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Arrhythmia

Clinical problems
Authors Learning objectives Introduction 1/ Assessing the normal ECG Specific indications for ECG monitoring Those with known cardiopulmonary disease e.g. Those exposed to a proarrhythmic environment Those with a history of unexplained collapse Potential problems with ECG monitoring General principles of ECG monitoring Standard limb leads The chest leads (V1-V6) Normal cardiac conduction Sinoatrial node (SAN) Atrioventricular node (AVN) His bundle Bundle Branches Mechanisms of cardiac arrhythmias Abnormal automaticity Abnormal conduction 2/ Diagnosis of rhythm disturbances Assessment of heart rate (= ventricular rate) Assessment of heart rhythm 3/ Managing the patient with rhythm disturbances Structure of ion channels Sodium currents Calcium currents Potassium currents Electrogenic pumps The Na+ /K+ pump The Na+ /Ca++ exchanger Treatment options Pacing Pharmacology 4/ Managing the patient with bradycardias Sinus node (SAN) dysfunction

Sinus node dysfunction in the context of acute myocardial infarction Atrioventricular (AV) conduction disease AV node dysfunction in the context of acute myocardial infarction (MI) Bundle branch block in the context of acute MI Cases for special consideration 5/ Managing the patient with supraventricular tachycardias Sinus tachycardia Causes Management Paroxysmal atrial tachycardia Causes Management Atrial flutter Causes Management Atrial fibrillation Diagnosis Causes Treatment Atrial fibrillation after cardiac and thoracic surgery Junctional tachycardias Circus movement tachycardia (CMT) Wolff-Parkinson-White (WPW) syndrome 6/ Managing the patient with ventricular tachycardias Ventricular extrasystoles Ventricular tachycardia (VT) Diagnosis Management Newer interventions for the management of VT/VF Torsade de pointes Conclusion Patient challenges Self-Assessment

Introduction
The diagnosis and management of patients with cardiac arrhythmias are undergoing rapid change. Better understanding of the mechanisms that initiate and perpetuate abnormal cardiac rhythms, and exciting new modes of treatment are the principal reasons. Appropriate and timely referral for specialist opinion may be life-saving Intensive care physicians should be thoroughly conversant with the diagnosis, appropriate investigation and treatment of patients with cardiac rhythm disturbances. They should also be aware of the indications for specialist intervention that a cardiologist and/or cardiac surgeon might have to offer. Two particularly useful and up-to-date reviews are to be found below.

1/ Assessing the normal ECG


Continuous electrocardiographic (ECG) monitoring should be employed routinely in all intensive care patients. The principal goals of ECG monitoring in the ICU are to: Alert staff to changes in cardiac rhythm which may herald life-threatening events Alert staff to sudden changes in cardiac rhythm which are themselves life-threatening Identify silent ischaemia

1/ Assessing the normal ECG


Continuous electrocardiographic (ECG) monitoring should be employed routinely in all intensive care patients. The principal goals of ECG monitoring in the ICU are to: Alert staff to changes in cardiac rhythm which may herald life-threatening events Alert staff to sudden changes in cardiac rhythm which are themselves life-threatening Identify silent ischaemia

Specific indications for ECG monitoring


ECG monitoring is mandatory in patients at high risk of cardiac arrhythmia. Such patients fall into three categories. Those with known cardiopulmonary disease Those exposed to a proarrhythmic environment Those with a history of unexplained collapse

Those with known cardiopulmonary disease e.g.


By definition, virtually all ICU patients require ECG monitoring Known or suspected ischaemic heart disease (including unstable angina and recent myocardial infarction) History of past cardiac arrhythmia Cardiothoracic surgery

Those exposed to a proarrhythmic environment


Electrocution Acute neurological disease Acute drug/ metabolic toxicity Specific endocrine disease At risk of profound bradycardia

Those with a history of unexplained collapse


See the references below.

Potential problems with ECG monitoring


Lead positioning can be difficult (e.g. the burned patient) Movement or muscle artefact may make traces unreliable (e.g. shivering) Single-lead monitoring may make detection of ECG components (such as the P wave) difficult if axis/rhythm alters Single-lead monitoring may not demonstrate changes in ST-segments in an (unmonitored) ischaemic zone Monitoring patients nursed in the prone position Arrhythmia detection software must be both sensitive and specific Diathermy interference - rare in ICU (but possible on patient having emergency surgery (e.g. remediastinotomy after heart surgery in ICU) A ventilated patient was about to be DC cardioverted from ventricular fibrillation. Fortunately, the disconnected lead (with transmission of 'mains hum' at 50 Hz) was detected in time. Always remember to check that the rhythm you observe is real: lead disconnections can cause apparent VF as well as asystole. Check the rhythm on two other leads and check the patient's pulse or the displayed arterial trace. A patient being prone ventilated for ARDS developed ventricular fibrillation. Substantial delay ensued whilst the patient was turned to allow defibrillation. In such circumstances, prophylactic application of an anterior chest 'stick-on-pad' prior to turning prone would have facilitated rapid defibrillation.

General principles of ECG monitoring


The surface ECG records changes in electrical potential of the heart as it depolarises and repolarises; by recording in multiple directions, summation and subtraction are performed to yield a 'net' activity in one region of the heart only (the axis). Each lead on an ECG printout represents this net activity in just one region. If the net activity is towards the lead, then the resulting deflection will be upwards (positive). If away from the lead, the deflection will be predominantly downwards (negative). Standard recording speed is 25 mm/sec. The trace is drawn on graph-paper which is composed of 5 mm 'large' squares, each divided into 5 'small' (1 mm) squares (each lasting 0.04 sec). The leads which are most commonly viewed are divided in two groups, the standard limb leads (I, II, III, aVR, aVL, aVF), and the chest leads (V1-V6).

In the next ten 'at risk' patients undergoing ECG monitoring in your ICU, try to determine on how many occasions this affected management, what abnormal cardiac rhythms occurred and in which patients?

Make a list of which factors might have predisposed to the abnormal rhythms. Address each factor in turn. Were appropriate precautions taken in each case?

Standard limb leads

Object 1

The chest leads (V1-V6)

A 12-lead ECG allows diagnosis of the nature and origin of almost any myocardial ischaemia (an exception would be e.g. right ventricular infarction) or the origin of an arrhythmia (e.g. ventricular tachycardia (VT) originating in either the right or left ventricle).Wherever possible, therefore, a 12-lead ECG recording should be obtained. Serial ECGs will be required in evolving situations.

Normal cardiac conduction


To understand the principles and concepts involved in the accurate diagnosis and treatment of arrhythmias, a brief review of the anatomy and physiology of the conducting system may be useful.

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

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) This is the normal situation. Intensivists need to think about bypass tracts. The impulse is then carried through the His-Purkinje system, and results in ventricular depolarisation.

Hampton JR. : The ECG Made Easy. Harcourt Publishers Ltd; 1997. Ellenbogen KA, Kay GN, Wilkoff BL, editors. : Clinical Cardiac Pacing and Defibrillation. 2nd ed.

WB Saunders Company; 2000. ISBN 0721676839 SAN, AVN, and His bundle depolarisation are electrically silent on the ECG.An increase in QRS duration is seen when: The conducting system is damaged (leading to bundle branch block) The ventricle is being activated through an alternative AV pathway (e.g. an accessory or nonHis- AV bundle) Ventricular activation originates in the ventricle itself (e.g. a ventricular escape focus, or VT) All areas of the heart have the capacity for automaticity, and therefore can become pacemakers. In general, the rate of pacemaker activity is lower the further down the heart one goes: An atrial pacemaker may 'fire' at rates of <250 bmp The SA node may have re-entrant cycles producing similar rates of <200 bpm The common His bundle generally "fires" at rates of <70 bpm With normal conduction, all of these will produce normal narrow QRS complexes. Lower His-bundle pacemaker sites fire at slower rates, and the apices of the ventricles at rates of 35-40 bpm and will produce wide complexes.

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) This is the normal situation. Intensivists need to think about bypass tracts. The impulse is then carried through the His-Purkinje system, and results in ventricular depolarisation.

Hampton JR. : The ECG Made Easy. Harcourt Publishers Ltd; 1997. Ellenbogen KA, Kay GN, Wilkoff BL, editors. : Clinical Cardiac Pacing and Defibrillation. 2nd ed.

WB Saunders Company; 2000. ISBN 0721676839 SAN, AVN, and His bundle depolarisation are electrically silent on the ECG.An increase in QRS duration is seen when: The conducting system is damaged (leading to bundle branch block) The ventricle is being activated through an alternative AV pathway (e.g. an accessory or nonHis- AV bundle) Ventricular activation originates in the ventricle itself (e.g. a ventricular escape focus, or VT) All areas of the heart have the capacity for automaticity, and therefore can become pacemakers. In general, the rate of pacemaker activity is lower the further down the heart one goes: An atrial pacemaker may 'fire' at rates of <250 bmp The SA node may have re-entrant cycles producing similar rates of <200 bpm The common His bundle generally "fires" at rates of <70 bpm With normal conduction, all of these will produce normal narrow QRS complexes. Lower His-bundle pacemaker sites fire at slower rates, and the apices of the ventricles at rates of 35-40 bpm and will produce wide complexes.

Mechanisms of cardiac arrhythmias


Abnormal automaticity and abnormal conduction are two major causes of cardiac arrhythmias.

Abnormal automaticity
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
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 reentrant tachycardia, atrioventricular re-entry tachycardia as observed in the Wolff-Parkinson-White Syndrome (see Task 5 ). The following section assumes a degree of competence in ECG interpretation.You will find the following references particularly helpful.

Ferry DR. : Basic Electrocardiography in Ten Days. McGraw-Hill Publishing Company; 2000

Brose JA, Auseon JC, Waksman D, Jarosick MJ. The Guide to EKG Interpretation. Ohio University

Press; 2000 Jelliffe RW. Fundamentals of Electrocardiography. Berlin: Springer-Verlag and Heidelberg GmbH & Co. KG. http://www.ecglibrary.com/ Practice makes perfect

Apprentice yourself to a cardiological colleague until you are familiar with the common ECG abnormalities. Abnormal conduction 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 reentrant tachycardia, atrioventricular re-entry tachycardia as observed in the Wolff-Parkinson-White Syndrome (see Task 5 ). The following section assumes a degree of competence in ECG interpretation.You will find the following references particularly helpful.

Ferry DR. : Basic Electrocardiography in Ten Days. McGraw-Hill Publishing Company; 2000 Brose JA, Auseon JC, Waksman D, Jarosick MJ. The Guide to EKG Interpretation. Ohio University

Press; 2000 Jelliffe RW. Fundamentals of Electrocardiography. Berlin: Springer-Verlag and Heidelberg GmbH & Co. KG. http://www.ecglibrary.com/ Practice makes perfect

Apprentice yourself to a cardiological colleague until you are familiar with the common ECG abnormalities.

This ECG was obtained from a 55-year-old man with typical ischaemic chest pain. Explain the ECG findings; in which circumstances would you consider intervention and what treatment options are available? This case illustrates an acute inferior wall myocardial infarction with an ST score (the total amount,

in millimetres, of ST elevation in the inferior leads II, III, aVF) of more than 7mm, indicating an extensive myocardial infarction. The additional recording of lead V4R would have been of help to identify the coronary involved, presence of right ventricular myocardial infarction and risk of developing AV nodal block. The latter was already present in this patient - indicating the proximal location of the obstruction in the right coronary artery, leading to a large inferior wall infarction with right ventricular involvement. When high-degree AV nodal block occurs in acute myocardial infarction the in-hospital mortality rate is two and one-half times that of inferior myocardial infarction without high-degree AV block. This patient should be referred for primary percutaneous coronary intervention.

This ECG was obtained from a 60-year-old man with typical ischaemic chest pain. Explain the ECG findings; in which circumstances would you consider intervention and what treatment options are available? This case illustrates an acute anterior myocardial infarction complicated by a left bundle branch block. The development of bundle branch block during the acute phase of myocardial infarction indicates extensive anterior wall infarction, because such conduction problems indicate an occlusion proximally in the LAD coronary artery. When anterior myocardial infarction is complicated by bundle branch block, early death occurs because of pump failure and ventricular tachycardia or fibrillation. The finding of a bundle branch block as a complication of anterior wall infarction calls for aggressive treatment. This patient should be referred for primary percutaneous coronary intervention. Development of second or third degree heart block in association with bundle branch block during anterior MI necessitates temporary pacing.

This ECG was obtained from a 22-year-old woman with a history of pyrexia, and rigors. On examination there were profuse splinter haemorrhages and a short early diastolic murmer at the lower left sternal edge. Explain the anatomy of the abnormality seen, what is the likely underlying diagnosis, and what investigation and treatment are indicated? The clinical features in this patient are those of an active infective endocarditis of the aortic valve. The development of high degree atrioventricular block indicates the development of an aortic root abcess. Using the knowledge of the anatomical relationships between the valve cusps and adjacent structures, the echocardiographer can more clearly define the perivalvular extension of infection. Extension of the infection beyond the valve leaflets into the surrounding tissue is an ominous step in the progression of infective endocarditis. In patients with endocarditis complicated by perivalvular extension of infection, cardiac surgery should be considered to debride invasive infection, ablate abscesses and reconstruct anatomical damage

This ECG was obtained from a 62-year-old lady admitted to ICU following a cardiac arrest. The only past medical history of note was treatment with antidepressants. What is the underlying ECG abnormality? What was the likely cause of her syncope? Tricyclic antidepressants may cause orthostatic hypotension and arrhythmias. Like quinidine, tricyclic antidepressants may prolong the Q-T interval as in this patient. Torsade de pointes was the underlying cause of her cardiac arrest.

We have now completed assessment of the normal ECG. Understanding of the normal anatomy and physiology of the conducting system has been emphasised, in order to allow interpretation of ECG changes in pathological conditions. These skills will now be used to interpret arrhythmias.

. 2/ Diagnosis of rhythm disturbances

2/ Diagnosis of rhythm disturbances


Assessment of heart rate (= ventricular rate) Standard recording speed is 25 mm/sec. An estimate of rate can be most easily determined by dividing the number of 'large' squares between QRS complexes into 300. counting the number of QRS complexes over 30 large squares (i.e. the number in 6 seconds) and multiplying by ten By convention, a rate of >100 bpm is classified as a tachycardia, and <60 bpm as a bradycardia. A 22-year-old fit rugby player was admitted with abdominal pain. His heart rate was 74 bpm, which reassured his carers. Suddenly several hours later he collapsed. At laparotomy, 400 ml of pus was drained from an appendix abscess. A 27-year-old patient was brought to the Accident and Emergency Department, complaining of a severe headache. She would intermittently scream inconsolably. Neurological examination was unremarkable. Heart rate was 65 bpm. Two hours later, neurosurgeons performed a shunt to treat her hydrocephalus. Remember, the heart rate must be put in the context of the individual patient. A 'normal' heart rate may be abnormal in certain circumstances.

Assessment of heart rhythm


Assessment of regularity Assessment of QRS duration P waves present - implies co-ordinated atrial electrical activity. See algorithm A below. P waves absent - ensure not 'hidden' after or within QRS complex. See algorithm B below. No P waves - absence of co-ordinated atrial electrical activity. Atrial flutter - atrial activity at 300 bpm - 'saw-tooth' baseline to ECG. Consider this if QRS rate is regular and is a division of 300 (explained later ). Atrial fibrillation (AF) - chaotic atrial activity and irregular QRS rate.

Algorithm A P wave activity present Algorithm B no clear P wave activity present

Describe the following ECG I Atrial fibrillation

3/ 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.

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. Knowledge of ionic currents is mandatory in the understanding of drug interactions and arrhythmias 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

Sodium currents
The sodium current is primarily responsible for the depolarisation phase of the action potential.

Calcium currents
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). You will find the following reference useful in this connection.

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 Adenosine CLASS Antiarrhythmic

INDICATIONS Arrhythmia/supraventricular arrhythmias DOSE Initial dose: 6 mg as rapid IV bolus (over 1-2 sec) if desired response is not achieved within 1-2 min 12 mg should be given as a rapid IV bolus (may be repeated). Another 12 mg dose is not recommended ADVERSE EFFECTS Facial flushing (18%) Dyspnoea (12%) Chest discomfort (7%) CONTRAINDICATIONS Second or third degree heart block or sick sinus syndrome (unless functioning pacemaker) COMMENT Inhaled adenosine induces bronchoconstriction in asthmatic patients

The 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. Conditions that increase intracellular Ca++ also increase the extrusion of Ca++ ; this depolarising process may produce early and/or late after-depolarisations.

Digitalis inhibits the enzyme sodium-potassium adenosine triphosphatase (ATPase) and thus interferes with the sodium pump, causing sodium to accumulate in the cell, which in turns alters sodium-calcium exchange. Digitalis intoxication results in enhanced impulse formation, based on triggered activity (early after-depolarisations). Common digitalis arrhythmias are atrial tachycardia, junctional tachycardia and VT. Digitalis also causes SA and AV block. Describe those conditions that may promote expressions of digitalis intoxication. What treatment is indicated? Conditions that may promote arrhythmic expressions of digitalis intoxication are increased sympathetic stimulation, which includes intracellular calcium overload, hypokalaemia, hypercalcaemia, hypomagnesaemia, diuretics, ischaemia and reperfusion, increased wall tension, and heart failure, all of which by themselves are capable of producing triggered activity. Treatment consists of discontinuation of digitalis, bedrest (no sympathetic stimulation), correction of potassium-magnesium deficits. If haemodynamically unstable, phenytoin is indicated unless digitalis antibodies are available. During treatment with phenytoin ventricular pacing is indicated since suppression of the tachycardia may be followed by asystole. The assessment and treatment of any cardiac arrhythmia must include full

clinical assessment of the patient. A number of factors that increase the likelihood of arrhythmias are commonly encountered in the intensive care setting: (before reading the following list you may wish to note down your own thoughts and then see how well you did!). Factors increasing arrhythmic risk are numerous in the ICU 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)

Determine, in the next ten patients admitted to your ICU, which proarrhythmic drugs are used and make a list of concomitant factors that might provoke arrhythmias. 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


All anti-arrhythmic drugs are potentially proarrhythmogenic. Is the patient haemodynamically compromised? If so, act now (e.g. broad complex tachycardia or profound bradycardia with significant hypotension). Is the patient likely to become haemodynamically compromised? (e.g. AF with impaired ventricular function). Wait and watch. Is the patient not haemodynamically compromised? Do you need to intervene at all?

Keep a diary of interventions for cardiac arrhythmias in your ICU for one month. Was the correct diagnosis of the underlying arrhythmia made in each case? Was intervention necessary on each occasion?

Rule 2. 'Electricity' is generally safer than drugs


In general, every anti-arrhythmic drug is proarrhythmogenic, nearly all are negatively inotropic, and many have long half-lives. If in doubt, 'electricity' is safer and quicker. Thus: If the rhythm and rate are fast and the patient haemodynamically compromised, consider cardioversion. If the rhythm and rate are slow and the patient haemodynamically compromised, consider pacing.

Rule 3. Correct all correctable abnormalities


Do this simultaneously with other treatment if the patient is haemodynamically compromised; otherwise, do this first: Check arterial blood gases and electrolytes 'Normal' isn't necessarily normal e.g. in patients with cardiac disease or recent cardiac surgery, maintaining potassium levels at the upper range of normal reduces the risk of arrhythmia (this does not apply after cardiac transplantation) Magnesium deficiency is common in ICU patients Blood levels do not reflect tissue levels, but care should be taken in replacement, as side effects occur with high levels. Shortly after arrival in the ICU, a patient with acute renal failure developed refractory VF. Defibrillation was unsuccessful until calcium gluconate, bicarbonate and intravenous insulin and glucose had been administered. A patient with severe burns suffered repeated runs of AF, despite all measured elec-trolytes being normal. The patient responded well to 4 mmol intravenous magnesium.

Iseri LT, Allen BJ, Brodsky MA. Magnesium therapy of cardiac arrhythmias in critical care medicine.

Magnesium 1989; 8 (5-6): 299-306. PMID 2693848 Moran JL, Gallagher J, Peake SL, Cunningham DN, Salagaras M, Leppard P. Parenteral magnesium sulfate versus amiodarone in the therapy of atrial tachyarrhythmias: a prospective, randomized study. Crit Care Med 1995; 23 (11): 1816-1824. PMID 7587256

Rule 4. Treat all treatable ischaemia


Myocardial ischaemia as a cause of arrhythmia must always be considered, and if thought to be the

cause, must be treated. Consider: Pharmacotherapy (-blockade, nitrates) Mechanical support (intra-aortic balloon pump) Temporary transvenous (or external) pacing Percutaneous intervention (angioplasty stent) Surgery

Ischaemia in the presence of hypotension and VT/atrial tachycardia may need additional urgent non-pharmacological intervention: inotropes increase BP (and hence coronary perfusion pressure) but in the presence of flow-limiting coronary disease, the increased coronary flow may be offset by increased cardiac work and the ischaemia persist. Moreover, the tachycardia may be perpetuated. In these situations, use of intraaortic balloon counterpulsation may be considered.

Rule 5. Consider your intravascular lines


Is a central venous pressure (CVP) line or pulmonary artery (PA) catheter 'tickling' the right atrium, tricuspid valve or right ventricle? If in doubt, withdraw it a few centimetres. Similarly, you may need to remove a PA catheter, or reposition temporary pacing wires. Is the patient 'under- or over-filled'? AF (in particular) responds to altered blood volume status.

Rule 6. Consider drug toxicity


Many drugs commonly used in the ICU are proarrhythmogenic All anti-arrhythmics may be proarrhythmogenic. Many other drugs (often those which affect neurotransmission e.g. antidepressants and anticonvulsants, and some anaesthetic agents) may be proarrhythmic.

A patient with paroxysmal AF was treated with regular (oral) amiodarone

. Four months later she

presented in sustained AF. Increasing amiodarone dosage resulted in repeated VT arrests. This was the ECG on admission to the ICU. What is the ECG abnormality and the cause of her arrhythmia? What treatment would you consider? Long QT syndrome, with possible torsade de pointes. Treat by stopping amiodarone and consider overdrive pacing the VT. The emergence of a sustained ventricular tachycardia after starting a Class IC anti-arrhythmic drug or after an increase in drug dose suggests an adverse drug effect. Lengthening of the membrane action potential duration prolongs the QT interval and may therefore promote the occurrence of early after-depolarisations and polymorphic ventricular arrhythmias (torsade de pointes). Their occurrence is promoted by hyperkalaemia and hypomagnesaemia. In this setting detection and treatment should be early and relatively easy. The offending drug should be stopped and electrolyte disturbances (potassium, magnesium) corrected. Intravenous magnesium (1-2 gm by intravenous bolus over five minutes) is suggested even in normomagnesaemia. If intravenous magnesium is unsuccessful, an increase in basic heart rate with isoproterenol or by ventricular pacing may be necessary. Amiodarone

CLASS Antiarrhythmic INDICATIONS Arrhythmias/Ventricular fibrillation Arrhythmias/Ventricular tachycardia INTERACTIONS DOSE Loading dose of 800-1600 mg PO qd for 1-3 weeks, 600-800 mg/d for one month, and then 200-400 mg qd For initial therapy: 150 mg over 10 min not >30 mg/min followed by 360 mg over next 6h (1 mg/min) followed by 540 mg over the next 18h (0.5 mg/min) DOSAGE ADJUSTEMENTS Reduce dose or discontinue therapy for interstitial/alveolar pneumonitis Elevation in hepatic enzymes >3 x normal (2 x baseline if baseline liver enzymes elevated) Hepatomegaly Hypothyroidism or hyperthyroidism Paroxysmal ventricular tachycardia (proarrhythmia) CHF Warfarin: hypoprothrombinemic effect -blockers: Bradycardia, hypotension Digoxin: serum digoxin level Flecainide: flecainide level Hydantoins: - hydantoin level and amiodarone level Procainamide: procainamide level Quinidine: quinidine level Theophylline: theophylline level

MONITORING Baseline work up should include thyroid function tests. Plasma concentrations (therapeutic: 1-2.5 mcg/ml) may be help-ful. Monitor closely after dosage adjustments due to long half-life (9-44 days) ADVERSE EFFECTS Oral: Peripheral neuropathy (20-40%) Gastrointestinal: Complaints most common nausea/vomiting (10- 33%), constipation, anorexia (4-9%) Visual disturbances (4-9%) Dermatologic reactions (15%), photosensitivity (10%), blue discoloration of skin CHF (3%), bradycardia Abnormal liver function tests (4-9%) Pulmonary inflammation or fibrosis (4-9%) Parenteral: ARDS (2%), hypotension (15.6%) Asystole, cardiac arrest, electro-mechanical dissociation (1.1%) Ventricular tachycardia (2.4%), cardiogenic shock (1%), bradycardia

(4.9%), congestive heart failure (2.9%), fever (2%), abnormal LFTs (3.4%), nausea (3.9%) Others include atrial fibrillation, nodal arrhythmia, prolonged QT interval, ventricular fibrillation (<2%), abnormal renal function, pulmonary oedema, Stevens-Johnson syndrome, thrombocytopoenia, diarrhoea, and vomiting (<2%) CONTRAINDICATIONS Oral: Severe sinus node dysfunction, second and third degree AV block, symptomatic bradyarrhythmias (except when used in conjunction with a pacemaker) Parenteral: Marked severe bradycardia, second- or third-degree AV block except when used in conjunction with a pace-maker, cardiogenic shock COMMENT If breakthrough arrhythmias occur, supplemental infusions of 150 mg over 10 min (not >30 mg/min) may be given and rate of maintenance infusion may be increased. Daily dose >2100 mg is associated with increased risk of hypotension

Treatment options
Electricity -pacing cardioversion, defibrillation Pharmacology Other (catheter ablation, ICD, surgical intervention).

Pacing
Cardiac pacing is a definitive life-saving treatment for bradyarrhythmias, in addition to its role for the termination of certain tachyarrhythmias. The modes available are: Mechanical Transcutaneous electrical Transvenous electrical Transoesophageal Transthoracic

Mechanical pacing Percussion pacing


Thought to work by mechanical stimulation of excitable myocardial tissue, either by direct or transmitted physical forces - performed with serial chest thumps, or cough-induced. Performed using serial thumps to the sternum with clenched fist 15-20 cm above the sternum 1/4-1/3 of the force used to cardiovert VF Rate: 60-90 bpm Confirmed by a palpable peripheral pulse or displayed arterial trace (ECG can be misleading)

Cough pacing (also known as cough CPR)


Precise mechanism unclear - possibly via mechanical stimulation. Witnessed arrest, in conscious patient Instruct patient to cough forcefully every 1-3 seconds May maintain cardiac output in asystole and VF Mechanical pacing can offer instantaneous and effective maintenance of cardiac output. Most successful when used early in witnessed arrests. In most instances secondary cardioversion is the ultimate solution. Although the above manoeuvres are important most serious arrhythmias in the ICU context require rapid initiation of more definitive measures.

Electrical pacing Transcutaneous pacing


Application of self-adhesive surface patch electrodes coated with high-impedance conductive gel allows rapid establishment of pacing. Skin should be cleaned to improve contact Patches secured anteriorly (negative) and posteriorly Safe to perform external cardiac massage during pacing Prominent muscle twitches in the unconscious patient may make palpation of the pulse difficult - confirm using intra-arterial line or Doppler

Hampton JR. The ECG Made Easy. Harcourt Publishers Ltd; 1997. Ellenbogen KA, Kay GN, Wilkoff BL, editors. Clinical Cardiac Pacing and Defibrillation. 2nd ed.

WB Saunders Company; 2000. ISBN 0721676839

During transcutaneous pacing sedation should be considered. Thresholds increase significantly after cardiac and thoracic surgery.

Which features of cardiac and/or thoracic surgery would you expect to increase thresholds during transcutaneous pacing? How would you treat them? Increased intrathoracic air (reduce positive pressure ventilation, treat pneumothorax),

pericardial effusion (drain), myocardial ischaemia/electrolyte disturbances (correct metabolic abnormalities and hypoxaemia, CPR if inadequate cardiac output).

Transvenous pacing
Used for atrial and/or ventricular pacing, this provides the most reliable means of temporary pacing, although it requires a degree of operator skill and may take some minutes to initiate. Right internal jugular approach is the fastest and easiest Femoral approach has the highest incidence of infection The more distal the approach, the higher the risk of lead displacement Defibrillator must always be at hand Usually ventricular single chamber pacing is adequate Perform under fluoroscopic guidance - aim to place ventricular lead in the right ventricular apex, and atrial lead in theatrial appendage (characteristic motion of the wire is seen). A simple 'pacing-only' catheter may be used but the 'SG pace-port' approach is most appropriate in the ICU. Confirm correct position with measurement of threshold parameters, stability, chest radiograph (see figure below) and 12-lead ECG recording Avoid the subclavian approach if possible, in patients likely to require subsequent permanent pacemaker implantation.

Chest radiograph showing correct position of pacing wires

What features of conduction would you expect to see in a 12-lead ECG in a correctly positioned ventricular lead? Since ventricular pacing is from the right ventricle the QRS complexes have the left bundle branch block configuration.

In addition to checking stability, thresholds and chest radiographic position at the time of temporary wire insertion, ensure the lead(s) is/are secure and then check the pacing thresholds daily.

In a patient who is undergoing temporary ventricular pacing, make sure you know how to assess the sensing mode, and the pacing threshold. In one such patient, if safe and appropriate: Adjust the rate of pacing, whilst looking at the haemodynamic monitoring. Is the patient's haemodynamic status improved with a faster rate, or paradoxically worse? If the patient has a stable sinus bradycardia underlying their paced rhythm, are they in fact better off with atrioventricular (AV) synchrony and their slower rate, than paced at a faster rate without AV synchrony? Drugs such as isoprenaline or dobutamine may also be considered but pacing is the preferred option. Instruction for checking pacing thresholds may be found in the following reference.

Isoprenaline (Arrhythmia) CLASS Short acting synthetic catecholamine with pure -adrenergic stimulating properties (1 > 2) INDICATIONS In emergencies to stimulate heart rate in patients with bradycardia or heart block INTERACTIONS None

DOSE 0.5-10 g/min ADVERSE EFFECTS Drop in diastolic blood pressure, headache, tremor, palpitations, arrhythmias and sweating CONTRAINDICATIONS Myocardial ischaemia and arrhythmias
Cardiac Pacemakers and antiarrhythmic devices. In: Braunwald E, Zipes DP, Libby P, editors. Heart

Disease: A Textbook of Cardiovascular Medicine. 6th ed. WB Saunders Company; 2001. p.775. ISBN 0721685617 If, despite successful pacing, the patient remains haemodynamically compromised, consider whether AV pacing would be more appropriate.

Causes for malfunctioning in pacing


Troubleshooting

Object 2

Antitachycardia pacing
In addition to its widespread use in the treatment of bradycardias, pacing may be used in the treatment of tachycardias: To prevent emergence of rhythm disturbances which occur during episodes of relative bradycardia (also used in arrhythmias due to repolarisation abnormalities - atrial flutter (Type I), AV node re-entry, AV re-entry, atrial tachycardia, VT). Overdrive/underdrive pacing Overdrive pacing - 20-30% faster than the tachycardia rate Underdrive pacing - pace asynchronously at a rate lower than the tachycardia (only useful if tachycardia rate >150 bpm). Antitachycardia pacing may terminate, re-initiate or accel-erate existing tachycardias. The risks of acceleration or fibrillation increase as the rate and duration of antitachycardia pacing increase.

Pharmacology
Efficacy of antiarrhythmic agents is unproven in the ICU population

No large clinical trials have been performed of the use of anti-arrhythmic therapies in the general ICU population. Care must be taken therefore when applying the results found in the non-critically ill and those on the coronary care unit, to those in the ICU setting. The choice of drugs, however, remains the same. Drug Classification APD: action potential duration RP: refractory period AVN: atrioventricular node SAN: sinoatrial node

Object 3

http://www.bnf.org

All anti-arrhythmic drugs are potentially proarrhythmogenic.


Examples

Although drug classification is easy, it is better to choose the drug for the diagnosis, rather than fit the diagnosis to the drug Class 1a: Quinidine, procainamide Class 1b: Lidocaine Class 1c: Flecainide Class 2: -blockers, bretylium Class 3: Amiodarone Class 4: Verapamil Other: Adenosine , disopyramide, sotalol , diltiazem , digoxin (high dose only) , phenytoin , encainide

Make a list of the most commonly used anti-arrhythmic drugs in your department and look for potential drug interactions. It is extremely important when caring for critically ill patients to be familiar with rhythm disturbances and be able to institute appropriate therapy. Optimal management of bradyarrhythmias and tachycardias requires expertise in electrocardiography, pharmacokinetics and pharmacodynamics as well as bedside clinical acumen. Digoxin CLASS Digitalis glycoside INDICATIONS Arrhythmias / Atrial fibrillation Arrhythmias / Atrial tachycardia / Paroxysmal (PAT) Heart failure INTERACTIONS Potassium depleting corticosteroids and diuretics: Likelihood of digitalis toxicity Rapid administration of IV calcium: Likelihood of serious arrhythmias Quinidine, flecainide, verapamil, amiodarone and propafenone: serum digoxin level Concomitant use of digoxin with sympathomimetics: likelihood of cardiac arrhythmias Succinylcholine: likelihood of arrhythmias -blockers and calcium channel blockers: Additive depressant effects on AV node conduction DOSE Loading: 10-15 mcg/kg total dose given 50% initially and remainder at 4-8h intervals Maintenance: 0.0625-0.375 mg qd. DOSAGE ADJUSTEMENTS The following conditions may require a lower maintenance dose: Renal insufficiency, hypokalemia, hypothyroidism, extensive myocardial damage, conduction disorders, and advanced age. In heart failure accompanying acute glomerulonephritis, relatively low loading doses and maintenance doses are usually necessary. MONITORING Therapeutic range is 0.5-2 ng/ml; patients with atrial fibrillation or atrial flutter require and tolerate higher levels. Sampling of serum concentrations should be obtained 6-8h after last dose.

ADVERSE EFFECTS Cardiovascular: Ventricular premature contractions (most common), ventricular tachycardia, AV dissociation, accelerated junctional rhythm, atrial tachycardia, progressive pulse slowing and AV block Gastrointestinal: Anorexia, nausea, vomiting, diarrhoea CNS: Visual disturbances, headache, weakness, dizziness, psychosis Other: Gynaecomastia, eosinophilia, and thrombocytopoenia are rare CONTRAINDICATIONS Ventricular fibrillation, ventricular tachycardia, digitalis toxicity, Beriberi heart disease, hypersensitive carotid sinus syndrome, hypersensitivity COMMENT In Wolff-Parkinson-White syndrome with atrial fibrillation, digoxin can accelerate transmission of impulse through accessory pathway; the risk of ventricular fibrillation discourages its use in this setting. Adenosine CLASS Antiarrhythmic INDICATIONS Arrhythmia/supraventricular arrhythmias DOSE Initial dose: 6 mg as rapid IV bolus (over 1-2 sec) if desired response is not achieved within 1-2 min 12 mg should be given as a rapid IV bolus (may be repeated). Another 12 mg dose is not recommended ADVERSE EFFECTS Facial flushing (18%) Dyspnoea (12%) Chest discomfort (7%) CONTRAINDICATIONS Second or third degree heart block or sick sinus syndrome (unless functioning pacemaker) COMMENT Inhaled adenosine induces bronchoconstriction in asthmatic patients Sotalol CLASS Antiarrhythmic INDICATIONS Arrhythmias / Ventricular INTERACTIONS Calcium channel blockers: Hypotension, bradycardia DOSE 80-320 mg bid ADMINISTRATION

Do not use in patients with hypokalaemia or hypomagnesaemia (can exaggerate the degree of QT prolongation and - risk of torsade de pointes) DOSAGE ADJUSTEMENTS Modify dosing interval based on renal function: CrCl >60 ml/min (q 12h), CrCl 30-60 ml/min (q 24h), CrCl 10-30 ml/min (q 36-48h), CrCl <10 ml/min Individualise dose: Dosage escalations in renal impairment should be after 5-6 doses at the appropriate intervals DISCONTINUATION QT interval >550 ms ADVERSE EFFECTS Cardiovascular: Bradycardia, heart failure, oedema, pulmonary oedema CNS: Dizziness, fatigue, headache, peripheral neuropathy, nervousness Urological: Sexual dysfunction, impotence, libido Endocrine: Hyperglycaemia, hypoglycaemia, Raynaud's phenomenon

CONTRAINDICATIONS Sinus bradycardia, >first degree heart block, overt heart failure, cardiogenic shock, congenital or acquired long QT syndrome Caution in patients with bronchospasm, peripheral vascular disease, or diabetes mellitus COMMENT After discontinuation of amiodarone, do not initiate sotalol until the QT interval is normalised. Proarrhythmic events can occur at initiation of therapy and with each upward dosage adjustment Verapamil CLASS Calcium channel blocker INDICATIONS Angina pectoris / Stable Angina pectoris / Unstable Angina pectoris / Variant Arrhythmias Hypertension

INTERACTIONS -blockers: Bradycardia, hypotension Digoxin: Lithium: Theophylline: Cyclosporine: serum digoxin level serum lithium level theophylline level cyclosporine level

Carbamazepine: DOSE

carbamazepine level

Oral: Digitalised patient with chronic atrial fibrillation: 240-360 mg/d in 3 or 4 divided doses; PSVT prophylaxis in non-digitalised patients: 240-480 mg/d in 3 or 4 divided doses; do not exceed 480 mg/d Parenteral: SVT: Initial: 5-10 mg (0.075-0.15 mg/kg), over 2 min, repeat 10 mg IV (0.15 mg/kg) 30 min after initial dose if response is not adequate ADVERSE EFFECTS CNS: Dizziness/lightheadedness (3.5%), headache (2.2%) Gastrointestinal: Constipation (7.3%), nausea (2.7%) CV: Hypotension (2.5%), peripheral oedema (2.1%), bradycardia (1.4%), AV block (1%), pulmonary oedema (1.8%) Other: Shortness of breath/dyspnoea/wheezing (1.4%) CONTRAINDICATIONS Sick sinus syndrome or second or third degree AV block except with a functioning pacemaker, ventricular tachycardia, hypotension (<90 mmHg systolic), severe left ventricular dysfunction, cardiogenic shock, and severe CHF unless secondary to supraventricular tachycardia amenable to verapamil therapy, atrial flutter or fibrillation with an accessory bypass tract (possibly - ventricular response). Do not give IV verapamil within a few hours of IV -blockers COMMENT IV verapamil may cause fatal hypotension if given during ventricular tachycardia Procainamide HCl CLASS Antiarrhythmic INDICATIONS Arrhythmias / Atrial fibrillation Arrhythmias / Atrial tachycardia / Paroxysmal (PAT) Arrhythmias / Perioperative Arrhythmias / Ventricular tachycardia

INTERACTIONS Propranolol: procainamide serum levels

Cimetidine and ranitidine: clearance of both procainamide and NAPA Quinidine, trimethoprim: the plasma levels of procainamide and NAPA Lidocaine, phenytoin, propranolol, quinidine: Cardiac effects may be additive or antagonistic, and toxic effects may be additive Amiodarone: respectively plasma procainamide and NAPA concentration up to 55% and 33%,

DOSE Initial control: IV doses of 50-100 mg may be given q 5-10 min until the arrhythmia is controlled, adverse effects occur, or 1.0 g has been given Alternatively, a loading dose IV infusion of 500 mg-1.0 g may be given at a constant rate over a 25-30 min period (rate not to exceed 25-50 mg/min) Maintenance: Continuous IV infusion of 1-6 mg/min DOSAGE ADJUSTEMENTS Reduce dose in renal insufficiency, congestive heart failure, and critically ill patients: QRS widening of >50% or marked prolongation of QT interval MONITORING dose if

Desired plasma concentrations of procainamide are 4-8 mcg/ml; toxicity associated with levels >12 mcg/ml NAPA's antiarrhythmic therapeutic concentrations are between 10-30 mcg/ml; toxic level is >30 mcg/ml ADVERSE EFFECTS Hypotension and serious disturbances of cardiac rhythm such as ventricular asystole or fibrillation (most common after IV administration) Skin: Angioneurotic oedema, urticaria, pruritus, flushing, maculopapular rash, and lupus-like syndrome after prolonged administration and in slow acetylators Positive ANA found in >50% of patients receiving long term therapy (usually within 2-18 months) Haematologic: Neutropoenia, thrombocytopoenia, haemolytic anaemia (rare), agranulocytosis CNS: Dizziness, giddiness, weakness, mental depression, psychosis with hallucinations Gastrointestinal: Anorexia, nausea, vomiting, abdominal pain, bitter taste, diarrhoea (3-4%) CONTRAINDICATIONS Complete heart block, idiosyncratic hypersensi-tivity, lupus erythematosus, torsade de pointes lidocaine CLASS Antiarrhythmic INDICATIONS Arrhythmias / Ventricular fibrillation Arrhythmias / Ventricular tachycardia INTERACTIONS -blockers: lidocaine levels

Cimetidine: lidocaine levels Procainamide: May have additive cardiodepressant action Succinylcholine: May prolong neuromuscular blockade DOSE

Acute management of ventricular arrhythmias: Single dose justified in following exceptional circumstances: When ECG is not available to verify diagnosis When facilities for IV administration are not available Patient in pre-hospital phase of suspected acute MI when directed by qualified medical personnel viewing transmitted ECG IM: 300 mg in deltoid muscle IV: Initial dose of 50-100 mg given at rate of 25-50 mg/min. If desired response not achieved, rebolus after 5 min. Do not give >200-300 mg/h. Continuous IV infusion: 1-4 mg/min (20-50 mcg/kg/min) DOSAGE ADJUSTEMENTS Reduce maintenance doses in heart failure, liver disease, receiving drugs known to clearance of lidocaine or accompanied by AV block. liver blood flow, patients >70 years of age, and digitalis toxicity

Widening of QRS complex and the appearance or aggravation of arrhythmias should be followed by dosage reduction and, if needed, discontinuation of drug MONITORING Constant ECG monitoring is essential Lidocaine plasma levels may correlate with CNS toxicity Metabolites can contribute to toxicity ADVERSE EFFECTS CNS: Lightheadedness, nervousness, drowsiness, confusion, mood changes, tremors, convulsions Cardiovascular: Hypotension, bradycardia, CV collapse CONTRAINDICATIONS Hypersensitivity to amide local anaesthetics, Stokes-Adams attacks, Wolff-Parkinson-White syndrome, and severe degrees of sinoatrial AV or intraventricular block in absence of an artificial pacemaker Flecainide CLASS Antiarrhythmic INDICATIONS Arrhythmias/Atrial fibrillation/Paroxysmal (PAF) Arrhythmias / Supraventricular tachycardia (PSVT) (Arrhythmias / Ventricular) INTERACTIONS Amiodarone: Cimetidine: flecainide level flecainide bioavailability

Disopyramide, verapamil: Smoking: Digoxin: Acidic urine: Alkaline urine: DOSE

negative inotropic effect

clearance of flecainide digoxin absorption elimination elimination

In patients without structural heart disease for PSVT and PAF associated with disabling symptoms: PSVT 50-150 mg bid, PAF 50-100 mg bid. Prevention of documented life-threatening ventricular arrhythmias: 100-200 mg bid ADMINISTRATION For treatment of sustained ventricular tachycardia, initiate therapy in the hospital DOSAGE ADJUSTEMENTS Renal impairment: CrCl <35 ml/min, initial dose 100 mg/d or 50 mg bid; less severe renal impairment initial dose is 100 mg q 12h Hepatic impairment: Do not use unless benefit outweighs risk. If used, cautious dose, appropriate at >4 day intervals MONITORING Trough levels associated with therapeutic effect 0.2-1mcg/ml Adverse effects - with levels >1 mcg/ml. DISCONTINUATION If second or third degree AV block or bifascicular block (RBBB + left hemiblock) occurs, discontinue therapy unless a ventricular pacer is in place ADVERSE EFFECTS Dizziness (18.9%), dyspnoea (10.3%), headache (9.6%), nausea (8.9%), fatigue (7.7%), palpitations (6.1%), chest pain (5.4%), asthenia (4.9%), tremor (4.7%), constipation (4.4%), oedema (3.5%), abdominal pain (3.5%) Ventricular tachycardia reported in 0.4% of patients treated for PAF. When used to suppress PVC's post-MI (CAST study) excessive mortality on non fatal cardiac arrest was seen in flecainide treated patients compared with placebo (5.1% vs 2.3% respectively) CONTRAINDICATIONS Pre-existing second or third degree AV block or bifasiclar block unless a pacemaker is present Others include recent MI or cardiogenic shock COMMENT Reserve use for patients in whom treatment benefits outweigh risk of proarrhythmic effects Not recommended for use in patients with chronic atrial fibrillation or non life-threatening ventricular arrhythmias Use only in extreme caution in sick sinus syndrome

May cause or worsen CHF, especially in patients with cardiomyopathy, pre-existing severe heart failure, or low ejection fractions Bretylium tosylate CLASS Antiarrhythmic INDICATIONS Arrhythmias / Ventricular INTERACTIONS Bretylium enhances pressor effects of catecholamines Digoxin toxicity may be worsened by the initial release of norepinephrine DOSE Initial dose 5 mg/kg by rapid IV injection (undiluted) If arrhythmia persists, dose to 10 mg/kg and repeat prn q 5-10 min up to 30-35 mg/kg For continued suppression, 1-2 mg/min, alternative - 5 to 10 mg/kg over >8 min q 6h IM Initial dose 5-10 mg/kg undiluted; may repeat at 1-2 h intervals if arrhythmia persists Maintenance: 5-10 mg/kg q 6-8h DOSAGE ADJUSTEMENTS Renal dysfunction: if CrCl 10-50 ml/min, ADVERSE EFFECTS Cardiovascular: Hypotension and postural hypotension (50%), bradycardia, frequency PVC's, transitory in BP, initial in arrhythmias (rare) Gastrointestinal: Nausea/vomiting (3% incidence with rapid IV administration) CONTRAINDICATIONS Not available COMMENT Avoid use in patients with fixed cardiac output (severe aortic stenosis or severe pulmonary hypertension). For a life-threatening arrhythmia in a digitalised patient, use bretylium only if digoxin toxicity is not the aetiology and other agents are ineffective Amiodarone CLASS Antiarrhythmic INDICATIONS Arrhythmias/Ventricular fibrillation Arrhythmias/Ventricular tachycardia INTERACTIONS Warfarin: hypoprothrombinemic effect -blockers: Bradycardia, hypotension dose by 50-75%

Digoxin: Flecainide:

serum digoxin level flecainide level amiodarone level

Hydantoins: - hydantoin level and Procainamide: Quinidine: Theophylline: DOSE procainamide level quinidine level theophylline level

Loading dose of 800-1600 mg PO qd for 1-3 weeks, 600-800 mg/d for one month, and then 200-400 mg qd For initial therapy: 150 mg over 10 min not >30 mg/min followed by 360 mg over next 6h (1 mg/min) followed by 540 mg over the next 18h (0.5 mg/min) DOSAGE ADJUSTEMENTS Reduce dose or discontinue therapy for interstitial/alveolar pneumonitis Elevation in hepatic enzymes >3 x normal (2 x baseline if baseline liver enzymes elevated) Hepatomegaly Hypothyroidism or hyperthyroidism Paroxysmal ventricular tachycardia (proarrhythmia) CHF

MONITORING Baseline work up should include thyroid function tests. Plasma concentrations (therapeutic: 1-2.5 mcg/ml) may be help-ful. Monitor closely after dosage adjustments due to long half-life (9-44 days) ADVERSE EFFECTS Oral: Peripheral neuropathy (20-40%) Gastrointestinal: Complaints most common nausea/vomiting (10- 33%), constipation, anorexia (4-9%) Visual disturbances (4-9%) Dermatologic reactions (15%), photosensitivity (10%), blue discoloration of skin CHF (3%), bradycardia Abnormal liver function tests (4-9%) Pulmonary inflammation or fibrosis (4-9%) Parenteral: ARDS (2%), hypotension (15.6%) Asystole, cardiac arrest, electro-mechanical dissociation (1.1%) Ventricular tachycardia (2.4%), cardiogenic shock (1%), bradycardia (4.9%), congestive heart failure (2.9%), fever (2%), abnormal LFTs (3.4%), nausea (3.9%) Others include atrial fibrillation, nodal arrhythmia, prolonged QT interval, ventricular fibrillation (<2%), abnormal renal function, pulmonary oedema, Stevens-Johnson syndrome,

thrombocytopoenia, diarrhoea, and vomiting (<2%) CONTRAINDICATIONS Oral: Severe sinus node dysfunction, second and third degree AV block, symptomatic bradyarrhythmias (except when used in conjunction with a pacemaker) Parenteral: Marked severe bradycardia, second- or third-degree AV block except when used in conjunction with a pace-maker, cardiogenic shock COMMENT If breakthrough arrhythmias occur, supplemental infusions of 150 mg over 10 min (not >30 mg/min) may be given and rate of maintenance infusion may be increased. Daily dose >2100 mg is associated with increased risk of hypotension

4/ Managing the patient with bradycardias


Watch and wait May be too late! These are common, but usually only transient in the ICU setting (i.e. related to airway manipulation etc). In this section we will cover diagnosis of the more common bradyarrhythmias and consider their treatment in the ICU.

Atrioventricular (AV) conduction disease


The nomenclature of AV conduction disease refers to the ECG patterns and not to the underlying pathophysiology or anatomy. Treatment based on an ECG diagnosis must be considered in the clinical context of the patient.

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). See the ECG.

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)

What degree of AV block is shown in the ECG rhythm strip? Second degree AV block type I Wenckebach.

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). See the ECG.

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.

Risk of progression to high-grade block


Although 1st degree and type I 2nd degree block rarely require pacing(low risk of progression), type I 2nd degree block associated with a wide QRS (especially in the context of anterior myocardial infarction) should have temporary backup pacing. In this context, what is the significance of the widened QRS complex, and what does it imply? 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.

Bundle branch block (BBB)


In the case of failure of conduction in the right or left bundles of His, the ECG changes are of bundle branch block (BBB). In the intensive care setting, the diagnosis of BBB on the ECG does not by itself usually indicate that any specific action is necessary, although the development of new BBB should alert the physician to the possibility of myocardial infarction.

Right bundle branch block (RBBB)


Due to delayed depolarisation of the right ventricular free wall: QRS duration >0.12 seconds Secondary positive lead in V1 (rsR) Deep slurred S wave in I, aVL, V4-6 Secondary ST, T changes in V1-V3

See the ECG

Left bundle branch block (LBBB)


Due to depolarisation of free wall of the left ventricle, together with reversal of the direction of septal depolarisation: QRS duration >0.12 seconds Absence of septal Q waves in I aVL and V4-V6 Absence of secondary R in V1 See the ECG

Sinus node (SAN) dysfunction

'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.

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.

Atrioventricular (AV) conduction disease


The nomenclature of AV conduction disease refers to the ECG patterns and not to the underlying pathophysiology or anatomy. Treatment based on an ECG diagnosis must be considered in the clinical context of the patient.

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). See the ECG.

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)

What degree of AV block is shown in the ECG rhythm strip? Second degree AV block type I Wenckebach.

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). See the ECG.

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.

Risk of progression to high-grade block


Although 1st degree and type I 2nd degree block rarely require pacing(low risk of progression), type I 2nd degree block associated with a wide QRS (especially in the context of anterior myocardial infarction) should have temporary backup pacing. In this context, what is the significance of the widened QRS complex, and what does it imply? 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.

Bundle branch block (BBB)


In the case of failure of conduction in the right or left bundles of His, the ECG changes are of bundle branch block (BBB). In the intensive care setting, the diagnosis of BBB on the ECG does not by itself usually indicate that any specific action is necessary, although the development of new BBB should alert the physician to the possibility of myocardial infarction.

Right bundle branch block (RBBB)


Due to delayed depolarisation of the right ventricular free wall: QRS duration >0.12 seconds Secondary positive lead in V1 (rsR) Deep slurred S wave in I, aVL, V4-6 Secondary ST, T changes in V1-V3

See the ECG

Left bundle branch block (LBBB)


Due to depolarisation of free wall of the left ventricle, together with reversal of the direction of septal depolarisation: QRS duration >0.12 seconds

Absence of septal Q waves in I aVL and V4-V6 Absence of secondary R in V1 See the ECG

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 Examples of AV block and BBB ECGs can be found on the following website:

Cases for special consideration


Certain conditions in the ICU merit special consideration when considering bradyarrhythmias.

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. This complication carries significant risk of abrupt develop-ment of high-grade block. Immediate temporary pacing wire insertion is indicated, together with discussion with a cardiologist and cardiac surgeon.

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. We have now covered the main bradycardias found in the ICU setting. In the next two chapters we will discuss diagnosis of tachycardias (supraventricular and ventricular).

5/ Managing the patient with supraventricular tachycardias


This section will deal exclusively with tachyarrhythmias arising above the AV node. By definition, the heart rate is >100 bpm for all causes, although in the critically ill, rates around and above 100 bpm are common, and may be entirely appropriate. All supraventricular tachycardias may be caused and/or exacerbated by inotropic agents. If possible, concomitant with treating the arrhythmia, proarrhythmic drugs should be reduced.

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).

Sinus tachycardia
The ECG will show normal P waves, normal QRS complexes (in the absence of BBB) with a constant PR interval between each beat.

Causes
Sinus tachycardia in the ICU-patient/physician/both? Consider those that are associated with an increase in sympathetic activity, or catecholamine drive: -agonists (such as inotropes, salbutamol, aminophylline) Pain and anxiety Hypovolaemia, left ventricular dysfunction, or any cause of reduced cardiac output Sepsis or other vasodilation, causing a reflex chronotropic response Anaemia Fever Thyrotoxicosis

Management
Correct the underlying cause Rarely, if ever, are small doses of -blocker indicated Ensure that the diagnosis is not paroxysmal atrial tachycardia (see the next screen) In a patient with severe left ventricular diastolic dysfunction and poor cardiac output, a tachycardia (even if only moderate) may significantly impair ventricular filling. Consider cautious !!! use of short-acting -blocking agents. What form of monitoring might be useful in this situation? Transoesophageal cardiography (TOE) can be a useful monitoring precaution

Paroxysmal atrial tachycardia


The terminology used here is different from that commonly used in the US, in which the term paroxysmal SVT is preferred to PAT. Paroxysmal SVTs are divided into those arising from an automatic focus and those resulting from reentry. 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. This arrhythmia ECG occurs when a site of atrial automaticity is discharging (an 'ectopic atrial focus'). Sudden abrupt rises in heart rate are seen, and P wave morphology or axis may change. If the P wave morphology is changing, the tachycardia is known as multifocal atrial tachycardia (MAT).

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 -blockers are effective. Note, however, that since chronic obstructive pulmonary disease is a common cause of MAT, -blockers may not be the best choice. In all cases, stop digoxin and treat toxicity if necessary.

Atrial flutter
Consider in any patient where the heart rate is a division of 300, and constant. Diagnosis is made on the characteristic 'saw-tooth' (not always) flutter waves on the 12-lead ECG. Not every impulse will be conducted. If every second impulse is conducted, then a heart rate of 150 bpm will be seen. If every third is conducted, then a heart rate of 100 results. Blockade may be variable, thus mimicking atrial fibrillation. See the ECG.

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). Design a clinical flow chart for the treatment of patients with persistent atrial flutter.

Atrial fibrillation
Diagnosis
If the atrial activity is chaotic, then atrial fibrillation is said to be present. The AVN is bombarded with erratic electrical activity, and impulses are intermittently conducted. An 'irregularly irregular' heart rhythm results: you cannot tell when a beat is coming next. The onset of AF commonly causes hypotension Why may atrial fibrillation cause haemodynamic deterioration? Because of loss of atrial systole and the decrease in diastolic filling time with a rapid heart rate.

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

Electrical cardioversion
DC cardioversion is safe and effective The natural history of AF in ICU, in a large proportion of cases, is spontaneous

reversion to SR. Cardioversion is often unsuccessful unless the underlying cause is corrected. You can find further information in the following references:

Peuhkurinen K, Niemela M, Ylitalo A, Linnaluoto M, Lilja M, Juvonen J. Effectiveness of

amiodarone as a single oral dose for recent-onset atrial fibrillation. Am J Cardiol 2000; 85 (4): 462-465. PMID 10728951 Donovan KD, Power BM, Hockings BE, Dobb GJ, Lee KY. Intravenous flecainide versus amiodarone for recent-onset atrial fibrillation. Am J Cardiol 1995; 75 (10): 693-697. PMID 7900662 Consideration must also be given to anticoagulation - international normalised ratio (INR) 2.03.0 (risk of embolisation with cardioversion >48 hours AF 5.5% with no anticoagulation, <1% with anticoagulation for 3 weeks). Transoesophageal echocardiography (TOE) (to exclude thrombus in the atrial appendage) may be useful. If cardioversion fails, amiodarone success. (300 mg/30 min) may increase the likelihood of

Chemical cardioversion
Clinical trials (but note, NOT in the ICU population) have demonstrated increased success rate of transthoracic electrical cardioversion for AF with ibutilide channel blocker), but note the increased risk of torsade de pointes. (class III potassium

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.

Rate control
To achieve rate control in atrial fibrillation acutely, digoxin and is not the drug of choice. Intravenous -blockers or verapamil rate response, but are negatively inotropic. In the non-ICU population, digoxin has the slowest onset of action

(0.075 mg/kg as a slow push) provide rapid

together with atenolol has been shown to be

effective in controlling ventricular response rate in AF. Amiodarone population. is also rapidly effective in control of ventricular response rate of AF in the ICU

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).

Are there any situations when verapamil

should never be given?

Verapamil should never be used with a -blocker, or if an accessory pathway is known or suspected.

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. Prevention is better than cure but how to prevent? 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. For data regarding the use of -blockers and sotolol in this context read:

Ibutilide fumarate CLASS Antiarrhythmic INDICATIONS Arrhythmias / Atrial fibrillation INTERACTIONS Not evaluated DOSE If patient weight >60 kg: 1 mg IV over 10 min; administer second dose if arrhythmia fails to terminate within 10 min of completing first dose If patient weight <60 kg: 0.01 mg/kg over 10 min Repeat prn as before MONITORING Continuous ECG monitoring for 4h following infusion or until OTC has returned to baseline ADVERSE EVENTS Sustained ventricular tachycardia (0.2-1.7%), non-sustained ventricular tachycardia (2.7-4.9%),

PVC or PAC2, (0.9-3.6%), hypotension (2%), bundle branch block (1.9%), AV block (1.5%), bradycardia, QT prolongation, hypertension (1.2%), nausea (>1%), palpitations (1%), CHF (0.5%), renal failure (0.3%) CONTRAINDICATIONS Hypersensitivity to ibutilide Atropine CLASS Antimuscarinic or muscarinic cholinergic blocking agent INDICATIONS Treatment of bradycardia, when it is accompanied by haemodynamic compromise or ventricular ectopy INTERACTIONS None DOSE 0.02 mg/kg May be repeated in 5 min up to 1 mg in a child and 2 mg in an adolescent/adult ADVERSE EFFECTS Dryness of mouth Inhibition of sweating In intoxication: Skin flushed, hot, dry and scarlet, blurring of near vision, restlessness and fatigue, difficulty in swallowing, hallucinations and delirium, coma CONTRAINDICATIONS Glaucoma

Junctional tachycardias 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 If the PSVT recurs, then verapamil may both slow the rhythm, or cardiovert it. is effective at terminating the rhythm and preventing

recurrence. Flecainide , -blockers, and sotalol are also effective.

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).

Treatment
Carotid sinus massage or adenosine may both slow the rhythm, or cardiovert it. Verapamil diltiazem or a -blocker are also effective. Digoxin ,

should not be given in the WPW syndrome because it may shorten the refractory may accelerate

period of the AP as well as the atrium. Such a caution is necessary because verapamil the ventricular rate during atrial fibrillation in a WPW syndrome.

6/ Managing the patient with ventricular tachycardias


Inotropes complicate management of VT As with all tachycardias, the ECG diagnosis and subsequent action taken, must take into account the clinical context. Any underlying or exacerbating factors must be addressed, and successful treatment of the tachycardia is more likely in the absence of high-dose inotropes.

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

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 Do not panic when confronted with a broad QRS tachycardia. Try to obtain a 12-lead ECG. If the patient is haemodynamically compromised with a broad complex tachycardia, it is safer to assume VT, and treat with cardioversion.

Find out whether there is agreement in your unit concerning the above approach to broad QRS tachycardia. If not, what alternative approaches are suggested? 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. The history of MI prevails over ECG criteria in the differential diagnosis and strongly suggests ventricular tachycardia.

Diagnosis
VT or SVT? That is the question

QRS configuration? Variation of RR interval is typically seen in SVTs, but minor variation (up to 20 ms) may also occur in VT

A negative praecordial pattern is always a VT.

Management Non-sustained VT
Always address exacerbating factors together 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).

American Heart Association; American College of Cardiology; North American Society for Pacing

and Electrophysiology 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices: http://circ.ahajournals.org/cgi/content/full/106/16/2145

Sustained VT
In the uncompromised and awake patient, consider intravenous lignocaine as first line drug (effective in around 24-40% only). If lignocaine fails, proceed rapidly to DC cardioversion. In sustained monomorphic VT, in the

absence of myocardial ischaemia or infarction procainamide is the treatment of choice (80% success rate for cardioversion, vs lignocaine 20%). In sustained polymorphic VT 24-48 hours post-infarction, and in the context of myocardial ischaemia, intravenous lignocaine is the treatment of choice.

Gorgels AP, van den Dool A, Hofs A, Mulleneers R, Smeets JL, Vos MA, et al. Comparison of

procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia. Am J Cardiol 1996; 78 (1): 43-46. PMID 8712116

Refractory ventricular tachycardia and fibrillation


Refractory polymorphic VT and VF may occur in the context of myocardial ischaemia, myocardial infarction and following coronary artery bypass grafting. These may be refractory to intravenous lignocaine, therefore consider: Overdrive or underdrive pacing Intra-aortic balloon counterpulsion Intravenous amiodarone Intravenous bretylium Coronary revascularisation Intubation Cardiac assist device

In the presence of significant left ventricular dysfunction this group of patients has a very poor outlook, and no intervention may be appropriate. Any patient who develops VT or VF >48h after myocardial infarction in the absence of ongoing myocardial ischaemia is at high risk for malignant arrhythmias and should be referred for cardiological assessment.

Consult with your cardiological colleagues as to what they would consider if confronted with such a referrral.

Drugs given for the treatment of supraventricular tachycardia may be dangerous in a patient with ventricular tachycardia. When in doubt about the origin of the tachycardia, do not use verapamil

; use procainamide IV verapamil

or lidocaine

instead. Severe haemodynamic deterioration will occur when

is administrated during ventricular tachycardia.

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

Consider cardiological referral in such patients 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) 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% 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.

Josephson ME, Callans DJ, Buxton AE. The role of the implantable cardioverter-defibrillator for

prevention of sudden cardiac death. Ann Intern Med 2000; 133 (11): 901-910. PMID 11103061

Catheter ablation for VT


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.

Torsade de pointes
Unpredictable and lethal 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

What would be examples of relevant antibiotics and toxins as listed above? Antibiotics (e.g. macrolides), toxins (e.g. arsenic poisoning).

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).

Conclusion

We have now covered the diagnosis, assessment and management of the major arrhythmias found in the intensive care unit. We strongly believe that a systematic and informed approach to the 12-lead electrocardiogram contributes to better outcome for many of our patients. The correct diagnosis of the underlying cause is the first step to optimal treatment. From time to time the development of arrhythmias may lead to the need for implementation of resuscitation following cardiac arrest. The following guidelines are valuable resources for necessary emergency skills.

Patient challenges
A 32-year-old male patient is transferred from the Emergency Department in your hospital to the Cardiac Intensive Care Unit suffering from wide complex tachycardia and dyspnoea. The patient, a well-trained sportsman, was well until one month earlier when he presented to his GP with progressive exertional dyspnoea and fatigue, accompanied by a feeling of heaviness in the limbs and the right upper quadrant. There was no history of chest pain. On the day of admission he awoke with a 'racing' heart, profuse sweating, nausea, vomiting and dyspnoea at rest.

On admission the patient's core temperature is 36.8C, pulse rate estimated at >150 bpm (pulse deficit detected), respiratory rate 26 breaths per minute and arterial blood pressure 106/82 mmHg. Arterial oxygen saturation is 100 percent with supplementary oxygen by mask. On examination the patient is pale and sweaty. The jugular venous pressure is 14 cm H2O. Rales are heard at both lung bases. The heart sounds appear normal but rapid. A wide complex tachycardia ECG with a ventricular rate of 160 bpm is evident on the 5 lead monitoring record of the Emergency Department. Diagnosis of rhythm disturbances ECG diagnosis of VT

Wellens HJJ, Conover MB. : The ECG in emergency decision making. WB Saunders; 1992. Chapter

What immediate actions should be taken when confronted with this patient suffering a regular broad QRS tachycardia? First, a 12-lead ECG must be obtained. Having performed a 12-lead ECG you note a

regular wide complex tachycardia with a left bundle-branch-configuration at a rate of 162 bpm (figure on the next screen). The next task now is to differentiate between ventricular tachycardia and supraventricular tachycardia with aberrant conduction (Bundle Branch Block). The emergency response to broad QRS tachycardia demands a calm, informed, and systematic approach. Certain morphological findings on this standard ECG can quickly and accurately pinpoint ventricular tachycardia. The figure shows the 12-lead ECG of this patient at admission. A further standard cardiological investigation will be helpful

Supposing a 12-lead ECG machine is not available at the time of this patient's arrival in the department and the ECG recording system in use does not have the capability of recording simultaneous leads, which leads would you consider to be of particular interest? For the diagnosis of ventricular tachycardia it is absolutely necessary to record at least V1; in many cases recordings of V2 and V6 are also necessary. If lead V1 does not conclusively demonstrate ventricular tachycardia: a) in the V1-positive configuration, lead V6 is needed; b) in the V1- negative configuration, leads V2 and V6 are needed. Leads I and II are useful for axis determination and P wave detection.

The poor haemodynamic status of this patient on admission to the Cardiac ICU prompts the attending physician to resort to immediate cardioversion. Measurement of arterial blood gases and serum electrolytes is performed by the bedside. Electrolyte disturbance is excluded. Simple rules in the treatment of arrhythmias

A trainee colleague from the department of Emergency Medicine follows with interest these activities in the department of Cardiac Intensive Care and asks you how to proceed when confronted with a patient suffering from a broad QRS tachycardia in an out-of-hospital situation. Your advice is that if the patient is haemodynamically unstable, cardiovert. If stable, determine the type of tachycardia by obtaining a history to establish the absence or presence of heart disease, doing a physical examination and by systematic evaluation of the 12-lead ECG. Careful clinical assessment of the patient in this manner will help you to differentiate between a supraventricular and a ventricular tachycardia. Intravenous verapamil will only be considered in the treatment of broad QRS tachycardia when the diagnosis of supraventricular tachycardia is 100% certain. When ventricular tachycardia is the diagnosis either procainamide or lidocaine the antiarrhythmic drug of choice. If medical therapy is unsuccessful, cardiovert. is

Careful history taking is mandatory when confronted with a wide QRS tachycardia (1) Careful history (2) Assessment of heart rhythm Clinical signs of AV dissociation (1) Clinical signs of AV dissociation (2) Management of SVT Management of VT

The presence of regular independent P waves cannot clearly be demonstrated on the 12lead ECG recording in your patient. Indeed, P wave identification is not always possible on the standard ECG recordings. How can we 'unmask' P waves 'hidden' after or within the QRS complex? In this situation intravenous adenosine can be useful to differentiate ventricular from supraventricular tachycardia with aberrant ventricular conduction. Presence/absence of P waves Diagnosis of supraventricular tachycardia

At the time of admission an echocardiogram on your patient showed a dilated, diffuse hypo- to

akinetic left ventricle (ejection fraction 20-25%) with a moderate to severe mitral valve insufficiency (see video on the next screen). Further investigation could not elucidate the cause of his cardiomyopathy and a coronary angiogram showed absence of marked coronary artery disease. The patient suffered recurrent episodes of sustained monomorphic VT despite chronic antiarrhythmic drug therapy (amiodarone ). An ICD was implanted one month later. Chronic treatment with ace-inhibitors, anticoagulants, loop-diuretics and canrenol was maintained. The patient remained stable until six months later when he was readmitted after he experienced multiple shocks. The patient suffers from concomitant acute laryngotracheobronchitis with core temperature <40C. Refresh your Echo interpretative skills - see PACT module on Haemodynamic monitoring

Implantable cardioverter defibrillator

What is the immediate course of action when confronted with electrical instability in your patient with an implantable cardioverter defibrillator. The sudden occurrence of multiple shocks requires immediate evaluation and hospitalisation of your patient. The differential diagnosis of multiple shocks in this case includes: recurrent ventricular arrhythmias, supraventricular arrhythmias, or ICD/lead malfunction. Revision of the ICD in the electrophysiology laboratory, however, cannot identify/prevent any system failure. Antitachycardia pacing function and VT detection criteria are considered appropriate.

Simple rules in the management of arrhythmias There are important ICD inter-actions with antiarrhythmic drugs that must be recognised by physicians who care for these patients Implantable cardioverter defibrillator

Given all shocks of the ICD were adequate what is the next priority? Is there any place for changing or initiating (additional) antiarrhythmic drugs in this patient? All correctable abnormalities (electrolyte imbalance, fever etc.) are tackled. Lidocaine is given by continuous intravenous infusion. Additional -blockade is not appropriate because of the haemodynamically poor condition of your patient. Simple rules in the treatment of arrhythmias Refractory VT

Dijkman B, den Dulk K, Wellens HJ. Management of electrical instability after ICD implantation.

Update in Nonpulmonary Critical Care. Pacing Clin Electrophysiol 1995; 18: 148-151. PMID 7724389

What are the appropriate plasma concentrations for lidocaine Appropriate drug levels of lidocaine 1.5-5 g/ml (6.4-21 mol/l).

in patients with electrical instability are

Despite this treatment the ventricular electrical storm cannot be controlled. Your patient needs to be sedated and ventilated. An intra-aortic balloon pump and Swan-Ganz catheter are put in place. The

patient is put on the waiting list for urgent heart transplant.

On reflection, the clinical course of this patient was complicated and involved progressively more sophisticated treatment.

From this account and your study of the topic what conclusions have you reached as to the role of the intensive care physician in potentially life threatening arrhythmias? You will have appreciated that interpretation of electrocardiographic findings must always be made in light of your patient's history and clinical condition. The importance of knowing when to act quickly and when to seek specialist opinion will also have been clear. Finally, when conservative measures finally fail, life support measures may be required to sustain the patient until heart transplant can be effected.

Q1. Regarding anti-arrhythmic drugs:

Your answers A. Calcium channel blockers prolong atrioventricular node refractoriness. The correct answer is : True B. Verapamil should not be used in Wolff-Parkinson-White syndrome. The correct answer is : True - it may shorten the refractoriness of the accessory pathway and increase the ventricular response rate. C. Phenytoin is useful in treating digitalis toxicity because it enhances nodal conduction. The correct answer is : True D. Amiodarone is a -blocker. The correct answer is : True - it is also a -blocker. E. Bretylium magnifies the effects of exogenous catecholamines but reduces the effects of indirect sympathomimetics. The correct answer is : True - this is because it depletes terminals and blocks reuptake Your total score is 0/5

Q2. A patient with a temporary transvenous pacemaker suddenly loses consciousness. ECG shows continuous pacing spikes but without capture. The heart rate is 40 beats.min-1
Your answers A. A likely cause is the displacement of the pacemaker electrode from the myocardium. The correct answer is : True B. Atropine or isoprenaline can be given in an attempt to increase the heart rate as an immediate, short-term measure. The correct answer is : True - these may not be effective, though.

C. The stimulating electrode should be advanced until there is capture. The correct answer is : True D. Cardioversion should be attempted if other measures fail. The correct answer is : False - cardioversion is not indicated, as this will not increase the rate. E. An external pacemaker is of no use in this situation. The correct answer is : False - an external pacer should be used if other measures fail to improve the heart rate. Your total score is 0/5

Q3. In atrial flutter


Your answers A. The atrial rate is commonly 230 bpm The correct answer is : False - when a conduction ratio of 2:1 or 3:1 exists, the ventricular rate becomes approximately 150 or 100 (atrial rate is classically 300 bpm). B. Digoxin often converts the rhythm to atrial fibrillation The correct answer is : True C. The heart is usually otherwise normal The correct answer is : False - atrial flutter is nearly always associated with organic heart disease. D. Carotid sinus massage usually slows the AV conduction The correct answer is : True - adenosine, verapamil or carotid sinus massage will temporarily block AV conduction and reveal the characteristic sawtooth atrial wave on the ECG.

E. The radial pulse is usually regular or regular irregular The correct answer is : True Your total score is 0/5

Q4. In a patient with broad complex tachycardia


Your answers A. Presence of any Q wave in V6 in LBBB pattern tachycardia is strongly suggestive of ventricular tachycardia. The correct answer is : True - qR pattern in V6 suggest VT. B. P waves just after every QRS complex are diagnostic of ventricular tachycardia. The correct answer is : False - AV dissociation (seen in ~ 25%) is suggestive of VT. C. Variation of the tachycardia cycle length by >10 ms between adjacent beats usually excludes ventricular tachycardia. The correct answer is : False - variation of RR interval is typically seen in SVTs, but minor variation (up to 20 ms) may also occur in VT. D. In a RBBB pattern tachycardia, if the QRS width is >140msec, it is likely to be ventricular. The correct answer is : True E. If no pre-excitation is seen on ECG during sinus rhythm, then it is not an atrioventricular re-entrant tachycardia. The correct answer is : False - absence of pre-excitation in sinus rhythm does not exclude atrioventricular re-entry tachycardia ('hidden' accessory pathway). Your total score is 0/5

Q5. Digoxin toxicity may cause


Your answers A. Prolongation of the PR interval

The correct answer is : True - most common toxic effects are sinus bradycardia, atrial tachycardia with block, AV block, ventricular bigeminy and VT. B. Prolongation of the QT interval The correct answer is : False - at therapeutic levels digoxin causes ST depression, reduction in size of the T wave and shortening of the QT interval. C. Diarrhoea The correct answer is : True - GI symptoms are nausea, vomiting, abdominal pain and diarrhoea. D. Photophobia The correct answer is : False - visual effects are xanthopsia, halo and visual blurring.

E. Blurred vision The correct answer is : True - visual effects are xanthopsia, halo and visual blurring. Your total score is 0/5