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Violation of the rhythm and conductivity of the heart: drugs
Last reviewed: 10.08.2022
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Treatment is not always required; The approach depends on the manifestations and danger of arrhythmia. Asymptomatic arrhythmias, not accompanied by high risk, do not require treatment, even if they occur with deterioration of survey data. At clinical displays therapy can be necessary for improvement of quality of a life of the patient. Potentially life-threatening arrhythmias are an indication for treatment.
Therapy depends on the situation. If necessary, an antiarrhythmic treatment is prescribed, including antiarrhythmic drugs, cardioversion-defibrillation, implantation of ECS, or a combination thereof.
Medicines used to treat arrhythmias. Most antiarrhythmic drugs are divided into four main classes (Williams classification), depending on their effect on the electrophysiological processes in the cell / digoxin and adenosine phosphate are not included in the Williams classification. Digoxin shortens the refractory period of the atria and ventricles and is a vagotonik, as a result of which it lengthens the conduction along the AV node and its refractory period. Adenosine phosphate slows or blocks conduction on the AV node and can stop tachyarrhythmias that pass through this node during circulation of the pulse.
I class
Sodium channel blockers (membrane stabilizing drugs) block fast sodium channels, slowing down the passage through tissues with fast ion channels (functioning atrial and ventricular myocytes, the His-Purkinje system). On the electrocardiogram, their effect can be expressed by the widening of the P wave, the complex by an extension of the PR interval, or by a combination of these features.
I class is subdivided depending on the speed of development of the effects of sodium channels, the lb class is characterized by fast kinetics, lc is the slow, la-average velocity. The kinetics of blockade of sodium channels determines the heart rate at which the electrophysiological effects of the subgroup of drugs are manifested. Since the lb class is characterized by rapid kinetics, their electrophysiological effects are manifested only at high heart rate. For this reason, an electrocardiogram recorded at a normal rhythm with a normal heart rate does not reflect a slowing down of the "fast-channel" heart tissue. Class lb preparations are not powerful antiarrhythmics and have minimal effect on atrial tissue. Since 1c class is characterized by slow kinetics, its electrophysiological effects are manifested at any heart rate. Thus, an electrocardiogram recorded at a normal rhythm and normal heart rate often shows a slowing down of the "fast-channel" tissue. Preparations of 1c class - more powerful antiarrhythmic drugs. Since class 1a has intermediate kinetics, their effect on the "fast-channel" impulse may be visible, but it may not be present on an electrocardiogram obtained at a normal rhythm with a normal heart rate. Class 1a preparations also block repolarized potassium channels, increasing the refractory period of the "fast-channel" tissue. According to the ECG, this effect is expressed by the prolongation of the QT interval even at normal heart rate. Class lb and 1c drugs do not directly block potassium channels.
Antiarrhythmic drugs (Williams classification)
A drug |
Doses |
Target concentration |
Side effects |
Comments |
1a class. Application: PES and VES, suppression of CBT and VT, suppression of AF, atrial flutter and FF
Dizopyranide |
Intravenous: first 1.5 mg / kg in more than 5 minutes, then continue infusion of 0.4 mg / kg per hour. Ingestion (immediate release preparation): 100 or 150 mg every 6 hours. Ingestion (slow release form): 200-300 mg after 12 hours |
2-7.5 μg / ml |
Anticholinergic effects (urinary retention, glaucoma, dry mouth, double vision, GI disorders), hypoglycemia, pirouette tachycardia, VT |
The drug should be used with caution in patients with impaired LV function. The dose is reduced with renal failure. Side effects can lead to a withdrawal from the drug. If the QRS complex expands (more than 50% at the initial <120 ms or> 25% at the initial> 120 ms), the amount of infusion or dose should be reduced (or cancel the drug). There is no intravenous form in the US |
Procainamide |
Intravenous: 10-15 mg / kg bolus at a rate of 25-50 mg / min, followed by a prolonged infusion of 1-4 mg / min. Ingestion: 250-625 mg (sometimes up to 1 g) every 3-4 hours |
4-8 g / ml |
Arterial hypotension (with the introduction), serological changes (predominantly AHA) in almost 100% of those taking 12 months, drug lupus (arthralgia, fever, pleurisy) in 15-20% of patients; agranulocytosis less than 1%, tachycardia of the type "pirouette", VT |
Medicinal forms with slow release can avoid frequent admission. If the complex is enlarged (more than 50% for the initial <120 ms or> 25% for the initial> 120 ms), the amount of infusion or dose should be reduced (or discontinued) |
Quinidine |
Ingestion: 200-400 mg after 4-6 hours |
2-6 μg / ml |
Diarrhea, colic and flatulence, fever, thrombocytopenia, violations of the liver, tachycardia of the type "pirouette", VT, the total proportion of side effects is 30% |
If the complex expands (more than 50% at the initial <120ms or> 25% at the initial> 120 ms), the amount of infusion or dose should be reduced (or cancel the drug) |
Lb class. Application: suppression of rhythm disturbances of the ventricles (VES, VT, VF)
Lidocaine |
Intravenous: 100 mg per 2 min followed by infusion of 4 mg / min (2 mg / min for patients over 65 years of age) |
2-5 μg / l |
Tremor, convulsions; with very rapid introduction of drowsiness, delirium, paresthesia |
To reduce the risk of toxicity, the dose or amount of administration should be reduced to 2 mg / min after 24 hours. Expressed metabolism at the first passage through the liver |
Mexiletin |
Ingestion (immediate release preparation): 100-250 mg every 8 hours. Ingestion (prolonged form): 360 mg every 12 hours. Intravenous: 2 mg / kg at a rate of 25 mg / min, then continue the administration of 250 mg per hour, 250 mg for the next 2 hours and continuously at a rate of 0.5 mg / min |
0.5-2 μg / ml |
Nausea, vomiting, tremor, convulsions |
Prolonged form for oral administration and form for intravenous administration are not available in the US |
1c class. Application: suppression of PES and VES, SVT and VT, AF or atrial flutter, as well as VF
Flecainide |
Ingestion: 100 mg every 8-12 hours. Intravenous administration: 1-2 mg / kg for 10 min |
0,2-1 m kg / ml |
Sometimes double vision and paresthesia; increases mortality in patients who underwent MI with asymptomatic or low-symptom VES |
The intravenous form is not available in the United States. If the QRS complex expands (more than 50% at the initial <120 ms or> 25% at the initial> 120 ms) or the QTk interval increases> 550 ms, the amount of infusion or dose should be reduced (or cancel the drug) |
II class (b-adrenoblockers). Application: SVT (PES, CT, CBT, AF, atrial flutter) and ventricular arrhythmias (often as ancillary drugs)
Proprano-lol |
Ingestion 10-30 mg 3-4 times a day. Intravenous 1-3 mg (can be repeated after 5 minutes if necessary) |
III class (membrane-stabilizing drugs). Application: any tachyarrhythmias, except VT by the type of "pirouette"
Amiodarone |
Ingestion 600-1200 mg / day for 7-10 days, then 400 mg / day for 3 weeks, then maintaining a dose (ideally - 200 mg / day). Intravenous injection of 150-450 mg for 1-6 hours (depending on the urgency), then maintain a dose of 0.5-2.0 mg / min |
1-2.5 μg / ml |
Fibrosis of the lung (approximately 5% of patients treated more than 5 years), which can be fatal; extension of QTk; sometimes tachycardia as pirouette, bradycardia |
The drug has a non-competitive b-adrenoblocking effect, long-term blocking calcium and sodium channels. Because of the prolonged refractoriness, amiodarone can lead to an adequate repolarization of the entire heart. A form for intravenous administration can be used to restore the rhythm |
Azimilide |
Ingestion 100-200 mg once a day |
200-1000 ng / ml |
ZT of the type "pirouette" |
|
Dofetilide |
Intravenous injection 2.5-4 m kg / ml. Ingestion 500 mcg 2 times a day, if KK> 60 ml / min; 250 μg 2 times a day, if the SC is 40-60 ml / min; 125 μg 2 times a day, if the SC is 20-40 ml / min |
Not determined |
ZT of the type "pirouette" |
The drug is contraindicated with an OTL elongation of more than 440 ms or if CC <20 ml / min |
Ibutilide |
Intravenous administration to patients with a body weight of 60 kg and more mg intravenous infusion, patients with a body weight of less than 60 kg 0.01 mg / kg for 10 min, then repeat after 10 min if the first administration is ineffective |
Not determined |
ZhT as "pirouette" (in 2% of cases) |
The drug is used to reduce the frequency of AF (the effect is manifested with a decrease in heart rate by 40%) and atrial flutter (65%, respectively) |
Sotalol |
Ingestion 80-160 mg through a 12h. Intravenous 10 mg for 1-2 min |
0.5-4 μg / ml |
Similar to Class II; possibly, depresses LV function and causes tachycardia by the type of "pirouette" |
The drug refers to b-adrenoblockers; racemic (DL) form possesses properties of class II, with the predominant activity of class III in the D-isomer. In clinical practice, only the racemic form of sotalol is used. The drug can not be prescribed for kidney failure |
Bretilia tosylate |
Intravenous administration: initial dose of 5 mg / kg, then 1-2 mg / min as a continuous infusion. With MI: first 5-10 mg / kg, can be repeated up to a total dose of 30 mg / kg. The maintenance dose at IM 5 mg / kg every 6-8 hours |
0.8-2.4 μg / ml |
Arterial hypotension |
The drug has properties of Class II. The effect can develop after 10-20 minutes. Brethilium tosylate is used to treat potentially lethal refractory ventricular tachyarrhythmias (resistant VT, recurrent VF), in which it is usually effective within 30 minutes after administration |
IV class (calcium channel blockers). Application: arresting SVT, slowing frequent AF and atrial flutter
Verapamil |
Ingestion 40-120 mg times or, when using the prolonged form, 180 mg once a day to 240 mg 2 times a day. |
Not determined |
May provoke the development of VF in patients with VT; has a negative inotropic effect |
Intravenous form is used to stop tachycardia with a narrow ventricular complex, including tachycardia from the AV node (the frequency of effectiveness is almost 100% with the application of 5-10 mg intravenously for 10 minutes) |
Diltiazem |
Ingestion (a drug with a slow release) 120-360 mg once a day. Intravenous administration of 5-5 mg / hour up to 24 hours |
0.1-0.4 μg / ml |
Can provoke VF in patients with VT; has a negative inotropic effect |
An abnormal form is most often used to reduce the incidence of ventricular contraction in AF or atrial flutter |
Other antiarrhythmic drugs
Adenosine phosphate |
6 mg rapidly intravenously bolus, repeat 2 times to a dose of 12 mg if necessary. Dissolve the bolus in 20 ml of isotonic sodium chloride solution |
Not determined |
Transient dyspnea, chest discomfort, redness of the face (in 30-60% of cases), bronchospasm |
The drug slows down or blocks the conduct at the level of the AV node. The duration of the action is extremely small. Contraindications include bronchial asthma and AV blockade of a high degree. Dipyridamole enhances the effect of the drug |
Digoxin |
Intravenous administration: loading dose 0.5 mg. Ingestion (maintenance dose) 0,125-0,25 mg / day |
0.8-1.6 μg / ml |
Anorexia, nausea, vomiting and often severe arrhythmias (ventricular extrasystole, ventricular tachycardia, atrial extrasystole, sinus tachycardia, AV blockade of 2nd and 3rd degree and a combination of these arrhythmias) |
Contraindications include antegrade conduction or the presence of functioning additional pathways (manifestation of ERW syndrome); may exert an excessive effect on the ventricular myocardium (digoxin reduces the refractory period in the cells of additional pathways) |
The main indication for the assignment of Classes 1a and 1c is SVT, and for the whole of Class I - VT. The most dangerous side effect is proarrhythmic, that is caused by the intake of the drug arrhythmia, which is more severe than the previous one. Class 1a can provoke the development of VT as a "pirouette", drugs 1a and 1c classes - cause atrial tachyarrhythmias to a sufficient extent to achieve atrioventricular conduction in a 1: 1 ratio with a pronounced increase in the frequency of conducting to the ventricles. All drugs of the first class are able to aggravate VT. They also tend to suppress ventricular contractility. Since these side effects of class I antiarrhythmic drugs are more likely to develop in patients with organic heart lesions, in general, these drugs are not recommended for such patients. These medications are usually prescribed only to patients without cardiac arrhythmias or patients with structural pathology that do not have an alternative in treatment.
Grade II
Class II drugs are represented by b-adrenoblockers, which predominantly act on tissues with slow channels (SP and AV nodes), where they lower the automatism, reduce the rate of conduction and prolong the refractory period. As a result, the heart rate slows down, the PR interval is prolonged, and the AV node conducts frequent atrial depolarization at a lower frequency. II class of antiarrhythmic drugs is used primarily for the treatment of SVT, including sinus tachycardia, re-entry at the level of the AV node, AF and atrial flutter. These drugs are also used to treat VT to increase the threshold for ventricular fibrillation (VF) and reduce ventricular pro-arrhythmic effects of b-adrenoreceptor stimulation. B-Adrenoblockers are generally well tolerated; side effects include rapid fatigue, sleep disorders and gastrointestinal disorders. These drugs are contraindicated in patients with bronchial asthma.
Grade III
It is predominantly calcium channel blockers, which prolong the duration of the action potential and refractoriness both in "fast channel" and in tissue with slow channels. As a result, the ability of all heart tissues to carry out impulses with high frequency is inhibited, but the conduct itself does not suffer much. As the action potential lengthens, the frequency of automatism decreases. The leading change in the electrocardiogram is the prolongation of the QT interval . Preparations of this class are used to treat SVT and VT. Ill class of drugs has a risk of proarrhythmias, mainly VT by the type of "pirouette".
IV class
Includes non-dihydropyridine calcium channel blockers that inhibit the calcium-dependent action potential in tissues containing slow calcium channels, and as a result, reduce automatism, slow down the ability to carry out, and prolong refractivity. The heart rate slows down, the PR interval is extended and the AV node conducts the atrial pulses at a lower frequency. Preparations of this class are used mainly for the treatment of CBT.
Attention!
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Description provided for informational purposes and is not a guide to self-healing. The need for this drug, the purpose of the treatment regimen, methods and dose of the drug is determined solely by the attending physician. Self-medication is dangerous for your health.