PHYSIOLOGICAL ADAPTATIONS DURING PREGNANCY William R. Camann, MD, and Gerard W. Ostheimer, MD Pregnancy involves major physiological and anatomical Adaptation by al the maternal organ systems. The anes thesiologist caring forthe pregnant patient nist under stand these physiological changes in order to provide Safe analgesia and anesthesia to the mother anel enable safe delivery of the fetus. CARDIOVASCULAR SYSTEM Gardiae Output ‘Oxygen consumption increases during pregnancy, and maternal cardiac output rises to meet these demands [1] (Table 1), The rise in cardiac output is result of in ‘creased heart rate and decreased slterload, as stroke vol lume does not change appreciably during normal preg: nancy [2], Cardiac ouput rises most rapidly during the second trimester (Fig I) and then remains steady until term, when labor sinc! uleroplacental transfusion of blood into the intravascular system cause further in creases in cardiae output Blood Volume Blood volume increases by 35% during pregnancy com pared with during the nonpregnant state [3}. ‘The Stimulus for this change is controversial. Increased mmineralocontcoid levels during pregnancy may predis pose to progressive sodium and water retention ith Consequent enlargement of the intravascular space (the ‘Ades eoreespande i Dr Caan, Brigham a ‘St tepartnci of Arcus 73 Pani Se Boon 2 Copyright © 1990 by Late, Brown and Company “overfill” hypothesis). Alternatively, primary enlarge iment of this space owing to hormonal (prostaglandin, progesterone) vasodilation and placental arteriovenous shunting may be the stimulus for secondary renal sodium and water retention (the “underfill” hypothesis) [4], Recent evidence seems to favor primary peripheral ‘vasodilation early in the frst trimester (underfill) us the cause of subsequent blood volume expansion [5] Uterine Sie and Vascuarity The gravid uterine blood flow is 20 to 40 times above the nonpregnant level, accounting for 20% of maternal car- dlige output at term, Uterine vascular resistance is marke edly reduced during gestation, producing 2 low-pressure CGreuit in "patalle!” with a niaersal circulation character iaed by reduced systemic vascular resistance The enlarged uterus produces mechanical compres sion of surrounding vascular structures, known a aor ocaval compression or the “maternal supine hypoten- sive syndrome” (6). In the supine position, compression fof the inferior vena cava decreases venous Feturn, result ing in decreased stroke volume and hypotension: com pression ofthe aorta further decreases uterine perfusion fnd may result in fetal distress. Normal maternal com pensatory responses to aprtocaval compression consist of tachycardia and lower-extremity vasoconstriction, The Pericardiun Recent noninvasive studies have demonstrated a high incidence of asymptomatie pericardial effusion during. nhormal pregnancy [7]. The stimulus is unknown, #8 plasma volume and protein fraction changes do not Seem fo correlate with the development of such effusion 6) Vascular Tone Normal parturients are less responsive to. vasopressor and chronotropic agonists 8.0]. Epinephrine, soproter fenol, and angiotensin TT all show dose-related blunting. Of effect during pregnancy, Dossn-regulation of alpha und beta-adrenergic receptors us been postulated as the ‘cause of these phenomens. However, the presence of ‘vasodilatory prostaglandins may play a role as wel, since (1) inhibitors of prostaglandin. synthesis have been shown to reverse vasculir unresponsiveness to catechol nines. and (2) toxemic patients whe have an abundance fof sasoconstricting prostaglandins (e.g.. thromboxane) fre more sensitive 10 exogenous catecholamines, Clinical Implications Aortocaval compression should always be avoided. Par turients should not be allowed o rest in the supine posi tion, but rather encouraged to maintain uterine disp ‘ment by a right or (preferably) left Lateral tile of the pels (Fig 2). Sympathetic blockade due to spinal or epidur anesthesia interferes with the mechanisms that compen sate for aortocaval compression, sometimes causing pro:Camano an Osher: Physical Adaplatons Daring Pregnancy $ change Weeks of Gestation Fig 1 Hemodynamic changes daring preg. (Map from Mashini tal (2) Table 1. Maternal Cardiccnlar Alterations a Te Variable Rave) Cardiac oupa we Heart rae 6 Systolic blood pressure 0-5 nm tg Diastolic blood pressire uw 10-20 Bg Total peripheral reaitance | 1s CGenl venous pressure 0 Pulmonary wedge pressure — ” jection fraction 0 Sear: Adopted fou Mashin ol at Sls! SN, Ost daeuhenis Reg Aniea MINED isc, Kepreaced wih pects itm 8 Lippe found hypotension in the absence of adequate uterine dlisplacerment and intravascui volume expansion. Con ditions involving a particularly lige uterus (e.g. mult ple gestation, polyhydramnios, diabetes mellitus) pre- dispose to the risk and consequences of aortocaval compression (6). Engorgement of the epidural vasculature (Batison's plexus) makes puncture oF cannulation of an epidural vein more likely than in the nonpregnant patient during initiation of epidural analgesia, Likewise, negative pres sure in the epidural space may not be consistently Found inthe parturient {10}, theoretically rendering the “hang- ing drop” technique for identification of the epidurs space less successful in the pregnant patient than in non pregnant patients Patients with cardiac disease may tolerate pregnancy poorly. The increased bloox! volume and decreased sys temic resistance may cause decompensation in patients with stenotic valvular lesions and may worsen tight-t left shunting in the presence of uncorrected congenital Postpartum weeks heart defects. In contrast, parturients with regurgitant valvular lesions usually do quite well during pregnancy Although coronary artery disease is rare among women of child-bearing age, gradual rend to older pari may increase the incidence of myoidil chemi, in farction, or both during gestation [11]. ‘The hyper metabolic demands of pregnaney suggest that invasive monitoring be considered in pattarients with known oF suspected atherosclerotic, spastic, or thrombotic core: nary artery disease. In addition, the differential dag: nosis of hemodynamic instability ftom any cardiac tiological factor should inclide echocardiographic evaluation to rule out pericardial etfusion, RESPIRATORY SYSTEM. The Upper Airway Whereas generalized peripheral edema is common i sance in pregnancy, edematous ehanges at the upper airway may be life threatening. Mucous membranes be come extremely friable during the third trimester, and ‘manipulation of the upper aitway, sch as may occur luring insertion of nasal airways or masogasttie tubes, oF heal intubation, should! be done with during nasotr great care to avoid severe bleeding. Toxemie patients are particularly susceptible to airway ane vocal cord eden [12}. The possibility of technically dificult intubation ve= ‘quiting small-diameter endotache 6.0 mm ‘or less) should always be kept inn such patients tubes tie nd when caring for Respiratory Mechanics The expanding uterus produces cephalad displacement of the diaphragm: thus, functional residual capacity (FRC) is decreased {13}, Total lang capacity, vita capa4 International Aneel Clini Vl 28 No 1 Winter 1990 Fig 2. Aetoavaldrcomprsan ih I lara Table 2. Maternal Respiratory Alterations a Ter Variable “Change Rate Minute veniaion i. 0 Alveolar ventilation tittt ‘Tidal volume ttt 0 Respiratory rate t 6 losing volume = 0 ‘Away resistance u 7 Vital expacty : ° Inspiratory hang capacity : ° Fantionalresdval capacity Ld Pn Total ung eapaciy = ” Expiratory reserve volume Lb Pn Residual volume uw 20 ‘Onygen consumption 1 20 Stare: Saree SoatoSN- Reprose ah ern fy Table 3 Acid Base Values in Pres er the Neng Site Variable ‘Nenpregnan State Pregnancy pH Ta Te TMT Pos (mm Ha won 0-110 Pes (mm Hg) ey ity, and inspiratory capacity all remain unchanged, bow fever, because of compensatory subcostal widening ad ‘enlarging of the thoracie anteroposterior diameter [14 ‘The increased oxygen consumption of pregnancy is ‘compensated by a 70% increase in alveolar ventilation at term [15], This is accomplished by increases in both tidal volume (408) and respiratory rate (15%). Enhancement of tidal volume is hargely dite to rib cage volume displace ment, and Jess $0 10 abo ment [14]. The rise in ‘oxygen demands of the parturient and i probably are sult of elevated. progesterone levels, which increase the ventilatory response to carbon dioside [16] (Table 2) Gas Exchange Ventilatory augmentation produces a respiratory al kalosis with compensatory renal excretion of bicarbonate and, hence, partial pH correction [15]. Oxygenation is improved during normal pre are typically slightly higher (fable 3). Physiological dead space at cerm is decreased [17]. This likely that increased cardiac output with favor- able ventilation: perfusion matching in upper lung zones accounts for both the increased Po. values and the de- ‘creased dead space. Clinical Implications “The decreased FRG is aswally of litle concern to the normal parturient. However, conditions that decrease losing volume (otherwise unchanged in normal preg- nan} stich as smoking, obesity, oF kyphoscoliosis, may result in airway closure and increasing hypoxemia as pregnancy. progresses [18]. The relationship beoveen ERC and closing volume may be further aggravated by the positions assumed using birth (Trendetenburg, lithotomy, andl supine) and by induetion of general anes: thesia [19]. One should therefore have a low threshold for administration of supplemental oxygen to the parte ent in labor, particularly during episodes of fetal dis tress oF prior to induction of general anesthesia. The decreased! FRC implies that preoxygenation (denitroge- nation) can occur more rapidly in the parturient than in the nonpregnant woman, and indeed thisis the case [20] However, the marked inevease in oxygen consumption contributes to the frighteningly rapid development of ‘maternal hypoxemia during periods of apnea (21). The decrease in dead space serves to enhance further the reliability of noninvasive respiratory monitoring (eap- ography and/or mass spectiomenty), as the yap De and arterial gas measurements narrows GASTROINTESTINAL SYSTEM Elevated levels of circulating progesterone dec trointestinal motility, decrease Tood absorption,lower esophageal sphincter pressure [23]. In addition, elevated gastrin levels (of placental origin) result in more acidic gastric contents [24]. The enlarged uterus in creases intragastric pressure and decreases the normal ‘oblique angle of the gastroesophageal junction. Clinical Implications ‘These gastrointestinal tract alterations mean that the parturient should always be considered to have a full stomach, regardless of the actual number of hours lapsed since the last meal. Consequently, pregant p tients should always be considered at risk for aspitation of gastric contents (Mendelson’s syndrome), and sures should be taken 10 minimize this risk, Moreover, pain, anxiety, and treatment with narcotic analgesics serve to retard further gastric emptying during labor [25]. Maternal "bearing down’ efforts and the lithotomy position during the second stage of labor and delivery. coupled with incompetence of the lower esophageal sphincter silent regurgitation and pul monary aspiration more common than we often realize Our practice i to require oral administration of 30 ml of a nonparticulate antacid (0.3 M sodium citrate oF its equivalent) belore the initiation of any anesthetic. This agent rapidly decreases the acidity of gastric contents and helps ameliorate the consequences of Histamine receptor (H2) antagonists such as cimetidine (Tagamet) oF ranitidine (Zantac) may be administered ‘orally the evening before, and orilly oF intravenously the morning of an elective procedure, Metoclopramid (Reglan) stimulates gastric emptying, increases lower ‘esophageal sphincter tone, and serves as a centally act ing antiemetic. Metoclopramide has been very” use ful in parturients who have eaten it large meal shortly before arriving atthe labor suite as wells in diabetic pa tients, whose disease results in inherently slow gastric emptying, HEMATOLOGICAL SYSTEM. volume and red cell mass increase above values, but the increase in the former fat ease in the later, A “dilutionsal” ane therefore ensues [3] (Fable 4). Blood viscosity ‘gen content both decrease. ated, as are coagulation faciors 1, VL, X, and XUL ‘Thrombocytopenia may, however, be seen nor imal pregnant patients in the absence of any other hhematopathology [26,27]. Systemic hbvinolysis i i decreased from normal levels Clinical plications ‘The physiological “anemia of pregnancy” (normal hema: toerit 35%) is usually of kite concern to the normal pa turient, as increases in cardiac output serve actuals 10 crease oxygen delivery to tissues. The increase in cosy ulation factors (Fable 5) renders pregnaney a “hypercor with a consequent increase in the in: Camann and Oxhvimer:Physlgcal Adaptations During Pregnancy Table 4 Maternal Hematologeat Aoratons tim Variable Change ae Blood wiume tit ™ Plasma volume tin % Enythroeste volume 1 0 Blood wea nitrogen ade ss Plana chobinesterase is 20 oral protein ' « Albumin 1 4 Globulin + 0 AST, ALT, LDH 1 Cholesterat 1 Allaline phomphatase tt produced by places) bit > Wie debsdrogenase Sure: Shatedll MN Onener GAY: Msg hangs daring Pj efles nao seial anes Reg Ate Tost 28—a Reproduccd wth ponte Lyon Cn sai rial Table 5. Congdon Fates and ohio slur Normal Propane Factor Tate Preguaney Factor I hibrinoen Factor I (prothrombi Factor V Factor V “10-150 mal Factor Factor IN Factor N Factor NI Factor NIL Platclers Bi ‘Slight 1 Siig ays dence of thrombotic events (e.g.. deep venous and cortical vein thrombosis), Enhanced clotting, coupled with the expanded blood volume, affords teleological protection to the parturient against the effects af bleed ing at the time of delivery RENAL SYSTEM Renal hemodynamics undergo profound changes dir ing gestation [28]. Marked increases in (80% above normal) occur by the midlle trimester and then decline slightly by term. Glomerular filtration rate (GFR) increases 10 5077 aboxe prepregiant values by the sixteenth gestational week atic remains 90 until delivery (Fig 3). Consequently, 24-hon clearance values are elevated, a chinge discern le6 International Anesthesiology Cher Vol 28 No 1 Winter 1990 ten Weeks of peru) pregant i Fig 3. Renal faction during pogo (Rrpraduce vith prison fram Daven (25). carly as the eigth week of gestation. Glyeosuria is com mon in normal pregnanes, owing to both alterations in tubular reabsorptive capacity and the increased load of ‘glucose presented by the increased GER. While these changes are noted in early pregnancy, implying a hor ‘onal stimulus, the exact mechanism is as yet unknown, Increased levels of aldosterine, cortisol, and human pl cental lactogen all contribute to the multifactorial renal adaptations to pregnancy. Pro uses dilation Of the renal pelvis and ureters, Hence, the incidence of urinary tract infections is increased, particularly alter i strumentation of the urinary bladder [29]. (Clinical plications Laboratory determinations of renal function are so ab tered that great care must be exercised when “normal nonpregnant values are applied to the pregnant woman, For example, “normal” values of blood urea nitrogen and creatinine in a preeclamptic or diabetic patient may actually indicate serious rensl compromise; in contrast Such values may indicate hypovolemia in a parturient with otherwise normal renal function. Although glucose excretion is enlunced during prey nancy, excessive administration of glucose to patients during labor may result in both maternal hyperglycemia and initial fetal hyperglycemia, Resultant fetal hyperin sulinemia persists after delivery, however, and a reactive neonatal hypoglycemia may’ ensue [30] Serum electrolyte values are unchanged during preg: nancy. Expansion of plasma volume must therefore be accompanied by electtolyte retention. A. primary reset ting of thirst and vasopressin osmoreceptors allows the pregnant womisn to maintain internal homeostasis dar ing this volume-expanded state, Le., the threshold for antidiuretic hormone secretion is reset at lower level of plasma sodium, thus allossing volume expansion without Accompanying diuresis. The antecedent stimulus for this ‘adaptation has yet to be elucidated [28} CENTRAL NERVOUS SYSTEM. Emotional, social, and cultural factors all contribute to the parturient’s psychological miliew during labor and delivery [31-34], Pregnancy is a stressful experience, and wide mood swings during gestation, delivery, and the postpartum period can be expected. hormonal basis for this emotional lability has been proposed inas- much as progesterone and endogenous endorphins act as both neurotransmitters and analgesis, Progesterone and endorphins also serve to decrease minimal alveolar concentration (MAG) ofall inhaled anesthetic agents [35 36]. In addition, reduced enzymatic degradation of opioids at term contributes (o elevated pain thresholds (37) Reduced doses of local anesthetic (LA) agents are re {quired for spinal and epidural anesthesia compared with doses for nonpregnant patients (38), Vascular conges tion in the epidural space contributes to the decreased LA requirement through thtee mechanisms 1, Reduced volume in the epidural space facilites spread of a given dose af LN aver wider number of dermatomes 2, Increased pressure within the epidural space facil tates dural diffusion aad higher cerebrospinal Hud levels of LA. 3. Venous congestion of the lateral foramina decreases ‘egress of LA via the dural root sleeves. The respiratory alkilosis of pregnaney may enhance LA action by increasing the relative concentration of un: charged LA. molecules, sshich facilitates. penetration through neural membranes, This decreased require ment for LA is seen as early as the first trimester, Hor rmonal changes may be operative xs well, since progester- fone has been shown ite with enhanced ‘conduction blockade in isl ations (39, 40). MISCELLANEOUS Musculoskeletal Placental procluction of the hormone relaxin stimulates generalized ligamentous vekasation [41]. Particularly no: table is the widening of the pelvis in preparation for fetal passage, resultant "hese-down” ult seen when the parturient assumes the literal position, and compensi tion should be mace wher the anesthesiologist performs regional anesthesia (Fig 4) Generalized vertebral collagenous softening, coupled with the burden of a gravid sterus, increases the lumbar lordosis. ‘echnical difficuliy with regional anesthesia tay result. In addition, these changes account for the high incidence of back pain and sciatica during. preg nancy, complaints whieh, per se, do not represent con: traindications to regional anesthesia [42]. Stress fractures of the weight-bearing bony pels have also been noted especially during difficult deliveries [43]ig 4, Pee wadening ad vata hed ltl ps tio daring organs Upper pune! = ogame) Dermatological Hyperpigmentation ofthe face, neck (chloasma or “mask ‘of pregnancy"), and abdominal midline (lives mgt) are due to the effects of melanocvte-stimabiting hornon (MSH), a congener of adrenoconticotropie horton (ACTH), Levels of MSH increase markedly during the first trimester and remain elevated until after delivery 44), Mammary Breast enlargement is typical in orm pregnancy and is a result of human placental hitogen secretin, Essangedd breasts in an obese parturient with a short neck may lea to difficult laryngoscopy and intubation, Use of short hhandled laryngoscope can be extremely helpful in these patients [45] (Fig 5) Ocular Conjunctival vasospasm ane subconjunetional hemor shage are occasionally seen, especially daring maternal expulsive efforts, and in preeelamptic patients [46}. The retina may manifest focal vaseular spasm, detachment and retinopathy associated with hypertensive disorders. Central setous choroidopathy, oF a breakdown of the blood-retina barrier, may occur even in the absence of hypertension, Intraocular pressure is lower duing pre perhaps a result of progesterone and rekixin fects (hich facilitate aqueous outflow) and human chorionic sxonadotropin (which depresses aqueous humor produc: tion). Corneal thickening. a manifestation ofthe gener ized eclema of pregnancy, may produce mild visual di turbances and contact lens intolerance during gestation (7) INTRAPARTUM CHANGES, Active labor magnifies many of the physiological vari ables already altered during gestation. Although the Cameun an Osthrins: Pela Adaptations During Prrgnanry 7 i ) » Fig 5. Use of sont honed arog for lane partnen owed ine dicate rein ary Ire tne eh ping rigors of labor are usually well raleated, the limited re serves of the term parturient may sonetianes be stressed in ways not benelicial to mother ot fetus, Cardiovascular Stem Cardiae output during. active labor rises uo approxi nately twice prelabor valies, with the ruaximval erease seen in the immediate postdelivery period (Fig 6). The rise in cardiac output is multifactorial. First, pain andl anxiety during labor inerease nsaternal circuk cholamines with st resultant tachycardia ann in stroke volume [48]. Second, uterine contractions resilt in eyelic autotranstusion and increased central blood vol lume, This augmentation of preload in the setting of nor imal (or hyperdynamic) ventricular funetion contributes to inereased cardiac output via Frank-Starling mecha: Adequate regions anesthesia can ameliorate manty the pain-mnediated hemodynamic consequences of libor. Uterine contractions. however, will sill case t autotransfusions of blood with elevation of central vase lar pressures, Respiratory Sistem Hyperventilation is common during labor. This may be natural response 10 pain or the result of various pte= pated childbirth methods in which repetitive, panting breathing techniques are useel. Hyperventilation during, labor in the setting of an already lowered material PaCOz at term may result in chngerons degrees of a kalemia. Women who have received narcotic analgesics during labor may alternate periods of hyperventilation with marked hypoventilation between eonitractions, re sulting in wid swings in PaCOs [49}, The lar response to hypocatbis is vasoconstriction an subse ‘quent decreased placental perfusion [50]. ‘Thus the potential for fetal hypoxemia exists during episodes of ‘maternal alkalemia, particularly if a fetus is already comm promised for other reasons. Regional anesthesia during labor obvi tes the need for8 International Anrtrilgy lines Vol 28 No E Winer 1980 Percent Change trom Cor ao ro Fig 6, Candivasculr aration during lab. Rented with pr tation fam Ser 8 evuson€. Anshan 2d Tatrmor: Willan & Watkny, 1987-040) breathing techniques" and eliminates pain-indueed hy perventilation, so patients with marginal placental re- Serve (from preeclampsia, diabetes, postiature pre nancy, oF small abruptio phicentae, for example) are strong, candidates for epicaral analgesia 1 la Metabolic Eject The homeostatic milieu that develops during gestation undergoes marked changes during labor. Metabolic acidosis may accur for several reasons. Ftst, prolonged labor, especially in the setting of inaclequate intravenous hhydration, sometimes contributes to elevated lactate andl pyruvate levels [31]. Secon, muscular activity, de 10 pin, shivering, oF respiratory muscle demands. a 0 cic metabobites in the maternal circulation. Lied. ma ternal alkalemia may predispose to compensatory acid retention, Overall maintenance of normal acid-base status during labor is accomplished by the balance of what may be markedly altered (es nonpregnant) levels of acidemic and alkalemic mediators, Thus, situations that Turther aggravate pH balance (e.g. dehydration, vomit ing. ketoacidosis, hypothermia, hemorrhage) may be poorly tolerated by the gravida in labor The common markers of physiological stess (epi nephrine, norepinephrine, and cortisol all increase dr ing labor (52, 53). The magnitude of this increase is blunted by regional anesthesia PUERPERAL RESOLUTION Gardiae output rises shaxply immediately after birth sustained contraction of the emptied uterus results autotranstusion of BIN! 4 750 mil of blood, coincident with elimination of the placental arteriovenous shunt The immediate postpartom period ist bighcrisk time for decompensation in patients with certain cardiae disease states (patticularly stenotic valvular lesions or pulmonary hypertension). Cardiac output xradually returns 10 non: pregnant levels by 2 to 4 acechs after delivery (3) Uterine evieutation and ivolition promote ¥ olution of many of the pulmonary changes induced by mechanical compression othe diaphragm aul Tangs by the gravid uterus. Thus, FRC and tesidual_ volume quickly ret 10 normal, The gradual decline in blood rial progesterone levels is mirrored by a slow rise i Peg and alveolar ventilation yeturns:e normal by 21033 weeks post partum [54 Postpartum diuresis counmon: this diuretic phase ‘contributes to 3 gradual decline in plasm: volume though edt cell mmass venians constant, Chu, the “lil tional” anemia of pregnanny resolves, and the he Crit rises to nonpretiant keels i 2 to seeks. Excessive blood los at delnery markedly alters the enue of hematological resohition. The GER, blood area nite igen, and creatinine levels verti 1 norma in ta 8 weeks [28] “Mechanical effects on the gastrointestinal tat rapidly resolve by 2 40 3 days post partum, However, elevated: levels of progesterone persist and may delay gastric emp: tying for several weeks, Precautions o minitnize the risk and consequences of acid aspitation should therefore be taken if surgery with petiod [55] restless is planed ving this REFERENCES 1. 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