Induction And Analgesia Druing Labor Flashcards

1
Q

Tocolytics vs oxytocics

A

Tocolytics = delay and prevent labor by reducing smooth muscle contractions

Oxytocics (uterotonics) = induce labor by promoting smooth muscle contractions

both pathways converge on myosin light-chain kinase (MLCK)

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2
Q

Myosin light chain kinase (MLCK)

A

Is essential in smooth muscle contraction

  • *myometrial cell relaxation is promoted by phosphorylation/inactivation of MLCK**
  • agonism of CRH, PGE2 and B2 receptors on the uterus all induce cAMP dependent phosphorylation
  • *MLCK is activated by Ca/calmodulin complex**
  • this induces contraction due to increased calcium levels
  • agonism of thrombin, oxytocin and PGF receptors promotes contraction
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3
Q

General principles of tocolytic agents

A

Used to arrest preterm deliveries

  • are 80% effective
  • usually only used between 24-34 weeks of labor
  • preterm deliveries are associated with neonatal respiratory distress syndrome, pulmonary HTN and intracranial hemorrhages
    • indicated when delaying delivery up to 48hrs is beneficial to the fetus and vertical dilation is not advanced**
  • generally are NOT indicated past 34 weeks gestation

are not agents used to decrease overall occurrence of preterm labor or alleviate complications

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4
Q

Contraindications of tocolytic agent use

A

note that tocolytic agents can only be used for 48hrs- 1week

Contraindications

  • previability
  • intrauterine fetal demise
  • lethal fetal anomaly
  • intrauterine infections
  • fetal distress
  • severe preeclampsia
  • vagina bleeding
  • maternal hemodynamically unstable
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5
Q

Two mechanisms of tocolytic agents

A

Decrease calcium/calmodulin complex availability

Increase phosphorylation of MLCK

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6
Q

COX inhibitors (indomethacin)

A

MOA: non-specific COX inhibitor/ antagonist tocolytic agent (used to block COX-2 in the uterus though but is not selective since selective agents have serious cardiac issues) which works to decrease available intracellular calcium
- 1st line treatment usually

ADRs:

  • inhibited platelet functions
  • nausea
  • GERD
  • emesis
  • fetal premature closure of the ductus arteriosus
  • fetal oligohydramnios

CONTRAINDICATED AFTER 32 WEEKS

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7
Q

Nifedipine

A

MOA: CBB blocker that is used for tocolytic between 32-34 weeks and also to treat maternal preeclampsia/eclampsia for its HTN properties
- 1st line if indomethacin is contraindicated or 32-34 weeks

safer than BB agonists which can cause cardiac damage (since Nifedapine doesnt affect nodal tissues)

ADRs:

  • peripheral vasodilator (headaches, flushing, dizziness, palpitations)
  • hypotension
  • NO fetal effects
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8
Q

Terbutaline and ritodrine

A

MOA: selective B2 agonists on the uterus to up-regulate cAMP phosphorylation of MLCK

  • terbutaline is also used for asthma treatments
  • both can be used as a 2nd-line agent for tocolytic use in 32-34 weeks gestation

ADRs:

  • tachycardia
  • hypotension
  • pulmonary edema
  • hypokalemia and hyperglycemia
  • CNS issues (tremor, headache, anxiety, sleep disturbances)
  • black box for maternal cardiotoxicity and death (due to also mild b1 agonism effects)
  • fetal tachycardia and hypotension
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9
Q

Atosiban

A

MOA: oxytocin receptor antagonists which work as tocolytic agent to decreased intracellular calcium and calcium/calmodulin complexes

Given IV only

Mimics the effectiveness of terbutaline but has fewer ADRs
- hypersensitivity is possible though!

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10
Q

Magnesium sulfate and nitric oxide

A

MOA: (magnesium) used as tocolytic agent to block calcium voltage-gated channels (similar to nifedipine). (NO) = used to activate PKG via increased cGMP signaling to up-regulate phosphorylation of MLCK

Are IM only and magnesium can also be used for preeclampsia

ADRs:

  • diaphoresis
  • flushing
  • magnesium toxicity (give calcium gluconate to protect)
  • fetal bone abnormalities for long-term exposure
  • adjust dose for renal impairment
  • *contraindications**
  • MG
  • cardiac issues present
  • hypotension (NO only)
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11
Q

Maternal factors that would signal indicated use for oxytocics/uterotonics

A
Preeclampsia (mild and severe) 
Eclampsia 
HELLP 
Poorly controlled diabetes (any) 
Chronic HTN 
Heart disease 
Intrauterine infection 
Augmentation of protracted labor 
postpartum hemorrhage due to uterine aTony
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12
Q

PGE2 and oxytocin

A

Are required for onset of parturition and are the most commonly used agents to promote cervical ripening

Produce dose-dependent increases in

  • uterine tone
  • frequency of contractions
  • intensity of contractions
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13
Q

Dinoprostone and Misoprostol

A

MOA: Both are PGE (PGE2 and PGE1 respectively) analogs used as uterotonic agents

Diniprostone = gel from that is administered intracervically or intravaginally
- remove 30 minutes prior to induction and induce with oxytocin

Misoprostol = tablets that are administered orally, vaginally or rectally
- allow for at least 4 hrs before induction with oxytocin

ADRs:

  • fetal bradycardia
  • fetal distress
  • nausea/vomiting
  • fever
  • peripartum infections
  • uterine hypertonicity and postpartum hemorrhage

Contraindications

  • history of asthma
  • glaucoma
  • MI history
  • unexplained vaginal bleeding
  • chorioamnionits
  • ROM
  • previous C-section
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14
Q

Oxytocin

A

MOA: directly agonist of oxytocin receptors on uterus which increases calcium/calmodulin complexes
- is enhanced by PGE2s

  • *always use lowest effective dose and precise IV administration with a continuous-infusion pump**
  • increase as needed every 30-60 minutes with a maximum of 20 mU/min

Always need constant observation

MUST discontinue If tachysystole of the uterus (> 5. Contractions/10 minutes) or fetal distress arises

ADRs:

  • serious toxicities below (super rare as long as you use low dose)
  • off target vasopressin receptor activation = excessive fluid retention and water intoxication (HF, seizures, hyponatremia, etc.)
  • excessive uterine contractions which causes transient placental blood flow reduction.
  • hypotension

Contraindications

  • fetal distress or malpresentations
  • placental abruption or risks of uterine ruptures
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15
Q

Non-pharmacologic methods for obstetric pain management

A

Continuous support during labor

  • provide best outcomes
  • proper number nurses, midwifes, coaches, educators (changes based on patient)
  • fewer operative vaginal or C-section deliveries
  • fewer requests for pain medication

Warm baths and acupuncture

little evidence for = acupressure, hypnosis, TENS, breathing techniques, but if it helps the psychology of the patient then go for it

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16
Q

General principles of obstetric analgesia and anesthesia

A

Psychologically prepared patients require less medications

Anticipate and addressed anxieties before and during labor

DONT promise painless labor

Treatment must be individualized to each patient
- variations in response, preference and adverse reactions in all patients

Know the limitations, ADRs and contraindications for all drugs that can be sued

17
Q

Analgesia vs anesthesia

A

Analgesia = loss of only pain perception

Anesthesia = loss of total sensory perception and potentially consciousness

both can be local or IV and are often combined

18
Q

Trans placental drug transfer of analgesia

A

ONLY occurs with systemic agents

- this can cause CNS depression in the fetus

19
Q

Non-systemic analgesia and major sites of placement

A

Indication = maternal request

Two main types:

1) Epidural analgesia
- catheter introduced into epidural space
- opioid and/or anesthetic administered
- less neurotoxicity
- increase3d risk for rapid absorption syndrome, postpartum backache and direct cardio toxicity

2) Spinal-epidural (intrathecal) analgesia
- injection of a single opioid bolus into the subarachnoid space followed by epidural catheter
- much faster onset and lower doses needed
- also lower risk of direct cardio toxicity
- risks = blockade of T1-T4 is reported which can cause hypovolemia and CHF (indirect cardio toxicity. the higher the block is place = great risk for cardiovascular complications
- increased risk for post spinal tap headaches

Both are patient-controlled analgesia with the epidural catheter
- major benefit is the patient controls analgesia and results in overall lower goal dose over the course of labor

20
Q

Risk of epidural analgesia

A

Prolongation of 1st and 2nd stages of labor

Higher numbers of instrumental deliveries and C-section rates for fetal distress

Maternal fever

21
Q

Regional anesthesia blocks

A

Types of nerve blocks on

  • lumbar epidural
  • subarachnoid block
  • combined spinal epidural block
  • pudendal block
  • *main drugs used are**
  • teracaine
  • Lidocaine
  • Bupicavine
  • chloroprocaine
  • ropivacaine

Anesthesia regional blocks are often mixed with narcotics to improve analgesia and reduce side effects**

Indications

  • labor analgesia a
  • C-section
  • obstetric operations that are intense
22
Q

Local anesthetic OD and toxicity

A

all are toxic if injected directly into vasculature

most are mixed with epinephrine also to increase the toxic dose threshold(make it safer)

Toxic central nervous system reaction = seizures

  • prodromal signs to this are tinnitus, diplopia, perioral numbness, deep and slurred speech
  • maintained airway and give 100% O2 sat
  • if convulsions = immediate IM injection of thiopental 50mg or midazolam 1-2 mg

Cardiotoxicity = ventricular tachycardia, cardiac arrest

  • bupivacaine is the #1 risk for this
  • treat with lipid emulsion infusions

Sympathetic block = hypotension
- coadminister with epinephrine to present this

23
Q

Pudendal nerve blocks

A

Injection of lidocaine into the pudendal nerve on each side
- achieves anesthesia for 30-45 minutes

Benefits

  • rapid onset
  • infant has no risk for depressed effects
  • blood loss is minimal

Risks

  • difficult to not puncture other areas
  • can show skip areas
  • discomfort with administration
24
Q

Anesthesia for C-section delivery

A

Most are performed with spinal, epidural or general anesthesia
- can still do this with the patients awake

Needs inhaled anesthetics, NMJ blockers and IV agents in combined

10% of mortality in C-sections are due to anesthesia and failure to incubate the trachea at induction of general anesthesia