Clinical and physiologic sequelae of large ventricular septal defects

Tikoff, Gerasim; Schmidt, Alexander M.; Thorne, Joseph L.; Kuida, Hiroshi

doi:10.1016/0002-9343(67)90050-2

Cited by 8 publications

(2 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…With PAm of greater than 40 mmHg, the negative correlation was observed in VSD and PDA, representing the reciprocal relationship of the pulmonary blood flow and the vascular resistance (Rudolph and Nadas 1962; Tikoff et al 1967). These patients frequently accompanied right-to-left shunt (reversed shunt).…”

Section: Discussionmentioning

confidence: 99%

Pulmonary Arterial Pressure-Flow Characteristics in Atrial Septal Defect: Comparative Study with Ventricular Septal Defect and Patent Ductus Arteriosus

Miyazawa

Haneda

Shirato

et al. 1977

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

Pulmonary arterial pressure-flow relation was studied in 142 patients with atrial septal defect (ASD) and was compared with that of 139 patients with ventricular septal defect (VSD) and 54 patients with patent ductus arteriosus (PDA).The incidence of pulmonary arterial mean pressure (PAm) over 25 mmHg was 21% in ASD, 36% in VSD and 43% in PDA, and that over 40 mmHg was 3%, 23% and 19%, respectively. Large left to right shunt over 50% was found more frequently in ASD (58%) than in VSD (22%) and PDA (30%).When patients were separated into 2 groups at a PAm of 40 mmHg, lower pressure group showed a positive correlation between PAm and left-to-right shunt in each disease, although the correlation was poor in ASD (r=0.23) as com pared with VSD (r=0.49) and PDA (r=0.47).The slope of the regression line was less steep in ASD (0.08) than in VSD (0.17) and PDA (0.14). It is considered that pulmonary hypertension in ASD develops on the basis of pulmonary vascular changes caused by prolonged hyperkinetic circulation.atrial septal defect; left-to-right shunt; pulmonary hypertension; pressure-flow diagram; congenital heart disease It has been known that the occurrence of severe pulmonary hypertension is less frequent in ASD than in VSD and PDA (Swan et al. 1954a;Wood 1958). Recently, much attention has been directed to ASD in elderly patients, and beneficial effects of surgical closure of the defect have been discussed in the presence of pulmonary hypertension to prevent the progressive increase in pul monary vascular resistance in some cases (Saksena and Aldridge 1970;Dave et al. 1973). It is therefore important to clarify the mechanism under which severe pulmonary hypertension develops in ASD. This study was undertaken to examine the relation between pulmonary arterial pressure and pulmonary blood flow in a large number of ASD patients and to compare the results with those obtained in VSD and PDA.

show abstract

Section: Discussionmentioning

confidence: 99%

Pulmonary Arterial Pressure-Flow Characteristics in Atrial Septal Defect: Comparative Study with Ventricular Septal Defect and Patent Ductus Arteriosus

Miyazawa

Haneda

Shirato

et al. 1977

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

show abstract

“…Irritation of the recurrent laryngeal nerves because of enlarged pulmonary arteries may result in hoarseness. 14 Physical examination. The physical examination of the lungs is usually normal, unless congestive heart failure is present.…”

Section: Pulmonarymentioning

confidence: 99%

Eisenmenger Syndrome

Previte

Haran

2001

Semin Cardiothorac Vasc Anesth

View full text Add to dashboard Cite

The incidence of congenital cardiovascular malformation is unknown but is estimated to be approximately 0.8% of live births. This figure does not include preterm infants (all of whom have a patent ductus arteriosus [PDA]) or stillborn infants (who have a high incidence of cardiovascular abnor malities). Approximately 9% of patients with congenital car diac disease and 11% of those with uncorrected left-to-right intracardiac shunts will develop the Eisenmenger syndrome (ES). ES develops at different rates, depending on the size and location of the cardiac lesion and the amount of in creased pulmonary blood flow and pressure. Onset in in fancy is common in patients with PDA or a large ventricular septal defect (VSD). ES is seen in up to 50% of patients with VSD larger than 1.5 cm in diameter, whereas there is only a 3% incidence in those with defects that are less than 1.5 cm in diameter. Children with Down syndrome and a VSD or atrioventricular canal defect are prone to early development of ES. They have abnormal upper airways that predispose them to chronic upper airway obstruction and sleep apnea, both of which promote hypoxemia, hypercarbia, and early development of pulmonary hypertension. ES develops early in nearly all patients with uncorrected transposition of the great arteries and truncus arteriosus, whereas most patients with uncorrected ASD who develop the syndrome do so in the second decade of life. The prognosis for survival through childhood with ES is relatively good. Patients usually lead remarkably active lives until shortly before they die. The goal of this article is to provide a detailed overview of the pathophysiology, clinical presentation, and medical and sur gical management of these patients. Particular focus on the anesthetic management of patients undergoing cardiac and noncardiac surgery is provided.

show abstract

Periglomerular Granulomatosis

Oliet¹

1988

Arch Intern Med

View full text Add to dashboard Cite

Clinical and physiologic sequelae of large ventricular septal defects

Cited by 8 publications

References 21 publications

Pulmonary Arterial Pressure-Flow Characteristics in Atrial Septal Defect: Comparative Study with Ventricular Septal Defect and Patent Ductus Arteriosus

Pulmonary Arterial Pressure-Flow Characteristics in Atrial Septal Defect: Comparative Study with Ventricular Septal Defect and Patent Ductus Arteriosus

Eisenmenger Syndrome

Periglomerular Granulomatosis

Contact Info

Product

Resources

About