Assuntos

RESUMO

Seventeen children with oxygen-dependent bronchopulmonary dysplasia, right ventricular hypertrophy, and Doppler echocardiographic evidence of pulmonary hypertension were studied by cardiac catheterization. Fifteen of these patients had pulmonary hypertension when placed in room air; six of these 15 patients were shown to have large systemic-to-pulmonary collateral vessels. The hemodynamic responses to oxygen and hydralazine were evaluated. Five patients developed normal pulmonary artery pressure while receiving supplemental oxygen and were not studied further. Of the remaining ten patients, the six patients with large, hemodynamically significant collateral vessels all had deleterious reactions to hydralazine. Two of the four patients without collateral pulmonary circulation responded to hydralazine with further reductions in mean pulmonary artery pressure. Five of the ten patients who had persistent pulmonary hypertension while receiving oxygen have died. Cardiac catheterization and angiography may provide important diagnostic, therapeutic, and prognostic information in patients with pulmonary hypertension complicating bronchopulmonary dysplasia.

Assuntos

Assuntos

RESUMO

Some newborn infants with either primary or secondary persistent pulmonary hypertension (PPHN) remain hypoxemic, hypercarbic, and acidotic despite therapeutic efforts. In autopsies of 23 infants who had PPHN, diffuse platelet-fibrin thrombi were present in the pulmonary microcirculation of eight (15.2 +/- 18.1 thrombi/cm2 lung tissue) and absent in 15 (0.2 +/- 0.3 thrombi/cm2 lung tissue), (P less than 0.004). Diagnoses in group A (thrombi) were pneumonia and sepsis (four patients), meconium inhalation (3), and primary PPHN (1); and in group B (no thrombi) pneumonia and sepsis (4), meconium inhalation (4), primary PPHN (4), hyaline membrane disease (2), and diaphragmatic hernia (1). The only significant differences between the two groups were the response to tolazoline infusion as assessed by changes in partial pressure of arterial oxygen (PaO2) and the platelet counts. Group A responded less favorably to tolazoline (14.8 mm Hg vs 83.6 mm Hg; P less than 0.05) and had lower platelet counts (51,000/microliter vs 128,000/microliter) (P less than 0.01) than group B. No significant differences could be detected in Apgar scores, duration or mode of mechanical ventilation, oxygen requirements, arterial blood gas tensions or pH, systemic arterial blood pressure, coagulation profile, amount of blood product transfusions, or intravascular catheter use. Pulmonary microthrombi should be added to the list of mechanisms for PPHN and may explain why some infants do not respond well to therapeutic efforts aimed at vasodilation. Thrombocytopenia and failure to respond to pulmonary vasodilators might suggest the diagnosis.

Assuntos

Assuntos

Assuntos

RESUMO

The hemodynamic effects of dobutamine were studied in 33 infants and children with cardiogenic or septic shock. Dobutamine was administered at doses of 2.5, 5.0, 7.5, and 10.0 micrograms/kg/minute. Significant increases above preinfusion values were observed in cardiac index, left ventricular stroke work index, and pulmonary wedge pressure. Significant decreases from preinfusion values were observed in systemic arteriolar resistance index. No significant differences occurred in heart rate, mean systemic arterial pressure, mean pulmonary arterial pressure, right atrial pressure, or pulmonary arteriolar resistance index. Analysis of the data also revealed significant effects of age and diagnosis on the hemodynamic responses. These data suggest that dobutamine is a useful drug in the pharmacologic management of children in shock, especially in children older than 12 months with cardiogenic shock not complicated by severe hypotension.

Assuntos

RESUMO

Although a right-to-left shunt via a patent ductus arteriosus is one criterion for the diagnosis of persistent pulmonary hypertension of the newborn infant, it cannot be demonstrated by simultaneous pre- and postductus arteriosus blood oxygen tensions in many infants with the clinical syndrome. In animals, exposure of the fetal ductus arteriosus to salicylates causes contriction and results in pulmonary hypertension. We postulated that maternal ingestion of salicylates and premature closure of the ductus arteriosus may explain why some infants with PPHN do not have right-to-left ductus shunts. Therefore, we studied serum salicylate levels in six groups of infants: I, normal infants' cord blood (0.73 +/- 0.44 mg/dl, N = 20); Ia, normal infants at 24 to 36 hours of age (0.08 +/- 0.1 mg/dl, N = 5): II, other cardiopulmonary diseases with no right-to-left ductus shunt (2.08 +/- 1.74 mg/dl, N = 26); III, other cardiopulmonary diseases and right-to-left ductus shunt (2.34 +/- 1.70 mg/dl, delta Pao2 70 +/- 71 mm Hg, N = 6); IV, PPHN and right-to-left ductus shunt (1.86 +/- 1.51 mg/dl, delta Pao2 39.6 +/- 58.9 mm Hg, N = 5); V, PPHN without right-to-left ductus shunt (7.77 +/- 5.18 mg/dl, delta Pao2 2.2 +/- 1.5 mm Hg, N = 6). Serum salicylate levels were significantly greater (P less than 0.01) in infants with PPHN without right-to-left ductus shunt, indicating that the ductus arteriosus may have been closed prematurely. No other factor, including serum bilirubin, amikacin, ampicillin, or furosemide levels, could be found to account for the difference in serum salicylate levels. Premature closure of the ductus arteriosus secondary to maternal ingestion of salicylates may be one cause of PPHN and may explain the absence of right-to-left ductus shunting in some infants with the clinical syndrome.

Assuntos