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96 Cards in this Set

  • Front
  • Back
Stage One of Labor
3 phases:
Latent Phase (0-4cm)
Active Phase (4-7cm)
Transition (7-10cm)
Stage Two of Labor
Full Dilation to delivery
of infant
Stage Three of Labor
Delivery of placenta
Period between conception and onset of labor
Period from onset of labor to delivery of placenta.
Stages I-III of labor)
Period from delivery of placenta to 4-6 weeks post-delivery
Physiology of Pain in
1st stage of labor
Visceral pain arises from uterine contractions and dilation of cervix. Pain carried through spinal segments/pathways T10-L1 via A-delta & C-fibers; Lumbar epidural works well during this stage
Physiology of Pain in
2nd stage of labor
Pain is somatic caused by stretching of the vagina and perineum. Pain is carried via S2-S3 segments via the pudendal nerve; Lumbar epidural doesn't always eliminate this pain
Contraction of Uterus can result in myometrial ischemia which can cause release of:
K+, bradykinin, histamine, and seratonin
Describe Maternal blood flow through placenta:
Blood arises in central circulation and then thru uterine artery to arcuate artery to radial arteries to spinal artery into intervillous space where maternal blood passes fetal villa; blood returns to uterine wall via uterine vein
Function of Spinal artery:
It is terminal branch of uterine artery & supplies 2/3 of endometrium and empties into intervillous space; it is important in halting hemorrhage after placental circulation b/c it collapses unto self as uterus contracts
3 Tissue layers in placental membrane:
1. Outermost layer: Fetal trophoblasts(cytotrophoblast & syncytiotrophoblast)
2. Fetal connective tissue
3. Fetal capillaries
Function of syncytiotrophoblast:
secretes HCG & progesterone; responsible for endocrine function of placenta
Mechanisms of exchange across placental membrane:
Active Transport
Bulk Flow
Small breaks in membrane
Determinants of Uterine blood flow:
uterine blood flow is directly r/t perfusion pressure;
Uterine blood flow = (mean uterine artery pressure-uterine vein pressure)/uterine vascular resistance;
Uterine Blood Flow
Non-pregnant: 50-100ml/min (5% of cardiac output)
Pregnant: 700-900ml/min
(12% of cardiac output)
Adrenergic Receptors affect on uterine blood flow:
Alpha-adrenergic receptors predominate uterine vessels;
Alpha-agonists or increased catecholamines will decrease uterine blood flow; No nervous system control over blood flow; Uterine vessels have lower sensitivity to vasoconstrictors than systemic circulation d/t progesterone effects-therefore vasopressors will shunt blood from systemic circulation to uterine circulation
Factors that decrease Uterine Blood flow:
1. Maternal hypotension
2. Vasoconstriction of uterine artery
3. Uterine contraction
Physiologic Anemia of Pregnancy
Blood volume increases 35%,
Plasma volume increases 50%,
RBC volume increases 20%
Normal Hgb: 11-12; Hct: 35%
Blood Loss with Birth
Vaginal: 200-500ml
C-Section: 750-1000ml
Laboratory Changes in Pregnancy
Increased WBC, Decreased Plasma Protein, Inreased turn-over of Platelets with decreased or normal platelet count, Increased coagulation/fibrinolysis = increased risk for thromboemboli
Cardiac Output in Pregnancy
CO increases 30-40% first trimester; 45% during labor; highest level can be 80% above prelabor level at 4 hours postpartum
Heart Rate and Stroke Volume in Pregnancy
HR increases 15%
SV increases 35%
Tidal Volume during Pregnancy
Increases by 45% by term
Which lung volume is most changed at term in the parturient?
FRC: decreases starting by 5th month (ERV decrease by 25% + RV decrease by 15%)
Respiratory Changes during pregnancy:
-Alveolar/Minute ventilation increase 70%
-FRC decrease 20%
-PaCo2 decrease 30%
-Upper airway edema & capillary engorgement
-Decreased airway resistence
Why do parturients desaturate so quickly when apneic?
-Decreased FRC
-Increased O2 consumption
-V/Q mismatch
Will maternal hyperventilation effect the fetus?
Yes, If severe d/t decreased placental blood flow r/o vasoconstriction and left shift in maternal O2-Hgb curve
How does maternal hypotension effect FHR?
-Decreased Uterine Blood flow leads to fetal hypoxia leads to decreased FHR;
Factors that decrease FHR:
-Maternal hypotension
-Umbilical cord compression
-Placental dysfunction
How does maternal hypertension impact FHR?
If maternal BP NOT >160/100 in first 20 weeks not issue; Severe HTN can lead to increased uterine artery resistance and decreased O2 delivery to fetus and decreased FHR
Which type of lung disease does pregnancy resemble?
Restrictive lung disease
Which respiratory parameters don't change during pregnancy?
-Dead space
-Lung compliance
-Arterial blood pH
-Vital capacity (ERV+TV+IRV)
-Total Lung Capacity
-Closing Volume
-Diffusing capacity
What are the complications of regional anesthesia in OB?
Hypotension, total spinal, seizure, N/V, dyspnea, H/A, nerve injury, backache
Is seizure a common complication of CLE?
How is LA toxicity treated?
Early recognition, prevention of progression, ABC, support circulation, treat cardiac arrest, assess fetal status
Which blocks can be used for the 1st stage of labor?
Paracervical, lumbar epidural, caudal, spinal
What are two disadvantages of a paracervical block?
Not effective in 2nd stage labor, fetal bradycardia may occur
Why give an epidural to a laboring woman?
CLE relieves pain & anxiety, it blunts increased CO, HR, B/P, & hyperventilation
Are there advantages to caudal anesthesia?
More rapid onset of perineal anesthesia and muscular relaxation; may be good late in labor
Why isn't caudal anesthesia used often in OB anesthesia?
Can't titrate drugs, risk of accidentally injecting the head of the fetus
Fetal Side of Placenta Blood Flow
Fetal blood is Oxygenated in the placenta (mixes in villa with maternal blood) and returns to fetus via one umbilical vein; fetal deoxygenated blood leaves fetus via two umbilical arteries to transverse thru villa again
Fetal side of placenta
Maternal side of placenta
What are the determinants of placental blood flow?
Placental blood flow is dependent on uterine artery blood flow; solely dependent on maternal blood pressure; (Uterine & Placental blood flow is not autoregulated)
Causes of fetal hypoxia and decreased FHR with normotensive mother:
Umbilical cord compression
Placental dysfunction
Maternal physiological changes first trimester d/t:
Hormonal changes
Maternal phsyiological changes third trimester d/t:
anatomical changes (gravid uterus)
Average weight gain with pregnancy:
First trimester 1-2kg
Second & third 5-6kg/each trimester
O2 consumption during pregnancy:
Increases 30-40% up to 60% b/c increased metabolic needs of fetus, uterus, and placenta and by increased cardiac and resp. work
Increased ventilation during pregnancy:
Increased Co2 production and hormones; progesterone increases sensitivity of the central resp. center to Co2 and acts as direct resp. stimulant
PaCO2 level in pregnancy
decreases to 30mmHg by 12 weeks gestation
HCO3 level in pregnancy
decreases to 20mEq/L d/t: metabolic compensation for respiratory alkalosis
Respiratory Changes During Active Labor:
MV increased 70-140% 1st stage & 120-200% 2nd stage; PaCo2 decreases to 10-15mmHg; O2 consumption increases 40% 1st stage 75% second stage d/t: hyperventilation, uterine activity, & maternal expulsion efforts
Which other nerve block can be given late in labor?
Pudendal nerve block can be given late in the 2nd stage
Which regional techniques block the pelvic plexus?
Pudendal nerve block
A parturient has been given an SAB with narcotics only-Why?
Appropriate in high risk patients who can't tolerate the functional sympathectomy associated with SAB or CLE; (i.e. heart dx, hypovolemia, TOF, AS, Pulm HTN, Eisenmnger's syndrome)
Is general anesthesia appropriate for elective vaginal delivery?
No-b/c risk of aspiration Aspiration is the greatest danger of GA in an obstetric setting
Which block is best choice for early labor analgesia?
CLE as compared to caudal or spinal b/c: segmented analgesia w/o paralysis, minimal LA requirements, maintencance of pelvic muscle tone so fetal head can be rotated
Which local anesthetics are used in OB?

(Prilocaine is NOT b/c it causes methemoglobinemia & crosses placenta)
What is the effect of IV Lidocaine on uterine tone?
In HIGH doses, lidocaine can cause uterine arterial vasoconstriction & high uterine tone
How is the CLE dose adjusted in a parturient?
The dose is reduced 25-50%; reduction needed d/t increased sensitivity of neurons during pregnancy as well as teh engorged epidural veins reducing the potential volume of the epidural space
Which LA degrades the efficacy of opiods?
Chloroprocaine; it competes with opioids at the Mu-receptor sites; could give kappa receptor opioid agonist-antagonists
Is an epidural appropriate in a multiple sclerosis patient?
Yes, exacerbations of M.S. are associated with SAB-- NOT CLE
What are the signs of a high spinal?
Unconsciousness & apnea
How to treat a high spinal:
communicate with patient, SLUD, 100% O2, PPV, support
After dosing a CLE the parturient becomes agitated and seizes-Why?
Most likely intravascular injection; Motor paralysis will not be seen with intravascular injection
S/S of LA toxicity:
tinnitus, circumoral numbness, metallic taste
1st sign of epidural catheter migration out of epidural space:
Loss of analgesia; remove catheter and re-administer
How does one minimize the incidence of LA toxicity or high block?
-Aspiration of catheter
-Use dilute doses of LA
-Incremental injection (5ml at a time)
-Epidural test dose [3cc of lido 1.5-2% (45-60mg) with 1:200 epi (15mcg)]

Intrathecal injection with test dose = profound paralysis
Intravascular injection = s/s of LA toxicity
Technique for CSE
Find epidural space as usual, pass spinal needle and aspirate CSF, remove and thread epidural catheter
Intrathecal opioid doses:
Morphine Sulfate: 0.1-0.3mg, Onset: 45-60min, DOA: 1-3hr;
Fentanyl: 10-25mcg, Onset: 2-3min, DOA: 70-75min;
Sufentanil: 5-10mcg, Onset: 2-3min, DOA: 70-120min;
Meperidine: 10mg, Onset: 2-3min, DOA: 30-60min;

Some clinicians choose to give less opioid & add low dose LA
How far to pass epidural catheter?
3-5cm is optimal
Common epidural infusions:
0.1-0.125% bupivacaine with 1-2mcg/ml Fentanyl
Potential complications of CSE?
respiratory depression, fetal bradycardia, dosing untested CLE catheters
When might the CSE technique be advantagous?
-nulliparous in early labor (Wong study showed speeds up labor)
-multiparous in late labor
-patients wanting to walk
-s/p spinal surgery & increased risk for "patchy epidural"
The patient reclines in bed after CLE is placed & B/P drops-Why?
-compression of vena cava= decreased return=decreased CO
-compression of aorta=decreased LE & uterine blood flow
What are the signs of aortocaval compression?
-Diaphoresis, N/V, changes in mentation, dizziness, tachycardia, vertigo, apprehension (all same s/s of hypotension)
How is aortocaval compression treated?
Left uterine displacement, elevate right hip 10-15cm while patient is supine
B/P continues to decrease, what is the drug of choice to treat the B/P?
Ephedrine, it is a weak alpha and mild beta-one agonist, therefore uterine blood flow is minimally effected.
What are three concerns when giving phenylephrine to a parturient?
1) Can cause vasoconstriction of uterine artery;
2)LARGE doses can cause tetanic uterine contractions; 3)If combined with ergot derivatives (methergine) can lead to severe HTN
Which B/P parameter needs to be maintained in the parturient?
Systolic pressure should be prevented from falling 20-30% from baseline or <100torr
Treatment of B/P in parturient consists of:
IV ephedrine, O2, SLUD, IVF bolus, IV phenylephrine
Is the treatment of hypotension different in pregnant M.S. patient?
When can amniotic fluid embolism (AFE) occur?
AFE can occur during labor, delivery, C-section, or post partum; occurs when there is a tear in the uteroplacental membrane and sufficient pressure to force amniotic fluid into the maternal circulation.
Is AFE a significant cause of maternal mortality?
AFE is the 3rd leading cause of maternal death; mortatlity is 50% within the first hour; hard to diagnose-by exclusion
How does an amniotic fluid embolism present?
Sudden onset of dyspnea, hypotension, progresses to cardiac arrest
What are the S/S of AFE?
Rapidly developing pulmonary distress, decreased CO, hypoxia, coma, DIC, uterine atony
What are the 3 principal pathophysiologic events occurring during AFE?
Acute pulmonary embolism, DIC, & uterine atony
Is AFE known by another name?
Anaphylactoid Syndrome of Pregnancy
Mechanical obstruction has minor effect on outcome; it is the activation of biochemical mediators that cause major effects
Treatment of AFE:
CPR, stabilization, supportive care
Specific actions to be taken in AFE:
Intubate/ventilate, 2 IV's, A-line, PA cath, F/c, monitor SpO2, ECG, PA, SBP, CO, neuro status; order FFP, Plts, blood, trt metabolic acidosis, deliver fetus/placenta, trt heart failure (lasix,digoxin), give hydrocortisone (1gm q 6h x 48hrs)
Which drugs may be given in AFE?
Sympathomimetcs, diuretics, digoxin, hydrocortisone, Amicar (epsilon-aminocaproic acid for DIC)
How to treat postpartum pain:
Central neuraxial opioids can be given for 12-24hours; PCEA & PCA, parenteral, oral
What is the principle concern in patients receiving a post-partum tubal ligation?
Aspiration: 8-12 hours should elapse between birth and tubal to allow CV stability and increase likelihood of gastric emptying; risk of aspiration can be reduced by using regional anesthesia