This document discusses obstetrical anesthesia and the physiological changes that occur during pregnancy. It notes that pregnancy causes changes to nearly all organ systems and outlines specific alterations to the respiratory, cardiovascular, hematologic, coagulation, hepatic, renal, gastrointestinal and central nervous systems. It also discusses the implications of these changes for providing safe anesthesia during labor and delivery, including considerations for fetal monitoring, pain management and neonatal resuscitation using the Apgar score.

1. OBSTETRICAL ANESTHESIA

2. OBSTETRICAL ANESTHESIA
• The anesthetic and analgesic management of
a pregnant patient will present unique
challenges for the anesthetist.
• The physiologic changes of pregnancy and the
potential effects on the fetus must be
considered when providing anesthesia for the
pregnant patient.
2

3. OBSTETRICAL ANESTHESIA
• Virtually all organ systems of the pregnant patient
are influenced by the hormonal changes of
pregnancy and/or the effects caused by the mass
of the gravid uterus.
• An understanding of the physiologic changes of
pregnancy and the potential for uteroplacental
transfer of drugs to the fetus will assist the
anesthetist in providing safe anesthesia for the
mother along with protection of the fetus.
3

4. Alterations in Maternal Physiology
• Respiratory
– Increased O2 consumption
– Decreased FRC and pCO2 (increased MV)
• Cardiovascular
– Cardiovascular changes begin 5-8 weeks into the pregnancy
– Increased blood volume and CO
– Dilutional anemia
– Possible aorto-caval compression (when supine)
– Heart rate usually increases about 15%.
– Systemic vascular resistance (SVR) decreases about 21%.
– Central venous pressure (CVP) usually remains normal throughout
pregnancy.
– Stroke volume increases about 30%.

5. SUPINE HYPOTENSIVE SYNDROME
• Supine hypotensive syndrome results from
occlusion of the inferior vena cava by the
gravid uterus which reduces right atrial
pressure and leads to hypotension.
• Supine hypotensive syndrome may begin to
develop in the second trimester. Incidence is
greater in twin pregnancies.
5

6. SUPINE HYPOTENSIVE SYNDROME
• Most women compensate for the decrease in
right heart filling by increasing heart rate and
increasing systemic vascular resistance.
• Compensation is frequently inadequate
causing about 10% of patients to become
symptomatic when supine.
6

7. SUPINE HYPOTENSIVE SYNDROME
• Symptoms of supine hypotensive syndrome:
• Hypotension
• Diaphoresis
• Nausea and vomiting
• Light-headedness
• Fetal distress
7

8. AORTOCAVAL COMPRESSION
• The gravid uterus may compress the aorta
which will cause uterine artery hypotension.
• A reduction in uteroplacental perfusion will
result in fetal distress even though maternal
brachial blood pressure remains normal.
8

9. AORTOCAVAL COMPRESSION
• Compression of the aorta and inferior vena
cava can be relieved by maintaining the
patient in a lateral tilt position or side lying
position.
• Usually the left lateral position is most
effective but a small percentage of patients
will have a better response to right tilt.
9

10. 10

11. 11

12. ANESTHETIC IMPLICATIONS OF SUPINE
HYPOTENSION SYNDROME
• Neuraxial anesthesia interferes with normal
compensation of the circulatory insufficiency
caused by aortocaval compression.
• Management includes generous fluid preload,
lateral tilt and possibly the titrated
administration of ephedrine.
12

13. HEMATOLOGIC CHANGES
• Red cells increase about 20% during pregnancy.
• Plasma volume increases between 45 and 50% as a
result of sodium retention.
• The greater increase in plasma volume compared to
the red cell increase leads to the relative “dilution
anemia” of pregnancy.
• The increase in plasma volume results in a decrease in
blood viscosity by approximately 20%.
• Hematocrit and hemoglobin are maintained at low
normal levels, averaging 35% HCT and 12gm Hgb.
13

14. COAGULATION
• Pregnancy induces a “hypercoaguable state” as a
result of increases in several clotting factors
(7,8,10).
• Fibrinogen level is elevated as much as 50% at
term making the pregnant patient susceptible to
the development of venous thrombosis.
• Fibrinogen levels which would be considered
normal in the non-pregnant patient may indicate
a deficiency in the pregnant patient.
14

15. HEPATIC CHANGES
• Most hepatic changes are minor, there is an
slight increase in liver enzymes at term.
• Albumin concentration is reduced which may
elevate levels of circulating free drug.
• Cholinesterase synthesis is reduced with
reductions of 20-30% during the first and
second trimesters.
15

16. RENAL CHANGES
• Mechanical obstruction caused by the gravid uterus and the relaxant
effect of progesterone will cause a progressive dilation of the ureters
beginning at twelve weeks.
• The increase in blood volume and cardiac output will induce a 50%
increase in glomerular filtration rate (GFR) and renal blood flow (RBF).
• Reduction of blood urea nitrogen (8-9mg/dl) and creatinine levels (0.5-
0.6mg/dl) are a result of the increased GFR and RBF.
• Small amounts of glucosuria and proteinuria are common during
pregnancy. Proteinuria greater than 300mg/day indicates potential PIH.
• Creatinine and BUN should be low during pregnancy. If lab studies reveal
normal (non-pregnant) levels of BUN and creatinine, pathology should be
suspected.
16

17. GASTROINTESTINAL CHANGES
• The enlarging uterus progressively displaces the stomach and intestines in
a cephalad direction which increases gastric pressure.
• Elevated progesterone levels reduce lower gastro-esophageal sphincter
(GES) tone and decrease gastric motility.
• An increased level of gastrin during pregnancy causes a reduction of
gastric pH and an increase in gastric volume.
• After delivery, several weeks are required for pregnancy induced
gastrointestinal changes to return to pre-pregnancy state.
17

18. GASTROINTESTINAL CHANGES
• Increased intragastric pressure
• Increased gastric acid production (low pH)
• Delayed gastric emptying (full stomach)
• Reduction of lower GES tone (reflux)
• The GI changes of pregnancy place the patient
at increased risk for aspiration. Always treat
the pregnant patient as having a full stomach.
18

19. ACID ASPIRATION PROPHYLAXIS
• The goal of prophylaxis is to decrease gastric
volume and increase the gastric pH.
• Raise gastric pH – administer non-particulate
antacid such as sodium citrate 30ml. The
effects of sodium citrate will last about two
hours.
19

20. ACID ASPIRATION PROPHYLAXIS
• Decrease acid secretion – administer H2
blocker such as famotidine 20mg
• Increase gastric motility and increase lower
GES tone – administer prokinetic, dopamine
antagonist such as metoclopromide 5-10mg
• Avoid general anesthesia when ever possible.
20

21. BLOOD GAS ANALYSIS
• PaCO2 26-32 mmHg – low, reflecting
hyperventilation (normal 35-40)
• PaO2 92-106 mmHg – normal, room air (normal
95-100)
• Arterial pH 7.44 – slight alkalosis (normal
7.38-7.44)
• Bicarb 16-21mEq/L – low, compensatory bicarb
excretion (normal 22-27)
21

22. ANESTHETIC IMPLICATIONS OF RESPIRATORY
CHANGES
• Increased incidence of difficult intubation, always have multiple plans
prepared. Consider awake fiberoptic intubation if significant difficulty is
anticipated or identified in patient history.
• Rapid development of hypoxia during periods of apnea due to decreased
FRC and increased oxygen demand.
• Prolonged pre-oxygenation with 100% oxygen before induction.
• Head up position, possibly use a modified “head elevated laryngoscopy
position”.
• Minimize periods of apnea.
22

23. ANESTHETIC IMPLICATIONS OF RESPIRATORY
CHANGES
• Avoid the use of nasal airways and perform
careful, deliberate laryngoscopy to avoid
trauma to friable tissues.
• Due to reduction in FRC (less dilution) the
MAC of volatile anesthetics is reduced.
• Short handled laryngoscope will help with
maneuvering around enlarged breasts.
23

24. CENTRAL NERVOUS SYSTEM CHANGES
• The placenta releases endorphins into the circulation.
• Peripheral nerves are more sensitive to local anesthetics.
• Progesterone produces a sedative effect.
• The epidural and subarachnoid spaces are less compliant, partly due to
the engorgement of epidural veins.
• The MAC of volatile anesthetics is reduced by about 40%.
• The sedative effect of progesterone and an elevated level of circulating
endorphins both contribute to an increased sensitivity to inhaled
anesthetics.
24

25. CENTRAL NERVOUS SYSTEM CHANGES
 The reduction in MAC of volatile anesthetics will
speed the induction of inhaled agents.
 Changes in the epidural and subarachnoid
spaces require the doses of neuraxial anesthetics
to be reduced by about one third.
 The administration of all anesthetic drugs may
have enhanced effects. All anesthetic drugs
should be titrated to effect when possible.
25

26. LABOR
• Labor is defined as increasing cervical dilatation and effacement with
descent of the fetal presenting part. Labor is divided into three stages.
• Stage 1 begins with the onset of regular contractions and ends with
complete cervical dilatation (10cm).
• Stage 2 begins with full dilatation of the cervix and terminates with
delivery of the infant.
• Stage 3 begins at delivery of the infant and ends at delivery of the
placenta.
26

27. LABOR
• Stage 1 is further divided into two phases.
• The latent phase begins with the onset of
regular contractions and ends when the cervix
is dilated to 3-4cm.
• The active phase of stage 1 begins at 3-4cm
and continues until complete cervical
dilatation is achieved.
27

28. PAIN OF LABOR
• The pain of first stage labor results from dilation and
effacement of the cervix and as a result of uterine muscle
ischemia during contractions.
• Stage 1 labor pain is primarily visceral. Uterine and cervical
pain transmission is via spinal nerves entering the spinal cord
at T-10 through L-1 levels.
• There is an addition of somatic pain during stage 2 resulting
from the stretching of the vagina and perineum.
• These pain impulses are transmitted by the pudendal nerves
entering the spinal cord at S-2 through S-4 levels.
28

29. 29

30. FETAL MONITORING
• Monitoring of fetal heart rate is the accepted
method for assessment of fetal wellbeing.
• Fetal heart rate can be monitored through
ultrasound or placement of an electrode on
the presenting fetal scalp if the cervix is open
and membranes are ruptured.
• The normal fetal heart rate continually varies
5 to 20 beats per minute.
30

31. FETAL MONITORING
• Normal fetal heart rate at term is 120-160
beats per minute. An immature fetal heart
rate will be slightly higher.
• Fetal heart rate less than 120bpm is
considered bradycardia.
• Fetal bradycardia of 100bpm is usually
tolerated unless the bradycardia lasts longer
than two minutes.
31

32. FETAL MONITORING
• A fetal heart rate under 100bpm requires
investigation.
• Fetal heart rate below 80bpm is indicative of
significant fetal compromise and requires
immediate intervention.
32

33. FETAL MONITORING
• Fetal heart rate above 160bpm is considered
tachycardia.
• Causes of fetal tachycardia include hypoxia, fever,
fetal dysrhythmias, drugs or fetal immaturity.
• Causes of fetal bradycardia include hypoxia,
drugs, fetal dysrhythmias, asphyxia, maternal
hypoxemia or a sustained decrease in placental
blood flow.
33

34. BEAT TO BEAT VARIABILITY
• The normal variability of the fetal heart rate is
indicative of an intact central nervous system,
vitally mediated, and a functioning cardiac
conduction system.
• Beat to beat variability is an assurance of fetal
wellbeing.
• Decrease in variability indicates fetal compromise
as a result of hypoxic myocardial depression.
34

35. BEAT TO BEAT VARIABILITY
• Hypoxia may also cause CNS depression which
will reduce variability.
• Other causes of the reduction or loss of beat
to beat variability include fetal acidosis, CNS
depressant drugs, defects in the fetal heart
conduction system, fetal CNS defects.
35

36. 36

37. 37

38. EARLY DECELERATIONS
• Early decelerations of fetal heart rate begin with
the onset of uterine contraction and return to
baseline by the end of contraction.
• Early decelerations are thought to be the result of
vagal stimulation as the fetal head is compressed
during uterine contraction.
• Early decelerations are not indicative of fetal
distress unless there is absence of beat to beat
variability.
38

39. 39

40. 40

41. LATE DECELERATIONS
• Late decelerations are indicative of fetal
distress as a result of uteroplacental
insufficiency.
• Maternal hypotension is the usual cause of
uteroplacental insufficiency.
41

42. LATE DECELERATIONS
• Late decelerations are most likely the result of
fetal myocardial hypoxia.
• The absence of beat to beat variability
represents an increased severity of fetal
decompensation.
• Maternal hypotension + uteroplacental
insufficiency= fetal distress
42

43. 43

44. VARIABLE DECELERATIONS
• Variable decelerations are variable in time of
onset, duration, and magnitude.
• Most variable decelerations are characterized by
rapid reductions in fetal heart rate in response to
uterine contraction and rapid return to baseline
after contraction.
• A response to umbilical cord compression is
thought to be the cause of variable decelerations.
44

45. VARIABLE DECELERATIONS
• Variable decelerations are usually benign
unless they are prolonged beyond 30 seconds
or bradycardia is lower than 70bpm.
• Variable decelerations are considered severe if
they last longer than 60sec, if the heat rate
decreases more than 60bpm from baseline or
the heart rate decreases below 60bpm.
• Repositioning the mother will usually reduce
or abolish variable decelerations.
45

46. 46

47. 47

48. 48

49. APGAR SCORE
• An organized initial assessment of the neonate
will identify the need for resuscitation.
• The Apgar score is a numerical value assigned
to five vital signs of the neonate which are
evaluated at one and five minutes after
delivery.
49

50. APGAR SCORE
• Heart rate, breathing, reflex irritability, muscle
tone and color are evaluated when
determining the Apgar score.
• The Apgar score is useful in helping to
communicate an identified need for neonatal
resuscitation.
50

51. APGAR SCORE 8 TO 10
• The majority of newborns have Apgar scores
in this range.
• Newborns with Apgar 8-10 may only require
routine suctioning of the mouth and nose,
drying and placement in a warm environment.
51

52. APGAR SCORE 5 TO 7
• Newborns scored in this category have most
likely experienced mild hypoxia before
delivery.
• Vigorous tactile stimulation and oxygen
directed toward the face will usually be
enough to encourage a response.
• If the newborn does not respond within 1-2
minutes or if bradycardia less than 100bpm
develops, ventilatory assistance should be
provided with bag-mask ventilation and 100%
O2 until response is achieved.
52

53. APGAR SCORE 3 TO 6
• Newborns scored in this range are pale or cyanotic as
a result of a more prolonged asphyxia.
• Immediate assistance with 100% O2 via bag-mask
ventilation (40-60bpm) is required until ventilatory
effort is sufficient to maintain saturation.
• If mask ventilation is difficult or the newborn does
not spontaneously breath within several minutes,
endotracheal intubation should be performed.
53

54. APGAR SCORE 0 TO 2
• An Apgar score this low indicates that the
newborn has been severely asphyxiated and
will require emergent resuscitation.
• This newborn requires immediate intubation
and ventilation with 100% oxygen at a rate of
40-60bpm.
54

55. APGAR SCORE 0 TO 2
• The heart rate should be evaluated and chest
compressions should be initiated if heart rate
is slower than 60bpm.
• Epinephrine 0.01-0.05ug/kg, via umbilical vein
catheter or ET tube, may be required if
bradycardia is sustained.
• Severely compromised newborns are often
hypoglycemic and may benefit from glucose
administration.
55

56. APGAR SCORE
zero one two
• Heart rate: absent <100 >100
• Breathing: absent slow crying
Irregular
• Reflex : no response grimace cough
sneeze
• Muscle tone: limp flex active
extremities
• Color: cyanotic body pink, pink
extremities cyanotic
56

57. HEMORRHAGE IN THE PARTURIENT
• Hemorrhage is the leading cause of mortality
in the parturient.
• Hemorrhage can result from placenta previa,
placental abruption, uterine rupture, retained
placenta or uterine atony.
57

58. PLACENTA PREVIA
• Undiagnosed placenta previa typically
presents in the 32nd week with painless
vaginal bleeding.
• Placental position should be identified with
ultrasound when previa is suspected.
58

59. PLACENTA PREVIA
• There is an increased incidence of previa in
patients who have experienced previa in a
previous pregnancy.
• The potential exists for rapid, excessive blood loss
to occur.
• The risk of postpartum bleeding is also greater
due to the placental location of uterine
implantation (lower segment doesn’t contract as
forcefully).
59

60. PLACENTA PREVIA
• Placenta previa is an indication for cesarean
section.
• Two large bore intravenous lines should be
established and blood for transfusion should be
available (2-4 units recommended).
• Regional anesthesia may be acceptable if the
placenta is intact at time of surgery and the
anesthetist is prepared to volume resuscitate in
the event of significant blood loss.
60

61. PLACENTA PREVIA
• When a patient with placenta previa presents
with active bleeding, regional anesthesia should
be avoided.
• Rapid sequence induction with low dose
thiopental (3mg/kg) or ketamine (1mg/kg) and
succinylcholine is the recommended choice
during acute hemorrhage. Nitrous oxide and low
concentration of volatile agent can be used for
maintenance.
61

62. PLACENTAL ABRUPTION
• Placental abruption refers to separation of a
normally implanted placenta before delivery.
• Vaginal bleeding may identify abruption but
often, significant blood loss can be concealed
within the uterus.
62

63. PLACENTAL ABRUPTION
• Symptoms of abruption include:
• Painful vaginal bleeding
• Uterine tenderness
• Uterine hypertonus
• Back pain
• Preterm labor
• Hypovolemia or shock
• Fetal distress or demise
63

64. PLACENTAL ABRUPTION
Chronic bleeding with clot formation between
the placenta and the uterine wall may induce
maternal disseminated intravascular
coagulation (DIC).
If the patient is experiencing uterine
hypertonus, it may be best to avoid ketamine
due to its potential for increasing uterine tone
(increased fetal compromise).
64

65. PLACENTAL ABRUPTION
• Rapid sequence induction and maintenance
with low concentration volatile agent in 50%
nitrous oxide is recommended until delivery.
• After delivery, maintenance of anesthesia with
the volatile agent should be discontinued and
nitrous oxide with an intravenous anesthetic
should be initiated.
65

66. PLACENTAL ABRUPTION
• Several large bore intravenous lines should be
inserted and blood for transfusion should be
available.
• Oxytocin and ergotamine should be available
for intravenous and intramyometrial injection
to facilitate uterine contraction.
66

67. DISSEMINATED INTRAVASCULAR COAGULATION
• DIC is an activation of the clotting cascade
throughout the circulatory system.
• Thrombin production is increased (converts
fibrinogen to fibrin), an increase of fibrin
enters the microcirculation, clotting factors
are consumed. Activation of the fibrinolytic
system further adds to the development of
severe coagulopathy.
67

68. D I C
• Two possible causes of the increased
production of thrombin may be the result of
excessive release of tissue thromboplastin, or
as the result of the introduction of a foreign
substance into the circulation.
• Diffuse bleeding and often thromboembolism
occur with the development of DIC.
• All lab studies involving the clotting cascade
will indicate deficiencies (all are exhausted).
68

69. D I C
• The development of shock causes further
tissue injury as a result of reduced blood flow.
• The accumulation of fibrin and cellular debris
within the renal filtration system will result in
renal failure.
69

70. D I C
• Conditions associated with DIC include :
• Placental abruption
• Amniotic fluid embolism
• Prolonged in utero fetal demise
• Sepsis
• Preeclampsia and eclampsia
• Massive blood transfusion
70

71. D I C MANAGEMENT
• Supportive care
• Elimination or treatment of the underlying
cause
• Possibly transfusion of blood products guided
by lab evaluation as the patient stabilizes.
71

72. UTERINE RUPTURE
• Uterine rupture is more common in patients
with uterine scar.
• There is also an increased incidence of uterine
rupture in patients who are cocaine abusers.
• Half of maternal mortality, attributed to
hemorrhage, is a result of uterine rupture.
72

73. UTERINE RUPTURE
• The gravid uterus receives about 10% (6-
800ml/min) of cardiac output (non-pregnant
percentage is 50ml/min).
• The large volume of blood flow to a ruptured
uterus can quickly lead to exsanguinations.
• Up to 3500ml of blood has been found in the
abdomen of patients with ruptured uterus.
73

74. UTERINE RUPTURE
• The classic progression of uterine rupture :
• Sudden, severe abdominal pain during hard
labor
• Labor stops
• Fetal distress rapidly develops
• Maternal shock occurs very quickly
74

75. POSTPARTUM BLEEDING
• Moderate postpartum bleeding is common.
• Persistent or excessive postpartum bleeding
may occur as a result of several conditions.
• Uterine atony, retained placenta, uterine
abnormalities, lacerations of the birth canal,
inversion of the uterus, and coagulopathy may
be responsible for postpartum bleeding.
75

76. POSTPARTUM BLEEDING
• Often, a brief anesthetic will be required for
the surgeon to identify the source of bleeding
and control it.
• Anesthesia may be required for evacuation of
retained placenta.
• Always be aware that a retained placenta may
evolve into something more significant.
76

77. POSTPARTUM BLEEDING
• If general anesthesia is required in the
immediate postpartum period, be prepared to
manage a potentially difficult airway.
• Take all precautions to avoid the possibility of
aspiration.
• Have smaller than normal ET tubes available
with all equipment checked and organized for
plan B,C etc.
77

78. AMNIOTIC FLUID EMBOLISM
• Amniotic fluid embolism is a rare occurrence
but has a very high mortality rate – 86% (50%
in the first half hour).
• Amniotic fluid embolism (AFE) may occur
during labor, vaginal or Cesarean delivery, and
the postpartum period.
• AFE is associated with placental abruption,
placenta previa and uterine rupture.
78

79. AMNIOTIC FLUID EMBOLISM
• AFE and air embolism have a similar
presentation but disseminated intravascular
coagulation (DIC) commonly occurs with AFE if
the patient survives the initial embolic event.
• Advanced age, multiparity, rapid labor,
pharmacologic induction of labor and large
fetal size have all been associated with AFE.
79

80. AMNIOTIC FLUID EMBOLISM
• Prodromal symptoms include nausea,
vomiting, agitation, chills, restlessness, and
apprehension.
• Symptoms quickly progress to respiratory
distress and severe hypotension, leading to
cardiac arrest.
80

81. AMINOTIC FLUID EMBOLISM
• Other presentations of AFE include chest pain,
tachy-dysrhythmias, seizures, and
coagulopathy.
• Immediate delivery is the only approach to
prevent fetal demise.
81

82. AMNIOTIC FLUID EMBOLISM
• Treatment of AFE :
• ABC’s
• Intubate and ventilate with 100% oxygen
• Fluid bolus, left tilt and drugs to treat
hypotension.
• CPR
• Immediate C-section
82

83. PREGNANCY INDUCED HYPERTENSION
• Pregnancy induced hypertension (PIH) or
preeclampsia refers to the triad of
hypertension, edema, and proteinuria
(>500mg/dl) which may occur after the 20th
week of gestation and resolves within 48
hours after delivery.
83

84. P I H
• A consistent systolic blood pressure greater
than 140mmHg (or 30mmHg above baseline) and
diastolic blood pressure greater than 90mmHg
(or 15mmHg above baseline) defines PIH.
• Eclampsia is the term used when seizures
develop during PIH.
84

85. CARDIOVASCULAR MANIFESTATIONS OF P I H
• Decreased intravascular fluid volume
• Increased arteriolar resistance (vasospasm)
• Hypertension
• Heart failure
85

86. PULMONARY MANIFESTATIONS OF P I H
• Upper airway edema
• Pulmonary edema
86

87. NEUROLOGIC MANIFESTATIONS OF P I H
• Headache
• Visual disturbances
• Hyperexcitability
• Seizures
• Intracranial hemorrhage
• Cerebral edema
87

88. HEPATIC MANIFESTATIONS OF P I H
• Impaired liver function
• Elevated enzymes
• Rupture
88

89. RENAL MANIFESTATIONS OF P I H
• Proteinuria
• Sodium retention
• Decreased GFR
• Oliguria (usually due to hypovolemia and renal
artery vasospasm)
• Renal failure
89

90. HEMATOLOGIC MANIFESTATIONS OF P I H
• Thrombocytopenia
• Platelet dysfunction
• Hemolysis
90

91. P I H
• There is an increased incidence of PIH in
young primigravidas but patients older than
35 years and those which have had previous
experience with PIH are susceptible.
• The exact pathophysiology of PIH is unknown
but an abnormality in the ratio of
prostacyclins and thromboxanes appears to be
a common finding in PIH patients.
91

92. P I H
• There is an increase in the levels of both
prostacyclins and thromboxanes (produced by
the placenta) during pregnancy.
• Thromboxanes are potent vasoconstrictors,
they promote platelet aggregation, increase
uterine activity, and decrease uteroplacental
blood flow.
• Prostacyclins have the exact opposite effect of
thromboxanes. 92

93. P I H
• Severe PIH is characterized by blood pressure
greater than 160/110, proteinuria 3+ to 4+,
urine output less than 20ml/hr, pulmonary
edema, visual changes, epigastric pain, and
changes in level of consciousness.
• Maternal mortality results from CVA as a
result of hypertension in most cases.
93

94. P I H
• Other causes of maternal mortality include
pulmonary edema, hepatic rupture, renal
failure, cerebral edema, and DIC.
• Seizures are the result of CNS irritability
caused by cerebral edema.
94

95. H E L P SYNDROME
• Hemolysis
• Elevated liver enzymes
• Low Platelet count
• HELP syndrome often accompanies severe
pregnancy induced hypertension.
95

96. TREATMENT OF P I H
• Delivery of the fetus and placenta is the only
definitive treatment of PIH.
• If the pregnancy is at least 37 weeks, most
obstetricians proceed with delivery.
• The main focus of treatment before delivery is
to control blood pressure, maintain
uteroplacental blood flow, promote organ
perfusion and prevent seizures.
96

97. TREATMENT OF P I H
• Hydralazine is a direct acting arteriolar
smooth muscle dilator which is a popular
antihypertensive for the treatment of PIH.
• Hydralazine improves renal and uterine blood
flow.
• Acute hypotension may occur in the presence
of hypovolemia.
97

98. TREATMENT OF P I H
• Labetolol is also a very popular choice for
blood pressure control in obstetrics.
• Labetolol reduces systemic vascular
resistance, uterine blood flow is maintained.
• There is no significant fetal adrenergic
blockade.
98

99. TREATMENT OF P I H
• Magnesium sulfate is the drug of choice for
anticonvulsant therapy.
• Magnesium sulfate is used to prevent seizures
in the preeclampsia patient and to treat
seizures in the eclamptic patient.
• Magnesium sulfate is given as a 4gm IV
loading dose (over 20min) followed by a 1-
3gm/hr infusion.
99

100. MAGNESIUM SULFATE PLASMA
CONCENTRATION
• 1.5-2.0 mEq/L normal range
• 4.0-8.0 therapeutic range
• 5.0-10 ECG changes - prolonged
• 10 loss of deep tendon reflexes
• 15 SA and AV block
• 15 respiratory paralysis
• 25 cardiac arrest
100

101. MAGNESIUM SULFATE
• Magnesium sulfate may cause tocolysis and
may contribute to uterine atony leading to
increased blood loss.
• Magnesium sulfate may also potentiate
nondepolarizing neuromuscular blocking
agents. Use peripheral nerve stimulator to
guide dosing.
101

102. ANESTHETIC MANAGEMENT OF P I H
• The patient with PIH will most likely arrive to
the operating room with a magnesium sulfate
infusion.
• A separate large bore intravenous line should
be inserted for volume replacement.
• Many PIH patients are hypovolemic. Urine
output should be used as a guide for volume
replacement.
102

103. ANESTHETIC MANAGEMENT OF P I H
• Spinal or epidural anesthesia is usually the
preferred choice of anesthetic for c-section if
no evidence of coagulopathy exists.
• A minimum platelet count of 100,000 is most
often used as a guide for preeclampsia.
• Coagulation profile (PT, PTT) should be
obtained with severe preeclampsia.
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104. ANESTHETIC MANAGEMENT OF P I H
• Advantage of regional anesthesia :
• Reduced risk of aspiration
• Neurologic status can be monitored
• Avoids increased ICP
• Less fetal drug exposure
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105. ANESTHETIC MANAGEMENT OF P I H
• Although dramatic hypertensive episodes can
be avoided by using regional anesthesia,
hypotension is possible.
• Replacement of intravascular volume with
crystalloid should be the initial approach to
preventing and correcting hypotension.
• If heart rate is less than 100bpm, ephedrine
may be used in 2.5-5mg increments. Caution
must be used to avoid rebound hypertension.
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106. GENERAL ANESTHESIA FOR P I H
• Edema may produce glottic swelling which
may make laryngoscopy very difficult.
• Evidence of potential airway difficulty includes
facial edema, hoarseness, difficulty
swallowing, respiratory distress.
• Be prepared for alternative approaches to
airway management.
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107. GENERAL ANESTHESIA FOR P I H
• Small endotracheal tubes should be available
(5.5, 6mm)
• A controlled, awake intubation may be the
safest approach.
• Labetalol, up to 1mg/kg, is a good choice for
blunting the hemodynamic response to
laryngoscopy without affecting uteroplacental
or fetal blood flow.
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108. GENERAL ANESTHESIA FOR P I H
• Fentanyl 100-200ug/kg has been used to blunt
the hemodynamic response to laryngoscopy
without causing neonatal respiratory
depression.
• Narcotics will increase the time of return to
spontaneous respiration in the event of failed
intubation.
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109. Pregnancy and Anaesthesia
• Understand the physiology
• Be prepared for GETA even if a spinal case
with styleted endotracheal tube
• Blood loss peripartum kills mothers fast
• With hemorrhage, do a general anesthesia
• Preeclampsia and eclampsia increase the risks
of anesthesia with C/S
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110. Questions?