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 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
Chapter 8
120
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 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 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-
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 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.)
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
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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 .
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ion concentration changes . J Clin Invest 1966 ; 45 :
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7 Adamsons K , Behrman R , Dawes GS , James LS , Koford CO .
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10 Press S , Tellechea C , Prergen S . Cesarean delivery of full - term infants:
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11 Miller DL , Oliver TK Jr . Body temperature in the immediate neonatal
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geal stimulation . J Pediatr 1971 ; 78 : 441 – 447 .
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infants immediately after birth . J Pediatr 2006 ; 148 : 585 – 589 .
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after birth . J Pediatr 2006 ; 148 : 590 – 594 .
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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
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 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 .
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 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
(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 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:

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 adminis-
tered, 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 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] .

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, 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.

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 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.

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 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 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 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 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
(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 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] .
P
a
O
2
levels of 80 torr result in very small changes in oxygen 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] .

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 con-
sumption 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 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)

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 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 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 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 breathing 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