Questions Flashcards
How do the maternal intravascular fluid,plasma,anderythrocyte volumes change during pregnancy?
How do
the coagulation status change during pregnancy?
What is the average maternal blood loss vaginal delivery delivery
The average maternal blood loss during vaginal delivery of a newborn is 300 to 500 mL. The average maternal blood loss during the delivery of a newborn by cesarean delivery is 800 to 1000 mL, but blood loss during a cesarean delivery 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. The contracted uterus after either type of delivery creates an autotransfusion of approximately 500 mL of blood, which decreases the overall effect of the blood loss on the mother. (515
Maternal cardiac output increases 10% by the tenth week of gestation, and at term pregnancy increases by approximately 40% to 50% of its prepregnancy value. Cardiac output is equal to the product of stroke volume andheart rate. The increase in cardiac output is primarily due to an increase in stroke volume. The increase in heart rate during pregnancy is less and is therefore only a minimal contributor to the increase in cardiac output. Labor is associated with further increases in cardiac output with output above prelabor values by 10% to 25% during the first stage and 40% in the second stage. The greatest increase in cardiac output occurs just after delivery, when it increases by as much as 80% above prelabor values. This is the maximal change in cardiac output in the woman. Cardiac output decreases substantially toward prepregnant values by 2 weeks postpartum. (515, Table 33-1)
The systolic blood pressure of the woman having an uncomplicated pregnancy does not exceed her prepregnancy blood pressure and typically decreases secondary to a 20% reduction in systemic vascular resistance at term. Systolic, mean, and diastolic blood pressure may all decrease 5% to 15% by 20 weeks gestational age and gradually increase toward prepregnant values as the pregnancy progresses towards term. Central venous pressure does not change during pregnancy despite the increased plasma volume because venous capacitance increases. (5
Supine hypotension syndrome, as the name implies, is the decrease in blood pressure seen when the pregnant patient lies in the supine position after midgestation. The supine hypotension syndrome occurs because of a decrease in cardiac output by approximately 10% to 20%. When the pregnant woman is in the supine position, the gravid uterus compresses the inferior vena cava, resulting in decreased venous return and decreased preload for the heart. Symptoms that accompany the hypotension include diaphoresis, nausea, vomiting, and possible changes in cerebration. Symptoms must be present for the patient to be considered susceptible to supine hypotension syndrome. (516, Figure 33-1)
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 vena 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. Dilation of the epidural veins may make unintentional intravascular placement of an epidural catheter more likely. A “test dose” is given before dosing an epidural catheter to decrease the likelihood of an unrecognized intravascular placement before initiating neuraxial blockade. 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. Regional anesthesia, however, can interfere with these compensatory mechanisms by causing sympathetic nervous system blockade, rendering the pregnant woman at term more susceptible to decreases in blood pressure. The gravid uterus can also compress the lower abdominal aorta and lead to arterial hypotension in the lower extremities, but maternal symptomsor decreases in systemic blood pressure as measured in the arms are often not reflective of this decrease. The major clinical significance of the aortocaval compression is the decrease in placental and uterine blood flow that results. The decrease in blood flow through the uteroplacental unit leads to a decrease in blood flow to the fetus. The aortocaval compression can be minimized by having the woman lie in the lateral position. 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 table tilt or the placement of a wedge or folded blanket under the right hip, elevating the hip by 10 to 15 cm. (516-517, Figures 33-1 and 33-2)
There is significant capillary engorgement of the mucosal layer of the upper airways and increased tissue friability during pregnancy. There is increased risk of obstruction from tissue edema and bleeding with instrumentation of the upper airway. Additional care is needed during suctioning, placement of airways (avoid nasal instrumentation if possible), direct laryngoscopy, and intubation. In addition, because the vocal cords and arytenoids are often edematous, smaller-sized cuffed endotracheal tubes (6.0 to 6.5 mm internal diameter) may be a better selection for intubation of the trachea for these patients. The presence of preeclampsia, upper respiratory tract infections, and active pushing with associated increased venous pressure further exacerbate airway tissue edema, making both intubation and ventilation more challenging. (517)
During pregnancy, the minute ventilation 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. An increase in tidal volume is the main contributor to the increase in minute ventilation seen, with only small increases in respiratory rate from prepregnancy. 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 or 32 mm Hg. Arterial pH, however, remains only slightly alkalotic (7.42 to 7.44) secondary to increased renal excretion of bicarbonate ions
Maternal hemoglobin has less of an affinity for binding oxygen during pregnancy, which facilitates downloading oxygen to the tissues and the fetus. The hemoglobin dissociation curve is thus shifted to the right with the P-50 increasing from 27 to approximately 30 mm Hg. (517)
Maternal lung volumes start to change in the second trimester. This is a result of mechanical compression by the gravid uterus as it enlarges and forces the diaphragm cephalad. This leads to a decrease in the woman’s functional residual capacity by approximately 20% at term. This decrease is a result of approximately equal decreases in both the expiratory reserve volume and residual lung volume. This can result in a functional residual capacity less than closing capacity and increased atelectasis in the supine position. There is no significant change in vital capacity seen during pregnancy. The rates of change in the alveolar concentration of inhaled anesthetics during induction and emergence from anesthesia are both increased secondary to the increase in minute ventilation and decrease in functional residual capacity. Clinically this, along with the decrease in MAC that accompanies pregnancy, leads to a more rapid achievement of an anesthetized state than when the patient is not pregnant. Apnea in the woman rapidly leads to arterial hypoxemia. There are at least two explanations for this. First, a decreased functional 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 cardiac output would lead to an increase in overall oxygen extraction and therefore decrease the level of oxygenation of blood returning to the heart. Third, maternal oxygen consumption is increased by 20% at term, with furtherincreases noted during labor. Because of the rapid decrease in maternal PaO2 with apnea or hypoventilation, preoxygenation with 100% O2 for 3 minutes or four maximal breaths over the 30 seconds just prior to the induction of emergent general anesthesia is recommended.
Maternal PaO2 changes during the progression from early gestation to term. Early in gestation, the PaO2 in the mother is slightly increased over prepregnancy values to over 100 mm Hg breathing room air. This is secondary to maternal hyperventilation and subsequent decreased PaCO2 during this time. As the pregnancy progresses, the PaO2 is normal or even slightly decreased. The decrease in PaO2 during the course of pregnancy likely results from airway closure and associated intrapulmonary shunt
There are at least four gastrointestinal changes in pregnancy that render the woman significantly vulnerable to the regurgitation of gastric contents beyond midgestation. The enlarged uterus acts to displace the stomach and pylorus cephalad from its usual position. This repositions the intraabdominal portion of the esophagus into the thorax and leads to relative incompetence of the physiologic gastroesophageal sphincter. The tone of the gastroesophageal sphincter is further reduced by the higher progesterone and estrogen levels of pregnancy. Gastric pressure is increased by the gravid uterus. Gastrin secreted by the placenta stimulates gastric hydrogen ion secretion. The pH of the woman’s gastric fluid is predictably low as a result. Reflux and subsequent esophagitis are common during pregnancy. During labor, gastric emptying is delayed and intragastric fluid volume tends to be increased as a result. (Epidural analgesia alone does not alter gastric emptying.) Anxiety, pain, and the administration of opioids can further decrease gastric emptying. Clinically, this means that the pregnant patient must always be treated as if she has a full stomach. Regardless of what amount of time has elapsed since her last ingestion of solids, she is at increased risk of regurgitation and aspiration of gastric contents. This includes the routine use of nonparticulate antacids, rapid sequence induction, cricoid pressure, and cuffed endotracheal intubation as part of general anesthesia induction sequence in a pregnant woman after approximately 20 weeks gestational age. Pharmacologic interventions that are recommended in the woman 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 pregnant women 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. Of note, the antacid must be nonparticulate, because aspiration of particulate matter contained in some antacids is in itself a hazard. Metoclopramide can be useful for decreasing the gastric fluid volume of pregnant women in active labor who require general anesthesia. It can significantly decrease gastric volume in as little as 15 minutes, although gastric hypomotility associated with prior opioid administration reduces the effectiveness of metoclopramide. H2 receptor antagonists increase gastric fluid pH in pregnant women approximately one hour after administration without producing adverse effects, and are additionally recommended by some
During pregnancy, both the epidural and intrathecal spaces are decreased in volume from their prepregnancy state. This occurs because of the engorgement of epidural veins and the increased intraabdominal pressure resulting from the progressive enlargement of the uterus. However, CSF pressure does not increase with pregnancy. The decrease in 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 decreased intrathecal space also facilitates the spread of spinal anesthetic and decreases the dose required from prepregnancy values.There appears to be an increased sensitivity to local anesthetics by women who are pregnant. The decreased local anesthetic requirement in pregnant women appears to have a biochemical component to it as well as a mechanical one. This is based on the observation of decreased neuraxial local anesthetic doses as early as the first trimester, before significant uterine enlargement.
Renal blood flow and glomerular filtration rate in the woman are both increased. By the third month of pregnancy the increase is about 50% to 60%. This results in a decrease in what is considered the normal upper limit of both the blood urea nitrogen and serum creatinine concentrations during pregnancy to about 50% of what it was in the prepregnancy state. (51
Liver blood flow does not change significantly with pregnancy. Plasma protein concentrations are reduced in pregnancy secondary to dilution. The decreased albumin levels can create increased blood levels of highly protein bound drugs. 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 postpartum. There is no clinical manifestation of this change in plasma cholinesterase activity, and no significant change in the duration of action of succinylcholine. (518)
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. Nutrient rich blood is returned from the placenta to the fetus via a single umbilical vein. The two most important determinants of placental function are uterine blood flow and the characteristics of the substances to be exchanged across the placenta. (519)
Uterine blood flow increases during gestation from approximately 100 mL/min before pregnancy to 700 mL/min at term. Adequate uterine blood flow must be maintained to ensure placental circulation is adequate and therefore guarantee fetal well-being. About 80% of the uterine blood flow perfuses the placenta and 20% supports the myometrium. (519
During pregnancy uterine blood flow has limited autoregulation, and the uterine vasculature is essentially maximally dilated under normal pregnancy conditions. Uterine blood flow is proportional to the mean blood perfusion pressure to the uterus and inversely proportional to the resistance of the uterine vasculature. Decreased perfusion pressure can result from systemic hypotension secondary to hypovolemia, aortocaval compression, or decreased systemic resistance from either general or neuraxial anesthesia. Uterine blood flow also decreases with increased uterine venous pressure. This can result from vena caval compression (supine position), uterine contractions (particularly uterine tachysystole as may occur with oxytocin administration), or significant abdominal musculature contraction (Valsalva during pushing). Additionally, extreme hypocapnia (PaCO2 <20 mm Hg) associated with hyperventilation secondary to labor pain can reduce UBF to the point of fetal hypoxemia and acidosis. Epidural or spinal anesthesia does not alter UBF as long as maternal hypotension is avoided. Endogenouscatecholaminesinducedbystressorpainandexogenousvasopressors have the capability of increasing uterine arterial resistance and decreasing UBF, although both ephedrine or phenylephrine are used clinically in moderate amounts to maintain uterine perfusion pressure when the pregnant patient is hypotensive. (519)
Transfer of oxygen to the fetus is dependent on a variety of factors including the ratio of maternal to fetal umbilical blood flow, the oxygen partial pressure gradient, the respective hemoglobin concentrations and affinities, the placentaldiffusing capacity, and the acid-base status of the fetal and maternal blood (Bohr effect
Transfer of drugs and other substances less than 1000 Da from the maternal circulation to the fetal circulation and vice versa is primarily by diffusion. Some factors that affect the exchange of substances from the maternal circulation to the fetus 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. (519)
Nondepolarizing neuromuscular blocking drugs have ahigh molecular weight and low lipid solubility. These two characteristics together limit the ability of nondepolarizing neuromuscular blocking drugs to cross the placenta. Succinylcholine is highly ionized, preventing it from diffusing across the placenta despite its low molecular weight. Additionally, both heparin and glycopyrolate have significantly limited placental transfer. Placental transfer of barbiturates, local anesthetics, and opioids is facilitated by the relatively low molecular weights of these substances. (519)
Fetal blood 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. 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 maintainedbetweenthe motherandthefetus. Inthe case of lidocaine administration, this may mean that if the fetus was distressed and acidotic and lidocaine was given in sufficient doses to the woman, lidocaine may accumulate in the fetus. (519)
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, drug contained in the umbilical vein blood 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 fetus, resulting in a decrease in the concentration of the drug that is in the inferior vena cava. In addition, despite decreased liver enzyme activity in comparison to adults, fetal/neonatal enzyme systems are adequately developed to metabolize most drugs. (520)
