11/11/13

Shock and Pregnancy

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Shock and Pregnancy
Author: Marie Rosanne Baldisseri; Chief Editor: David Chelmow, MD more... Updated: Jan 4, 2012

Background
Shock is a state of compromised tissue perfusion that causes cellular hypoxia. It is defined as a syndrome initiated by acute hypoperfusion, leading to tissue hypoxia and vital organ dysfunction. Shock is a systemic disorder affecting multiple organ systems. Perfusion may either be decreased globally or distributed poorly, as in septic shock. During shock, perfusion is insufficient to meet the metabolic demands of the tissues; consequently, cellular hypoxia and end organ damage ensue.[1] The treatment of shock in a pregnant person differs in 2 important respects from the treatment of shock in adults who are not pregnant. First, normal physiologic changes occur in the most organ systems during pregnancy. Second, 2 patients are vulnerable, the mother and the fetus. Therefore, obstetric critical care involves simultaneous assessment and management of both patients (mother and fetus), who have differing physiologic profiles. See the image below.

Determinants of cardiac function and oxygen delivery to tissues. Adapted from Strange GR. APLS: The Pediatric Emergency Medicine Course. 3rd ed. Elk Grove Village, Ill: American Academy of Pediatrics ; 1998:34.

For excellent patient education resources, visit eMedicine's Shock Center, Pregnancy and Reproduction Center, and Public Health Center. Also, see eMedicine's patient education articles Shock, Pregnancy, and Cardiopulmonary Resuscitation (CPR).

Cardiovascular Physiology During Normal Pregnancy
During pregnancy, significant cardiovascular changes occur, including changes in the blood volume, heart rate, stroke volume, cardiac output, and systemic vascular resistance. Furthermore, pregnant women also experience respiratory changes in lung volumes, minute ventilation, and acid-base status. Understanding and appreciating the normal physiologic adaptations to gestation are important for treating pregnant women.

Blood volume
Maternal blood volume increases from 25-52% by late pregnancy.[2] The plasma volume increases by 45-50%,
emedicine.medscape.com/article/169450-overview 1/15

the hypervolemia of pregnancy. when it should be approximately 110/60 mm Hg.[7] Alternate hypotheses for the increase in left ventricular stroke volume have been suggested. caused by compression of the pelvic veins and inferior vena cava by the uterus. The supine hypotensive syndrome manifests as dizziness. The heavy gravid uterus compresses the descending aorta and the inferior vena cava. these promote sodium retention and an increase in total body water. a fall in cardiac output. During pregnancy. Turning the mother to her side quickly restores the pooled blood to the circulation.5 L. Blood pressure Both the systolic and diastolic blood pressures decrease until mid pregnancy. Effect of maternal posture on maternal hemodynamics The uterine blood flow increases from approximately 50 mL/min prepregnancy to 500 mL/min at term. even when the blood pressure of the arm measures normal.com/article/169450-overview 2/15 . this represents a change of systemic cardiac output from 2% normally to 18% during the third trimester. 6] This increase occurs by 10 weeks' gestation and peaks at the end of the second trimester. sweating.medscape.[3] The blood pressure decrease likely occurs because of decreased vascular resistance. Cardiac output and stroke volume Maternal cardiac output increases 30-50% during pregnancy. a decrease in venous return to the heart. In pregnancy. Intrapartum hemodynamics emedicine. The expansion in blood volume and extracellular fluid volume is required for optimal uteroplacental circulation. marked hypotension and syncope may be experienced with sudden standing from a sitting or lying position.[8. interpret the blood pressure relative to gestational age. Elevated levels of estrogen and progesterone increase plasma aldosterone levels and renin activity. nausea. thereby increasing diastolic filling. the cardiac output is increased due to the tachycardia rate. The measurement of brachial artery pressure is not indicative of the uterine arterial blood pressure because the uterine arterial pressure can be extremely low. The 2 important factors that reduce systemic vascular resistance are the dilatation of peripheral blood vessels and the presence of the placental circulation. pallor. with a progressive rise towards the baseline value at term. In late pregnancy. this reaches and stays at 120% of the baseline by 32 weeks of pregnancy. The venous pressure in the legs increases progressively during pregnancy. The increase in cardiac output during gestation is the result of an increase in heart rate and stroke volume. tachycardia. 4 L of which is extracellular. and hypotension. The erythropoiesis occurs secondary to progesterone and other placental hormones. 9] A pregnant woman has a greater tendency for pooling of venous blood. and hypotension that occur when a pregnant woman lies on her back.[4] The maternal tachycardia may be secondary to cardiac adaptation to volume overload and elevated free thyroxine serum levels. The placental vascular bed is a low-resistance vascular system perfused with a large portion of the maternal cardiac output. In the first half of pregnancy. Heart rate The maternal heart rate becomes elevated by 12 weeks' gestation. the ventricular pressure volume curve may be shifted to the right because of a hormonally dilated heart. Uterine veins increase enormously in size and number during gestation.[5. the stroke volume is increased primarily as the uteroplacental circulation acts as an arteriovenous shunt. total body sodium levels increase by 950 mEq/L. This disproportionate increase in plasma volume accounts for the hemodilution or anemia of pregnancy. A blood pressure measurement of 130/80 mm Hg may be normal at term but is abnormal at 28 weeks' gestation. with gradual recovery to nonpregnant values by late gestation. Nonreassuring fetal status may occur from decreased uteroplacental perfusion. blood volume increases 1-1. and uterine vascular resistance is greatly decreased during pregnancy. The elevated femoral venous pressure returns to a normal level following labor. which is at its maximum by 32 weeks' gestation. and the volume of total body water is 6-8 L. This results in pooling of blood in the legs.11/11/13 Shock and Pregnancy compared with a 20% increase in red blood cell mass . Systemic vascular resistance Systemic vascular resistance decreases and reaches a nadir by the 24th week of pregnancy.

The increased circumference of the thoracic cage allows the vital capacity to remain unchanged.[13] Cardiac output remains elevated for at least 48 hours postpartum due to the stroke volume increase despite maternal bradycardia. beginning in the first trimester and reaching 20-40% above baseline at term. and diaphragmatic excursion is not reduced. 16. Cardiac output increases during various phases of labor. analgesia. resulting in 3 kg of weight loss during the first week. and peripartum blood loss. Approximately 500 mL of blood loss occurs with vaginal delivery and 1000 mL with cesarian delivery.11/11/13 Shock and Pregnancy Maternal cardiovascular responses can be further modified by uterine contractions. adversely affecting fetal oxygenation by reducing uterine blood flow. pregnancy does not appear to change lung compliance. The uterine contractions augment cardiac output. capillary congestion. severe pain and anxiety can lead to rapid shallow breathing with alveolar hypoventilation. As the uterus expands.[12] The hypervolemia of pregnancy allows women to lose as much as 30% of predelivery blood volume. producing hyperemia. and mild hypoxemia. mucosal edema. Alveolar ventilation increases 50-70%. Postpartum diuresis peaks between the second and fifth day after delivery. Diaphragm function remains normal. 17] Ventilation The minute ventilation increases significantly. hypersecretion. but this finding is not consistent. Each uterine contraction expresses from 300-500 mL of blood. The respiratory rate remains relatively constant or increases slightly. increasing the chest wall circumference. with little change in postpartum hematocrit values.[15.47. In some patients. The fetal emedicine. hyperventilation increases and tachypnea caused by pain and anxiety might result in marked hypocapnia and respiratory alkalosis. surgery. maintaining an arterial pH in the range of 7.40-7. and the total lung capacity decreases only minimally by term. but chest wall and total respiratory compliance are reduced at term. atelectasis.[18] In active labor. and increased mucosal friability. The magnitude of cardiac output gained during contraction is 11% less in women laboring under epidural analgesia. The arterial carbon dioxide pressure reaches a plasma level of 28-32 mm Hg. a decreased expiratory reserve volume is a definite change. Arterial blood gases Physiological hyperventilation results in respiratory alkalosis with compensatory renal excretion of bicarbonate. Estrogen is probably responsible for producing tissue edema.[10] The infusion of blood back into the maternal circulation increases venous return and augments stroke volume. Pulmonary functions Anatomical changes to the thorax produce a progressive decrease in functional residual capacity (FRC). Hormonal changes do not significantly affect airway function. The return of blood volume from the lower extremities results in approximately 1 L of autotransfusion at the time of delivery. Mild hypoxemia might occur in the supine position. which is reduced by 10-20% by term.com/article/169450-overview 3/15 . the diaphragm is displaced cephalad by as much as 4 cm. and bicarbonate is decreased to 1821 mmol/L. Uteroplacental and Fetal Physiology A basic understanding of fetal physiology is required to care for pregnant patients who are critically ill.[14] Respiratory Physiology Anatomical changes Hormonal changes in pregnancy affect the upper respiratory tract and airway mucosa. pain. The residual volume can decrease slightly during pregnancy. The enlarging uterus and the hormonal effects produce anatomical changes to the thoracic cage. The increase in ventilation occurs because of increased metabolic carbon dioxide production and an increased respiratory drive due to the increased serum progesterone level.medscape. an increase in the anteroposterior diameter and transverse diameter of the thorax occurs. Maternal cardiac output increases by approximately 20-30% above prelabor values during the first 24 hours following delivery. Oxygen consumption increases at the beginning of the first trimester and increases 20-33% by term because of fetal demands and increased maternal metabolic processes. The tidal volume increases 30-35%. and hyperplasia of mucous glands. labor.[11] This concept is important for patients with cardiac disease who may not tolerate hemodynamic fluctuations during labor.

the degree of matching of maternal and fetal blood flows. Fetal pH monitoring can only be performed when emedicine. fetal bradycardia may indicate hypoxia secondary to uteroplacental insufficiency. This is partially compensated by a high fetal cardiac output relative to oxygen consumption. maternal oxygen delivery to the placenta. amniotic fluid volume. A 50% decrease in uterine blood flow may be tolerated for brief periods. limb tone. ie. resulting in decreased fetal oxygen delivery. The causes of hypovolemia include supine position. The interaction of maternal and fetal circulations in the placenta most likely follows a concurrent exchange mechanism. whereas a pH greater than 7. Vasoconstriction of the uterine arteries occurs in preeclampsia[19] or with vasoconstrictor drugs. and reactivity to nonstress testing. small changes in maternal PaO2 may cause significant changes in fetal oxygen content.[20] Fetal monitoring Fetal monitoring is performed via continuous electronic fetal heart rate (FHR) monitoring to identify any changes in fetal physiology. The baseline FHR is in the range of 120-160 beats per minute.11/11/13 Shock and Pregnancy oxygen delivery is dependent on maternal arterial oxygen content and uterine blood flow. which depends on maternal cardiac output Thus. Despite low umbilical vein PaO2. Variations in maternal pH also influence oxygen delivery. Although fetal tachycardia may be a nonspecific finding. brain damage. which is determined by maternal PaO2 Maternal hemoglobin concentration and saturation Uterine blood flow. Fetal acid-base measurements from scalp blood sampling are used in labor to assess the state of fetal physiology.com/article/169450-overview 4/15 . and the oxygen reserve is approximately 42 mL. vasoconstriction of the placental bed. Therefore. a decreased PaO2 in the mother can be offset somewhat by augmentation of the blood hemoglobin concentration or cardiac output.25 predicts a favorable outcome. The oxygen consumption of the fetus is 20 mL/min. However.[20] Determinants of fetal oxygen delivery Oxygen delivery to fetal tissues can be affected at many levels. and oxygen transport from the placenta to fetal tissues. and fetal death. late or variable decelerations. and further reduction produces anaerobic metabolism. alkalosis causes vasoconstriction of the uterine artery. The other placental factors that determine fetal oxygenation are the amount of intraplacental shunt. These factors are hypotension. Absence of beat-to-beat variability in the FHR may be another indication of fetal asphyxia and anemia. the fetus has the capability of surviving longer by redistributing blood flow to the vital organs. thus maintaining abundant oxygen delivery to the tissues. and the presence of any placental abnormalities such as placental infarcts. The fetal biophysical profile consists of an ultrasound determination of fetal movements. The major determinants of oxygen delivery to the placenta are the following: The oxygen content of uterine blood. This is less efficient than a countercurrent exchange mechanism. A combination of maternal hypoxemia and decreased cardiac output has a profoundly deleterious effect on fetal oxygenation. and the fetal blood flow may decrease by as much as 20% with vasoconstriction. hypovolemia. therefore. This level of PaO2 is sufficient to saturate fetal hemoglobin to 80-85% because of the left shift in the hemoglobin oxygen dissociation curve. placental transfer. factors affecting either the arterial oxygen content or uterine blood flow also affect fetal oxygenation. fetal breathing movements. The fetal arterial blood has an even lower PaO2 than umbilical vein blood. The umbilical vein PaO2 is approximately 3540 mm Hg because it is mixed with deoxygenated blood in the fetal inferior vena cava. far lower than the uterine vein PaO2. sepsis. particularly when recurrent and combined with decreased variability. this helps explain why the PaO2 of the fetal umbilical vein is in the range of 32 mm Hg. are highly suggestive of fetal hypoxia. The umbilical vein PaO2 values of less than 30 mm Hg are saturated on the steep part of the fetal oxyhemoglobin dissociation curve. A pH less than 7. While early decelerations of FHR are benign.20 indicates fetal hypoxia.medscape. and medications. Abnormalities of FHR patterns may be further evaluated using results from a fetal biophysical profile. The uterine blood flow increases during pregnancy from 2% of cardiac output in a nonpregnant patient to 18% of cardiac output by the third trimester in a pregnant patient. fetal oxygen content is actually quite close to maternal oxygen content because of the shape of the oxyhemoglobin saturation curve of the fetal hemoglobin. and uterine contractions.

pulmonary edema. oropharyngeal. Critical Care Monitoring and Support of the Pregnant Patient The pregnant patient is unique in an intensive care environment. cardiomyopathy. is known to increase uterine blood flow and maternal blood pressure. In normal pregnancy . and magnesium overdose. hence. obstetric hemorrhages are responsible for 13. cause vasoconstriction of uterine arteries and should be avoided if possible. Endotracheal intubation must be performed quickly because pregnant patients have lower oxygen reserves because of the decrease in FRC. such as phenylephrine and norepinephrine. the normal level during pregnancy. and AFE. maternal hypercapnia has not been reported to be harmful to the fetus. Benzodiazepines may be used. or penetrating injuries. norepinephrine. Fetal pulse oximetry has been approved for use with the conventional fetal monitor only on patients with nonreassuring heart rates. but the cardiac filling pressures are unchanged. intubation and suctioning may lead to mucosal injury and bleeding. meperidine and fentanyl are commonly used. This technique directly and objectively measures fetal oxygen status during labor and delivery. the cardiac output increases as much as 30-50% compared to prepregnancy levels. In the United States. Intubation and mechanical ventilation During pregnancy. place pregnant patients in a left lateral tilt position to avoid supine hypotension. Therefore. severe cardiac disease. experience with propofol is limited. Cardiopulmonary resuscitation In an arrest situation. 23] emedicine. which is expected to provide a more complete and accurate assessment of the fetal condition. A pregnant patient who is critically ill and in shock requires special expertise because of the extraordinary underlying physiology. Placental abruption occurs in 1-5% of patients with minor trauma and 20-50% of patients with major trauma.com/article/169450-overview 5/15 . and epinephrine adversely affect uterine blood flow. Animal data suggest that dobutamine. the nasopharyngeal. Advanced cardiac life support (ACLS) is provided according to ACLS standard protocols. A patient who is critically ill and in shock requires vasoactive drugs. and respiratory tract mucosa swell. The pure alpha-adrenergic agents.11/11/13 Shock and Pregnancy membranes are ruptured.4% of all maternal deaths. septic shock . pulmonary embolism (PE). Avoid high ventilatory pressures at the expense of a rise in PaCO2. The precipitating events for cardiac arrest in pregnancy include amniotic fluid embolism (AFE). but these may have depressive effects on fetal respiration. acute respiratory distress syndrome (ARDS).[22. assaults.[21] Antepartum hemorrhage can occur from disruption of the placenta and spontaneous or traumatic uterine rupture. Fetal oxygen saturation is a new intrapartum fetal monitoring technology. Ephedrine. This can be achieved by placing a pillow or wedge under the patient's right hip. fetal oxygenation. this new technology requires further study to assess its role in the management of different clinical situations. Because the degree of nonreassuring rates differs. anesthetic complications. falls. Drug therapy For sedation. The cause of trauma can be vehicular accidents. Dopamine and ephedrine have been shown to increase maternal blood pressure and uterine flow. Hemodynamic monitoring Pregnant patients who are critically ill and in shock may require insertion of a pulmonary artery catheter. which has both beta-2 properties and alpha-1 agonist properties.medscape. The indications for pulmonary artery catheterization are severe preeclampsia with oliguria. myocardial infarction. It is the vasoactive drug of choice to treat hypotension in pregnant patients. Insufficient human data are available to assess the effects of these drugs in pregnancy and labor. Avoid respiratory alkalosis because it may decrease uterine blood flow and. Hemorrhagic Shock Trauma and resultant hemorrhage causes 6-7% of all deaths in pregnancy. Ventilate pregnant patients to maintain their PaCO2 at approximately 30 mm Hg.

manifesting as uterine pain and hemorrhage. and hypoxemia. Postpartum hemorrhage may be worsened by thrombocytopenia. transient buttock ischaemia. and blood typing and crossmatching to replace packed red blood cells. resulting in inadequate perfusion of certain organs. The ultrasound confirms if the hemorrhage is due to placenta previa or placental abruption. preservation of the uterus and fertility. placement of 2 intravenous lines. viruses. and decreased rebleeding from collaterals. Pseudomonas aeruginosa. ventilation-perfusion mismatch. intravenous volume replacement. uterine atony can be treated with uterine massage. Most obstetric hemorrhages occur postpartum and are primarily due to uterine atony and cervical or vaginal lacerations. Uterine rupture commonly occurs when high doses of oxytocin or prostaglandins are infused for induction. nontender uterus. coagulopathy secondary to AFE. The commonest complication is low-grade fever but.11/11/13 Shock and Pregnancy Placenta previa is implantation of the placenta in the lower uterine segment. and hypotension. initiating an inflammatory response. Furthermore. Several advantages of uterine artery embolization include easy identification of the bleeding site. in an antepartum patient. Transcatheter arterial embolization has been a recognized method of hemorrhage control and has been used successfully in the control of postpartum hemorrhage.2 mg).2 mg intramuscularly. vasoconstriction. In postpartum hemorrhage. excessive blood loss diminishes uteroplacental blood flow and induces fetal distress.medscape. The signs and symptoms of uterine rupture include vaginal bleeding. which should be treated with appropriate blood product support. low peripheral vascular resistance. Patients requiring a large amount of volume replacement may develop coagulopathy. emedicine. multiorgan failure. Management The management of hemorrhagic shock requires immediate resuscitative measures.com/article/169450-overview 6/15 . The dose is 0. Once the patient is stable. Excessive blood loss results in hypovolemic shock. Gram-negative bacteria such as Escherichia coli. and hypotension. with a classic presentation of painless vaginal bleeding and a soft. If medical management fails. such as hypertension. and death. tachycardia. Adverse effects include bronchospasm.[25] In emergencies. pelvic infection. Fetal monitoring should be performed via continuous FHR monitoring to detect fetal distress or fetal hypoxia. prostaglandins increase myometrial intracellular free calcium concentrations and enhance the activity of other oxytocic agents. transient foot ischaemia and bladder gangrene may occur. The normal blood loss of vaginal delivery (500 mL) or cesarian delivery (1000 mL) is generally well tolerated. groin hematoma. the presence of which should lead to prompt fetal delivery by the safest possible method. therapeutic embolization of the internal iliac or uterine artery has been used to control obstetric hemorrhage. and increased pulmonary artery pressures. rarely. Oxytocin is the first-line drug and is often administered as an infusion (20-40 U/L) because bolus administration can cause peripheral vasodilation. immediately perform an abdominal ultrasound to definitely diagnose the cause of uterine bleeding. lower abdominal pain. or sepsis. The uterine pain is present between contractions. The microorganisms produce endotoxins that activate complement systems and cytokines.9% and a complication rate of 8. blood that is type-specific and not crossmatched can be administered. blood flow is poorly distributed. Hemabate (15-methyl prostaglandin F2-alpha) at a dose is 250 mcg administered intramuscularly every 15-30 minutes as necessary (not to exceed 2 mg) is the frequently used agent. leading to cellular damage. The next step is prostaglandin administration. The mediators of sepsis are responsible for vasodilation. and a nonreassuring fetal tracing.7% in 138 cases of PPH treated by arterial embolization. Surgical exploration to repair lacerations and decrease blood loss by arterial ligation or hysterectomy may be required as a life-saving measure. and intravenous oxytocin infusion. antepartum hemorrhage is less common. including administration of oxygen. Abruptio placenta may occur in a normally implanted placenta. Klebsiella species.[24] The uterine fundus feels boggy and tender upon palpation. intramuscular administration of methylergonovine (0. A recent review revealed a success rate of 94. Ergonovine and methylergonovine are the ergot alkaloids that produce rapid tetanic uterine contraction and are used to treat refractory uterine atony. and the uterus is tender. iliac artery perforation. or fungi. Septic Shock Septic shock may occur during pregnancy because of overwhelming infection caused by gram-positive bacteria. and Serratia species cause most cases of septic shock. These drugs can cause serious cardiovascular problems.

aminoglycoside. Optimum mean arterial pressure. Prolonged rupture of membranes. Intravaginal mifepristone in medical abortions has resulted in fulminant and lethal septic shock due to Clostridium sordellii. 7. In summary.[27] Cultures of sputum. The clinical illness is consistent with toxic shock and had evidence of endometrial infection with C sordellii. 6. and urine are sent prior to antibiotic administration. hypotension.or third-generation cephalosporin combined with metronidazole. This approach results in recruitment of alveoli. The causes of septic shock are septic abortion. the incidence of death is lower compared to nonobstetric patients with septic shock (0-3% in obstetric patients vs 10-80% in nonobstetric patients). Patients with septic shock present with chills. Ephedrine.11/11/13 Shock and Pregnancy The mediators of inflammation result in increased capillary permeability. lowering lung compliance. and clindamycin or metronidazole. maintain adequate tissue oxygenation. By blocking both progesterone and glucocorticoid receptors. and treatment with antimicrobial therapy. These patients require aggressive resuscitation with crystalloids and colloids to maintain sufficient intravascular volume before considering vasopressor therapy. bradycardia. and instrumentation of the genitourinary tract are other significant risk factors for sepsis. Treatment Treatment of septic shock requires immediate resuscitation. causing leakage of intravascular fluid throughout the body. the goals of mechanical ventilation are the use of a low tidal volume and a high positive endexpiratory pressure. the patient develops cool clammy skin. 2. circulating blood volume. Because patients with septic shock often develop ARDS. an alpha and beta agonist. and producing severe hypoxemia. Later. cardiac output. and sufficient oxyhemoglobin saturation are required. and cyanosis. Early recognition Early and adequate antibiotic therapy Source control Early hemodynamic resuscitation and continued support Corticosteroids (refractory vasopressor-dependent shock) Drotrecogin alpha (Severely ill if APACHE II > 25) Tight glycemic control Proper ventilator management with low tidal volume in patients with ARDS Other Causes Of Shock In Pregnancy emedicine. chorioamnionic and postpartum infections. blood. which is necessary to prevent the endometrial spread of C sordellii infection. A usual combination used often is penicillin. During sepsis.[26] Although septic shock remains one of the major causes of death in obstetric patients. Thus. tachypnea. may be the preferred vasopressor in patients with acute hypotension during pregnancy. Concomitant release of potent exotoxins and an endotoxin from C sordellii contribute to the rapid development of lethal septic shock. 5. mifepristone interferes with the release and function of cortisol and cytokines. pyelonephritis. 4. the principles in the management of septic shock. In puerperal sepsis. specifically the pulmonary parenchyma. antibiotic therapy is adjusted based on the patient's response to therapy and the results of culture and sensitivities. and respiratory tract infections. This constellation of clinical and physiological features is described as ARDS. Patients in septic shock require hemodynamic support with restoration of adequate circulating volume followed by the administration of vasoactive drugs. the failed release of cortisol and cytokine responses impairs the body's defense mechanism. makes the lungs more compliant. As the septic shock progresses. and flushed skin. similar to treatment of any other case of septic shock.medscape. a gram-positive. mental confusion. Piperacillin-tazobactam is another combination that provides fairly comprehensive coverage for an intra-abdominal source of sepsis. and improves oxygenation. and resulting in noncardiac or low-pressure pulmonary edema. also provide anaerobic coverage. Provide empiric antibiotic coverage intravenously for both gram-negative and gram-positive bacteria. fever. Although dopamine has been used in the past in patients with septic shock. This may be achieved at a cost of reduced uterine blood flow. include the following components: 1. injury to type II pneumocytes impairs surfactant production. Patients in respiratory distress or those with severe hypoxemia may need to be intubated and mechanically ventilated. An alternate combination is a second.com/article/169450-overview 7/15 . 3. retained products of conception. identification of the underlying cause of septic shock. toxin-forming anaerobic bacteria. causing alveolar collapse. 8. tachycardia. In septic shock. norepinephrine achieves better perfusion pressure and maternal hemodynamics and helps restore oxygen delivery to hypoperfused organs.

coagulopathy. AFE is totally unpredictable. Whether the pathogenesis occurs secondary to embolization of particulate cellular contents or secondary to humoral factors has not been established. and this may well be the first indication of AFE. Postpartum patients may have a localized abscess. pulmonary venous congestion. A small percentage of these patients are found to have inflammatory myocarditis after analysis of endomyocardial biopsy specimens. In cardiogenic shock. and death. This may lead to pulmonary arterial vasospasm and transient pulmonary hypertension. at times. Uterine manipulation or trauma may often precede AFE. Management of coronary artery disease in a pregnant patient is similar to that for a nonpregnant patient. or delivery. The fetal substance may initiate an anaphylactoid reaction. Treatment consists of oxygenation and hemodynamic support.[28] This disease tends to recur in subsequent pregnancies. A recent analysis of 46 verified cases of AFE had none of the previously cited predisposing factors: 12% of the cases occurred in women with intact membranes. the presence of a third heart sound. but of those who do. AFE is a rare disorder. shock. but. and neurological manifestations such as confusion. The risk factors include old age. a rare event.11/11/13 Shock and Pregnancy Cardiogenic shock Cardiogenic shock may also be observed during pregnancy. resistant organism. occurring in 1 case in 20. and generalized edema occur. tachypnea. and generalized edema. multiparity. and death. The diagnosis of AFE is based on a characteristic clinical picture. Coronary artery disease is uncommon in reproductive-aged women. dyspnea. but myocardial infarction has occurred because of the excessive hemodynamic stress of pregnancy. The acute left ventricular dysfunction may be caused by humoral mediators or cytokines contained in amniotic fluid released during the anaphylactoid reaction. digoxin. myocardial infarction. these patients have signs and symptoms of congestive heart failure. although most cases occur after the onset of labor. Inflammatory myocarditis may respond to immunosuppressive therapy. Seizure activity may. the left ventricle is not able to pump sufficient blood to meet the metabolic demands of the tissues. tachycardia. multiorgan failure. Approximately 50% of patients do not survive this cardiopulmonary catastrophe. causes myocardial ischemia and sudden death in younger age groups and especially postpartum women. The major cause of cardiogenic shock is severe valvular disease. The treatment is usually tailored to the individual patient's needs. and AFE is extremely difficult to predict or prevent. Patients often require invasive monitoring to assess the adequacy of intravascular volume emedicine. hypervolemia.000-30. Respiratory distress and cyanosis occur suddenly within the first few minutes and are quickly followed by hypotension. eventually. systolic or diastolic murmurs. Upon presentation.com/article/169450-overview 8/15 . No specific cardiac risk factors have been associated with its occurrence. 70% during labor. the diagnosis may be suggested by findings from a CT scan of the pelvis. be the first manifestation. The clinical signs of cardiogenic shock are distended neck veins. cardiogenic shock.[29] AFE may occur at any point during pregnancy. the possible mechanism for dissection is thought to be pregnancy-induced degeneration of collagen and the additional stresses of parturition. Peripartum cardiomyopathy is an idiopathic disorder that occurs during the last month of pregnancy and up to 6 months postpartum. twin gestation. labor. but it accounts for 10% of all maternal deaths. and preeclampsia. decreased cardiac output. 11% after vaginal delivery. The mortality rate associated with peripartum cardiomyopathy is 25-50%. Spontaneous coronary artery dissection. hypoxemia. The clinical presentation includes angina. or septic pelvic thrombophlebitis. Inadequate oxygen delivery leads to cellular damage. 40-50% develop coagulopathy and hemorrhage up to 4 hours later. and seizures. vasodilators for afterload reduction. resulting in endogenous mediator release and causing hypotension. Patients with septic pelvic thrombophlebitis usually develop persistent fever. hypoxemia.medscape. The treatment consists of diuretics. and seizures. Amniotic fluid embolism AFE is a catastrophic peripartum syndrome that manifests as a sudden onset of severe dyspnea. and 19% during cesarean delivery with or without labor. followed by left ventricular failure. More than 80% of patients experience cardiorespiratory arrest at the onset.000 pregnancies. The incidence of this disease is 1 case in 1500-4000 deliveries. The compensatory response is tachycardia. pulmonary edema. In postpartum patients. some may occur outside of labor. loss of consciousness. and seizures. Treatment consists of a broad spectrum of antibiotics and standard anticoagulation. and hydrostatic pulmonary edema. hemodynamic collapse. and careful follow-up.

Chest radiograph findings are abnormal in 80% or more of patients with PE. A clinical guideline is to maintain systolic blood pressure at or higher than 90 mm Hg. the mother should be placed in the left lateral position.com/article/169450-overview 9/15 . Obtaining the appropriate diagnostic study in pregnancies is mandatory.005 Gy.5-2 times the baseline value. Administration of blood transfusions and blood components is considered the first line of treatment for correcting coagulopathy associated with AFE. Management Immediately treat patients. with acceptable organ perfusion. Extensive clinical experience and cohort studies establish heparin as the safest anticoagulant to use during pregnancy because it does not cross the placenta. The patient may need to be intubated and ventilated. A complete and adequate evaluation to document the presence or absence of PE requires less than 0. breathing. impedance plethysmography is adequate. This is particularly true in pregnancies because the diagnosis of DVT or PE requires the following: Prolonged therapy (potentially heparin for the entire 40 wk of pregnancy) Prophylaxis during future pregnancies Avoidance of oral contraceptive pills The first objective diagnostic test should be compression ultrasonography. The initial loading dose should be 5000-10.11/11/13 Shock and Pregnancy status and to guide inotropic therapy. If findings from the noninvasive leg studies are negative. Perfusion scanning alone is recommended initially. Monitor and keep the activated partial thromboplastin time in the therapeutic range. can be administered once a day and does not require monitoring. Intravenous steroids to treat underlying inflammatory response and similarities of AFE to anaphylaxis may be helpful. but they are nonspecific. The initiation of fluid therapy and the administration of pharmacological agents to maintain optimal blood pressure and cardiac output is next step. Corticosteroids have been used. proceed to ventilationperfusion lung scanning. and circulation. adding ventilation scanning when perfusion defects are noted.000 live births in white females and 2.[30] The signs and symptoms of PE are more problematic because dyspnea and tachypnea are common in pregnancy. and (3) correcting coagulopathy.000 U. 86% of patients may succumb to this disorder. chest pain (pleuritic). Management includes supportive measures and should begin emergently. Following loading. low molecular weight heparin (LMWH). pregnant or not. The fetus should be monitored continuously for signs of compromise. if it is not available. Pulmonary angiography might be necessary if lung scan findings are of low probability or indeterminate but clinical evidence is strong. and placental abruption is found in 50% of the cases. Electrocardiogram findings are abnormal in 70% of patients with PE. Although data are relatively modest. The first priority is resuscitation of the mother and administration of oxygen (100% concentration). The initial principles of dealing with obstetric emergencies include: airway. in whom PE is strongly considered.5-fold higher in black females. which is 1. tachypnea. and the findings are nonspecific. The 3 main goals of treatment are (1) oxygenation. (2) maintaining cardiac output and blood pressure. Incidence increases markedly following cesarean delivery compared to vaginal delivery. unless a high risk or contraindication to the use of any anticoagulants exists. Arterial oxygen tension is low in most patients with PE. and crackles are present in only 50% or more of patients. which does not cross the placenta. Objective diagnostic testing As with DVT. LMWH has not been shown to have an emedicine. Treatment is with intravenous unfractionated heparin. but their benefit has not been established. Pulmonary embolism The risk for developing deep venous thrombosis (DVT) and PE increases markedly during the advanced stages of pregnancy and is greatest during postpartum. Approximately 40% of cases have fetal death at the time of presentation.medscape. apprehension. Several studies show no increased risk of teratogenicity in patients undergoing radiological procedures for the diagnosis of maternal venous thromboembolic disease. Rates of maternal mortality from PE have been reported at 2. In order to ensure optimal uterine perfusion. PE requires objective diagnostic testing to confidently confirm or exclude the diagnosis. In nonpregnant patients. The mortality rate for AFE is high. Volume replacement and therapy for left ventricular dysfunction should be directed toward improving inotropy. start an infusion of 18 U/kg. as indicated by a urine output of 25 mL/h or more.6 cases per 100. dyspnea.

FRCPC Professor and Head. In one report. American College of Physicians-American Society of Internal Medicine. in a small number of patients. Associate Professor. Vena cava filters (Greenfield. bird's nest. St Boniface General Hospital Sat Sharma. or vitamin D supplementation. After delivery.2 U/mL. University of Pittsburgh Medical Center Marie Rosanne Baldisseri is a member of the following medical societies: American College of Physicians. including cesarian deliveries. Site Director. The teratogenic effects are particularly common during the first trimester. New York Presbyterian Hospital. Contributor Information and Disclosures Author Marie Rosanne Baldisseri MD. MD. Department of Internal Medicine.1-0. cases of epidural hematoma have occurred after epidural anesthesia. or neonatal problems. Canadian Medical Association. The problem of osteopenia and osteoporosis might be less severe if LMWH is used. and insufficient information on risks of obstetric. cleft lip. MD Assistant Professor. No information is available about the beneficial effects of concomitant multivitamins. both fatal and nonfatal complications have been reported. Continue the warfarin for at least 6 weeks postpartum or until at least 3 months of anticoagulant therapy have been completed. FRCPC is a member of the following medical societies: American Academy of Sleep Medicine. and World Medical Association Disclosure: Nothing to disclose. and hemorrhage. Warfarin crosses the placenta. Fatal complications are rare. University of Manitoba. but providing optimum calcium and vitamin D supplementation to all patients receiving long-term heparin administration during pregnancy is reasonable. data on the use of LMWH during pregnancy are limited. Additionally. Division of Pulmonary Medicine. Complications of treatment Osteopenia has been reported with unfractionated heparin administered for more than 6 months. it can cause fetal and neonatal hemorrhage and placental abruption. cleft palate. Duration of anticoagulation Patients who develop DVT or PE antepartum should receive anticoagulation therapy with heparin throughout pregnancy. and Society of Critical Care Medicine Disclosure: Nothing to disclose. Vena cava filters and filter placement are associated with a favorable safety profile. Royal College of Physicians and Surgeons of Canada. Weill Cornell Medical College emedicine.com/article/169450-overview 10/15 . and most nonfatal complications are of minimal clinical significance. American College of Chest Physicians. however. the heparin can be discontinued once an adequate International Normalized Ratio is achieved. The recommended dose was 5000 U. Department of Critical Care Medicine. However. fetal. FCCM. Specialty Editor Board Steven David Spandorfer. Department of Obstetrics and Gynecology. Society of Critical Care Medicine. no optimal dose regimen. most come from diverse case series involving prophylaxis rather than therapy. Coauthor(s) Sat Sharma. Neurocritical Care Society. Patients with documented venous thromboembolic disease who have contraindications to anticoagulation therapy or in whom conventional therapy has failed are candidates for inferior vena cave filter placement. Respiratory Medicine. Warfarin should be avoided throughout pregnancy because it can cause embryopathy characterized by mental retardation. calcium. MD. optic atrophy. dalteparin was used safely and effectively for prophylaxis in 47 women throughout their pregnancies. once or twice daily. stainless steel or titanium.11/11/13 Shock and Pregnancy increased risk of bleeding with surgical procedures.medscape. warfarin should be started. cataracts. American Thoracic Society. Simon-Nitinol) are positioned within the infrarenal inferior vena cava to trap thrombi arising from the lower extremities. These data provide no clear conclusions as to the efficacy and adverse effects of LMWH. Royal Society of Medicine. with a target trough plasma heparin level of 0.

Society for Gynecologic Investigation. Lees MM.37(2):395-407. 5. Jan 1980. American Society for Colposcopy and Cervical Pathology. Blood pressure survey in pregnancy. American Medical Association. Severe obstetric morbidity in the United States: 1998-2005. Barfield WD. Meikle SF. Clin Sci. the renin-aldosterone system and sex steroids throughout normal pregnancy. Zervoudakis I. [Medline].32(3):453-65. MD is a member of the following medical societies: American College of Obstetricians and Gynecologists. Blood volume during pregnancy. Jun 1967. Phi Beta Kappa. 3. [Medline]. Sigma Xi. [Medline].113(2 Pt 1):293-9. Sigma Xi. Blood pressure. Wilson M. University of Nebraska Medical Center College of Pharmacy. Virginia Commonwealth University Medical Center David Chelmow. and Society for Medical Decision Making Disclosure: Nothing to disclose. Katz R. MD is a member of the following medical societies: American College of Obstetricians and Gynecologists. Morganti AA. Medscape Drug Reference Disclosure: Medscape Salary Employment David Chelmow. MD Leo J Dunn Distinguished Professor and Chair. MD is a member of the following medical societies: American College of Obstetricians and Gynecologists. Effects of a natural volume overload state (pregnancy) on left ventricular emedicine. Resnik R. American Society for Reproductive Medicine. St Louis University School of Medicine Timothy D Rice. Obstet Gynecol. Scott DB. 2.98(3):394-403.com/article/169450-overview 11/15 .68(1):97-104. The circulatory effects of recumbent postural change in late pregnancy. Editor-in-Chief. Kerr MG. 6.74(3):319-28. Kuklina EV. Jun 1 1967. Am J Med. Lees MM. American Medical Association. Lund CJ. MacGillivray I. Hillis SD. 4. Karliner JS. [Medline]. Chief Editor David Chelmow. Virginia Commonwealth University Medical Center David Chelmow. Taylor SH. Rose GA. et al. et al. PhD Adjunct Assistant Professor. Timothy D Rice. American Society for Colposcopy and Cervical Pathology. Clin Sci. MD Associate Professor. Jamieson DJ. Taylor SH. and Endocrine Society Disclosure: Nothing to disclose. Francisco Talavera. A study of cardiac output at rest throughout pregnancy. Rowe B. J Obstet Gynaecol Br Commonw. Phi Beta Kappa. MD Leo J Dunn Distinguished Professor and Chair. [Medline]. Donovan JC. PharmD. Scott DB. Department of Obstetrics and Gynecology. Jun 1967. Significance of plasma and red cell volumes. and Society for Medical Decision Making Disclosure: Nothing to disclose. Kerr MG. Association of Professors of Gynecology and Obstetrics. Department of Obstetrics and Gynecology. 7. Society for Gynecologic Investigation. Council of University Chairs of Obstetrics and Gynecology. References 1. Whiteman MK. Oct 1969. Council of University Chairs of Obstetrics and Gynecology.11/11/13 Shock and Pregnancy Steven David Spandorfer. Am J Obstet Gynecol. MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians Disclosure: Nothing to disclose. Association of Professors of Gynecology and Obstetrics. [Medline].medscape. Feb 2009. Departments of Internal Medicine and Pediatrics and Adolescent Medicine.

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