Maternal Physiology
and the Anesthetized
Pregnant Patient
Kimberly Babiash, MD, MBA
Oct 7, 2015
Overview Neuraxial Anesthesia
Epidurals vs spinals
How they work
Physiologic alterations
Contraindications
Patient factors
Febrile patient
Pre-eclampsia
Anesthetic choices for Cesarean Sections
Neuraxial vs General Anesthesia
Physiologic alterations and why they matter
Gastric emptying
Airway
Hemodynamic control
Epidural and Spinals
Neuraxial Anatomy
Neuraxial Anatomy
Understanding Neuraxial
Anesthesia
Epidurals
Slow onset
Long duration
VOLUME dependent
Better hemodynamic control
Spinals
Rapid onset
Short duration
DOSE (mass) dependent
Poor hemodynamic control
Understanding Neuraxial
anesthesia
How do local anesthetics work?
Understanding Neuraxial
Anesthesia Differential Blockade
clinical phenomenon that nerve fibers with different
functions have different sensitivities to local anesthetic
blockade.
Length of each nerve in the thecal space
Depth of the nerve fiber
Distribution of Na+ and K+ channels on each nerve type
Understanding Neuraxial
Anesthesia
Understanding Neuraxial
Anesthesia
Differential Blockade
Sympathetics: most sensitive to local anesthetic
agents (2-4 levels beyond motor)
Pain/touch: moderately sensitive (2-3 levels beyond
motor)
Motor fibers: least sensitive
Dermatome goals Labor (T10 usually achieved with 10-15 ml)
Stage I = T10 – L1
Stage II = S2-S4
Cesarean Section
T2-S4 (higher for exteriorization of uterus)
Pain sensations from pelvic organs and visceral pain fibers
from other abdominal structures including the peritoneum
enter spinal cord at T10-L1; however, some pelvic nerves
accompany sympathetic fibers to reach the spinal cord as
far as T2
Traction on uterosacral ligaments and bladder require
anesthesia as low as S4
Achieved with dose of 12 mg bupivacaine
Why add neuraxial opioids?
Factors affecting block height
Dose
Site of injection
Baricity
Dextrose added for hyperbaric (sinks)
Position of patient
Extremes of height (minor)
Lumbosacral CSF volume (interindividual variability)
Explains variability in spinal with similar doses
Physiologic Disturbances with Neuraxial
Anesthesia
Cardiovascular disturbances take the cake
Hyotension and bradycardia (33% and 13%)
Primary Cause = Sympathectomy
SNS arises from the middle of the SC in the interomedial nucleus of the
lateral grey column beginning at T1 and extends to L2 (thoracolumbar
outflow)
Extends approx 2 dermatomes above the sensory level
Venous and arterial dilation
Venodilation predominates (75% of TBV)
Redistributes central blood volume to splanchnics and lower extremities
Vascular smooth muscle on the arterial side retains considerable tone
If normal cardiac output is maintained, PVR should only
decrease by 15% in the normovolemic patient
Physiologic Disturbances with Neuraxial Anesthesia
Modulation of vasomotor tone
A complex process that relies on much more than
just simple augmentation or attenuation of SNS
Simple thought: hypotension should lead to reflex
tachycardia and vasoconstriction….
But bradycardia is more commom….
Shift towards vagal predominance
Level of block? Cardioaccelerator fibers (t1-t4)
Bezold Jarisch Reflex (a cardioinhibitory reflex)
Mechano/chemosensitive receptors located in the ventricles
Involved in the restorative response to reduced cardiac filling
A sudden decrease in VR and PVR triggers bradycardia to
preserve cardiac filling
Physiologic Disturbances with
Neuraxial Anesthesia Respiratory Effects
Decrease in Vital Capacity (IRV+ VT +ERV) due to
decrease in ERV from paralysis of abdominal
muscles necessary for forced expiration
Nothing to do with diaphragm or phrenic nerve
Therefore, expiration >inspiration
Consideration for severe asthmatic
High Spinal and respiratory arrest
Unrelated to phrenic nerve or respiratory function
Hypoperfusion of the respiratory centers of the brainstem
Respiratory Volumes in Pregnancy
Contraindications
Absolute
Patient refusal
Obstructive intracranial hypertension
Infection at the site
Frank coagulopathy
Regional Anesthesia in the
infected febrile patient
Despite the apparent low risk of central nervous
system infection after regional anesthesia,
anesthesiologists have long considered sepsis to
be a relative contraindication to the
administration of spinal or epidural anesthesia.
Sepsis = SIRS + suspected or documented infection
There is no evidence to suggest that neuraxial
anesthesia is contraindicated in chorioamnionitis
alone
Recommendations:
Serious central neuraxial infections such as arachnoiditis, meningitis, and abscess
after spinal or epidural anesthesia are rare (Grade B).
The decision to perform a regional anesthetic technique must be made on an
individual basis considering the anesthetic alternatives, the benefits of regional
anesthesia, and the risk of CNS infection (which may theoretically occur in any
bacteremic patient) (Grade C).
Despite conflicting results, many experts suggest that, except in the most
extraordinary circumstances, central neuronal block should not be performed in
patients with untreated systemic infection (Grade C).
Available data suggest that patients with evidence of systemic infection may safely
undergo spinal anesthesia, provided appropriate antibiotic therapy is initiated before
dural puncture and the patient has shown a response to therapy, such as a decrease
in fever (placement of an indwelling epidural (or intrathecal) catheter in this group of patients remains controversial) (Grade A).
Anesthetic Choices for Cesarean
Delivery
Neuraxial vs General Anesthesia (GA)
Considerations
GA fastest induction to delivery time
GA lower APGAR scores
Neuraxial is preferred to GA in most cases
study done by Mancuso et al. (Spinal vs GA)
179 healthy elective
Umbilical cord artery pH, Apgar score and need for assisted
ventilation were evaluated and found spinal anesthesia superior
to general in fetal outcome.
Anesthetic Choices for Cesarean Delivery
The relative risk of fatality during GA has increased to more
than 8 times that for regional anesthesia
Failed intubation
incidence of failed intubation in OB patient is 1:300
whereas incidence in general population is 1:2,230 (8 fold
increased risk)
Increased difficulty (vascular engorgement, obesity, breast size,
preeclampsia)
Rapid time to desaturation
Increased oxygen consumption and decreased FRC
Pulmonary aspiration
*see next slide
Maternal awareness
Neonatal depression
Gastric Changes in Pregnancy
Decreased tone and motility progesterone
possibly due to decreased levels of motility
Conflicting info about delayed gastric emptying
Reduced tone of the gastroesophageal junction sphincter Increased intraabdominal pressure leads to acid reflux
Preeclampsia and Neuraxial
1950s evidence that preeclampsia actually attenuates spinal-anesthesia
hypotension
1990s clinical trials demonstrate safety of spinals in this population
3 prospective trials
Less severe and less frequent hypotension and smaller doses of
vasopressors
Early epidural placement in laboring preeclamptic parturients is ideal
Complications of GA
Hypertensive crisis (common with RSI)
Stroke (difficult to recognize under GA; conflict in management
between RSI and deep plane of anesthesia/stable induction to
maintain CBF)
Difficult airway management (pharyngeal and subglottic edema along
with traumatic laryngoscopy and further bleeding)
Preeclampsia and Neuraxial
Spinal compared to GA in severe preeclampsia
with nonreassuring FHT
Dyer et al:
70 parturients prospectively compared
Spinal greater mean neonatal umbilical artery base deficit (7.1 vs
4.7) and lower median umbilical artery pH (7.2 vs 7.23)
Spinal group had higher ephedrine use (fetal pH)
1 min APGAR significantly lower in GA (but at 5 min no
statistical difference)
No significant intergroup differences in other markers of
neonatal compromise
Need for resuscitation, APGAR <7, pH <7.2, need for PPV
Anesthetic Choices for Cesarean
Delivery GA
APGAR scores are lower at 1 and 5 min
Equivocal regarding differences in umbilical artery pH values
Reduces the time to skin incision
Greater maternal complications
Epidural
Increases time to skin incision
Reduces the quality of anesthesia compared to spinal
CSE vs epidural
No difference in frequency of hypotension or 1 minute APGAR
Better anesthesia
Faster time to skin incision
Failed Epidural, Now What?
Epidural anesthesia is less reliable that spinal
Concern with spinal after a failed epidural
High spinal from compression of intrathecal space
Especially when >20 ml in epidural space less than 30
minutes before spinal
Reduction in spinal dose of 20-30%
Anesthetic Medications
Volatile anesthetics
Dose dependent decrease in uterine smooth muscle contractility and
blood flow
Only modest at 0.5 MAC
Rapidly cross placenta but quickly exhaled in neonate
Propofol
GABA agonist
Potent myocardial depressant and inhibits sympathetic tone
Distributes quickly to the vessel rich placenta
Studies with barbiturates indicate optimal timing of fetal delivery 4-8
minutes post induction
However, in a poorly perfused placenta, time is of the essence
Pre-induction Fentanyl?
Peak effect 3-5 minutes
Rapid placental transfer
Though not associated with lower umbilical artery
pH or APGAR scores after 1mcg/kg on induction
Nitrous?
Peak effect lags the start of its administration by 50 sec
Uterine contractions typically peak 30 sec after they start
Reductions in pain scores seem similar to that of systemic opioids, which some
authors suggest have little effect on labor pain
Its use does not seem to appreciably affect the rates of maternal nausea or emesis
during labor
The direct respiratory depressant effect along with maternal hypocapnea may increases
the rate of maternal oxygen desaturation between contractions
It does NOT affect uterine contractility
The effects of the fetus exposed to nitrous in utero is unknown
With rising concern about the subtle long-term effects of perinatally administered
anesthetics, the role of nitrous certainly demands judiciuos scrutiny
Thank You!