Welcome to the Maternal Physiology presentation. I am Beth Ann Clayton, and I will be reviewing the significant anatomic and physiologic changes that occur in pregnancy. Our learning objective for this presentation is to review anatomic and physiologic changes of the perturiate. I have no financial relationships with any commercial interest related to the content of this activity, and I will not discuss off-label use during my presentation. Pregnancy is a physiologic state where most physiologic parameters are abnormal. Therefore, it is important to be familiar with the various changes in order to deliver optimal anesthesia care. Most of these changes are driven by hormones. The first hormone we will discuss is the beta-human chorionic gonadotropin hormone, or HCG. It's known as the pregnancy hormone because HCG is produced in the placenta after a fertilized egg implants in the uterus, and the HCG tells the body that conception has occurred, which ultimately creates a chain of events, including continued ovarian production of progesterone. Your HCG is found in blood and urine, which this is the hormone that's detected in the typical over-the-counter pregnancy test that we utilize. And the beta-HCG hormone peaks in the first trimester, as you can see here demonstrated on the chart on the right. Progesterone is the principal hormone responsible for the most significant changes that we see during pregnancy. It is produced in the ovaries, and it's responsible for maintaining uterine lining and preventing menstruation. It rises throughout the pregnancy and ends up being about 20 times the non-pregnant value by the end of the pregnancy. And the fall in progesterone is actually an effect that's associated with the onset of labor in the third trimester. The body composition changes during pregnancy. The mean weight increase is approximately 17% of the pre-pregnant weight, leading to 10 to 14 kilograms, or 25 pounds of overall weight gain. During the first trimester, the normal weight gain is approximately 1 to 2 kilograms. And in the second trimester and the third trimester, the protein will gain an additional 5 to 6 kilograms. The components that add to the additional weight gain include the uterus and its contents, including the amniotic fluid, the overall increase in blood volume and interstitial fluid, the fetus and the placenta itself, and then the deposition of fat and protein. There are various respiratory anatomical changes that occur during pregnancy. The thoracic AP diameter increases by 5 to 7 centimeters, and there is an actual flaring of the ribs, as you can see by the image on the right. The diaphragm also will elevate approximately 4 centimeters due to the growing uterus that pushes the diaphragm up. And there also is an increase in airway dilation, and that occurs due to the hormone progesterone. Normal respiratory tract changes that occur during pregnancy include capillary engorgement. There is swelling of the mucosa throughout the entire respiratory tract, and because of this, frequently, the Parcherians have symptoms of upper respiratory infections. In addition, they may notice laryngitis and voice changes as well. Exacerbation of symptoms can happen when there is a fluid overload or they actually have an upper respiratory infection or the presence of pregnancy-induced hypertension. The airway can also change during pregnancy. In fact, airway exams can be deceiving and may even change significantly during labor. This is due to the engorgement that we discussed and also the distribution of weight gain. Historically, airway loss was the leading cause of anesthetic-related morbidity and mortality in Parcherians. Therefore, the popularity of regional anesthesia occurred, and it is recommended that if you need to intubate the patient due to general anesthesia, that you use video laryngoscopy. Increased ventilation during pregnancy results from hormonal changes and increased carbon dioxide production. The arterial partial pressure of carbon dioxide is actually closely related to the blood level of the progesterone. This hormone increases the sensitivity of the central respiratory center to carbon dioxide and actually acts as a direct respiratory stimulant. Estrogen hormones also may contribute to the increased ventilation. Hyperventilation occurs with the Parcherian because of the significant increase in progesterone, which decreases the carbon dioxide, leading to a mild compensated respiratory alkalosis with normal pH. There is also an increase in minute ventilation and oxygen consumption that begins as early as the seventh week of pregnancy, actually before the development of the demands of fetus, and it continues to rise to 60% above normal by the third trimester. There are significant changes to the lung volumes and respiratory parameters. You will see that the minute ventilation, alveolar ventilation, tidal volume, respiratory rate, and arterial oxygen level all increase. There is an increase as well in the oxygen consumption. There is no change in the arterial pH because of the compensation, but there is a decrease in your total lung capacity and functional residual capacity and also decreases in your expiratory reserve volume and residual volume. You see demonstrated on this chart the changes in the arterial blood gas of the pregnant patient compared to the non-pregnant patient. You can see that in the pregnant patient, your carbon dioxide level does decrease and your PaO2 level increases. You remain at a higher pH with the 7.44 and your bicarbonate level decreases to 20. Pregnant women become hypoxemic more rapidly than non-pregnant women during episodes of apnea. This is caused by the reduced functional residual capacity and the higher oxygen consumption of pregnant women. Therefore, during the apnea associated with a rapid sequence induction of general anesthesia, the PaO2 of prarturient falls at more than twice the rate in the non-pregnant women. You can see demonstrated by this graph that pre-oxygenation results in a PaO2 of approximately 500 millimeters of mercury and that pregnant patients become hypoxemic after three minutes of apnea, whereas non-pregnant women maintain a PaO2 above 100 for approximately seven to nine minutes. The pain of labor causes significant changes in ventilatory values. You can see demonstrated here that the respiratory rate, tidal volume, minute ventilation, and PaO2 all increase significantly. The PaCO2 actually decreases due to the hyperventilation. During the first stage of labor, where the prarturient is dilating from zero to 10 centimeters, the minute ventilation goes up 70 to 140 percent. And during the second stage of labor, which is the delivery of the fetus, the minute ventilation increases by 120 to 200 percent. As you can imagine, the oxygen consumption in labor goes up significantly as well. In the first stage, the oxygen consumption goes up by 40 percent, and in the second stage of labor, at delivery, the oxygen consumption increases to greater than 75 percent. This puts the prarturient in an anaerobic metabolism, increasing the blood lactate. Moving on to heart and circulation changes in the prarturient. Cardiovascular changes in the maternal patient provide support for the fetus and also prepare the mother for blood loss associated with delivery. The heart will increase in size, both due to an increase in blood volume and also an increase in stretch and force of contractions. The displacement of the diaphragm by the uterus also displaces the heart. Therefore, you can hear the apical impulse cephalad to the fourth intercostal space and also laterally. On auscultation, you may notice a murmur. There is an extenuation of the first heart sound due to an exaggerated and splitting of the mitral and tricuspid components. You may also hear a third heart sound, which typically will disappear at term. Approximately 96 percent of women do have a systolic ejection murmur, either at a grade one or grade two. On echocardiography, left ventricular hypertrophy can be detected by 12 weeks of gestation. This is due to an increase in cardiac output by 23 percent during the first through third trimester. And by term, the cardiac output has increased to 50 percent. The annular diameters do also increase of the mitral, tricuspid, and pulmonic valves. Therefore, 94 percent of term pregnant women exhibit tricuspid and pulmonic regurgitation, and 27 percent exhibit mitral regurgitation. The EKG changes that you can see with the proturient include sinus tachycardia with a shortening of the PR and QT intervals. There may also be a mild transient ST segment depression and T wave inversion. And PACs and PVCs are not uncommon. There is also a low threshold for reentrant SVT. One should be suspicious for cardiovascular disease if you notice a systolic murmur greater than three, or a diastolic murmur, the presence of severe dysrhythmias, or unequivocal cardiac enlargement on a chest X-ray. The hemodynamic parameters that are noticed with the proturient is that the stroke volume and heart rate increases by approximately 25 percent, and the left ventricular and diastolic volume and injection fraction also increase. There is an overall decrease of 20 percent in the systemic vascular resistance, and this is due to the progesterone level that causes overall vasodilatation throughout the body. Cardiac output increases throughout the pregnancy. There is a 35 to 40 percent increase in cardiac output by the end of the first trimester, and 50 percent by the end of the second trimester. In labor, you will notice that the cardiac output increases as well. Throughout the latent phase of labor, the active phase of labor, and also the expulsive phase. Ultimately, the cardiac output is greatest, increased to greater than 80 percent immediately post-delivery due to the autotransfusion and increased venous return after the uterine invulsion. The cardiac output overall does not return to normal until two weeks after delivery. To review the central hemodynamic values, you can see that the cardiac output and heart rate increase in the pregnant patient, and you see a decrease in your systemic vascular resistance and also in your colloid osmotic pressure. It is important to measure blood pressure accurately in the periturian due to the various hypertensive disease processes that can occur. In the brachial measurement, the blood pressure is highest in the supine position and it's lowest in the lateral position. Typically, blood pressure does decrease in the periturian due to the downregulation of alpha and beta receptors and also, as we discussed, the circulating progesterone, which causes vasodilatation. In advanced maternal age patients, there is a higher median systemic vascular resistance. However, in women that smoke, there is a lower systemic vascular resistance compared to non-smoking patients. The uterus receives 5-12% of the overall increased cardiac output in the periturian, therefore leading an increase of 50 mL per minute of blood flow to the uterus up to 700-900 mL per minute in the term periturian. Uterine blood flow is not autoregulated, therefore it is essential that we maintain normal pressure so that you can maintain uteroplacental blood flow. The uterine artery branch supplies the majority of blood flow to the uterus, with the ovarian arteries comprising about a sixth of the blood flow, ultimately leading, as I said, to a 700-900 mL per minute in the term parturient. The uterine arteries then will divide into the spiral arteries and the spiral arteries are elongated and dilate and they spurt blood into the intervallous space that you can see here illustrated. Two umbilical arteries take blood from the fetus to the placenta. They divide then into the chorionic arteries and the capillaries within the fetal villi. The blood is exchanged with the maternal blood in the intervallous space and then the clean blood or nourished and nourished blood will return to the fetus via the umbilical vein. It is essential to maintain normal uterine blood flow so that the placenta can be supported appropriately. The things that decrease uterine blood flow include a decreased uterine arterial pressure that can be caused by maternal aortic cable compression, hypovolemia, or a sympathectomy that you may have induced with administration of your neuraxial anesthetic. In addition, increased uterine venous pressure caused by uterine contractions or uterine hypertonics such as induced by the administration of oxytocin or skeletal muscle hypertonics that can occur with valsalva or seizures can all increase the uterine venous pressure, ultimately decreasing uterine blood flow. And lastly, an increased vascular resistance can also decrease uterine blood flow. This may be caused by endogenous catecholamines that can occur when a patient is in pain from labor or vasopressin release. Exogenously, the administration of epinephrine or an alpha-1 agonist could also increase vascular resistance. Aortic cable compression begins as early as 13 to 16 weeks gestation and is usually evident by the 20th week gestation. Supine hypotensive syndrome is when there is nearly complete vena cable compression at term in the supine position, causing a 10 to 20% decrease in cardiac output leading to hypotension. Aortic cable compression can be decreased once the fetal head is engaged and also contractions of labor will actually rise the uterus off the vena cava. By term, the periturian has a 35 to 40% expansion of their blood volume, leading to approximately 1,000 to 1,500 milliliters more. This is due to the metabolic needs of the fetus and also the preparation of blood loss during delivery for the maternal patient. A vaginal delivery normal blood loss is 500 to 600 milliliters and a twin delivery or cesarean delivery leads up to about 1,000 milliliters of blood loss. As you can see demonstrated by the chart on the right, there is a significant increase in plasma volume. It almost doubles from 40 milliliters per kilo to 70 milliliters per kilo. However, the red blood cell volume does increase but it is not as significant. You can see that it goes from 25 milliliters per kilo to 30 milliliters per kilo. Red blood cell mass does increase during pregnancy due to elevated erythropoietin. However, there is a physiologic anemia that occurs because there's a greater increase in the plasma volume compared to the red blood cell mass volume, therefore creating a dilutional anemia. In addition, anemia can occur in pregnancy also due to iron deficiency. Overall, the maternal blood volume of the patient increases by 45%. This is due to the increasing plasma volume of 55% and the red blood cell volume increasing by 30%. The hemoglobin concentration and hematocrit fall after conception until they are approximately 11 and 35, respectively, by mid-gestation. Pregnancy is considered a hypercoagulable state. This is because almost all factors increase. Fibrinogen increases most significantly from 400 to 650 milligrams per deciliter. Factor 7 and factor 8 also increase, causing a shortening of the PT and PTT, which is consistent with an elevation of most factor concentrations. This situation places the patients at risk for thrombolic events. The platelet count typically in a pregnant patient remains stable. This is because there is an increase in platelet production but also an increase in platelet consumption. However, in the third trimester, some patients are prone to gestational thrombocytopenia because of an increase in platelet destruction present. Due to the increase in plasma volume in the maternal patient, you also will note that there is a decrease in plasma proteins due to the dilutional effect, much like what you saw with the red blood cells. Therefore, there is a decrease in total protein and a decrease in albumin, noting that the albumin-globulin ratio also goes down. In addition, you will notice that there is a plasma cholinesterase deficiency as well. This is due partially to, again, the plasma dilution, but also there is lower production of plasma cholinesterase in a pregnant patient. Typically, this decrease will peak three days postpartum, but it will return to normal at the six weeks postpartum. Due to this plasma cholinesterase deficiency, you will notice that if you use succinylcholine, it will last longer, and therefore you may not need to re-administer it during a case. The various immune system changes that you will see in the maternal patients is that the leukocyte production increases throughout pregnancy, peaking at the first day postpartum and returning at the sixth day postpartum to a more normal level. Even though the leukocyte production goes up, the actual function of the succulocytes, though, goes down, leading the parturient more at risk to infections. In addition, the pregnant patient will be in an immunosuppressed state. Therefore, if they have any type of autoimmune disease, they may notice that their symptoms during pregnancy actually decrease, but then when they're not pregnant, they may rebound. Due to the growing uterus, there can be changes in the gastrointestinal system as well. The uterus displaces the stomach upward and leftward and also displaces the intra-abdominal segment of the esophagus into the thorax. The lower esophageal high pressure zone decreases while there is an increase in intergastric pressure. The increase in intergastric pressure causes approximately 45 to 70% of women to claim plain of heartburn by the third trimester. And it is normally seen in the last few weeks of pregnancy, and it's even further exaggerated in pregnancy that the patient may be obese or have an enlarged uterus due to multiples. Gastric emptying, however, is unaltered during pregnancy, but during labor it is slowed. Due to the gastrointestinal changes, it's imperative that you try to avoid aspiration pneumonia if you need to administer general anesthesia. Therefore, it's essential to provide the patient aspiration pneumonia prophylaxis, such as administering a non-particular antacid such as Bicitra, 30 millimeters of it, 30 to 45 minutes prior to surgery. In addition, you may consider metoclopramide in your high-risk patients 30 to 90 minutes prior to surgery. You want to consider patients that are past the first trimester as a full stomach and utilize a rapid sequence induction with cricoid pressure. It is recommended that you use video laryngoscopy for your first attempt to intubate. In addition, you want to try to avoid or minimize positive pressure mask ventilation and ensure that you extubate the patient fully awake. The hepatic changes that you may see in the maternal patient include a mild increase in enzymes, the upper limits of normal. There will also be noted, as described before, a decrease in your plasma pseudocolonesterase by about 25%, so you want to be mindful of the medications that you administer that are metabolized by plasma colonesterase. There also can be a decrease in the serum albumin, and it is noted that in some pregnant patients, there's delayed gallbladder emptying due to the antagonistic effects of progesterone. This causes an increase in the concentration of bile higher than normal, therefore leading to cholestasis. Due to the increase in blood volume and cardiac output, the kidneys also receive additional blood volume, causing the kidneys to be enlarged and also dilating the ureters and renal pals. Notice that the renal blood flow will increase by approximately 60% at term, therefore leading to an increase in your glomerular filtration rate by about 50%. Because of this increase in glomerular filtration rate, you will see that your creatin clearance is also improved. So when looking at renal values, a non-pregnant renal value is almost pathological because you will note that the BUN and creatin in the pregnant patient are significantly lower, and that if you actually have a normal BUN and creatin in a pregnant patient, that is showing that there is compromise to the kidneys. During pregnancy, there is increased vascularity and hyperplasia to the thyroid gland. Therefore, if the patient has an existing goiter, it will usually grow in size, and it's important to do a thorough airway assessment and of the neck in a patient with a goiter to determine if you can have displacement of the trachea. The patient will remain euthyroid. However, the thyroid stimulating hormone typically falls in the first trimester, but then returns to normal. In the parathyroid gland, the parathyroid hormone levels will increase significantly for the provision of calcium for fetal growth. So you'll notice that the total serum calcium decreases by about 10%, but the ionized calcium remains unchanged. The maternal patient's bone density is not affected with these calcium changes during pregnancy. During pregnancy, insulin secretion increases, demonstrated by the chart to the right. Also, the parturient has a reduced tissue sensitivity to insulin. These changes are mediated by hormones secreted by the placenta, primarily placental lactogen. You will notice that glucose metabolism returns to normal at 24 hours after delivery. It is important to understand that maternal insulin does not cross the placenta. Therefore, the fetus will secrete its own insulin in response to a maternal glucose load. Therefore, it's essential that normal glycemia in the mother is present immediately prior to delivery, because if the fetus is secreting extra insulin to handle the maternal hyperglycemia, once the fetus is separated from the maternal patient, they will not have the glucose for their overproduction of insulin to respond to, causing them to be hypoglycemic. There are maternal vertebral column changes during pregnancy. The most noted thing that you will see is an enhanced lumbar lordosis. Because of this lumbar lordosis, there may be a reduced vertebral inner spinous gap and change in the lumbar angulation of the spinous processes, therefore increasing the difficulty to place neuroxial anesthesia. In addition, the cerebral spinal fluid pressure does not alter in pregnancy, but the cerebral spinal fluid rate may actually increase during uterine contractions. Due to the anatomical changes during pregnancy, there is compression of the inferior vena cava by the uterus, which causes the blood to be diverted through the vertebral plexus into the epidural space, ultimately distending the epidural veins and decreasing the cerebral spinal fluid. The distended epidural veins place the patient at a higher risk for the development of an epidural hematoma if we inadvertently hit the vein with a needle or the epidural catheter. Lastly, there are neurologic changes that occur in the pregnant patient. These are primarily due to changes in hormone levels and also endorphins and encephalins. Displayed by the patient due to these changes is often emotional changes. You also may notice an increased sensitivity to some of the pharmacologic agents that we use, decreasing your MAC by almost a third. There can be pregnancy-induced analgesia by effects again of progesterone and increasing endorphins and encephalins in labor. In conclusion, there are numerous physiologic and anatomical changes that occur with the maternal patient. Throughout our lecture series, we will be addressing the various anesthetic considerations related to these changes. Thank you for your time and attention.

pregnancy

hormonal influences

physiological changes

cardiovascular adaptations

respiratory changes

anesthesia challenges