Cardiopulmonary Bypass 199 evaluates the placenta as an oxygenator as blood is pumped through it by the CPB machine. As the CPB techniques are changed, the blood gases of the fetus are evaluated. Some research- ers believe that information gained from this model should translate to CPB techniques of the human parturient because placental function is still being evaluated, albeit from the other side [40] . By comparing the vasoactive effects of acetylcholine (endothe- lium dependent) and nitroprusside (endothelium independent), this model has shown that non - pulsatile fl ow bypass selectively inhibits endothelium - dependent vasodilation [52] . In other words, non - pulsatile fl ow and the absence of sheer stress on the vessel inhibits the placental endothelium ’ s ability to synthesize nitric oxide. In contrast, pulsatile fl ow bypass preserves nitric oxide synthesis of the placental endothelium [53,54] . With the placental vasoconstriction that occurs with non - pulsatile CPB, higher fl ows and increased mean arterial pressures may be neces- sary to perfuse the placenta. Myometrial a ctivity d uring CPB The onset of sustained contractions during CPB can lead to fetal distress and possible fetal death [20] . When the uterus contracts, placental vascular resistance increases, placental perfusion decreases, and if relaxation does not occur subsequent fetal hypoxia ensues. The mechanism(s) responsible for these uterine contractions have not been clearly delineated. The dilutional effect of CPB has been postulated to reduce the hormonal levels of progesterone resulting in increased uterine excitability [18,40,49] . Sabik and coworkers [55] have implicated the pro- duction of vasoactive prostaglandins. Further, both the cooling and rewarming phases of CPB are associated with sustained uterine contractions [18] . Normothermic (versus hypothermic) CPB demonstrates increased fetal survival which may partially be a result of preventing the contractions associated with tempera- ture change [19] . hypothermia resulting in fetal bradycardia, fetal hypoxia from hemodilution acutely decreasing the maternal oxygen content, and uterine contractility at the onset of CPB increasing the uterine vascular resistance and decreasing placental suffi ciency [45] . Whatever the cause of the initial fetal bradycardia seen with initiation of CPB, many reports indicate that FHR directly cor- relates with perfusion throughout CPB such that when fl ow rate is increased, the FHR is restored [19,38,46 – 50] . Thus, when the fetus is beyond about 25 weeks gestational age, most anesthesi- ologists monitor fetal heart rate throughout CPB and attempt to establish adequate fl ow to maintain a normal FHR (110 – 160 bpm). Temperature manipulation during hypothermic CPB has also been thought responsible for the FHR changes [45] . It has been known for some time that maternal temperature change results in fetal heart rate changes with hyperthermia causing fetal tachy- cardia and hypothermia causing fetal bradycardia as shown in Figure 14.2 [51] . However, multiple cases of normothermic CPB demonstrate the characteristic initial bradycardia and post - CPB tachycardia, sustaining the theory that although temperature infl uences FHR, the typical changes observed during CPB are likely a result of uteroplacental insuffi ciency. At the conclusion of CPB, the fetal heart rate often becomes tachycardic with minimal beat - to - beat variability which is pre- sumed to be secondary to fetal acidosis developing from con- tinuous uteroplacental insuffi ciency throughout CPB. The uteroplacental insuffi ciency throughout bypass is likely from multiple causes. Gas or debris could embolize to the placenta during CPB resulting in decreased perfusion. It is also known that CPB may cause regional alterations in fl ow in particular vascular beds. Studies are indicating that the non - pulsatile fl ow that occurs during non - pulsatile CPB incites placental vasoconstriction. Animal studies researching placental function during CPB place an animal fetus on CPB and evaluate the effects of various bypass techniques on this exquisitely sensitive model. The bypass machine in these models does not have an oxygenator, but instead 1 12 0 20 40 60 80 100 120 140 160 180 200 0 20 40 60 80 100 120 140 160 180 200 3456789 10 2 MATERNAL INTRA ARTERIAL BLOOD PRESSURE (mmHg) FETAL HEART RATE (BPM) TIME (HRS) Fetal Heart Rate Maternal Systolic Blood Pressure Maternal Diastolic Blood Pressure Mean Perfusion Pressure 3 Figure 14.1 Fetal heart rate as related to maternal hemodynamics during cardiopulmonary bypass. 1, induction of anesthesia; 2, ventilatory rate adjustment; 3, median sternotomy; 4, pericardotomy; 5, heparin administration; 6, aortic cannulation and manipulation of the heart; 7, scopolamine and pancuronium administration; 8, start of cardiopulmonary bypass; 9, fall in maternal blood pressure and FHR with start of non - pulsatile fl ow; 10, cardiopulmonary bypass discontinued. (Reproduced by permission from Levy DL, Warriner RA, Burgess GE. Fetal response to cardiopiulmonary bypass. Obstet Gynecol 1980; 56: 112 – 115.) Chapter 14 200 allow the obstetric attendant to detect signifi cant decreases in fetal heart rate and suggest the need for interventions [58] . Besides fetal bradycardia, other fetal heart rate features, such as diminished variability, fetal tachycardia and a sinusoidal - like pattern, have also been described in association with decreased perfusion during CPB and may be amenable to pump manipula- tion, as described previously [43,44,49,59] . Fetal decelerations or diminished variability occurring despite increased CPB fl ow in normothermic patients with normal acid – base status may be sec- ondary to fetal exposure to drugs administered during anesthesia [48,60 – 62] . Such FHR changes will recover after anesthetic recov- ery and do not indicate fetal distress. If technically feasible, uterine activity also should be monitored during CPB. Uterine contractile activity should be anticipated, especially during periods of reduced mean arterial pressure during and after CPB. If consistent uterine contractions or pro- longed tetany of the uterus is detected, prompt treatment as previously discussed is warranted. Tocodynamometry should continue into the immediate postoperative days. Anesthesia and s urgery in the p arturient Lateral uterine displacement during surgery is essential to avoid aortocaval compression, and decreased cardiac output and utero- placental perfusion [63] . A lateral tilt of at least 30 – 40 ° has been recommended during CPB [18,64] . This is especially crucial because CPB often involves periods of hypotension, and such The anesthesiologist and obstetrician should monitor in order to detect uterine contractions so they can be treated immediately and appropriately. The routine prophylactic use of tocolysis before CPB surgery is controversial, especially because of the cardiac effect of the ß 2 - sympathomimetic agents [50,56] . Progesterone, ß 2 - sympathomimetic agents such as ritodrine or terbutaline, indomethacin, nitroglycerin, intravenous ethanol, and magnesium sulfate have all been described with some effect in decreasing uterine contractions associated with CPB [40,46,49,57] . In general, uterine contractions should be treated fi rst with increased perfusion pressure and fl ow, then by increas- ing the potent volatile anesthetic agent to reduce uterine tone or by administering a tocolytic agent such as magnesium, nitroglyc- erin, ritodrine or terbutaline depending upon the hemodynamics at the time and recognizing the cardiac effects of the latter two ß 2 - sympathomimetic agents. Fetal m onitoring d uring c ardiopulmonary b ypass Consideration for fetal monitoring is important whether or not the fetus is viable. In the presence of bradycardia, alterations in pump fl ow, pressure or temperature may improve fetal status and outcome. Such monitoring is often most easily performed with continuous external electronic fetal heart rate monitoring, assum- ing fetal size, fetal movement and maternal habitus do not pre- clude such a technique. Otherwise, intermittent auscultation may Figure 14.2 Maternal temperature and fetal heart rate (FHR). The FHR plot directly parallels the maternal temperature. The arrow at 0800, 1/1/86, represents the nadir of maternal BP: 87/46 mmHg (mean arterial pressure, 69). Within 20 minutes the BP was 94/57 mmHg (mean arterial pressure, 69). The mean arterial pressure during the rest of the illustrated time ranged from 64 to 76. Previous and subsequent pressures during this pregnancy ranged from 90/50 to 110/65 mmHg (mean arterial pressure, 63 – 80). BPM, beats per minute. (Reproduced by permission from Jadhon ME, Main EK. Fetal bradycardia associated with maternal hypothermia. Obstet Gynecol 1988; 72: 496.) Cardiopulmonary Bypass 201 Hemodilution and subsequent changes in hormone concentra- tions, such as a decrease in progesterone, may play a role in trig- gering uterine contractions [49] . Korsten and coworkers suggested that the addition of progesterone to the prime may be helpful in avoiding preterm uterine activity, but this approach requires further investigation before incorporation into clinical practice. Mannitol is often added to the CPB prime in order to promote an osmotic diuresis and to scavenge oxygen free radicals from the circulation. For parturients, some recommend omitting mannitol in the CPB prime to decrease the risk of hemoconcentrating fetal blood [71] . As the osmotic pressure of the maternal blood increases, water would be pulled from the fetal into the maternal blood within the placenta. On the other hand, one case of fetal hydrocephalus and hydrops detected after CPB at 19 weeks gesta- tion has been reported [39] . Perhaps the maternal hemodilution that occurs during CPB results in overhydration of fetal blood and resulting hydrops in some cases. Mannitol may prevent this. Further investigation is needed regarding the use of mannitol in CPB prime. Hypothermia Hypothermia was considered an important component of CPB for many years in order to decrease systemic and vital organ oxygen consumption and minimize organ damage. Animal studies initially demonstrated safety in the parturient, because the fetal sheep in pregnant ewes cooled to 29 ° C did not exhibit fetal distress as long as maternal acidosis and hypoxia were avoided [72] . Likewise, hypothermic CPB and even deep hypothermic circulatory arrest have been described with successful maternal – fetal outcomes [56,73,74] . However, its use is now deemed less benefi cial and perhaps unnecessary. It may also be harmful in the parturient, resulting in fetal bradycardia and possibly asystole, the provocation of uterine contractions, decreased placental blood fl ow and interference with placental function. As maternal temperature decreases, FHR also decreases as demonstrated in Figure 13.2 . Whether this is related to a decrease in fetal metabolism, changes in the placental vasculature, or fetal distress is not known. If hypothermic CPB is performed, decreases in FHR should be expected. An attempt to bring the FHR back into the normal range (110 – 160 bpm) by increasing fl ow may be prudent, but may not be successful as described in one case report in which the FHR decreased to 50 beats per minute [56] . The fetal heart rate in this case increased only after rewarming and the fetus survived. Two case reports describe the loss of fetal heart tones and presumed fetal asystole during hypothermia that were detected again after the surgery with subsequent fetal survival [62,74] . A fetal bypass study placed eight fetal ewes on CPB with the placenta working as an oxygenator [75] . Four fetuses had CPB performed at 37 ° C at various fl ow rates and four at 25 ° C at various fl ow rates. Although PCO 2 was lower in the hypothermic ewes, fetal oxygenation was signifi cantly worse. This indicates that the placenta acts as a poor oxygenator during hypothermic CPB. compression is enhanced during periods of hypotension, further worsening a hypotensive episode. A combination of a wedge and table tilt is generally adequate to achieve appropriate lateral uterine displacement. Anesthesiologists should also be aware that parturients have increased rates of failed intubation compared to non - pregnant patients [65,66] . Edema of the airway structures as pregnancy progresses may impede the anesthesiologist ’ s laryngoscopic view. Because of reduction in functional residual capacity and an increase in oxygen consumption, an apneic parturient will drop their PaO 2 at twice the rate of a non - pregnant woman [67] . Therefore, careful attention should be paid to the obstetric airway. Mechanical positive - pressure ventilation is instituted routinely in patients undergoing cardiac surgery, and various degrees of hyperventilation are frequently produced, either intentionally or inadvertently. Blood gas disturbances can affect sympathetic activity and thus indirectly affect UBF. In addition, hyperventila- tion may decrease uteroplacental perfusion either through mechanical means by increasing intrathoracic pressure and decreasing cardiac output, or through the induction of hypocap- nia, which decreases UBF. Thus, hyperventilation should be minimized or avoided in the pregnant surgical patient unless specifi cally indicated. The presence of pre - eclampsia and eclampsia complicate the anesthetic management of the parturient signifi cantly. These patients are exquisitely sensitive to sympathetic stimulation, probably from impaired endothelial function. Cerebral vascular accident from malignant hypertension must be avoided with adequate antihypertension therapy, a deep induction for laryn- goscopy, adequate anesthesia throughout surgery, and careful titration of sympathomimetic agents. This complex disease state and its anesthetic implications are reviewed elsewhere [68,69] . Cardiopulmonary b ypass t echnique Priming the p ump The various components of the CPB apparatus (e.g. tubing) require approximately 2 L of priming solution in most adult cir- cuits. Priming of the CPB circuit produces hemodilution which is an important element of CPB. It decreases blood product uti- lization and its attendant costs and risks. Hemodilution also improves the rheology of blood by decreasing its viscosity, result- ing in a lower arterial resistance and improved peripheral perfu- sion [70] . Other purported benefi ts of hemodilution during CPB include decreases in major organ complications, such as cerebral vascular accident, and renal and pulmonary dysfunction. In the pregnant cardiac surgical patient, or any anemic patient for that matter, CPB - associated hemodilution may result in severe anemia. This can compromise the oxygen - carrying capacity of blood as well as oxygen delivery. Anemic patients with poor cardiac function may not tolerate severe hemodilution. Whole blood or RBCs can be added to the prime of the CPB circuit so that the resultant hematocrit is no less than 21 – 26% [61] . Chapter 14 202 used to improve fetoplacental perfusion after CPB. In the second, the pump was inserted during the bypass period to produce pul- satility and thereby improve fetoplacental perfusion. Both patients did well. In spite of these potential benefi ts, clinical application of pulsatile fl ow during CPB is uncommon. Flow and p erfusion p ressure Because normal cardiac output in pregnant women is often greater than 6 L/min [81] , the usual fl ows ( ∼ 2.5 L/m 2 ) employed during CPB may be too little. Changes in baseline fetal heart rate have been identifi ed after initial fl ow rates as high as 80 mL/kg/ min, even in the absence of maternal hypotension [50] . Increases in CPB fl ows to 3.0 – 4.0 L/m 2 have been successfully (if only tem- porarily) employed during surgery in the pregnant patient, espe- cially in response to fetal bradycardia [18,50,82] . For example, Koh and associates [43] were the fi rst to describe improvement in fetal bradycardia by increasing fl ow rate by 16%. Other inves- tigators have since confi rmed the value of increasing pump fl ow rate to improve fetal bradycardia [20,46 – 49,82] . Further, fetal bypass animal models have shown that moderately high fl ow rates improve placental function [83] . The ideal mean arterial pressure (MAP) during CPB is not fi rmly established for cardiac surgical patients in general. In the pregnant patient, the use of moderate to high arterial pressures during CPB is recommended. Some recommend that MAP should initially be maintained at a level of 70 mmHg or greater. It is preferable to produce elevations in MAP with fl uid volume administration and high fl ow rates as opposed to vasopressor administration, which could have an adverse effect on UPBF. It should be anticipated that on institution of CPB, transient but signifi cant hypotension occurs and frequently produces fetal bradycardia [43,44,48,82] . This is generally correctable by appropriate manipulations of pump fl ow and pressure. Cardioplegia Myocardial protection during CPB is essential to reduce periop- erative cardiac morbidity. Both cold and warm blood cardiople- gia have been shown to reduce cardiac morbidity [84] . The application of cardioplegia may need to be more frequent with the maintenance of high fl ows during CPB, especially if normo- thermia or only mild hypothermia is employed. Normothermic perfusion often results in early rewarming of the left ventricle leading to diffi culties with myocardial protection [40] . Cardiac activity may return as frequently as every 10 minutes under these circumstances. In one study, 3.5 L of cardioplegia was required to adequately suppress cardiac activity [49] . The use of cold car- dioplegia has been associated with fetal bradycardia [85] and continuous cold pericardial irrigation or warm blood cardiople- gia have been suggested as effective alternatives [86] . Concomitant tocolytic therapy may potentially also increase the need for car- dioplegia and it is generally avoided as an elective prophylactic measure. Hypothermia has been shown to decrease umbilical blood fl ow velocity in the human fetus. Goldstein et al. [45] measured umbil- ical artery fl ow velocities during hypothermic CPB (nadir 29 ° C) and found an absence of end - diastolic uterine artery blood fl ow from 10 minutes after initiation of CPB until the patient began rewarming. Because the diastolic fl ow returned after rewarming but before the end of CPB, he related the decrease in uterine blood fl ow to temperature, not just the effects of non - pulsatile CPB itself. Rewarming is associated with increased frequency of uterine contractions [18] and reports of fetal heart rate decelerations have been reported in association with rewarming. Mahli and coworkers [62] suggest that these fetal decelerations may be sec- ondary to defi cient delivery of heat to the fetus during rewarming as a result of vasoconstriction of the umbilical vessels. Current knowledge and practice has been to avoid aggressive rewarming strategies. Such strategies were more often practiced in the past and have more recently been associated with increased CNS adverse effects [76] . The most infl uential study demonstrating the potential fetal benefi t of normothermic CPB retrospectively evaluated 69 reports of CPB during pregnancy from 1958 to 1992 [19] . In evaluation of the 40 most recent cases, hypothermic CPB was associated with a fetal mortality of 24.0% while normothermic CPB was associ- ated with no fetal losses. Because of this demonstrated improve- ment in fetal survival as well as the reports of fetal asystole, uterine contractions, and decreased placental blood fl ow during hypothermic CPB, normothermic CPB is preferred. Pulsatility Non - pulsatile fl ow is most commonly employed during CPB. It can be argued that pulsatile fl ow could be superior, providing a more normal physiologic milieu and better tissue and organ per- fusion than non - pulsatile blood fl ow. For example, differences in vascular resistance, oxygen delivery, and myocardial lactate pro- duction indicate the superiority of pulsatile CPB [48,77,78] . As discussed earlier, non - pulsatile fl ow and the absence of sheer stress on the vessel inhibits the placental endothelium ’ s ability to synthesize nitric oxide [52] . These same researchers also demon- strated that although the levels of endothelin - 1, a potent vaso- constrictor, were increased after 60 minutes of both pulsatile and non - pulsatile CPB, the levels were signifi cantly higher in the non - pulsatile group. Pulsatile fl ow has also been shown to maintain placental perfusion through decreasing the activation of the fetal renin – angiotensin – aldosterone axis, decreasing vasoconstriction of the fetal placental vasculature [78] . Non - pulsatile perfusion is performed during CPB at most institutions [79] . Pulsatile fl ow has been attempted in human par- turients. In one case, a roller pump was used in a pulsed mode to produce maternal arterial pulse pressures of about 35 mmHg [80] . Two cases of intra - aortic balloon pump use in parturients have also been described [71] . In one case, the balloon pump was Cardiopulmonary Bypass 203 alkalemia decreases fetal oxygenation [89] . Therefore, maternal PaCO 2 should be kept as close to 30 mmHg as possible and maternal alkalosis or acidosis avoided. Cardiopulmonary b ypass d uration The technical profi ciency and speed of the cardiac surgical team are two of the primary determinants of outcome in cardiac surgery. With regard to the pregnant cardiac patient, fetal mor- bidity and mortality also appear to increase with CPB duration. Thus, it is essential that CPB time be minimized in the pregnant patient. Postoperative c ourse The most common problems cardiac surgery patients experience in the immediate postoperative period involve hemostasis, and cardiovascular and respiratory function. Less commonly, renal function may deteriorate and renal failure signifi cantly worsens the prognosis. In the pregnant patient, such problems, if severe, may necessitate postoperative emergency cesarean delivery [90] . Patients undergoing CPB can suffer signifi cant neurologic complications after heart surgery. Defi cits can occur in up to 50% of patients, with a much smaller percentage (2 – 3%) experiencing permanent focal or cognitive problems [1 – 3] . In pregnant patients, these problems also are likely to be of concern for several reasons. Emergency procedures, and especially open heart opera- tions, will increase neurologic complication rates. Systemic embolization and stroke will also be increased in pregnant patients if their condition includes rheumatic valvular disease with bacterial endocarditis and the presence of vegetations. Once postoperative bleeding has resolved, and depending on the type of valvular prosthesis employed, mothers may require continued and consistent anticoagulation postoperatively. The complex issues surrounding the use of heparin versus warfarin derivatives in these patients is discussed elsewhere in this text. Delivery of the fetus may take place several months after cardiac operation. At the time of delivery, the cardiac team should be made aware and complete evaluation of the mother ’ s cardio- vascular status should be undertaken even if maternal outcome after cardiac surgery has been excellent. The team should be prepared for treatment of any cardiac problems (e.g. hemor- rhage) that may arise during or after delivery. Summary Cardiopulmonary bypass during pregnancy is safe for the partu- rient but poses signifi cant risk to the fetus. If possible, delaying the surgery until after delivery is best for the neonate, but can result in increased morbidity and mortality for the mother. High - Anticoagulation and h ematologic c onsiderations Anticoagulation is essential during CPB. It is generally accom- plished with heparin therapy which has posed little risks to the fetus when used for CPB. Such anticoagulation is typically reversed with protamine sulfate following successful weaning and separation from the CPB pump. This drug has also not been shown to harm the fetus. The use of antifi brinolytic agents to reduce blood loss in cardiac surgery during pregnancy has not been studied. Because pregnancy is associated with physiologic enhancement in clot- ting, the parturient likely relies upon fi brinolysis to prevent thrombotic adverse events such as placental infarction or deep venous thrombosis formation. Therefore, the use of antifi brino- lytic therapy in pregnancy may not be prudent. When transfusing red blood cells to the parturient, it is impor- tant to maintain the physiologic anemia of pregnancy (hemoglo- bin about 11.6 g/dL or hematocrit 35.5%). Teleologically, the decreased viscosity likely occurs to maintain uteroplacental per- fusion. This is illustrated by the fact that elevations of maternal hematocrit are associated with placental infarction [87] . Acid – b ase s tatus Acid – base status may vary signifi cantly during CPB. The most common approaches to the management of acid – base status during CPB are called alpha STAT and pH STAT. Briefl y, alpha STAT management attempts to maintain a normal enzymatic milieu. This is accomplished by targeting normocarbia, as deter- mined by blood gas analysis of a blood sample at a temperature of 37 ° C. pH STAT management attempts to maintain a pH of 7.4, no matter what the patient ’ s temperature. This usually involves the addition of carbon dioxide to the CPB oxygenator to maintain a calculated patient blood PCO 2 of 40 mmHg at the patient ’ s temperature during hypothermic CPB. While com- monly practiced in the past, pH STAT approaches have become less popular in the adult cardiac surgical patient population. During pregnancy, PaCO 2 decreases to 30 mmHg by week 12, bicarbonate concentration decreases to about 20 mEq/L, the base excess decreases to 2 – 3 mEq/L, and the blood pH increases by 0.02 to 0.06 units [88] . Normally, the fetal pH is 0.1 units lower than that of the mother. Maintenance of a normal acid – base balance is paramount for the parturient and her fetus. Maternal acidosis can result in fetal acidosis, and the fetus is unable to compensate for acidemia by compensatory respiratory and renal responses like the adult. Therefore, maternal pH should be kept as close to 7.44 as possible. Likewise, hyperventilation and alka- losis should be avoided because this shifts the oxyhemoglobin dissociation curve to the left with subsequent decreased unload- ing of oxygen from mother to fetus. 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Open heart surgery for thrombosis of a prosthetic mitral valve during pregnancy. Fetal hydrocephalus . J Cardiovasc Surg (Torino) 1986 ; 27 : 217 – 220 . 37 Leyse R , Ofstun M , Dillard DH , Merendino KA . Congenital aortic stenosis in pregnancy, corrected by extracorporeal circulation, offering a viable male infant at term but with anomalies eventuating in his death at four months of age – report of a case . JAMA 1961 ; 176 : 1009 – 1012 . 38 Westaby S , Parry AJ , Forfar JC . Reoperation for prosthetic valve endocarditis in the third trimester of pregnancy . Ann Thorac Surg 1992 ; 53 : 263 – 265 . 39 Khandelwal M , Rasanen J , Ludormirski A , Addonizio P , Reece EA . Evaluation of fetal and uterine hemodynamics during maternal car- diopulmonary bypass . ACOG J 1996 ; 88 : 667 – 671 . 40 Parry AJ , Westaby S . Cardiopulmonary bypass during pregnancy . Ann Thorac Surg 1996 ; 61 : 1865 – 1869 . 41 Skillman CA , Plessinger MA , Woods JR , Clark KE . Effect of graded reductions in uteroplacental blood fl ow on the fetal lamb . Am J Physiol 1985 ; 249 : H1098 – 1105 . 42 Bilardo CM , Nicolaides KH , Campbell S . Doppler measurements of fetal and uteroplacental circulations: relationship with umbilical venous blood gases measured at cordocentesis . Am J Obstet Gynecol 1990 ; 162 : 115 – 120 . 43 Koh KS , Friesen RM , Livingstone RA , Peddle LJ . Fetal monitoring during maternal cardiac surgery with cardiopulmonary bypass . Can Med Assoc J 1975 ; 112 : 1102 – 1104 . 44 Levy DL , Warriner RA , III , Burgess GE , III . Fetal response to cardio- pulmonary bypass . Obstet Gynecol 1980 ; 56 : 112 – 115 . 45 Goldstein I , Jakobi P , Gutterman E , Milo S . Umbilical artery fl ow velocity during maternal cardiopulmonary bypass . Ann Thorac Surg 1995 ; 60 : 1116 – 1118 . 46 Werch A , Lambert HM , Cooley D , Reed CC . Fetal monitoring and maternal open heart surgery . Southern Med J 1977 ; 70 : 1024 . 47 Veray FX , Hernandez CJJ , Raffucci F , Pelegrina IA . Pregnancy after cardiac surgery . Conn Med 1970 ; 34 : 496 – 499 . 48 Trimakas AP , Maxwell KD , Berkay S , Gardner TJ , Achuff SC . Fetal monitoring during cardiopulmonary bypass for removal of a left atrial myxoma during pregnancy . Johns Hopkins Med J 1979 ; 144 : 156 – 160 . 49 Korsten HH , Van Zundert AA , Mooij PN , De Jong PA , Bavinck JH . Emergency aortic valve replacement in the 24th - week of pregnancy . Acta Anaesth Belg 1989 ; 40 : 201 – 205 . 50 Chambers CE , Clark SL . Cardiac surgery during pregnancy . Clin Obstet Gynecol 1994 ; 37 : 316 – 323 . 51 Jadhon ME , Main EK . Fetal bradycardia associated with maternal hypothermia . Obstet Gynecol 1988 ; 72 : 496 . 52 Reddy VM , McElhinney DB , Rajasinghe HA , Liddicoat JR , Hendricks - Munoz K , Fineman JR , Hanley FL . Role of the endothelium in Chapter 14 206 82 Lamb MP , Ross K , Johnstone AM , Manners JM . Fetal heart monitor- ing during open heart surgery. Two case reports . Br J Obstet Gynaecol 1981 ; 88 : 669 – 674 . 83 Hawkins JA , Clark SM , Shaddy RE , Gay WA , Jr. Fetal cardiac bypass: improved placental function with moderately high fl ow rates . Ann Thorac Surg 1994 ; 57 : 293 – 296 . 84 Fremes SE , Tamariz MG , Abramov D et al. Late results of the Warm Heart Trial: the infl uence of nonfatal cardiac events on late survival . Circulation 2000 ; 102 : 19 ( Suppl 3 ): 339 – 345 . 85 Garry D , Leikin E , Fleisher AG , Tejani N . Acute myocardial infarction in pregnancy with subsequent medical and surgical management . Obstet Gynecol 1996 ; 87 : 802 – 804 . 86 Lichtenstein SV , Abel JG , Panos A , Slutsky AS , Salerno TA . Warm heart surgery: experience with long cross - clamp times . Ann Thorac Surg 1991 ; 52 : 1009 – 1013 . 87 Naeye RL . Placental infarction leading to fetal or neonatal death. A prospective study . ACOG J 1977 ; 50 : 583 – 588 . 88 Templeton A , Kelman GR . Maternal blood gases, (PAO 2 – PaO 2 ), physiological shunt, VD/VT in pregnancy . Br J Anaesth 1976 ; 48 : 1001 – 1004 . 89 Levinson G , Shnider SM , Delorimier AA , Steffenson JL . Effects of maternal hyperventilation on uterine blood fl ow and fetal oxygenation and acid - base status . Anesthesiology 1974 ; 40 : 340 – 347 . 90 Baraka A , Kawkabani N , Haroun - Bizri S . Hemodynamic deteriora- tion after cardiopulmonary bypass during pregnancy: resuscitation by postoperative emergency Cesarean section . J Cardiothorac Vasc Anesth 2000 ; 14 : 314 – 315 . 72 Matsuki A , Oyama T . Operation under hypothermia in a pregnant woman with an intracranial arteriovenous malformation . Can Anaesth Soc J 1972 ; 19 : 184 – 191 . 73 Plunkett MD , Bond LM , Geiss DM . Staged repair of acute type I aortic dissection and coarctation in pregnancy . Ann Thorac Surg 2000 ; 69 : 1945 – 1947 . 74 Buffolo E , Palma JH , Gomes WJ et al. Successful use of deep hypo- thermic circulatory arrest in pregnancy . Ann Thorac Surg 1994 ; 58 : 1532 – 1534 . 75 Hawkins JA , Paape KL , Adkins TP , Shaddy RE , Gay WA . Extracor- poreal circulation in the fetal lamb. Effects of hypothermia and perfusion rate . J Cardiovasc Surg 1991 ; 32 : 295 – 300 . 76 Grigore AM , Grocott HP , Mathew JP et al., the Neurologic Outcome Research Group of the Duke Heart Center. The rewarming rate and increased peak temperature alter neuroco gnitive outcome after cardiac surgery . Anesth Analg 2002 ; 94 : 4 – 10 . 77 Philbin DM . Pulsatile Blood Flow . Baltimore : Williams and Wilkins , 1993 : 323 – 337 . 78 Vedrinne C , Tronc F , Martinot S et al. Effects of various fl ow types on maternal hemodynamics during fetal bypass: is there nitric oxide release during pulsatile perfusion? J Thorac Cardiovasc Surg 1998 ; 116 : 432 – 439 . 79 Farmakides G , Schulman H , Mohtashemi M , Ducey J , Fuss R , Mantell P . Uterine - umbilical velocimetry in open heart surgery . Am J Obstet Gynecol 1987 ; 156 : 1221 – 1222 . 80 Tripp HF , Stiegel RM , Coyle JP . The use of pulsatile perfusion during aortic valve replacement in pregnancy . Ann Thorac Surg 1999 ; 67 : 1169 – 1171 . 81 Clark SL , Cotton DB , Lee W et al. Central hemodynamic assessment of normal term pregnancy . Am J Obstet Gynecol 1989 ; 161 : 1439 – 1442 . 207 Critical Care Obstetrics, 5th edition. Edited by M. Belfort, G. Saade, M. Foley, J. Phelan and G. Dildy. © 2010 Blackwell Publishing Ltd. 15 Non - Invasive Monitoring Michael Cackovic 1 & Michael A. Belfort 2 1 Division of Maternal - Fetal Medicine, Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT, USA 2 Department of Obstetrics and Gynecology, Division of Maternal - Fetal Medicine, University of Utah School of Medicine, Salt Lake City, UT and HCA Healthcare, Nashville, TN, USA Introduction The appropriate management of critically ill patients requires frequent observation of biophysical parameters. The most impor- tant of these parameters describe the delivery of oxygenated blood to the peripheral tissues. Peripheral oxygen saturation and markers of hemodynamic function are essential prerequisites in the provision of intensive care, the development of which was initially based upon the accuracy and utility of pulmonary artery catheters as an investigative tool. While this technology has remained synonymous with critical care practice it is now recog- nized that the invasive nature of this monitoring is associated with a range of complications. Newer, non - invasive technologies have been developed that now provide similar, or more extensive data with fewer risks. Non - invasive hemodynamic assessment has permitted the col- lection of diagnostic and research data beyond the arena of criti- cal care. Information derived from the use of echocardiography in particular has helped to expand our understanding of many conditions including the physiological events of normal preg- nancy, the pathogenesis of pre - eclampsia, the abnormalities characteristic of various forms of heart disease, and a variety of medical disorders. In some circumstances, echocardiography has become an integral part of the prepregnancy and antenatal assess- ment of women with heart disease. This chapter will review some aspects of this technology and the clinical issues associated with the use of non - invasive moni- toring that may be encountered in obstetric practice. The measurement of cardiac output An adequate cardiac output is essential to deliver oxygenated blood to the peripheral tissues. Low output will refl ect either hypovolemia or ventricular failure. Knowledge of the cardiac output will determine management and will also allow calcula- tion of other derived hemodynamic values including vascular resistance and oxygen delivery and consumption indices. In the past, cardiac output was measured using the Fick prin- ciple. This principle states that the amount of a substance taken up by the body per unit time equals the difference between the arterial and venous levels multiplied by the blood fl ow. Hence, oxygen consumption by the body divided by the arteriovenous oxygen difference equals the cardiac output. CO O uptake arterial O venous O= [] − [] () 222 This principle has been modifi ed to use other markers includ- ing dye dilution techniques and the thermodilution principle of the pulmonary artery catheter. In the latter case, iced water is the marker injected into the right atrium with a probe measuring the temperature of the blood fl owing through the pulmonary artery thus allowing the derivation of the cardiac output from the area under the curve. This technique, although clinically sound, may produce results that are confounded by variations in catheter position, variations in injectate temperature and volume, and differences in the rate of saline injection. These technologies have nevertheless contributed to our understanding of physiology and pathophysiology and remain the gold standard against which newer techniques are assessed. The need to cannulate peripheral and central vessels has been associated with some risk of injury and justifi ed the search for safer technology. Ultrasound in the form of echocardiography allows estimation of cardiac output by measuring changes in left ventricular dimen- sions during systole measured in the plane below the level of the mitral valve. By assuming that the ventricle is ellipsoid in shape and that the long axis is double the short axis, stroke volume can be calculated from the cube of the change in left ventricular dimension. This measurement is inaccurate when the assump- tions upon which it is based are no longer true. Hence, the dilated ventricle and the pregnant woman with an increased volume and Chapter 15 208 tion of this technology to specifi c situations including intraopera- tive and postoperative care. Other techniques of measuring cardiac output include imped- ance cardiography based upon changes in transthoracic electrical resistance associated with the ejection of blood into the pulmo- nary circulation. This technique has been shown to overestimate low cardiac output with the opposite error in high cardiac output states. Doppler ultrasound and the physiology of pregnancy Doppler techniques have confi rmed the increased cardiac output and stroke volume of pregnancy associated with progressive increases in left atrial dimension and function. Both fi lling phases of the left ventricle show increased fi lling velocities (E - and A - wave velocity). The increase in early wave velocity occurs by the end of the fi rst trimester whereas the peak A - wave velocity changes occur in the third trimester. The E/A ratio increases in the fi rst trimester but falls again as the A - wave velocity increases and is accompanied by decreasing left ventricu- lar isovolumetric relaxation time [5,6] . Left ventricular mass increases signifi cantly while fractional shortening and velocity of shortening diminish throughout preg- nancy [7] . Systolic function is preserved by falling systemic (including uterine artery) resistance [5,6] . Peak left ventricular wall stress, an indicator of afterload, has been demonstrated in early pregnancy and normalizes as ventricular mass increases in the mid - trimester [5] . Geva et al. [8] similarly report a 45% increase in cardiac output in normal pregnancy accompanied by an increase in left ventricular end - diastolic volume and increased end - systolic wall stress accompanied by transient left ventricular hypertrophy. These authors also report a reversible decline in left ventricular function during the second and third trimesters. Systemic arterial vascular compliance is thought to diminish because of reduced vascular tone [9] . The pulmonary circulation shows increased fl ow during preg- nancy with some reduction in vascular resistance without any signifi cant alteration in blood pressure. These changes are evident by 8 weeks gestation without any subsequent alteration and return to prepregnancy values by 6 months postpartum [10] . Doppler ultrasound and critical care There are few studies that address this issue, and non - invasive techniques for the routine estimation of stroke volume and ven- tricular fi lling pressures have only been recently reported in the obstetric literature. Validation studies have, however, been con- ducted and show reliable correlation between non - invasive tech- niques and values derived by the use of pulmonary artery catheters. Two - dimensional and Doppler echocardiography was used to demonstrate this in a group of 11 critically ill obstetric end - diastolic dimensions violate these assumptions and may overestimate stroke volume and cardiac output. Doppler ultrasound has added to the utility of echocardiogra- phy by allowing an estimation of blood velocity. The Doppler principle measures the frequency of a refl ected ultrasound beam striking moving erythrocytes where the change in frequency detected is proportional to the velocity of the red cells moving in the axis of the beam. The velocity of a column of red cells mul- tiplied by the period of ejection provides a measure of the dis- tance traveled by a column of blood during systole. The use of ultrasound to measure the diameter of the vessels containing the blood will allow calculation of cross - sectional area with subse- quent derivation of stroke volume and cardiac output. The veloc- ity of blood fl ow can also be related to the pressure gradient down which the blood is moving thus providing a way of calculating intracardiac pressure gradients and pulmonary artery pressures. Doppler probes may be pulsed (range - gated) to allow the mea- surement of a signal from a given depth of tissue. The pulsed Doppler signal usually allows simultaneous ultrasound imaging and estimation of the angle of insonation between the Doppler probe and the vessel. This latter measurement is important because the calculation of velocity from the refl ected Doppler signal requires a knowledge of the angle between the ultrasound beam and the column of blood from which the signal is being refl ected. Where the signal is perpendicular to the moving column of blood, no movement will be detected, and the closer the beam moves to being parallel to the vessel, the more completely the refl ected vector represents the velocity of the cells in the path of the beam. The combination of cross - sectional echocardiography and Doppler measurement of fl ow velocity at specifi c points in the heart and great vessels allows the determination of volumetric fl ow. The mitral and aortic valve orifi ces and the root or arch of the aorta have all been studied using both suprasternal and intra- esophageal Doppler probes. Potential for error exists in these techniques both in the calculation of the insonation angle and in the measurement of the cross - sectional area of the vessel. Of the different sites studied, the best correlation between the Doppler technique and thermodilution studies was documented in the aortic valve orifi ce measurements. Although transthoracic Doppler studies are the most widely accessible tool, transesopha- geal Doppler allows the posterior structures of the heart to be more clearly imaged with more accurate diagnosis of cardiac pathology and precise alignment to the aortic valve in both the long and short axis as well as providing long axis views of the ascending aorta [1] . The use of multiplanar transesophageal echocardiography allows precise measurements of asymmetric ventricles that cannot be reliably imaged using a transthoracic probe [2] . It provides high spatial resolution and access to struc- tures such as the left atrial appendage, the thoracic aorta, and the pulmonary veins that are not well seen by transthoracic echocar- diography on routine exam [3] . The probe has particular utility in the diagnosis of aortic dissection and thromboembolism [4] although the need for esophageal endoscopy limits the applica- . Maternal - Fetal Medicine, Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT, USA 2 Department of Obstetrics and Gynecology,. Uterine - umbilical velocimetry in open heart surgery . Am J Obstet Gynecol 1987 ; 156 : 1221 – 1222 . 80 Tripp HF , Stiegel RM , Coyle JP . The use of pulsatile perfusion during aortic valve. assessment of normal term pregnancy . Am J Obstet Gynecol 1989 ; 161 : 1439 – 1442 . 207 Critical Care Obstetrics, 5th edition. Edited by M. Belfort, G. Saade, M. Foley, J. Phelan and G. Dildy.