I. Tachyarrhythmias
Atrial premature beats: Atrial premature beats are those in which the ectopic excitation point is located in the atrium. The electrocardiogram is characterized by: (1) early appearance of ectopic external P(P) waves; (2) P-R interval ≥0.12 seconds; (3) QRS wave group morphology is generally normal, but it may show abnormal morphology when accompanied by intraventricular differential conduction, or it may show no QRS wave group after P waves because the excitation is blocked in the atrioventricular junction area (atrial premature beats are not transmitted downward). ) ④ The compensatory interval after premature beats is often incomplete.
(1) QRS waveform: The QRS wavegroup of intraventricular differential conduction (referred to as differential conduction) often shows RBBB (right bundle branch block) pattern, that is, ①Vl lead QRS wavegroup with triphasic waveform (rSR, rsR or rsi) is mostly differential conduction, and those with monophasic (R) or biphasic (qR, RS or QR) ventricular premature beats (referred to as ventricular premature) are more likely to be ②V1 lead QRS wavegroup onset vector often The possibility of differential transmission is high in those who have the same QRS start vector as normal, and the possibility of ventricular premature is high in those whose start vector is fixed and different from normal QRS start vector. (3) The possibility of differential transmission is high in those with irregular QRS waveforms and the possibility of ventricular prematureness is high in those with fixed morphology (except for multi-source ventricular prematureness).
(2) Length of cardiac cycle: Generally, the length of the overdue period of heartbeat is proportional to the length of the previous cardiac cycle, that is, the premature beats after long cardiac cycles are prone to differential conduction, while ventricular premature beats do not have this rule.
In conclusion, to distinguish atrial premature with differential conduction from ventricular premature beats, the above points must be taken into consideration to make a more accurate judgment, and errors are inevitable based on one point alone.
The main difference between the two is the presence or absence of P waves in front of the QRS waves of premature beats, whether the P waves are retrograde or not, and whether the P`-R interval is >O.12 seconds.
In ventricular premature beats, the QRS wave deformation is obvious and is the easiest to determine clinically, but in atrial premature beats with intraventricular differential conduction, the morphology of the QRS wave group is also more variable and should be distinguished from each other (see previous section).
(B) Tachycardia
1, sinus tachycardia: adults with sinus heart rate more than 100 beats/min is sinus tachycardia, its etiology in addition to various organic heart disease and heart failure, more common is the physiological factors only exercise, excitement, sympathetic excitation, etc.) and other systemic diseases (such as hyperthermia, hyperthyroidism, drug effects, etc.).
(1) sinus tachycardia and atrial tachycardia to distinguish; ① start and stop; sinus tachycardia (hereinafter referred to as sinus tachycardia) start and stop are gradual changes, while paroxysmal atrial tachycardia (referred to as atrial tachycardia) start and stop suddenly; ② P wave morphology: sinus tachycardia and after the onset of the P wave morphology is the same, while atrial tachycardia is different; ③ heart rate: sinus tachycardia heart rate is generally <160 beats/min, face atrial tachycardia heart rate (3) heart rate: the heart rate is usually <160 beats/min in sinus tachycardia and 160-220 beats/min in atrial tachycardia; (4) post-episode ECG: the ECG is often without atrial premature beats after sinus tachycardia, while the ECG is often with atrial premature beats after termination of atrial tachycardia; (5) stimulation of vagal response: pressing the carotid sinus or stimulating the pharynx during sinus tachycardia can slow down the heart rate, but it cannot return to the normal heart rate, while atrial tachycardia can terminate or invalidate the attack.
2, paroxysmal supraventricular tachycardia: paroxysmal supraventricular tachycardia (PSVT) refers to tachycardia originating from the atrial or atrioventricular junctional zone, including paroxysmal atrial tachycardia and paroxysmal junctional tachycardia, because the two in the clinical manifestations and treatment principle Yun no significant differences, and because of the faster heart rate, the electrocardiogram P wave and the T wave fusion of the previous heartbeat, so often collectively referred to as paroxysmal The two are often referred to as paroxysmal supraventricular tachycardia.
The duration of paroxysmal supraventricular tachycardia varies from seconds or minutes to hours, days or months, but generally does not exceed two weeks. The frequency of seizures varies from person to person, from once a few years to many times a day. During an attack, there is a sudden change in position, deep inhalation, and stimulation of the pharynx. Pressing on the eyeballs and massaging the carotid sinus can cause the attack to stop suddenly.
Paroxysmal supraventricular tachycardia should be differentiated from the following rhythms.
(2) Atrial flutter (AF): Atrial flutter, especially those with 2:1 regular conduction, is sometimes difficult to distinguish from paroxysmal supraventricular tachycardia and can be differentiated according to the following points: ① combined organic heart disease: paroxysmal supraventricular tachycardia is often absent, atrial flutter is often present; ② stimulation of the vagus nerve response: can make paroxysmal supraventricular tachycardia episodes suddenly stop or ineffective, atrial flutter is mostly ineffective; ③ atrial (3) Atrial rate: 160-220 beats/min in paroxysmal supraventricular tachycardia and 250-350 beats/min in atrial flutter; (4) ECG isoelectric lines: isoelectric lines can be seen between P-Q-S-T in paroxysmal supraventricular tachycardia and no isoelectric lines in atrial flutter; (5) Atrioventricular conduction ratio: mostly 1:1 in paroxysmal supraventricular tachycardia and 2:1 or 3:1 or 4:1 in atrial flutter, rarely 1:1. (6) Ventricular rate: 160-220 beats/min in paroxysmal ventricular tachycardia and often 150 beats/min or less in atrial flutter.
3, paroxysmal qualitative tachycardia (PVT) paroxysmal ventricular tachycardia is a relatively rare but very important clinical arrhythmia, because it is often seen in patients with organic heart disease, and may induce ventricular fibrillation, so the clinical importance. In paroxysmal ventricular tachycardia, depending on the ventricular rate, the hemodynamic impact on patients varies greatly, from mild palpitations or no discomfort at all in mild cases to shortness of breath, precordial pain, decreased blood pressure and even syncope or convulsions (A-Syndrome) in severe cases. The patient’s heart rate is often increased (150-200 beats/min), mostly around 160 beats/min, the rhythm is relatively regular, but may not be regular when there is a ventricular seizure; the first heart sound varies greatly in strength (atrioventricular disconnect caused by different levels of ventricular filling causes varying systolic pressure, sometimes the fourth heart sound can be heard, stimulation of the vagus nerve has no effect on paroxysmal ventricular tachycardia.
(1) paroxysmal supraventricular tachycardia with intraventricular differential conduction: in this case you which wide deformity, can be confused with paroxysmal ventricular tachycardia, but paroxysmal supraventricular tachycardia with intraventricular differential conduction is mostly seen in young people, often meta-organic heart disease history, faster ventricular rate during the attack (160-220 times/min), regular and uniform electrocardiogram QRS wave, RR interval difference <0.01 These characteristics are different from paroxysmal ventricular tachycardia, such as the absence of ventricular seizure and ventricular fusion waves, and the stimulation of the vagus nerve can terminate the attack or be ineffective.
(iii) Flutter or fibrillation
The atrial rate (F-wave frequency) of atrial flutter is about 300 beats/min (250-350 beats/min but these excitations are only partially (2:l-41) transmitted to the ventricles, especially 2:l conduction is the most common, so the ventricular rate of patients with atrial flutter is often about 150 beats/min. The diagnosis of atrial flutter mainly relies on the electrocardiogram, which is characterized by the disappearance of P waves and their replacement by regular and uniform flutter waves (F waves), the ventricular rate can be regular or irregular depending on whether the atrioventricular conduction ratio is fixed, but the glottal wave pattern is generally normal. Atrial flutter should be clinically differentiated from sinus tachycardia and paroxysmal supraventricular tachycardia (see previous section).
Ventricular flutter should be distinguished from ventricular tachycardia, in which the ventricular rate is also often around 180 beats/min, but the QRS waves are clear, there are isotonic lines between the waves, and the QRS waves can be distinguished from the T waves, and the QRS wave time frame is shorter than that of ventricular flutter waves.
Atrial fibrillation is one of the more common types of clinical arrhythmias, and the diagnosis can often be established based on the typical “three unequal” signs during physical examination, i.e., unequal heart sounds, absolute rhythm irregularity, and unequal pulse rate and heart rate (pulse dwarf). However, the diagnosis should be determined clinically on the basis of ECG examination, which is characterized by the disappearance of P waves and their replacement by irregular (size and interval) fibrillation waves (f waves) with an f frequency of 350-600 beats/min, absolute irregularity of ventricular rhythm, QRS wave groups with a morphology similar to normal, but with slight differences between waves due to different degrees of ventricular filling and the influence of f waves, and with intraventricular differential conduction, which may also be broad The pattern of QRS waves is similar to normal, but the waves are affected by different degrees of ventricular filling and f waves.
(iv) Pre-excitation syndrome
This syndrome can be seen at any age and has a degree of familial onset. It may or may not be associated with evidence of organic heart disease, but it is usually detected clinically during electrocardiography for other conditions, and paroxysmal supraventricular tachycardia may occur. The prognosis is generally good, but many people have complications, including paroxysmal supraventricular tachycardia, atrial fibrillation, atrial flutter, and premature atrial contractions. Among them, paroxysmal supraventricular tachycardia is the most common, with an incidence of 36%-64%, and the mechanism of occurrence is almost always related to excitation folding.
The preexcitation syndrome is divided into two types, A and B.
Typical preexcitation syndrome can be diagnosed by electrocardiographic examination, when the preexcitation pattern intermittently occurring do not misdiagnose as bundle branch block; and combined with paroxysmal supraventricular tachycardia, especially in the atrioventricular junction area retrograde type of RS was widened deformity, easily confused with paroxysmal ventricular tachycardia, at this time can be distinguished according to the following points: ① ventricular rate during the attack: preexcited often > 200 times / min, paroxysmal ventricular tachycardia is often < 200 beats/min; ② history: pre-excited people have a history of tachycardia episodes, while ventricular tachycardia people have a history of organic heart disease; ○3 electrocardiogram P wave: pre-excited people can have P' wave, and P-P flat spacing < 50% of the r-r spacing, ventricular tachycardia atrial separation or no P wave; ④ electrocardiogram p="" δ wave, ventricular tachycardia morphology is basically the same; ⑤ r-r interval: pre-excited people uniformly consistent (difference of r-r interval <0.01 sec), mildly uneven in ventricular tachycardia (difference of r-r interval 0.02-0.03 sec); ⑤ ECG before and after the attack: preexcitation waves can be found in preexcitation (also can occur intermittently), and ventricular premature beats with similar patterns can be seen in ventricular tachycardia. <="">
(I) Choked bradycardia
The electrocardiographic presentation of sinus bradycardia is relatively simple, i.e., it first conforms to two features of sinus rhythm (normal P-wave morphology and direction, P – R interval > 0.12 seconds).
R interval >0.12 s), but the P-wave frequency is <60 beats/min. Sinus bradycardia should be distinguished from the following rhythms.
2. Atrial premature beats without downward transmission
Especially when frequent atrial premature beats are not transmitted, it is easy to be misdiagnosed as sinus bradycardia, which should be distinguished by careful observation of T-wave morphology (with or without deformation, including sharp, rounded, bimodal, and tangential) and by searching for occult P-wave, and comparing with previous ECG if necessary.
(ii) Stuffed arrest
Sinus arrest can be caused by vagal reflexes, but more commonly (especially in the elderly) it is due to sinus node pacing dysfunction. The presence or absence of clinical symptoms depends on the duration of the pacing stop and the ability of the potential pacing point to replace the excitation (escape beat).
The main difference between sinus arrest and sinus block is whether the length of this long interval is an integer multiple of the basic cardiac cycle; if they are integer multiples, sinus block is more likely, and vice versa, sinus arrest is more likely, but a long interval of more than two times the basic cardiac cycle is almost always considered as sinus arrest.
(C) Atrioventricular block (AVB)
1.One degree Sinus or atrial excitation can all be transmitted to the ventricle through the junctional area, but the conduction time is prolonged, and the ECG shows prolonged P-R interval (>0.20 seconds) Type I refers to the second degree AV block with Wen’s phenomenon, that is, the P-R interrogation period is gradually prolonged until one atrial excitation is blocked and cannot be transmitted down to the ventricle, then the PR interval is restored to the shortest, and then gradually prolonged, and so on and so forth.
Third degree AV block is a phenomenon in which atrial excitation (or sinus excitation) cannot reach the ventricles at all. In this case, atrial excitation is controlled by sinus node, while ventricular excitation is controlled by the pacing point below the junctional area, and atrial and ventricular activities are completely cricket. The ECG shows that both P and QRS waves have their own rhythm, but they are not related to each other, and generally the P wave frequency is faster than the QRS wave frequency.
However, when the P-R interval is excessively prolonged or the heart rate is fast resulting in T-P fusion, the ECG changes should be distinguished from the junctional rhythm.
The symptoms of third-degree AV block depend on the speed of the ventricular rate and the patient’s underlying cardiac function. The closer to the atrioventricular junction zone, the closer to normal QRS wave pattern, the closer to 60 beats/min and the more stable the rhythm; the closer to the distal end of the conduction system, the more obvious the QRS deformation, the slower the heart rate and the more unstable the rhythm, even leading to cardiac arrest and the onset of A.S. syndrome in patients.