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
What gastrointestinal changes occur in pregnancy women after 20 weeks gestation?
Stomach and pylorus are moved cephalad, and intraabdominal esophagus becomes intrathoracic (increases gastric pressure and decreases competence of LES)
Decreased LES tone (estrogen, progesterone)
More acidic gastric fluid (placenta secretes gastrin)
All together, these changes lead to a greater propensity for gastric reflux and heartburn in pregnant women with a large, gravid uterus.
According to the current guidelines from the ASA, uncomplicated laboring women may consume..
According to the current guidelines from the ASA, uncomplicated laboring women may consume a moderate amount of clear liquids.
NOTE:
Complicated patients excluded from these restrictions include those with diabetes, morbid obesity, difficult airway, or increased risk of operative delivery.
ASA recommends avoiding solid foods in laboring patients and fasting for 6-8 hours in those undergoing elective CS.
According to the current guidelines from the ASA, uncomplicated patients scheduled for an elective cesarean section may consume..
According to the current guidelines from the ASA, uncomplicated patients scheduled for an elective cesarean section may consume clear liquids up to two hours prior to induction of anesthesia.
NOTE:
Complicated patients excluded from these restrictions include those with diabetes, morbid obesity, difficult airway, or increased risk of operative delivery.
ASA recommends avoiding solid foods in laboring patients and fasting for 6-8 hours in those undergoing elective CS.
Why do pregnant women have decreased oxygen reserve compared to average adults?
Many respiratory changes occur in the obstetric patient due to both anatomic and hormonal alterations.
As the pregnancy progresses, the diaphragm moves more cephalad which causes a decrease in the functional residual capacity.
In order to compensate for this change, the thoracic rib cage increases in anteroposterior and transverse diameter which aids to cause only a slight decrease in the total lung capacity overall.
The functional residual capacity decreases by about 20-30% as does the expiratory reserve volume and residual volume. In addition, there is an increase in the inspiratory reserve volume.
Airway resistance remains unchanged as progesterone relaxes the bronchiolar smooth muscle which combats the increased airway resistance due to upper airway edema.
These changes contribute to a rapid desaturation during apnea and necessitate prompt airway intervention to avoid complications.
Risk factors for preterm labor (<37 week)?
Risk factors for preterm labor (<37 week):
Previous preterm delivery
Extremes of age (<18, >35)
Race (black)
Low BMI
Short cervix
Multiple gestations (eg twins)
Tobacco/substance abuse
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.
Indications for general anesthesia for CS include
Immediate delivery for fetal or maternal concerns WITHOUT an epidural already in place
Severe hypovolemia or coagulopathy
Surgery involving massive hemorrhage
Intracranial or spinal conditions that preclude neuraxial
Patient refusal of neuraxial anesthesia
NOTE:
General anesthesia is generally avoided due to increased difficult airway risk, adverse risks to the fetus, uterine relaxation from volatile anesthetics, and risk of intraoperative awareness.
Factors that can affect the block height during spinal anesthesia include:
Factors that can affect the block height during spinal anesthesia include:
-Baricity (most important factor for the spread of local anesthetic and the level of block)
- Medication (dose and baricity)
- Patient (cerebrospinal fluid volume, older age, and pregnancy),
- Procedure (patient position, epidural injection before or after spinal injection) factors.
Mechanism by which epidurals reduce risk of postoperative ileus?
Epidurals containing a local anesthetic (with or without opioid) for postoperative analgesia reduces risk of postoperative ileus.
The proposed mechanism is increased gastrointestinal peristalsis (Sympatholytic) and reduced overall opioid use.
The increased gastrointestinal motility is thought to come from regional blockade of sympathetic nervous system (sympathectomy) and the epidural leaving the parasympathetic nervous system innervation of the gastrointestinal tract unopposed.
NOTE:
Single dose neuraxial opioids do not offer sympathectomy and are not superior to epidurals in regards to risk of post-op ileus.
Rank the following in terms of analgesic effectiveness:
Nurse administed medication (PRN)
Patient Controlled Epidural Analgesia (PCEA)
Continuous Epidural Infusion (CEI)
Patient Controlled Analgesia (PCA)
Rank the following in terms of analgesic effectiveness:
1 Continuous Epidural Infusion (CEI)
2 Patient Controlled Epidural Analgesia (PCEA)
3 Patient Controlled Analgesia (PCA)
4 Nurse administed medication (PRN)
What is more effective for pain relief, local based or opioid base epidurals?
Local based epidural
Epidural administration of any anesthetic agent including local anesthetics and opioids has been shown to produce superior analgesia to the same medications administered systemically, regardless of the type of surgery being performed. The proposed mechanism for this significantly improved pain control involves the direct effect of administration on nociceptive inputs into the central nervous system.
The use of a local anesthetic based epidural regimen has been shown to provide the best postoperative pain control. Opioid-based epidural analgesics provide superior pain control to systemic opioid-based analgesic regimens, though they are inferior to a local anesthetic based epidural regimen. The hydrophilicity of opioids plays a role in this superior pain control, with epidural administration of hydrophilic opioids generally equating an equianalgesic dosing of systemic hydrophilic opioids. Therefore, some suggest only using lipophilic opioids such as fentanyl in the epidural space for immediate postoperative pain control.
The use of opioids in combination with local anesthetics in epidural analgesia may be beneficial, however, definitive data on this point are lacking.
Furthermore, patient-controlled epidural analgesia (PCEA) has been shown to be inferior to continuous epidural infusions (CEI) of analgesic medications. Proposed mechanisms for this finding include the delayed action of local anesthetics in the epidural space, as well as benefits of a continual bathing of the pertinent nerve roots in CEI when compared to the intermittent coverage provided by PCEA. CEI may have increased incidences of medication-related side effects secondary to the increased amounts of medication administered in CEI compared to PCEA, and the benefits of CEI should be weighed against these possible complications. In clinical practice, many choose an epidural regimen that combines both CEI and PCEA.
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).
MORE:
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.
Does closing capacity change during pregnancy?
NO, CC remains unchanged. However, FRC can fall below CC resulting in atelectasis and hypoxemia.
How does minute ventilation change during pregnancy?
Minute ventilation increases primarily due to large TVs and to a lesser extent higher RR.
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.
MORE:
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.
The risk of Meconium Aspiration Syndrome (MAS) is highest in..
The risk of Meconium Aspiration Syndrome (MAS) is highest in post-term deliveries (>41 weeks).
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.
In the first stage of labor, describe the latent and active phase.
Latent phase (0-6cm dilation)
Characterized by mild and irregular contractions.
Active phase (6-10cm dilation)
Characterized by strong and frequent contractions.
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.
Does labor epidural analgesia prolong the first stage of labor?
NO
Does labor epidural analgesia prolong the second stage of labor?
YES
Neuraxial labor analgesia does cause a prolongation of the second stage of labor. However, this is of modest magnitude at approximately 15 min. It may be due to decreased motor nerve transmission to abdominal and pelvic skeletal muscle (decreased pushing).
Risk factors for failed neuraxial anesthesia during cesarean delivery include:
Risk factors for failed neuraxial anesthesia during cesarean delivery include:
Increasing maternal size
Late labor epidural placement
Rapid decision-to-incision interval
NOTE:
About 3% of blocks fail during cesarean deliveries.
Spinal block after a failed epidural is a risk factor for
Spinal block after a failed epidural is a risk factor for high spinal.
NOTE:
Cut spinal dose in half.
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).
For each anesthetic technique, describe whether they provide analgesia for first, second, or first and second stage of labor:
Epidural
Lumbar sympathetic block
Paracervical block
Pudendal block
For each anesthetic technique, describe whether they provide analgesia for first, second, or first and second stage of labor:
Epidural- first & second
Lumbar sympathetic block- first only
Paracervical block- first only
Pudendal block- second only
Pudendal nerve blocks provide analgesia for what stage of labor?
Second stage of labor
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.
Somatic nerve fibers from the perineum, pelvic floor, lower vagina, and vulva come together to form the pudendal nerve entering the neuraxis at S2-S4. Pudenal nerve blocks block 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
____________ is a uterotonic that is relatively contraindicated in patients with hypertensive disorders as it can concomitantly increase systemic blood pressure (by increasing systemic vascular resistance).
Methylergonovine (Methergine) is a uterotonic that is relatively contraindicated in patients with hypertensive disorders as it can concomitantly increase systemic blood pressure (by increasing systemic vascular resistance).
In the Neonatal Resuscitation Algorithm, when should baby be intubated and chest compressions initiated?
When HR < 60 bpm
Does neuraxial analgesia prolong labor?
YES, neuraxial labor analgesia does cause a slight (~15 min) prolongation of the *second stage *of labor.
It is also believed to cause maternal fever and higher instrumental delivery rate.
Describe the mechanism of neuraxial opioid administration.
1) During neuraxial opioid administration, the binding of neuraxial opioids at presynaptic and postsynaptic neurons within the substantia gelatinosa of the spinal cord lead to suppression of substance P and glutamate secretion. The transmission of nociceptive information arising from the dorsal horn toward the brain (ie, ascending pathway) is inhibited via this process.
2) Effects in the brain and brainstem also occur through systemic absorption and passage through the cerebrospinal fluid, resulting in projections into the spinal cord that inhibit pain transmission from the dorsal horn as well. Direct effects on the medulla and periaqueductal gray areas that project neurons into the spinal cord cause inhibition of ascending pain transmission from the dorsal horn as well.
Steps in managing patients with accidental high spinal include…
High/total spinal blockade occurs when the level of anesthesia rises and results in paralysis of the respiratory muscles and diaphragm (C3-5).
High/total spinal blockade can occur after an unintentional injection of local anesthetic into the subarachnoid or subdural space, often occurring around the initial spinal injection or epidural placement (or later with epidural overdose). Although initial aspiration of the epidural and negative test dose limit the possibility of intrathecal injection via the epidural catheter, migration into the intrathecal space can result in delayed high/total spinal blockade.
Patients will often present with symptoms such as agitation, dyspnea, difficulty with phonation, severe hypotension, bradycardia, and loss of consciousness. If high/total spinal blockade is suspected, communication should occur immediately with the patient.
**In pregnant patients, the patient should be placed in the left lateral position to avoid aortocaval compression (increasing blood return to the heart). If it is not already happening, maternal and fetal monitoring should occur (fetal heart rate and maternal heart rate, blood pressure, oxygen saturation, and electrocardiogram). The patient should be given 100% oxygen. If the patient cannot oxygenate or protect the airway, intubation should immediately occur. Cardiovascular stability should be maintained with vasopressors and intravenous fluids.
**
High/total spinal blockade does not equate to brain anesthesia, so, if general anesthesia does not occur, additional anesthetic agents are often required. Moreover, the loss of consciousness results from decreased cerebral perfusion, not brain anesthesia.
Although it is rarely used, CSF lavage is an alternative treatment for high/total spinal blockade.
TrueLearn Insight: As the neuraxial block rises, patients may experience a feeling of dyspnea. If the level increases to C6-8, the patient may feel numbness and weakness of the fingers. If the level rises to C3-5, the diagram may become paralyzed, and the patient may require intubation to protect the airway. When patients do experience the feeling of dyspnea, an assessment of grip strength can be performed rapidly. If the grip strength is strong, the diaphragm is unlikely to be affected; if it is weak, the patient should be continuously assessed to ensure the block does not continue to rise.
What happens to platelet count during pregnancy?
Due to the increase in plasma volume, there is a dilutional effect on platelets, leading to a slight decrease (a 0%-10% decrease from baseline in most patients).
Why is pregnancy considered a hypercoaguable state?
Pregnancy is a hypercoagulable state due to significant increases in procoagulant factors I (fibrinogen) and VII and smaller increases in other procoagulation factors. Anticoagulant factors such as antithrombin III and protein S are also decreased tilting the scale toward a hypercoagulable state.
These changes lead to a 20% decrease in prothrombin time (PT) and in partial thromboplastin time (PTT).
Which coagulation factors are decreased during pregnancy?
XI, XIII
Which coagulation factors are increased during pregnancy?
I, VII, VIII, IX, X, XII, von Willebrand factor
Which anticoagulants are decreased during pregnancy?
Antithrombin III and Protein S
No Change in Protein C
(activated protein C resistance occurs but levels do not typically decline.)
During pregnancy, cardiac output increases up to ____% above the nonpregnant state.
During pregnancy, cardiac output increases up to **50% **above the nonpregnant state.
Maternal blood volume is increased up to _____% during pregnancy. This effect is mediated by sodium retention via the renin-angiotensin system..
Maternal blood volume is increased up to 45% during pregnancy. This effect is mediated by sodium retention via the renin-angiotensin system..
APGAR Score
The Apgar scoring system is a standardized, easy to perform, and relatively objective way to assess a newborn while performing neonatal care. Apgar scores are traditionally obtained at 1 and 5 minutes after delivery. If scores are low, further scoring can be done in 5- or 10-minute intervals as needed. The Apgar score includes the assessment of five parameters with a score of 0, 1, or 2 for each. See the table below for details.
Apgar scores help determine whether a neonate requires routine post-delivery care or more involved neonatal resuscitation. A score of 8-10 is considered a normal score where only routine post-delivery care is needed. A score of 4-7 suggests the need for close observation and more advanced care. A score of 0-3 suggests the need for immediate resuscitation. The Apgar score is not considered a true predictor of long-term neurologic outcome.
Define preeclampsia
Preeclampsia is diagnosed by new-onset hypertension during pregnancy (after 20 weeks gestation) with proteinuria OR with severe features.
Diagnostic criteria for preeclampsia:
1) New-onset hypertension of systolic >140 mm Hg, or diastolic >90 mm Hg occurring after 20 weeks of gestation on at least 2 occasions at least 4 hours apart
and
2) Proteinuria of 300 mg >24 hours or a protein:creatinine ratio of ≥0.3
OR
Preeclampsia with severe features is diagnosed with signs and/or symptoms of end-organ ischemia:
1. Systolic >160 mm Hg or diastolic >110 mm Hg
2. Visual or cerebral symptoms (blurry vision, headache, altered mental status)
3. Thrombocytopenia <100,000 μL
4. Creatinine >1.1 or greater than 2 times the baseline creatinine level
5. Aminotransferase and alanine aminotransferase levels >2 times normal or right upper quadrant (RUQ) pain (due to hepatic inflammation and the stretching of the liver capsule)
6. Pulmonary edema
The diagnosis of preeclampsia can be made without the presence of proteinuria with the presence of elevated blood pressure plus any of the severe features listed above for points 2 through 6.
MORE:
Part of the pathophysiology of preeclampsia is thought to involve abnormal implantation of myometrial spiral arteries. Spiral arteries generally remodel during pregnancy to increase blood flow by increasing their diameter. However, during preeclampsia, the arteries are unable to remodel adequately, resulting in high resistance in arterial flow through these arteries causing an overall stress response that leads to the release of vascular mediators that dramatically increase the vascular tone causing an increase in vascular resistance. This increase in overall uterine vascular resistance decreases uterine blood flow. Because uterine blood flow is not autoregulated but rather blood pressure dependent, the maternal systemic vasculature will increase to provide an optimal pressure gradient of blood flow to the uterus. Preeclampsia affects approximately 5% of all pregnancies.
Overall, there are high levels of inflammatory cytokines that lead to a hypervasoconstricted state. Thromboxane increases both vascular tone and platelet aggregation, which increases the risk of thrombosis. Prostacyclin normally decreases both vascular tone and platelet aggregation, which decreases the risk of thrombosis. The high systemic vascular resistance leads to decreased renal blood flow causing renal insufficiency. Pulmonary edema can occur secondary to capillary leakage.
Define severe features of preeclampsia
Preeclampsia - Severe Features:
- Severe HTN (greater than or equal to 160/110 mm Hg)
- Thrombocytopenia (less than 100,000/microliter)
- Elevated liver enzymes
- Persistent right upper quadrant abdominal pain
- Persistent cerebral symptoms, including visual
- Renal insufficiency (serum creatinine twice normal
- Pulmonary edema
How does magnesium treat preeclampsia?
Magnesium cause vasodilation by inhibiting calcium channels in the vasculature.
Preeclampsia risk factors:
A list of risk factors follows, with the most important factors at the top of the list:
- Antiphospholipid antibody syndrome
- Prior preeclampsia
- Chronic hypertension
- Diabetes mellitus (pre-gestational, type 1 or type 2)
- Obesity (pre-gestational or early pregnancy BMI > 30)
- Assisted reproductive technique (postulated to be due to limited preconception exposure to paternal sperm)
- History of placental abruption
- Multifetal pregnancy
- Chronic renal disease
- Prior stillbirth
- Advanced maternal age > 40 years
- Nulliparity
- Systemic lupus erythematosus
- Family history of preeclampsia
- African-American race
- Partner who fathered a preeclamptic pregnancy in another woman (through fetal genes)
- Teenage mother, primipaternity (postulated to be due to limited preconception exposure to paternal sperm)
- Hispanic ethnicity
Identification of risk factors is important because one intervention to prevent preeclampsia is available, namely administration of low-dose aspirin. Aspirin causes a 10% to 20% reduction in the risk of developing preeclampsia, possibly by reducing the thromboxane-to-prostacyclin ratio. Currently, the ACOG suggests daily low-dose aspirin, beginning in the late first trimester, specifically for women with a history of preeclampsia leading to prior preterm delivery before 34 weeks’ gestation, or preeclampsia in more than one prior pregnancy. However, as new studies help better delineate the risk factors for preeclampsia, more women could become candidates for prophylactic therapy in the future.
NOTE:
Smoking, however, is actually a dose-dependent protective factor for the development of preeclampsia. This effect may be due to nicotine inhibition of thromboxane A2 synthesis or stimulation of nitric oxide release.
Risk factors for preeclampsia include..
Extremes of age (< 18, > 40)
Nulliparity
African American Race
Hispanic ethnicity
Chronic HTN
Diabetes
Obesity (BMI >30)
Antiphospholipid syndrome (APLS)
Lupus
Prior of preeclampsia
Family history of preeclampsia
Prior of placental abruption
Prior still birth
Multifetal pregnancy
Chronic kidney disease
NOTE:
Smoking is NOT a risk factor actually is a dose-dependent protective factor for development of preeclampsia. This effect may be due to nicotine inhibition of thromboxane A2 synthesis or stimulation of nitric oxide release.
What is the only intervention that has been shown to prevent preeclampsia?
Low dose Aspirin
Aspirin causes a 10-20% reduction in the risk of developing preeclampsia, possibly by reducing the thromboxane-to-prostacyclin ratio. Currently, ACOG suggests daily low dose ASA beginning in the late first trimester specifically for women with a history of preeclampsia leading to prior preterm delivery before 34 wks gestation or preeclampsia in more than one pregnancy.
What is the leading cause of maternal death due to preeclampsia?
Stroke
Placental abruption risk factors:
Risk factors for placental abruption include
* Maternal hypertension
* Preeclampsia
* Advanced maternal age (age > 35 years at time of delivery)
* Increasing parity
* Maternal and paternal tobacco use
* Cocaine use
* Trauma
* Premature rupture of membranes
* Chorioamnionitis
* Bleeding in early pregnancy
* History of prior abruption
* Increased incidence of placental abruption has been noted in African-American populations and in patients hospitalized for acute and chronic respiratory disease.
Placental abruption is characterized by complete or partial placental separation from the decidua basalis prior to fetal delivery. Placental abruption commonly presents with painful vaginal bleeding, uterine tenderness, increased uterine activity, and possible nonreassuring fetal heart rate patterns (secondary to loss of sufficient placental oxygen and nutrient exchange with the fetus). It can also present as idiopathic preterm labor. Diagnosis is predominantly clinical and while ultrasonography is not very sensitive (24%), it can aid in confirming diagnosis due to high specificity (96%).
The Placenta Accreta Spectrum (PAS) include what three conditions?
Placenta Accreta
Placenta Increta
Placenta Percreta
NOTE:
Most cases of PAS involve >2000cc of blood loss during delivery. Increasing risk of peripartum mass hemorrhage with increasing from accreta < increta < percreta)
Anesthetic management of patients with known or suspected PAS should include large bore IV access, consideration of arterial line placement, use of GA (or the ability to convert quickly), and the ready availability of blood products (in room).
Prophylactic measures to decrease blood loss include balloon occlusion or embolization of the internal iliac arteries.
What is Placenta Accreta?
Placenta Accreta is when the placenta adheres to the myometrium without invasion of the uterine muscle.
What is Placenta Increta ?
Placenta increta occurs when the placenta adheres to the myometrium and invades the uterine muscle.
What is Placenta Percreta?
Placenta percreta is when the placenta invades through the uterine serosa and potentially into pelvic structures.
A major risk factor for placenta accreta is
A major risk factor for placenta accreta is the umber of previous cesarean deliveries.
0 = 3% incidence
1= 11% incidence
2= 40% incidence
3= 61% incidence
4 or more = 67% incidence
Risk factors for placenta previa?
Previous C-Section
Previous uterine surgery
Smoking
Advanced maternal age
Multiple gestations
Multiparity
Cocaine abuse
A blood gas taken from the umbilical artery of a term fetus would have the approximate values:
pH
PaCO2
PaO2
HCO3-
A blood gas taken from the umbilical artery of a term fetus would have the approximate values:
pH: 7.27
PaCO2: 50
PaO2: 18
HCO3: -2.7
A past history of _________ is the greatest predictor of a successful trial of labor after cesarean (TOLAC).
A past history of vaginal birth after cesarean (VBAC) is the greatest predictor of a successful trial of labor after cesarean (TOLAC).
Factors that tend to predict a successful TOLAC include
* Prior VBAC
* Younger maternal age
* TOLAC during spontaneous labor without augmentation or induction
* Advanced cervical dilation on presentation
* Lower prenatal BMI
* White race
* Nonrecurrent indication for the initial cesarean section such as breech positioning or fetal bradycardia
* Longer interdelivery interval since prior CS
Factors that tend to predict an unsuccessful (failed) TOLAC include
* Prior cesarean section for anatomic issues such as dystocia, cephalopelvic disproportion, or failed induction
* The requirement for augmentation or induction
* Postterm gestational age
* No history of vaginal delivery
* Geriatric mothers (age > 35 years)
* Nonwhite race
* Prenatal maternal obesity
* Fetal macrosomia (> 4,000 g estimated fetal weight)
Risk factors for uterine rupture?
MATERNAL
Prior CS
Myomectomy
Abnormal placentation
Congenital uterine anomalies
Grand multiparity
FETAL
Macrosomia
Malpresentation
Multifetal gestation
Labor induction/augmentation
Uterine instrumentation/manipulation
Trauma
NOTE:
True uterine rupture is a rare event with estimates of incidence ranging from 0.012-0.07%.
Risk factors for placenta accreta?
Prior uterine surgery (including C-sections)
Previous myometrial tissue damage (myomectomy, Asherman syndrome)
Advanced maternal age
Multiparity
Smoking
NOTE:
Treatment is usually a cesarean hysterectomy
_____________ is recommended as a fast and efficient tocolytic that resolves quickly.
Nitroglycerin is recommended as a fast and efficient tocolytic that resolves quickly.
An appropriate dose and route is 0.4 mg sublingual. If IV dosing is required, then 50 to 200 mcg IV is typical.
Postdural puncture headache (PDPH) can present as early as the first time the patient sits up, but the typical presentation timing is ________ to _________ after dural puncture.
Postdural puncture headache (PDPH) can present as early as the first time the patient sits up, but the typical presentation timing is **6 to 72 hours **after dural puncture.
The incidence is approximately 50% when the dura is accidentally punctured with the epidural needle, but only in the low single digits if using a spinal needle, particularly when using a small-diameter pencil-tip needle. Therapeutic blood patch is very effective (90%)
Usually after traumatic dural puncture (with large bore Touhy needle) or lumbar puncture / drainage but can also occur with
regular spinal anesthesia using a 25G spinal needle
Incidence of PDPH?
1/100
PDPH Presentation
- Positional headache (worse with standing, better with laying flat) often frontal/occipital
- Associated with neck stiffness, nausea, and photophobia
Risk factors for PDPH
Risk factors for PDPH
* Female sex
* Pregnancy
* History of headaches
* Extremes of age
* Volume of CSF removed
* Kow BMI
Describe the MOA of magnesium as it pertains to treatment of preclampsia/eclampsia
Magnesium Sulfate (VAST):
* V: Vasodilator, smooth muscle relaxation
* A: Anticonvulsant
* S: Sedative, skeletal muscle relaxant (decreases release of ACh and decreases sensitivity of
motor endplate to ACh)
* T: Tocolytic, decreases uterine activity which increases uterine blood flow
Symptoms of hypermagnesemia
Normal serum magnesium levels are between 1.5-2.5 mg/dL. Hypermagnesemia is > 2.5 mg/dL and can result from kidney impairment, overuse of magnesium-based laxatives or enemas, over-infusion of magnesium in preeclampsia treatment, and disorders such as milk-alkali syndrome. Hypermagnesemia results in neurotoxicity by decreasing transmission of the impulse across the neuromuscular junction resulting initially in diminished deep tendon reflexes. As the magnesium levels rise (see table below), the reflexes disappear. Cardiotoxicity results from magnesium acting as a calcium and potassium channel blocker, disrupting cardiac function and leading to complete heart block and cardiac arrest (> 12 mg/dL). Due to its calcium channel blocker effects, elevated magnesium levels can lead to hypotension, bradycardia, and ECG changes including prolonged PR interval and widened QRS. Of note, respiratory failure typically occurs prior to cardiac arrest.
Though magnesium toxicity from preeclampsia treatment is rare in women with good renal function, toxicity can still occur. Despite there being no consensus on the optimal treatment regimen, magnesium sulfate is commonly started at the onset of labor, induction, or prior to and during cesarean delivery. Usually, a loading dose is intravenously administered followed by a maintenance dose. In women with renal insufficiency, the maintenance dose should be lowered or not given. Clinical assessment of magnesium sulfate treatment should occur every one to two hours by assessing the presence of the patellar reflex. The loss of the reflex is the first sign of symptomatic hypermagnesemia. When renal function is normal and there are no signs of magnesium toxicity (see table below), serum magnesium levels are not required. Serum magnesium levels are checked if a seizure occurs during treatment, renal insufficiency is present (creatinine > 1.1 mg/dL), or there are signs of magnesium toxicity. If no toxicity occurs, total treatment should is usually for 24 hours postpartum with the therapeutic range for serum magnesium between 5-9 mg/dL.
High magnesium can result in cardiotoxicity by blocking calcium and potassium channels leading to complete heart block and cardiac arrest above what level?
Magnesium > 12 mg/dL
NOTE:
Also muscle paralysis and respiratory failure >12 mg/dL.
EKG changes including bradycardia, prolonged PR, prolonged QRS, prolonged QT are seen at what magnesium level?
Magnesium 7-12 mg/dL
Diminished DTRs can be seen at what magnesium level?
Magnesium 5-7 mg/dL
NOTE:
Clinical evaluation of magnesium sulfate pre-eclampsia treatment should occur every 1-2 hours by assessing the patellar reflex.
The loss of patellar reflex is the first sign of symptomatic hypermagnesemia.
Physiologic changes during normal pregnancy include:
The most reliable (sensitive and specific) sign of uterine rupture during labor is _____________________.
The most reliable (sensitive and specific) sign of uterine rupture during labor is** non-reassuring fetal heart rate (FHR) patterns.
**
Uterine rupture occurs when the integrity of the entire thickness of the myometrial wall is compromised, usually at the location of a previous uterine wall defect. It can result in fetal compromise or maternal hemorrhage and accordingly, requires timely cesarean delivery or postpartum laparotomy. Uterine rupture typically presents with vaginal bleeding, maternal tachycardia and hypotension, cessation of labor, abdominal pain, and/or fetal compromise. Among these, non-reassuring FHR patterns (e.g. fetal decelerations) are the most sensitive and specific sign of uterine rupture and occur in approximately 75% of cases. Diagnosis is then confirmed by manual exploration of the uterus or with a laparotomy. Risk factors for uterine rupture include a history of prior cesarean section, grand multiparity, fetal malpresentation, bicornuate uterus, prior myomectomy, and labor induction with oxytocin or prostaglandin.
Which epidural local anesthetic has the fastest onset and shortest duration of action?
Epidural 2-chloroprocaine has an onset time of approximately 6-12 minutes, as a result of the high concentration of local anesthetic that is used.
The ester local anesthetic 2-chloroprocaine is most frequently used in the setting of obstetric epidural analgesia. Compared to other commonly used local anesthetics, is has the fastest onset of action time. 2-chloroprocaine has an onset time of 6-12 minutes, and that may be shortened slightly when high volumes are used. It is available in a 2% and 3% concentration. Duration of action is 45-60 minutes plain and 60-90 minutes when mixed with epinephrine (1:200,000 dilution). Chloroprocaine is hydrolyzed rapidly by plasma cholinesterases (half-life elimination of 21 seconds). However, metabolism is decreased in patients with a pseudocholinesterase deficiency. Chloroprocaine is commonly used to obtain rapid analgesia for an emergency cesarean section, when a working epidural catheter is already in place.
TrueLearn Insight: Administration of 2-chloroprocaine may decrease the efficacy of subsequently administered neuraxial drugs including bupivacaine, morphine, and fentanyl. Chloroaminobenzoic acid (the metabolite of 2-chloroprocaine) may be responsible for decreasing the efficacy of subsequent bupivacaine administration. Chloroaminobenzoic acid may also act as an antagonist of the µ-opioid receptor, leading to reduced efficacy of subsequent opioid neuraxial administration.
Maximum allowable dose of the commonly used local anesthetic agents:
Lidocaine (plain): mg/kg
Lidocaine (with epinephrine): mg/kg
Bupivacaine (plain): mg/kg
Bupivacaine (with epinephrine): mg/kg
Ropivacaine (plain only): mg/kg
Chloroprocaine (plain only): mg/kg
It is important to know the approximate maximum allowable dose of the commonly used local anesthetic agents. These maximum dosages are irrelevant to the site of injection, and toxicity may occur at lower dosages if inadvertent direct vascular injection is made. Although not all sources agree on the maximum allowable dose, these doses are generally quoted:
Lidocaine (plain): 5 mg/kg
Lidocaine (with epinephrine): 7 mg/kg
Bupivacaine (plain): 2.5 mg/kg
Bupivacaine (with epinephrine): 3 mg/kg
Ropivacaine (plain only): 3 mg/kg
Chloroprocaine (plain only): 12 mg/kg
Which epidural opioid lasts the longest? Fentanyl or Morphine
Fentanyl
Onset: 5-10 minutes
Duration: 1-2 hr duration
Morphine
Onset: 30-60min
Duration: 12-24 hr
Which of the following spinal needles has a cutting tip?
Sprotte
Whitacre
Quincke
Quincke
Sprotte and Whitacre are pencil-point needles and are also known as noncutting point needles. Since they are noncutting they reduce the risk of postdural puncture headache.
“Quincke Cuts”
NOTE:
The use of smaller guage needles is associated with decreased risk of postdural puncture headaches. On the other hand, higher guage needles provide better tactile sensation and have a lower failure rate than small guage needles.
What is the most commonly used epidural needle?
Tuohy
Which opioid has the greatest CSF spread when injected intrathecally? Fentanyl or Morphine?
Morphine
Transient Neurological Symptoms (TNS)
Presentation?
Risk factors?
Transient neurologic symptoms (TNS) are characterized by unilateral or bilateral radiating pain in the buttocks and legs. Symptoms occur within 24 hours of intrathecal injection and usually resolve within 1 week.
Risk factors:
- Use of lidocaine over bupivicaine or tetracaine
- Addition of phenylephrine to 0.5% tetracaine
- Lithotomy position w/ knee flexion
- Patients undergoing outpatient procedures
Spinal blockade above what level can result in sympathectomy and significant hypotension?
T5
Why should epidural dosing be reduced in the elderly?
Increased dura permeability
At what magnesium level do DTRs become absent
7-12
How do the following change during pregnancy?
Plama Albumin
Plasma Volume
Red blood cell volume
How do the following change during pregnancy?
Plama Albumin- decreases
Plasma Volume- increases
Red blood cell volume- increases
NOTE:
Maternal colloid oncotic pressure decreases due to the decreased plasma albumin resulting in edema.
Although both plasma volume and red blood cell volume increase, plasma volume increases more than red blood cell volume resulting in physiological anemia of pregnancy.
Why do some patients have nausea/vomiting immediately after spinal anesthesia?
Unopposed splanchnic parasympathetic stimulation of the stomach and intestines causing hyperperistalsis
What are the three primary causes of hypothermia with neuraxial anesthesia?
Core to peripheral shift of warm blood
Depression of the shivering threshold
Patient unable to experience cold sensation
How do the following lung volumes change during pregnancy?
IRV
TV
IC
ERV
VC
RV
TLC
IRV - increases
TV - increases
IC - increases
ERV- decreases
VC - unchanged
RV- decreases
TLC- decreases
Elevation of the diaphragm from the growing uterus decreases FRC as early as how many weeks gestation?
Elevation of the diaphragm from the growing uterus decreases FRC as early 20 weeks gestation.
What gastrointestinal effects does progresterone have during pregnancy?
Decreased LES tone
More acidic gastric pH
Increased total gastrointestinal transit time
Uterine blood flow =
Uterine blood flow = Uterine perfusion pressure/ Uterine vascular resistance
Uterine blood flow = (Uterine arterial pressure - Uterine venous pressure)/ Uterine vascular resistance
NOTE:
Maternal blood pressure is the most important determinant of uterine blood flow.
In a pregnant patient, what anti-muscarinic should be given to prevent fetal bradycardia when neostigmine is used to reverse NMBAs?
Atropine
At term, what percent of the maternal cardiac output does the uterus receive?
20%
At term, 20% of the maternal cardiac output is provided to the uterus.
Review physiologic cardiovascular changes seen at term in pregnancy.
NOTE:
SVR decreases due to decreased response to endogenous vasopressors, vasodilatory effects of progesterone and prostaglandins, and the low resistance of the uteroplacental vascular bed.
Define Post-Partum Hemorrhage (PPH).
Post-Partum Hemorrhage (PPH) is defined as an estimated blood loss >500cc for vaginal deliveries and >1000cc for C-Sections.
The most common cause of post-partum hemorrhage is
Uterine Atony
Risk factors for uterine atony?
C-Section
Prolonged labor
Labor induction/augmentation
High parity
Multiple gestations
Macrosomia
Polyhydramnios
Chorioamnionitis
Retained products of conception
The hypercoagulable state during pregnancy is due to an increase in what two factors?
Factor VII
Fibrinogen
Epidural coverage between what levels is required to prevent pain from uterine contractions and cervical dilation during a vaginal delivery?
T10-L1
Epidural coverage between what levels is required to prevent pain from vaginal and perineal distension during a vaginal delivery?
S2-S4
The initial treatment of choice to induce rapid uterine relaxation during an obstetric emergency in a patient who is not under general anesthesia is…
Nitroglycerin
Other pharmacologic options for uterine relaxation include inhaled anesthetic, inhaled amyl nitrite, and beta adrenergic agonists (IV ritodrine, IV salbutamol, IV terbutaline).
During obstetric emergencies, there is often a requirement for rapid and transient relaxation of the cervix and the uterus to allow obstetric maneuvers. Examples include facilitation of vaginal delivery of a twin in an abnormal positions, breech presentations to deliver the fetal head, cesarean delivery of a fetus with an abnormality (such as hydrocephalus), inverted uterus, removal of retained placenta, and oxytocic overdose.
Tocolytics include
Beta agonists (Terbutaline)
Oxytocin antagonists
Magnesium sulfate
Prostaglandins inhbitors
Calcium channel blockers
Methylergonovine maleate (Methergine) is contraindicated in patients with…
Hypertensive disorders (including preeclampsia)
NOTE:
Because Methergine is a synthetic ergot alkaloid and may lead to hypertensive emergency.
Oxytocin (Pitocin)
Side effects?
Hypotension
Tachycardia
Coronary vasoconstriction
Myocardia ischemia
NOTE:
No contraindications exist
Carboprost trometamine (Hemabate) is contraindicated in patients with…
Reactive airway disease
NOTE:
Because Carboprost has prostaglandin-like effects and can cause bronchospasm.
Methylergonovine maleate (Methergine)
MOA?
Induces uterine contractions by increasing intracellular calcium.
Dose: 0.2mg IM
Methylergonovine maleate (Methergine)
Side effects?
Severe hypertension
Bradycardia
Coronary vasospasm
Cardiogenic pulmonary edema
Carboprost trometamine (Hemabate)
Side effcts?
Nausea
Diarrhea
Bronchospasm
Labile blood pressures
Carboprost trometamine (Hemabate)
MOA?
Prostaglandin-like (F2-alpha) effects
Dose: 0.25mg (250mcg) IM
Paracervical nerve blocks may provide analgesia during the first stage of labor by injecting local (Chloroprocaine or Mepivacaine) at the 3 O’clock and 9 O’clock position of the cervix blocking the Frankenhauser ganglion effectively anesthetizing the upper part of the vagina, cervix, and uterus.
What is the most common complication of paracervical nerve blocks?
Fetal bradycardia (unknown mechanism)
What 5 factors determine placental transfer of drugs?
1) Size
2) Lipid solubility
3) pKA of drug
4) Protein binding
5) Maternal drug concentration
Size- small drugs (molecular weight < 500 Da more readily corss the placenta while drugs > 1000 Da (eg heparin, protamine, insulin) do not readily cross
Lipid solubility- lipophilic drugs (eg fentanyl) readily cross, highly ionized drugs (sux, NDMAs) do not easily cross
pKA- defined as the pH at which a drug exists in 50% ionized and 50% non-ioniized form. Only the non-ionized fraction of a drug will cross the placenta.
Protein binding- highly bound drugs do not cross, unbound crosses
Maternal drug concentration- the higher the concentration of a drug in the maternal circulation, the greater the rate of transfer through the placenta
NOTE:
Some important drugs that do not cross the placental include: Heparin, Insulin, Glycopyrrolate, Nondepolarizing muscle relaxants, Succinylcholine (“He is Going Nowhere Soon”)
Fetal acidosis promotes the conversion of local anesthetics to what form? (ionized or non-ionized)?
Fetal acidosis promotes the conversion of local anesthetics from non-ionized to ionized form in the fetal circulation resuliting in “ion trapping”.
NOTE:
Most local anesthetics are slightly basic and have a pKA between 7-9
Does atropine cross the placenta?
Yes
Why should atropine be used with neostigmine reversal as opposed to glycopyrrolate?
Glycopyrrolate does not cross the placenta. Neostigmine DOES cross the placenta. If glycopyrrolate is administered with neostigmine, the fetus will accordingly be exposed to more neostigmine than glycopyrrolate and can become bradycardic. For this reason, atropine may be preferred in combination with neostigmine to antagonize non-depolarizing NMB in pregnant patients.
Risk factors for development of Amniotic Fluid Embolism (AFE)?
Risk factors for development of Amniotic Fluid Embolism (AFE) include any condition that might impair the barrier between the mother and amniotic or fluid cells:
Advanced maternal age
Multiple pregnancy
Multiparity
Abnormal placentation
C-Section
Induction of labor
Eclampsia
Trauma
Pathophysiology and treatment of Amniotic Fluid Embolism (AFE)?
See picture for pathophysiology
Treatment is mainly supportive; intubation, 100% FiO2, access, inotropes, reverse coagulopathy often consistent with DIC (FFP, cryo, platelets, RBCs)
Define Gestational Hypertension.
Gestational hypertension is hypertension (>140/90 on two separate occasions) that occurs during pregnancy AFTER the 20th week WITHOUT signs of proteinuria (<300mg/24, PC ratio < 0.3, urine dipstick < 1+) or end-organ dysfunction.
The patient must have been normotensive before 20wks of gestation. If hypertension occurs before 20 weeks of gestation this is called chronic hypertension.
25% of patients with gestational hypertension will develop preeclampsia.
Gestational hypertension typically resolves by postpartum week 12.
Define Preeclampsia.
Preeclampsia is hypertension (>140/90 on two separate occasions) that occurs AFTER 20 wks gestation plus proteinuria (>300mg/24, PC ratio >0.3, urine dipstick > 1+) or end-organ dysfunction or end-organ signs/symptoms (known as severe features).
Preeclampsia can be broken down into preeclampsia without severe features and preeclampsia with severe features. Differentiate the two..
Preeclampsia WITHOUT severe features have hypertension with proteinuria.
If proteinuria is not present then 1 of the following severe features must be present: persistent epigastric or RUQ pain, fetal growth restriction, SBP >160, thrombocytopenia <100K, impaired renal function (Cr >1.1), impaired liver function (doubles of transaminases), pulmonary edema, or severe neurologic or visual changes.
HELLP syndrome is a severe form of preeclampsia that occurs during pregnancy that results in
Hemolysis
Elevated Liver enzymes
Low Platelets
Causes of variable decelerations on HFR tracing include
Variable decelerations are commonly caused by umbilical cord compression, leading to decreased umbilical flow to the fetus.
Variable decelerations can lead to fetal asphyxia when severe. They may progress to late decelerations or severe fetal bradycardia due to ischemia of the fetal myocardium, both of which indicate the need for emergent intervention.
Variable decelerations are transient decreases in FHR that characteristically vary in duration, shape, and magnitude. They are not typically associated with the patient’s underlying contraction pattern.
Causes of early decelerations on HFR tracing include
The most common cause of early decelerations is a vagal response from fetal head compression during contractions.
Early decelerations occur simultaneously with uterine contractions and often appear as a mirror image of them on tracing.
Causes of late decelerations on HFR tracing include
Late decelerations are associated with fetal hypoxia and acidosis. Common causes of this pattern of deceleration are maternal hypotension or uteroplacental insufficiency due to longstanding preeclampsia or gestational hypertension.
Late decelerations represent drops in FHR that occur 15-30 seconds after uterine contractions.
Maternal hypotension from a chemical sympathectomy induced by labor analgesia may cause what kind of FHR trace?
Late decelerations
Maternal hypotension from a chemical sympathectomy induced by labor analgesia may cause late decelerations.
Rapid administration of a fluid bolus and a vasoactive agent is often needed to correct this derangement and ensure adequate placental perfusion and oxygen delivery to the placenta.
The primary goal of fetal assessment in the intrapartum period is to ensure adequate fetal oxygen delivery. In general, a decrease in fetal blood flow is the primary cause of fetal hypoxia, which most commonly manifests as…
Fetal bradycardia
The primary goal of fetal assessment in the intrapartum period is to ensure adequate fetal oxygen delivery. In general, a decrease in fetal blood flow is the primary cause of fetal hypoxia, which most commonly manifests as fetal bradycardia.
Fetal acidosis is defined as
pH < 7.21 or a lactate > 4.8
NOTE:
Normal pH > 7.25
Normal lactate < 4.2
What is the PaO2 and PCO2 of the umbilical artery?
Umbilical Artery
PaO2= 20
PaCO2= 50
Surgery during what trimester carries the lowest risk of premature labor and abnormal fetal organogenesis?
Second trimester
Surgery during the second trimester carries the lowest risk of premature labor (highest in third trimester) and abnormal fetal organogenesis (highest in first trimester).
Factors that tend to predict a successful TOLAC include
Prior VBAC (#1)
Younger maternal age
TOLAC during spontaneous labor without augmentation or induction
Advanced cervical dilation on presentation
Lower prenatal BMI
White race
Nonrecurrent indication for the initial CS such as breech positioning or fetal bradycardia
Factors that tend to predict an unsuccessful (failed) TOLAC include
Prior CS for anatomic issues such as dystocia, cephalopelvic disproportion, or failed induction
The requirement for augmentation or induction
Postterm gestational age
No history of vaginal delivery
Mothers aged > 35 years
Nonwhite race
Prenatal maternal obesity
Fetal macrosomia (>4000g)
Is MAC increased or decreased in pregnancy?
MAC is decreased by up to 40% in pregnancy
Does nitrous oxide affect uterine blood flow?
NO
NOTE:
Nitrous oxide has demonstrated teratogenicity in animal studies, but not in the third trimester of pregnancy. In fact, in a few institutions in the US and around the world NO is used as labor analgesia.
Aortocaval compression may be observed as early as how many weeks gestation?
Aortocaval compression may be observed as early as 20 weeks gestation.
Should defibrillation be preformed in a pregnant women with the same energy as in a nonpregnant patient?
YES
NOTE:
Transthoracic impedenance remains the same in pregnant and non-pregnant patients. Any fetal monitors should be removed prior to defibrillation. During chest compressions, the uterus should be manually displaced to the left to reduce aortocaval compression and improve cardiac output. IV access should be obtained above the diaphragm because of concern for aortocaval compression. If magnesium is running it is possible that it is the cause of arrest and should be stopped and calcium should be given as the treatment for magnesium toxicity.
What are the leading causes of DIC in pregnancy?
Placental abruption
Postpartum hemorrhage
Hypertensive disorders of pregnancy
Transfusion goals for patients in DIC?
Hgb > 7
Plts > 50K
INR < 1.5 (via FFP)
Fibrinogen >300 (via cryo)
Is neuraxial contraindicatd in patients in suspected DIC?
YES, general anesthesia is required.
What is the primary mechanism of action of neuraxial opioids?
Neuraxial opioids inhibit presynaptic release of neurotransmitters (substance P and glutamate) in the substantia gelatinosa of the dorsal horn.
During cardiac arrest of a pregnant patient, perimortem delivery of the fetus should be prefromed if there is no ROSC after how many mintutes?
Four minutes
Review changes in coagulation factors at term.
