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Tachycardia, sinus tachycardia and tachyarrhythmiasTachycardia is a heart rate >100 beats per minute.
Pathophysiologic mechanisms of tachyarrhythmiasTachyarrhythmias. like all arrhythmias, are caused by disorders of impulse formation or disorders of impulse propagation.
Tachycardias caused by disorders of impulse formation are called focal tachycardias. In focal tachycardias, an ectopic (not the sinus node) site generates impulses, that propagate in the myocardium and overdrive the sinus node. This means that the sinus node undergoes overdrive suppression, which is the inhibition of pacing activity of an area of the myocardium, due to the higher frequency of the electrical impulses originating from another site. The increased frequency of depolarizations of a site in the myocardium by electrical impulses conducted by adjacent cells has the following consequences. If that frequency of depolarization of a myocardial area exceeds its intrinsic pacing rate, that leads to an increase in intracellular sodium ions in this area. This increased sodium stimulates the Na+-K+-ATPase and because this pump is electrogenic it increases the amount of hyperpolarizing currents, driving the membrane potential more negative.This prevents the depolarizing pacemaker currents (If) of the cells from depolarizing the cell membrane to its threshold potential, and thereby prevents the spontaneous generation of action potentials.
On the contrary, in normal sinus rhythm, the sinus node, as the pacemaker with the highest intrinsic rate, exerts overdrive suppression to all other cardiac foci that have a capability of pacemaker function, by the above mechanism.
Disorders of impulse formation causing tachyarrhythmias consist of abnormal automaticity and triggered activity.
Early afterdepolarizations (EADs): Occur during the plateau (phase 2), or repolarization (phase 3) of the action potential and are probably associated with calcium overload. They are associated with prolonged QT and torsades de pointes
Delayed afterdepolarizations (AEDs): Occur after repolarization (phase 3) is complete.They are associated clinically with digoxin toxicity.
Fibrillation is the chaotic, disorganized electrical activation of the muscle. It may involve both abnormal impulse formation and abnormal impulse propagation.
Tachyarrhythmias are classified in:
Supraventricular where the origin of the abnormal rhythm is confined to the atrium (atrial arrhythmias) or the mechanism that generates the arrhythmia is not confined to the atria but includes various supraventricular structures (paroxysmal supraventricular arrhythmias-PSVTs). A better definition is that supraventricular tachyarrhythmias originate from or are dependent on conduction through the atrium, or atrioventricular (AV) node to the ventricle. In supraventricular arrhythmias, the arrhythmia circuit always involves supraventricular tissue and depending on the type of the arrhythmia it may also involve ventricular tissue or not.
Ventricular: The abnormal rhythm originates in ventricular structures (usually ventricular myocardium, but may also originate in the His-Purkinje system). The arrhythmia circuit involves only ventricular tissue.
Symptoms of supraventricular arrhythmia depend on the rate, duration, associated heart disease, and comorbidities and include palpitations (which is the most common presenting symptom), fatigue or diminished exertional capacity, dyspnea, chest pain and rarely syncope. Rarely, a supraventricular arrhythmia can precipitate cardiac arrest in patients with the Wolff-Parkinson-White syndrome, or in patients with severe heart disease, such as hypertrophic cardiomyopathy, or severe aortic valve stenosis.
Most supraventricular tachyarrhythmias produce tachycardia with a narrow QRS complex (QRS duration <120 ms). The presence of a narrow QRS is characteristic of ventricular activation over the physiologic route, the His- Purkinje system.
A nonsustained supraventricular tachycardia is one of brief duration with spontaneous termination.
Paroxysmal supraventricular tachycardia (PSVT):is characterized by episodes of tachycardia that occur with sudden onset and termination. It includes atrioventicular node reentry tachycardia (AVNRT), atrioventricular reentry tachycardia using an accessory pathway (AVRT) and some cases of atrial tachycardia (AT).
Differential Diagnosis for Narrow QRS-Complex Tachycardia
If ventricular activation (QRS) is narrow (less than 120 msec), then the tachycardia is almost always supraventricular. To diagnose its mechanism (the specific type of the tachycardia) one must know the following: If no P waves or evidence of atrial activity is apparent and the RR interval is regular, then the tachycardia is more commonly an atrioventricular nodal reentry tachycardia AVNRT. Sometimes P-wave activity in AVNRT may be only partially hidden within the QRS complex and may deform the QRS to give a pseudo-R wave in lead V1 and/or a pseudo-S wave in inferior leads (II, III,avF).
If a P wave is present in the ST segment and separated from the QRS by 70 ms or more, then the tachycardia is most likely an atrioventricular reentry tachycardia AVRT . Typical AVNRT and AVRT are tachycardias with a short RP (i.e. a short time interval from the QRS to the next P wave: the P wave is nearer to the preceding than the next QRS).
Tachycardias with RP longer than PR (the P waves are near the next QRS complex), are the following : sinus tachycardia, atypical AVNRT, permanent form of junctional reciprocating tachycardia (PJRT, which is a type of AVRT via a slowly conducting accessory pathway, or atrial tachycardia (AT).
Differential Diagnosis for Wide QRS-Complex Tachycardia:
Atrioventricular nodal reentry tachycardia (AVNRT)
In AVNRT there are two functionally different pathways predominantly within the atrioventricular node (AV node). This is termed "dual AV nodal physiology". In order to understand the physiology of reentry one must remember the concept of the refractory period. Once a myocardial cell has an action potential (electrical activation) its sensitivity to further stimulation decreases for a time interval, called the refractory period. The first part of the refractory period, during which complete insensitivity to any stimulus exists, is called the absolute refractory period. The second part of the refractory period, called the relative refractory period, follows the absolute refractory period. During the relative refractory period the cell can be stimulated but a stronger than usual electrical signal is needed to achieve stimulation of the cell and initiation of a new action potential. In AVNRT the two functionally different pathways that exist predominantly within the AV node are the following: There is a pathway with a short refractory period and slow conduction and another pathway with a longer refractory period and fast conduction. In sinus rhythm, the atrial impulse is usually conducted to the ventricles through the fast pathway. If an atrial impulse (an atrial premature beat) occurs early when the fast pathway is still refractory, the impulse is conducted to the ventricles through the slow pathway (since it has a shorter refractory period)
Meanwhile, the fast pathway has the time to recover its excitability and so the electrical impulse travels back through the fast pathway. Then it is conducted again through the slow pathway and this circular movement of the impulse continues. initiating the most common "slow-fast", or typical, AVNRT.
In atrioventricular nodal reentry tachycardia (AVNRT) the ECG shows regular QRS complexes, usually at a rate of 140–240/minute. The QRS complexes are usually narrow but sometimes they have a typical bundle branch block morphology.
In AVNRT P waves are either:
Not visible ("buried" in the QRS complex- this is common) or
seen immediately before the QRS complex (this is rare and is manifested by pseudo-q waves in the inferior leads) or
seen immediately after the QRS complex (this is common and is manifested as pseudo -r wave in V1, and small pseudo-s waves in leads II, III, and avF).
This close proximity of the P wave to the QRS, occurs because the reentrant circuit is in the AV node- in proximity to both the atria and the ventricles- and retrograde atrial activation is usually through the fast pathway. Thus, in AVNRT there is almost simultaneous atrial and ventricular activation.
An exception to the above, is fast-slow or atypical AVNRT (5% of cases), where the electrical stimulus is conducted antegradely, from atria to ventricles, through the fast pathway and retrogradely from the ventricles to the atria through the slow pathway. This causes the P wave to be near the next QRS complex (since conduction from the atria to the ventricles is rapid, through the fast pathway) and away from the previous QRS complex (since conduction from the ventricles to the atria is through the slow pathway). This situation is the opposite of what is happening in the usual (typical) form of AVNRT (which is a tachycardia with a short RP interval). Thus, the atypical fast-slow AVNRT is a supraventricular tachycardia with a short PR and long RP interval, thus mimicking an atrial tachycardia or a permanent junctional reciprocating tachycardia (PJRT).
P wave morphology in AVNRT : In all kinds of AVNRT (typical slow-fast, or atypical fast-slow) the P wave (when it is identifiable) is negative in leads II, III and aVF, and biphasic with a terminal positive component in V1. (These characteristics are opposite of those of the sinus P wave).
|ECG: atrioventricular nodal reentry tachycardia AVNRT (Click on the photo to see it larger )|
Atrioventricular reentry (or atrioventricular reciprocating) tachycardia -AVRT
It is the most common arrhythmia that can occur in Wolff Parkinson White (WPW) syndrome. (The second most common arrhythmia in WPW is atrial fibrillation.) The mechanism of AVRT involves a reentrant circuit that includes the atrioventricular (AV) node and an accessory pathway.
AVRT is classified into orthodromic or antidromic depending on the direction of conduction over the atrioventricular (AV) node.
Orthodromic AV reciprocating tachycardia (Orthothromic AVRT): The antegrade conduction of the electrical impulse (from the atria towards the ventricles) occurs down the AV node and retrograde conduction (from the ventricles to the atria) occurs through the accessory pathway.This is the most common form of AVRT (95%)
Orthodromic AVRT may occur with a manifest or concealed accessory pathway. A manifest accessory pathway is one that has the capability of antegrade conduction (from the atria to the ventricles) and usually these pathways have the capability of retrograde conduction (from the ventricles to the atria) as well. It is called a manifest accessory pathway because in sinus rhythm its presence can be recognized from the ECG findings (short PR interval < 120 msec, a slurring of the initial part of the QRS called delta wave, prolonged QRS and secondary ST-T wave changes. This the ECG pattern of the Wolff-Parkinson -White syndrome).
Tachycardia conducts antegrade down the accessory pathway and retrograde up the AV node, or a second accessory pathway. Antidromic AVRT, since ventricular activation occurs via the accessory pathway and not via the normal conduction system, shows on the ECG broad QRS complexes >120 msec. Thus antidromic AVRT is a wide- complex tachycardia which can be mistaken for a ventricular tachycardia. It is rare (about 5 % of AVRT).
What kind of rhythm is that?
The initial ECG and the ECG after administration of intravenous adenosine is shown
The first ECG shows a regular narrow complex supraventricular tachycardia. P waves cannot be seen . It can be AVNRT or orthodromic AVRT After the administration of adenosine the tachycardia stopped and the second ECG shows sinus rhythm with short PR interval and a delta wave (a slurring at the onset of the QRS) can be seen clearly in some leads. So this is a case of a patient with Wolff Parkinson White syndrome and the tachycardia in a patient with a by-pass tract (accessory pathway) probably was AVRT
THIS CASE IS FROM THE SITE: LIFE IN THE FAST LANE , LINK https://lifeinthefastlane.com/ecg-library/pre-excitation-syndromes/
Acute management of narrow QRS paroxysmal supraventricular tachycardia (AVNRT or AVRT)Acute treatment is guided by the clinical presentation. If the patient is hemodynamically stable (without significant hypotension or symptoms of acute heart failure) termination of the tachycardia is accomplished with vagotonic maneuvers or drugs. In the presence of hypotension with unconsciousness or respiratory distress, QRS-synchronous direct current cardioversion is indicated. Generally this is rarely needed, because intravenous adenosine can terminate the tachycardia promptly in most situations.
Beta blockers, verapamil, or diltiazem can also be given orally (PO) and they can be taken by the patient on an as-needed basis to terminate the tachycardia, or to facilitate tachycardia termination by theValsalva maneuver. PO drugs have a slower onset of action than IV treatment, but it can be an option in stable cases, where the arrhythmia is well tolerated by the patient.
Atrial fibrillation (AF)AF is a supraventricular arrhythmia with uncoordinated atrial activation and as a consequence, there is no effective atrial contraction. ECG) characteristics of AF include:
1) Absolutely irregular R-R intervals (This is the general rule, with an exception in the rare occasion of a patient with AF and a complete atrioventricular block: then the RR intervals will be regular and the heart rate low),
2) Absence of distinct repeating P waves, and
3) Irregular atrial activity (irregular waves of low amplitude are seen between QRS complexes).
The duration of an arrhythmia with the above characteristics on the ECG must be at least 30 seconds in order for the diagnosis of AF to be made (according to the ESC guidelines 2016).
AF is associated with increased risk of stroke, heart failure exacerbation, and all-cause mortality. The mortality rate in patients with AF is about twice that of patients with sinus rhythm. However, in patients with AF the treatment strategy of maintaining sinus rhythm does not decrease mortality in comparison to the treatment strategy of controlling heart rate.
Etiology: AF is most commonly associated with advanced age, hypertension, valvular heart disease, congestive heart failure (CHF), and coronary artery disease (CAD), cardiomyopathy, chronic lung disease, hyperthyroidism, obesity and sleep apnea and cardiac surgery (cardiac surgery is associated with a high risk of postoperative atrial fibrillation). There are also idiopathic cases of AF without any clear underlying etiology. The term lone AF is used to describe cases of AF without evidence of an underlying cardiopulmonary disease.
Pathophysiologically, factors that contribute to the development of Atrial Fibrillation (AF) are the following : Atrial fibrosis, reduced atrial contractility, atrial dilation, pulmonary vein dilation, local conduction heterogeneities within the atrial myocardium and increased sympathetic stimulation. This substrate permits the development of multiple small reentrant circuits in the atria that induce and stabilize the arrhythmia. Recent data support that the mechanism of AF involves both increased automaticity and multiple reentrant wavelets, occurring predominantly in the left atrium around the pulmonary veins.
The RR intervals are completely irregular, there are no distinguishable P waves, only small uneven fluctuations of the baseline. Therefore, it is atrial fibrillation. Also a mild non-specific repolarization disorder is noted (slightly negative T waves and a minimal ST depression) are observed in leads II, aVF, V4-V6) These non specific ST-T changes are not diagnostic for a certain disease and in the setting of a tachyarrhythmia, they cannot even be evaluated. The heart rate is markedly accelerated (there is a rapid ventricular response). Since the arrhythmia is of recent onset (less than 48 hours) , cardioversion can be attempted either with an antiarrhythmic drug, or electrical synchronized DC cardioversion. The patient is hemodynamically stable (no hypotension) and there are no symptoms of acute heart failure or cardiac ischemia, so an immediate emergency electrical DC cardioversion is NOT required. An initial attempt to control the heart rate ( with intravenous administration of a beta-blocker or digoxin ), while administering also an antiarrhythmic drug for cardioversion (usual options include flecainide or propafenone PO, if the patient does not have significant structural heart disease, or IV amiodarone in cases of concomitant structural heart disease). In addition, anticoagulation is initiated ( a vitamin K antagonist such as acenocoumarol, or warfarin, or one of the newer anticoagulants-dabigatran, apixaban, or rivaroxaban). If pharmaceutical cardioversion fails. then electrical cardioversion (synchronized DC cardioversion). can be attempted.
Alternatively, one could choose not to attempt cardioversion, but only to control (slow) the heart rate, for example with a beta-blocker, verapamil or digoxin and start PO anticoagulation with one of the anticoagulants mentioned above. However, in recent onset atrial fibrillation, the success rate of cardioversion is high and it is usually attempted. We should also schedule to check for possible underlying causes of atrial fibrillation (hyperthyroidism, valvular heart disease, hypertensive heart disease, ischemic heart disease). This testing includes blood levels of TSH (thyroid stimulating hormone), echocardiography and possibly, depending on indications and the degree of clinical suspicion, a scheduled functional test for ischemia detection (eg exercise test or myocardial perfusion scintigraphy).
Management of atrial ﬁbrillationTreatment of atrial fibrillation consists of:
a) Anticoagulation to prevent embolic complications (mainly stroke) on the short term for new-onset atrial fibrillation converted to sinus rhythm, or on the long term for people who have risk factors that increase the thromboembolic risk.
b) Rate control (control of the ventricular rate)
c) Rhythm control when appropriate and feasible (restoration and maintanance of sinus rhythm).
Atrial fibrillation (AF) is a factor that increases a person's risk for embolic stroke (embolic cerebrovascular accident -CVA). For a discussion of anticoagulation in atrial fibrillation see below in this chapter, but some general facts are the following. As a general rule therapy with an oral anticoagulant (OAC) can prevent the majority of ischemic strokes in AF patients and can prolong life (according to the ESC guidelines 2016). OAC treatment is superior to no treatment or aspirin in patients with AFwith risk factors for stroke.
Apart from the issue of anticoagulation, two strategies are available for AF treatment:
1) Rate control without conversion to sinus rhythm (AV nodal slowing agents to control the resting heart rate at about 70-100 beats per minute (bpm) and heart rate during exercise <140 bpm, plus oral anticoagulation if the CHA2DS2-VASc stroke risk score is ≥ 1, to prevent thromboembolic complications of AF, such as an embolic stroke). For the CHA2DS2-VASc score see below...
2) Rhythm control : Antiarrhythmic drugs and if needed direct current (DC) cardioversion, to convert to sinus rhythm and continuation of antiarrhythmic drugs for maintenance of sinus rhythm, plus oral anticoagulant for at least 4 weeks in sinus rhythm after cardioversion. The decision if the anticoagulant will be discontinued after 4 weeks of sinus rhythm or if it will be continued permanently depends on the presence or absence of risk factors for thromboembolism. If there are no risk factors, the anticoagulant will be stopped after 4 weeks : Generally, if AF does not recur and the CHA2DS2-VASc stroke risk score is 0 or 1, anticoagulation can be discontinued. Anticoagulation will be permanent if the CHA2DS2-VASc risk score is ≥ 2, even if the arrhythmia does not reccur, or if the patient has CHA2DS2-VASc score=1 and a high likelihood of AF recurrence (e.g. history of AF recurrences, significant enlargement of the left atrium) in order to prevent embolic complications.
Major randomized studies in patients with atrial fibrillation (AF) predominantly over the age of 65 years (AFFIRM), or in patients with heart failure (AF-CHF) have shown that there is no net mortality or symptom beneﬁt to be gained from one strategy (rhythm control or rate control) compared with the other. Which strategy to adopt needs to be assessed and decided for each individual patient. Factors considered in order to make this decision, include: The likelihood of maintaining sinus rhythm (low likelihood favors rate control and the opposite is true for high likelihood),
The safety and tolerability of antiarrhythmic drugs in a particular patient (if there is problematic safety or tolerability of antiarrhythmics this favors rate control),
If there is a history of failed cardioversions or many AF recurrences (this favors rate control),
The age of the patient (younger age usually favors rhythm control whereas older age rate control)
If AF is accompanied by symptoms and their intensity (significant symptoms with AF favor rhythm control)
Generally, a rhythm control strategy is prefered in younger and more symptomatic patients and if AF is of new onset.
Risk Score for embolic risk in non-valvular atrial fibrillation (AF): The CHA2DS2-VASc score is calculated by summing the points corresponding to the risk factors present in given patient: Risk factors for thromboembolism included in this score (the name of the score stems from the initial letters of these factors) are :
Congestive heart failure or left ventricular dysfunction= 1 point,
Hypertension= 1 point,
Age >75 =2 points,
Diabetes mellitus= 1 point,
Stroke (history of previous stroke or transient ischemic attack-TIA, or other arterial thrombo-embolism) = 2 points
Vascular disease (a prior myocardial infarction, peripheral arterial disease, aortic plaque) = 1 point
Age 65–74 = 1 point
Sex category (female sex) = 1 point.
(Maximum score= 9 / minimum score=0)
Hence, there are 2 major risk factors (history of previous thromboembolic event or stroke and age >75) each having a value of 2 points in the score. The rest of the risk factors are minor risk factors (1 point each)
Patients with paroxysmal AF should be regarded as having a stroke risk similar to those with persistent or permanent AF, in the presence of risk factors. (Let's remember this fact, it is important).
Patients aged ≤ 60 years, with lone AF, i.e. no clinical history or echocardiographic evidence of cardiovascular disease, have a very low stroke risk, about 1.3% over 15 years. However, the probability of stroke will increase with advancing age or development of hypertension, therefore re-assessment of risk factors for stroke over time is important. In general, patients without clinical stroke risk factors do not need antithrombotic therapy, while patients with stroke risk factors (i.e. CHA2DS2-VASc score of 1 or more for men, and 2 or more for women) are likely to benefit from oral anticoagulants.
Another important note is that the CHA2DS2-VASc score does not cover all cases. In patients with AF that have significant structural heart disease (for example valvular, or congenital heart disease, or hypertrophic cardiomyopathy, etc / or in patients with uncontrolled hyperthyroidism (thyrotoxicosis) anticoagulation is definitely needed regardless of the CHA2DS2-VASc score.
Another consideration in such cases is the type of anticoagulation.
The term "valvular AF" in the guidelines does not include all patients with AF that have significant valvular heart disease. It is used to indicate which AF patients are treated only with vitamin K antagonists and should not be treated with the new oral anticoagulants (NOACS):
The distinction between "valvular" and "non-valvular" AF remains a matter of debate. Currently, "valvular AF" refers to patients with moderate or severe mitral stenosis (MS) or mechanical heart valves (and valve repair in North American guidelines only). These patients with AF should be treated with a vitamin K antagonist -not with a new oral anticoagulant (NOAC). Other valvular heart diseases, such as mitral regurgitation, aortic stenosis, and aortic regurgitation, do not result in conditions of low flow in the left atrium and do not apparently increase as much the risk of thromboembolism brought by AF. These patients should receive anticoagulation in case of AF, but both vitamin K antagonists and NOACs are acceptable alternatives ( in contrast to patients with MS, or prosthetic valves, or a history of valve repair, for whom only vitamin K antagonists are recommended).
In case of a new patient presenting with atrial fibrillation the management is as follows: If the patient is hemodynamically unstable (systolic blood pressure < 90, acute pulmonary edema, ischemic chest pain) give heparin and proceed quickly to synchronized DC cardioversion.
If the patient is not unstable and the heart rate is fast, an AV node slowing medication is given ( a beta-blocker, or verapamil, or diltiazem, or digoxin either intravenously or orally, to slow the ventricular response) and also a decision must be made about the treatment strategy (rate control, or rhythm control).
If rate control is chosen then a rate slowing medication is prescribed and if CHA2DS2-VASc score is ≥ 1 an anticoagulant medication should also be included in the treatment ( a vitamin K antagonist with target INR 2-3, or dabigatran, or apixaban, or rivaroxaban).
If a rhythm control strategy is chosen, we should carefully define from patient's history the time of onset of AF:
If it is a new onset AF (<48 hours) then we can proceed to cardioversion (restoration of sinus rhythm) either electrically (synchronized DC cardioversion) or with an antiarrhythmic medication. (If the patient has risk factors for thromboembolism, before cardioversion therapeutic dose of unfractionated heparin, or low molecular weight heparin or of one of the new oral anticoagulants should be given, but if the patient does not have significant risk factors this is not necessary). After cardioversion, anticoagulation is given for at least 4 weeks, but if the patient has moderate to high risk for thromboembolism (CHA2DS2-VASc score ≥ 2) anticoagulation is continued permanently.
If AF duration is > 48 hours, or if it is unknown, or we have reasonable doubt, then there is a risk that a thrombus may already be present in the left atrium or in the left atrial appendage. In such case, cardioversion to sinus rhythm leading to the resumption of atrial contraction, may "push" thrombus into the circulation and lead to an arterial thromboembolic complication. Hence, to avoid that, in AF of > 48 hours duration or of unknown duration we have the following two choices:
1) Give therapeutic anticoagulation for 3-4 weeks, then cardiovert (electrically or pharmacologically) and then continue anticoagulation for at least 4 weeks (permanently if there are risk factors for thromboembolism).
2) Give heparin (unfractionated or low molecular weight) and conduct a transesophageal echocardiogram (TEE) to assess the left atrium (LA) and the left atrial appendage: If there is no thrombus proceed to cardioversion and then give anticoagulation for at least 4 weeks (or permanently if there are is moderate or severe risk for thromboembolism with CHA2DS2-VASc ≥ 2). If there is thrombus in the LA or its appendage, give anticoagulation for 4 weeks and then carry out a new TEE. If there is no thrombus then proceed to cardioversion and continue anticoagulation for at least 4 weeks.
The choices of oral (PO) anticoagulation are either a vitamin K antagonist (target INR 2-3), or one of the newer oral anticoagulants (dabigatran, apixaban, or rivaroxaban-for dosages see below)
The newer oral anticoagulants (NOACS) are at least as efficacious as warfarin in preventing stroke and are associated with a lower risk of intracranial bleeding. However, they are excreted primarily by the kidney, therefore renal function should be assessed before treatment initiation (and after treatment initiation at regular time intervals e.g. 2 times/year) and they are not readily monitored with standard laboratory tests.
Recommendations for chronic antithrombotic prophylaxis (anticoagulation) for atrial fibrillation (AF) :
There is benefit from anticoagulation for AF patients with risk factors (i.e. men with CHA2DS2-VASc score ≥1 or women with CHA2DS2-VASc score ≥2).
There is an absolute (class I) indication for anticoagulation in AF patients having at least 1 major or 2 minor risk factors for thromboembolism (except female sex), i.e. men with CHA2DS2-VASc score ≥ 2 and women with score ≥ 3.
In patients having only 1 minor clinical risk factor (except from female sex) , i.e in men with score =1, or women with score =2, there is generally a logical, but not absolute, indication for anticoagulation (class IIa indication).
The above guidelines are applied if there is no contraindication for anticoagulation (e.g. active pathological bleeding, severe hepatic disease, etc)
Dabigatran 150 mg x 2 times/day (150 mg bid), or 110 mg x 2 /day if there is a high estimated bleeding risk, or if age > 75 years. Dabigatran is a direct thrombin inhibitor.
Dosages of the new oral anticoagulants (NOACS) for patients with non-valvular atrial fibrillation with risk factors for thromboembolism :
Caution is needed for patients with moderate renal impairment (CrCl or GFR 30-50 mL/min).
European Medicines Agency (EMA) based primarily on pharmacokinetic evidence, recommends a reduction of the daily dabigatran dose to 150 mg (75 mg x 2) if patients are aged >75 years and have a CrCl between 30 and 50 mL/min, or need treatment with verapamil or amiodarone (these two drugs have an interaction with dabigatran). Reduce the dose of dabigatran (to75 mg twice daily) in patients with severe renal impairment (CrCl 15-30 mL/min). The drug should not be administered to patients with CrCl < 15 mL/min or on dialysis.
Discontinuation for surgery and other interventions, that can cause bleeding: In patients with CrCl ≥ 50 mL/min) discontinue dabigatran 1 to 2 days before invasive or surgical procedures because of the increased risk of bleeding. For patients with less adequate renal function (CrCl < 50 mL/min) discontinue dabigatran for 3 to 5 days. In case of emergency surgery use the specific reversal agent (antidote) idarucizumab for reversal of the anticoagulant effect of dabigatran.
If creatinine clearance (CrCl) or glomerular filtration rate (GFR) is 15-50 mL/min, then rivaroxaban dosage is 15 mg 1 time per day.
It is contraindicated in very severe renal failure with CrCl < 15 mL/min). Rivaroxaban was tested in patients with non valvular AF in the ROCKET AF trial.
Discontinuation for surgery and other interventions, that can cause bleeding: Dabigatran should be stopped at least 24 hours before the intervention and restarted as soon as possible after the procedure, provided the clinical situation allows and adequate haemostasis has been established.
Apixaban (a factor Xa inhibitor), dosage: 5 mg x 2 times per day, swallowed with water, with or without food. Reduced dosage of 2.5 mg x 2 times/day is prescribed if
a) 2 or more of the following factors are present : age > 80, body weight ≤ 60 kg, creatinine ≥ 1.5 mg/dL).
b) there is severe renal impairment (creatinine clearance 15-30 mL/min)
Apixaban must not be used in patients with serum creatinine >2.5 mg/dL, or CrCl <15 mL/min (these were exclusion criteria
The drug was tested for patients with non valnular AF in ARISTOTLE study.
Discontinuation for surgery and other interventions, that can cause bleeding: Apixaban should be discontinued at least 48 hours prior to elective surgery or invasive procedures with a moderate or high risk of bleeding (interventions for which clinically significant bleeding cannot be excluded or for which the risk of bleeding would be unacceptable).
In case of surgery or invasive procedures with a low risk of bleeding (interventions for which any bleeding that occurs is expected to be minimal, non-critical in its location): apixaban should be discontinued at least 24 hours before the procedure .
Note: Great caution is needed in patients on treatment with anticoagulants who need epidural or spinal anesthesia because if an epidural or spinal hematoma occurs, it can cause long term paralysis. The discontinuation of any anticoagulat drug in such cases should be such as to avoid any periprocedural anticoagulant effect
What is the type of rhythm shown on this ECG ?
For ventricular rate control the same drugs are used as in atrial fibrillation, but it is more difficult to achieve with atrial flutter than with atrial fibrillation.
Cardioversion and anticoagulation:The risk of thromboembolism in atrial flutter is generally considered equivalent to the risk in atrial fibrillation and anticoagulation treatment for atrial flutter follows the same rules as for atrial fibrillation. As with atrial fibrillation, precardioversion anticoagulation is not necessary in atrial flutter when the arrhythmia is of <48 hours duration, except in the setting of mitral valve disease.
In atrial flutter anticoagulation must be continued at least 4 weeks after electrical or chemical cardioversion. Long term anticoagulation is indicated in patients with risk factors for thromboembolism (CHA2DS2-VASc score ≥ 1). Note that these rules are the same, as for atrial fibrillation.
For the pharmacological cardiovesion of atrial flutter the most effective drug is ibutilide, an intravenous (IV) class III antiarrhythmic agent. Within 60-90 minutes following IV ibutilide 1-2 mg, conversion to sinus rhythm occurs in about 50–70% of patients.
For the conversion of atrial flutter to sinus rhythm amiodarone (a class III antiarrhythmic agent), or class I antiarrhythmic drugs can also be used. Conversion of atrial flutter with class I antiarrhythmic drugs is difficult to achieve (relatively low success rates). When these drugs are used, (e.g. drugs of the category Ic such as flecainide or propafenone) concomitant administration of rate lowering drugs that lower AV conduction (such as beta-blockers, verapamil, diltiazem, or digoxin) is indicated. This is advised in order to avoid the following rare but dangerous complication: Administration of class I drugs can slow the atrial flutter rate and this in some cases can reach a point where 1:1 atrioventricular (AV) conduction of the atrial flutter waves to the ventricles can occur, with a resulting ventricular rate of 200 beats/minute or higher, leading to hemodynamic collapse.
Another risk associated with the use of antiarrhythmic drugs and especially sotalol and drugs of class Ic (flecainide, propafenone) is the risk of proarrhythmia (the relatively rare but dangerous possibility of the occurence of ventricular arrhythmias as a result of these drugs). This risk is probably greatest in the first 24-48 hours after the initiation of antiarrhythmics, therefore careful assessment of the patient with repeated ECGs is needed during of the first days of treatment or after dose increments.
The most effective treatment (with the highest success rate) to achieve cardioversion of atrial flutter is eletrical cardioversion. With a synchronized electric shock of low energy, 25-50 Joules (J), conversion to sinus rhythm is accomplished in about 90% of patients.
Catheter ablation is a highly successful treatment for atrial flutter to prevent recurrences. It is the prefferred treatment option for patients with reccurent typical atrial flutter.
Radiofrequency ablation (RFA) is often used as first-line therapy to permanently restore sinus rhythm. For patients with recurrent symptomatic isthmus-dependent atrial flutter the current success rate is ≥ 95%.
Ventricular tachycardia (VT)A tachycardia with a heart rate of 120 / minute or greater comprising of at least three or more consecutive systoles of ventricular origin.
Ventricular tachycardias originate from sites located distally to the bifurcation of the bundle of His. The circuit from which the tachycardia originates may include specialized conductive myocardial tissue, common contractile myocardium, or both types of myocardial tissue.
A VT is called sustained (persistent) when it lasts> 30 seconds, or if electrical DC cardioversion is required to manage the hemodynamic consequences, whereas when none of these two conditions is fulfilled, the tachycardia is called non sustained(non-persistent).
Ventricular tachycardia (VT) is also divided into monomorphic in which the morphology of QRS waves is stable and polymorphic, with a varying QRS.morphology.
Nonsustained VT: May be asymptomatic or cause palpitations
Sustained VT: It is more likely to cause palpitations, and it may also present with lightheadedness, near-syncope, syncope, or cardiac arrest.
A tachycardia with a frequency of 120 / minute or more (some electrophysiologists set the heart rate threshold at 100 beats/ minute) and wide QRS (120 msec or greater) should be considered as ventricular tachycardia, unless proven otherwise.
Less commonly, a tachycardia with wide QRS may be of supraventricular origin, if one of the following occurs:
a) There is aberrant conduction, i.e. it is a supraventricular tachycardia with bundle branch block , a preexisting block, or one that appears only at an increased heart rate, or
b) There is a supraventricular tachycardia with pre-excitation, i.e. conduction of the electrical impulse to the ventricles through an accessory pathway
c) An antidromic AV reentry tachycardia (antidromic AVRT) which is the least common type of AV re-entrant tachycardia, in which the impulse is conducted downward (anterogradely) from the atria to the ventricles through an accessory pathway and then retrogradely from the ventricles to the atria through the normal conduction system (ie the bundle of His and the atrioventricular node).
d) A supraventricular tachycardia with wide QRS due to the effect of an antiarrhythmic drug that causes QRS prolongation. ( Class Ic antiarrhythmics, such as flecainide and propafenone).
If there is doubt whether it is a ventricular or supraventricular tachycardia, an intravenous calcium receptor blocker (verapamil or diltiazem).should never be administered for diagnostic purposes. The calcium channel blocker if the tachycardia is supraventricular,will usually terminate it, but if it is ventricular it may cause severe hypotension, or frank circulatory collapse (shock).
The ECG in ventricular tachycardia and ECG criteria for the differential diagnosis of a wide QRS tachycardia
ECG findings suggestive of a ventricular origin of the tachycardia are the following:
1) P waves that have no temporal relationship to the QRS. This is called atrioventricular dissociation and strongly favours the diagnosis of VT.
2) The presence of fusion beats: The presense of one or more beats within the tachycardia with a QRS morphology originating from the concomitant occurence of a ventricular and supraventricular beat. Fusion beats have a QRS morphology with features intermediate between these two beats. This is due to the simultaneous stimulation of the myocardium by an impulse of supraventricular origin and one of ventricular origin and strongly suggests VT.
3) The presence of capture beats is also strongly suggestive of VT: This is the occurence between the wide QRS complexes of the tachycardia, of one or more supraventricular beats with a narrow QRS complex.
4) Concordance (relative uniformity) in the appearance of the QRS in the precordial leads (i,e. when QRS is positive or negative in all the precordial leads)
6) Occasionally in ventricular tachycardia there may be a temporal relationship between the QRS and P waves, when the atria are stimulated retorgradely from the ventricles, resulting in P waves following the QRS complexes. Then, if there is evidence that the atrial depolarizations (P waves) have a temporal dependence on the ventricular ones (QRS complexes), i.e. when there is a degree of a ventriculoatrial conduction block, this is suggestive of VT. (E.g., a 2: 1 ventriculoatrial block, where there is 1 P wave for every 2 QRS complexes).
In contrast, if the ventricular depolarizations show a temporal dependence on atrial depolarizations, e.g. a 2: 1 block of AV conduction, where every second P-wave is followed by a QRS complex, the diagnosis of supraventricular tachycardia is supported.
7) A QRS duration > 140 msec when the tachycardia has a right bundle branch block morphology, or > 160 msec when there is a left bundle branch block QRS morphology suggests a ventricular tachycardia.
8) In the case of a tachycardia with wide QRS complexes and a right bundle branch block (RBBB) morphology, i.e. a positive QRS in lead V1, the presence in this lead of a monophasic or biphasic QRS (consisting of only one positive wave or two waves, a positive and a negative one) is an indication of VT, as is the presense in lead V6 of a deep S wave with an R / S ratio <1.
Therefore, if a three-wave ( rSR') morphology is present in V1 with the first R being smaller than the second (R'), this is suggestive of a supraventricular tachycardia, as is a R / S ratio > 1 in V6 in the presence of an RBBB morphology of the QRS.
9) In the case of a tachycardia with a wide QRS, showing a left bundle branch block (LBBB)-like QRS morphology , i.e. a positive QRS in left-oriented leads (I, aVL, V5, V6), one can use the following rules: When there is an initial r wave in leads V1, V2 , the following criteria can be applied: If r in V1 or V2 has
10) In case of a tachycardia with a LBBB morphology, the presence of an initial q wave in lead V6 is an indication of VT (This criterion is based on the fact that in a true left bundle branch block, there is no q wave in this lead).
A history of structural heart disease, if present, also increases the likelihood that a broad QRS tachycardia is of ventricular origin (VT).
A male 73 years old with a history of diabetes-type 2 , permanent atrial fibrillation with an adequately controlled heart rate (ventricular response) and known mild global left ventricular systolic dysfunction (ejection fraction EF= 45%). He did not have a history of smoking , or increased alcohol consumption. He was on treatment with ramipril, metoprolol (sustained relase tablets) and acenocoumarol (a vitamin K antagonist- same drug category with warfarin). A recent coonary angiography showed no significant stenoses of the coronary arteries, and he had no history of chronic unregulated hypertension or a history of cardiac valvulopathy.
He presented for examination because he was feeling fast pulpitations, fatigue and a mild nonspecific and poorly described precordial discomfort of approximately one hour. He did not have breathlessness or chest pain. Blood pressure was 120/90 mmHg and a brief targeted physical examination was without significant findings except from tachycardia. What is the type of the observed tachycardia (a reasoned answer is requested), in the context of which heart disease did the arrhythmia propably occur and what is the proposed treatment?
A tachycardia with a regular rhythm, heart rate around 140 beats per minute (bpm) and wide QRS complexes in a patient with a history of structural heart disease (mild global reduction of systolic left ventricular function). A regular tachycardia with wide QRS, (especially in a patient with structural heart disease) is very likely to be a ventricular tachycardia (VT). In this case, some of the morphological criteria of VT are also present (see above): The tachycardia has a left bundle branch block morphology and a QRS duration marginally exceeding 160 msec [QRS width here, is more clearly discerned on leads V2-V4 , while in leads V1, V2 there is an r wave clearly more than 40 msec wide and the interval from the beginning of the QRS to the deepest point (the nadir) of the S wave is greater than 70 msec]. The above findings are suggestive of a ventricular tachycardia (VT). Since the patient is hemodynamically stable, initial treatment can be by intravenous infusion of amiodarone or lidocaine. If this fails to terminate the VT, then electrical cardioversion is employed by administering an electric shock (initially 100-200 Joules) synchronized to the R wave of the QRS complex (synchronized cardioversion-press the defibrillator's sync button).
Regarding the underlying heart disease, diabetic cardiomyopathy would be most likely and as a second possibility idiopathic dilated cardiomyopathy (often resulting from unrecognized prior viral myocarditis, but a genetic predisposition is also commonly involved). One can arrive to these two possibilities, relying upon the patient's history, since from the history other common causes of systolic left ventricular dysfunction (such as coronary heart disease, chronic uncontrolled hypertension, chronic severe valvular disease, alcoholic cardiomyopathy, cardiomyopathy due to chronic tachyarrhythmia) propably can be ruled out.
These depend on the presence of underlying structural heart disease. The most common causes of VT are ischemic heart disease and cardiomyopathies (dilated or hypertrophic) but there are also other more rare causes.
Prognosis and treatment of ventricular tachycardia (VT):
In ischemic heart disease the underlying substrate for VT is usually a scar in ventricular myocardium, i.e an area of fibrosis due to a previous myocardial infarction (MI), arround which the reentrant impulse propagates. Another cause is acute myocardial ischemia or an acute MI, which can produce non-homogeneous electrophysiologic properties (slow conduction, differences in refractory period) in areas of the ventricular myocardium), which can lead to the occurence of VT.
In dilated cardiomyopathy the most common underlying substrate, responsible for ventricular tachycardia (VT) is myocardial fibrosis. However, there is also another important mechanism causing VT in some of the patients with dilated cardiomyopathy, called "bundle branch reentry". In these cases VT is caused by a reentrant circuit, which uses the bundle of His and its branches. Since the electrical impulse uses the bundle branches to enter the ventricles, the ECG, unlike the usual pattern of VT, shows a typical bundle branch block morphology, usually LBBB and rarely RBBB. Appart from dilated cardiomyopathy, VT from bundle branch reentry can also occur in patients with aortic or mitral valve disease. This is attributed to the anatomical proximity between the annuli of these valves and the bundle of His and the proximal parts of its branches.
Less common causes of VT include congenital heart disease, arrhytmogenic right ventricular dysplasia-ARVD (better term: arrhytmogenic right ventricular cardiomyopathy), mitral valve prolapse (very rarely it can cause VT) and various genetic disorders of ion channels of the myocardial cell membrane (Brugada syndrome, congenital long QT syndrome, etc).
Idiopathic ventricular tachycardia is a VT occuring in otherwise healthy people, with structurally normal hearts and it is usually benign (good prognosis). The most common type of idiopathic VT is right ventricular outflow tract (RVOT) ventricular tachycardia.
In patients with a diagnosed ventricular arrhythmia, the next step is a careful evaluation to exclude or confirm the presence any structural heart disease. Evaluation for structural heart disease is necessary and besides a careful history (including family history) physical examination and ECG it should always include echocardiography. Note that the family history can provide clues for an inherited cardiomyopathy, or an inherited disorder of the ion channels. Depending on the specific characteristics of each case and the suspected probable etiology, additional studies can include stress testing with ECG or imaging, cardiac computed tomography-angiography or conventional coronary angiography. Cardiac magnetic resonance imaging (CMR) is indicated only in selected cases, when there is a suspicion of arrhythmogenic right ventricular cardiomyopathy (ARVC) or sarcoidosis.
Diagnostic assessment of a patient with ventricular arrhythmias
Idiopathic ventricular tachycardiaDespite a comprehensive evaluation, about 10 to 15% of patients with VT will not have an identifiable cause. Most of the idiopathic monomorphic VTs are in one of two categories, defined by the absence of indications of an underlying heart disorder and by ECG morphology. These most prevalent categories of idiopathic VT are VTs that arise in the right or left ventricular outﬂow tract. The ECG in those VTs typically shows an inferiorly directed frontal axis (the QRS is markedly positive in inferior leads)
Inherited Arrhythmia Syndromes
These are inherited syndromes that can be manifested with ventricular tachycardia (VT), ventricular fibrillation (VF) and sudden death. They incude the congenital long QT syndromes (LQTS), the short QT syndrome, the Brugada syndrome and catecholaminergic polymorphic VT
The congenital long QT syndromes form a family of disorders characterized by prolongation of cardiac repolarization with a prolonged QT interval. These patients have a tendency to develop
polymorphic VT (torsades de pointes) which is often transient (self-terminating) causing syncope but in some cases it can degenerate to ventricular fibrillation causing sudden death. These patients, although they have structuraly normal hearts and they are usually otherwise healthy individuals, have an increased risk for syncope and sudden cardiac death.
The estimated prevalence of the LQTS in the general population is about 1 in 3000 - 5000 people. The LQTS are caused by mutations in genes that encode ion channel proteins, with the resultant ion channel dysfunction leading to a prolonged repolarization phase of the ventricular action potential.A prolonged QT is defined in women as a QTc >460 ms and in men a QTc >450 ms. A congenital long QT syndrome is suspected in a person with a prolonged QTc (particularly if QTc>480ms) if there is not any reversible cause of QT prolongation (metabolic, drug, ischemia, or cardiomyopathy). Some other findings that are supportive of this diagnosis are the following: The presence of T wave alternans (beat to beat variation in the morphology of the T wave), syncope, family history of long QT or family history of sudden death, ECG screening of family members (marked
prolongation of QTc in a family member).
In people with congenital long QT syndrome (LQTS), factors associated with higher risk for polymorphic VT and sudden death are: QTc > 500 ms, syncope despite treatment with a beta-blocker, age-gender interactions (increased event rate in males during childhood and females after onset of adolescence), LQTS genotype (LQT3, which responds less to beta blocker treatment). There are also some factors that can further prolong repolarization in people with LQTS and thereby they can trigger an episode of VT or sudden death. Such factors are electrolyte disorders, bradycardia or pauses, sudden sympathetic stimulation, and drug effects.
|ECG: Congenital Long QT syndrome (LQTS). Leads V1 and II are shown here. Note the very prominent QT prolongation in this example|
|ECG: another case of a congenital long QT syndrome (LQTS). The limb leads are shown here.|
A congenital short QT syndrome has also been described. The cause is a mutation enhancing a repolarizing potassium current. To date, mutations in six genes have been implicated in the pathogenesis. The syndrome has most often an autosomal dominant inheritance, but some de novo sporadic cases have also been described. This uncommon syndrome, first described in 2000, is characterized by a short QT interval (usually QT ≤ 320 msec or QTc ≤ 340msec ), a high incidence of syncope and atrial fibrillation and an increased risk for sudden death. Symptoms, including syncope or cardiac arrest, occur most often during periods of rest or sleep. Atrial fibrillation occurs in approximately a third (1/3 ) of the patients.
ECG features consists of a short QT interval (QTc ≤340 msec), an ST segment which is absent or short and T waves in the precordial leads are usually tall and peaked. In some cases T waves can be inverted.
The Brugada syndrome is another familial condition associated with sudden death. It is caused by a mutation in an ion- channel gene (causing reduced function of a sodium channnel) .The inheritance is autosomal dominant but the mutations are heterogenous. It usually affects males (90% of the affected people are males).
The ECG shows an incomplete or complete right bundle branch block with a coved ST-segment elevation in leads V1 and V2.
There are three types of Brugada ECG pattern, but only type 1 is associated with a risk of clinical events such as VT, syncope or sudden death. These patients can manifest episodes of polymorphic VT and ventricular fibrillation (but not monomorphic VT) often during sleep, or at rest, or during a febrile illness (fever can trigger polymorphic VT in these patients).
Type 1: coved ST elevation ≥ 2mm at the J point in at least two of the leads V1-V3, with T‐wave inversion
Type 2: saddleback ST elevation >1mm with upright or biphasic T wave
Type 3: coved ST< 2mm or saddleback ST<1mm
Brugada ECG patterns can be transient and they can be unveiled by Na channel blockers, such as flecainide, or by fever, propofol, cocaine, or tricyclic antidepressant use.
The spontaneous type 1 Brugada pattern is the one most specifically associated with sudden death and this is called Brugada syndrome. The other two patterns are suspicious but may often be seen in absolutely healthy individuals and they require provocative testing with flecainide to make the diagnosis of Brugada syndrome. Provocation of type 1 pattern with flecainide establishes the diagnosis, but provoked type1 Brugada has a much lower event risk than the spontaneous type 1. The spontaneous type 1 Brugada pattern is associated with a syncope/sudden death rate of approximately 0.5% per year.Types 2 and 3 are not clearly associated with an increased event rate.
In asymptomatic type 1 Brugada pattern, an electrophysiologic study may be performed, during which an inducible VF implies a higher risk of sudden death, although this is still controversial.
Asymptomatic type 2 or 3 patterns do not require any specific workup and are normal variants rather than specific predictors of life‐threatening
In persons with the Brugada syndrome the risk of VT can be reduced by treatment with quinidine.
Indications for ICD implantation include patients who have been resuscitated from an episode of cardiac arrest, or patients with Brugada type 1 (spontaneous or inducible) and a history of syncope.
Catecholaminergic polymorphic VT
Catecholaminergic polymorphic ventricular tachycardia (CPVT), a rare genetic condition resulting from abnormal calcium homeostasis in the myocardial cells, is an inheritable cardiac channelopathy, i.e. a genetic disorder of the ion channels of the cardiac myocytes. CPVT is considered as a highly malignant channelopathy because it predisposes to sudden cardiac death. It is thought to affect 1 in 10,000 people and is estimated to cause 15% of all unexplained sudden cardiac deaths in young people.
CPVT results from mutations in the genes encoding the cardiac ryanodine receptor type II or encoding calsequestrin and also some other mutations (mutations in the genes encoding the calcium signaling protein calmodulin, another gene located in the chromosome 7, etc). These mutations cause an increased intracellular calcium and this predisposes to an increased risk of ventricular arrhythmias.
Symptom onset most often occurs in the first two decades of life, with a median age at diagnosis of 15 ± 10 years but there is also a type with delayed symptom onset in patients aged 30-50 years. The older age group has a larger proportion of females.
Arrhythmiogenic right ventricular cardiomyopathy :
See the chapter on cardiomyopathies, where this entity is described. (link: The cardiomyopathies)
Impantable cardioverter defibrillator (ICD) for the secondary prevention of sudden cardiac death (SCD) and ventricular tachycardia (VT):
ICDs are implantable electronic devices highly effective for termination of VT and ventricular fibrillation (VF), which also provide pacing in case of bradycardia. The main benefit of ICDs is that they decrease mortality in patients with structural heart diseases, with increased risk for sudden death.
The components of an ICD are the following: The ICD generator which is implanted in the subcutaneous tissue of the upper chest at the subclavicular area, an atrial pacing lead which is placed in the right atrium, and a ventricular pacing and defibrillating lead in the right ventricle. If it is a unit also capable of biventricular pacing (used in patients with symptomatic heart failure with EF<35% and prolonged QRS duration, see chapter on heart failure) then it also includes a lead for pacing the left ventricle, usually placed in the left ventricular branch of the coronary sinus (LV lead).
ICDs can terminate ventricular arrhythmias in two ways:
a) They can terminate a monomorphic VT by antitachycardia pacing, which is a burst of rapid pacing, at a rate faster than the VT.
b) An electric shock is delivered if antitachycardia pacing fails, or in case of rapid VT or VF. Shocks are often lifesaving, but they are also painful.
The most common complication is the delivery of inappropriate (unnecessary) shocks in response to a rapid supraventricular tachycardia or to electrical noise (resulting from an ICD lead fracture).
Another complication is infection of the device ( in about 1% of patients).As a general rule ICDs are implanted only if there is also a reasonable expectation for survival of at least 1 year (with the planned treatment), with acceptable functional capacity.
ICD implantation is recommended in patients with documented VF or haemodynamically not tolerated VT in the absence of reversible causes and not within 48 h after myocardial infarction, who are receiving chronic optimal medical therapy.
This is class I recommendation and is based on a meta-analysis of three trials, Antiarrhythmic drugs Versus Implantable Defibrillator(AVID), Cardiac Arrest Study Hamburg (CASH) and Canadian Implantable Defibrillator Study (CIDS), conducted in patients who had suffered a cardiac arrest or hemodynamically unstable VT, or VT with syncope. These studies, compared treatment with an ICD with anti-arrhythmic drug therapy, predominantly amiodarone.
ICD implantation should be considered in patients with recurrent sustained VT (not within 48 h after myocardial infarction) who are receiving chronic optimal medical therapy, even if they have a normal left ventricular EF (class IIa).
In patients with VF or VT and an indication for ICD, amiodarone may be considered as an alternative treatment (instead of the ICD), when an ICD is not available, contraindicated for concurrent medical reasons or refused by the patient.
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Links and bibliography
Brugada J. Katritsis DG, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. European Heart Journal, 2020;41,(5):655–720. LINK2019 ESC Guidelines for the management of patients with supraventricular tachycardia
Tang PT, Do DH, et al. Team Management of the Ventricular Tachycardia Patient. Arrhythmia & Electrophysiology Review 2018;7(4):238–46. LINK Team Management of the Ventricular Tachycardia Patient
Brugada J, Diez DP. How to recognise and manage idiopathic ventricular tachycardia. The e-journal of the ESC Council for Cardiology Practice 2010;8 (26)
LINK How to recognise and manage idiopathic ventricular tachycardia
Medi C, Kalman JM, Freedman SM. Supraventricular Tachycardia. Med J Aust 2009;190 (5): 255-260 LINK Supraventricular Tachycardia
Guidelines on supraventricular tachycardias
2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS
Guidelines on ventricular arrhythmias and the prevention of sudden cardiac death- ESC 2015
ACCF/HRS/AHA 2013 Appropriate Use Criteria for Implantable Cardioverter-Defibrillators and Cardiac Resynchronization Therapy
HRS/ACC/AHA Expert Consensus Statement on the Use of Implantable Cardioverter-Defibrillator Therapy in Patients Who Are Not Well Represented in Clinical Trials
Atrial Fibrillation Guideline ESC 2010
Focused update of the guidelines for atrial fibrillation .2012- ESC
Atrial Fibrillation Guideline2014 AHA/ACC/HRS -Click on the link and download PDF !
Guideline on atrial fibrillation -NICE
2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care