46: Abnormal Blood Gas

An abnormal blood gas value for a neonate is reported by the laboratory.

1. What component of the blood gas is abnormal? Accepted normal values for an arterial blood gas on room air are pH 7.35–7.45 (pH varies with age, a pH >7.30 is generally acceptable), Paco₂, 35–45 mm Hg (slightly higher accepted if the blood pH remains normal), and Pao₂ 50–95 mm Hg (depends on gestational age). (See Table 8–1) Blood gas measures pH, Pco₂, and oxygen (O₂), and all the other components (base excess, bicarbonate concentration, and oxygen saturation) are calculated based on the 3 levels measured. General blood gas concepts are as follows:

   1. pH is proportional to HCO₃ (base excess)

      1. Metabolic acidosis. Abnormal ↓ in HCO₃ with ↓ pH.

      2. Metabolic alkalosis. Abnormal ↑ HCO₃ with ↑ pH.

   2. pH is inversely proportional to Pco₂

      1. Respiratory acidosis. Abnormal ↑ Pco₂with ↓ pH.

      2. Respiratory alkalosis. Abnormal ↓ Pco₂ with ↑ pH.

2. Is this blood gas value very different from the patient's previous blood gas determination? If the patient has had metabolic acidosis on the last 5 blood gas measurements and now has metabolic alkalosis, it might be best to repeat the blood gas measurements before initiating treatment. Do not treat the infant on the basis of one abnormal gas value, especially if the infant's clinical status has not changed.

3. How was the sample collected? Blood gas measurements can be reported on arterial, venous, or capillary (heelstick) blood samples.

   1. Arterial blood samples. Best indicator of pH, Paco₂, and Pao₂. The gold standard of obtaining a blood gas is to obtain one from an indwelling arterial catheter (peripheral or umbilical). Blood gases by intermittent arterial punctures may not accurately reflect the infant's respiratory status. A sudden decrease in the Paco₂ and Pao₂ can occur during the puncture. Crying can decrease the Paco₂, HCO₃ and oxygen saturation.

   2. Venous blood samples. Give a lower pH value, significantly lower Po₂, and a higher Pco₂ than arterial samples. It is good for HCO₃ estimation,

   3. Capillary (heelstick) samples. Give a satisfactory assessment of the infant's pH and Pco₂ but do not give an accurate Pao₂. Capillary samples give a similar or lower pH value (not as low as venous pH), similar or slightly higher Pco₂, and lower Po₂ than arterial samples; capillary blood gas measurements are not reliable in an infant who is hypotensive or in shock.

4. Is the infant on ventilatory support? Management of abnormal blood gas levels is approached differently in an intubated infant than in a patient breathing room air.

1. Metabolic acidosis (pH <7.30–7.35 with a normal to low CO₂). After birth it is normal for an infant to have a mild metabolic acidosis. The 3 main causes of metabolic acidosis are loss of base (mainly bicarbonate) from renal or gastrointestinal (GI) cause, decreased renal excretion of acid, or an increased production of acid. Metabolic acidosis is classified as anion gap (increased, high) or non–anion (normal) gap acidosis. Determining the anion gap will help decide the cause of the acidosis.

   1. Anion gap. Difference in measured cations and anions in serum or plasma. Calculated by:

      

      1. Normal. 8–16 mEq/L (up to 18 mEq/L in premature infants <1000 g).

      2. Increased. >16 mEq/L in infants (>18 mEq/L in premature infants <1000 g).

   2. Common causes of metabolic acidosis in the newborn

      1. Increased anion gap metabolic acidosis (normal chloride)

         1. Lactic acidosis associated with clinical evidence of decreased tissue perfusion is common in the neonate. A serum anion gap >16 mEq/L is highly predictive of lactic acidosis (<8 mEq/L lactic acidosis is highly unlikely). Some infants may not have an increased anion gap with lactic acidosis. Causes: asphyxia, hypoxia, respiratory distress syndrome (RDS), sepsis, compromised cardiac output (cardiogenic, septic, and hypovolemic shock), circulatory or respiratory failure, massive hemorrhage/severe anemia, periventricular hemorrhage (PVH)/intraventricular hemorrhage (IVH), hypothermia/cold stress, hypotension,patent ductus arteriosus (PDA), necrotizing enterocolitis (NEC) or any intestinal ischemia, excessive ventilator pressures with decreased cardiac output, seizures, and ascites/third spacing of fluids.

         2. Inborn errors of metabolism. Inborn errors have lactic acidosis not associated with clinical evidence of poor tissue perfusion. An anion gap of >16 is seen in many inborn errors of metabolism such as organic acidemias (most common), galactosemia, hereditary fructose intolerance, maple syrup disease, congenital/primary lactic acidosis, type I glycogen storage disease and pyruvate dehydrogenase/carboxylase deficiency, mitochondrial respiratory chain defects, multiple carboxylase deficiency, and fatty acid oxidation defects.

         3. Renal failure. Kidney failure with renal bicarbonate losses.

         4. Late metabolic acidosis of prematurity (first to third week of life). Excessive acid load from high-protein formula (casein-based formulas), amino acid intake, or intravenous alimentation.

         5. Toxins and medications. Maternal use  of salicylates and maternal acidosis. Benzyl alcohol in doxapram. Others: alcohols and glycols, acetaminophen, β-adrenergic agents, cocaine, nitroprusside, ibuprofen, iron, isoniazid, paraldehyde, sulfasalazine, valproic acid.

      2. Normal or non–anion gap metabolic acidosis (normal anion gap, elevated serum chloride, hyperchloremic acidosis). A low serum potassium indicates loss of base; a high serum potassium suggests renal tubular acidosis. Most common causes are renal tubular acidosis (RTA) and diarrhea.

         1. Renal loss of bicarbonate

            • (a) Immature kidneys. Bicarbonate wasting.

            • (b) RTA. Defect in either the reabsorption of bicarbonate or the secretion of the hydrogen ion. (Most common cause in preterm infants is proximal RTA).  Check urine pH, <7 suggests proximal RTA, >5.5 suggests distal RTA.

            • (c) Renal failure.

            • (d) Renal dysplasia.

            • (e) Medications.  Carbonic anhydrase inhibitors  can cause reduced uptake of bicarbonate ions (acetazolamide, dorzolamide, methazolamide, hydroxyurea). Aldosterone inhibitors: spironolactone and eplerenone.

            • (f) Hypoaldosteronism. Low Na⁺, elevated K⁺.

            • (g) Hyperparathyroidism.

         2. GI loss of bicarbonate

            • (a) Diarrhea (usually secretory).

            • (b) Urologic and GI procedures. Surgery for NEC, ileostomy, enterocutaneous or bowel fistula, small bowel or pancreatic drainage, any bowel diversion in contact with urine.

            • (c) Medications. Ion exchange resins, cholestyramine, calcium chloride, magnesium sulfate.

         3. Dilutional acidosis. Rapid volume expansion with lactated Ringer's solution, saline, or dextrose with dilution of bicarbonate.

         4. Factitious acidosis. Due to excessive heparin in the syringe. Air contamination can give a large base deficit.

         5. Excessive chloride in IV fluids.

         6. Hyperalimentation acidosis caused by the acid load.

         7. Potassium-sparing diuretics and hyperkalemia.

      3. Low anion gap metabolic acidosis. (Low or negative anion gap.) Rare, usually caused by laboratory error or hypoalbuminemia.

2. Metabolic alkalosis (pH >7.45 with base excess of >5). Usually iatrogenic and uncommon, it is due to an excess of base (HCO₃) or loss of acid. There are 2 types: Chloride resistant and chloride responsive. Obtain a spot urinary chloride to help determine the etiology.

   1. High urinary chloride >20 mEq/L (chloride-resistant metabolic alkalosis; increased extracellular fluid [ECF] volume). Hypokalemia, early diuretic therapy (especially furosemide), excess alkali administration, large blood transfusion, Bartter syndrome (mineralocorticoid excess), exogenous steroid therapy, Cushing, Conn, or Liddle syndrome, primary aldosteronism, congenital adrenal hyperplasia variant (DOC excess syndrome), milk-alkali syndrome.

   2. Low urinary chloride <10 mEq/L (chloride-responsive metabolic alkalosis; low serum chloride and decreased ECF volume). Loss of gastric secretions (persistent vomiting, continuous nasogastric/orogastric suction), secretory diarrhea (congenital chloride wasting diarrhea), acute correction of chronically compensated respiratory acidosis, late diuretic therapy, posthypercapnia syndrome.

   3. Common causes of metabolic alkalosis in the newborn

      1. Prolonged NG/OG suction

      2. Diuretic therapy (especially Lasix in patients with bronchopulmonary dysplasia/chronic lung disease [BPD/CLD])

      3. Excess alkali administration (eg, sodium bicarbonate, citrate, acetate, or lactate infusion) as in parenteral nutrition or increased alkali load from feedings

      4. Potassium depletion

      5. Compensation for respiratory acidosis (eg, infant with BPD/CLD/chronic ventilation)

   4. Less common causes. Pyloric stenosis (persistent vomiting), Bartter syndrome (rare), primary hyperaldosteronism, diarrhea with chloride loss, congenital adrenal hyperplasia (certain types).

3. Low CO₂. Respiratory alkalosis: a decrease in CO₂ with an increase in pH.

   1. Overventilation by the ventilator. Most common cause in NICU.

   2. Air bubble in the blood gas collection syringe. This can falsely lower the Pao₂ and Paco₂. Heparin can falsely lower the Paco₂.

   3. Hyperventilation therapy. As used in persistent pulmonary hypertension.

   4. Central hyperventilation. Central nervous system (CNS) stimulation of the respiratory drive caused by a CNS disorder or transient hyperammonemia (ammonia stimulates the respiratory center resulting in hyperventilation).

   5. Hypoxemia can cause a low CO₂. Respiratory centers are stimulated through chemoreceptors.

   6. Hyperventilation. Seen in a spontaneously breathing infant secondary to sepsis, fever, aspiration pneumonia, retained fluid.

   7. Compensation for a primary metabolic acidosis.

4. High CO₂. Respiratory acidosis: increase in Paco₂ with decrease in pH.

   1. Obstructed ETT (eg, mucus plug).

   2. Improper ETT position. An endotracheal tube positioned in the oropharynx, down the right main stem bronchus, or at the carina.

   3. Ventilator malfunction or insufficient respiratory support.

   4. Ventilator strategy that allows permissive hypercapnia (controlled mechanical hypoventilation) is controversial. Use caution with permissive hypercapnia until further studies are done. Severe hypercapnia or hypocapnia should be avoided. In infants with BPD/CLD, higher CO₂ is sometimes tolerated to wean them from mechanical ventilation.

   5. Increasing respiratory failure; lung diseases such as RDS, pneumonia, transient tachypnea (TTN), BPD/CLD, pleural effusion, pulmonary hypoplasia, atelectasis.

   6. Pneumothorax.

   7. Hypoventilation or poor respiratory effort from maternal anesthesia, medications, neuromuscular disorders, congenital central hypoventilation syndrome, sepsis, intracranial hemorrhage, or hypoglycemia.

   8. PDA with pulmonary edema. Suspect a PDA if the infant has a systolic murmur, active precordium, bounding pulses, and increased pulse pressure. Other clinical signs and symptoms may include congestive heart failure, deteriorating blood gases with an increase in the ventilator settings, and cardiomegaly with increased pulmonary vascularity on chest radiograph.

   9. Others. Congenital diaphragmatic hernia, phrenic nerve paralysis, and other causes.

5. Low O₂ (hypoxia). See also Chapter 51.

   1. Agitation

   2. Improper ETT position or inadequate ventilatory support

   3. Congenital heart disease (cyanotic)

   4. Respiratory diseases

      1. Primary lung disease. RDS, TTN, BPD/CLD, others.

      2. Airway obstruction. Mucus plug, choanal atresia, other congenital malformations (macroglossia, cystic hygroma, etc.).

      3. External compression of the lungs. Air leak syndrome (eg, pneumothorax) or congenital defects (eg, congenital diaphragmatic hernia).

   5. Apnea of prematurity

   6. Pulmonary hypertension

   7. CNS/neuromuscular disorders

   8. Metabolic abnormalities

   9. Hematologic disorders

   10. Sepsis /hypotension

1. Physical examination. Evaluate for signs of sepsis (eg, hypotension or poor perfusion). Check for equal breath sounds; asymmetric breath sounds suggest pneumothorax or incorrect ETT placement. Observe for chest wall movement. Listen for breath sounds over the chest versus the epigastric region, which may help determine whether the ETT is malpositioned. Listen to the heart for any murmur, and palpate for cardiac displacement.

2. Laboratory studies

   1. Repeat blood gas measurement. Repeat if the result is unexpected. Do not make a major clinical decision based on a venous or capillary blood gas values or on 1 arterial gas result.

   2. Serum electrolytes. To include blood urea nitrogen, creatinine, glucose, potassium (severe metabolic alkalosis can cause hypokalemia). Serum Na, K, Cl, and bicarbonate (from arterial blood gas) to determine anion gap.

   3. Urine chloride. To evaluate metabolic alkalosis. May not be valid in the setting of diuretic use.

   4. Urinary ketones. If absent or small, think lactic acidosis; if moderate or large, suspect organic acidemias (maple syrup urine disease, glycogen storage disease, disorders of pyruvate metabolism, others).

   5. Plasma ammonia level. If normal, may be RTA; may be increased in urea cycle defects, may be increased in some organic acidemias (acidosis and hyperammonemia).

   6. Serum potassium level. Severe metabolic alkalosis can cause hypokalemia.

   7. Measure the anion gap. Correct for hypoalbuminemia by adding 2.5 mEq/L to the anion gap for every gram per deciliter that the concentration of serum albumin is reduced below the normal value of 3.5 g/dL.

   8. Plasma lactate. Increased in lactic acidosis. It is important to do this in infants who have a normal anion gap but in whom lactic acidosis is suspected. Infants with lactic acidosis do not always have an increased anion gap. Normal and elevated lactate can be seen in organic acidemias.

   9. Complete blood count with differential. If sepsis is being considered.

   10. Further sepsis workup if indicated. Blood culture, urinalysis and culture, lumbar puncture if indicated.

   11. Metabolic screen if indicated. Urine and plasma for amino acids and organic acids.

3. Imaging and other studies

   1. Pulmonary mechanics. Check the tidal volume (Vt) delivered on the ventilator. The normal Vt is 5–6 mL/kg. If the Vt is low, it could mean that not enough pressure is given or there is an obstruction in the ETT.

   2. Transillumination of the chest. If pneumothorax is suspected (see Chapter 70).

   3. Chest radiograph. Should be performed if an abnormal blood gas value is reported, unless there is an obvious cause. An anteroposterior view should be obtained to check ETT placement (see Figure 11–7), rule out air leak (eg, pneumothorax, see Figure 11–20), check heart size and pulmonary vascularity (increased or decreased) and determine whether the infant is being hypoventilated or hyperventilated.

   4. Abdominal radiograph. If NEC is suspected in a patient with severe metabolic acidosis. See Figure 11–23.

   5. Ultrasonography of the head. To diagnose IVH. See Figures 11–1, 11–2, 11–3, 11–4 for examples of IVH.

   6. Echocardiography. May detect PDA or other cardiac abnormality and can be used to diagnose low cardiac output.

   7. Ultrasonography of the abdomen with color Doppler studies. To evaluate for NEC and bowel necrosis.

1. Overall plan. Verify the blood gas result, find the cause of the problem, and provide treatment for the specific cause. First, examine the infant. If the infant's clinical status has not changed, repeat blood gas measurements to verify the report. If the clinical status has changed, the abnormal report is probably correct; repeat blood gas measurements and begin further evaluation of the infant.

2. Specific management

   1. Metabolic acidosis. The primary treatment is to treat the underlying cause. Correct hypoxia, hypovolemia, low cardiac output, and anemia. Treatment with bicarbonate is not recommended as a supportive therapy and its use is very controversial. It has been quoted as “basically useless therapy” and associated with adverse sequelae (hypernatremia, intracranial hemorrhage, fluctuations in cerebral blood flow, cardiac deterioration, and worsening acidosis).

      1. Important and controversial points in the treatment of metabolic acidosis

         1. Sodium bicarbonate in the delivery room (controversial). American Academy of Pediatrics and American Heart Association guidelines state that the use of sodium bicarbonate is controversial during resuscitation in the delivery room. It is not recommended early on, and if used later in resuscitation or during a prolonged resuscitation not responding to therapy, make sure the lungs are adequately ventilated. Sodium bicarbonate is hyperosmolar and may cause IVH if given rapidly. Cochrane review states there are insufficient data to make a recommendation on using sodium bicarbonate during resuscitation.

         2. Sodium bicarbonate in an asphyxiated newborn (controversial). If metabolic acidosis is severe or persistent, some institutions may use sodium bicarbonate. Rapid infusion increases serum osmolality, and alkalinization may decrease cerebral blood flow. Some institutions only do 24-hour corrections in patients with profound postasphyxia acidosis.

         3. Sodium bicarbonate in preterm infants (controversial). Cochrane review states there is insufficient evidence to state that use of sodium bicarbonate in preterm infants with metabolic acidosis reduces mortality and morbidity.

         4. Sodium bicarbonate in a cardiac arrest (controversial). May cause harm and there is no evidence of benefit.

         5. If sodium bicarbonate is given and the infant does not respond, think inborn error of metabolism.

         6. Watch for hypokalemia as metabolic acidosis is corrected.

         7. Do not treat metabolic acidosis with hyperventilation.

         8. Replacement of base for ongoing GI and renal losses. Not proven but is often accepted as reasonable therapy.

         9. Fluid therapy for metabolic acidosis. Volume expansion should not be used to treat acidosis unless there are signs of hypovolemia. Severe acidosis causes a decrease in myocardial contractility. Cochrane review states that there is insufficient evidence to state that a fluid bolus reduces morbidity and mortality in preterm infants with metabolic acidosis.

      2. Medications for metabolic acidosis. It is best to correct the underlying cause of the metabolic acidosis. Some institutions treat acidosis if severe with an alkali infusion if the base excess is >–5 to – 10 or if the pH is ≤7.25 (controversial). The alkali can be given as IV push, 1 dose over 30 minutes, or can be given as an 8–24-hour correction. If the acidosis is mild, usually only 1 dose is given and repeat blood gas measurements are obtained. If the acidosis is severe, a dose is given and correction is started at the same time. One of 3 medications is used:

         1. Sodium bicarbonate can be used if the infant's serum sodium and Pco₂ are not high. It is the most common medication used. If used, it is recommended to give a diluted formulation and a slow correction. If given to a premature infant, it is important to give it slower than recommended.

            • (a) One-time dose. 1–2 mEq/kg/dose, given as a 4.2% solution (0.5 mEq/mL); infuse at 1 mEq/kg/min max over at least 30 minutes.

            • (b) IV push (for cardiac arrest, routine use not recommended, controversial). 1 mEq/kg slow IV push, given as 0.5 mEq/mL (4.2% concentration). Maximum rate in neonates and infants is 10 mEq/min. May repeat with a 0.5-mEq/kg dose in 10 minutes one time as indicated by patient's unstable acid-base status.

            • (c) Slow correction should be given over 8–24 hours in IV fluids. Give half the correction at first, then reassess. The total dose required to correct the base deficit is as follows:

              

         2. Tromethamine (THAM) can be used in infants who have a severe metabolic acidosis but have a high serum sodium (>150 mEq/L) or high Pco₂ (>65 mm Hg) despite aggressive assisted ventilation. It does not increase CO₂ or sodium as bicarbonate does. It is not indicated for metabolic acidosis caused by bicarbonate deficiency. Use only in infants with good urine output (hyperkalemia risk) and monitor for hypoglycemia. (Controversial: Many institutions do not use THAM because of side effects: higher osmolar load, risk of hypoglycemia, others). See dose in Chapter 148.

         3. Polycitrate (Polycitra) (oral solution). This alkali can be helpful in patients with acidosis associated with chronic renal insufficiency, intrinsic renal disease, or renal wasting or on medications that promote acidosis such as acetazolamide (Diamox). It consists of 1 mEq Na⁺, 1 mEq K⁺, and 2 mEq citrate. Each 1 mEq citrate equals 1 mEq bicarbonate. The dose is 2–3 mEq/kg/d polycitrate in 3–4 divided doses; adjust to maintain a normal pH.

         4. Sodium or potassium acetate (IV preparations) can be used to treat chronic metabolic acidosis through the conversion of acetate to bicarbonate. It is used in hyperalimentation for bicarbonate replacement as part of urinary losses in preterm infants and treatment of metabolic acidosis. See doses in Chapter 148.

      3. Specific treatments for metabolic acidosis

         1. Sepsis. Initiate a septic workup and consider broad-spectrum antibiotics. (See Chapter 130.)

         2. NEC. See Chapter 113.

         3. Hypothermia or cold stress. See Chapter 7.

         4. Periventricular-intraventricular hemorrhage. Weekly ultrasonographic examinations of the head and daily head circumferences are indicated. Monitor the infant for signs of increased intracranial pressure (convulsions, vomiting, and/or hypotension). (See Chapter 104.)

         5. PDA. If hemodynamically significant, PDA should be treated. (See Chapter 118.)

         6. Shock/ low cardiac output. Give volume expansion if hypovolemic or vasoactive medications based on cardiac function. (See Chapter 65.)

         7. Renal tubular acidosis. Treated with alkaline therapy such as sodium bicarbonate or one of citrate and citric acid solutions.

         8. Inborn errors of metabolism. Rare cause (see Chapter 101).

         9. Maternal use of salicylates. Acidosis usually resolves without treatment.

         10. Renal failure. See Chapter 123.

         11. Congenital lactic acidosis. Supportive care, correction of the metabolic acidosis with sodium bicarbonate.

         12. Parenteral hyperalimentation. Preterm infants usually need acetate supplementation in hyperalimentation to correct for ongoing bicarbonate losses. It should be given to infants with a base deficit >–5. The use of acetate in total parenteral nutrition reduces the severity of the acidosis and the incidence of hyperchloremia.

   2. Metabolic alkalosis. Mild or even moderate alkalosis may not require correction. First treat any underlying cause. Volume replacement can be used in cases of volume contraction and chloride depletion. If hypokalemia is present, that should be treated. Chloride replacement as KCl can be used, but infusion rate may have to be limited. HCL or ammonium chloride can be considered in severe persistent cases but must be given carefully. Acetazolamide has been used in some pediatric cardiac patients with chloride-resistant metabolic alkalosis.

      1. Excess administered alkali. Adjust or discontinue the dose of THAM, sodium bicarbonate, or polycitrate; reduce acetate in hyperalimentation.

      2. Hypokalemia. This can cause a shift of hydrogen ions into cells as potassium is lost. The infant's potassium level should be corrected (see Chapter 63).

      3. Prolonged nasogastric suction. Treated with IV fluid replacement, usually with 1/2 normal saline with 10–20 mEq KCl/L, replaced mL/mL each shift.

      4. Vomiting and loss of chloride from diarrhea. Give IV fluids and replace deficits.

      5. Compensation for respiratory acidosis. Correct ventilation.

      6. Diuretics. These can cause mild alkalosis; no specific treatment is usually necessary. Stop the dose temporarily, or decrease the diuretic dose if necessary, or add a potassium-sparing diuretic such as spironolactone.

      7. Bartter syndrome. Treated with indomethacin and potassium supplements. Replace electrolyte losses.

      8. Primary hyperaldosteronism. Treatment depends on the cause. Acute therapies include diuretics, angiotensin-converting enzyme inhibitors, and steroids.

   3. Other causes of abnormal blood gases

      1. ETT problems. Determine whether there are any changes on the pulmonary function test measurements on the ventilator that may indicate a problem with the ETT. Colorimetric CO₂ detectors can be used to determine airway patency, with a color change from purple to yellow if there is exhaled CO₂ gas. If no color change, there is airway obstruction and possible ETT problem. Mark position on the ETT when it is correctly placed to note whether the tube is out of position.

         1. Mucus plug. With decreased bilateral breath sounds and retractions, a plugged ETT is possible. Pulmonary function measurements on specific ventilators may also define this if the Vt is low. The infant can be suctioned, and, if clinically stable, repeat blood gas measurements can be obtained. If the infant is in extreme distress, replace the tube.

         2. ETT placement problems. An infant with a tube placed down the right main stem bronchus has breath sounds on the right only. An infant with a tube that has dislodged has decreased or no breath sounds on chest auscultation.

      2. Ventilator issues. Changes in blood gas levels based on changes in routine ventilator settings can be found in Table 46–1. Advanced ventilator management for high-frequency devices can be found in Chapter 8.

         1. Overventilation. If the blood gas levels reveal overventilation, the ventilation parameters need to be adjusted. Deciding which parameter to adjust depends on the patient's lung disease and the disease course.

            • (a) If the oxygen level is high. Decrease the Fio₂. Other options include decreasing the positive end-expiratory pressure (PEEP), peak inspiratory pressure (PIP), inspiratory time, rate and flow.

            • (b) If the CO₂ level is low. Decrease the rate. Other options include decreasing the PIP, expiratory time, or flow.

         2. Insufficient respiratory support. If the infant's chest is not moving, the PIP is not high enough; an adjustment of the ventilator setting is needed. Also check the Vt; if it is low, it could mean not enough pressure is given.

            • (a) If the oxygen is low. One or more of the following can be increased: Fio₂, PIP, PEEP, inspiratory time, rate, and flow rate.

            • (b) If the CO₂ is high. One or more of the following can be increased: rate, PIP, flow rate, or expiratory time. Decreasing PEEP will increase tidal volume and decrease CO₂.

         3. Ventilator malfunction. Notify respiratory therapy to check the ventilator and replace it if necessary.

      3. Agitation. May cause the infant to drop in oxygenation; sedation may be needed (controversial) or ventilator settings adjusted. See also Chapter 76.

         1. Note: Agitation can be a sign of hypoxia, so a blood gas level should be obtained before ordering sedation. If there is documented hypoxia, attempt to increase oxygenation.

         2. Sit by the bedside and try different ventilator rates. To see whether the infant fights less.

         3. Routine sedation. Usually not recommended because in very low birthweight infants and premature infants, it is associated with an increase in severe IVH, delay in diuresis, and ileus. If sedation is used, use the preferred agent at your institution (see Chapter 76 for agents used: diazepam, lorazepam, midazolam, fentanyl, chloral hydrate, morphine).

      4. Acute change in clinical pulmonary status

         1. Pneumothorax. See Chapter 70.

         2. Atelectasis. Treatment consists of percussion and postural drainage and possibly increased PIP or PEEP. Avoid percussion in small preterm infants; a study showed a strong link between IVH and porencephaly with chest physiotherapy in extremely premature infants.

         3. Pulmonary edema. Diuretics (eg, furosemide) are the primary treatment with mechanical ventilation as indicated.

         4. Persistent pulmonary hypertension. See Chapter 120.