First Semester - Ob Extras

Front 1

Why is maternal HOTN a concern? (Describe supine hotn syndrome)

Back 1

When parturient is in supine position, the gravid uterus compresses the Vena Cava decreasing venous return to the heart --> decreased CO and HOTN. Sx may include N/V, diaphoresis and changes in cerebration

Gravid uterus may compress lower abdominal aorta leading to HOTN in LEs (despite normal BP reading in arm), and decreased uteroplacental perfusion.

Front 2

Describe the tx for supine HOTN syndrome and aortocaval compression.

Back 2

Prevention preferred to tx - term parturient should be encouraged to assume a lateral position

Alternatively, LUD in the supine position, accomplished by elevating the right hip 10-15 cm with a wedge or blanket. Tipping the OR or delivery table 15 degrees to the left is also effective for displacing uterus off of aorta and vena cava.

Drugs causing vasodilation or techniques that induce sympathetic blockade decrease venous return during aortocaval compression.

Front 3

During labor, when does the largest increase in CO occur?

Back 3

The largest increase in CO occurs immediately after delivery. Typically, CO/HR/SV return to nonpregnant levels within 2 weeks after delivery.

CO During Labor
Latent Phase Increases 15%
Active Phase Increases 30%
Second Stage Increases 45%
Postpartum Increases 80%

Front 4

What causes anemia during pregnancy?

Back 4

A relative anemia occurs.

An increase in maternal intravascular fluid volume begins in the first trimester and results in an average expansion of about 1000-1500ML at term. The Plasma volume increases 45-50%, whereas RBC volume increases only 15-30%. This disproportionate increase in plasma volume accounts for the relative dilutional anemia of pregnancy. It takes about 8 weeks after delivery for the blood volume to return to normal.

A hb level less than 11 g/dL or Hct <33% represents anemia s/t Iron deficiency.

Front 5

How does CO change during pregnancy?

Back 5

CO increases, the result of increased SV. By 28-32 weeks gestation, the HR also increases 10-15 bpm

Front 6

Discuss typical upper airway findings in the parturient.

Back 6

Capillary engorgement leads to swelling of the oral and nasal larynx, pharynx and trachea. Parturient may have nasal congestion& voice changes.
Manipulation of the upper airway requires special care. Aggressive suctioning & placement of airways and careless laryngoscopy can lead to trauma and bleeding.
A nasal airway is especially prone to causing epistaxis.
When an ett is placed, a smaller 6.5 -7.0 cuffed oral tube is required b/c swelling of the false vocal cords narrows the glottic opening.

Front 7

Is inhalational agent uptake affected by pregnancy?

Back 7

The combination of increase Ve and decreased FRC increases the rate at which changes in alveolar concentration of inhaled anesthetics can be achieved. Induction, emergence and changes in depth of anesthesia are faster in parturients.

Front 8

How is the parturient's minute ventilation affected by pregnancy?

Back 8

Minute ventilation is increased by 50% above nonpregnant levels at term, primarily the result of increased tidal volume. Progesterone sensitizes the respiratory center to CO2. Ventilatory augmentation produces a respiratory alkalosis with compensatory renal excretion of bicarb and partial pH correction.

Front 9

What happens to the FRC during pregnancy?

Back 9

S/T enlargement of the uterus, the diaphragm is forced cephalad, decreasing the FRC.
FRC is decreased further with supine, lithotomy & trendelenburg positions and with obesity. The reduced FRC, in conjunction with the increased O2 consumption associated with pregnancy can lead to a precipitous decline in PaO2, especially during periods of apnea. Supplemental oxygen during labor and an increased fraction of inspired oxygen during general anesthesia are prudent. Patients will desat FAST...they got no reserve.

Front 10

What happens to the oxyhb disassociation curve during pregnancy?

Back 10

The oxyhemoglobin disassociation curbe shifts to the right, with P50 values increasing from 26-30 mmHg by term; this facilitates oxygen unloading to the fetus.

Front 11

Why are parturients at risk for aspiration?

Back 11

The enlarging uterus changes the angle of the gastroesophageal jx leading to relative incompetence of the physiological sphincter mechanism. Progesterone also decreases GI motility.

Parturients are vulnerable to regurgitation of gastric contents (Mendelson's syndrome). Maternal "bearing down" efforts & the lithotomy position during the second stage of labor and delivery make silent regurg a threat.
Opioids, diazepam (valium) and atropine all decrease LES tone and prolong gastric emptying time.

Front 12

Discuss what can be done to prevent pulmonary aspiration.

Back 12

Parturients should always be considered to have a full stomach regardless of time of last meal.
Use of nonparticulate antacid (NaCitrate 30 ml, 0.3Mol/L) is recommended.
Reglan 10 mg or an H2 receptor antagonist is often administered before rgional or GA.
The mechanical efforts of the gravid uterus on the stomach are resolved ina few days postpartum.

The other GI changes revert back to nonpregnant states within 6 weeks postpartum.

Front 13

Are the required doses of LA agents for spinal and epidural anesthesia different in the parturient?

Back 13

The anesthetist should reduce the doses of LAs in the pregnant patient by 30-40%.

There may be increased sensitivity to LAs for spinal and epidural anesthesia for up to 36 hours postpartum.

Front 14

Why is the parturient at risk for DVT?

Back 14

The blood of the parturient is hypercoagulable. Plasma levels of PLTs, the clotting factors VII/VIII/IX/X; and thrombin are increased. This "hypercoagulable state" is beneficial in limiting blood loss at delivery, but it places the parturient at risk for thromboembolic complications.

Front 15

On what does the integrity of the uteroplacental circulation depend?

Back 15

UBF = [uterine arterial pr - uterine venous pr]/uterine vasc. resistance

The integrity of uteroplacental circulation depends on adequate uterine blood flow and normal placental fx.
At term, UBF represents 10% of CO, or 700-800 ml/min (vs 50 ml/min in a nongravid uterus) .
At least 80% of the UBF supplies the placenta and the remainder goes to the mymetrium.

Front 16

How does progesterone affect the CNS?

Back 16

Progesterone has a sedative effect on the mother. There is an increase in the parturients sensitivity to inhalational anesthetic agents. (Need less.)
Anesthesia requirements for inhalational agents in the postpartum period return to normal in 3-5 days.

Front 17

What are the major factors that ↓ uterine blood flow?

Back 17

Pregnancy maximally dilates uterine vessels, so autoregulation is absent.
Any condition that decreases maternal MAP or increases uterine vascular resistance decreases uterine blood flow.

FACTORS THAT:
Decrease uterine arterial pressure - hypovolemia/hemorrhage, HOTN induced by drugs or sympathetic blockade, aortocaval compression

Increase Uterine Arterial Resistance - catecholamines (stress), vasopressors (phenylephrine), severe hypocapnia (PaCO2 <20 mmHg).

Increase Uterine Venous Pressure - Uterine contractions & drug induced hypertonus (oxytocin), skeletal muscle hypertonus (seizures), vena caval compression.

HOTN, vasoconstriction and contractions are the major factors that decrease UBF.

Front 18

What is an appropriate drug to treat sustained HOTN in a parturient pt.?

Back 18

Ephedrine is the DOC for tx of sustained HOTN b/c it increases BP through inotropic and chronotropic effects on the heart w/o decreasing UBF. (My note: Ephedrine stimulates both alpha-and beta-receptors, causing increased heart rate, unchanged or augmented stroke volume, enhanced cardiac output, and increased BP. Causes relaxation of smooth muscle via B2 effects, stimulation of cerebral cortex, and pupil dilation.)

The uterine muscles has alpha1 receptors (uterine contraction) and beta 2 receptors (uterine relaxation). Maternal release of catecholamines or admin of an alpha-adrenergic (methoxamine, metaraminol, mephentermine) may increase BP but paradoxically reduce UBF s/t uterine contraction.
Low-dose phenylephrine (40 mcg) may be an alternative to ephedrine if tachycardia is contraindicated.

Front 19

Define the determinants of diffusion across the placenta.

Back 19

Although placenta acts as a barrier to drugs: LOW mol weight, HIGH lipid solubility, NONionized drugs may be transferred rapidly from mother to fetus.

Miminizing the maternal blood concentration of a drug is the most important method of ultimately limiting the amt of drug that gets to a fetus.

Transfer of a drug to a fetus can be minimized by IV injection of a drug during uterine contraction b/c maternal blood flow to the placenta is markedly decreased at that time.

Front 20

Define ion-trapping.

Back 20

Fetal uptake of a substance that crosses the placenta may be facilitated by the lower pH of fetal blood compared with maternal blood. The lower fetal blood pH means that weakly basic drugs (LAs, opioids) that cross the placenta in their nonionized form become ionized and trapped in the fetal circulation.
B/C an ionized drug cannot readily cross the placenta back to maternal circulation, this drug accumulates in fetal blood.

Front 21

Describe fetal oxygen balance.

Back 21

Fetal O2 transfer depends on oxygen-affinity and oxygen-carrying capacity of fetal and maternal blood.

To aid O2 transfer, the fetal oxyhg disassociation curve shifts to the left, producing greater fetal hb affinity for oxygen compared with maternal hb.
Also, fetal hb is usually 15 g/dL vs 12 g/dL in the mother.
The higher oxygen-affinity and oxygen-carrying capacity of the fetal blood benefits the fetus.

Front 22

Summarize mechanisms that can produce fetal acidosis during maternal hyperventilation.

Back 22

1st stage labor: No pain relief/mom hypervents --> maternal hypocapnia --> uteroplacental vasoconstriction --> fetal hypoxia.

Late 1st stage to 2nd stage labor: Severe pain/↑ maternal Ve --> respiratory alkalosis --> hypoventilation between painful contractions --> left shift on maternal oxyhb curve --> O2 tightly bound to maternal hb --> fetal acidosis.

General Anesthetic --> need to hyperventilate mother --> increased intrathoracic pressure --> decreased venous return & CO --> decreased placental perfusion --> fetal acidosis.

Front 23

Describe the effects of inhalational agents on the fetus.

Back 23

The volatile halogenated anesthetic agents can DIRECTLY DEPRESS the fetal CV system and central nervous system.

Volatile anesthetics may INDIRECTLY affect fetus by producing maternal HOTN --> decreased UBF which may lead to fetal asphyxia.

N2O may have negative impact on DNA synthesis. This proposed effect is controversial, but as a precaution, many practitioners avoid N2O during the first two trimesters.

Front 24

Discuss common uterotonic agents.

Back 24

Oxytocin (Pitocin): A synthetic preparation that selectively acts on the muscle cells of the uterus to produce uterine contractions. It is commonly used to induce or augment labor & prevent postpartum hemorrhage. To avoid HOTN, a dilute IV mixture (2U/100 ml of solution) is recc. In large doses, pitocin has been shown to exert an antidiuretic effect.

Ergot alkaloids: considered DoC when oxytocin fails to produce a uterine contraction. Uterine tone is increased through direct alpha adrenergic stimulation. Ergonovine maleate (Ergotrate) and methylergonovine maleate (methergine) may precipitate maternal hypertension via direct peripheral vasoconstriction. Admin IM or very slowly IV.

Prostaglandins (prostaglandin F2a): used if uterine contraction . Smooth muscle constriction may produce hypertension, bronchoconstriction & pulmonary vasoconstriction. A common choice is carboprost tromethamine (hemabate) 250 mcg IM.

Front 25

Describe the stages of labor.

Back 25

First Stage: begins with onset of reg contractions and concludes when the cervix is fully dilated. The stage is subdivided into the latent and active phases, lasting 7-13 hours in the primigravida and 4-5 hours in the multigravida.

The latent phase is a preparatory phase of labor, during which, despite reg contractions, there is little cervical dilation. The contractions cause softening and thinning (effacement) of the cervix.

The active phase is characterized by rapid changes in cervical dilation.

Front 26

List the advantages of regional anesthesia in the parturient.

Back 26

*Ability to achieve segmental bands of analgesia during labor, reducing levels of catecholamines in the maternal circulation.

*Unlikely to produce drug-induced depression i the fetus or mother

*Avoid the risks of GA (aspiration, failed intubation); maternal airway reflexes remain intact.

*Means to provide surgical anesthesia if neccessary.

*Mother remains awake and can react to her newborn early in postpartum period.

Front 27

Review obstetrical epidural local anesthetics.

Back 27

Bupivicaine
Lidocaine (Xylocaine)
Chloroprocaine
Ropivicaine (Naropin)
Levobupivicaine (Chirocaine)

Front 28

Discuss important considerations for regional anesthesia for caesarion sections.

Back 28

Regional anesthetic (lumbar epidural or spinal) is often chosen for elective c-section, particularly when pt awareness is desirable.
A regional anesthetic minimizes newborn depression and avoids risk of general anesthesia (aspiration, failed intubation).

A sensory level of T4 is desirable for c-section, although an awake parturient may experience some discomfort with exteriorization of the uterus of the abdominal viscera at this level.

Epidural anesthesia for C-section requires large doses of LAs, which may cross placenta and affect the fetus. The anesthesia provider must ensure proper catheter placement with a test dose before administering a full local anesthetic dose.

Administer a nonparticulate oral antacid (Na-citrate 15-30 ML) w/in 1 hour of the procedure.

Administer IV dextrose free balanced salt solution immediately before the regional technique (at least 500 ml for an epidural; 1000-2000 ml for a spinal anesthetic).

Supplemental oxygen to the mother.

After regional block placement, position with left uterine displacement.

Compare maternal blood pressure and FHR with baseline. Prepare to treat HOTN with additional volume expansion & 5-10 mg of ephedrine as needed.

Front 29

What should be done if regional block fails?

Back 29

.If the sensory block isn't satisfactory, supplemental analgesia can be achieved safely by incremental admin of low-dose opioids or ketamine (0.1-0.25 mg/kg) or inhaled N2O in oxygen. It is paramount that maternal laryngeal reflexes remain intact. GA & endotracheal intubation may be required.

Front 30

Summarize important considerations for general anesthesia for C-section.

Back 30

Evaluate airway in advance. If difficulties are anticipated, consider an awake oral fiberoptic tracheal intubation.

Admin 15-30 ml of a nonparticulate oral antacid within 1 hour of induction.

Place mother in Left Uterine Displacement.

Preoxygenate mother for 3-5 minutes or have 4-5 deep breaths with a well-fitting mask.

Administer cricoid pressure and initiate RSI (thiopental or propofol, followed by Sux 80-100 mg IV; if sux can't be used may use Roc 0.6 mg/kg IV). No defasciculating dose needed b/c increased pregesterone levels seem to prevent fasciculations.

Inability to intubate the trachea and provide effective ventilations is the leading cause of maternal death r/t anesthesia.

When ett placement is confirmed by capnography, OB may proceed with skin incision. In the predelivery interval, anesthesia may be maintained with a 50/50 O2-N2O flow rate with 0.5 MAC of a halogenated agent. The small dose of volatile agent decreases risk of maternal awareness but does not increase maternal blood loss. A few minutes before delivery is anticipated, concentration of volatile anesthetic may be increased to provide uterine relaxation.

Avoid maternal hyperventilation b/c it may decrease uterine blood flow.

After cutting of the cord, a narcotic and amnestic may be given to deepen the anesthesia.

Extubate only when the patient is fully awake and able to manage the airway.