Home > Flashcards > Print Preview
The flashcards below were created by user
on FreezingBlue Flashcards. What would you like to do?
Increase metabolic demands of both the mother and the fetus are met by an increase in cardiac output. How much is this increased?
CO increases 40%, mostly d/t increased SV (30-35%) and slightly because of increased HR (15-30%)
In pregnancy does SVR increase or decrease?
Blood volume increases how much during pregnancy?
- Blood volume increases progressively after 7weeks gestation and peaks at approximately 33weeks
Why don't we see circulatory overload during pregnancy with the increase in CO?
It's more of a shift of volume (1000-15000ml) to the uterus, kidneys, breasts, and striated muscle
What causes dilutional anemia in the pregnant patient?
Although both increase, Plasma volume increases more (45%) than red cell mass (25%)
Why is dilutional anemia good in pregnancy?
- Facilitates maternal and fetal exchange of nutrients, gases, and metabolites (decreased viscocity)
- Reduces the impact of maternal blood loss at delivery (500ml vag; 1000ml Csec)
What is autotransfusion mean during labor?
- The contracting uterus auto transfuses 300-500ml of blood which helps compensate for the maternal blood loss during labor
- This causes a further increase in CO up to 50% (SV increases so HR decreases to compensate)
What is aortocaval compression (supine hypotension syndrome)?
- Uterus compresses on IVC and lower aorta when the mom lies supine
- Reduces venous return and can decreases CO by 25%
How does the mom compensate for supine hypotension syndrome?
- Unanesthetised state-mom compensates with increase SVR and HR
- Also, blood begins to flow through collateral veins at the paravertebral venous plexous (including epidural veins)
- Mom can change position d/t symptoms she feels
What happens under anesthesia during supine hypotension syndrome?
- compensatory mechanisms aren't there so resultant hypotensioinReduced blood flow to kidneys, lower extremities, and to the uteroplacental unit, compromising the fetus
What are the s/s of supine hypotension syndrome?
N/V, pallor, anxiety, & sweating
How do we treat supine hypotension syndrome?
- Left tilt, RIGHT HIP ROLL
When is the MOST CRITICAL TIME for the paturient?
immediate post partum period when CO is highest and greatest strain on heart
Why is immediately after birth the most critical time?
The auto transfusion from the uterus, complete sudden relief of IVC obstruction, and high circulating endogenous catecholamines
Hematologic effects of pregnancy create a hypercoagulable state which helps limit blood loss during delivery. What two coagulation factors DON'T increase?
11 & 13 (board question)
What happens to oxygen consumption and minute ventilation during pregnancy?
Increases throughout and peaks at 50% above normal at end of 2nd trimester
How do we get the increase in minute ventilation in pregnancy?
TV increases 40% & RR increases 15%
Anatomic dead space is unchanged by physiologic dead space decreases during pregnancy, why?
- some non-functional alveoli improve because of the increased TV/MV
- This decrease narrows the arterial EtCO2 graident (more effective release of CO2)
Overall, alveolar ventilation is about ___% higher at the end of gestation
The arterial and alveolar CO2 tensions are decreased by this increased ventilation during pregnancy so what happens to the PaCO2?
Since PaCO2 decreases, the mom develops alkalosis, what happens to compensate for that?
- Serum bicarbonate decreases 15% as well
- Increase in maternal levels of 23DPG (because alkalosis causes left shift and we don't want the mom holding on to O2)
What is the Bohr effect
- At the lung, CO2 goes from blood to alveoli, so less pCO2 and less H+ in the blood because a decrease in blood carbonic acid
- Shifts the curve to the left which helps uptake of oxygen from the alveolus
- Opposite occurs at fetus, CO2 from fetus goes to mom's blood, increases carbonic acid in mom so increase H+ and right shift so it releases oxygen to the fetus
What is the Double Bohr Effect? (enhances the transport of Oxygen to the fetus)
- HgB carry more oxygen at a low PCO2 than at a high PCO2
- Fetal blood entering placenta has high PCO2 but it goes to mom's blood
- Transfer of CO2 makes fetal blood alkalotic and mom's blood acidic so mom's blood gets a right shift and releases oxygen easier to the fetal blood (which is relatively alkaline and has affinity for the oxygen)
How much does FRC decrease in pregnancy and what does that mean to us?
- Decreases 20%
- Reduction in oxygen storage capacity, combined with increased oxygen consumption, leads to a rapid desaturation in apnic parturient
Why is the pregnant patient difficult to intubate?
- Engorgement of resp mucosa predisposes the upper airway to trauma & obstruction during DL
- Gentle technique & small ETT is prudent
Why is the pregnant patient an RSI?
- Uterus causes gradual cephalad displacement of abdominal contents
- Incompetent gastoesophageal sphincter (d/t displacement and elevated progesterone levels)
- Placental gastrin secretion increases maternal gastric output
When are ALL PARTURIENTS considered an RSI?
All parturients are considered at risk for aspiration and subsequent Mendelson's syndrome after 8-10weeks gestation
What is Mendelson's syndrome?
Gastric contents >25cc with a pH <2.5
How do we pre-tx for aspiration risk?
- Non particulant antacid (30cc NaCitrate) prior to induction
- Reglan 10mg 15-30min prior to induction
- Zantac 150mg night before or morning of delivery
Renal Plasma Flow and Glomerular Filtration Rate increase then decrease, when does this happen?
- Begin to increase after the 4th month and by term they are elevated 50-60%
- Decreases in 3rd (D/t compression of aorta)
Elevations in renal blood flow and GFR result in increased creatinine clearance. Both blood urea and creatinine are reduced by ___%.
Why would you see glycosuria and/or proteinuria in the parturient?
Increased GFR overwhelms the ability of the renal tubules to reabsorb glucose and amino acids
Why do parturients have fluid retention (think renal)
increased levels of renin and aldosterone promote sodium reabsorption and thus fluid retention
Why should we be very cautious to check twitches after Succinylcholine?
Serum pseudocholinesterase falls during the first trimester and remaines low throughout gestation
Pregnancy enhances inhalation agent uptake by as much as ___% (MAC increase)
How does pregnancy increase inhalation agent uptake?
- 1) Increase in MV delivers more volatile agent into the alveoli per unit time
- 2) Parturients reduction in FRC favors rapid replacement of alveolar content with inspired agent
Why is there increased sensitivity to local anesthetic?
- d/t hormonally mediated or possibly r/t acid base changes CSF
- Also d/t engorged epidural venous plexus
The natural compensatory mechanism to offset obstructed venous return through these collateral veins has 3 efffects on the CNS, what are they?
- 1) Decreased CSF volume
- 2) Decreased potential epidural space
- 3) Increased epidural space pressure
The natural compensatory mechanism to offset obstructed venous return through these collateral veins has 3 efffects on the CNS, what do these changes do to epidural placement?
- Increase the cephalad spread of LAs
- Epidural catheter placement more difficult
- (higher incidence of dural puncture & epidural catheter migration into veins)
What alterations in IV agents do we see in pregnancy?
- Elimination 1/2 lifes are longer
- 45% increase in plasma there is a resultant greater volume of distribution
- Elimination 1/2 life of Thiopental is doubled
What maternal hormonal changes contribute to increased CNS sensitivity? (think nature's way to help in the birthing process)
- Progesterone (naturally sedating) increases 20x normal by term
- Endogenous opiate levels are also increased
- Beta endorphin levels surge as well delivery
What are the changes to the muscular skeletal system?
- Increased hormone Relaxin (secreted by the ovaries and placenta to prepare the mom for delivery)
- Relaxin softens the cervix, inhibits uterine contractions during gestation, relaxes the pubic symphysis, and pelvic joints
- Relaxin also contributes to back pain of pregnancy
Uterine blood flow accounts for __% of the maternal cardiac output
Uterine vasculature is already max dilated so autoregulation is absent, but what is it sensitive to??
- Uterus remains somewhat sensitive to ALPHA AGONISTS
- Extreme hypocapnia <20Torr also causes vasoconstriction
Blood flow to the uterus is directly proportionate to the difference between what two pressures? what is it inversely proportional to?
- uterine artery and venous pressures
- Inversely proportional to the uterine vascular resistance
What are the three major factors that decrease uterine blood flow?
- Systemic hypotension
- Uterine vascular vasoconstriction
- Uterine contractions
What are some common causes of maternal systemic hypotension?
- Aortacaval compression (supine hypotensive syndrome)
- Sympathetic blockade after regional anesthesia
How do we minimize maternal systemic hypotension?
- Ephedrine pre-tx (25mg IM)
- Epidural w/minimal LA concentration/vol + narcotic for pain control
- Right uterine dysplacement
- Oxygen supplementation
We should do frequent monitoring after epidural placement, especially for the first __min post-block
What causes uterine vascular vasoconstriction?
Caused by stress release of endogenous catecholamines (sympathetic discharge) or exogenous sympathomimetics
Why do uterine contractions cause decreased uterine blood flow?
decreased blood flow by elevating uterine venous pressure brought on by the increased intramural pressure of the uterus, this action even compresses the arterial vesssels in the myometrium (so transfers to the baby and cord as well)
How many arteries and veins are in the cord?
- 2 umbilical arteries
- 1 umbilical vein (vein visits the fetus)
What % of the fetus CO goes to the placenta (via the two umbi arteries)?
What are the villi in the placenta? (what is it's purpose)
- The villi are projections of fetal tissue
- The placenta blood goes to the capillaries in the villi where exchange occurs
- This is where the fetal blood is cleaned and oxygenated before returning to the fetus via the umbi vein
- Maternal blood goes through the uterine arteries into the large maternal sinuses surrounding and bathing the villus again where exchange occurs and then flows back into the uterine veins into the maternal systemic circulation
Umbilical blood flow is what?
At term is 120ml/kg/min or about 360ml/min
What are the 5 mechanisms by which substances are exhcanged across the placenta?
- Diffusion (Resp gases, fatty acids, small ions)
- Bulk flow (d/t hydrostatic or osmotic gradient-water)
- Active Transport (AA, water soluble vitamins, some ions)
- Pinocytosis (lg molecules, pinched off enclosed vesicles)
When might we see breaks in the plasma (which is when thin filmy villi may break off within the intervillous space and the contents may be extruded into the maternal circulation)??
When fetal Rh+ red cells are deposited in the vascular system of the Rh- mom
___% of uterine blood flow passes in to the intervillous space of the placenta while ___% supplies the actual myometrium of the uterus
Oxygen has the lowest storage to utilization ratio to the fetus but the fetus can survive up to 10min of oxygen deprivation, why???
- Redistribution of fetal blood flow to the brain, heart, & placenta
- Decreased oxygen consumption
- Anaerobic metabolism
Transfer of oxygen across the placenta is dependent on...........
- the ratio of maternal blood flow to fetal umbilical blood flow.
- Well oxygenated blood from the placenta has a PaO2 of 40torr (maternal is 95-104torr)
What 3 things aid in the oxygen transfer from mother to fetus?
- Fetal HgB is left shifted and Maternal is Right shifted (with increased 23DPG)
- HgB concentration in the fetus is about 50% more than the mother
- Double Bohr Effect
The HgB of the fetus is mainly fetal hemoglobin and is synthesized by the fetus prior to birth. Fetal HgB can carry as much as __-___ more oxygen than maternal HgB (left shift)
20-30%, this means that at at given PO2, the fetal HgB can carry as much as 20-30% more oxygen than the maternal HgB
What is the main goal of the fetal shunts?
to maximally perfuse the placenta and to bypass nearly all of the nonfunctional lung and liver
What are the three fetal shunts?
- ductus venousus
- Foramen Ovale
- Ductus arteriosus
What is the average oxygen saturation of the blood in the umbi vein; what about after it mixes with the ductus venosus?
80%; sats drop to 67% after mixing
What is the septum primum?
- A small valve located on the left side of the atrial septum that overlies the foramen ovale
- Helps to prevent blood from moving in reverse direction
The first breath of the newborn generates initial negative intrathoracic pressures in the range of __-___cmH2O
How much does the pulmonary blood flow increase from fetal to newborn?
5fold; because of vasodilation of the pulmonary blood vessels
Which shunt closes d/t pressure and which d/t O2 level?
- Foramen ovale closes d/t LA > RA pressure and so septum primum has blood forcing it to close the PFO
- Ductus arteriosus is closed when the muscular walls of the ductus arteriosus constrict because of increased oxygen in the area (fetal PaO2 20torr & newborn PaO2 100torr)
How does the ductus venosus close?
Not sure why but when blood flow through the umbi vein stops, the muscular walls of the ductus venosus contract strongly within 1-3 hrs and consequently the portal venous pressure rises from 0 to 10 torr, which forces blood through the liver sinuses
What is persistent fetal circulation (aka persistent pulmonary HTN)
- if the neonate experiences hypoxia or acidosis during first few days of life
- R->L shut across PFO or PDA causes more hypoxia and acidosis which causes more shunting, etc.
- ***Avoid acidosis and hypoxia!**
Who is more at risk for pregnancy induced HTN?
primigravidas uner 20yrs of age (under 20 have 5fold increased risk)
What is pregnancy induced HTN?
Multi-organ disease process primarily marked by an increase in BP (SBP>140/DBP>90)
What does HELLP stand for?
- Liver Enzymes
What are the potential maternal complications with pregnancy induced hTN?
- acute renal failure
- Cerebral hemorrhage
- Pulmonary edema
When does preeclampsia usually occur?
After the 20th week gestation
What end organ involvement is there in pre-eclampsia?
- hyperdynamic CV state: generalized vasoconstriction and increase in CO
- Plasma volume is decreased (hypovolemia)
- SubQ tissue edema (also CNS and larynx)
- Tissue hypoxia causes renal and hepatic dysfunction
- Decreased GFR and CC, lg amt of serum proteins are lost in urine
- Mild hepatic involvement (unless HELLP)
- Uterine activity is increased and the uterus can become hyperactive and markedly sensitive to oxytocin
When does severe preeclampsia progess to ecclampsia?
When seizures /convulsions occur
What might the initial stages of ecclampsia be? What happens next?
- mom may roll her eyes while facial and hand muscles twitch slightly
- Tonic stage occurs soon after the initial stage and includes twitching and teeth clenching, arms and legs go rigid, lasts for up to 30sec
- Clonic stage the spasm stops but the muscles jerk violently, these seizures can last up to 2min after which the patient may lose consciousness
What is the first priority in the eclamptic patient?
- to control convulsions
- Magnesium (2-4g)
- Benzodiazepines (Valium 2-5mg or Versed 1-4mg)
- Barbiturates (Thiopental 50-100mg)
- If not able to control seizures, GA is initiated to protect the airway and deliver the fetus
What is the main problem in HELLP?
- Activation of the coagulation cascade
- Cross linking of fibrin in the liver's sm. vessels leads to hemolytic anemia as the RBC pass through-plts are also destroyed this way
- Liver portal necrosis->elevated liver enzymes
What are the symptoms of HELLP?
- Gradual w/onset of HA, Blurred vision, N/V, "band pain" around upper abdomen and tingling in the extremities
- HTN may be seen but can be mild
- DIC is 20% of HELLP patients
What is the definitive therapy for pregnancy induced HTN?
- delivery of the fetus and placenta
- Maturation of the fetus is rate limiting factor so control of the disease is the 2nd best choice
Why is magnesium so good in the parturient?
Extremely efffective anticonvulsant, tocolytic, & mild vasodilator
How is Mg a good anti convulsant?
depression of the CNS & through cerebral artery vasodilation
Why is Magnesiums tocolytic actions so helpful in the parturient?
In PIH often see a hyperactive uterus so it helps with that but does not appear to be associated with prolongation of either induced or spontanous labor
How does Mg help lower BP?
depresses both smooth muscle contractions and CNS catecholamine release (results in lower BP and improved uterine blood flow)
What are the SE associated w/Mg?
Abnormal neuromuscular transmission resulting in maternal muscle weakness (including resp)
What type of analgesia can be helpful in pregnancy induced HTN patients?
Lumbar epidural analgesia (if it isn't contraindicated by coagulation abnormalities, maternal refusal, septicemia, and untreated hypovolemia)
What is the proper technique when placing a lumbar epidural in the pregnancy induced HTN patient?
- Management of HTN
- Eval for absence of coagulopathy
- Supplemental oxygen
- Adequate pre-hydration (500ml NS for T10 or 50-100ml of 25% Albumin)
What monitoring should be available when placing a lumbar epidural analgesia in the pregnancy induced HTN patient?
- Pulse ox
- Continuously recorded FHR/Uterine contractions
- Occasionally CVP
How can we convert a lumbar epidural for analgesia into a profound block for C sec? (what do we do to prepare?)
- prehydrate w/1-2L NS for expected T4 level
- Always have ephedrine available (2.5-5mg) to tx hypotension
How should we position the patient during GA?
displace the uterus off major vessels leading to and from the heart (usually a right hip roll to displace the uterus to the left)
What sedative do we use for induction in the parturient (think PIH, emergent C sec)
- Propofol or Thiopental but at reduced doses
- NO KETAMINE--contraindicated!
Do we need to use a non-depolarizing MR to defasciculate in a PIH patient undergoing emergency Csec?
No, Mg is already given
After the RSI, do we redose MR in the emergency Csec patient?
No, further use of MR is not usually required (decreased muscle tone)
How do we use our volatile in an emergent C sec?
- 100% oxygen and 1.5MAC for 1st min
- 2/3 MAC to 1/2 MAC after until the delivery of the fetus
Is the use of short term low concentrations of inhalation anesthetic drugs associated w/decreased uterine activity?
NO, it is not associated with decreased uterine activity, increased uterine bleeding, or neonatal depression
After delivery of fetus, how do we manage our anesthetic in a true C sec?
Opioids are further supplemented as tolerated and inhaled agents are reduced or eliminated (N2O or TIVA w/propofol)
What kind of extubation conditions do we want in the patient after emergency Csec?
Use opioids , magnesium, lidocaine, or (more frequently) anti-HTN agents usually BB
What are our concerns about the neonate born to the mother with pregnancy induced HTN?
- Usually born small for gestational age
- high risk for asphyxiation
- Drug depression
- Meconium aspiration
What are the immediate complications in the neonate after being born from a mother w/pregnancy induced HTN?
- respiratory distress
- instability toward maintaining body temp
- poor feeding
After delivery, the pregnancy induced HTN patient is still prone to convulse or develop pulmonary edema within ___hrs of delivery
Why might the pregnancy induced patient convulse or develop pulmonary edema even after delivery? What do we do to try and prevent it?
- the sympathetic block/analgesia from the epidural begins to dissipate
- Magnesium is weaned off over 48hrs
- Anti-HTN therapy is continued PRN