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
Epidurals Understanding Neuraxial Anesthesia 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 Differential Blockade Anesthesia 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 Differential Blockade Anesthesia 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 Propofol Only modest at 0.5 MAC Rapidly cross placenta but quickly exhaled in neonate 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
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