Obstetrics Flashcards
What happens to cardiac output during pregnancy? How does it change from fetal development until birth of the child? What factors influence the initial change in CO? What factors influence the dramatic change after labor? What can this mean for a mom with a history of heart problems, then?
Cardiac output increases in pregnancy due to an increase in stroke volume (increase blood volume) and an intrinsic increase in HR. It is increased by about 40% throughout pregnancy due to these factors.
Immediately after delivery CO increases as much as 80% due to blood volume and the now contracted uterus.
The increased demands on the heart associated with pregnancy can place a mom with heart disease at risk for heart failure.
Does Hct increase or decrease with pregnancy? Does this lead to anemia? Why or why not?
Hct actually increases, but d/t the increase in blood volume a relative dilutional anemia exists.
What happens to SVR during pregnancy? Why?
SVR and PVR decrease to promote perfusion
What happens to MAP during pregnancy? Explain why
MAP remains relatively constant due to increased CO and decreased SVR
What is average blood loss for a vaginal delivery? Uncomplicated Csection?
Vaginal: 500 ml
Csection: 750-1000 ml
What is Aortocaval compression? What steps should be taken to avoid this complication when patients are supine?
Gravid patients lying supine may allow the uterus to compress the inferior vena cava and the aorta reducing blood return to the heart and blood flow to the uterus. This in return can reduce cardiac output and lead to hypotension and poor uterine perfusion.
Left uterine displacement. Place a ramp on the patients RIGHT side at 15 degrees to displace the uterus to the left
Speak to the clotting situation for the parnutrient: What happens to coag factors? What happens to fibrinogen? What does all this mean for the parturient in terms of clotting?
Both. They are hypercoagable as coag factors and fibrinogen increase. This, however, is accompanied by increased fibrinogen breakdown. Overall, moms are considered to be hypercoagulable and at increased risk for clotting.
What happens to platelets in the parnutrient? Why? What does this put the mom at risk for?
Platelet levels may decrease due to a number of possible factors including dilution and accelerated platelet breakdown. Usually this throbmobcytopenia is not a problem and considered normal with pregnancy. As a general rule of thumb practitioners may refuse to place epidural catheters if platelet values drop below 100K
What makes parturients more susceptible to airway complications? What are the concerns?
Engorgement of the mucosa d/t increase in blood volume can lead to a higher malampati score, a narrowed glottic opening, and increased risk of bleeding with instrumentation
How does pregnancy effect the following respiratory considerations: oxygen consumption, respiratory rate, tidal volume, minute ventilation, PaCO2, FRC, ERV, RV
O2 consumption: increased RR: increased Minute Ventilation: increased Tidal Volume: increased PaCO2: decreased FRC: decreased ERV: decreased RV: decreased
Why are FRC, ERV, and RV decreased in pregnancy? In terms of respiratory pathophysiology how can this be thought of as?
Due to upward displacement of the diaphragm restricting the lungs. It can be thought of as restrictive disease (not letting air in)
What effect does progesterone have on MAC for anesthetics and dosing of local anesthetics both peripherally and neuroaxially?
MAC is decreased by 30-40%
Local anesthetic dosing is reduced as nerves are more sensitive to locals
Neuroaxial dosages are reduced d/t engorgement and reduction in the neuroaxial space increasing spread of the local both in the epidural and subarachnoid space
What are the three considerations that make parturients a higher risk for aspiration? What causes these risks to occur?
Increased gastric volume d/t slow motility
Decreased pH of gastric content d/t gastrin
Decreased LES tone d/t progesterone
At what point in pregnancy are parturients considered an increased aspiration risk and RSI with a secured and protected airway advised? At what point is the risk normalized?
Beginning in the 2nd trimester.
What happens to GFR in pregnancy? Why does this occur?
GFR is increased d/t an increase in CO.
Describe blood flow to the uterus in pregnancy (autoregulation, %CO,
There is NO autoregulation and thus it is dependent on a maternal MAP.
It is 10% of cardiac output.
What are disadvantages to IV analgesics for laboring parturients?
Typically provides subpar pain relief
Leads to maternal and fetal respiratory depression
Associated with nausea and vomiting in the face of a lowered LES tone —> aspiration risk
Will the following opioid analgesics cause respiratory depression in the fetus? (Meperidine, Morphine, Fentanyl, Ketamine, Remifentanil)
All of them can cause respiratory depression in the neonate if administered in utero
Describe each stage of labor in regards to vaginal changes, delivery process, and analgesia needs (stage 1, stage 2, stage 3)
Stage 1: dilation and effacement from 1-9 cm, pain is typically T10-L2
Stage 2: complete dilation (10 cm) until delivery of the fetus, pain is T10-L2 and S2-S4
Stage 3: delivery of the placenta
What is fetal heart rate variability? What is a normal FHR? What is normal variability (mild, moderate, marked)?
When a fetus is well oxygenated there will be variability in the fetal heart rate from 110-160 bpm. Variability is an assurance of fetal well being. Variability is described as mild (< 5bpm variability), moderate (6-24 bpm variability), and marked (25+ bpm variability)
What are the advantages and disadvantages of Bupivicaine for epidural anesthesia
Produces more sensory then motor block (differential blockade); ADVANTAGE
Associated with more severe cardiotoxicity with LAST
What are the advantages and disadvantages of lidocaine for use in parturients?
It has a quick onset with dense block for Csection; ADVANTAGE
The dense block is not ideal for vaginal delivery; DISADVANTAGE
Lidocaine is associated with potential neurotoxicity, cauda equina syndrome, and transient neurological symptoms when administered in the subarachnoid space (spinal) and for this reason it is often avoided for spinal anesthesia; DISADVANTAGE
What unique phenomenon must be considered with the use of morphine and chloroprocaine
It has been show to reduce the effectiveness of neuroaxial morphine
What is a common “test dose” for placement of an epidural catheter in obstetric anesthesia? What is the idea behind this test dose?
45 mg of lidocaine (3 cc of 1.5%) in 1:200,000 epinephrine. It is a means of assessing if the catheter is intrathecal or intravascular. Intrathecal will create a dense lower extremity block (undesired) and intravascular will created an increase in HR and possibly early signs of systemic toxicity (lip numbness, metallic taste, ringing in ears). In pregnant patients an increase in HR with bolus test dose is non-specific due to contractions and pain.
What is the advantage of adding an opioid to an epidural or spinal block? What are the disadvantages?
Opioids allow lower concentrations of local anesthetic, thus creating less motor blockade, while maintaining effective analgesia.
What are indications that an epidural catheter may have migrated into the intrathecal space? What about the intravascular space?
Intrathecal —> If motor block becomes dense, sensory block remains adequate, and segmental spread less distinct
Intravenous —> sensory block lost and possible signs of system toxicity (though low concentration epidural bags make this unlikely
What are common solutions for epidural anesthesia (Bupivicaine and Ropivicaine)? What is a common rate?
Bupivicaine: 0.0625% - 0.125% w/ 1-3 mcg of fentanyl
Ropivicaine: 0.1% - 0.2% w/ 1-3 mcg of fentanyl
Rate is 8-12 ml/hr with bolus interval
What are common side effects of neuroaxial opioid administration?
Respiratory depression, pruritus, urinary retention, nausea
What is a “subdural injection” during epidural? What are the signs and symptoms? How can it be avoided? What is the treatment?
Placement of the catheter between the dura and the arachnoid (subdural). Spread will occur within 5-15 minutes to cause hypotension, respiratory compromise, and/or unconsciousness.
It can not be avoided. Treatment involves support: stop infusion, provide hemodynamic support, intubate and respiratory support if needed.
Describe the two common uses of Mg Sulfate infusion in the obstetric population. What are the therapeutic levels for the therapy?
Tocolytic: used to stop/slow uterine contractions in preterm pregnancy. Therapeutic level is 4-8 mg/dL
Anti-convulsant: used to prevent seizures in cases of severe pre-eclampsia. Therapeutic levels are 8-10 mg/dL
What are the common side effects of Mg Sulfate infusion that should be monitored for?
Pulmonary Edema Hypotension Loss of Reflexes Muscle Weakness CNS Depression
How does Mg Sulfate work as a Tocolytic? What about as a treatment for pre-eclampsia?
Mg Sulfate reduces the amount of Ca for uterine contraction
It is a CNS depressant
Describe what is observed at the following Mg levels: 1-3, 4-8, 8-10, 10+, 18+
1-3: normal Mg blood level 4-8: useful as a tocolytic 8-10: useful as an anticonvulsant 10+: deep tendon reflexes are suppressed 18+: respiratory depression
What is the use of betamethasone in pregnancy for the neonate? How long does it take before it begins to take effect with benefits?
It is given to hasten the lung development of the neonate in cases of possible premature labor. It takes 8-48 hrs before results will be beneficial.
What class of drug is Terbutaline? What is it used for? What are common side effects? Why has it fallen out of favor?
It is a beta-agonist used as a tocolytic. Common side effects include transient low blood sugar and hypokalemia. It also causes fetal tachycardia as it crosses the placenta. It has fallen out of favor d/t fetal tachycardia and its lack of efficacy as a tocolytic.
What must be taken into consideration in regards to the following IV pharmacological agents given concurrently with a Mg Sulfate infusion…
- Depolarizing Muscle Relaxant
- Non-Depolarizing Muscle Relaxant
- Alpha Agonists (phenylephrine, ephedrine, etc)
All muscle relaxants will be potentiated by Mg; this means smaller doses are needed to elicit muscle relaxation
Alpha agonists efficacy is decreased; it may take more then usual to elicit desired effects when a Mg Sulfate infusion is in use.
Describe Placenta Previa, Placenta Accreta, Placenta Precreta, and Placenta Increta
Placenta Previa: the placenta covers the cervical os, this leads to painless vaginal bleeding, and depending to the severity of cervical os coverage a c-section may be indicated. Patients are at a higher risk for sudden rupture and bleeding and higher post-partum bleeding.
Placenta Accreta: the placenta is adhered to the myometrium and placenta delivery results in an increase in hemorrhage and bleeding.
Placenta Precreta: the placenta is adhered into the myometrium and placenta delivery results in an increase in hemorrhage and bleeding.
Placenta Increta: the placenta is adhered through the myometrium and placenta delivery results in an increase in hemorrhage and bleeding. Bleeding may be so intense and fast that a hysterectomy in the face of massive blood infusion is indicated
What is placental abruption? What are the signs and symptoms? What are complications of abruption? What disease states are most likely to lead to abruption?
When the placenta tears away from the uterine and internal bleeding occurs. Signs and symptoms may include abdominal pain, loss of positive fetal assurance d/t hypoperfusion, external bleeding may or may not be noted. Parturients with pre-eclampsia or a history of uncontrolled HTN are more likely to have placental abruption.
What is diagnostic for pre-eclampsia (Mild and Severe)
Mild is new onset HTN and proteinuria (>3g) at 20+ weeks gestation, other signs and symptoms are rare if present
Severe is BP >/= 160 mm Hg and proteinuria >5g. Other signs and symptoms may include visual disturbances, RUQ pain, headache, thrombocytopenia, etc.
When should BP management be initiated for a mom diagnosed with pre-eclampsia? What is the aim of this management? When should Mg Sulfate infusion be initiated? Why? What is the therapeutic value?
BP management should be administered when BP exceeds 160 systolic or 110 diastolic. This is to reduce occurrences of thrombolitic stroke and/or decreased placental perfusion.
Mg Sulfate is initiated with severe pre-eclampsia to reduce chances of seizure. A therapeutic value is 8-10 mg/dL
How is Mg toxicity treated?
With 10% calcium gluconate (10 ml)
