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70 Cards in this Set

  • Front
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Describe the hematological and cardiovascular changes in pregnancy and how they relate.
* Increased Progesterone causes prostaglandin release and arterial VD. This decreases SVR.
* DECREASED SVR causes mom to increase plasma blood volume via RAAS to maintain BP. CO also increases due to an increased preload/SV and a mild increase in HR. (It will gradually increase and will be highest just after delivery 180% due to cat release and autotranfusion of blood from contracted fetus.). After delivery, CO will return to normal in 2 weeks.
* INCREASED PLASMA BLOOD VOLUME will leads to a DILUTIONAL ANEMIA. (low Hgb and Hct). This offsets the blood loss in labor (300-500 mL for vaginal delivery, 500-1000mL for a C-section). This anemia is also compensated by the mother's right shift of the oxyHgb diss. curve. There is increased O2 extraction at the tissue level.
* At delivery, mom is in a HYPERCOAGULABLE STATE. There are increased fibrinogen, factor VII, and plts. This aids in stopping blood loss after delivery but also puts them at risk for DVT, PE, thrombosis, especially if they are bedridden.
*Increased CO will cause ventricular hypertrophy. An S3 Split or Grade I or II systolic murmur may occur. This is normal. But if it's a diastolic murmur, accompanied by chest pain, SOB or if it's a grade IIII or IV..get a cardiac workup.
* Edema occurs due to progesterones effect on capillary permeability.
* Baroreceptor sensitivity is increased, causing more lability of vital signs. (more tachycardia with HOTN). If pt is tachycardic after an epidural, consider BP drops.
* More dependent on RAAS to maintain BP. Do not preload mom more than 500-1000mL of fluid before an epidural...will knock out RAAS and accentuate the HOTN with sympathectomy.
* Increased clearance of vasopressin = increase urine output.
* Maternal MAP is the pressure head for placental blood flow. Therefore, maternal BP must be at least 100 to maintain blood flow to the fetus.
*Aortocaval Depression - when baby presses on Inferior Vena Cava and Abdominal Aorta when mom is LYING DOWN ONLY. This causes supine HOTN syndrome.
Describe Aortocaval Syndrome
When mom lies down, baby compresses on Inferior Vena Cava and Abdominal Aorta. Arterial blood flow is maintained via collateral circulation (paravertebral venous plexuses/ azygos vein). Venous return is reduced, causing decreased CO and supine HOTN. Venous blood stagnates in extremities, causing foot swelling, varicose leg veins, and an increased risk for DVT.
*Supine HOTN decreases uterine placental blood flow. SBP< 90-100 FOR MORE THAN 10-15 MIN CAN LEAD TO FETAL ACIDOSIS.
*The first sign of this HOTN is NAUSEA. (also sweating and AMS).
*Arterial blood flow back to the heart via the paravertebral venous plexuses will dilate epidural veins...putting mom at increased risk of venous puncture and hemmorhage with epidural placement.
*Epidural LA will pvt increased SVR with supine HOTN syndrome...be very careful of any signs of nausea and check BP.
* TX: Staged...
----1) HEAD UP!!!! OR SEMIFOWERS POSITION ASAP.
----2) PLACE MOM ON LEFT SIDE. DISPLACE UTERUS TO THE LEFT WITH A PILLOW (ELEVATE RIGHT HIP)
----3) Give volume (IVF)
----4) Give pressors (Ephedrine)
Pulmonary Changes with Pregnancy
* UPPER AIRWAY EDEMA - due to capillary engorgement. More prone to bleeding with intubation and a more difficult intubation. Use a 1/2 SIZE SMALLER ETT. to prevent post op stridor and edema. If this occurs, tx with racemic epi.
* Large breasts and edematous airway make a difficult intubation.
* Minute ventilation increased by 50% due to increase O2 consumption and metabolic demands. (Increased tidal volume in first trimester). This causes resting PaCO2 to decrease from 40 to 32 mmHg. (Pt will be slightly alkalotic due to hyperventilation...but the kidneys excrete more bicarb so pH stays w/n normal range.) Dec PaCO2 can also cause systemic VC, which can reduce uterine BF. A PaCO2 LESS THAN 20 WILL HAVE A NEG IMPACT ON THE FETUS!!!! GIVE MOM A BROWN PAPER BAG WHEN HYPERVENTILATING.
*DECREASED O2 RESERVE: Later in pregnancy: Diaphragm is forced cephalad causing decreased FRC (below closing capacity) , ERV, TV and RV. This causes atelectasis and a decreased PaO2. Mom increases RR to maintain minute ventilation and O2 levels. Right shift of oxyHgb dissociaton curve will increase unloading at tissues but will inhibit loading when preoxygenating. Mom also has increased O2 consumption - up to 33% more demand over baseline at term & 100% during Stage Two labor. All these things will make mom desat quicker on induction...makes intubation more difficult. You must preoxygenate longer.
*Conversely, the increase minute ventilation will allow for a FASTER inhalational induction. (MV increases up to 300% during labor....GET A BROWN PAPER BAG!)
Gastrointestinal Changes with Pregnancy
*HIGHER RESIDUAL VOLUME:
* INCREASED RISK OF ASPIRATION
* INCREASED RISK OF CHEMICAL PNEUMONITIS
*Progesterone decreases gastric motility. Displacement of pylorus cephalad by uterus delays gastric emptying...especially during labor.
* Progesterone decreases LES tone: premedicaid with antacids, H2 antagonists, zofran, and reglan. Avoid opiods, which will decrease gastric motility.
* DONT use cimetidine because it will inhibt CYP450's and decrease LA metabolism leading to toxicity.
* Sudden onset nausea - check BP...could be supine HOTN syndrome
Pharmacology and Altered Drug Responses of Parturient
* Sedative effects of Progesterone will require smaller doses of sedatives, local and general anesthetics. (MAC levels for mom are decreased).
* Increased sensitivity to local AND general anesthetics. (peripheral nerves more sensitives to LA's, less space for spread..can use smaller doses for epidurals. ).
* HOTN shoud be treated with IVF, then with Ephedrine.
* Neosynephrine should be used as a last resort tx of HOTN in mom...ONLY USE SMALL DOSES (40 mcg) GIVEN AT LARGE INTERVALS. This will pvt decreased uterine blood flow and reflex bradycardia.
* Do not give Ephedrine for a HR > 100.
* Fentanyl is the opiod of choice due to it's potency and short duration.
* Ketamine is good for sedation in parturients who are not preeclampsic. It helps maintain BP, is short acting, and has no resp depression. It DOES NOT decrease uterine blood flow.
* Oxytocin (pitocin) is used to induce labor and to contract the uterus after delivery (boggy uterus). It is GIVEN IV INFUSION ONLY. (can cause HOTN and stroke if given IV Push).
* Methergine is given IM ONLY to cause uterine contraction AFTER birth. (0.2 mg IM)
* Hemabate is given DIRECTLY INTO UTERUS or IM to stimulation contractions AFTER delivery. (250 mg)
* Terbutaline is a tocolytic given SUBQ to arrest preterm labor. It is the first line tx for preterm contractions. It is a selective beta 2 agonist. Can cause reflex tachycardia due to VD of skeletal muscle beds. Will also cause bronchodilation. (10 mcg/min, titrate to 80 mcg/min)
* Ritodrine is a tocolytic used to arrest preterm labor and can also be used to tx preeclampsia.
* Magnesium sulfate is tocolytic use to arrest RESISTANT preterm labor. This med can be given IV INFUSION ONLY and requires hospital admission, as pt's BP must be monitored.
Nervous System Changes in Parturient
* Sedation via progesterone
* Increased SNS tone
* Impaired upper airway reflexes increase aspiration risk.
* Decreased size of epidural space and decreased CSF requires smaller doses of LA for epidural (decrease by 30%).
* Dilated epidural veins increases risk of hemmorhage with epidural.
*Peripheral nerves more sensitive to LA.
Hepatic Changes in the Parturient
* DECR PLASMA PROTEINS (dilutional): Protein bound drugs will need smaller doses.
* DECR PLASM ACHESTERASE (dilutional): Increased duration of Succs, Esmolol, Remifentanyl, etc. (Tab says not relavant).
* INCR FIBRINOGEN, FACTORS, AND PLTS
Renal Changes in the Parturient
* GFR and RBF increased by 50%-60%.
* BUN and creatinine DECREASE by 50% (due to increased GFR and clearance).
* Small amts of glucose in the urine are normal.
* Mechanical obstruction of ureter can occur by uterus leading to stent placement.
Uterine blood flow is ___ mL/min or ___% of CO.
Uterine blood flow is 800 mL/min or 10% of CO.
What effects the ability of drugs to cross the placenta?
1) Amount of protein binding (must be free, unbound form to cross
2) Lipid Solubility: Only unionized form of the drug is lipid soluble and can cross the membrane. This is pH dependent (acidosis can cause more ionization. In the fetus this can lead to ion trapping of the drug). (NMB's will not cross because they are ionized.)
3) Size of the molecule (molecular weight). Must be < 500 daltons. (most meds are).
4) Concentration Gradient (ion trapping create a conc gradient for the unionized form...encouraging more to cross and toxifiying an acidotic fetus.).
What effects CO2/O2 exchange across the placenta?
It's PERFUSION LIMITED, not diffusion limited.

That means it's entirely dependent on MAP of mom and unobstructed blood flow of cord and placenta.
What problem occurs with epidurals...what danger can the LA pose to the fetus and what can you do about this?
LA's are weak bases. They are ionized at acidotic pH's. In fetal acidosis, they will cross the placenta in their unionized form and ionized in the fetus (fetal blood pH is acidotic compared to mom). This creates a conc gradient for more unionized form to cross over...leading to toxic doses in the fetus.

To prevent this, use an ESTER LA, one that is rapidly hydrolyzed in maternal blood before it can get to fetus. Example: Chloroprocaine...the fastest acting ester and shortest duration. 2- CHLOROPROCAINE is the drug of choice.

Or you can use dilute amts and add fentanyl.
What are some ways the the placenta and fetal circulation protect the fetus from toxicity of drugs that cross the placenta?
* Placenta dilutes the drugs in blood, buffering them.
* Drug is absorbed into placental tissue.
* Drug distribution in mom and fetal circulation will dilute it and partition it away.
* Shunting of blood via FA, DV, and DA keep drug from some tissues of fetus.
* Fetal liver metabolizes some drugs (barbs)

THE MAIN THING IS DILUTION.
Explain what happens in labor...the stages of labor. Explain the physiology of pain with labor. What are the two types of labor pain and how to treat them.
Stages of Labor:
STAGE 1: Starts with contraction and ends with full dilation (10 cm).
STAGE 2: From full dilation (10 cm) to delivery of the infant.
STAGE 3: From delivery of the infant to delivery of the placenta.

Pain causes excessive catecholamine release. Each contraction is like an autotranfusion of cats to mom. This causes VC and decreased BP to baby. It will also increase nausea and delay gastric emptying. ...puts mom at risk of aspiration!!!!!!!! MV increases by 300% due to increased O2 demands/ consumption. Hyperventilation can cause VC and decreased uterine blood flow. So each contraction potentially causes fetal hypoxia.

Labor Pains:
STAGE 1 LABOR PAINS = VISCERAL PAIN(from contractions to full dilation): Stimulation of unmyelinated C-fibers, travels via SNS up nerves from T10-L2). Associated with uterine ischemia (due to contractions) and cervical dilation. (can be treated with an epidural).
STAGE 2 LABOR PAINS = SOMATIC PAIN (from full dilation to delivery of baby): Stimulation of somatic pain fibers up the pudendal nerve (S2-S4). Associated with perineal and vaginal stretching and stretching of pelvic ligaments. (Can be treated with a saddle block).

*Start with an epidural in stage 1, then, at stage 2, sit mom up and infuse a LARGER VOLUME of LA to get to S2-S4 (hyperbaric).
Musculoskeletal Changes in pregnancy
* Increased lumbar lordosis to hold the baby. This causes a narrowing of interspinous spaces, making spinal or epidural placement more difficult.
Describe uterine blood flow and uterine changes in pregnancy
2 Uterine Arteries - supply BF to the uterus.

Uterine blood Flow increases to a max of 800 mL/min (10% of CO).

2 Umbilical Arteries: Take blood from fetus to mom. (Deoxygenated)

Umbilical Vein: Take blood from mom to fetus. (Oxygenated).

Perfusion limited: Decreases in mom's MAP or increases in placental vascular resistance will decrease fetal oxygenation.

A maternal SBP < 100 will cause fetal distress!!!! (this # is higher with preeclampsia).
Describe the two "modes" of pain perceived by women in the first stage of labor.
1) A non-localized cramping referred to the appropriate surface dermatomes on the abdomen from the level of the umbilicus to the inguinal ligament.
2) "Back Labor" - sharp localized back pain that results from referred pain to dermatomes (cutaneous innervation) and sclerotomes (innervation of bone and muscle). Sclerotomes are located several inches below the actual vertebral level of involvement, causing the pain of stage 1 to be felt over the L5-S1 region. . Can be tx w/ a lumbar sympathetic block, a pericervical block, or an epidural up to T10.
When should an H&P be performed?
BEFORE mom is in labor/ has labor pains.

If mom IS already in labor...get a thorough H&P before medicating for pain...it's better to know all you can and have a mom in pain then to medicate too early and not have a thorough history.
In a healthy paturient who desires labor analgesia, a preanesthetic evaluation should include the following additional information....
1) The extent of the pt's cervical dilation and percent effacement
2) The station of the fetal presenting part.
3) Fetal heart rate and it's degree of variability (require fetal heart monitoring preop)
4) Amniotic membrane (ruptured?)
5) Gestation age of fetus
6) Gravity (# preg) and parity (# live births) of mom
Why should you ask about a mom's last po intake?
Potential for dehydration due to N/V, HOTN with an epidural, fluid losses from hyperventiliation.
T/F Baseline labs are mandatory before inserting an epidural on mom.
False.
review of baseline labs is not mandatory unless mom has had no prenatal care or if there is a coexisting pathology.
Describe invasive and non-invasive fetal HR monitoring.
Non-invasive: Abdominal Ultrasound Probe aimed at fetal heart.

Invasive: Spiral Electrode inserted in utero 2mm from fetal scalp. This method requires a ruptured amniotic sac and a partially dilated cervix through which you can place the electrode.
What is the limiting factor of fetal oxygenation...uteroplacental blood flow or maternal oxygenation?
Uteroplacental blood flow (it's perfusion limited).
What is normal fetal HR and what is fetal bradycardia?
Normal HR = 120-160 bpm

Bradycardia < 120 (A hr DOWN TO 100 is well tolerated if it lasts less than 2 min.)(Fetal bradycardia <100 bpm is a cause for concern) (HR < 80 is severe regardless of the duration.)
What is the single best indicator of fetal well being?

Describe it thoroughly...
Fetal HR Variability

*Can only be ACCURATELY recorded with an INVASIVE fetal HR monitor. (monitor records the diff b/n r waves), but a noninvasive can also be used...just avoid artifacts.

*Baseline FHR variability increases w/ gestational age.

*Short term beat to beat variability (5-10 bpm change with every beat) (the instantaneous change in rate that occurs b/n two consecutive heartbeats.) is normal and reflects a healthy CNS with good responses and compensatory capacity.

*Long-term beat to beat variability (acceleration of the HR for short periods followed by a return to baseline HR) is associated with fetal movement. It is normal when the baseline HR varies by 15 bpm for 15s on a frequent and regular basis. Anything LESS than this is abnormal. (no fetal movement or activity).

Therefore, during sleep, beat to beat varibility continues but long term varibility will decreases for periods up to 40 min (baby is not moving).

*FHR varibility is indicative of FETAL RESERVE. Decreased beat to beat variability is seen with hypoxia, decreased MAP of mom, acidiosis, anencephalopathy, drugs (opiods), and fetal cardiac defects. It can also be a sign that the fetus is beginning to decompensate.

* A sinusoidal fetal HR pattern is seen with fetal anemia. (squiggles). This is associated with butorphanol (Stadol) - an opiod agonist used for labor pain. It can last for 1.5 hours.
Early Decellerations ....translate.
Slowing of fetal HR (20bpm) with the onset of contractions, returns to baseline when contraction is over.

They are uniform in appearance and have a loss of beat-to-beat variability with each contraction/deceleration.

Indicate head compression..which causes a vagal response. This is NORMAL as long as HR drops < 20 bpm.
Variable Decelerations ...translate.
Decelleration in HR that varies in occurence, onset, depth, duration, and appearance. (Just happen when and where they want to.)

Not uniform, do not occur after every contraction. Abrupt. HR can plunge 60 bpm in 2s.

UMBILICAL CORD COMPRESSION - causes a baroreceptor reflex.

Usually these are benign unless:
1) If HR decreases by 60 bpm from baseline
2) If HR drops below 60bpm,
3) if the decellerations are sustained for 60s or longer.
4) If beat to beat variability is absent.
5) If the variable decelerations occur for longer than 30 min.

**1) Place mom on left side and put head up, 2) Give IVF, 3) Give pressor to manage HOTN.
Late Decellerations....translate
Decellerations in HR with contraction that occur 10-30s after the onset of the contraction (lagtime).

They are smooth and regular.
Beat to beat variability may or may not be present.

UTEROPLACENTAL INSUFFICIENCY!! This will ALWAYS cause fetal hypoxia and acidosis. Pt needs an emergency C-section.

BE CAREFUL with an epidural in these pts....can cause HOTN and only increase the fetal distress!!!
Regional Anesthesia Types and Info
* Pre-hydrate with a 500 mL bolus of NS.
* Epidural spread is volume related so depends on where you put it in and how much volume you give.
*Can use the hanging drop or the loss of resistance technique to place.

*Commonly used drugs for epidural are bupivacaine (o.1%) and Ropivacaine (0.2%) because both of these cause a differential blockade. Both are given diluted.
*Bupivacaine has a longer elimination halflife (10.9 hours) and can become cardiotoxic.
* Ropivacaine has a shorter elimination halflife and is not cardiotoxic (it's the S-isomer of Bupicvacaine.) It also produces a better differential block. (it's less potent but less toxic.).
* A test dose will reveal subarachnoid or intravascular injection of LA w/o producing systemic toxicity or systemic block.
*Fentanyl is added to the solution to add analgesia (mophine is avoided because it is water soluble ..is not absorbed well by the neural tissue and can therefore spreadup to the brain...also not as short-acting.) Fentanyl allows you to give less LA, which decreases the amt of motor block.
* Chloroprocaine is used for spinal b/c of least risk of toxcity to the fetus.
* An epidural infusion with a loading dose ensures a steady state.
* PCA gives the highest level of pt satisfaction.
* After insertion check the level of block with an alcohol swab. Watch for nausea or fetal distress which could indicate HOTN.
* Saddle block - use when baby has crowned...hyperbaric lidocaine in sitting postion.
* Pudendal Block: give transvaginally behind the sacrospinous ligament for an episiotomy.
* Paracervical Blocks: in stage 1 of labor during cervical dilation...but assoc with bad fetal outcomes (bradycardia).
* A spinal is not desired because of the inability to titrate LA to effect. (but can be used in morbidly obese pts. ). A combined technique also works well, and spinal dose is given in Stage II.
* After given LA in a spinal, fetal bradycardia may occur...this is most likely due to the rapidly decreasing maternal catecholamines after the onset of analgesia.
* For an epidural, higher concentrations would increase the density of the block and cause a motor block..so you want dilute solution and large volumes to influence spread.
* For a spinal, you want hyperbaric solutions and smaller quanities. spread depends on curvature of spine and gravity.
Summarize important considerations for general anesthesia for cesarean section
*Denitrogenate for 3-5 min or 4 VC breaths.
* INduce with thiobarbital, propofol, ketamine, or etomidate. (Thiopenthal is the drug of choice for induction).
* Sux is okay. NMB's are okay (dont' cross placenta).
*Edematous airway will mean a smaller sized ETT.
* RSI induction due to increased gastric volume.
* Use up to 2/3 of MAC of volatile agent (however this will depress uterine contractility after delivery). Give Oxytocin to help it contract later. Get volatile agent off as soon as possible after delivery.

* If fetal distress is present or if maternal O2 saturation is below 97%, high concentrations of O2 should be used WITHOUT NITROUS OXIDE. Otherwise, use 50% O2 and 50% N2O b/c too much O2 is bad for the fetus.
* Use a Sux drip to paralyze or a NDMR (cannot cross placenta). But mom might not even need to be paralyzed d/t muscles being stretched out.
* The length of time from incision to delivery correlates with neonatal acidosis. Should not take longer than 3 min.
* After cord is clamped, if uterus contracts, you can leave the gas on and use some opiods and N2O at that point. If uterus is not contracting, turn off agent and give opiods and N2O.
*Give oxytocin as soon as placenta is delivered. (30 to 40 units over 1st hour). If thsi doesn't work give methergine, hemabate, or prostaglandins.
*Suction stomach with an OGT to prevent aspiration upon emergence.
Discuss important considerations for regional anesthesia for cesarean section
EPIDURAL
* Slower onset means less dramatic changes in BP. More time to tx the HOTN.
* Pain coverage is not as reliable/ intense as a spinal and does not cover upper levels of the spinal cord.
* Add epinephrine 1:400,000 conc to increase the duration of the block.
* Add Sodium Bicarb 1 mL/ 10 mL of LA to increase the onset of the block (increased unionized fraction).
* LA's used:
---> Lidocaine (2-3%)
---> Bupivacaine ( 0.5%)
---> Chloroprocaine (3%)
* Adding fentanyl can increase the intensity of the block.
* Don't forget left uterine displacement and a 500 mL fluid bolus preop.

SPINAL
* Hyperbaric solutions and smaller amts. (LA mixed with dextrose or glucose).
---> Lidocaine 5%
--->Bupivacaine 0.5%
---> Tetracaine 1%
* Add epinephrine 0.2 mg (1:1000 in 2 cc's ) to prolong duration.
* Add fentanyl to allow you to give less LA.
* YOu want blockage to T4.
* HIgh spinal: ring and pinky numbness - low cervical and diaphragm innervation is being effected. If pt stops breathing and has HOTN, Bradycardia...intubate and ventilate. Give 1 mg epi.
Describe the effects of inhalational agents on the fetus
All inhalational agents cause direct CNS and CV depressant effects on the fetus, and they have indirect effects by lowering maternal BP and decreasing perfusion.
Thromboembolism in the parturient is associated with
Bedrest
C-sections
Obesity
Increasing age or parity.
Symptoms of a PE
chest pain
dyspnea
hyperventilation
hypocapnia
coughing
hemopysis
distention of neck veins
Venous Air embolism
* Can occur with all types of delivery and is assoc with placenta previa.

*Air is entrained into open maternal venous sinuses in the uterine wall when the placenta separates or at the site of a surgical incision. ..gets stuck in the lungs.

S/S:
* Mill-wheel murmur detected over the precordium.
* Chest pain.
* Decreased ETCO2
* Dyspnea
* Elevated CVP.

Tx:
* PPV and 100% O2 via an ETT.
* D/C N2O - will expand the embolism.
* IVF to increase preload to overcome increased PVR.
* Left lateral position, head up traps air in right atrium..aspirate from central line if possible.
Amniotic Fluid Embolism
Associated with placental abruption. Most always fatal.
*Symptoms similiar to venous air embolism. with the addition of:

* DIC can occur even after survival of the embolism.
* Chill, shivering, anxiety, cough, dyspnea, cyanosis, tachypnea, pulmonary edema, cardiovascular collase.

* Tx: PPV and 100% O2.
* Immediate support of maternal circulation (epinephrine, dopamine).
* Tx for coagulopathy ASAP.
* Large volume infusion devices on hand in case DIC Develops.
Placenta Previa
Placenta has implanted in lower uterine segment and partially or completely covers the cervical opening.

Three types: Total, Partial, and Marginal.

* More common in women who have had it in the past. Increases the risk of placental abruption.

* S/S: PAINLESS BLEEDING - not large amts. DO NOT do a pelvic exam...this could cause sudden hemmorrhage..don't mess with the placenta at all!!

* Post partum bleeding is often increased as well b/c the lower uterine segment does not contract as well as the rest of the uterus.

*: Tx: C-Section!! Prepare for HEAVY blood loss. GETA preferred due to risk of heavy blood loss....don't want to increase the risk by potentially causing a spinal hemmorrhage as well.
Explain Placenta accretia, increta, and percreta.
Normally the placenta implants into the endometrium. With these..the placenta implants deeper and separation from the uterine wall will be difficult and can cause severe bleeding. More common in women with placenta previa and previous C-section.

Placenta accreta - implants ON the myometrium
Placenta increta - implants INTO the myometrium
Placenta percreta - implants completely THROUGH the myometrium.
Placental Abruption
Placenta begins to separate from the uterus before delivery. Bleeding behind the placenta occurs and can be CONCEALED. This jeapardizes fetal blood supply.

S/S:
* Abdominal Pain (painful bleeding)
* Hypertonic uterus (cramping)
* Concealed bleeding
* Fetal Distress adn or death.
* Can cause a thromboembolism or amniotic fluid embolism, leading to DIC, hemmorage, and death. (50% of cases).

* High incidence in women with HTN, smokers, and drugs abusers.
* Fetal death can increase mortality of mom.

Tx: Vaginal delivery may still be possible if mom is stable and no signs of fetal distress. Otherwise, with unstable mom or fetal distress - emergency C-section.

*DO NOT use regional anesthesia...potential for DIC coagulopathy exists and risk of fetal hypoxia will only be increased.
* Prepare for massive blood tranfusions (when the baby dies, maternal blood loss can be as much as 5 LITERS!!...this can be concealed blood. ) Also give large volume of crystalloids and colloids as needed.

* GETA with ketamine or etomidate for induction. (If uterus is hypertonic..DO NOT use ketmaine...will cause uterine contraction and fetal hypoxia.)
* Volatile agent will decrease uterine tonicity, but after delivery need to titrate it off to pvt boggy uterus. Give oxytocin after delivery.
Excessive postpartum bleeding is associated with
Uterine atony (boggy uterus...most common cause).
Placental retention (manually remove to stop the bleeding).
uterine abnormalities
lacerations of the delivery channel
Uterine inversion
Coagulopathies
Uterine atony (boggy uterus) is caused by

Treatment?
Multiparity
Prolonged infusions of oxytocin before delivery
Polyhydraminos
Mx gestation

Tx:
Fundal massage
Oxytocin
Methergine
Hemabate
IV prostaglandin
How to you relax the uterus for placental extraction of retained fragments?
Nitroglycerin

(give volume before to pvt HOTN).
Uterine Rupture
Happens during vaginal delivery in a woman who has had a prevous C-section. Also has a high incidence in cocaine abusers.

S/S Sudden severe tearing and abd. pain. ...so bad you feel it with an epidural. Labor will cease and SHOCK and FETAL DISTRESS will rapidly develop due to severe bleeding. (800 mL/min) lost. Fetal mortality is 80%. This is the cause of death from hemmorage for 50% of moms.

*Most common sign is an ABNORMAL FHR TRACING.

TX:
* Emergency C-section adn hemostasis.
* Prepare for massive blood transfusions.
Emergency C-section and Hysterectomy Anesthesia
Trauma Anesthesia - primary purpose is the maintain vital signs adn perfusion, oxygenation...forget amnesia and analgesia.

Use Etomidate, Ketamine, Benzo's, and opiods...they cause minimal hemodynamic depression. CONVERT A REGIONAL ANESTHESIA TO GENERAL ASAP!!...RSI induction.
Disseminated Intravascular Coagulation
DIC - a generalized activation of the clotting system. ...large vascular damage or thromboplastic material in circulation. ...starts with some type of infection or foreign substance in the blood.

* Three causes:
1) Retention of a dead fetus
2) Placental abruption
3) Amniotic Fluid Embolism.

*Accompanied by circulatory shock due to uncontrolled bleeding because of consumption of clotting factors. Decreased fibrinogen, plts, increased fibrin degradation product.s

Tx:
1) Aggressive IVF - dilutes the clotting factors and slows the process. It increases hepatic and peripehral perfusion, pvting cell damage there. Hepatic perfusion increases clearance of the clotting factors.

* DO NOT give clotting factors!! will fuel the effects.
Breech Postion delivery Anesthesia..
C-section is preferred but is elective.

If vaginal delivery...use regional anesthesia for muscle relaxation and analgesia.

Will have more blood loss than a normal delivery due to forceps and birth canal tears. .
Mx Gestation Delivery Anesthesia
RISKS:
*Aortocaval compression is magnified. ...left uterine displacement a priority.
*Risk of need for emergent C-section..be prepared.
*Usually babies are premies.
* Risk of boggy uterus post delivery due to stretched out muscles...need to use larger than usual doses of oxytocin. (DO NOT GIVE UNTIL ALL BABIES ARE DELIVERED.)

VAGINAL DELIVERY: an epidural is required...must relax the birth canal as much as possible.

C-SECTION: regional or general anesthesia is appropriate.
Prolapsed Umbilical Cord
Cord protrudes from cervix ahead of the fetus...compression can cut off blood flow to fetus.

Tx:
1) Get pt off the cord. Put it back in the uterus if possible (as long as fetus is not in distress. Anesthesia will be needed for uterine relaxation (epidural).
2) If fetal distress is present...emergency c-section.
Preeclampsia
1) HTN (BP> 140/90 or more than 3o above systolic baseline or 15 above diastolic baseline.)
2) Proteinuria (1+ or 2+)
3) Edema
AFTER the 20th wk of gestation. (Dx is made when 2 of the 3 signs are present).

SEVERE PREECLAMPSIA:
* BP> 160/110
* Proteinuria (3+ or 4+)
*Urine output < 20 mL/hr
* Blurred vision or altered mentation
* Pulmonary Edema
* Epigastric Pain

The severity of the HTN parallels the severity of the disease. Preeclampsia increases mother, fetal, and neonatal morbidity and mortality. Most common in primigravidas < 20yrs old or > 35 years old or those who have had preeclampsia in the past.

MECHANISM: unknown. Involves an abnormality in the ratio of thromboxanes (more) to prostacyclins (less). Thromboxanes are potent VCrs & plt aggregators. Prostacyclins are VDrs and plt inhibitors. These are both produced by the placenta during pregnancy.

Maternal mortality -Main cause is CEREBRAL HEMMORAGE due to HTN. Other causes are pulmonary edema, renal failure, hepatic rupture, cerebral edema, adn DIC. (Brain edema can cause seizures and an increase sensitivity to depressant drugs.) Seizure - eclampsia.

Fetal death: due to PLACENTAL ABRUPTION OR INFARCT.

Tx: Deliver fetus!!!
Preeclamptic pts have increased levels of what plasma agent?
Thromboxane A2

Levels are correllated with disease severity. (So is BP).
Describe the pathophysiology of preeclampsia
Abnormal ratio of Thromboxane A2 and prostacyclin. (Too much thromboxane).

*increased vascular permeability results in extravasation of fluid and protein (proteinuria.)
* HTN causes decreased blood volume...fluid contraction by 40%.
* Vascular damage from HTN causes increased risk of thrombus, DVT, stoke, and DIC.
* Mx organ system dysfunction d/t HTN.
* Total body water is increased due to edema
* Marked peripheral and end organ vasoconstriction.
* Increased vascular sensitivity to ADH, ANG II, and catecholamines.
* Increased catecholamine levels....decreased perfusion to uterus, placenta, and fetus.
* Increased SVR and left ventricular work.
* Low/ normal CVP due to contracted blood volume.
* Wedge pressure is high due to increased SVR and does not correlate with CVP.
* Placental perfusion may decrease by 70% !!!!! This can cause INTRAUTERAL GROWTH RESTRICTION, FETAL HYPOXIA, AND PLACENTAL INFARCTION.
* below normal plt function, but increased plts.
Tx for preeclampsia:
Magnesium Sulfate helps but DELIVERY OF FETUS is the only way to cure preeclampsia. It is a tocolytic, causes venodilation, mild CNS depression, and a decrease in the rate of fibrin.

*If fetus is under 37 weeks or delayed development..delivery is delayed for development.

Mg sulfate decreasing fibrin deposition pvts further decay in organ perfusion and often greatly decreases liver pain in parturients with HELLP syndrome.

Continue Mg sulfate after delivery b/c preeclampsia can continue for days after delivery.
What type of anesthesia should you use for preeclampsia and delivery of fetus?
Epidural

Helps control maternal HTN and may improve maternal bloodflow.
Avoids stimulation of induction, which can increase BP.

Reconsider if plts are < 100,000...this only happens with severe preeclampsia.

Avoid HOTN, HOTN will occur at higher #'s for women who are severe preeclampsics.
What type of anesthesia is best for vaginal delivery with preeclampsia?
Epidural with bupivacaine.
What would cause you to have to use GETA for a C-section with a preeclamptic pt?
Coagulopathy or a decay in maternal or fetal condition.

Becareful with induction!!! Can increase BP and cause a cerebral hemmorhage...can be lethal.

Airway Edema will make the intubation difficult.

Give FENTANYL before induction to attenutate the sympathetic response.

Labetalol can be given before induction to pvt the HTN.

Other drugs that can be used are
Hydralazine (not for emergent cases though).
Nitroglycerin (quick onset)..does not cross placenta.
Esmolol at low doses only. (high doses cross the placenta causing fetal bradycardia).
What is special and NDMR's and preeclamptic women?
NDMR's are markedly potentiated in women with preeclampsia and therapeutic levels of magnesium.

Half the normal dose will cause a 100% block.

Why??
What is HELLP Syndrome?
Hemolysis
Elevated Liver Enzymes
Low platelets

Occurs in the most severe cases of preeclampsia. they have acute epigastric pain, proteinuria, jaundice, N/V.

DIC can develop.
What gas is a tetrogen?
Nitrous oxide.
Fetal viability occurs at how many weeks gestation?
26 weeks.
What are therapeutic levels of MgSo4
4-7 mEq/L
What does magnesium sulfate to to NMB's?
Makes the patient MORE sensitive to NDMR's and LESS sensitive to sux.
What effect can a epidural hematoma have on a spinal or epidural block?
It can cause a prolonged block.

Time becomes of the essence...the longer the microcirculation the peripheral nerve is impaired, the more the risk of permanent damage.
HOw long should you d/c coags before sx?
Heparin: 6 hrs before
Coumadin: 3-5 days before
LMWH: 12 hrs before.
What post partum problems can MgSO4 cause?
Prolonged NM blockade. (increases their risk of resp distress and aspiration).

May need to keep intubated and sedated in ICU until it wears off.

S/S of preeclampsia can last days or hours post partum.
MgSo4 can last 24 hours postpartum.
When would you want to give nitroglycerin sublingual?
Shoulder distocia - need relaxation in the pelvic floor to get the baby out. (Can also give a perineal epidural with nesicaine.

Retained placental fragments.
Discuss management of the HIV Positive/AIDS parturient
60% is transferred during labor (intrapartum).
40% is via breastfeeding.

Solution: zidovudine given pre-partum will decrease the risk of this transmission.
Smoking/ Tobacco and pregnancy
20% of pregnant women smoke during pregnancy.

Can cause: miscarriages, intrauterine growth retardation, increased risk of premature rupture of membranes, placental previa, abruption placentae, preterm delivery, impaired respiratory function in newborns, and sudden infant death syndrome.

Nicotine induced vasoconstriction - decreased placental blood flow.

Doesn't effect anesthesia.
Opiod addiction
Mom can have hepatitis, endocardititis, thrombophlebitis.

Increased risk of developing preeclampsia and third trimester bleeding.

Precipitated withdrawal with Naxolone.

Management: Opiod use throughout surgery.

Neonates will have neonatal abstinence syndrome.
Marjiuana
THC crosses the placenta.

Preterm labor.
Growth retardation.
Cocaine
Congential anomalies, premature labor, growth retardation, abruptio placentae,

HTN, tachycardia, MO

Avoid beta antagonists - can worsen the HTN due to unopposed alpha stimulation.

Anesthesia depends on pt and planned delivery.

Regional anesthesia would only increase the systemic toxicity, especially amides. .