OB Flashcards
(216 cards)
1
Q
Uterine sensory neurons carrying pain during the first stage oflabor enter the cord at what segments? What is the cause of pain during the first stage of labor?
A
Pain is carried through spinal segments TlO- L l by somatic afferent (sen- sory) nerves during the first stage oflabor. This is visceral pain. Visceral pain, arising during the first stages oflabor, is caused by uterine contrac- tions and dilation of the cervix. [Stoelting and Miller, Basics, 1994, p364j
2
Q
What nerve carries pain during the second stage of labor? What causes pain during the second stage oflabor?
A
Pain is carried to spinal segments S2-S4 by the pudendal nerve during the second stage oflabor. This is somatic pain. Somatic pain is caused by stretching of the vagina and perineum by descent of the fetus. [Birnbach, Gott and Datta, Textbook ofOb. Anes., 2000, p19; Morgan and Milduil, Clinical Anesthesiology, 1996, p705; Stoelting and Miller, Basics, 1994, p364]
3
Q
A patient in the first stage oflabor will need spinal anesthesia for what levels?
A
TlO- Ll. [Barash Handbook, Clinical Anesthesia, 1997, p584]
4
Q
A patient in the second stage of labor will need a spinal level of anesthesia for what levels?
A
S2-S4. [Barash Handbook, Clinical Anesthesia, 1997, p584]
5
Q
What dermatome level should be reached for a C-section?
A
T4. [Barash Handbook, Clinical Anesthesia, 1997, p585]
6
Q
What is the PaC02 and Pa02 in the normal fetus?
A
8 mmHg PaC02 (40-45 mmHg in maternal blood), 30 mmHg PaO2 (fetal blood leaving placenta). [Guyton, TMP, 1996, pp1036-1037]
7
Q
If a pregnant patient is placed on 100% oxygen (F,O, ~ 1.0), by how much will fetal 02 change?
A
A maternal F10 2 = 1.0 will cause maternal P02 to rise from 90 to 500 mmHg, which is an increase of about 1 mrnol in arterial oxygen content. Because increasing F10 2 will not cause uterine blood flow to increase, uterine venous oxygen content should also increase by I mmol. There- fore, uterine venous P02will increase by about 10 mmHg(ll.S mmHg, to be exact). Since uterine venous P02 is the primary determinant of umbili- calvenousP02, thefetalP02willincreasebyabout10mmHg.[Birnbach, Textbook Ob. Anes., 2000, p54]
8
Q
Describe how maternal blood circulates through the placenta.
A
The maternal blood is carried initially in the uterine arteries. Blood is spurted into the intervillous space. Blood in the intervillous space passes fetal villi before draining back to the veins of the uterine waH (myometri- um). [Shnider and Levinson, Anes. for OB., 1993, p19; Morgan and Mi- khail, Clinical Anesthesiology, 1996, p697]
9
Q
Fetal blood and maternal blood are separat~ ed by the placental membrane. How many microscopic tissue layers are found in the placental membrane?
A
Three. Fetal trophoplasts (which consists of cytotrophoblast and syncytio- trophoblast), fetal connective tissue, and the endothelium of the fetal capillaries are the three microscopic layers of the placental membrane. [Shnider and Levinson, Anes. for OB., 1993, pp 19,20]
10
Q
What determines uterine blood flow?
A
Uterine blood flow is directly related to perfusion pressure (uterine mean arterial pressure- uterine venous pressure) and inversely related touter- ine vascular resistance. Mathematically: uterine blood flow == (mean uterine artery pressure- uterine vein pressure)/uterine vascular re- sistance. Note that uterine artery pressure depends on maternal arterial pressure. [Birnbach, Galt and Datta, Textbook Ob. Anes., 2000, p62; Longnecker eta!., PPA, 1998, p1991]
11
Q
What determines placental blood flow?
A
Placental blood flow is directly dependent on the pressure in the uterine artery. Since uterine artery blood pressure depends on maternal blood pressure, placental blood flow depends solely on maternal blood pressure. [llirnbach, Galt and Datta, Textbook Ob. Anes., 2000, pp62,96]
12
Q
Is the uterine and placental vasculature under appreciable neural control? Is utero- placental blood flow autoregulated? What is the significance of this?
A
Uterine and placental blood flows are not under appreciable neural con- trol; uterine bloodflow is not autoregulated. Uterine blood flow is deter- mined by mom’s arterial blood pressure and SVR. When mom becomes hypotensive, uterine and placental blood Oows decrease. Likewise, when mom’s arterial vessels constrict (increased SVR) as they would if phe- nylephrine were administered, uterine and placental blood flows decrease. [Barash, Clinical Anesthesia, 1997, pp 1063-1065; Stoelting and Miller, Basics, 1994, p359; Morgan and Mikhail, Clinical Anesthesiology, 1996, p695]
13
Q
Identify the predominant adrenergic recep- tor in the uterine vasculature, and state the significance of this.
A
Alpha-adrenergic receptors predominate in the uterine vasculature. Ma- ternal release of catecholamines or administration of an alpha-adrenergic agonist drug such as phenylephrine will reduce uterine and placental blood flows. [Morgan and Mikhail, Clinical Anesthesiology, I996, p695]
14
Q
List three factors that decrease uterine blood flow.
A
(1) Maternal hypotension, (2) vasoconstriction of uterine vasculature (by phenylephrine, for example), and (3) uterine contractions. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p695]
15
Q
Which maternal hemodynamic parameter shows the greatest decrease during normal gestation?
A
During normal gestation, the greatest decrease in a hemodynamic param- eter occurs in the systemic vascular resistance (-20% SVR). [Chestnut, Ob. Anes., 3’’ ed., 2004, p18t]
16
Q
Which maternal hemodynamic parameter shows the greatest increase during normal gestation?
A
During normal gestation, the greatest increase in a hemodynamic param- eter occurs in the cardiac output (+50% CO). [Chestnut, OB Anes. 3e. 2004 pp18t]
17
Q
How does extreme maternal hyperventila- tion affect uterine oxygenation? Give two reasons for this change.
A
Extreme maternal hyperventilation will result in fetal hypoxemia and acidosis because of (1) vasoconstriction and reduced umbilical blood flow and (2) increased affinity of maternal hemoglobin for oxygen secondary to a leftward shift in the oxyhemoglobin dissociation curve; this left shift results in reduced transfer of oxygen across the placenta from the mother to the fetus. [Miller, Anesthesia, 1994, p2035]
18
Q
How does mild hyperventilation affect the fetus?
A
Mild hyperventilation is probably safe, but fetal heart rate should be monitored to detect any adverse effects of a mild maternal hyperventila- tion. [Shnider and Levinson, Anes.Jor OB., 1993, p556j
19
Q
How and why does fetal heart rate normally fluctuate with maternal blood pressure?
A
If maternal blood pressure falls, uterine blood flow decreases. Fetal heart rate decreases when fetal hypoxia develops secondary to decrements in uterine blood flow. [Shnider and Levinson, Anes. for OB., 1993, pp23, 25, 661]
20
Q
If the mother is hypertensive, how and why will fetal heart rate fluctuate with maternal blood pressure?
A
Mothers with blood pressures not exceeding 160/100 mmHg before and during the Orsl20 weeks of pregnancy usually have no problems. Mothers with hypertension have a lower cardiac index and a decreased blood volume. Increased uterine arterial vascular resistance is associated with increasingly severe hypertension. This can result in decreased oxygen delivery to the fetus with resultant bradycardia. [Shnider and Levinson, Anes.for OB., I993, pp23, 509, 661]
21
Q
What is the normal fetal heart rate? Fetal bradycardia is defined as a heart rate less than how many beats per minute? Fetal tachycardia is defined as a heart rate more than how many beats per minute?
A
Normal fetal heart rate ranges between 120 and 160 beats per minute. Fetal bradycardia is diagnosed when heart rate is less than 120 beats per minute, and fetal tachycardia is present when heart rate exceeds 160 beats per minute. [Shnider and Levinson, Anes. for OB., 1993, p660]
22
Q
dentify 3 maternal physiological disturb- ances that pose the greatest risk to the fetus.
A
The greatest risk to the fetus occurs following maternal catastrophes involving (l) severe hypoxia, (2) hypotension, and (3) acidosis.[Chestnut, Ob. Anes., 3’’ ed., 2004, p283]
23
Q
What is the most serious fetal risk associ- ated with maternal surge1y during pregnan- cy?
A
The most serious fetal risk associated with maternal surgery during preg- nancy is that of uterine asphyxia. [Chestnut, Ob. Anes., 3”1 ed., 2004, p263]
24
Q
What are two signs of fetal hypoxia (asphyx· ia)?
A
Fetal bradycardia and late decelerations indicate fetal hypoxia (asphyxia). [Shnider and Levinson, Anes. for OB., 1993, pp661,663]
25
Urgent delivery of the fetus is indicated by what fetal heart rate deceleration pattern and what heart rate?
Urgent delivery is usually necessary when prolonged late decelerations without beat-to-beat variability and baseline fetal heart rate is below 70 beats per minute. [Datta, Ob. Anes. Handbook, 1995, p112]
26
Describe the mechanism of physiological anemia of pregnancy.
Physiological anemia of pregnancy occurs because plasma volume in- creases 75% (from 40 mL!kg before pregnancy to 70 mL!kg during late pregnancy) and red cell volume increases only 20% (from 25-30 mL!kg). Hematocrit falls to 35% and hemoglobin to 11-12 mg/100 mL because plasma volume increases more than red blood celt volume. [Barash, Clini- cal Anesthesia, 1997, pl061; Miller, Anesthesia, 1994, pp2033-2035]
27
When does the greatest increase in cardiac output occur in the pregnant patient? What happens to cardiac output during pregnancy and during labor?
The greatest increase in cardiac output associated with pregnancy occurs immediately after deliveiy, being elevated by as much as 80% above pre- labor values. Cardiac output increases about 30-40% by the lOth week and falls toward normal levels by the third trimester. During labor, cardi- ac output increases another 45%. [Shnider and Levinson, Anes. for OB., 1993, pp8-9]
28
Describe plasma cholinesterase (pseudo- cholinesterase) changes in the pregnant patient.
Plasma cholinesterase (pseudocholinesterase) levels wilt decrease by 24% before delivery and decrease further (to 33% less) by 3 days postpartum. Plasma cholinesterase (pseudocholinesterase) levels will return to normal levels in 2-6 weeks postpartum. [Hughes, Shnider Anes.for OB., 4e, 2002, p13]
29
What causes supine hypotensive syndrome?
Compression of aorta and inferior vena cava (aortocaval compression) occurs when the pregnant patient is in the supine position. Decreased venous return and hypotension result. [Miller, Anesthesia, 1994, p2033]
30
What are eight signs and symptoms of su- pine hypotensive syndrome (aortocaval compression)?
1) Diaphoresis, (2) nausea, (3) vomiting, (4) changes in cerebration,
(5) dizziness, (6) vertigo, (7) tachycardia, and (8) apprehension. [Stoelting and Miller, Basics, 1994, p356l
31
Describe the treatment for aortocaval com- pression (supine hypotensive syndrome).
Right hip up. Left uterine displacement by elevating the right hip 10-15 em with a blanket or foam rubber wedge while supine is effective in treat- ing this problem. [Shnider and Levinson, Anes, for OB., 1993, pll; Stoelt- ing and Miller, Basics, 1994, p375]
32
he patient in labor has a history of mulliple sclerosis. She becomes hypotensive. What is the agent of choice to treat this hypotension?
The primary concern with any mulliple sclerosis patient is in regard to exacerba- tion of the disease and is typically focused on drugs and/or techniques potentially causing neurotoxicity and on preventing an increase in body temperature. A specific interaction between multiple sclerosis and the treatment of hypertension is not discussed in textbooks. Therefore, treat the hypotension as you would for the normal obstetric patient: (1) left uterine displacement, (2) IV hydration, (3)vasopressors of which ephedrine is the pressor of choice in most obstetric situations. [Norris, Obstetrical Anestheshl, 1999, pp74-76,48l-482,595-596j
33
List four respiratory changes that occur during pregnancy.
(l) Increased alveolar ventilation (70%), (2) decreased FRC (20%),
(3) airway edema, (4) decreased P,CO, (30%). [Barash Handbook, Clinical Anesthesia, 1997, p58l; Guyton, TMP, 1996, pl040; Barash, Clinical Anes- thesia, 1997, pl06]
34
How does minute ventilation change during pregnancy?
Minute ventilation increases by up to 45% during pregnancy. [Chestnut, OB Anes. 4th. 2009 pp20; Morgan, eta!., Clin. Anesth. 4e. 2006 pp875]
35
#What respiratory parameter changes most to increase minute ventilation during pregnancy? What physiological factors prompt the increase in minute ventilation during pregnancy?
During pregnancy, resting minute ventilation increases (up to 45%) ow- ing primarily to an increase in tidal volume, with minimal, if any, change in inspiratory rate and pattern. The rise in minute ventilation results from hormonal changes (increased progesterone) and increased C02 produc- tion. Progesterone acts as a direct respiratory stimulant and the proges- terone-induced increase in chemoreceptor sensitivity results in a steeper and leftward shifted C02 ventilatory response curve. [Chestnut, OB Anes. 4th. 2009 pp20; Morgan, eta!., Clin. Anesth. 4e. 2006 pp875]
36
What lung capacity is changed most at term in the pregnant patient?
Functional residual capacity (residual volume+ expiratory reserve vol- ume) is most decreased (15% to 20%) at term in the pregnant patient. Vital capacity, total lung capacity, and closing volume are not changed. [Miller, Anesthesia, 1994, p203l]
37
How much is FRC decreased in the pregnant patient at term, compared to the non- pregnant patient?
FRC is decreased 15-20% at term compared with the non-pregnant pa- tient. [Stoelting and Miller, Basics, 1994, p357]
38
State three reasons why hypoxemia is more likely to develop during a period ofapnea in the pregnant patient compared with the non-pregnant patient?
The pregnant patient is more susceptible to hypoxemia because of:
(l) a decrease in functional residual capacity, {2) an increase in 02 con- sumption, and (3) development of a ventilation-perfusion inequality, as suggested by an increased P AOri\02 gradient. The decrease in functional residual capacity is probably the most important of these. [Yao and Artu- sio, Problem Oriented Patient Management, 1993, p48l; Authors]
39
Does pregnancy mimic restrictive or ob- structive disease? Explain.
Restrictive. With increasing enlargement of the uterus, the diaphragm is forced to assume a more cephalad position, causing a 20% reduction in functional residual capacity. [Stoelting, Co-Existing, 1993, pp54l-543]
40
Define pre-eclampsia.
Pre-eclampsia is a syndrome of pregnancy-induced hypertension> pro- teinuria, and edema occurring after the 20th week of gestation and resolv- ing within 48 hours after delivery. [Morgan and Mikhail, Clinical Anesthe- siology, 1996, p717]
41
Define eclampsia.
When seizures are associated with the syndrome of pregnancy-induced hypertension, the syndrome is termed eclampsia. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p717]
42
What does HELLP stand for?
Hemolysis, Elevated Liver enzymes, and Low Platelet count. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p718]
43
When does the HELLP syndrome usually occur? What should be done if this syn- drome develops?
The HELLP syndrome usually occurs before 36 weeks gestation. Its diagnosis calls for immediate delivery, regardless of gestation due to high maternal and fetal mortality. [Shnider and Levinson, Anes. for OB., 1993, pp32-34j
44
Severe pregnancy-induced hypertension (pre-eclampsia) is characterized by what seven signs and symptoms?
(1) Hypertension (arterial blood pressure greater than 1601!10 nun Hg); (2) proteinuria (greater than 5 grams per day); (3) oliguria (urine now less than 500 mL/day); (4) systemic and pulmonary edema; (5) CNS dysfunc- tion (headaches, visual disturbances, seizures); (6) hepatic tenderness; and (7) presence ofHE!.LP syndrome. [Morgan and Mild1ail, Clinical Anesthesiology, 1996, p718; Shnider and Levinson, Anes. for OB., I993, pp306-314]
45
List the diagnostic triad (most characteristic signs and symptoms) of pre-eclampsia.
1) Hypertension (2) proteinuria, and (3) generalized edema. [Stoelting, Co-Existing, 1993, p783]
46
The pregnant patient presents with maternal hypertension, hyperreflexia, and convul- sions. Your immediate diagnosis is pregnan- cy-induced hypertension (PIH).What other diagnosis must be included in your differen- tial diagnosis?
Cocaine abuse. Maternal hypertension, hyperreflexia, and convulsion due to cocaine abuse can mimic pregnancy-induced hypertension (PIH) and must be included in your differential diagnosis. [Hughes Shnider and Levinsons Anes. for OB., 2002, p605]
47
The patient with pregnancy-induced hyper- tension (pre-eclampsia) is in danger of developing what six very serious complica- tions?
(I) Pulmonary edema, (2) cerebral hemorrhage, (3) renal failure,
(4) cerebral edema, (5) disseminated intravascular coagulopathy, and (6} airway obstruction are serious complications of pregnancy-induced hypertension. [Datta, Ob. Anes. Handbook, 1995, p200I
48
In the pre-eclamptic patient, what are the best tests to evaluate bleeding? Why?
PT and PTT might be best because prolongation of PT and PTT indicates consumption of coagulant factors. Platelets, fibrinogen, and fibrin split products might also be assessed to check for disseminated intravascular coagulation (DIC). [Yao and Artusio, Problem Oriented Patient Manage~ ment, 1993, p501; Stoelting, Co-Existing, 1993, pp562, 1281; Barash, Clinical Anesthesia, 1997, p1070-1074]
49
What is the number one cause of maternal death in pregnancy-induced hypertension (PII-I = pre-eclampsia)? The second most common cause?
The number one cause of maternal death in pregnancy-induced hyperten- sion is cerebral hemorrhage. The second leading cause of death is puhno- nary edema. [Yao, POPM, 5th ed. 2003, p815; Stoelting & Dierdorf, Co- Existing, 4th ed. 2002, p661]
50
How does pre-eclampsia affect the uteropla- cental circulation?
Uterine vascular resistance increases in pre-eclampsia, so uterine blood flow decreases. The uteroplacental circulation is compromised in pre- eclampsia. [Shnider and Levinson, Anes. for OB., 1993, pp306-314]
51
The mother has pre-eclampsia. What causes the variations in fetal heart rate? What caus- es the mother's increased blood pressure?
The placenta develops a vasculitis, and placental perfusion decreases. Decreased blood Oow to the fetus with associated hypoxia c;tuscs variations in fetal heart rate. Pregnancy-induced hypertension is thought to be due to decreased placental perfusion. Placental ischemia and placental dysfunction result in release into the circulation of a variety of mediators including thromboxane, renin, angiotensin, aldosterone, catecholamines and thromboplastin. These mediators lead to gener- alized vasoconstriction and hypertension. [Morgan and Mikhail, Clinical Anesthe- siology, 1996, p7l7; Davison, Eckhardt, and Perese, Mass General, 1993, pp466- 467]
52
List 8 antihypertensive agents used prophy- lactically to prevent hypertension during induction of general anesthesia or to treat severe hypertension in the pre-eclamptic patient.
All of the following antihypertensive drugs are used in the patient with pregnancy-induced hypertension (pre-eclampsia): (1) hydralazine (the "standard" agent for tl1is condition); (2) labetalol; (3) sodium nitroprus- side (briefly for hypertensive emergencies); (4) nifedipine (a calcium channel blocker); (5) trimethaphan (Arfonad), which may be useful be- cause it does not cause cerebral vasodilation and increased intracranial pressure; (6) alpha-methyldopa; (7) nitroglycerin; and (8) diazoxide. Note that all of these agents have vasodilating properties. [Hurford, Bailin, Davison, Hospel, Rosow, Mass General, 1998, pp535-536; Barash, Clinical Anesthesia, 1997, pp1073-1074; Longnecker eta!., PPA, 1998, p499; Stoelting, Co-Existing, 1993, p563]
53
What are concerns with using sodium nitro- prusside or nitroglycerin in the pre- eclamptic patient?
Cyanide toxicity in fetal lambs occurs with high-dose nitroprusside. Tox- icity in human fetuses, however, has not been demonstrated with short- term use of recommended doses of nitroprusside. The actions of nitro- glycerin are unpredictable. In pre-eclamptic patients with severe hyper- tension and low pulmonary capillary wedge pressure, either nitroprusside or nitroglycerin can precipitate profound hypotension. [Datta, Ob. Anes. Handbook, 1995, p211; Longnecker eta!., PPA, 1998, p499]
54
What is the mainstay therapy for hyperten- sion in the pre-eclamptic patient? Why?
Hydralazine, which may be given IM, PO, or IV, has been the intrapartum mainstay antihypertensive therapy. Hydralazine is popular because it lowers blood pressure and increases uteroplacental blood flow. [Datta, Ob. Anes. Handbook, 1995, p211; Longnecker eta!., PPA, 1998, p499]
55
Which drug on the following list would you NOT give to treat severe hypertension in the pre-eclamptic patient: hydralazine, sodium nitroprusside, nitroglycerin, esmolol, labetalol, or trimethaphan? Why?
Esmolol should be avoided in the treatment of hypertension in the pre- eclamptic patient. "Unlike labetalol, esmolol can have significant, poten- tially adverse fetal effects." [Morgan and Mikhail, Clinical Anesthesiology, 1996, p718]
56
What drug(s) would you administer to a pre-eclamptic patient with cerebral edema prior to cesarean section?
Hydralazine or labetalol are the most popular drugs to reduce hyperten- sion in the pre-eclamptic patient. Cerebral blood Oow and intracranial pressure are maintained with both of these antihypertensives. Antihyper- tensive with reported adverse effects during pregnancy which may be avoided include esmolol, clonidine, nifedipine, and ACE inhibitors. [Nor- ris,Ob.Anes.,1999,pp509-511;HughesShniderandLevinsons Anes.for OB., 2002, pp306-307; Omoigui, Anesthesia Drug Handbook, 1999, pp206, 234]
57
18. Why is the fetus at increased risk in the patient with pregnancy-induced hyperten- sion (preeclampsia)?
The fetus is at increased risk because of mmginal placental function. [Stoelting, Co-Existing, 1993, p562]
58
List six complications during pregnancy- induced hypertension (Pill pre-eclampsia) that necessitate immediate delivery of the fetus.
Six complications during pregnancy-induced hypertension (PIH, pre- eclampsia) that necessitate immediately delivery of the fetus are:
(I) severe hypertension (systolic~ 160 mmHg or diastolic~ 110 mmHg), persisting for 24-48 hours, (2) progressive thrombocytopenia, (3) liver dysfunction, (4) progressive renal dysfunction, (5) premonitory signs of eclampsia, and (6) evidence of fetal jeopardy. [Chestnut, Ob. Anes., yJ ed., 2004, p807]
59
Should either a general or regional anesthet- ic be used to lower blood pressure in the pre-eclamptic patient?
No. [Stoelting and Miller, Basics, 1994, p370)
60
What is the most common cause of morbidi- ty and mortality in pregnancy?
Pre-eclampsia and eclampsia, often referred to as toxemia of pregnancy and now referred to as pregnancy-induced hypertension, are among the leading causes of maternal morbidity and mortality. [Miller, Anesthesia, 1994, pp2061-2062)
61
Pre-eclampsia and eclampsia, often referred to as toxemia of pregnancy and now referred to as pregnancy-induced hypertension, are among the leading causes of maternal morbidity and mortality. [Miller, Anesthesia, 1994, pp2061-2062)
Hyperreflexia and CNS irritability occur in pre-eclampsia, accounting for the TMJ rigidity. Anesthesia can be managed by epidural, spinal or gen- eral anesthesia. Continuous epidural lumbar anesthesia is a useful method of analgesia for labor and vaginal delivery for the volume-depleted pre- eclamptic patient. [Yao and Artusio, POPM, 1993, pp499, 507-513; Stoelt- ing, Co-Existing, 1993, p564)
62
What is the normal serum magnesium concentration, and what is the therapeutic anticonvulsant range in the treatment of preeclampsia?
Normal serum magnesium is 1.4-2.0 mEq/liter, and the therapeutic range for the treatment of preeclampsia/eclampsia is 4-7 mEq/!iter. [Longneck- er eta!., PPA, 1998, p973)
63
How can you convert a magnesium concen- tration reported in mEq/liter to mg/dL? If serum magnesium is 4 mEq/liter, what is the concentration in mg/dL?
Divide mEq/liter by 0.8 to convert to mg/dL. 4 mEq/liter/0.8 ~ 5 mg/dL. [Longnecker eta!., PPA, 1998, p973)
64
State the loading and maintenance doses of magnesium sulfate administered for seizure prophylaxis in pregnancy-induced hypertension (PIH).
For seizure prophylaxis in pregnancy-induced hypertension (preeclamp- sia), magnesium sulfate is administered at a loading dose of 4-6 g over 20-30 minutes, followed by a maintenance dose of 1-2 g/hr., continued for up to 24 hours postpartum. [Chestnut, OB Anes. 4th. 2009 pp986)
65
What is magnesium sulfate's anticonvulsive mechanism of action in edampsiH and pre- eclampsia?
Magnesium depresses the CNS and increases the threshold for seizure activity. Magnesium produces these effects by decreasing the presynaptic release of acetylcholine and reducing the sensitivity of postsynaptic mem- lH'anes to acetylcholine. (Shnider and Levinson, Anes. for OB., 1993, p315; Stoelting, Co-Existing, 1993, p563)
66
List, in order of appearance, seven clinical manifestations of progressive hy- permagnesemia.
Signs ofhypermagnesemia are: {I) diminished deep tendon reOexes
(4-5 mEq/liter); (2) ECG changes including prolonged PR and ST inter- vals, widened QRS complexes, and/or elevated T waves (4-7 mEq/liter); (3) somnolence (5-7 mEq/liter); (4) loss of deep tendon reOexes, or myo- tonia (8-!0 mEq/liter); (5) heart block (!2 mEq/liter); (6) respiratory arrest (15 mEg/liter); and {7) cardiac arrest and cardiovascular collapse (20 mEq/liter). [Longnecker eta!., PPA, 1998, p973)
67
What are cardiovascular signs and symp- toms ofhypermagnesemia? At what serum magnesium levels are these cardiovascular signs and symptoms manifested?
ECG changes are seen when serum magnesium is 4-7 mEq/liter. Severe hypermagnesemia produces hypotension secondary to vasodilation, bradycardia, and myocardial depression. These signs and symptoms develop when serum magnesium exceeds 20 mEq/liter. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p540)
68
When the plasma concentration of magnesi- um rises above the therapeutic range, as suggested by the absence of the knee jerk (patellar tap) reflex, what three things can happen?
(1) Hearl block, (2) ventilatory failure, and (3) cardiac arrest. [Stoelting,
Co-Existing, 1993, p563; Longnecker et al., PPA, 1998, p973]
69
30. ; ( W h a t is the earliest sign of magnesium toxicity?
Clinically, the therapeutic effects of magnesium therapy are estimated by the response to deep tendon reflexes. Marked depression ofdeep tendon reflexes is an indication ofimpending magnesium toxicity. At therapeutic magnesium levels (4-6 mEq/L), letharb>y, nausea & vomiting, and facial flushing may occur. At magnesium levels greater than 6 mEq/L, loss of deep tendon reflexes and hypotension ensue. [Miller & Stoelting, Basics. Se. 2007 pp494; Hines, Stoelting's Co-existing. Se. 2008 pp358]
70
What specific changes are often seen in the ECG when magnesium levels reach 10 mEq/L?
At magnesium levels of 10 mEq/L, prolonged P-Q intervals and widened QRS complexes may be observed. Asystole occurs at 20 mEq/L. [Yao, Yao & Artnsio's POPM. 6e. 2008 pp917]
71
The pre-eclamptic mother who has been receiving IV magnesium and displays de- pression of deep tendon reflexes delivers her infant by Caesarean section. What signs wi!l the infant exhibit?
Magnesium crosses the placenta. Hypermagnesemia in the neonate re- sults in drowsiness, decreased muscle tone (atonia), and hypovenlilation requiring assisted ventilation. [Yao and Artusio, Problem Oriented Pa- tient Management, 1993, p506]
72
33. What is the treatment for magnesium toxici- ty in the pre-eclamptic/eclamptic patient if supportive therapy is inadequate?
Magnesium toxicity is treated with IV calcium gluconate. [Shnider and Levinson, Anes. for OB., 1993, pp349-350; Stoelting, Co-Existing, 1993, p563]
73
The parturient with pregnancy-induced hypertension (pre-eclampsia) has been treated with magnesium sulfate and has now delivered the baby. Oxytocin has been given, but uterine atony persists. What is your next action?
This is a "toughie." Magnesium sulfate is often given prophylactically to the patient with pregnancy-induced hypertension (Pil-I) to prevent seizures. Magne- sium sulfate is often continued for up to 24 hours p.illi!.partum for seizure prophy- laxis. Recall, though that Mg$0.1 is also a tocolytic (relaxes the uterus). Tocolytics (e.g., MgS01, beta-adrenergic agonists, and calcium channel blockers) given before or during labor have been implicated as causative agents of uterine atony. A careful review of medications that the patient has received or is receiving should be made and the offending agent should be stopped immediately. You might have considered giving methylergonovine to treat the uterine atony. However, even the baby has been delivered-which is definitive treatment for PHI-ergot alkaloids are relatively contraindicated in PIH, due to their hypertensive effects (Chestnut). [Datta, Anesthetic and Obstetric Management of High-Risk Pregnancy, 3'J ed., 2004, pl2l; Chestnut, Ob. Anes., yJ e(l., 2004, p67l; Authors]
74
The pre-eclamptic patient should generally not receive which general anesthetic? Why?
Ketamine should be avoided because it can aggravate the hypertension. [Barash, Clinical Anesthesia, 1997, p1074]
75
36. What is the definitive treatment for preg- nancy-induced hypertension (pre- eclampsia)?
The definitive treatment ofpregnaucy-induced hypertensior1 is delivery of the fetus and placenta. The pregnancy is allowed to continue as long as the intrauterine environment supports growth and maturation of the fetus without endangering the mother. Hospitalization and bed-rest in the lateral decubitus position are begun. Adequate hydration and IV volume expansion with a balanced salt solution are also initiated. [Shnider and Levinson, Anes.for OB., 1993, pp314-315]
76
Why is ritodrine given to a parturient? How does ritodrine stop premature labor?
Ritodrine is administered to stop premature labor. Ritodrine relaxes uterine smooth muscle and stops contractions. It does this by stimulating uterine adrenergic beta-2 receptors. [Shnider and Levinson, Anes. for OB., 1993, pp341-342; Barash Handbook, Clinical Anesthesia, 1997, pl076]
77
What are the four side-effects associated with a ritodrine administration to stop premature labor?
Side-effects of ritodrine, a beta-2 adrenergic agonist, include hyperglyce- mia, hypokalemia, tachycardia and possibly pulmonary edema. [Barash Handbook, Clinical Anesthesia, 1997, pl076]
78
Does ritodrine (Yutopar) cross the placenta? What effects could ritodrine have on the fetus?
Ritodrine (Yutopar) readily crosses the placenta such that cardiovascular and metabolic side effects may occur in the mother and fetus. You should know the side-effects of ritodrine for mom (MemoryMaster 2004, IB6b:Q10). As a reminder they arc: (1) hypokalemia, (2) hyperglycemia, and (3) tachycardia. Thus the fetus could experience hypokalemia, hyper- glycemia, and/or tachycardia. [Stoelting, PPAP, 3'" ed. 1999, p276; Au· thorsl
79
Should atropine be administered to the pregnant patient receiving ritodrine? Why or why not?
No, do not administer atropine. Ritodrine has side-effects including tach- ycardia sufficient to produce pulmonary edema. Atropine will exacerbate the problem. [Barash Handbook, Clinical Anesthesia, 1997, pl076l
80
Your obstetric patient is receiving magnesi- um sulfate. How does magnesium interact with nondepolarizing muscle relaxants? With a depolarizing muscle relaxant (suc- cinyldlOline)?
Magnesium sulfate increases the mother's sensitivity to both nondepolar- izing and depolarizing muscle relaxants. Muscle relaxants need to be titrated carefully. IShnider and Levinson, Anes. for OB., 1993, pp315-3l6]
81
Does magnesium sulfate cross the placenta? What effects can magnesium sulfate have on the fetus?
Magnesium sulfate may cross the placenta and potentially cause hy- pennagncsemia in the fetus. Hypermagnesemia in the fetus results in loss of beat-to-beat variability in fetal heart rate, hyporeflexia, muscle weak- ness, and respiratory depression (apnea). [Yao & Artusio, Yao & A rtusio's POPM, Se, 2003, p819; Hurford, Mass Gen Handbook, 6e, 2002, p502l
82
What is the effect of intravenous lidocaine on uterine tone?
Uterine arterial vasoconstriction and high uterine tone occur with high increased intravenous doses of lidocaine. Low levels ofcirculating lido- caine do not produce vasoconstriction. [Shnider and Levinson, Anes. for OB., 1993, pp35-37, 273-275]
83
How does fetal ion trapping of a local anes- t-hetic occur? Ion trapping is signiftcant when fetal pH falls into what range?
The non-ionized form of the local anesthetic crosses the placental barrier. Since the fetus has a lower pH than is found in the mother, the non- ionized form of the local anesthetic is converted to the ionized form (a weak base made more acidic yields more ionized drug), and the ionized form is trapped in the fetus. The more acidotic the fetus, the greater the ion trapping. When fetal pH falls into the range of 7.03-7.23, significant ion trapping occurs. tShnider and Levinson, Anes. for OB., 1993, p75; Authors]
84
The amount of local anesthetic diffusing across the placental barrier to the fetus will be increased if mother is acidotic of if moth~ er is alkalotic? Explain your answer.
Maternal alkalosis favors diffusion of local anesthetic across the placental barrier. Un-ionized drug diffuses across barriers such as the placental barrier. Hence, maternal conditions that shift the drug to its un-ionized form will cause the rate of diffusion from Mother to fetus to increase. Local anesthetics are weak bases and follow the rule: a weak base made more basic becomes more un-ionized (base+ base= un-ionized). There- fore, maternal alkalosis results in greater diffusion of local anesthetic to the fetus. IAuthors]
85
Ion trapping of local anesthetic by the fetus is facilitated by fetal acidosis or fetal alkalo- sis? Explain your answer.
Fetal acidosis (decrease in fetal pH) facilitates ion trapping. Local anes- thetics, which are weak bases, become progressively more ionized as pH falls (base+ acid = ionized). The lower the fetal pH, the greater the amount oflocal anesthetic in ionized form in the fetus, and the greater the amount of ion trapping. Ionized drug does not cross the placenta from the fetus to the mother. IAuthors]
86
Which of the following sets of conditions most facilitates trapping of local anesthetic by the fetus: (a) maternal alkalosis and fetal alkalosis, (b) maternal alkalosis and fetal acidosis, (c) maternal acidosis and fetal acidosis, or (d) maternal acidosis and fetal alkalosis?
Ion Trapping is facilitated by maternal alkalosis (which favors the diffusion of un-ionized drug across the placenta to the fetus) and fetal acidosis (which favors the formation of ionized drug and trapping in the fetus). IAuthors; Barash Handbook, Clinical Anesthesia, 1997, p103]
87
What local anesthetics are used in obstet- rics? Which of these crosses the placental barrier in smatlest amounts? Why?
Lidocaine, chloroprocaine and bupivacaine are commonly used in obstet~ rics. Chloroprocaine, an ester, is rapidly hydrolyzed by cholinesterase in plasma and liver, so virtually no chloroprocaine is available to cross the placental barrier. Of the amides, bupivacaine least crosses the placental barrier because it is most protein bound. Main point: Chloroprocaine crosses the placental barrier in the smallest amounts. [Morgan and Mi- khail, Clinical Anesthesiology, 1996, p708; Stoelting, Handbook PPAP,
l995, pl28; Stoelting, PPAP, 1991, p153]
88
What local anesthetic accumulates the least in the fetus? Why?
Chloroprocaine (Nesacaine) is rapidly hydrolyzed by pseudocholinester- ase and does not accumulate with repeated epidural injections in the maternal circulation; furthermore, it is metabolized in the fetal circula- tion. !Barash, Clinical Anesthesia, 1997, p1065]
89
Why is chloroprocaine a suitable anesthetic for obstetric practice?
Chloroprocaine is not too potent, and it is rapidly metabolized by plasma cholinesterase. Thus, the plasma levels of chloroprocaine wil! normally be kept low. This is important because local anesthetics cross the placenta. In summmy, chloroprocaine has low fetal toxicity and rapid onset. [Shnider and Levinson, Anes. for OB., 1993, pp84-86j
90
Which local anesthetic is the least cardiotox- ic, fastest acting, and one of the safest for use in obstetrics? Why?
Chloroprocaine is safest and least toxic because it is metabolized by plas- ma cholinesterase. Minimal amounts of cl1loroprocaine cross the placen- tal barrier. The maternal half-time of elirnination of chloroprocaine is 1.5 to 6.4 minutes. {Shnider and Levinson, Anes. for OB., 1992, p84J
91
Which local anesthetic would be best to consider for a gravida, with an epidural in place, and an acidotic fetus? Why?
Chloroprocaine (Nesacaine). When chloroprocaine crosses into the fetal blood it is metabolized rapidly and substantial accumulation is avoided, even in acidosis. [Barash, Clinical Anesthesia, 1997, pl065)
92
Rank the amide local anesthetics, from greatest to least, according to their ability to cross the placenta.
Mepivacaine > etidocaine > lidocaine> ropivacaine > bupivacaine. Mne- monic: "Maternal Elevated Locals are Risky to Baby." [Hughes, Shnider Anes.for OB., 4e, 2002, p77]
93
Why does bupivacaine pass less readily across the placental barrier than the other amide local anesthetics?
Bupivacaine has the greatest protein binding (95% is protein bound). Because it is the free, or unbound, portion of the drug that crosses lipid bilayers, only small quantities ofbupivacaine cross the placental barrier. [Barash, Clinical Anesthesia, !997, pp!062-!063; Stoelting, PPAP, 1991, pi53)
94
Do the ester-linked local anesthetics have much placental transfer? Why or why not?
No. Ester local anesthetics have little placental transfer because they are metabolized by plasma pseudocholinesterase before reaching the placen- ta. [Shnider and Levinson, Anes.Jor OB., 1993, p84)
95
Is prilocaine appropriate for use in obstet- rics? Why or why not?
Prilocainc is a poor choice for obstetrics. Ils breakdown product, alpha- ortho-toluidine, causes methemoglobinemia, and it readily crosses the placental barrier. [Shnider and Levinson,Anes.for OB., 1993, p87; Wood and Wood, Drugs and Anesthesia, !990, p360I
96
What is the best choice for early labor; spi- nal, epidural, or caudal? Why?
Epidural. Advantages of continuous lumbar epidural anesthesia via an appropriately placed epidural catheter include (1) the ability to achieve segmented analgesia (Tl 0-Ll) during the first stage of labor when total anesthesia is not required, (2) minimal local anesthetic requirements, and (3) maintenance of pelvic muscle tone so the fetal head can be more easily rotated. [Stoelting and Miller, Basics, 1994, p36SI
97
When giving an epidural to a parturient, how much should you decrease the dose?
A reduction in dosage of 25-50% is required in pregnancy. Barash states that the dose should be reduced 33-40% Reducing the dosage by one- third may be a good rule of thumb. [Davison, Eckhardt, and Perese, Mass General, 1993, p208; Morgan and Mikhail, Clinical Anesthesiology, 1996, p226; Bamsh, Clinical Anesthesia, !997, p659l
98
Identify 2 factors that decrease local anes- thetic dosing by 30% to 50% in the obstetric patienl.
Two factors that decrease local anesthetic dosing by 30% to 50% in the obstetric patient are: (1) engorgement ofepidural veins, producing a decrease in the size of the epidural space and decreased CFS volume, which facilitates the spread ofthe agent, and (2) increased peripheral sensi- tivity to local anesthetics. [Stoelting & Miller, Basics.4e, 2000, p344l
99
What is the drug of choice for treatment of hypotension during a C-section? Why?
Ephedrine. It does not constrict umbilical vessels. It has very weak alpha- receptor agonist activity (thus minimal or no vasoconstriction) and mild beta-one receptor agonist activity. It is a mild drug. [Miller, Anesthesia, 2ooo, p2043I
100
What vasopressor has a minimal effect on uterine blood flow?
Ephedrine. [Stoelting and Miller, Basics, !994, p360 I
101
evere hypertension may occur if the preg- nant patient is given a pure alpha-adrenergic agonist (phenylephrine) and the patient is also receiving what other medication?
Particularly dangerous in the pregnant patient is the combination of a purely alpha-adrenergic agent such as phenylephrine or methoxamine, and the ergot derivatives ergonovine and methylergonovine. [Shnider and Levinson, Anes.Jor OB., 1993, pl43]
102
What are the key determinants of the amount of drug transferred across the pla- centa?
A concentration gradient (diffusion force), lipid solubility, molecular weight of the drug, and total uterine blood flow. [Shnider and Levinson, Anes.for OB., 1993, pp7l-74]
103
IdentifY the drugs that are compatible with the mother who is breast-feeding her infant.
Most drugs are safe during lactation. TypicaiJy only 1% to 2% of the ma- ternal dose appears in breast milk. Lithium and ergotamine are best avoided during lactation. [Chestnut, Ob. Arzes., 3nl ed., 2004, pp223-225]
104
When is ketamine used for Cesarean sec- tion? Specify the ketamine dose.
Ketamine is used instead of thiopental if the mother is hypovolemic. Ketamine at doses of 0.2-0.5 mg/kg IV produce excellent analgesia for labor and delivery. [Morgan and Mikhail, Clinical Anesthesiology, 1996, pp7ll, 714; Barash Handbook, Clinical Anesthesia, !997, p1067; Stoelting, PPAP, 1995, pill]
105
What is the maximum dose ofketamine to be used on a pregnant woman during a rapid sequence induction? What happens with larger doses?
The maximum dose ofketamine for rapid sequence induction of a preg- nant women is 1 mg/kg. Above this dose, uterine tone increases enough to endanger the fetus. [Barash, Clinical Anesthesia, !997, pl067]
106
What is the major concern for a patient who is scheduled for tubal ligation in the early post-partum period?
The major concern is aspiration. [Stoelting, Co-Existing, 1993, p575; Stoelting and Miller, Basics, 1994, p378]
107
How can the risk of aspiration be reduced in the patient who is scheduled for tubal liga- tion in the early post-partum period?
The risk of aspiration is diminished if the surgery was anticipated and continuous epidural analgesia or spinal was used. When regional anesthe- sia had not been used, wait 8-12 hours post-parturn to allow the patient to reach cardiovascular stability and increase the likelihood of gastric emptying. Give antacids or H2 antagonists. [Stoelting, Co~Existing, 1993, p575; Stoelting and Miller, Basics, 1994, p378]
108
What are 5 major anesthetic concerns for the pregnant patient scheduled for nonob- stetric surgery?
Five major concerns for the pregnant patient scheduled for nonobstetric surgery are: (I) maternal safety, (2) fetal well-being, (3) avoid or prevent pre-term labor, (4) fetal and uterine monitoring, and (5) maintaining uteroplacental perfusion. [Kirby, eta!., Clinical Anesthesia Practice, 2002, pll68]
109
What are your concerns for the fetus in or after nonobstetric surgery in the pregnant patient?
Perinatal mortality is a common complication from elective surgery in the pregnant patient and your concern for the fetus includes possible terato- genic effects of anesthetic agents, intrauterine fetal asphyxia, and prema- ture labor (rare, according to Kirby). Nitrous oxide has been associated with inhibition of DNA synthesis avoid N20 if possible. Maternal diaze- pam administration is associated with cleft lip/palate avoid benzodiaze- pines if possible. There is an increased risk of spontaneous abortion if elective surgery is done during the first or second trimester (most organ~ agenesis occurs in the first trimester). [Duke, Secrets, 2000, p319; Kirby, et a!., Clinical Anesthesia Practice, 2002, pp1167-1168; Barash, Clinical Anesthesia, 2001, p1164]
110
What are nine concerns related to anesthe- tizing the pregnant patient for non-obstetric surgery during the third trimester?
(1) Requirements for local or inhaled anesthetics are decreased; (2) func- tional residual capacity is reduced; (3) metabolic rate is high; (4) gastric emptying is slowed; (5) aortocaval compression is high; (6) teratogenicity of anesthetic drugs is possible; (7) uteroplacental circulation needs to be monitored; (8) premature labor can be inadvertently initiated; and (9) fetal heart rate needs to be monilored. [Barash Handbook, Clinical Anes- thesia, 1997, pp593-594; Barash, Clinical Anesthesia, 1997, pp1061-1062, 1087]
111
The pregnant patient requires an appendec- tomy emergently. How do you premedicate this patient?
A non~particulate antacid, such as 30 mL of0.3 M sodium citrate, is given about one-half hour before the procedure. If necessary, a barbiturate may be given for sedation, and glycopyrrolate, which does not cross the pla- cental barrier, can be used as a vagolytic and antisialagogue. Note: Ap- pendicitis is the most common surgical emergency procedure during pregnancy. [Yao and Artusio, POPM, 1998, pp722,726]
112
Why is Bicitra given to the pregnant patient?
Bicitra (sodium citrate) is an acid neutralizing buffer that raises gastric pH, which is advantageous should aspiration occur. {Omoigui, Anesthesia Drug Handbook, 1995, p326]
113
What is the most common indication for using inhalational anesthesia for vaginal delivery?
The most common indication for general anesthesia for vaginal delivery is t·he necessity for uterine relaxation. Uterine relaxation, usually with a potent volatile agent, is necessary for intrauterine manipulations (turning the baby), complete breach extraction, manual removal of the placenta, and replacement of an inverted uterus. [Shnider and Levinson, Anes. for OB., 1993, p194; Barash, Clinical Anesthesia, 2005, p1161]
114
How does N20 affect uterine tone?
Nitrous oxide does not significantly affect uterine tone. [Omoigui, Anes- thesia Drugs Handbook, 1995, p384]
115
Is general anesthesia appropriate for elective vaginal delivery? Why or why not?
General anesthesia is not indicated for elective vaginal delivery because of the inherent risk of aspiration. [Morgan and Mikhail, Clinical Anesthesi- ology, 1996, p711l
116
What are the primary concerns when a general anesthetic is used on the obstetric patient?
Decreased FRC and mucosal congestion may cause problems in the pa- tient awakening from anesthesia. Laryngeal spasm or edema after extuba- tion, rapid desaturation, opioid depression of respiration, and chance of vomiting or regurgitation with aspiration are potential problems. {Barash, Clinical Anesthesia, 1997, pp!068-1070]
117
What drugs are appropriate for general anesthesia for an emergency vaginal deliv- ery?
(I) Thiopental (4 mg/kg) and succinylcholine (1.5 mg/kg) are most com- monly used for induction. If the patient is hypotensive, use ketamine (I mg/kg) in place of thiopental. (2) After intubation, 1-2 MAC of any po- tent volatile inhalation agent may be administered with 100% 02. (3) If skeletal muscle relaxation is necessary, atracurium, cisatracurium, vecu- ronium, rocuronium, and/or succinylcholine infusion may be used. 4) Once the fetus and placenta are delivered, the concentration of a vola- tile agent is decreased to less than 0.5 MAC or discontinued; an oxytocin infusion is started (20-40 units/L of IV fluid) and a nitrous oxide opioid technique can be used. [Morgan and Mild1ail, Clinical Anesthesiology, !996,p71l]
118
What two physiologic changes lead to rapid oxygen desaturation during periods of apnea (e.g., induction with thiopental and suc- cinylcholine} in the near-term pregnant patient?
the combination of a decreased functional residual capacity and an in- creased oxygen consumption leads to rapid oxygen desaturation during periods of apnea. At term, maternal oxygen consumption has increased 20% and maternal functional residual capacity has decreased 20%. [Mor- gan and Mikhail, Clinical Anesthesiology, 1996, p693]
119
What are five advantages of volatile anes- thetic agents for the patient undergoing elective cesarean section?
ow dose halothane (0.5%), isoflurane (0.75%), or enflurane ( l.O%) supplemented with nitrous oxide (1) decreases awareness and recall,
(2) pennits higher inspired 0 2, (3) may improve uterine blood flow,
(4) does not increase uterine bleeding, and (5) does not depress the new- born. [Shnider and Levinson, Anes. for OB., 1993, p234]
120
Describe the best induction/intubation technique for a C-section with a full stom- ach.
After pre-oxygenation, induce with thiopental (3-5 mg/kg) and succinyl- choline (1-1.5 mg/kg). Within 90 seconds, intubation is possible, having applied cricoid pressure. [Stoelting and Miller, Basics, 1994, p376]
121
List three actions that can be taken to pre- vent hypotension during a C-section.
1) Increase the effective intravascular volume by fluid loading with 500- 1000 mL 15-30 minutes prior. (2) Left uterine displacement. (3) Possibly use vasopressors, preferably ephedrine, a mixed agonist which increases blood pressure while restoring uterine blood flow. [Davison, Eckhardt, and Perese, Mass General, 1993, pp258, 259, 262]
122
What is the most common cause of maternal death during obstetric general anesthesia?
Hemorrhage is the most common cause of maternal death. [Stoelting and Miller, Basics, 1994, p372]
123
Which is more important to neonatal out- come: the induction of anesthesia-to- delivery interval or the uterine incision-to- deliveryinterval?
The uterine incision-to-delivery interval seems to be more important to neonatal outcome than the induction of anesthesia-to-delivery interval. The uterine incision-to-delivery interval is ideally less than3 minutes (180seconds).[HughesSlmiderandLevinsons Anes.forOB.,2002, pp223-225, 651-652; Norris, Ob. Anes., 1999, pp392, 405; Barash, Clinical Anesthesia, 2001, pll50]
124
What are the primary concerns when a regional anesthetic is used to anesthetize an obstetric patient?
Regional anesthetic complications include hypotension, total spinal anes- thesia, convulsions induced by local anesthetics, nausea, vomiting, breathing difficulties, headache, effects of nerve injury. [Barash, Clinical Anesthesia, 1997, pl067-1068, 1080]
125
he pregnant patient has been given a sub- arachnoid block with opioids only and no local anesthetics. What conditions may have necessitated this technique?
Subarachnoid block with opioids only would be most useful (appropriate) in high risk patients who may not tolerate the functional sympathectomy associated with spinal or epidural anesthesia. Patients who have signifi- cant cardiovascular disease, such as hypovolemia, aortic stenosis, tetralogy of Fallot, Eisenmenger's syndrome, or pulmonary hypertension, are can- didates for this technique. [Morgan and Mild1ail, Clinical Anesthesiology, !996, p707; Norris, Obstetrical Anesthesia, 1999, p444l
126
Which types of block can be used for the first stage of labor?
Paracervical, lumbar epidural, caudal, and spinal (modified saddle) blocks all can block TIO-Ll. [Stoelting and Miller, Basics, !997, ppl 067- !069]
127
At what stage ollabor is a pudendal block given?
A pudendal nerve block is given just before delivery (end of second stage), [Bonica, p487]
128
hich regional techniques would block the pelvic plexus?
Pudendal nerve block, lumbar epidural or caudal block, low subarachnoid block. [Shnider and Levinson, Anes. for OB., !993, pp!S0-!5! J
129
What are two disadvantages of paracervical block during labor and delivery?
(1) Paracervical block is not effective during the second stage oflabor. (2) The major disadvantage of a paracervical block is the 8~40% incidence of fetal bradycardia that develops 2~lO minutes after injection, Fetal acido- sis often accompanies the bradycardia, [Stoelting and Miller, Basics, 1994, pp364, 365)
130
The efficacy of epidural opioids is impaired when used in conjunction with which local anesthetic?
Chloroprocaine is not a suitable agent for use with epidural opioids, be- cause studies suggest that chloroprocaine interferes with the effectiveness (efficacy) of the opioid agonists. Opioid agonists with nm-receptor activi- ty such as fentanyl and morphine have reduced effect because chloropro- caine or its metabolites compete for opioid mu receptors in the spinal conL [Shnider and Levinson, Anes. for OB., 1993, p85; Morgan and Mi- khail, Clinical Anesthesiology, !996, p7!0]
131
Which opioids would be most effective when used epidurally with chloroprocaine, opioid agonists, opioid agonist-antagonists, or opioid antagonists?
The opioid agonist-antagonists, which have their actions predominately on kappa receptors, are more effective than opioid agonists such as fenta- nyl or morphine which have strong mu receptor actions. I3utorphanol or nalbuphine are the opioid agonist-antagonists appropriate to use with chloroprocaine; however, the opioid agonist-antagonists have a short duration of action and can cause heavy sedation. [Shnider and Levinson, Anes.forOB., l993,p85]
132
List five disadvantages of redosing the ob- stelric patient with epidural chloroprocaine.
Why would you choose to give a laboring woman an epidural?
An epidural or spinal anesthetic will relieve pain and anxiety initially and then during the first and second phases of labor, epidural analgesia blunts the increases in maternal cardiac output, heart rate and blood pressure. This may convert a dysfunctional labor pattern to normal. This may benefit the fetus by eliminating maternal hyperventilation which leads to reduced fetal arterial oxygen tension. [Barash Handbook, Clinical Anes- thesia, !997, pl274]
133
What do you want to maintain in the healthy (nontoxemic) pregnant patient undergoing lumbar epidural anesthesia: systolic pressure, diastolic pressure, or mean arterial pressure?
Systolic pressure. You want to prevent the systolic pressure from decreas- ing from baseline by 20 to 30% or falling below !00 nun Hg. [Shnider and Levinson, Anes.for OB., 1993, p397; Morgan and Mildrail, Clinical Anes- thesiology, 1996, p709; Miller, Anesthesia, 1994, p2047]
134
I'The parturient has received a neuraxial opioid and is experiencing nausea and vom- iting. Which drug is effective for opioid- induced nausea in laboring women, but has the most significant side-effects?
Droperidol is effective for the treatment of nausea in laboring women, but it has significant side-effects, namely dysphoria, akathisia (an unpleasant sensation of "inner restlessness" accompanied by the inability to sit still), and oculogyric crisis. Furthermore, the FDA has issued a "black box" warning because of the concern that the administration of droperidol may result in an increased risk of cardiac arrhythmias. [Chestnut, OB Anes. 3e. 2004 pp358; Authors]
135
The APGAR scoring system for the standard evaluation of newborn infants during the first 60 seconds after delivery assesses what five parameters?
1) Heart rate, (2) respiratory effort, (3) reflex irritability, (4) muscle tone, and (5) color. [Barash Handbook, Clinical Anesthesia, 1997, p592]
136
List seven actions that should be taken if the newborn's APGAR score is 4-6.
l) Oropharyngeal airway inserted, and (2) 0 2 applied under pressure of 16-20 em H20 for l-2 seconds. If no response, (3) visualize airway with laryngoscope, (4) insert endotracheal tube, (5) ventilate through tube gently at 25-35 em I-hO, (6) start spontaneous respiration, (7) withdraw endotracheal tube after the infant has taken five or six breaths. [Barash Handbook, Clinical Anesthesia, 1997, p!082]
137
List five actions that should be taken i f the newborn's APGAR score is 0-3.
(1) Establish ventilation without delay; (2) inspect glottis with scope; (3) if meconium is present, suction at once before lungs are infiated; (4) severe- ly depressed infants may require 3-8 minutes of artificial ventilation before spontaneous gasp is taken; and (5) severe acidosis (pH15 mEq/1} should be corrected promptly with sodium bicar- bonate infused over two minutes to a total dose of2 mEq/kg. [Barash Handbook, Clinical Anesthesia, 1997, p1082-1083]
138
What APGAR scores indicate that the neo- nate is severely depressed? What drugs might be appropriate for resuscitating the neonate with an APGAR score of3?
An APGAR score of 0-3 indicates a severely depressed neonate. Epineph- rine should be given for asystole or a spontaneous heart rate less than 80 (some sources suggest atropine sulfate for bradycardia). Naloxone is given to reverse respiratory depression if opioids were given to the mother in the last four hours of labor, and the mother is not addicted to opioids. Other drugs that may be indicated for specific situations include sodium bicarbonate if the fetus is acidotic (pH
139
What is the neonatal dose of epinephrine for treatment of asystole?
Epinephrine, 0.01-0.03 mg/kg (0.1-0.3 mL!kg of a 1:!0,000 solution), should be given for neonatal asystole or neonatal spontaneous heart rate
140
What is the appropriate drug for the neonate with an APGAR score of 3 after 5 minutes?
odium bicarbonate. Sodium bicarbonate may be administered during prolonged resuscitation (>5 minutes), particularly i f blood gas measure- ments are not available. [Morgan and Mikhail, Clinical Anesthesiology, 1996, pp724-725]
141
The pregnant patient delivered baby under general anesthesia; what factor(s) correlates most with a depressed APGAR score at one minute?
The general anesthetic factors which most depress the APGAR score at one minute are low F10 2 and high N20. Initial lower APGAR scores under general anesthesia are probably due to transient sedation rather than asphyxia. The incidence of depressed APGAR scores at one minute can be markedly reduced by techniques that include: (1) higher r.o,, (2) reduced N20, (3) lower dose (0.5 MAC) halogenated agents, (4) continuous lateral tilt, and (5) expeditious delivery time. Note: the fears that high maternal P02 may cause uterine vasoconstriction are unfounded (Norris). (Hughes Shnider and Levinsons Anes.for OB., 2002, pp223-225, 651-652; Norris, Ob. Anes., 1999, pp392, 405]
142
What is done for the infant who is born with thin meconium in the mouth?
For watery thin meconium found only in the mouth, a bulb syringe is used to suction the orophatynx followed by suctioning of each naris. [Cote, ed., PAIC, 2e, p214; Barash, Clinical Anesthesia, 1997, pp 1093- 1094]
143
If a newborn has meconium and blood below the cords, what are the appropriate actions?
If meconium is below the cords, intubate and suction. [Davison, Eck- hardt, and Perese, Mass General, 1993, pp513-514]
144
What should be monitored during meconi~ urn suctioning?
Heart rate should be monitored during suctioning. "Suctioning should not be carried out to the point of severe bradycardia or cardiac arrest." [Cote, ed., PAIC, 2e, p214]
145
What is the most common musculoskeletal complaint of the pregnant person?
The most common musculoskeletal complaint during pregnancy is low back pain. [Chestnut, Ob. Anes., 3'' ed., 2004, p856]
146
What is the major potential complication of a D&C (dilation & curettage)'
From a surgical standpoint, the major risk of diagnostic D&C is perfora- tion and subsequent hemorrhage. [Longnecker, Tinker, and Morgan, PPA, 2e, 1998, p2036]
147
A pregnant patient receives a caudal block and suddenly becomes agitated, dyspneic and her legs thrash. Shortly after this she becomes unconscious and apneic. Why?
Intravascular injection oflocal anesthetic may have occurred. These are signs and symptoms of seizures. [Davison, Eckhardt, and Pcrese, Mass General, 1993, p464]
148
A pregnant patient receives a caudal block and suddenly becomes agitated, dyspneic and unable to move her legs. She then be- comes unconscious and apneic. Why?
High spinaL The key here is the motor paralysis, which indicates that the local anesthetic caused paralysis, which would not be seen with intravas- cular injection. [Authors}
149
The fetus of a parturient presenting with abruptio placenta is bradycardic. The patient is morbidly obese and has modest tem- poromandibular joint immobility. She can open her mouth two fingerbreadths. How should the patient be anesthetized for deliv- ery of thefetus?
The fetal bradycardia signals severe fetal distress, which is an emergency. An emergency cesarean section should be performed. A rapid sequence induction with cricoid pressure is performed using thiopental (4 mg/kg) or ketamine (1 mg/kg) and succinylcholine (l.S mg/kg). Ketamine is used instead of thiopental if the patient is hypotensive or hypovolemic. [Mor- gan and Mikhail, Clinical Anesthesiology, 1996, pp713-714,716; Shnider and Levinson, Anes.forOB., 1993, pp390,386]
150
Define "fetal distress." What common moni- tors are used to determine fetal well-being intrapartum?
Fetal distress has been an imprecisely and poorly defined term applied to many fetal conditions including abnormal fetal heart rate patterns, meco- nium-stained amniotic fluid, and newborns with low APGAR scores. fetal distress is now more accurately defined as "persistent fetal asphyxia, that, if not corrected or circumvented, will resull in permanent neurologic damage or death" (Norris). Fetal heart rate monitoring (FHR) is com- monly used to assess fetal well-being. Fetal pH, monitored via scalp blood samples, is also used to monitor fetal well-being. [Norris, Obstetrical Anesthesia, 2'"1ed. 1999, pp6l9-624; Miller, Anesthesia, 5th ed. 2000, pp2023-2033; l
151
What are the early signs and symptoms of fetal distress (persistent fetal asphyxia)?
The hallmarks of fetal distress have traditionally been fetal bradycardia and the passage of meconium in utero. Fetal heart rate (FHR) is normally 120-160 beats/min. The loss of beat-to-beat variability coupled with variable or late decelerations significantly increases the likelihood of significant fetal hypoxia. [Norris, Obstetrical Anesthesia, 2nd ed. 1999, pp619-624]
152
What is placenta accreta? What patients are at increased risk for placenta accreta?
Placenta accreta describes any condition in which the placenta adheres to, invades, or penetrates the uterine myometrium. The combination of placenta previa and previous cesarean section is associated with increased risk of placenta accrcta. The risk increases further when more than one previous cesarean section has been performed. [Stoelting, Co-Existing, 1993, p567; Miller, Anesthesia, 1994, p2065]
153
What should be done once the diagnosis of placenta accreta is made?
The anesthetist should be prepared for rapid blood and fluid replacement prior to surgery. This preparation should include placement ofseveral large-bore intravenous catheters and the immediate availability ofblood. [Miller, Anesthesia, !994, p2065]
154
What are six anesthetic considerations for the patient with an inverted uterus during vaginal delivery?
(1) Use large bore catheters for Ouid resuscitation, (2) have blood typed, crossed and ready for infusion, (3) administer warm fluids, (4) administer oxygen, (5) provide general anesthesia with a volatile agent, and (6) use rapid sequence induction with oral endotracheal tube placement after oral antacid. fOstheimer, Manual ofOb. Anes., 1992, p232; Shnider and Levin- son, Anes. for OB., 1993, p393]
155
Consider the pregnant patient who is at- tempting a trail of labor for vaginal birth after cesarean section (VBAC): what is a major concern?
Uterine rupture is a potentially life-threatening complication that may occur with vaginal birth after cesarean section (VBAC). The incidence of uterine rupture with VBAC labor is higher than once thought, now ap- proaching l %. Maternal or fetal morbidity or mortality is lO% to 25%, and fetal mortality may approach 80%. [Miller, Anesthesia, 6e, 2005, p2336; Nagelhout & Zaglauiczuy, NA, 3'" ed., 2004, pl085]
156
Identify the signs and symptoms of uterine rupture. What is the treatment for uterine rupture?
Signs and symptoms of uterine rupture are often nonspecific, but they almost always include fetal bradycardia, or an abnormal fetal heart rate. Maternal hypotension, abrupt onset of continuous abdominal pain-even with epidural anesthesia, and changes in uterine tone or contraction pattern herald the onset of uterine rupture. Treatment of uterine rupture requires volume resuscitation and emergency laparotomy under general anesthesia. [Miller, Anesthesia, 6e, 2005, p2336; Morgan, Mikhail, and Murray, Clinical Anesthesiology, 3"1 ed., 2002, pp823, 835-836]
157
In the past, general anesthesia with halogen~ ated agents was commonly used during replacement of an inverted uterus (uterine inversion). What drug (and dose) may sup- plement or replace general anesthesia for correction of uterine inversion? What is your anesthetic concern?
The combined use oflow-concentration inhaled agents with nitroglycerin (50-100 meg) has been used for successful correction of uterine inver- sion. Nitroglycerin alone may be ideal owing to its rapid onset and short duration of action. Hypotension is of concern, especiaUy if both NTG and GA are used. [Hughes, Shnider Anes. for OB., 4e, 2002, p367; Chestnut, Ob. Anes., Jfd ed., 2004, p674; Datta, Anesthetic and Obstetric Manage- ment ofHigh-Risk Pregnancy, 3'' ed., 2004, pl29]
158
A patient with an inverted uterus comes to the operating room immediately after deliv- ery. Blood pressure is 80/50 and heart rate 150. Blood loss during delivery was 3liters. What is the induction of choice?
Ketamine. It supports blood pressure better than all other induction agents. [Davison, Eckhardt, and Perese, Mass General, 1993, pi 54]
159
Damage to which of the three layers of the uterus is of greatest concern to the anesthe- tist? Explain your answer.
The middle (muscular) layer. The middle muscular coat, or myornctrium, consists of 12 to 15 mm of smooth muscle. The thickness of the myome- trium increases greatly during pregnancy. The main branches of the blood vessels and nerves of the uterus are located in this layer. "If blood has extravasated into the myometrium, the uterus may not contract, bleeding may continue, and a DIC syndrome may occur." [Moore, Clinically Ori- entedAnatomy,yded.,p284;Miller,Anesthesia, 1994,p2064]
160
Uterine atony is associated with what per- cent of vaginal births? How much blood can be lost?
Uterine atony occurs in about 2 to 5% of vaginal births. Two liters of blood may be lost in five minutes. [Shnider and Levinson, Anes. for OB., 1993, p393]
161
List five requirements for the anesthetic management of uterine atony.
Anesthetic management for an inverted uterus requires: (I) replacing blood loss initially with crystalloid or col!oid; (2) giving IV infusion of oxytocin (Pitocin) to cause uterine contraction; (3) giving 0 2 by face mask; (4) placing the patient in the Trendelenburg position; and (5) close- ly monitoring vital signs including central venous pressure and urine output. [Shnider and Levinson, Anes. for OB., 1993, p393]
162
Should severe maternal hypotension exist, what IV anesthetic would you use for indue- lion and intubcltion?
Ketamine may be used for induction of general anesthesia and endotra- cheal intubation for emergency delivery usually from hemorrhage causing maternal hypotension. Ketamine is indicated in hypotensive states due to its ability to maintain cardiac output and elevale blood pressure. [Os- theimer, p58; Firestone, Mass General, 1993, p154; Shnider and Levinson, Anes. for OIJ., 1993, p128]
163
A patient with a ruptured ectopic pregnancy becomes hypotensive. What should be done first?
Increase delivery of IV iluids. The patient with a ruptured ectopic preg- nancy usually has postural signs of hypovolemia and will need intravascu- lar volume restored. [Anesthesia and Uncommon Diseases, 1990, p165]
164
Is the incidence of morbidity and mortality associated with seizures and convulsions during epidural anesthesia for labor and delivery high or low?
The reported incidence of convulsions during obstetrical regional anes- thesia is low (0.03-0.5%). The incidence of morbidity and mortality asso- ciated with intravascular injection oflocal anesthetic is also very low. [Shnider and Levinson, Anes. for OB., 1993, p141]
165
To what is the low incidence of morbidity and mortality in the patient who seizes during labor and delivery with epidural anesthesia attributed?
Early recognition and proper management usually lead to good outcomes. [Shnider and Levinson, Anes.for OB., 1993, p141; Morgan and Mikhail, Clinical Anesthesiology, 1996, p709]
166
List six steps in the treatment of local anes- thetic toxicity in the obstetric patient under- going epidural anesthesia.
Treatment of local anesthetic toxicity involves: (I) early recognition of the reaction (accomplished by observing the patient and her vital signs and by talking to her); (2) prevention of the progression of the reaction (accomplished by giving small doses of thiopental or a benzodiazepine); (3) maintenance of oxygenation (accomplished by maintaining a patent airway and, if necessary, intubating with succinylcholine and cricoid pressure); (4) supporting the circulation (accomplished by elevating the legs, displacing the uterus to the left, and rapid administration of intrave- nous fluids if needed); (5) treatment of cardiac arrest; and (6) assessing the condition of the fetus as soon as possible after the convulsions {prompt maternal resuscitation usually will restore uterine blood flow and fetal oxygenation). [Shnider and Levinson, Anes. for OB., 1993, p142]
167
The patient receives a spinal for C-seclion and develops numbness in fingers and dyspnea. What four actions should be taken? What caused this?
(l) Give 0 1; (2) support blood pressure; (3) provide reassurance; (4) initi- ate assisted ventilation and general anesthesia. Cause: High spinal. The cervical segments supply sensory nerves to the fingers and thumb. [Barash, Clinical Anesthesia, 1997, pp664, 10801
168
If a maternity patient begins getting short of breath with a high spinal, what four actions should be taken?
Treatment consists of (1) establishing an airway and ventilating with oxygen, (2) intubating to protect the airway, (3) placing in Trendelenburg position and left uterine displacement to increase venous return to the heart, and (4) giving fluid and ephedrine (as necessary) to maintain blood pressure at a normal level. [Miller, Anesthesia, 1994, p2054; Shnider and Levinson, 2002, pp142-143l
169
An OB patient is experiencing a difficult labor, then suddenly exhibits dyspnea, tach- ycardia, cyanosis, and hypotension; what is the most likely cause?
Abnormal presentation, or multiple births, could compress aortocaval structures and induce these symptoms. {Stoelting and Miller, Basics, 1989, pp378-379; Davison, Eckhardt, and Perese, Mass General, 1993, p273]
170
The fetus is considered acidotic when fetal pH is below what value? What is the lowest blood pH the fetus may have and still be considered normal?
A fetal pH belaw 7.20 indicates fetal acidosis. A fetal capillary blood pl-I of 7.25 is the lowest limit of normal. Values beLween 7.20 and 7.24 are con- sidered pre-acidotic. [Barash, Clinical Anesthesia, 1997, ppl080-1081]
171
What causes fetal acidosis?
Fetal hypoxia leads to anaerobic metabolism and systemic fetal acidosis. [Yao and Artusio, POPM, 1993, p523J
172
What is measured by the fetal scalp moni- tor? What is assessed by the fetal scalp mon- itor?
Petal scalp monitoring involves taking blood samples from the scalp of the fetus and measuring blood pH. Fetal scalp blood sampling is used to assess the degree of fetal acidosis for asphyxia when abnormal heart rate pat- terns cannot be corrected or their significance is unclear. [Hurford et al, Mass General, 1998, p525; Barash, Clinicnl Anesthesia, 1997, p1079]
173
List five complications associated with placement of the fetal scalp electrode, and indicate which complication is the most common.
etal complications related to placement ofscalp electrodes include: (I) ecchymoses, (2) lacerations, (3) leakage ofcerebrospinalfluid, (4) sepsis, and (5) scalp abscesses. The most common fetal complication is scalp abscess. Maternal complications of placement of the fetal scalp electrode may include damage to the wall of the vagina such as lacerations. Note: Fetal acidosis is not a complication of fetal scalp monitoring; fetal acidosis is assessed by the fetal scalp monitor. [Barash, Clinical Anesthesia, 1997, pl079; Authors]
174
What is normal fetal heart rate and normal beat-to-beat variability? What treatments can restore utero placental circulation when variations in fetal heart rate occur?
Normal fetal heart rate is 120-160 beats/minute. Baseline beat-to-beat variabilityof3-6 beats/minute is normal. Aortocaval compression, ma- ternal hypoxemia, maternal hypotension, or excessive uterine activity can compromise fetal circulation. Fetal asphyxia can lead to wide variations in fetal heart rate. Changes in maternal position to avoid aortocaval com- pression, IV ephedrine and fluid or adjustment of oxytocin infusion can improve utero placental flow. Wide variability in fetal heart rate necessi- tates immediate delivery. [Morgan and Mikhail, Clinical Anesthesiology,
!996, pp720-72!]
175
Describe early (Type I) decelerations of fetal heart rate. Are early decelerations a sign of fetal distress?
Early decelerations are characterized by the slowing of the fetal heart rate that begins with the onset of uterine contractions. Decreases in heart rate are usually not more than 20 bpm or below an absolute rate of 100 bpm. This deceleration pallern is thought to be caused by vagal stimulation secondary to compression of the fetal head. Early decelerations are NOT associated with fetal distress. [Hines, Stoelting's Co-existing. Se. 2008 pp577; Nagelhout & Plaus, NA. 4th. 2009 pptlll-1112)
176
Describe late (type II) decelerations.
Late (type II) decelerations are characterized by decreases in heart rate that begin at the peak of uterine contraction force; the decreases in fetal heart rate may be small (5 beats/min) and are greatest after the peak of uterine contraction force. [Morgan and Mikhail, Clinical Anesthesiology, !996, p720]
177
Stale what causes late (type II) decelerations. Is the fetus compromised when late deceler- ations are present?
Late decelerations are thought to be due to low fetal Pa02. When late decelerations are present, the fetus is compromised. [Morgan and Mi- khail, Clinical Anesthesiology, 1996, p720]
178
Describe the cause and significance of late (type II) decelerations with normal beat-to- beat variability in heart rate.
Late decelerations with normal beat-to-beat variability in heart rate are associated with acute insults such as maternal hypotension or maternal hypoxemia; these are usually reversed with treatment. [Morgan and Mi- ldlail, Clinical Anesthesiology, 1996, p720]
179
Describe the cause and significance of late (type II) decelerations with diminished beat- to-beat variability in heart rate.
Late decelerations with reduced beat -to-beat variability in heart rate are associated with prolonged fetal asphyxia; these are an indication for fur- ther assessment such as fetal pH scalp sampling. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p720]
180
Describe the cause and significance oflate (type II) decelerations with no beat-to-beat variability in heart rate. What action should be taken?
Late decelerations without beat-to-beat variability signifies severe decom- pensation; immediate delivery is imperative. [Morgan and Mikhail, Clini- cal Anesthesiology, 1996, p720]
181
Describe variable (type III) decelerations.
The onset, magnitude, and duration of theses decelerations are variable. Onset is abrupt and may occur at any time during the uterine contraction. The duration of the deceleration may be short or long. The magnitude of the deceleration varies, but the decrease in heart rate often exceeds 30 beats/min. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p720]
182
State what causes variable (type III) deceler- ations.
Variable (type III) decelerations are thought to be due to uterine-induced umbilical cord compression which causes a decrease in umbilical blood flow. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p720]
183
When are variable (type III) decelerations typically associated with fetal asphyxia?
Fetal asphyxia is associated with variable decelerations when the decrease in heart rate is greater than 70 beats/minute, more than 60 seconds long, or when the pattern persists for more than 30 minutes. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p720]
184
Identify the most common cause of anes- thesia-related maternal mortality on the obese parturient.
The most common anesthesia-related cause of maternal mortality in the obese parturient is airway complications. [Chestnut, Ob. Anes., 3rd ed., 2004, p901]
185
You are confronted with an unexpected difficult intubation of the pregnant patient. The parturient is anesthetized, but you were unable to intubate the trachea. Mask ventila- tion is adequate and there is no fetal distress. What are your options? What is mandatory during mask ventilation?
In the parturient who cannot be intubated but can be ventilated by mask and with no fetal distress either awaken the patient or perform a cricothy- rotomy or tracheostomy. During positive mask ventilation, maintenance of cricothyroid pressure is mandato1y. Establishment of a surgical airway is an acceptable alternative because emergence may be accompanied by difficulty maintaining adequate mask ventilation. [Chestnut, Ob. Anes., Y" ed., 2004, pp549-550]
186
You are confronted with an unexpected difficult intubation of the pregnant patient. The parturient is anesthetized, but you were unable to intubate the trachea. Mask ventila- tion is adequate, but fetal distress is present. What are your three options?
In the parturient who cannot be intubated but can be ventilated by mask with fetal distress, three options are available. (I) Awaken the patient. This option will likely preserve the mother's life, but may result in the demise of the fetus. (2) Perform a cricothyrotomy or tracheostomy. (3) Continue anesthesia by mask ventilation while an assistant maintains cricoid pres- sure (the "failed intubation drill"). The objective of the failed intubation drill is to achieve spontaneous ventilation and oxygenation by mask, without aspiration. (See reference for full failed intubation drill.) [Chest- nut, Ob. Anes., 3'' ed., 2004, pp550-551]
187
You are confronted with an unexpected difficult intubation of the pregnant patient. The parturient is anesthetized, but you were unable to intubate the trachea and mask ventilation is inadequate. What are four rescue options for this situation?
For the parturient who cannot be intubated or ventilated by mask there are four rescue options: ( l) insertion of an esophageal-tracheal Com- bitube, (2) insertion of la>yngeal mask airway (LMA), (3) transtracheal jet ventilation (TTJV), and (4) emergent cricothyrotomy or tracheostomy. [Chestnut, Ob. Anes., 3"1 ed., 2004, pp55l-552j
188
For the cannot-intubate cannot-ventilate situation in the prior question, why might the laryngeal mask airway (LMA) be your first choice?
The laryngeal mask airway (LMA) is often the first option in the cannot· intubate cannot-ventilate situation because of the small incidence of failure-the exact position is not critical for establishing an acceptable airway. [Chestnut, Ob. Anes., 3'' ed., 2004, pp549-552]
189
Can an intubating laryngeal mask airway (ILMA or Fastrach LMA) be used in the cannot-intubate cannot-ventilate scenario? What is the potential advantage of the IL- MA/Fastrach?
The intubating laryngeal mask airway (ILMA or Fastrach) is an acceptable option in the rescue attempt of a cannot -intubate cannot-ventilate diffi- cult airway. The advantage of the ILMA/Fastrach is that it also functions as a conduit for the blind passage of an endotracheal tube. [Chestnut, Ob. Anes., 3"1ed., 2004, ppSSl-552]
190
Amniotic fluid embolism is the first, second, third, fourth, or fifth leading cause of ma- ternal death? What is the mortality rate for patients with amniotic fluid embolism?
Amniotic fluid embolism is the third leading cause of maternal death. Patients who develop amniotic fluid embolism die within one hour if not diagnosed and treated. The mortality rate for patients with amniotic fluid embolism is greater than 50% in the first hour. [Kirby, Taylor, and Civetta, Handbook ofCritical Care, 1997, p608; Morgan and Mikhail, Clinical Anesthesiology, 1996, p719]
191
When does amniotic fluid embolism occur? The classic presentation of amniotic fluid embolism consists of what three elements?
Amniotic fluid embolism occurs when there is a tear through the amnion or chorion (which opens uterine or endocervical veins) and pressure is sufficiently high to force amniotic fluid into the venous circulation. The classic presentation consists ofsudden onset ofdyspnea and hypotension followed by cardiopulmonaty arrest. [Davison, Eckhardt, and Perese, Mass General, 1993, p470; Kirby, Taylor, and Civetta, Handbook ofCritical Care, 1997, p 608; Morgan and Mikhail, Clinical Anesthesiology, 1996, p719]
192
What are six signs and symptoms of amniot- ic fluid embolism?
( 1) Rapidly developing respiratory distress (pulmonary embolism, tach- ypnea, hyperventilation), (2) decreased cardiac output (systemic hypoten- sion), (3) hypoxia (marked ischemia), (4) coma, (5) disseminated intra- vascular coagulopathy (DIC), and (6) uterine atony. [Shnider and Levinson,Anes.forOB., 1993, pp377-78]
193
What three pathophysiological problems are responsible for the presenting signs and symptoms seen in the patient with amniotic fluid embolism?
Three major pathophysiological events responsible for the signs and symptoms associated with amniotic fluid embolism are: (I) acute pulmo- nary embolism, {2) disseminated intravascular coagulopathy (DIC), and (3) uterine atony. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p719]
194
List five specific actions in treating amniotic fluid embolism. (You will be asked in the next question to identify five more actions.)
Treatment ofamniotic fluid embolism consists ofaggressive cardiopulrno- nary resuscitation, stabilization and supportive care. (1) Intubate and ventilate with 100% Oz, (2) begin cardiopulmona1y resuscitation, if there is no pulse, (3) insert two large bore intravenous lines, a pulmonary artery catheter, a bladder catheter, and an arterial line, (4) monitor SaC)2, EKG, pulmonary and systemic blood pressures, cardiac indices, and neurologic function, and (5) notify the blood bank for probable need of fresh frozen plasma and platelets. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p719; Shnider and Levinson, Anes.for OB., 1993, p381]
195
List five additional actions you might take in treating amniotic fluid embolism.
(1) Sodium bicarbonate can be administered for acidosis, (2) deliver the fetus and the placenta as soon as feasible, (3) administer sympathomimet- ics for left ventricular failure, (4) if central venous pressure is rising, digoxin or deslanoside and furosemide may be given, and (5) administer hydrocortisone. [Morgan and Mild1ail, Clinical Anesthesiology, 1996, p719; Shnider and Levinson, Anes. for OB., 1993, p381 I
196
What is the appropriate positioning for the parturient with amniotic fluid embolism if the fetus has not yet been delivered?
For the parturient with amniotic fluid embolism (AFE) from whom the fetus has not been delivered, !eft uterine displacement is appropriate, along with slight head-opposition, with left lateral tilt of at least 15 de- grees. [Nagelhout & Zaglaniczny, NA, 3'" cd., 2004, pp 1083-1084]
197
What drugs may be used to treat amniotic fluid embolism?
Sympathomimetics (dopamine, dobutamine, isoproterenol, norepineph- rine) if there is left ventricular failure; digitalis (digitoxin or deslanoside) and furosemide if central venous pressure is rising; hydrocortisone in 1- gram intravenous boluses every 6 hours for 48 hours. [Shnider and Levin- son, Anes.for OB., 1993, p381]
198
What drug is recommended for the treat- ment of disseminated intravascular coagula- tion (DIC) associated with amniotic fluid embolism? How does this drug work?
Epsilon-aminocaproic acid (Amicar) administered in 4 to 6 g doses every 4 to 6 hours is recommended for the treatment of the DIC component of the disorder. Amicar decreases the breakdown of fibrin (inhibits fibrinolysis) by inhibiting plasminogen and plasmin. [Kirby, Taylor, and Civetta, Handbook ofCritical Care, 1997, p610; Omoigui, Anesthesia Handbook, 1995, p7]
199
Identify 5 signs and symptoms of venous air embolism in the pregnant patient.
Signs and symptoms of venous air embolism in the pregnant patient are (l) milt-wheel murmur detected over the pericardium, (2) chest pain,
(3) dyspnea, (4) decreased end-tidal C02, and (5) elevated central venous pressure. Late signs of venous air embolism are hypotension, tachycardia, and cardiac dysrhythmias. [Stoelting & Miller, Basics, 5e, 2007, p460; Chestnut, Ob. Anes., 3'" ed., 2004, p691]
200
The obstetric patient develops a venous air embolism-in what position will you place the parturient?
The parturient who develops a venous air embolism (incidence as high as 95%) should be placed in a slight anti-Trendelenburg position with left- lateraltilt of 15. This position increases the likelihood of trapping air in the right atrium, from which it can be aspirated via a central venous catheter. [Nagelhout & Zaglaniczny, NA, 3"1 cd., 2004, p1083]
201
A routine antenatal ultrasound reveals poly- hydramnios in the pregnant patient. What is polyhydramnios and what are the implica- tions for the fetus?
Polyhydramnios is the presence of excessive amniotic Ouid around the unborn infant. Polyhydramnios occurs when the infant fails to swaltow and absorb amniotic fluid in normal amounts. The most common causes are gastrointestinal obstruction and neurological problems. Esophageal atresia, as seen in tracheoesophageal fistula (TEF) is o fgreatest concern for the infant. If polyhydramnios is present, check for TEF by passing a nasa- gastric tube shortly after delivery. Note: Polyhydramnios also appears antenatally in 30% of congenital diaphragmatic hernia cases. (Barash, Handbook). Ifboth answers appear and no other pertinent information is given, choose tracheoesophageal fistula as the BEST answer. [Barash, Clinical Anesthesia, 2001, pp1184, 1187; Barash, Handbook, 2001, p629; Authors]
202
o u r patient has mitral stenosis and is being prepared for an emergent cesarean section. The patient has not been adequately hydrated and hypotension is a concern- which anesthetic technique will you use?
A general anesthetic would be the technique of choice for emergent cesar- ean section when hypotension is a major concern. Although regional and neuraxial techniques are viable options, hypotension is more common with these techniques, compared to general anesthesia. Hypotension is most common with a spinal anesthetic, less common with epidural anes- thetics, and modestly less common with a regional technique; a general anesthetic is associated with the least likelihood of hypotension. [Chest- nut, OB Anes. 3e. 2004 pp440; Yao, Yao & Artusio's POPM. 6e. 2008 pp942]
203
What medication should be used to treat a hypotensive episode in the parturient who has mitral stenosis?
Phenylephrine (Nco-Synephrine) is preferred as a vasoconstrictor because tachycardia is not well tolerated. [Longnecker eta!., PPA, 1998, p20l3]
204
The pregnant patient with mitral stenosis develops atrial fibrillation during labor and delivery. When would you consider drug therapy? What drug should be used?
The patient should be treated immediately if evidence of hypotension, left ventricular failure, or myocardial ischemia exists. Direct current cardia- version is the first choice for treating acute life-threatening atrial fibrilla- tion. If this is not possible, a drug with a rapid onset should be selected. A beta-blocker such as propranolol is the choice in this situation. [Shnider and Levinson, Arws.for OB., !993, p5!6]
205
Polyhydramnios is associated with trache- oesophageal fistula, as you know. Identify four other maternal and fetal concerns when polyhydramnios is present.
In addition to tracheoesophageal fistula, four other maternal and fetal concerns associated with polyhydramnios are: (1} umbilical cord pro- lapse-polyhydramnios and decreased fetal heart rate are indicative of umbilical cord prolapse; (2) possible breech presentation with a single gestation; (3) possible malpresentation in multiple gestation (twins, tri- plets, etc.); and, (4) polyhydramnios is associated with uterine atony. [Chestnut, Ob. Anes., 3'd ed., 2004, pp633, 64!, 670; Miller, Anesthesia, 6e, 2005, p2336]
206
What vasopressor should be selected to maintain blood pressure in the pregnant patientwhohasaorticstenosis?
Since hypotension is poorly tolerated, maternal blood pressure should be sustained with fluids, or phenylephrine, if hypotension does not respond tovolume.!Norris,ObstetricalA1testhesia, 1999,p444]
207
An epidural or intrathecal opioid instead of an epidural or intrathecal local anesthetic is should be given to the pregnant patient with what valve problem (aortic regurgitation, aortic stenosis, mitral regurgitation, mitral stenosis)?
Aortic stenosis. Epidural or spinal opioid techniques are most useful for high risk patients who may not tolerate the functional sympathectomy associated with spinal or epidural anesthesia. This group includes patients with significant cardiovascular disease such as hypovolemia, aortic stow- sis, tetralogy ofFallot, Eisenmenger's syndrome, or pulmonary hyperten- sion. [Morgan and Mikhail, Clinical Anesthesiology, !996, p707; Norris, Obstetrical Anesthesia, !999, p444]
208
The patient undergoes a vaginal hysterecto- my. If, at the end of the case the patient is unable to dorsiOex the foot, what nerve was injured?
The common peroneal nerve was injured. This nerve can be compressed between the head of the fibula and a lithotomy stirrup when the patient is in the lithotomy position. Footdrop, or inability to dorsiflex the foot, results. [Martin and Warner, Positioning, 1997, pp275-276; Gravenstein and Kirby, Complications in Anesthesiology, 1996, p588; Ellis & Feldman, Anatomyfor Anaesthetists. 8e. 2004 pp205]
209
What nerve is responsible for loss ofsensation to the lateral thigh during vaginal hysterectomy?
Lateral femoral cutaneous. [Authors]
210
What nerve is most commonly injured in the patient undergoing an abdominal hys- terectomy?
The femoral nerve. [Jaffe and Samuels, Anaesthesiologist's Manual of Surgical Procedures, 19941
211
Nerve injury to the mother during labor and delivery usually occurs for what two rea- sons?
In obstetrics, nerve injury to the mother is usually due either to: (1) com- pression o f the lumbosacral trunk between the head of the fetus and the sacrum, or (2) kinking or compression of the femoral, lateral femoral cutaneous, or peroneal nerves when the patient is in the lithotomy posi- tion. [Miller, Anesthesia, 1994, p2054j
212
What nerve injury is most commonly asso- ciated with vaginal delivery?
The lumbosacral nerve probably is most commonly injured during vaginal delivery. The ASA Closed Claim study revealed that the ulnar, brachial plexus and lumbosacral nerve root injuries predominated. The lumbosa- cral injury-related claims were most commonly filed by women. Clear documentation for this question is difficult to find. [Long11ecker et al., PPA, 1998, p620]
213
A pregnant patient presents with thrombo- cytopenia. What are the likely reasons for the thrombocytopenia?
Of pregnant patients who present with a platelet countless than 150,000/mm3, 74% had incidental thrombocytopenia (also known as
gestational thrombocytopenia), 21% had pre-eclampsia/eclampsia (HELLP syndrome), and 4% had an autoimmune disease such as systemic lupus erythematosus (SLE) or autoimmune thrombocytopenia, also known as either idiopathic thrombocytopenia or immune thrombocytopenia. In the pregnant patient presenting with thrombocytopenia, the most likely cause is incidental, or gestational, thrombocytopenia. The next most likely reason for onset of thrombocytopenia during pregnancy is preeclamp- sia/eclampsia (HELLP syndrome). Recognize that there is an additional long list of additional reasons the pregnant patient may develop thrombo- cytopenia. [Norris, Obstetrical Anesthesia, 1999, p457; Birnbach, Gatt and Datta, Textbook Ob. Anes., 2000, pp588-590]
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Describe the etiology of idiopathic thrombo- cytopenic purpura.
Idiopathic thrombocytopenic purpura (autoimmune thrombocytopenic purpura) is characterized by persistent thrombocytopenia caused by antiplatelet antibodies that bind to platelet membranes, causing prema- ture rupture of the platelets. [Stoelting & Dierdorf, Co-Existing, 4e, 2002, p502]
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How common is incidental or gestational thrombocytopenia?
Incidental or gestational thrombocytopenia occurs in 7.6% of pregnant patients. This mild thrombocytopenia does not appear to be associated with adverse consequences to the mother or the fetus. [Birnbach, Galt and Datta, Textbook Ob. Anes., 2000, pp588-590j
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A parturient has gestational diabetes me!litus and is hyperglycemic on admission for labor and delivery. Wi!l her infant be normoglycemic, hypoglycemic, or hypergly- cemic? Why?
Neonatal hypoglycernia occurs in 5% to 12% of cases of pregestational and gestational diabetes mellitus (DM). The neonatal hypoglycemia is pre- sumed to result from sustained fetal hyperinsulinemia that develops in response to chronic intrauterine hyperglycemia. Decreased fetal oxygen secondary to uncontrolled maternal DM may also promote hypoglycemia in the fetus and newbom. [Chestnut, OB Anes. 3e. 2004 pp739, 740t; Datta, OB Anes. Handbook. 3e. 2000 pp247; Stoelting, PPAP. 4e. 2006 pp309J
