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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

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arrhythmias

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
College of Intensive Care Australia New ZealandELECTRICAL 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
College of Intensive Care Australia and New Zealand 2008Basic 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.
college of intensive care australia and new zealand 2008 basic science short answer1
College of Intensive Care Australia and New Zealand 2008Basic Science Short Answer
  • 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.
slide5
‘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
  • Extensive autonomic innervation
  • 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

slide6
‘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
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
Conduction velocity and refractory periods
  • Conduction Velocity
  • Atrial/ventricular muscle fibers: 0.3-0.5 meters per second
  •  Specialized fibers for action potential propagation through the heart (e.g. Purkinje fibers): 0.02-4 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 = 0.25-0.3 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
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 channels1
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
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.
college of intensive care australia and new zealand 2007 basic science short answer
College of Intensive Care Australia and New Zealand 2007Basic Science Short Answer
  • 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 -
slide14
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
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
College of Intensive Care Australia New ZealandANTI-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
college of intensive care australia and new zealand 2007 basic science short answer2
College of Intensive Care Australia and New Zealand 2007Basic Science Short Answer
  • 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.
college of intensive care australia and new zealand 2007 basic science short answer3
College of Intensive Care Australia and New Zealand 2007Basic Science Short Answer
  • 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
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
slide20
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
slide21
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
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
'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
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
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'
  • Commonly occurs at the level of the AV node (narrow QRS)
  • 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
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
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
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
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
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
slide31
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
  • 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

slide33
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
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
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
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 fibrillation1
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
Rate controlfor 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
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
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

slide41
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
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
College of Intensive Care Australia and New Zealand 2009SHORT 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

college of intensive care australia and new zealand 2009 short answer question paper 11
College of Intensive Care Australia and New Zealand 2009SHORT ANSWER QUESTION PAPER 1
  • 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
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
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
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
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 vf1
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

college of intensive care australia and new zealand 2010 short answer question paper 1
College of Intensive Care Australia and New Zealand 2010SHORT ANSWER QUESTION PAPER 1
  • 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.
college of intensive care australia and new zealand 2010 short answer question paper 11
College of Intensive Care Australia and New Zealand 2010SHORT ANSWER QUESTION PAPER 1
  • 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
college of intensive care australia and new zealand 2010 short answer question paper 12
College of Intensive Care Australia and New Zealand 2010SHORT ANSWER QUESTION PAPER 1
  • 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
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
college of intensive care australia and new zealand 2009 short answer question paper 12
College of Intensive Care Australia and New Zealand 2009SHORT ANSWER QUESTION PAPER 1
  • 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.
college of intensive care australia and new zealand 2009 short answer question paper 13
College of Intensive Care Australia and New Zealand 2009SHORT ANSWER QUESTION PAPER 1
  • 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
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
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 pointes1
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).
pharmacologic management of atrial fibrillation af
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
Risk for Ischemic Stroke and Intracranial Bleeding as a Function of Anticoagulation Intensity

Ischemic StrokeIntracranial 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:e257-354.

antithrombotic therapy for patients with af
Antithrombotic Therapy for Patients With AF

*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:e257-354.

heart rate control versus rhythm control in persistent af
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

Rate control

Cumulative Mortality (%)

60

50

0

0

6

12

18

24

30

36

Months

No. at Risk

Rate control 256 239 232 222 212 99 25

Rhythm control 266 243 224 218 207 85 24

No. of Deaths number (percent)

Rate control 0 80 (4) 175 (9) 257 (13) 314 (18) 352 (24)

Rhythm control 0 78 (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;347:1834-1840.

2. Wyse DG, et al. N Engl J Med. 2002;347:1825-1833.

rate control versus rhythm control where we are now
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
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;43:1201-1208.

drug therapy for hr control in af acute management
Drug Therapy for HR Control in AF: Acute Management

BP = blood pressure; HB = heart block; HR = heart rate; HF = heart failure.

Fuster V, et al. Circulation. 2006;114:e257-354.

drug therapy for hr control in af long term management
Drug Therapy for HR Control in AF: Long-term Management

Fuster V, et al. Circulation. 2006;114:e257-354.

ventricular rate control in af additional caveats
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
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;43:1201-1208.

rhythm control pharmacologic conversion of af duration of 7 days
Rhythm Control: Pharmacologic Conversion of AF (Duration of ≤7 Days)

Fuster V, et al. Circulation. 2006;114:e257-354.

outpatient therapy for recent onset af pill in the pocket approach
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;351:2384-2391.

pharmacologic therapy to maintain sinus rhythm typical dosages and adverse effects
Pharmacologic Therapy to Maintain Sinus Rhythm: Typical Dosages and Adverse Effects

*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:e257-354.

maintaining sinus rhythm an algorithm based on underlying heart disease
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:e257-354.

antiarrhythmic drug proarrhythmia an extension of pharmacologic effects
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
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
Risk Factors for Ventricular Proarrhythmia

*Some of these factors may develop later after the initiation of drug treatment.

VW = Vaughan-Williams.

Fuster V, et al. Circulation. 2006;114:e257-354.

risk factors for ventricular proarrhythmia cont d
Risk Factors for Ventricular Proarrhythmia (Cont'd)

*Some of these factors may develop later after the initiation of drug treatment.

Fuster V, et al. Circulation. 2006;114:e257-354.

on the horizon
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
Inhibition of Angiotensin II Signaling to Prevent AF:a Meta-analysis

.1 .2 1 5

Favors treatment Favors control

RR = relative risk; CI = confidence interval.

Healey JS, et al. Am Coll Cardiol. 2005;45:1832-1839.

inhibition of angiotensin ii signaling to prevent af a meta analysis cont d
Inhibition of Angiotensin II Signaling to Prevent AF: a Meta-analysis (Cont'd)

.1 .2 1 5

Favors treatment Favors control

Healey JS, et al. Am Coll Cardiol. 2005;45:1832-1839.

use of statins and af in patients with coronary artery disease
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;92:1379-1383.