐ cardiac contusion Hypothyroidism Hyperbillirubinaemia Hypothermia Raised intra‐cranial pressure (cushingoid reflex) Glaucoma Drugs: beta‐blockers, opioids (fentanyl), digoxin, calcium channel blockers, organophosphates Treatment: Asymptomatic Observe Correct underlying cause ‐ address pharmacotherapy, electrolyte abnormalities, myocardial ischaemia Symptomatic: a) Pharmacological Anticholinergics ‐ atropine, glycopyrolate B‐agonists ‐ isoprenaline, dobutamine, adrenaline Measures to control intra‐cranial hypertension Thyroxine replacement (slowly) b) Non‐pharmacological Pacing ‐ trans‐venous, external Warm to normothermia (if feasible)

4.2 Conduction Block

Conduction block in the AV node is classified as 1st, 2nd or 3rd degree.

1st Degree AV block ‐ prolonged PR interval (> 210 msec) 2nd Degree AV block ‐ Mobitz Type I ‐ Wenkebach phenomenon (progressive increase in the PR interval until a QRS complex is dropped) ‐ Mobitz Type II ‐ Intermittent complete AV block whereby no QRS follows the P‐wave ‐ 3:1, 4:1 AV block 3rd Degree AV block ‐ characterised by complete AV dysynchrony

AV block causing haemodynamic compromise will require the insertion of a temporary pacing wire. These are usually trans‐venous (via an R IJ approach), although external pacing should be employed as an interim measure while this is being undertaken. Chronotropic drugs such as atropine and isoprenaline may be of limited benefit.

Bundle branch patterns can also frequently be seen in ICU patients. Examples of a L BBB and R BBB pattern are provided below. Left Bundle Branch:

Common causes include: Ischaemic heart disease, hypertension, left ventricular hypertrophy, aortic stenosis, aortic regurgitation, hypertrophic obstructive cardiomyopathy.

Right Bundle Branch:

Common causes include: Ischaemic heart disease, hypertensive heart disease, rheumatic heart disease, COPD, interstitial lung disease, pulmonary embolism, congenital heart disease, can be a normal variant.

5.0 Tachycardia

5.1

This is a VERY frequent arrhythmia in the intensive care unit. Common causes and treatment options are summarised below:

Causes of Sinus Tachycardia: Acute myocardial infarction / ischaemia Sick sinus syndrome Trauma ‐ cardiac contusion Hyperthyroidism Fever Pain, anxiety, discomfort Hypovolaemia Systemic Inflammatory Response Syndrome/ sepsis Seizures Drugs: Isoprenaline, Salbutamol, Adrenaline, Theophylline/Aminophylline, NMS, Serotonin syndrome Treatment: Asymptomatic Observe Correct underlying cause ‐ address pharmacotherapy , fluid status, myocardial ischaemia Symptomatic: a) Pharmacological B‐blockers Sedation / Analgesia Management of Seizures b) Non‐pharmacological Fluid resuscitation Cooling measures

5.2 Narrow Complex Tachycardia (including Atrial Fibrillation)

Atrial fibrillation is the most commonly encountered SVT the intensive care unit, particularly post . In the general ICU, it mostly occurs in combination with other features of multi‐ system disease, and is not the 'primary' reason for admission. The key feature is a irregular narrow complex arrhythmia where no p‐waves can be identified. The following gives some examples of common causes, but is not exhaustive:

Myocardial infarction / ischaemia Valvular heart disease (particularly mitral stenosis / regurgitation) Myocarditis Blunt cardiac trauma Hypokalaemia, hypomagnesaemi Fever Thyrotoxicosis Severe Sepsis Use of pro‐arrhythmic agents

The main consequences of AF relate to an added risk of thrombo‐embolism and cerebro vascular accident, myocardial ischaemia (rate related) and haemodynamic instability. The urgency of treating this arrhythmia is largely determined by the presence of hypotension or rate related ischaemia. The following table outlines the treatment options for both recent onset and chronic AF.

Recent onset / Paroxysmal AF Haemodynamics ‐ unstable (hypotension) ‐ DC cardioversion (50 J) ‐ stable / poor LV function ‐ Digoxin ‐ symptomatic (chest pain) ‐ or Beta‐blocker ‐ asymptomatic ‐ observe, correct electrolytes (K and Mg) Duration < 48hrs ‐ attempt cardioversion (chemical or electrical) > 48hrs ‐ anti‐coagulation prior to cardioversion

DC cardioversion is unlikely to be successful if: AF > 1yr, LA diameter > 45mm, ongoing cause (untreated sepsis). Chemical cardioversion is best achieved with Amiodarone Chronic AF Rate Control ‐ Digoxin (most suitable where there is a history of poor LV function) ‐ Beta‐blocker (only in the absence of hypotension) ‐ Amiodarone (useful with haemodynamic instability) ‐ (consider if history of asthma or airways limitation) Anti‐coagulation < 60 yrs ‐ Asprin > 75 yrs ‐ warfarin (consider earlier with a history DM, previous emboli, and hyptension)

The risk of significant intra‐cranial haemorrhage with warfarin therapy for AF is 0.3% / yr.

Other forms of SVT are also encountered in the ICU, such as atrial flutter, and re‐entry tachyarrhythmias.

As with all arrhythmia management, the presence of haemodynamic instability dictates urgent consideration of DC cardioversion (typically 50‐100J). In the absence of hypotension, other useful manoeuvres to help terminate the arrhythmia include: a) Cold water emersion (less than practical in the ICU) b) Carotid sinus massage (should only be performed in the absence carotid vascular disease, always auscultate for a bruit beforehand) c) Valsalva manoeuvre ‐ difficult in the intubated patient d) Correction of electrolytes ‐ Mg, K e) Administration of ‐ 6mg, 12mg, 18mg IV Adenosine should always be administered via a large peripheral vein or central line, and must be followed by a 10‐20ml saline flush. Its half‐life is < 2min as it is taken up by RBCs and rapidly de‐ aminated. It stimulates A1 receptors on the surface of cardiac myocytes, causing slowing of the sinus rate and prolonging AV conduction. Extreme care should be taken in those with a history of significant asthma, and its administration is contra‐indicated post cardiac transplant (where the effects can be significantly prolonged). There is a 90% expected reversion rate with AVNRT and AVRT, while the presence of flutter waves can often be better appreciated following the administration of adenosine.

5.3 Wide Complex Tachycardia

An important distinction (that is not always immediately obvious) is to determine whether the rhythm represents a ventricular focus (VT) or is in fact an SVT with aberrancy. The following criteria favour a diagnosis of VT as compared with SVT. a) Width of the QRS > 140msec b) Presence of fusion or capture beats (representing AV dissociation, as seen on the rhythm strip below indicated by arrows) c) Ventricular concordance in the chest leads d) Absence of a typical BBB pattern e) Significant axis deviation

True ventricular tachycardia is categorised as being either 'monomorphic' (where each complex has a similar appearance) or 'polymorphic' (Torsades des Pointes), which is characterised by cyclical changes in the appearance of the QRS complex around an isoelectric axis. The most common cause of monomorphic ventricular tachycardia is previous myocardial infarction resulting in scarring in the ventricular muscle. This sets up a re‐entry loop, similar to that seen with supra‐ventricular tachyarrhythmia.

The following rhythm strip demonstrates monomorphic VT with fusion or capture beats marked by arrows:

Although commonly associated with a prolonged QT interval, polymorphic VT can be seen without such a feature post cardiac surgery or in the setting of acute myocardial infarction.

The causes of a prolonged QT interval are summarised below:

Acquired: MI / Ischaemia Cardiomyopathy Mitral valve prolapse Myocarditis Acute cerebral injury (adrenergic surge) Electrolyte abnormality (hypomagnesaemia, hypokalaemia, hypocalcaemia) Hypothermia Drugs: Class IA agents, Class III agents, tricyclic anti‐depressants, macrolides, quinolones, phenothiazines, anti‐histamines, cisapride Idiopathic: Familial ‐ 90% Romano‐Ward Syndrome Jervell and Lang Nielsen Syndrome Sporadic ‐ 10%

The principles of managing these arrythmias following standard resuscitation guide lines (see below). Evidence of haemodynamic instability should be treated by prompt DC Cardioversion. Consideration can be given to the administration of amiodarone in the setting of monomorphic VT without hypotension, although continuous cardiac monitoring is essential. In the setting of polymorphic VT, the anti‐arrhythmic agent of choice is intra‐venous magnesium, and agents that prolong the QT interval (, amiodarone) should be avoided. The use of isoprenaline and over‐ drive pacing are second line agents.

Beta‐blockers can be used in those with congenital long QT syndromes as secondary prevention, as episodes can be precipitated by surges in catecholamines.

5.3 Ventricular Fibrillation

This represents a medical emergency, and must be treated promptly by electrical . Standard resuscitation guidelines (including commencing CPR) should be followed.

2.0 Cardiopulmonary Resuscitation

The Australian Resuscitation Council has produced guidelines for both adult and paediatric cardiopulmonary resuscitation. Importantly these documents are regularly being updated, and the ARC website (www.resus.org.au) should be checked regularly for any new additions.

2.1 Adult Advanced Cardiac Life Support

Some hospitals will modify these guidelines to suit the equipment that is available in their institution. Knowledge of the guidelines does not obviate the need for good clinical assessment and appropriate orientation to resuscitation equipment.

2.2 Paediatric Advanced Cardiac Life Support

3.0 Bibliography

Morley PT. Adult cardiopulmonary resuscitation. In Oh's Intensive Care Manual, 6th edition. Eds: Berston AD and Soni N. Butterworth Heinemann Elsevier, 2009.

Holt A. Management of cardiac arrhythmias. In Oh's Intensive Care Manual, 6th edition. Eds: Berston AD and Soni N. Butterworth Heinemann Elsevier, 2009.

Delacretaz E. Supraventricular tachycardia. N Engl J Med 2006, 354: 1039‐51.

Falk RH. Atrial Fibrillation. N Eng J Med 2001, 344: 1067‐78.

Roden DM. Long‐QT syndrome. N Eng J Med 2008, 358: 169‐76.

4.0 MCQ Questions

1) Causes of Atrial fibrillation include the following, except: a) Hypothyroidism b) Mitral stenosis c) Sepsis d) Blunt thoracic trauma e) Myocarditis

2) Which of the following features is NOT useful in distinguishing VT from SVT with aberrancy: a) QRS width > 140msec b) Marked change in Axis c) Typical bundle branch pattern d) Ventricular concordance e) Fusion or capture beats

3) Which anti‐arrhythmic agent should be considered first line in the management of polymorphic ventricular tachycardia: a) Adrenaline b) Magnesium c) Amiodarone d) Digoxin e) Metoprolol

4) Adenosine: a) Has a prolonged effect lasting weeks b) Binds to A3 receptors causing an increase in heart rate c) Can be used freely in the intensive care unit d) Is the treatment of choice for ventricular tachycardia e) Has a half‐life of < 2min