559 Critical Care Obstetrics, 5th edition. Edited by M. Belfort, G. Saade, M. Foley, J. Phelan and G. Dildy. © 2010 Blackwell Publishing Ltd. 40 Hypovolemic and Cardiac Shock Scott Roberts Department of Obstetrics and Gynecology, The University of Texas Southwestern Medical Center (UTSMC) at Dallas, TX, USA Introduction Hemorrhage is one of the leading causes of pregnancy - related mortality in the United States (2.0/100 000 live births) second only to embolism (2.3/100 000 live births) (Table 40.1 ) [1] . Almost 99% of maternal deaths occur in developing countries. Immediate postpartum hemorrhage (PPH), defi ned as excessive blood loss within 24 hours after childbirth, is the single most important cause of maternal death worldwide, accounting for almost half of all postpartum maternal deaths in developing countries [2,3] . In the United States, hemorrhage was the leading cause of death after stillbirth (from abruptions and uterine rupture), and accounted for 93% of deaths associated with ectopic pregnancies. Hemorrhage was also prominent as a cause of death in pregnan- cies ending in induced or spontaneous abortion (21.8%) [1] . These deaths are mediated through hypovolemic shock which is also responsible for a number of other serious non - fatal compli- cations, including acute renal failure, acute respiratory distress syndrome (ARDS), and more rarely, postpartum pituitary necro- sis. The parturient undergoes several important physiologic adaptations during pregnancy to protect her from the bleeding expected at the time of delivery. Peripartum complications can occur quickly and since the uterus receives a blood fl ow of 450 – 650 mL/min quick, decisive, and coordinated action on the part of the practitioner and supporting staff can be life - saving [4] . Shock is perhaps best defi ned as reduced tissue oxygenation resulting from poor perfusion [5] . Low fl ow or unevenly distrib- uted fl ow from hypovolemia and disproportionate vasoconstric- tion are major causes of inadequate tissue perfusion in the acutely ill patient with circulatory dysfunction or shock. In hemorrhagic shock, the disparity is a result of blood loss that leads to both compensatory neurohormonal activation as well as the release of various endogenous mediators, which may aggravate the primary physiologic effects of hypovolemia [6 – 8] . Because the purpose of the circulation is to provide oxygen and oxidative substrates for metabolic requirements, insuffi cient tissue perfusion and oxy- genation to support body metabolism is the common circulatory problem of acute critical illness. This inadequate perfusion leads to local tissue hypoxia, organ dysfunction, multiple organ failure, and death. Blood fl ow to the capillary beds of various organs is controlled by arterioles, which are resistance vessels that in turn are con- trolled by the CNS. On the other hand, 70% of the total blood volume is contained in venules, capacitance vessels controlled by humoral factors. Hypovolemic shock evolves through several pathophysiologic stages as body mechanisms combat acute blood volume loss (Table 40.2 ). The diagnosis of shock is most often made by the presence of hypotension, oliguria, acidosis, and col- lapse in the late stage, when therapy is frequently ineffective. Early in the course of massive hemorrhage, there are decreases in mean arterial pressure (MAP), cardiac output (CO), central venous pressure (CVP), pulmonary capillary wedge pressure (PCWP), stroke volume and work, mixed venous oxygen saturation, and oxygen consumption. Increases are seen in systemic vascular resistance (SVR) and arteriovenous oxygen content differences. These latter changes serve to improve tissue oxygenation when blood fl ow is reduced [9] . Catecholamine release also causes a generalized increase in venular tone, resulting in an autotransfu- sion effect from the capacitance reservoir. These changes are accompanied by compensatory increases in heart rate, SVR and pulmonary vascular resistance, and myocardial contractility. Redistribution of CO and blood volume occurs via selective arte- riolar constriction mediated by the CNS. This results in dimin- ished perfusion to the kidneys, gut, skin, and uterus, with relative maintenance of blood fl ow to the heart, brain, and adrenal glands. In the pregnant patient, such redistribution may result in fetal hypoxia and distress, even before the mother becomes overtly hypotensive. In such situations, the uterus is, from a teleologic viewpoint, relatively less important than the essential life - saving organs systems. Regardless of the absolute maternal BP, Chapter 40 560 signifi cant maternal shock is highly unlikely in the absence of fetal distress [10] . Peripheral vasoconstriction caused by the adreno- medullary stress response is an initial reaction to blood loss that maintains pressure in the presence of decreasing fl ow. This vaso- constriction, however, is disparate and leads to unevenly distrib- uted microcirculatory fl ow. These early changes precede the development of organ failure. In the presence of continued hypo- volemia, the stress response may result in poor tissue perfusion, tissue hypoxia, covert clinical shock, organ dysfunction, ARDS, and other organ failure [11,12] . As the blood volume defi cit approaches 25%, such compensa- tory mechanisms become inadequate to maintain CO and arterial pressure. At this point, small additional losses of blood result in rapid clinical deterioration, producing a vicious cycle of cellular death and vasoconstriction, organ ischemia, loss of capillary membrane integrity, and additional loss of intravascular fl uid volume into the extravascular space [13,14] . Increased platelet aggregation is also found in hypovolemic shock. Aggregated platelets release vasoactive substances, which cause small vessel occlusion and impaired microcirculatory per- fusion. These platelet aggregates can embolize to the lungs and be a factor contributing to respiratory failure, which is often seen following prolonged shock. Table 40.2 Clinical classifi cation of maternal hemorrhage. Class Blood loss (mL) Volume defi cit (%) Signs and symptoms I ≤ 1000 15 Orthostatic tachycardia ( ↑ 20 bpm) II 1001 – 1500 15 – 25 ↑ HR 100 – 120 bpm Orthostatic changes ( ↓ 15 mmHg) Cap refi ll > 2 sec Mental changes III 1501 – 2500 25 – 40 ↑ HR (120 – 160 bpm) Supine ↓ BP ↑ RR (30 – 50 rpm) Oliguria IV > 2500 > 40 Obtundation Oliguria - anuria CV collapse BP, blood pressure; bpm, beats per minute; CV, cardiovascular; rpm, respirations per minute; RR, respiratory. From Eisenberg M, Copass MK, eds. Emergency Medical Therapy . Philadelphia: WB Saunders, 1982: 40. Table 40.1 Causes of pregnancy - related death, by outcome of pregnancy and pregnancy - related mortality ratios (PRMR * ) – United States, 1991 – 1999. Cause of death Outcome of pregnancy (% distribution) All outcomes (n = 4200) Livebirth Stillbirth Ectopic Abortion † Molar Undelivered Unknown Percent PRMR (n = 2519) (n = 275) (n = 237) (n = 165) (n = 14) (n = 438) (n = 552) Embolism 21.0 18.6 2.1 13.9 28.6 25.1 18.3 19.6 2.2 Hemorrhage 2.7 21.1 93.3 21.8 7.1 8.7 8.7 17.2 2.0 PIH § 19.3 20.0 0 0.6 0 12.3 11.8 15.7 1.8 Infection 11.7 18.9 2.5 33.9 14.3 11.0 12.9 12.6 1.5 Cardiomyopathy 10.1 5.1 0.4 1.8 0 3.4 11.2 8.3 1.0 CVA ¶ 5.7 0.7 0 1.2 0 3.9 8.5 5.0 0.6 Anesthesia 1.8 0.7 1.3 9.7 0 0 0.4 1.6 0.2 Other * * 17.1 14.9 0.4 16.4 50.0 33.6 27.9 19.2 2.3 Unknown 0.6 0 0 0.6 0 2.1 0.4 0.7 0.1 Total † † 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 * Pregnancy - related deaths per 100 000 livebirths. † Includes spontaneous and induced abortions. § Pregnancy - induced hypertension. ¶ Cerebrovascular accident. * * The majority of the other medical conditions were cardiovascular, pulmonary, and neurologic problems. † † Percentages might not add to 100.00 because of rounding. From Centers for Disease Control and Prevention. Pregnancy - related mortality surveillance – United States, 1991 – 1999. MMWR 2003; 52: 55 – 62. Hypovolemic and Cardiac Shock 561 gland may undergo ischemic necrosis. Sheehan and Murdoch fi rst described the syndrome of hypopituitarism secondary to postpartum hypotension as result of hemorrhage [19] . This con- dition is now a rare complication in modern obstetrics. The clini- cal presentation can vary, but secondary amenorrhea resulting from loss of pituitary gonadotrophs is usually present. In severe cases, thyrotropic and adrenotropic pituitary hormones also may be defi cient. A typical or partial defi ciency syndrome of both anterior and posterior pituitary hormones has been reported. Hypovolemia from any cause leads to reduced renal perfusion, which can result in acute tubular necrosis. In one series, hemor- rhage and hypovolemia were precipitating factors in 75% of obstetric patients with acute renal failure [20] . Prompt blood and fl uid replacement is essential in order to avoid such sequelae. Lung injury may result from hypovolemic shock [21] . In the non - pregnant state, a critical cardiac output exists below which oxygen extraction becomes impaired, and this critical oxygen delivery has been implicated in the pathogenesis of ARDS in humans. The question of a critical oxygen delivery point in human pregnancy is unclear although it has been suggested as a component of the pathology of severe pre - eclampsia [22] . Evans and colleagues pre- sented evidence that in the pregnant sheep model, such a critical cardiac output does not exist [23] . Causes of o bstetric h emorrhage Any disruption in the integrity of the maternal vascular system during pregnancy has the potential for devastating blood loss. As an overview, ectopic pregnancy is the leading cause of life - threatening obstetric hemorrhage in the fi rst half of gestation (see Table 40.1 ). Beyond the fi rst trimester, antepartum obstetric hemorrhage usually results from a disruption of the placental attachment site (involving either a normally implanted placenta or placenta previa) or uterine rupture (spontaneous or trauma related). During the intrapartum period, the likelihood of clini- cal shock is enhanced in patients with pre - eclampsia. Because of the intravascular volume depletion associated with this condition, even the usual blood loss associated with delivery may result in clinical instability. Another pathophysiologic change often associated with pre - eclampsia is thrombocytope- nia, which when severe, may contribute to postpartum blood loss [24] . Most serious obstetric hemorrhage occurs in the postpartum period. The most common cause is uterine atony following pla- cental separation. Under normal conditions, shortening myome- trial fi bers act as physiologic ligatures around the arterioles of the placental bed. Thus, uterine atony with failure of myometrial contraction results in arterial hemorrhage. Factors that predis- pose a patient to uterine atony include precipitous or prolonged labor, oxytocin augmentation, magnesium sulfate infusion, cho- rioamnionitis, enlarged uterus resulting from increased intra- uterine contents, and operative deliveries [10,25] . Physiologic c hanges in p reparation for p regnancy b lood l oss The pregnant woman undergoes profound physiologic changes to prepare for the blood loss that will occur at the time of parturi- tion. By the end of the second trimester of pregnancy, the mater- nal blood volume has increased by 1000 – 2000 mL [15] . The maternal CO increases by 40 – 45% while total peripheral resis- tance decreases [16] . This decreased peripheral resistance results from hormonal factors (progesterone, and prostaglandin metab- olites such as prostacyclin) that reduce overall vasomotor tone and from the development of a low - resistance arteriovenous shunt through the placenta. The decreased peripheral resistance is maximal in the second trimester. About 20 – 25% of the mater- nal CO goes to the placental shunt to yield a blood fl ow of approximately 500 mL/min. Placental blood fl ow is directly pro- portional to the uterine perfusion pressure, which in turn is pro- portional to systemic BP. Any decrease in maternal CO results in a proportionate decrease in placental perfusion. The uterine arte- rioles are very sensitive to exogenous vasopressor substances but because of an incompletely understood pregnancy - related stimu- lus of the renin – angiotensin system, the vasopressor effect of angiotensin appears to be blunted during pregnancy [17] . Thus, during her pregnancy, the mother has been prepared for a blood volume loss of up to 1000 mL. Following a normal spontaneous vaginal delivery, a fi rst - day postpartum hematocrit usually is not altered signifi cantly from the admission hematocrit. In practice, blood loss at delivery is often underestimated. Actual measure- ments show that the average blood loss after normal spontaneous vaginal delivery is over 600 mL [18] . With a postpartum blood loss of less than 1000 mL, the parturient ’ s vital signs may refl ect acute blood loss (i.e., hypotension and tachycardia). During the antepartum period, the obstetrician must be con- cerned with both patients. Fetal oxygenation decreases in propor- tion to the decrease in maternal CO. The catecholamine output from the mother ’ s adrenal medulla may preferentially increase arteriolar resistance of the spiral arterioles in the placental bed, thus further decreasing oxygenation. Under such circumstances, the fetus may be in jeopardy, even though compensatory mecha- nisms maintain stable maternal vital signs. Thus, even in the absence of overt hypotension, the healthcare team must act quickly to preserve fetal well - being by expanding the intravascu- lar volume of an antepartum patient who has lost a signifi cant amount of blood. Although all vital organs receive increased blood fl ow during pregnancy, three organs (other than the placenta) are particularly susceptible to damage when perfusion pressure decreases as a result of hemorrhagic shock. These organs are the anterior pitu- itary gland, the kidneys, and the lungs. During pregnancy, the anterior pituitary enlarges and receives increased blood fl ow. Under the condition of shock, blood fl ow is shunted away from the anterior pituitary gland. As a result, the anterior pituitary Chapter 40 562 Oxygenation The most frequent cause of maternal death from shock is inad- equate respiratory exchange leading to multiple organ failure [11] . The duration of relative tissue hypoxia is important in the accumulation of byproducts of anaerobic metabolism. Thus, increasing the partial pressure of oxygen across the pulmonary capillary membrane by giving 8 – 10 L of oxygen per minute by tight - fi tting mask may forestall the onset of tissue hypoxia and is a logical fi rst priority. Also, increasing the partial pressure of oxygen in maternal blood will increase the amount of oxygen carried to fetal tissue [27] . If the airway is not patent, or the tidal volume is inadequate, the clinician should not hesitate to perform endotracheal intubation and institute positive - pressure ventila- tion to achieve adequate oxygenation. Studies in adult critical care indicate that tissue oxygen debt resulting from reduced tissue perfusion is the primary underlying physiologic mechanism that subsequently leads to organ failure and death [28,29] . It seems that early identifi cation and treatment of hypovolemic shock and its inciting cause is imperative to improving outcome. One approach commonly used to assist the clinician is to classify the degree of hemorrhage from I to IV based on the patient ’ s signs and symptoms (Table 40.2 ). Volume r eplacement Protracted shock appears to cause secondary changes in the microcirculation; and these changes affect circulating blood volume. In early shock, there is a tendency to draw fl uid from the interstitial space into the capillary bed. As the shock state progresses, damage to the capillary endothelium occurs and is manifested by an increase in capillary permeability. Capillary permeability further accentuates the loss of intravascular volume. This defi cit is refl ected clinically by the disproportionately large volume of fl uid necessary to resuscitate patients in severe shock. Sometimes, the amount of fl uid required for resuscitation is twice Obstetric trauma is another common cause of postpartum hemorrhage. Cervical and vaginal lacerations are more common with midpelvic operative deliveries, and as a consequence of an extension of a uterine incision for cesarean birth. Other causes of postpartum hemorrhage (Table 40.3 ) include uterine inversion, morbidly adherent placenta (accreta/percreta), amniotic fl uid embolism, retroperitoneal bleeding from either birth trauma or episiotomy, and coagulopathies of various causes [10,25,26] . Management of h ypovolemic s hock in p regnancy Fundamentally the most important and prerequisite manage- ment tool in approaching hypovolemic shock is a complete understanding of maternal blood volume and how that volume is affected by pregnancy. In 1989, Clark et al. presented central hemodynamic parameters of normal - term pregnancy and contrasted them with non - pregnant values (Table 40.4 ). The calculation and demonstration of a 50% increased blood volume in term pregnancy was delineated by Pritchard et al. in 1965 [15] . So we are to understand that the average pregnant woman has 4.5 – 5 L of total blood volume, not 3 – 3.5 L as in the non - pregnant state. Further, there is a rise in CO of 50% in the term patient, a result of an increased heart rate and stroke volume. There is also a dramatic decrease in SVR and pulmonary vascular resistance. Clark et al. were not able to document increases in left ventricular contractility and we are left with the knowledge that pregnancy is not a hyperdynamic state, but rather a fi nely written (evolved) and adapted symphony of perfect resilience and capacity to perpetuate the gestation. Excesses have also been built into the system to withstand the blood loss of labor and delivery. After delivery, the low resistance placental shunt is turned off and a process of autotransfusion helps to replenish lost volume from the delivery phase. We are fortunate to have repro- duction occur at the zenith of human health in the early adult years. Table 40.3 Common causes of obstetric hemorrhage. Antepartum and intrapartum Placental abruption Uterine rupture Placenta previa Postpartum Retained placenta Uterine atony Uterine rupture Genital tract trauma Coagulopathy Table 40.4 Central hemodynamic changes. Non - pregnant Pregnant Cardiac output (L/min) 4.3 ± 0.9 6.2 ± 1.0 Heart rate (beats/min) 71 ± 10.0 83 ± 10.0 Systemic vascular resistance (dyne/cm/sec − 5 ) 1530 ± 520 1210 ± 266 Pulmonary vascular resistance (dyne/cm/sec − 5 ) 119 ± 47.0 78 ± 22 Colloid oncotic pressure (mmHg) 20.8 ± 1.0 18.0 ± 1.5 Colloid oncotic pressure – pulmonary capillary wedge pressure (mmHg) 14.5 ± 2.5 10.5 ± 2.7 Mean arterial pressure (mmHg) 86.4 ± 7.5 90.3 ± 5.8 Pulmonary capillary wedge pressure (mmHg) 6.3 ± 2.1 7.5 ± 1.8 Central venous pressure (mmHg) 3.7 ± 2.6 3.6 ± 2.5 Left ventricular stroke work index (g/m/m − 2 ) 41 ± 8 4 8 ± 6 Reproduced with permission from Clark S, Cotton D, Lee W, et al. Central hemodynamic assessment of normal term pregnancy. Am J Obstet Gynecol 1989; 161: 1439 – 1442. Hypovolemic and Cardiac Shock 563 risk of FFP includes disease transmission, anaphylactoid reac- tions, alloimmunization, and excessive intravascular volume [34] . Massive blood replacement is defi ned as transfusion of one total blood volume within 24 hours. The NIH consensus confer- ence report noted that pathologic hemorrhage in the patient receiving a massive transfusion is caused more frequently by thrombocytopenia than by depletion of coagulation factors. This fi nding was demonstrated in a prospective study of 27 massively transfused patients in whom levels of factors V, VII, and IX and fi brinogen could not be correlated with the number of units of whole blood transfused [35] . A study of combat casualties sug- gested the thrombocytopenia was more important than depletion of coagulation factors as a cause of bleeding in massively trans- fused patients [36] . In this report, restoration of the prothrombin times (PT) and partial thromboplastin times (PTT) to normal with FFP had little effect on abnormal bleeding; however, platelet transfusions were effective. There is no evidence that routine administration of FFP per a given number of units of RBCs decreases transfusion requirements in patients who are receiving multiple transfusion and who do not have documented coagula- tion defects [37] . Thus, during massive blood replacement, cor- rection of specifi c coagulation defects (fi brinogen levels < 150 mg/ dL) and thrombocytopenia (platelet count < 30 000/mL) will minimize further transfusion requirements. With massive obstet- ric hemorrhage (the usual reason for hypovolemic shock) coagu- lation factors as well as red blood cells are lost. Specifi c replacement with PRBC ’ s and crystalloid solution may lead to dilutional coag- ulopathy and subsequently more blood loss. In acute hemorrhagic shock, central venous pressure (CVP) or pulmonary capillary wedge pressure (PCWP) refl ect intravas- cular volume status and may be useful in guiding fl uid therapy. In the critically ill patient, however, CVP may be a less reliable indicator of volume status due to compliance changes in the vein walls [38] . The clinician must use resources on hand to correct the volume defi ciency. Central hemodynamic monitoring equipment, and personnel to introduce and maintain it, are not commonly present in the obstetric delivery suite or labor area. Again, we digress to the obstetrician ’ s fundamental knowledge of maternal volume in pregnancy, and how that may be authenticated by her current condition (e.g. pre - eclampsia or abruption). In the absence of diuretic use (an unusual if not proscribed therapy during the conduct of labor and delivery, or preparations for elective cesarean delivery); urine output measured with indwelling Foley catheter and drainage will provide approximate and important information about maternal volume and intravas- cular status in real time. The operative or treating physician ’ s time is best confi ned to eliminating the focus of hemorrhage and relying on simple and adequate techniques for assessing patient response to resuscitation measures. Serial hematocrit, platelets, fi brinogen, PT, and PTT can monitor the hemoglobin and coagu- lation integrity in the maternal vascular tree. Urine fl ow should be maintained between 30 and 60 cc/h. the amount indicated by calculation of blood loss volume. Prolonged hemorrhagic shock also alters active transport of ions at the cellular level, and intracellular water decreases. As can be appreciated from Table 40.3 most instances of hypo- volemic shock in obstetrics are hemorrhagic and immediate. Although optimal measurements of this process may certainly document its severity, quick action and volume replacement is essential to optimizing outcome of the patient. The two most common crystalloid fl uids used for resuscitation are 0.9% sodium chloride and lactated Ringer ’ s solution. Both have equal plasma volume - expanding effects. The large volumes of required crystal- loids can markedly diminish the colloid osmotic pressure (COP). Fluid resuscitation in young, previously healthy patients can be accomplished safely with modest volumes of crystalloid fl uid and with little risk of pulmonary edema. The enormous volumes of crystalloids necessary to adequately resuscitate profound hypo- volemic shock, however, will reduce the gradient between the COP and PCWP and may contribute to the pathogenesis of pul- monary edema [30] . Unfortunately, only 20% of infused crystalloid solution remains intravascular after 1 hour in the critically ill patient. Their use should be limited to immediate resuscitation and perfu- sion as the clinician orders and awaits the arrival of blood prod- ucts. Crystalloid solutions such as lactated ringers and normal saline also help to replenish intracellular water and electrolytes, and help to correct metabolic derangement created by the hemor- rhagic and resuscitative event [31] . Recently, data supporting the use of colloid solutions (e.g. 5% albumin) in the active resuscita- tion of patients have come under re - evaluation. No trial or analy- sis has purported to show any benefi t for the use of colloids over crystalloids and some have suggested increased mortality with the use of colloids [32] . The most effective replacement therapy for lost blood volume is its replacement with whole blood. The immediacy of obstetric hemorrhage may, at times, demand this. Modern blood transfusion practice emphasizes the use of cell components or component hemotherapy rather than whole blood. Red blood cells are administered to improve oxygen deliv- ery in patients with decreased red cell mass resulting from hemor- rhage. A National Institutes of Health (NIH) consensus conference concluded that transfusion of fresh frozen plasma (FFP) was inappropriate for volume replacement or as a nutritional supple- ment [33] . In the past, up to 90% of FFP use was for volume replacement. The other 10% was for the following conditions approved by the NIH consensus conference: replacement of iso- lated coagulation factor defi ciencies, reversal of coumarin effect, antithrombin III defi ciency, immunodefi ciency syndromes, and treatment of thrombotic thrombocytopenic purpura. The current concern for excessive use of FFP is at least threefold. Firstly, the high profi le of cost containment has caused blood banks to reevaluate use of blood products and the time involved in their preparation. Second, the routine use of FFP compromises the availability of raw material for preparation of factor VIII concen- trates for hemophiliacs. Third, with regard to recipient safety, the Chapter 40 564 and aroyl preparations delivered in the third stage of labor were more effective than rectal misoprostol in the prevention of post- partum hemorrhage [42] . In cases of persistent vaginal bleeding, careful exploration of the vagina, cervix, and uterus is performed. The clinician looks for retained products of conception or lacerations. For hemor- rhage resulting from uterine atony that has failed to respond to the previously described conservative measures, as well as in cases of extensive placenta accreta or uterine rupture not amenable to simple closure, laparotomy and hysterectomy may be indicated. If the patient does desire future fertility and is clinically stable, uterine artery ligation or stepwise uterine devascularization has been favorably described [43,44] . The fundus compression suture as described by B - Lynch has also been reported to abate uterine hemorrhage in many cases [45] . Rarely, hypogastric artery ligation is surgically necessary. Balloon occlusion and embolization of the internal iliac arteries have also been described in cases of placenta percreta [46,47] . A good discussion of many of these techniques, as well as a more comprehensive discussion of techniques for achieving medical and surgical hemostasis in patients with postpartum bleeding, have been described elsewhere [48,49] . It should be emphasized that preventable surgical death in obstetrics may, on occasion, represent an error in judgment and a reluctance to proceed with laparotomy or hysterectomy, rather than defi ciencies in knowledge or surgical technique. Proper management of serious hemorrhage requires timely medical and surgical decision - making as well as meticulous attention to the aforementioned principles of blood and volume replacement. Cardiogenic s hock This type of shock is caused by failure of the heart as an effective pump. In the obstetric patient this most often occurs in the patient with pre - existing myocardial disease, peripartum cardio- myopathy, congenital or acquired valvular heart disease, and certain cardiac arrhythmias. It is important to remember that ischemic changes in the heart may be induced in the settling of hypovolemic and septic shock [50] . Common causes of cardiogenic pulmonary edema in preg- nancy are diastolic heart failure due to chronic hypertension and obesity, leading to left ventricular hypertrophy [51,52] . Cyanotic congenital heart disease leads to ischemic changes with increasing right to left shunting due to normal decreases in systemic vascular resistance in pregnancy [53] . Patients with Eisenmenger syn- drome can develop right heart failure and cardiogenic shock as pulmonary hypertension worsens temporarily [54] . Pathogenesis Cardiogenic shock is characterized by systemic hypoperfusion in the setting of an adequate intravascular volume. Hemodynamic criteria include sustained hypertension (i.e. systolic blood pres- sure < 90 mmHg), reduced cardiac index ( < 2.2 L/min/m 2 ), and an Initial type and screening of labor and delivery patients can provide valuable information if the need for blood replacement arises in hemorrhagic morbidity. Type - specifi c blood to the patient with Coombs negative blood screens is associated with an acceptably low level of incompatibility of 0.01% [39] . Pharmacologic a gents During the antepartum and intrapartum periods, only correction of maternal hypovolemia will maintain placental perfusion and prevent fetal compromise. Although vasopressors may temporar- ily correct hypotension, they do so at the expense of uteroplacen- tal perfusion. Thus, vasopressors are not used in the treatment of obstetric hemorrhagic shock. Further e valuation After the patient ’ s oxygenation and expansion of intravascular volume have been accomplished and her condition is beginning to stabilize, it is essential for the healthcare team to evaluate the patient ’ s response to therapy, to diagnose the basic condition that resulted in circulatory shock, and to consider the fetal condition. Serial evaluation of vital signs, urine output, acid – base status, blood chemistry, and coagulation status aid in this assessment. In select cases, placement of a pulmonary artery catheter should be considered to assist in the assessment of cardiac function and oxygen transport variables. In general, however, central hemody- namic monitoring is not necessary in simple hypovolemic shock. Evaluation of the fetal cardiotocograph may indicate fetal dis- tress during an acute hemorrhagic episode. As a rule, maternal health trumps fetal health. This means that delivery, under these circumstances, should not be considered until maternal condi- tion has been stabilized. Once the pregnant woman is stabilized and the fetus continues to demonstrate persistent signs of fetal distress, the clinician should then consider delivery. It is impor- tant to realize that as the maternal hypoxia, acidosis, and under- perfusion of the uteroplacental unit are being corrected, the fetus may recover. Serial evaluation of the fetal status and in utero resuscitation are preferable to emergency delivery of a depressed infant from a hemodynamically unstable mother. Hemostasis In certain situations, such as uterine rupture with intraperitoneal bleeding, defi nitive surgical therapy may need to be instituted before stabilization can be achieved. With postpartum hemor- rhage resulting from uterine atony that has not responded to the conventional methods of uterine compression and dilute intra- venous oxytocin, the physician should consider intramuscular methergine or 15 methyl prostaglandin F 2 α . The latter is admin- istered as a 250 - µ g dose, which may be repeated as necessary for up to a maximum of eight doses at 15 – 90 - min intervals. In a small series of patients, rectal administration of misopro- stol, a PGE 1 analogue, has been found effective in the treatment of uterine atony [40] . Other data indicate that rectal misoprostol is no more effective than intravenous oxytocin in preventing postpartum hemorrhage [41] . In a systematic review oxytocin Hypovolemic and Cardiac Shock 565 Pregnancy - associated spontaneous coronary artery dissection (P - SCAD) is the most common cause of myocardial infarction in the immediate postpartum period. In one report 78% of women with peripartum P - SCAD had no risk factors for coronary artery disease and 84% of lesions involved the left anterior descending artery [68] . Successful treatment includes coronary stenting and emergency bypass grafting [69,70] . One review of P - SCAD man- agement concluded that approximately one - third of women could be managed medically with antiplatelet therapy and β - blocker administration and achieve excellent clinical and angio- graphic results [71] . Women who have evidence of atherosclerotic or intracoronary thrombosis are candidates for coronary stenting or the adminis- tration of tissue plasminogen activator (TPA). This large molecu- lar weight molecule should not cross the placenta and has been used successfully in thrombolysis of intracoronary thrombosis during pregnancy [72] . However, TPA is contraindicated in the early postpartum period because the risk of postpartum hemor- rhage is greater than the risk of angioplasty and coronary artery stenting. The foregoing discussion should emphasize the useful- ness of early coronary angiography after acute myocardial infarc- tion in pregnancy. Peripartum c ardiomyopathy Peripartum cardiomyopathy (PPCM) is cardiomyopathy that develops in the last gestational month of pregnancy or in the fi rst 5 months postpartum. By defi nition, it requires that there be no identifi able cause for heart failure and no identifi able heart disease. It is rare in the United States (1 in 3000 to 1 in 15 000) but more prevalent in Africa (1 in 3000), and Haiti (1 in 350). Risk factors include, but are not limited to, the following: older women, obesity, multiparous mothers with multifetal gestation [73] , and may also include pre - eclampsia and severe hyperten- sion during pregnancy [74] . Prior to delivery PPCM presents as a patient with NYHA class III or IV functional status [75] . Patients who present after delivery often have dramatic signs of congestive heart failure. Symptoms may include, but are not limited to, dyspnea, orthopnea, persistent weight retention or weight gain, peripheral edema, nocturnal cough, and profound fatigue post- partum. Evaluation of left ventricular size and systolic function should be performed with echocardiography. Every attempt should be made to rule out other causes of cardiomyopathy. Cunningham et al. evaluated 28 cases of peripartum heart failure of obscure etiology and was able to ascribe underlying causes to all but 7 (25%). The majority of cases on this cohort were due to underlying chronic hypertension, obesity, and forme fruste mitral stenosis that were eliminated by thorough evaluation. In this study, peripartum heart failure was usually precipitated by, or may even have been caused by, a constellation of complications common to pregnancy, namely pre - eclampsia, cesarean delivery, anemia, and infection [76] . elevated fi lling pressure (pulmonary capillary wedge pressure > 18 mmHg). Cardiogenic shock is characterized by a vicious cycle in which decreased myocardial contractility, usually due to ischemia, results in reduced cardiac output and arterial pressure. The cycle continues with hypoperfusion of the myocardium and further depression of maternal cardiac output. Systolic myocardial dys- function reduces stroke volume and, together with diastolic dys- function, leads to elevated LV end - diastolic pressure and PCWP as well as to pulmonary congestion. Reduced coronary perfusion leads to worsening ischemic and progressive myocardial dysfunc- tion and a rapid downward spiral, which, if uninterrupted, is often fatal [55] . Due to the unstable condition of these patients, supportive therapy must be initiated simultaneously with diagnostic evalua- tion. In this circumstance, clinical evaluation of the patient is important in helping to establish a diagnosis and to guide patient management. Blood work including baseline ABG, cardiac tro- ponin, metabolic profi le, hematocrit, and live enzymes should be sent to the lab. ECG, chest X - ray, and echocardiogram should be obtained. There is a split of opinion with respect to the use of pulmonary artery catheterization in patients with suspected car- diogenic shock. However, many clinicians believe that the use of the pulmonary artery catheter provides diagnostic clarity and guidance for clinical management [56 – 59] . Acute m yocardial i nfarction Acute myocardial infarction in pregnancy is a rare event. Recent studies place the incidence at 2.8 – 6.2 per 100 000 deliveries [60,61] . The three strongest independent predictors of myocar- dial infarction in one population were chronic hypertension, diabetes, and advanced maternal age [60] . Case fatality rates have been estimated from 5.1% to 37%; and the most dangerous time for the gravida is in the last trimester of gestation or puerperium [60 – 62] . Women who sustain an infarction less than 2 weeks prior to labor are at especially high risk of death [64] . Myocardial infarction is more common during the third trimester or puer- perium of the fi rst or second pregnancies [65] . Patients typically present with ischemic chest pain in the pres- ence of an abnormal ECG and elevated specifi c cardiac troponin I. Initially the maternal condition should be stabilized by medical management. Nitroglycerin and morphine sulfate should be administered. Oxygen is also a potent vasodilator and should be administered initially by nasal cannula. Ventricular arrhythmia may occur and if left unchecked, can lead to cardiogenic shock or sudden cardiac death. Ventricular defi brillation should be effective in this case. Lidocaine should be started to prevent arrhythmias. In the case where left ventricular dysfunction occurs as a result of ischemic changes, intra - aortic balloon pump has been used to improve left ventricular output and coronary artery perfusion [66,67] . Calcium channel blockers and β - blockers may be used to help decrease afterload. Chapter 40 566 are common in mitral stenosis and should be treated aggressively with intravenous verapamil (5 – 10 mg) or cardioversion, if neces- sary. Because of the increased risk of systemic embolism in patients with mitral stenosis and atrial fi brillation, anticoagulant therapy is indicated. Intrapartum, carefully controlled epidural anesthesia with attention to minimizing preload will decrease anxiety, which causes tachycardia and pulmonary congestion. Choice of route of delivery should be left to the patient as both vaginal delivery and elective cesarean are obstetrically acceptable options. Assuming the patient does not elect a cesarean using a regional anesthetic, instrumental vaginal delivery should be considered to shorten the second stage. Once delivered, the low resistance uterine shunt disappears and “ autotransfusion ” may bring about pulmonary edema (Figure 40.1 ). During pregnancy diuretic therapy may be used to decrease preload along with prophylactic β - blockers to slow the heart rate response to activity and anxiety [83] . Acute pulmonary edema in pregnancy may also occur with the use of tocolytics, pre - eclampsia, and fl uid overload [84] . Arrhythmias Management of cardiac arrest attributable to life - threatening ventricular tachyarrhythmias is essential to prevent sudden cardiac death in the mother and fetus. This requires a correct diagnosis and is usually possible with a 12 - lead surface ECG. Clinical errors can occur in circumstances where medical person- nel believe that a young healthy woman is unlikely to develop a life - threatening ventricular arrhythmia. Ventricular tachycardia (VT) is rare in pregnant women but can originate from either the right or left ventricle in structurally normal hearts [85,86] . If the Treatment of peripartum cardiomyopathy is similar to the treatment of acute and chronic heart failure due to other causes of left ventricular systolic dysfunction. Patients who are con- gested but have adequate perfusion will require treatment with intravenous diuretics alone or in combination with vasodilators such as nitroglycerin or nitroprusside. Patients with diminished perfusion will require augmentation of their cardiac output with inotropic agents such as dobutamine [77] . Beta - blockers are used, since high heart rate, arrhythmias, and sudden death often occur with PPCM. Digitalis, an inotropic agent, is also safe during pregnancy and may help to maximize contractility and rate control. Because of the high incidence of thromboembolism in these patients, the use of heparin is considered medically neces- sary, followed by warfarin (when not pregnant) in those with left ventricular ejection fractions less than 35%. After pregnancy is over, ACE inhibitors are used to reduce afterload by vasodilata- tion. Angiotensinogen receptor blockers may be substituted for those patients intolerant of ACE inhibitors. The acute treatment aims to reduce preload and afterload, and increase contractility. In the setting of cardiogenic shock, invasive hemodynamic monitoring may be helpful in making decisions regarding maternal responses to therapy and the need for additional therapeutics. Since an immune pathogenesis has been postulated, immune modulation with intravenous immu- noglobulin has been proposed [77,78] . However, no consistent benefi t has been demonstrated. If patients remain in cardiogenic shock despite aggressive medical therapy, additional therapies to maintain circulatory support and organ perfusion should be considered. Intra - aortic balloon counterpulsation can be used acutely. Where resources exist, left ventricular assist devices and heart transplantation may be used if clinically indicated [79,80] . Mitral s tenosis Rheumatic mitral stenosis (MS) is the most common clinically signifi cant valvular abnormality in pregnant women and may be associated with pulmonary congestion, edema, and atrial arrhyth- mias during pregnancy or soon after delivery. The contracted valve impedes blood fl ow from the left atrium to the ventricle. The left atrium is dilated, left atrial pressure is chronically ele- vated, and signifi cant passive pulmonary hypertension may develop. Twenty - fi ve per cent of women have cardiac failure for the fi rst time during pregnancy [81] . This has been confused with peripartum cardiomyopathy [76] . With signifi cantly tight MS (surface area < 2.5 cm 2 ) symptoms usually develop [82] . The most common complaint is dyspnea and others may include, but are not limited to, fatigue, palpita- tions, cough, and hemoptysis. Tachycardia shortens diastolic fi lling time and increases the mitral gradient, which raises left atrial and pulmonary venous and capillary pressures and may result in pulmonary edema. Sinus tachycardia is often treated with β - blockers. Atrial tachyarrhythmias, including fi brillation, A 10 20 30 40 3 8 4 7 6 5 2 BC Time PCWP (mm Hg) DE Figure 40.1 Intrapartum alterations in pulmonary capillary wedge pressure (PCWP) in eight patients with mitral stenosis. (a) First - stage labor; (b) second - stage labor, 15 – 30 min before delivery; (c) 5 – 15 min post partum; (d) 4 – 6 h post partum; (e) 18 – 24 h post partum. (Reproduced with permission from Clark SL, Phelan JP, Greenspoon J, et al. Labor and delivery in the presence of mitral stenosis: central hemodynamic observations. Am J Obstet Gynecol 1985; 152: 986.) Hypovolemic and Cardiac Shock 567 pressure) associated with labor. The combined α - and β - blocker labetolol can be titrated (1 – 10 mg/kg/min) to allow rapid control of mean arterial blood pressure during labor and delivery. A split of opinion exists as to the optimal anesthetic for cesarean delivery in these patients. General anesthesia may be indicated in anticoagulated patients, but the hypertensive response to intuba- tion and surgical stimulation may increase cardiovascular stress, promoting rupture or progression of a pre - existing dissection [65] . Summary Cardiogenic shock is quite different from hypovolemic shock, the latter requiring increased preload and the former inotropic support and decreased afterload. Cardiogenic shock occurs infre- quently and calls for consultation, timely decision - making, and diagnostic integration. Pulmonary congestion is the usual pre- senting symptom and has multiple etiologies. Although there is a split of opinion as to the effectiveness of invasive hemodynamic monitoring, accurate diagnosis as to the etiology of heart failure is essential and many experts feel comfortable with this diagnostic modality. Others have demonstrated that non - invasive echocar- diographic modalities to estimate cardiac parameters are reason- ably accurate [97] . Obstetricians should have a working knowledge of maternal hemodynamics in pregnancy and should avail them- selves of frequent cardiology and maternal – fetal medicine con- sultation. Responding to postpartum hemorrhage should be fairly straightforward in most but not all instances. Cardiogenic shock (and its imitators) should be suspected in the setting of pulmonary congestion and myocardial infarction. In many of these circumstances, timely consultation and a multidisciplinary approach can enhance maternal and fetal outcome. References 1 Center for Disease Control and Prevention . Pregnancy - related mortality surveillance – United States . MMWR 2003 ; 52 (Suppl 2 ): 1991 – 1999 . 2 McCormick M , Sanghvi H , Kinzie B . Preventing postpartum hemor- rhage in low - resource settings . Int J Gynecol Obstet 2002 ; 77 : 267 – 275 . 3 Li X , Fortney J , Katelchuk M , et al. The postpartum period: the key to maternal mortality . Int J Gynecol Obstet 1996 ; 54 : 1 – 10 . 4 Edman C , Toofanian A , MacDonald P , et al. Placental clearance rate of maternal plasma and rostenedione through placental estradiol for- mation . Am J Obstet Gynecol 1981 ; 141 : 1029 – 1037 . 5 Shoemaker W . Diagnosis and treatment of shock and circulatory dysfunction . In: Grenvik A , Ayers S , Holbrook P , Shoemaker W , eds. Textbook of Critical Care , 4th edn . Philadelphia : WB Saunders : 2000 . 6 Pullicino E , Carli F , Poole S , et al. The relationship between circulat- ing concentrations of interleukin - 6, tumor necrosis factor, and the acute phase response to elective surgery and accidental injury . Lymphokine Res 1990 ; 9 : 231 – 238 . pregnant patient has structural heart disease VT carries a poor prognosis [87] . Acutely, it is important to determine whether VT is hemody- namically stable or unstable. If at any time the patient becomes unstable or there is evidence of fetal compromise direct - current (DC) countershock (50 – 100 J) should be delivered immediately [88] . Conservative therapy is appropriate for sustained VT and stable hemodynamics. Acute therapy should be initiated with procainamide (50 – 100 mg intravenously). Another potential antiarrhythmic drug is lidocaine. Neither is known to be terato- genic. Life - threatening ventricular fi brillation (VF) or ventricular fl utter can occur in any stage of pregnancy and is associated with a high risk of sudden cardiac death [89] . In these patients DC defi brillation is the method of choice (100 – 360 J). Prompt car- diopulmonary resuscitation and early defi brillation by either DC countershock or an automated external defi brillator signifi cantly improves the likelihood of successful resuscitation from VF [89,90] . The implantable cardioverter - defi brillator (ICD) is an excellent approach to terminal tachyarrhythmias and prevents sudden death [91] . Ventricular premature beats (VPBs) in pregnant women with structurally normal hearts are benign and do not usually require therapy [87] . Exacerbating chemical stimulants (e.g. caffeine, cocaine) should be eliminated, and cardiology and maternal – fetal medicine consultation should be considered. If patients remain highly symptomatic a selective β - blocker such as metoprotol may be used. Aortic d issection Acute aortic dissection may occur in pregnancy in association with severe hypertension due to pre - eclampsia, coarctation of the aorta, or connective tissue disease such as Marfan ’ s syndrome [92,93] . Although rare, aortic dissection during pregnancy accounts for 50% of all dissections in women under 40 years of age [94] . Classic symptoms include severe retrosternal and/or abdominal pain. The patient may present with cardiogenic shock due to aortic incompetence or hemopericardium and tampon- ade. Diagnosis is made with computed tomography or trans- esophageal echocardiography. Maternal outcome is poor with mortality as high as 25% [93,95] . If the dissection is limited to the descending aorta some patients can be managed successfully to term and surgery performed postpartum. Before 28 weeks gestation, aortic repair with the fetus kept in situ is warranted, given the high mortality (80%) of non - opera- tive treatment in this setting [93,96] . After 32 weeks gestation (fetal viability) primary cesarean followed by repair is appropriate [93,95] . Controlled vaginal delivery with regional anesthesia has been described [95] . Management between 28 and 32 weeks is controversial. If there is hemodynamic instability or non - reassur- ing fetal status, then cesarean followed by operative repair should be affected. Epidural anesthesia reduces increases in vessel shear stress (cardiac output) and wall tension (mean arterial blood Chapter 40 568 27 Dildy G , Clark S , Loucks CA . Intrapartum fetal pulse oximetry: the effects of maternal hyperoxia on fetal arterial oxygen saturation . Am J Obstet Gynecol 1994 ; 171 : 1120 – 1124 . 28 Thangathurai D , Charbonnet C , Wo C , Shoemaker WC , et al. Intraoperative maintenance of tissue perfusion prevents ARDS . New Horiz 1996 ; 4 : 466 – 474 . 29 Taylor RW . Pulmonary Artery Catheter Consensus Conference Participants: Pulmonary Artery Catheter Consensus Conference consensus statement . Crit Care Med 1997 ; 25 : 910 . 30 Harms B , Kramer GC , Bodai BI . The effect of hypoproteinemia and pulmonary and soft tissue edema formation . Crit Care Med 1981 ; 9 : 503 . 31 Chiao J , Minei J , Shires G , et al. In vivo myocyte sodium activity and concentration during hemorrhagic shock . Am J Physiol 1990 ; 258 : R684 – R689 . 32 SAFE Study Investigators . A comparison of albumin and saline for fl uid resuscitation in the intensive care unit . N Engl J Med 2004 ; 350 : 2247 – 2256 . 33 National Institutes of Health Consensus Development Conference . Fresh frozen plasma. Indications and risks . JAMA 1985 ; 253 : 551 – 553 . 34 Oberman HA . Uses and abuses of fresh frozen plasma . In: Garrity A , ed. Current Concepts in Transfusion Therapy . Arlington, VA : American Association of Blood Banks , 1985 . 35 Counts R , Haisch C , Simon TL , et al. Hemostasis in massively trans- fused trauma patients . Ann Surg 1979 ; 190 : 91 – 99 . 36 Miller R , Robbins T , Tong MJ , et al. Coagulation defects associated with massive blood transfusions . Ann Surg 1971 ; 174 : 794 – 801 . 37 Mannucci P , Federici A , Sirchia G . Hemostasis testing during massive blood replacement: a study of 172 cases . Vox Sang 1982 ; 42 : 113 – 123 . 38 Shippy C , Appel P , Shoemaker WC . Reliability of clinical monitoring to assess blood volume in critically ill patients . Crit Care Med 1984 ; 12 : 107 – 112 . 39 Boral L , Hill S , Apollon CJ , et al. The type and antibody screen, revisited . Am J Clin Pathol 1979 ; 71 : 578 – 581 . 40 O ’ Brien P , El - Refaey H , Gordon A , et al. Rectally administered miso- prostol for the treatment of postpartum hemorrhage unresponsive to oxytocin and ergotomine: a descriptive study . Obstet Gynecol 1998 ; 92 : 212 – 214 . 41 Gerstenfeld T , Wing DA . Rectal misoprostol versus intravenous oxy- tocin for the prevention of postpartum hemorrhage after vaginal delivery . Am J Obstet Gynecol 2001 ; 185 : 878 – 882 . 42 Villar J , G ü lmezoglu A , Hofmeyr GJ , et al. Systematic review of randomized controlled trials of misoprostol to prevent postpartum hemorrhage . Obstet Gynecol 2002 ; 100 : 1301 – 1312 . 43 AbdRabbo SA . Stepwise uterine devascularization: a novel technique for management of uncontrolled postpartum hemorrhage with preservation of the uterus . Am J Obstet Gynecol 1994 ; 171 : 694 – 700 . 44 O ’ Leary JA . Uterine artery ligation in the control of postcesarean hemorrhage . J Reprod Med 1995 ; 40 : 189 – 193 . 45 B - Lynch C , Coker A , Lawal AH , et al. The B - Lynch surgical technique for the control of massive postpartum hemorrhage: an alternative to hysterectomy? Br J Obstet Gynaecol 1997 ; 104 : 372 – 375 . 46 Dubois J , Burel L , Brignon A , et al. Placenta percreta: balloon occlu- sion and embolization of the internal iliac arteries to reduce intraop- erative blood loss . Am J Obstet Gynecol 1997 ; 176 : 723 – 726 . 47 Shih J , Liu K , Shyu MK . Temporary balloon occlusion of the common iliac artery: new approach to bleeding control during cesarean hyster- 7 Abraham E . Physiologic stress and cellular ischemia: relationship to immunosuppression and susceptibility to sepsis . Crit Care Med 1991 ; 19 : 613 – 618 . 8 Hoch R , Rodriguez R , Manning T , et al. Effects of accidental trauma on cytokine and endotoxin production . Crit Care Med 1993 ; 21 : 839 – 845 . 9 Bassin R , Vladeck B , Kim S , et al. Comparison of hemodynamic responses of two experimental shock models with clinical hemor- rhage . Surgery 1971 ; 69 : 722 – 729 . 10 Clark SL . Shock in the pregnant patient . Semin Perinatol 1990 ; 14 : 52 – 58 . 11 Shoemaker W , Appel P , Kram HB . Role of oxygen debt in the devel- opment of organ failure, sepsis, and death in high risk surgical patients . Chest 1992 ; 102 : 208 – 215 . 12 Shoemaker W , Appel P , Kram HB . Hemodynamic and oxygen trans- port responses in survivors and nonsurvivors of high risk surgery . Crit Care Med 1993 ; 21 : 977 – 990 . 13 Shoemaker WC . Pathophysiologic basis for therapy for shock and trauma syndromes: use of sequential cardiorespiratory measurements to describe natural histories and evaluate possible mechanisms . Semin Drug Treat 1973 ; 3 : 211 – 229 . 14 Slater G , Vladeck B , Bassin R , et al. Sequential changes in the distribu- tion of cardiac output in various stages of experimental hemorrhagic shock . Surgery 1973 ; 73 : 714 – 722 . 15 Pritchard JA . Changes in the blood volume during pregnancy and delivery . Anesthesiology 1965 ; 26 : 393 . 16 Clark S , Cotton D , Lee W , et al. Central hemodynamic assessment of normal term pregnancy . Am J Obstet Gynecol 1989 ; 161 : 1439 – 1442 . 17 Greiss FC . Uterine vascular response to hemorrhage during preg- nancy and delivery . Anesthesiology 1965 ; 26 : 393 . 18 Pritchard J , Baldwin R , Dickey JC , et al. Blood volume changes in pregnancy and the puerperium, 2. Red blood cell loss and changes in apparent blood volume during and following vaginal delivery, cesar- ean section, and cesarean section plus total hysterectomy . Am J Obstet Gynecol 1962 ; 84 : 1271 . 19 Sheehan H , Murdoch R . Postpartum necrosis of the anterior pitu- itary: pathologic and clinical aspects . Br J Obstet Gynaecol 1938 ; 45 : 456 . 20 Smith K , Browne J , Shackman R , et al. Renal failure of obstetric origin . Br Med Bull 1968 ; 24 : 49 . 21 Mabie WC , Barton JR , Sibai BM . Adult respiratory syndrome in preg- nancy . Am J Obstet Gynecol 1992 Oct; 167 ( 4 pt 1 ): 950 – 957 . 22 Belfort M , Anthony J , Saade G , et al. The oxygen consumption: oxygen delivery curve in severe preeclampsia: evidence for a fi xed oxygen extraction state . Am J Obstet Gynecol 1993 ; 169 : 1448 – 1455 . 23 Evans W , Capelle S , Edelstone DI . Lack of a critical cardiac output and critical systemic oxygen delivery during low cardiac output in the third trimester in the pregnant sheep . Am J Obstet Gynecol 1996 ; 175 : 222 – 228 . 24 Haddad B , Barton JR , Livingston JC , et al. Risk factors for adverse maternal outcomes among women with HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome . Am J Obstet Gynecol 2000 Aug; 183 ( 2 ): 444 – 448 . 25 Naef R , Chauhan S , Chevalier S , et al. Prediction of hemorrhage at cesarean delivery . Obstet Gynecol 1994 ; 83 : 923 – 926 . 26 Zelop C , Harlow B , Frigoletto FD , et al. Emergency peripartum hysterectomy . Am J Obstet Gynecol 1993 ; 168 : 1443 – 1448 . . 559 Critical Care Obstetrics, 5th edition. Edited by M. Belfort, G. Saade, M. Foley, J. Phelan and G. Dildy postpartum pituitary necro- sis. The parturient undergoes several important physiologic adaptations during pregnancy to protect her from the bleeding expected at the time of delivery. Peripartum. [18] . With a postpartum blood loss of less than 1000 mL, the parturient ’ s vital signs may refl ect acute blood loss (i.e., hypotension and tachycardia). During the antepartum period, the