A general theory of the causes of murmurs in the cardiovascular system

Bruns, David L.

doi:10.1016/0002-9343(59)90002-6

Cited by 105 publications

(28 citation statements)

References 16 publications

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“…Cavitation may be generated when blood moves through a narrow orifice at very high velocities and therefore at reduced lateral pressures [72,73]. R obiczek et al [72] and Bruns 173] have suggested that cavitation may injure the vessel wall and thereby produce post-stenotic dilatations.…”

Section: Localized Enlargementsmentioning

confidence: 99%

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Vascular Caliber

Rodbard¹

1975

Cardiology

232

135

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Many aspects of vascular caliber can be accounted for on the basis of interactions between the frictional drag generated by the stream, and the sensitivity of the endothelial cells to this force. When the drag force on endothelial cells is at its critical set-point, these lining cells are at rest with respect to factors that affect caliber. An increase in flow rate increases the drag and appears to induce the endothelium to generate a signal that triggers relaxation of the subjacent medial smooth muscle. The resulting functional dilatation of the vessel reduces the stream velocity and returns the drag to its set-point. If the drag stimulus is persistent or recurrent, vasodilatation is soon followed by anatomical reorganization of the vessel around its enlarged lumen. This sequence can account for gradual, generalized and regional vascular growth, and for the opening of collateral vessels. This sequence may also play a role in the enlargement of veins, lymphatics, airways and other vessels. Turbulence greatly increases drag per unit volume of flow. Aneurysms and and post-stenotic dilatations are considered to result from an increased drag. Jets increase drag to an even greater extent and may account for saccular aneurysms and for ‘jet lesions’. Conversely, reduced flow diminishes drag and thereby triggers constriction of the vascular smooth muscle. Persistent reduction of drag permits proliferation of the subendothelial connective tissue, which reduces vascular caliber until the drag on the lining cells is returned to its set-point. Progressive localized narrowings (stenoses) may also be attributed to a reduced drag. Thus high velocity flow around an irregularity such as a plaque may separate the streamlines from the wall at the downstream end of the narrowing. In this region of separation the cells respond to the reduced local flow and drag by subendothelial proliferation and ingrowth, producing further narrowing. These mechanisms may be operative in

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Section: Localized Enlargementsmentioning

confidence: 99%

“…A number of workers have held that stream turbulence triggers vascular widening [60,[67][68][69][70][71][73][74][75][76][77], Turbulence develops Rodbard when the inertial forces (due to velocity, caliber, and density) exceed the viscous forces that tend to maintain laminar (streamline) flow ( fig. 15).…”

Section: Localized Enlargementsmentioning

confidence: 99%

Vascular Caliber

Rodbard¹

1975

Cardiology

232

135

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“…Bruns has suggested on theoretical grounds that the intensity should be related to the fourth power of the veloc- ity. 10 Dexter and co-workers, 11 however, were unable to find a direct correlation between the intensity of the murmur of clinical aortic stenosis and the calculated velocity of flow through the valve. In an attempt to clarify this point, the velocity of flow through the stenotic portion of the pulmonary artery in .…”

Section: Resultsmentioning

confidence: 97%

Study of the Murmur Produced by Acute Pulmonary Artery Constriction

Moedjono

Little

Orlando

et al. 1962

Circulation Research

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• Pulmonary artery constriction has been utilized as an experimental method of stressing the right ventricle 1 " 4 or producing changes in the systemic circulation. "7 As a result, the basic circulatory features of pulmonary artery constriction have been documented. The murmur that is produced by this procedure has not received as much attention. It therefore seemed desirable to investigate this aspect of pulmonary artery constriction. The purpose of this report is to summarize these observations. MethodsDogs were anesthetized with intravenous sodium pentobarbital (30 ing. per Kg.) and the chest opened using a sternal-splitting procedure under mild positive pressure respiration. The right ventricle was cannulated through the azygos vein and the left pulmonary artery via a side branch. A phonocatheter* was also placed in the pulmonary artery by way of a second side branch. This was connected to a Electronics-for-Medicine logarithmic heart sound amplifier. Right ventricular and pulmonary artery pressures were measured electrically using Stathani strain gauges and, together with the intrapulmonary sounds, were recorded photographically using 1 both an Electronics-for-Medicine recorder and a Sanborn twin-beam recorder. Respirations were interrupted during all recordings to avoid artifacts due to lung inflation. The zero level for nil pressure recordings was the level of the right atrium.A ligature was placed around the base of the main pulmonary artery and attached to a screw device similar to that described by Finberg and Wiggers.1 By tightening this instrument, the loop around the pulmonary artery was reduced in size. This instrument was calibrated so that the reduction in the size of the loop was known for each From the Department of Physiology, Seton Hall College of Medicine and Dentistry, Jersey City, New Jersey.Supported in part by a grant from the American Heart Association and from the Burlington County Heart Association.'Manufactured by American Electronic Laboratories, Inc., Philadelphia, Pennsylvania.setting. In addition, immediately following each experiment, the segment of the pulmonary artery containing the stenosis was removed without disturbing the ligature, and the internal diameter was measured for each degree of constriction utilized in that study. As a result, it was possible to quantitate with considerable accuracy the internal cross sectional area of the constriction that was produced in the pulmonary artery by each setting. During a typical experiment the ligature was tightened. Sound and pressure recordings were made and other data obtained. The ligature was then loosened to permit a recovery period before the procedure was repeated at an increased degree of constriction.Cardiac output was determined in some animals during each of the experimental procedures. The dye-dilution technique, as modified by Opdyke and Sniffen, 8 was utilized with tricarbocyanine dye (Cardio-Green*) as the indicator. The dye was injected into the right atrium via a cannula in the right jugular vein, and blood was wi...

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“…It has been postulated that the source of the disturbed flow, and of the CVH itself, is vibrations which lead to periodic wave fluctuations arising from the convergence of tributaries (the left innominate and right subclavian veins which enter the SVC) [4,18], We therefore selec tively occluded each of these veins in several of our ini tial subject studies by applying pressure to the left innominate vein with the head of the transducer as we visualized the vessel ultrasonically and by restricting venous flow from the right arm with a blood pressure cuff. We found no change in SVC velocity pattern to indicate that convergent streams contributed to the flow disturbance.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamic Factors Associated with the Cervical Venous Hum

Schwartz¹,

Goldberg²,

Hegesh³

1987

Am J Noninvas Cardiol

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The etiology of the cervical venous hum (CVH) has been long debated. Our purpose was to elucidate hemodynamic factors associated with the presence of a CVH. Forty-three normal children were studied, 28 with a CVH detected by auscultation and 15 who had no CVH. Pulsed Doppler and imaging echo were used to measure superior vena cava (SVC) and aortic diameters and velocities at different head positions (straight forward and turned left) and body positions (upright, supine, and the critical angle at which the CVH disappeared). As expected, age and body surface area were significantly lower for the CVH group. Mean indexed cardiac output (CO) in both supine and upright positions was significantly higher in the CVH group (mean ± SD = 4,487 ± 1,095 and 4,144 ± 845 ml/min, respectively) as compared to the controls (supine CO = 3,184 ± 538, upright CO = 2,509 ± 580 ml/min). The incidence of marked instantaneous velocity spread in the upright-head straight position was significantly greater in the CVH group (73%) than in controls (27%; p < 0.0005). No important differences in SVC diameter or velocity were found between the two groups. A unique cyclically elevated waveform, unrelated to respiration, was observed in both subject groups (p > 0.05). Within each group, body position significantly affected mean peak SVC velocity by the hydrostatic effect, while head position did not. These findings indicate that increased CO resulting in higher SVC flow and a flow disturbance in the SVC are major factors associated with the presence of the CVH.

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A general theory of the causes of murmurs in the cardiovascular system

Cited by 105 publications

References 16 publications

Vascular Caliber

Vascular Caliber

Study of the Murmur Produced by Acute Pulmonary Artery Constriction

Hemodynamic Factors Associated with the Cervical Venous Hum

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