OB

Question 1

ABG in preggos:

Answer 1

OB patients have a baseline decreased paCO2 due to increased minute volume (increased tidal volume and mildly increased respiratory rate). To compensate, the kidneys excrete bicarbonate leading to a mildly decreased bicarbonate level. A normal ABG of pregnancy shows mild alkalosis (~7.45), hypocarbia (30-32), and mildly decreased bicarb (~19).

Question 2

Creatinine is 0.5 and BUN of 8 in a pregnant woman cool right?

Answer 2

Yup! When we start talking about preeclampsia, renal effects are very important, therefore it is important to know what is normal for OB patents. The threshold for glycosuria (normally around 190 g/ dL) is decreased and mild glycosuria is very normal. The same is true for protein. Above 300 mg/day of protein, preeclampsia should be considered.

Question 3

Respiratory changes in preggo-TV, respiratory rate, changes in the chest and oxygen saturation curve

Answer 3

In pregnancy, tidal volumes increase due to a changing of the chest shape in which the higher positioned diaphragm (due to uterus compression) can, not only be compensated for, but operates more efficiently. Both tidal volume and respiratory rate increases, thereby increasing minute volume and decreasing PaCO2 (see OB 2). It is also worth noting that near term physiologic dead space also decreases, which also contributes to lowering the CO2 (less wasted ventilation plus a higher minute volume). Despite this, the oxygen-haemoglobin saturation curve is shifted to the right in pregnancy, this is due to increased production of 2,3-DPG.

Question 4

In OB, we know preggos have a decreased FRC, but are both volumes decreased?

Answer 4

Yes. Both RV and ERV are decreased

Question 5

Tell me about SV in preggo:

Answer 5

Universally, stroke volume increased in pregnancy, making it the most likely finding. Cardiac output increases in pregnancy, and rises to 50% above pre-labor values by the end of the second trimester. Another 25% rise happens with labor and the very highest cardiac output occurs immediately following delivery. The rise in cardiac output is due to a 30% increase in stroke volume and 15% increase in heart rate. Increased stroke volume is due to increased preload (left ventricular end diastolic volume (LVEDP) (Starlings Law)) and decreased SVR (afterload).

Question 6

Uterine perfusion-what’s the equation, what affects it?

Answer 6

In pregnancy, the uterine blood flow (via the uterine arteries and spiral arteries) is pressure dependent, in other words, there is NO autoregulation. The arterial system of the gravid uterus is essentially maximally dilated and unable to significantly dilate further in response to hypercarbia (answer B). Perfusion, therefore is uterine MAP – uterine venous pressure. Contraction of the uterus significantly increases uterine venous pressure, decreasing perfusion. Extreme hypocapnea, but not moderate, can lead to uterine arterial vasoconstriction, especially with paCO2s under 20 mm Hg. Catecholamine induced vasoconstriction, as with labor, can decrease blood flow as well. The most significant risk for poor perfusion of a normal gravid uterus is systemic hypoperfusion, from any cause including uterine compression of the IVC.

Question 7

Maternal shifts and fetal shifts with 2,3 DPG

Answer 7

Oxygen transfer from mom to fetus occurs at the placenta where well oxygen saturated blood is delivered by mom to the placenta and diffuses to placental blood. Therefore to aid in oxygen transfer, the maternal oxygen –haemoglobin disassociation curve is shifted towards the RIGHT, favoring oxygen release. Fetal oxygen-haemoglobin disassociation curve is shifted towards the LEFT, favoring oxygen uptake. Placental oxygen tensions are around 40 mm Hg, so the right-left shifting is very important. Maternal levels of 2,3-DPG are increased to favor this right shift (as maternal hypocarbia favors a left shift, see OB 3). Fetal Hb is unable to bind 2,3-DPG, leading to a left shift (see Neonatology Quetion 5). Increased maternal cardiac output (answer C) would lead to more oxygen being supplied to the placenta (see ICU section), not less. Adding a volatile agent to the inspired gas would not effect gas exchange in any significant way, assuming maternal cardiac output did not significantly drop.

Question 8

Hgb in preggo-what happens to Hgb and why? How can someone’s hgb actually go up?

Answer 8

Pregnancy is associated with a decrease in Hb level (from around 14 to 12) to a disproportionately increased plasma volume to RBC mass (both are increased in pregnancy, but plasma volume is increased more leading to a dilutional anaemia). Women with iron-deficiency anemia (from normal causes, not parasites, GI bleeding, etc) have two problems: blood loss from menses and insufficient iron intake. With pregnancy, the lack of menses combined with iron supplementation (as part of prenatal vitamins) can lead to a normal Hb level (which is increased for this patient). If the iron deficiency anaemia is not treated effectively during pregnancy, preterm birth, low birth weight, and neonatal health problems are more likely.

Question 9

Aorticaval compression-when does it start? Why does it happen? How can you fix it?

Answer 9

Aortalcaval (especially IVC) compression generally becomes an issue around 28 weeks (answer A), although has been reported at 20 weeks. IVC compression leads to decreased venous return and therefore decreased preload, and hence decreased stroke volume, and consequently decreased cardiac output. Decreased cardiac output leads to decreased oxygen delivery to the placenta, leading to fetal hypoxia with resultant bradycardia (answer C). The treatment is to increase preload, and the most effective way to do that is lift the uterus off the IVC by shifting the uterus towards the left (answer D) as the IVC lies to the right of the aorta. Aorta compression can also become a problem, especially late in pregnancy. Trendelenberg position leads to greater compression when supine as compared to other positions (answer B).

Question 10

1 hour prior to delivering, a 100 kg woman receives 50 mcg of fentanyl intravenously. Expected findings?

Answer 10

Less respiratory depression than if an equipotent dose of morphine was given IV

Pound, for pound, morphine leads to slightly more respiratory depression in this setting than fentanyl or meperidine. Opioids, and especially lipid soluble opioids, readily cross the placenta and can cause respiratory depression in neonates (answer D & E). The risk for respiratory depression increases the closer the dose is given to delivery. Morphine and meperidine can have more late peaking respiratory depression and can occur more than 2 hours after birth (answer C), whereas fentanyl is more likely to present near the time of delivery.

Question 11

Which of the following anesthetic agent, given in full induction, intubation, or maintenance doses to the mother will have the LOWEST relative blood concentration in the newborn:
A. Rocuronium
B. Sevoflurane
C. Ketamine
D. Thiopental
E. Propofol

Answer 11

Muscle relaxants, both succinylcholine and nondepolarizers, are charged hydrophilic chemicals that do not cross the placenta and therefore are almost immeasurable in the fetus. All other agents can cross the placenta. Induction agents such as propofol, ketamine, and thiopental rapidly redistribute and doses that reach the fetus are minimal. Volatile agents such as sevoflurane or nitrous oxide easily crosses the placenta and after about 10 minutes, fetal end-tidal levels can be at anesthetic doses. This is one of the reasons that quick delivery after induction of general anesthesia is important

Question 12

Transfer of local anesthetics across the placenta is a long-time boards favorite. Do tell: if chloroprocaine was given IV, how would the concentration be in mom be baby? What about for bupi or ropi?

Answer 12

Concentration would be lower in baby than in mom. understanding the fetal pH is LOWER than maternal pH and in this setting, local anesthetics are IONIZED (donation of proton from low pH environment) and TRAPPED inside the fetus. Therefore, for most anesthetics, with the notable exceptions of chlorprocaine, bupivacaine, and ropivicaine, answer B would be correct. Chlorprocaine is rapidly metabolized in the maternal circulation by plasma cholinesterase and therefore very little of the drug reaches the fetus (answer A). Bupivicaine and ropivicaine are highly protein bound, limiting placental transfer. Both bupivacaine and ropivicaine can avidly bind to sodium channels on the myocardium leading to bradycardia and widened QRS cardiovascular collapse resistant to chest compressions, epinephrine and electrical defibrillation (answer C). Intralipid can bind these two drugs, effectively removing them from sodium channels.

Question 13

What do you tell women when they fear that their epidural will prolong labor?

Answer 13

There is no more misinformation given to patients than on the L&D floor. Epidurals, when used in dilute doses (~0.125% bupivicane), and especially with opioid supplementation, do not prolong labor or increase the rate of C-sections. Older solutions utilizing 0.25% bupivicane (or even stronger) did prolong labor as well as lead to more forceps deliveries.

Question 14

Terbutaline is a ______ that can cause:

Answer 14

Tocolytic that can cause tachycardia and hypokalemia -hypokalemia is beta 2 mediated

Question 15

Ephedrine in preggo-good and bad:

Answer 15

Ephedrine has also been found to be safe in pregnancy. Ephedrine crosses the placenta and increases fetal metabolism and oxygen consumption, leading to decreased umbilical arterial oxygen tensions. These decreased tensions, however, are without clinical significance.

Question 16

Motor, temp, and sensing in order of ease of blockade

Answer 16

the principle of sympathetic temperature sensing conduction is blocked easier than pain conduction, which is blocked easier than motor block.

Question 17

Pt with epidural says she’s still having pain. She has t9 sensation block. What can you do, and what does this mean?

Answer 17

You can increase rate of infusion

The patient has a T9 level on temperature discrimination. The rule of thumb is that pain block will lag below temperature discrimination by about 2 dermatome levels. Therefore, at least a T8 level on alcohol swab would be needed for blockade of T10 pain conduction.

Question 18

What’s the latent phase of labor, and what mediates that pain? Active phase nerve roots? How can the second stage of labor be more effectively blocked? What could be negative side effects with effectively blocking second stage?

Answer 18

The latent phase of labor (from about 0-3 cm dilation) is primarily mediated by low thoracic pain pathways (T10-11). As labor continues into the active phase, lumbar (T10-L1) nerve roots account for an increasing amount of the painful stimulation. Dilute epidural solutions (~0.125% bupivacaine) with opioid supplementation effectively relieve the pain carried by the small visceral afferent fibers which travel ALONG SIDE the sympathetic nervous system (answer B). In fact, the pain pathways can be traced through the hypogastric and aortic nerve plexuses. The second stage of labor (when the child is being delivered) involves the addition of the pudendal nerve (S2-4) (answer D) which is not as easily blocked with dilute bupivacaine as the thin afferent fibers mentioned above. Increasing the dose of bupivicaine to 0.25% (or higher) can reliably block pain sensation (answer C), although motor block and arrest of labor can also occur. Lumbar, gluteal, and upper leg pain can also occur with labor and are effectively treated by blockade of T10-L1 afferent fibers

Question 19

How does toradol work? Why is it a big no on pregnant women? Is there any need to get platelets? Are NSAIDS a tocolytic? What to do about this?

Answer 19

Ketorlac can also lead to increased bleeding (by inhibiting COX mediated prostaglandin production
It’s a big no because-NSAIDS can theoretically lead to ductus arteriosis closure in the fetus which would be rapidly fatal (see Neonatal 6 for a detailed description of fetal circulation). There are no known cases of this when NSAIDS are used only for labor pain.
There is no evidence for platelet transfusion or need to cross and type patients after ketorolac. NSAIDS are also a weak tocolytic, but again, no evidence exists that oxytocin would be needed to supplement contractions

Question 20

Eisenmeiger’s syndrome and pregnancy: can you do an epidural? Why or why not? Concerns? How to treat pain?

Answer 20

With any right to left shunt, decreasing left sided intraventricular pressures will result in increasing right to left flow, and thus cyanosis. Epidural local anesthetics can precipitously drop preload and afterload, leading to this complication. Running a very dilute strength of bupivacaine may limit the sympathectomy, but will also not relieve pain, so what’s the point? Decreasing the epidural rate in half will likely not cover labor pain (T10-L4) adequately. Pure opioid techniques can provide mild to moderate pain relief without a sympathectomy (answer D).

Question 21

So, if you decide to give opioids to a patient through an epidural, which opioid should you avoid? Why?

Answer 21

Meperidine has weak local anesthetic properties which can lead to a variable sympothectomy. In the setting of Eisenmenger’s syndrome, any loss of left ventricular afterload (due to systemic vascular resistance) can lead to cyanosis and fetal demise. The same concern is true with intathecal meperidine. The other opioids are devoid of local anesthetic-like effects.

Question 22

Epinephrine as part of a block in preggo is NOT safe:

Answer 22

False, it is

Question 23

Symptoms of a migraine? Are they common after pregnancy?

Answer 23

Migraines are classically unilateral, intense, long lasting, proceeded by a prodromal aura, have associated photophobia, throbbing, and nausea. Both migraines and tension-type headaches are VERY common post-partum and should be considered before diagnosis of post-dural headache is made.

Question 24

Two reasons for headache in PDPH:

Answer 24

First, the loss of CSF through the dural puncture leads to downward displacement of the brain and stretching of the meninges. Secondly, there is compensatory vasodilation leading to pain.

Question 25

Is PDPH risk lessened by threading the catheter?

Answer 25

Not significantly according to some studies

Question 26

Can you place an epidural in a patient with IIH?

Answer 26

IIH, also known as pseudotumor cerebri (by our outdated textbooks) and is safe and effective for neuraxial anesthesia (answer A). If IIH has been treated with a lumbo-peritoneal shunt (LPS), then the best practice is probably to avoid lumbar epidural or spinal placement (to avoid damage to the shunt). This procedure is done to relieve the symptoms of IIH (headache, nausea, vomiting, tinnitus, double vision, etc). Treatment of IIH includes lumbar puncture as well as LPS, so answers C & D are incorrect. There is no evidence that dose modifications need to be made with IIH other than the standard dose reductions used for pregnancy

Question 27

Maternal fever and epidural placement? What does that have to do with chorio?

Answer 27

Maternal fever has a high association with epidural placement, possibly secondary to inhibition of shivering or sweating, and most likely accompanying nulliparity.

Chorioamnionitis is an obstetric emergency that should be treated with antibiotics and immediate delivery. Risk factors include premature rupture of membranes and concomitant GI/GU infections. The presence of a slowly increasing mild fever with membrane rupture occurring only 30 minutes prior makes chorioamnionitis an unlikely source for the fever in this setting. Infection of the epidural space can lead to abscess and spinal cord compression as well as fever, but would likely not occur this soon after epidural placement (spinal cord syndrome component). Furthermore, mild leg weakness is a normal finding of a functioning labor epidural (answer C). Chorioamnionitis has an association with cerebral palsy

Question 28

When comparing doses of spinal anesthetics in preggo people to obese people, does the dose need to be changed?

Answer 28

Obese patients do not require a dose reduction in spinal anesthetic as epidural vascular congestion is less pronounced and they do not have increased sensitivity to local anesthetics.

Question 29

Nitrous for GA in preggo? What about after baby is delivered?

Answer 29

Prior to delivery of the fetus high concentrations of nitrous oxide (>50%) should be avoided due to the risk of diffusion hypoxia of the newborn. Nitrous oxide (as well as sevoflurane) can easily pass through the placenta to the fetus. After birth, the fetus must breath off the anesthetic gas.
Nitrous oxide has the advantage of not causing (clinically significant if any) uterine relaxation, allowing the dose of halogenated volatile anesthetics (which do decrease uterine tone) to be minimized. This is most important following delivery of the fetus where uterine contractions are needed to prevent excessive bleeding.

Question 30

Emergency C section on hemodynamically unstable patient. What do you induce with?

Answer 30

With hypotensive patients in this setting, especially due to hypovolaemia, induction must occur prior to resuscitation as the fetus may not survive (answer A). Of the available choices, ketamine is the best choice as it preserves sympathetic tone.

Propofol (afterload reducer) and thiopental (preload reducer) will significantly exacerbate the hypotension (answers D & E). Spinal anesthesia also will significantly decrease preload and worsen hypotension.

Question 31

Why should you be around for a breech version?

Answer 31

External version of breech presentation can result in placental abruption or umbilical cord compression, both necessitating an emergency C-section. Nitroglycerin can improve the success rate of external version (especially in nulliparous women), but does not require an anesthesiologist to administer the drug. Nitroglycerine is a short acting, effective uterine relaxant.

Question 32

Loss of variability in association with late decelerations:

Answer 32

Loss of variability, especially in association of late decelerations in fetal HR is widely considered rather specific for fetal hypoxia.

Question 33

Drugs that can lead to decreased variability in a non hypoxia fetus

Answer 33

Opioids, magnesium, benzodiazepines, lidocaine, atropine, esmolol, among others, can lead to decreased variability in the setting of a non-hypoxic fetus.

Question 34

FHRM has three types of decelerations you need to know:
Early:
Late: 
Variable: 
What does variability tell us?

Answer 34

First, early decels are associated with increased vagal tone of the fetus due to head compression with uterine contraction and occur with contractions
Late decelerations are more likely due to uteroplacental insufficiency, especially in the setting of loss of variability.
Variable decelerations lack a sustained pattern in association with uterine contraction and are due to brief but reversible periods of fetal hypoxia due to umbilical cord compression (not utero-placental insufficiency).

Question 35

What does scalp pH tell you?

Answer 35

Scalp pH is an invasive monitor for fetal well being, and a pH above 7.25 is considered normal and below 7.20 abnormal

Question 36

Patholophys of ORs-eclampsia as it relates to the teophiblast and spiral arteries.

What stuff is released? And because of what dysfunction? That dysfunction leads to what proba with platelets and proteinuria?

Answer 36

the problem of preeclampsia likely begins with trophoblast migration into the endometrium. The trophoblast is genetically the fetus, and the migration into the endometrium may initiate an unknown immunologic mechanism where the trophoblast (and therefore placenta) is not completely seated in the endometrium. Normally, the trophoblasts invade the spiral arteries of the uterus and remove their ability to constrict (“adrenergic denervation”) so that blood flow to the placenta is copious and unrestricted. In preeclampsia this is incomplete and the spiral arteries are un-dilated, high resistance, & low flow

This sets off a systemic cascade of endothelial dysfunction (skipping a couple steps in the story here) where vasodilating NO and PGI2 are decreased and vasoconstricting TxA2 and ET-1 are increased

Endothelial dysfunction also leads to aggregation of platelets (TxA2 release, serotonin release, and thrombocytopaenia). Endothelial dysfunction can also lead to capillary permeability and oedema, and in the kidney can lead to proteinuria. Unchecked vasoconstriction can lead to hypertension, decreased cardiac output, sodium retention, left ventricular failure, pulmonary oedema, and cerebral haemorrhage.

Question 37

Pre-eclampsia is generally assoc with what SVR and CO? How is it that they actually are still hypovolemic and intravascularly depleted? Why must you be careful with a single shot spinal?

Answer 37

Severe preeclampsia is generally associated with a high adrenergic state with increased systemic vascular resistance (SVR) and venous tone that causes hypertension despite a decreased cardiac output (CO)
In this setting, vascular capacitance is decreased and the actual intravascular blood volume is decreased. With the sympathectomy of a spinal anesthetic, venous and arterial dilation leads to profound hypotension and uteroplacental insufficiency. In fact, left ventricular end diastolic volume (LVEDV, aka preload) can decrease to the point of cardiovascular collapse.

Question 38

Pre-eclampsia and platelet count for epidural. How low can you go?

Answer 38

A platelet count of 70,000 is generally regarded as safe for spinal placement, assuming the platelet count is not rapidly falling

Question 39

Platelet count in parturient vs pre-eclamptic. But still prothrombotic-how sway?

Answer 39

It is often stated that preeclamptic patients have a defect in the number and function of platelets, and this is most certainly the correct answer for the boards

Despite this, like normal pregnancy, preeclamptics have an overall pro thrombotic state. In fact, thrombocytopaenia (not thrombocytosis, answer B) is often a result of platelet consumption (as well as factor consumption), kind of like a slow, controlled disseminated intravascular coagulation

Question 40

Pre-eclamptics have which type of anemia?

Answer 40

Preeclamptics are more likely to have haemolytic anaemia (HELLP), but this is typically a normocytic anaemia

Question 41

Explain how renal failure works in pre-eclampsia, and what is the ultimate solution??

Answer 41

First, cardiac output, and therefore renal perfusion, tends to decrease in preeclampsia. Second, endothelial and mesangial cell hypertrophy (called glomerular capillary endotheliosis- surprised that endothelial cells are invlolved?) nearly occludes the afferent artioles to the glomeruli, starving them from perfusion. This means, that even if cardiac output was increased, the glomeruli would remain poorly perfused. Delivery of the fetus (and placenta!) is the ultimate treatment for preeclampsia, in that the underlying pathophysiology is interrupted and recovery (of organ systems) quickly improves.

Question 42

Safe anti-hypertensives in preggo? What about a woman with severe PET pulmonary rales, and who is set to deliver via c section in an hour?

Answer 42

Well-studied and safe antihypertensives in pregnancy other than labetalol include alpha-methyldopa, hydralazine, and short acting oral nifedipine. In this situation, with only an hour before surgery and hypertension so severe that left ventricular (LV) dysfuction (leading to pulmonary rales) is likely present, hydralazine (not listed as an option) or nicardipine gtt are the top choices.

Nicardipine gtt, (especially with the use of data from an arterial line) can be carefully titrated for afterload reduction which will hopefully decrease LV dysfunction and help treat the pulmonary oedema prior to C-section. Hydralazine is predictably effective in lowering afterload in this situation, although titration is difficult to achieve in only one hour, as maximum effect does not occur for 20-30 minutes after administration. Nifedipine (answer E) is generally less effective than hydralazine and rarely used in severe preeclampsia for this reason. Alpha-methyldopa (answer B) onset of action is about 6 hours and would not be useful at this time. Esmolol gtt (answer C) can lead to profound fetal bradycardia and is generally contraindicated in obstetrics.

The American College of Obstetrician and Gynecologists (ACOG) guidelines (yes I read them!) infer that in this situation hydralazine and labetalol is first line therapy, and in the rare circumstance where it does not work, consultation with an anesthesiologist or intensivist should be sought to start a labetolol gtt or (cringe) nicardipine gtt for second line. The ACOG algorithm goes along the lines of this: if hypertension not controlled give some IV labetolol, if that doesn’t work give more. If that doesn’t work more again. If that doesn’t work, give more and then some hydralazine. If that doesn’t work, get a consult.

Question 43

The most common cause of preeclampsia mortality is

Answer 43

cerebral haemorrhage.

Question 44

Cushing’s triad:

Answer 44

HTN, bradycardia, apnea

Question 45

How does magnesium work for PET patients? Is it more effective than diazepam or phenytoin?

Answer 45

Magnesium has been shown to be more effective than diazepam or phenytoin. Its calcium inhibition leads to a few important BOARD WORTHY effects. First, it is a muscle relaxant (calcium inhibitor), and decreases deep tendon reflexes (which is how it is clinically followed, see below (answer E)), prolongs muscle relaxants (both depolarizing and nondepolarizing) and can lead to respiratory failure. Secondly, it venodilates and helps reduce blood pressure (again by calcium inhibition). Thirdly, it has tocolytic effects.

Question 46

So why does hypermagnesemia prolong the PR and QT?

Answer 46

Think about what hypocalcaemia looks like on ECG: prolonged QT! Therefore, think about magnesium inhibiting calcium, and you’ll remember magnesium’s effects: weakness & QT prolongation

Question 47

Magnesium’s effects at 4-7
7-10
10-13
15-25
Over 25
How to treat hypermagnesiumeia

Answer 47

Hypermagnesaemia has very predictable effects based on plasma level. At 4-7 mEq/L preeclampsia tends not to progress to eclampsia, and flushing and vasodilation are present. At 7-10 mEq/L deep tendon reflexes (DTRs) are lost. 10-13 mEq/L, respiratory depression. 15-25 mEqL heart block can occur, and above 25 mEq/L cardiac arrest is expected.

Hypermagnasaemia should be immediately treated with calcium intravenously.

Question 48

PTT and Neuraxial Anesthesia?

Answer 48

There is not a strong consensus regarding elevated PTT, but some sources say 1.5 X normal as a cut off. In this case, assuming no heparin is being used, an elevated PTT may be an early sign of an underlying coagulopathy as well.

Question 49

Would you not place an epidural in a patient who has elevated liver enzymes 2x base levels? RUQ Pain?

Answer 49

you do NOT withhold an epidural so you can follow abdominal pain (risk of liver subcapsular haemoatoma)

Question 50

NTG and preggo. What does it do? Side effects? Typical dosing?

Answer 50

NTG is a short acting, potent uterine relaxant that can help in the setting of difficult extraction of the fetus from the uterus (both with C-section or forceps delivery), external version of a breech presentation, and a variety of other indications (uterine inversion, etc). Its primary side effect is maternal hypotension, which is short lived. Doses of 50-300 mcg are often effective.

Question 51

One hour following C-section, the patient is found to have copious clotted blood expressed from her uterus but no bright red blood currently. Vitals: BP 80/50, HR 125, Sat 95% on room air. The patient is cold to touch and pale, but conversing appropriately. There has been no urine output since the C-section ended. She is type and screened, and conversion to type and cross will take 30-40 minutes. The obstetrician wants to examine the uterus under anesthesia immediately in the OR. What is the next BEST step:

A. Copious crystalloid administration
B. Draw a CBC, and await results
C. Phenylephrine administration
D. Take the patient to the OR and sedate with ketamine and face mask
E. Take the patient to the OR and induce general anesthesia with etomidate and succinylcholine

Answer 51

The correct answer is: A: Copious crystalloid administration

The problem here is volume, and the determination that must be made now is if she is bleeding faster than fluid can be administered and is she stable enough to induce general anesthesia. The patient is hypotensive but neurologically intact, so phenylephrine (a temporizing measure) is probably not needed at this time. The patient appears to be in hypovolaemic shock due to bleeding and awaiting CBC results is wasting time. Taking the patient to the OR is risky as she is severely hypovolaemic and increasing intravascular volume with crystalloid (or colloid) will make induction of anesthesia safer. The absence of bright red blood makes the possibility of the patient bleeding to death prior to some degree of fluid resuscitation very unlikely.

Question 52

Three types of abnormal placental attachments

Answer 52

Accrete - chorionic villi attach to the myometrium

Increta — chorionic villi invade the myometrium

Percreta — chorionic villi invade through the myometrium, often also invading rectum or bladder

Question 53

What is placenta previa? How does it present?

Answer 53

one of the more common obstetric presentations that can be associated with massive blood loss. In previa, the placenta attaches to the uterus low, near or on the os, leading to antepartum painless bleeding

Question 54

How does bleeding occur in placenta previa?

Answer 54

Birth of the fetus injures the placenta which can lead to uteroplacental insufficiency and massive bleeding. Furthermore, after the fetus is delivered, the lower uterine segments have inefficient contractions leading to further postpartum haemorrhage

Question 55

Obstetric management of previa. Regional or CS?

Answer 55

Obstetric management is typically elective C/S at ~ 37 weeks (answer E). Anterior placenta can make even C/S challenging and difficult (as it is located where the incision is typically placed). Most authors appear to suggest general anesthesia in preference to regional anesthesia for C/S, due to the combination of a sympathectomy and significant bleeding have an increased risk for hypotension. Nearly all sources do say, however, that regional anesthesia is not contraindicated and may be appropriate in some cases

Question 56

Risk factors for previa:

Answer 56

Risk factors for placenta previa are prior C/S, multiparity, prior uterine surgery, and advanced maternal age (answer C). Placenta previa is a risk factor for accreta.

Question 57

Why would someone not want to place an epidural for VBAC!

Answer 57

Because VBAC is a risk for uterine rupture, and people are scared that it might dull that pain. First, the obstetric literature supports a diagnosis of uterine rupture be made by risk factors, fetal heart rate monitor, and ultrasonography. Abdominal pain is not very sensitive or specific. Second, uterine rupture in VBAC is typically wound dehiscence, which is prototypically painless as the scar is deinnervated.

Question 58

Risk factors for uterine rupture:

Answer 58

VBAC, Other risk factors for uterine rupture are excess oxytocin (which is easier to do with labor epidurals), myomectomy, trauma, and forceps delivery.

Question 59

The combination of mitral stenosis and obstetrics is a boards classic, and even today it’s seen occasionally (often following rheumatic fever as a child). Tell me about it in pregnancy. Why is it a problem with Neuraxial?

Answer 59

The most likely cause of death was decreased preload secondary to the sympathectomy generated from the spinal anesthetic. Decreased venous return to the left atrium decreases pressures. In mitral stenosis, high left atrial pressures are required for flow across the stenotic valve. Decreased flow leads to a decreased (not increased) pressure gradient across the mitral valve

Question 60

Why is tachycardia in MS a problem?

Answer 60

Tachycardia can precipitate flash pulmonary oedema in mitral stenosis (by requiring higher flows across the valve to maintain cardiac output, thereby generating higher left atrial pressures)

Question 61

What are the ways that ACLS is different in pregnant patients?
3 things
Should you use fetal assessment during this time?

Answer 61

First, and most importantly, the uterus should be displaced off the inferior vena cava (and aorta) with manual left uterine displacement throughout resuscitation
emergent delivery, at any age (answer E), should be undertaken to save the life of the mother (since both mother & fetus will die otherwise). If hysterotomy is to be undertaken, it should be done within the first 4 minutes (answer A) as it is assumed that irreversible neurologic injury starts to occur at 5 minutes after cardiac arrest
Chest compression rates and pressor & defibrillation doses are the same for both pregnant and non-pregnant patients (answer B & C), with the exception that chest compressions should be performed higher up on the chest for effective cardiac massage.

No fetal assessment during this time

Question 62

When should surgery happen in a preggo woman?

Answer 62

Loss of the fetus is most likely to occur during the first trimester, followed by third. Therefore, when possible, urgent and elective surgery should be timed for the second trimester

Question 63

When does organogenesis happen? Risk of aspiration is when? Supine hypotension syndrome? How should partirient be positioned during surgery? How should you monitor the fetus, and at what age can you do that?

Answer 63

Organogenesis is the time of the greatest teratogenesis and occurs from gestational age 2-8 weeks, with weeks 2-5 being the most at risk (answer B). Risk of aspiration by gestational age of the mother is not well defined, but around the beginning of the second trimester (week 13) most authors seem to draw a line in the sand of increased risk of aspiration (answer C). Supine hypotension syndrome (question 10) is usually a concern around 20 weeks gestational age, but theoretically can occur at an earlier point in the pregnancy. The patient should be in the left uterine displacement position throughout surgery. Fetal heart rate monitoring should be used prior and after surgery to document viability (if nothing else) of the fetus before and after surgery. When possible it should be used intraoperatively as well (non-abdominal surgery). Fetal heart rate monitoring can typically be used after 16 weeks of pregnancy

Question 64

Category A, C, D, X in fetus and drugs

Answer 64

This is a tricky concept actually, as only category A and X have conclusive data on human pregnancy to help guide you. Category A drugs have been studied in pregnancy and proven to be of no risk. Category B drugs have EITHER been studied in animals and shown to be safe OR animal studies have shown risk while human studies have not. Category C (most drugs) are where there are no acceptable data in humans and animal studies are also lacking OR show risk but potential benefits likely outweigh the risks. Confused yet, wait until category D. Category D shows possible risk to human pregnancy, but potential benefits may outweigh the risks. Category X are drugs with clear risk to the fetus that outweighs any benefit to the mother.

Question 65

Can APGARs be decreased after delivery of fetus if nidazolam was given?

Answer 65

APGARs could be decreased if midazolam was administered just prior to birth (anesthetizing the fetus)

Question 66

Laparoscopic surgery for preggo women? Main goals for PaCO2 in preggo surgery?

Answer 66

Both open and laproscopic surgery for appendectomy have been used safely in pregnancy.
One of the primary goals of laparoscopic surgery in pregnancy is to keep the PaCO2 near baseline through hyperventilation as needed. Hypercarbia of the fetus may result in a right shift of fetal haemoglobin oxygen dissociation curve leading to inadequate oxygen uptake from the placenta (no evidence). Maternal hypocarbia can lead to left shifting of the oxygen haemoglobin dissociation curve, again leading to decreased transplacental oxygen transfer as well as umbilical vascular vasoconstriction (lots of evidence)

Question 67

Emergent surgery in patient with full term baby. What’s our goal here?

Answer 67

In the setting of emergency surgery of a term fetus, the baby should be delivered prior to the non-obstetric portion, regardless of anesthetic technique

Question 68

33 year old G5P5 woman has received a lidocaine spinal anesthetic for tubal ligation 1 day after giving birth. Testing the abdomen at the level of the umbilicus for incision elicits pain. What is the best management for this patient:

Answer 68

The patient received an inadequate spinal that could be due to inadequate dose, ineffective (denatured, etc) medication, or placement of the needle was not intrathecal. If absolutely no effects of anesthesia are present after ~10-15 minutes, the discretion of the anesthesiologist may be to retry the spinal anesthetic. However, if any portion of blockade is present (any means absolutely any), then the spinal should be allowed to wear off before attempted again to avoid high spinal (answer A). In this stem you were only given information about the level of anesthesia (not even temperature discrimination) at a T10 level, therefore the case should be delayed at least 1-2 hours. Dosing an epidural (answer B) can compress the dural sac and push the intrathecal lidocaine to a higher level (high spinal). Conversion to general anesthesia is not recommended for an elective patient either pregnant or pregnant within the past 6 weeks due to increased risk of aspiration and difficult intubation (answer D).