Nagelhout Chapter 51- Lesson 4

Obstetric Anesthesia: Key Concepts and Changes During Pregnancy

• Parturients present unique challenges; pain relief techniques are continually refined to provide the best possible care.
• Thorough understanding of the anatomic and physiologic changes during pregnancy is crucial for safe and effective anesthesia.

Anatomic and Physiologic Changes During Normal Pregnancy

• Changes result from increased metabolic demands, hormonal shifts, and anatomic alterations, starting early and continuing postpartum.
• These changes have significant implications for anesthesia.

Cardiovascular Changes

• Begin as early as the fourth week of pregnancy and persists into the postpartum period.
• Heart rate increases by 20%-30% at term, beginning in the first trimester and peaking at 32 weeks of gestation.
• Cardiac output increases by approximately 40% over nonpregnant values, starting in the fifth week, resulting from increased stroke volume (20%-50%) and, to a lesser extent, heart rate.
• Cardiac output consistently increases throughout pregnancy; prior studies suggesting a decrease in the third trimester were likely affected by aortocaval compression.
• At term, approximately 10% of cardiac output perfuses the gravid uterus.
• Cardiac output increases during uterine contractions due to autotransfusion from the uterus to the central circulation.
• Immediately after delivery, cardiac output increases as much as 80% above prelabor values due to autotransfusion and decreased venous return from aortocaval decompression.
• Patients with preexisting cardiac anomalies face increased risks of decompensation in the immediate postpartum period.
• Cardiac output gradually normalizes within 14 days as heart rate and stroke volume return to baseline.
• The diaphragm rises during pregnancy, shifting the heart up and to the left, enlarging the cardiac silhouette on x-ray.
• Ventricular walls thicken and end-diastolic volume increases.
• Benign grade 1 or 2 systolic murmurs or third heart sounds may be heard on auscultation.
• Systolic murmurs greater than grade 3 or accompanied by chest pain or syncope warrant further evaluation.
• Diastolic murmurs and cardiac enlargement are considered pathologic.
• Normal pregnancy may manifest as exercise intolerance, shortness of breath, and edema.
• Total blood volume increases 25% to 40% throughout pregnancy to prepare for normal blood loss during delivery.
• Plasma volume increases 40% to 50%, and red blood cell volume increases by only 20%, leading to relative or dilutional anemia.
• Increased plasma volume is likely due to elevated progesterone and estrogen levels that enhance renin-angiotensin-aldosterone activity.
• Red blood cell volume increases as a result of elevated erythropoietin levels after the eighth week of gestation.
• Normal blood loss for vaginal delivery is less than 500 mL while for cesarean section is 800 to 1000 mL.
• Healthy parturients generally tolerate normal blood losses at delivery due to compensatory mechanisms.
• Each contraction during labor moves approximately 300 to 500 mL of blood from the uterus to the central circulation.
• Pregnant women exhibit greater baroreflex-mediated changes in heart rate at term compared to 6 to 8 weeks postpartum.
• With adequate neuraxial analgesia and minimal sympathetic stimulation, maternal heart rate may decrease during contractions due to increased preload.
• Systemic vascular resistance (SVR) decreases as much as 21% by the end of a term pregnancy, mainly because of decreased resistance in the uteroplacental, pulmonary, renal, and cutaneous vascular beds.
• Term gestation shows 10% of cardiac output perfusing the low-resistance intervillous space of the uterus.
• Baseline central sympathetic outflow is twice as high in term pregnant women versus nonpregnant women.
• Venous capacitance system loses tone, allowing pooling of the larger blood volume.
• Minimal overall systolic blood pressure change occurs during normal pregnancy despite the increased blood volume.
• Diastolic blood pressure may decrease up to 15 mm Hg, decreasing mean pressure.

Aortocaval Compression

• Supine hypotension syndrome was identified in term or near-term pregnant women in the early 1950s.
• Gravid uterus compresses the vena cava and aorta, restricting venous return to the heart in the supine position.
• Compression can be more severe with a tense abdomen or larger-than-normal uterus, as in polyhydramnios or multiple gestation pregnancies.
• Decreased venous return results in a significant reduction in stroke volume, and ultimately, cardiac output.
• Severe hypotension can cause loss of consciousness.
• Maximal decreases in blood pressure may take up to 10 minutes to develop; some women experience an almost immediate decrease.
• Normal physiologic responses to aortocaval compression involve tachycardia and vasoconstriction of the lower extremities.
• Uterine blood flow is lessened, therefore fetal oxygenation is reduced.
• Shifting the uterus to the left (left uterine displacement) or lying on the side relieves compression of the aorta and vena cava.
• Left uterine displacement can be accomplished with a 15-degree rotation or an under the right hip and back.
• Many clinicians choose the lateral position to facilitate both maternal and fetal hemodynamics.
• Cardiac index is improved in both the left and right lateral positions when compared to the sitting flexed position in healthy pregnant women.
• Although positioning for neuraxial anesthesia may influence maternal hemodynamic variables, there were no differences indices among positions.
• These changes are not clinically significant.

Hematologic Changes

• Parturients are in a hypercoagulable state.
• Concentrations of factors VII through X and fibrinogen are increased, while fibrinolytic activity is decreased.
• Fibrinogen levels: nonpregnant state averages 200-400 mg/dL; late pregnancy at least 400 mg/dL, potentially as high as 650 mg/dL.
• Increased levels place the parturient at risk for thromboembolic events.
• Platelet count remains stable or slightly decreases in the third trimester.
• Maternal thrombocytopenia prevalence (platelet count less than 150 109/L) in normal pregnancy has been shown to be 11.6%.
• Pathogenesis is not well understood, but it may involve hemodilution or accelerated platelet clearance.
• White blood cell count rises in pregnancy. The third trimester mean is 10,500/mm3, and in labor it may increase to 20,000-30,000/mm3.

Respiratory Changes

• Capillary engorgement in the upper airway narrows the glottic opening and causes edema in the nasal and oral pharynx, larynx, and trachea.
• Airway tissues are susceptible to damage and bleeding during placement of airway adjuncts.
• Nasal intubation in the parturient generally should be avoided.
• A 6.5- to 7.0-mm cuffed oral endotracheal tube is recommended when intubation is necessary.
• Obese patients with use a short-handled laryngoscope.
• Term is accompanied by an increase in oxygen (O2) consumption by up to 33% at rest and 100% or rest during the second stage of labor.
• Minute increases by 50% at and is primarily due to a 40% increase in tidal volume, whereas respiratory rate remains unchanged or increases by just 10%.
• Normal PaCO2 decreases to approximately 30-32 mm Hg by 12 weeks' weeks' and stays this way throughout pregnancy
• Metabolic is rarely seen because there is a compensatory decrease in the serum bicarbonate from 26 to 22 mEq/L.
• The normal arterial partial pressure of O2 is than 100 mm Hg.
• Functional residual capacity (FRC), expiratory reserve volume, and residual volume are results functionally similar to restrictive lung disease.
• The decrease in FRC (20%) combined with the increase in O2 results in arterial desaturation in the apneic pregnant patient.
• Preoxygenation with 100% O2 prior to induction of general anesthesia (CA) is important.
• Closing capacity does not change and CC ratio often leading before tidal volume has been exhaled.
• PaCO2 can drop below 15 can cause hypoventilation between contractions, resulting hypoxemia .
• Hyerventilation to of 20 harm the fetus.
• The fetus develop hypoxia or acidosis by analysis of a scalp blood presence of a compromised labor with preexisiting effects could arise.

Nervous System Changes

• In the first women have an increased sensitivity to local and general anesthetics.
• The exact mechanism unclear, but studies demonstrated a in rats effects on pain .
• In women nerves to local anesthetics pregnancy.
• Mechanical veins become a both the the spaces

Gastrointestinal Changes

• Parturients are at increased risk for regurgitation and aspiration of gastric contents because changes .
• Gastric volumes in excess of and gastric have been during .
• In of neuraxial and in the who had not eaten in for
• During higher increased by displacement by the mechanical obstruction to outflow through the progesterone a smoothrelaxant to the This explains normal .
• Changes do Several postpartum.
• Accompanied can ingest a

Table 51.1 Summary of the Physiologic Changes in Pregnancy at Term

• No Change or a Small Decrease

Box 51.1 Key Points Regarding Physiologic Changes in Pregnancy

• Cardiac out-put increase.

Uterine Blood Flow

• Placental flow during .
• Autoregulation of blood This means on maternal spiral do not be to

Placental Transfer and Fetal Effects of Drugs

• Transfer of drugs from diffusion. favor
• Factors: Low weight, water to not contain a

• The of first . can from to spinal. can be second . to of with women with a makes .
• The defined as cervical progressive has in spinal the is only can depression . with to be for with for from for of is, is is

Important Key Points from Box 51.1

.can

This lesson covers the interpretation of fetal heart rate (FHR) tracings. It focuses on identifying baseline rates, variability, and concerning patterns. Additionally, it explains the limitations of external monitoring and the advantages of internal monitoring.