Pharmacologic doses of glucocorticoids are administered to patients with adrenal insufficiency during operative procedures to prevent hemodynamic instability, cardiovascular collapse, and death. Since these supraphysiologic doses might not be necessary and might have adverse effects, we examined the effects of different doses ofglucocorticoids on hemodynamic adaptation during surgical stress in adrenalectomized primates. Sham-adrenalectomized placebo-treated animals served as controls. Adrenalectomized monkeys were maintained for 4 mo on physiologic glucocorticoid and mineralocorticoid replacement. The adrenalectomized monkeys were then stratified into three groups receiving, respectively, subphysiological (one-tenth the normal cortisol production rate), physiological, or supraphysiological (10 times the normal cortisol production rate) cortisol (hydrocortisone) treatment. 4 d later a cholecystectomy was performed. The intraoperative hemodynamic and metabolic parameters, perioperative survival rates, and postoperative wound healing were compared. The subphysiologically treated group was hemodynamically unstable before, during, and after surgery and had a significantly higher mortality rate than control. In this group, arterial blood pressure was low, and the cardiac index, systemic vascular resistance index, and left ventricular stroke work index were all reduced, suggesting decreased cardiac contractility and blood vessel tone. In contrast, the physiologically replaced group was indistinguishable from either supraphysiologically treated animals or sham-operated controls. All groups had similar metabolic profiles and normal wound healing. These findings suggest that the permissive actions of physiologic glucocorticoid replacement are both necessary and sufficient for primates to tolerate surgical stress. Supraphysiological glucocorticoid treatment has no apparent advantage during this form of stress in the primate.
Pulmonary venous blood and pulmonary venous pressure were obtained by catheterization technic in a case of Eisenmenger's complex with anomalous pulmonary venous drainage into the right auricle. This made possible measurement of the true total pulmonary vascular resistance and evaluation of a pulmonary factor in the cyanosis accompanying this anomaly. No evidence for inadequate oxygenation in the lungs was apparent, and it is concluded that the cyanosis in Eisenmenger's complex is due solely to venoarterial shunting.T HE pathologic anatomy of the heart in Eisenmenger's complex has been known for more than 50 years1 and considerable progress has been made in its clinical recognition.2 Recently, striking morphologic changes in the intrapulmonary vessels have been demonstrated in this anomaly3-5; yet the pathophysiology underlying many of its manifestations, for example, delayed cyanosis, has remained confused. It has been postulated that the cyanosis may result from (a) some congenital abnormality of the pulmonary epithelium or capillaries which interferes with the complete oxygenation of the blood in the lungs6' or (b) that blood is sucked from the right ventricle directly into the aorta by the vigorous pumping action of the left ventricle.2The application of cardiac catheterization to the investigation of congenital heart disease has provided the means for a physiologic approach to the study of the clinical features of this disease. From such studies it has been learned that pulmonary hypertension and systemic arterial unsaturation are two of the physiologic derangements consistently present in Eisenmenger 's complex.
The ECGs of 104 normal children from a few hours old to 5 years of age were studied. These ECGs consisted of the standard limb leads, the aV limb leads and six precordial leads: V4R, V1, V2, V4, V5 and V6. While the number of cases in each group are small, the following conclusions are suggested by this study: 1. ECGs of the newborn infant present important variations from those seen in later life. This is especially true during the first week of life. Thereafter the contour evolves [SEE FIG. 2 IN SOURCE PDF] in a definite manner until the adult-like pattern is reached. 2. The vertical and semivertical "electric" positions were the most frequently encountered in this age group. 3. P-waves present a rather permanent pattern in this age range: a. is usually upright in lead 1 and 2, aVF, V4, V5 and V6. b. is usually inverted in lead 2 and aVR. c. is either upright, inverted or diphasic in lead 3, aVL, V4R, V1 and V2. 4. The P-R interval varies from 0.10 sec. minimum to 0.16 sec. maximum with the average being 0.12 sec. in this age range. It tends to become greater in the older age groups. 5. QRS duration is shorter in the younger age groups and increases slowly with age. 6. Polyphasic, M-shaped or slurred QRS complexes are not uncommon in the ECGs of normal children in this age range. 7. A Q wave is frequently absent in lead 1 and in all chest leads during the first week of life. Thereafter up to 5 years of age the pattern of the Q wave is as follows: a. Q is generally absent in lead 1, V4R, V1, V2 and V4. b. Q is generally present in lead 3, V4R, aVF, V5 and V6. 8. There is a distinct pattern of right ventricular dominance in leads from the sternum and to its right at birth. This pattern gradually undergoes involution, probably related to normal physiologic development, until the left ventricle becomes dominant. Thus the evolution of the S-wave parallels a gradual involution of the R-wave in right precordial leads and probably also in aVR. This dominance of the left ventricle over the entire precordium is usual by about 3 years, but may be delayed normally until 5 years of age. 9. The T-wave is upright or diphasic in V4R, V1, and V2 and inverted in V5 and V6 for the first 24 hours of life; it gradually alters so that by the fourth day it is inverted in V4R, V1 and V2 and upright in V5 and V6 and thereafter. 10. The transition zone of QRS varies from one age group to another and tends in some ages to be broad. In some instances no real transition zone can be determined.
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