Details of the case
The patient, a 40-year-old male, was admitted to the hospital mainly due to "prolonged palpitations".
He has a history of atrial acrobatic attacks and has experienced cardiac arrest after receiving adenosine treatment for persistent supraventricular tachycardia and tachycardia cardiomyopathy. Cardiac ultrasound suggests LVEF 63%, aortic and mitral valves with mild reflux. Cardiac MRI at sinus rhythm shows mild thickening of the left ventricular wall (maximum thickness of 14 mm) and no specific abnormalities.
In view of the frequent episodes of atrial arrhythmias in patients, sotalol is given. Prior to taking sotalol, the patient's 12-lead ECG (Figure 1) showed sinus rhythm, 57 beats/min, and no abnormalities were seen in the QRS wave width and QT interval.
Figure 1. Electrocardiogram before taking sotalol
After oral administration of sotalol, telemetry monitoring (figure 2) shows an increase in QRS waves.
Figure 2. Telemetry monitors the ECG
The main reasons for distinguishing the patient's ECG changes are: 1) frequency-dependent transmission; 2) ventricular autonomic rhythm; 3) 4 phase difference transmission; 4) pre-excitation syndrome.
Given that there is no significant change in the ECG during sinus rhythm, 3-phase or 4 phase phase transfer is unlikely; ventricular autonomic rhythm needs to be consistent with the P-wave rhythm, that is, isofrequency separation to have a constant PR interval, which is not very likely; and pre-excitation syndrome can have ST-T changes with PR interval shortening with ventricular pleus abnormalities.
The patient's first ECG is absent from pre-shock, suggesting occult pre-excitation, but pre-shock after taking sotalol at constant heart rate suggests pre-transmission via bypass.
The mechanism considered is that sotalol slows down AV nodal conduction and prevents occult conduction from entering the bypass, resulting in such ECG changes, when the time for sinus node descent through AV nodal descent is roughly equal to that for down passage via bypass. Patients who later review the ECG (figure 3) confirm the presence of pre-excitation syndrome.
Figure 3. Electrocardiogram after load dose of sotalol
The patient terminates tachycardia after Valsalva maneuver and undergoes radiofrequency ablation (posterior spacer sidewalk) during hospitalization, with ablation in the coronary sinus. After discharge, treatment was continued with metoprolol and lisinopril.
Pharmacokinetics of sotalol
The FDA recommends the preferred class III antiarrhythmic agent for patients with organic heart disease, of which amiodarone is a typical representative, but amiodarone cardiac toxicity side effects are high and should not be used for long time.
Another important anti-arrhythmic drug is sotalol, and sotalol has a class II antiarrhythmic effect, including a variety of ventricular arrhythmias, atrial flutter, atrial fibrillation and so on.
Sotalol is a water-soluble drug, which is absorbed in the small intestine after oral administration, and the blood concentration reaches a peak in 2 to 3 hours, without liver first-pass effect.
In the blood and tissues sotalol exists as a free type of drug, does not bind to plasma proteins. It can pass through the placental barrier, but it is not easy to cross the blood-brain barrier and has no significant effect on the central nervous system.
Sotalol is excreted mainly by the kidneys, in addition to partial excretion through bile and intestinal secretions. For those with normal renal function, the half-life of sotalol is 15 to 20 h, and in those with abnormal renal function, the half-life will be prolonged.
Pharmacological effect of sotalol
Sotalol is a competitive inhibitor of rapid activation delayed rectification potassium channels (IKr) and does not inhibit slow activation delayed rectifier potassium channels (IKs). In addition to inhibiting IKr, sotalol increases the late sodium current (INa-L) and is time-dependent, and the arrhythmia-inducing effect of sotalol is also associated with increased late sodium current.
Sotalol has both β receptor blocking effect and class III antiarrhythmic action characteristics, when the plasma concentration is greater than 800 ng/mL, the β receptor blocking effect is obvious, the blocking effect is 1/3 of propranolol;
Sotalol exhibiting a class III antiarrhythmic effect requires doses higher than 80 mg, by specifically blocking IKr, resulting in prolonged APD and ERP in the atrium and ventricles, slowing sinus frequencies, inhibiting AV conduction, and prolonging the refractory period of the atrium and atrioventricular node.
In this case, the atrioventricular node is suppressed due to the loading dose reached when sotalol is treated for arrhythmias, and the time for the sinus node to pass down the atrioventricular node is roughly equal to the time of down transmission through the bypass, so the ECG has a pre-excitation syndrome.
Notes on sotalol
Adverse effects of sotalol include fatigue, bradycardia, dyspnea, arrhythmias, weakness, and dizziness.
If severe bradycardia occurs, isoproterenol or temporary cardiac pacing can be given;
When a heart block occurs (second-degree type II or third-degree AV block), temporary cardiac pacing may be given;
If severe hypotension is concomitant, epinephrine may be used instead of isoproterenol or norepinephrine to boost blood pressure;
Bronchospasm is administered aminophylline or beta2 agonists;
If torsades de pointes are present, vVD should be given immediately with DC cardioversion and, if necessary, treatments such as temporary cardiac pacing or epinephrine and/or potassium supplementation and magnesium sulfate. Dialysis treatment may also be performed.
Sotalol causes arrhythmia side effects, the most common is bradycardia, and atropine therapy is ineffective, the most serious side effect is torsades de pointes ventricular tachycardia, QT interval prolongation is an important cause.
Electrolyte monitoring is required during sotalol and should be kept with blood magnesium >2 mmol/L and serum potassium >4 mmol/L.
Sotalol is contraindicated in patients with baseline QT interval prolongation (QT interval > 450 ms), other contraindications include cardiogenic shock or uncontrolled decompensated heart failure, bronchial asthma attack, bradycardia, second-degree type II without pacemaker protection, third-degree atrioventricular block, and Ccr
In addition, the combination of sotalol with the acid-making agents alumina or magnesium hydroxide reduces bioavailability by about 20% to 25%; the combination with digoxin increases the risk of arrhythmias; the combination with non-dihydropyridine calcium antagonists can aggravate conduction disorders, further inhibit ventricular function, and lower blood pressure; and the combination of use with the consumption of catecholamines (eg, reserpine, guanethidine) can produce hypotension and severe bradycardia.
Combination with these drugs should be avoided as much as possible, and ECG monitoring may be performed if necessary.
Summary
In this case, sotalol is given to control frequent episodes of atrial arrhythmias, which is in line with the indications for the administration of sotalol.
Although the basal heart rate before taking sotalol is 57 bpm, there is sinus bradycardia, but after taking the dose of sotalol load, there is no significant change in heart rate compared to the basal heart rate and there is no symptom of cerebral insufficiency such as vertigo and black oak, so it can be treated with sotalol.
I didn't expect that the patient had an occult pre-excitation, and the use of sotalol made the pre-excitation syndrome "expose the horse's foot". Therefore, after the discharge from the hospital, metoprolol was used to continue treatment.
Sotalol is a class II and class III antiarrhythmic agent with minimal toxic side effects. Indications cover a variety of ventricular arrhythmias, atrial flutter, and atrial fibrillation.
Oral dose of sotalol begins with 40 to 80 mg bid and is gradually increased to 160 mg bid, and the QT interval should be monitored for the first 3 days of administration. Clinical data used by sotalol in Chinese populations are still small and need to be further accumulated and summarized.
This article was reviewed: Feng Huiping Chief Physician of the Department of Cardiology of the Affiliated Hospital of Hebei University
Curated: ly
Caption: Stand Cool Helo
bibliography:
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Pu Jielin, Wu Lin, Wu Yongquan, Yang Xinchun, Yang Yanmin, Zhang Ping, Zhu Wenqing. Sotalol antiarrhythmia Chinese expert consensus[J]. China Cycle Magazine,2019,34(08):741-751.