Unf Anesthesia - Ob

Front 1

What physiologic and anatomical changes happen during pregnancy: Cardiovascular

Back 1

HR: Increased 20-30%
SV: Increased 20-50%
CO: Increased 30-50%
Contractility: variable + OR -10%
CVP/PCWP Unchanged
SVR: Decreased 20%
SBP: Slight decrease (midtrimester 10-15mm Hg, then rises)
PVR: Decreased 30%
Pulmonary artery pressure: slight decrease
Cardiomegaly, enlarged left atrium by 12-14%, increased left ventricle end diastolic dimensions by 6%-10%, Common murmurs: split S1 (early closure of mitral valve), S3 by 20 wks, S4, benign grade I/II systolic, trivial tricuspid regurgitation (up to 43%-94% at term), pulmonary regurgitation (up to 94% at term), mitral regurgitation (28% at term), pericardial effusion (40% postpartum)
(BIG MILLER, 7TH ED, PP 2204-2205)
"

Front 2

What physiologic and anatomical changes happen during pregnancy: Hemapoietic

Back 2

EBL vag delivery 300-500 ml; C-sec 800-1000 ml
*uterine blood flow: 500-700 ml/min (not autoregulated, DIRECTLY proportional to mean perfusion pressure across the uterus and INVERSELY proportional to uterine vascular resistance
physiologic anemia of preg: plasma vol expansion increase exceeds that of the RBC vol increase

Front 3

What physiologic and anatomical changes happen during pregnancy: Respiratory

Back 3

upper airway: capillary engorgement (mucosal lining, UR tract); edematous vocal cords and arytenoids
minute ventilation: increased ~50% during the 1st trimester (TV 40%, RR 10%); progesterone-stimulus; results in a decreased resting maternal PaCO2 (from 40-30mmHg; no change in pH [renal excretion of bicarb ions])
lung volume: 3rd month of pregnancy, diaphragm cephalad (decreased FRC -20% at term, FRC < closing capacity; atelectasis when supine)
anesthetic considerations: increased MV, decreased FRC→inc alveolar concentrations of inhaled anesthetics; select a smaller cuffed ETT (6-7); avoid nasal airways (vascular congestion); wt gain, short neck, and large breasts (consider difficult airway); rapid alveolar concentrations of IA; rapid desat with apnea; prexoygenate, oxygenate during regional anesthesia
arterial oxygenation: early PaO2 above 100mmHg (hyperventilation); later PaO2 normal or slightly decreased (airway closure); marked decrease in PaO2 with apnea
decreased FRC; decreased CO r/t aortocaval compression; increased oxygen consumption

Front 4

What physiologic and anatomical changes happen during pregnancy: Renal

Back 4

3rd month: 50% increase (RBF, GFR); 50% decrease (BUN, creat)

Front 5

What physiologic and anatomical changes happen during pregnancy: Gastrointestinal

Back 5

upward & backward displacement of pylorus (retards gastric emptying)
decrease in gastric motility r/t progesterone (increase gastric fluid vol)
gastrin (placenta) stimulates gastric H+ secretion→lower pH of gastric fluid
incompetent physiologic sphincter mechanism
anesthetic considerations: commonly experience esophagitis, GERD; gastric fluid vol and gastric fluid pH; “full stomach”; reglan, zantac, bicitra

Front 6

What physiologic and anatomical changes happen during pregnancy: Central nervous system

Back 6

Progesterone in the CSF increases 10-20 fold in late pregnancy. Progesterone is sedating and potentates the effects of volatile anesthetics

Front 7

What physiologic and anatomical changes happen during pregnancy: Peripheral nervous system

Back 7

engorgement of epidural veins as intra-abdominal pressure increase w/ progressive enlargement of the uterus results in a decrease in the size of the epidural space and decrease volume of CSF in the subarachnoid space; decrease volume of these spaces facilitates the spread of LA

Front 8

What physiologic and anatomical changes happen during pregnancy: Endocrine

Back 8

Increased Glucose excretion, Reduced tissue sensitivity to insulin

Front 9

What is the effect of pregnancy on plasma protein content? How does this affect protein bound drugs?

Back 9

Plasma protein content decreases secondary to the dilutional effect of the increased intravascular fluid volume. Decrease in protein subsequently decreases the amount of protein that drugs can bind to and will increase the amount of free drug.

Front 10

What electrocardiogram (ECG) changes may be normally seen with pregnancy?

Back 10

Increase in hr, shortening of both the PR interval and the uncorrected QT interval, which can affect women with long QT syndrome; axis shift to the R during the 1st T but may shift to the L during the 3rd trimester as a result of the displacement by the expanding uterus. Depressed ST segments and isoelectric low-voltage T waves in the left-sided precordial and limb leads.

Front 11

How will pregnancy affect a woman’s response to drugs; that is: inhalational agents, intravenous anesthetics, and local anesthetics?

Back 11

Pregnancy decreases MAC by 30-50% (decreased FRC). Local anesthetic dosages need to be reduced by 30%. Normal doses of opiods may be used.

Front 12

What factors affect maternal uptake and elimination of anesthetics?

Back 12

Decreased protein binding associated with low albumin may result in larger fractions of unbound drug, with the potential for greater drug toxicity during pregnancy. Decreased FRC and increased MV leads to faster alveolar concentration equilibrium.

Front 13

Identify motor nerve supply to the uterus.

Back 13

Sympathetic supply comes directly from the ovarian and inferior hypogastric plexuses, and parasympathetic comes from the pelvic splanchnic nerves

Front 14

Which factors influence placental transfer of drugs?

Back 14

Lipid solubility, protein binding, tissue binding, pKa (Degree of Ionization), pH, Fetal/Maternal concentration gradient, Placental blood flow, Molecular weight of the drug, placental efflux transporter proteins (fetal-to-maternal direction)

Front 15

Does the placenta metabolize the commonly used anesthetic drugs?

Back 15

The high molecular weight and poor lipid solubility of nondepolarizing neuromuscular blocking drugs result in limited ability of these drugs to cross the placenta. Succinylcholine has a low molecular weight but is highly ionized and therefore does not readily cross the placenta. Thus, during administration of a general anesthetic fir c-section, the fetus/neonate is not paralyzed. Placental transfer of barbiturates, local anesthetics, and opioids is facilitated by the relatively low molecular weights of these substances. Drugs that readily cross the blood-brain barrier also cross the placenta (atropine, scopolamine, benzos, propofol, thiopental, halothane, isoflurane, nitrous oxide, local anesthetics, opioids, vasopressors, epherinde). There was much written about the placental transfer of drugs, but nothing that I found on the actual metabolism of drugs by the placenta. ( From chestnut pg 63).

Front 16

If a woman is in active labor, at what point can drugs be administered intravenously to decrease fetal exposure and uptake (this means during a uterine contraction)?

Back 16

- stage one in early phase of labor

Front 17

How will fetal acidosis affect drug delivery in the fetus?

Back 17

Fetal academia will greatly enhance maternal to fetal transfer (ion-trapping) of many BASIC drugs, such as local anesthetics and opiods.

Front 18

Is uteroplacental blood flow autoregulated? What is the significance of this?

Back 18

uterine blood flow lacks autoregulation and is dependent on maternal blood pressure/cardiac output. Maternal blood pressure is autoregulated which increases or decreases the uteroplacental blood flow by a pressure-flow relationship. Pg 39-40 of chestnut

Front 19

List three factors to decrease uterine blood flow?

Back 19

Uterine contractions, systemic hypotension, aortocaval compression, unintential intravenous injection of LA,

Front 20

What are the causes of pain during the first stage of labor? Which dermatomes is this associated?

Back 20

.Caused by uterine contractions and dilation of the cervix. Transmitted by uterocervical afferents having cell bodies pass through the paracervical region, the hypogastric nerve and plexus, and the lumbar sympathetic chain and enter the spinal cord at T10 to L1 region.

Front 21

What are the causes of pain during second stage of labor? What nerve fibers are involved? How does pain affect uterine blood flow?

Back 21

(Stoelting p. 481) Perineal pain, fetal descent, stretching and compression of pelvic and perineal structures. T10-S4. Pain stimulates endogenous release of catecholamines.

Front 22

What is the sedative of choice during C/Section with a regional anesthetic?

Back 22

Benzodiazepines are typically avoided during awake c-section, but with severe anxiety, small doses of midazolam or opiod may be used. (Chestnut, p. 530)

Front 23

What causes supine hypotensive syndrome? What are 8 signs and symptoms of supine hypotensive syndrome (Aorto-caval compression)? Describe the treatment for aorto – caval syndrome/compression?

Back 23

Compression of the inferior vena cava and aorta by the gravid uterus while lying supine. This causes ↓ venous return, ↓ CO, and ↓ systemic BP.
LE venous stasis, ankle edema/varices, diaphoresis and pallor, N/V, ↓ venous return (↓ preload), ↓ CO and hypotension, ↑ afterload r/t aortal compression, tachycardia, ▲'s in cerebration, fetal distress d/t ↓ uterine blood flow, dilation of epidural veins.
Tx is left lateral displacement of the uterus which can be accomplished manually or by elevating the right hip 10-15 cm with a wedge or blanket.

Front 24

What nerves carry pain during the first, second, and third stages of labor?

Back 24

Uterus and cervix: innervated by T10-L1; pain impulses carried in visceral afferent
type C fibers (1st stage)
Perineum: S2-4; pain impulses carried by somatic nerve fibers, pudendal nerves (2nd
stage)
Somatic pain (incision pain, 2nd stage labor pain) is well localized and described as
“sharp.” Visceral pain (uterine contractions in the 1st stage of labor) is poorly
localized and usually described as “dull but intense aching.”

Front 25

What are the three stages of labor and what is the physiologic process involved?

Back 25

1st stage: onset of regular contractions and subdivided into the latent (irreg in contraction pattern) and active stages (start active labor); give epidural during this stage
2nd stage: begins with complete dilation (opening) and effacement (thinning) of the cervix; hard to get pain relief
3rd stage: delivery of baby until the placenta is expelled

Front 26

What are the determinants of uterine blood flow? What is the significance of this?

Back 26

UBF= (Uterine arterial-uterine venous pressure)/uterine vascular resistance
Uterine blood flow may decline when the perfusion pressure decreases because of decreased uterine arterial pressure which occurs during systemic hypotension, when perfusion pressure decreases because of increased uterine venous pressure, or because of increased vascular resistance. See pg. 40 of Chestnut
Uterine blood flow is related to perfusion pressure and vascular resistance according to the following formula:
UBF = Uterine arterial – Uterine venous pressure / Uterine vascular resistance
Systemic blood pressure, uterine venous pressure, and uterine vascular resistance are the determinants of an acute change in uterine blood flow.
Most anesthetic drugs are passively transferred, with blood flow rates (hence drug delivery) affecting the amount of drug that crosses the placenta.

Front 27

How does extreme maternal hyperventilation affect uterine oxygenation? Give 2 reasons for this change.

Back 27

Decreased uterine blood flow d/t a reduction in venous return, cardiac output, and uterine perfusion pressure.

Front 28

What are the advantages and disadvantages of regional anesthesia for Cesarean sections? General anesthesia?

Back 28

Regional:
Adv: (spinal) reliable in providing surgical anesthesia, low incidence of post-dural h/a, safe with pts with preeclampsia, good for cardiac pts (epidural),
Dis: maternal hypotension (spinal), may not alleviate visceral pain and may need adjunct (epidural)
General:
Adv: used when regional is contraindicated (coagulopathy, certain cardiac lesions, hemorrhage) or for emergencies (placental abruption, uterine rupture, fetal bradycardia, prolapsed umbilical cord) because of rapid and predictable action
Dis: affects the fetus
Spinal advantages: simplicity, rapid onset, dense neural blockade, negligible maternal risk of systemic local anesthetic toxicity, minimal transfer of drug to infant, and negligible risk of local anesthetic depression of infant.
Spinal disadvantages: rapid onset of sympathetic blockage may result in abrupt severe hypotension, recovery time may be prolonged if procedure is shorter than anticipated.
Epidural advantages: can be administered in incremental doses and the total dose can be titrated to the desired sensory level, decreased risk of severe hypotension and uteroplacental perfusion due to slower onset of anesthesia allowing for maternal CV system to compensate for the occurrence of sympathetic blockade, less intense motor blockade- advantageous for pts w/pulmonary disease b/c high level may impair ventilation.
Epidural disadvantages: slower onset when pt has breech presentation o active labor, larger oses are required which results in an increased risk of systemic local anesthetic toxicity.
General anesthesia risks: failed intubation, failed ventilation, pulmonary aspiration of gastric conents, lower 1-min Apgar scores but 5-min Apgars do not differ from regional anesthesia infants

Front 29

When is general endotracheal anesthesia the technique of choice for a C/Section? When might you avoid GETA, if possible? Describe a routine induction for a general anesthetic and C/Section.

Back 29

GETA is technique of choice for dire fetal distress in the absence of preexisting epidural anesthesia, acute maternal hypovolemia, significant coagulopathy, inadequate regional anesthesia, maternal refusal of regional anesthesia.
Avoid GETA if difficult airway, history of MH, or severe asthma
Routine induction: H2 receptor antagonist or PPI and/or metoclopramide IV→ clear antacid orally→ left uterine displacement→ application of monitors→ denitrogenation with 100% O2 x 3-5 mins→ cricoid pressure→ IV induction: thiobarbiturate, propofol, ketamine, or etomidate; sux (roc or vec if sux is contraindicated)→ intubation w/6-7mm cuffed ETT

Front 30

Which local anesthetics are used in obstetrical anesthesia? Which of these cross the placental barrier in the smallest amounts? Why?

Back 30

Lidocaine, mepivacaine, etidocaine, bupivacaine, ropivacaine, 2-chloroprocaine, tetracaine are used in OB.
Bupivicaine and etidocaine cross the placenta in smaller amts b/c of their higher protein binding.

Front 31

Which local anesthetic is the least cardiotoxic, fastest acting, and one of the safest for use in obstetrics. Why?

Back 31

"Of the common OB LA's (ED: Bupivacaine+Ropivicaine; Lidocaine, Chloroprocaine) Lidocaine is the least cardiotoxic b/c it dissociates from cardiac Na channels more rapidly during diastole. (Chestnut, p251)
When considering Epidural Anesthesia:
Bupivicaine and Lidocaine have equal Tmax in epidural use but Bupiv has 2x the duration. (Barash, p539,541)
Chloroprocaine has a rapid onset and very short half-life in maternal and fetal blood because it is metabolized by plasma esterases, thus it may be the safest of the commonly used local anesthetics; However its short duration limits its usefulness. (Duke, Secrets 4th ed p421; Chestnut, p441)
Best answer:
Ropivacaine is slightly less potent than bupivacaine. Onset, duration, and sensory block are similar to equipotent doses of bupivacaine. Motor blockade is slightly less than bupivacaine and may be an advantage. It has less cardiotoxicity (if inadvertently injected IV) because it binds less avidly to sodium channels of cardiac conduction tissue. It is currently approved for epidural use and is available in 2-, 5-, 7.5-, and 10-mg/mL preparations. Ropivacaine costs significantly more than bupivacaine. (Duke, Secrets, p421)"

Front 32

List amide local anesthetics from those that most extensively cross the placental barrier to those that least extensively cross the placental barrier.

Back 32

Mepivacaine, Lidocaine, bupivacaine, etidocaine, ropivacaine

Front 33

When giving an epidural to a parturient, how much should we decrease the amount of local anesthetic given? Why?

Back 33

The concentration of local is much less for bupivicaine the concentration is 0.0625-0.25% as opposed to normal concentration of 0.5-1%. The concentration is therefore 1/8th -1/2 the dose given a non-pregnant person. It had been thought that the enhanced spread caused by the local in the epidural venous engorgement caused the increase reaction. Recently the theory is that during pregnancy neuronal sensitivity to local anesthetics is enhanced.

Front 34

In what 3 ways do drugs cross the placental barrier?

Back 34

According to MMM there are 5ways to cross the placental barrier…
1.Bulk Flow→Water moves across the placenta in this manner(not really a way drugs can move across)
2. Active Transport→Amino Acids and vitamins move across the placenta
3. Pinocytosis→ Large molecules are surrounded and taken in, immunogloblulins are absorbed primarily this way.
4. Breaks → breaks in the placental memebrane are thought to be responsible for Rh sensitization.
5.****Diffusion→(what we need to know) Most anesthesia medications are absorbed this way. Diffusion is the process of small molecules crosses and respiratory gasses as well cross through diffusion. Most anesthetic medications are small enough to cross the placenta in this way.
***Determinants are as follows… the transfer of a drug across the placented is determined by the ratio of its fetal umbilical vein to maternal venous concentrations(UV/MV). Uptake by the fetus is determines by the fetal artery to the umbilical vein (UA/UV). Factors that help determine the amount of effect on the fetus are the route of administration and maturity of the fetal organs.

Front 35

How do most drugs cross the placental membranes?

Back 35

Anesthetic compounds cross the placenta mostly by simple diffusion.

Front 36

What are the three determinants of the amount of drug transferred across the placenta?

Back 36

Lipid solubility, protein binding, tissue binding, pKa, pH, blood flow

Front 37

Describe the physiologic mechanisms behind “ anemia of pregnancy”?

Back 37

Increased glucose excretion and Reduced Tissue Sensitivity to Insulin

Front 38

When does the greatest increase in cardiac output occur in the pregnant patient?

Back 38

Increase of 40-50% in 3rd trimester with further increase with onset of labor.

Front 39

What happens to cardiac output immediately after delivery?

Back 39

The cardiac output can increase up to 75% immediately following deleviery. It decreases the next hour by 30%. AN increase in CVP and stroke volume due to relative hypervolemia and increase venous return result from relief of caval compression and decrease lower extremity venous pressure which enhances transcapillary fill. Cardiac output increases 75% of pre-delivery, which is 50% higher than pre-pregnancy.

Front 40

Does pregnancy mimic restrictive or obstructive disease? Explain?

Back 40

Pregnancy mimics a restrictive lung disease, as the gravid uterus displaces the diaphragm cephalad, both reducing the volume of the lungs and restricting their maximum expansion.

Front 41

List six respiratory system variables that do NOT change during pregnancy?

Back 41

FEV 1, FEV1/FVC, Flow-volume loop, Closing capacity,Flow volume loops, Respiratory rate.

Front 42

What is the most frequent complication of epidural/spinal anesthesia for labor and delivery?

Back 42

Systemic hypotension secondary to sympathetic nervous system block

Front 43

List the contraindications for spinal/epidural anesthetics.

Back 43

Contraindications- infection over the site, coagulopathy, thrombocytopenia, marked hypovolemia, pt refusal, inability to cooperate
Relative contraindications- preexisting neuro diagnosis, back disorder, some forms of heart disease.

Front 44

Discuss the advantages and disadvantages of epidural versus spinal anesthesia for the parturient undergoing an elective C/Section. An emergency C/Section.

Back 44

Epidural- more gradual decrease in bp, continous rate allows better control of level, takes longer to place in emergency, slower onset
Spinal- easier to perform, more rapid predictable onset, may produce more intense block, less potential for systemic toxicity because use less drug

Front 45

Explain what is meant by the terms: Induction to delivery time.

Back 45

The time between induction and when the cord is clamped

Front 46

Explain what is meant by the terms: Uterine incision to delivery time.

Back 46

Actual incision of uterus until baby is out of womb, cord is clamped and separation of mother and baby

Front 47

Explain what is meant by the terms: What are the obstetrical and anesthesia implications of both terms?

Back 47

Healthy fetus: the interval from induction to delivery is not as important as the interval from uterine incision to delivery (when uterine blood flow may be compromised and fetal asphyxia may occur).
A long time from induction to delivery may result in a lightly anesthetized neonate, but not an asphyxiated neonate.

Front 48

What is your decision making process for the choice(s) of local anesthetics for epidurals and spinal anesthesia for vaginal delivery? C/Sections?

Back 48

(Chestnut 177). The urgency and anticipated duration of surgery dictate the choice of local anesthetic agent
Vaginal delivery/ epidural- (baby miller 486) 6-10 ml of 0.125%- 0.25% of bupivacaine or ropivacaine is the choice anesthetic to relieve the visceral pain in the first stage of labor b/c they are motor sparing and long duration of action. If you add narcotics to the mix the local concentration will drop to 0.0625- 0.01%.
Vaginal delivery/ spinal- (baby miller 487) done immediately before- produces a rapid onset of analgesia and skeletal muscle relaxation. A dose of a dilute solution of hyberbaric Lidocaine (20-30mg), tetracaine (2-4mg), or bupivacaine (5-6 mg) is used for profound and rapid anesthesia for the perineum and vagina areas with a shorter duration.
C-section/epidural-(baby miller 490, 491).
Lidocaine, 1.5%-2%, plus epinephrine, 1:200,000.
Bupivacaine, 0.5%.
Chloroprocaine, 3%
(chestnut 178). The most popular choice of local anesthetic when giving epidural anesthesia for C-section is 2% lidocaine with epinepherine-this addition of epi causes a modest prolongation of the block and improves the quality of epidural lidocaine anesthesia
C-section/spinal- (baby miller 490,491) used more often- more reliable to provide surgical anesthesia from midthoracic to sacrum.
Bupivacaine (12-15mg)- 1.6-2 ml 0.75% bupivacaine in 8.25% glucose; most common choice
8-10 mg tetracaine- hyperbaric – 0.8- 1ml 1% tetracaine with equal val. Of 10% glucose in water
60-75 mg Lidocaine- 1.2-1.5 ml 5% Lidocaine in 7.5% glucose diluted with equal volumes of cerebral spinal fluid.
Epinephrine 0.1-0.2 MG added to the local anesthetic solution may prolong and/or improve the quality of the block

Front 49

You should have an understanding of the following terms relative to fetal monitoring: Variability

Back 49

Variability means small changes in FHR (fetal heart rate)

Front 50

You should have an understanding of the following terms relative to fetal monitoring: Range of fetal heart rate

Back 50

Normal baseline fetal heart rate is defined as 110-160 beats per minute (bpm) and is determined by assessing the mean heart rate over a 10-minute period rounded to increments of 5 bpm. - pg 143 of chestnut.

Front 51

You should have an understanding of the following terms relative to fetal monitoring: Fetal heart decelerations: (early, late, and variable)

Back 51

Early decelerations-Characterized by slowing of the FHR that begins with the onset of uterine contraction, Not indicative of fetal distress. Late decelerations-Characterized by slowing of the FHR that begins 10 to 30 seconds after the onset of uterine contraction. Associated with fetal distress. Variable decelerations- Variable in magnitude, duration, and time of onset. Generally characterized by a steep descent of FHR. Thought to be caused by umbilical cord compression. Unless prolonged, they are usually benign. Consider changing maternal position

Front 52

You should have an understanding of the following terms relative to fetal monitoring: Fetal scalp pH

Back 52

Fetal scalp pH- Not commonly performed-used when abnormal fetal heart rate patterns occur. It is used to confirm or exclude the presence of fetal compromise
A pH value are near 7.0= depression of fetus
A pH value higher than 7.2-7.25 = vigorous infant at birth

Front 53

What are the components of an Apgar score? What does it all mean?

Back 53

The Apgar score is a system of assessing the clinical status of a newborn. There are 5 parameters that are assessed at 1 and 5 minutes after birth, and can have a score of 0, 1, or 2. They parameters are: heart rate, respiratory effort, muscle tone, reflex irritability, and color. A score of 8 to 10 means normal; 4 to 7 indicates moderate impairment; 0 to 3 indicates immediate resuscitation.

Front 54

Understand what is included in basic and advanced neonatal resuscitation.

Back 54

(M&M p917) Normal: Respir: begins w/in 30sec & sustained w/in 90sec, 30-60 breaths/min, HR 120-160bpm, BP 50/25mmHg-70/40mmHg, Apgar score 8-10 @ 1 and 5 mins, thin/watery meconium. Indications for PPV: apnea, gasping respirations, persistent central cyanosis w/ 100% O2, HR <100bpm. Ventilate @ 30-60 breaths/min @ <30cm H2O pressure, chest compressions if HR 60-80bpm or less @ 120/min. Intubate with Miller 00, 0, or 1; 2.5-3.5mm ETT. Can cannulate umbilical vein for vascular access or umbilical arteries for BP and PaO2 monitoring. IVF if hypovolemic: 10mL/kg of LR, NS, or type-O negative blood. Epinephrine 0.01-0.03mg/kg of 1:10,000 for asystole or HR <60. Naloxone 0.1mg/kg prn for respir depressant effects of opioids (in mother). Sodium bicarb only for severe metabolic acidosis w/adeq ventilation per ABG.

Front 55

Which drug should be avoided in a baby born to a heroin – addicted mother?

Back 55

1. Morphine, b/c the active metabolite is heroin (morphine is pharmaceutical heroin)
2. Possibly opiates due to the synergistic RT depression. Heroin races to regions of the brain that control breathing. Too much heroin dangerously slows breathing, starving the heart of oxygen and causing it to stop beating.

Front 56

What are the causative factors involved in the following complications of obstetrical regional anesthesia and discuss treatment for each: Hypotension

Back 56

Neuraxial anesthesia induced sympathetic blockade leads to peripheral dilation and increased venous capacitance. Leads to reduced venous return and therefore decreased blood pressure and CO. To prevent, typically pre-treat with 0.5 L of crystalloid solution just prior to initiation of block. Treatment includes administration of additional crystalloids and placement of mother in complete lateral and trendelenberg position. If this fails, administeres ephedrine 5-10mg. Phenylephrine may also be considered based on the mother's heart rate. (Chestnut, p455-6)

Front 57

What are the causative factors involved in the following complications of obstetrical regional anesthesia and discuss treatment for each: Total spinal

Back 57

Total spinal: term applied to excessive sensory and motor anesthesia assoc w/ loss of consciousness. May be a direct consequence of LA effect above the foramen magnum. Manifested soon after injection into the the subarachnoid space.
Treatment: maintain airway and ventilation as well as circulation w/ sympathomimetics and IV fluids. Pts are placed a head-down position to facilitate venous return. For pregnant pts, intubation is warranted due to their high risk of aspiration.

Front 58

What are the causative factors involved in the following complications of obstetrical regional anesthesia and discuss treatment for each: Convulsions

Back 58

In OB, risk is low at 0.5%. CNS toxicity causes convulsions and is due to a high brain concentration of LA 2° to accidental IV administration, accumulation of LA during repeated injections over a prolonged period of time, or rapid systemic absorption of LA from highly vascular areas.
Tx: prevent progression of the reaction (small doses of barbs may prevent convulsions); maintain oxygenation with 100% O2 and a + pressure bag--be ready to give succs 80-100mg and intubate if necessary to provide an adequate airway and prevent aspiration; maintain CV status by elevating legs, placing the pt in left lateral position, and rapidly administering IV fluids and pressors if needed; check condition of fetus after incident to decide subsequent course of action.

Front 59

What are the causative factors involved in the following complications of obstetrical regional anesthesia and discuss treatment for each: Headaches

Back 59

Headaches: Cause: The puncture into the dura results in a loss of CSF at a rate exceeding production (production rate = 0.35Ml/min). The loss of CSF in the subarachnoid space, causes the medulla and the brain stem to drop into the foramen magnum. The subsequent stretching of the meninges and pulling on the tentorium caused by the mvmt may cause a headache. Pain also results from distention of the blood vessels, which must compensate for the loss of CSF b/c of the fixed volume of the skull. (Chestnut, 3rd ed, pp. 564-567)

Manifestations: pain begins 12-48hrs after. Lasts less than 1 week typically. The characteristic feature of PDPH is the postural component: it appears or intensifies w/ sitting or standing and is partially relieved by recumbency. Pain is in frontal and occipital regions and radiates to the neck (which may be stiff). (Chestnut, 3rd ed, pp. 564-567)

Risk Factors: Age: uncommon older than 60 years. Most common in patients < 40. Females are twice as susceptible.
Incidence is correlated with the diameter of the needle used to pierce the dura. (Chestnut, 3rd ed, pp. 564-567)

Treatment: bed rest, fluids, analgesics, and caffeine (500mg IV), epidural blood patch, epidural saline, epidural morphine, Abdominal binder – basically increasing pressure in the CSF will alleviate pain, whether it be through fluids, position, abdominal binder, vasoconstriction (caffeine). (Chestnut, 3rd ed, pp. 564-567)

Front 60

What are the causative factors involved in the following complications of obstetrical regional anesthesia and discuss treatment for each: Nerve injury

Back 60

Incidence ~ 0.03-0.1%; May result from trauma, either directly provoked by a needle or catheter or indirectly by compression from hematoma or abscess. LA if administered in sufficient quantity can induce permanent injury. Transient neurological symptoms are a common occurrence after the subarachnoid administration of certain local anesthetics, particularly lidocaine. (Barash, p948)
Nerve root irritation may have protracted recovery, lasting weeks to months. (Barash, p1149)
Tx: there is no specific treatment: symptoms resolve in 4-6wks for about 92% of pts and 99% in one year. (No source)

Front 61

What is organogenesis? What are the anesthetic implications?

Back 61

Organogenesis: is the process by which the ectoderm, endoderm, and mesoderm develop into the internal organs of the organism. Internal organs initiate development in humans within the 3rd to 8th weeks in utero. Most structural abnormalities result from exposure during the period of organogensis. Functional abnormalities are associated w/ exposure during late pregnancy or even after birth, b/c the CNS continues to mature during this period.
There is concern that anesthetics are teratogenic at clinical concentrations due to their potential harmful effects on cells which include reversible decreases in cell motility, prolongation of DNA synthesis, and inhibition of cell division. However, anesthetics nor any other drug routinely used in anesthesia is considered a teratogen.

Front 62

What are your major concerns for the obstetrical patient undergoing non-obstetrical surgery? Review how anesthetic management would be managed for a pregnant patient at 8, 20, and 37 weeks gestation undergoing an appendectomy.

Back 62

Non OB Most Common Surgical procedures: (Goal is to preserve the pregnancy until term. Management is directed at prevention of fetal loss.)
Trauma: leading cause of maternal death
Appendicitis
Ovarian cyst
Cholecystectomy
Breast biopsy
Abdominal laparoscopic procedures
Cervical cerclage: is the surgical intervention used to prevent 2nd trimester fetal loss from cervical incompetence.
Laparocopic surgery concerns: CO2 pneumoperitoneum
limit abd insufflation pressure to 15-20 mmHg
increase minute ventilation
Risk and concerns
Risk of fetal morbidity, spontaneous abortion, congentital malformations
Avoid: hypoxia, hypercarbia, hypotension, and elective operations until 6wks postpartum.
Review how anesthetic management would be managed for a pregnant patient at 8, 20, and 37 weeks gestation undergoing an appendectomy.
8wk gestation:
This week marks the end of organogenesis. Most structural abnormalities result from exposure during the period of organogensis. It is preferred to not do surgery during this time due the possible effects to the fetus.

20 wk gestation:
o If possible, postpone surgery until 2nd semester
o Consult an obstetrician
o Use a nonparticulate antacid for aspiration prophylaxis
o Document fetal heart tones before and after surgery
o Starting at about 20-24wks gestation, fetal monitoring during surgery is suggested if it doesn’t interfere w/ the surgical field.
o Blood glucose should also be checked if the procedure ends up taking longer.

37 wk gestation:
Airway:For general anesthesia, a cuffed ETT is indicated w/ RSI b/c this pt is at higher risk for aspirtion. Airway problems tend to occur more frequently w/ OB pts than healthy pts. (failure to intubate in OB pts is 1:250) This is true due to the soft-tissue edema often present in the hypopharynx. Breast enlargement and cephalad displacement of the thorax often makes maneuvering the laryngoscope into the mouth more difficult. Placement of a rolled towel lengthwise along the thoracic spine or widthwise under the shoulders helps to elevate the chest off the operating table.
Induction: Propofol produces no greater neonatal depression than STP and is rapidly cleared from the neonate. All induction agents gross the placenta rapidly, but neonatal depression is infrequently a problem when the cited doses are used. Traditionally induction of anesthesia has been delayed until prep for the surgery is completed. Surgery starts immediately after verification of ETT. This is due to the least amount of exposure of the fetus to induction agents.
Intubation: Succs remains the preferred muscle relaxant of choice. If succs is contraindicated, then a fast-acting NDMR is used and often an awake intubation is attempted. After relaxation, the trachea must be intubated expeditiously. B/c the pt’s FRC is decreased by 25% and her whole-body O2 demand is up to 30% greter than normal, desaturation occurs rapidly. Once apnea occurs, maternal O2 partial pressure drops three times as quickly as it would in a nonpregnant woman.
Maintenance: General can be maintained by Propofol or low doses of VAA (1/2 MAC). Maintenance of uterine perfusion and maternal oxygenation preserves fetal oxygenation (this is key) Above all avoid hypotension and hypoxia
Emergence: Even when given drugs to empty the stomach, a pregnant pt often has a large volume of gastric contents. Suctioning of the stomach w/ an OGT while the patient is anesthetized decreases the incidence of vomiting after awake extubation.

Front 63

Ion trapping of a local anesthetic in the fetus will be the greatest in which of the following situations: mom is alkalotic, mom is acidotic, fetus is alkalotic, fetus is acidotic?

Back 63

Most drugs, including locals, readily cross the placenta. Locals cross the placental membrane based on simple diffusion described by Fick’s Law.
The degree of ionization affects the rate of placental diffusion because the unionized molecule is more lipid soluble than the ionized molecule. Locals are wek bases; they have a relatively low degree of ionization and considerable lipid solubility at physiologic pH. The relationship between pH and pK(baby) may affect drug accumulation in the fetus. For the amide locs anesthesthetics in particular, pKbaby values are sufficiently close to physiological pH that changes in fetal acid-base status may significantly alter the balance between ionized and unionized drug. In the acidotic fetus, a greater proportion of drug in the ionized from results in a larger total amount of local anesthetic in fetal plasma. This is b/c of ion trapping. Also, accumulation of anesthetic, lidocaine for example, may be greater in the fetal tissues, where the pH is even lower than that of fetal blood.
Thus,unionized local anesthetics molecules freely pass through the placenta. Since fetal pH is lower than mater pH, more local anesthetics become ionized in fetal circulation and become trapped

Front 64

What is hemolytic disease of newborn? Erythroblastosis fetalis?

Back 64

Erythroblastosis fetalis is hemolytic anemia in the fetus or neonate caused by transplacental transmission of maternal antibodies to fetal RBCs. The disorder usually results from incompatibility between maternal and fetal blood groups, often Rh0 antigens

Front 65

Define and differentiate the following: Preeclampsia

Back 65

2-6% of parturients; Higher in primagravidas under 20 years of age or older than 35 years of age; exact cause is unknown; abnormality in the ratio of thromboxanes to prostacyclins; Hypertension, edema, and proteinuria; Diagnosis is sustained B/P > 140/90, 2+ or greater proteinuria, pretibial edema; magnesium used to treat;

Front 66

Define and differentiate the following: Eclampsia

Back 66

Eclampsia (826) is defined as those characteristics of preeclampsia w/ szs. “convulsions and/or coma not caused by a coincidental neurologic disease, which occurs during pregnancy or the peurperium (The time immediately after the delivery of a baby) in a woman whose condition also meets the criteria for preeclampsia.”
Epidemiology: most often occurs suddenly, in the the 3rd trimester near term.
Approximately 50% of all pts have sever preeclampsia; however, the classic triad HTN, proteinuria, and edema may be absent.
Risk factors:nulliparity, multiple gestation, molar pregnancy, triploidy, preexisting HTN or renal disease, nonimmune hydrops fetalis, and lupus.
Patho:Cerebral vasospasm, ischemia, edema, hemorrhage, and hypertensive encephalopathy, and DIC have been implicated in the pathogenesis of szs.

Front 67

Define and differentiate the following: Severe Preeclampsia (I think she made a typo here)

Back 67

Features of severe preeclampsia
1. BP > or = 160 mmHg systolic or > or = 110 mmHg diastolic on 2 occasions at least 6 hrs apart while the pt is on bed rest. Dx not delayed if the diastolic BP exceeds 110mmHg
2. Proteinuria > or = to 5g in a 24 hr urine specimen
3. Oliguria: urine output <500 mL in 24 hrs
4. Cerebral or visual disturbances: HA, blurred vision, or altered consciousness
5. Pulmonary edema or cyanosis
6. Epigastric or RUQ pain: believed to be caused by stretching of Glisson’s capsule by hepatic edema
7. Impaired liver function or Hepatic rupture: a rare complication
8. Thrombycytopenia
9. Fetal growth restriction

Front 68

Define and differentiate the following: HELLP syndrome

Back 68

HELLP syndrome: Hemolysis, elevated liver enzymes, and a low plt count. 5-10% of the sickest women w/ preeclampsia develop HELLP syndrome.
Clinical signs: include epigastric pain, upper abd tenderness, HTN, jaundice, N/V. Some experts believe that a degree of compensated DIC is present in all pts w/ HELLP syndrome.

Front 69

Discuss obstetrical management of preeclampsia and eclampsia. What are the essential pharmacologic interventions?

Back 69

The essential pharmacologic interventions are those that maintain uterine blood flow, treat hypertension, and maximize organ perfusion. Magnesium is used nearly universally.

Front 70

What are the first and second causes of death in preeclampsia?

Back 70

#1 seems to be CVA , #2 is a toss up between Hemorrhage, Renal and hepatic failure, pulmonary edema

Front 71

How does preeclampsia affect uteroplacental circulation?

Back 71

Preeclampsia can impair uteroplacental blood flow. Downstream resistance in the uteroplacental bed increases, diastolic flow velocity decreases, and the systolic-to-diastolic flow velocity ratio increases in preeclampsia. The systolic-to-diastolic blood pressure ratio, calculated from Doppler ultrasonographic determination of blood flow velocities, reflects intrinsic arterial resistance. Pathophysiologic changes can lead to intrauterine fetal growth restriction in some cases of preeclampsia. Chestnut (pg,984)

Front 72

Discuss anesthetic implications and choices for patients with preeclampsia, eclampsia, and HELLP syndrome for patients undergoing both vaginal delivery and C/Sections.

Back 72

M&M pgs 910-912
Pregnancy induced hypertension (PIH) more accurately describes preeclampsia, eclampsia, and HELLP. Patients with mild PIH generally require only extra caution during anesthesia; standard anesthetic practices may be used. Spinal and epidural anesthesia are associated with similar decreases in arterial blood pressure in these patients. Patients with severe disease, however, are critically ill and require stabilization prior to administration of any anesthetic.
HTN should be controlled and hypovolemia corrected before anesthesia. In the absence of coagulopathy, continuous epidural anesthesia is the 1st choice for most patients with PIH during labor, vaginal delivery, and cesarean section. Continuous epidural anesthesia avoids increased risk of a failed intubation due to severe edema of the upper airway. Platelet count and coagulation profile should be checked before regional anesthesia. Recommended to avoid regional anesthesia if platelet count is < 100,000/μL, as low as 70,000 may be acceptable. Continuous epidural anesthesia can decrease catecholamine secretion and improve uteroplacental perfusion up to 75%. Judicious colloid boluses before epidural may be better for hypovolemia correction than crystalloids; central line can guide replacement; pulmonary artery catheter needed for severe cases (marked htn, refractory oliguria, hypoxemia, or frank pulmonary edema). Hypotension should be treated with small doses of vasopressors (epinephrine 5 mg) because of sensitivity to these agents.
Intraarterial blood pressure should be monitored in severe hypertension for general and regional anesthesia. IV nitroprusside, trimethaphan, or nitroglycerin is usually necessary to control bp during general anesthesia. IV labetalol can help to decrease htn in response to intubation.
Magnesium potentiates muscle relaxants, so, nondepolarizing muscle relaxant doses should be reduced and guided by peripheral nerve stimulators.

Front 73

What is uterine atony? List 5 requirements for anesthetic management of uterine atony. Review three primary pharmacologic interventions for uterine atony. What are these drugs dosages, side effects and complications?

Back 73

M&M pgs 912-913; Baby Miller pgs 496-497; Chestnut pgs 559-560
Uterine atony is a loss of tone in the uterine musculature. It is the most common cause of postpartum hemorrhage, peripartum hysterectomy, and is often associated with uterine overdistention (multiple gestation and polyhydramnios). Other causes include: macrosomia, high parity, prolonged labor, chorioamnionitis, precipitous labor, augmented labor, tocolytic agents, high doses VAA.
Anesthetic management may be to assist in venous access or fluid resuscitation; provide anesthesia for careful examination of the vagina, cervix, and uterus; perineal lacerations repaired with local anesthesia or pudendal nerve blocks; residual anesthesia from epidural or spinal facilitates exam as well as supplemented opiods, nitrous oxide, or both may be needed; do not induce spinal or epidural in hypovolemia; general anesthesia usually required for bimanual massage of the uterus, manual extraction of a retained placenta, reversion of an inverted uterus, or repair of a major laceration
Pharmacologic interventions should include treatment with oxytocin (20-30 U/L of IV fluid at 10 mL/min), methylergonovine (0.2 mg intramuscularly) if oxytocin is ineffective, 15-Methyl prostaglandin F2α (carboprost or hemabate) (0.25 mg intramuscularly), prostaglandin E1 (misoprostol) (600 μg orally or sublingually).
Side effects and complications
Dilute solutions of synthetic oxytocins exert no cardiovascular effects, but rapid IV injections may be associated with tachycardia, vasodilation, and hypotension. These cardiovascular effects are avoided by infusion of 10 to 15 units of synthetic oxytocin in 500 mL of balanced salt solution until uterine contraction is adequate.
Methylergonovine should be used with great caution because intense vasoconstriction may lead to acute hypertension, seizures, CVA, retinal detachment, myocardial arrest, N&V.
15-Methyl prostaglandin F2α can cause diarrhea, HTN, vomiting, fever, flushing, and tachycardia, bronchospasm, pulmonary vasoconstriction, and oxyhemoglobin desaturation can also occur.
Prostaglandin E1 can cause hyperthermia.

Front 74

Placenta Previa: Define

Back 74

placenta implants in advance of the fetal presenting part; abnormally low implantation of the placenta in the uterus; total placenta previa completely covers the cervical os; parcial placenta previa covers part but not all of the cervical os; marginal placenta previa lies close to, but does not cover, the cervical os

Front 75

Placenta Previa: Incidence

Back 75

Incidence of placenta previa is 1:200 pregnancies (take from Dr. Harmon's powerpoint slides)

Front 76

Placenta Previa: Symptoms

Back 76

1. • Symptoms: Painless hemorrhage (***Painless vaginal bleeding - #1 sign) any bleeding seen in the third trimester is always assumed to be caused from a placenta previa until ruled otherwise.
2. The blood appears fresh devoid of clots

Front 77

Placenta Previa: Diagnosis

Back 77

See above. Classic sign is painless vaginal bleeding during 2nd or 3rd trimester; 1st bleeding episode usually occurs preterm and without contractions and is not related to any particular event. 1st episode typically stops spontaneously and fetal distress is uncommon with 1st episode of hemorrhage.

Front 78

Placenta Previa: “Double Setup”

Back 78

examination performed in the OR with all members of the obstetric care team present, including the anesthesia provider, obstetrician, and pediatrician making full preparation for cesarean delivery. Full preparation consists of application of maternal monitors, insertion of 2 large-gauge IV cannulae, administration of a nonparticulate antacid, and sterile preparation and draping of the abdomen; 2 units of PRBCs should be available in OR; obstetrician performs a careful vaginal exam; c-section performed if significant bleeding occurs or if placenta previa confirmed in woman with mature fetus; the accuracy of ultrasonography for the identification of placenta previa has almost eliminated the need for double setup exam

Front 79

Placenta Previa: Anesthetic management

Back 79

regional anesthesia is appropriate for elective cesarean delivery in a woman with known placenta previa; the use of 2 large-bore IV lines is suggested to allow rapid infusion of fluids or blood, if needed; for emergency situations with active hemorrhage, general anesthesia may be required, and ketamine (1 to 1.5 mg/kg IV) is a useful drug for induction of anesthesia.

Front 80

Define placenta accreta, increta, and percreta. What the predisposing factors for placenta accreta? What are the complications? Discuss anesthetic management.

Back 80

1. Placenta accrete vera = adherence to the myometrium w/o invasion of – or passage through – uterine wall
2. Placenta increta – invasion of the myometrium
3. Placenta percreta – invasion of the uterine serosa or other pelvic structures
Predisposing factors: previous cesarian sections, uterine trauma, current placenta previa or low lying placenta.
Anesthetic mgmnt:maintain hemodynamics, plan for blood loss, use c-section.

Front 81

Abruptio Placenta: Definition

Back 81

complete or partial separation of the placenta from the decidus basalis before delivery of the fetus

Front 82

Abruptio Placenta: Incidence

Back 82

There is an incidence of 0.4% to 1% with the incidence increasing among black women.

Front 83

Abruptio Placenta: Etiology

Back 83

(M&M p 908) Bleeding into the basal layers of the decidua causes placental separation. Expansion of the hematoma can progressively extend the separation possibly into the myometrium. Risk factors: HTN, trauma, short umbilical cord, multiparity, ETOH, cocaine, abnormal uterus, prolonged premature ROM.

Front 84

Abruptio Placenta: Symptoms

Back 84

vaginal bleeding, uterine tenderness, and increased uterine activity; in some cases may manifest as idiopathic preterm labor; may have variety of nonreassuring fetal heart rate patterns, including bradycardia, late or variable decelerations, and/or loss of variability; in concealed abruption, vaginal bleeding may be absent, and a gross underestimation of maternal hypovolemia can occur

Front 85

Abruptio Placenta: Diagnosis

Back 85

Usually diagnosed by classic presentation of vaginal bleeding, uterine tenderness and increase uterine activity. Ultrasound can also confirm the diagnosis. (Chestnut, p.815)

Front 86

Abruptio Placenta: Obstetrical management

Back 86

FHR should be monitored, and if feasible, an internal scalp electrode and intrauterine pressure catheter should be placed; a large-bore IV catheter should be inserted, and blood should be obtained for cross-match and assessment of hct and coagulation; supplemental oxygen should be administered, and left uterine displacement should be maintained; placement of urethral catheter helps the physician assess the adequacy of renal perfusion; definitive treatment is delivery of the infant

Front 87

Abruptio Placenta: Anesthetic implications

Back 87

First consider severity of abruption and urgency of delivery. For vaginal delivery, epidural if coag profile is WNL. Ensure pt has adequate IV access and is T&C for 2 units PRBC minimally and other blood units are available. For stat C/S 2° fetal distress, GA is preferred. Ketamine (1 mg/kg) and etomidate (0.2 mg/kg) are better choices than STP and propofol b/c of their minimal effect on BP. Aggressive volume resuscitation with crystalloids and colloids is common. If coagulopathy is suspected or confirmed, CVP monitoring should be accessed via AC (antecubital) vein and NOT IJ or SC vein. All should have A-line placed prior to induction of anesthesia.

Front 88

Amniotic Fluid Embolism: Definition

Back 88

Amniotic fluid embolism is a devastating condition that is unique to pregnancy. First reported in 1926, it was not until 1941 that a series of autopsies described the syndrome of sudden peripartum shock characterized by pulmonary edema (Chestnut, 3rd ed, pp. 688).

Front 89

Amniotic Fluid Embolism: Incidence

Back 89

4-6 per 100000 live births; may be higher in multiple gestation births 14.5/100000
Parturient mortality between 25-80%
(Chestnut, p844)

Front 90

Amniotic Fluid Embolism: Symptoms

Back 90

sudden tachypnea, cyanosis, shock, and generalized bleeding; seizures and pulmonary edema may develop

Front 91

Amniotic Fluid Embolism: Hemodynamic consequences

Back 91

biphasic response; early phase consists of transient pulmonary vasospasm (pulmonary hypertension), which most likely results from the release of vasoactive substances and may account for the often fatal right heart dysfunction; low cardiac output leads to increased ventilation-perfusion mismatch; second phase consists of left ventricular failure and pulmonary edema in women who survive initial insult

Front 92

Amniotic Fluid Embolism: Why does DIC occur

Back 92

unclear, but some suggest that circulating trophoblast may be responsible for the disruption of the normal clotting cascade; in addition, uterine atony occurs in some women; massive hemorrhage may also contribute to a consumptive coagulopathy

Front 93

Amniotic Fluid Embolism: Predisposing factors

Back 93

Advanced maternal age, multiple pregnancies, macrosomic fetuses, short duration of labor, and intense contractions often augmented with a uterine muscle stimulant such as oxytocin

Front 94

Amniotic Fluid Embolism: How is diagnosis made

Back 94

diagnosis of exclusion; definitive diagnosis is extremely difficult or impossible, even postmortem; can only firmly be established by demonstrating fetal elements in the maternal circulation (usually at autopsy or less commonly by aspirating amniotic fluid from a central venous catheter); should always be suggested by sudden respiratory distress and circulatory collapse

Front 95

Amniotic Fluid Embolism: What other pathophysiologic events could mimic AFE

Back 95

pulmonary thromboembolism, venous air embolism, inhalation of gastric contents, overwhelming septicemia, or hepatic rupture or cerebral hemorrhage in a patient with toxemia

Front 96

Amniotic Fluid Embolism: Treatment

Back 96

1. Initiate CPR if necessary
2. Support maternal circulation
3. Perform IV volume resuscitation
a. Establish IV access with several large bore IV’s
b. Insert A-line
c. Begin inotropic support (dopamine, norepinephrine etc.)
4. Perform fetal monitoring (Make decision regarding delivery either before impending maternal demise or to improve maternal resuscitation efforts)
5. Treat the coagulopathy
a. Decide between component therapy or fresh whole blood
b. Obtain early consultation with hematologist and blood bank pathologist
6. Manage sequelae of shock (i.e. cardiac failure, pulmonary edema, ARDS, renal failure, hepatic failure, neurological sequelae)
7. Anticipate a prolonged ICU stay

Front 97

Uterine rupture: etiology, risk factors, symptoms, management, and anesthesia implications. Should women at risk for uterine rupture receive epidurals for labor?

Back 97

Baby Miller pg 496; M&M pgs 908-909
Uterine rupture - associated with separation of a previous cesarean section and healed incision (scar) in the uterus, rapid spontaneous delivery, or excessive oxytocin stimulation; 80% spontaneous without an obvious explanation
Risk factors – result of (1) dehiscence of a scar from a previous cesarean section, extensive myomectomy, or uterine reconstruction; (2) intrauterine manipulations or use of forceps; (3) spontaneous rupture following prolonged labor in patients with hypertonic contractions, fetopelvic disproportion, or a very large, thin and weakened uterus
Symptoms – frank hemorrhage, fetal distress, loss of uterine tone, and/or hypotension with occult bleeding into the abdomen; abrupt onset of continuous abdominal pain and hypotension
Management – volume resuscitation and immediate laparotomy under general anesthesia; ligation of the internal iliac (hypogastric) arteries, with our without hysterectomy, may be necessary to control intraoperative bleeding
Anesthetic implications – local anesthetics for epidural anesthesia during labor may mask early recognition of uterine rupture
Women at risk for uterine rupture should receive a diluted concentration of local anesthetics for epidural anesthesia.

Front 98

What are the risks to mothers presenting with the following heart pathology: Pulmonary hypertension

Back 98

Risks to mothers include: SOB, syncope, peripheral edema, cor pulmonale (right heart failure).

Front 99

What are the risks to mothers presenting with the following heart pathology: Mitral stenosis

Back 99

prevents filling time of the left ventricle, which decrease SV and CO leading to decreased left atrial emptying and possible pulmonary edema

Front 100

What are the risks to mothers presenting with the following heart pathology: Tetralogy of Fallot

Back 100

1) a VSD, 2) right ventricular hypertrophy, 3) pulmonic stenosis with right ventricular outflow tract obstruction, and 4) overriding aorta (receives blood from both right and left ventricles). Any decrease in SVR increases severity of R-L shunt leading to maternal-fetal hypoxemia. The goal in anesthesia is to maintain volume and SVR and prevent increase in PVR. M&M (pg.482)

Front 101

What are the risks to mothers presenting with the following heart pathology: Marfan Syndrome

Back 101

in addition to MVP, pt’s may develop dilation of ascending aorta (possibly progressing to dissecting aneurysm, aortic incompetence, rupture of aorta). Possibly associated with cervical incompetence, abnormal placentation and postpartum hemorrhage.

Front 102

What are the risks to mothers presenting with the following heart pathology: Aortic stenosis

Back 102

women with mild aortic stenosis are able to tolerate pregnancy, though at risk for infective endocarditis after delivery. Sever stenosis causes a limited ability to compensate for increased demands of pregnancy, and may develop dyspnea, syncope or angina.

Front 103

What is amniotic fluid? What a normal amount? What is a L-S ratio?

Back 103

Clear slightly yellowish liquid that surrounds the unborn baby (fetus) during pregnancy. Composed of fetal urine, lung fluid, skin transudate, and water that is filtered across the amniotic membranes. It contains electrolytes, proteins, and desquamated fetal cells. The average amount is 800 mL at 34 weeks; the average amount is 600 mL at 40 weeks The L-S ratio (Lecithin-Sphingomyelin) ratio is a test for assessing fetal lung maturity

Front 104

Differentiate between chronic hypertension, gestational hypertension and preeclampsia.

Back 104

- Gestational hypertension• Systolic blood pressure ≥ 140 mm Hg or diastolic blood pressure ≥ 90 mm Hg at or after 20 weeks of gestation in a previously normotensive woman, but without proteinuria
- Chronic hypertension• Systolic blood pressure ≥ 140 mmHg or diastolic blood pressure ≥ 90 mm Hg that is documented prior to the 20th week of gestation
- preecalmpsia- the triad of hypertension, proteinuria (>500mg/d) and edema (hand/face) occuring after 20 weeks of gestation and resolving within 48h after delivery (M&M p 910)

Front 105

What is gestational diabetes? What is the White classification system for diabetes? Why is diabetes a significant disorder during pregnancy?

Back 105

What is gestational diabetes? Develops when a pt can’t mount a sufficient compensatory insulin respoinse dudring pregnancy. In some, GDM can be a preclinical state of glucose intolerancethat isn’t detectable before pregnancy. After delivery, most pts return to normal but with increase chance of developing DM (mostly Type 2) later in life. What is the White classification system for diabetes? A system developed to emphasize the relatonship among the duration of type 1 DM, vascular complication of type 1 DM, and poor fetal outcome. See Table. Why is diabetes a significant disorder during pregnancy? Pregestational and GDM are associated with increased incidence of PIH, polyhydramnios, and c-section (three to ten fold increased incidence in pregestational and 1.5 times that in GDM). Preterm labor and delivery.

Front 106

What is chorioamnionitis? What are your anesthesia concerns with parturients with infections?

Back 106

Chorioamnionitis (amnionitis, intraamniotic infection) occurs in approximately 1 to 5 percent of term pregnancies. In patients with preterm delivery, frequency of clinical or subclinical infection may approach 25 percent. Although chorioamnionitis may result from hematogenous dissemination of microorganisms, it more commonly is an ascending infection caused by organisms that are part of the normal vaginal flora. The principal pathogens are Bacteroides and Prevotella species, E. coli, anaerobic streptococci, and GBS. Several clinical risk factors for chorioamnionitis have been identified. The most important are young age, low socioeconomic status, nulliparity, extended duration of labor and ruptured membranes, multiple vaginal examinations, and preexisting infections of the lower genital tract. Diagnosis of chorioamnionitis requires either a fever (

Front 107

What is a tocolytic drug? Identify 3 tocolytic agents. Should atropine be administered to a pregnant patient receiving ritodrine? Why or why not?

Back 107

A tocolytic drug is a drug that is used to stop labor. “stopping labor is termed tocolysis”
Magnesium sulfate, B-adrenergic receptor agonists, nitric oxide donors, calcium channel blockers, prostaglandin synthesis inhibitors, and oxytocin antagonists.
Ritodrine is a tocolytic drug used to stop labor….. Why or why not? No, do not administer these two together. This is why Ritodrine is a beta 2 selective adrenergic agonist. Despite this classification it also stimulates beta 1 adrenergic receptors. Because of this is elicits the all the effects of beta adrenergic agonists. Atropine is a muscarinic antagonist, so since stimulation of cardiac muscarinic receptors decreases heart rate, blockade of these receptors with atropine will cause the heart rate to increase. Atropine causes the heart rate to increase.

Front 108

Magnesium sulfate: Why is it used?

Back 108

It is used as a tocolytic drug, to stop labor, preeclampsia/eclampsia

Front 109

Magnesium sulfate: When is it used?

Back 109

pre-eclampsia treatment in pregnant women. Delays labor in the case of premature labor, to delay preterm birth.

Front 110

Magnesium sulfate: What is the pharmacology of magnesium sulfate?

Back 110

Magnesium relaxes uterine and vascular smooth muscle, which contributes to an increase in uterine blood flow. Magnesium works in the obstetric patient who has preeclampsia by decreasing the irritability of the central nervous system, which decreases the likelihood of seizures. Magnesium also decreases hyperactivity at the neuromuscular junction, presumably by decreasing the presynaptic release of acetylcholine, as well as by decreasing the sensitivity of postjunctional membranes to acetylcholine.

Front 111

Magnesium sulfate: What are clinical assessments of the effects of MgSO4?

Back 111

The effects are estimated by the response of the deep tendon reflexes (DTR). Depression of the DTRs indicates magnesium toxicity.

Front 112

Magnesium sulfate: Discuss lab values for magnesium sulfate.

Back 112

(N'hout p. 1129) Normal: 1.8-3mg/dL. Therapeutic as tocolytic: 4-8mg/dL. Anticonvulsant: 7-9.5mg/dL. Eliminates patellar reflex: 10-12mg/dL. Respiratory depression: >12mg/dL. Apnea: >18mg/dL. Cardiac Arrest: >25mg/dL

Front 113

Magnesium sulfate: Discuss treatment of magnesium sulfate toxicity

Back 113

Calcium gluconate 1 gram over 10 mins (Chestnut, p. 986)

Front 114

The preeclamptic patient should not receive which general anesthetic?

Back 114

The maternal brain is edematous and more sensitive to CNS-depressant drugs. THIS WAS FOUND IN NAGELHOUT PP. 1138,confirmed this during lecture with Prof. Hogan…… note**DO NOT GIVE PREECLAMPITC patients Ketamine because it stimulates the sympathetic nervous system and increases systemic BP, HR, and cardiac output. Baby miller page 490.

Front 115

Identify 2 pharmacologic treatments for a hypertonic uterus.

Back 115

Terbutaline IV or NTG (nitroglycerine) IV 60-90 mcg. Both relax the uterus.

Front 116

What is the therapeutic action of oxytocin? What are the adverse effects associated with oxytocin?

Back 116

Oxytocin produces selective stimulation of uterine smooth muscle. The principal uses of oxytocin are to induce labor at term and to counter uterine hypotonicity and decrease hemorrhage in the postpartum or postabortion period. (Stoelting and Hiller, Handbook of Pharmacology, 2nd ed. Pp 487)

Side effects: high doses of oxytocin produce a direct relaxant effect on vascular smooth muscles (hypotension, flushing, reflex tachycardia). (Stoelting and Hiller, Handbook of Pharmacology, 2nd ed. Pp 487)

Oxytocin is one of two hormones secreted by the posterior pituitary (arginine vasopressin the other). It causes ejection of milk and nuclei uterine contraction. (Stoelting and Hiller, Handbook of Pharmacology, 2nd ed. Pp 945)

The primary role of oxytocin is to eject milk from the lactating mammary gland. Large amounts of oxytocin cause the sustained uterine contraction necessary for postpartum hemostasis. (Stoelting and Hiller, Handbook of Pharmacology, 2nd ed. Pp 949)

Front 117

Which local anesthetic accumulates the least in the fetus and why?

Back 117

Ester-linked LAs (procaine, chloroprocaine, tetracaine) are rapidly metabolized by plasma cholinesterase, thus limiting the risk for maternal toxicity and placental drug transfer.
2-Chloroprocaine has a rapid onset time and short-lived duration of action. Its rapid metabolism by ester hydrolysis (t1/2 = 45 seconds) makes it a safe agent in obstetrics b/c almost no drug crosses the placenta.
(mostly Evers, p527)

Front 118

Should the obstetrical patient be pre - curarized prior to the delivery of general anesthesia for an Emergency c/Section?

Back 118

Since all pregnant patients are treated as if they have a full stomach,RSI is the usual, succinylcholine 1 to 1.5 mg/kg is the standard neuromuscular blocker of choice. Baby miller page 492, under neuromuscular blocking drugs

Front 119

Which maternal nerve block will cause the most fetal bradycardia? Why?

Back 119

A paracervical block is associated with a relatively high incidence of fetal bradycardia after the block. The cause of this phenomenon is unclear but probably involves decreased uterine blood flow secondary to the vasoconstrictive properties of local anesthetics.

Front 120

Which types of blocks can be used for first stage of labor pain?

Back 120

Epidural segmental bands of analgesia T10-L1., paracervical block.

Front 121

What is meconium aspiration? What is treatment or protocols?

Back 121

Meconium aspiration is a common neonatal outcome of intrauterine asphyxia and requires expert and prompt management to avoid the risks associated with meconium aspiration pneumonitis. Immediate ET intubation and tracheal/bronchial sxn should be performed in all depressed newborns born through meconium staining. This will remove particulate material that is impossible to dislodge through smaller suction catheters and should be repeated until suctioning through the ett retrieves no meconium.

Front 122

What are 6 anesthetic considerations for the patient with an inverted uterus during a vaginal delivery?

Back 122

EMERGENCY; need a large bore IV for rapid fluid resusitation; sevo, halo, iso are uterine relaxants; The uterus is most commonly inverted when too much traction is applied to the umbilical cord in an attempt to deliver the placenta. Excessive pressure on the fundus during delivery of the placenta, a flaccid uterus, or placenta accreta (abnormally adherent placenta) can contribute. Treatment is immediate manual reduction by pushing up on the fundus until the uterus is returned to its normal position. If the placenta is still attached, the uterus should be replaced before the placenta is removed. Because of discomfort, IV analgesics and sedatives or a general anesthetic are sometimes needed relaxes the uterus. Terbutaline (BRETHINE, BRICANYL).. MAGNESIUM SULFATE, nitroglycerin. IF attempts to return the uterus are unsuccessful, a laparotomy may be necessary; the fundus is manipulated vaginally and abdominally to return it to its normal position.

Front 123

List 6 steps in the treatment of local anesthetic toxicity in the OB patient undergoing epidural anesthesia.

Back 123

The most serious complications of regional anesthesia are due to accidental IV or subarachnoid injection of LAs. Accidental injection can result in maternal seizures and possible cv collapse. Resusctiation and support of the mother will reestablish uterine bld flow and allow adequate fetal oxygenation and excretion of the LA.
Also, systemic hypotension secondary to SNS block is a common complication. Prophylactic measures include adequate hydration, avoidance of supine position, and leftward displacement of the uterus off the abdominal aorta and vena cava. Treament include more uterine displacement, IV fluids, and administration of a vasopressor. Ephedrine 5-15 mg or Phenylephrine 25-50mcg can be used to tx hypotension. Seizures can be treated with Thiopental 50-100mg.
An excessive level of neural blockade (high or total spinal) may develop during initiation of a spinal, epidural, or caudal block or during continuous influsion and lead to block of the motor nerves to the respiratory muscles. Treatment consists of intubation and ventilation. (M+M, 899)

Front 124

What nerve is most commonly associated with vaginal delivery and why?

Back 124

Pudendal nerve b/c it includes somatic nerve fibers from the anterior primary divisions of the second, third, and fourth sacral nerves, and it represents the primary source of sensory innervation for the lower vagina, vulva, and perineum.

Front 125

How would you best assess a patient’s ability to have a labor epidural is there is a concern relative to a bleeding disorder?

Back 125

Concern exists that an epidural hematoma may develop after the administration of regional anesthesia in pts with coagulopathy. There are only 8 published cases of epidural or spinal subdural hematoma after the administration of epidural anesthesia in pregnant pts. This suggests that epidural hematoma after regional anesthesia is either very rare or underreported.
Remember, frank coagulopathy represents an absolute contraindication to the administration of epidural or spinal anesthesia. Clinical judgment represents the most impt means of assessing the risks for epidural hematoma in an individual pt.
In addition, pts on minidose heparin is controversial..Epidural should not be performed 6-8 hours of a SQ dose of unfractionated heparin or 12-24 hours of a LMW heparin such as lovenox. Use of antiplatelet drug such as Plavix or ASA also increases the risk of spinal hematoma. (M+M, 897)

Front 126

Review common causes of premature labor. How would premature labor be treated?

Back 126

Common causes include: extremes of maternal age, ETOH, tobacco, illicit drugs, multiparity, fertility drug use, infection, trauma. Tocolytics (turbutaline) are used to temporarily halt labor.

Front 127

Discuss the usage of intravenous opioids for treatment of labor pain.

Back 127

Used to help tolerate labor pain but are unable to provide complete analgesia. Use can lead to Maternal sedation and nausea, and neonatal respiratory depression and neurobehavioral changes. PCA may be better choice than bolus dosage.

Front 128

What are the side effects of intrathecal opioids and their treatment?

Back 128

• Increased risk for PDPH b/c additional doses require repeat dural punctures or the presence of an intrathecal catheter
• Neurotoxicity – potential for irritation and outright damage to neural structures
• Effect on the progress of labor – may prolong labor and increase the risk of operative delivery
• Sensory changes – (with sufentanil) pts may feel that they cannot breathe or swallow; afferent information from A-delta and C fibers to the spinal cord are blocked, but the efferent nerve impulse is unaffected…so motor function is not impaired; symptoms usually subside in 30-60 minutes
• Hypotension - vasopressors
• N/V – antiemetics (reglan, zofran, scopolamine, cyclizine, decadron)
• Pruritus – narcan, Benadryl, nubain, propofol, prophylactic zofran
• Respiratory depression
• Urinary retention – bladder catheterization, narcan
• Delayed gastric emptying
• Recrudescence of herpes simplex viral infection
• Fetal side effects – effects on FHR and respiratory depression after delivery
M&M (pg. 266-270)

Front 129

What is considered normal blood loss for vaginal delivery? C/Section?

Back 129

Vaginal delivery is 300-500 ml C/Section? 800-1000 ml. (Baby Miller, 476)

Front 130

What the most common causes of fetal distress?

Back 130

Fetal distress is a widely used but poorly defined as a progressive fetal asphysxia that if not corrected will result in decompensation of the physiologic responses (primarily redistribution of blood flow to preserve oxygenation of vital organs) and cause permenant central nervous system and other damage or death.

Front 131

How is the management of pregnant patient different 24 hours post delivery for an anesthetic for a PPTL?

Back 131

PPTL = Post Partum Tubal Ligation The placenta is the primary site of progesterone production, and progesterone concentrations fall rapidly after the delivery of the placenta. Typically progesterone concentrations decline within 2 hours of delivery, and by 24 hours postpartum, progesterone levels are similar to those found in the luteal phase of the menstrual cycle. Remember progesterone produces sedation and may require a decrease in MAC before induction- without the placenta, requirements may return to normal. Also, progesterone causes a decreases gastric motility, so with the loss of the placenta, gastic motility should be restored.

Front 132

What are the effects of positioning the pregnant patient? Each trimester

Back 132

"Compression of the inferior vena cava by the gravid uterus occurs in all patient positions, but venal cava compression is greatest in the supine position. Aortocaval compression is caused by the gravid uterus compressing the inferior vena cava and the aorta and manifests principally as hypotension and tachycardia. Aortic compression may lead to decreases in uterine and placental blood flow resulting in fetal distress. Aortocaval compression is prevented by uterine displacement (lateral position or a wedge under the right hip) to increase venous return. Symptoms may be treated with intravenous fluid administration, supplemental oxygen, and ephedrine.

• Supine – Up to 20% of women at term develop the supine hypotension syndrome, which is characterized by hypotension, associated with pallor, sweating, nausea and vomiting. The cause of this syndrome appears to be the complete or near complete occlusion of the inferior vena cava by the gravid uterus. The treatment is typically turning the patient on her side, because it restores venous return from the lower body and corrects the hypotension.
• Trendelenburg – may exacerbate caval compression

• Lithotomy – FRC is reduced (which is already reduced starting in the 2nd trimester) with this position predisposiing to ateletasis and hypoxia, increase venous return acutely but can lead to CHF, MAP increases, but cardiac output is relatively unchanged, rapid lowering of legs can lead to hypotension, take BP immediately after lowering the legs for this reason

• Right lateral decubitus uteroplacental perfusion and fetal condition often improve after the patient has assumed the lateral decubitius position. In some cases of cord compression the fetus will tolerate the left but not the right lateral decubitus position or vice versa. (chestnut 451)
"

Front 133

What are the effects of positioning the pregnant patient? Supine

Back 133

"Compression of the inferior vena cava by the gravid uterus occurs in all patient positions, but venal cava compression is greatest in the supine position. Aortocaval compression is caused by the gravid uterus compressing the inferior vena cava and the aorta and manifests principally as hypotension and tachycardia. Aortic compression may lead to decreases in uterine and placental blood flow resulting in fetal distress. Aortocaval compression is prevented by uterine displacement (lateral position or a wedge under the right hip) to increase venous return. Symptoms may be treated with intravenous fluid administration, supplemental oxygen, and ephedrine.

• Supine – Up to 20% of women at term develop the supine hypotension syndrome, which is characterized by hypotension, associated with pallor, sweating, nausea and vomiting. The cause of this syndrome appears to be the complete or near complete occlusion of the inferior vena cava by the gravid uterus. The treatment is typically turning the patient on her side, because it restores venous return from the lower body and corrects the hypotension.
• Trendelenburg – may exacerbate caval compression
"

Front 134

What are the effects of positioning the pregnant patient? Lithotomy

Back 134

Lithotomy – FRC is reduced (which is already reduced starting in the 2nd trimester) with this position predisposiing to ateletasis and hypoxia, increase venous return acutely but can lead to CHF, MAP increases, but cardiac output is relatively unchanged, rapid lowering of legs can lead to hypotension, take BP immediately after lowering the legs for this reason

Front 135

What are the effects of positioning the pregnant patient? Right lateral decubitus

Back 135

Right lateral decubitus uteroplacental perfusion and fetal condition often improve after the patient has assumed the lateral decubitius position. In some cases of cord compression the fetus will tolerate the left but not the right lateral decubitus position or vice versa. (chestnut 451)

Front 136

Discuss management of an “epidural wet tap”

Back 136

conservative treatment involves recumbent position, analgesics, intravenous or oral fluid administration, and caffeine. Keeping the patient supine will decrease the hydrostatic pressure driving fluid out the dural hole and minimizing the headache if postdural puncture headache (PDPH) develops from the wet tap. Analgesic medication may range from acetaminophen to NSAIDs. Hydration and caffeine work to stimulate production of CSF. Caffeine further helps by vasoconstricting intracranial vessels. An epidural blood patch is a very effective treatment for PDPH. 15-20 ml of autologous blood is injected into the epidural space at, or one interspace below the level of the dural puncture. Pg 319 of M&M. With a wet tap, the catheter can be replaced at an alternate interspace or continuos spinal analgesia may be given through the existing catheter. - pg 461 of chestnut.

Front 137

What signs and symptoms of Post dural puncture headache?

Back 137

Occipital and frontal HA's, stiff or painful neck. symptoms worse standing up, better lying down. nausea and vomiting

Front 138

How do manage a patient with PDPH?

Back 138

Mild H/A are cured with best rest, hydration, oral analgesics, epidural injection of 50 ml of saline(preservative-free I would think)and caffeine sodium benzoate 500mg IV.
Discuss technique and risks of an epidural blood patch. Moderate to severe H/A require aTo a blood patch, up to 15-20 mL of the patient's blood is placed in the epidural space to seal the dural hole and to elevate low CSF pressure. If the first patch fails, a second can be done. If symptoms fail to resolve, alternative diagnoses should be excluded. Risks include infection, menegitis, seizures, back pain, late onset ecclampsia. Some controversy has arisen regarding the optimal volume of blood to be injected; however, most practitioners use 15 to 25 mL and stop injection of the blood if severe pain occurs. Although the incidence of complications (especially back pain) increases with increased volume, it appears that increased volume also increases the success rate. The lateral position is more comfortable for the patient during the procedure and for 1-2 hours afterwards. (M+M, 900)

Front 139

Discuss technique and risks of an epidural blood patch.

Back 139

The lateral position is more comfortable to the patient during the procedure that is done using sterile/ aseptic technique. If unsure about the location of the dural puncture, the more caudad (toward the feet) space should be chosen. The epidural space is identified. Then an assisting nurse draws 10 -20 ml of blood from the patient, then the patient’s blood is injected slowly through the epidural needle. If back, leg, or neck pain occurs, the procedure should be terminated. Back pain is sometimes resolved by slowing the rate of the injection. Occasionally a small amount of CSF is noted upon entry of the needle into the epidural space leading to doubt of correct placement. In this case a small test dose of local anesthetic may be administered, sufficient to cause a rapid onset of spinal anesthesia if the needle tip is in the intrathecal space. If w/o neuroblockade the blood patch can be done. After the procedure the patient should rest quietly in the horizontal position for 1 to 2 hours. Ambulation can occur after the 1- 2 hour mark, but no vigorous physical activity for several days. Pt. should be counseled to report severe back pain, fever, or radiating lower extremity pain. RISKS to OB patients: Meningitis, cauda equina, subdural hematoma, radicular back pain, pneumocephalus, arachnoiditis, seizures.

Front 140

What are the etiologies and precipitating factors of pre-eclampsia?

Back 140

(N'hout p.1135) Etiologies: Exact cause unknown but probably involves abnormality in ratio of thromboxanes (vasoconstrictor & plt aggregator) to prostacyclins (vasodilator & inhibitor of plt aggregation). Precipitating Factors: primigravidas <20yo or >35yo, previous preeclampsia, women with vascular disorders (M&M p910).

Front 141

What are the PaO2 and the PaCO2 in the normal fetus?

Back 141

In the fetus, the umbilical artery (UA) is traveling to the placenta. It therefore carries with it the metabolic waste products of the fetus. Hence, it has low PaO2, SpO2, and pH values, and high PaCO2 values.
Conversely, the umbilical vein (UV) is returning blood from the placenta. It therefore has higher values for PO2, SpO2, and pH, and low values for pCO2. See the table below
PO2 PCO2 SpO2 pH
UA 12-18 48-54 28% 7.24-7.29
UV 26-32 38-42 70% 7.30-7.35
For simplicity in remembering the UA/UV pO2/pCO2 values, remember that UA PaO2 value is the lowest at approximately 20 torr. These values increase by 10 in a counter clockwise fashion until you reach a high value fo 50 torr in the UA pCO2 column. See table below:
pO2 pCO2
UA 20 50
UV 30 40

Front 142

How and why does the fetal heart rate normally fluctuate with maternal blood pressure? How is that affected if mother is hypertensive?

Back 142

Maternal blood pressure changes affect uteroplacental blood flow. If too low or too high, the blood getting to the fetus is decreased and therefore causes fetal hypoxemia. Bradycardia is the initial fetal response to hypoxemia. After prolonged hypoxemia, fetus may experience tachycardia. (Chestnut, p. 143)

Front 143

How and why does the fetal heart rate normally fluctuate with maternal blood pressure? What is normal fetal heart rate?

Back 143

120-160 bpm

Front 144

How and why does the fetal heart rate normally fluctuate with maternal blood pressure? What is fetal bradycardia and tachycardia?

Back 144

Uteroplacental perfusion is proportional to maternal BP. Normal fetuses have 15-40 accelerations in HR per hour, thought to be d/t ↑ in catecholamine secretion with ↓ in vagal tone. Normal FHR= 110-160 bpm. Fetal bradycardia is < 100 bpm and tachycardia is > 160. Uteroplacental perfusion is ↓ in PIH (preg-induced HTN) which can lead to fetal hypoxia and ↓ HR variability.

Front 145

What are two signs of fetal hypoxia?

Back 145

Late type 2 decelerations, variable type 3 decelerations (M&M, 4th ed. pp 915)

Front 146

Your pregnant patient is preeclamptic and has temporomandibular joint (TMJ) rigidity. What would be safe anesthetics to consider?

Back 146

"Cannot find an answer to this question.
Ketamine should be avoided in PreE due to cardioacceleratory effects.
Muscle relaxants may have prolonged effects if magnesium is being administered."

Front 147

What is definitive treatment for pregnancy – induced hypertension?

Back 147

Definitive treatment of PIH is delivery of the fetus and placenta. (M&M, p. 911)

Front 148

When is ketamine used for Cesarean section? Specify what does is used.

Back 148

Ketamine is a good bronchodilator and therefore may be helpful when pregnancy complicates asthma or other airway diseases. Low IV doses of ketamine are within the range of 10 to 25mg, up to a total of 1mg/kg. Neonatal depression has not been demonstrated after maternal ketamine doses of up to 1mg/kg. (Nagelhout, p. 1115)

Front 149

What is the risk of aspiration in the early post partum period?

Back 149

The patient continues to be at an increased risk for aspiration if they have been NPO for at least 6-8hours postpartum before tubal ligation in hope of improving the likelihood of gastric emptying. Evaluation of the pt to include assessment of hemodynamic status (blood loss) and consideration of anesthetic technique (regional vs. general). Consider also if opioids were used and has blunted some of their reflexes. No time period guarantees the postpartum patient will be free from the risk of aspiration. The pt should be given zantac, raglan and bicitra and rapid sequence intubation used. (S&M, p. 502; Nagelhout)

Front 150

How can that risk of aspiration be managed for a post partum tubal ligation?

Back 150

The patient planning to have an elective PPTL within 8 hours of delivery should have no oral intake of solid food during labor, or postpartum until the time of surgery. Two important questions to address during the preanesthetic evaluation of a PPTL are: 1. What is the duration of the fast for solids? 2. Were parenteral opioids administered during labor? No time interval guarantees the postpartum patient is free from risk of aspiration. Per the PPT give zantac, reglan and bicitra and proceed with rapid sequence intubation. As always hold cricoid pressure until tube is in place and secured.

Front 151

What are 5 advantages of volatile agents for the patient undergoing elective C/section?

Back 151

The speed of induction, control of the airway, superior hemodynamics, great for preventing maternal recall, fetal concentration of drug depends on the concentration and duration of anesthetic administered to the mother. (S&M, p.492)

Front 152

List three actions to prevent hypotension during a C/section.

Back 152

Prehydration, avoidance of aortocaval compression, and aggressive use of ephedrine (even as a prophylactic) may minimize the risk for hypotension. (S&M, p.490)

Front 153

What is the greatest maternal/fetal danger of using general anesthesia for deliveries?

Back 153

Placental transfer of volatile anesthetics is rapid. If excessive concentrations of volatile anesthetics are given for prolonged periods, neonatal effects of these drugs will be evident by flaccidity, cardio-respiratory depression, and decreased tone may be anticipated.

Front 154

What are the primary concerns when a regional anesthetic is used to anesthetize an obstetric patient?

Back 154

Systemic hypotension secondary to sympathetic nervous system block. Systemic toxicity through accidental intravascular injection of the LA, an excessive level of neural blockade during initiation of a block that can lead to a block of the motor nerves to the respiratory muscles, and altered progress of labor b/c of decrease in uterine tone and prevention of contraction. (S&M, p. 490; Nagelhout)

Front 155

The efficacy of epidural opioids is impaired when used in conjunction with which local anesthetic?

Back 155

Recent studies have demonstrated that the addition of a lipid soluble opioid such as fentanyl or sufentanil decreases the MLAC for epidural bupivacaine, predominantly by a spinal site of action. Administration of a reduced concentration of LA results in less maternal motor block, which is especially important during the second stage of labor. Epidural 2-chloroprocaine may affect the efficacy of other drugs given in the neuroaxis. 2-Chloroprocaine may reduce the quality and duration of analgesia produced by subsequent injection of morphine or fentanyl epidurally due to the low pH of 2-chloroprocaine which may cause the acidification of the epidural space, and it favors formation of the poorly diffusible, charged form of the opioid” (Chestnut, p. 199).

Front 156

What are six anesthetic considerations for the patient with an inverted uterus during vaginal delivery? How is it managed?

Back 156

"Relaxation us the uterus may be necessary to facilitate replacement, this can be accomplished by inducing general anesthesia with a VAA.
Estimated Blood loss is expected to be very high requiring replacement with blood transfusions and fluids.
Hypovolemia requiring replacemement with crystalloids, Hypotension requiring pressors such as ephedrine, 3rd space loss and deficit
Once uterus has been replaced a firm and well contracted uterus is desired. Uterine tone increased with oxytocin 20 U/ L"

Front 157

What does the fetal scalp monitor measure? What can the fetal scalp monitor assess?

Back 157

A fetal scalp electrode is placed by screwing a tiny sire into the top layers of the baby's scalp, then relaying the baby's heart rate to the fetal monitor. This is more accurate because it does not use ultrasound. It goes between the uterine wall and the baby. This also allows the midwife or doctor to know the exact force from the contractions, rather than a simple graphical representation given by external monitoring. This is very useful in the case of induction.
Internal monitoring can also prevent an unnecessary cesarean for fetal distress if it shows the baby is healthy, compared to the less accurate external monitoring.

Front 158

What nerve injury is most commonly associated with vaginal delivery?

Back 158

Peroneal nerve injury

Front 159

How do the physiologic and anatomical changes during pregnancy effect nonobstetric surgery for the OB patient?

Back 159

Physiological and anatomical changes that can affect the OB patient in other surgeries are:
 Changes in the CV system such as an increase in intravascular fluid volume, increase in CO and decreased SVR.
 The decreases in blood pressure are because of aortocaval compression by the gravid uterus associated with the supine position. Also related to the vena cava compression which contributes to venous stasis and thereby resulting in decreased venous return.
 Pulmonary changes are enlargement of the upper airway, increased in minute ventilation, decreased FRC (therefore a decrease in lung volumes), and decreased arterial oxygenation.
 Renal blood blood flow and GFR are increased; therefore, the normal upper limits in blood urea nitrogen and serum creatinine concentrations are decreased
 Plasma protein concentrations are reduced because of dilution resulting in higher free blood levels of highly protein bound drugs. So they may have slightly elevated liver function tests
 Displacement of the pylorus cephalad by the enlarged uterus retards gastric empyting, and progesterone decreases GI motility. In addition gastrin, which is secreted by the placenta, stimulates gastric hydrogen ion secretion such that the pH of gastric fluid is predictably low in OB women. Puts them at an increased risk for aspiration.
Their airways may be edematous, short neck, decreased FRC, increased intravascular volume, increased cardiac output,…all of which makes the patient difficult to intubate, induce anesthesia, and position.

Front 160

What are the most common procedures performed on the OB patient that are considered nonobstetric in nature? Less common?

Back 160

Laparoscopy for acute appendicitis, cholecystectomy, and adnexal surgery.

Front 161

What are the concerns and how are OB patients evaluated in terms of nonobstetric surgery when related to trauma?

Back 161

"Anesthetic management of pregnant trauma patients incorporates the principles of anesthesia for trauma patients with those pregnant patients undergoing non-OB surgery. Principles of anesthetic management of pregnant trauma patients includes:
• Optimization of gas exchange
• Restoration of blood volume and tissue perfusion
• Protection of the brain and spinal cord
• Maintenance of uteroplacental circulation and fetal oxygenation
• Prevention of maternal awareness
• Detection of unrecognized injuries
• Correction of coagulopathy
• Maintenance of normothermia
• Avoidance of tertatogenic drugs during the first trimester
• Prevention of preterm labor
"

Front 162

What are the concerns and how are OB patients evaluated in terms of nonobstetric surgery when related to appendectomy?

Back 162

Optimization of gas exchange, Restoration of blood volume and tissue perfusion, Protection of the brain and spinal cord, Maintenance of uteroplacental circulation and fetal oxygenation, Prevention of maternal awareness, Detection of unrecognized injuries, Correction of coagulopathy, Maintenance of normothermia, Avoidance of tertatogenic drugs during the first trimester, Prevention of preterm labor

Front 163

What are the guidelines regarding laparotomy versus laparoscopic surgery on the OB patient?

Back 163

Deferring surgery until the second trimester, Obtain preopt info, Use intermittent pneumatic compression devices to prevent thrombosis resulting from lower extremity stasis, Monitor fetal HR and uterine status as well as maternal end tidal CO2 and arterial blood gas measurements, Using an open technique to enter the abdomen, Avoid aortacaval compression, Maintain low pneumoperitoneum pressures (8-12 mmHg not to exceed 15), Protect the uterus with a lead shield

Front 164

Understand the purpose of cervical cerclage and the contraindications.

Back 164

An inherent or traumatic deficiency in the structure or function of the uterine cervix results in an incompetent cervix which is unable to substain a pregnancy until full term. Typically the women will suffer second trimester pregnancy losses that are characterized with painless cervical dilation, herniation followed by rupture of the fetal membranes, and a short labor with delivery of a live, immature infant. The cerclage treatment is usually done transvaginally. A ligature is placed around the cervix at or near the level of the internal cervical os. Contraindications it include preterm labor, vaginal bleeding, fetal abnormalities, fetal death, rupture of the membranes, placental abruption, and chorioamnionitis. Immediate complications of include rupture of the membranes, hemorrhage, and stimulation of labor.

Front 165

Discuss appropriate anesthetic measures to perform fetal surgery, including risk and outcomes.

Back 165

"Unlike other surgical procedures performed during pregnancy, fetal surgery requires both complete uterine relaxation (i.e. atony) and fetal anesthesia. Fetal surgery also entails a high risk of preterm labor, preterm rupture of membranes, and preterm delivery.
Local anesthetic infiltration of the abdominal wall is sufficient to reduce maternal discomfort for many percutaneus procedure(e.g., amniocentesis, cordocentesis, and intrauterine blood transfusion). Supplemental maternal analgesia and anxiolysis can be provided by administration of an opioid and/or benzodiazepine. Administer supplemental O₂ whenever conscious sedation is employed
Cordocentesis occasionally results in prolonged fetal bradicardia, especially if the needle punctures the umbilical artery rather than the umbilical vein. Emergency c-section should always be planned. General anesthesia is preffered when surgical exposure requires uterine exteriorization for, both for maternal comfort and to block the uterine response to the increased manipulation. Open Fetal Surgery:
When corrective fetal surgery or an utero procedure requires hysterotomy, high concentration of a volatile halogenated agent is administered to provide both maternal and fetal anesthesia and to provide the required uterine relaxation. In summary, anesthetic considerations for intrauterine fetal surgery are similar to those for nonobstetric surgery in pregnant patient plus 1.) fetal surgeries entails greater requirement for intraoperative monitoring, 2.) the fetus should be anesthetized and immobile, 3.) intraopertive uterine relaxation is essential, and 4.) the pt is at high risk for preterm labor during or after surgery; many minimally invasive intrauterine procedures can be performed with use of local or regional anesthesia, but open surgeries requires general anesthesia. - pg 129 of chestnut

Front 166

Describe the risk changes related to gestational age when exposed to anesthetics.

Back 166

"Gest – 14 days: any adversity likely results in embryo death-i.e. chromosomal abnormalities.
<8 wks organogenesis: structural or developmental abnormalities possible
>13 wks: less developmental risk, during the second trimester. Brain is still being developed.
3rd trimester: Preterm labor is greatest risk
"

Front 167

Describe how best to avoid contributing to malformation of the fetus during surgery.

Back 167

Fetal activity may render the procedure technically difficult or impossible. Fetal movement may be hazardous for the fetus because displacement of the needle or catheter may lead to trauma, bleeding, or compromise of the umbilical circulation. Fetal movement is controlled by use of direct fetal intramuscular or IV administration of pancuronium or vecuronium (0.3 mg/kg im or 0.05-0.1 mg/kg IV). The onset of fetal paralysis occurs in 2 min, with a duration of 1-2 hours.

Front 168

List the four major objectives of anesthetic management in the OB patient which corresponds to fetal wellbeing.

Back 168

Maintaining maternal oxygenation, cardiac output, oxygen delivery, and uterine blood flow OR can be viewed as avoiding hypoxemia, hypotension, acidosis, and hyperventilation

Front 169

Describe the complication during late gestation or the OB patient undergoing nonobstetric surgery.

Back 169

(from ppt) Intubation difficulties with or without gastric acid aspiration, unrecognized esophageal intubation, high or complete spinal block during regional, unintended deep inhalational anesthesia.

Front 170

Know the US FDA risk classification of pharmacologic use in the OB patient.

Back 170

In 1979, the US FDA introduced a drug classification system to discourage nonessensial use of medications during pregnancy:
1. Category A: Well controlled studies in pregnant women have not shown and increased risk of fetal abnormalities.
2. Category B: Animal studies have revealed no evidence of harm to fetus but, no adequate studies have been conducted in pregnant women.
3. Category C: Animal studies have shown an adverse effect but, no adequate studies have been conducted in pregnant women. GIVE DRUG ONLY IF POTENTIAL BENEFIT OUTWEIGHS THE RISK.
4. Category D: Well-controlled studies in pregnant women have demonstrated a risk to the fetus. HOWEVER, BENEFITS MAY OUTWEIGH THE RISKS. GIVE THE DRUG ONLY IF THE DRUG IS NEEDED FOR LIFE-THREATENING SITUATION OR SERIOUS DISEASE FOR WHICH OTHER DRUGS CANNOT BE USED OR ARE INEFFECTIVE.
5. Category X: Well-controlled studies in animals or pregnant women have demonstrated evidence of fetal abnormaliites. USE OF THE PRODUCT IS CONTRAINDICATED.

Front 171

Define teratogencity. Identify documented teratogens.

Back 171

Any significant postnatal change in function or form in an offspring after prenatal treatment. Examples included ace inhibitors, cocaine, coumadin, lithium, tetracycline (Chestnut., p. 341)

Front 172

Know the FDA classification of commonly used anesthetic drugs.

Back 172

Cat B- sevoflurane, desflurane, Propofol, Lidocaine, Ropivacaine, Rocuronium, Nimbex,
Cat C-Morphine, Fentanyl, sufentanil, alfentanil, Remifentanil,Meperedine, Thiopental, Isoflurane, Etomidate, Bupivacaine, Succinylcholine, Pancuronium, Atracurium, Vecuronium
Cat D-Midazolam, Lorazepam, Diazepam, Ketamine,
No anesthetic agent is proven teratogen in humans, although some anesthetic agents, specifically nitrous oxide, are teratogenic in animals

Front 173

Understand the pre-anesthesia assessment of all patients of child bearing age.

Back 173

Obtain thorough reproductive hx to include last menstrual period and possibility of pregnancy. A pregnancy test should be obtained on ALL women of reproductive age with an intact uterus.

Front 174

Discuss the preoperative period of the OB patient and ways in which to alleviate anxiety without drug use.

Back 174

"""Natural childbirth"" stems from a phrase coined by Grantley Dick-Read in 1933; he believed that childbirth was a painless process that did not need medical intervention if the mother was adequately prepared.The Pavlovian methods of childbirth used in Russia were adapted by the French obstetrician Fernand Lamaze in the late 1950s, and ""natural childbirth"" was popularized as an option for parturtients. This method focuses on teaching the mother conditioned reflexes to overcome the pain and fear of childbirth. It also uses an education program, human support during labor, breathing techniques, relaxation techniques of voluntary muscles, a strong focus of attention, and specific activities to concentrate on during contractions to block pain. Indeed, even the effect of the presence of another woman during labor to support the expectant mother has been shown to have a positive effect on outcomes, including the duration of labor. (BIG MILLER, 7TH ED, PP. 2211)

TENS is thought to reduce pain by nociceptive inhibition at a presynaptic level in the dorsal horn by limiting central transmission. Electrical stimulation preferentially activates low-threshold myelinated nerves. Afferent inhibition effects inhibit propagation of nociception along unmyelinated small ""c"" fibers by blocking impulses to target cells in the substantia gelatinosa of the dorsal horn. TENS is also thought to enhance release of endorphins and dynorphins centrally.Placement of electrode pads over the lower back region in the distribution of T10-L1 provides analgesia for some patients in early labor. However, other reports have failed to demonstrate its effectiveness for labor analgesia or as an adjunct to epidural analgesia. (BIG MILLER, 7TH ED, PP. 2212)

Most women do not require sedatives before administration of anesthesia for c-section, and they are usually avoided until after the delivery of the infant. If necessary, a small dose of midazolam 0.5-2 mg and or opioid- fentanyl 25 mcg to 50 mcg. can be given. A major disadvantage of benzodiazepins is amnesia; most pt wants to remember their childbirth experience. If anticholinergic is needed to lessen the likelihood of bradicardia, Glycopirolate is drug of choice (does not readily cross the placenta). All patients receive pharmacologic aspiration prophylaxis. (Chestnut 3RD ED p. 421)



"

Front 175

Describe the goals in anesthetic management which support maternal and fetal safety.

Back 175

The anesthesia management of the pregnant surgical patient should focus on the avoidance of hypoxemia, hypotension, acidosis, and hyperventilation. When possible, local or regional anesthesia is preferred; this permit administration of drugs with no laboratory or clinical evidence of teratogenecity. In addition, maternal respiratory complications occur less frequently.

Front 176

Understand aspiration precautions and the prevention methods for the OB patient. At what point is the OB patient no longer considered an OB patient?

Back 176

Pregnant women undergoing c-section or other surgical procedure are at increased risk for aspiration pneumonitis and should receive pharmacological prophylaxis. Decreased LES tone and an increased risk of difficult intubation are the primary factors that increase the risk of aspiration during C-section and surgery. The most effective way to decrease the risk is to avoid the administration of general anesthesia. When possible, all mothers should be encouraged to have regional anesthesia for c-section. Mothers with potential difficult airways who require general anesthesia, should have an awake fiberoptic intubation. For elective c-section, a suitable antiacid regimen is given at bedtime (e.g. H₂-receptor antagonist: 300 mg cimetidine, 150 mg ranitidine, or 20 mf famotidine po) or a PPI (omeprazole 40 mg) at bedtime and again 60-90 min before the induction of anesthesia. Metoclopramide 10 mg po is given at the same time or iv at least 15 min before induction. Metoclopramide not only increases LES tone and accelerates gastric empting but also decreases the incidence of nausea and vomiting. For emergency c-section under GA, 30 ml of sodium citrate should be administer just after transferring patient to the OR, because it has a relatively short duration of action. In addition, 10 mg Metoclopramide, and 50 mg Ranitidine IV should be given. The goal of pharmacologic therapy is to decrease gastric volume and increase pH. Pt requiring GA, RSI is performed, while cricoid pressure is applied to prevent aspiration during induction and loss of protective reflexes. At the end of surgery pt is extubated awake with intact airway reflexes.
Remember from an anesthetic point of view, all obstetric patients have a full stomach.

Front 177

Understand positioning of the OB patient and how best to achieve optimal positioning.

Back 177

(Chestnut, p. 423)
Aortocaval compression must be avoided before and during the performance of c-section and surgery. When the pregnant woman lies supine, the gravid uterus compresses the aorta and the IVC against the bodies of the lumbar vertebrae. This results in decreased uteroplacental perfusion by: 1.) decreased venous return, which can cause decreased maternal CO and BP, 2.) the obstruction of uterine venous drainage increases uterine venous pressure and decreases uterine artery perfusion pressure, 3.) the compression of the aorta or common iliac arteries results in decreased uterine artery perfusion pressure. Therefore, it is necessary to maintain left uterine displacement before and during the procedure, regardless of the anesthetic techniques. This may be easily accomplished by placing a wedge beneath the right buttock. The qualitative effectiveness can be assessed by palpating the R femoral pulse, and monitoring BP and SaO₂ on a lower extremities.

Front 178

Discuss fetal monitoring, signs and symptoms of fetal distress and the potential causes.

Back 178

Continuous FHR monitoring (using transabdominal Doppler) is feasible beginning at approximately 18 weeks’ gestation. Transabdominal monitoring may not be possible during abdominal procedures or when the mother is very obese; use of transvaginal Doppler ultrasonography then is considered. FHR variability, which is typically a good indivcator of fetal well-being, is present by 25 to 27 weeks’ gestation. Changes in the baseline FHR and FHR variability caused by anesthetic agents or other drugs must be distinguished from changes that result from fetal hypoxia. Persistent severe fetal bradicardia typically indicates true fetal distress. There should be always a plan that addresses how to proceed in the event of persistent fetal distress, including whether to perform emergency cesarean delivery. An unexplained change in FHR mandates the evaluation of maternal position, blood pressure, oxygenation, acid-base status and the inspection of the surgical site to ensure that neither surgeon or retractors are impairing uterine perfusion.

Front 179

List the six ‘H’(s) to avoid during induction and maintenance of the OB patient.

Back 179

"Hypoxemia,
Hypercapnea
Hyperventilation
Hypotension
Hypovolemia
Hyperoxia