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55 Cards in this Set

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2. What are 4 aspects of the cardiovascular system that undergo physiologic change in the parturient1
2. Aspects of the cardiovascular system that undergo physiologic change in the parturient include the intravascular fluid volume,
the constituents of theintravascular fluid voluIre,
the cardiac output,
and the peripheral circulation.
3. How does the maternal intravascular fluid volume change? During which trimester does this change lake place?
3. The maternal intravascular fluid volume increases from its prepregnancy volume. The increase in intravascular volume begins in the first trimester of pregnancy. By tenn the total increase in intravascular fluid volume is approximately 1000 mL.
4. By what percent does the plasma volume change in the Parturient? By what percent does the erythrocyte volume change?
4. Plasma volume in the parturient patient increases by approximately 45%. The erythrocyte volume in the paturient patien ncreases by approximately 20%.
5. What is the explanation for the relative anemia of pregnancy?
5. Because the plasma volume increases by over twice as much as the erythrocyte volume, the parturient has a relative physiologic anemia. That is, the hematocrit of the parturient patient is relatively less than her prepregnancy state. Thii is termed be physiologic anemia of pregnancy.
6. What is the coagulation status of the term parturient?
6. The term parturient is In a hypercoagulable state secondary to increases in factors Vll, Vlll, X, and plasma fibrinogen.
7. What is the average maternal blood loss during the vaginal delivery of a newborn? What is the average maternal blood loss during cesarean section?
7. The averagi! maternal blood loss during the vaginal delivery of a newborn is 400 to 600 mL. The average maternal blood loss during the delivery of a newborn by cesarean section is 1000 mL, but blood loss during a cesarean section is greatly variable. The increase in intravascular fluid volume and the hypercoagulable state of the mother help to counter the blood losses incurred during this time
8. How does the maternal total plasma protein concentration change during pregnancy?
8. The maternal total plasma protein concentration decreases during pregnancy. This is secondary to a dilutional effect of the increased intravascular fluid volume. (341; 2029)
9. How does the maternal cardiac output change from nonpregnant levels? At what week of gestation does this change take place?
9. The maternal cardiac output during pregnancy increases by approximately 40% of its prepregnancy value. This increase has taken place by the tenth week of gestation.
110. Given that cardiac output equals stroke volume times heart rate, how much of the change in cardiac output can be attributed to a change in stroke volume? How much can be attributed to a change in heart rate?
10. The cardiac output, which increases by about 40% in pregnancy, is equal to stroke volume times heart rate. The 40% increase in cardiac output is primarily due to an increase in stroke volume. The increase in heart rate during pregnancy is minimal and is therefore only a minimal contributor to the increase in cardiac output. The augmentation and maintenance of cardiac output in the pregnant patient is believed to be due to circulating placental and ovarian steroids released during pregnancy.
11. How does cardiac output change with the onset of labor? When is the maximal change in cardiac output in the parturient?
11. With the onset of labor, cardiac output increases to approximately 45% above prelabor values. The cardiac output increases further just after delivery, to about 60% above prelabor values. This is the maximal change in cardiac output in the parturient.
12. How does a regional anesthetic affect the cardiac output of the parturient in labor? When might this effect be useful?
12. Regional anesthesia may attenuate the increase in cardiac output normally seen in the laboring parturient. This effect may be useful ill parturients during the peripartum period who have a compromised cardiovascular system. (342)
13. In what time course postpartum does the cardiac output return to prepregnancy values?
13. Cardiac output returns to prepregnancy values by about 2 weeks post partum
14. In an uncomplicated pregnancy, what changes occur in the systolic blood pressure of the parturient?
14. The systolic blood pressure of the parturient having an uncomplicated pregnancy does not exceed her prepregnancy blood pressure.
15. In an uncomplicated pregnancy, what changes occur in the systemic vascular · resistance of the parturient?
15. The systolic blood pressure does not increase during pregnancy and usually stays about the same as prepregnancy values in an uncomplicated pregnancy. Cardiac output, however, increases by approximately 40%. Given that, the systemic vascular resistance must decrease to maintain an equal systolic blood pressure. Systemic vascular resistance does decrease, by approximately 20%
16. How does the central venous pressure change during pregnancy?
16. Central venous pressure does not change during pregnancy. ln the presence of increased intravascular fluid volume, the lack of change of central venous pressure presumably reflects a decrease in the resistance of the systemic and pulmonary vasculature.
17. What is the supine hypotension syndrome? What symptoms accompany the syndrome? Approximately what percent of pregnmt females have this syndrome?
17. The supine hypotension syndrome, as the name implies, is the decreaie in blood pressure seen in the parturient when she lies in the sIPire position at or near term. Symptoms that accompany the hypotension include diaphoresis, nausea, vomiting, and pmsnle :hanges in cerebration. This syndrome occurs m approximately 10% of pregnant women. Symptoms must be present for the patient to conside-ed susceptite to the supine hypotension syndrome.
18. What is the mechanism for the supine hypotension syndrome?
18. The supine hypotension syndrome occurs because of a decrease in cardiac output. When the term or near-term parturient lies in the supine position, the gravid uterus compresses the inferior vena cava, resulting in decreased venous return. The decreased venous return to the heart leads to a decreased preload for the heart. The cardiac output subsequently decreases.
19. What compensatory mechanisms do most women have that prevents them from experiencing the supine hypotension syndrome? How are these compensatory mechanisms affected by regioral anesthetic techniques?
19. Most pregnant women, when lying in the supine position, are able to compensate for the possible decrease in blood pressure that results from the compression of the inferior vern cava by the gravid uterus. One compensatory mechanism includes maintaining venous return by diverting blood flow from the inferior vena cava to the paravertebral venous plexus. The blood then goes to the azygos vein and returns to the heart via the superior vena cava. Another compensatory mechanism is an increase in peripheral sympathetic nervous system activity. This increases peripheral vascular tone and helps to maintain venous return to the heart. Because of these compensatory mechanisms only about 10% of pregnant women at or near term suffer from the supine hy?otension syndrOJ:re. Regional anesthesia, however, can interfere with these compensatory mechanisms by causing sympathetic nervous system blockade, rendering the pregnant wonan at term more susceptible to decreases in blood pressure
20. What maternal symptoms result from compression of the aorta by the gravid uterus?
20. Compression of the aorta by the gravid uterus does not typically lead to any symptoms in the pegrunt woman. The blood pressure in the lower extremities may decrease, whereas the blood pressure measured from the upper extrem- I hies remains unchanged
21. What is the major clinical significance of the supine hypotension syndrome? What maternal blood pressure is worrisome?
21. The major clinical significance of the supine hypotension syndrome is the , decrease in placental and uterine blood flow that results. The decrease m blood flow tluough the uteroplacental unit leads to a decrease in blood Bow to the fetus. Indeed, progressive fetal distress and bradycardia may result from decreases in systolic blood pressure to below 100 mm Hg for longer than 10 to 15 minutes.
22. How can the supine hypotension syndrome be minimized?
22. The supine hypotension syndrome can be minimized by having the parturient lie in the lateral pmition. Uterine displacement can also be used, typically with displacement being to the left because the inferior vena cava sits just to the right of and anterior to the spine. Left uterine displacement is easily accomplished by the placement of a foam rubber wedge or folded blanket under the light hip, elevating the hip by 10 to 15 cm
23. What are some aspects of tie pulmonary system that undergo physiologic change in the parurient?
23. Aspect of the pulmonary system that undergo physiologic change in the parturient include the upper airway, minute ventilation, lung volumes, and arterial oxygenation.
24. Why is the need for gentleness emphasized when instrumenting the upper airway of a parturient? Why might it be prudent to select a smaller cuffed endotracheal tube for intubation of the trachea?
24. Instrumentation of the upper airway of the parturient, whether by laryngoscope, nasal airway, oral airway, or suctioning, must be done gently. Capillary engorgement of the mucosal layer of the upper airways in these patients makes them sus~ptible to trauma and bleeding. In addition, because the vocal cords and arytenoids are often edematous, smaller-sized cuffed endotracheal tubes m~y be a better selection for intubation of the trachea for these patients. Endotrachetl. cubes with internal dianeters of 6.5 to 7.0 mm may be appropriate.
25. Why might insertion of the laryngoscope in the mouth of the parturient be difficult?
25. Insertion of the laryngoscope into the parturient's mouth may be made physically difficult because of a short neck and large breasts.
26. How is the milUtf ventilation changed from nonpregnant levels in the parturient? During which trimesmdret~lltange tale place?
26. The minute ventilation of the parturient increases to about 50% above prepregnancy levels. This change occurs in the first trimester of pregnancy and remains elevated for the duration of the pregnancy.
27. Given that minute ventilation equals tidal volume times respiratory rate, how much of the change in minute ventilation in parturients can be attributed to a change in tidal volume? How much can be attributed to a change II respiratory rate?
27. Minute ventilation is a factor of tidal volume and respiratory rate. Minute ventilation increases in the parturient by about 50%. An increase in tidal volume is the main contributor to the increase in minute ventilation seen. · The respiratory rate of the parturient does not change significantly from the prepregnancy rate.
28. What is presumed to be the stimulus for the change in minute ventilation during · pregnancy?
28. The stimulus for the change in minute ventilation that is observed during pregnancy is thought to be the increased levels of progesterone circulating in the mother's blood.
29. How does the resting maternal Paco2 change as a result of the change in minute ventilation?
29. During the first trimester, as a result of the increase in minute ventilation, the resting maternal Paco2 decreases from 40 mm Hg to about 30 mm Hg.
30. How does maternal arterial pH change as a result of the change in minute ventilation?
30. As a result of the change in minute ventilation, the maternal Paco2 decreases to about 30 rom Hg. A respiratory alkalosis is not seen in the parturient, however, because of increased renal excretion of bicarbonate ions. This · allows for maintenance of a normal arterial pH in the parturient.
34. What are two possible explanations for the rapid decrease in PaO2 during apnea, as in during the induction of general anesthesia, in the parturient? What precautionary measure must be taken before the induction of general anesthesia in the parturient?
34. Apnea in the parturient rapidly leads to aeria.! hypoxemia. There are at least two explanations for this. First, a decreased flll(tional residual capacity and subsequent decreased oxygen reserve are contributors. Second, aortocaval compression and decreased venous return leading to decreases in cardiac output may also contribute. The decrease in cardilc output would lead to an increase in oxygen extraction md therefore decrease the le,el of oxygenation of blood returning to the heart. Because of the rapid decrease in maternal Pa02 with apnea or hypoventilation, supplemental oxnen should be administered to the Parturient during a regional anesthetic. In addition, before the induction of general anesthesia preoxygenation with 100% 02 for 3 minutes or for eight deep breaths over 60 seconds is recommended. (3
35. How is the minimum alveolar concentration (MAC) altered in tie pregnant patient? Why is this thought to occur
35. The minimum alveolar concentration (MAC) is decreased in the parturient. This is thought to be due at least in part to the sedative effects of progesterone.
36. What is the important clinical consequence of the change in MAC in pregnant Women?
36. The important clinical consequence of the change in MAC in the pregnant WOffiU is that concentrations of inhaled anesthetics that would not produce 1 unconsciousness in a woman before pregnancy may be sufficient to do so during pregnancy. The change in MAC is compounded by the increased rate of induction of anesthesia with inhaled agents secondary to a decreased functional residual capacity. These together can quickly lead to dangers to the ability of the parturient to protect her airway and render her subject to the consequences of pulmonary aspiration
37. How does the epidural space change in parturients? How does the change in the epidural space of parturients affect the dosing requirements for epidural anesthesia?
37. The epidural space of parturients is decreased from its prepregnancy state. This occurs because of both the engorgement of epidural veins and the increased intra-abdominal pressure resulting from the progressive enlargement of the uterus. The decrease i1 the epidural space decreases the required volume of local anesthetic necessary to achieve a particular level of anesthesia , by facilitating its spread in the epidural space. The decrease in the dose ()f local anesthetic required is estimated to be 30% to 50%.
38. How does the subarachnoid space change in parturients? How does the change in the subarachnoid space of parturients affect the dosing requirements for spinal anesthesia?
38. The subaraclnoid space of parturients is decreased from its prepregnancy state. Just as the epidural space decreases as a result of the progressive enlargement of the uterus increasing intra-abdominal pressure, so does the 1. subarachnoid space decrease. The decreased space facilitates the spread of I local anesthetic and decreases the dose required by 30% to 50% from prepregnancy values.
39. How is the sensitivity to local anesthetics different in the pregnant versus nonpregnant patient?
39. There appears to be an increased sensitivity to local anesthetics by women I who are pregnant. The decreased local anestheic requirement in parturients I appears to have a biochemical component to it as well as a mechanical one_
40. How do renal blood flow and glomerular filtration rate change in pregnancy? At what gestational month of pregnancy is this effect at a maximum? How does this affect the normal upper limits of creatinine and blood urea nitrogen in parturients?
40. Renal blood flow and glomerular filtration rate in the parturient are both increased. By the fourtlt month of pregnancy the increase is 40%. This results in a decrease in what is considered the normal upper limit of both the blood urea nitrogen and serum creatinine concentrations in parturients to about 50% · of what it was in the prepregnancy state.
41. How is plasma cholinesterase activity altered by pregnancy? How does this manifest clinically?
41. Plasma cholinesterase, or pseudocholinesterase, decreases in activity by about 25% during pregnancy. This decrease in activity is first noted by about the tenth week of gestation and persists for as long as 6 weeks post partum. There is no clinical marifestation of this change in plasma cholinesterase activity. There is unlikely to be a significant change in the duration of action of succinylcholine or rnivacurium, for instance.
42. What are four gastrointestinal changes in pregnancy that render the parturient vulnerable to the regurgitation of gastric contents? What other factors during labor can further retard ga>tric emptying? What clinical significance does this have?
42. There are at least four gastrointestinal changes in pregnancy that render the Parturient vulnerable to the regurgitation of gastric contents

Two of these result from the enlarged uterus, which acts to displace the pylorus upward and backward from its usual position. First, this retards gastric emptying.

Second, it also leads to a change in the angle of gastroesophageal junction, leading to relative incompetence of the physiologic gastroesophageal sphincter. Gastroesophageal reflux and subsequent esophagitis are common in parturients.

A third cause is from circulating progesterone, which decreases gastrointestinal motility. Gastric fluid volume tends to be increased as a result, even in the fasting state.

Finally, gastrin secreted by the placenta stimulates gastric hydrogen ion secretion. The pH of the parturient's gastric fluid is predictably
43. What pharmacological interventions are recommended in the parturient to help minimize the risk of pulmonary aspiration?
43. Phannacologic interventions that are recommended in the parturient to help minimize the risks of pulmonary aspiration are aimed at decreasing the severity of acid pneumonitis should aspiration occur. The administration of antacids to the parturients before the induction of anesthesia is common practice. This is as an attempt to increase the pH of gastric contents. Sodium citrate is the antacid commonly used. A single administration is reCOIDmended, because repeated doses of antacid have not been proven to provide any additional benefit. Of note, the antacid must be nonparticulate, because aspiration of particulate matter contained in some antacids is in itself a hazard. Histamine-2 receptor antagonists can increase the pH of gastric fluid. They do not increase the pH of gastric contents already present, unlike antacids. Some reports indicate that combining histamine-2 receptor antagonists with antacids may work better than antacids alone in maintaining the increase in pH of gastric contents.
44. What is the function of the placenta? How is maternal blood delivered to the placenta?
44. The function of the placenta is to unite maternal and fetal circulations. The union allows for the physiologic exchange of nutrients and waste. Maternal blood is delivered to the placenta by the uterine arteries. Fetal blood is delivered to the placenta by the two umbilical arteries. The two most important determinants of placental function are uterine blood flow and the characteristics of the substances to be exchanged across the placenta.
45. What is uterine blood flow at term? How much can uterine blood flow decrease before fetal distress is detected?
45. Uterine blood flow at term is 500 to 700 ml/min. Uterine blood flow must be maintained to ensure placental circulation is adequate and therefore guarantee fetal well-being. In a normal placenta, uterine blood flow can decrease by about 50% before fetal distess, diagnosed by the presence of fetal acidosis, is detected.
46. What are the determinants of uterine blood flow
46. Uterine blood flow is not autoregulaled. Uterine blood flow is proportional to the mean blood pressure of the blood supplying the uterus and inversely proportional to the resistance of the uterine vasculature. Drugs that alter either of these, such as drugs ttat decrease systerroc blood pressure, affect uterine blood flow.
47. How does maternal hypotension affect uterine blood flow? How do anesthetics . delivered to the mother during labor and delivery affect uterine blood flow? How I do epidural and spinal anesthesia affect uterine blood flow?
47. Maternal hypotension, of any cause, results in a decrease in uterine blood flow. Uterine blood flow is decreased by a decrease in the perfusion pressure of blood supplying the uterus. Anesthetics delivered to the parturient during labor and delivery that decreiSe maternal tlood pressure could decrease uterine blood ftCI.'. Epdural and spinal anesthesia do not, in and of themselves, decrease uterine blood flow in the absence of maternal hypotension.
48. How co alpla-adrenergic agonists affect uterine blood flow? How do endogenous catecholamines affect uterine blood flow?
48. Alpha-adrenergic agonis~, such as phelylephrine, inclease uterine vascular resistance and therefore decrease uterine blooc flow. Endogenous catecholamines, as with maternal pain or aniety, also increase uterine vascular resistance and decrease uterine blood flow
49. How does ephedrine affect uterine blood flow?
49. Ephedrine administration does not result in any change in uterine blood flow. Ephedrine is therefore useful for increasing blood pressure when the parturient is hypotensive.
50. How do uterine contractions affect uterine blood flow?
50. Uterine contractions increase uterine venous pressure, thereby decreasing uterine blood flow.
51. How does the placental exchange of substances occur? What are some factors that affect this exchange? What is the most reliable way to nnmnuze fetal transfer of a drug?
51. Diffusion from the ma~ma1 circubtioll to the fetal circulation and vice versa is the pnmar: My in which the placental exchange of substances occurs. Some factors that affect the exchange of substances from the maternal circulation to the f~tus include the concentration gradient of the substance across the placenta, maternal protein binding, molecular weight, lipid solubility, and degree of ionization of the substance. The most reliable way to minimize the amount of drug that reaches the fetus is by minimizing the concentration of the drug in the maternal blood.
52. Why is maternal protein binding of local anesthetics important? At typical clinical concentrations, what percent of lidocaine is bound to protein? What percent of bupivicaine?
52. Protein binding of local anesthetics in the parturient is important because only the free form, or unbound portion, of the drug is available for diffusion across the placenta to the fens. At typical clinical concentrations, lidocaine is 50% to 70% protein bound. This compares with bupivacaine, which is 95% protein bound. This means that at typical clinical concentrations the 1 decreased bound fraction of ido(aine results in more loct! anesthetic being available to diffuse across the placenta.
53. How does the molecular weight of nondepolarizing neuromuscular blocking drugs affect their ability to transfer across the placenta? Does succinylcholine cross the placenta?
53. Nondepolarizing neuromuscular blocking drugs, such as vecuronium, have a high molecular .. e~ht and low lipd solubility. These two characteristics together limit the ability of nOildepolarizing neuromuscular blocking drugs to cross the placenta. Succinylcholine is highly ionized, preventing it from diffusing across the placenta despite its low molecular weight.
54. Do barbiturates cross the placenta? Do opioids cross The placenta?
54. Barbiturates opioids both readily diffuse across he placenta, owing to their relatively low molecular weights.
55. What pH of drug is facilitated in crossing the placenta?
55. Fetal bloed is slightly more acidic than maternal blood, with a pH about 0.1 unit less than maternal blood pH. The lower pH of fetal blood facilitates the fetal uptake of drugs that are basic.
56. What is ion trapping? \What is the potential clinical consequence of this with respect to lidocaine administration to the mother?
56. Weakly basic drugs, such as local anesthetics and opioids, that cross the placenta in the nonionized state become ionized in the fetal circulation. This results in an accumulated concentration of drug in the fetus for two reasons. First, once the drug becomes ionized it cannot readily diffuse back across the placenta. This is known as ion trapping. Second, a concentration gradient of nonionized drug is maintained between the mother and the fetus. In the case of lidocaine administration, this may mean that if the fetus was distressed and acidotic and lidocaine was given in sufficient doses to the parturient, lidocaine may accurnulae in the fetus
57. How well do the neonatal enzyme systems metabolize most drugs? Which local anesthetic is a pos~ible exception to this?
57. Neonatal enzyme activity is decreased in comparison to the enzyme activity of an adult. Despite the decreased activity, however, neonatal enzyme systems are sufficiently developed for the metabolism of most drugs delivered to the mother.
58. What are two ways in which the fetal circulation is protective against the distribution of large doses of drugs to vital organs?
58. There are two ways in which the fetal circulation inherently provides some protection to vital Jrgans against large doses of drugs. First, about 75% of the blood that is coming to the fetus via the umbilical vein passes through the liver. This allows for a significant amount of metabolism of the drug to take place before going to the fetal arterial circulation and delivery to the heart and brain. Second, blood with drug in it from the umbilical vein enters the inferior vena cava via the ductus venosus. This blood is diluted by drugfree blood returning from the lower extremities and pelvic viscera of the I fetus, resulting in a decrease in the concentration of the drug that is in the inferior vena cava
59. What types of medications may be admirristered systemicall~ b the mother during labor and clivery to help decrease pain and anxiety? What inftuences the degree of fetal depression that may result?
59. Systemic medications that are most often administered to the parturient to help decrease pain and anxiety during labor include opioids, benzodiazepines, and ketamine. Although different drugs will produce varied level; of depression in the fetus, the administration of any systemic medication to a parturient will result in the transfer of drug to the fetus to some extent. Other factors that influence the degree of fetal depression include the dose of the drug administered, the route of administration, and the time of administration before delivery.