CHAPTER 24 Anesthesia for Obstetrics

Introduction

Pregnancy is unique to all clinicians because of the responsibilities of two lives. Physiological changes occur in pregnancy due to hormones secreted by corpus luteum and placenta, like progesterone, and the mechanical effects by the gravid uterus. Interaction between mother and fetus both at physiological as well as pharmacokinetic level make anesthetic management challenging in such a group of patients. Following is the detailed discussion about physiological changes in pregnancy:

1. Cardiovascular system

Changes occur to provide the growing needs of the fetus, to maintain adequate fetal oxygenation, as well as to compensate for reduced venous return in the mother. These changes in the cardiovascular system are illustrated in Table 24.1.

Table 24.1 Cardiovascular changes in pregnancy
Table 24.1 Cardiovascular changes in pregnancy

Cardiovascular parameter

Change

Anesthetic implication

Heart rate

+20–30%

Due to hyperdynamic circulation—more prone to CHF

Stroke volume

+20–50%

Cardiac output

+30–50%

  • Increases from 5th week onwards

  • Reaches maximum by 32 weeks during pregnancy

  • Highest is in the immediate postpartum period (increase by up to 75%)

Uterine perfusion

Increased to 10% of cardiac output

Uterine perfusion not autoregulated

Supine hypotension syndrome

  • IVC compression by 13–16 weeks

  • Aortic compression by 28–30 weeks

Supine hypotensive syndrome requires left lateral tilt by wedge placement of 15–20°, exacerbates hypotension caused due to GA and RA

Central venous pressure

Unchanged

Pulmonary capillary wedge pressure

Unchanged

Systemic vascular resistance

–20%

Hypotension common under RA and GA

Blood pressure

A slight decrease in the second trimester by 10–15 mm Hg. Both systolic as well as diastolic pressure fall

Pulmonary vascular resistance

–30%

Pulmonary artery pressure

–30%

Wide, loud, and split S1, S3 and soft ejection systolic murmur on auscultation

ECG: Left axis deviation—due to upward displacement of heart by the uterus

Arrhythmias: Sinus tachycardia, ventricular ectopics, paroxysmal supraventricular tachycardia, paroxysmal atrial complexes, ventricular arrhythmias

Abbreviations: CHF, congestive heart failure; GA, general anesthesia; IVC, inferior vena cava; RA, regional anesthesia.

Note: Remember diastolic murmur in preg­nancy is always pathological.

Supine hypotension syndrome: In this pheno­menon, circulatory collapse occurs due to diminished venous return and because of gravid uterus compressing over inferior vena cava (IVC) in the supine position in parturients by 13 to 15 weeks. This causes hypotension and decreased cardiac output. Turning the patient to lateral position (left) restores venous return and corrects hypotension. The gravid uterus also compresses over the aorta, which occurs by 28 to 30 weeks, compromising uteroplacental flow which, in turn, leads to reduced fetal perfusion in the supine position. This aortocaval compression is a preventable because of fetal distress; hence, left uterine displacement should be done with a wedge (Crawford wedge) of >15° under the right hip as a precaution in the OT.

2. Hematological system

Maternal hematological changes begin to occur early in pregnancy as mentioned in Table 24.2.

Table 24.2 Hematological changes in pregnancy
Table 24.2 Hematological changes in pregnancy

Parameter

Change

Anesthetic implication

Blood volume

+45%

Dilutional/physiological anemia of pregnancy

Plasma volume

+55%

Red blood cell volume

+30%

Coagulation factor

Change/effect

Factor II

Unchanged

Factor VII

Increased

Factors VIII, IX, X, XII

Increased

Factor XI

Reduced

Fibrinogen

Increased

Platelets

Dilutional thrombocytopenia

↑ Coagulation factors

Thromboembolic complications (DVT prophylaxis)

↓ Albumin and colloid osmotic pressure

Edema, decreased protein binding of drugs

Abbreviation: DVT, deep vein thrombosis.

3. Respiratory System

Changes in the respiratory system during pre­gnancy are summarized in Table 24.3.

Table 24.3 Changes in the respiratory system during pregnancy
Table 24.3 Changes in the respiratory system during pregnancy

Parameter

Change

Cause

Anesthetic implication

1. Respiratory mechanics

Pulmonary resistance

Decreases by 50%

Due to bronchiolar dilatation by progesterone

FEV1, FEV1/FVC

No change

Type of breathing

Diaphragmatic type

Limited thoracic cage movement and pressure of gravid uterus and upward displacement of the diaphragm

The potential risk of hypoxemia in the supine and Trendelenburg positions

Mucosal edema and increased friability

  • Difficult laryngoscopy and intubation; bleeding during attempts

  • Smaller endotracheal tube preferred (size 6–7 mm OD)

  • Increased work of breathing

2. Respiratory physiology at term gestationa

Tidal volume, minute and alveolar ventilation

Respiratory rate unchanged

+45%

Increased oxygen demand and increased requirement for CO2 elimination

Faster inhalation induction

FRC

–20%

Shorter apnea time during intubation; hence, parturients desaturate faster

Preoxygenation for 5 mins reduces the rate of desaturation

Closing capacity

Unchanged

Total lung capacity, expiratory reserve volume, residual volume

Reduced

Table 24.3 (Continued)
Table 24.3 (Continued)

3. Blood gas parameterb

Nonpregnant

First trimester

Second trimester

Third trimester

Comments

PaCO2 mm Hg

40

30

30

30

PaO2 mm Hg

100

107

105

103

Increase is due to increase in minute ventilation

pH

7.40

7.44

7.44

7.44

Respiratory alkalosis of pregnancy

Bicarbonate

24

21

20

20

Abbreviations: FEV, forced expiratory volume; FRC, functional residual capacity; FVC, forced vital capacity; OD, outer diameter.

Notes: aProgesterone sensitizes the respiratory center to CO2 and is responsible for the increase in ventilation.

bThe rightward shift of the oxygen dissociation curve occurs during pregnancy.

4. Gastrointestinal system

Changes in the gastrointestinal (GI) system are tabulated in Table 24.4.

Table 24.4 Gastrointestinal changes in pregnancy
Table 24.4 Gastrointestinal changes in pregnancy

Gastrointestinal parameter

Cause

Anesthetic implication

↑Intragastric pressure

  • Progesterone and gastrin relaxes smooth muscles and impairs gastric and intestinal motility

  • Reduced motilin

  • Gravid uterus causes upward displacement of stomach and diaphragm

  • ↑ Aspiration risk

  • Antacid prophylaxis

  • RSI with cricoid pressure

  • After 12 weeks gestation, parturients should be considered full stomach

  • ETI preferred over LMA insertion—for airway protection

  • RA preferred over GA

↓ Barrier pressure

Residual volume of the stomach ↑

Increased gastrin secretion

Increased cortisol and human placental lactogen

Reduced glucose tolerance

Hyperglycemia and ketosis can be encountered

Abbreviations: ETI, endotracheal intubation; GA, general anesthesia; LMA, laryngeal mask airway; RA, regional anesthesia; RSI, rapid-sequence intubation.

Mendelson’s syndrome: It is the most common cause of death during general anesthesia (GA) in obstetrics. It is caused by pulmonary aspiration of gastric contents. It can be prevented by:

  • Empty stomach: Fasting for solids > 6 hours, clear liquids > 2 hours, before any anesthesia induction.

  • Reduction in gastric acid secretion by administering H2 blockers like ranitidine.

  • Neutralization of any acid produced in the stomach by giving 30 mL of 3M non­particulate antacid, like sodium citrate, 30 minutes before the induction of anesthesia.

  • Increasing lower esophageal sphincter tone and increasing gastric emptying by prokinetic drugs like metoclopramide.

  • Sellick maneuver (backward pressure on cricoid cartilage).

5. Renal system

Renal system changes in pregnancy are as men­tioned in Table 24.5.

Table 24.5 Renal changes in pregnancy
Table 24.5 Renal changes in pregnancy

Renal parameter change

Cause

Anesthetic implication

↑ Renal plasma flow ↑ GFR by 50%

  • Increased cardiac output during pregnancy

  • Elevated creatinine and uric acid clearance

Normal urea and creatinine may mask impaired renal function

↓ Reabsorptive capacity

  • Glycosuria up to 1–10 g/day

  • Proteinuria up to 300 mg/day

Dilatation of calyces, pelvis, ureters

Leads to urinary stasis—frequent UTI

Abbreviations: GFR, glomerular filtration rate; UTI, urinary tract infection.

6. Central nervous system

Pregnancy-related central nervous system (CNS) changes are summarized in Table 24.6.

Table 24.6 CNS changes in pregnancy
Table 24.6 CNS changes in pregnancy

CNS change

Cause

Anesthetic implication

1. RA

↑ Epidural vein engorgement

Due to the compression of IVC by gravid uterus—swelling of epidural veins and increased CSF pressure due to raised intraabdominal pressure

Bloody tap more common

↓ Epidural and subarachnoid space volume

More extensive local anesthetic spread in subarachnoid space leading to an increased chance of high spinal

↑ Sensitivity to LA

Dose requirement of LA reduced by 30%

↑ Lumbar lordosis

More cephalad spread of LA

2. GA

↑ Sensitivity to opioids and sedatives

Production of endogenous opioids and production of progesterone

The lesser requirement of those drugs

Reduced MAC of volatile anesthetics by 25–40%

Altered pain threshold

Abbreviations: CNS, central nervous system; CSF, cerebrospinal fluid; GA, general anesthesia; IVC, inferior vena cava; LA, local anesthesia; MAC, minimum alveolar concentration; RA, regional anesthesia.

Placental Transfer of Anesthetic Drugs

The drugs given to pregnant women may cross the placenta and have adverse effects on the fetus.

  • The processes by which this transfer can happen are:

    • Simple diffusion: Transfer occurs along concentration gradient following Fick’s principle, for example, paracetamol and midazolam.

    • Facilitated transport: Simple diffusion requiring carrier molecule, for example, glucocorticoids.

    • Active transport: Transfer occurs against concentration and requires carrier and energy, for example, dopamine and norepinephrine.

    • Pinocytosis: Molecule gets engulfed by placental membrane.

  • The extent of transfer depends on:

    • Molecular weight: <500 D cross pla­centa, for example, bupivacaine and succinylcholine.

    • Degree of lipid solubility: Lipid-soluble drugs easily cross the placenta, for example, thiopentone, benzodiazepines, and local anesthetics (LAs).

    • Protein binding: Highly protein-bound molecules do not cross the placenta, for example, bupivacaine and succinylcholine.

    • Degree of ionization and pKa: Ionized drugs are not able to cross the placenta, for example, glycopyrrolate, succinylcholine, neostigmine, and non­depolarizing muscle relaxants.

    • Other factors: Route of administration, maternal metabolism, maternal pH, placental blood flow, fetal pH, and fetal circulation.

Once a drug crosses the placenta, the fetal pH and protein binding affect drug disposition. The fetal liver gets exposed first. Hepatic drug uptake by a fetus may protect it from the harmful effects of certain drugs. Hence, to avoid the placental transfer of drugs, regional anesthesia (RA) is preferred over GA.

There is no anesthetic agent known to cause any teratogenicity in humans directly.

Table 24.7 enlists drugs with the differential capability to cross the placenta.

Dec 11, 2022 | Posted by in ANESTHESIA | Comments Off on CHAPTER 24 Anesthesia for Obstetrics

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