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55 Cards in this Set

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138. What is pregnancy-associated hypertension? How frequently does it occur?
l38. Pregnancy-associated hypertension is a term used to describe a range of disorders that present in pregnancy and have in common the clinical presenta
139. What is the cause of predampsia?
139. The exact cause):jl:Clipi~lunlaC\ll. Iti;beUeved that preeclampsia nay involve darruge tl endothelial cells that triggers vasoconstriction, platelet activation, and an imbalance between prostacyclin and throm- I boxane. The endothelial cell damage also results in a loss of capillary integrity, leading to generalized edema. (3
140. What effects does preeclampsia have on the major organ systems?
140. Preeclampsia is a major cause of morbidity ane mortality for both the parturient ani the leonatf. hoo:lmSJ ~ it foowing potential effects on the major organ system!

multiple prob
141. What are the diagnostic criteria for mild preeclampsia?
141. Preeclampsia can be diagnosed after the twentieth week of gestation. The criteria that must be met to diagnose mild preeclampsia include hypertension with a blood pressure higher than 140/90 mm Hg, proteinuria of over 0.3 g/day, and generalized edema. (3:
143. What are the diagnostic criteria for eclampsia? What percent of parturients with preeclampsia get eclampsia?
143. When a parturient with preeclampsia has a seizure her disease has progressed to eclampsia. The exact mechanism for eclamptic seizures is unknown, but they may occur from vasospasm, hypertensive encephalopathy, or cerebral edema. Approximately 5% of parturients with preeclampsia develop eclampsia
144. What is the approximate percent maternal mortality of parturients with edamJdsia? What are some causes of maternal mortality from eclampsia?
144. The approximate maternal mortality of parturients with eclampsia is 10%. Some ClUses of maternal mortality from eclampsia include congestive heart failure aJid cerebral hemorrhage.
145. How should eclampsia be managed?
145. Eclanpsla should be managed supportively by first ensuring adequate oxygen- I ation and circulation. Suppkmental oxygen should be applied md the parturient positioned with left uterine displacement. Magnesium can be administered to control the seizures. In the event that seizures persist, oxygenation is inadequate, or the airway is unprotected, intubation of the trachea may be necessary. Delivery of the fetus may be indicated if the fetus becomes distressed
146. What is the definitive treatment for pregnancy-associated hypertension?
The definitive treatment for pregnancy-associated hypertension is delivery of fetus and placenta
147. When do the manifestations of preeclampsia resolve? .
147. The manifestations of preeclampsia usually resolve within 48 hours of delivery of the fetus
148. What are the goals of the pharmacologic management of preeclampsia?
148. The goals of the pharmacologic management of preeclampsia include blood pressure control and seizure prophylaxis.
149. What are some of the effects of magnesium on the parturient when administered for pregnancy-associated hypertension? What is the anesthetic implication of this?
149. The goal of the administration of magnesium in parturients with pregnancyassociated hypertension is to decrease central nervous system irritability, which in tum decreases the likelihood of seizures. Magnesium also relaxes uterine and vascular smooth muscle tone, resulting in increases in uterine blood flow. There are several other effects of magnesium that require understanding by the anesthesiologist for the appropriate management of anesthesia. First, magnesium decreases activity at the neuromuscular junction, possibly rll~l, llli:lgllCMUUl UCvlCi:lI;CS acuvuy at me neuromusculaIJunctOl, possibly post junctional membrane sensitivity to acetylcholine. ClinicaDy, this can enhance the neuromuscular blo(cade produced by nondepolarizing neuromuscular blocking drugs. Second, magnesium-induced relaxation of uterine and vascular smooth musce tone may contribute to uterine atony and increased bleeding after abiy. ThiI, magnesium can enhance the effects of opioids and sedatives. Finally, magnlSium readily crosses the placenta. Neonatal muscle tone may be decreased at birth as a result of magnesium administration to the mother
150. What is the therapeutic level of magnesium when administered for pregnancyassociated hypertension? How can the levels of magnesium be monitored clinically?
150. The therapeutic serum level of magnesium when administered for pregnanc)associated hypertension is 4 to 6 mE(~. Clinical monitoril!)f the lagnesium level can be achieved by evaluating the parturint's deep tendon reflex response. Marked depression of the deep tendon reflexes gives evidence for impending magnesium toxicity.
151. What are some signs af increasing magnesium toxicity? What is the antidote for magnesium toxicity?
151. When toxic levels of serum magnesium are reached the parturient may experience severe skeletal muscle weakness, twx~ !<aniac arrest. The therapeutic serum level of magnesUn is 4 to 6 mEqlL. A prolonged PQ interval and QRS complex widening on the electrocardiogram indicate that serum levels of magnesium are 5.0 to 10 mEqlL. The loss of the parturient's deep tendon reflex response occurs when serum levels are about 10 mEqlL. Sinoatrial and arioventricular block and respiratory paralysis may become eviden: Wlen serum magnesium levels reach about 15 mEq/ L, and at serum levels of 25 rnEq/L cardiac arrest may occur. The antidote for magnesium in the event of magnesium toxicity is the intravenous adminisration of calcium
152. How is magnesium cleared from the body?
152. Magnesium is cleared by renal excretion. The parturient with pregnancyassociated hypertension who also has renal (~rution should have her serum magnesium levels closely monitored
153. What antihypertensives are commonly used to treat maternal hypertension?
153. Antihypertensive therapy for the parturient with pregnancy-associated hypertension is likely to be initiated when the mkna diaS:ooc blood pressure is more than 110 mm Hg. An~ptrtensive> that rre commonly used to treat pregnancy-associated hypertension include hydralazine and a beta-adrenergic antagonist such as labetalol. Hydralalineiso:u;hosen because of its rapid onset and its preservation of renal blood flow. Labetalol is often chosen because of its ability to block a reflex tachycardia.
154. What is the concern regarding the administration of nitroprusside to parturients?
154. Nitroprusside is generally avoided in parturients because of the concern with cyanide accumulation in the fetus. Cyanide results from the degradation of I I on the fetus. (356) on the fetus. (356)
155. Why is it important to continuously monitor fetal heart rate while administering antihypertensives?
155. The continuous monitoring of fetal heart rate during the administration of antihypertensives gives information about the well-being of the fetus while decreases in maternal blood pressUIe may result in decreases in the uterine decreases in maternal blooo pressure may result in decreases in the uterine perfmion plS1IJe The effect on uteroplacental circulation could manifest as changes in fetal heart rate.
165. What is placenta previa? How does it present? How can the diagnosis be confirmed?
165. Placenta previa is the implantation of the placmta in the uterus in an abnonnally low positon ?lacenll previa classic illy resents as painless vaginal bleeding. This usually occurs around the thirty·se~ond week of gestation when the lower uterine segmentisbe~jrnilgto fom. The diagnosis of placenta previa can be made by ultrasound examination of the placenta. If ultrasound is not satisfactory for a diagnosis of placenta previa, diagnosis can be made by direct examination of the os. The anesthesiologist may better manage the parturient for labor and delivery with knowledge of the position of the placenta. For example, in cases of cesarean delivery there may be excessive intraoperative blood loss if the position of the placenta requires that the Obstetrical cut through the placenta to access the fetus. (3:
166. What are some risk factors for placenta previa?
166. Risk factors for placenta previa include advanced age, multiparity, previous cesarean section, and a history of prior placenta previa. (20:
167. How should examination of the cervical os of a woman suspected of having placenta previa be undertaken?
167. The direct examination of the cervical os of a woman suspected of having a placenta previa should only be undertaken in the operating room while prepared to proceed with an emergent cesarean section with acute blood loss This is tenned a double set-up, in which the obstetrician and anesthesiologist are present and prepared to proceed with erItIgJt(:a! delivery of the I newborn. Two large-bore peripheral intravenous catheters should be in place.
168. What is abruptio placentae? What are the possible clinical presentations of abruptio placentae?
168. Abruptio placentae is the separation of a normally implanted placenta leading to bleeding behind the placenta after the twentieth week of gestation. The parturient often has painful, frequent uterine contractions. The separation can involve only the placental margin, presenting as vaginal bleeding. Abruptio placentae can also occur without vaginal bleeding. In these cases, blood can accumulate in large volumes and be entirely sequestered within the uterus. Therefore, the degree of vaginal bleeding may not reflect the total amount of blood loss from the placenta. In cases of severe abruption, the parturient '. may have clotting abnormalities and disseminated intravascular coagulation, uterine hypertonicity and pain, and hypotension in addition to fetal distress or death.
170. What is the definitive treatment of abruptio placentae?
170. The definitive treatment of abruptio placentae is delivery of the fetus and emptying the uterus of the placenta. (35
174. What are some options for the anesthetic management of patients with retained placenta?
174. The anesthetic management of patients with retained placenta has as its goal uterine relaxation as well as decreasing the pain and anxiety of the patient. Anesthetic methods balle usee to ItCOmplilh tis ioclude intravenous sedation, epidural anesthesia, spinal anesthesia, and general anesthesia. The patient's protective airway reflexes must be retained when intravenous sedation is administered.
173. What approximate percent of vaginal deliveries are associated with some amount of retained placenta? What is the treatment?
173. Retained placenta occurs when some portion of the placenta has not been spontaneously delivered within 1 hour of delivery of the fetus. Uterine bleeding continues due to tile inability of the uterus to contract around adherent placenta. Approximately I % of all vaginal deliveries are associated with some retained placenta. The treatment involves manual exploration of the uterus fa: the removal of retained placental parts.
175. What is uterine atony? When does it present?
175. Uterine atony is the most:ommon cause of postpartum hemorrhage. It occurs when inadequate contraction of the uterus after delivery of the placenta leads to ongoing blood loss from the uterus. It can present immediately after delivery or can occur several hours after delivery.
176. What are some risk factors for uterine atony?
176. Risk factors for uterine atony rid/I prolonged liOO£, multiJle gestations, grand mutripa.ity, and the administration of tocolytics to the parturient. Tocolytics include beta-2-adrenergic agonists, magnesium, and inhaled anesthetics
177. How should uteine atony be managed?
177. The treatment of uterine atony is by the administration of agents that increase uterine tone. Such agents include synthetic oxytocins,methylergonovine, andJ or Hemabate, an analog of prostaglandin F2a
178. What is the risk of the rapid administration of synthetic oxytocin? How can this risk be avoided?
178. Rapid intravenous administration of synthetic oxytocin can result in vasodilation, hypotension, and tachycardia in the patient. This risk can be avoided by administering synthetic oxytocin in a cor.tinuoul infusion ~: 10 to 15 units in 500 mL of crystalloid. (358)
179. Why is it important that the synthetically made oxytocin drugs do not contain vasopressin?
179. It is important that synthetically made oxytocin does not contain vasopressin. If it did, parturients who had been previously treated with sympathornimetics may have responded to its administration with exaggerated increases in blood pressure.
180. What is the clinical Presentation of an amniotic fluid embolism? What are some out? out?
180. The clinical presentation of an amniotic fluid embolism that is sufficiently large to cause symptoms is the sudden onset of respiratory distress, hypotension, and arterial hypoxemia. Amniotic fluid embolisms may obstruct pulmonary blood flow leading to pulmonary hypertension and decreased cardiac output. Hemorrhage often develops due to disseminated intravascular coagulation. Some conditions that may mimic an amniotic fluid embolism include the inhalation of gastric contents, air embolism, pulmonary embolism, and local anesthetic toxicity. (358)
183. What is the treatment of an amniotic fluid embolism?
183. The treatment of an amniotic fluid embolus is supportive, including cardiopulmonary resuscitation and te correction of arterial hypoxemia
186. Are anesthetics teratogenic?
:6. Most data regarding the administration of anestheils to pregnant women in the first trim~ter ~e retrospective. In most cases the anesthetic was administered before the knowledge that the patient was pregnant. After retrospective analysis, there is no eviderce to suppat a teratogenic effect of inhaled or regional anesthetics administered during pregnancy, nor is there evidence to support an adverse effect on the later mental and neurologic development of neonates.
190. What is the definition of premature labor in the parturient?
190. Premature laboLs defined as being at least eight uterine contractions every hour combined vith cervical effacement greater than 75% in a parturient between 20 and 35 weeks of gestation
192. How can premature labor be treated?
192. Premature labor can be treated through the administration of tocolytics. Beta2 agonists such as terbutaline or ritodrine are commonly used for this purpoie. Beta-2 agonists relax uterine smooth muscle and thereby inhibit uterine contractions while improving uteroplacental blood flow. Side effects of the treatment of premature labor with beta-2 agonists include maternal hypokalema lid cardiac dysrhytbrnias. Side effects for the fetus include fetal tachycardia and hypoglycemia.
193. When should elective nonobstetric surgery be performed in the parturient?
193. Elective nonobstetric surgery in the parturient should be performed some time after the delivery of the fetus. (3
194. What is the preferred trimester for surgery to take place when surgery in the parturient is not elective! What type of anesthetic is preferred if possible?
194. If surgery is necessary during the course of a woman's pregnancy, the preferred time for the surgery to take place is during the second or third trimester. Spinal anesthesia limits the amount of anesthetic a fetus is exposed to, making spinal anesthesia the preferred method of anesthesia if possible in parturients undergoing surgical procedures
196. How might cocaine and/or heroin abuse affect the outcome of the newborn?
196. Cocaine and/or heroin abuse in the parturient often leads to a neonate who is delivered prematurely and who is depressed at delivery. C
197. What is the preferred method of anesthesia during labor and delivery in the parturient who has been known to abuse drugs?
197. Regional anesthesia may be the preferred method for providing anesthesia to the parturient who has been known to abuse drugs, to mnimize possible interactions with unknown drugs the parturient may have ingested.
198. How is fetal well-being best evaluated?
198. Fetal well-being is best evaluated by monitoring the fetal heart rate with particular interest in the number and type of fetal heart rate decelerations and in the beat-to-beat variability. The beat-to-beat variability is computed from R wave intervals on a fetal electrocardiogram.
200. What is the normal fetal heart rate?
200. The normal fetal heart rate is between 120 and 160 beats per minute. (359)
201. What is the normal! fetal heart rate variability per minute?
201. The normal fetal heart rate variability is between 5 to 20 beats per minute.
202. What types of fetal distress may be reflected as a decrease in the fetal heart rate beat-to-beat variability?
202. Types of fetal distress that may be reflected as a decrease in the fetal heart rate beat-to-beat variability include distress due to arterial hypoxemia, acidosis, or central nervous system damage.
203. What types of drugs often administered by an anesthesiologist may result in a decrease in the fetal heart rate beat-to-beat variability1 What is the clinical implication of this?
203. Fetal heart rate beat-to-beat variability may be decreased by the administration of drugs to the mother, such as local anesthetics and opioids used for continuous lumbar epidural analgesia, and intravenous opioids, benzodiazepines, beta-adrenergic blockers, and anticholinergics. Clinically, the administration of these drugs may produce effects on the fetus that may be confused with fetal distress. Conversely, true fetal distress may be masked by the administration of these drug:
204. What are early decelerations in fetal heart rate? What are they thought to be due to?
204. Decelerations in fetal heart rate are defined by their timing with the uterine contraction. An early deceleration in fetal heart rate is a slowing of the fetal heart rate whose onset begins with :he onset of the uterine contraction. Early decelerations are thought t> be due to COlllpresS:cn of the fetal heal and a resultant reflexive vagal stimulation. Early decelerations are not considered to be an indication of fetal distress. (:
205. What are late decelerations in fetal heart rate? What are they thought to be due to? What further diagnostic intervention can be made in this circumstance?
205. Decelerations in fetzl nem ra~ a.re renel by their timing with the uterine contraction. A late deceleration in fetal heart rate is a slowing of the fetal heart rate whose onset begins 10 to 30 seconds after the onset of the uterine contraction. Late decelerations are thought to be due to arterial hypoxemia and/or uteroplacental insufficiency, as may result from maternal hypotension. Late decelerations are indicative of fetal distress, and under these circumstances the fetal scalp pH may be obtained for further evaluation of fetal wellbeing
206. What are variable decelerations in fetal heart rate? What are they thought to be due to?
206. Variable decelerations in fetal heart rate are decelerations in the fetal heart rate whose timing, magnitude, and duration vary vith respect to the timing of the onset of the uterine contraction. Umbilical cord compression is believed to be a ,:ause d rtiltl:lecelenlUJs in fetal heart rate. Prolongation of the fetal heart rate deceleration to more than 30 seconds or fetal bradycardia that is slower than 70 beats per minute are both factors that make variable decelerations worrisome. Under these conditions changing maternal position alone is often sufficient treatment for the deceleration.
207. What is the value of the Apgar score? What is its use?
207. The Apgar score is an assigned numerical value to the status of a newborn at various intervals after the time of delivery. The Apgar score is useful as a guide in identifying infants who require intervention or resuscitation at birth, although one should not wait until the I-minute Apgar score to begin necessary resuscitation.
209. What type of intervention is usually sufficient for infants with an Apgar score of 8 to 10?
209. Most newborns have an Apgar score between 8 and 10. These infants require only suctioning of the mouth and nose and placement on a heated bed
210. What type of neonatal injury is most likely to be associated with Apgar scores between 5 and 7? What type of intervention is usually necessary for these infants? When should ventilation of the newborn's lungs be instituted under these circumstances?
210. Newborns with Apgar scores between 5 and 7 have most likely suffered from some mild asphyxia before birth. The only intervention usually required for these infant; is external stimulation and the delivery of supplemental oxygen. Ventilation of the lungs of the newborn should be instituted only if the newborn does not respond within 1 to 2 minutes or if the heart rate is less than 100 beats/min.
211. How does the newborn with Apgar scores between 3 and 6 appear? What intervention may be necessary for this newborn?
211. Newborns with Apgar scores between 3 and 6 appear cyanotic and have poor breathing efforts. Hand ventilation of the lu~ t mask mllSt usually be instituted, although increased airway resistance may make this difficult. If this is the case, intubation of the trachea may become necessary.
212. What type of neonatal injury is most likely to be associa1ed with Apgar scores between 0 and 2? What type of intervention is usually necessary for these infants?
212. Newborns with Algar scores between 0 and 2 have suffered from severe asphyxia. Prom{t, aggressive resuscitative measures must be taken, including intubation of the trachea, ventilltiQn, aJld supJOrt of the cardiovascular system as necessary. I
213. At what rate should the lungs of a neonate be ventilated? How should the adequacy of ventilation be tvaluated? .
213. The lungs of a neonate should be ventilated at a rate of 30 to 60 breaths/min. The maintenance of 3 to 5 cm H20 positive end-expiratory pressure may also be useful
218. What is the risk of meconium-stained amniotic fluid for the neonate? How should it be managed?
['he risk of meconium-stained amniotic fluid for the neonate is meconium aspiration and respiratory compromise at birth. These neonates should have their tracheas intubated and suctioned at birth before ventilation occurs, in an attempt to minimize the meconium reaching the distal airways. Further management of the neonate should be guided by the cardiopulmonary status.
225. What sensory dermatomal level must be achieved for patient comfort during a postpartum rubal ligaton undel regional anesthesia?
225. Postpartum tubal ligation performed under regional anesthesia requires a sensory dermatomal level of T5 anesthesia to ensure patient comfort. (362)
226. Why is it common to wait 8 - 12 hours post partum before performing a tubal ligation?
226. Studies have ShoWl that partui.ents have little change in their gastric fluid I volume and pH in tte first ~ hours after vaginal delivery. Despite this, it is I common to wait 8 to 12 hours postpartum before peforming a tubal ligation in an effort to allow for increased gastric emptying and thereby minimize the risk of the pulmonary aspiration of gastric contents.