OBGYN Flashcards
Risk factors for aspiration during pregnancy include:
Risk factors for aspiration during pregnancy include:
* Weakened lower esophageal sphincter tone; increased progesterone levels can weaken lower esophageal sphincter tone and increase the risk of gastroesophageal reflux in pregnant patients.
* Increased incidence of difficult airway due to swelling, airway mucosal friability, and weight gain
* Gastrointestinal system anatomical alterations due to enlarged uterus resulting in increased abdominal pressure and upward displacement
Justification for general vs. neuraxial anesthesia?
The choice of which type of anesthesia is administered for cesarean delivery (CD) depends on the urgency and patient factors, but, ultimately, experience and clinical judgment should always be used. When there is currently an epidural in place (whether it be an epidural alone, combined spinal anesthesia and epidural, or a dural puncture epidural), the epidural can be used for the CD.
If the patient does not have an epidural, the following questions must be answered:
* Does the patient require immediate delivery for maternal and/or fetal health?
* Is massive hemorrhage expected?
* Are there any contraindications to neuraxial anesthesia?
If the answer is “yes” to any of these questions, general anesthesia should be performed.
If the answer is “no” to all of these questions, the following questions must be answered:
* Is the duration of CD > 1.5 hours, or are multiple procedures planned?
* Does the patient have abdominal surgeries or previous CD (uterine scar)?
* Does the patient have risk factors that increase the risk of a poor outcome with general anesthesia (severe obesity, difficult airway, or history of malignant hyperthermia)?
If the answer is “yes” to any of these questions, an epidural can be placed and used for the CD. If the answer is “no” to all of these questions, spinal anesthesia can be performed.
The acid-base status of an otherwise healthy parturient is ________________.
The acid-base status of an otherwise healthy parturient is respiratory alkalosis with metabolic compensation.
Due to the effects of progesterone during pregnancy, maternal tidal volume increases by 50%, while respiratory rate remains mostly the same. The increased tidal volume increases minute ventilation with the levels of partial pressure of carbon dioxide in the arterial blood ranging from 27 to 32 mmHg in full-term parturients.
The respiratory alkalosis of pregnancy is compensated for by increased renal excretion of bicarbonate, and these combined physiologic changes result in a pH of approximately 7.44 to 7.46.
The changes in tidal volumes during pregnancy affect ventilation, oxygenation, and anesthesia management. The increased minute ventilation increases maternal oxygenation and causes a high-normal or slightly increased partial pressure of oxygen in the arterial blood. However, the decreased functional residual capacity and residual volume that also occur as the uterus expands during pregnancy render pregnant women more susceptible to hypoxemia in the supine or lithotomy position and during the induction of general anesthesia.
Additionally, the increase in tidal volume with the subsequent decrease in functional residual capacity and residual volume allows quicker equilibration of volatile anesthetics.
Describe the challenges with intubation of pregnant women.
The upper airway in pregnant patients becomes friable due to capillary engorgement. Edema of the oropharynx, larynx, and trachea begins to occur in the first trimester. Thus, when the airway is manipulated, there is an increased risk of bleeding. Because of this edema, mask ventilation, laryngoscopy, and intubation are more difficult. In addition, upon extubation, the edema can compromise the airway, leading to obstruction. Repeated attempts at laryngoscopy should be minimized, and a small diameter endotracheal tube (6-7-mm internal diameter) should be used.
The decreased FRC and RV that also occur as the uterus expands during pregnancy render pregnant women more susceptible to hypoxemia in the supine or lithotomy position and during the induction of general anesthesia.
Describe the changes that occur to minute ventilation in a pregnant woman?
To meet the increased metabolic demands during pregnancy, a woman’s minute ventilation increases throughout pregnancy to approximately 145% of normal nonpregnant minute ventilation. This effect is primarily due to increased tidal volume (from 450 to 600), with a small contribution from increased respiratory rate by 1-2 breaths/min). It is driven by the respiratory stimulant effects of progesterone, which shifts the carbon dioxide–ventilatory response curve to the left. Respiratory alkalosis occurs as the arterial partial pressure of carbon dioxide (PaCO2) is decreased by ∼ 10 mm Hg (from 40 to 30 mm Hg) by the end of the first trimester.
The respiratory rate then remains relatively constant for the remainder of the pregnancy. Despite respiratory alkalosis, the pH remains normal to only slightly elevated (7.40-7.44) due to compensatory metabolic acidosis. Serum bicarbonate (HCO3-) decreases to 20-21 mEq/L, and the serum base excess falls by 2-3 mEq/L. The increased minute ventilation improves alveolar ventilation, leading to an increase in PaO2. This increase is also due to the decrease in PaCO2 and a lower arteriovenous oxygen difference (which decreases the effect of venous admixture on PaO2).
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The increased progesterone during pregnancy leads to an increase in minute ventilation (as much as 50% at term), tidal volume (30%-50%), and respiratory rate (0%-15%). One to three weeks after pregnancy, ventilation returns to the nonpregnant levels.
The oxyhemoglobin dissociation curve shifts to the ______ during normal pregnancy.
The oxyhemoglobin dissociation curve shifts to the right during normal pregnancy (increased p50), allowing a greater volume of oxygen to be unloaded to the tissues (fetus) at a given arterial oxygen pressure.
TrueLearn Insight: The P50 of maternal hemoglobin during pregnancy increases from 26.8 mm Hg in the prepregnant state, to 30 mm Hg. This results in a rightward shift of the maternal oxyhemoglobin dissociation curve. The fetal oxyhemoglobin dissociation curve sits to the left of the normal adult and maternal dissociation curves. The P50 of fetal hemoglobin is 19-21 mm Hg. The increase in this gradient between P50 values of the mother and fetus facilitates oxygen unloading from maternal hemoglobin to fetal hemoglobin.
The normal FHR range is _____-______ bpm.
The normal FHR range is 110-160 bpm.
The normal FHR can vary from beat to beat and is referred to as “short-term variability” or “beat-to-beat variability.” The normal variation from one beat to another is 5-25 bpm. Variability in the FHR is a sign of a healthy autonomic nervous system, chemoreceptors, baroreceptors, and cardiac responsiveness. The FHR becomes nonreassuring if the variability is < 5 or > 25 bpm. A decrease in FHR variability can be due to fetal sleep state, fetal acidosis, or maternal sedation from drugs.
* Minimal variability is an amplitude of 5 bpm or less.
* Moderate variability is normal, with an amplitude range is 6 to 25 bpm.
* Marked variability has an amplitude range > 25 bpm.
Tachycardia may be secondary to fetal hypoxia, maternal fever, chorioamnionitis, anticholinergics, beta-agonists, fetal anemia, or tachyarrhythmias.
Bradycardia could be due to congenital heart block, beta-antagonists, hypoglycemia, hypothermia, or fetal hypoxia.
Variability of FHR is primarily influenced by ____________.
Variability of FHR is primarily influenced by the parasympathetic tone, with increasing tone exerting an increased effect on the heart rate, and therefore increasing variability.
This is evidenced by the fact that the maternal administration of atropine, which effectively eliminated the vagal tone in the fetus as it readily crosses the placenta, causes a decrease in FHR variability. Conversely, maternal administration of a beta-blocker which also readily crosses the placenta has minimal effect on the FHR variability.
How is early deceleration differentiated from late deceleration on FHR monitoring?
Early deceleration:
Early decelerations occur simultaneously with uterine contractions. The onset, nadir, and offset of each deceleration coincide with the onset, nadir, and offset of the uterine contraction. Head compression can precipitate early decelerations which are believed to result from reflex vagal activity secondary to mild hypoxia. Early decelerations are not ominous/not associated with fetal distress.
Late deceleration:
**Late deceleration starts after the onset of a uterine contraction with a nadir > 30 seconds after the onset of a contraction. **Late deceleration is most likely due to uteroplacental insufficiency/response to hypoxemia. The severity is determined by the magnitude of the deceleration. The delayed onset of the deceleration reflects the time needed for the chemoreceptors to detect decreased oxygen tension and change FHR via the vagus nerve. Late decelerations may also result due to myocardial failure secondary to decreased coronary blood flow.
VEAL CHOP
Variable - Cord compression
Early - Head compression
Accelerations - Okay
Late - Placental insufficiency
How are sustained variable decelerations treated?
Amnioinfusion (shown to decrease rate of C-Section)
Variable decelerations, as the name suggests, vary in depth, shape, and duration. They often are abrupt in onset and offset without coinciding with uterine contractions. Variable decelerations result from baroreceptor or chemoreceptor-mediated vagal activity. Umbilical cord occlusion, either partial or complete, results in variable decelerations.
A healthy fetus can typically tolerate mild to moderate variable decelerations without decompensation. With sustained, severe variable decelerations or persistent fetal bradycardia, it is difficult for the fetus to maintain cardiac output and umbilical blood flow.
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A variable deceleration reflects the fetal autonomic reflex response to transient mechanical compression of the umbilical cord. Umbilical vein and umbilical artery compression both occur. Initially, compression of the umbilical cord occludes the thin-walled and compliant umbilical vein. This results in decreased fetal venous return which triggers a baroreceptor-mediated reflex rise in FHR. Further compression occludes the umbilical arteries, causing an abrupt increase in fetal peripheral resistance and blood pressure. Baroreceptors detect the abrupt rise in blood pressure, triggering an increase in parasympathetic outflow and an abrupt decrease in heart rate. The reverse occurs as cord decompression begins. Prompt attention is required because ongoing hypoxic injury cannot be excluded.
In-utero resuscitation is indicated for fetal distress, with the goal of improving fetal oxygenation. Measures of in-utero fetal resuscitation include:
In-utero resuscitation is indicated for fetal distress, with the goal of improving fetal oxygenation. Measures of in-utero fetal resuscitation include:
* Repositioning of the mother to a lateral or “hands and knees” position
* Administration of supplemental oxygen (which is controversial)
* Administration of intravenous fluids
* Administer vasopressors if the patient is hypotensive
* Discontinuation of uterotonic drugs if these have been administered
* Administration of a tocolytic if sustained uterine contraction is suspected.
Fetal hypoxia mnemonic:
SPOILT: Stop oxytocin, Pressure (treat hypotension), Oxygen, Intravenous fluid bolus, Left lateral decubitus (or all fours), Tocolytics
Refractory late decelerations are an indication for emergent cesarean delivery after failure of in-utero resuscitation.
Describe the three stags of labor
Labor is divided into 3 stages.
The first stage begins with the maternal perception of regular, painful uterine contractions and ends with complete dilation of the cervix.
The second stage begins with complete dilation of the cervix and ends with the birth of the baby.
The third stage begins with the birth of the baby and ends with the delivery of the placenta.
Epidural analgesia is effective for treating pain in the first and second stages of labor.
What spinal segment coverage is required to relieve the pain of contractions and cervical dilation?
Epidural analgesia is effective for treating pain in the first and second stages of labor. T10 to L1 spinal segment coverage is required to relieve the pain of contractions and cervical dilation.
Note, S2-S4 spinal segment coverage is required to relieve the pain of vaginal and perineal distention. Not covered by epidurals.
Although spinal analgesia is effective for treating pain in the first and second stages of labor, it is not commonly employed because…
Although spinal analgesia is effective for treating pain in the first and second stages of labor, it is not commonly employed because it may affect the ability of the mother to push during delivery (may be used as a low-dose rescue technique near the time of delivery).
Pudendal nerve block helps relieve pain during the second stage of labor.
The pudendal nerve blocks somatic nerve fibers from what levels?
Pudendal nerve block helps relieve pain during the second stage of labor. The pudendal nerve includes somatic nerve fibers from S2-S4.
The lumbar sympathetic block is an effective regional anesthetic technique for first-stage analgesia. A lumbar sympathetic block interrupts the transmission of pain impulses from the cervix and lower uterine segment to the spinal cord.
The lower uterine and cervical visceral afferent sensory fibers join the sympathetic chain at what levels?
The lumbar sympathetic block is an effective regional anesthetic technique for first-stage analgesia. A lumbar sympathetic block interrupts the transmission of pain impulses from the cervix and lower uterine segment to the spinal cord.
The lower uterine and cervical visceral afferent sensory fibers join the sympathetic chain at **L2 and L3. **
How does pregnancy affect MAC?
The MAC of volatile anesthetics is reduced by about 30% during pregnancy.
Do volatile anesthetics cross the placenta?
YES, due to their high lipid solubility, non-ionized nature, and low molecular weight, volatile anesthetics rapidly cross the placenta.
How do volatile anesthetics affect uterine blood flow?
Volatile anethetics relax the uterine muscle and thus increase uterine blood flow.
Due to their tendency to cause uterine smooth muscle relaxation (decreased uterine tone), they are associated with increased blood loss during cesarean section. It is therefore recommended to use less than 1 MAC of volatile anesthetic and combine it with other agents such as nitrous oxide for maintenance of general anesthesia during cesarean section.
Pruritus is a side effect of opioids and is particularly prevalent with neuraxial opioids (60-80%). __________ is the drug of choice for the treatment of pruritus induced by neuraxial opioids.
Pruritus is a side effect of opioids and is particularly prevalent with neuraxial opioids (60-80%). ** Nalbuphine (mixed opioid agonist/antagonist) **is the drug of choice for the treatment of pruritus induced by neuraxial opioids.
When given in small doses (3 mg) Nalbuphine does not reverse the analgesic effect of neuraxial morphine.
Antihistamines actually have little or no effect on pruritis induced by neuraxial opioids (other than causing sedation).
By definition, amniotic fluid embolism (AFE) symptoms (hypotension in this case) must occur during or within _________ min/hour of labor, during cesarean delivery, during dilation and evacuation, or postpartum.
By definition, amniotic fluid embolism (AFE) symptoms (hypotension in this case) must occur during or within 30 minutes of labor, during cesarean delivery, during dilation and evacuation, or postpartum.
Amniotic fluid embolism is a diagnosis of exclusion but describes a syndrome of sudden peripartum shock characterized by pulmonary edema that has a mortality rate (up to 80%).
Amniotic fluid embolism accounts for up to 10% of all deaths for maternal mortality as a whole.
The etiology of AFE is unclear but may be due to the transfer of arachidonic acid metabolites (especially leukotrienes) and other vasoactive substances found in amniotic fluid to the maternal circulation. There may also be an immune-mediated response with massive mast cell activation.
The characteristic cardiac signs and symptoms of AFE may be divided into 2 stages.
Early-stage AFE generally lasts less than 30 minutes and is characterized by transient, often intense, pulmonary vasospasm. The resultant right heart dysfunction can progress to fatal right heart failure. The low cardiac output then leads to ventilation-perfusion mismatch, hypoxemia, and hypotension.
The second phase of AFE is characterized by left ventricular dysfunction or failure and pulmonary edema due to the previous right heart dysfunction. Right heart function may return to close to normal during this phase. Left or biventricular failure is often fatal unless supportive care is initiated.
Maternal coagulopathy occurs in most cases due to disruption of the normal clotting cascade, although the etiology is unclear. This can lead to massive hemorrhage, which then causes consumptive coagulopathy. The onset of maternal symptoms is quickly followed by spontaneous uterine hypertonus, which decreases placental perfusion and leads to profound fetal bradycardia (if the patient is still gravid). Therefore, fetal monitoring should be promptly initiated, and emergent cesarean section should be considered if AFE occurs while the fetus is in utero. Prompt diagnosis and initiation of supportive or resuscitative efforts are critical for maternal and fetal survival. Most mothers will require intubation for mechanical ventilation and oxygen. Cardiopulmonary resuscitation is often required, and cardiogenic shock must be managed. Large quantities of blood products are usually required, and efforts should be made to prevent or reverse coagulopathy via blood product transfusion.
Commonly used uterotonics include:
Commonly used uterotonics include:
* Oxytocin (Pitocin)
* Methylergonovine (Methergine)
* Carboprost (Hemabate)
* Misoprostol (Cytotec)
Asthma is a relative contraindication to the use of which uterotonic?
Asthma is a relative contraindication to the use of which carboprost.
Carboprost should be carefully administered to patients with a history of reactive airway disease as it can trigger bronchoconstriction. It is safe in patients with mild, asymptomatic cases of reactive airway disease