Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
33 Cards in this Set
- Front
- Back
What are the hypertensive disorders of pregnancy?
|
Gestational HTN-b/p >140/90, with no proteinuria (after 20 weeks)
Preeclampsia Eclampsia Superimposed preeclampsia Chronic HTN |
|
What is preeclampsia?
|
Syndrome of pregnancy induced HTN, proteinuria, generalized edema, sustained SBP>140, 300mg or protein in 24 hr collection, S/S appear after 20weeks gestation, resolves 48 hours after delivery
|
|
What causes preeclampsia?
|
Occurs only in the prescence of placental tissue, endothelial cell dysfunction central to pathogenesis-pt. produces deficient levels of vasodilator prostacyclin & excessive levels of vasoconstrictor thromboxane, vasospasm central to physiology of preeclampsia; trophoblass (outermost layer of placenta) fail to implant into spiral arteries=hypoperfusion=endothial damage/vascular hyperreactivity=maternal HTN & decreased placental perfusion
|
|
How does preeclampsia impact the patient'S CV & RESP SYSTEMS?
|
CV: HTN d/t generalized vasoconstriction, increased SVR, hemoconcentration, hypoalbuminemia; Pulmonary: low colloid oncotic pressure d/t hypoproteinemia and increased vascular permeability, increasaed risk of pulmonary edema and difficult airway;
|
|
How does preeclampsia impact the patient's CNS, Renal, Hepatic, Hematologic systems?
|
CNS: vasospasm +/- cerebral edema can cause visual disturbance, H/A, hyperreflexia; Renal: decreased GFR, RBF, proteinuria; Hepatic: risk of hepatic hematoma, rupture; Hematologic: hemoconcentration, thrombocytopenia, increased fibrinolysis
|
|
What causes the maternal HTN in preeclampsia?
|
Placental ischemia leads to the release into maternal circulation of vasoactive substances (thromboxane, renin, angiotensin, aldosterone, catecholamines, and thromboplastin) which increase maternal B/P
|
|
What is eclampsia?
|
Seizures associated with pregnancy induced HTN; treat with magnesium sulfate
|
|
What is HELLP syndrome?
|
Hemolysis, Elevated Liver enzymes, Low Platelet count
|
|
When does HELLP syndrome occur?
|
Before the 36th week of gestation, dx is indication for delivery
|
|
What are the signs of severe preeclampsia?
|
Hypertension >160/110, oliguria <500ml/d, pulmonary edema, hepatic tenderness, proteniuria, systemic edema, CNS dysfunction, HELLP syndrome
|
|
The most serious complications of pre-eclampsia are?
|
Pulmonary edema, renal failure, airway obstruction, cerebral hemorrhage, DIC, cerebral edema
|
|
What are the two leading causes of maternal death in preeclampia?
|
Cerebral hemorrhage, pulmonary edema, (then renal failure, DIC, airway obstruction)
|
|
How does preeclampsia effect circulation?
|
Protein content is decreased, intravascular space is contracted, usually not under filled, associated vasoconstriction d/t increased renin, angiotensin, & aldosterone
|
|
What is the impact of pre-eclampsia on the uteroplacental circulation/
|
uterine vascular resistance increases d/t vasculitis=decreased uterine blood flow
|
|
In the preeclamptic patient what is the best test to evaluate bleeding?
|
PT/PTT, platelets, fibrinogen, & FSP
|
|
Which drugs are used to control B/P in the preeclamptic patient?
|
Hydralazine, SNP, Trimethaphan, NTG, Labetolol, Nifedipine, Methyldopa, diazoxide
|
|
What are the concerns when giving SNP or NTG to preeclamptic patients?
|
SNP can cause cyandie toxicity,
NTG can be unpredictable, In patients with HTN & low PAOP, SNP or NTG can precipitate profound decrease in B/P |
|
Why is hydralazine used so commonly in preeclamptic patients?
|
Hydralazine can reduce maternal B/P and increase uterine blood flow simultaneously
|
|
Which anti-hypertensive techniques should be avoided in the preeclamptic patient?
|
Esmolol should NOT be used, adverse fetal effects;
General or regional anesthetics should NOT be used to reduce the B/P in this population |
|
What is the drug of choice to control preeclampsia?
|
Magnesium Sulfate
|
|
What are the normal serum levels for Magnesium Sulfate?
|
Norm: 1.4-2.0mEq/L
Therapeutic range for preeclampsia/eclampsia is 4-7mEq/L; (divide by 0.8 to convert mEq/L to mg/dl); Loading dose 4-6gm over 20min; gtt 2-3gm/hour |
|
In order of prgression, what are the signs of hypermangnesemia?
|
Least-to-worst: decreased deep tendon reflex (DTR), ECG changes, somnolence, loss of DTR, heart block, respiratory arrest, cadiac arrest
|
|
If the patellar reflex is absent in patients on Magnesium Sulfate what can happen to the patient?
|
Heart block
Ventilatory failure Cardiac arrest |
|
How does MgSO4 work as an anticonvulsant?
|
increases the seizure threshold by decreasing the presynaptic releaseof acetylcholine and reducing the sensitivity of post synaptic receptors to Ach; can also act as NMDA receptor antagonist
|
|
The patient shows signs of MgSO4 toxicity, should you give Ca+?
|
IV Ca+ gluconate should be given only if supportive therapies are ineffective; it reverses magnesium toxicity but increases risk of seizures; supportive measures first (intubation)
|
|
Does magnesium toxicity impact the neonate?
|
Yes, it can cross the placenta, neonate can be somnolent, atonic, and need ventilation assistance
|
|
What is the definitive treatment for preeclampsia?
|
Delivery of fetus and placenta
|
|
Considering pt. hx (preeclampsia)-which anesthetic technique is most appropriate?
|
CLE, SAB, or GA can be used, CLE best choice
|
|
When is GA appropriate for delivery of a preeclamptic?
|
coagulopathy present, fetal distress,
|
|
What issues complicate fluid management in preeclamptics?
|
plasma volume may be decreased in preeclampsia-filling pressures maintained by increased capacitance, colloid oncotic pressure is reduced, capillary permeability is increased
|
|
What induction agent should be AVOIDED in PIH patients?
|
Ketamine
|
|
How does Magnesium Sulfate interact with muscle relaxants?
|
It increases sensitivity to both depolarizing & non-depolarizing
|
|
How long should you continue MgSO4 after delivery?
|
24-48hrs d/t risk of seizures remains
|