Ventricular Premature Systoles Research Articles

The Evolution of the vectorcardiogram and electrocardiogram of the normal infant: I. The normal newborn ∗

1. 1. Vectorcardiograms and electrocardiograms were obtained in fifty normal newborn infants. 2. 2. Typically, the vectorcardiographic findings were similar to those found in cases of pathologic right ventricular hypertrophy in older children and adults with two possible exceptions: (1) T sÊ loops were almost always concordant with the QRS sÊ loops in all planes in the normal newborn; and (2) the QRS sÊ loop was usually inscribed in a clock-wise direction in the sagittal plane in the normal newborn. 3. 3. Variations from the typical vectorcardiographic findings were seen including: (1) QRS sÊ loops oriented predominantly to the left in some, superiorly in others and posteriorly in still another group; (2) counterclockwise direction of inscription of the QRS sÊ loop in the frontal and horizontal planes. 4. 4. In general, the electrocardiograms showed varying degrees of right axis deviation and evidence of “right ventricular preponderance” in the precordial leads. 5. 5. Deviations from typical electrocardiographic findings were also encountered including: (1) precordial lead patterns suggestive of “left ventricular preponderance”; and (2) T wave changes heretofore described as indicative of pathologic ventricular hypertrophy. These included upright T waves in right precordial leads of infants more than one day old and inverted T waves in left precordial leads of the same age group. 6. 6. Arrhythmias were present as follows: five infants with ventricular premature systoles, one with nodal premature systoles, one with atrial premature systoles and one with a wandering pacemaker. 7. 7. Because of the wide range of normal, conservatism is urged in the interpretation of the vectorcardiogram and electrocardiogram of the newborn infant.

Electrical activation and mechanical asynchronism in the cardiac cycle of the dog.

Dissociation of electrical and mechanical asynchronism in the right and left ventricle of the dog has been studied by simultaneous registration of the precordial electrocardiogram and right and left ventricular pressure curves. Observations were made during sinus rhythm and during digitalis-induced ventricular premature beats with widened aberrant QRS complexes. Measurements were made of the time of onset of isometric contraction in the ventricles, relative to each other, and to the onset of the QRS complex. The results indicate that mechanical asynchronism in onset of isometric contraction is not a necessary consequence of the asynchronous electrical depolarization of ventricular premature systoles. Submitted on November 10, 1958

Electrical activation and mechanical asynchronism in the cardiac cycle of the dog.

Right and left ventricular pressure curves and electrocardiogram were recorded in the dog during sinus rhythm and during mechanically induced right and left ventricular premature systoles. The normal range during sinus rhythm for the relationship between onset of right and left ventricular contraction was determined. At one extreme, right ventricular contraction commenced 0.02 second before the left; at the other extreme, left ventricular contraction started 0.03 second before the right. In most instances, the onsets of ventricular contraction were either temporally identical or one ventricle contracted 0.01 second prior to the other.

Management of cardiac arrhythmias during anaesthesia

Disorders of cardiac rhythm may be described as supraventricular or ventricular in origin. The former for the most part are innocuous. Ventricular premature systoles may be the forerunner of ventricular tachycardia or ventricular fibrillation. Ventricular tachycardia if persistent is accompanied by failing circulation. The majority of the arrhythmias observed during anaesthesia can be attributed to hypoxia or accumulation of carbon dioxide. In the opinion of certain anaesthetists, if these two causes of arrhythmia are avoided there is no need for an antiarrhythmia drug. Procaine amide has proven of value in the control of the ventricular arrhythmias which occur during cyclopropane anaesthesia. Rapidly acting digitalis preparations, particularly acetyl strophanthidin, may be needed to slow a rapidly beating heart (supraventricular tachycardias). The ventricular arrhythmias which accompany digitalis toxicity are caused by loss of intracellular potassium. Potassium chloride is effective in the control of digitalis-induced arrhythmias and should be considered in other instances as well.

Mechanisms of intermittent ventricular bigeminy. I. Appearance of ectopic beats dependent upon length of the ventricular cycle, the "rule of bigeminy".

In order to analyze the cause for the appearance and disappearance of ventricular premature systoles giving rise to temporary bigeminal rhythm, the electrocardiographic material was divided into two major groups: group A, consisting of ectopic beats with fixed coupling occurring during grossly irregular dominant rhythms, and group B, consisting of ectopic beats with varying coupling occurring during regular dominant rhythms. Analysis of group A, the subject of the present report, shows a definite relationship between the duration of the ventricular cycle and the occurrence of ventricular premature systoles, in that long cycles favor their appearance whereas short cycles tend to preclude it. This "rule of bigeminy" is best explained on the basis of a re-entry mechanism of the ventricular premature systoles. Criteria are given for the differential diagnosis between ventricular premature systoles and aberrant ventricular conduction of supraventricular impulses which is prone to occur under similar circumstances. The analysis of group B is presented in a subsequent report.

Mechanisms of intermittent ventricular bigeminy. II. Parasystole, and parasystole or re-entry with conduction disturbance.

In a previous report dealing with intermittent ventricular bigeminy due to ventricular premature systoles with fixed coupling in the presence of a grossly irregular dominant pacemaker, it was shown that the appearance and disappearance of the ectopic beats were dependent upon the length of the ventricular cycle ("rule of bigeminy"). In the present report, dealing with ventricular premature systoles with varying coupling in the presence of a regular dominant rhythm, the mechanism of ectopic impulse formation is shown to be either parasystole or re-entry, and the intermittence of bigeminy is due to simple interference or to a disturbance in conduction of a parasystolic or of a re-entrant impulse. Intermittent parasystole is illustrated and presented as a possible link between the two fundamental mechanisms of parasystole and re-entry.

The clinical and electrocardiographic differentiation of supraventricular and ventricular tachycardias with regular rhythm

1. 1. The differentiation of a supraventricular from ventricular tachycardia can usually be made by careful bedside auscultation, if particular care is paid to splitting of the heart sounds. 2. 2. In a case of rapid regular tachycardia, if the first and second sounds are single or normally split, the diagnosis of supraventricular tachycardia can be made with confidence, and ventricular tachycardia can be excluded with confidence. 3. 3. In a case of rapid regular tachycardia, if there is wide splitting of both sounds, ventricular tachycardia is usually present. 4. 4. In a case of rapid regular tachycardia, if there is wide splitting of both sounds, variation in the intensity of the first sound and independent, irregular “Cannon A” waves in the jugular venous pulse, the diagnosis of ventricular tachycardia can usually be made with confidence. 5. 5. The wide splitting of both heart sounds is a manifestation of ventricular asynchrony; the variation in the intensity of the first sound and the independent, irregular “Cannon A” waves is a reflection of auriculoventricular dissociation. 6. 6. Supraventricular tachycardia with bundle branch block, ventricular tachycardia with auricular fibrillation and ventricular tachycardia with retrograde conduction are all rare conditions, in which ventricular asynchrony occurs without auriculoventricular dissociation. Wide splitting of both heart sounds without variation in the intensity of the first sound is therefore encountered. Differentiation is difficult but can be made by careful study, as discussed. 7. 7. The great value of the esophageal lead in the electrocardiographic diagnosis has been clearly demonstrated. 8. 8. In a case of rapid regular tachycardia, if the electrocardiogram reveals a QRS interval of normal duration, the diagnosis of supraventricular tachycardia is established. Auricular activity can usually be demonstrated by standard electrocardiograms and esophageal leads are rarely necessary. 9. 9. In a case of rapid regular tachycardia, if the electrocardiogram reveals a widened QRS, supraventricular tachycardia with bundle branch block cannot be differentiated from ventricular tachycardia, unless auricular activity is demonstrated. Whereas clinical evidence of auricular activity can be readily detected, the diagnosis cannot usually be made by the conventional electrocardiogram, as the P waves are often obscured by the widened QRS-T complexes. The esophageal leads, however, will clearly demonstrate P waves and thus overcome this problem. 10. 10. The esophageal lead is essential in the differentiation of supraventricular tachycardia with bundle branch block, ventricular tachycardia with independent auricular activity, ventricular tachycardia with retrograde conduction, and ventricular tachycardia with auricular fibrillation. 11. 11. The same clinical features that help to differentiate supraventricular tachycardia from ventricular tachycardia help to differentiate auricular from ventricular premature systoles.

The intraventricular conduction time (QRS duration) of ventricular premature systoles.

The intraventricular conduction time (QRS duration) of ventricular premature systoles.

Ventricular premature systoles with postponed compensatory pause

Several examples of a physiologic phenomenon accompanying ventricular premature systoles are presented and analyzed. The term postponed compensatory pause is proposed for this infrequent disturbance.

The effect of induced ventricular premature systoles upon the precordial QRS pattern in a case of right ventricular hypertrophy

The effect of induced ventricular premature systoles upon the precordial QRS pattern in a case of right ventricular hypertrophy

A study of the central and peripheral arterial pressure pulse in man; correlation with simultaneously recorded electrokymograms.

This communication describes and discusses the results obtained in studying central and peripheral arterial pressure pulses in man by means of retrograde aortic catheterization. The pressure pulse transformation and pulse transmission in the aorticobrachial system are presented and compared with comparable tracings reported in the dog. Several normal subjects and patients with hypertension, aortic regurgitation and coarctation of the aorta were studied. The genesis of the central pulse contour in aortic regurgitation is reconsidered. The changes in central pulse pressure, produced by the Valsalva-like maneuver, and ventricular premature systoles have been investigated, especially in their relationship to cycle length, end-diastolic volume and peripheral resistance. The technic of obtaining pulse pressure recordings by retrograde aortic catheterization is recommended for determining the location, size and dynamic significance of coarctation of the aorta. As an additional study, aortic densograms and border electrokymograms from the aortic arch and left ventricular border were correlated with simultaneously recorded central aortic pressure tracings.

Aberrant ventricular conduction

1. 1. Examples are presented of aberrant ventricular conduction of supraventricular impulses dependent upon the duration of the preceding ventricular cycle. 2. 2. The criteria for the differential diagnosis of ventricular premature systoles and aberrant ventricular conduction in cases of auricular fibrillation and auricular flutter with irregular ventricular rate are pointed out. 3. 3. The clinical importance of the recognition of aberrant ventricular conduction, particularly in the differential diagnosis of paroxysmal tachycardia, is pointed out.

Ventricular premature systoles occurring at rapid heart rates.

Ventricular premature systoles occurring at rapid heart rates.

Factors Influencing the Time of Appearance of Premature Systoles (Including a Demonstration of Cases with Ventricular Premature Systoles due to Re-entry but Exhibiting Variable Coupling)

The genesis of the most common cardiac arrhythmia, that due to premature systoles, still remains obscure. Observations made upon two patients with ventricular premature systoles are reported because of some unusual features of their timing which shed some light upon the mechanism behind the appearance of premature systoles, regardless of the extrasystolic impulse. The theories of the extrasystolic irregularities are reviewed with particular attention to the criterion of "fixed coupling" generally used to distinguish between premature systoles explained by a re-entry mechanism and those explained by a parasystolic pacemaker.

The role of anemia in the experimental production of heart block and auricular fibrillation in the dog

1. 1. The minimal dose of acetylcholine required to produce second degree A-V block (the minimal standardizing dose) was determined in thirty-one dogs. Although the minimal standardizing dose varies widely from animal to animal, it remains relatively constant for the same animal over long periods of time. The minimal standardizing dose bears a crude relationship to the hemoglobin level. Doses ten times and twenty times the minimal standardizing dose were also given. With such doses auricular fibrillation occurred in approximately 50 per cent of the animals tested. 2. 2. Anemia was produced by phenylhydrazine, n-propyl disulfide, and hemorrhage. An increased sensitivity toward the development of A-V block and auricular fibrillation which roughly paralleled the course of the anemia was observed. Fifty per cent of the dogs which did not fibrillate with control injections of acetylcholine fibrillated following the onset of the anemia. Animals which fibrillated with control injections fibrillated during anemia with smaller doses of acetylcholine. 3. 3. It is suggested that the increased sensitivity of the heart to acetylcholine in anemia is due to anoxia of the myocardium. Decreased concentration of effectiveness of cholinesterase may also play a role. 4. 4. In dogs in which acetylcholine causes auricular fibrillation, there is a semidirect relationship between the dosage of acetylcholine given and the length of time during which the auricles fibrillate. There is also a relationship between the magnitude of the dose and the length of time during which the A-V block persists. 5. 5. The development of auricular fibrillation was preceded in almost every instance by the occurrence of intra-auricular block and A-V block. It is suggested on the basis of the contour of our records and in support of previous reports from this department that auricular re-entry is the mechanism of the genesis of auricular fibrillation. 6. 6. Electrocardiographic changes seen after the administration of acetylcholine included changes in the contour of the P waves and the T waves and shifts in the P-Q and S-T segments. Arrhythmias seen included auricular fibrillation and flutter, ventricular tachycardia, auricular and ventricular premature systoles, nodal rhythm, and A-V dissociation.

Auricular premature systole: I. Aberration of the ventricular complex in the electrocardiogram

1. 1. The electrocardiograms of 201 patients who had auricular premature systoles (APS) were analyzed. One thousand three hundred six APS were found, and were divided into five groups according to the degree of their prematurity. Multiple APS of the same degree of prematurity occurring in one record were counted as one “type.” Multiple APS of different degrees of prematurity were counted as different “types.” The total number of “types” of APS was 525. Eight of these were blocked. 2. 2. APS with aberration of the ventricular complexes were three times as frequent as APS without aberration. 3. 3. If no aberration is present, the APS may be overlooked, or the irregularity may be misinterpreted as sinus arrhythmia. 4. 4. Aberration, especially of the T wave, is often more marked in the chest leads. Chest leads may thus aid in the recognition of APS. 5. 5. Forty-three types showed no aberration of QRS, but showed aberration of the RS-T segments or the T waves. 6. 6. Three hundred thirty-seven types of APS showed aberration of the QRS complexes. 7. 7. If aberration of QRS was of slight degree, increase or decrease in amplitude was the most frequent single change: changes in configuration (slurring, notching, appearance of a Q wave) were next in frequency; changes in duration occurred seldom except in conjunction with other changes; a reversal of direction never occurred alone. 8. 8. The higher degrees of aberration were less frequent than the lower. They consisted of changes in amplitude combined with changes in configuration, or various combinations of changes in amplitude, configuration, duration, and direction. 9. 9. The highest degree of aberration (twenty-eight types) affected all four characteristies of the QRS complex, amplitude, configuration, duration, and direction. APS with such bizarre ventricular complexes are commonly mistaken for ventricular premature systoles. 10. 10. The degree of prematurity of an APS is a major factor in determining the degree of its aberration. This was shown by the following facts: 10.1. a. None of the twenty-eight types of APS with very marked aberration occurred late in diastole. 10.2. b. None of the thirty-five types of APS without any aberration occurred very early in diastole. 10.3. c. None of the 101 types of APS occurring late in diastole showed more than moderate aberration. 10.4. d. None of the six types of APS occurring very early in diastole were free from aberration. 11. 11. The degree of prematurity is not the only factor which determines the degree of aberration. This was shown by the following facts: 11.1. a. Of one hundred types of APS occurring early in diastole, eleven showed no aberration. 11.2. b. Most electrocardiograms showing different types of APS in the same record revealed a lack of parallelism between aberration and the degree of prematurity; aberration often remained the same or became less marked as the degree of prematurity increased. 12. 12. No definite relationship was found to exist between the number of APS in a given record and the aberration of their ventricular complexes. 13. 13. P-R interval changes in APS had no influence on the aberration of their ventricular complexes. 14. 14. The patient's age had no influence on aberration. APS with marked aberration were found in children. APS without any aberration were found in patients over 70 years of age. 15. 15. Aberration occurred in normal and abnormal electrocardiograms. Aberration of all degrees occurred in noncardiac patients as frequently as in cardiac patients. Aberration was no more frequent in the presence of congestive heart failure than in its absence. 16. 16. Three cases are reported. Their serial records showed that significant changes in the degree of aberration of the APS occurred within a few days. In two cases, the change was probably brought about by the administration of quinidine, and, in the third, by a severe infection (pneumonia). 17. 17. Aberration of the ventricular complexes of APS reflects changes in intraventricular conduction; these changes may be physiologic; or they may be pathologic and may then be produced by diseases or by drugs affecting the conduction system, e. g., quinidine. 18. 18. Quinidine selectively affects APS by increasing their aberration, especially the duration of QRS. 19. 19. A change in the degree of aberration is more significant than aberration itself. It indicates a change in the condition of the heart which the remainder of the electrocardiogram may not clearly reveal.

Reciprocal beating initiated by ventricular premature systoles: Langendorf, R., Katz, L. N., and Simon, A. J.: Brit. Heart J. 6: 13, 1944

Reciprocal beating initiated by ventricular premature systoles: Langendorf, R., Katz, L. N., and Simon, A. J.: Brit. Heart J. 6: 13, 1944

An unusual effect of interpolated ventricular premature systoles

1. 1. A case of interpolated ventricular premature systoles is presented in which there was unusual prolongation of the postextrasystolic P-R intervals; they attained 0.78 second in one instance, and over 0.60 second in three others. 2. 2. The marked prolongation of the postextrasystolic P-R interval after interpolated ventricular premature systoles had a hitherto undescribed effect on the second postextrasystolic beat, namely, prolongation of its P-R and, on one occasion, dropping out of the second postextrasystolic ventricular complex. 3. 3. Analysis showed that the P-R of the first postextrasystolic beat did not depend exclusively on the interval between the beginning of QRS of the premature systole and the next sinus P wave which occurred; some other factor was involved. Reasons are given for the view that this most likely depended upon variations in the retrograde conduction from the point of origin of the ventricular premature systole. The P-R of the second postextrasystolic beat, on the contrary, depended exclusively on the interval between its P and the beginning of the preceding QRS.