Paroxysmal Tachycardia

PAROXYSMAL TACHYCARDIA, attacks of rapid heartbeat characterized by a sudden onset, an equally sudden cessation, and an extremely high heart rate—up to 200 and more beats per minute. Thus, "paroxysmal tachycardia" is a symptomatological concept, a clinical symptom complex. In 1876, Cotton first described a case of paroxysmal tachycardia, but this symptom complex was named in 1889 by Bouveret, who considered paroxysmal tachycardia a special vagal neurosis and called it essential paroxysmal tachycardia. With the development of the doctrine of cardiac arrhythmias due to the introduction into clinical practice of graphic methods for studying cardiac activity—namely, venous pulse recording and especially electrocardiography—it became clear that paroxysmal tachycardia is based on various cardiac rhythm disturbances. Currently, based on pathogenesis, paroxysmal tachycardia is divided into extrasystolic (A. Hoffmann) and paroxysmal tachycardia resulting from attacks of atrial fibrillation or flutter. However, some authors (e.g., Edens, Fogelson) do not classify attacks of tachycardia due to fibrillation and flutter as paroxysmal tachycardia. The existence of a form of paroxysmal tachycardia in which impulses originate from the sinus is controversial. Hering and Lewis do not recognize this form, whereas Wenckebach and others describe cases where attacks of tachycardia were caused by a significant, more or less rapidly developing and terminating acceleration of impulses generated in the sinus. In view of the fact that of all parts of the heart, the sinus is under the greatest influence of extracardiac nerves, one can imagine that the sinus itself can become a source of particularly accelerated impulse generation as a result of impaired innervation by extracardiac nerves. On the other hand, it can be assumed that another site of the Tawara node, rather than the one that normally generates impulses, can become the site of origin of accelerated impulses. In the latter case, sinus paroxysmal tachycardia could be attributed to the extrasystolic group of paroxysmal tachycardia. Within this extrasystolic group of paroxysmal tachycardia, depending on the site of origin of heterotopic impulses, the following types of paroxysmal tachycardia are distinguished: atrial, atrioventricular, and ventricular. Atrial tachycardias are the most frequent form of paroxysmal tachycardia. Impulses for heart contraction originate from the atria at an average rate of 150–200 beats per minute. The ventricular contraction rate is usually the same as that of the atria. The atrial wave (P) is positive, located in front of R, but often of altered shape (depending on the site in the atria from which the impulses originate). Very often, the P wave coincides with the T wave of the preceding contraction and is hidden by the latter. The ventricular complex of the electrocardiogram is usually normal—of supraventricular origin (see electrocardiogram in Figure 1); in rare cases, due to functional block of the conduction system branches, the ventricular complex may change, which makes it difficult to distinguish atrial tachycardias from ventricular ones. More frequently, the shape of T changes due to P being superimposed on it. When the number of impulses arising in the atria reaches a high frequency—300–400 beats per minute—the ventricular contraction rate can be either the same as that of the atria (1:1 conduction) or twice (2:1), three times less (3:1), etc. (diagram 3). The difference in the contraction rates of the ventricles and atria is caused by the fact that the conduction system is capable of conducting on average only about 200 impulses per minute, as a result of which not all impulses arising in the atria reach the ventricles and cause their contraction. The pulse rate in this form of paroxysmal tachycardia is 180–200 beats per minute. The ratio between the number of P waves and the QRST group of the electrocardiogram can be 1:1, 2:1, 3:1, etc. (electrocardiogram in Fig. 2). Atrioventricular (junctional) tachycardias. Impulses for heart contraction originate not from the sinus, but from the Aschoff-Tawara node; furthermore, impulses can arise in the upper, middle, and lower parts of the node. In the first case, the excitation wave reaches the atria earlier, and the atrial wave (P)—as a rule, negative—is located directly in front of the ventricular complex (electrocardiogram in Fig. 3). When the impulse for heart contraction arises in the middle part of the node, it simultaneously reaches both the ventricles and the atria, which leads to their simultaneous contraction, i.e., to the fusion of the P and R waves of the electrocardiogram (electrocardiogram in Fig. 4). When impulses arise in the lower part of the node, the excitation reaches the ventricles earlier, and then the atria. In these cases, the negative wave P is located behind the initial group of ventricular waves (P after R—electrocardiogram in Fig. 5). In all the listed forms of tachycardia, the ventricular complex is of supraventricular origin, as a result of which these forms of tachycardia are also called supraventricular tachycardias. The ventricular form of paroxysmal tachycardia is the least common form, but prognostically the most unfavorable, since it most often appears in severe lesions of the heart muscle, especially during occlusion of the lumen of the coronary arteries. Out of 65 cases of ventricular paroxysmal tachycardia collected and described by Strauss, 53 cases had organic changes in the cardiovascular system, including 12 cases of coronary artery disease. This form of paroxysmal tachycardia also frequently develops after the administration of large doses of digitalis, which indicates its toxic origin in a number of cases (in the presence of severe organic changes in the cardiovascular system). This form is observed predominantly at an advanced age, but isolated cases have also been described at a young age, in the absence of organic changes in the cardiovascular system. A characteristic feature of ventricular paroxysmal tachycardia is a sharp distortion of the ventricular complexes of the electrocardiogram, having the shape of right- or left-sided ventricular extrasystoles, depending on whether the automatic excitation center arises in the right or left ventricle (electrocardiogram in Fig. 6). The atrial rhythm is significantly slower than the ventricular rhythm. Sometimes impulses arising in the ventricles retrogradely penetrate into the atria and cause their contractions (negative P, delayed behind QRS even more than in the atrioventricular form with impulse origination in the lower part of the Aschoff-Tawara node). In rarer cases, the automatic excitation center arises simultaneously in both the right and left ventricles, which is reflected on the electrocardiogram by the alternation of right- and left-sided ventricular extrasystoles. Finally, cases of short paroxysms of ventricular tachycardia interrupted by paroxysms of atrial or junctional tachycardias have been described. As for attacks of tachycardia caused by atrial fibrillation, they differ from all previous forms of paroxysmal tachycardia by an irregular rhythm. In atrial flutter, the rhythm can be regular or irregular; flutter is very characteristic for changes in rhythm frequency with doubling or another regular ratio (1:3, 1:4) of the faster and slower rhythms to its initial frequency, depending on changes in the conduction of excitations from the atria to the ventricles (transition of every second, third, etc. impulse). Etiology of paroxysmal tachycardia. In experiments, attacks can be caused by clamping the aorta (increase in intraventricular pressure), closing the lumen of the coronary arteries (Lewis), the action of medicinal substances (digitalis, strophanthin, chloroform, nicotine), the action of heavy metal preparations (barium, calcium), irritation of the vagus and sympathetic nerves. In clinical practice, from an etiological point of view, one can distinguish: 1) Paroxysmal tachycardia in the absence of other pathological changes on the part of the heart. This form corresponds to the concept of "essential" paroxysmal tachycardia. According to A. Hoffmann and Schrumpf, it accounts for 2/3 of all cases of "paroxysmal tachycardia." 2) Paroxysmal tachycardia observed in various cardiac and cardiovascular diseases (valvular heart disease, hypertension, coronary sclerosis of the heart, etc.). There is no clear boundary between these two forms, since transitional forms are often observed—i.e., forms where other pathological phenomena on the part of the heart are present, but indistinctly expressed. Sometimes attacks of paroxysmal tachycardia occur in individuals with organic lesions of other systems—the central nervous system (syphilis, brain tumor) and the gastrointestinal tract. Of the various forms of paroxysmal tachycardia by pathogenesis, atrial and atrioventricular paroxysmal tachycardias are observed more frequently in the absence of other pathological changes on the part of the cardiovascular system; in other words, "essential" paroxysmal tachycardia most often has the character of an extrasystolic auricular or atrioventricular form. Figure 5. Atrioventricular tachycardia (lower part of the node). Figure 6. Ventricular form of paroxysmal tachycardia. Sinus paroxysmal tachycardia belongs to the same category, but is very rare. Conversely, in the presence of other pathological phenomena on the part of the heart or vessels, paroxysmal tachycardia due to attacks of fibrillation or flutter is observed more frequently, and the ventricular extrasystolic form of paroxysmal tachycardia is rare.

The occurrence of attacks in all types of paroxysmal tachycardia is undoubtedly favored by neuro-functional factors: physical and mental overstrain, excesses of various kinds, nervous and psychic excitement, etc. Of particular importance are internal secretory disorders, for example during menopause and puberty, when attacks occur especially frequently and easily. However, it is hardly possible to ascribe exclusive importance to neuro-functional factors in the onset of attacks. Most likely, one must assume that excitation of the nervous system or intoxication factors (digitalis) particularly predispose to the onset of attacks in the presence of organic changes in the cardiovascular system, especially the atrial musculature. These changes, however, are in a number of cases difficult to detect or are not detected at all. This refers in particular to the so-called essential paroxysmal tachycardia.* The mechanism of the "slipping" of the normal heart rhythm to heterotopic centers in the extrasystolic form of paroxysmal tachycardia cannot be considered finally elucidated. Many tend to equate the mechanism of occurrence of paroxysmal tachycardia attacks with the mechanism of extrasystole, reducing this mechanism to the enhanced activity of the heterotopic center; others reduce all forms of paroxysmal tachycardia to the pathogenesis of atrial fibrillation and flutter. The clinical picture of a paroxysmal tachycardia attack is determined not so much by the pathogenesis of tachycardia as by the working capacity of the heart muscle, primarily depending on the existing pathological changes in the cardiovascular system and on the presence of sclerosis of the coronary arteries of the heart. The degree of heart failure developing during the attacks depends on this. Otherwise, the clinical picture of the attacks themselves for various forms of paroxysmal tachycardia is more or less the same. The duration of the attacks varies from several seconds to many hours, days, weeks, and even months. Among 177 cases of paroxysmal tachycardia collected by Gallavardin and Froment (Gallavardin, Froment), the duration of attacks was less than 12 hours in 113 cases; from 12 to 48 hours in 43 cases; from 2 to 10 days in 10 cases; from 10 days to 2 months in 10 cases; and about a year in one case. The intervals between individual attacks vary widely—from one or several days to many years—as well as the frequency of their occurrence, ranging from a single one in a lifetime to recurring daily. The frequency of attacks is often inversely proportional to their duration, or at the beginning of their appearance they are short and frequent, and over time become rarer and more prolonged. Attacks occur equally often in men and women at any age, most frequently at middle age. The clinical manifestations of paroxysmal tachycardia are diverse. Subjective sensations and objective changes in the cardiovascular system during and after attacks usually have a definite correlation with the duration of attacks and the frequency of their occurrence, and also depend on the nature and degree of changes in the cardiovascular system. In mild, short-lived attacks, subjective sensations are usually not very typical or are entirely absent. Patients feel the onset of the attack as a sudden blow to the chest, followed by a sharp palpitation—cardiac "racing" (Herzjagen). Sometimes the attacks are preceded by prodromal phenomena, a kind of "aura," in the form of a series of general sensations. In a number of cases, however, patients endure the attack extremely hard: fatigue appears, shortness of breath, a feeling of air hunger, pressure and pain in the chest, dizziness—up to a fainting condition, cold sweat, dragging pains in the limbs. The pulse rate during the attack is from 180 to 300 beats per minute. The pulse is of small volume, often difficult to count. Systolic blood pressure usually decreases—venous pressure increases. Heart sounds are loud, often slapping, the difference in pauses between the first and second sound disappears (embryocardia), sometimes a systolic murmur appears (in some cases, murmurs present in patients disappear). When the heart rate is not very high and the attack is short, and the heart is otherwise healthy, in particular the coronary arteries are not sclerosed, then phenomena of heart weakness may not occur; in this case, the size of the heart due to insufficient diastolic filling even decreases somewhat in cross-section. In more prolonged attacks with a sharp increase in the number of heart contractions, especially in patients with organic changes in the cardiovascular system (mainly in sclerosis of the coronary arteries), the high heart rate, by reducing the duration of pauses between ventricular systoles, i.e., shortening diastole, leads to rapid exhaustion of the contractile capacity of the heart muscle, resulting in heart dilation and the development of heart failure. Circulatory failure, in particular blood stagnation in the veins of the systemic circulation, is significantly promoted by a phenomenon that Wenckebach called Vorhofspfropfung (atrial plugging). The fact is that in cases where the heart rate reaches a certain critical value (about 200), the atrial systole of each heart contraction begins to coincide with the ventricular systole of the preceding heart contraction. In this case, the atria upon their contraction cannot transfer their contents into the ventricles and empty them into the venae cavae. This is manifested by particularly high atrial waves of the venous pulse. In these cases, severe phenomena of heart failure usually develop: shortness of breath and cyanosis increase, neck veins swell and pulsate, urine output decreases, blood congestion in the lungs and liver appears, along with edema. With the end of the attack in mild cases, both subjective sensations and objective changes disappear; at the same time, the end of the attack is often accompanied by belching, sometimes vomiting, and abundant urination. By some patients, the very end of the attack is perceived as the most unpleasant sensation during the entire attack, but following the end of the attack, as a rule, subjective relief and cessation of objective manifestations of heart failure quickly ensue. Only in severe cases of circulatory disorders can the disorders also be prolonged after the end of the attack and pass only gradually. With frequent attacks, persistent phenomena of heart failure can develop. In exceptional cases, death occurs during the attack from heart failure. The diagnosis of paroxysmal tachycardia usually does not present difficulties and can be made on the basis of clinical observation of the attack or anamnesis. Difficulties are encountered in the differential diagnosis of paroxysmal tachycardia attacks from sinus tachycardias. The latter, as is known, often occur with elevated temperature, nervous excitations, thyrotoxicoses, etc. Of importance here are: 1) pulse rate, which in sinus tachycardias is usually low—100–150 beats per minute, while in heterotopic tachycardias it is extremely high—200 or more beats per minute; 2) fluctuation of the pulse rate in one direction or another in sinus tachycardias and its constancy in heterotopic tachycardias, and 3) the onset and end of attacks: sudden in heterotopic, gradual in sinus tachycardias. Electrocardiography helps to accurately determine the origin of the tachycardia. The prognosis in paroxysmal tachycardia accompanying other cardiovascular diseases depends on the nature of the underlying disease. The paroxysmal tachycardia attacks themselves in such cases can, if they are frequent and prolonged, contribute to the deterioration of the patient's condition. In the absence of pronounced organic changes in the cardiovascular system (atherosclerosis of the coronary arteries, degeneration of the heart muscle), the prognosis of paroxysmal tachycardia is usually favorable. In these cases, paroxysmal tachycardia attacks accompany the patient sometimes from early childhood to deep old age, being the only manifestation of the disease in them and often without significantly disrupting their working capacity. There are frequent patients who, having become accustomed to their attacks, do not even interrupt their normal work during them. True, there are, on the other hand, cases where, even without other pronounced pathological changes on the part of the heart under the influence of prolonged attacks, a picture of heart failure develops and where death can occur during attacks. The treatment of paroxysmal tachycardia can be reduced to: 1) preventing the appearance of attacks, 2) terminating them, and 3) prophylaxis and treatment of diseases directly or reflexively causing the appearance of attacks. Prevention of attacks can be achieved by avoiding all those factors which, according to the observations of the patients themselves, cause attacks in them. These factors include alcohol and nicotine abuse, sexual excesses, overwork, immoderate eating and drinking, flatulence, strong psychic excitations. * One can assume in these cases a congenital anomaly in the structure, innervation, or blood supply of certain areas of the heart muscle, which under the influence of fluctuations in the tone of extracardiac nerves become a source of impulse generation.

Various methods have been proposed to terminate the attacks, aiming to affect the vagus nerve and thereby correct the disturbance of extracardiac innervation which was the ultimate cause of the onset of the attack. Mechanical irritation of the vagus nerve is achieved by compressing it in the neck [pressure should be applied with the thumb at the anterior edge of the sternocleidomastoid muscle, at the level of the upper edge of the thyroid cartilage, towards the spine; one can be guided by the pulsation of the carotid artery, upon compression of which in the indicated direction the vagus nerve is also compressed (to avoid a fainting state, pressure must be produced on one side only)]. Pressure on the eyeballs, proposed by Czermak, in a number of cases, especially when applied early and with sufficient force, leads to the rapid termination of the attack. Also, other physical techniques, such as the Valsalva maneuver, deep inhalation, straining, squatting (Erb's phenomenon), a specific position of the torso, turning the neck, hanging the torso, as well as vomiting induced by tickling the pharynx, can stop the attack. Medicinal substances proposed for terminating the attack are divided into two groups: 1) cardiotonica and 2) cardioparalytica. The former obviously act also through irritation of the vagus nerve; these include the intravenous administration of strophanthin ¹/₄--¹/₂ cm³ (with caution, especially when the patient has been taking digitalis for a long time—possibility of cumulation), digalen (¹/₂-1 cm³), physostigmine (0.5-1.0 mg pro die), and choline in the form of Acetylcholine (1-2 cm³ of a 20% original solution intramuscularly or intravenously) or choline chloride (5% solution 0.5 cm³). In markedly pronounced changes of the coronary vessels, as well as the heart muscle, all these agents must be used with caution. From the cardioparalytica group, quinine and quinidine have recently become widespread. Quinine lowers the basic functions of the heart, and consequently the automatism of the excited center. However, the use of quinine requires caution, as it is a protoplasmic poison that paralyzes the heart. It is therefore contraindicated in diseases accompanied by pronounced cardiovascular insufficiency. Quinine or quinidine is used at 0.2-0.4 two to three times a day. Quinine can also be used intravenously in the form of soluble preparations of Chininum bihydrochloricum, Merck's urethan-quinine, and intramuscularly—Hamburg solvochin (2 cm³). During attacks, it is also necessary to observe strict bed rest, proper bowel function, and a non-irritating diet. Finding a connection between attacks and diseases of individual organs or body systems is very difficult; in some cases, however, such a connection can be detected (helminths, meteorism, diseases of the gastrointestinal tract and central nervous system). In these cases, the elimination of these diseases can also lead to the disappearance of paroxysmal tachycardia.