Critical Care Obstetrics part 14 ppsx

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

solution of epinephrine be used via the endotracheal route If epinephrine is given via an umbilical venous catheter, the recom-mended 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 epi-nephrine 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 admin-istered intramuscularly, but this route of administration is associ-ated with a delayed onset of action

It is important to note that the duration of action of the nal-oxone may be signifi cantly shorter than the duration of action of the narcotic analgesic Therefore, repeated doses may be neces-sary 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

com-pression Thus, in a 2 - second period, 3 compressions and 1

breath are given This provides 90 compressions and 30

respira-tions in each minute Intermittently, chest compressions should

be stopped to check for a spontaneous heart rate If the

spontane-ous 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

place-ment The umbilical catheter is inserted slightly past the level of

the skin – only to the point where blood is fi rst able to be

aspi-rated 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

bra-dycardia 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

gen stores, especially myocardial glycogen stores, and it is impor-tant to provide fuel to such an infant The glucose infusion also prevents the hypoglycemia that is frequently associated with peri-natal compromise

Fluids

The urine output of any infant undergoing an episode of depres-sion 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 ade-quate 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 con-centration 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 develop-ment 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 intracerecere-bral 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

compro-mise 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

assis-tance 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

inter-mittent 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-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 pneumo-thorax 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 - pres-sure 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

dis-tress 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 compli-ance 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 sig-nifi 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

amni-otic 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

approxi-mately 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

venti-lation 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.)

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

pres-ence of 15 – 20 mL of gastric contents on initial aspiration raises

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

resuscita-tion? 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

strate-gies 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

Critical Care Obstetrics, 5th edition Edited by M Belfort, G Saade,

M Foley, J Phelan and G Dildy © 2010 Blackwell Publishing Ltd.

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

respi-ratory 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

respira-tory 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/pul-monary 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

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:

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

ven-tilation/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:

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:

Under the clinical circumstances where the P a O 2 value is less than 60 mmHg, and especially when oxygen therapy is adminis-tered, it is acceptable to discount the respiratory quotient dispar-ity and use the simplifi ed version of the ideal alveolar gas equation:

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 essen-tial substrates to tissues Oxygen delivery is dependent upon oxy-genation 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]

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:

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,

vas-cular 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

ven-tilatory 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

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

globin is altered structurally in such a fashion as to have a dimin-ished 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 hemo-globin 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

mL O d

a 2 a 2 a 2

2

16 22

= −

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

arte-rial 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

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

pH DPG Temp

pH DPG Temp

{

{

O 2 tension (mmHg)

P50

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.)

Assessing o xygenation

Arterial blood gas (ABG) sampling is performed to obtain accu-rate 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 - inva-sively 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 infra-red light than infra-reduced hemoglobin The degree of oxygen satura-tion of the hemoglobin thereby determines the ratio of red to infrared light absorption The estimates are generally very accu-rate and correlate to within 2% of measured arterial O 2 saturation

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 poison-ing 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 mea-sured by the pulse oximeter, correlation of the pulse rate deter-mined 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]

satu-ration, 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]

The oxygen extraction ratio (OER) is the fraction of delivered

oxygen that actually is consumed:

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

con-sumption decreases The level of oxygen delivery at which oxygen

consumption begins to decrease has been termed the “ critical

glycolysis, with resultant lactate production and metabolic

acido-sis [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

depen-dent 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

preg-nant 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)

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 pul-monary toilet, position change, and antibiotic therapy Since ven-tilation perfusion mismatching is frequently a component of hypoxemia, an increase in F i O 2 usually results in some improve-ment 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%), increas-ing F i O 2 does not signifi cantly improve P a O 2 This clinical situa-tion usually arises in condisitua-tions 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 oxygen-ation is adequate and there is no evidence of depressed cardiac function and carbon dioxide retention CPAP prevents the devel-opment of alveolar collapse and increases the pressure in the small airways (including those in which the critical closing pres-sure has been elevated) thus increasing functional residual capac-ity CPAP has the advantages of convenience, lower cost, and morbidity - sparing potential when compared with standard inva-sive 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 ven-tilation 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 breath-ing efforts with the ventilator so that spontaneous breathbreath-ing is assisted even during sleep This type of ventilatory assistance is particularly effi cacious in treating patients with chronic obstruc-tive sleep apnea

Non - invasive approaches have been most effective for manag-ing episodes of acute respiratory failure in which rapid improve-ment 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

pulmo-nary 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

second-ary 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

alve-olar – arterial oxygen tension gradient is increased is a more

accu-rate 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

gener-ally achieved with a P a O 2 of 60 mmHg or arterial oxygen

satura-tion (S a O 2 ) of greater than 90% Isolated hypercapnia is usually