Unit 11 ACROSS LIFESPAN FLASHCARDS
(107 cards)
1
Q
How does pregnancy affect minute ventilation? By How much is VT and RR increased?
A
Progesterone is a respiratory stimulant. It increases minute ventilation up to 50%.
Vt increases by 40%
RR increases by 10%
2
Q
How does pregnancy affect the mother’s arterial blood gas?
A
Progesterone is a respiratory stimulant. It increases minute ventilation up to 50%. In consequence, mom’s PaCO2 falls and she develops a respiratory alkalosis. Renal compensation eliminates bicarbonate to normalize blood pH.
3
Q
What explains the mild increase in PaO2 in pediatrics
A
A small reduction in physiologic shunt explains the mild increase in PaO2. This increases the driving pressure of oxygen across the fetoplacental interface and improves fetal gas exchange.
4
Q
How does pregnancy affect the oxyhemoglobin dissociation curve?
A
Right shift (↑ P50) → Facilitates O2 unloading to the fetus
5
Q
How does pregnancy affect the lung volumes and capacities?
A
Functional residual capacity is reduced as a function of a decrease in expiratory reserve volume and residual volume (ERV decreases more than RV).
6
Q
What about pregnancy makes patient more likely to desat?
A
An increased oxygen consumption paired with a decreased FRC hastens the onset of hypoxemia. Failure to reverse hypoxemia results in brain death of the mother and the fetus.
7
Q
Uterus receives what % of the CO
A
10%
8
Q
Uterine contraction causes
A
Autotransfusion (increase preload)
9
Q
Compared to pre-LABOR values, CO during labor, 1st stage
A
CO increase 20%
10
Q
Compared to pre-LABOR values, CO during labor, 2nd stage
A
CO increase 50%
11
Q
Compared to pre-LABOR values, CO during labor, 3rd stage
A
CO increases 80%
12
Q
CO return to pre-labor values when
A
In 24-48 hours
13
Q
CO returns to pre-pregnancy values when?
A
In approximately 2 weeks
14
Q
Twins cause CO to increase
A
20% above a single fetus pregnancy
15
Q
How do blood pressure and systemic vascular resistance change during pregnancy? MAP, SBP, DBP
A
MAP no change
SBP no change
DBP decrease by 15%
16
Q
What causes the no change effect in MAP
A
Increase blood volume + Decrease SVR = NO CHANGE (effect) on MAP
17
Q
How do PVR and SVR change during pregnancy?
A
SVR decrease by 15%
PVR decrease by 30%
18
Q
Progesterone causes
A
Increase in nitric oxide –> Vasodilation
Decrease response to angiotensin and NE
19
Q
Who is at risk for aortocaval compression, and how do you treat it?
A
In the supine position, the gravid uterus compresses both the vena cava and the aorta. This decreases venous return to the heart as well as arterial flow to the uterus and lower extremities. Decreased cardiac output compromises fetal perfusion and can also cause the mother to lose consciousness.
20
Q
How do you treat aortocaval compression?
A
By displacing the uterus away from the vena cava and aorta, we can reduce its compressive effect. We can accomplish this by elevating the mother’s right torso 15 degrees. It should be used for anyone in their 2nd or 3rd trimester
21
Q
How does the intravascular fluid volume change during pregnancy? What creates the dilutional anemia?
A
Intravascular fluid volume increase by 35% to prepare mom for hemorrhage w/ labor
Plasma volume increase by 45%
Erythrocyte volume increase by 20%
CREATE DILUTIONAL ANEMIA
22
Q
What hematologic changes accompany pregnancy?
A
Pregnancy creates a HYPERCOAGULABLE STATE
23
Q
DVT in pregnant vs non-pregnant
A
6 times higher in pregnant women
24
Q
Consumption coagulopathy in mom
A
Mom makes more clot but breaks it down faster. Explains tendency to develop consumption coagulopathy
25
Factors decrease in pregnant women
Factor XI and XIII
Protein C and S
26
Factors increase in pregnant women
1,7,8,9,10,12
27
How does MAC change during pregnancy?
MAC is decreased by 30-40%. This is probably due to increased progesterone.
28
How does pregnancy affect gastric pH and volume?
Pregnancy increases gastric volume and decreases gastric pH. This is due to increased gastrin.
29
How does pregnancy affect gastric emptying? Before and after onset of labor?
Before onset of labor = No change
After onset of labor = Slowed
30
How does pregnancy affect uterine blood flow?
At term, uterine blood flow increases to 500-700 mL/min (10% of CO).
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Uterine blood flow does NOT
autoregulate - therefore it is dependent on MAP, cardiac output, and uterine vascular resistance.
32
One of the 2 causes of reduced uterine blood flow: 1. Decreased perfusion --> causes are
Maternal hypotension (sympathectomy, hemorrhage, aortocaval compression)
33
One of the 2 causes of reduced uterine blood flow:
2. Increased resistance -->
Uterine contraction, hypertensive conditions that increase UVR
34
Uterine Blood flow formula
Uterine blood flow = Uterine artery pressure - uterine venous pressure/ Uterine Vascular resistance
35
Discuss the use of phenylephrine and ephedrine in the laboring patient.
Classic teaching states that phenylephrine increases uterine vascular resistance and reduces placental perfusion. More recent evidence suggests that phenylephrine is as efficacious as ephedrine in maintaining placental perfusion and fetal pH in healthy mothers. In fact, mothers that received phenylephrine had higher fetal pH values (less fetal acidosis).
36
Which law determines which drugs will pass through the placenta?
The Fick principal determines which drugs can pass across the placenta.
37
Drug characteristics that favor placental transfer:
Low molecular weight < 500 Daltons (most anesthetic drugs are smaller than 500 Daltons)
High lipid solubility
Unionized
Nonpolar
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Ficks diffusion formula
Rate of diffusion = Diffusion coefficient x Surface area x concentration gradient/ Membrane thickness
39
3 stages of labor Stage 1 is
Stage 1: Beginning of regular contractions to full cervical dilation (10 cm)
40
3 stages of labor Stage 2 is
Stage 2: Full cervical dilation to delivery of the fetus (Pain in the perineum begins during stage 2)
41
3 stages of Labor Stage 3 is
Stage 3: Delivery of the placenta
42
How does uncontrolled labor pain affect the fetus? Why?
Uncontrolled pain may result in:
Increased maternal catecholamines → hypertension → reduced uterine blood flow
Maternal hyperventilation → leftward shift of oxyHgb curve → reduced delivery of O2 to the fetus
43
Compare and contrast the pain that results from the first and second stages of labor.
First Stage: Pain begins in the lower uterine segment and the cervix. Origin: T10-L1 posterior nerve roots.
Second Stage: Adds in pain impulses from the vagina, perineum, and pelvic floor.
Origin: S2-S4 posterior nerve roots.
44
Compare and contrast the pain that results from the first and second stages of labor.
First Stage: Pain begins in the lower uterine segment and the cervix.
Second Stage: Adds in pain impulses from the vagina, perineum, and pelvic floor.
45
2nd stage of labor pain origin
Origin: S2-S4 posterior nerve roots.
46
1st stage of labor pain origin
Origin: T10-L1 posterior nerve roots.
47
Compare and contrast the regional anesthetic techniques that can be used for first and second stage labor pain.
Neuraxial techniques that provide analgesia to T10-L1 during the first stage of labor must be extended to cover S2-S4 during the second stage of labor.
48
Quality of pain from the perineum during 2nd stage of labor
Well localized and Sharp
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Quality of pain from the perineum during 1st stage of labor
Diffuse, dull , cramping
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Pain carried via
Afferent pathway
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Affarent pathway for 1st stage
Visceral C-fibers, --> Hypoglastric plexus
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Affarent pathway for 2nd stage
Pudental nerve.
53
Describe the "needle through the needle" technique for CSE.
The CSE technique provides the dual benefit of a rapid onset of spinal anesthesia and the ability to prolong the duration of anesthesia with an indwelling epidural catheter. This technique is particularly useful in labor and delivery. The "needle through the needle" technique is the most common approach.
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CSE , The epidural space
The epidural space is identified with the epidural needle.
A spinal needle is placed through the epidural needle, and then LA and/or opioid is injected into the intrathecal space.
The spinal needle is removed.
An epidural catheter is threaded through the epidural needle.
55
Compare and contrast bupivacaine and ropivacaine for labor.
Ropivacaine less risk of CV toxicity
decrease potency than bupivacaine
decrease motor block
56
Discuss the use of 2-chloroprocaine for labor.
Useful for emergency C/S when epidural is already in place (very fast onset)
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2-Chloroprocaine for labor
Metabolized by pseudocholinesterase in the plasma – minimal placental transfer
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2-Chloroprocaine antagonizes
Antagonizes opioid receptors (mu & kappa) and reduces efficacy of epidural morphine
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2-Chloroprocaine for spinal
Risk of arachnoiditis when used for spinal anesthesia due to preservatives
60
Solutions without methylparaben and metabisulfite do not cause
neurotoxicity
61
Discuss the consequences of an epidural that is placed in the subdural space.
Although a rare and unpreventable event, it is possible to position the tip of the epidural catheter in the subdural space - between the dura and the arachnoid. Neither catheter aspiration or a test dose will rule out subdural placement.
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Won't rule out subdural placement
Neither catheter aspiration or a test dose will rule out subdural placement.
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If subdural placement, Within 10 - 25 minutes after the epidural is dosed, the patient will
experience symptoms of an excessive cephalad spread of local anesthetic. Because the subdural space is a potential space, it holds a very low volume. For this reason, the block height for a given amount of local anesthetic will be much higher than if the same volume was administered in the epidural space.
64
Causes of a total spinal?
A total spinal may result from:
An epidural dose injected into the subarachnoid space.
An epidural dose injected into the subdural space.
A single shot spinal after a failed epidural block.
65
What is the treatment for a total spinal?
Initial treatment includes: vasopressors, IVF, left uterine displacement, elevation of the legs, and intubation if LOC.
66
Discuss the fetal heart rate? What does it provide?
The fetal heart rate is a surrogate measure of overall fetal wellbeing. It provides an indirect method to assess fetal hypoxia and acidosis. Use of this modality guides clinical decision making, so that we can minimize the risk of fetal injury and demise.
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Fetal oxygenation is a function of
uterine and placental blood flow. The fetus responds to stress with peripheral vasoconstriction, hypertension, and a baroreceptor mediated reduction in heart rate.
68
Bradycardia in the fetus is caused by
Asphyxia and Acidosis, can be causes by drugs that decrease uteroplacental perfusion
69
Which type of fetal decelerations are unremarkable? Which cause concern?
Early decelerations do not present a risk of fetal hypoxemia, while late and variable decelerations require urgent assessment of fetal status.
70
What are the common causes of fetal deceleration patterns? VEAL CHOP
Variable decels: Cord compression
Early decels: Head compression
Accelerations: OK or give oxygen
Late decels: Placental insufficiency
71
Define premature delivery, and list of the potential complications from its occurrence.
Premature delivery is defined as delivery before 37 weeks gestation or less than 259 days from the last menstrual cycle.
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It is the leading cause of perinatal morbidity and mortality
PREMATURE DELIVERY., and this risk is even higher for newborns weighing less than 1500g.
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The incidence of prematurity rises with
multiple gestations and premature rupture of membranes.
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Complications of premature delivery include:
Respiratory distress syndrome
Intraventricular hemorrhage
NEC
Hypoglycemia
Hypocalcemia
Hyperbilirubinemia
75
Discuss the use of steroids in the prevention of premature delivery.
Corticosteroids (betamethasone) hasten fetal lung maturity. These drugs begin to take effect within 18 hours, with a peak benefit at 48 hours.
76
Discuss the use of tocolytic agents in the prevention of premature delivery.
Tocolytic agents stop labor ~ 24 - 48 hours. They provide a bridge that allows the corticosteroids time to work. Antibiotic prophylaxis for chorioamnionitis is also given at this time. Tocolytic agents or corticosteroids are seldom given after 33 weeks gestation.
77
Name 2 beta agonists used in pregnancy
Beta-2 agonists: Terbutaline, Ritodrine
78
What are the side effects of beta-2 agonists when used for tocolysis? Side effects:
Hypokalemia results from an intracellular potassium shift.
Beta-2 agonists cross the placenta and may increase FHR.
79
Beta 2 agonists and blood sugar
Hyperglycemia results from glycogenolysis in the liver.
80
The newborn of a hyperglycemic mother is at risk of
post-delivery hypoglycemia. The mother's glucose supply is gone, but the insulin in the neonatal circulation remains.
81
How does the serum magnesium level correspond with its clinical effects? mEq/L LOSS OF PATELLAR REFLEXES
4 - 6.5
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How does the serum magnesium level correspond with its clinical effects? mEq/L CARDIAC ARREST
>10
83
How does the serum magnesium level correspond with its clinical effects? mg/dL CARDIAC ARREST
>25
84
How does the serum magnesium level correspond with its clinical effects? mg/dL LOSS OF PATELLAR REFLEXES
10-12
85
How does the serum magnesium level correspond with its clinical effects? mg/dL RESP DEPRESSION and APNEA
12-18
>18 APNEA
86
Magnesium normal level mg/dL
1.8 - 3
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How does the serum magnesium level correspond with its clinical effects? mg/dL ANTICONVULSANT
7-9.5
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How does the serum magnesium level correspond with its clinical effects? mg/dL TOCOLYSIS
4-8
89
What are the side effects of magnesium?
Pulmonary edema
Hypotension
Skeletal muscle weakness (synergism with non-depolarizers)
CNS depression
Reduced responsiveness to ephedrine and phenylephrine
90
What is the treatment for hypermagnesemia?
Supportive measures
Diuretics (to facilitate excretion of Mg+2)
IV calcium (to antagonize Mg+2)
91
Where is oxytocin synthesized?
Oxytocin is synthesized in the supraoptic and paraventricular nuclei of the hypothalamus. It is released from the posterior pituitary gland.
92
How can oxytocin be administered? What are the potential side effects?
You can give it IV (diluted in IVF) or the OB can inject it directly into the uterus.
93
Side effects of oxytocin
Water retention
Hyponatremia
Hypotension
Reflex tachycardia
Coronary vasoconstriction
94
How can methergine be administered? What can IV administration cause
Methegine is a ergot alkaloid. It can be given 0.2 mg IM (not IV). IV administration can cause significant vasoconstriction, hypertension and cerebral hemorrhage.
95
What are the pros and cons of general anesthesia for cesarean section?
Pros: Fast onset , secured airway ,greater hemodynamic instability
Cons: Risk for difficult mask ventilation, difficult laryngoscopy, risk for aspiration, potential for MH, Absence of maternal awareness.
96
Describe aspiration prophylaxis for the patient scheduled for a cesarean section.
Triple prophylaxis against aspiration:
-Sodium citrate to neutralize gastric acid
- H2 receptor antagonist (ranitidine) to reduce gastric acid secretion
Gastrokinetic agent (metoclopramide) to hasten gastric emptying and increase LES tone
97
How does sodium citrate protect against aspiration?
Neutralize gastric acid
98
How does H2 receptor antagonist protect against aspiration?
- H2 receptor antagonist (ranitidine) to reduce gastric acid secretion
99
How does metoclopramide protect against aspiration?
Gastrokinetic agent (metoclopramide) to hasten gastric emptying and increase LES tone
100
When is the pregnant patient who presents for non-obstetric surgery at risk for aspiration?
Consider aspiration prophylaxis if mom is beyond 14 weeks gestation.
101
How to prevent aspiration?
Administer an antacid (sodium citrate 15 - 30 mL) within 30 min of induction, ranitidine 1 hour prior to induction, and consider metoclopramide to facilitate gastric emptying.
102
If mom is beyond 14 weeks gestation, secure the airway with a
rapid sequence intubation and a 6.0-7.0 endotracheal tube.
103
What is the risk of NSAIDs when used in the pregnant patient?
Avoid NSAIDS after the first trimester, as they may close the ductus arteriosus.
104
Compare and contrast the diagnostic criteria for gestational hypertension, preeclampsia, and eclampsia.
GH --> occurs After 20 weeks, HTN
Preeclampsia --> occurs After 20 weeks, HTN , Proteinuria, EDEMA
Eclampsia --> occurs After 20 weeks, HTN , Proteinuria, EDEMA, and SEIZURES
105
The classic triad of preeclampsia consists oft should be noted that
hypertension that develops after 20 weeks gestation
proteinuria
generalized edema
(Anesthesia and Co-Existing Disease states that edema is no longer required for diagnosis)
106
Discuss the balance of prostacyclin and thromboxane in the patient with preeclampsia.
The healthy placenta produces thromboxane and prostacyclin in equal amounts, however the patient with preeclampsia produces up to 7 times more thromboxane than prostacyclin.
107
Increased thromboxane favors
vasoconstriction, platelet aggregation, and a reduced placental blood flow.
