Breech Presentation, Fetal Distress, and Mitral Stenosis
Jill Fong
A 25-year-old unregistered primigravida at 38 weeks of gestation presented to the labor room contracting. The patient had a history of rheumatic fever with no subsequent medical follow-up. On physical examination, she had a diastolic murmur and an opening snap. She reported having shortness of breath when climbing two flights of stairs. She was attached to an external fetal heart rate (FHR) monitor and tocodynamometer; recurrent variable decelerations without any beat-to-beat variability were noted. Simultaneously, the patient was found to have ruptured membranes, meconium-stained amniotic fluid, a fetal foot in her vagina, and a prolapsed umbilical cord. She was rushed to the operating room for an emergency cesarean section. Her blood pressure was 100/60 mm Hg; pulse rate, 100 beats per minute; and respiratory rate, 18 breaths per minute.
A. Medical Disease and Differential Diagnosis
How are fetal lie, presentation, and position defined and determined?
What is the approximate frequency of the various lies and presentations at or near term?
What are the different types of breech presentation, and what is their incidence?
What is the cause of breech presentation?
What are the perinatal problems associated with breech presentation?
What is the usual obstetrical management for patients with breech presentation?
What is the incidence of heart disease in pregnancy and the mortality rate associated with maternal cardiac disease?
What classifications may help predict an individual pregnant woman’s cardiac risk?
What are the cardiovascular changes of pregnancy?
What changes may normally occur in heart sounds during pregnancy?
What are the normal electrocardiographic and echocardiographic changes seen during pregnancy?
What causes rheumatic heart disease?
What are the physiologic consequences of mitral stenosis?
What are the auscultatory findings associated with mitral stenosis?
What may be seen on the electrocardiogram (ECG) in patients with mitral stenosis?
What are the echocardiographic findings associated with mitral stenosis?
What is the effect of the physiologic changes of pregnancy on patients with mitral stenosis?
If mitral stenosis is first recognized during pregnancy and symptoms develop, how would you treat the patient?
What are the determinants of fetal oxygenation?
What are the determinants of uterine blood flow?
B. Preoperative Evaluation and Preparation
How is fetal well-being assessed during labor?
How are FHR and maternal contractions monitored?
What is the normal FHR with beat-to-beat variability?
What are periodic decelerations?
How accurate is FHR monitoring in predicting fetal well-being?
In the fetus with a nonreassuring FHR pattern, what other modalities can be used to assess fetal well-being?
What is the significance of meconium-stained amniotic fluid?
What is meconium aspiration syndrome?
What are the usual noninvasive tests used to evaluate the pregnant cardiac patient?
What preoperative medications would you give this patient?
C. Intraoperative Management
What monitors would you use in this functional New York Heart Association (NYHA) class II patient during her cesarean section?
When would you use invasive monitoring in a pregnant patient with cardiac disease?
What are the hemodynamic goals of intraoperative management of the pregnant patient with mitral stenosis?
What anesthetic technique would you use for this emergency cesarean section?
What technique could you use for general anesthesia in this patient?
If you had unexpectedly been unable to intubate this patient, how would you have managed the airway?
Would this patient benefit from the use of β-blockers?
What is the effect of the inhalation agents on uterine contractility?
What is the Apgar scoring system?
What is the significance of Apgar scores?
At birth, what should be done to minimize an infant’s risk of meconium aspiration syndrome?
The Apgar score of the newborn was 3 at 1 minute. How would you treat the newborn?
Blood gases are sent immediately after delivery. What are the normal values for umbilical vein and artery blood gases?
D. Postoperative Management
Immediately after the baby was delivered, the mother’s oxygen saturation decreased. What is the differential diagnosis?
A. Medical Disease and Differential Diagnosis
A.1. How are fetal lie, presentation, and position defined and determined?
Fetal lie describes the position of the long axis of the fetus in relative to the long axis of the mother. Longitudinal, transverse, and oblique lies exist. Longitudinal lies are either cephalic or pelvic (breech) depending on which fetal structure enters the maternal pelvis. Transverse lies are either back up or back down with the long axis of the fetus perpendicular (90 degrees) to the mother’s long axis. An oblique lie results when the long axis of the fetus is at an acute angle to that of the mother. It is usually only transitory and converts to a transverse or longitudinal lie when labor begins.
Presentation describes the part of the fetus that is lowermost in the pelvis: cephalic, breech, or shoulder. Cephalic presentations are further subdivided into vertex, brow, and face presentations.
Position of the presenting part is described as a relationship between a certain pole of the fetal presenting part and the maternal surrounding pelvis.
Fetal lie, presentation, and position can often be determined by manual pelvic and abdominal examination. Ultrasonography is also useful, particularly, when palpation is inconclusive, as can occur with maternal obesity, multiple gestations, placenta previa, and hydramnios.
Cunningham FG, Leveno KJ, Bloom SL, et al, eds. Williams Obstetrics. 24th ed. New York: McGraw-Hill; 2014:433-438.
A.2. What is the approximate frequency of the various lies and presentations at or near term?
Longitudinal lie, >99%, including cephalic presentation, 97%; breech presentation, 3% to 4%; transverse lie, 0.3%; compound presentation, 0.1%; face presentation, 0.05%; and brow presentation, 0.01%.
Cunningham FG, Leveno KJ, Bloom SL, et al, eds. Williams Obstetrics. 24th ed. New York: McGraw-Hill; 2014:434.
A.3. What are the different types of breech presentation, and what is their incidence?
Frank breech: Both fetal lower extremities are flexed at the hips and extended at the knees. The incidence is approximately 60% (48% to 73%) of breech presentations.
Complete breech: The knees are flexed, as are the hips. The incidence is approximately 10% (4.6% to 11.5%).
Incomplete or footling breech: One or both hips are extended and a foot or knee hangs below the breech. The incidence is approximately 30% (12% to 38%).
Gabbe SG, Niebyl JR, Simpson JL, et al, eds. Obstetrics: Normal and Problem Pregnancies. 6th ed. Philadelphia, PA: Elsevier/Saunders; 2012:396-402.
A.4. What is the cause of breech presentation?
The etiology of breech is unknown, but certain factors are associated with this presentation including prematurity, hydramnios, uterine relaxation associated with high parity, multiple fetuses, oligohydramnios, hydrocephaly, anencephaly, uterine anomalies, pelvic tumors, placenta previa, cornual-fundal placenta implantation, and previous breech delivery. Ford et al. found that the rate of breech recurrence after a previous breech pregnancy was 9.9%, and after two prior breech deliveries, the incidence of another breech presentation was 27.5%. After a prior cesarean delivery, a twofold increase in the incidence of breech presentation has been reported.
Cunningham FG, Leveno KJ, Bloom SL, et al, eds. Williams Obstetrics. 24th ed. New York: McGraw-Hill; 2014:559-560.
Ford JB, Roberts CL, Nassar N, et al. Recurrence of breech presentation in consecutive pregnancies. BJOG. 2010;117(7):830-836.
A.5. What are the perinatal problems associated with breech presentation?
There is an increased incidence of prolapsed cord, perinatal morbidity and mortality resulting from difficult delivery, preterm delivery, fetal anomalies, placenta previa, and uterine anomalies.
Cunningham FG, Leveno KJ, Bloom SL, et al, eds. Williams Obstetrics. 24th ed. New York: McGraw-Hill; 2014:561.
A.6. What is the usual obstetrical management for patients with breech presentation?
An external cephalic version is attempted to convert the breech to a vertex presentation in nonlaboring patients who are candidates for vaginal deliveries. In general, the American College of Obstetricians and Gynecologists (ACOG) recommends that external version should be considered in patients when a breech presentation is recognized prior to labor at or after 36 weeks’ gestation. The reported success rates vary from 35% to 86%. Successful version is more commonly associated with multiparity, abundant amniotic fluid, a non-engaged presenting part, fetal size ranging from 2,500 to 3,000 g, a posterior placenta, and non-obesity. Tocolysis has been shown to be variably effective in improving version success rates; there is
more evidence to support betamimetic tocolysis than the use of nifedipine or nitroglycerin. Epidural anesthesia during version has been shown by Schorr et al. and Mancuso et al. to improve the success rate of external cephalic version. While others have found no improvement in version success associated with neuraxial analgesia/anesthesia, Collaris and Oei found that maternal and fetal complications increased when conduction anesthesia had been used, and they concluded that the decreased maternal pain associated with these versions encouraged an overzealous application of force. A meta-analysis of six randomized trials involving 508 attempted versions found that spinal or epidural anesthesia improved the rate of success to 59.7% compared to 37.6% for those receiving intravenous or no analgesia. According to ACOG in 2014, there is evidence that success may be enhanced by regional anesthesia. If the version is successful, labor and vaginal delivery may proceed.
more evidence to support betamimetic tocolysis than the use of nifedipine or nitroglycerin. Epidural anesthesia during version has been shown by Schorr et al. and Mancuso et al. to improve the success rate of external cephalic version. While others have found no improvement in version success associated with neuraxial analgesia/anesthesia, Collaris and Oei found that maternal and fetal complications increased when conduction anesthesia had been used, and they concluded that the decreased maternal pain associated with these versions encouraged an overzealous application of force. A meta-analysis of six randomized trials involving 508 attempted versions found that spinal or epidural anesthesia improved the rate of success to 59.7% compared to 37.6% for those receiving intravenous or no analgesia. According to ACOG in 2014, there is evidence that success may be enhanced by regional anesthesia. If the version is successful, labor and vaginal delivery may proceed.
The 2006, and reaffirmed in 2012, recommendation from ACOG for breech delivery of the singleton fetus states “the decision regarding mode of delivery should depend on the experience of the health care provider,” and “planned vaginal delivery of a term singleton breech fetus may be reasonable under hospital-specific protocol guidelines.” Cesarean delivery is commonly used in the following circumstances: lack of operator experience, incomplete or footling breech, hyperextended fetal head, fetal macrosomia, unfavorable pelvic shape, severe fetal growth retardation, fetal anomaly incompatible with vaginal delivery, healthy preterm fetus with maternal labor or with indicated delivery, previous perinatal death/trauma, maternal cesarean section request, and possibly previous cesarean delivery. The availability of skilled operators to safely deliver breech fetuses vaginally seems to be declining at least in Australia. The rates of planned vaginal delivery attempts, at least in Dublin, Ireland, are also declining.
American College of Obstetricians and Gynecologists. External cephalic version. ACOG Practice Bulletin Number 13 February 2000. Obstet Gynecol. 2000;95(2). Reaffirmed 2012.
American College of Obstetricians and Gynecologists, Society for Maternal-Fetal Medicine. Obstetric care consensus no. 1: safe prevention of the primary cesarean delivery. Obstet Gynecol. 2014;123(3):693-711.
American College of Obstetricians and Gynecologists Committee on Obstetric Practice. ACOG Committee Opinion No. 340. Mode of term singleton breech delivery. Obstet Gynecol. 2006;108(1):235-237. Reaffirmed 2012.
Collaris RJ, Oei SG. External cephalic version: a safe procedure? A systematic review of version related risks. Acta Obstet Gynecol Scand. 2004;83:511-518.
Cunningham FG, Leveno KJ, Bloom SL, et al, eds. Williams Obstetrics. 24th ed. New York: McGraw-Hill; 2014:558, 562, 570-541.
Goetzinger KR, Harper LM, Tuuli MG, et al. Effect of regional anesthesia on the success rate of external cephalic version: a systematic review and meta-analysis. Obstet Gynecol. 2011;118(5):1137-1144.
Mancuso KM, Yancey MK, Murphy JA, et al. Epidural anesthesia for cephalic version: a randomized trial. Obstet Gynecol. 2000;95(5):648.
Schorr SJ, Speights SE, Rose EL, et al. A randomized trial of epidural anesthesia to improve external cephalic version success. Am J Obstet Gynecol. 1997;177:1133.
A.7. What is the incidence of heart disease in pregnancy and the mortality rate associated with maternal cardiac disease?
The incidence of cardiac disease is around 1% and is now the leading cause of indirect maternal deaths accounting for 20% of the deaths. Worldwide, rheumatic fever is the main cause of the cardiac valvular disease encountered during pregnancy. Congenital heart disease, not rheumatic heart disease, is now the major cause of heart disease in pregnancy in the developed world. In the developing world and in immigrants to developed countries, rheumatic heart disease continues to be a major problem. Small et al. also found that cardiovascular disease was a leading obstetrical cause for intensive care unit admission.
Chestnut DH, Wong CA, Tsen LC, et al, eds. Chestnut’s Obstetric Anesthesia: Principles and Practice. 5th ed. Philadelphia, PA: Elsevier Saunders; 2014:881.
Cunningham FG, Leveno KJ, Bloom SL, et al, eds. Williams Obstetrics. 24th ed. New York: McGraw-Hill; 2014:958, 973.
Small MJ, James AH, Kershaw T, et al. Near-miss maternal mortality: cardiac dysfunction as the principal cause of obstetric intensive care unit admission. Obstet Gynecol. 2012;119(2 pt 1):250-255.
A.8. What classifications may help predict an individual pregnant woman’s cardiac risk?
The NYHA classification of a complete diagnosis of cardiovascular disease is not widely used now. The grading of dyspnea and/or fatigue resulting from heart failure is, however, often still classified using the old functional NYHA classification.
Class I: no limitation of physical activity
Class II: slight limitation of physical activity; symptoms with ordinary activity
Class III: marked limitation of physical activity; symptoms with less than ordinary activity
Class IV: unable to carry on any physical activity without discomfort; symptoms may be present at rest
On the basis of an analysis of 562 pregnant patients with heart disease, Siu et al. expanded on the NYHA classification and developed a system for predicting complications during pregnancy. Their predictors of cardiac complications included the following:
Prior heart failure, arrhythmia, transient ischemic attack, or stroke
A baseline NYHA III or IV classification or cyanosis
A left-sided heart obstruction defined as a mitral valve area less than 2 cm2, aortic valve area less than 1.5 cm2, or an echocardiographically demonstrated peak left ventricular outflow tract gradient exceeding 30 mm Hg
Less than 40% ejection fraction
Their cardiac disease in pregnancy (CARPREG) scoring system helps predict maternal cardiac events. Each predictor is 1 point. With one of these factors, the risk of sustained arrhythmia, pulmonary edema, stroke, or cardiac death was increased, and if two or more factors existed, the risk was enhanced. The cardiac complication rate associated with 0 point is 5%, with 1 point is 27%, and with ≥2 points is 75%. There were no maternal deaths in patients in NYHA class I or II. Similarly, Stangl et al. found that pregnant patients with acquired and congenital cardiac disease were at increased risk of maternal and fetal morbidity and mortality if they had a left ventricular ejection fraction <50%, an NYHA class >II, a peak left ventricular outflow gradient >60 mm Hg, or were cyanotic. The CARPREG risk score has been validated in several studies and appears to be a valuable tool to predict maternal risk in acquired and congenital heart disease. Drenthen et al. investigated populations with congenital heart disease that has yet to be validated by other studies and outlined created a ZAHARA point system for predicting maternal cardiovascular events.
The European Task Force recommends that maternal risk assessment be based on the World Health Organization risk classification for cardiovascular disease in pregnancy (Table 29.1).
Maternal cardiac disease is associated with a 20% to 28% neonatal complication rate; neonatal and maternal adverse events are highly correlated. In women with cardiac disease, maternal predictors of increased neonatal adverse events include a baseline NYHA class >II, cyanosis, smoking during pregnancy, left-sided heart obstruction, multiple gestations, oral anticoagulation during pregnancy, and mechanical valve prosthesis.
Cunningham FG, Leveno KJ, Bloom SL, et al, eds. Williams Obstetrics. 24th ed. New York: McGraw-Hill; 2014:976-977.
Drenthen W, Boersma E, Balci A, et al. Predictors of pregnancy complications in women with congenital heart disease. Eur Heart J. 2010;31(17):2124-2132.
Regitz-Zagrosek V, Blomstrom Lundqvist C, Borghi C, et al. ESC guidelines on the management of cardiovascular diseases during pregnancy: the Task Force on the Management of Cardiovascular Diseases during Pregnancy of the European Society of Cardiology (ESC). Eur Heart J. 2011;32(24):3147-3197.
Siu SC, Sermer M, Colman JM, et al. Prospective multicenter study of pregnancy outcomes in women with heart disease. Circulation. 2001;104(5):515-521.
Stangl V, Schad J, Gossing G, et al. Maternal heart disease and pregnancy outcome: a single-centre experience. Eur J Heart Fail. 2008;10(9):855-860.
TABLE 29.1 Modified World Health Organization (WHO) Risk Classification for Cardiovascular Disease in Pregnancy | ||||||||||||||
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A.9. What are the cardiovascular changes of pregnancy?
During the first trimester of pregnancy, the cardiac output increases to between 40% and 50% above the normal nonpregnant level and plateaus at approximately 28 weeks of gestation. It remains fairly stable until the stresses imposed by labor increase it further. The increase in cardiac output is due to a 30% increase in stroke volume and a 15% increase in heart rate. Blood pressure, however, is not elevated because peripheral vascular resistance decreases. Central venous pressure, pulmonary capillary wedge pressure, pulmonary artery diastolic pressure, and left ventricular stroke work index are unchanged when compared to nonpregnant values.
During labor, cardiac output increases approximately 15% with uterine contractions during the latent phase, 30% in the active phase, and 45% in the expulsive phase when compared to prelabor values. The greatest increase in cardiac output occurs immediately postpartum when it increases an average of 80% above prelabor values. Cardiac output and heart rate decline to prelabor values within 1 hour of delivery, and by approximately 24 hours, mean blood pressure and stroke volume return to their prelabor values. In the first 3 to 6 months
after delivery, the cardiovascular changes of pregnancy resolve. It can take a year, however, for the residual effects of cardiovascular remodeling to subside.
after delivery, the cardiovascular changes of pregnancy resolve. It can take a year, however, for the residual effects of cardiovascular remodeling to subside.
Cunningham FG, Leveno KJ, Bloom SL, et al, eds. Williams Obstetrics. 24th ed. New York: McGraw-Hill; 2014:59-60, 974.
Walsh RA, Fang JC, Fuster V, eds. Hurst’s The Heart: Manual of Cardiology. 13th ed. New York: McGraw-Hill; 2013:628-629.
A.10. What changes may normally occur in heart sounds during pregnancy?
In a study of 50 normal pregnant women at varying stages in pregnancy, a phonocardiographic study found that the first heart sound might have an exaggerated split with increased loudness of both components. In up to 84% of pregnant patients, a third heart sound is also evident. In 16% of pregnant women, a fourth heart sound may be heard, but it typically disappears by term. Functional systolic murmurs, which disappear shortly after delivery, occur in more than 90% of pregnant women. Soft transient diastolic murmurs occur in 18% of these women, and 10% have continuous murmurs apparently arising from the breast vasculature. These murmurs alone, therefore, are not indicative of organic heart disease. Similarly, venous distention, tachycardia, edema, and breathlessness may be seen with pregnancy and not be a sign of heart disease. Audible diastolic murmurs on auscultation are uncommon, however, and warrant further investigation.
Chestnut DH, Wong CA, Tsen LC, et al, eds. Chestnut’s Obstetric Anesthesia: Principles and Practice. 5th ed. Philadelphia, PA: Elsevier Saunders; 2014:16. Walsh RA, Fang JC, Fuster V, eds. Hurst’s The Heart: Manual of Cardiology. 13th ed. New York: McGraw-Hill; 2013:628-631.
A.11. What are the normal electrocardiographic and echocardiographic changes seen during pregnancy?
Premature atrial and ventricular contractions can occur. The QRS axis may shift to the right during the first trimester and then to the left, -15 degrees, in the third trimester. A true left axis deviation, -30 degrees, implies heart disease. In lead III, inverted P waves and small Q waves may be seen that disappear with inspiration. Some ST-segment depression and flattening or inverting of the T waves may occur. ST elevations, however, do not occur normally during pregnancy and should be considered pathologic.
Normal echocardiographic findings include an increase in atrial diameters bilaterally. Left ventricular wall mass is increased. Left ventricular function is unchanged or slightly improved. During end-diastole and end-systole, the left and right ventricular chamber sizes are increased; left ventricular mass increases. The annuli of the pulmonary, tricuspid, and mitral valves dilate progressively, and term pregnant women may have mild tricuspid, pulmonic, and/or much more infrequently mitral regurgitation. A small pericardial effusion may develop as well.
Chestnut DH, Wong CA, Tsen LC, et al, eds. Chestnut’s Obstetric Anesthesia: Principles and Practice. 5th ed. Philadelphia, PA: Elsevier Saunders; 2014:16, 961, 964-965.
Cunningham FG, Leveno KJ, Bloom SL, et al, eds. Williams Obstetrics. 24th ed. New York: McGraw-Hill; 2014:976.
Desai DK, Moodley J, Naidoo D. Echocardiographic assessment of cardiovascular hemodynamics in normal pregnancy. Obstet Gynecol. 2004;104(1):20-29.
Walsh RA, Fang JC, Fuster V, eds. Hurst’s The Heart: Manual of Cardiology. 13th ed. New York: McGraw-Hill; 2013:632.
A.12. What causes rheumatic heart disease?
Rheumatic heart disease may occur in patients who have had acute rheumatic fever (ARF). ARF is an immune-mediated illness that may develop after some group A streptococcal infections. It predominantly affects the heart and joints and may lead to chronic rheumatic heart disease. In individuals who appear to be genetically susceptible, ARF may follow an untreated pharyngeal group A streptococcal infection. ARF occurs most commonly in 5- to 15-year-old children and occurs most commonly in the winter or spring. It is much less common in developed countries than it was a few decades ago. Treatment of ARF includes
an anti-inflammatory agent for those with arthritis and/or mild carditis, an agent such as phenobarbital, diazepam, haloperidol, etc. for those with chorea, and a prophylactic antibiotic. Long-term antibiotic prophylaxis is indicated because ARF frequently recurs with subsequent group A streptococcal infections. The duration of this secondary prophylaxis against recurrent rheumatic fever depends on the presence or absence of carditis and/or valvular disease.
an anti-inflammatory agent for those with arthritis and/or mild carditis, an agent such as phenobarbital, diazepam, haloperidol, etc. for those with chorea, and a prophylactic antibiotic. Long-term antibiotic prophylaxis is indicated because ARF frequently recurs with subsequent group A streptococcal infections. The duration of this secondary prophylaxis against recurrent rheumatic fever depends on the presence or absence of carditis and/or valvular disease.
The diagnosis of ARF is a clinical one, and the manifestations are extremely variable. There are no specific laboratory tests to confirm the diagnosis, and the exact pathogenetic mechanism is unknown. The diagnosis is made using the original Jones criteria and the 1992 American Heart Association committee update. In addition to the requirement of supporting evidence of an antecedent group A streptococcal tonsillopharyngitis infection, there are five major criteria: carditis, polyarthritis, Sydenham chorea, erythema marginatum, and subcutaneous nodules. Several minor criteria exist. The presence of one major and two minor or two major criteria are needed for the diagnosis.
Rheumatic heart disease is the only long-term sequela of ARF. With the improved ability to prevent recurrent attacks, the prognosis of these patients has improved greatly. An individual’s prognosis is related directly to the severity of cardiac involvement during the acute phase. On 10-year follow-up after ARF, only 6% of patients with no history of carditis had heart murmurs. Heart disease occurred, however, in 30%, 40%, and 68% of the patients who had apical systolic murmurs, basal diastolic murmurs, and pericarditis and/or congestive heart failure, respectively, during the initial attack. With the use of echocardiography and based on screening 5,800 randomly selected schoolchildren in Colombia and Mozambique, studies have found that the prevalence of rheumatic heart disease in developing countries is about 10-fold greater than that recognized by conventional screening.
In almost all adults, mitral stenosis is caused by a previous rheumatic carditis. Approximately 60% of the patients with rheumatic mitral valve disease report no history of rheumatic fever or chorea. In about 40% of all patients with rheumatic heart disease, an isolated mitral stenosis occurs. Mitral valve insufficiency and aortic valve stenosis and insufficiency can also occur in these patients.
Bennett JE, Dolin R, Blaser MJ, eds. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases. 8th ed. Philadelphia, PA: Saunders/Elsevier; 2015:2300.e3-2309.e3.
Mann DL, Zipes DP, Libby P, et al, eds. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 10th ed. Philadelphia, PA: Saunders/Elsevier; 2015:1834-1842.
Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Thorac Cardiovasc Surg. 2014;148(1):e1-e132.
Walsh RA, Fang JC, Fuster V, eds. Hurst’s The Heart: Manual of Cardiology. 13th ed. New York: McGraw-Hill; 2013:380.
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