Everyone Loves Youfit. Cardiac Arrhythmia Ablation The need for the treatment of arrhythmias depends on the symptoms and severity of the arrhythmia. Treatment is aimed at the causes of the disease. If necessary, direct antiarrhythmic therapy is carried out, which includes antiarrhythmic drugs, cardioversion-defibrillation, implantable cardioverter-defibrillators (ICD), pacemakers (and a special form of stimulation - resynchronization cardiac therapy ), catheter ablation, surgical intervention, or a combination thereof.
With tachyarrhythmia resulting from additional pathways or ectopic foci of automatism, the focus can be deliberately destroyed (removed) for the effectiveness of treatment. There are several ablation methods.
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| Everyone Loves Youfit. Cardiac Arrhythmia Ablation |
Ablation is usually performed using a transvenous catheter, to which a low-voltage, high-frequency (300–750 MHz) radio-frequency (RF) electromagnetic energy is supplied. RF energy heats and necrotic tissue1 cm in diameter and to a depth of 1 cm.
During cryoablation, tissue freezing is used (up to –70 ° C) to achieve the effect of tissue destruction. For intraoperative use, other delivery systems have been developed.
Before the application of energy, the ablation zone should be noted during an electrophysiological study.
Ablation efficiency is >90% for reciprocal supraventricular tachycardia (atrioventricular [AV-nodal] or involving additional conduction pathways), focal atrial tachycardia and atrial flutter, focal idiopathic ventricular tachycardia (VT from the exit tract of the right ventricle, septal duct from the VT or VT Gisa). Since atrial fibrillation (AF) most often occurs and/or is supported by arrhythmogenic zones in the pulmonary veins, this source can be electrically isolated by circumferential ablation of the mouth of the pulmonary veins or in the left atrium. An alternative in patients with symptomatic, refractory to drug therapy of AF with a high heart rate can be implantation of a permanent pacemaker followed by ablation of the AV compound.
Transcatheter ablation is safe; mortality 1/2 000.
Complications include damage to the heart valves, stenosis or occlusion of the pulmonary veins (in the treatment of AF), stroke or other embolic complications, cardiac perforation, tamponade (1%), and unintended ablation of the AV compound.
Antiarrhythmic drugs
Most antiarrhythmic drugs are grouped into 4 main classes based on their cellular electrophysiological action ( Antiarrhythmic drugs.
Class I: Class I drugs are divided into subclasses a, b and c. Class I: sodium channel blockers (membrane-stabilizing drugs) block fast sodium channels, slowing down the conduction in the corresponding areas of the myocardium (working cardiomyocytes of the atria and ventricles, His-Purkinje system).
Class II: drugs of class II - β-blockers, which mainly act on tissues with slow conduction (sinoatrial [CA] and atrioventricular [AB] node), where they reduce the frequency of automatism, slow down conductivity and increase refractoriness.
Class III: Class III drugs are primarily potassium channel blockers, which increase the duration of the action potential and refractoriness in slow and fast channels.
Class IV: Class IV drugs are calcium channel blockers that inhibit the calcium-dependent action potential in slow channels, therefore they reduce automatism, slow down the rate of electrical conductivity and increase refractoriness.
Digoxin and adenosine are not included in this classification. Digoxin shortens the atrial and ventricular refractory period, lengthening AV conduction and its refractoriness. Adenosine slows or blocks atrioventricular conduction and can prevent tachyarrhythmias, the mechanism of which is supported by the work of the AV connection.
Antiarrhythmic drugs.
Drug Dosage Target level Selective side effects Notes
Class Ia
Application: suppression of PES, Zhe, NZhT, ZhT, FP, TP, FZ
Of disopyramide* Intravenously: initially 1.5 mg / kg for > 5 min, after which - infusion 0.4 mg / kg / hour
Inside - Short-acting: 100 or 150 mg every 6 hours
Inside - prolonged action: 200 or 300 mg every 12 hours
2-7.5 μ g / ml
Anticholinergic effects (urinary retention, glaucoma, dry mouth, impaired vision, intestinal disorders), hypoglycemia, bidirectional VT, negative inotropic effects (which may exacerbate heart failure or lead to hypotension)
The drug should be used with caution in patients with impaired LV function.
Dosage should be reduced in patients with renal failure.
Side effects can occur with a violation of the treatment regimen.
When expanding the QRS complex ( > 50%, if the initial interval120 ms, or > 25%, if the initial interval > 120 msec), or if the corrected QT-interval is lengthened > 550 msec, the infusion rate or the dose should be reduced or administration of the drug suspended.
Procainamide * Intravenously, 10-15 mg / kg, jet (25-50 mg / min) followed by continuous intravenous infusion at a rate of 1-4 mg / min
Inside: 250-625 mg (rarely up to 1 g) every 3 or 4 hours
Inside with prolonged action: for patients <55 = "" kg, = "" 500 = "" mg; = "" for = "" patients = "" 55-91 = "" kg, = "" 750 = "" mg ; = "" or = "" for = "" patients = ""> 91 kg, 1000 mg every 6 hours
4-8 mcg / ml
Hypotension (with intravenous infusion), serological abnormalities (especially ANA) occur in almost 100% of cases when taking the drug > 12 months, lupus erythematosus (arthralgia, fever, first effusion) occur in 15-20%, agranulocytosis in1% of cases, polymorphic VT
There is no need for frequent dosing since the active substance is slowly excreted.
When expanding the QRS complex ( > 50%, if the initial interval120 ms, or > 25% if the initial interval is > 120 ms) or if the corrected QT interval is longer > 550 ms, the infusion rate or dose should be reduced or the administration of the drug should be stopped.
Quinidine * Inside: 200-400 mg every 4-6 hours
2-6 μ g / ml
Diarrhea, colic, flatulence, fever, impaired liver function, ventricular tachycardia "torsades de pointes", the overall frequency of side effects - 30%
If the QRS interval lengthens ( > 50%, if the initial interval120 ms, or > 25% if the initial interval is > 120 ms) or if the corrected QT interval is longer > 550 ms, the infusion rate or dose should be reduced or the administration of the drug should be stopped.
Class ib * Application: suppression of ventricular arrhythmias (ventricular ES, VT, VF)
Lidocaine* Intravenously: 100 mg for 2 minutes, then continuous infusion at a rate of 4 mg/min (2 mg/min in patients > 65 years of age) and 5 minutes after the administration of 1 dose - jet administration of 50 mg of the drug
2–5 μ g / l
Tremor, cramps; with too rapid administration - drowsiness, delirium, paresthesia; possibly increased risk of developing bradyarrhythmias after acute myocardial infarction
To reduce the risk of intoxication after 24 hours, the dose or rate of administration should be reduced to 2 mg/min.
Marked metabolism in the liver during the initial passage.
Mexiletine* Inside for quick release: 100-250 mg every 8 hours Inside for slow release: 360 mg every 12 hours
Intravenously: 2 mg/kg at a rate of 25 mg/min, then administration of 250 mg for an hour, 250 mg for a second hour, a maintenance dose of 0.5 mg/min
0.5–2 μ g / ml Nausea, vomiting, tremors, cramps
Class ic
Application: suppression of PES, Zhe, NZhT, ZhT, FP, TP, FZ
Flecainide* Inside: 100 mg every 8 or 12 hours
Intravenously: 1-2 mg / kg over 10 minutes
0.2–1 μ g / ml Occasionally visual impairment and paresthesia
If the QRS interval lengthens ( > 50%, if the initial interval120 ms, or > 25% if the initial interval is > 120 ms), the dose should be reduced or the administration of the drug should be suspended.
Propafenone* Inside: initially from 150 mg 3 times / day with dose titration up to 150-300 mg 3 times / day
Intravenously: 2 mg / kg, by stream; subsequently, administration at a rate of 2 mg / min
0.1-1.0 mcg/ml Beta-blocking activity, respiratory distress may occur; rarely gastrointestinal upset
Non-linear pharmacokinetics; dose increase should not be more than 50% of the previous one.
Bioavailability and protein binding are different; the drug has a cumulative effect.
Class II (beta-blockers)
Application: supraventricular tachyarrhythmias (PES, sinus tachycardia, NRT, flutter, and atrial fibrillation) and ventricular tachyarrhythmias (often for prophylaxis)
Acebutolol* Inside, 200 mg 2 times / day
Beta-blockers do not have the recommended dosage; titration is carried out to reduce the heart rate by more than 25%
As a rule, when taking beta-blockers, gastrointestinal upsets, insomnia, scary dreams, lethargy, erectile dysfunction, disturbances in AV conduction are possible
Beta-blockers are contraindicated in patients with bronchospastic disorders.
Atenolol* Inside: 50-100 mg, 1 time / day
Betaxolol* Inside: 20 mg, 1 time / day
Bisoprolol* Intravenously: 5–10 mg, 1 time / day
Carvedilol* Oral: initially 6.25 mg 2 times / day, followed by titration up to 25 mg 2 times / day
Esmolol* Intravenously: 50-200 mcg / kg / min
Metoprolol* Intravenously: 50–100 mg, 2 r / day
Intravenously: 5 mg every 5 min until 15 mg is reached
Nadolol* Inside: 60-80 mg, 1 time / day
Propranolol* Inside: 10-30 mg 3-4 times / day
V \ in 1-3 mg (injection can be repeated after 5 minutes, if necessary)
Timolol* Oral: 10-20 mg twice daily
Class III (membrane-stabilizing drugs)
Application: any tachyarrhythmias except spindle-shaped VT
Amiodarone* Inside, 600-1200 mg / day for 7-10 days, then 400 mg / day for 3 weeks, followed by a maintenance dose (best, up to ( ≤ ) 200 mg / day)
Intravenously: 150–400 mg after 1–6 hours (depending on urgency), with a further maintenance dose of 0.5–2.0 mg/min
1–2.5 μ g / ml
Pulmonary fibrosis (up to 5% of patients treated > 5 years) can be fatal; QT interval lengthening; polymorphic VT (rarely); bradycardia; gray and cyanotic skin pigmentation; photosensitivity; impaired liver function; peripheral neuropathy; micro-deposits on the cornea (in almost all patients) - usually without serious visual impairment, they disappear after discontinuation of treatment; changes in thyroid function; an increase in creatinine up to 10% without changes in glomerular filtration rate; slow clearance, possibly increasing the duration of side effects
The drug has a non-competitive beta-blocking effect, the properties of calcium and sodium channel blocker with a delayed effect.
By lengthening refractoriness, the drug can lead to a homogeneous state of cardiac repolarization.
Intravenous forms can be used for rhythm conversion.
Azimilide * Inside, 100-200 mg 1 time / day
200-1000 ng / ml
Spindle-shaped VT
Brethilium * Intravenously: initially, 5 mg / kg, then continuous infusion at a rate of 1-2 mg / min
V / m: initially, 5-10 mg / kg, administration can be repeated until a concentration of 30 mg / kg is reached
V / m maintenance dose of 5 mg/kg every 6-8 hours
0.8–2.4 mg / ml
Hypotension
Has the properties of class II drugs.
Effects can last 10-20 minutes.
The drug is used to treat potentially life-threatening persistent ventricular tachyarrhythmias (non-stopping VT, recurrent VF), in which it usually acts for 30 minutes after administration.
Dofetilide* Oral: 500 mcg twice / day if creatinine clearance > 60 ml / min; 250 mcg two times / day if creatinine clearance is 40-60 ml / min; 125 mcg twice daily if creatinine clearance is 20–40 ml / min
Not used
Spindle-shaped VT
The drug is contraindicated if the corrected QT interval > 440 ms or creatinine clearance <20 = "">
Dronedarone* Inside: 400 mg twice / day
Not used
Elongation of the corrected QT interval, bidirectional VT (rare), bradycardia, gastrointestinal disturbances, possible hepatotoxic effect (rare), creatinine level increase to 20% without changes in glomerular filtration rate
The drug is a modified amiodarone molecule (deiodinated) with a shorter half-life, less distribution volume, fewer side effects, and less effectiveness.
The drug is better not to use in patients with heart failure or a constant form of atrial fibrillation.
Ibutilide* Intravenously: for patients weighing more than or equal to 60 kg, 1 mg infusion, or, for patients weighing less than 60 kg, 0.01 mg/kg in 10 min, with repeated administration after 10 minutes if the first infusion is unsuccessful
Not used
Spindle-shaped VT (in 2%)
The drug is used to stop atrial fibrillation (successful in about 40%) and atrial flutter (effective in almost 65% of patients).
Totalol* Inside: 80-160 mg every 12 hours
Intravenously: 10 mg in 1–2 minutes
0.5-4 μ g / ml
Like class II; possible deterioration of the function of the left ventricle and spindle-shaped VT
The racemic [ dl ] form has class II properties (beta-blocking), the [ d ] form does not. Both forms are similar in activity to class III. Only racemic sotalol is available for clinical use.
The drug should not be used in patients with renal failure.
Class IV (calcium channel blockers)
Application: relief of supraventricular tachycardia and heart rate control for atrial fibrillation and flutter
Diltiazem* Prolonged form for oral administration (Diltiazem CD): 120-360 mg 1 time / day
Intravenously: 5-15 mg / h for up to 24 hours
0.1-0.4 mcg / ml
Perhaps the occurrence of ventricular fibrillation in patients with ventricular tachycardia, a negative inotropic effect
The intravenous form is most often used to reduce the frequency of ventricular contractions in AF and TP.
Verapamil* Inside, 40-120 mg 3 times / day; for prolonged forms, 180 mg once or 240 mg 2 times a day
Intravenously, 5-15 mg, after 10 minutes
Inside for prevention, 40-120 mg, 3 times / day
Not used
Perhaps the occurrence of ventricular fibrillation in patients with ventricular tachycardia, a negative inotropic effect
The IV form is used to stop tachycardia with a narrow QRS complex, including nodular (almost 100% effective with 5-10 mg intravenously in 10 minutes).
Other antiarrhythmic drugs
Adenosine* 6 mg rapidly intravenously in a jet, repeated twice 12 mg, if necessary; in a jet of 20 mg of isotonic solution
Not used Transient respiratory disorders, chest discomfort, and (30-60%) transient bronchospasm
The drug slows or blocks the conduct in the AV connection.
The duration of action is extremely short.
Contraindications include asthma and high degree atrioventricular block.
Dipyridamole enhances the effect of the drug.
Digoxin* B \ in loading dose: 0.5 mg
Inside, maintenance dose: 0.125-0.25 mg / day
0.8-1.6 mg / ml
Anorexia, nausea, vomiting, and often serious arrhythmias (ventricular extrasystoles and tachycardia, atrial extrasystoles and tachycardia, atrioventricular blockade 2 and 3 degrees, a combination of these rhythm disturbances)
Contraindications include the presence of an antegrade-conducting additional route (manifesting Wolf-Parkinson-White syndrome), since the occurrence of atrial fibrillation will lead to severe ventricular tachysystole (digoxin shortens the refractory period of the additional atrial ventricular connection).
* Abbreviations.
AF = atrial fibrillation; ANA = antinuclear antibodies: PES = atrial extrastistol; AB = atrioventricular; CrCl = creatinine clearance; LV = left ventricle; QTk = corrected QT interval; NRT = supraventricular tachycardia; VF = ventricular fibrillation; ZhE = ventricular extrasitol ; VT = ventricular tachycardia.
Antiarrhythmic drugs Class I
Sodium channel blockers (membrane-stabilizing drugs) block fast sodium channels, slowing down the conduction in the corresponding areas of the myocardium (working cardiomyocytes of the atria and ventricles, His-Purkinje system). On the ECG, this effect can be reflected by the expansion of the P-wave, QRS-complex, lengthening of the PR-interval, or a combination thereof.
The separation of class I drugs is based on the kinetic effects of sodium channels:
Class Ib drugs have fast kinetics.
Class Ic drugs have slow kinetics.
Class Ia drugs have intermediate kinetics.
The kinetics of sodium channel blockers is determined by the frequency of contractions of the heart, at which their electrophysiological effect is manifested. Since class Ib drugs have fast kinetics, they show their electrophysiological effect only with a fast heart rate. Thus, an ECG recorded during the normal rhythm and normal heart rate usually does not show any signs of a slowdown in the myocardium. Class Ib drugs are not very strong antiarrhythmics and have minimal effect on the atrial myocardium. Since class Ic drugs have slow kinetics, their electrophysiological effect is noticeable at any rhythm. Therefore, on the ECG with normal heart rate and normal rhythm, a slowdown in the myocardium is usually seen. Class Ic drugs are the most powerful antiarrhythmics. Class Ia drugs have intermediate kinetics, their effect on cardiomyocyte conduction in fast channels can be noticeable or imperceptible on an ECG recorded against a normal rhythm and heart rate. Class Ia drugs also block the repolarization of potassium channels, increasing the refractory periods of fast channel cardiomyocytes. On the ECG, this effect is reflected as an extension of the QT interval even at a normal rhythm. Class Ib and class Ic drugs do not directly block potassium channels.
The main indications for the use of drugs of classes Ia and Ic are the treatment of supraventricular tachycardia (CBT); ventricular tachycardia (VT) - for all drugs of class I.
Side effects of class I drugs include proarrhythmia, drug-induced arrhythmia obtained during treatment, which is the most alarming side effect. All class I drugs can aggravate the course of ventricular tachycardia. Class I drugs also tend to decrease ventricular contractility. These side effects are more characteristic in patients with structural heart disease; class I is not recommended for the treatment of such patients. Thus, these antiarrhythmics are usually used in patients who do not have structural heart disorders or in patients with structural disorders who have no other therapeutic alternative. There are other side effects of class I drugs that are specific to a subclass or individual drug.
Antiarrhythmic drugs Class Ia
Class Ia drugs have kinetics that is intermediate between fast class Ib kinetics and slow class Ic kinetics. Their effect on the conduction of cardiomyocytes in the fast channels can be noticeable or imperceptible on an ECG recorded against a normal rhythm and heart rate. Class Ia drugs block the repolarization of potassium channels, increasing the refractory periods of cardiomyocytes with fast channels. On the ECG, this effect is reflected as an extension of the QT interval even at a normal rhythm.
Class Ia drugs are used to reduce atrial extrasystole (PES), ventricular extrasystole (VES), supraventricular tachycardia, ventricular tachycardia, atrial fibrillation (AF), atrial flutter, and ventricular fibrillation. The main indications are supraventricular and ventricular tachycardia.
Class Ia drugs can cause polymorphic ventricular tachycardia. Taking class Ia drugs induces and slows down atrial tachyarrhythmias, which is sufficient for 1: 1 atrioventricular conduction with an increase in ventricular response.
Antiarrhythmic drugs Class Ib
Class Ib drugs have fast kinetics, they show their electrophysiological effect only with a fast heartbeat. Thus, an ECG recorded during the normal rhythm and normal heart rate usually does not show any signs of a slowdown in the myocardium. Class Ib drugs are not very strong antiarrhythmics and have minimal effect on the atrial myocardium. Class Ib drugs do not directly block potassium channels.
Class Ib drugs are used to reduce ventricular arrhythmias ( ventricular extrasystoles, ventricular tachycardia, ventricular fibrillation ).
Antiarrhythmic drugs Class Ic
Class Ic drugs have slow kinetics: their electrophysiological effect is noticeable at any rhythm. Therefore, on the ECG with normal heart rate and normal rhythm, a slowdown in the myocardium is usually seen. Class Ic drugs are more potent antiarrhythmics than class Ia or Ib drugs. Class Ic drugs do not directly block potassium channels.
Class Ic drugs can induce and slow down atrial tachyarrhythmias, which is enough to achieve 1: 1 AV conduction with an increase in the rate of ventricular response.
Class Ic drugs are used to suppress atrial extrasystoles , ventricular extrasystoles , supraventricular tachycardia , ventricular tachycardia , atrial fibrillation , atrial flutter, and ventricular fibrillation .
Antiarrhythmic drugs Class II
Class II drugs are beta-blockers that primarily act on tissues with slow conduction (sinoatrial and atrioventricular nodes), where they reduce automatism, slow down conduction and increase refractoriness. Thus, the heart rate slows down, the PR interval increases, AB-connection reduces the conduct of the fast atrial activity.
Class II drugs are mainly used to treat supraventricular tachycardia, including sinus tachycardia, atrioventricular nodular reciprocal tachycardia, atrial fibrillation, and atrial flutter. These drugs are also used to treat ventricular tachycardia to increase the threshold for ventricular fibrillation (VF) and reduce the pro-arrhythmic effect of beta-adrenoreceptor stimulation.
Beta-blockers are generally well tolerated; side effects include fatigue, sleep disturbances, and gastrointestinal upsets. These drugs are contraindicated in patients with asthma.
Antiarrhythmic drugs Class III
Class III drugs are membrane-stabilizing drugs, primarily potassium channel blockers, which increase the duration of the action potential and refractoriness in tissues with slow and fast channels. Thus, the ability of muscle fibers in the heart to transmit impulses at high frequencies deteriorates, but the speed of the conduction does not significantly change. Therefore, the action potential is lengthened, automatism is reduced. The predominant effect on the ECG is to lengthen the QT interval.
These drugs are used to treat SVT and VT. Class III drugs have a risk of ventricular proarrhythmic, especially bidirectional spindle-shaped (like “pirouette”) ventricular tachycardia, and are not used in patients with this type of VT.
Antiarrhythmic drugs Class IV
Class IV drugs are calcium channel blockers of the non-dihydropyridine series, which inhibit the calcium-dependent action potential in slow channels and, therefore, reduce automatism, slow the rate of electrical conductivity and increase refractoriness. The heart rhythm slows down, the PR interval lengthens, and the AV connection conducts an atrial rhythm to the ventricles with a lower frequency. These drugs are used primarily for the treatment of SVT. They can also be used to slow atrial fibrillation or flutter. One form of VT (left-sided septal flutter or Belhassen-type VT) can be treated with verapamil.
Lidocaine* Intravenously: 100 mg for 2 minutes, then continuous infusion at a rate of 4 mg/min (2 mg/min in patients > 65 years of age) and 5 minutes after the administration of 1 dose - jet administration of 50 mg of the drug
2–5 μ g / l
Tremor, cramps; with too rapid administration - drowsiness, delirium, paresthesia; possibly increased risk of developing bradyarrhythmias after acute myocardial infarction
To reduce the risk of intoxication after 24 hours, the dose or rate of administration should be reduced to 2 mg/min.
Marked metabolism in the liver during the initial passage.
Mexiletine* Inside for quick release: 100-250 mg every 8 hours Inside for slow release: 360 mg every 12 hours
Intravenously: 2 mg/kg at a rate of 25 mg/min, then administration of 250 mg for an hour, 250 mg for a second hour, a maintenance dose of 0.5 mg/min
0.5–2 μ g / ml Nausea, vomiting, tremors, cramps
Class ic
Application: suppression of PES, Zhe, NZhT, ZhT, FP, TP, FZ
Flecainide* Inside: 100 mg every 8 or 12 hours
Intravenously: 1-2 mg / kg over 10 minutes
0.2–1 μ g / ml Occasionally visual impairment and paresthesia
If the QRS interval lengthens ( > 50%, if the initial interval120 ms, or > 25% if the initial interval is > 120 ms), the dose should be reduced or the administration of the drug should be suspended.
Propafenone* Inside: initially from 150 mg 3 times / day with dose titration up to 150-300 mg 3 times / day
Intravenously: 2 mg / kg, by stream; subsequently, administration at a rate of 2 mg / min
0.1-1.0 mcg/ml Beta-blocking activity, respiratory distress may occur; rarely gastrointestinal upset
Non-linear pharmacokinetics; dose increase should not be more than 50% of the previous one.
Bioavailability and protein binding are different; the drug has a cumulative effect.
Class II (beta-blockers)
Application: supraventricular tachyarrhythmias (PES, sinus tachycardia, NRT, flutter, and atrial fibrillation) and ventricular tachyarrhythmias (often for prophylaxis)
Acebutolol* Inside, 200 mg 2 times / day
Beta-blockers do not have the recommended dosage; titration is carried out to reduce the heart rate by more than 25%
As a rule, when taking beta-blockers, gastrointestinal upsets, insomnia, scary dreams, lethargy, erectile dysfunction, disturbances in AV conduction are possible
Beta-blockers are contraindicated in patients with bronchospastic disorders.
Atenolol* Inside: 50-100 mg, 1 time / day
Betaxolol* Inside: 20 mg, 1 time / day
Bisoprolol* Intravenously: 5–10 mg, 1 time / day
Carvedilol* Oral: initially 6.25 mg 2 times / day, followed by titration up to 25 mg 2 times / day
Esmolol* Intravenously: 50-200 mcg / kg / min
Metoprolol* Intravenously: 50–100 mg, 2 r / day
Intravenously: 5 mg every 5 min until 15 mg is reached
Nadolol* Inside: 60-80 mg, 1 time / day
Propranolol* Inside: 10-30 mg 3-4 times / day
V \ in 1-3 mg (injection can be repeated after 5 minutes, if necessary)
Timolol* Oral: 10-20 mg twice daily
Class III (membrane-stabilizing drugs)
Application: any tachyarrhythmias except spindle-shaped VT
Amiodarone* Inside, 600-1200 mg / day for 7-10 days, then 400 mg / day for 3 weeks, followed by a maintenance dose (best, up to ( ≤ ) 200 mg / day)
Intravenously: 150–400 mg after 1–6 hours (depending on urgency), with a further maintenance dose of 0.5–2.0 mg/min
1–2.5 μ g / ml
Pulmonary fibrosis (up to 5% of patients treated > 5 years) can be fatal; QT interval lengthening; polymorphic VT (rarely); bradycardia; gray and cyanotic skin pigmentation; photosensitivity; impaired liver function; peripheral neuropathy; micro-deposits on the cornea (in almost all patients) - usually without serious visual impairment, they disappear after discontinuation of treatment; changes in thyroid function; an increase in creatinine up to 10% without changes in glomerular filtration rate; slow clearance, possibly increasing the duration of side effects
The drug has a non-competitive beta-blocking effect, the properties of calcium and sodium channel blocker with a delayed effect.
By lengthening refractoriness, the drug can lead to a homogeneous state of cardiac repolarization.
Intravenous forms can be used for rhythm conversion.
Azimilide * Inside, 100-200 mg 1 time / day
200-1000 ng / ml
Spindle-shaped VT
Brethilium * Intravenously: initially, 5 mg / kg, then continuous infusion at a rate of 1-2 mg / min
V / m: initially, 5-10 mg / kg, administration can be repeated until a concentration of 30 mg / kg is reached
V / m maintenance dose of 5 mg/kg every 6-8 hours
0.8–2.4 mg / ml
Hypotension
Has the properties of class II drugs.
Effects can last 10-20 minutes.
The drug is used to treat potentially life-threatening persistent ventricular tachyarrhythmias (non-stopping VT, recurrent VF), in which it usually acts for 30 minutes after administration.
Dofetilide* Oral: 500 mcg twice / day if creatinine clearance > 60 ml / min; 250 mcg two times / day if creatinine clearance is 40-60 ml / min; 125 mcg twice daily if creatinine clearance is 20–40 ml / min
Not used
Spindle-shaped VT
The drug is contraindicated if the corrected QT interval > 440 ms or creatinine clearance <20 = "">
Dronedarone* Inside: 400 mg twice / day
Not used
Elongation of the corrected QT interval, bidirectional VT (rare), bradycardia, gastrointestinal disturbances, possible hepatotoxic effect (rare), creatinine level increase to 20% without changes in glomerular filtration rate
The drug is a modified amiodarone molecule (deiodinated) with a shorter half-life, less distribution volume, fewer side effects, and less effectiveness.
The drug is better not to use in patients with heart failure or a constant form of atrial fibrillation.
Ibutilide* Intravenously: for patients weighing more than or equal to 60 kg, 1 mg infusion, or, for patients weighing less than 60 kg, 0.01 mg/kg in 10 min, with repeated administration after 10 minutes if the first infusion is unsuccessful
Not used
Spindle-shaped VT (in 2%)
The drug is used to stop atrial fibrillation (successful in about 40%) and atrial flutter (effective in almost 65% of patients).
Totalol* Inside: 80-160 mg every 12 hours
Intravenously: 10 mg in 1–2 minutes
0.5-4 μ g / ml
Like class II; possible deterioration of the function of the left ventricle and spindle-shaped VT
The racemic [ dl ] form has class II properties (beta-blocking), the [ d ] form does not. Both forms are similar in activity to class III. Only racemic sotalol is available for clinical use.
The drug should not be used in patients with renal failure.
Class IV (calcium channel blockers)
Application: relief of supraventricular tachycardia and heart rate control for atrial fibrillation and flutter
Diltiazem* Prolonged form for oral administration (Diltiazem CD): 120-360 mg 1 time / day
Intravenously: 5-15 mg / h for up to 24 hours
0.1-0.4 mcg / ml
Perhaps the occurrence of ventricular fibrillation in patients with ventricular tachycardia, a negative inotropic effect
The intravenous form is most often used to reduce the frequency of ventricular contractions in AF and TP.
Verapamil* Inside, 40-120 mg 3 times / day; for prolonged forms, 180 mg once or 240 mg 2 times a day
Intravenously, 5-15 mg, after 10 minutes
Inside for prevention, 40-120 mg, 3 times / day
Not used
Perhaps the occurrence of ventricular fibrillation in patients with ventricular tachycardia, a negative inotropic effect
The IV form is used to stop tachycardia with a narrow QRS complex, including nodular (almost 100% effective with 5-10 mg intravenously in 10 minutes).
Other antiarrhythmic drugs
Adenosine* 6 mg rapidly intravenously in a jet, repeated twice 12 mg, if necessary; in a jet of 20 mg of isotonic solution
Not used Transient respiratory disorders, chest discomfort, and (30-60%) transient bronchospasm
The drug slows or blocks the conduct in the AV connection.
The duration of action is extremely short.
Contraindications include asthma and high degree atrioventricular block.
Dipyridamole enhances the effect of the drug.
Digoxin* B \ in loading dose: 0.5 mg
Inside, maintenance dose: 0.125-0.25 mg / day
0.8-1.6 mg / ml
Anorexia, nausea, vomiting, and often serious arrhythmias (ventricular extrasystoles and tachycardia, atrial extrasystoles and tachycardia, atrioventricular blockade 2 and 3 degrees, a combination of these rhythm disturbances)
Contraindications include the presence of an antegrade-conducting additional route (manifesting Wolf-Parkinson-White syndrome), since the occurrence of atrial fibrillation will lead to severe ventricular tachysystole (digoxin shortens the refractory period of the additional atrial ventricular connection).
* Abbreviations.
AF = atrial fibrillation; ANA = antinuclear antibodies: PES = atrial extrastistol; AB = atrioventricular; CrCl = creatinine clearance; LV = left ventricle; QTk = corrected QT interval; NRT = supraventricular tachycardia; VF = ventricular fibrillation; ZhE = ventricular extrasitol ; VT = ventricular tachycardia.
Antiarrhythmic drugs Class I
Sodium channel blockers (membrane-stabilizing drugs) block fast sodium channels, slowing down the conduction in the corresponding areas of the myocardium (working cardiomyocytes of the atria and ventricles, His-Purkinje system). On the ECG, this effect can be reflected by the expansion of the P-wave, QRS-complex, lengthening of the PR-interval, or a combination thereof.
The separation of class I drugs is based on the kinetic effects of sodium channels:
Class Ib drugs have fast kinetics.
Class Ic drugs have slow kinetics.
Class Ia drugs have intermediate kinetics.
The kinetics of sodium channel blockers is determined by the frequency of contractions of the heart, at which their electrophysiological effect is manifested. Since class Ib drugs have fast kinetics, they show their electrophysiological effect only with a fast heart rate. Thus, an ECG recorded during the normal rhythm and normal heart rate usually does not show any signs of a slowdown in the myocardium. Class Ib drugs are not very strong antiarrhythmics and have minimal effect on the atrial myocardium. Since class Ic drugs have slow kinetics, their electrophysiological effect is noticeable at any rhythm. Therefore, on the ECG with normal heart rate and normal rhythm, a slowdown in the myocardium is usually seen. Class Ic drugs are the most powerful antiarrhythmics. Class Ia drugs have intermediate kinetics, their effect on cardiomyocyte conduction in fast channels can be noticeable or imperceptible on an ECG recorded against a normal rhythm and heart rate. Class Ia drugs also block the repolarization of potassium channels, increasing the refractory periods of fast channel cardiomyocytes. On the ECG, this effect is reflected as an extension of the QT interval even at a normal rhythm. Class Ib and class Ic drugs do not directly block potassium channels.
The main indications for the use of drugs of classes Ia and Ic are the treatment of supraventricular tachycardia (CBT); ventricular tachycardia (VT) - for all drugs of class I.
Side effects of class I drugs include proarrhythmia, drug-induced arrhythmia obtained during treatment, which is the most alarming side effect. All class I drugs can aggravate the course of ventricular tachycardia. Class I drugs also tend to decrease ventricular contractility. These side effects are more characteristic in patients with structural heart disease; class I is not recommended for the treatment of such patients. Thus, these antiarrhythmics are usually used in patients who do not have structural heart disorders or in patients with structural disorders who have no other therapeutic alternative. There are other side effects of class I drugs that are specific to a subclass or individual drug.
Antiarrhythmic drugs Class Ia
Class Ia drugs have kinetics that is intermediate between fast class Ib kinetics and slow class Ic kinetics. Their effect on the conduction of cardiomyocytes in the fast channels can be noticeable or imperceptible on an ECG recorded against a normal rhythm and heart rate. Class Ia drugs block the repolarization of potassium channels, increasing the refractory periods of cardiomyocytes with fast channels. On the ECG, this effect is reflected as an extension of the QT interval even at a normal rhythm.
Class Ia drugs are used to reduce atrial extrasystole (PES), ventricular extrasystole (VES), supraventricular tachycardia, ventricular tachycardia, atrial fibrillation (AF), atrial flutter, and ventricular fibrillation. The main indications are supraventricular and ventricular tachycardia.
Class Ia drugs can cause polymorphic ventricular tachycardia. Taking class Ia drugs induces and slows down atrial tachyarrhythmias, which is sufficient for 1: 1 atrioventricular conduction with an increase in ventricular response.
Antiarrhythmic drugs Class Ib
Class Ib drugs have fast kinetics, they show their electrophysiological effect only with a fast heartbeat. Thus, an ECG recorded during the normal rhythm and normal heart rate usually does not show any signs of a slowdown in the myocardium. Class Ib drugs are not very strong antiarrhythmics and have minimal effect on the atrial myocardium. Class Ib drugs do not directly block potassium channels.
Class Ib drugs are used to reduce ventricular arrhythmias ( ventricular extrasystoles, ventricular tachycardia, ventricular fibrillation ).
Antiarrhythmic drugs Class Ic
Class Ic drugs have slow kinetics: their electrophysiological effect is noticeable at any rhythm. Therefore, on the ECG with normal heart rate and normal rhythm, a slowdown in the myocardium is usually seen. Class Ic drugs are more potent antiarrhythmics than class Ia or Ib drugs. Class Ic drugs do not directly block potassium channels.
Class Ic drugs can induce and slow down atrial tachyarrhythmias, which is enough to achieve 1: 1 AV conduction with an increase in the rate of ventricular response.
Class Ic drugs are used to suppress atrial extrasystoles , ventricular extrasystoles , supraventricular tachycardia , ventricular tachycardia , atrial fibrillation , atrial flutter, and ventricular fibrillation .
Antiarrhythmic drugs Class II
Class II drugs are beta-blockers that primarily act on tissues with slow conduction (sinoatrial and atrioventricular nodes), where they reduce automatism, slow down conduction and increase refractoriness. Thus, the heart rate slows down, the PR interval increases, AB-connection reduces the conduct of the fast atrial activity.
Class II drugs are mainly used to treat supraventricular tachycardia, including sinus tachycardia, atrioventricular nodular reciprocal tachycardia, atrial fibrillation, and atrial flutter. These drugs are also used to treat ventricular tachycardia to increase the threshold for ventricular fibrillation (VF) and reduce the pro-arrhythmic effect of beta-adrenoreceptor stimulation.
Beta-blockers are generally well tolerated; side effects include fatigue, sleep disturbances, and gastrointestinal upsets. These drugs are contraindicated in patients with asthma.
Antiarrhythmic drugs Class III
Class III drugs are membrane-stabilizing drugs, primarily potassium channel blockers, which increase the duration of the action potential and refractoriness in tissues with slow and fast channels. Thus, the ability of muscle fibers in the heart to transmit impulses at high frequencies deteriorates, but the speed of the conduction does not significantly change. Therefore, the action potential is lengthened, automatism is reduced. The predominant effect on the ECG is to lengthen the QT interval.
These drugs are used to treat SVT and VT. Class III drugs have a risk of ventricular proarrhythmic, especially bidirectional spindle-shaped (like “pirouette”) ventricular tachycardia, and are not used in patients with this type of VT.
Antiarrhythmic drugs Class IV
Class IV drugs are calcium channel blockers of the non-dihydropyridine series, which inhibit the calcium-dependent action potential in slow channels and, therefore, reduce automatism, slow the rate of electrical conductivity and increase refractoriness. The heart rhythm slows down, the PR interval lengthens, and the AV connection conducts an atrial rhythm to the ventricles with a lower frequency. These drugs are used primarily for the treatment of SVT. They can also be used to slow atrial fibrillation or flutter. One form of VT (left-sided septal flutter or Belhassen-type VT) can be treated with verapamil.
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