In today’s dizzying world of interventional therapy, although more and more tachyarrhythmias can be cured by catheter ablation and the placement of pacemakers in slow arrhythmias is not a concern, pharmacological therapy remains the cornerstone and mainstay of antiarrhythmic treatment, covering the majority of antiarrhythmic therapy, often as the first choice and long-term maintenance therapy. Therefore, the rational application of antiarrhythmic drugs has become a topic of widespread concern among clinicians.
1. Risk stratification first, then decide on the program
In the face of patients with arrhythmias, the first step is to make a clear diagnosis and risk stratification before deciding on immediate and long-term treatment options according to the degree of risk.
1.1 Malignant and potentially malignant arrhythmias
For malignant and potentially malignant arrhythmias, the decision on what antiarrhythmic drugs to use and how to use them should be based on the preferential selection of appropriate nonpharmacologic therapy. For example, for patients eligible for implantable cardioverter-defibrillator (ICD) placement, the decision on how to apply β-blockers and/or amiodarone must be made on the basis of ICD placement; for patients eligible for pacemaker placement, it is even more important to talk about pacemaker therapy before applying antiarrhythmic drugs, otherwise the drugs will lead to increased arrest or conduction disturbance; for patients with ventricular tachycardia, it is even more important to consider In patients with ventricular tachycardia, it is more important to consider the necessity of transcatheter ablation therapy.
1.2 Arrhythmias that do not require treatment
These patients should be educated to avoid unhealthy lifestyles, such as avoiding or reducing the use of alcohol, coffee, tea and other stimulants that can aggravate arrhythmias, and avoiding overexertion, staying up late, excitement and anger. In addition, it is also crucial to instruct patients on how to regularly review and self-monitor their pulse to assess arrhythmias. The application of anti-arrhythmic drugs in these patients is not only unhelpful, but in some cases aggravates the existing arrhythmia or even induces new arrhythmias (arrhythmogenic effects of anti-arrhythmic drugs).
2, intravenous drugs need to pay attention to the method and strengthen monitoring
Intravenous medication is generally used for acute arrhythmia attacks, or to restore existing arrhythmias. Because of its rapid and powerful effect, attention must be paid to strengthen monitoring when applying.
2.1 Adequate knowledge of the organism before drug administration
In the most urgent cases, it is important to quickly understand the patient’s body condition (of course, in more urgent cases, electrical resuscitation is chosen), such as what disease? What medications are being taken? What is the current heart rate? How long has the arrhythmia lasted? Are there any electrolyte disturbances? For example, in patients with atrial fibrillation (AF), if QTc is prolonged, hypokalemia is present, or AF has not been detected by transesophageal echocardiography for several days, and anticoagulants are not used, the medication is like walking a tightrope before applying eptifibrotide or amiodarone.
2.2 Appropriate prolongation of monitoring time
Some drugs require prolonged electrocardiographic monitoring, for example, when ibrate is used to revert atrial flutter or atrial fibrillation, even if it has been reverted to sinus rhythm, the monitoring time should be extended appropriately to observe the changes in QTc and the presence of premature ventricular beats and tip-twisting ventricular tachycardia.
2.3 Pay attention to the necessary protective measures
In elderly patients, especially those with slow heart rate and long duration of tachyarrhythmia on weekdays, they must be alert to the presence of sinus node dysfunction, and the sinus node is inhibited by rapid ectopic rhythm point for too long, therefore, the moment of drug diversion is likely to have a longer period of sinus arrest or even secondary malignant ventricular arrhythmia, so they must be prepared for temporary pacing. It is also possible that when the atrial flutter is reversed with drugs, the frequency of atrial flutter may slow down slightly (e.g. from 300 beats/min to 260 beats/min) due to the drug slowing down the intra-atrial conduction, and the original 2:1 downward transmission (ventricular rate of 150 beats/min) may suddenly become 1:1 downward transmission (ventricular rate of 260 beats/min), and the patient may have an immediate onset of As syndrome, which requires electrical resuscitation (I have encountered two cases). The author has also encountered patients with prolonged sinus arrest after pharmacological conversion of atrial flutter.
2.4 Give adequate loading volume
When amiodarone is used to revive atrial fibrillation, a sufficient loading dose must be given to be effective. Generally speaking, the loading dose of amiodarone is 5-7 mg/kg, such as at least 300 mg for a patient with a body weight of 60 kg, and if 300 mg is not reversed, an additional 150 mg can be administered, preferably with a micro-chestnut or infusion pump to ensure uniform input within the required time. The author has observed that when applying Ebritt to revert atrial fibrillation, if a large syringe is used for pushing, ventricular premature beats or even tip-twisting ventricular tachycardia may occur when the speed is fast.
2.5 The correct method of drug administration
The use of the same drug for the same arrhythmia may have very different results. For example, when applying adenosine or ATP to revert paroxysmal supraventricular tachycardia, it is necessary to use a projectile injection to be effective, i.e., push the drug in the fastest way within 12 seconds, and then immediately push it in the fastest way with 5 ml of saline, so that the effect can be immediate and can be reverted in about 1 minute. For example, ATP was previously administered at 20mg (1 stick) in a rapid intravenous push, but the scientific usage should be administered according to body weight, 0.1~0.3mg/kg, with an average of 0.2mg/kg (for a patient weighing 60kg, only 12mg is needed), which can significantly reduce the occurrence of adverse reactions.
2.6 Safety and non-safety are relative
Since the repolarization prolongation of the inner, middle and outer layers of the myocardium by amiodarone is relatively homogeneous, QT interval prolongation or even tip-twisting ventricular tachycardia caused by the other three types of drugs rarely occurs after application, plus it is effective for both supraventricular tachycardia and ventricular tachycardia, and can be used in patients with myocardial infarction and heart failure, many doctors consider it a safe ” panacea”. In fact, in patients with prolonged QTc and hypokalemia, the tip-twist ventricular tachycardia can also occur. For the three types of drugs that are more prone to tip-twisting ventricular tachycardia (such as Ibutilide), they are safe to use in relatively safe patients (no QTc prolongation, blood potassium not less than 4.0 mmol/L), and pay attention to the method of administration.
3, clinical application of oral drugs should be long-term vision
In the application of oral antiarrhythmic drugs, it is advisable to take a long-term view and think long term.
3.1 Class I drugs are not eliminated
In the process of clinical use, many doctors think that although class I drugs are effective in antiarrhythmia, they are not useful or even harmful to reduce death, so they give up applying them even to patients without cardiac structural or functional abnormalities, and instead abuse the second-line drug amiodarone as an all-purpose first-line drug, which is groundless. Clinical studies that are unfavorable to class I drugs are for patients with myocardial infarction and heart failure, and class I drugs are still essential first-line therapeutic drugs as long as the patients do not belong to these two conditions.
In contrast, quinidine is the only drug on the market that has a significant Ito inhibitory effect, and the Ito inhibitory effect of this drug is stronger than the sodium ion flow inhibitory effect. Studies have confirmed that quinidine restores the epicardial action potential dome, normalizes the elevated ST segment, and inhibits the formation of 2-phase folding and the onset of ventricular tachycardia. Quinidine normalizes the ST segment in patients with Brugada syndrome and effectively inhibits the development of ventricular fibrillation and spontaneous arrhythmias during electrophysiological examinations. Quinidine is also an effective alternative to ICD therapy in patients who have been fitted with an ICD but have had multiple therapeutic shocks, in patients with Brugada syndrome who present with electrical storms, and in pediatric patients. The current recommended dose is 10001500 mg/d. The efficacy and safety of quinidine compared to the effects of an ICD are yet to be further confirmed in clinical trials. And another study in 6 patients with short QT syndrome compared the effect of flucarbamide, sotalol, Ibutilide, and quinidine, and found that only quinidine could prolong the QT interval from (290±13) ms to (405±26) ms, while the other three drugs did not have this effect, which is expected to be the drug for short QT syndrome.
3.2 Caution is needed for combination drug use
When antiarrhythmic drugs are combined, extra care should be taken to pay attention not only to the inhibition of sinus node autoregulation, atrioventricular node conduction, and myocardial contractility, but also to the synergistic effect on QTc interval prolongation, especially in women, patients with heart failure, patients with organic heart disease, and when macrolide antibiotics and tricyclic antidepressants that can prolong the QT interval are also applied, more attention should be paid to enhance Monitoring.
4, pay attention to the monitoring of adverse drug reactions
Regular monitoring of electrocardiogram, blood and urine routine, liver and kidney function, chest X-ray, dynamic electrocardiogram, echocardiogram, etc. should be performed after the use of drugs. It is very important to ask relevant symptoms, conduct detailed physical examination and compare with baseline data during outpatient review, which can help early detection and timely treatment.
5.The timing of medication should be individualized
Some patients have arrhythmias concentrated in the daytime, others in the night, and most have them both day and night. For patients with daytime attacks only, they are often associated with increased sympathetic tone, so medium-acting beta-blockers are preferred, and one morning dose is sufficient, avoiding long-acting drugs. For patients with nocturnal episodes only, sleep apnea monitoring should be performed to exclude secondary arrhythmias caused by sleep apnea. The arrhythmias will improve significantly with the application of continuous positive pressure ventilation (CPAP) and other treatments, and if antiarrhythmic drugs must be used, one dose of antiarrhythmic drugs after dinner or at bedtime is sufficient. Considering the convenience and compliance of patients in taking medication and reducing the stimulation of the gastrointestinal tract, even if Q6H medication is required daily, it can be taken after three meals and before bedtime.
Since antiarrhythmic drugs have arrhythmogenic effects, their indications and adverse effects must be strictly grasped and applied correctly. First of all, it should be determined whether it is necessary to use antiarrhythmic drugs and avoid abuse. Try to use drugs with high efficacy and low side effects. Before using antiarrhythmic drugs, attention should be paid to correct myocardial ischemia and heart pump failure, and correct electrolyte disorders, especially hypochondriasis. The drugs should be started in small doses and gradually increased when they are ineffective, and the combination of drugs should be minimized. When combining antiarrhythmic drugs and other drugs, attention should be paid to the mutual adverse effects and contraindications. When antiarrhythmic drugs are applied intravenously, electrocardiographic monitoring should be performed. For long-term use, blood concentration should be monitored if available. Once the arrhythmia is aggravated or new arrhythmia occurs, the arrhythmogenic drugs should be stopped immediately.
In conclusion, the focus of pharmacological treatment of cardiac arrhythmias is to skillfully grasp the mechanism of action, efficacy, side effects and treatment principles of each antiarrhythmic drug and to individualize its use according to the patient’s condition. As research progresses and various new antiarrhythmic drugs are developed, their clinical application value still needs to be verified, and the use of classical antiarrhythmic drugs still needs to be mastered by clinicians. As long as patients are carefully evaluated, risk stratified, personalized drug administration, monitoring is strengthened, and necessary protective measures are taken, antiarrhythmic drug therapy is still safe and effective.