The fetus maintains a blood glucose value of 70%–80% of maternal levels by facilitated diffusion across the placenta. There is a build-up of glycogen stores in the liver, skeleton, and cardiac muscles during the later stages of fetal development, but little gluconeogenesis. The newborn must depend on glycolysis until exogenous glucose is supplied. After delivery, a healthy full-term baby depletes his or her hepatic glycogen stores within 2–3 hours, with plasma glucose levels falling rapidly upon birth, stabilizing at an average of 55 mg/dL in the first 1–2 hours of life. The newborn is severely limited in his or her ability to use fat and protein as substrates to synthesize glucose. When total parenteral nutrition (TPN) is needed, the glucose infusion rate should be initiated at 4–6 mg/kg/min and advanced 1–2 mg/kg/min to a goal of 12 mg/kg/min, although this can sometimes be higher in postsurgical patients with high caloric demands for growth.

Calcium is actively transported across the placenta. Of the total amount of calcium transferred across the placenta, approximately two-thirds are transferred in the third trimester, which partially accounts for the high incidence of hypocalcemia in preterm infants. Data on the incidence of neonatal hypocalcemia varies. However, one small cohort study conducted in VLBW infants born at less than 32 weeks of gestation reported the incidence of early-onset hypocalcemia to be 37% at 12 hours of life, 83% at 24 hours, and 89% by 36 hours. Neonates are predisposed to hypocalcemia due to limited calcium stores, renal immaturity, and relative hypoparathyroidism secondary to suppression by high fetal calcium levels. Some infants are at further risk for neonatal calcium disturbances owing to the presence of genetic defects, fetal growth restriction, hypomagnesemia, pathologic intrauterine conditions, birth trauma, and perinatal asphyxia. Hypocalcemia is defined relative to birth weight. For neonates born weighing 1500 g or more, hypocalcemia is defined as an ionized calcium less than 1.1 mmol/L (4.4 mg/dL). If less than 1500 g, hypocalcemia is defined as ionized calcium less than 1 mmol/L (4 mg/dL). At greatest risk for hypocalcemia are preterm infants, newborn surgical patients, and infants born to mothers with complicated pregnancies, such as those with diabetes or those receiving bicarbonate infusions. Calcitonin, which inhibits calcium mobilization from the bone, is increased in premature and asphyxiated infants.

Routine tests for calcium levels are not indicated. Infants with risk factors such as VLBW and ELBW, congenital heart disease, and clinical signs of hypocalcemia should be screened. Signs of hypocalcemia are nonspecific and similar to those of hypoglycemia; they may include jitteriness, seizures, cyanosis, vomiting, and myocardial arrhythmias. Ionized calcium is the screening test of choice for these infants, with levels sent at 24 hours of life and repeated at 48 hours if indicated. Following confirmation of hypocalcemia, phosphate levels, parathyroid hormone (PTH) levels, vitamin D, and urine calcium should be checked for a complete evaluation. Hypocalcemic infants will demonstrate increased muscle tone, which helps differentiate infants with hypocalcemia from those with hypoglycemia. Symptomatic hypocalcemia is treated with 10% calcium gluconate administered intravenously at a dosage of 1–2 mL/kg (100–200 mg/kg) over 30 minutes while monitoring the electrocardiogram for bradycardia. Asymptomatic hypocalcemia is best treated with calcium gluconate in a dose of 50 mg of elemental calcium/kg/day added to the maintenance fluid: 1 mL of 10% calcium gluconate contains 9 mg of elemental calcium. If possible, parenteral calcium should be given through a central venous line, as skin and soft tissue necrosis may occur should the peripheral IV infiltrate.

Magnesium is actively transported across the placenta. Half of the body’s total magnesium resides in plasma and soft tissues. Hypomagnesemia is observed with growth retardation, maternal diabetes, after exchange transfusions, and with hypoparathyroidism. Although the mechanisms by which magnesium and calcium interact are not clearly defined, they appear to be interrelated. The same infants at risk for hypocalcemia are also at risk for hypomagnesemia. Magnesium deficiency should be suspected and confirmed in an infant who has seizures that do not respond to calcium therapy. Emergent treatment consists of magnesium sulfate 25–50 mg/kg IV every 12 hours until normal levels are obtained.

Total RBC volume is at its highest point at delivery. Estimations of blood volume for premature infants, term neonates, and infants are summarized in Table 1.5 . By about 3 months of age, total blood volume per kilogram is nearly equal to adult levels as infants recover from their postpartum physiologic nadir. The newborn blood volume is affected by shifts of blood between the placenta and the baby before clamping the cord. Infants with delayed cord clamping, defined as greater than 1 minute after birth, have higher hemoglobin levels. A hematocrit greater than 50% suggests placental transfusion has occurred. Although this effect on hemoglobin levels does not persist, iron stores are positively impacted for up to 6 months of age by delayed cord clamping, while the increased risk of jaundice only impacts infants in the short term. Other benefits of delayed cord clamping include decreased risk of intraventricular hemorrhage, necrotizing enterocolitis, and late-onset sepsis, as well as decreased need for blood transfusions, surfactant, and mechanical ventilation in preterm and low-birth-weight infants. ⁴¹

Hemoglobin

At birth, nearly 60%–80% of circulating hemoglobin is fetal (a2Aγ2F). When infant erythropoiesis resumes at about 2–3 months of age, most new hemoglobin is adult. When the oxygen level is 27 mmHg, 50% of the bound oxygen is released from adult hemoglobin ( P ₅₀ = 27 mmHg). Reduction of the affinity of hemoglobin for oxygen allows more oxygen to be released into the tissues at a given oxygen level as shown in Fig. 1.2 .

The oxygen dissociation curve of normal adult blood is shown in red . The P ₅₀ , the oxygen tension at 50% oxygen saturation, is approximately 27 mmHg. As the curve shifts to the right, the affinity of hemoglobin for oxygen decreases and more oxygen is released. Increases in PCO ₂ , temperature, 2,3-DPG, and hydrogen ion concentration facilitate the unloading of O ₂ from arterial blood to the tissue. With a shift to the left, unloading of O ₂ from arterial blood into the tissues is more difficult. Causes of a shift to the left are mirror images of those that cause a shift to the right: decreases in temperature, 2,3-DPG, and hydrogen ion concentration.

Modified from Glancette V, Zipursky A. Neonatal hematology. In: Avery GB, ed. Neonatology . JB Lippincott; 1986. p. 663.

Fetal hemoglobin has a P ₅₀ value 6–8 mmHg lower than that of adult hemoglobin. This lower P ₅₀ value allows more efficient oxygen delivery from the placenta to the fetal tissues. The fetal hemoglobin equilibrium curve is shifted to the left of the normal adult curve. Fetal hemoglobin binds less avidly to 2,3-diphosphoglycerate (2,3-DPG) compared with adult hemoglobin, causing a decrease in P ₅₀ . This is somewhat of a disadvantage to the newborn because lower peripheral oxygen levels are needed before oxygen is released from fetal hemoglobin. By 4–6 months of age in a term infant, the hemoglobin equilibrium curve gradually shifts to the right and the P ₅₀ value approximates that of a normal adult.

Pathologic anemia of the newborn is defined by a hemoglobin level less than 13.5 g/dL within the first month of life, anemia with a lower hemoglobin level than is observed with physiologic anemia, signs of hemolysis, or symptoms of anemia. Anemia in the newborn can be caused by hemolysis, blood loss, or decreased erythrocyte production ( Table 1.6 ). In a newborn, testing for anemia is indicated in the setting of symptoms (irritability or poor feeding) or signs of hemolysis (jaundice, scleral icterus, dark urine).

Jaundice is common in the neonatal period and is due to a myriad of reasons. The severity can range from a slight benign rise in plasma bilirubin levels to severe hyperbilirubinemia at risk for bilirubin-induced neurologic disorder. In the hepatocyte, bilirubin created by hemolysis is conjugated to glucuronic acid and rendered water soluble. Conjugated or direct bilirubin is excreted in bile. Unconjugated bilirubin interferes with cellular respiration and is toxic to neural cells. Subsequent neural damage is termed kernicterus and produces athetoid cerebral palsy, seizures, sensorineural hearing loss, but rarely death.

Healthy full-term infants usually have an elevated unconjugated bilirubin level. This is often referred to as physiologic jaundice. This is due to the breakdown of fetal RBCs and the relative immaturity of the neonatal liver to handle this level of metabolism in the newborn period. This entity peaks about the third day of life at approximately 6.5–7.0 mg/dL and does not return to normal until the 10th day of life. A total bilirubin level greater than 7 mg/dL in the first 24 hours or greater than 13 mg/dL at any time in full-term newborns often prompts an investigation. There are different nomograms for bilirubin levels used and these data can be different across ethnic and racial backgrounds, so it is important to normalize for these differences. Breast-fed infants usually have serum bilirubin levels 1–2 mg/dL greater than formula-fed babies. Various factors have been associated with breast milk jaundice including substances in breast milk (e.g., steroids, fats, cytokines, β-glucuronidase, and epidermal growth factor), difficulties with breastfeeding, and infant weight loss. However, new studies also implicate differences in extrahepatic UDP-glucuronosyltransferase 1A1. ^, The common causes of prolonged indirect hyperbilirubinemia are listed in Table 1.7 .

Pathologic jaundice within the first 36 hours of life is usually due to excessive production of bilirubin. In 2022, the AAP established clinical practice guidelines for initiating treatment of neonatal hyperbilirubinemia with hour-specific total serum bilirubin thresholds that varied based on gestational age and risk factors for neurotoxicity (prematurity, albumin less than 3.0 g/dL, hemolytic disease, sepsis, or significant clinical instability in the previous 24 hours). Prompt treatment should be initiated for patients with total serum bilirubin levels at or above the corresponding thresholds for phototherapy, and, if meeting the higher set of thresholds, exchange transfusion.

Newborns have difficulty maintaining body temperature for a multitude of reasons. They have a relatively large surface area to body mass ratio, a relatively low proportion of subcutaneous fat, and immature skin, resulting in increased evaporative water and heat losses, greater body water content, and poorly developed metabolic mechanisms for responding to the cold, as they do not shiver. Instead, nonshivering thermogenesis occurs through the metabolism of their relatively increased stores of brown adipose tissue. Brown adipose tissue is highly innervated, allowing for a brisk uncoupling of mitochondrial oxidation from phosphorylation in response to hypothalamic stimuli, which allows for heat production from free fatty acid oxidation.

As such, newborns are particularly susceptible to hypothermia. Neonatal hypothermia is defined as a body temperature of less than 36.5°C. Strategies to prevent heat loss include maintaining the delivery room at a minimum of 26°C, thoroughly drying the baby at birth, removing wet blankets and replacing them with warm towels, encouraging early skin-to-skin contact, and delayed cord clamping. ^, Following birth, strategies implemented in the neonatal intensive care unit to prevent hypothermia include the use of double-walled incubators, plastic bags/wraps, caps and mattress warming. ^,

At the opposite end of the temperature spectrum, neonatal fever is also critical to detect and manage. Neonatal fever is defined as a rectal temperature of 100.4°F or higher. Rectal temperatures are the gold standard for detecting fever in neonates less than 3 months old, as axillary, temporal artery, and tympanic membrane temperatures are felt to be less reliable in this population. Management of neonates who meet fever criteria should include a swift and thorough work-up to determine etiology.

The glomerular filtration rate (GFR) is the volume of plasma that is filtered through the kidney over time. The glomerular filtration rate of newborns is slower than that of adults. From 26 mL/min/1.73 m ² at birth in the term infant, GFR quickly increases to 54 mL/min/1.73 m ² by 2 weeks of age. GFR reaches adult levels by 18 months to 2 years of age. A preterm infant has a GFR that is only slightly slower than that of a full-term infant. In addition to this difference in GFR, the concentrating capacity of preterm and full-term infants is well below that of adults. Importantly, GFR in the newborn is best calculated by measuring creatinine clearance levels, as blood urea nitrogen (BUN) levels vary more widely for premature infants. An infant responding to water deprivation increases urine osmolarity to a maximum of 600 mOsm/kg. This is in contrast to the adult, whose urine concentration can reach 1200 mOsm/kg. It appears that the difference in concentrating capacity is due to the insensitivity of the collecting tubules of the newborn to antidiuretic hormone. Although the newborn cannot concentrate urine as efficiently as the adult, the newborn can excrete very dilute urine at 30–50 mOsm/kg. Urine output typically averages 3–4 mL/kg per hour and does not vary based on gestational or postnatal age. Newborns are unable to excrete excess sodium, an inability thought to be due to a tubular defect. Term babies conserve sodium, but premature infants are considered “salt wasters” because they have an inappropriate urinary sodium excretion, even with restricted sodium intake.

To estimate fluid requirements in the newborn requires an understanding of (1) any preexisting fluid deficits or excesses, (2) metabolic demands, and (3) losses. Because these factors change quickly in the critically ill newborn, frequent adjustments in fluid management are necessary. Daily fluid requirements in the newborn vary based on birth weight and postnatal age. Hourly monitoring of intake and output allows early recognition of fluid balance that will affect treatment decisions. This dynamic approach requires two components: (1) an initial hourly fluid intake that is safe and (2) a monitoring system to detect the patient’s response to the treatment program selected.

The typical fluid choice in newborns has a 10% glucose concentration to provide for the child’s glycemic needs. After administering the initial hourly volume for 4–8 hours, depending on the patient’s condition, the newborn is reassessed by observing urine output and concentration. With these two factors, it is possible to determine the state of hydration of most neonates and their responses to the initial volume. In more difficult cases, changes in serial serum osmolarity and sodium (Na ⁺ ), creatinine levels, along with urine osmolarity and Na ⁺ and creatinine levels, make it possible to assess the infant’s response to the initial volume and to use fluid status to guide the fluid intake over the next 4–8 hours.

Surgical neonatal patients have unique fluid demands. Generally, these patients have higher daily fluid volume requirements as they have significant insensible losses from surgery, ostomy output, exposed viscera, and higher catabolic requirements from factors such as postoperative inflammation, sepsis and third spacing. ^, Gastrointestinal losses can be gastric (emesis or suction), proximal bowel ostomy, or distal bowel (ostomy or water loss stools). In all circumstances, these fluid losses should be quantified and replaced 1 mL for 1 mL with isotonic fluid. Gastric and proximal stoma output are high in sodium, potassium, and magnesium. The sodium levels will generally autocorrect with fluid repletion, but these patients should be aggressively repleted with magnesium and potassium as well. Distal stoma output tends to be high in bicarbonate and potassium, and repletion should also include potassium.

Maturation of the lungs is generally divided into five periods:

• Embryonic phase (begins approximately week 3)

• Pseudoglandular phase (5–17 weeks)

• Canalicular phase (16–25 weeks)

• Terminal saccular phase (24 weeks to full-term birth)

• Alveolar phase (late fetal phase to childhood)

Pulmonary development begins in the third week (embryonic phase) when a ventral diverticulum develops off the foregut (laryngotracheal groove), initiating tracheal development. During the pseudoglandular phase, all major elements of the lung form, except those involved in gas exchange. The dichotomous branching of the bronchial tree that develops during the fourth week from the primitive trachea is usually completed by 17 weeks of gestation. Fetuses born during this phase are unable to survive because respiration is not possible. In the canalicular phase, respiration is made possible because thin-walled terminal sacs (primordial alveoli) have developed at the ends of the respiratory bronchioles and the lung tissue is well vascularized. No actual alveoli are seen until 24–26 weeks of gestation, during the terminal saccular phase. The air-blood surface area for gas diffusion is limited should the fetus be delivered at this age. The terminal saccular phase is defined by the establishment of the blood-air barrier that allows gas exchange for the survival of the fetus, should it be born prematurely. Between 24 and 28 weeks, the cuboidal and columnar cells flatten and differentiate into type I (lining cells) and/or type II (granular) pneumocytes. Between 26 and 32 weeks of gestation, terminal air sacs begin to give way to air spaces. At the same time, the phospholipids that constitute pulmonary surfactants begin to line the terminal lung air spaces. Surfactant is produced by type II pneumocytes and is extremely important in maintaining alveolar stability. During the alveolar phase, further budding of these air spaces occurs and alveoli become numerous, a process that continues postnatally until the age of 3–8 years.

Fetal lung maturity can be assessed with prenatal biochemical and biophysical testing. The available tests include lamellar body count, phosphatidylglycerol, and the lecithin/sphingomyelin ratio. These tests measure the concentrations of pulmonary surfactant components or evaluate the surface tension properties of these phospholipids. Once commonly performed, fetal lung testing is no longer used in most clinical settings, as the degree of fetal lung maturation often will not change the recommended clinical course of action. For newborns at risk of lung immaturity, an antenatal course of corticosteroids has been shown to provide lung maturation benefits without additional risk. The rare instances in which fetal lung testing continues to be performed involve predicting the level of neonatal care required after birth and for semielective but medically indicated births at gestational ages less than 39 weeks.

The change in the ratio of the amniotic phospholipids (lecithin:sphingomyelin) is used to assess fetal lung maturity. A ratio greater than 2 is considered compatible with mature lung function. Absence of an adequate surfactant leads to hyaline membrane disease (HMD) or respiratory distress syndrome (RDS). HMD is present in 10% of premature infants. Other conditions associated with pulmonary distress in the newborn include delayed fetal lung absorption, meconium aspiration syndrome, intrapartum pneumonia, and developmental structural anomalies (e.g., CDH and congenital lobar emphysema). In all these conditions, endotracheal intubation and mechanical ventilation may be required for hypoxia, CO ₂ retention, or apnea. Ventilator options and management depend on the clinical context and are discussed further in Chapter 7 .

To accelerate fetal lung maturity, a maternal dose of corticosteroids is the standard of care for threatened preterm delivery between 23 0/7 and 33 6/7 weeks of gestation. This antenatal course can be given as two 12 mg doses of intramuscular betamethasone given 24 hours apart or four 6 mg doses of intramuscular dexamethasone sodium phosphate given 6 hours apart. This therapy reduces the incidence of perinatal death as well as RDS, intraventricular hemorrhage (IVH), and necrotizing enterocolitis (NEC). Proposed pathways for the effect of corticosteroids on lung maturity include stimulation of surfactant production through enzymatic induction, increasing pulmonary blood flow, and increasing air space volume by decreasing perialveolar tissue volume. ^, Studies are ongoing to investigate concerns regarding the short- and long-term effects of antenatal corticosteroid administration as well as the consequences of repeated doses. There is thought to be a risk of hypoglycemia in newborns with diabetic mothers who receive antenatal steroids that may lead to neurodevelopmental issues later in the child’s life. The most recent data support short-term respiratory benefits for newborns of females who remained at risk for preterm birth 7 days or more after an initial course of corticosteroids and received a second course of steroids, and no significant harm for the mother or child in early and mid-childhood. Data detailing the long-term risks and benefits of receiving antenatal corticosteroids remains inconclusive. The Society for Maternal-Fetal Medicine and the American College of Obstetricians and Gynecologists (ACOG) recommend a single course of antenatal steroids for patients who meet inclusion criteria for the Antenatal Late Preterm Steroids Trial, and ACOG supports a single rescue course of antenatal corticosteroids if the initial course was more than 2 weeks prior, and birth is thought to occur within the next week. ^,

Respiratory distress syndrome (RDS) is caused by insufficient pulmonary surfactants in the immature lung and commonly affects preterm newborns. In fetal development, pulmonary surfactant begins to accumulate in the lungs at around 20 weeks of gestation and is progressively expressed as the fetus reaches term. As such, preterm birth is the most common cause of RDS. The pathophysiology in RDS is a direct result of high end-tidal surface tension due to surfactant deficiency, resulting in ventilation/perfusion mismatch and resulting hypoxemia. Inflammation is also thought to play a role in promoting pulmonary edema and worsening respiratory distress. Additionally, worsening pulmonary edema promotes surfactant inactivation, catalyzing a cascade of worsening pulmonary function and gas exchange. The incidence of RDS decreases with increasing gestational age, reportedly occurring in 93% of preterm infants born at 28 weeks or less, 10.5% of infants born at 29–34 weeks, 6% of infants born at 30–35 weeks, 2.8% of infants born at 36 weeks, 1% of infants born at 37 weeks and 0.3% of infants born at 38 weeks or more. ^, The natural course of RDS is characterized by symptoms peaking at 48–72 hours and resolving within 1 week of age, as more and more endogenous pulmonary surfactant is produced. Management of RDS includes delivery of exogenous surfactant and supportive care. High-frequency oscillatory ventilation has been shown to improve the disease course, and extracorporeal membrane oxygenation can be used in cases that do not respond to conventional treatment and meet inclusion criteria.

The development of exogenous surfactants in the 1990s significantly advanced the field of neonatology, resulting in reductions in the rates of neonatal mortality. As previously mentioned, surfactant deficiency is the major cause of RDS. Surfactant replacement therapy reduces the surface tension on the inner surface of the alveoli, preventing the alveoli from collapsing during expiration and thereby improving air exchange.

Indications for the use of surfactants include (1) intubated infants with RDS, (2) intubated infants with meconium aspiration syndrome requiring more than 50% oxygen, (3) intubated infants with pneumonia and an oxygen index great than 15, and (4) intubated infants with pulmonary hemorrhage who have clinically deteriorated. Its efficacy is uncertain in neonates with pulmonary hemorrhage and pneumonia. Worse outcomes are associated when surfactant is used in CDH. ^, The acute pulmonary effects of surfactant therapy are improved lung function and alveolar expansion leading to improved oxygenation, which results in a reduction in the need for mechanical ventilation and extracorporeal oxygenation.

Several adverse outcomes have been associated with the use of surfactan ( Table 1.8 ). Intraventricular hemorrhage is one of the most worrisome potential side effects. However, meta-analyses of multiple trials have not shown a statistically significant increase in this risk. ^,

Arterial oxygen tension (PaO ₂ ) is most commonly measured by obtaining an arterial blood sample and measuring the partial pressure of oxygen with a polarographic electrode. In the term newborn, the general definition of hypoxia is PaO ₂ below 50 mmHg, whereas hyperoxia is greater than 70 mmHg.

Capillary blood samples are “arterialized” by topical vasodilators or heat to increase blood flow to a peripheral site. Blood flowing sluggishly and exposed to atmospheric oxygen falsely raises the PaO ₂ from a capillary sample, especially in the 40–60 mmHg range. Capillary blood pH and carbon dioxide tension (PCO ₂ ) correlate well with arterial samples, unless perfusion is poor. PaO ₂ is least reliable when determined by capillary blood gas. In patients receiving oxygen therapy in which arterial PaO ₂ exceeds 60 mmHg, the capillary PaO ₂ correlates poorly with the arterial measurement. ^,

In newborns, umbilical artery catheterization provides arterial access. The catheter tip should rest at the level of the diaphragm or below L3. The second most frequently used arterial site is the radial artery. Complications of arterial blood sampling include repeated blood loss and anemia. Distal extremity or organ ischemia from thrombosis or arterial injury is rare but can occur. Changes in oxygenation are such that intermittent blood gas sampling may miss critical episodes of hypoxia or hyperoxia. Due to the drawbacks of ex vivo monitoring, several in vivo monitoring systems have been used.

The noninvasive determination of oxygen saturation (SaO ₂ ) gives moment-to-moment information regarding the availability of O ₂ to the tissues. If PaO ₂ is plotted against the oxygen saturation of hemoglobin, the S-shaped hemoglobin dissociation curve is obtained (see Fig. 1.2). From this curve, it is evident that hemoglobin is 50% saturated at 27 mmHg PaO ₂ and 90% saturated at 50 mmHg. Pulse oximetry has a rapid (5–7 seconds) response time, requires no calibration, and may be left in place continuously.

Pulse oximetry is not possible if the patient is in shock, has peripheral vasospasm, or has vascular constriction due to hypothermia. Inaccurate readings may occur in the presence of jaundice, direct high-intensity light, dark skin pigmentation, and greater than 80% fetal hemoglobin. Oximetry is not a sensitive guide to gas exchange in patients with high PaO ₂ due to the shape of the oxygen dissociation curve. On the upper horizontal portion of the curve, large changes in PaO ₂ may occur with little change in SaO ₂ . For instance, an oximeter reading of 95% could represent a PaO ₂ between 60 and 160 mmHg.

A study comparing pulse oximetry with PaO ₂ from indwelling arterial catheters has shown that SaO ₂ greater than or equal to 85% corresponds to a PaO ₂ greater than 55 mmHg, and saturations less than or equal to 90% correspond with a PaO ₂ less than 80 mmHg. Guidelines for monitoring infants using pulse oximetry have been suggested for the following three conditions:

• 1.

  In the infant with acute respiratory distress without direct arterial access, saturation limits of 85% (lower) and 92% (upper) should be set.

• 2.

  In the older infant with chronic respiratory distress who is at low risk for ROP, the upper saturation limit may be set at 95%; the lower limit should be set at 87% to avoid pulmonary vasoconstriction and pulmonary hypertension.

• 3.

  As the concentration of fetal hemoglobin in newborns affects the accuracy of pulse oximetry, infants with arterial access should have both PaO ₂ and SaO ₂ monitored closely. A graph should be kept at the bedside, documenting the SaO ₂ each time PaO ₂ is measured. Limits for the SaO ₂ alarm can be changed because the characteristics of this relationship change.

Measuring expired CO ₂ by capnography provides a noninvasive means of continuously monitoring alveolar PCO ₂ . Capnometry measures CO ₂ by an infrared sensor either placed in-line between the ventilator circuit and the endotracheal tube or off to the side of the air flow, both of which are applicable only to the intubated patient. A comparative study of end-tidal carbon dioxide in critically ill neonates demonstrated that both sidestream and mainstream end-tidal carbon dioxide measurements approximated PaCO ₂ . When the mainstream sensor was inserted into the breathing circuit, the PaCO ₂ increased by an average of 2 mmHg.

Indications for central venous catheter placement include (1) hemodynamic monitoring, (2) inability to establish other venous access, (3) TPN, and (4) infusion of inotropic drugs or other medications that cannot be given peripherally. Measuring central venous pressure (CVP) to monitor volume status is frequently used in the resuscitation of a critically ill patient. A catheter placed in the superior vena cava or right atrium measures the filling pressure of the right side of the heart, which usually reflects left atrial pressure and filling pressure of the left ventricle. Often, a wide discrepancy exists between left and right atrial pressure when pulmonary disease, overwhelming sepsis, or cardiac anomalies are present. Positive-pressure ventilation, pneumothorax, abdominal distention, or pericardial tamponade all elevate CVP. Less invasive options for vascular access include umbilical lines and peripherally inserted central catheter (PICC) lines. Long-term central access such as Broviac catheters are also options.