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:
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.
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.
Maternal hematological changes begin to occur early in pregnancy as mentioned in Table 24.2.
Abbreviation: DVT, deep vein thrombosis.
Changes in the respiratory system during pregnancy are summarized in Table 24.3.
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.
Changes in the gastrointestinal (GI) system are tabulated in Table 24.4.
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.
Renal system changes in pregnancy are as mentioned in Table 24.5.
Abbreviations: GFR, glomerular filtration rate; UTI, urinary tract infection.
Pregnancy-related central nervous system (CNS) changes are summarized in Table 24.6.
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.
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.
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