Critical Care Obstetrics part 14 ppsx

Neonatal Resuscitation 119 solution of epinephrine be used via the endotracheal route. If epinephrine is given via an umbilical venous catheter, the recommended dose is 0.1 – 0.3 mL/kg of a 1 : 10 000 solution. Given concern about adverse outcomes when high - dose epinephrine has been used for adult resuscitations, routine use of higher epinephrine doses cannot be recommended. When epinephrine alone is not effective, consideration should be given to the possibility of hypovolemic shock. There is no role for the use of sodium bicarbonate in an acute neonatal resuscitation. Volume e xpanders After administration of epinephrine, if the infant exhibits signs of shock such as poor capillary refi ll, weak pulses or a pale appear- ance, or there is evidence or suspicion of acute blood loss a volume expander may be indicated. With a placental abruption or a placental previa, blood loss may be obvious. However, an infant may lose blood into the maternal circulation and this may not be obvious. The recommended volume expander, and the most easily available is normal saline at a dose of 10 mL/kg via the umbilical vein given over 5 – 10 minutes. Ringer ’ s lactate can also be used. If severe fetal anemia is documented or expected, type O Rh - negative packed red blood cells should be used, if available. The d rug - d epressed i nfant Although relatively uncommon, respiratory depression may occur in the infant whose mother received inhalational anesthetic before cesarean section delivery or who was given a narcotic analgesic less than 4 hours before delivery. With the inhalational anesthetics, adequate ventilation will effectively clear them from the infant. If the infant ’ s mother received a narcotic analgesic less than 4 hours before delivery and there is continued respiratory depression after effective positive - pressure ventilation has restored the heart rate and color, naloxone (Narcan) may be useful in antagonizing the narcotic agent ’ s respiratory depression. The standard dose is 0.1 mg/kg of a 1.0 mg/mL solution. The referred route of administration is intravenous. It may be administered intramuscularly, but this route of administration is associated with a delayed onset of action. It is important to note that the duration of action of the naloxone may be signifi cantly shorter than the duration of action of the narcotic analgesic. Therefore, repeated doses may be necessary. Narcan should never be given to the infant born of a mother with a narcotics addiction. The infant may have acute withdrawal symptoms, including seizures. If an infant is not breathing, it is important to stress that the fi rst intervention is the administration of positive - pressure ventilation to establish a good heart rate and color, regardless of how sure you are of the fact that narcotics were given to the mother within 4 hours before delivery. Only then, in the face of recent narcotic administration, should a narcotic antagonist be considered. administer adequate chest compressions. However, regardless of the method used, those responsible for chest compressions and for continued ventilation of the infant must position themselves so that they do not interfere with one another. It is helpful for a third team member to monitor for palpable pulses during compressions. It is currently recommended that chest compressions occur 90 times a minute with ventilation interposed after every third compression. Thus, in a 2 - second period, 3 compressions and 1 breath are given. This provides 90 compressions and 30 respirations in each minute. Intermittently, chest compressions should be stopped to check for a spontaneous heart rate. If the spontaneous heart rate is greater than 60 beats/min compressions may be stopped. If well - coordinated chest compressions and ventilation do not raise the infant ’ s heart rate above 60 beats/min within 30 seconds, support of the cardiovascular system with medications is indicated. Medications If the heart rate remains below 60/min, despite ventilation and chest compression, the fi rst action should be to ensure that ventilations and compressions are well coordinated and optimal and 100% oxygen is being used before proceeding with medications. Epinephrine is indicated when, in the rare infant, positive - pressure ventilation and chest compressions fail to correct the neonatal bradycardia. Where the infant appears to be in shock, there is evidence of blood loss and the infant is not responding to resuscitation, volume expanders may be indicated. Clearly, the best choice for giving epinephrine or volume expanders is via an umbilical venous catheter. If, while preparing for placement of the venous catheter, epinephrine is needed, it can be given via an endotracheal tube. Resuscitative placement of the umbilical vein catheter differs from postresuscitative placement. The umbilical catheter is inserted slightly past the level of the skin – only to the point where blood is fi rst able to be aspirated. This avoids the devastating complication of hepatic necro- sis caused by infusion of medications through a catheter inadvertently wedged in a hepatic vein. Any doubt about the position of the umbilical catheter should prompt removal and reinsertion of the catheter to just past the level of the skin. Epinephrine Epinephrine should be used as the fi rst - line agent for persistent bradycardia in the face of adequate positive - pressure ventilation with 100% oxygen. It may be given via intravenous catheter or via endotracheal tube while intravenous access is being acquired. It may be re - administered every 3 – 5 minutes as needed for bradycardia. It remains uncertain as to whether an increase in the standard IV epinephrine dosage should routinely be given when epinephrine is administered via the endotracheal tube. The most current recommendations are that 0.3 – 1 mL/kg of a 1 : 10 000 Chapter 8 120 gen stores, especially myocardial glycogen stores, and it is important to provide fuel to such an infant. The glucose infusion also prevents the hypoglycemia that is frequently associated with perinatal compromise. Fluids The urine output of any infant undergoing an episode of depression should be carefully monitored. Oliguria may occur in asphyxiated infants, and an infant can easily be overloaded with fl uid. Fluid should be restricted until there is evidence of adequate urine output. The need to restrict fl uid and yet give glucose emphasizes the importance of considering glucose infusion in terms of milligrams per kilogram of body weight per minute, rather than in the amount of 10% glucose to be given. The concentration of glucose will depend on how much fl uid can be given to the infant. Thermal m anagement Any infant who has undergone an active resuscitation should be carefully observed. This requires that the infant be clothed only in a diaper and kept in either an incubator or a radiant warmer so that thermal neutrality can be maintained. The temperature of the infant should be monitored frequently. As important as it is to prevent hypothermia, it is equally important to avoid hyperthermia. Feeding During the asphyxial process, ischemia of the intestine may occur as a result of vasoconstriction of the mesenteric blood vessels. Due to the association between gut ischemia and the development of necrotizing enterocolitis, it may be prudent to withhold enteral feedings from the asphyxiated infant for anywhere up to a few days. Other p roblems Other complications of the post - asphyxial infant include hypo- calcemia, disseminated intravascular coagulation, seizures, cere- bral edema, and intracerebral hemorrhage. Special p roblems d uring r esuscitation Meconium a spiration Infants with meconium - stained amniotic fl uid are at an increased risk for aspiration of meconium. Although not all infants who pass meconium are depressed or have problems, it is true that if meconium is present in the amniotic fl uid, there is a chance that the meconium will enter the mouth of the fetus and be aspirated into the lungs. Aspiration of meconium into the lungs may create ball - valve obstructions throughout the lung, leading to possible air trapping and pneumothorax. Aspirated meconium may further create a reactive infl ammation in the lungs that will hinder gas exchange and may be associated with persistent pulmonary hypertension. This perpetuates the fetal circulation Immediate c are a fter e stablishing a dequate v entilation and c irculation Once an infant is stabilized after resuscitation, the next steps require deliberate consideration. The future course of the infant ’ s resuscitation is related to the degree of cardiorespiratory compromise. Many infants will quickly improve, and develop good lung compliance, adequate pulmonary blood fl ow and spontaneous respiratory drive. In these infants, assisted ventilation can be withdrawn in a matter of minutes. Attention must be paid to the amount of assistance they receive as they improve. There is a tendency to overventilate the recovering infant after a successful resuscitation. Furthermore, some degree of inspired oxygen may be all that is necessary to support the recovering infant after an effective resuscitation. Prolonged a ssisted v entilation Prolonged ventilatory assistance is often linked to the time required to resume spontaneous respirations. Some asphyxiated infants, as well as premature infants, may also demonstrate some degree of lung disease and, hence, may require ventilatory assistance even after the resumption of spontaneous respirations. At times, infants with lung disease start out well on their own, but very shortly require ventilatory assistance, in the form of intermittent mechanical ventilation (IMV) or continuous positive airway pressure (CPAP), to maintain adequate ventilation and oxygenation. Whenever an infant requires prolonged ventilatory support, the infant should be managed by physicians and nurses who are comfortable providing assisted ventilation to infants. The use of arterial blood gases taken from an umbilical arterial catheter or peripheral arterial line should be used to guide further ventilatory management. Dopamine There are times when the severely asphyxiated infant will have suffered so much compromise despite the previous steps in the resuscitation that poor cardiac output and hypertension remain in spite of the volume boluses which were given. For such infants, dopamine should be used. starting at an intravenous infusion rate of 5 µ g/kg/min, increasing, if necessary, to 20 µ g/kg/min. If the dose of 20 µ g/kg/min is reached without improvement, further increases in the infusion rate are unlikely to make a difference. By the time one is far enough into the resuscitation to reach the point at which dopamine is needed, there should have been some consultation with a neonatologist or pediatrician who is experi- enced in taking care of sick newborns. Glucose As soon as the hypoxia has been corrected, an infusion of glucose at about 5 mg/kg/min should be started (approximately 80 cc/kg/ day of 10% glucose). Adjustment of the glucose infusion rate should be made in response to serial, follow - up blood glucose measurements. The asphyxiated infant may have depleted glyco- Neonatal Resuscitation 121 all infants who appear to be improving and then suddenly dete- riorate. The infant with a pneumothorax may present with unequal breath sounds and distant heart sounds, or the heart sounds may be shifted from the normal position in the left side of the chest. The affected side of the chest may appear to be slightly more distended and less mobile with ventilation than the unaffected side. Acute oxygen desaturation and cyanosis may be noted. If the pleural air generates enough tension, cardiac venous return may be impaired. This may result in hypotension due to a signifi cant drop in cardiac output. The signs and symptoms of a pneumothorax are usually easily recognized in the otherwise stable infant who suddenly takes a turn for the worse. A high index of suspicion for early pneumothorax must, however, be maintained in the unstable infant requiring resuscitation, for in this circumstance the signs and symptoms are not as obvious. Diaphragmatic h ernia Congential diaphragmatic hernia undiagnosed before birth is an unusual, but not uncommon, event in the contemporary practice of perinatal medicine. In any infant known or suspected to have a diaphragmatic hernia, one should always use an endotracheal tube for ventilation to prevent gas from entering the intestines. Forcing air into the intestine with bag - and - mask positive - pressure ventilation increases the chances of infl ating the intratho- racic bowel and further compromising pulmonary function. An orogastric tube should be placed as soon as possible to remove as much air as possible from the intestines. Erythroblastosis/ h ydrops The hydropic infant is likely not only to be severely anemic, but also to have marked ascites, pleural effusions and pulmonary edema. These infants are also more likely to be asphyxiated in utero as well as to be born prematurely, adding respiratory distress syndrome to the list of complications. Thus, successful resuscitation of an infant with hydrops demands preparation of a coordinated team with preassigned responsibilities. The team should be prepared at delivery to perform a thoracentesis, paracentesis, and a complete resuscitation, in addition to an immediate partial exchange transfusion, with O - negative blood cross - matched against the mother, if available. Establishment of adequate positive - pressure ventilation with immediate tracheal intubation is essential as poor lung compliance and marked pulmonary edema are the rule in this setting. If adequate ventilation cannot be established and signifi cant abdominal distension is noted, paracentesis with removal of signifi cant ascites will often allow improved diaphragmatic excur- sion and improve ventilation and oxygenation. Consideration should be given to performing a thoracentesis for removal of signifi cant pleural effusions if evidence for signifi cant fl uid accu- mulations exists. Information obtained from prenatal ultrasound examinations can help predict the amount of fl uid present. Careful attention must be paid to the maintenance of pattern and further impairs ventilation and oxygenation of the infant. The management of infants born through meconium - stained amniotic fl uid has represented a controversial area, with varying recommendations over time. Current recommendations [1] take into account recent studies showing no advantages from tracheal suctioning in vigorous, term infants born through meconium - stained amniotic fl uid [38] . The current recommendations are based upon two observations: the presence of meconium of any kind and the baby ’ s level of activity. A vigorous infant is defi ned as an infant with strong respiratory efforts, good muscle tone and a heart rate of > 100/min. Vigorous, term infants born through meconium - stained amniotic fl uid, thick or thin, need not be handled in a special way. If an infant is born through meconium - stained amniotic fl uid and has depressed respirations, depressed muscle tone and/or a heart rate of less than 100/min then the infant should have the mouth and trachea suctioned. The best method to remove meconium from the trachea is to insert an endotracheal tube and attach an adapter so that suction can be directly applied, using regulated wall suction at approximately 100 mmHg, as the tube is withdrawn (Figure 8.8 ). The trachea can then be reintubated and suctioned again, if necessary. One should not try to use a suction catheter inserted through the endotracheal tube to suction meconium. Because some infants with thick meconium - stained amniotic fl uid may be severely asphyxiated, it may not be possible to clear the trachea completely before beginning positive - pressure ventilation. Clinical judgment determines the number of reintuba- tions needed. Pneumothorax Whenever positive - pressure ventilation is used a pneumothorax is a potential problem. A pneumothorax should be suspected in Figure 8.8 Adapter to connect endotracheal tube to mechanical suction. (Reproduced by permission from Textbook of Neonatal Resuscitation . Elk Grove, IL; American Academy of Pediatrics/American Heart Association, 1994, rev. 1996: 5 – 68.) Chapter 8 122 the possibility of a high intestinal obstruction. The same tube can then be removed and inserted into the anal opening. Easy passage of the tube for 3 cm into the anus makes anal atresia unlikely. A minute or so spent screening for congenital defects in this way may help avert many future problems. References 1 American Heart Association . 2005 American Heart Association (AHA) Guidelines for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC) of Pediatric and Neonatal Patients: Neonatal Resuscitation Guidelines . Pediatrics 2006 . www. pediatrics.orgt/cgi/doi/10.1542/peds . 2006 – 0349 2 Kattwinkel J , ed. Textbook of Neonatal Resuscitation , 5th edn. Elk Grove Village, IL : American Academy of Pediatrics , 2006 . 3 Rudolph AM , Yuan S . Response of the pulmonary vasculature to hypoxia and H + ion concentration changes . J Clin Invest 1966 ; 45 : 339 – 411 . 4 Rudolph AM . Fetal cardiovascular response to stress . In: Wiknjosastro WH et al., eds. Perinatology . New York : Elsevier Science , 1988 . 5 Morin CM , Weiss KI . Response of the fetal circulation to stress . In: Polin RA et al., eds. Fetal and Neonatal Physiology . Philadelphia : WB Saunders Co , 1992 : 620 . 6 Downing SE , Talner NS , Gardner TH . Infl uences of arterial oxygen tension and pH on cardiac function in the newborn lamb . Am J Physiol 1966 ; 211 : 1203 – 1208 . 7 Adamsons K , Behrman R , Dawes GS , James LS , Koford CO . Resuscitation by positive pressure ventilation and tris - hydroxy- methylaminomethane of rhesus monkeys asphyxiated at birth . J Pediatr 1964 ; 65 : 807 . 8 Dawes GS . Birth asphyxia, resuscitation, brain damage . In: Foetal and Neonatal Physiology . Chicago : Year Book Medical , 1968 : 141 . 9 Pearlman JM , Risser R . Cardiopulmonary resuscitation in the delivery room: Associated clinical events . Arch Pediatr Adolesc Med 1995 ; 149 : 20 – 25 . 10 Press S , Tellechea C , Prergen S . Cesarean delivery of full - term infants: identifi cation of those at high risk for requiring resuscitation . J Pediatr 1985 ; 106 : 477 – 479 . 11 Miller DL , Oliver TK Jr . Body temperature in the immediate neonatal period: The effect of reducing thermal losses . Am J Obstet Gynecol 1966 ; 94 : 964 – 969 . 12 Bruck K . Temperature regulation in the newborn infant . Biol Neonate 1961 ; 3 : 65 . 13 Adamsons K , Gandy GM , James LS . The infl uence of thermal factors upon oxygen consumption of the newborn human infant . J Pediatr 1965 ; 66 : 495 . 14 Cordero L Jr , Hon EH . Neonatal bradycardia following nasopharyn- geal stimulation . J Pediatr 1971 ; 78 : 441 – 447 . 15 Omar C , Kamlin F , Colm PF et al. Oxygen saturations in healthy infants immediately after birth . J Pediatr 2006 ; 148 : 585 – 589 . 16 Rabi Y , Yee W , Chen SY et al. Oxygen saturation trends immediately after birth . J Pediatr 2006 ; 148 : 590 – 594 . 17 Clark RH , Gerstmann DR , Jobe AH et al. Lung injury in neonates: causes, strategies for prevention and long - term consequences . J Pediatr 2001 ; 139 : 478 – 86 . 18 Dreyfuss D , Soler P , Basset G et al. High infl ation pressure pulmonary edema . Am Rev Respir Dis 1988 ; 137 : 1159 – 1164 . intravascular volume and the prevention of shock, especially after the removal of large amounts of peritoneal or pleural fl uid. A hematocrit obtained in the delivery room will determine the need for an exchange transfusion (usually partial) in the delivery room. If the infant is extremely anemic and in need of immediate oxygen - carrying capacity, catheters should be inserted into both the umbilical artery and vein to permit a slow, isovolemic exchange with packed red cells. This should result in minimal impact on the hydropic infant ’ s already tenuous hemodynamic status. These lines can also be transduced for central venous and central arterial pressures. Then critical information for managing the hydropic infant ’ s volume can be more easily attained. This information is even more essential if large fl uid volumes are removed from either the chest or the abdomen. Screening for c ongenital a nomalies Two to three per cent of infants will be born with a congenital anomaly that will require intervention soon after birth. Those that commonly require some form of immediate intervention include bilateral choanal atresia, congenital diaphragmatic hernia, or aspiration pneumonia as a complication of esophageal atresia or a high intestinal obstruction. A rapid screen for congenital defects can easily be performed by the delivery room staff to help identify many of these defects, as well as those that are not life - threatening but require recognition and intervention. External p hysical e xamination A rapid external physical examination will identify obvious abnormalities such as abnormal facies, and limb, abdominal wall or spinal column defects. A scaphoid abdomen may be a clue to the presence of a diaphragmatic hernia, whereas a two - vessel umbilical cord should alert the examiner to the increased prob- ability of other congenital abnormalities. Internal p hysical e xamination Because infants are preferentially nose breathers, bilateral choanal atresia of the nares will present with respiratory distress and require a secure airway at birth. This defect can be quickly ruled in or out by assessing the infant ’ s ability to breathe with its mouth held closed. Some infants with unilateral choanal atresia will appear normal and only exhibit respiratory distress when the mouth is held closed and the patent nostril is occluded. The inability to insert a soft nasogastric tube, with obstruction noted within 3 – 4 cm, suggests possible choanal atresia. An examination of the mouth will reveal a cleft palate. Insertion of a nasogastric tube may help identify esophageal atresia or a high intestinal obstruction. If the tube does not reach the stomach, an esophageal atresia, commonly associated with a tracheoesoph- ageal fi stula, should be suspected. If the tube passes into the stomach, the contents of the stomach may be aspirated. The presence of 15 – 20 mL of gastric contents on initial aspiration raises Neonatal Resuscitation 123 28 Jobe AH , Kramer BW , Moss TJ et al. Decreased indicators of lung injury with continuous positive expiratory pressure in preterm lambs . Pediatr Res 2002 ; 52 : 387 – 392 . 29 Avery ME , Tooley WH , Keller JB et al. Is chronic lung disease in low birth weight infants preventable? A survey of eight centers . Pediatrics 1987 : 79 : 26 – 30 . 30 Van Marter LJ , Allred EN , Pagano M et al. Do clinical markers of barotrauma and oxygen toxicity explain interhospital variation in rates of chronic lung disease? Pediatrics 2000 ; 105 : 1194 – 1201 . 31 Halamek LP , Morley C . Continuous positive airway pressure during neonatal resuscitation . Clin Perinatol 2006 ; 33 : 83 – 98 . 32 Morley C . New Australian Neonatal Resuscitation Guidelines . J Paediatr Child Health 2007 ; 43 : 6 – 8 . 33 Saugstad OD , Ramji S , Vento M . Oxygen for neonatal resuscitation: How much is enough? Pediatrics 2006 ; 118 : 789 – 792 . 34 Richmond S , Goldsmith JP . Air or 100% oxygen in neonatal resuscitation? Clin Perinatol 2006 ; 33 : 11 – 27 . 35 Saugstad OD , Rootwelt T , Aalen O . Resuscitation of asphyxiated newborn infants with room air or oxygen: An international controlled trial: The Resair 2 Study . Pediatrics 1998 ; 102 : el. www.pediatrics. org/cgi/contnet./full/102/1/el 36 Davis PG , Tan A O ’ Donnell CPF . Resuscitation of newborn infants with 100% oxygen or air: a systematic review and meta - analysis . Lancet 2004 ; 364 : 1329 – 1333 . 37 Canadian NRP Steering Committee . Addendum to the 2006 NRP Provider Textbook: Recommendations for specifi c treatment modifi - cations in the Canadian Context. Updated: Nov 2006. www.cps.ca/ english/proedu/nrp/addendum.pdf 38 Vain NE , Szyld EG , Prudent LM et al. Oropharyngeal and nasopha- ryngeal suctioning of meconium - stained neonates before delivery of their shoulders: multicentre, randomized controlled trial . Lancet 2004 ; 364 : 597 – 602 . 19 Wada K , Jobe AH , Ikegami M . Tidal volume effects on surfactant treatment responses with the initiation of ventilation in preterm lambs . J Appl Physiol 1997 ; 83 ( 4 ): 1054 – 1061 . 20 Bjorklund LJ , Ingimarsson J , Curstedt T et al. Manual ventilation with a few large breaths at birth compromises the therapeutic effect of surfactant replacement in immature lambs . Pediatr Res 1997 ; 42 : 348 – 355 . 21 Dreyfuss D , Saumon G . Ventilator - induced lung injury: lessons from experimental studies . Am J Respir Crit Care Med 1998 ; 157 : 294 – 323 . 22 American Heart Association . 2005 American Heart Association (AHA) Guidelines for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC) of Pediatric and Neonatal Patients: Neonatal Resuscitation Guidelines . Pediatrics 2006 : 3 – 22 . www.pediatrics.orgt/cgi/doi/10.1542/peds.2006 - 0349 23 Musceedere JG , Mullen JBM , Gan K , Slutsky AS . Tidal ventilation at low airway pressure can augment lung injury . Am J Respir Crit Care Med 1994 ; 149 : 1327 – 1234 . 24 Tremblay L , Valenza F , Ribeiro SP et al. Injurious ventilatory strategies increase cytokines and c - fos M - RNA expression in an isolated rat lung model . J Clin Invest 1997 ; 99 : 944 – 952 . 25 Dreyfuss D , Saumon G . Role of tidal volume, FRC and end - inspiratory volume in the development of pulmonary edema following mechanical ventilation . Am Rev Respir Dis 1993 ; 148 : 1194 – 1203 . 26 Frose AB , McCulloch P , Sugiura M et al. Optimizing alveolar expan- sion prolongs the effectiveness of exogenous surfactant theapy in athe adult rabbit . Am Rev Respir Dis 1993 : 148 : 569 – 577 . 27 Michna J , Jobe AH , Ikegami M . Positive end - expiratory pressure pre- serves surfactant function in preterm lambs . J Appl Physiol 1999 ; 160 : 634 – 649 . 124 Critical Care Obstetrics, 5th edition. Edited by M. Belfort, G. Saade, M. Foley, J. Phelan and G. Dildy. © 2010 Blackwell Publishing Ltd. 9 Ventilator Management in Critical Illness Luis D. Pacheco 1 & Labib Ghulmiyyah 2 1 Departments of Obstetrics, Gynecology and Anesthesiology, Maternal - Fetal Medicine - Surgical Critical Care, University of Texas Medical Branch, Galveston, TX, USA 2 Maternal – Fetal Medicine, Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston, TX, USA Introduction Respiratory failure remains one of the leading causes of maternal mortality [1,2] . Thromboembolism, amniotic fl uid embolism, and venous air embolism together account for approximately 20% of maternal deaths. Other causes of respiratory failure prob- ably account for a further 10 – 15% of maternal deaths [1] . Not only does maternal respiratory failure affect the mother but it also contributes heavily to fetal morbidity and mortality. This chapter reviews the general principles of airway management in the gravid patient with respiratory failure. In addition, it will provide the reader with information to facilitate a timely recognition and management of respiratory compromise and describes the most recent advances in mechanical support. Respiratory f ailure Respiratory failure is a syndrome that develops when one or both functions of the respiratory system (oxygenation (O 2 ) and carbon dioxide (CO 2 ) elimination) fail. Respiratory failure is classifi ed as either hypoxemic or hypercapnic. Hypoxemic respiratory failure is characterized by an arterial partial pressure oxygen (P a O 2 ) of less than 60 mmHg with a normal or low arterial partial pressure of carbon dioxide (P a CO 2 ). On the other hand, hypercapnic respiratory failure is characterized by a P a CO 2 of more than 50 mmHg. The most commonly encountered causes of acute respiratory failure in pregnancy are listed in Table 9.1 . Hypoxemic respiratory failure is the most frequently seen of these. It is important to remember that respiratory failure during pregnancy leads to a decrease in oxygen delivery not only to the mother but also to the fetus. Ventilation/ p erfusion ( V / Q ) m ismatch Shunt ( Q S / Q T ) The V/Q ratio, otherwise known as the alveolar ventilation/pulmonary perfusion ratio, determines the adequacy of gas exchange in the lung. When alveolar ventilation matches pulmonary blood fl ow, CO 2 is eliminated and the blood becomes fully saturated with oxygen. However, a mismatch of ventilation to perfusion (V A /Q) is a major cause of lung dysfunction [3] . When the V/Q ratio decreases ( < 1), arterial hypoxemia occurs. As the mismatch worsens, the resultant hyperventilation produces either a low or normal arterial partial pressure of CO 2 (P a CO 2 ). The hypoxemia caused by low V/Q areas is responsive to supplemental oxygen administration. The lower the V/Q ratio, the higher the inspired fraction of oxygen (F i O 2 ) required to raise the arterial partial pressure of oxygen (P a O 2 ). The most extreme case of V/Q mismatching (V/Q ratio = 0) is known as intrapulmonary shunting. Oxygenation does not occur in an area of the lung without ventilation even in the face of normal perfusion. This perfused but non - ventilated area of the lung is known as a shunt. The shunt fraction (Q S /Q T ) is the total amount of pulmonary blood fl ow that perfuses non - ventilated areas of the lung. In normal lungs, the value of the shunt fraction is 2 – 5% [4] . A shunt of 10 – 15% is evidence of signifi cant impairment in oxygenation. A shunt fraction of > 25%, in spite of therapy, suggests active acute respiratory distress syndrome (ARDS). The P a O 2 /F i O 2 ratio is a sometimes used as indicator of gas exchange. A P a O 2 /F i O 2 < 200 correlates with a shunt fraction greater than 20% and is indicative of ARDS. A P a O 2 /F i O 2 of between 200 and 300 is termed acute lung injury (ALI) and suggests marginal lung function. The causes of pulmonary shunting include alveolar consolida- tion or edema, alveolar collapse and atelectasis, and anatomic right to left shunt (e.g. thebesian veins, septal defects). The shunt fraction (Q S /Q T ) can be calculated using the following formula: Q Q CO CO CO CO ST c a c v =− () − () 22 22 Ventilator Management in Critical Illness 125 is the major factor in determining blood oxygen content. P a O 2 changes with position and age, and is increased during pregnancy [5,6] . Pulmonary disorders that impair oxygen exchange affect P a O 2 . These include impaired diffusion, increased shunt, and ventilation/perfusion mismatch. The degree of mixed venous oxygen saturation also affects P a O 2 especially in the presence of an increased shunt [3] . Hypercarbia also affects the P a O 2 (especially when breathing room air), since CO 2 displaces oxygen. Alveolar – a rterial o xygen t ension g radient The alveolar – arterial oxygen tension gradient (P (A – a) O 2 ) is a sensi- tive measure of impairment of oxygen exchange from lung to blood [3] . Alveolar – oxygen tension (P a O 2 ) is estimated as: PO P P FO PCO RQ aBHOia2222 =− () ×− where P B is barometric pressure, P H2O is water vapor pressure, and RQ is the respiratory quotient. The alveolar – arterial oxygen tension gradient (P (A – a) O 2 ) is equal to: PO PO aa22 − Under the clinical circumstances where the P a O 2 value is less than 60 mmHg, and especially when oxygen therapy is administered, it is acceptable to discount the respiratory quotient dispar- ity and use the simplifi ed version of the ideal alveolar gas equation: PO P P FO PCO aBHOia2222 =− () ×− This is best measured when the patient is breathing 100% oxygen [3] ). Under these circumstances, the alveolar – arterial oxygen tension gradient is less than 50 torr on when the F i O 2 is 1.0 (or less than 30 torr on room air). Oxygen d elivery and c onsumption All tissues require oxygen for the combustion of organic com- pounds to fuel cellular metabolism. The cardiopulmonary system serves to deliver a continuous supply of oxygen and other essential substrates to tissues. Oxygen delivery is dependent upon oxygenation of blood in the lungs, the oxygen - carrying capacity of the blood, and the cardiac output [7] . Under normal conditions, oxygen delivery (DO 2 ) exceeds oxygen consumption (VO 2 ) by about 75% [8] . DO CO C O normal range mL a22 10 700 1400=× × =− () min Arterial oxygen content (C a O 2 ) is determined by the amount of oxygen that is bound to hemoglobin (S a O 2 ) and by the amount of oxygen that is dissolved in plasma (P a O 2 × 0.0031): C c O 2 is the oxygen content of pulmonary capillary blood. Directly measuring pulmonary capillary blood (CcO 2 ) is diffi cult; therefore, CcO 2 is assumed to be 100% when F i O 2 equals 1. Therefore, using an F i O 2 of 1.0 (100%) simplifi es the calculation of the shunt fraction [3] . C a O 2 is the oxygen content of arterial blood. C v O 2 is the oxygen content of mixed venous blood. Dead s pace It is normal for a small percentage of air in the lungs not to reach the blood. The lung is ventilated but not perfused, creating what is known as “ dead space ” . Air in the nasopharynx, trachea and bronchi does not reach the alveoli before exhalation. Too much dead space, however, can lead to hypoxia. The portion of tidal volume (V t ) that is dead space (V d ) is calculated as a ratio, V d /V t ( ∼ 0.30) and can be calculated by the following formula: V V PCO PCO PCO dt a e a =− () 222 where P e CO 2 is CO 2 in exhaled gas. P e CO 2 is measured by collecting expired gas in a large collection bag and using an infrared CO 2 analyzer to measure the PCO 2 . Causes of increased dead space include shallow breathing, vascular obstruction, pulmonary hypertension, pulmonary emboli, low cardiac output, hypovolemia, ARDS, impaired perfusion, positive - pressure ventilation, and increased airway pressure. Acute increases in physiologic dead space signifi cantly increase ventilatory requirements and may result in respiratory acidosis and ventilatory failure. Increased dead space may impose higher minute ventilation, and hence higher work of breathing. A dead space to tidal volume ratio > 0.6 usually requires mechanical ventilatory assistance [3] . Arterial o xygen t ension ( P a O 2 ) P a O 2 is a measure of the amount of oxygen dissolved in plasma. P a O 2 determines the percentage saturation of hemoglobin, which Table 9.1 Causes of lung injury and acute respiratory failure in pregnancy. Hypoxic Thromboembolism Amniotic fl uid embolism Venous air embolism Pulmonary edema Aspiration of gastric contents Pneumonia Pneumothorax Acute respiratory distress syndrome (ARDS) Hypercapnic/hypoxic Asthma Drug overdose Myasthenia gravis Guillain – Barr é syndrome Chapter 9 126 globin is altered structurally in such a fashion as to have a diminished affi nity for oxygen [9] . It must be kept in mind that the amount of oxygen actually available to the tissues is also affected by the affi nity of the hemoglobin molecule for oxygen. Thus, when attempts are made to maximize oxygen delivery one must consider the oxyhemoglobin dissociation curve (Figure 9.1 ) and those conditions that infl u- ence the binding of oxygen either negatively or positively must be considered [10] . An increase in the plasma pH level, a decrease in temperature or a decrease in 2,3 - diphosphoglycerate (2,3 - DPG) will increase hemoglobin affi nity for oxygen, shifting the oxyhemoglobin dissociation curve to the left ( “ left shift ” ) and resulting in diminished tissue oxygenation. If the plasma pH level falls or temperature rises, or if 2,3 - DPG increases, hemoglobin affi nity for oxygen will decrease ( “ right shift ” ) and more oxygen will be available to tissues [10] . In certain clinical conditions, such as septic shock and ARDS, there is maldistribution of blood fl ow relative to oxygen demand, leading to diminished delivery and consumption of oxygen. The release of vasoactive substances is hypothesized to result in the loss of normal mechanisms of vascular autoregulation, producing regional and microcirculatory imbalances in blood fl ow [11] . This mismatching of blood fl ow with metabolic demand causes hyperperfusion to some areas, and relative hypoperfusion to others, limiting optimal systemic utilization of oxygen [11] . The patient with diminished cardiac output secondary to hypovolemia or pump failure is unable to distribute oxygenated blood to the tissues. Therapy directed at increasing volume with normal saline, or with blood if the hemoglobin level is less than 10 g/dL, increases oxygen delivery in the hypovolemic patient. The patient with pump failure may benefi t from inotropic support and afterload reduction in addition to supplementation of intravascular volume. It is taken for granted that in such patients every effort will be made to ensure adequate oxygen saturation of the hemoglobin by optimizing ventilatory parameters. C O Hgb S O P O normal range mL O d aaa222 2 1 34 0 0031 16 22 =×× () +× ()( =− LL ) . It is clear from the above formula that the amount of oxygen dissolved in plasma is negligible (unless the patient is receiving hyperbaric oxygen therapy) and, therefore, the arterial oxygen content is largely dependent on the hemoglobin concentration and the arterial oxygen saturation. Oxygen delivery can be impaired by conditions that affect cardiac output (fl ow), arterial oxygen content, or both (Table 9.2 ). Anemia leads to a low arterial oxygen content because of a lack of hemoglobin binding sites for oxygen. Likewise, carbon monoxide poisoning will decrease oxyhemoglobin because of blockage of the oxygen binding sites. The patient with hypoxemic respiratory failure will not have suf- fi cient oxygen available to saturate the hemoglobin molecule. Furthermore, it has been demonstrated that desaturated hemo- Table 9.2 Causes of impaired oxygen delivery. Low arterial oxygen content Anemia Hypoxemia Carbon monoxide Hypoperfusion Shock Hemorrhagic Cardiogenic Distributive Septic Anaphylactic Neurogenic Obstructive Tamponade Massive pulmonary emboli Hypovolemia 100 90 80 70 60 50 40 30 20 10 0 10 20 30 40 50 60 70 80 90 100 pH DPG Temp pH DPG Temp { { O 2 tension (mmHg) P 50 Percent oxyhemoglobin Figure 9.1 The oxygen - binding curve for human hemoglobin A under physiologic conditions (middle curve). The affi nity is shifted by changes in pH, diphosphoglycerate (DPG) concentration, and temperature, as indicated. P 50 represents the oxygen tension at half saturation. (Reproduced by permission from Bunn HF, Forget BG: Hemoglobin: Molecular, Genetic, and Clinical Aspects . Philadelphia, Saunders, 1986.) Ventilator Management in Critical Illness 127 Assessing o xygenation Arterial blood gas (ABG) sampling is performed to obtain accurate measures of P a O 2 , P a CO 2 , blood pH and oxygen saturation. Usually, the radial artery is used. Arterial blood gas values differ in pregnancy compared with non - pregnant values [21] (Table 9.3 ). Interpreting the ABG is useful for identifying respiratory and metabolic derangements. Measuring P a O 2 is required for cal- culating P (A – a) O 2 . In addition, acid – base disturbances can be diag- nosed [22] . An indwelling arterial line is useful for obtaining arterial blood gas measurements and monitoring blood pressure when patients are receiving ventilatory support. However, arterial oxygen saturation can be assessed continuously and non - invasively by pulse oximetry. End - tidal CO 2 can also be measured non - invasively. Pulse o ximetry Transcutaneous pulse oximetry estimates O 2 saturation (S P O 2 ) of capillary blood based on the absorption of light from light - emit- ting diodes positioned in a fi nger clip or adhesive strip probe. The usual sites for measurement are the ear lobe or the fi nger nail bed. Oxyhemoglobin absorbs much less red and slightly more infrared light than reduced hemoglobin. The degree of oxygen saturation of the hemoglobin thereby determines the ratio of red to infrared light absorption. The estimates are generally very accurate and correlate to within 2% of measured arterial O 2 saturation (S a O 2 ) [23] . Results may be less accurate in patients with highly pigmented skin, those wearing nail polish, and those with arrhythmias or hypotension, in whom the amplitude of the signal may be dampened. Hyperbilirubinemia and severe anemia may lead to oximetry inconsistencies [3] . Carbon monoxide poisoning will lead to an overestimation of the P a O 2 . In addition, if methemoglobin levels reach greater than 5%, the pulse oximeter no longer accurately predicts oxygen saturation. When assessing the accuracy of the arterial saturation measured by the pulse oximeter, correlation of the pulse rate determined by the oximeter and the patient ’ s heart rate is an indication of proper placement of the electrode. Pulse oximetry is ideal for non - invasive monitoring of the arterial oxygen saturation near the steep portion of the oxygen hemoglobin dissociation curve, namely at a P a O 2 of 70 torr [3] . P a O 2 levels of 80 torr result in very small changes in oxygen saturation, namely 97 – 99%. Large changes in the P a O 2 value in the range of 90 torr to a possible 600 torr can occur without signifi - cant change in arterial oxygen saturation (Figure 9.1 ). This Relationship of o xygen d elivery to c onsumption Oxygen consumption (VO 2 ) is the product of the arteriovenous oxygen content difference (C a – v O 2 ) and cardiac output. Under normal conditions, oxygen consumption is a direct function of the metabolic rate [12] . VO C O CO normal range mL av22 10 180 280=×× =− () − min . The oxygen extraction ratio (OER) is the fraction of delivered oxygen that actually is consumed: OER VO DO= 22 The normal oxygen extraction ratio is about 25%. A rise in OER is a compensatory mechanism employed when oxygen delivery is inadequate for the level of metabolic activity. A sub- normal value suggests fl ow maldistribution, peripheral diffusion defects, or functional shunting [12] . As the supply of oxygen is reduced, the fraction extracted from the blood increases and oxygen consumption is maintained. If a severe reduction in oxygen delivery occurs, the limits of O 2 extraction are reached, tissues are unable to sustain aerobic energy production, and consumption decreases. The level of oxygen delivery at which oxygen consumption begins to decrease has been termed the “ critical DO 2 ” [13,14] . At the critical DO 2 , tissues begin to use anerobic glycolysis, with resultant lactate production and metabolic acidosis [13] . If this oxygen deprivation continues, irreversible tissue damage and death ensue. Oxygen d elivery and c onsumption in p regnancy The physiologic anemia of pregnancy results in a reduction in the hemoglobin concentration and arterial oxygen content. Oxygen delivery is maintained at or above normal in spite of this because of the 50% increase that occurs in cardiac output. It is important to remember, therefore, that the pregnant woman is more dependent on cardiac output for maintenance of oxygen delivery than is the non - pregnant patient [15] . Oxygen consumption increases steadily throughout pregnancy and is greatest at term, reaching an average of 331 mL/min at rest and 1167 mL/min with exercise [16] . During labor, oxygen consumption increases by 40 – 60% and cardiac output increases by about 22% [17,18] . Because oxygen delivery normally far exceeds consumption, the normal pregnant patient is usually able to maintain adequate delivery of oxygen to herself and her fetus even during labor. When a pregnant patient has low oxygen delivery, however, she very quickly can reach the critical DO 2 during labor, compromising both herself and her fetus. Pre - eclampsia is known to have a signifi - cantly adverse effect on oxygen delivery and consumption, a con- dition that is believed to result from a tissue level disturbance that makes oxygen consumption dependent on oxygen delivery, i.e. there is loss of the normal reserve [19,20] . The obstetrician, therefore, must make every effort to optimize oxygen delivery before allowing labor to begin in the compro- mised patient. Table 9.3 Arterial blood gas values in the pregnant and non - pregnant woman. Status pH P a O 2 (mmHg) P CO 2 (mmHg) Non - pregnant 7.4 93 35 – 40 Pregnant 7.4 100 – 105 30 Chapter 9 128 well tolerated and is not a threat to the organs unless accompa- nied by severe acidosis (pH < 7.2). Hypoxemia is treated by increasing the fraction of inspired oxygen (F i O 2 ) while attempting to correct the underlying problem. Disorders causing increased shunting, such as atelectasis and bronchial pneumonia, can usually be treated effectively with pulmonary toilet, position change, and antibiotic therapy. Since ventilation perfusion mismatching is frequently a component of hypoxemia, an increase in F i O 2 usually results in some improvement in oxygenation [3] . Table 9.4 lists some available non - invasive oxygen delivery systems and the approximate F i O 2 obtained with each [24] . When the shunt is large ( > 25%), increasing F i O 2 does not signifi cantly improve P a O 2 . This clinical situa- tion usually arises in conditions such as ARDS or cardiogenic pulmonary edema, and in such cases mechanical ventilation is indicated. Continuous p ositive a irway p ressure ( CPAP ) Continuous positive airway pressure (CPAP) is the most widely used method of non - invasive positive pressure ventilatory support. This method consists of a continuous high fl ow of gas and an expiratory resistance valve attached to a tight - fi tting mask. Airway pressure in CPAP is consistently higher than atmospheric pressure even though all of the patient ’ s breaths are spontaneous. The fl ow of air creates enough pressure during inhalation to keep the airway patent. The best CPAP level is one in which oxygenation is adequate and there is no evidence of depressed cardiac function and carbon dioxide retention. CPAP prevents the development of alveolar collapse and increases the pressure in the small airways (including those in which the critical closing pressure has been elevated) thus increasing functional residual capacity. CPAP has the advantages of convenience, lower cost, and morbidity - sparing potential when compared with standard invasive positive - pressure ventilation. Unfortunately, CPAP also suffers from the disadvantage of a heightened risk of volutrauma and hypotension. An additional problem is the potential for developing pressure sores from the tight - fi tting mask [25] . Non - i nvasive p ositive - p ressure v entilation Another type of non - invasive ventilation is called non - invasive positive - pressure ventilation (NPPV). In contrast to CPAP, which does not provide ventilatory assistance and which applies a sustained positive pressure, non - invasive positive - pressure ventilation delivers intermittent positive airway pressure through the upper airway and actively assists ventilation [25] . Non - invasive positive - pressure ventilation requires patient cooperation [26] . Patients must learn to coordinate their breathing efforts with the ventilator so that spontaneous breathing is assisted even during sleep. This type of ventilatory assistance is particularly effi cacious in treating patients with chronic obstructive sleep apnea. Non - invasive approaches have been most effective for managing episodes of acute respiratory failure in which rapid improvement is expected such as during episodes of cardiogenic technique, therefore, is useful as a continuous monitor of the adequacy of blood oxygenation and not as a method to quantitate the level of impaired gas exchange. Mixed v enous o xygenation The mixed venous oxygen tension (P V O 2 ) and mixed venous oxygen saturation (S V O 2 ) are parameters of tissue oxygenation [12] . Normally, the P V O 2 is 40 mmHg with a saturation of 73%. Saturations less than 60% are abnormally low. These parameters can be measured directly by obtaining a blood sample from the distal port of the pulmonary artery catheter when the catheter tip is well positioned for a wedge pressure reading and the balloon is not infl ated (distal pulmonary artery branches). The S V O 2 also can be measured continuously with a special fi beroptic pulmonary artery catheter. Mixed venous oxygenation is a reliable parameter in the patient with hypoxemia or low cardiac output, but fi ndings must be interpreted with caution. When the S V O 2 is low, oxygen delivery can be assumed to be low. However, normal or high S V O 2 does not guarantee that tissues are well oxygenated. In conditions such as septic shock and ARDS, the maldistribution of systemic fl ow may lead to abnormally high S V O 2 in the face of severe tissue hypoxia [11] . The oxygen dissociation curve must be considered when interpreting the S V O 2 as an indicator of tissue oxygenation [9] (Figure 9.1 ). Conditions that result in a left shift of the curve cause the venous oxygen saturation to be normal or high, even when the mixed venous oxygen content is low. The S V O 2 is useful for monitoring trends in a particular patient, as a signifi cant decrease will occur when oxygen delivery has decreased secondary to hypoxemia or a fall in cardiac output. Impairment of o xygenation A decrease in arterial oxygen saturation (P a O 2 ) below 90% is one defi nition of hypoxemia. However, the degree to which the alveolar – arterial oxygen tension gradient is increased is a more accurate measurement of the degree of impairment. A shunt of greater than 20% refl ects respiratory failure. This degree of shunt will result in an alveolar – arterial oxygen tension gradient of greater than 400 torr [3] . It is important to understand the interrelation- ship between shunt, the level of mixed venous oxygen saturation, and the arterial oxygen saturation. As more oxygen is extracted from the blood, the mixed venous oxygen saturation decreases resulting in a lower P a O 2 (depending on the severity of the shunt). Therefore, a marked change in P a O 2 can occur in the absence of any change in lung pathology [3] . Therapy Hypoxemia is a major threat to normal organ function. Therefore, the fi rst goal is to reverse and/or prevent tissue hypoxia. The goal is to assure adequate oxygen delivery to tissues, and this is generally achieved with a P a O 2 of 60 mmHg or arterial oxygen saturation (S a O 2 ) of greater than 90%. Isolated hypercapnia is usually . Pacheco 1 & Labib Ghulmiyyah 2 1 Departments of Obstetrics, Gynecology and Anesthesiology, Maternal - Fetal Medicine - Surgical Critical Care, University of Texas Medical Branch, Galveston,. . 124 Critical Care Obstetrics, 5th edition. Edited by M. Belfort, G. Saade, M. Foley, J. Phelan and G. Dildy. © 2010 Blackwell Publishing Ltd. 9 Ventilator Management in Critical Illness. delivery at which oxygen consumption begins to decrease has been termed the “ critical DO 2 ” [13 ,14] . At the critical DO 2 , tissues begin to use anerobic glycolysis, with resultant lactate