The First Heart Sound in Normal and Ectopic Ventricular Contractions

Little, Robert C.; Hilton, James G.; Schaefer, Roy D.

doi:10.1161/01.res.2.1.48

Cited by 32 publications

(6 citation statements)

References 9 publications

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“…Secondly, it has been shown that a properly placed atrial systole can show its influence, whether or not the mitral valve is closed before the onset of ventricular systole (Little, Hilton and Schaefer, 1954;Sarnoff, Gilmore and Mitchell, 1962;. During ventricular pacing, as conducted in these experiments, atrial systole was not properly placed (Fig.…”

Section: Discussionmentioning

confidence: 78%

SYNCHRONICITY OF VENTRICULAR CONTRACTION: OBSERVATIONS COMPARING HAeMODYNAMIC EFFECTS OF ATRIAL AND VENTRICULAR PACING

Gilmore¹,

Sarnoff²,

Mitchell³

et al. 1963

Heart

189

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In the course of earlier investigations it was noted that when the heart was paced by ventricular stimulation, mean left atrial pressure was higher for any given cardiac output, aortic pressure, and stroke work than when the atrium was paced at the same rate. Although the changes observed in those initial observations were not always striking, it was felt desirable to clarify the mechanisms by which they took place and to find what influenced their magnitude. Accordingly, a more systematic investigation was undertaken.Two explanations were entertained that it was thought might account for the observed phenomena. The first was that, as suggested by Koch (1920) and Wiggers (1925), ventricular stimulation does not produce as well-organized a wave of ventricular depolarization as is the case when the impulse is normally propagated, and so results in a less synchronous ventricular contraction. Secondly, it was reasoned that if the ventricle had perchance been stimulated at such a rate and at such a time in the cardiac cycle that the paced ventricle and the spontaneously beating atrium were contracting simultaneously, the atrium would have been contracting against a closed atrio-ventricular valve, thus depriving the ventricle of that portion of its filling and the consequent influence on contraction which normally results from atrial systole (Sarnoffand Mitchell, 1961). The results of experiments designed to examine the validity of these two explanations over the whole range of ventricular function and to ascertain the effects of such changes on flow are the subject of this communication. A preliminary report on a portion of these data has been previously presented (Linden et al., 1959). METHODSMongrel dogs of both sexes weighing 17-5 to 31-5 kg. were anesthetized with morphine, chloralose, and urethane. The chest was opened under intermittent positive pressure breathing and the appropriate cannulations made so as to be able to record continuously aortic blood flow and heart rate, as well as right atrial, left atrial, aortic, and pulmonary arterial pressures and left ventricular diastolic pressure. The techniques used were essentially the same as those described (Samoff et al., 1960a) with the following additions. After pericardiotomy, pacing electrodes were placed on the right or left atrium or both, on the right or left ventricle or both, and sometimes on all four chambers. Each cardiac electrode, as well as the indifferent electrode, was connected to a multiplexing switch so that the impulse could be applied to the atrium and then instantaneously changed from atrium to ventricle and back again as desired. No special effort was made to apply the ventricular electrode to any particular place on the ventricular myocardium although generally it was applied to the lateral wall of the ventricle near the atrioventricular sulcus rather than in the vicinity of the ventricular septum. The electrodes for atrial pacing were applied on or near the atrial appendage.

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Section: Discussionmentioning

confidence: 78%

SYNCHRONICITY OF VENTRICULAR CONTRACTION: OBSERVATIONS COMPARING HAeMODYNAMIC EFFECTS OF ATRIAL AND VENTRICULAR PACING

Gilmore¹,

Sarnoff²,

Mitchell³

et al. 1963

Heart

189

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“…The effect of atrial systole on closure of the A-V values has been emphasized by Little et al, 14 Sarnoff and Mitchell,15 and others. 10 Whether absence of atrial facilitation of valve closure does in fact impair ventricular function and whether any such impairment would be comparable to the effect on ventricular function of loss of atrial augmentation of end diastolic filling has not been demonstrated as yet.…”

Section: Ditcuitionmentioning

confidence: 93%

Atrial Contribution to Stroke Volume in Dogs with Chronic Heart Block

Snyder

Bender

Kitchin

et al. 1966

Circulation Research

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In dogs studied without thoracotomy, under morphine-pentobarbital anesthesia and with an average heart rate of 71 beats/minute, atrial systole contributes to ventricular function to a small but significant degree. Stroke volume increased by 7 to 8% when atrial systole was timed to occur 0.1 second prior to closure of the atrioventricular valves, and decreased a similar magnitude when the contribution of atrial systole to ventricular filling was rendered ineffective by the use of an A-V delay of zero so that atrial emptying into the ventricles was prevented by the closed A-V valves. Increases or decreases in right atrial pressure of several centimeters of water induced by infusion of 6% dextran and by hemorrhage, respectively, were not associated with demonstrably significant alterations in these effects. ADDITIONAL KEY WORDSbypass of bundle of His hypovolemia hypervolemia nonthoracotomized dogs electrical pacing of atria and ventricles effective and ineffective atrial contraction stroke volume determined from pulse pressure • Although it is generally agreed that late diastolic distention of the ventricles produced by atrial contraction improves ventricular performance, there is considerable variability in the results of experiments designed to quantitate this effect. Gesell 1 in 1916 found that the ventricular filling effect of atrial systole averaged about 50*. Wiggers and Katz 2 in 1922 assessed the atrial contribution to ventricular filling as 18 to 60$, averaging 35%. Jochim 8 in 1938 calculated the maximal net atrial contribution as 21$ of ventricular filling when the atrial systolic-ventricular systolic interval was 0.1 second.Because of the variability in the results and because open-chest preparations were used in all but one of these studies, we have investigated the effect of atrial contraction on stroke volume and venous pressure in dogs with chronic heart block studied without thoracotomy. An electronic bypass was substituted for the bundle of His, atrial action potentials being used to trigger stimuli to the right ventricle through a variable delay circuit, a technic employed by Hellerstein and associates. 4 MethodsNine experiments were performed in seven dogs (body wt 13 to 15 kg) in which chronic atrioventricular block had been produced 6 to 12 months before, by ligating the bundle of His at open atriotomy during temporary caval occlusion. All the animals were in good condition and free of congestive failure. They were premedicated with morphine (5 mg/kg subcutaneously) and 30 minutes later anesthetized with sodium pentobarbital (15 mg/kg intravenously). Occasional supplementing doses of the barbiturate (25 to 50 mg) were required during long experiments. The dogs were positioned on their backs on a padded animal board with their front legs flexed along the thorax. Positive pressure respiration equal to 6 to 9 cm saline at 35 to 40 cycles/

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“…Acoustic cardiography permits simultaneous acquisition of ECG and heart sound information and provides a computerized interpretation of these findings. Although, the application of heart sounds in prediction of the origin of VA has been intensively investigated, it is not clinically available because of the lack of objectivity 2 , 10 , 11 . The present study was designed to test whether acoustic cardiography could provide information in differentiating the origin of VA in clinical practice.…”

Section: Introductionmentioning

confidence: 99%

Predicting the Origin of Ventricular Arrhythmia Using Acoustic Cardiography

Lin

Chang

et al. 2017

Sci Rep

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This study aimed to examine the relationship between measurements related to heart sounds and the origin of ventricular arrhythmia. We retrospectively evaluated 45 patients undergoing catheter ablation with contemporaneous digital acoustic cardiography of the first heart sound (S1) and the second heart sound (S2). The patients with baseline wide QRS morphology (>120 ms or aberrant conduction), heart failure, valvular heart disease, chronic pulmonary disease, and obesity were excluded. Ventricular arrhythmias from the left ventricle had an increased S1 complexity score and S1 duration in comparison to adjacent sinus beats. On the other hand, ventricular arrhythmia from right ventricle had decreased S1 complexity score and S1 duration in comparison to adjacent sinus beats. The difference of S1 (ΔS1) parameters between premature ventricular complex and sinus beat was significantly smaller in right ventricular arrhythmia group compared with and left ventricular arrhythmia group. For predicting the origin of ventricular arrhythmia, the ΔS1 duration provide better predictive accuracy (sensitivity: 100%, specificity: 100%, cutoff value: −1.28 ms) in comparison to ΔS1 complexity score (sensitivity 71.4%, specificity 75.0%, cutoff value: −0.13). The change of S1 complexity and duration determined from acoustic cardiography could accurately predict the ventricular arrhythmia origin.

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The First Heart Sound in Normal and Ectopic Ventricular Contractions

Cited by 32 publications

References 9 publications

SYNCHRONICITY OF VENTRICULAR CONTRACTION: OBSERVATIONS COMPARING HAeMODYNAMIC EFFECTS OF ATRIAL AND VENTRICULAR PACING

SYNCHRONICITY OF VENTRICULAR CONTRACTION: OBSERVATIONS COMPARING HAeMODYNAMIC EFFECTS OF ATRIAL AND VENTRICULAR PACING

Atrial Contribution to Stroke Volume in Dogs with Chronic Heart Block

Predicting the Origin of Ventricular Arrhythmia Using Acoustic Cardiography

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