Arrhythmias are common diseases in cardiovascular medicine, and their onset can be rapid or slow, the disease can be mild or severe, the light is initially hidden, does not cause symptoms or only mild discomfort, and the severe sudden onset of illness, causing serious hemodynamic disorders, and even sudden death. Therefore, the identification of high-risk arrhythmias is crucial for clinicians.
1 What is a high-risk arrhythmia?
Due to the occurrence of arrhythmias caused by obvious changes in hemodynamics, endangering the patient's vital signs and consciousness, if not treated in time will cause a sharp deterioration, or the original severe organic heart disease of patients due to the occurrence of arrhythmia, the original heart disease and cardiac function significantly aggravated, worsening, so that the patient is in a very unstable state, these arrhythmias should be regarded as high-risk arrhythmias.
2 How are high-risk arrhythmias classified?
It is usually divided into two categories: tachyarian high-risk arrhythmias and slow high-risk arrhythmias according to the speed of the ventricular rate at the time of the attack.
1) How to identify rapid high-risk arrhythmias?
First of all, the type of arrhythmia is the most important, such as the most typical is persistent ventricular tachycardia or ventricular fibrillation, because the ventricular rate is extremely fast and irregular, the amount of blood exuded from the heart is almost zero, so that important organs due to acute severe ischemia and impaired function, loss of consciousness, loss of aortic pulse, blood pressure is almost undetectable, so urgent treatment is needed.
Second, the patient's underlying disease is critical, such as in patients with severe coronary heart disease or severe cardiac insufficiency, even rapid supraventricular arrhythmias can rapidly worsen hemodynamically, causing life-threatening.
Third, the speed of the ventricular rate during arrhythmia attack is also important, such as slow-frequency ventricular tachycardia can last for hours or days, and when antiarrhythmic drugs are applied, the 2:1 down-pass atrial flutter suddenly becomes 1:1 down-pass ventricle, and the rapid ventricular rate can cause the patient to develop A-S syndrome.
2) How to identify slow, high-risk arrhythmias?
Bradyacarias at high risk include severe sinus arrest, sinus atrial block, severe sinus bradycardia (< 35 beats/min), atrial fibrillation with one or more ventricular arrests for at least 5 seconds, and third-degree AV block with very slow ventricular self-paced rhythms.
Because the amount of heart discharge is directly proportional to the ventricular rate, the extremely slow ventricular rate makes the heart discharge drop sharply, the blood pressure drops significantly or cannot be detected, and the clinical manifestations are dizziness, black oak, loss of consciousness, etc., and need to be rescued immediately.
3 How to deal with common high-risk arrhythmias?
1) Malignant ventricular arrhythmias
Figure 1. Ventricular fibrillation: QRS-T disappears completely and is replaced by ventricular fibrillation waves of different shapes, sizes, and intervals, with frequencies ranging from 250 to 500 beats per minute
When malignant ventricular arrhythmias such as ventricular flutter, ventricular fibrillation, polymorphism, and torsades de pointes are persistent, they quickly cause syncope, convulsions, and Ass syndrome, and the success rate of electrical cardioversion can reach 94% within 1 minute, and for every 1 minute, the ventricular fibrillation threshold is increased by 10%, and the success rate of defibrillation is reduced by 7% to 10%.
Therefore, once impaired consciousness occurs and the aortic pulse is significantly weakened or disappeared, electrical cardioversion should be performed immediately, and effective cardiocardial compressions (frequency > 100 beats/minute, depth > 5 cm) should be performed persistently before the cardioversion device can be applied.
Electrical cardioversion
Electrical cardioversion is the preferred method of stopping malignant ventricular arrhythmias. Generally, the reference energy of the first electrical cardioversion is: room velocity 100 to 150 J, ventricular flutter and ventricular fibrillation 300 to 400 J, in vivo electrical cardioversion 20 to 30 J, transesophageal electrical cardioversion 20 to 50 J, children's electrical cardioversion should be < 50 J, and the energy can be halved during biphasic wave cardioversion.
To repeat defibrillation, it should be done after 5 CPR chest compressions and ventilation cycles.
drug therapy
Lidocaine: rapid ventricular arrhythmias that occur early in acute myocardial infarction (within 48 hours) are often more effective and can improve the success rate of electrical cardioversion and electrical defibrillation, but the efficacy of rapid ventricular arrhythmias caused by other causes is not as good as amiodarone, and is often used when amiodarone is ineffective or contraindicated.
Intravenous: 50 to 100 mg, may be repeated 3 to 5 times at intervals of 5 to 10 minutes. After onset of action, intravenous instillations of 1 to 4 mg/min are maintained, and the total dose is ≤ 3 mg/kg (or ≤ 200 to 300 mg/h) for a short period of time, and the total amount ≤ 1.0 to 1.5 g for 24 hours. Usually onset for 20 s and lasts for about 20 min.
Adverse effects: dizziness, drowsiness, excitement, etc., occur in 6%.
Amiodarone: may be used as the drug of choice without QT interval prolongation, especially in patients with cardiac anatomical abnormalities and cardiac insufficiency.
Intravenous medication: the usual dose is 5 to 7 mg/kg slow intravenous (within 10 minutes), followed by 1 to 2 mg/min continuous intravenous instillation, gradually reduced after effectiveness, the total amount of 24 hours < 2 to 3 g. Usually onset action in 10 min to 1 h, peak in 4 to 6 h, and last for a long time.
Adverse reactions: pulmonary interstitial fibrosis, hyperthyroidism or hypothyroidism, sinus bradycardia, etc., the incidence is low.
β receptor blockers: indicated for rapid ventricular arrhythmias due to acute coronary syndromes and primary long QT interval syndromes. It has the effects of central anti-arrhythmia, inhibition of sympathetic storms, and blocking multiple ion channels of cardiomyocytes. The ventricular fibrillation threshold can be raised by 60% to 80%.
Intravenous: metoprolol injection 5 mg/5 min, if necessary, may be repeated once at intervals of 5 min, for a total of 3 times a total of 15 mg, 15 minutes after 15 minutes to start oral administration, 50 mg each time, 2 times a day.
2) Pre-excitation syndrome with atrial fibrillation with rapid ventricular rate
Figure 2. Pre-excitation syndrome with atrial fibrillation, the arrow in the figure refers to the "Δ" wave
In patients with pre-excitation syndrome, when the bypass has a fronthaul function, the refractory period is short, and atrial fibrillation occurs, the very fast and unaligned atrial fibrillation waves will selectively pass down the ventricles along the bypass, causing fast and untidy wide QRS group tachycardia, especially when the patient's bypass prequel refractory period is too short, and the rapid ventricular response caused by atrial fibrillation may deteriorate into ventricular fibrillation and sudden death.
For pre-excitation with atrial fibrillation, synchronized cardioversion is preferred if hemodynamically unstable, and amiodarone is preferred if hemodynamics are stable, verapamil and digitalis are contraindicated.
3) Atrial flutter with rapid atrioventricular node transmission
Figure 3. Atrial flutter in 2:1 AV conduction, where one of the F-waves overlaps with the QRS wave group and is easily overlooked
Hemodynamics deteriorate rapidly due to impaired cardiac function during atrial flutter, sympathetic activation, and abrupt 2:1 down transmission to a 1:1 down-pass ventricle after the application of antiarrhythmic drugs. Synchronous electrical cardioversion should be given immediately, generally selecting an energy of 50 to 150 J.
At present, ibutilide is the most effective drug for terminating atrial flutter, with a success rate of up to 70%, but the occurrence of torsades de pointes should be vigilant, and potassium and magnesium supplementation should be given if necessary.
4) Atrial fibrillation with extremely fast ventricular rate
Figure 4. Rapid atrial fibrillation (ventricular rate 200 beats/min): normal P waves disappear and are replaced by a series of f-waves of varying shapes, sizes, and intervals, with absolutely uneven ventricular rhythms
Studies have shown that 18% of ventricular fibrillation and 3% of ventricular tachycardia are metamorphosed by atrial fibrillation. Rapid ventricular rate activates the sympathetic nervous system and lowers the ventricular fibrillation threshold; shortens the diastolic period, worsens cardiac function, and increases the chance of ventricular early triggering of ventricular fibrillation; and increases the risk of ventricular fibrillation due to absolute irregularities in the RR interval during atrial fibrillation.
Generally, β receptor blockers, digitalis, and diltine are generally selected to control the ventricular rate of atrial fibrillation.
5) Malignant bradyarrhythmia
Figure 5. Atrial flutter with third-degree AV block, junctional escape rhythm: F-R is not fixed, ventricular rate is slow, R-R rules are characteristic of atrial flutter with third-degree AV block; although the ventricular rate is < 40 beats/min (36 beats/min), the QRS wave group morphology is normal, so it should still be considered as a bordering escape rhythm
When the heart rate is less than 40 beats per minute, even if the heart is normal, the compensatory effect of increasing the amount of strokes can no longer completely offset the effect of slow heart rate on the volume of heart output, and patients may have symptoms of ischemia such as dizziness, forgetfulness, fatigue, chest pain, and in the long run, bradyarrhythmic cardiomyopathy.
Therefore, an intravenous infusion of isoproterenol or atropine may be temporarily given and a temporary pacemaker can be implanted. Long-term treatment involves the implantation of a permanent pacemaker.
bibliography:
Gu Fusheng, Hu Dayi. Clinical and practical cardiovascular diseases[M]. Beijing: Peking University Medical Press,2015:199-212.]
Huang Congxin, Zhang Shu, Huang Dejia, et al. Atrial fibrillation: Current understanding and treatment recommendations-2018[J]. Chinese Journal of Cardiac Pacing and Electrophysiology,2018,32(4):5-8.
Ge Junbo, Xu Yongjian, Wang Chen. Internal Medicine [M]. Beijing: People's Medical Publishing House, 2018:166.
Zhang Xinmin, Shen Chengxing, Zhi Hong, et al. Clinical ECG analysis and diagnosis[M]. Beijing: People's Medical Publishing House, 2007:191-199.
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This article was first published on Lilac Garden's professional platform: Cardiovascular Time