1: Obstetrics
Physiologic Changes During Pregnancy: Respiratory
The parturient is at higher risk of difficult mask ventilation, difficult laryngoscopy, and difficult intubation.
Factors that complicate airway management include:
Increased Mallampatti score.
Upper airway vascular engorgement.
Narrowing of the glottic opening.
Increased oxygen consumption and decreased Functional Residual Capacity (FRC) lead to a faster onset of hypoxemia during apnea.
Functional Residual Capacity falls below closing capacity, resulting in airway closure during tidal breathing.
Progesterone increases minute ventilation by up to 50% causing:
Mild compensated respiratory alkalosis in the mother.
Clinical Scenario Analysis
A patient requires an emergency cesarean section. The MOST likely cause for rapid arterial oxygen desaturation during intubation is:
Decreased expiratory reserve volume
Other options:
Increased inspiratory reserve capacity
Increased residual volume
Decreased vital capacity
Physiologic Changes During Pregnancy: Respiratory (Upper Airway)
Increased levels of progesterone, estrogen, and relaxin result in vascular engorgement and hyperemia, leading to:
Upper airway swelling affecting the nasal passages, oropharynx, epiglottis, larynx, and trachea.
An anesthetic plan must account for these changes.
The Mallampatti score increases during pregnancy.
Difficult and failed intubation is 8 times higher in full-term patients.
Narrowing of the glottic opening necessitates the use of a downsized (6.0 - 7.0) endotracheal tube.
A short-handled laryngoscope (Datta handle) may assist women with larger breasts.
Airway manipulation can cause tissue trauma and bleeding.
The tissue in the nasopharynx is notably friable; avoid unnecessary insertion of artificial airways in this area.
Airway edema is exacerbated by factors such as preeclampsia, tocolytics, and prolonged Trendelenburg position.
Lung Physiology
Relaxin leads to relaxation of rib cage ligaments early in pregnancy, allowing a more horizontal rib position and increasing the anterior-posterior diameter of the chest for lung expansion.
As the uterus expands, it shifts the diaphragm cephalad, impacting lung physiology:
Functional residual capacity reduces due to decreases in:
Expiratory reserve volume
Residual volume
The combination of increased oxygen consumption and decreased FRC hastens the onset of hypoxemia.
Prolonged hypoxemia may lead to brain death in the mother and fetus.
An FRC that falls below closing capacity causes airway closure during tidal breathing.
Arterial Blood Gas (ABG) Changes
Progesterone acts as a respiratory stimulant, leading to significant changes:
Minute ventilation increases by up to 50%.
Maternal PaCO2 decreases, leading to respiratory alkalosis.
Renal compensation occurs through bicarbonate elimination to normalize blood pH.
A negligible reduction in physiologic shunt contributes to the mild increase in PaO2, enhancing oxygen transfer across the fetoplacental interface and improving fetal gas exchange.
Key parameters in ABG changes:
Parameter
From Baseline
Key Information
Arterial pH
No change
PaO2
▲ 20%
Facilitates O₂ transfer to the fetus
PaCO2
▼ 20%
Due to O₂ consumption and CO2 production
HCO3
No change
OxyHgb Dissociation
-
P50 right shift
Minute Ventilation
-
Tidal volume
▲ 20%
Respiratory rate
▲ 75%
Lung Capacities
-
Total lung capacity
No change
Vital capacity
▼ 20%
Functional residual
▼ 20-25%
Expiratory reserve
▼ 40%
Residual volume
No change
Closing capacity
-
Oxygen Consumption
-
- Term: Up 40% over prelabor
- First stage: Up 75%
- Second stage:
Physiologic Changes During Pregnancy: Cardiovascular
Maternal oxygen consumption increases throughout pregnancy to secure the developing fetus.
Cardiac Output (CO) dynamics during labor relative to pre-labor values:
1st stage: CO increases by 20%
2nd stage: CO increases by 50%
3rd stage: CO increases by 80%
Hemodynamic stability is seen as Mean Arterial Pressure (MAP) and Systolic Blood Pressure (SBP) remain stable; however:
Diastolic Blood Pressure (DBP), Systemic Vascular Resistance (SVR), and Pulmonary Vascular Resistance (PVR) decrease.
Expansion of plasma volume leads to dilutional anemia despite increased RBC production:.
Hypercoagulability during pregnancy increases the risk for DVT.
In the supine position, the gravid uterus compresses both the vena cava and aorta:
Aortocaval decompression by left displacing the uterus enhances hemodynamics, advisable during the second and third trimesters.
Hemodynamic Variables
Which hemodynamic variables are anticipated to increase during pregnancy? (Select 2.)
Heart rate
Stroke volume
Systemic vascular resistance
Pulmonary artery occlusion pressure
Physiologic Changes During Pregnancy: Cardiovascular (Continued)
Systemic alterations in obstetric patients result from anatomical, hormonal, and metabolic changes related to pregnancy, necessitating understanding for effective anesthetic planning.
Parameter Table:
Parameter
From Baseline
Key Information on Changes & Implications
O₂ Consumption
▲ 20%
- Increased demand for maternal-fetal oxygenation
Cardiac Output
▲ 40%
- Heart Rate: ▲ 30% - Stroke Volume: ▲ 15%
Uterine blood flow
10% of CO
Autotransfusion during contractions increases preload
CO during labor
1st stage: ▲ 20%
- 2nd stage: ▲ 50% - 3rd stage: ▲ 80%
CO return to pre-labor
24-48 hours
CO returns to pre-pregnancy values in ~ 2 weeks
Twin pregnancies
CO increases by ▲ 20% over single gestation
Blood volume increases with reduced SVR = negligible effect on MAP
Blood Pressure:
MAP: No change
SBP: Stable - DBP: ▼ 15%
Vascular Resistance:
SVR: ▼ 15%
PVR: ▼ 30%
Filling Pressures:
CVP: No change
PAOP: No change
Cardiac Axis: Left deviation
Role of Progesterone:
- Increases nitric oxide production leading to vasodilation
-RAAS activity ↑
- Increased minute ventilation
Aortocaval Compression
Awareness of aortocaval compression syndrome, also referred to as supine hypotension syndrome, is crucial.
In the supine position, the uterus exerts pressure on the vena cava and aorta, leading to:
Diminished venous return - Reduced arterial flow to the uterus and lower extremities.
This compression reduces cardiac output, compromising fetal perfusion, and poses a risk for the mother’s loss of consciousness.
To mitigate this, the uterus can be displaced laterally, improving hemodynamics by elevating the mother's right torso by 15° to 30°.
Note: Historical goals aimed for a 15-degree lateral tilt; however, recent MRI studies indicate significant increases in vena cava volume at term with a 30-degree lateral tilt.
Hematologic Changes
Changes in fluid volume during pregnancy:
Parameter
Change from Baseline
Key Information
Intravascular volume
▲ 35%
Prepares mother for blood loss during labor
Plasma volume
▲ 45%
Leads to dilutional anemia
Erythrocyte volume
▲ 20%
Clotting Factors
1, 7, 8, 9, 10, 12
Pregnancy creates a hypercoagulable state
Antithrombin, Protein S, No A Protein C, ↑ Fibrin breakdown (11 and 13)
Platelet count remains unchanged or decreases up to 10%
Hemodilution and consumption
Common cause of thrombocytopenia during pregnancy is gestational thrombocytopenia
Risks are minimal
Other causes include
Hypertensive disorders of pregnancy and idiopathic thrombocytopenia
Physiologic Changes During Pregnancy: Neurologic, GI, Renal, and More…
Minimum Alveolar Concentration (MAC) decreases by 30-40% beginning at 8-12 weeks gestation due to increased progesterone.
Gastric emptying is unchanged before labor onset but slows post-labor.
Factors expected to increase during pregnancy (Select 3):
Creatinine clearance
Lower esophageal sphincter tone
Sensitivity to local anesthetics
MAC
Gastric pH
Urine glucose
Physiologic Changes During Pregnancy: The Uterus
Uterine blood flow increases up to 700 - 900 mL/min at term, relevant in maternal hemorrhage cases.
Uterine blood flow does NOT autoregulate; it's dependent on MAP, CO, and uterine vascular resistance, a low-resistance system.
Effective uterine blood flow is influenced primarily by MAP and CO.
Key Drug Characteristics Favoring Placental Transfer
Low molecular weight (< 500 Daltons)
High lipid solubility
Non-ionized and non-polar compounds can more readily cross the placenta.
Most anesthetic agents cross into the placenta; however, neuromuscular blockers, glycopyrrolate, heparin, and insulin do not cross.
Effects of Vasopressors on Uterine Perfusion: Phenylephrine vs. Ephedrine
Administering a vasopressor is essential during general anesthesia in cesarean delivery to restore MAP and uterine blood flow, often using phenylephrine or ephedrine.
Classic teachings assert phenylephrine escalates uterine vascular resistance and diminishes placental perfusion.
Recent evidence suggests phenylephrine is equally effective as ephedrine in preventing hypotension, causing no fetal pH depression in healthy mothers.
Mothers receiving phenylephrine presented with higher fetal pH values (indicating less fetal acidosis).
Despite this, phenylephrine can provoke reflex bradycardia and reduce cardiac output. Norepinephrine is gaining usage as an alternative.
Transfer of Anesthetic Drugs Across the Placenta
A drug’s transit across biological membranes follows the Fick principle:
Rate of diffusion = (Diffusion coefficient × Surface area × Concentration gradient (between mom and fetus)) / Membrane thickness
Key factors for placental transfer include drug characteristics and concentration gradients. Fetal acidosis may increase these gradients, potentially causing fetal ion trapping.
Route of administration significantly affects peak plasma levels; intravenous routes yield higher levels than intramuscular or subcutaneous.
Drug Characteristics Favoring Placental Transfer
Significant placental transfer drugs include local anesthetics (excluding chloroprocaine), IV anesthetics, volatile anesthetics, opioids, benzodiazepines, atropine, and magnesium (non-lipophilic but small).
Drugs Not Transferred to the Placenta: Neuromuscular blockers, glycopyrrolate, heparin, insulin.
Stages of Labor
Labor is divided into three stages:
Stage 1: Beginning of regular contractions to full cervical dilation (10 cm).
Stage 2: Full cervical dilation to delivery of the fetus. - Perineal pain begins during this stage.
Stage 3: Delivery of the placenta.
A laboring mother is always regarded as a full stomach.
The ASA Practice Guidelines permit a healthy laboring mother to:
Consume moderate amounts of clear liquids throughout labor.
Eat solid food up to the entry of neuraxial block.
An epidural does not prolong the first stage of labor nor increases c-section necessity.
Clinical Assessment
Identify which stage of labor begins with perineal pain onset:
Latent stage
Active stage
First stage
Second stage
NPO Guidelines
Labor is strenuous; hence, adequate maternal nutrition and hydration are critical.
A laboring mother is considered a full stomach regardless of the time since her last intake.
The ASA Guidelines indicate:
Healthy laboring mothers can drink moderate clear liquids.
Solid food intake is permissible until neuraxial block placement.
However, patients should remain NPO when surgical interventions necessitating general anesthesia are probable.
Pain Pathways
Assessing labor pain requires understanding the labor stage. The pain pathophysiology includes:
First-stage labor pain stems from T10 - L1 regions.
Second-stage labor pain arises from T10 - S4 regions, including the vagina, perineum, and pelvic floor.
Options for first-stage labor analgesia include neuraxial blockade, paravertebral lumbar sympathetic block, and paracervical block.
Second-stage labor pain can be managed via neuraxial blockade or pudendal nerve block.
Nitrous oxide (50% N2O and 50% O2) serves as a non-invasive labor analgesia method.
The Combined Spinal Epidural technique (CSE) allows for rapid spinal anesthesia onset and prolongs anesthesia via an epidural catheter.
Neuraxial Analgesia
Common Local Anesthetics in obstetrics:
Bupivacaine
Ropivacaine
Lidocaine
2-Chloroprocaine
Cautions:
0.75% bupivacaine is contraindicated via epidural due to IV toxicity risk.
Ropivacaine presents lower cardiovascular toxicity risk compared to bupivacaine.
Neuraxial opioids provide:
No loss of sensation or proprioception.
No sympathectomy (better hemodynamic stability).
They do not compromise the mother's ability to bear down for delivery.
Meperidine possesses local anesthetic properties.
Potential side effects of neuraxial opioids:
Pruritus (most common)
Nausea/Vomiting
Sedation
Respiratory depression (minimal systemic impact on the fetus).
Dosing Regimens for Labor Analgesia
Local Anesthetics
Anesthetic
Spinal Bolus
Epidural Bolus
Bupivacaine
1.25 - 2.5 mg
-
Ropivacaine
2 - 3.5 mg
-
Lidocaine
-
-
2-Chloroprocaine
-
-
Opioids
Opioid
Dosage
Route
--------------------
----------------
--------
Fentanyl
15-25 mcg
-
Sufentanil
1.5 - 5 mcg
-
Morphine
50-100 mcg
-
Meperidine
5-10 mcg
-
Total Spinal
Total spinal may occur in patients due to:
An epidural dose being injected into the subarachnoid space.
An epidural dose being injected into the subdural space (symptoms may be delayed).
A single-shot spinal following a failed epidural block.
Management requires supportive care including airway management, IV fluids, vasopressors, left uterine displacement, and leg elevation.
Hypotensive Episode Post Epidural
15 minutes after an epidural dosing, a patient's hypotension and respiratory arrest suggest multiple etiologies:
Epidural catheter migration
Loss of accessory respiratory muscle strength
Subdural injection
Eclampsia
Fetal Heart Rate Monitoring
Fetal heart rate serves as a surrogate for fetal wellbeing, linking to fetal hypoxia and acidosis.
Notable Factors:
Fetal oxygenation relies on uterine and placental blood flow.
Responses to stress include peripheral vasoconstriction, hypertension, and baroreceptor-mediated heart rate reduction.
Normal FHR Disturbances
Normal FHR values: - Normal: 110-160 bpm
Bradycardia: ≤ 110
Tachycardia: ≥ 160
Variability indicates intact CNS and normal SNS and PNS functioning, reflecting oxygenation and acid-base balance.
Variability absence suggests fetal distress, which may stem from CNS depressants, hypoxemia, or acidosis.
Types of Deceleration Phenomena
Fetal deceleration types include:
Early: Head compression (no fetal risk), coinciding with contractions.
Late: Placental insufficiency (requires more urgent fetal status assessment), occurring post-peak fetal heart rate.
Variable: Umbilical cord compression (assess urgency), showing no consistent relationship with contractions.
Fetal Heart Rate Categories
The American College of Obstetricians and Gynecologists has established a three-tier classification system for fetal heart rate evaluation:
Category 1: Normal acid-base status with no oxygen threat (Baseline 110-160 bpm, moderate variability, no late or variable decelerations).
Category 2: Indeterminate; can't conclude normality or abnormal acid-base status.
Category 3: Abnormal status indicating significant fetal oxygenation risks.
Prematurity and Tocolysis
Premature delivery: Before 37 weeks gestation, correlating with perinatal morbidity/mortality, especially for infants < 1500g.
Complications: Include respiratory distress syndrome, intraventricular hemorrhage, and necrotizing enterocolitis (NEC) and are more frequent in multiple gestations or preterm rupture of membranes.
Tocolytic agents: Used to suppress contractions temporarily, allowing corticosteroid administration for fetal lung maturation.
Examples:
Beta-agonists
Magnesium sulfate
Calcium channel blockers
Nitric oxide donors
Clinical Dosing for Magnesium
Reflex testing assists in assessing hypermagnesemia. Presence of deep tendon reflexes indicates low risk for complications; diminished reflexes could signify magnesium toxicity.
Magnesium concentrations and corresponding effects:
| Magnesium Level | Clinical Effect |
|----------------------|------------------|
| 8 mg/dL | Seizures |
| 5 mg/dL | Drowsiness |
| 1 mg/dL | Loss of patellar tendon reflex |
| 15 mg/dL | Respiratory depression |
Obstetric Hypertensive Disorders: Pathophysiology
Classifications include chronic hypertension, gestational hypertension, preeclampsia, and eclampsia:
Chronic Hypertension: Pre-existing, present before 20 weeks gestation, not normalizing postpartum.
Gestational Hypertension: Develops post-20 weeks without proteinuria returning to normotensive after delivery.
Preeclampsia: Hypertension after 20 weeks with proteinuria; categorized further into mild (>140/90) or severe (>160/110).
Eclampsia: Seizures occur in preeclampsia cases.
HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets) has similar treatment and presentation as severe preeclampsia.
Elevated thromboxane activities could reduce prostacyclin levels in preeclampsia.
Key Clinical Factors to Monitor
Preeclampsia can be marked by symptoms such as seizures, increased thromboxane, vasoconstriction, and proteinuria.
Medical Treatment & Anesthesia for Preeclampsia
Definitive treatment for preeclampsia is fetal delivery; severe cases may require kombosing with medications for management (labetalol, hydralazine, nifedipine, and nicardipine) for blood pressure control.
Neuraxial anesthesia aids in blood pressure management and uteroplacental perfusion but must be evaluated based on platelet counts (≥ 70,000 μL generally lower risk, < 50,000 μL increased hematoma risk).
Magnesium sulfate is the drug of choice for seizures .
Anesthetic Management for Eclampsia
Differences arise in animating procedures for managing acute preeclampsia and eclampsia, notably the role of magnesium sulfate in seizure management and HELLP syndrome correlation with thrombocytopenia risk affecting neuraxial interventions.
Maternal Cocaine Abuse: Anesthetic Implications
Cocaine affects both CNS and cardiovascular systems, thus presenting maternal risks of complications during anesthesia.
Labetalol may be effective for hypertension associated with cocaine.
Considerations all around
Assess for thrombocytopenia prior to neuraxial anesthesia and manage appropriately.
Disorders of the Placenta
Abnormal implantation categories include:
Accreta: Attachment to myometrium surface.
Increta: Invasion into myometrium.
Percreta: Extending beyond the uterus.
Monitoring significant bleeding indicates the need for both surgical expertise and prompt intervention during labor and parturition processes.
Apgar Score and Neonatal Resuscitation
The Apgar score assesses newborns at 1 and 5 minutes after delivery, determining the necessity for resuscitation based on parameters: heart rate, respiratory effort, muscle tone, reflex irritability, and color.
Normal scoring: 8-10; Moderate: 4-7; Critical: 0-3.
Resuscitation Guidelines
Most newborns are healthy; however, 10% require varying degrees of resuscitation, with room air recommended for initial interventions. Absent severe hypoxia or bradycardia, non-invasive measures are indicated.
Normal parameters and actions for neonatal resuscitation can significantly impact outcomes.