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OB Flashcards

1
Q

What does magnesium do to blood vessels and catecholamines? why do people even use mag in preggo?

A

It vasodilates them, and inhibits catecholamine release. It’s used because it is a tocolytic

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2
Q

Less than 0.8 of magnesium?

A

Arrhythmia, and disorientation if also with hypocalcemia

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3
Q

Magnesium of 1.4-2.1

A

Normal

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4
Q

Magnesium of 2.1-4.2

A

Typically asymptomatic

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5
Q

Magnesium of 4.2-5.8

A

Lethargy, drowsiness, flushing, nausea and vomiting, diminished DTRs

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6
Q

Magnesium of 5.8-10

A

Somnolence, complete loss of DTRs (10), hypotension and EKG changes

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7
Q

Magnesium of 10-20

A

Respiratory arrest, AV conduction block, QRS widening, bradycardia

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8
Q

Magnesium of >25

A

Cardiac arrest

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9
Q

When is excessive magnesium eliminated? How?

A

Eliminated within 4-8 hours by the kidneys, and can be done via fluid loading followed by diuresis

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10
Q

How exactly does magnesium work?

A

Acts at NMDA receptor-so an option for pain, acts at nicotine AcH receptor-prolonging non depolarize gets NM blockade, and L type calcium channels causing antagonism

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11
Q

Why are methylergovine and Carboprost contraindicated in HTN and asthma (respectively)?

A

Methykergovine-ergot derivative that could cause HTN

Carboprost-prostaglandin like effects that can cause bronchospasm

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12
Q

SEs of mwthykergovine and carbaorost

A

Methyl-cardiogenic pulmonary edema, bradycardia, coronary vasospasm, HTN

Carboprost-nausea, diarrhea, bronchiapasm

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13
Q

How does oxytocin work?

A

Activated uterine myosin

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14
Q

Placenta accreta, increta, and percreta

A

Placenta implants with absent decidua-accreta

Increta-invades myometrium

Percreta-invades surrounding structures

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15
Q

Risk factors for accreta-worse one being:

A

AMA, multiparty, previous myomectomy, Asherman’s syndrome, but number one is precious c section with placenta overlying the scar

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16
Q

Definition of PET:

A

Elevated BP (even postpartum), with some kind of end organ dysfunction

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17
Q

Can PET happen without fetal development? What Can NOT cross the placenta?

A

Yes

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18
Q

What are the two most important parts of placental transfer? What does this mean?

A

Degree of ionization at physiological pH and amount of protein binding. Protein bound drugs have a more difficult time crossing the placenta. And Bupi has a pKa of 8.1, making it ionized at the physiologic pH of 7.4

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19
Q

What’s the difference in the difficult airway algorithm between regular adults and pregnant adults?

A

If the baby is in Fetal distress, you have to do stuff differently and if that means you have to mask ventilate during the section, then so be it.

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20
Q

Describe late decelerations. What does it mean, and what can cause the meaning?

A

Deceleration in heart rate at or after the peak of uterine contraction. Associated with uteroplacental insufficiency which is indicative of fetal hypoxia. Maternal hypotension is a cause of fetal hypoxia

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21
Q

What are variable decelerations? What causes them?

A

They are when the heart rate abruptly decreases-NOT associated with uterine contractions, and they are due to core compression.

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22
Q

Why are early decelerations?

A

Gradual deceleration in heart rate that is associated with the beginning of uterine contractions. Fetal head compression

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23
Q

Explain the anemia of preggo. Which coach factors decrease and which ones increase? When are pregnant women considered anemic?

A

Anemia is because RBC mass increases to increase oxygen carrying capacity, but plasma VOLUME increases disproportionately. Pregnant women are anemic when Hgb falls below 11. Factors 8,9, and 10 and fibrinogen are increased while protein S is decreased=hypercoagulable state.

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24
Q

If patient is getting subcutaneous heparin and then wants an epidural, then how long do they have to wait for an epidural? What about if she was getting 7500 to 10000? More than 10000 per dose or 20000 per day?

A

6 hours for subcutaneous
12 hours fir high dose
24 hours for therapeutic

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25
Q

In the absence of coagulation issues and anticoagulation issues, does a prolonged PTT mean you can’t place NA?

A

No

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26
Q

Labor pain from first vs second stage of labor-whetebis it from?

A

First: T10-L1
Second: s2-S4

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27
Q

T/F magnesium raises the seizure threshold

A

True-via action at NMDA receptors

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28
Q

Why is minute ventilation increased in pregnancy? And due to why?

A

Progesterone, increases tidal volume

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29
Q

Why do pregnant women desaturate so easily?

A

Decreased FRC and increased o2 consumption (which is increased in pregnancy).

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30
Q

PET is associated with increased thromboxane A2 levels-T/F? How is there platelet activation but also low platelets? What happens to prostaglandin levels?

A

True. There’s platelet activation, but a decreased number of platelets. Prostaglandin levels decrease.

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31
Q

Morbid obesity and PDPH?

A

Obesity decreased risk of PDPH

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32
Q

So, vaginal delivery and uterine rupture vs c section and uterine rupture.

A

Pat who deliver vaginally are more likely to rupture than those who get elective c sections due to uterine contractions. However, a c section increases your chance of uterine rupture.

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33
Q

Increase in ____ and decrease in ___ lead to vasoconstricted state in pre-eclampsia

A

Increase in thromboxane A2 and decrease in prostacyclin.

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34
Q

Why do pregnant women have lower serum albumin?

A

due to an increase in total plasma volume and NOT due to decrease in actual albumin

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35
Q

What happens to alpha and beta globulins during preggo?

A

They both increase, and the albumin: globulin ratio decreases

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36
Q

which two coagulation factors increase the most during preggo when compared to all other factors?

A

Fibrinogen and factor 7 increase the most compared to all other factors.

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37
Q

What happens to transferrin and serum iron, and TIBC during preggo?

A

Transferrin rises, serum iron falls, and TIBC rises

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38
Q

uterine flow during pregnancy is dependent on what? And what does this mean as far as arterial and venous pressure?

A

Perfusion pressure. this means that anything that decreases uterine arterial pressure (hemorrhage, hypovolemia, sympathetic blockade), or increases uterine venous pressure (caval compression, contractions) will reduce placental perfusion.

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39
Q

Does hypercarbia affect uterine vascular tone?

A

No

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40
Q

Does the epidural prolong any stage of labor? If so, which stage?

A

It prolongs the second stage of labor

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41
Q

Does hypocarbia affect blood flow?

A

Hypocarbia can increase uterine vascular resistance and cause decreases in uterine blood flow

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42
Q

Magnesium and calcium-what does magnesium do to calcium? What does it do to NO and Prostaglandin I2?

A

It blocks calcium channels. it causes dilation and prevents some actin/myosin crosslinking. Magnesium also increases nitric oxide and prostaglandin I2 (both of which vasodilate)

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43
Q

Does magnesium affect sodium channels?

A

No. It affects calcium channels

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44
Q

Loss of FHR variability means what? Variability is most influenced by:

A

Fetal hypoxia. Variability is most influenced by: PS tone via vagus nerve.

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45
Q

If a mom is on Mag and needs to be intubated are you giving lower doses of either sux or roc?

A

Lower doses of roc but same dose of sux. Mag does potentiate the action of both depolarizing and non-depolarizing muscle relaxants

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46
Q

AFE is likely due to:

A

a maternal immune reaction

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47
Q

Two phases of AFE:

A

CV collapse followed by consumptive coagulopathy.

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48
Q

We know that maternal blood volume is increased durign pregnancy, but why?

A

Because of sodium retention mediated by the RAAS.

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49
Q

Platelets and Leukocytes during pregnancy

A

Platelet count maintained, however a 10% decrease can be seen, and leukocytosis of up to 21K can be observed during the 3rd trimester.

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50
Q

Should you ever give a baby naloxone while trying to resuscitate the baby?

A

NO

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51
Q

If the neonatal HR is less than ___, then it’s time to put on a pulse ox, add o2, and give PPV.

A

100.

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52
Q

So, brief NALS. Once PPV is not enough AND HR drops below ___. What do you do then? If they’re STILL not showing improvement?

A

If positive pressure ventilation fails to revive the infant, and if the heart rate is < 60 beats per minute, chest compressions should be started as well. Chest compressions and ventilation should be coordinated and given in a 3:1 ratio, with 90 compressions and 30 breaths per minute. Once chest compressions have begun, endotracheal intubation is recommended in order to ensure adequate ventilation during resuscitation. Both ventilation and chest compressions should continue until the heart rate improves to >60 beats per minute. If still no improvement, then you can give epi, but drugs are not routinely given.

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53
Q

So, what exactly is AFE and the pathophys behind it?

A

AFE leads to intense pulmonary vasospasm, and also pulmonary edema and cardiogenic shock. 1st phase: RV dysfunction. 2nd phase: LV dysfunction

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54
Q

What happens to uric acid levels in pregnancy?

A

they decrease for the same reason creatinine does. Increased GFR

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55
Q

which coagulation factor decreases in pregnancy?

A

Factor XI

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56
Q

d- dimer sensitivity is decreased in pregnant women-explain.

A

Well, fibrinogen and fibrin split products increase in pregnancy, this means d-dimer levels are increased in pregnancy, meaning this test is less sensitive in preggo

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57
Q

What is placental abruption? Is it painful?

A

It’s when the placenta separates from the uterus. It is painful

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58
Q

If there’s no NTG, and the placenta still needs to relax, then what:

A

Other options include inhaled amyl nitrite and beta-adrenergic agonists (IV ritodrine, IV salbutamol, IV terbutaline).

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59
Q

Should you suction a baby stained with meconium

A

Apparently not

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60
Q

How can you prevent meconium aspiration?

A

Use theearliest gestational age for estimating delivery, because that issue is more common in later gestational age babies.

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61
Q

MCC of postpartum hemorrhage:

A

Uterine atony

62
Q

Does chorio increase chances of PPH?

A

Yes

63
Q

ABG pH in pregnant third trimester woman

A

7.44

64
Q

Umbilical venous blood is deox or oxygenated

A

actually oxygenated

65
Q

How to remember the PO2 and PCO2 of umbilical artery and vein? When are we concerned about fetal scalp pH?

A 
20-30-40-50
PO2-20 in artery, 30 in vein 
PCO2: 50 in artery, 40 in vein 
Umbilical vein is the oxygenated one. KIM! 
Fetal scalp pH <7.20=no bueno
66
Q

Can you use inhalational agents with a MAC >0.5 in preggo

A

YUP!

67
Q

Adequate anesthesia for c section vs labor

A

Adequate neuraxial anesthesia for a cesarean section is best achieved through sensory blockade of the T4-S4 dermatomes.

TrueLearn Insight : For adequate analgesia for stage I labor, the T10-L1 dermatomes should be covered. The second stage of labor requires additional coverage at S2-4.

68
Q

Which factors increase in preggo? What about protein s?

A

11 and 13. Only factor 11 and 13 increase. Protein s decreases

69
Q

two mcc for delay in latent phase of labor?

A

An unripe cervix and false labor are two of the most common causes for a delay in the latent phase of labor.

70
Q

3 stages of labor:

1st stage is divided into:

A
  • Stage I is the onset of true labor (regular contractions) until the cervix is completely dilated.
    • Stage II occurs once fully dilated until the baby is delivered.
    • Stage III starts after delivery of the baby and ends with delivery of the placenta.
      Stage I is further divided into the latent and active phase of cervical dilation. The active phase is further subdivided into the acceleration and deceleration phases, see figure below
71
Q

Normal amount of diation in 1st stage for nuliparous vs multiparous:

A

The latent phase for primigravida parturients may last 20 hours, while multiparous women should labor less than 14 hours before transitioning to the active phase. Once active phase cervical dilation begins, nulliparous women typically dilate by 1.2 cm per hour and multiparous women usually dilate by least 1.5 cm per hour.

72
Q

What happens to bicarb and base excess in pregnant women? Increased O2 in preggo?

A

Serum bicarbonate (HCO3-) and the serum base excess both decrease. Increased minute ventilation in pregnancy leads to a respiratory alkalosis with a compensatory metabolic acidosis (pH may remain normal or be slightly elevated). Increased alveolar ventilation also leads to an increase in PaO2

73
Q

what causes a leftward shift of the CO2 ventilatory response curve?

A

Factors that cause a leftward shift of the carbon dioxide-ventilatory response curve include, but are not limited to: pregnancy, arterial hypoxemia, acidosis, increased intracranial pressure, and pain or surgical stimulus. Note that these are not the same as factors that shift the hemoglobin-oxygen dissociation curve (e.g. acidosis in particular)

74
Q

Why would you add epi to an epidural? why wouldnt you?

A

Advantages of including dilute epinephrine in local anesthetic/opioid solutions for epidural labor analgesia include more rapid onset and longer duration of analgesia, enhanced analgesia due to α-1 receptor stimulation, and decreased local anesthetic/opioid requirements. Disadvantages include increased intensity of motor blockade, cost, and increased risk of drug error. Epinephrine may also cause a clinically insignificant reduction in uterine activity via uterine β-2 receptor stimulation
Epinephrine has also been shown to decrease the minimum local anesthetic concentration (MLAC) of epidural bupivacaine.

75
Q

Cervical cerclage anesthetic plan:

A

Prophylactic cervical cerclage is usually performed under neuraxial anesthesia. When cervical dilation and bulging membranes are present, general anesthesia may be preferable if acceptable to the patient. In the absence of studies showing fetal outcomes, no technique is contraindicated, however, general anesthesia has the advantage of causing uterine relaxation which facilitates replacement of membranes.

76
Q

Treating fetal hypoxia:

A

Delivery of oxygen to the fetus during labor is controlled by oxygen carrying capacity (oxyhemoglobin saturation and hemoglobin concentration) and uterine blood flow. In addition to increasing FiO2, the provider can reposition the mother, hold the oxytocin infusion, and administer a tocolytic. A fluid bolus or leg raise to increase venous return and improve cardiac output may be indicated if the mother is hypotensive or has abnormal placentation. Refractory late decelerations are an indication for emergent cesarean delivery.

77
Q

Beta agonists classically cause hyperglycemia and hypokalemia T/F

A

TRUE

78
Q

Define PET and inclusion criteria

A

It is defined classically as the new-onset of hypertension with proteinuria (0.3 g in 24 hours) after 20 weeks gestation up to 4-6 weeks post-partum. It should be noted that proteinuria is not required if severe features exist.

In a new-onset hypertensive parturient without proteinuria, any one of the following additional criteria not only implicate the presence of preeclampsia but indicate severe features as well:

  • Platelets < 100,000
  • Serum creatinine >1.1
  • Doubling of baseline serum creatinine
  • Doubling of baseline liver transaminase levels
  • Pulmonary edema
  • Cerebral or visual symptoms
79
Q

leading COD in PET and maternal death in US

A

Stroke in PET and cardiac conditions in us for all preggo

80
Q

when are pregnant women aspiration risks? what are the major risk factors?

A

Any pregnant patient undergoing general anesthesia after the 18th week of pregnancy is at risk for aspiration. The major risk factors are a volume > 0.4 mL/kg, gastric pH less than 2.5, and particulates in the aspirate.

81
Q

asymptomatic SVT in preggo? how does adenosine wor? beta blockers in preggo?

A

Vagal maneuvers should be utilized first to treat asymptomatic SVT in pregnant patients. If these fail, adenosine is the recommended first-line pharmacologic treatment. Digoxin, calcium channel blockers, or β-blockers may then be considered. Amiodarone should be used as a last resort due to numerous potential fetal risks.

TrueLearn Insight : Adenosine is a nucleotide that transiently blocks the atrioventricular node. It is commonly used to diagnose and/or treat SVTs and regular wide-complex tachycardias. Adenosine should not be used in the presence of irregular wide-complex tachycardias (e.g. polymorphic ventricular tachycardia, ventricular fibrillation, and atrial fibrillation with aberrancy or Wolff-Parkinson-White syndrome) since it can result in hemodynamic instability and an increase in the ventricular rate. BB class c in preggo. dont give them if ou dont have to.

82
Q

CSE vs CLE

A

A CSE is associated with a more rapid onset of analgesia (especially for the second stage of labor), a decreased incidence of failed epidural analgesia, a higher risk of pruritus compared to CLE alone, and complete analgesia for early labor may be provided with opioid alone.

83
Q

APGAR

A

EYE ROLL EMOJI

84
Q

BLOCK needed for epidural

A

The T12-L1 and S2-4 dermatomes need to be covered during the second stage of labor for a patient to remain comfortable.

85
Q

Can intralipid be used for a high spinal?

A

No-its for intravascular complications

86
Q

How can you attempt to reverse a high spinal? what about reverse t berg?

A

CSF lavage (remove 40 mL of csf and replace with saline) is a method to quickly reverse a high spinal from an inadvertent placement of a subarachnoid catheter. NO to reverse t berg

87
Q

What is the bezold jerisch reflex?

A

The Bezold-Jarisch reflex occurs when stretch and chemo-receptors in the heart are stimulated. This results in bradycardia and hypotension. This reflex has been implicated as one of the causes for bradycardia, hypotension, and the cardiovascular collapse seen with spinal anesthesia.

88
Q

Normal average values for uterine artert=y blood gas

A

The normal average values of an umbilical artery blood gas sample are approximately: pH 7.2-7.3, PaCO2 50-55 mm Hg, PaO2 18-25 mm Hg, bicarbonate 22-25 mEq/L, base excess -2.7 to -4.7 mEq/L

89
Q

why do pre-eclamptics take asa?

A

Endothelial cells become abnormal and dysfunctional during preeclampsia. The dysfunctional endothelial cells produce less nitric oxide during preeclampsia and more thromboxane. This imbalance of nitric oxide and thromboxane production causes vasoconstriction. This is the reason why patients at high risk for preeclampsia or a history of preeclampsia often take aspirin. Aspirin decreases thromboxane production, which helps balance vasodilating and vasoconstricting elements.

90
Q

Is calcium metabolism dysfunctional in PET?

A

no

91
Q

Why would anyone use indomethacin as a tocolytic?

A

Indomethacin is a non-steroidal anti-inflammatory drug (NSAID) that can be used as a tocolytic agent. Indomethacin inhibits cyclooxygenase, which is a crucial enzyme in the formation of prostaglandins. Prostaglandins cause uterine irritability and increase uterine contractions. Therefore indomethacin causes tocolysis by inhibiting prostaglandin synthesis, specifically prostaglandin E2 and F2alpha. Side effects of indomethacin can include platelet dysfunction and renal dysfunction. For this reason, indomethacin should not be used for longer than 72 hours. Indomethacin is also associated with patent ductus arteriosus closure when used after 32 weeks gestation.

92
Q

Can you use magnesium as a toclytic in patiemts with myasthenia gravis?

A

NO-it is contraindicated

93
Q

Why does nifedipine work as a tocolytic?

A

Nifedipine (D) is a calcium channel blocking agent. Specifically, nifedipine blocks voltage-gated calcium channels and therefore decreases intracellular calcium. Decreased intracellular calcium subsequently reduces uterine contractions. Nifedipine has a very low affinity for myocardial calcium channels. However, nifedipine should be avoided in patients with AV conduction block. Otherwise, nifedipine has few side effects, but it is associated with nausea and flushing. Nifedipine has been associated with pulmonary edema in some instances. Some authorities recommend nifedipine as a first line agent for preterm labor.

94
Q

why do beta agonists cause hyperglycemia?

A

Hyperglycemia is a side effect of terbutaline. Hyperglycemia is caused by beta agonism in the liver and pancreas. Beta agonism in the liver causes glycogenolysis and beta agonism in the pancreas causes glucagon secretion and suppresses insulin release.

95
Q

progesterone and GERD

A

Increased progesterone in pregnancy causes smooth muscle relaxation, decreases LES tone and gastric motility, and increases the risk for GERD in parturients.

96
Q

When do you start chest compressions on a neonate?

A

Neonatal resuscitation guidelines call for initiation of chest compressions as the first intervention if a neonate’s heart rate has a sustained drop below 60 bpm.

97
Q

How should you perform chest compressions?

A

Chest compressions should be performed in a 3:1 ratio with ventilation at a rate of 120 events per minute (i.e. 90 chest compressions and 30 breaths total per minute), and full chest recoil should be allowed after each compression. This should continue until the neonate’s heart rate is > 60 bpm.

98
Q

HR less than 100 in neonates?

A

If a neonate’s heart rate is less than 100 bpm, positive pressure ventilation should be initiated. The most common cause of bradycardia in neonates is hypoxia, so improving oxygenation typically improves heart rate. Room air or 100% oxygen may be used for assisted ventilation, but if supplemental oxygen is used, the FiO2 should be lowered as soon as possible. High FiO2 use in neonates can create oxygen free radicals which can lead to hypoxia-reoxygenation injury, retinopathy of prematurity, and pulmonary toxicity.

99
Q

AFE vs PE:

A

Unlike a pulmonary embolism, AFE triggers the maternal immune system response due to inflammatory mediators that are found in the amniotic fluid. Patients with AFE present more like systemic inflammatory response (SIRS) than a pulmonary embolism. The presence of an AFE results in mast cell degranulation and complement activation. This leads to the clinical signs that are seen with AFE: hypotension, coagulopathy, and noncardiogenic pulmonary edema.

100
Q

Tx of AFE:

A

Treatment of AFE is primarily resuscitative and involves controlling the airway, stabilizing the hemodynamics, and correcting the coagulopathy.

AFE is almost always associated with hypoxia, and it is recommended to have an endotracheal tube placed and start positive pressure ventilation on 100% FiO2

101
Q

Criteria for recognizing AFE:

A

The criteria for recognizing AFE are:

1) Acute hypotension or cardiac arrest
2) Acute hypoxia (dyspnea, cyanosis, respiratory arrest)
3) Coagulopathy or severe hemorrhage
4) Occurs at the onset of labor, during a cesarean delivery, or within 30 minutes post-partum

102
Q

Pressors and AFE

A

Along with fluid resuscitation for the management of hypotension, vasopressors and inotropes are generally needed. Phenylephrine (alpha-1 agonist) is a good choice during the early phase of AFE where hypotension is secondary to systemic vasodilation. Norepinephrine, epinephrine, and dopamine should be considered later where left ventricular dysfunction may be the cause of hypotension. If right ventricular function is severely reduced, milrinone should be considered.

103
Q

Phases of AFE:

A

1) pulmonary hypertension with right ventricular dysfunction, 2) left ventricular failure and coagulopathy.

104
Q

go back to the OR with AFE or give products?

A

Blood products (red blood cells, fresh frozen plasma, platelets, cryoprecipitate) should be available and administered early in the course of AFE. Recombinant factor VII has been used, however it can increase the risk of intravascular thrombosis

105
Q

What does placental abruption look like? (symptoms)

A

painful vaginal bleeding, uterine tenderness, increased uterine activity, and possible nonreassuring fetal heart rate patterns

106
Q

What is placental abruption?

A

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, and 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.

107
Q

Contraindications to cerclage placement include:

A

preterm labor, vaginal bleeding, fetal anomalies, fetal death, rupture of membranes, placental abruption, and chorioamnionitis. BAsically stuff where the baby would need to come out anyway.

108
Q

Risk factors for developing GERD during pregnancy

A

gestational age, GERD symptoms prior to pregnancy, and multiparity

109
Q

Is the gastric emptying of liquid and solid materials altered during pregnancy?

A

No.

Gastric emptying is only slowed during labor

110
Q

Why has esophageal peristalsis and intestinal transit been shown to be slowed during pregnancy?

A

Due to INHIBITION of gastrointestinal contraction by increased progesterone and a decrease in plasma concentration of motilin (D).

111
Q

Do BMI, weight gain during pregnancy, and rate of weight gain correlate with reflux symptoms?

A

NO

112
Q

How does metoclopramide work? Does it do anything to tone? what about anti-emetic and gastric emptying?

A

Metoclopramide increases lower esophageal tone and has both anti-emetic and increased gastric emptying effects.

113
Q

What is CVP? Does it change in pregnancy?

A

Central venous pressure is the pressure transduced in the right atrium of the heart.

114
Q

Which components of CO increase during pregnancy?

A

Both HR and SV

115
Q

What happens to proteins C and S during pregnancy?

A

A resistance develops to Protein C, And protein S levels decrease.

116
Q

What happens to fibrinogen in preggo?

A

It doubles

117
Q

What is uterine rupture?

A

the integrity of the entire thickness of the myometrial wall is compromised

118
Q

Greatest risk factor for uterine rupture:

Other risk factors:

A

Greatest risk: Prior scar (with upper scars being worse) uterine hypercontractility, oxytocin use, prostaglandin use, prolonged labor, dystocia, multiparity, multiple gestations, congenital uterine anomalies, polyhydramnios, and trauma.

119
Q

Saddle anesthesia (different from the technical saddle block)

A

Saddle anesthesia occurs from sitting up after a spinal block with hyperbaric local anesthetic as gravity in the context of positioning causes the medicine to selectively target the sacral nerve roots.

120
Q

uterotonic means:

A

Makes the uterus contract

121
Q

Oxytocin is the star of the show-when? When is it first line? When are the others first line? half life of oxytocin (short vs long) and side effects?

A

Oxytocin is the first-line drug recommended for prophylaxis against uterine atony in the third trimester due to the high number of oxytocin receptors that develop near term. Alternative uterotonics are more effective in the first and second trimester.

The synthetic analog of oxytocin, typically administered IV, has a very short half-life (approximately six minutes) and a variety of side effects; most common are hypotension, tachycardia, and myocardial ischemia.

122
Q

When should all of the things be measured in preggo? FHR, Aspiration precautions (not asp risk?) , Left uterine displacment

A

Starting at 18-20 weeks gestation, aspiration precautions, left uterine displacement, and FHR monitoring (at minimum, pre- and post-op) should be utilized.

123
Q

Oropharynx suctioning prior to delivery and routine intubation for tracheal suctioning are no longer recommended.

A

Well, okay then!

124
Q

Does vital capacity change during pregnancy?

A

NO.

125
Q

In preggo (IP): IRV

A

Increase

126
Q

IP: Tidal volume

A

Increase

127
Q

Expiratory reserve volume (IP)

A

Decrease

128
Q

Residual volume IP

A

decrease

129
Q

IP: Inspiratory capacity:

A

Increase

130
Q

IP: FRC

A

decrease

131
Q

IP: Total lung capacity:

A

decrease

132
Q

IP: Dead space:

A

Increase

133
Q

IP: Resp rate

A

increase then plateau

134
Q

IP: Minute ventilation

A

Increase by 45%

135
Q

Look at chart with uterine contractions and baby decels

A

okay!

136
Q

What is a sinusoidal FHR pattern and what does it mean?

A

Sinusoidal FHR pattern: a smooth sine wave (no variability present). It is rare, however, is associated with high rates of fetal morbidity and mortality (C). This pattern is indicative of severe fetal anemia.

137
Q

What is normal beat to beat variability?

A

5-25 bpm

138
Q

what electrolyte is affected by oxytocin?

A

igh-dose oxytocin has antidiuretic and natriuretic effects which can cause hyponatremia.

139
Q

Why do pregnant women have faster inhalational inductions compared to normal people?

A

Inhalational induction will be faster in a pregnant patient compared with a non-pregnant patient. The combination of increased minute ventilation, with a decreased FRC, and decreased MAC requirements causes a significantly faster inhalational induction

140
Q

Rate of inhalational induction is inverse to what? Explain.

A

The rate of inhalational induction is inversely related to functional residual capacity (FRC). FRC is the volume of air in lungs at the end of passive exhalation. When describing an inhalational induction, FRC can be thought of as the lung volume diluting volatile anesthetics.(uts like FRC is pure or something) A pregnant patient at term has a 20% reduction in FRC, thereby increasing the speed of an inhalational induction.

141
Q

The speed of inhalational induction is related to what ratio? And that ratio is made faster by which type of anesthetics?

A

The speed of an inhalation induction is related to the rise in FA/FI of volatile anesthetics. The FA/FI is faster when using agents with a low blood gas coefficient. The rate of inhalational induction is directly proportional to minute ventilation and pregnant patients have an increased minute ventilation, which increases the FA/FI and speeds inhalational induction. Pregnant patients can have up to a 40% reduction in minimum alveolar concentration (MAC) when compared to non-pregnant patients. The decrease in MAC is likely related to progesterone levels.

142
Q

What does CO typically do to rate of inhalational induction? does it do that during preggo? Which anesthetics does this

A

Cardiac output is increased during pregnancy, which can decreased the rate of inhalational induction. However, this change is not enough to compensate for the other changes (minute ventilation, FRC, MAC requirement). Also, this would most affect the soluble inhalational anesthetics like isoflurane and halothane. An inhalational induction with more insoluble agents, like sevoflurane and nitrous oxide, is a more likely scenario and also is less likely to be affected by increases in cardiac output.

143
Q

Emphysema and inhalational induction compared to preggo:

A

it would take longer for emphysema patients because they have increased FRC

144
Q

explain ion trapping as it relates to lidocaine. What about bupi and ropi?

A

A phenomenon known as “ion trapping” may result in higher ratios of local anesthetic accumulating in an acidotic fetus. Lidocaine is a basic drug with a pKa of 7.8. As a patient’s pH drops, the ionized form of lidocaine (NH3+) is increasingly favored over the non-ionized form (NH2). The charged form does not cross the placenta membrane as readily as the neutral form (NH2) and gets trapped. This may result in higher levels of local anesthetic accumulating in the fetus.

Bupi and ropi are so highly protein bound, that they wo’t cross the placenta the way lidocaine will

145
Q

If baby’s stressed at birth, you could consider

A

local anesthetic toxicity if mom got too much

146
Q

So defffffff look at chart with side effects of terbutaline-they evn said pay close attention to the cardiac and endocrine effects. What are te ones you can name that arent’ as comon

A

myocardial ischemia
vasodilation and hypotension

Endocrine: altered thyroid function
antidiuresis

147
Q

Herpes and delivery: what are risk factors for neonatal transmission? Are neuraxial anesthetics contraindicated?

A

Risk factors for increased neonatal transmission of genital HSV2 include parturients with primary infections, active disease at labor, use of invasive fetal monitoring, and vaginal delivery with active disease. Neuraxial anesthesia is not contraindicated with recurrent maternal HSV2 disease.

148
Q

In placental abruption, is pain a warnign sign?

A

Yes

149
Q

What is the most common (and reliable) sign of uterine rupture during labor?

A

non-reasuring FHR

150
Q

Look at cardiac and respiratory changes in preggo charg

A

Ok

151
Q

P50 of mom vs baby, and how does mom’s change in preggo?

A

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.

152
Q

What is critical during an EXIT procedure? Why? How can you do that? most common side effects of the anesthesia needed for that procedure?

A

Adequate uterine relaxation is critical during an EXIT procedure in order to maintain uteroplacental circulation and fetal gas exchange. This can be accomplished with high-dose volatile anesthetics and/or nitroglycerin. The most common maternal side effects are maternal hypotension and uterine atony (which increases the risk for postpartum hemorrhage).

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