Ebook A practical approach to obstetric anesthesia (2/E): Part 1

(BQ) Part 1 book “A practical approach to obstetric anesthesia” has contents: Physiologic changes of pregnancy, local anesthetics and toxicity, obstetric medications, ethical and legal considerations in obstetric anesthesia, nonobstetric surgery during pregnancy, fetal assessment and monitoring,… and other contents.

examination of each patient and consideration of, among other things, age, weight, gender, current or prior medical conditions, medication history, laboratory data, and other factors unique to the patient The

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To the memory of Dr Geraldine O’Sullivan

A PRACTICAL A PPROACH TO O BSTETRIC A NESTHESIA, 2ND E DITION

There is certainly no shortage of obstetric anesthesia texts currently available,from introductory handbooks to encyclopedic treatises What has been lacking is

a book that straddles the middle ground between those extremes, a book thatwould serve to supply both experienced and novice clinicians with guidance formanaging routine and complicated parturients, as well as providing an

section Key points are noted at the beginning of each chapter Clinical Pearls areembedded within the text Each chapter also contains a list of current and

relevant references The use of color in this edition highlights important sections

to improve readability

This book would not have been possible without the commitment and hard work

of more than 40 contributors as well as the production staff at Wolters Kluwer

I would like to dedicate this book to the memory of Sol Shnider, who started me

on my career in obstetric anesthesia; to my parents, Roy and Mary Lee, whoseresources and encouragement helped make my career in medicine a reality; to

my children, Charles and Katherine, who have honored me by pursuing careers

as physicians; and to my wife Mary, whose love and support I receive daily

Curtis L Baysinger

I would like to dedicate this book to my husband, Uli, my parents, and all of thelearners who study obstetric anesthesiology

Brenda A Bucklin

I would like to acknowledge two important mentors, Professor Graham

McMorland and Professor Joanne Douglas, who facilitated my understanding ofobstetric anesthesia I dedicate this book to the memory of my father Gordon and

to acknowledge the love and support of my wife Kimberley; my children

Carwyn, Jake, and Samantha; and my mother Sadie

David R Gambling

Bryan S Ahlgren, DO

Assistant Professor

University of Colorado School of MedicineAurora, Colorado

Mrinalini Balki, MB, BS; MD

Associate Professor

University of Toronto

Department of Anesthesia and Pain ManagementDepartment of Obstetrics and GynaecologyMount Sinai Hospital

Wake Forest School of Medicine

Winston-Salem, North Carolina

James P.R Brown, MBChB(Hons), MRCP, FRCAConsultant Anesthesiologist, Clinical Instructor

Laurie A Chalifoux, MD

Assistant Professor of Anesthesiology

Northwestern University Feinberg School of MedicineChicago, Illinois

Debnath Chatterjee, MD

Associate Professor of Anesthesiology

Children’s Hospital Colorado/University of Colorado School of MedicineAurora, Colorado

Consultant Anesthetist

University College London Hospitals NHS Foundation TrustLondon, United Kingdom

Dominique Moffitt, MD

Instructor in Anaesthesia

Pharmacology and Physiology

A Increased minute ventilation and reduced functional residual capacity

3. Increases in progesterone result in decreased lower esophageal sphinctertone and render the parturient at high risk for aspiration of gastric

contents

4. Renal blood flow increases during pregnancy, resulting in increased

glomerular filtration rate This leads to increased creatinine clearance anddecreased blood urea nitrogen (BUN) and creatinine (normal ~0.5 to 0.6

mg per dL at term)

5. Pain tolerance increases throughout pregnancy Hormonal changes lead todecreases in anesthetic requirements and an approximately 30% decrease

in minimum alveolar concentration (MAC)

NORMAL PREGNANCY IS MARKED BY significant physiologic changes in everyorgan system in order to meet the metabolic demands of the growing uterus,fetus, and placenta Knowledge of these changes is critical for the obstetricanesthesiologist because they have significant implications for anesthetic

management of the parturient In addition, these physiologic changes can have asignificant impact on preexisting pathophysiology

In this chapter we describe the system-based physiologic changes of pregnancy

as well as the anesthetic considerations that result from these changes Eachsection in this chapter discusses potential impact of normal physiologic changes

on relevant preexisting patient comorbidities

I. Cardiovascular system

A Central hemodynamic changes

Pregnancy is associated with profound adaptive changes in

1 Blood volume

a Blood volume increases during pregnancy1,2 (Table 1.1).This increase begins in early pregnancy, rises rapidly inthe second trimester, and peaks and stabilizes around 34weeks’ gestation Plasma volume increases more than redblood cell volume, resulting in a “physiologic anemia ofpregnancy” with a normal hemoglobin concentration of11.6 g per dL at term pregnancy.3 This level may be less ifthere is superimposed iron deficiency anemia

stroke volume (SV) and heart rate (HR) during pregnancy

HR peaks at 10 to 20 beats per minute (bpm) above theprepregnancy rate at term During labor, SV increasesdramatically, whereas HR increases slightly, leading to up

b Left ventricular hypertrophy (LVH) occurs progressively

throughout pregnancy, with a 23% increase in mass fromthe first to third trimesters.7

c Although an increase in myocardial contractility is

suggested by an increase in the velocity of LV

circumferential fiber shortening, this can be explained on

Intrinsic contractility as measured by left ventricularstroke work index (LVSWI) is unchanged

d HR increases steadily throughout pregnancy, peaking at

10 to 20 bpm above baseline at term Further increases areseen as a result of the pain and stress of labor

C Aortocaval compression

1 Compression of the inferior vena cava against the vertebral

column by the enlarged uterus (significant once the uterusmoves out of the pelvis between 16 and 20 weeks’ gestation)when in a supine position will lead to a reduction in venousreturn Although this is partially compensated by collateralblood flow, for example, through the azygos system, the netresult is a decrease in venous return to the heart and

subsequently CO is decreased

2 Compression of the aorta by the enlarged uterus may increase

measured blood pressure in the arm, by a mechanismanalogous to an aortic cross clamp Because the hypogastricartery, of which the uterine artery is a branch, arises distal tothe point of compression, uteroplacental perfusion may bedecreased in spite of an apparently increased systemic bloodpressure as described earlier Significant aortoiliac arterycompression by the gravid uterus is seen in 15% to 20% ofpregnant women In many nonlaboring patients, this isasymptomatic

3 A recent study evaluated the degree of tilt necessary to

minimize aortocaval compression in term, nonlaboringpatients prior to cesarean delivery (CD) CO and pulsepressure were highest at 15 degrees of left tilt, equal to full90-degree left lateral position This was significantly higherthan at 0 and 7.5 degrees of left tilt, suggesting that 15degrees is sufficient to restore CO.11

4 As a result, the supine position should be avoided in all pregnant patients at 20 weeks’ gestation or greater, and especially in all term parturients This applies even more following placement of a neuraxial anesthetic.

The enlarged uterus causes aortocaval compression in the supine position and may lead to decreased

venous return, decreased CO, and severe hypotension When the

supine position is required, the patient must be placed with at least a 15-degree left lateral tilt One of the most effective ways to assess for effective left uterine displacement is to visualize the

displacement of the uterus from the perspective of the head of the patient’s bed.

II. Respiratory system

A Arterial blood gases

1 Progesterone sensitizes central respiratory centers, increasing

the ventilatory response to CO2.12 Both tidal volume (majorcontributor) and respiratory rate (negligible to 1 to 2 bpm) areincreased and contribute to pregnancy-induced increasedminute ventilation A recent study has shown that thehyperventilation of human pregnancy is the result ofpregnancy-induced changes in wakefulness and centralchemoreflex drives for breathing, acid–base balance,metabolic rate, and cerebral blood flow.13 This explains whynormal PaCO2 in a pregnant patient is 30 to 32 mm Hg (Table1.3) Although there is increased urinary excretion of

bicarbonate (normal pregnant level 20 mm Hg), pH ispartially corrected; normal pH is 7.41 to 7.44.14

2 Hyperventilation causes decreased alveolar CO2, which, bythe alveolar gas equation, leads to an increase in PaO2 (normal

103 to 107 mm Hg)

B Lung volumes and capacities and respiratory mechanics8

(Table 1.4)

thoracic cage causes decreased chest wall excursion

C Mechanisms of hypoxemia in pregnancy16

1 Oxygen consumption (Table 1.5)

placenta, and the fetus cause oxygen consumption toincrease throughout pregnancy, increasing 40% to 60%above prepregnancy levels at term.17

minutes 25 seconds in nonpregnant subjects In

addition, the time taken for SaO2 to fall to 40% from 90%was 35 seconds in pregnant subjects and 45 seconds innonpregnant subjects During pregnancy, the hypoxicventilatory response is increased due to elevations inestrogen and progesterone

c Fetal hemoglobin has a P50 of approximately 18 mm Hg,

providing very effective loading of oxygen (and

unloading of maternal hemoglobin) in the uteroplacentalbed In addition, fetal hemoglobin does not interact with2,3-diphosphoglycerate, which also favors loading ofoxygen molecules from maternal hemoglobin Thus, thefetus effectively extracts the maximum amount of oxygenpossible from maternal blood

2 Decreased functional residual capacity Elevation of the

diaphragm during pregnancy leads to increased basilaralveolar atelectasis Functional residual capacity (FRC)essentially represents the stores of oxygen available during aperiod of apnea; therefore, a decrease in FRC shortens thetime to development of hypoxemia

Parturients are susceptible to rapid decreases in oxygen saturation with periods of apnea due to

decreases in FRC and increased oxygen consumption.

Preoxygenation of the parturient prior to general anesthesia and

endotracheal intubation is essential and will help alleviate severe arterial oxygen desaturation.

3 Compared to sitting or standing, FRC is significantly lower in

the supine position due to further cephalad movement of thediaphragm and increased posterior basilar atelectasis In thesupine position, FRC exceeds closing capacity This leads tosmall airway closure, an increase in ventilation/perfusion () mismatch, and decreased O2 saturation

4 Decreased CO in the supine position will cause decreased

mixed venous saturation and therefore decreased arterial O2saturation Appropriate left uterine displacement will helpmaintain adequate venous return and subsequent CO

Hg This extreme degree of hypocarbia may cause subsequent

2 At the same time, oxygen consumption is increased (i.e., a

doubling of ventilation by the parturient can increase oxygenconsumption by as much as 50%).19 As a result, significanthypoxemia can occur between contractions Maternal bloodlactate increases, indicating that aerobic oxygen requirementsexceed oxygen consumption during labor Although hypoxicventilatory drive is increased during pregnancy, it may not bepossible to match oxygen consumption without supplementaloxygen

F Oxygen delivery

1 The mild increase in dissolved oxygen in maternal blood

during pregnancy does not improve oxygen delivery to thefetus

2 However, oxygen delivery to the fetus is improved by a shift of the maternal oxygen dissociation curve to the right.21 The maternal P50 increases from 26 to 30 mm Hg atterm

3 As mentioned earlier, fetal ability to extract oxygen from

maternal hemoglobin is augmented by the higher oxygenaffinity of fetal hemoglobin, which has a P50 of 18 mm Hg

A Dilutional anemia

1 Red cell mass is increased during pregnancy Plasma volume

increases to a greater extent, however, producing the so-calleddilutional anemia of pregnancy

the coagulation and fibrinolytic systems (Table 1.6)

2 Although physiologic procoagulant changes serve to

minimize intrapartum blood loss, they also increase the risk ofthromboembolism during pregnancy and the postpartum

demonstrate an increase in endogenous thrombin potentialthroughout pregnancy.25 The CAT test measures protein Slevels and activity, which are reduced significantly duringpregnancy, and is able also to indicate increases in

plasminogen activator inhibitor-1, thrombin–antithrombincomplex, and tissue factor pathway inhibitor during

pregnancy Antithrombin levels and protein C levels remainstable throughout pregnancy It is unknown whether theseobserved changes correlate with thromboembolic disease

Pregnancy is associated with hyperfibrinogenemia Decreases in serum fibrinogen, especially

pregnancy, increasing from 6,000 per mm3 to 9,000 to 11,000per mm3 The increase is mostly due to polymorphonuclearcells, whereas lymphocyte, eosinophil, and basophil countsfall The monocyte count is unchanged Further increases inthe leukocyte count are seen during labor and may reach15,000 per mm3 on the first day postpartum

2 Polymorphonuclear leukocyte function is impaired during

pregnancy, which may account for the increased incidenceand severity of infection during pregnancy as well as thereduction of symptoms in some pregnant women withautoimmune disease.26 Impaired immune response is likely anevolutionary development to prevent maternal cells fromattacking fetal tissue in a host-versus-graft reaction

3 However, autoantibody production is unchanged during

pregnancy Serum levels of immunoglobulin A, G, and M areunaltered during pregnancy, whereas humoral antibody titers

to certain viruses, such as measles, influenza A, and herpessimplex, are decreased

IV. Gastrointestinal system

A Gastric position and pressure

1 As the uterus enlarges, it displaces abdominal contents,

including the stomach, in a cephalad direction This not onlyimpacts the interaction of the lower esophageal sphincter(LES) and diaphragm (see subsequent text) but also causesintragastric pressure to increase

B Lower esophageal sphincter tone

1 Progesterone (and to some degree estrogen) relaxes the

smooth muscle of the LES,27 decreasing the barrier pressurethat normally prevents gastroesophageal reflux Elevation androtation of the stomach by the enlarging uterus eliminates the

“pinch valve” at the entry point of the esophagus through the

diaphragm, further decreasing the barrier to reflux All of

these changes increase both the risk of regurgitation and