ARRHYTHMIAS Keith Tiong Registrar Intensive Care, John Hunter Hospital

ARRHYTHMIAS Keith Tiong Registrar Intensive Care, John Hunter Hospital
(Patient Centred Acute Care Training, ESICM)

College of Intensive Care Australia New Zealand ELECTRICAL PROPERTIES OF THE HEART
1. General Instructional Objectives An understanding of the basis of electrical activity of cardiac muscle and its relationship to basic mechanical events 2. Required Abilities a. To explain the ionic basis of spontaneous electrical activity of cardiac muscle cells (automaticity) b. To describe the normal and abnormal processes of cardiac excitation c. To explain the physiological basis of the electrocardiograph in normal and common pathological states d. To describe the factors that may influence cardiac electrical activity e. To describe and explain the mechanical events of the cardiac cycle and correlate this with physical, electrical and ionic events

College of Intensive Care Australia and New Zealand 2008 Basic Science Short Answer
Question 7 - Outline normal impulse generation and conduction in the heart. Describe the features present in a normal heart that prevent generation and conduction of arrhythmias. Answer This question required description of the SA node, its primary role and generation of the pacemaker potential and the influence of the autonomic nervous system.

A diagram of the conducting pathways, highlighting specialized tissues with fast or slow conduction velocities would have been appropriate. The importance of the AV node in preventing retrograde conduction and high rates conducted to the ventricles (>220 / min) was often neglected in answers. A discussion of the Purkinje Fibres with particular reference to the absolute and relative refractory periods was essential. Additional marks were awarded for mention of the atrial internodal pathways, conduction within the ventricles from the endocardial to epicardial surfaces and the significance of the compensatory pause in response to ectopic beats. Syllabus C1b 2.a, b; Reference: Cardiovascular Physiology, “Electrical Activity of the Heart” (Chapter 2), Berne and Levy. 1 candidate (33%) passed this question.

‘An understanding of the basis of electrical activity of cardiac muscle and its relationship to basic mechanical events’ Sinoatrial node (SAN) Sited in the supepicardium, junction of right atrium (RA) and superior vena cava (SVC) Extensive autonomic innervation Abundant blood supply via SA nodal artery (proximal branch of RCA in 55% population) or left circumflex coronary artery Atrioventricular node (AVN) Subendocardial structure within interatrial septum Blood supply via AV nodal artery (distal branch of RCA, 90-95% population) His bundle Formed by Purkinje fibres emerging from distal AV node, forming tubular structure which runs through the membranous septum to the muscular septum and divides into the bundle branches Sparse autonomic innervation Blood supply from AV nodal artery and septal branches of LAD artery Patient-Centred Acute Care Training European Society of Intensive Care

‘An understanding of the basis of electrical activity of cardiac muscle and its relationship to basic mechanical events’ Bundle Branches Anatomy varies Right bundle extends down right side of interventricular septum to base of anterior papillary muscle where it divides Left bundle usually divides into two or three distinct fibre tracts - a left posterior and a left anterior hemibundle Little autonomic innervation Extensive blood supply from RCA and LCA Normal conduction is initiated by the SA node, and results in a wave of depolarisation that spreads through the atria, causing atrial contraction Atria and ventricles are electrically isolated from one another in all but one site - the AV node which serves to: delay conduction between atria and ventricles, allowing time for the atrial component of ventricular filling protect against the development of ventricular fibrillation (VF) Patient-Centred Acute Care Training European Society of Intensive Care

Managing the patient with rhythm disturbances
Knowledge of the ionic currents responsible for the action potential and the nature of cell-to-cell electrical transmission are important for a comprehensive understanding of the cardiac action potential and the interaction of drugs and hormones with the ion channels Patient-Centred Acute Care Training European Society of Intensive Care

Conduction velocity and refractory periods
Atrial/ventricular muscle fibers: meters per second Specialized fibers for action potential propagation through the heart (e.g. Purkinje fibers): m per second Refractory Period Definition: amount of time following an action potential during which the normal cardiac impulse cannot re-excite the previously excited tissue: this is the absolute refractory period Duration -- normal absolute refractory period = seconds Relative refractory period: Cardiac muscle may be excited, but with greater difficulty than normal. Duration: approximately 0.05 seconds (adds somewhat to the absolute refractory period) Atrial refractory period (absolute refractory = 0.15 seconds; relative refractory = 0.03 seconds) -- shorter than ventricular refractory period. As a consequence, atrial contraction rates may be significantly higher than ventricular contraction rates

Structure of ion channels
Ion channels are proteins that traverse the plasma membrane. The major function of ion channels is the rapid and selective movement of ions in and out the cell. The selective permeability of a channel for a particular ion in preference to others is the basis for the classification of ion channels into Na+ , K+ , Ca++ channels among others. The sodium current is primarily responsible for the depolarisation phase of the action potential There are two major Ca++ currents in cardiac cells, the L-type and the T-type. L-type currents (slow inward current).T-type current is faster and smaller than the L-type current. Potassium currents. Several K+ currents are important in the cardiac tissue. Two key currents are involved in the process of repolarisation (phase 3) during the action potential and diastolic depolarisation (phase 4).

Structure of ion channels
Phase 0: Activation of fast Na+ channel-- initial depolarization; slope & magnitude of a 0 will be dependent on the resting membrane potential (A in the diagram on the right) Phase 1: Partial repolarization; K+ efflux Phase 2: Ca2+ entry with continued K+ efflux = "plateau phase". Initial Ca2+ influx through slow L- type Ca2+ channels initiates further Ca2+ release from and sarcoplasmic reticulum stores: Free Ca2+ binds to contractile proteins (e.g. troponin C) promoting/enhancing muscle contraction catecholamines (sympathomimetic amines e.g. epinephrine, norepinephrine (Levophed)) increase slow-inward Ca2+ currents-- a mechanism by which sympathomimetic agents enhance inotropism Phase 3 This phase is dominated by K+ efflux, i.e. repolarization. The membrane potential moves towards the original resting level. Phase 3 ccorresponds to the effective/absolute refractory period. Restoration of ionic gradients to "pre-action potential" levels requires the action of the Na+/K+ membrane ATPase-dependent transporter Phase 4 This phase is between action potentials. In some cell types, phase 4 depolarization (diastolic depolarization) can occur {especially, for example in "pacemaker" cells}.

SA nodal action potential characteristics/ Automaticity :
"Slow-response" type, consistent with limited fast-sodium channel activation involvement second inward current carried by Ca2+, (ICa2+), which is also depolarizing and a third outward current carried by K+ (IK+), the conductance of which tends to decrease during phase 4, those leading to a net depolarizing effect. Characteristic phase 4 depolarization (unstable membrane potential drifting towards threshold– phase 4 depolarization slope influenced by sympathetic/parasympathetic stimulation as well as other factors.

Q: Classify antiarrhythmic drugs, including their mechanisms of action, and give an example of one drug from each group. A: This question again highlighted the importance of candidates utilising a predetermined format or structure to their questions. Well structured responses were less likely to overlook important details, which was the predominate weakness for some candidates. A table format was one useful way of displaying a good answer, for example -

Quinidine: blocking the fast inward sodium current (INa)
Quinidine: blocking the fast inward sodium current (INa). blocks the slowly inactivating tetrodotoxin-sensitive Na current, the slow inward calcium current (ICa), the rapid (IKr) and slow (IKs) components of the delayed potassium rectifier current, the inward potassium rectifier current (IKI), the ATP-sensitive potassium channel (IKATP) and Ito. Lignocaine: Block fast voltage gated sodium (Na+) channels

Electrogenic pumps In addition to the various ion channels, there are electrogenic transporters which contribute to the membrane potential The Na+ /K+ pump: Adenosine triphosphatase (ATPase) dependent, inhibited by digitalis glycosides, exchanges two potassium ions for three sodium ions. The pump is electrogenic and increases the intracellular negative potential. It promotes repolarisation and maintains a low Na+ and high K+ inside the cell. Na+ /Ca++ exchanger: The Na+ /Ca++ exchanger extrudes three Na+ ions for each entering Ca++ ion when the membrane potential is more positive than -40 mV, thereby increasing intracellular negativity Patient-Centred Acute Care Training European Society of Intensive Care

College of Intensive Care Australia New Zealand ANTI-ARRHYTHMIC DRUGS
1. General Instructional Objectives An understanding of the physiological and pharmacological basis of antiarrhythmic therapy An understanding of the pharmacology of antiarrhythmic agents and their clinical applications 2. Required Abilities a. To classify antiarrhythmic agents by their electro-physiological activity and mechanisms of action b. To describe the pharmacology, with particular reference to the antiarrhythmic properties, of: · the sodium channel blocking agents (eg. lignocaine and flecainide) · the beta blockers · amiodarone, sotalol and ibutilide · the calcium antagonists · digoxin · adenosine · magnesium c. To describe the adverse effects of the anti-arrhythmic agents with particular reference to the potential pro-arrhythmic properties

5. Outline the pharmacology of amiodarone. Successful candidates applied, a systematic approach/format to answer questions that refer tooutlining pharmacology of select drugs. A number of useful mnemonics are suggested in the recommended texts for use when answering such a question. All candidates correctly stated what amiodarone is used for but most were not structured methodically and thus suffered from significant omission.

Amiodarone is an important class III anti-arrhythmic (with some characteristics of all 4 Vaughan-Williams classes). For a good pass candidates were expected to explain actions of amiodarone (eg blocks inactivated Na channels, decreases Ca current, noncompetitive adrenergic blocking effect, blocks myocardial K channels which contributes to slowing of conduction and prolongation of refractory period in AV node, prolongs refractory period in all cardiac tissues, prolongs cardiac action potential duration) and it’s pharmacokinetics (eg bioavailability, large volume of distribution, high protein binding, complex metabolism and long elimination half life – 29 days) Syllabus: C2c Reference Text: Goodman and Gillman’s The Pharmacological basis of Therapeutics 11th ed 2006 and Pharmacology and Physiology in Anaesthetic Practice / Stoelting 4th ed 2006

Mechanisms of cardiac arrhythmias
Abnormal automaticity and abnormal conduction are two major causes of cardiac arrhythmias Automatic arrhythmias, such as automatic atrial tachycardia, require no specific stimulus for initiation and may be persistent. Enhanced phase 4 depolarisation would provoke such arrhythmias. Abnormal conduction may promote re-entry in heart muscle. Re-entry is responsible for most clinically important arrhythmias including VT associated with coronary artery disease, atrial flutter, AV nodal re-entrant tachycardia, atrioventricular re-entry tachycardia as observed in the Wolff-Parkinson-White Syndrome Patient-Centred Acute Care Training European Society of Intensive Care

Factors that increase the likelihood of arrhythmias are commonly encountered in the intensive care setting: Pre-existing cardiac disease Treatment with anti-arrhythmics (this is with reference to the potential for proarrhythmias e.g. class Ic) Recent macrovascular (i.e. occlusive coronary) event Microvascular disease causing ischaemia (e.g. diabetes mellitus, sepsis) Altered acid-base status High CO2 Abnormal electrolyte balance Endogenous catecholamines (pain, anxiety) Exogenous catecholamines (inotropes) Presence of intracardiac catheters or pacing wires Suctioning, bronchoscopy, airway manipulation Deep anaesthesia (especially young patients) Anaesthetic drugs (e.g. pancuronium, methoxamine) Patient-Centred Acute Care Training European Society of Intensive Care

Management of arrhythmias in the critically ill is complex, and for this reason we need some safe and simple rules. Rule 1. Not all arrhythmias need to be treated Rule 2. 'Electricity' is generally safer than drugs Rule 3. Correct all correctable abnormalities Rule 4. Treat all treatable ischaemia Rule 5. Consider your intravascular lines Rule 6. Consider drug toxicity Patient-Centred Acute Care Training European Society of Intensive Care Patient Centred Acute Care Training, ESICM

Managing the patient with bradycardias
'Sinus node dysfunction' encompasses a heterogeneous group of conditions, including: Sinus bradycardia Sinus arrest Sino-atrial block Sick sinus syndrome Sinus node dysfunction may be exacerbated by many medications, but rarely needs treatment in the ICU setting. Patient-Centred Acute Care Training European Society of Intensive Care

'Sinus node dysfunction'
More Common Sinus node fibrosis Atherosclerosis of the SA artery Congenital heart disease Excessive vagal tone Drugs Less Common Familial SSS (due to mutations in SCN5A) Infiltrative diseases Pericarditis Lyme disease Hypothyroidism Rheumatic fever

Sinus node dysfunction in the context of acute myocardial infarction
This is a relatively common finding (5-30%) and is often associated with concomitant AV nodal block. Usually no treatment is required, unless in the case of cardiac failure, significant hypotension, or continuing myocardial ischaemia. Intermittent sinus node dysfunction may respond to small doses of atropine (note: rate response is unpredictable). If the bradycardia is prolonged, severe, aggravating ventricular irritability, and not responding to atropine and isoprenaline then temporary pacing may be indicated. Patient-Centred Acute Care Training European Society of Intensive Care

Atrioventricular (AV) conduction disease
1st degree AV block This refers to prolongation of the PR interval (>0.21 sec), and is strictly speaking not conduction block, merely conduction delay. The QRS duration is normal (narrow QRS). 2nd degree AV block This results from intermittent failure of atrial depolarisation to reach the ventricles. Ventricular beats that do occur result from normal conduction pathways.. Type I (Mobitz I or Wenckebach) Progressive prolongation of the PR interval, then a 'dropped beat' Commonly occurs at the level of the AV node (narrow QRS) Type II (Mobitz II) Normal, constant PR interval, with intermittent 'dropped beats' 3rd degree AV block (complete heart block) In complete heart block, although the atria depolarise normally, none of the atrial depolarisations reach the ventricles, which beat independently in response to an infranodal pacemaker (wide QRS). Patient-Centred Acute Care Training European Society of Intensive Care

AV node dysfunction in the context of acute myocardial infarction (MI)
A degree of AV block occurs in 12-25% of patients with acute myocardial infarction, most commonly in the context of inferoposterior MI (with right ventricular involvement). AV block in this context usually results from AV nodal ischaemia, is usually transient and usually resolves. In anterior MI, AV nodal block usually occurs in the bundles and can progress suddenly and without warning to complete AV block. Risk of progression to higher degrees of heart block/asystole, and therefore requirement for temporary backup pacing varies. Patient-Centred Acute Care Training European Society of Intensive Care

Risk of progression to high-grade block
Although 1 st degree and type I 2 nd degree block rarely require pacing(low risk of progression), type I 2 nd degree block associated with a wide QRS (especially in the context of anterior myocardial infarction) should have temporary backup pacing. Type II 2nd degree heart block (wide QRS), or type II 2nd degree heart block with wide or narrow QRS complex in the context of anterior myocardial infarction should have temporary backup pacing. Anterior MI with anything more than low-grade block may exhibit abrupt transition to high-grade block with slow, unreliable ventricular escape rhythm. This combination is associated with severe left ventricular dysfunction and high mortality. Patient-Centred Acute Care Training European Society of Intensive Care

Bundle branch block in the context of acute MI
Development of BBB in anterior MI signifies a poorer prognosis (due to large infarct size, left ventricular dysfunction and conduction abnormalities). It is, however, difficult to predict those patients who will need temporary pacing. Insertion of a backup temporary pacing wire should be considered in the case of 1st degree AV block + BBB New bifasicular block Alternating BBB Patient-Centred Acute Care Training European Society of Intensive Care

Cases for special consideration
Infective endocarditis: Development of new AV block/BBB in a patient with infective endocarditis implies an aortic root abscess (usually the non-coronary cusp). All patients with aortic valve endocarditis should have daily 12-lead ECGs performed specifically to look for conduction abnormalities Lyme disease: The commonest manifestation of the myocarditis of this condition is AV block. This frequently resolves with antibiotic treatment, but may require temporary pacing wire insertion. Patient-Centred Acute Care Training European Society of Intensive Care

Managing the patient with supraventricular tachycardias
All supraventricular tachycardias may be caused and/or exacerbated by inotropic agents. If possible, concomitant with treating the arrhythmia, proarrhythmic drugs should be reduced. Patient-Centred Acute Care Training European Society of Intensive Care

Various clinical skills may be useful in the diagnosis of supraventricular tachycardias, in addition to interpretation of the ECG Carotid sinus massage may increase AV block, and help in distinguishing some tachycardias. Only perform if both carotid pulses are present and of equal strength and there are no bruits. Perform gently to one side only but consider the risks in the older patient or those with a history of transient ischaemic attacks or other manifestations of cerebrovascular disease. Intravenous adenosine also increases AV block. This may help in diagnosis. Examination of the CVP line trace may be helpful in revealing the absence of an a-wave (for instance in AF), or the presence of cannon waves (in the case of av dissociation). If the patient has temporary pacing wires inserted (either epicardially at time of surgery, or transvenously as endocardial wires), simultaneous recordings can be made from these to aid in diagnosis. For instance, the absence of P waves can confirm atrial flutter or fibrillation in difficult cases: retrograde P waves - occurring after the onset of each ventricular depolarisation - can be identified (via the atrial ECG recording). Patient-Centred Acute Care Training European Society of Intensive Care

Paroxysmal SVTs Paroxysmal SVTs are divided into those arising from an automatic focus and those resulting from re-entry. Of these, 8-10% result from increased automaticity, about 60% from AV nodal re-entry, and 30% from AV junctional re-entry involving an accessory pathway, often concealed. Junctional tachycardial refers to accelerated junctional activity, and is uncommon except with digoxin toxicity. Patient-Centred Acute Care Training European Society of Intensive Care

SVT The following are types of supraventricular tachycardias, each with a different mechanism of impulse maintenance: SVTs from a sinoatrial source: Inappropriate sinus tachycardia, sinoatrial reentrant tachycardia SVTs from an atrial source: Atrial tachycardia, flutter, fibrillation SVTs from an atrioventricular source (junctional tachycardia): AVRNT AV reentrant tachycardia (AVRT) - visible or concealed (including Wolff-Parkinson-White syndrome)

Paroxysmal atrial tachycardia
Causes May derive from a number of general proarrhythmic factors in ICU patients, or underlying structural heart disease. One of the commonest causes is digoxin toxicity. Management Adenosine has been known to cardiovert some such patients. If tolerated, intravenous β -blockers are effective. Note, however, that since chronic obstructive pulmonary disease is a common cause of MAT, β -blockers may not be the best choice. In all cases, stop digoxin and treat toxicity if necessary. Patient-Centred Acute Care Training European Society of Intensive Care

Atrial flutter Causes In addition to the causes described above, specific additional causes to remember include under/overfilling, and pulmonary embolism. Atrial flutter may be resistant to chemical cardioversion. Management Digoxin is sometimes helpful in converting atrial flutter to atrial fibrillation, which is easier to manage. Note, however, that the primary rationale for using digoxin is to increase AV blockade. Overdrive atrial pacing may be used to cause cardioversion, if an atrial wire is in use. Otherwise, management is similar to that of atrial fibrillation. Atrial flutter carries a risk of embolisation - anticoagulation may be advisable before and after cardioversion (same guidelines as AF). Patient-Centred Acute Care Training European Society of Intensive Care

Atrial fibrillation Causes
Specific causes to remember include under/overfilling, and pulmonary embolism. Fever and sepsis should also be considered in the ICU population. Treatment Therapeutic objectives in patients with atrial fibrillation in order of importance are: Heart rate control Conversion to sinus rhythm Prevention of embolic complications Treatment of underlying (precipitating) cause Patient-Centred Acute Care Training European Society of Intensive Care

Atrial fibrillation Chemical cardioversion
Clinical trials (but note, NOT in the ICU population) have demonstrated increased success rate of transthoracic electrical cardioversion for AF with ibutilide (class III potassium channel blocker), but note the increased risk of torsade de pointes. Amiodarone (5 mg/kg slow 'push') may also result in cardioversion. In the perioperative state, magnesium-sulphate (34 mg/kg over 20 min, 0.1 mmol/kg) may be effective. Flecainide is contraindicated in patients with left ventricular dysfunction or ischaemic heart disease. Up to 10% of patients may develop acceleration of rate, or a proarrhythmic response. Patient-Centred Acute Care Training European Society of Intensive Care

Rate control for atrial fibrillation
To achieve rate control in atrial fibrillation acutely, digoxin has the slowest onset of action and is not the drug of choice. Intravenous β -blockers or verapamil (0.075 mg/kg as a slow push) provide rapid rate response, but are negatively inotropic. In the non-ICU population, digoxin together with atenolol has been shown to be effective in controlling ventricular response rate in AF. Amiodarone is also rapidly effective in control of ventricular response rate of AF in the ICU population. If ventricular response is uncontrolled, causing significant haemodynamic compromise, and resistant to all conventional manoeuvres, discussion with an electrophysiologist may be helpful (with the potential for AV nodal ablation and insertion of a permanent pacemaker). Patient-Centred Acute Care Training European Society of Intensive Care

Atrial fibrillation after cardiac and thoracic surgery
Post-operative AF is a significant problem on the ICU, and many trials have attempted to address this issue. Currently, the use of prophylactic drugs at the time of cardiac surgery is not routine, however: Amiodarone (pre-operatively, 600 mg by mouth for 1 week prior to cardiac surgery, and continued at 200 mg by mouth until discharge) reduces the risk of AF. Amiodarone (intravenous immediately post-operatively and continued for 48 hours) also reduces the risk of AF. Ibutilide successfully cardioverts patients with AF following cardiac surgery. Patient-Centred Acute Care Training European Society of Intensive Care

AV nodal reentrant tachycardia
These are usually based upon re-entry, two separate pathways within the AV node having two different refractory periods and different conduction velocities. These two pathways are connected proximally (close to the atrium) and distally (close to the His bundle). Diagnosis Fast regular rhythm (classically rates of >150 bpm), paroxysmal, small QRS (less than 0.12 sec). There will be no P waves preceding the QRS complex: most often P waves are hidden within the QRS complex (common form), although (retrogradely-conducted) negative P waves may sometimes be seen following the QRS complex in leads (II, III, aVF) with a RP interval that is equal to or longer than the PR interval (rare form). Treatment Carotid sinus massage or adenosine may both slow the rhythm, or cardiovert it. If the PSVT recurs, then verapamil is effective at terminating the rhythm and preventing recurrence. Flecainide , β -blockers, and sotalol are also effective. Patient-Centred Acute Care Training European Society of Intensive Care

AVRT Orthodromic AVRT (More common) – Narrow complex tachycardia in which the wave of depolarization travels down the AV node and retrograde up the accessory pathway. Antidromic AVRT (Less common) – Wide complex tachycardia in which the wave of depolarization travels down the accessory pathway and retrograde up the AV node.

Circus movement tachycardia (CMT) Wolff-Parkinson-White (WPW) syndrome
These are based upon the existence of an accessory AV connection (Accessory Pathway, AP) between the atria and the ventricles. These pathways not only lead to earlier activation of the ventricle following a supraventricular impulse than during conduction over the AV node (so-called pre-excitation), but also create the substrate for the re-entry circuit (CMT). Diagnosis Only patients with anterograde conduction have a delta wave on the electrocardiogram. This ECG manifestation of pre-excitation is seen in approximately 3/1000 ECGs. CMT may result in narrow or broad QRS tachycardia. Orthodromic CMT: most often small QRS tachycardia unless pre-existing bundle branch block, paroxysmal, regular rhythm, P waves are always separate from QRS: usually RP<PR (fast conducting AP), RP>PR (slow conducting AP). Patient-Centred Acute Care Training European Society of Intensive Care

College of Intensive Care Australia and New Zealand 2009 SHORT ANSWER QUESTION PAPER 1
Examine the ECG provided a. List 3 abnormalities on this ECG b. Name 2 drugs which are contraindicated in this disorder c. Name 2 complications of this disorder

a. List 3 abnormalities on this ECG ° Short PR ° Delta wave ° Wide QRS ° J wave (candidates mentioning this also received credit) ° Tall R wave in V1 b. Name 2 drugs which are contraindicated in this disorder ° Verapamil ° Digoxin c. Name 2 complications of this disorder ° VF arrest ° Syncope ° AF/tachyarrhythmias

Managing the patient with ventricular tachycardias
Ventricular extrasystoles In the context of the ICU, these should alert the physician to the possibility of cardiac disease or irritability (mechanical or chemical) of the heart. Appropriate management includes: Rigorous attention to correcting electrolyte imbalance Consider repositioning of any intracardiac lines In patients who have undergone cardiac surgery, or with underlying ischaemic heart disease, potassium and magnesium should be supplemented Patient-Centred Acute Care Training European Society of Intensive Care

Ventricular tachycardia (VT)
Always consider the possibility of VT in a broad complex rhythm, even if the heart rate is below 100bpm, especially if the patient is being, or has been treated with anti-arrhythmic drugs, and also in the context of known or suspected ischaemic heart disease. A broad complex tachycardia may be due to: Ventricular tachycardia Supraventricular tachycardia with aberrant conduction The likelihood of VT (vs SVT with aberrant conduction) increases if: Heart rate >170 bpm QRS duration >0.14 seconds The likelihood of SVT with aberrant conduction (vs VT) increases if the morphology of the QRS complex on the 12-lead ECG is identical to that seen prior to the onset of tachycardia. Patient-Centred Acute Care Training European Society of Intensive Care

Management Non-sustained VT
Asymptomatic, normal left ventricular function - low risk of sudden death or serious ventricular arrhythmias. Treat as for ventricular extrasystoles. Ischaemic heart disease with left ventricular ejection fraction <40% - high risk of sudden death or serious ventricular arrhythmias. Address all treatable exacerbating factors, seek cardiological opinion regarding catheterisation, possible intervention (angioplasty or surgical referral), choice of anti-arrhythmic agent and consideration for implantable cardioverter defibrillator (ICD). Recurrent non-sustained VT causing haemodynamic compromise. Address all treatable exacerbating factors, consider lignocaine infusion, amiodarone infusion or ventricular pacing (especially if VT emerges during period of relative bradycardia). Patient-Centred Acute Care Training European Society of Intensive Care

Newer interventions for the management of VT/VF
Implantable cardioverter defibrillator (ICD) The development of smaller devices, with more sophisticated software, together with increasing ease of implantation, and emerging evidence that ICDs improve survival in certain patient groups is leading to increasing rates of implantation. ICDs: Implantable subcutaneously (pre-pectoral), with transvenous leads Able to diagnose ventricular tachycardia and ventricular fibrillation Able to deliver antitachycardia pacing and/or defibrillation Can be interrogated to determine number and length of arrhythmic episodes May be deactivated by placing a magnet directly over the generator site Do not preclude an operator delivering standard cardioversion/defibrillation transcutaneously (take care not to place paddles over the device) Patient-Centred Acute Care Training European Society of Intensive Care

Newer interventions for the management of VT/VF
Patients with improved survival with ICDs include: Reduced ejection fraction and inducible VT during electrophysiological testing Survivors of arrests attributed to sustained VT with syncope, or sustained VT and ejection fraction <40% Consider cardiological referral in such patients As increasing numbers of patients are fitted with these devices, and those with ICDs are likely to come under the care of critical care physicians at some stage during the course of their illness, it is important that critical care physicians have some knowledge of their potential functions and problems. Patient-Centred Acute Care Training European Society of Intensive Care

Q: The following questions refer to implantable cardiac pacemakers and implantable cardiac defibrillators. a) What is the effect of applying a magnet to these devices? b) What information can you gain from a chest X-Ray in a patient with an implantable cardiac device? c) What are the advantages of DDD pacing compared to VVI pacing? d) List 4 benefits of cardiac resynchronisation therapy.

Q: The following questions refer to implantable cardiac pacemakers and implantable cardiac defibrillators. a) What is the effect of applying a magnet to these devices? ICD: it turns off antiarrhythmic programme but has no affect on backup pacemaker Pacemaker: It defaults to asynchronous mode or a fixed rate. Rate depends on battery life. b) What information can you gain from a chest X-Ray in a patient with an implantable cardiac device? • Single v dual chamber • Biventricular or left ventricular (cardiac resynchronisation) • Lead displacement or injury • Number of devices present

c) What are the advantages of DDD pacing compared to VVI pacing? • AV synchronisation maintained • Avoids pacemaker syndrome • Reduced incidence of AF • Possible decreased thrombotic events d) List 4 benefits of cardiac resynchronisation therapy. • improved LVEF,CO and haemodynamics • improved exercise tolerance • decreased NYHA class • decreased hospitilisation • improved quality of life Pass rate 6% Highest mark 5.5

AV dyssynchrony syndrome ? Pacemaker syndrome
Furman redefined pacemaker syndrome in a 1994 editorial in which he included the following elements: Loss of AV synchrony Retrograde ventriculoatrial (VA) conduction Absence of rate response to physiologic need

This ECG trace was taken from a 68 year old man, one hour following aortic valve replacement for aortic stenosis. Atrial and ventricular epicardial pacing wires are in place, and the pacing mode is DDD. a) What problem is demonstrated? b) Outline the steps that you could take to address the problem.

a) What problem is demonstrated? Intermittent failure of ventricular capture. b) Outline the steps that you could take to address the problem. Increase the ventricular output Check the connections to the pacemaker and pacing connector leads Reverse the polarity of the pacing to the ventricle Replace pacemaker box and pacing connector leads Unipolar pacing, with a cutaneous pacing stitch. This may fix the problem if one lead is faulty. Chronotropic therapy eg isoprenaline Alternative pacing method: transcutaneous, transvenous Open the chest and replace the epicardial wires

Consider referral for cardiological opinion in:
Right ventricular outflow tract (RVOT) VT: Consider in a young patient with RVOT VT (LBBB, right axis) that may terminate with adenosine , in the context of a structurally normal heart. Idiopathic left ventricular tachycardia: Consider in VT with RBBB, left axis morphology that terminates with verapamil , and a structurally normal heart. Bundle branch re-entrant VT: Consider in a patient with LBBB, syncope and dilated cardiomyopathy Patient-Centred Acute Care Training European Society of Intensive Care

Torsade de pointes This ECG is a polymorphic ventricular tachycardia with a sinusoidal electrocardiographic appearance due to the QRS complex undulating around the baseline. The arrhythmia arises from prolonged myocardial repolarisation (seen on the surface ECG as a prolonged QTc), which may be congenital or acquired. The tachycardia is paroxysmal and may result in VF and sudden death Causes Electrolyte abnormalities especially hypomagnesaemia Anti-arrhythmic agents Hereditary long QT syndrome Bradyarrhythmias Myocardial ischaemia Neurological events Neuroleptics Antibiotics Toxins

Torsade de pointes Management
Make the diagnosis and correct all exacerbating or causative factors. Consider temporary pacing; intravenous magnesium; ICD (although rarely necessary for torsades except in patients with hereditary long QT).

ARRHYTHMIAS THE END

Pharmacologic Management of Atrial Fibrillation (AF):
Prevention of thromboembolism Heart rate control versus rhythm control Optimizing the ventricular response Cardioversion of AF Maintenance of sinus rhythm Emerging therapies

Risk for Ischemic Stroke and Intracranial Bleeding as a Function of Anticoagulation Intensity
Ischemic Stroke Intracranial bleeding 20 15 10 Odds Ratio 5 1 1.0 2.0 3.0 4.0 5.0 6.0 7.0 8.0 International Normalized Ratio Fuster V, et al. Circulation. 2006;114:e

Antithrombotic Therapy for Patients With AF
Risk Category Recommended Therapy No risk factors One moderate-risk factor Any high-risk factor or more than 1 moderate-risk factor Aspirin, 81 to 325 mg/d Aspirin, mg/d, or warfarin (INR , target 2.5) Warfarin (INR , target 2.5)* Less Validated or Weaker Risk Factors Moderate-Risk Factors High-Risk Factors Female sex Age y Coronary artery disease Thyrotoxicosis Age 75 y Hypertension Heart failure LV ejection fraction ≤35% Diabetes mellitus Previous stroke, TIA, or embolism Mitral stenosis Prosthetic heart valve *If patient has a mechanical valve, target INR is >2.5. INR = international normalized ratio; LV = left ventricular; TIA = transient ischemic attack. Fuster V, et al. Circulation. 2006;114:e

Heart Rate Control Versus Rhythm Control in Persistent AF
RACE1 AFFIRM2 100 P = .08 Rate control 90 80 Rhythm control Rhythm control Event-free Survival (%) 70 Cumulative Mortality (%) Rate control 60 50 6 12 18 24 30 36 Months No. at Risk Rate control Rhythm control No. of Deaths number (percent) Rate control 0 80 (4) 175 (9) 257 (13) 314 (18) 352 (24) Rhythm control (4) 148 (7) 210 (11) 275 (16) 306 (21) RACE = Rate Control Versus Electrical Cardioversion for Persistent AF; AFFIRM = AF Follow-up Investigation of Rhythm Management. 1. Van Gelder IC, et al. N Engl J Med. 2002;347: 2. Wyse DG, et al. N Engl J Med. 2002;347:

Rate Control Versus Rhythm Control: Where We Are Now
Rate control is a reasonable strategy in elderly patients with minimal symptoms Deleterious effects of antiarrhythmic drugs may outweigh the benefits of sinus rhythm There are no differences in quality of life, development of heart failure, or thromboembolic events AF in the younger, more symptomatic patient was not addressed Effective strategies to maintain sinus rhythm with fewer side effects are needed

Ventricular Rate Control in AF (As Defined in AFFIRM)
Average heart rate at rest ≤80 beats/min and Either Maximum heart rate ≤110 beats/min during a 6-minute walk or Average heart rate ≤100 beats/min during 24-hour ambulatory Holter ECG monitoring (at least 18 hours of interpretable monitoring) and no heart rate >110% of the maximum predicted age-adjusted exercise heart rate ECG = electrocardiography. Olshansky B, et al. J Am Coll Cardiol. 2004;43:

Drug Therapy for HR Control in AF: Acute Management
Loading Dose Onset Maintenance Dose Major Adverse Effects Patients without accessory pathway Esmolol Metoprolol Diltiazem Verapamil 500 μg/kg IV over 1 min 2.5-5 mg IV bolus over 2 min; up to 3 doses 0.25 mg/kg IV over 2 min mg/kg IV over 2 min 5 min 2-7 min 3-5 min μg/kg/min IV NA 5-15 mg/h IV ↓BP, HB, ↓HR, asthma, HF ↓BP, HB, HF Patients with accessory pathway Amiodarone 150 mg over 10 min Days 0.5-1 mg/min IV ↓BP, HB, pulmonary toxicity, skin discoloration, hypothyroidism, hyperthyroidism, corneal deposits, optic neuropathy, warfarin interaction, sinus bradycardia Patients with heart failure and without accessory pathway Digoxin 0.25 mg IV q2 h, to 1.5 mg 60 min mg/d IV or po Digitalis toxicity, HB, ↓HR Dosing, onset, and major adverse effects as above BP = blood pressure; HB = heart block; HR = heart rate; HF = heart failure. Fuster V, et al. Circulation. 2006;114:e

Drug Therapy for HR Control in AF: Long-term Management
Loading Dose Onset Maintenance Dose Major Adverse Effects Heart rate control Metoprolol Propranolol Diltiazem Verapamil Same as maintenance dose 4-6 h 60-90 min 2-4 h 1-2 h mg bid, po mg/d in divided doses, po mg/d in divided doses, po ↓BP, HB, ↓HR, asthma, HF ↓BP, HB, HF ↓BP, HB, HF, digoxin interaction Heart rate control in patients with heart failure and without accessory pathway Digoxin Amiodarone 0.5 mg/d po 800 mg/d for 1 wk, po 600 mg/d for 1 wk, po 400 mg/d for 4-6 wk, po 2 days 1-3 wk 0.125 to mg/d po 200 mg/d po Digitalis toxicity, HB, ↓HR ↓BP, HB, pulmonary toxicity, skin discoloration, hypothyroidism, hyperthyroidism, corneal deposits, optic neuropathy, warfarin interaction, sinus bradycardia Fuster V, et al. Circulation. 2006;114:e

Ventricular Rate Control in AF: Additional Caveats
Digoxin is useful for patients with CHF or LV dysfunction and for sedentary individuals Digoxin can be combined with -blockers or calcium channel blockers to minimize bradycardia Amiodarone can be useful to control ventricular response (but consider adverse effects) IV procainamide or ibutilide is useful to slow the ventricular response in patients with preexcited AF (digoxin and AV-nodal blockers are contraindicated) Permanent pacing may be necessary for bradycardia CHF = congestive heart failure; AV = atrioventricular.

Long-term Therapy With Rate Control Drugs: Efficacy of -Blockers
Patients Without a Change of Therapy (%) Log rank = 77.02 P<.0001 -blocker Calcium channel blocker Digoxin alone N, Events (%) BB: 777, 0 (100) 598, 147 (81) 500, 191 (75) 315, 210 (71) 164, 213 (70) 35, 216 (68) CCB: 631, 0 (100) 461, 139 (77) 379, 187 (69) 246, 220 (62) 128, 238 (56) 20, 247 (48) Digoxin: 315, 0 (100) 190, 104 (66) 142, 140 (53) 92, 160 (45) 43, 165 (42) 5, 172 (29) Olshansky B, et al. J Am Coll Cardiol. 2004;43:

Rhythm Control: Pharmacologic Conversion of AF (Duration of ≤7 Days)
Drug Route of Administration Agents with proven efficacy Dofetilide Flecainide Ibutilide Propafenone Amiodarone Less effective or incompletely studied agents Disopyramide Procainamide Quinidine Should not be administered Digoxin Sotalol Oral Oral or intravenous Intravenous Fuster V, et al. Circulation. 2006;114:e

Outpatient Therapy for Recent-Onset AF: “Pill-in-the-Pocket” Approach
Single-dose self-administration of propafenone or flecainide for AF of <48 hours in duration Excluded: structural heart disease, sinus/AV-nodal dysfunction, QRS >120 ms, ventricular rhythm <70 bpm, Brugada syndrome, systolic BP <100 mm Hg Initial treatment given in hospital with monitoring Therapy was successful in 534 episodes (94%) Emergency room visits significantly reduced Pretreatment with -blocker or calcium channel blocker usually required Alboni P, et al. N Engl J Med. 2004;351:

Potential Adverse Effects
Pharmacologic Therapy to Maintain Sinus Rhythm: Typical Dosages and Adverse Effects Drug Daily Dose Potential Adverse Effects Amiodarone* Disopyramide Dofetilide† Flecainide Propafenone Sotalol† mg mg μg mg mg mg Photosensitivity, pulmonary toxicity, polyneuropathy, GI upset, bradycardia, torsades de pointes (rare), hepatic toxicity, thyroid dysfunction, eye complications Torsades de pointes, HF, glaucoma, urinary retention, dry mouth Torsades de pointes VT, HF, conversion to atrial flutter with rapid conduction through the AV node Torsades de pointes, HF, bradycardia, exacerbation of chronic obstructive or bronchospastic lung disease *A loading dose of 600 mg/d is usually given for 1 month or 1000 mg/d for 1 week. †Dose should be adjusted for renal function and QT-interval response during in-hospital initiation phase. GI = gastrointestinal; VT = ventricular tachycardia. Fuster V, et al. Circulation. 2006;114:e

Maintenance of Sinus Rhythm
Maintaining Sinus Rhythm: An Algorithm Based on Underlying Heart Disease Maintenance of Sinus Rhythm No (or minimal) heart disease Hypertension Coronary artery disease Heart failure Flecainide Propafenone Sotalol Substantial LVH Dofetilide Sotalol Amiodarone Dofetilide No Yes Amiodarone Dofetilide Catheter ablation Flecainide Propafenone Sotalol Amiodarone Amiodarone Catheter ablation Catheter ablation Amiodarone Dofetilide Catheter ablation Catheter ablation LVH = left ventricular hypertrophy. Fuster V, et al. Circulation. 2006;114:e

Antiarrhythmic Drug Proarrhythmia: an Extension of Pharmacologic Effects
Class IC toxicity: Atrial flutter with 1:1 AV conduction Class IA/III toxicity: Torsades de pointes

Proarrhythmia With Antiarrhythmic Drugs
Ventricular Torsades de pointes (class IA, III) Sustained monomorphic VT (class IC) Sudden death in coronary disease (class IC) Atrial Increased arrhythmias Conversion to atrial flutter (usually class IC) Abnormal conduction/impulse formation Increased ventricular rate during AF (class IA, IC) Sinus/AV-nodal dysfunction (nearly all drugs) Altered defibrillation thresholds (class I)

Risk Factors for Ventricular Proarrhythmia
VW Types IA and III Agents VW Type IC Agents Long QT interval (QTc 460 ms) Long QT interval syndrome Structural heart disease, substantial LVH Depressed LV function* Hypokalemia/hypomagnesemia* Female sex Renal dysfunction* Bradycardia* 1. (Drug-induced) sinus node disease or AV block 2. (Drug-induced) conversion of AF to sinus rhythm 3. Ectopy producing short-long R-R sequences Wide QRS duration (more than 120 ms) Concomitant VT Structural heart disease Depressed LV function Rapid ventricular response rate 1. During exercise 2. During rapid AV conduction *Some of these factors may develop later after the initiation of drug treatment. VW = Vaughan-Williams. Fuster V, et al. Circulation. 2006;114:e

Risk Factors for Ventricular Proarrhythmia (Cont'd)
VW Types IA and III Agents VW Type IC Agents Rapid dose increase High dose (sotalol, dofiletide), drug accumulation* Addition of drugs* 1. Diuretics 2. Other QT-prolonging antiarrhythmic drugs 3. Nonantiarrhythmic drugs listed in Previous proarrhythmia After initiation of drug Excessive QT lengthening High dose, drug accumulation Addition of drugs 1. Negative inotropic drugs Excessive (150%) QRS widening *Some of these factors may develop later after the initiation of drug treatment. Fuster V, et al. Circulation. 2006;114:e

On the Horizon Prevention of arrhythmogenic remodeling (structural remodeling/fibrosis, inflammation, oxidative stress, atrial tachycardia remodeling): ACE inhibitors/ARBs/aldosterone antagonists Statins Omega-3 polyunsaturated fatty acids (fish oil) Anti-inflammatory agents Atrial-selective agents Modifiers of gap junction coupling 5-Hydroxytryptamine 4 receptor antagonists ACE = angiotensin-converting enzyme; ARB = angiotensin-receptor blocker.

Inhibition of Angiotensin II Signaling to Prevent AF: a Meta-analysis
Study Treatment, n/N Control, n/N RR (95% CI) Weight, % Heart Failure Ven Den Berg SOLVD VaHeFT CHARM Subtotal (95% CI) 2/7 10/186 116/2209 179/2769 307/5171 7/11 45/188 173/2200 216/2749 441/5148 1.7 4.8 11.8 12.5 0.45 ( ) 0.22 ( ) 0.67 ( ) 0.82 ( ) 30.9 0.56 ( ) Test for heterogeneity chi-square = df = 3 P = .0018 Test for overall effect z = P = .007 Hypertension CAPP LIFE STOPH2 117/5492 179/4417 200/2205 11.4 12.6 13.0 37.1 0.87 ( ) 0.71 ( ) 1.12 ( ) 0.88 ( ) 496/12,114 Test for heterogeneity chi-square = df = 3 P = .0013 Test for overall effect z = P = .4 Favors treatment Favors control RR = relative risk; CI = confidence interval. Healey JS, et al. Am Coll Cardiol. 2005;45:

Inhibition of Angiotensin II Signaling to Prevent AF: a Meta-analysis (Cont'd)
Study Treatment, n/N Control, n/N RR (95% CI) Weight, % AF Madrid Ueng Subtotal 9/79 18/70 27/149 22/75 32/75 54/150 4.3 7.0 11.4 0.39 ( ) 0.60 ( ) 0.52 ( ) Test for heterogeneity chi-square = df = 1 P = .31 Test for overall effect z = P = .002 Post-MI TRACE GISSI 22.790 665/8865 6897/9655 42/787 721/8846 763/9633 6.6 14.0 20.7 0.52 ( ) 0.92 ( ) 0.73 ( ) Test for heterogeneity chi-square = df = 3 P = .0013 Test for overall effect z = P = .4 Total 1517/27,089 2002/29,220 100.0 0.72 ( ) Test for heterogeneity chi-square = df = 10 P = Test for overall effect z = P = .0002 Favors treatment Favors control Healey JS, et al. Am Coll Cardiol. 2005;45:

Use of Statins and AF in Patients With Coronary Artery Disease
Probability of AF-free Survival Nonusers Statin Users Young-Zu Y, et al. Am J Cardiol. 2003;92:

ARRHYTHMIAS Keith Tiong Registrar Intensive Care, John Hunter Hospital

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