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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.

To achieve adequate arterial BP, adequate capillary filling time, and adequate peripheral pulses, hypotensive newborn infants often require higher doses of dopamine that reportedly reduce urine output in adults. Whether these larger doses of dopamine also reduce urine output in newborns is not known. Therefore, we determined the effects of administering high-dose dopamine (more than 20 micrograms/kg X min) on the urine output of 15 newborn infants. Five infants were studied prospectively and ten retrospectively. In the prospective study, urine output was determined as the dose of dopamine was increased; in the retrospective study, urine output was determined as the infants were being weaned from high doses of dopamine. Both data sets demonstrate that administering high-dosage dopamine does not reduce the urine output of sick newborn infants. Therefore, we conclude that doses of dopamine previously reported to decrease urine output in adults do not do so in sick newborn infants. Consequently, when necessary, high doses of dopamine may be used in sick newborn infants to achieve cardiovascular stability without reducing urine output.

We studied the separate and combined effects of hyperventilation and administration of dopamine and tolazoline in five infants with pulmonary hypertension managed with indwelling pulmonary artery catheters. In five infants the right-to-left shunt reversed during ventilator-induced respiratory alkalosis (pH greater than 7.6). Response to drugs was variable and unpredictable. One infant could be oxygenated at normal pH during combined dopamine and tolazoline infusion. Other infants showed no response to drugs, or became worse during infusion. The ratio of pulmonary artery to systemic artery pressure averaged 1.14 with standard therapy, but decreased to 0.98 following respiratory alkalosis alone, to 0.87 following drug infusions, and to 0.70 following the combination of alkalosis and drug infusion. These changes were significant by analysis of variance at P less than 0.02, P less 0.001, and P less than 0.001, respectively. Systemic oxygenation was satisfactory in all cases when the pulmonary to systemic pressure ratio was less than 1.0.

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.

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.

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.

Colloid osmotic pressure (COP) is an important regulator of fluid movement and can now be measured simply and reliably. The authors used the 4100 Wescor Colloid Osmometer to define COP values and its relation to total protein concentration (TP) in different groups of newborns. The mean COP was 19.4 +/- 2.2 (SD) torr in 99 term infants delivered vaginally and 16.0 +/- 2.1 in 40 term infants delivered by cesarean section (p less than 0.005). The COP was lower in those born operatively without preceding labor (14.9 +/- 1.8). COP correlated well with TP (r = 0.92) in term infants. In 60 sick preterm infants with 362 determinations, COP (12.5 +/- 2.5) was different from term infants (p less than 0.001) and the correlation with TP was poor (r = 0.64). Different therapeutic modalities were found to affect COP widely. Crystalloid infusion decreased COP by 22% and surgery by 32%. The authors conclude that COP varies not only with gestational age but also with mode of delivery and experience of labor. In critically ill preterm neonates, because estimations form TP are inadequate, the only way to obtain a quantitative measure of COP is by direct measurement. Repeated measurements of COP will permit precise selection of the fluids and will warn of changes that may lead to pulmonary edema.

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).

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.