Induction And Analgesia Druing Labor Flashcards
Tocolytics vs oxytocics
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)
Myosin light chain kinase (MLCK)
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
General principles of tocolytic agents
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
Contraindications of tocolytic agent use
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
Two mechanisms of tocolytic agents
Decrease calcium/calmodulin complex availability
Increase phosphorylation of MLCK
COX inhibitors (indomethacin)
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
Nifedipine
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
Terbutaline and ritodrine
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
Atosiban
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!
Magnesium sulfate and nitric oxide
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)
Maternal factors that would signal indicated use for oxytocics/uterotonics
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
PGE2 and oxytocin
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
Dinoprostone and Misoprostol
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
Oxytocin
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
Non-pharmacologic methods for obstetric pain management
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
General principles of obstetric analgesia and anesthesia
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
Analgesia vs anesthesia
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
Trans placental drug transfer of analgesia
ONLY occurs with systemic agents
- this can cause CNS depression in the fetus
Non-systemic analgesia and major sites of placement
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
Risk of epidural analgesia
Prolongation of 1st and 2nd stages of labor
Higher numbers of instrumental deliveries and C-section rates for fetal distress
Maternal fever
Regional anesthesia blocks
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
Local anesthetic OD and toxicity
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
Pudendal nerve blocks
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
Anesthesia for C-section delivery
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
