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144 Cards in this Set
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- Back
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what are the benefits of the apgar scoring system
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*reproducible numerical mesurement
*objective criteria for neonatal resuscitation *refocused outcome on neonatal as well as maternal well-being |
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in pregnancy CO increases when
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from the 5th week to a max at 32 weeks
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in pregnancy CO remains stable after increasing when
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after its max at 32 weeks until L&D and the immediate postpartum period
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there is what amt of increase in CO at 8 wks gestation
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25 %
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there is what amt of increase in CO at the start of the 3rd trimester in pregnancy
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50 %
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there is what amt of increase in CO in active labor
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~ 100%
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there is what amt of increase in CO in the immediate postpartum period
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~ 150 %
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CO decreases to pre-labor values by when postpartum
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~ 48 hrs
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CO decreases to 10% above pre-pregnant values by when
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2 weeks postpartum
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CO returns to normal when postpartum
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12 and 24 weeks postpartum
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in pregnancy CO increases d/t what
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increased SV and HR
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HR changes how in pregnancy
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increases ~20% by 2nd trimester and then remains stable
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what is the major contributor to increased CO in pregnancy
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increased STROKE VOLUME
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what occurs to stoke volume with pregnancy
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*~20% increase by 4 wks gestation
*25-50% increase by term |
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how do pregnant pts have an increased ejection fraction
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LVEDV increases with NO change in end-systolic volume = increased ejection fraction
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the increased ejection fraction in pregnancy is d/t what
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*reduction in afterload
(not increased myocardial contractility) |
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pregnancy has what effect on SVR
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~ 20% reduction
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what are the ways in pregnancy effects SVR
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*development of the intervillous space, a low resistance vascular bed
*vasodilation caused by prostacyclin, estrogen and progestrone |
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compression of the IVC occurs as early as when in the pregnancy
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13-16 wks gestation
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compression of the IVC in pregnancy is evidenced by what
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increased femoral venous pressure
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with compression of the IVC in pregnancy collateral flow develops how
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primarily through the intraosseous vertebral veins, paravertebral veins and epidural venous plexus
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what is supine hypotensive syndrome in pregnancy
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vena caval compression results in sig hypotension in ~ 10 % of pts at term in the supine position
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overall aortic compression does what in pregnancy
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does not result in maternal symptoms but may result in decreased uteroplacental blood flow
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what are factors affecting BP in pregnancy
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*maternal age
*parity *position |
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クレジット
カード |
(n.) credit card [会L10]
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with pregnancy elevation of the diaphragm shifts the heart how
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anteriorly and to the LEFT
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what is heard with heart sounds with pregnancy
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*accentuation of the 1st heart sound
*exaggerated splitting of mitral & tricuspid components |
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what extra heart sound in heard in many pregnant women
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S3
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what is seen on echo with pregnancy
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L vent hypertrophy by 12 wks gestation with up to 50% increase in mass by term
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plasma volume changes how in pregnancy
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increases by ~ 45% at term
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estrogens do what regarding plasma volume in pregnancy
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increase plasma renin activity which enhances renal Na reabsorption & H20 retention by the renin-angiotension-aldosterone system
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progesterone enhances production of what during pregnancy regarding plasma volume
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ALDOSTERONE
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in pregnancy there is increasing erythropoeitin production why
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d/t progesterone, prolactin and placental lactogen
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during pregnancy when in there increasing erythropoietin concentration
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beginning at 8-12 wks
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during pregnancy erythropoietin concentration increaseses by how much at term
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~30 %
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what is the avg H&H at term with pregnancy
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*Hgb= 11.6
*Hct= 35.5 |
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why is oxygen transport not compromised with physiologic anemia of pregnancy
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d/t:
*increased maternal CO *increased pp of art O2 *R shift in oxyhemoglobin dissociation curve |
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what in pregnancy may be a protective mechanism against placental thrombosis and infarction
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HEMODILUTION
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pregnancy represents what kind of state of intravascular coagulation
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accelerated but compensated
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with pregnancy there is what kind of platelet consumption
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INCREASED
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with pregnancy there is what kind of changes in fibrinogen and factor VII
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marked INCREASES
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with pregnancy there is what kind of change in PT and PTT
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SHORTENING
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what remains the number one cause of death during pregnancy
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THROMBOEMBOLISM
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hemoglobin concentration does what for the first 3 postpartum days
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DECREASES
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after the first 3 postpartum days hemoglobin concentration does what
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RISES RAPIDLY
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hemoglobin concentration gradually returns to pre-pregnant levels when postpartum
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~ 6 wks
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during the first 3-5 postpartum days what occurs with fibrinogen and plt counts--this is concurrent with what
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*they begin to RISE
*concurrent with increased incidence of thromboembolic events |
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with pregnancy coag return to normal when postpartum
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~ 2 wks
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what is the typical blood loss with a vaginal delivery
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~ 600 ml
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what is the typical blood loss with a c-section
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~ 1000 ml
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colliod osmotic pressure does what during pregnancy
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decreases by ~ 5mmHg
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colloid osmotic pressure changes during pregnancy are d/t what
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*reduction in albumin from 4.5 to 3.3
*reduction in total protein from 7.8 to 7 |
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what occurs with minute ventilation during pregnancy
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it increases by 45%
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what causes minute ventilation to change during pregnancy
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*progesterone sensitizes the resp center to Co2
*increased Co2 production |
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PaCo2 does what by the 12th wk of pregnancy
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falls to ~ 30
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tidal volume does what in pregnancy
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increases by ~ 50%
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resp rate does what in pregnancy
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does NOT change
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type of respirations change how in pregnancy
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resp become more diaphragmatic secondary to the gravid uterus and decreased thoracic cage movement
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FRC changes how during pregnancy
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DECREASES by ~ 20%
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closing capacity does what during pregnancy
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remains UNCHANGED
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HYPERventilation with painful contractions leads to what
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periods of HYPOventilation b/t contractions resulting in transient materanal and fetal hypoxemia
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HYPERventilation in labor may do what
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reduce uterine blood flow
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the hyper/hypoventilation cycle is broken how
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with effective pain relief (i.e. labor epidural)
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gastric emptying is slowed during pregnancy or labor
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LABOR
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esophageal peristalsis and intestinal motility are slowed during pregnancy why
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d/t increased progesterone levels
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the stomach is displaced how during pregnancy
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*upward & to the LEFT
*45 degree axis rotation to the LEFT |
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with the stomach displacment changes that occur during pregnancy this displaces the intrabdominal segment of the esophagus where
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into the thorax
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d/t the displacement changes that occur with the stomach during pregnancy what happens that normally prevents reflux
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it reduces tone in the LEHPZ
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during pregnancy intragastric pressure is elevated when
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3rd trimester
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gastric emptying returns to normal when after delivery
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~ 18 hrs
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its common for liver function tests to do what in pregnancy
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to increase to the upper limits of normal
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alkaline phosphatase may do what in pregnancy
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show a 2-4x increase
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what occurs with the gallbladder during pregnancy
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*volumes markedly increase
*rate of emptying slows |
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what occurs with bile during pregnancy
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it becomes concentrated predisposing to gallstones
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plasma cholinesterase does what during pregnancy
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decreases 25% during the 1st trimester and remains at that level for up to 6 wks postpartum
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how is MAC changed in pregnancy
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REDUCED ~ 30% from early pregnancy
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when does MAC return to normal after pregnancy
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~ 3 days postpartum
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what are the proposed mechanisms for the change in MAC with pregnancy
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*increased progesterone has a sedative effect
*increased CNS serotonergic activity *increased endorphin levels during pregnancy |
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there is an INCREASED pain threshold when during pregnancy
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*late pregnancy
*labor |
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regarding pregnancy induced analgesia there are elevated levels of what in plasma and CSF of pregnant pts
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*endorphins
*enkephalins |
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during pregnancy there is a dependence on what for maintenance of hemodynamic stablity and this increases progressively during pregnancy & reaches a peak at term/primarily on venous capicitance of lower extremities
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sympathetic nervous system
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pregnant women display what kind of response to a carb load
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HYPERINSULINEMIC
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pregnant womens response to a carb load is more than compensated for by what
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a reduced tissue sensitivity to insulin
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during late pregnancy fasting glucose is what and why
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*DECREASED
*d/t high glucose utilization of placenta and fetus |
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blood leukocyte count does what during pregnancy
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progressively rises throughout pregnancy to ~ 11,000
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polymorphonuclear leukocyte function is what in pregnancy
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IMPAIRED
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polymorphonuclear leukocyte function is consistent with what in pregnancy
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*increased incidence of infection
*decreased s/s of autoimmune dz |
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pregnant pts have what kind of lumbar lordosis
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EXAGGERATED
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what increases the mobility of the sacroliliac, sacrococcygeal and pubic joints during pregnancy
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RELAXIN
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incidence of carpal tunnel increases during pregnancy why
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r/t changes in nature of connective tissue
(absorption of more fluid) |
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propofol has what changes in elimination half life with pregnancy
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NO significant change
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in pregnancy there is what change in plasma cholinesterase activity
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25% decrease in activity
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faster rate of recovery from succinlycholine with pregnancy is explained how
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by an increased volume of distribution
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after delivery what alters succinlycholine pharmacokinetics
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decrease in plasma cholinesterase activity and plasma volume
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pregnant pts have what kind of response to aminosteroid MR vec and roc
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enhanced sensitivity
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in pregnancy the pharmacokinetics of atracurium are altered how
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UNALTERED
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what class of drug is atracurium
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bisquaternary ammonium benzylisoquinoline compound
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at term 40% of women will experience what in the supine position
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sig decrease in femoral arterial BP d/t aortic compression in the supine position
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what is uterine flow in the NON-pregnant woman
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50-100 ml/min
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what is uterine flow in the pregnant woman
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700-900 ml/min
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what is the formula for uterine blood flow
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ute art press - ute ven press
--------------------------------------- uterine vascular resistance |
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what are factors that cause impairment of uterine blood flow
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*decreased uterine art pressure d/t systemic hypotension
*increased uterine venous pressure *increased uterine vascular resistance |
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there is what kind of change in angiotension II during pregnancy
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2-3 fold increase in blood concentration
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with angiotension II and pregnancy the vasoconstictor response is changed how
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it is attenuated
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uterine vasculature is less or more responsive to angiotension II than systemic vasculature
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LESS
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what are the mechanisms for the change in response of uterine vasculature to angiotension II compared to sytemic vaculatures response
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*angiotension II receptor alteration
*local antagonism effects of angiotension II (prostacyclin, NO) |
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there is decreased or increased sensitivity to alpha-adrenergic agonists during pregnancy
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DECREASED
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uterine vasculature is less or more responsive than systemic vasculature to alpha-adrengeric agonists
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MORE
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regarding alpha-adrenergic agonists there can be a potential for impairment of uterine blood flow with what
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*release of endogenous catecholamines d/t stress, hemorrhage
*exogenous admin of vasoconstrictors for management of hypotension |
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what occurs with prostaglandins during pregnancy
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increased production and circulation during pregnancy particularly PGI2
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nitric oxide is produced where
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vascular endothelium
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nitric oxide stimulates what
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*guanylate cyclase
*increasing cGMP |
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nitric oxide causes what to occur
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VASODILATION
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there is increased nitric oxide production where in pregnancy
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uterine vs systemic vasculature
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estrogen does what to uterine blood flow
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INCREASES it
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estrogens changes in uterine blood flow appear to be mediated by what
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vasodilation produced by increased NO and cGMP production
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progesterone does what to uterine blood flow
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INHIBITS the normal increase
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in pregnancy ANP and BNP do what to the vasoconstrictive response to angiotension II
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attentuate it
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atrial natiuretic peptide infusion is useful in pre-eclampsia why
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*to decrease BP
*increase uterine blood flow |
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what is protein kinase like in pregnancy
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decreased in uterine but not systemic arteries in pregnant ewes
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what is the likely mechanism of ephedrines protection of uterine perfusion
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enhanced release of NO from uterine artery endothelium
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ephedrine is preferred by most why
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d/t:
*apparent protection of uterine blood flow *hx of safety *ease of use |
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some studies have shown a higher cord pH following tx with which drug ephedrine or phenylephrine
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*PHENYLEPHRINE
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what is an appropriate choice ephedrine or phenylephedrine in small increments in a pt in whom tachycardia whould be detremental
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PHENYLEPHRINE
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what are the mechanisms for placental transfer
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*simple diffusion
*active transport(requires energy) *pinocytosis |
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drug transfer across the placenta is dependent on what
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*molecular wt
*protein binding *lipid solubility *maternal drug concentration *maternal & fetal pH *pka of drug |
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early decels begin when
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with onset of uterine contractions
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early decel is what kind of bpm decrease
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usually < 20 decrease, or not < 100
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early decels are what kind of response
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vagal response d/t fetal head compression
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what type of decels are NOT associated with fetal distress
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EARLY
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LATE decels begin when
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10-30 secs after onset of contraction
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what is a mid-late decel
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<20 bpm decel
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what is a profound late decel
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> 40 bpm decel
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what is the cause of LATE decels
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likely uteroplacental insufficiency
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what is reassuring with LATE decels
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beat to beat variability
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what is the most common kind of decel
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VARIABLE
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what are VARIABLE decels
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variable in
*magnitude *duration *time of onset |
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what is the cause/etilogy of VARIABLE decels
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umbilical compression
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what type of decels are usually well tolerated in a healthy fetus
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VARIABLE
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severe persistant VARIABLE decels are associated with what
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FETAL DISTRESS
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what is the NORMAL heart rate variability of a fetus
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5 - 20 bpm
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maitained beat to beat variability in a fetus implies what
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fetal well being
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loss of beat to beat variability is a fetus is associated with what
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fetal distress d/t
*hypoxemia *acidosis *CNS damage |
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what are things that affect beat to beat variability in a fetus
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*bzd
*opioids *barbs *anticholinergics *LA *prematurity *fetal sleep cycles |
