LIFE-THREATENING CARDIAC ARRYTHMIAS Raluca Tat, Adela Golea

Educational objectives What you need to know  What is a life-threatening arrhythmia  How life-threatening arrhythmias are classified  What are the signs/symptoms of hemodynamic instability  What are the therapeutic options  What are the indications of synchronized electrical cardioversion  What are the indications of cardiac pacing  What are the main indications of antiarrhythmic drugs used in the management patients with arrhythmia  What is the antiarrhythmic dosing recommended for the management of patients with arrhythmia

What you need to do  Identify arrhythmia  Identify patients with instability signs/symptoms  Choose the appropriate therapeutic option for treating arrhythmia in accordance with the clinical status of the patient and the type of identified arrhythmia

Definition Cardiac arrhythmia is a disturbance of the heart rate which may affect the frequency (the alteration of the succession of heartbeats), the regularity of cardiac frequency (the alteration of the ratio between atrial and ventricular rhythms) or both. These changes occur due to a disturbance of myocardial automatism, excitability and contractility, as the heart (body) is subjected to a wide range of pathological (stress) events, such as ischemia, hypoxia, acidosis, electrolyte imbalances, excessive intake of catecholamines, toxic substances etc.

Classification:  according to origin: sinus, atrial, junctional and ventricular  

Treatment principles  The initial assessment and treatment ABCDE principle o o o o o o – o Figure 1.

Figure 2. o

 Antiarrhythmic slower less reliable electrical cardioversion life-threatening tachyarrhythmia hemodynamic instability  Signs / Symptoms of hemodynamic instability: o Shock – o Syncope – o Acute heart failure – o Acute myocardial ischemia – cause angina (chest pain) or may only lead to isolated changes of the T waveform (sometimes linked to ST segment elevation myocardial infarction), highlighted by 12-lead ECG (silent ischemic lesion or acute coronary syndrome). In case of an underlying coronary or structural heart disease, myocardial ischemia increases the likeliness of severe complications, including heart arrest.  Therapeutic options: Once the rhythm has been assessed and the presence/absence of signs/symptoms of hemodynamic instability have been established, the immediate treatment options are: o electrical therapy (cardioversion, pacing) o medication therapy (antiarrhythmics and other drugs)

I. Tachyarrhythmias 1. Hemodynamically unstable patient If the patient is hemodynamically unstable (showing any sign/symptom of hemodynamic instability caused by cardiac arrhythmia) and the clinical condition deteriorates, the first treatment choice is synchronized electrical cardioversion. In patients with no cardiovascular conditions in their medical history, instability signs and symptoms are not present at a ventricular rate < 150 beats/minute. Conversely, patients with comorbidities and cardiac dysfunction may be symptomatic and hemodynamically unstable at lower heart rates. If conversion fails to restore normal heart rate and the patient is still unstable, 300 mg IV may be given over 10-20 minutes and electrical cardioversion may be repeated if the arrythmia persists. The initial bolus of amiodarone may be followed by a loading dose of 900 mg of amiodarone within the first 24 hours. Repeated electrical cardioversion attempts are not indicated in recurrent atrial fibrillation paroxysmal episodes. These are mostly recommended for critical patients with arrhythmia exacerbation factors, such as sepsis and metabolic dysfunctions. In the mean time, it should be mentioned that electrical cardioversion therapy does not prevent recurrence of arhythmias. If arrhythmia recurrence periods do occur, these are treated with antiarrhythmia medication. Synchronized electrical cardioversion Electrical cardioversion is used for the conversion of atrial or ventricular tachyarrhythmias with pulse. The administered shock is synchronized with the R waveform on the ECG, and not with the T waveform (thus avoiding the relative refractory period and minimizing the risk of inducing ventricular fibrillation). Patients in an aware state require analgesia and sedation prior to the performance of syncrhonized cardioversion. In case of wide complex tachycardia (Figure 3) and atrial fibrillation (AFib, Figure 4), cardioversion is initiated with a 120-150 J biphasic energy. If the initial attempt fails, the energy is increased gradually for the next shocks. Atrial flutter (Figure 5) and paroxysmal supraventricular tachycardia (PSVT, Figure 6) are usually converted at lower energy levels, starting with biphasic 70-120 J.

Figure 3. Ventricular tachycardia: wide QRS tachycardia

Figure 4. Atrial fibrillation: irregular beat, no P waveform, with F waveform

Figure 5. Atrial fibrillation: regular beat, no P waveform, with waveform

Figure 6. Supraventricular tachycardia: tachycardia rate, QRS complexes 2. Hemodynamically stable patient – –

a. Wide QRS tachycardia

 Wide QRS tachycardia with regular rhythm infusion of 900 mg over 24 hours. Expert advice should be sought before considering the use of alternative antiarrhythmic medication such as , or (class III ).

 Wide QRS complex tachycardia with iregular rhythm A wide complex tachycardia with irregular rhythm is most likely to be an AFib with bundle branch block, but can also be an AFib with ventricular pre-excitation (WPW syndrome - Wolff- Parkinson-White). In this case, there is a wider variation in the shape and width of the QRS complex than in the case of AFib with bundle branch block. Another possible cause is polymorphic TP (torsade de pointes). The treatment of AFib with bundle branch block is identical to the narrow complex AFib. If AFib/atrial flutter with pre-excitation mechanism is suspected, avoid , , or (blocking of AV node causes a rapid ventricular response, which may lead to severe tachycardia). In this case, syncronized electrical cardioversion is preferred. The immediate treatment of torsade de pointes consists of ceasing all known medication causing the extension of the QT interval, correcting electrolyte imbalances, especially hypokalaemia, IV magnesium sulphate 2 g administered over 10 minutes and expert cardiologic check up (including potential pacing overdrive). If the patient's status is getting worse (as it often happens), treatment consists of synchronized electrical cardioversion or immediate defibrillation. If loss of consciousness and of central pulse occurs, the ACLS algorithm is applied.

a. Narrow QRS complex tachycardia The first step in approaching a narrow complex tachycardia consists of establishing whether the rhythm is regular or irregular. Regular narrow complex tachycardias:  sinus tachycardia  AV nodal reentrant tachycardia (the most common SVT)  AV reentrant tachycardia, associated with WPW syndrome  atrial flutter with regular AV conduction (often 2:1). Irregular narrow complex tachycardias:  AFib   Narrow QRS, regular tachycardia o Sinus tachycardia – o AV nodal reentrant tachycardia – PSVT o AV reentrant tachycardia – o Atrial flutter with regular conduction –

The treatment of narrow complex, regular tachycardia o . carotid bruit in order to avoid rupturing an atherosclerotic plaque and a subsequent cerebral embolism (stroke). . the Valsalva manoeuvre (forced exhalation against a closed airway) . A 12-lead ECG monitoring is recommended during each of the aforementioned manoeuvres. o If the arrhythmia persists and is not atrial flutter, quickly dose 6 mg of adenosine; a subsequent 12 mg bolus dose can be given, followed by another 12 mg if arrhythmia conversion is not achieved. o The successful stopping of the tachyarrhythmia through vagal manoeuvres and adenosine medication indicates that the arrhythmia is most probably a reentrant circuit tachicardia. The patient should be monitored in case of a recurrent arrhythmia or the occurrence of another rhythm disorder. Recurrences should be treated with adenosine or extended release drugs with AV node blocking action (e.g. diltiazem, verapamil). o If adenosine is contraindicated or fails to restore sinus rhythm in a narrow complex, regular tachycardia, and no atrial flutter is demonstrated, use calcium channel blockers (e.g. verapamil or diltiazem).

 Narrow QRS irregular tachycardia Narrow complex arrhythmia with irregular rhythm is most likely an atrial fibrillation with an uncontrolled ventricular response or an atrial flutter with variable conduction. If the patient is hemodynamically unstable as a result of arrhythmia, synchronized cardioversion should be performed as soon as possible. If no instability signs are present, therapeutic options include: o dug controlled cardiac frequency o rhythm control through drug-induced cardioversion o rhythm control through electrical cardioversion o specific complication prevention treatments (e.g. anticoagulants) Expert advice should be sought as soon as possible. The more the patient is in AFib, the higher the risk to develop clots in the atrium. In general, patients in AFib > 48 years should not undergo drug-induced or electrical cardioversion before being subjected to efficient anticoagulation or before the presence of an atrial clot has been excluded through transesophageal echocardiogram. If the duration of the arrhythmia cannot be determined or if the clinical status of the patient requires cardioversion, the decision upon the anticoagulant to be used as well as on the duration of the treatment should be made together with the specialized cardiologist. Beta-blockers and diltiazem may be used for attempting to maintain control of the frequency. Digoxin and amiodarone may be used in patients with cardiac failure. If the duration of AFib is > 48 hours, the control of cardiac rhythm may be achieved through drug-induced cardioversion, using , or . Although amiodarone may also be used, it is less efficient (300 mg IV bolus over 20-60 min, followed by 900 mg over 24 hours). Special care should be given to patients with atrial fibrillation with known or discovered ventricular preexcitation - WPW syndrome and to those with atrial flutter. The use of adenosine, diltiazem, verapamil and digoxin should be avoided since these drugs block the AV node and lead to the relative increase of pre-excitation. Assess patient in accordance with ABCDE principle Administer O2 and obtain quick IV access Monitor rhythm, AT, SpO2, 12-lead ECG Syncrhonized external electrical shock The energy depends Assess hemodynamic instability signs on the QRS size and Unstabl rhythm e 1. Shock 3. Myocardial Up to 3 attempts ischemia Analgosedation or Stable

300 mg IV Narrow QRS complex (< 0.12 sec)? Amiodarone over 10- 20 min with repeated electrical shock if Wide required, followed by: Narro 900 mg Amiodarone w over 24 hours Wide QRS Narrow QRS QRS is regular? Rhythm is regular?

Regular Irregular Irregular Regular

Irregular narrow complex tachycardia Use vagal manoeuvres Probably AF Adenosine 6 mg IV Frequency control with: Specialized quick bolus, in case of check-up Beta-blockers/Diltiazem failure, increase to 12 Digoxin/Amiodarone in mg case of heart failure signs Continuous ECG ! Anticoagulants if monitoring arrhythmia lasts > 48 hours

Normal Specialized NO rhythm check-up

YES ! Possibilities If TP include: (or rhythm uncertain): AF with bundle 300 mg IV Amiodarone branch block Over 20-60 minutes, Probably PSVT treat like narrow then 900 mg over 24 reentrant circuit QRS hours tachycardia: Polymorphic TP If SVT with bundle ECG record in sinus (e.g. Torsade de branch block is rhythm Possible Atrial pointes - give previously confirmed: If arrhythmia flutter Magnesium Give Adenosine like in reoccurs, give Control 2 g over 10 min) the case of ventricular Adenosine again and frequency (e.g. tachycardia with narrow consider beta-blockers) and regular QRS antiarrhythmic

Figure 7. The algorithm of pulse tachycardia II. Bradyarrhythmias A cardiac frequency of less than 60 beats per minute is considered to be a bradycardia. The nature of bradycardia causes may be: a) cardiac (e.g. myocardial infarction, myocardial ischemia, sick sinus syndrome); b) non-cardiac (vasovagal response, hypothermia, hypoglycaemia, hypothyroidism, increased intracranial pressure); c) medicine induced toxicity (e.g. digoxin, beta-blockers, calcium channel blockers). Bradycardias are caused by the decreased stimulation of the sinoatrial node or by the failure of the atrioventricular conduction system (AV blocks). The decrease in the sinoatrial node stimulation occurs with sinus bradycardia (caused by the increased vagal tone), sinus arrest and sick sinus syndrome (sinus node dysfunction, Figure 8),

Figure 8. Sinus bradycardia: 50 rpm rhythm, P wave highlighted Atrioventricular blocks are classified as first degree, second degree and third degree blocks and may be caused by medication, electrolyte disturbances or may be secondary to structural changes in myocardial infarction or myocarditis. The first degree AV block is defined as the prolongation of the P-R interval (> 20 s) and is usually benign (fig. 7).

Figure 9. First degree AV block The second degree AV block is subclassified as Mobitz type I and II; a) In Mobitz I second degree AV block (Figure 10), the conduction is blocked at the AV node, the block is usually transient and may be non-symptomatic. b) In Mobitz II second degree AV block (Figure 11), the block most commonly occurs under the AV node, in the bundle of Hiss or in the Hiss bundle branches (right or left), it is often non-symptomatic and may lead to complete AV block (Figure 12). Figure 10. Mobitz I second degree AV block: the PR interval increases up to the point where a P wave is not followed by a QRS complex

Figure 11. Mobitz II second degree AV block: every second P wave is followed by a QRS complex (Mobitz II second degree intermitent AVB) The third degree AV block is defined as an atrioventricular dissociation which may be permanent or transient, depending on the triggering cause.

Figure 12. Third degree (complete) AV block: the P waves and QRS have different periodicities (complete atrioventricular dissociation)

1. Initial assessment The bradycardia patient shall be assessed according to the ABCDE principle, considering the potential causes of the bradycardia, as well as the identification of signs/symptoms of hemodynamic instability. Treat any identified reversible cause during initial assessment and if hemodynamic instability signs are present, start treatment. Medication is the first treatment option; pacing should be considered only for patients who fail to respond to medication or for patients with asystole risk factors.

2. Medication If there are signs/symptoms of hemodynamic instability, give 0.5 mg IV - dosing may be repeated every 3-5 minutes if the arrhythmia persists for up to 3 mg (complete vagolytic dose). Atropine doses smaller than 0.5 mg may have a paradoxical effect of lowering the ventricular frequency. Precaution should be taken when using atropine in case of acute coronary ischemia or myocardial infarction (the increase of the cardiac frequency may aggravate ischemia or may increase the infarction area). If atropine treatment is not effective, second line drugs should be considered: isoprenaline 5µg/min, initial dose, adrenaline 2-10µg/min or dopamine 2-10µg/kg/min. Theophylline (100-200 mg IV administered slowly) may be considered if bradycardia is caused by an inferior myocardial infarction, in case of cardiac transplant or spine lesion. Consider IV glucagon if potential causes of bradycardia include beta-blocker or calcium overdose. Atropine should not be given to patients with cardiac transplant (due to risk of high AV block or sinus arrest).

3. Percutaneous transthoracic pacing Percutaneous transthoracic pacing should be initiated if the response to atropine is not satisfactory or is less likely to have the expected effect. Pacing may be painful and may fail to produce mechanical capture, which is why the patient requires procedural analgosedation. Assessment of paced patient shall be carried out by watching pacing and mechanical capture, sensing and the evolution of the clinical status by ABCDE reassessment. If atropine is ineffective and pacing is not readily available, one might attempt heart stimulation by applying serial thumps to the lower half of the sternum, at a physiological pace of 50-70 thumps per minute (precordial thump). Immediately seek advice from cardiologist when initiating temporary transvenous pacing, especially if the patient has a history of asystole, Mobitz II second degree AV block, complete AV block (notably in the case of wide QRS, cardiac frequency lower than 40 bpm or ventricular pause > 3s).  Assess patient in accordance with ABCDE principle

 Administer O2 and obtain quick IV access

 Monitor rhythm, AT, SpO2, 12-lead ECG

 Identify and treat reversible causes

Assess presence of hemodynamic instability signs 1. Shock 3. Myocardial ischemia 2. Syncope 4. Cardiac failure

YES NO

Atropine 500 µg IV Asystole risk? Asystole in recent history Satisfactory response? NO Mobitz II second degree AV block NO Complete AV block with wide QRS Ventricular pause> 3s Additional measures 0.5 mg IV Atropine repeated until up to 3 mg IV Isoprenaline 5µg/min IV Adrenaline2-10µg/min NO Alternative medication* Or Transthoracic percutaneous pacing Monitoring

Specialized check-up *Alternative Provisions for transvenous medication: pacing Aminophylline ! Dopamine Glucagon (beta- blocker or overdose) Glycopyrrolate (may Figure 13. The algorithm of bradycardia III. Classification of antiarrhythmic medication. Antiarrhythmic drugs 1. Classification of antiarrhythmic drugs Class I. Sodium channel blocers I.A - increase the duration of action potential: , procainamide, , aprinidine, I.B - decrease the duration of action potential: , , , , moricizine I.C - no influence on the duration of action potential: propafenone, flecainide, , lorcainid, indecainide Class II. Beta-adrenergic blockers (beta-blockers): , , labetalol, , esmelol Class III. Potassium channel blockers: amiodarone, sotalol, tosylate, ibutilide, aimilide, nifekalant Class IV. Calcium channel blockers Other non-classifiable antiarrhythmics: digoxin, adenosine, magnesium sulphate

2. Antiarrhythmic drugs used in critical emergency patients 1. Adenosine - is a natural purine nucleotide. It slows down the transmission through the AV node, but has low effect on other myocardial cells or on the myocardial conduction pathway. It is highly efficient for stopping PSVT with reentrant circuit which includes AV node. In other tachycardias with narrow complexes, Adenosine will reveal the hidden atrial rhythm by slowing down the ventricular response. Due to the very short half-life, of about 10-15s, it is dosed in 6 mg IV boluses, quickly followed by a 10 mL saline infusion and will produce an asystole episode of which the patient should be made aware in order not to panic and breathe normally. The initial effective dose is 6 mg. If this dose does not produce the expected result, up to two more doses of 12 mg each may be given within 1-2 minutes. Patients must be warned of potential transient adverse reactions which may occur, such as nausea, flushing and chest pain. In some European countries, Adenosine is available as adenosine triphosphate. 2. Amiodarone – αβ Give 300 mg of IV amiodarone dissolved in 5% gluccose over 10-60 min (in hemodynamically unstable emergency, over 20 min) depending on the circumstances of arrhythmia onset and hemodynamic stability of the patient. Severe adverse reactions of amiodarone include hypotension and bradycardia, which are reversible upon slowing down the infusion rate. 3. Calcium channel blockers: verapamil and diltiazem – Initial dose of verapamil is 2-5 mg IV, given over 2 min. If the therapeutic response fails to appear, unless adverse reactions occur, repeated doses of 5-10 mg may be given every 15-30 minutes, up to a total of 20 mg. 4. Adrenergic beta-blockers – – α β β – β– ββ – β– 5. Magnesium – (Self-)Assessment form

Identification of life-threatening arrhythmia (brady/tachyarrhythmia) Establishing presence/absence of instability signs: shock, left sided ventricular failure, acute coronary syndrome, syncope Choosing the therapeutic option – electrical/medication-based depending on the highlighted instability signs Describing the chosen therapy: indication, dose, route of administration, adverse reactions