Resuscitation of the newborn

Effective resuscitation of the newborn requires knowledge of the cause of depression. Four major causes are trauma, asphyxia, medication, and malformation. More than one of these may contribute to depression in a single infant. The first principles of resuscitation are to avoid cooling the infant and to establish an airway. Infants with an Apgar score of 3 to 4 at one minute usually need bag-and-mask ventilation, while those with scores of 0 to 2 require immediate ventilation, preferably by means of endotracheal intubation. Severely depressed infants may also require chemical resuscitation and closed cardiac massage. Fetal depression caused by narcotic analgesics given to the mother can be reversed with the use of naloxone hydrochloride (Narcan). Infants asphyxiated on the basis of malformations may benefit from expeditious diagnostic and therapeutic procedures performed in the delivery room.     

Resuscitation of the newborn

The cause of respiratory depression in a newborn must be quickly determined so that effective therapy can be given. Need for assisted ventilation is dictated by the condition of the infant. Whether bag and mask or endotracheal intubation is used to deliver oxygen depends on the degree of neonatal depression and the experience of the resuscitator.     

Resuscitation of the newborn infant

Perinatal asphyxia may occur prior to or at the time of birth, leading to hypoxia and acidosis with persistence of the fetal circulatory pattern. Resuscitation facilitates transition to the adult circulatory pattern by restoring normal oxygenation, ventilation, and perfusion. Assessment of the degree of asphyxia should utilize the Apgar score, and resuscitation should proceed in a stepwise fashion to an extent determined by the degree of depression. Aspects of resuscitation unique to the newborn are reviewed, in addition to situations requiring specific intervention.     

Resuscitation with 21% or 100% oxygen is equally effective in restoring perfusion and oxygen metabolism in the liver of hypoxic newborn piglets

The differential effects of the use of high or low oxygen levels during resuscitation on the neonatal liver are unknown. We compared the hepatic hemodynamics and oxygen metabolism in hypoxic newborn piglets resuscitated with 21% or 100% oxygen. Twenty-seven piglets (age, 1-3 days; weight, 1.5-2.0 kg) were acutely instrumented to measure cardiac output, hepatic artery, and portal venous blood flows (hepatic artery flow index [HAFI] and portal venous flow index [PVFI], respectively). The animals underwent 2 h of hypoxia (fraction of inspired oxygen, 0.10-0.15), then reoxygenation with 21% (n = 9) or 100% (n = 9) oxygen for 1 h, then 1 h with 21% oxygen. The controls (n = 9) were sham-operated without hypoxia-reoxygenation. Oxygen transport and plasma lactate concentrations were studied. Hypoxic animals had hypotension and decreased cardiac index with metabolic acidosis (mean pH, 7.00-7.02; P < 0.05 vs. controls). The PVFI and the total hepatic blood flow (THFI = PVFI + HAFI), despite the absence of significant change in HAFI, decreased to 16 +/- 2 mL/min/kg and 19 +/- 3 mL/min/kg, respectively (versus 24 +/- 2 mL/min/kg and 28 +/- 2 mL/min/kg of controls; P < 0.05). Fifteen minutes after reoxygenation, the cardiac index improved, PVFI recovered, HAFI was maintained, and THFI was not different between the groups. The hepatic oxygen consumption decreased (59%; P < 0.05) and the extraction increased (89%; P < 0.001) during hypoxia. Similarly, on reoxygenation, the hepatic oxygen consumption improved; however, extraction decreased versus controls on 100% but not on 21% oxygen (P < 0.05). The plasma lactate concentrations increased in both groups with hypoxia and were not different during reoxygenation between the group administered with 21% oxygen and the group administered with 100% oxygen. The hypoxic neonatal liver has reduced hepatic blood flow but has relatively preserved HAFI, and oxygen consumption recovered similarly on reoxygenation with 21% and 100% oxygen. The increased oxygen extraction during hypoxia normalized in 21% but reduced in 100% reoxygenation, with no differences in plasma lactate concentrations.     

Continuous in vivo oxygen saturation in newborn infants with pulmonary disease: a new fiberoptic catheter oximeter.

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.     

Ventricular size in newborn infants

Cranial ultrasound examinations were performed on 533 infants of between 48 and 96 hours of age to establish the range of ventricular size in neonates of different gestational ages in whom there was no evidence of intraventricular hemorrhage or neural tube defects. It was found that ventricular size did not vary in infants with gestational age of 26 weeks or more. Only 15 (2.8 per cent) neonates had a ventricular width of greater than 3 mm. Of these 15 infants, 13 were re-examined within the first year of life and found to be neurologically and developmentally normal.     

Resuscitation from experimental heatstroke by hyperbaric oxygen therapy

OBJECTIVE: Heatstroke is characterized by hyperthermia, vasoplegic shock, and cerebral ischemia and hypoxia. Hyperbaric oxygen (HBO) has been shown to reduce brain ischemia and behavioral dysfunction during cerebral artery occlusion. The efficacy of HBO therapy for resuscitation from heatstroke remains to be determined in the laboratory. DESIGN: Anesthetized rats were randomized to several groups and administered: 1) no resuscitation (normobaric air) after onset of heatstroke, 2) HBO for 1 hr (100% oxygen at 253 kPa for 1 hr), 3) cyclic HBO intermitted by a 5-min air break for 1 hr of treatment (100% oxygen at 253 kPa), 4) hyperbaric air (air at 253 kPa for 1 hr), 5) normobaric hyperoxia (100% oxygen at 101 kPa for 1 hr), or 6) 8% HBO (hyperbaric 8% oxygen at 253 kPa for 1 hr). SETTING: Laboratory investigation. SUBJECTS: Sprague-Dawley rats (300- to 400-g males). INTERVENTIONS: Rats were exposed to an ambient temperature of 43 degrees C to induce heatstroke. Their colonic temperature; mean arterial pressure; heart rate; arterial blood levels of pH, Paco2, Pao2, So2%, and tumor necrosis factor-alpha; the cortical levels of ischemic and damage markers, and cortical neuronal damage scores were determined. The moment at which mean arterial pressure began to decrease from peak levels was arbitrarily taken as the onset of heatstroke. MAIN RESULTS: Survival time (interval between onset of heatstroke and animal death) was 19 +/- 1 (n = 10), 131 +/- 18 (n = 14), 159 +/- 28 (n = 13), 72 +/- 14 (n = 10), 68 +/- 12 (n = 10), and 45 +/- 11 (n = 10) mins, respectively, for normobaric air, HBO for 1 hr, cyclic HBO, hyperbaric air, normobaric hyperoxia, and 8% HBO groups. The heatstroke induced arterial hypotension and bradycardia, decreased arterial levels of pH, Pao2, and So2%, increased arterial levels of tumor necrosis factor-alpha, and increased values of cellular ischemia and damage markers. In addition, neuronal damage scores in the cortex were significantly reduced by HBO for 1 hr and cyclic HBO resuscitation. CONCLUSION: We successfully demonstrated that HBO and, to some extent, hyperbaric air, normobaric hyperoxia, or HBO 8% was found beneficial in resuscitating rats with experimental heatstroke. HBO effectively reduced heatstroke-induced arterial hypotension, hypoxia, plasma tumor necrosis factor-alpha overproduction, and cerebral ischemia and damage and improved survival.     

Transcutaneous carbon dioxide and oxygen tension in newborn infants: Reliability of a combined monitor of oxygen tension and carbon dioxide tension

We evaluated a new combined sensor for monitoring transcutaneous carbon dioxide tension (PtcCO₂) and oxygen tension (PtcO₂) in 20 critically ill newborn infants. Arterial oxygen tension (PaO₂) ranged from 16 to 126 torr and arterial carbon dioxide tension (PaCO₂) from 14 to 72 torr. Linear correlation analysis (100 paired values) of PtcO₂ versus PaO₂ showed anr value of 0.75 with a regression equation of PtcO₂=8.59+0.905 (PaO₂), while PtcCO₂ versus PaCO₂ revealed a correlation coefficient ofr=0.89 with an equation of PtcCO₂=2.53+1.06 (PaCO₂). The bias between PaO₂ and PtcO₂ was –2.8 with a precision of ±16.0 torr (range, –87 to +48 torr). The bias between PaCO₂ and PtcCO₂ was –5.1 with a precision of ±7.3 torr (range, –34 to +8 torr). The transcutaneous sensor detected 83% of hypoxia (PaO₂ <45 torr), 75% of hyperoxia (PaO₂ >90 torr), 45% of hypocapnia (PaCO₂ <35 torr), and 96% of hypercapnia (PaCO₂ >45 torr). We conclude that the reliability of the combined transcutaneousPo ₂ andPCo ₂ monitor in sick neonates is good for detecting hypercapnia, fair for hypoxia and hyperoxia, but poor for hypocapnia. It is an improvement in that it spares available skin surface and requires less handling, but it appears to be slightly less accurate than the single electrodes.     

Characteristics of anesthesia in newborn infants

The paper describes the specific features of anesthetic maintenance in preterm and full-term neonates, intraoperative monitoring, and the effects of inhaled anesthetics, narcotic analgesics, sedatives, and myorelaxants with emphasis on the anatomic and physiological features of a developing organism.