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248 Cards in this Set
- Front
- Back
there is a...% in cardiac output due to increase in.. and ....
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40% increase in cardiac output due to increase in SV of 30-30% and HR 15-30%
|
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secondary increase in co in pregnancy are due
|
increased catecholamines and auto transfusion from uterus
|
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increase in BV of
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35%
|
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blood volume increases progressively after
|
7 weeks gestation and reaches peak at 33 weeks w little change after
|
|
the shift in volume of goes to uterus, kidneys, breasts and striated muscle
|
1000-1500cc
|
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of the total blood volume increase, the increase in plasma volume of...is relatively greater than the increase in rbc mass of and this results in..
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45%-25%/hemodilution and a relative decrease in hg-dilutional anemia
|
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increased blood volume serves two purposes
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facilitates maternal and fetal exchange of nutrients, gases and metabolites (increased viscosity)
reduces the impact of maternal blood loss at delivery |
|
ebl at delivery
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vaginal is 500, csex is 1000
|
|
what is autotransfusion
|
during labor , the contracting uterus, auto transfuses 300-500 cc of blood compensating for the usual maternal blood loss at birth.
|
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autotranfusion can increase co by
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50%
|
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in normal pregnancy, ...and...remain unchanged
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syst bp, pulmonary artery p
|
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aortocaval compression is otherwise called
|
supine hypotension syndrome
|
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whent he parturient lies supin,e the ..and the ..is compressed
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inferior vena cava, lower aorta
|
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....% decrease in CO can occur from aortocaval compression
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25
|
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in the awake state, this....compensates for the decreased co seen due to aortocaval compression
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increased svr and hr; blood flow increase through collateral veins at the paravertebral venous plexus incuding epidural veins
|
|
tx for aortocaval compression
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pressors/ left tilt/right hip roll
|
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the most critical time for the parturient is the and why
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immediate postpartum period when cardiac output is at its highest and thus places the greatest strain on the heart
auto transfusion of the uterus, complete and sudden relief of inferior vena caval obst, high circultating catecholamines |
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cardiac output returns to normal wihtin
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2 weeks post partum
|
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all coag factors except for..increase
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11/13
|
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...and..increase throughout pregnancy and peak at 50% above normal by end of second trimester (respt)
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mv, o2 consumption
|
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..space increased due to increased vt/mv
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physiological
|
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overall alveolar vent is ...higher at end of gestation
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70
|
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pac02 decreases
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15%
|
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the development of alkalosis due to decreased co2 tension is prevented by
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a compensatory decrease in serum bicarb
|
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pa02 increases
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10%
|
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hyperventilation would shift the oxyghemoglobin curve to..and cause the maternal blood to
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left to hold on to oxygen
|
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two things offset the effects of hyperventilation and shift the curve to the right allowing o2 to be released to fetus
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increase in bicarb and increase in 23dpg
|
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p50
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the po2 required for 50% saturation on the dissasociation curve
|
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the bohr effect is..and shifts the curve to the...
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as co2 diffuses from blood to alveoli, there is a reduction in pco2 and hydrogen ions---decreased carbonic acid and a left shift resulting in an uptake of 02 and a left shift
|
|
how does the fetal placental interface effect the o2 diss curve
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co2 from fetus enters blood, forms increased carbonic acid, increased h+ ions, right shift with release of oxygen where its needed.
|
|
hg can carry more oxygen at a
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low pco2
|
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decrease of ...% of FRC and resultant
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20%, resultant reduced oxygen storage capacity combined with increased oxygen consumption leads to an unusual rapid decline in arterial oxygen in the apneic patient
|
|
elevated gi r/t hormones in pregnancy
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progesterone-decreases gastroesophogeal sphincter tone and gastrin increases maternal gastric output
|
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mendelson syndrome
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gastric contents over 25 cc, ph < 2.5,
|
|
tx for mendeslons syndrome
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non particulant anatacid 30 cc sodium citrate
|
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non particulant
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clear
|
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all parturients are at risk for aspiration after
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8-10 weeks gestation
|
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w/an elective c sextion npo status is
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6 hrs
|
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scopolamine reduces..
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lower gastroesophogeal sphincter tone and may promote passive regurg
|
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gfr increases after the fourth month and at term is
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elevated 50-60%
|
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blood urea and creatine is reduced by
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40%
|
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serum psudocholinestarase levels will fall during the first trimester and remain low throughout gestation bu
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there is a reserve so only 10% of women are really at risk
|
|
effects of preg on induction and depth of anes
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increased induction speed and depth
|
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pregnancy enhances inhalation agent uptake as mush a
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40%
|
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why does induction occur faster
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increase in MV delivers more VA, decreased frc favors the rapid replacment of alveolar content with inspired agent
|
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mac returns to normal by
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third postpartum day
|
|
why is there an increased sens to LA
|
changes in csf ph, likely due to engorged venous plexus of epidural veins
|
|
why is there an engorgment of the epidural venous plexus
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obst of the inferior vena cava by enlarging uterus and the increase in circulation blood volume
|
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effects of the engorged venous plexus
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decreased csf volume, decrease in potential epidural space, increase in epidural space pressure
|
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how does the engorged epidural plexus effect the spread of la
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cephelad, placement difficulty (higher incidence of dural puncture and the epidural catheter migration into the epidural veins
|
|
why does thiopental have a doubling of the elimantion half life
|
because of the 45% increae in plasma with a resultant increase in greater volume of destribution
|
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progesterone has ...effects on sedation
|
increase
|
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at term uterine blood flow accounts for about % of the maternal cardiac output
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10
|
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because uterine vasulature is max dilated,...is absent
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auto regulation
|
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uterine blood flow is proportional to
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mean perfusion pressure
ap-vp/vascular restistance= blood flow |
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blood flow is directly proportional to the difference between the uterine artery and inv. propr to
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venous pressures but inversly prop to uterine vascular resitance
|
|
three major factors that decrease uterine blood flow
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systemic hypotension, uterine vascular vasconstriction and uterine contraction
|
|
common causes of maternal hypotension includie
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aortocaval compression, hypovolemia, sympathetic blockade after regional anesthesia.
|
|
how can systemic hypotension in the praturient be minimized
|
fluid loading, ephedrine pre treat,epidural with minimal la concentration and + narcotics to supplement, right uterine displacement and oxygen supplementation
|
|
...causes uterine vascular vasconstriction
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release of endogeneous catecholamines and exogenous sympathomimetics
|
|
uterine contrations decrease blood flow by
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elevating uterine venous pressure brought on by the increased intramural pressure of the uterus.
|
|
50% of fetal cardiac output flows with little resistance through
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two umbilical arteries towards the placenta
|
|
where is fetal blood cleaned and oxygenated
|
in the villi
|
|
blood from the placenta to fetus goes through
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one umbilical vein
|
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at term blood flow is
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120 ml/kg/min 360 ml/min
|
|
substances are exchanged across the placental membrane by 5 mechanisms
|
diffusion, bulk flow, active transpot, pinocytosis, breaks
|
|
...are transported by diffusion
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respiratory gases, fatty acids, small ions.
|
|
water is transported by
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bulk flow
|
|
positive rh blood type denotes that the individual carries the
|
d type antigen
|
|
..% of uterine blood flow passes to the intervillous space of the placenta and
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80%, 20% supplies the actual myometrium of the uterus.
|
|
the fetus can survive up to 10 minutes w/out oxygen due to
|
redistribution of fetal blood flow to the brain and the placenta
decreased oxygen consumption anaerobic metabolism |
|
the fetus can survive up to ten minutes without oxygen because of
|
redistribution of blood flow to the brain, heart and placenta
decreased oxygen consumption anaerobic metabolism |
|
transfer of oxygen across the placenta is dependent upon the
|
ratio of maternal blood flow to fetal umbilical blood flow
|
|
well oxygenated blood from the placenta has a pa02
|
of only 40 torr.
|
|
normal maternal pa02 is
|
95-104 torr
|
|
to aid oxygen transfer (3)
|
fetal hg curve is left shifted
hemoglobin conc in fetus is 50% greater that the mother doublebohr effect |
|
double bohr effect
|
the fetal blood entering the placenta has a high pc02, which diffuses into the maternal blood which then releases more oxygen because it becomes more acidic. so even more oxygen is diffused into the blood of the fetus. the bohr effect allows even maternal blood to give up more oxygen that is typical and encourages the fetal blood to take up more oxygen than would be typically possible thus doubling the effect.
|
|
carbon dioxide diffuses across the placenta by
|
gradient
|
|
fetal hemoglobin has..affinity for co2 than maternal
|
less
|
|
fetal hemoglobin can carry...%..o2 than maternal
|
20-30 more
|
|
goal of the anatomic shunt is
|
to maximally perfuse the placenta and bypass nearly all of the nonfunctional lung and liver
|
|
blood from the placenta through the one umbilical vein passes through the
|
ductus venosus on its way to the inferior vena cava
|
|
from the ductus venosus through the inferior vena cava blood then flows through the...inot the ... and then to
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right atrium into the foramen ovale into the left atrium
|
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the well oxygenated blood from the left atrium enters the ...throught the and pumped by the ..into the vessels of the head and forelibms
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left ventricle thorugh the mitral valve and the left ventricle
|
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blood entering the right atrium via the superior vena cava is preferentially directed into the ..via the
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right atrium via the tricuspid valve
|
|
blood is pumped from the right ventricle into the
|
pulmonary artery
|
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from the pulmonary artery blood flows into the
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ductus arteriosus into descending aorta and through two umblical arteries to oxygante the placenta
|
|
average oxygen saturation of blood in umblical vein is..after it mixes with blood in the ductus venosus it is
|
80%, 67%
|
|
ductus arteriosis connects the....to the...and protects the
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connects the main pulmonary artery to the desending aorta and thus protects the lungs against circulatory overload
|
|
the foramen ovales helps prevent
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blood from moving in the reverse direction
|
|
all circulatory adjustments during the first few hours of life shunt an ever increasing amount of blood through the
|
liver
|
|
primary changes of circulation at birth are
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loss of tremendous blood flow through the low resistance placenta which double the SVR of the fetus. , increasing pressure of the left ventricle and atrium. Pulmonary vascular resitance decreases due to the expansion of lungs with the first breath. FA/DA closure
|
|
the first breath of the new born generates initial negative intrathoracic pressure of
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40-60 cmh20
|
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functional closure of the da occurs due to
|
increased oxygen in the area
|
|
another name for persistent fetal circulation is
|
persistent pulmonary hypertension
|
|
right to left shunt causes
|
hypoxia and acidosis
|
|
...WOULD cause right to lefts shunt
|
anything that would cause the pulmonary vascular resitance to be higher than the systemic vascular resistance
|
|
..%of pregnancies are complicated by pregnancy induced hypertentsion
|
6-8
|
|
most patients with pih
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under 20 , primigravidas
|
|
pih is characterized by
|
preeclampsia, eclampsia, HELLP ( hemolytic elevated liver enzymes and low platelets)
|
|
potential maternal complications of pih are
|
arf, cerebral hemorrage from hypertension, pulmonary edema
|
|
pre eclampsia occurs after the
|
20th week of gestation
|
|
pre eclampia features
|
intravascular depletion with increased caridac output and generalized vasoconstriction
|
|
severe preeclampsia progresses to eclampsia when
|
seizures occur
|
|
first priority of the eclamptic patient is to
|
control convulsion
|
|
increased PVR results frm and in
|
from hypoxemia and acidosis and results in Results in RV failure with R to L shunts across the foramen ovales and left V failure with a R to left shunt across the ductus arteriosus
|
|
preeclampsia results in a uterus that is
|
hyperactive
|
|
the main problem of the HELLP syndrome starts with activation of the
|
coagulation cascade
|
|
symptoms of hellp are
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gradual w the onset of headaches, blurred vision, n/v, band pain around the upper abomen and tinglinging in the extremities.
|
|
definitive therapy for PHI is
|
delivery of the fetus and the placenta
|
|
...is an extremely effective anticonvusant, tocolytic, and mild general vasodilator.
|
magnesium
|
|
the cns depression effects of mag are due to
|
cerebral artery vasodilation
|
|
magnesium depresses both
|
smooth muscle contraction and cns catecholamine release with the result of lowering of the bp and improved blood flow
|
|
side effects associated with the use of magnesium are
|
abnormal muscle contraction resulting in muscle weakness including resp insufficiency.
|
|
...provides superb analgesia during the labor and delivery of a parturient with PIH and why
|
LEA. Decreased maternal endogenous catecholamines helps to lower maternal oxygen requirments and improves uterine blood flow by decreasing the maternal hyperventilation. Decrease in BP. Assists overall with the hyperdynamic state
|
|
managment technique of the PIH patient
|
managment of hypertension, evaluation of the absence of the severe coagulopathy, supplemental oxygen, adequate prehydration with great caution . Monitoring should include use of pulse oximeter and cont recorded fetal heart rate/uterine contractions and occ. CVP
|
|
prehydration for the PIH patient
|
50o cc NS for T10 level or 50-100 cc of 25% albumin
|
|
add benefit for LEA for the PIH patient secondary to systemic benefits
|
provides block for cesarean section
|
|
prehydration/med for level of LEA required for Csextion
|
1-2 L NS, for t4 level and ephedrine 2.5-5.0 mg
|
|
approx size of tube for ETT for GA for the parturient PIH
|
5.5-6.0
|
|
induction for GA for the patrient with PIH
|
reduced propofol and thiopental and no ketamine. no def dose for succ because of magnesium dosing. succ 1.5 mg/kg. no further MR-decrease muscle tone and not required. initial maint is best achived with IA with a 100% oxygen delivery 1.5 mac for the first minute and 2/3 to 1/2 mac until delivery.
|
|
anes tx of the parturient with PIH after delivery
|
opiods are further supplemented as tolerated and IA are reduced or eliminated. N20/TIVA Propofol as tolerated. blunt hypertensive resopnse to intubation, surgical stimulation and expected light extubation condiitions w opiods, mag, lidocaine and more frequently bb or antihypertensives.
|
|
the PIH parturients are prone to...within 24 hrs of delivery and why
|
prone to convulse and develop pulmonary edema. because the sympathetic block from the epidural begins to dissapate. and mag is weaned over 48 hrs, antihypertensiv therapy is cont as needed
|
|
three stages of labor
|
first stage ( latent-4 cm cervical dilation) and active greater than 4 cm dilation)
second- complete dilation of the cervix till delivery involving the descent of the fetus through the pelvis and out of canal third- involves delivery of the placenta |
|
what is an actual shunt
|
patent foramen ovale
|
|
regular contractions are..apart
|
10 cm
|
|
the epidural can generally be placed in the ...
|
latent phase
|
|
innervation at...occurs with pain during the first stage
|
t10-l1
|
|
pain caused by fetal descend through the pelvis and the placental delivery stretches the pelvic and peritoneal structures with inervation at
|
s2-s4
|
|
epidural is usually placed
|
l2-3
|
|
nearly all opiod analgesics..
|
cross the placenta and can effect the fetus and cause resp depression w/ acidosis and sedation.
|
|
opiods are typically used
|
earlly in labor, w/in 4 hours of delivery
|
|
...are seldom used because
|
benzo ... amensia
|
|
most common side effect of labor epidurals is
|
hypotension secondary to sympathetic blockade and result in vasodilation
|
|
prior to placing epidurals it is essential to
|
establish the ptient with their pain relief expectations
|
|
epidurals should only be attempted in a location where
|
complete anestethia equipment and resuscitative drugs are available
|
|
absolute contraindications to epidural include
|
patient refusal, coagulopathy, plt count less than 100,000, skin infection at side, rasied ICP, hypovolemia. which may lead to circulatory collapse
|
|
relative contraindications to epidurals
|
uncooperative patients, prex nuerological disorders as such a MS maybe contraindicated because of any new neurolgical symptoms .
fixed cardiac output states including aortic stensois, hypertrophic obstructive obstructie cardiomyopathy, mitral stenosis and complete heart block. patients are unable to increase cardiac output in response to the symp. blockade and subsequent peripheral vasodilation caused by epidural blockade. anatomical abnormalities such as scoliosis previous back surgery ( ***infection) |
|
labor epidurals are...procedures
|
elective
|
|
prior to epidural positioning and placement...administer....
|
non particulant (clear) antaci and 500-1000 cc LR fluid bolus
|
|
spinal cord ends at
|
l1-l2
|
|
typical depth from skin to lumbar epidural space is
|
5 cm
|
|
test dose i
|
lido 1.5 % and epi 1:200,000 3 cc (45 mg LIDO and 27 mcg EPI)
|
|
intravascular placement o EPI woulld
|
give you increase in HR and BP unless the pt is BB
|
|
lido test dose ( ...% occurence) will give you a
|
.5-2.5% occurence will give you a fast block o t8-10
|
|
after pt positioning with an epidural, give
|
5 cc of .25% bupicivacine and 100 mcg of Fentanyl and begin frequent monitoring for of BP and watch for signs of hypotension
|
|
begin epidural infusion with
|
.1% bupivicaine and fentanyl 2-5 mcg per cc at 6-10 cc/hr
|
|
inadequate analgesia as labor progresses can be treated with
|
an additional bolus of .25% bupivicaine 5-10 cc
|
|
if pt is completely ditated and ready to push or i the process its pref to treat epidural w
|
Fentanul 50-100 mcg to avoid using la and maint the greatest motor function
|
|
when the epidural tip is removed than..
|
document
|
|
maintain the now recognized intrathecal catheter as you would
|
any other spinal or as an epidural with 1/10 of the mg volume dose. label the cather as intrathecal and cont to communicated with anyone who may handle the catheter.
|
|
pres free intentional intrathecal opiod placement is reseved for the
|
multip parturient as tehir progress through labor is typically fast and this is a one shot technique and the duration can not be extended or converted for emergency C/S.
|
|
one shot intrathecal opiods have no
|
have no side effects of sympthetic blockade.
|
|
side effects of intrathecal opiods
|
n/v urticaria.
|
|
ex of small gage needles to elimnate post dural puncture headaches
|
pencan 25 G or whitacre 25 G
|
|
...are typically not used due several reported cases of cauda equina syndrome
|
cont spinal catheters 28 gage.
|
|
the FHR is controlled by the
|
autonomic nervous system
|
|
the inhibitoryt influence on the HR is conveyed by the
|
vagus nerve
|
|
excitatory influence on the HR is conveyed by the
|
symp. nervous system
|
|
progressive vagal dominance on fetal hr occurs as the
|
fetus approaches term and after birth this results in a gradual decrease in the baseline FHR
|
|
...influence the FHR through the vagus nerve in response to change in fetal blood pressure
|
baroreceptors
|
|
almonst any stressful situation in the fetus evokes the...which ellicits
|
baroreceptor reflex..which ellicits selective peripheral vasoconstriction and hypertension with a resultant bradycardia.
|
|
vasonstriction due to stressful stimuli with resultant bradycardia in the fetus may be caused by
|
hypoxia, uterine contractios, fetal head compression, perhaps fetal grunting or defaction.
|
|
chemoreceptors located in the...of the fetus resond to tachycardia and hypertension, excess co2 and acidosis and produce
|
aortic and carotoid bodies/produce tachycarida and hypertension
|
|
a...or...refects a healthy fetal nervous system
|
variable FHR or baseline variability
|
|
variability should be normal after
|
32 weeks
|
|
sustained decreased baseline variability is a
|
potential sign of fetal asphixia and thus a nonreassuring FHR
|
|
FHR accelerations of...beat/min for more than..sec are normal and considered reassureing
|
a15 beats/min for more than 15 sec
|
|
accelerations reflect
|
normal oxygenation and are related to fetal activity in response to uterine pressure
|
|
absence of acelerations is
|
nonreassuring
|
|
the timing for FHR decelerations is relative to
|
the uterine contraction and has specific corresponding etiologies
|
|
early decelerations of (10-40 beats/min are simultaneous to contractions and re the result of
|
vagal reflex and head compression
|
|
early decelerations are not associated with
|
fetal distress and are thus reassuring
|
|
late decelerations have an onset of
|
10-30 seconds after contractionsbegin and end 10-30 seconds after the conraction ends. this is a sign of uteroplacental insuficiency and overall fetal circulatory decompression.
|
|
all late decelerations are considered/ late deceleration with a decrease in variability
|
potentially threatening to the fetus
|
|
variable decelerations may be a sign of
|
head and umbilical cord compression
|
|
variable decelerations are shown by an acute fall in the
|
FHR and a rapid down slope and a variable recovery phase and may not be in a constant releationsip with the contraction
|
|
...are the most commonly encountered patterns during labor and occur frequently in patient who have experienced premature rupture of membranes and decreased amniotic fluid volume
|
variable decelerations
|
|
variable decelerations are caused by
|
compression of the umbilical cord
|
|
a....if not corrected may lead to acidosis and fetal distress and is non reassuring
|
persistent variable decelration
|
|
nonreassuring variable decelerations associated with the loss of...are non reassuring and represent a threat to the fetus
|
beat to beat variability
|
|
non reassuring hr
|
decrease in variability, late deceleration w/ persistent decrease in variability, no variability fetal bradycardia.
|
|
implied with any regional anes. is a potential for
|
general anes.
|
|
any regional anes required a
|
t4 sensory level for cesarean section
|
|
cardiac accelerator fibers originate from
|
1st to 5th thoracic spinal nerves.
|
|
diaphragm innervation is at
|
c3,4,,5
|
|
sensory dennervation to the thoraci region which is partially blocked can lead to the
|
quiet respirations causing the pt to feel that they can not breath.
|
|
tingling or weak ability to grasp the hands implies
|
low cervical blockade for c5,6,7
|
|
ability of the patient to lift their head implies that
|
muscles of accessory breathing are intact
|
|
with routine or scheduled c sections, ..is pref over..due to..
|
spinal v. epi, due to faster placement and consistent dense sensory and motor blockade.
|
|
typical spinal dose
|
.75% bupivicaine 7.5mg/cc 10.5-15 mg with addition of fentanyl 12.5 mg or PF morphine .15 mg
|
|
true emergent c/x is treated at
|
RSI GETA
|
|
only induce GA after confirmation with
|
surgical team readiness.
|
|
incision with c/x occurs
|
after you confirm an established airway
|
|
an emergent c/x in a pt with a previously dosed labor epidural ca be dosed with
|
increments of 15-20 cc chloroprocaine 3% or alkanized 2% PF lido (1cc sodium bicarb 8.4% per 10 cc of LIdo) epi is not used because it can slow the onset of the block
|
|
why is epi not used for cx dosing of epidural
|
it ca slow the onset of block
|
|
migration of labor epidural catheters can result in
|
high spinal or toxic blood levels respectively and should be treated with RSI GETA.
|
|
inadequate or patchy sensory level of labor epidural catheters should be treated with
|
IV ketamine 10-25 mg or 30-50% N20. and the SR can infilrate with 1% lidocaine
|
|
GETA in the parturient has an increased risk because of
|
difficult airway, increased risk of aspiration
|
|
incidence of failed intubaation is x higher in the parturient
|
8
|
|
dosing for RSI induction for the parturient
|
succ 1.5 mg/kg/ propofol 2 mg/kg
|
|
incision is pertmitted after
|
confirmation of proper ETT placement
|
|
...given after fetal delivery
|
antibiotics, oxytocin 20 u/LTR PSR. Methergine 0.2 mg IM or Hemabate 025 mg IM PRS for uterine atony.
|
|
extubate the praturient w
|
awake with protective reflexes intact
|
|
normal apgar score, moderate, needs res.
|
normal is 7-10
mod 4-6 need res 1-3 |
|
..apgar score is defin
|
2nd
|
|
all elective surgeries should be
|
postponed until 6 weeks after delivery
|
|
with surgery during preg. during first signs of labor
|
give tocoltics such as torbutaline and ritordine
|
|
FHR for intra gestational surgery should be included
|
pre and post op 10-16 weeks gestation
|
|
for intra gestational surgery, rSI GETA should be utilized with GA after
|
10-16 weeks gestation
|
|
maintaine uterine displacement with the parturient in the supine position for intra gestational surgery...
|
after 24 weeks gestation
|
|
most common surgeris for the parturient
|
cerclage and lap
|
|
..prevents or blocks fetal delivery in .5% inc
|
placenta previa
|
|
..presents typically with painless vaginal bleedng
|
placenta previa
|
|
..previa that aheres to the uterine surface
|
placental accreta
|
|
placenta previa that invades the muscle
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placental increta
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...placenta previa that completely invades the uterine muscle and surrounding tissue
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placental pecreta
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..premature superation of the life giving placenta from the uterine wall witha ...inidence
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abpruption placentae with a 1-2 % incidence
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...indicated by painful vaginal bleeding
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abruptio placentae
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risk factor for abpurtio placenta
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hypertension, traum, short umbilical cord, multiparty, prolonged rupture of membraes, cocaine and etoh abuse
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severe abruptio requires
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emergency RSI GETA, C/S and aggresive volume managment
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uterine rupture may occur with
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parturients whith any history or previous extensie uterine manipulation particulary VBAC (vag birth after cesarean)
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presentation of uterine rupture
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loss of uterine tone, bleediing, fetal distress.
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treatment for uterine rupture
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emergency open hysyterectomy with aggresive volume managmenti
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incidence of post partum hemmorage
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4%
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tx post partum hemmorage
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oxytocin 2030 U/L, Methergine .2 mgIM (uterine an smooth muscle constrictor) Hemabate (form of prostogland/uterine/smooth muscle constricotor/increase BP)
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problem with prolapsed cord and %
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1%, cord compression and fetal demise
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risk factors for prolapsed cord
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excess lenght of cord, multiparty, multgestations. low birth weight, malpresentation. * premature or artifical rupture of membranes
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treatment for cord prolapse
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immediate c/s with RSI
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dystocia or inneffecive labor is caused by
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inadequate uterine contractions, abnormal fetal presentationor cephalopelvic disproportion
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prolonged latent phase is defined as
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greater that 20hrs in prima and 14 hrs in multi
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in the prolonged latent phase, the cervix remains
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dilated to 4cm but completely effeaced.
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most common abrnormal fetal presentation and %
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breech 3-4%
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typically breech presentation is due to
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multiple gestations and fetal prematurity
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cord prolapse occurs in % of breech presentation
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10
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..are often placed with external cephalic version
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epidurals
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why are epidurals placed for external cephalic version
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discomfort, manipulation can result in placental rupture/distress and requires immediate cx-placement avoid the need for RSI and GETA.
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csec rate for breech
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80-100
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amniotic fluid embolism has a greater than...mortality rate with a ...% rate
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80
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amniotic fluid embolism in a parturient presents with
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sudden respiratory distress, tachypnea, cyanosis, cardiovascular collapse and bleeding.
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chest compressions are at best ..in a parturient
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innafective due to pisiton
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risk of uterine rupture after VBAC is
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.2-1.5 %
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...%of patients w a dural puncture will develop a PDPH
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30-70%
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zero-24 hrs following a dural puncture, encourage the pt to
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increase fluid intake/helps to ensure that the rate of CSF production is adequate
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....can be used as tx for PDPH
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intravenous caffeine 500 mg/ caffeine sodium benzoate in one liter iv fluid and infuse this over one hour, may be repeated every 8. 300 mg oral caffeine will provide temp analgesia
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epidural blood patch is performed
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24-48 hrs following dural puncture with a severe PDPH
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epidural bloodpatch uses and is effective
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15-20 ml of blood in the patch, 95% of the time.
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after a blood patch, the pt should
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remain in the decubitus position for 30 minutes after placement before they are allowed to ambulate
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