Ventricular Septal Defect in Infants and Children

Fyler, Donald C.; Rudolph, Abraham M.; Wittenborg, Martin H.; Nadas, Alexander S.

doi:10.1161/01.cir.18.5.833

Cited by 73 publications

(14 citation statements)

References 11 publications

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“…Children with ventricular septal defect (VSD)' often demonstrate failure to thrive (FfT) (1)(2)(3). While several mechanisms have been proposed to explain this phenomenon (4)(5)(6)(7)(8)(9)(10), the observation that patients with the largest intracardiac shunts demonstrate the most growth retardation suggests a cardiac cause (8)(9).…”

Section: Introductionmentioning

confidence: 99%

Mechanism of decreased forward stroke volume in children and swine with ventricular septal defect and failure to thrive.

Corin¹,

Swindle²,

Spann³

et al. 1988

J. Clin. Invest.

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Children with ventricular septal defect (VSD) often demonstrate failure to thrive (Ff1'). Such patients usually have reduced systemic cardiac output which has been postulated as a cause for their growth retardation. This study was conducted to ascertain the mechanism of the reduced cardiac output in children with VSD and FT1'1 and also in a porcine model of VSD. Forward stroke volume was reduced in VSD-F'IT children, 31±8 ml/m2, compared to normal children, 49±15 ml/m2 (P < 0.05), but was not reduced in children with VSD and normal growth and development (41±16 ml/m2). Forward stroke volume was also reduced in swine with VSD compared to controls. Contractility assessed by mean velocity of circumferential shortening (Vd) corrected for afterload was similar in normals and VSD-FT'I children. Contractile performance was also similar in normal and VSD swine. Afterload assessed as systolic stress was similar in FIT-VSD children and normal subjects. Preload assessed as end-diastolic stress was increased in the VSD-FI' group. End-diastolic volume was not larger in the VSD-FTI' group. We conclude that the reduced stroke volume seen in VSD-FT'I children and VSD-swine was not due to reduced contractility, increased afterload or reduced preload. The reduced stroke volume may have been due to failure of end-diastolic volume to increase adequately.

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Section: Introductionmentioning

confidence: 99%

Mechanism of decreased forward stroke volume in children and swine with ventricular septal defect and failure to thrive.

Corin¹,

Swindle²,

Spann³

et al. 1988

J. Clin. Invest.

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“…The record does not seem to bear out this contention. In our own material (Fyler et al, 1958), less than 5 % of ventricular defects died and most of them with bronchopneumonia, prematurity, and associated anomalies. An 18% 'medical death rate' was found and contrasted with 25% 'surgical death rate' by Ritter et al (1965), but in only half of the 18% was death attributable to congestive failure; in the others pneumonia, prematurity, and arrhythmias were the underlying causes of death.…”

Section: Natural Historymentioning

confidence: 56%

“…6). The middiastolic rumble usually follows the third sound and thus is separated appreciably from the pulmonary closure; though, by and large, the louder the rumble, the greater the left-to-right shunt, this relation is far from linear (Fyler et al, 1958). It should also be mentioned that mid-diastolic rumbles due to increased mitral valve flow alone, V~s eldom, if ever, assume a presystolic crescendo configuration (Fig.…”

Section: Clinical Pictuimentioning

confidence: 98%

Ventricular septal defect. A review of current thoughts.

Nadas¹,

Fyler²

1968

Archives of Disease in Childhood

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“…complete destruction of the free wall of the right ventricle produces no immediate effect on the circulation (Starr, Jeffers, andMeade, 1943 Bakos, 1950;Kagan, 1952). Experimental excision of the pulmonary valves in dogs (Barger, Roe, and Richardson, 1952;Ratcliffe, Hurt, Belmonte, and Gerbode, 1957;Fowler and Duchesne, 1958) produced remarkably little alteration in function but cannot be regarded as benign. In man, foetal congestive cardiac failure due to pulmonary incompetence has been described (Smith, DuShane, and Edwards, 1959).…”

Section: Discussionmentioning

confidence: 99%

“…is established, viz., Fallot's tetralogy (Gasul, Dillon, Vrla, and Hait, 1957;Fyler, Rudolph, Wittenborg, and Nadas, 1958;Lynfield, Gasul, Arcilla, and Luan, 1961;Becu, Ikkos, Ljungqvist, and Rudhe, 1961).…”

mentioning

confidence: 99%

The Surgical Treatment of the Tetralogy of Fallot

Barnard¹,

Schrire²

1961

Thorax

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Maldevelopment of the bulbus cordis may be associated with right ventricular outflow stenosis and a ventricular septal defect. The pathological anatomy in this group of anomalies varies from severe obstruction to the right ventricular outflow, with a small ventricular communication, to a large ventricular septal defect dominating the picture with mild obstruction.When the pulmonary stenosis is mild, whether the ventricular septal defect is small or large, a left-to-right shunt is always present, giving the clinical picture of a ventricular septal defect. On the other hand, if the stenosis is severe and the ventricular septal defect is small, anatomically or functionally (McCord, Van Elk, and Blount, 1958;Vogelpoel and Schrire, 1960a;Hoffman, Rudolph, Nadas, and Gross, 1960), the clinical picture is that of severe pulmonary stenosis with an intact ventricular septum.When the septal defect is large and the stenosis severe, a haemodynamic spectrum develops, dependent on whether the pulmonary stenosis or the systemic resistance is the greater. If the systemic resistance is greater, a dominant left-toright shunt is present, i.e., ventricular septal defect with pulmonary stenosis; if the pulmonary resistance is greater, a right-to-left shunt is present, i.e., Fallot's tetralogy; if the resistances are balanced, acyanotic tetralogy is present.The differentiation of ventricular septal defect with severe pulmonary stenosis and Fallot's tetralogy thus becomes a matter of semantics. Moreover, the haemodynamic state is not static. An infant may present with the dynamics of ventricular septal defect with a large left-to-right shunt. As the crista supraventricularis hypertrophies, progressive infundibular narrowing develops, so that the left-to-right shunt diminishes, the heart becomes smaller, right ventricular hypertrophy develops and, finally, a right-to-left shunt is established, viz., Fallot's tetralogy (Gasul, Dillon, Vrla, and Hait, 1957;Fyler, Rudolph, Wittenborg, and Nadas, 1958;Lynfield, Gasul, Arcilla, and Luan, 1961;Becu, Ikkos, Ljungqvist, and Rudhe, 1961).In this paper, by Fallot's tetralogy we mean severe right ventricular outflow stenosis, i.e., stenosis of the infundibulum of the right ventricle, pulmonary valve area, or pulmonary arteries, with a large ventricular septal defect, and right and left ventricular pressures of the same order. Even in acyanotic patients, the stenosis is relatively severe, permitting bidirectional ventricular shunt or, at most, a small left-to-right shunt at rest (<30%). PATHOLOGYBy the time the heart is examined at operation, the pathological features observed are not only the result of the primary maldevelopment but are also consequent on changes secondary to the abnormal haemodynamics. The important defects, from the surgical point of view, are the right ventricular outflow stenosis and the incomplete development of the ventricular septum.RIGHT VENTRICULAR OUTFLOW STENOSIS.-The normal development of the infundibulum depends on the inclusion of the bulbus cordis into the embryoni...

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Ventricular Septal Defect in Infants and Children

Cited by 73 publications

References 11 publications

Mechanism of decreased forward stroke volume in children and swine with ventricular septal defect and failure to thrive.

Mechanism of decreased forward stroke volume in children and swine with ventricular septal defect and failure to thrive.

Ventricular septal defect. A review of current thoughts.

The Surgical Treatment of the Tetralogy of Fallot

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