Biomedical subjects
Publications and source records attributed to G A Gregory.
A newborn infant with agenesis of the left lung and critical distal tracheal stenosis required tracheal resection and reanastomosis. This case illustrates the combined use of flow-volume curves, radiology and endoscopy in the diagnosis and management of airway obstruction in infants. It also establishes the feasibility of complete tracheal reconstruction in small babies.
We used a new, rapidly responding in vivo catheter oximeter to continuously measure arterial oxygen saturation (Sao2) in 34 newborns with cardiopulmonary disease. The Sao2 was compared with the oxygen tension (Pao2) of blood sampled through the catheter in 2 groups. We evaluated the oxygen dissociation curves of 24 untransfused infants whose hemoglobin F (HbF) concentration was greater than or equal to 80%. We also examined the Sao2 curves of 20 extensively transfused infants who had greater than or equal to 80% hemoglobin A (HbA). We found a wide variation in Sao2 at levels of arterial Po2 between 30 and 90 mmHg. Although the oxygen dissociation curve of the transfused group was significantly to the right of the untransfused group, there was considerable overlapping between the 2 curves. This dispersion reflected the wide range of clinical states encountered in newborns with cardiopulmonary disease, and the changes in blood oxygen affinity. In some newborns, when Pao2 was less than 50 mmHg, Sao2 could be > 90% whereas in others, Sao2 could be < 75%. When both Pao2 and Sao2 were low, Sao2 reflected arterial oxygen contents more precisely because of the shape of the individual oxygen dissociation curves in both groups. Opinions vary as to the safe upper limit of Pao2 at which retrolental fibroplasia does not occur. The Sao2 at 2 upper limits of Pao2 (100 and 80 mmHg) was estimated by probit analysis of simultaneous measurements of Pao2 and in vivo Sao2. In both the untransfused and extensively transfused groups of newborns, Pao2 was < 100 mmHg when Sao2 was < 96%. The Pao2 was < 80 mmHg, when the Sao2 was < 92%, if the HbF was greater than equal to 80%, and when Sao2 was < 91%, if HbA was greater than equal to 80%, (95% confidence limits). The findings suggested a caveat against the practice of calculating Sao2 from measurements of pH, Pao2, and Paco2. This can be quite inaccurate when taking samples of arterial blood from newborns.
After creating "fontanelles" in infant rhesus monkeys, we measured intracranial pressure of these monkeys directly with an indwelling cannula and indirectly with a Ladd 1700 sensor. Values obtained with the Ladd sensor placed over the shaven fontanelle closely approximate directly measured pressure in acute experiments in these animals and in human cadavers. Application of the device is simple and application pressure need not always be the same for multiple determinations. The response time is 1.6 cm H2O/sec, which is adequate to record changes in intracranial pressure caused by changes in the partial pressure of CO2 in arterial blood.
We measured the in vivo oxygen saturation of hemoglobin in the arterial blood of 34 sick newborn infants with a new, rapidly responding, continuously recording, catheter oximeter. The oxygen saturation, SaO2, was found to fluctuate between 85 and 95% in infants with pulmonary disease who are in a stable condition and breathing spontaneously. Severe disaturation occurred during apnea and after procedures such as chest percussion and suctioning of the endotrachael tube. The effects of changes in respiratory therapy were quickly manifested by changes in SaO2. This was particularly useful in guiding resuscitation of newborn infants who were asphyxiated at birth. Blood sampling for measurement of PaO2 can be done less frequently, reducing the need for blood transfusions in small infants.
Improved accuracy of continuous arterial oxygen tension (PaO2) measurement is obtained if allowance is made for the response time of the electrode. Recalibration is necessary only when PaO2 measured in a blood sample differs from the electrode value by more than +/- 11.5 mmHg (1.5 kPa).
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In summary, our findings support and confirm the concerns of many investigators that present methods of cardiorespiratory monitoring are inadequate for the detection of many forms of apnea. Nurses underrecord both the frequency and duration of apneic episodes. Bradycardia is an unreliable index of hypoxemia. Thoracic impedance monitors are unreliable because they detect only a fixed duration of respiratory pause and are sensitive to many artifacts unavoidable in a clinical setting. Finally, ineffective breathing patterns such as disorganized breathing, obstructive apnea, and paradoxical breathing are undetectable by thoracic impedance monitoring. We warn against the reliance on heart rate and thoracic impedance monitoring alone for infants with recurrent apnea.
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We investigated the clinical use and limitations of the transcutaneous oxygen electrode described by Huch, Lübbers and Huch in 30 sick infants. One hundred and fifty-nine measurements of arterial oxygen tension (PaO2) and transcutaneous oxygen tension (tcPO2) were made. During the comparisons, arterial blood pressures, heart rate thoracic impedance were continuously recorded, skin axillary and environmental temperatures, hematocrit and skin thickness were measureed and the degree of peripheral perfusion noted. Despite a wide range of these variables, values of tcPO2 and PaO2 were similar (slope 0.963). Two groups of infants were identified in whom tcPO2 was lower than PaO2. These were infants receiving an intravascular infusion of tolazoline and infants with mean arterial blood pressures more than 2.5 s.d. below the predicted average value. Both of these situations represent extreme alterations in peripheral blood flow and give important information regarding the limitations of the method. Less extreme alterations in flow caused by mild hypotension, hypothermia, anemia, radiant warmers, and bilirubin lights did not adversely affect the transcutaneous PO2--arterial PO2 correlation. Advantages of transcutaneous oxygen monitoring over more conventional monitoring methods were assessed. We conclude that the transcutaneous oxygen electrode is safe, is easy to use, has few limitations and provides data which can help improve the management of most sick infants.
The clinical usefulness of the transcutaneous O2 electrode was investigated in 30 sick infants; 159 simultaneous measurements of arterial PO2 and transcutaneous PO2 were made. During the comparisons, arterial blood pressure, heart rate, and thoracic impedance were continuously recorded, and skin axillary and environmental temperatures and hematocrit were noted. Despite a wide range of arterial blood pressure and hematocrits, arterial PO2 and transcutaneous PO2 were similar (slope, 0.963), except for 2 groups of sick infants. Some infants with severe, persistent pulmonary hypertension who were receiving an intravascular infusion of tolazoline and infants with mean arterial blood pressures more than 2.5 SD less than the predicted average had values for transcutaneous PO2 that were lower than PO2. The surface O2 electrode is safe and relatively easy to use and provides data that can help in the management of most sick infants.
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Persistent pulmonary hypertension of the newborn infant can be difficult to distinguish from other cardiopulmonary causes of cyanosis during the newborn period. Infants with PPHN have cyanosis, tachypnea, acidemia, normal pulmonary parenchymal markings on the chest radiography, and anatomically normal hearts. We have identified and treated 11 infants and have noted several signs and symptoms not previously emphasized. These are cineangiocardiographic evidence of atrioventricular valve insufficiency in association with systolic murmurs and slow ventricular emptying, apnea, hypocalcemia, only a small rise in abdominal aortic blood oxygen tension during breathing of 100% oxygen, and no response to continuous positive airway pressure. Right-to-left shunting through the patent ductus arteriosus was documented in nine infants: in all six of those in whom simultaneous temporal and abdominal aortic blood oxygen tension measurements were made; in three by means of cardiac catheterization. Ten infants survived after variable courses and treatments which makes it difficult to ascribe improvement to any one therapy. The distinct increase in blood oxygen tension with tolazoline HCl and curare in some instances is discussed.
We determined the incidence of pneumothorax in 295 infants (mean birthweight, 1,917 gm) with the respiratory distress syndrome (RDS) treated according to the same protocol. Fifty-five infants (mean birthweight, 1,594 gm) developed pneumothorax (incidence, 19%); incidence varied with severity of RDS and intensity of respiratory assistance. Pneumothorax occurred in 3.5% (2 of 58) of infants who received no assisted ventilation and in 11% (14 of 124) of infants who received continuous positive airway pressure (CPAP) as the only form of assisted ventilation; the difference between these two groups is not significant. Forty-nine infants initially treated with CPAP later required mechanical ventilation with positive end-expiratory pressure (PEEP). Pneumothorax occurred in 12 of the 49 (24%) and in 21 of 64 (33%) of those infants initially treated with PEEP; the incidence of pneumothorax for both these groups was significantly higher than for those treated with no assisted ventilation or CPAP only. To assess the value of frequent measurement of vital signs, blood gas tensions, and pH in the recognition of pneumothorax, we analyzed these variables by the cumulative sum statistical technique. We noted the following significant changes associated with pneumothorax: arterial blood pressure, heart rate, and respiratory rate decreased in 77% of cases; pulse pressure narrowed in 51% of cases; Po2 decreased in 17 of 20 cases in which ventilatory settings were constant for at least three hours prior to pneumothorax. However, pH and Pco2 showed consistent changes. Frequent measurements of vital signs and Po2 aid in the early diagnosis of pneumothorax.
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We measured aortic and central venous pressures beginning soon after birth in 40 prematurely born infants with moderate or severe erythroblastosis fetalis, including 13 with severe and 10 with mild hydrops fetalis. All but four were asphyxiated at birth and this affected intravascular pressures. Before resuscitation, aortic or central venous pressure or both were elevated in more than one third. All but two of the remaining infants had normal initial pressures. Following resuscitation which relieved acidosis, hypoxia, and anemia, but did not reduce blood acidosis, hypoxia, and anemia, but did not reduce blood volume, the high pressures usually fell to normal and occasionally to subnormal levels, normal pressures fell to subnormal in almost one half, and those with initial subnormal pressures remained hypotensive. In all, 40% were hypotensive after resuscitation; treatment with blood volume expanders consistently returned these pressures to normal. Only two of the 13 severely hydropic infants and none of the mildly hydropic had findings indicative of hypervolemia and myocardial failure which persisted after treatment of asphyxia.
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Continuous positive airway pressure (CPAP) was used to support the ventilation of infants less than 3 months of age who had undergone thoractomy for cardiovascular surgery. The functional residual capacity, which was approximately 30 per cent of predicted at zero CPAP, increased 35 per cent in cyanotic and 33 per cent in acyanotic infants with the application of 5 mm Hg pressure. Increasing airway pressure from zero to 5 mm Hg increased PaO2 4 per cent in cyanotic and 13 per cent in acyanotic infants. There was no change in heart rate, respiratory rate, mean arterial pressure, pH or PaC02 under similar circumstances, but central venous pressure increased 1.5 mm Hg in cyanotic and 0.8 mm Hg in acyanotic infants.