What Is an Antiarrhythmic?

Medicines that can prevent tachycardia, bradycardia or arrhythmia. But generally refers to the prevention and treatment of tachycardia and some arrhythmic drugs.

Chinese name: Antiarrhythmics
Foreign name: antiarrhythmic drugs
Attend: Treating cardiac rhythm disorders

Pathological mechanism: Excitability and conductivity of cardiomyocytes
proposer: Vaughan Williams
Classification basis: Electrophysiological characteristics of drug action

Introduction to antiarrhythmic drugs

English name: antiarrhythmic drugs

Antiarrhythmic drugs are a class of drugs used to treat cardiac rhythm disorders. With the understanding of the electrophysiological properties of the heart and the mechanism of action of anti-arrhythmic drugs, great progress has been made in the medical treatment of arrhythmias.

Arrhythmias are abnormalities in the frequency and rhythm of the heart, which can be divided into two types, fast and slow. Bradyarrhythmias can be treated with atropine or epinephrine. Tachycardia is more complicated, and it includes atrial premature contraction, atrial tachycardia, atrial fibrillation, atrial flutter, paroxysmal supraventricular tachycardia, ventricular premature beats, ventricular tachycardia, and ventricular fibrillation. Wait. This chapter mainly discusses drugs for treating tachyarrhythmias.

Pathogenesis of antiarrhythmic drugs

heart Cardiomyocytes can be roughly divided into two categories. One type is working cells, including atrial and ventricular muscles, which mainly play a mechanical contractile role and are excitatory and conductive. The other type is autonomic cells, which have the ability to automatically generate rhythms, as well as excitability and conductivity. These specially differentiated cells also form a special conduction system, including the sinoatrial node, atrial conduction bundle, atrioventricular node (atrioventricular junction zone), atrioventricular bundle, and Purkinje fibers.

Antiarrhythmic cell membrane potential

1. Resting potential refers to the potential state in which the myocardial cells are in the resting state and negative in the membrane, which is also called polarization state. Its shape is because the sodium channel is closed, the potassium channel is open, and intracellular high potassium At rest, it is mainly a result of permeability to K +.

2. Action potentials When cardiomyocytes are stimulated and excited, depolarization and repolarization occur, membrane potentials rise, and action potentials occur when the threshold potential is reached. Taking ventricular myocytes as an example, the entire action potential can be divided into:

Phase O: It is the depolarization process. The fast sodium channel of the membrane is opened, and a large number of Na's inflows cause depolarization, and even the polarized action potential rapidly rises from -90mv to + 30mv during the resting state. The depolarization phase is very short, about 1 ~ 2ms.

Phase 1: It is the early stage of rapid repolarization, which is mainly caused by the transient outflow of K + and the inflow of C1-. Membrane potential drops rapidly from + 30mV to about Omv.

Phase 2: For the slow repolarization period, the membrane potential basically stagnates at about 0mv, also known as the plateau phase. This period is mainly due to the slow inflow of Ca2 + and a small amount of Na +, accompanied by a small outflow of K + and an inflow of Cl-.

Phase 3: It is the end of rapid repolarization, which is caused by rapid outflow of K +.

Phase 4: After repolarization, the ventricular myocytes are at rest. Due to the action of Na + and K + -ATPase, the cells pump out Na + and take in K + to restore the ion distribution of resting potential. After the autonomic myocardial cells such as sinoatrial node, atrioventricular node, atrioventricular bundle and Purkinje fiber reach the maximum diastolic potential, they are slowly depolarized automatically, and the membrane potential rises. Action potential and excitement.

Electrophysiological properties of antiarrhythmic drugs

1. Excitability Excitability is the ability to generate action potentials after stimulation of the myocardium. The threshold of excitability can be used as an indicator. A large threshold indicates low excitability, and a small threshold indicates high excitability. Cardiac cell membrane action potentials have different excitability in each phase, which can produce periodic excitatory changes such as effective refractory period, relative refractory period, and extraordinary period.

2. Autonomy The sinoatrial node, the atrioventricular node and the atrioventricular conduction system are all autonomic cells, that is, after reaching the maximum diastolic potential of 4 phases, it can slowly and automatically depolarize, and the action potential occurs after reaching the threshold potential. This is due to the slow outflow of K + and slow inflow of Na + or Ca2 + in 4-phase potential. Autonomy is affected by the speed of automatic depolarization, maximum diastolic potential, and threshold potential. According to the speed and amplitude of O phase depolarization, it can be divided into fast-responding autonomous cells and slow-responding autonomous cells. The former includes atrial conduction tissue, atrioventricular bundle, and Purkinje fiber (non-autonomous atrial muscle, ventricle). Myocytes are fast-responding cells), which include the sinoatrial node and the atrioventricular node. The main difference between the two types of cells is that the autonomy of fast-responding cells is mainly caused by Na + influx, while slow-responding cells are caused by Ca2 + influx.

3. Conductivity The speed at which action potentials spread along the cell membrane can be used as an indicator of conductivity. Since the conductivity of various cardiomyocytes varies, the speed at which excitement spreads in these parts is also not equal. The conduction velocity of the same cell is affected by a variety of factors. Among them, the factor that affects the resting potential (or maximum diastolic potential) and the excitation threshold potential to change the difference has the greatest effect on the conduction velocity. The action rate of the 0-phase depolarization of the action potential determines the conductivity. The O-phase depolarization of the fast-responding autonomous cells is determined by Na-influx, and the O-phase depolarization of the slow-reaction autonomous cells is determined by the Ca2 + influx. Generally, the membrane potential is large. Phase 0 rises fast, the amplitude is large, and the conduction speed is fast; otherwise, the conduction is slow. Therefore, blocking Na + inflow or Ca2 + inflow can inhibit conduction.

Electrophysiological mechanism of antiarrhythmic drugs

Arrhythmias are mainly due to impulse formation abnormalities, impulse conduction abnormalities, or both.

1. Impulsive abnormalities -increased autonomy is related to the 4-stage diastolic depolarization speed, maximum diastolic potential, and threshold potential. The 4-phase diastolic depolarization speeds up, the threshold potential moves down or the maximum diastolic potential becomes smaller, that is, the gap with the threshold potential decreases, and the autonomy increases. For example, the sympathetic nerve excitement reduces the K + outflow of 4 phases, promotes the inflow of Na + and Ca2 +, and accelerates the speed of 4 phase diastolic depolarization. When myocardial ischemia and hypoxia, the energy supply of the myocardium is insufficient, and the Na + -K + pump is incomplete, causing intracellular Loss of K + decreases the maximum diastolic potential, and at the same time 4-phase K + efflux decreases, increasing autonomy; digitalis poisoning Na +, K + -ATPase is severely inhibited, and intracellular K + loss also increases autonomy. Various pre-period contractions and paroxysmal tachycardia can occur.

2. Impulse conduction abnormality -reentry formation of reentrant excitement refers to _ times of impulse transmission, which can be re-excited along another circular path to excite the original excited myocardium again. Reentrant excitement forms various types of arrhythmia. Important reason. The ventricular "Purkinje fiber-ventricular muscle loop" is taken as an example to illustrate it (Figure 23-1).

Under normal circumstances, the impulses transmitted by the sinoatrial node pass through the two branches of Purkinje fiber A and B, reach the ventricular muscles at the same time, and disappear during the refractory period of the adjacent myocardium. The impulses cannot continue to conduct and disappear (Figure 23-1a) . However, under pathological conditions, one-way conduction block may occur in the branch of Purkinje fibers. For example, when the B branch is affected, the impulse is transmitted to the two branches A and B when the impulse is transmitted to the two branches A and B. The impulse can only pass down the A branch. After the ventricular muscles are excited, the impulse can be retrogradely transmitted to the A branch through the B branch; at this time, the refractory period of the A branch has passed, and excitement occurs again, resulting in reentrant excitement. Single reentry causes pre-period contraction, and continuous reentry causes paroxysmal tachycardia, flutter, or tremor. Reentry occurs not only in the ventricle, but also in the atria, atrioventricular junctions, etc., resulting in various types of tachycardia.

In addition, when local lesions, the effective refractory period (ERP) of a branch fiber is shortened or conduction is reduced, or when the ERP of adjacent myocardial fibers is uneven, reentry can also be formed.

Antiarrhythmic Drug Mechanism

Medical staff monitors arrhythmias with ECG It is mainly to correct the arrhythmia by affecting the Na +, Ca2 + and K + transport of the myocardial cell membrane, affecting the various phases of myocardial action potential, inhibiting autonomy and / or stopping reentry.

Because the mechanism of arrhythmia is more complex, and the effects and side effects of various antiarrhythmic drugs are also different, comprehensive consideration must be taken when choosing a drug, and the dosage and method of the drug should be paid attention to in order to achieve the expected results.

Antiarrhythmic Drug Classification

Classification basis of antiarrhythmic drugs

The classification of antiarrhythmic drugs has been used for nearly 30 years, proposed by Vaughan Williams, and supplemented by Harris et al. Vaughan Williams classification classifies drugs into four categories based on their electrophysiological characteristics.

Specific classification of antiarrhythmic drugs

Class I

Blocking the sodium channels of the myocardial and cardiac conduction systems has membrane stabilization, reduces the rate and amplitude of the 0-phase depolarization of the action potential, slows the conduction rate, and prolongs the APD and ERP. No effect on resting membrane potential. According to the different effects of drugs on the blockade of sodium channels, they are divided into three subclasses, namely a, b, c.

(1) Class a moderately blocks sodium channels with a resuscitation time constant of 1 to 10 s, which is most significant in prolonging ERP. Drugs include quinidine, procainamide, and propiramine.

(2) Class Ib mildly blocks sodium channels, with a resuscitation time constant of <1s, reducing autonomy. Drugs include lidocaine, phenytoin, and mexiletine.

(3) Type Ic significantly blocks sodium channels, and the reactivation time constant is> 10s, which has the strongest effect of slowing conductivity. Medications include propafenone, enkani, flukani, etc.

Class II

Beta blockers inhibit the increase of pacing current, sodium current, and L-type calcium current caused by sympathetic nerve excitability, which is manifested by slowing down the 4-phase diastolic depolarization rate, reducing autonomy, and lowering the action potential 0 Rate while slowing conductivity. Drugs include propranolol, atenolol, metoprolol, and others.

Class III

Prolonged action potential duration drugs, inhibit a variety of potassium currents, including amiodarone, sotalol, benzyl bromide, ibutiri and dofetil.

Class IV

Calcium channel blockers, including verapamil and diltiazem.

Antiarrhythmic drugs commonly used drugs

Antiarrhythmic sodium channel blockers

Quinidine

Antiarrhythmic drugs [Indications] For a variety of tachyarrhythmias. Including atrial and ventricular premature contractions; conversion of atrial flutter and atrial fibrillation, conversion of supraventricular and ventricular tachycardia; preexcitation syndrome.

[Contraindications] Heart failure, hypotension, severe sinus node disease, high AV block, pregnancy.

[Adverse reactions] Common gastrointestinal reactions, nausea, vomiting, diarrhea, etc. at the beginning of administration. For long-term use, "cinchonism" may occur, manifested as headache, dizziness, tinnitus, blurred vision, mental disorders and other symptoms, as well as allergic reactions such as drug fever and rash. Quinidine syncope usually occurs within the first few days of medication, is a specific response, and has no parallel relationship with the dose of the drug. It may be related to hypokalemia, cardiac insufficiency, or sensitivity to this drug.

Procainamide

[Indications] It is a broad-spectrum antitachycardia drug. Its effect is similar to quinidine, but its strength and toxicity are small. It is mainly used for ventricular arrhythmias, such as preventricular contraction and ventricular tachycardia, especially ventricular arrhythmias in acute myocardial infarction. It can also be used for cardioversion. treatment.

[Adverse reactions] Gastrointestinal reactions may be caused orally; intravenous administration may cause hypotension. Large doses have a cardiac mechanism. Allergic reactions are more common, such as rash, fever, leukocytopenia, and myalgia. Central adverse reactions include hallucinations and mental disorders. With long-term application, a few patients develop lupus erythematosus syndrome.

Disopyramide

[Indications] Propylamine is a broad-spectrum antiarrhythmic drug, which can be used to treat a variety of supraventricular or ventricular arrhythmias, and is particularly suitable for preventing recurrence of atrial fibrillation after cardioversion and arrhythmia after myocardial infarction.

[Contraindications] Glaucoma, prostatic hypertrophy, heart failure, atrioventricular block, or cardiogenic shock.

[Adverse reactions] Anticholinergic effects cause dry mouth, constipation, poor urination or urinary retention. A few may have rash, hypoglycemia, and granulocytopenia.

Lidocaine

[Indications] Reversion and prevention of ventricular tachyarrhythmias, such as myocardial infarction, ventricular tachycardia, and ventricular tachycardia, ventricular flutter, and ventricular fibrillation.

[Contraindications] Allergic to lidocaine, high AV block, heart failure, etc.

[Adverse reactions] More common central symptoms, such as drowsiness, dizziness, excitement, speech and swallowing difficulties, irritability at large doses, muscle convulsions, hypotension, and conduction block.

Mexiletine

[Indications] The chemical structure and electrophysiological effects of mexiletine are similar to lidocaine, and are used for various ventricular arrhythmias, for cardiac glycosides poisoning, ventricular premature beats caused by myocardial infarction or surgery, ventricular tachycardia, etc. effective.

[Contraindications] Severe heart failure, cardiogenic shock, slow arrhythmia, and ventricular block.

[Adverse reactions] Less and less. Large doses can cause gastrointestinal reactions, nervous system reactions such as dizziness, ataxia and so on. Intravenous medication can occasionally produce hypotension, bradycardia, and conduction block.

Phenytoin

[Indications] Phenytoin works similarly to lidocaine. It competes with cardiac glycosides for Na + -K + -ATPase and inhibits the triggering activity caused by cardiac glycoside poisoning. This medicine is mainly used to treat ventricular arrhythmias, especially effective for ventricular arrhythmias caused by cardiac glycoside poisoning. It can also be used for ventricular arrhythmias caused by myocardial infarction, cardiac surgery, cardiac catheterization, etc., but the effect is not as good as that of Lido Caine.

[Contraindications] Pregnancy, hypotension, sinus bradycardia, and degree atrioventricular block.

[Adverse reactions] Common central adverse reactions include dizziness, dizziness, tremor, and ataxia. Intravenous phenytoin can easily cause hypotension, and high concentrations can cause bradycardia.

Propafenone

[Indications] Propafenone is a class Ic antiarrhythmic drug with local anesthesia, and belongs to a broad spectrum of antiarrhythmic drugs. For a variety of supraventricular and pre-ventricular contractions, supraventricular and ventricular tachycardia, pre-excitation syndrome associated with tachycardia and atrial fibrillation.

[Contraindications] Pregnant and lactating women, sick sinus node syndrome, heart failure, atrioventricular block. This medicine is generally not suitable for combination with other antiarrhythmic drugs to avoid cardiac depression.

[Adverse reactions] Gastrointestinal reactions, a small number of patients with bradycardia, atrioventricular block, can also cause orthostatic hypotension. QT interval prolongation should be reduced or discontinued.

Flecainide

[Indications] Broad-spectrum antiarrhythmic drugs with membrane stabilization. It is effective for both supraventricular and ventricular arrhythmias, and for atrioventricular reentrant tachycardia, the effective rate is above 90%.

[Contraindications] Sick sinus syndrome, conduction block, heart failure, etc.

[Adverse reactions] Dizziness, fatigue, nausea, etc. The heart is mainly arrhythmogenic.

Antiarrhythmic drugs beta blockers

Beta blockers have an antiarrhythmic effect by blocking the beta receptors in myocardial cells. Its electrophysiological effects include slowing down the diastolic automatic depolarization speed, inhibiting cardiac autonomy and conductivity, and shortening the action potential duration. At the same time, it has membrane stabilization effect.

Propranolol

[Indications] Sinus tachycardia, especially sympathetic hyperthyroidism, hyperthyroidism and pheochromocytoma are effective. It can also be used for supraventricular and preventricular contractions and tachycardia, arrhythmia caused by pre-excitation syndrome and LQTS. Reduces arrhythmias caused by hypertrophic cardiomyopathy.

[Adverse reactions] This medicine can cause sinus bradycardia, atrioventricular block, and may induce heart failure, asthma, hypotension, etc. Long-term application has adverse effects on lipid metabolism and glucose metabolism, so patients with hyperlipidemia and diabetes should be used with caution. Sudden withdrawal can cause a rebound phenomenon.

Antiarrhythmic calcium channel blocker

This class of drugs mainly reduces the excitability of the sinoatrial node and the atrioventricular node conductivity by blocking the slow calcium channels and reducing the influx of calcium ions, and the refractory period is prolonged. It is mainly used for the treatment of supraventricular arrhythmias, and is a narrow-spectrum antiarrhythmic drug.

Verapamil

[Indications] The treatment of arrhythmia caused by supraventricular and atrioventricular node reentry is effective, and it is the first choice for paroxysmal supraventricular tachycardia. Effective for early myocardial infarction, myocardial ischemia and cardiac glycoside poisoning.

[Contraindications] Patients with and degree atrioventricular block, cardiac insufficiency, and cardiogenic shock.

[Adverse reactions] Dry mouth, nausea, bloating, diarrhea, headache and dizziness are common. Intravenous injection may cause blood pressure drop, bradycardia, and severe cases may cause cardiac arrest.

Antiarrhythmic drugs

Amiodarone

[Indications] atrial arrhythmias, such as atrial fibrillation and atrial flutter reversion; nodular arrhythmias; ventricular arrhythmias, including ventricular premature contractions, treatment of ventricular tachycardia, and ventricular tachycardia Prevention of tachycardia or ventricular fibrillation; A small dose is suitable for arrhythmias with organic heart disease, such as combined ventricular arrhythmias with acute myocardial infarction and heart failure.

[Contraindications] Sinus bradycardia and sinoatrial block; high conduction block; abnormal thyroid function; iodine allergy; pregnancy and lactation.

[Adverse reactions] Adverse reactions are dose-related. Common cardiovascular reactions include sinus bradycardia, atrioventricular block, and prolonged QT interval. Long-term application of this product shows corneal brown particles, usually asymptomatic; a few patients with hyperthyroidism or hypothyroidism and liver necrosis; individual patients with interstitial pneumonia or pulmonary fibrosis.

Other antiarrhythmic drugs

Adenosine

Adenosine acts on G protein-coupled adenosine receptors, activates acetylcholine-sensitive potassium channels, and reduces autonomy. At the same time, ICa (L) was inhibited, and atrioventricular node ERP was prolonged. It is clinically used to quickly terminate reentrant supraventricular tachycardia, which requires rapid intravenous injection when used.

Antiarrhythmic drugs are safe

Antiarrhythmics

The arrhythmogenic effect of antiarrhythmic drugs refers to that these drugs can cause the occurrence of new arrhythmias or increase the original arrhythmia, such as ventricular

Use of antiarrhythmic drugs requires safety Increased frequency of premature beats (3 to 10 times), accelerated ventricular tachycardia rate (more than 10%), changed from non-sustained VT to continuous VT, from monomorphic to apical torsional VT or Worsened to ventricular fibrillation.

All antiarrhythmic drugs have arrhythmogenic effects, the incidence rate is 6% ~ 36%, and the mechanism is related to the formation of ECG impulse or conduction disorder. Susceptible factors or causes include recurrent or persistent ventricular tachycardia, left ventricular dysfunction, myocardial ischemia, conduction block, prolonged QT interval, electrolyte (potassium, magnesium, etc.) disorders, inappropriate use of drugs, poor liver and kidney function, Drug compatibility is unreasonable. The antiarrhythmic and arrhythmic effects of these drugs coexist almost, the antiarrhythmic effect on normal myocardium is small, and the arrhythmogenic effect on pathological (ischemia, hypertrophy, heart failure) myocardium is greater.

Medical evidence of antiarrhythmic drugs

From 1993 to 2004, researchers completed a total of 138 clinical trials of related drugs, including 98,000 patients.

A total of 59 class I antiarrhythmic drug-related trials of class antiarrhythmic drugs found that the mortality rate in the drug treatment group (5.6%) was significantly higher than that in the control group (5.0%). Of these, 16 trials involved Class Ia drugs, and the results showed that the treatment group (13,292 patients) had a higher mortality rate than the control group (13,290 patients) (7.7% vs. 6.6%). There were 25 studies involving class Ib drugs, and there was no statistical difference in mortality between the treatment group (7068 cases) and the control group (6945 cases) (P> 0.05). In the study of class c antiarrhythmic drugs, the CAST test showed that the arrhythmia mortality rate in the flucaramide / incaline group was significantly higher than the control group (4.5% vs. 1.2% P <0.05), and the total mortality rate was also significantly increased (7.7% vs. 3.0%, P <0.05), Morexazine also increased mortality. Studies such as IMPACT have reached similar conclusions.

Data from 55 related clinical trials of class II antiarrhythmic drugs show that the beta-blocker group (26,973 patients) has a significantly lower mortality rate than the control group (26,295 patients) (5.4%). P> 0.05 for 6.6%).

In 13 related clinical trials (6553 cases) of class III antiarrhythmic drugs, the overall mortality rate of patients with myocardial infarction or congestive heart failure who were randomized to amiodarone was 13% lower than that of the control group, and the incidence of arrhythmic death or sudden death was reduced. 29%.

A total of 24 related clinical trials (20,342 cases) of class IV antiarrhythmic drugs found that the mortality rate of the verapamil-treated group was 10.1% and that of the control group was 10.6%.

Application Principles of Antiarrhythmic Drugs

The understanding of arrhythmia and the concept of diagnosis and treatment have been updated. At present, it is generally believed that most of the ventricular premature beats are functional. Unless symptomatic treatment is needed, the majority of premature beats should not require antiarrhythmic drugs.

Premature beats Most non-cardiac heart beats require no treatment. If you want to remove the inducement, you can take a sedative or beta blocker to eliminate tension. Drugs with less adverse reactions can be selected for treatment, such as -receptor blockers, mexiletine, morrelizine, propafenone, etc., and can also be supplemented with proprietary Chinese medicine. Organs such as amiodarone or quinidine are highly toxic and have a high risk of arrhythmia. They are generally not used during treatment. Organic premature ventricular premature beats should be targeted at basic heart disease treatment, control the cause, and correct the causes of low potassium, low magnesium, digitalis poisoning, and so on.

Ventricular tachycardia studies have shown that the use of amiodarone in the rescue of out-of-hospital cardiac arrest has a higher survival rate and a lower relapse rate than with lidocaine. Therefore, the current guidelines advocate amiodarone for VT. If the patient's hemodynamics is unstable, he should immediately undergo cardioversion or defibrillation, prepare for cardiopulmonary resuscitation, correct the inducement, and treat the primary disease. Amiodarone or sotalol can be used as a secondary preventive agent for malignant ventricular arrhythmias or in combination with an embedded defibrillator (ICD).

Amiodarone has class ~ antiarrhythmic drugs. It is mainly used to treat life-threatening ventricular tachycardia or ventricular fibrillation (survivors of sudden death), improve the effect of electrical defibrillation, treat arrhythmia with cardiac dysfunction, and atrial fibrillation, Atrial flutter rhythm and sinus rhythm maintenance. The incidence of adverse reactions of amiodarone is about 80%, but only 10% to 15% of them need to be discontinued. Among them, the incidence of lung toxicity is 1% to 15%, and the incidence of lung toxicity is low when maintained at low doses (0.4 g / day). You can also see abnormal thyroid function, in which the incidence of hyperthyroidism is about 2%, which can disappear after several weeks to several months, a few patients need antithyroid drugs; the incidence of hypothyroidism is 1% to 4%, more common in the elderly Patients, remission after months of withdrawal. Patients may also suffer liver damage with elevated transaminase and alkaline phosphatase, hepatitis, and cirrhosis, with an incidence of less than 3%. The adverse reactions are also cardiotoxicity. Patients may have sinus bradycardia, sinus arrest, sinoatrial block or atrioventricular block, and occasionally prolong QT interval with apical torsional ventricular tachycardia. In addition, hypotension can occur when the IV is fast.

Antiarrhythmic drugs use and side effects

Lidocaine

Uses: Acute myocardial infarction with ventricular tachycardia

Side effects: lethargy, dizziness, psychiatric symptoms at high doses, hypotension, respiratory depression

2.Mexiletine

Uses: Ventricular tachycardia, arrhythmia

Side effects: dizziness, nausea, tremor, less blood cell loss, high-dose intravenous administration can cause psychiatric symptoms and cardiovascular depression (bradycardia, conduction block, heart failure, hypotension)

3. Morexizine

Uses: Ventricular and supraventricular premature beats and various types of tachycardia

Side effects: gastrointestinal reactions, nervous system irritation (drowsiness, dizziness, tremor), cardiovascular depression at high doses

4. Propafenone

Uses: all types of premature beats, tachycardia, pre-excitation syndrome

Side effects: dizziness, headache, dry mouth, nausea, vomiting, large doses have cardiovascular inhibitory effects (sinus node suppression, atrioventricular block, hypotension), may increase bronchospasm, heart failure, metallic taste in the mouth, eyes flash, Finger tremor

5.Metoprolol (Betalock)

Uses: hypertension, coronary heart disease with premature beats, tachycardia

Side effects: insomnia, cold at the extremities, bloating, constipation, cardiovascular depression at high doses

6. Amiodarone

Uses: various premature beats, tachycardia, atrial flutter, atrial fibrillation, pre-excitation syndrome

Side effects: gastrointestinal irritation, microkeratosis, thyroid dysfunction, pulmonary interstitial fibrosis (most severe), large doses can cause cardiovascular depression and torsional ventricular tachycardia, elevated transaminase, and occasionally cirrhosis

7. Verapamil (Varidium)

Uses: supraventricular premature beat, supraventricular tachycardia, slow ventricular rate of atrial fibrillation, atrial flutter

Side effects: dizziness, headache, gastrointestinal reactions, bradycardia, atrioventricular block, and hypotension

8. Diltiazem