Tocolytics and Uterotonics Flashcards
tocolytic drugs include
magnesium sulfate CCB's Beta adrenergic agonists nitric oxide donors cyclooxygenase inhibitors oxytocin antagonists
how do tocolytics inhibit labor
generation or alteration of intracellular messengers or inhibiting synthesis or block action of myometrial stimulant
magnesium sulfate MOA
alter calcium transport and availability for muscle contraction. compete with intracellular calcium, reducing myometrial contractility, hyper polarization of plasma membrane leads to inhibition of myosin light chain kinase activity. depresses motor endplate sensitivity, and muscle membrane excitability.
what does magnesium sulfate relax.
relaxation of vascular, bronchial, uterine smooth muscle. decreases SVR and BP. decreases fibrin deposition, improving circulation to visceral organs
what does magnesium sulfate treat
preeclampsia, seizures
neonatal SE from mag sulfate
hypotonia, respiratory depression. rare
tocolytic magnesium sulfate therapeutic range
4-9mg/dL (P-Q lengthened, QRS widened)
magnesium sulfate SE
decreased BP, antagonism of alpha agonist, potentiation of NMB drugs.
flushing, transient hypotension, palpitations, chest pain, nausea, blurred vision, sedation, pulmonary edema, skeletal muscle weakness, CNS depression, vascular dilation
Magnesium sulfate OD:
discontinue IV, secure airway, IV admin of calcium chloride, diuresis
magnesium sulfate anesthetic implications
exaggerated hypotension after administration of epidural or general anesthesia
succinylcholine dose is not reduced for intubation. defasciculating doses are not required. reduce maintenance doses of non depolarizing muscle relaxants.
symptomatic hypocalcemia and respiratory compromise have occurred in cases of myotonic dystrophy.
during spinal/epidural: block pain fibers, ANS. can’t vasoconstrict.
Nifedipine drug class and MOA
CCB, blocks influx of calcium ions through cell membrane. block release of calcium from SR. inhibit calcium dependent MLCK mediated phosphorylation (leads to myocetrial relaxation). also can act on K channels. when used as tocolytic, birth is delayed for 2-7 days
SE of nifedipine
hypotension, dyspnea, pulmonary edema, tachycardia, headache. enhances NMB effects affecting respiratory and cardiac function
Nifedipine anesthetic implications
expect hypotension with administration of neuraxial or general anesthesia. potential uterine atony that may be refractory to oxytocin and prostaglandins. both act through CCB’s.
what should be used if uterine atony occurs
methylergonovine (methergine) IV
B2 Agonists MOA and effects
smooth muscle relaxation. inhibition of myometrial contractility, increase in progesterone production. progesterone causes histologic changes in myometrial cells that limit spread of contractile impulses.
common B2 agonists used
terbutaline ritodrine (no longer marketed in US)
hazards of B2 stimulation
increase blood sugar and insulin levels in mom within a few hours, returns to baseline by itself in 72h
potassium is redistributed to intracellular compartment, lowering K levels to as low as 3mEq/L. returns to normal in 72h
neonatal hypoglycemia r/t increased insulin secretion in response to hyperglycemia. following delivery, glucose load from mother ceases leading to rebound hypoglycemia.
fetal tachycardia is common
SE of terbutaline
maternal and fetal tachycardia dysrhythmias ischemia hypotension p edema (rarely) headache hyperglycemia hypokalemia increased plasma renin and vasopressin
terbutaline anesthetic implications
delay anesthesia for 60 min to allow HR to decrease
if not possible, all drugs that increase HR should be avoided
treat hypotension with phenylephrine and ephedrine
which drugs increase HR
ketamine, atropine, glycopyrrolate, thiopental, pancuronium, etomidate.
Nitroglycerine drug class and MOA
nitric oxide donor. nitric oxide is necessary for smooth muscle tone. acts by increasing cycling guanosine monophosphate (cGMP)
inactivates MLCK causing smooth muscle relaxation.
SE of nitroglycerine
maternal hypotension, headache
NSAIDS drug class and MOA
cyclooxyrgenase inhibitors. converts arachidonic acid to prostaglandin H2 which is a substrate for tissue specific enzymes critical to giving birth. prostaglandins enhance formation of myometrial gap junctions. increase available intracellular calcium via raising transmembrane influx and sarcolemmal release, reduce prostaglandin levels by inhibiting cyclooxyrgenase enzymes which results in decreased uterine contraction
cyclooxygenase inhibitors of use
indomethacin (nonselective)
celecoxib (cox 2 inhibitor) (tocolytic efficacy equal to mag sulfate in preventing preterm birth within 48h.
