Obstetrics Flashcards
Cardiovascular and respiratory changes associated with normal pregnancy?
CV
- Increase CO
- highest CO right after delivery d/t autotransfusion of empty uterus that now contracts and release of aorta-caval compression (baby not on IVC now)
RISKY time for CV hx pts (ex: fixed valvular stenosis/pHTN) → huge sudden increase in CO
- Decrease SVR, SBP
- S1 and S3 toward end pregnant
- Left axis deviation
- Left ventricular hypertrophy
- Aortacaval compression- uterus sitting on IVC → decreases BP
- Hypercoaguble state - increase fibrinogen, factor 7
- Gestational thrombocytopenia d/t hemodiluation
Respiratory
- Decrease FRC, arterial CO2 tension
- Increase mV, alveolar ventilation, O2 consumption, CO2 production, arterial O2 tension
- Capillary engrogement causing difficult AW
Effects of pregnancy on:
plasma volume?
total blood volume?
hemoglobin?
fibrinogen?
serum cholinesterase activity?
plasma volume- increase 40-50%
total blood volume- increase 25-40%
hemoglobin- dilutional decrease. 11-12 g/dL normal in pregnancy
fibrinogen- increase 100%
serum cholinesterase activity- decrease 20-30%
Effect of pregnancy on blood volume/composition?
Increase intravascular fluid volume in 1st trimester
- Rising progesterone levels → increased RAAS
- more Na reabsorption → H2O retention
Albumin – 25 % dec
Total protein- 10% dec
- decrease colloidal osmotic pressure
Plasma volume 50% increase→ prepare for BL during delivery
- Blood volume normalize 6-9 Postpartum
What is the impact of aortocaval compression during pregnancy?
Uterus sitting on IVC → decrease BP
- Supine hypoTN syndrome – decrease MAP > 15 mmHg w/ increase HR > 20bpm
- CV sig changes:
- diaphoresis
- N/V
- mental status change
- Tx: LUD position (elevate R hip 10-15 cm w/ wedge/tilt)- anyone after 20 wks
- Prevents hypoTN and increase fetal BF
Airway changes during pregnancy and anesthetic implications
- Capillary engorgement
- DAW
- Avoid instruments
- Most expert
- Small ETT
- Position optimal
- Decrease FRC… → reserve dec
Coagulation changes during pregnancy?
- Hypercoagulable state → increase fibrinogen, factor 7
- Factor 11 & 13 decreased
- ATIII, Protein S- decreased
- Protein C- unchanged
- Plt normal- but dec 10% d/t dilutional effect
- Gestational thrombocytopenia -d/t hemodilution and rapid plt turnover
- r/o: ITP, hemolysis, elevated liver enzymes, HELLP → do TEG on at risk pt
- PLT usually not < 70k unless problem
- Normal pregnancy: PT and aPTT decreased by 20%
What are the physiologic effects progesterone has on a pregnant mother?
- Increase RAAS Activity –> increase BV –> increase CO
- Vascular Muscle Relaxation –> decrease SVR & PVR –> increase BF
- increase mV (Vt > RR) –> decrease PaCO2 –> Kidneys secrete Hco3 to preserve pH
Describe the stages of labor and the pain innervation associated with those stages.
Stages of Labor (3)
-
First
- Start: regular painful contractions
- End: complete cervical dilation
- Length: ~ 2 - 20 hours
-
Second
- Start: complete cervical dilation
- End: birth
-
Third
- Start: Birth
- End: Placenta delivery
-
Fourth (New)
- Placenta to hemostatic stabilization
Labor Pain
-
1st Stage - visceral
- Cervical distention and stretching of lower uterine segment
- Latent phase: T10 – T12
- Active Phase: T10 – L1
- Non-specific nociceptor – unmyelinated C fibers
- Visceral afferent fibers travel w/ sympathetic nerve fibers to uterine & cervical plexus and then through hypogastric & aortic plexus
- Cervical distention and stretching of lower uterine segment
-
2nd Stage – somatic
- Mediation:
- Pudendal nerve (S2-4)
- Somatic afferent fibers – myelinated A delta
- Pain impulse from perineum, pelvic floor, vagina
- Mediation:
Inhaled Anesthetics and pregnancy
N2O
- Onset immediate
- duration minutes
- minimal effect on mother/fetus, may only be partially effective
- Impact on B12 synthesis
VA:
- MAC reduced up to 40% d/t progesterone
Regional anesthesia options for labor pain?
- Spinal opioids alone
- Single vs intermittent injection
- Good in high-risk patients – cardiac patients
- Local anesthetic +/- opioids
- Epidural
- Local only vs. local + opioids
- Dural puncture epidural can inadvertently do CSE and do wet tap and do this technique unintentionally
- Place epidural – puncture dura with spinal needle
- Bolus epidural
- Risks: typically these are result of wet-tap (unintentional tech)
- Epidural
- Combined spinal epidural (CSE)
- frequent technique for quick analgesia and follow up with epidural for continued labor
- Walking epidural – low dose local +/- opioid intrathecal
- Thread epidural catheter – initiate epidural at later moment
- Uses: quick analgesia and need bolus epidurals after
- Saddle block – pudendal nerve (somatic pain)
- Bupivacaine 2.5 mg and fentanyl 25 mcg
DOSING: Decreased!
- Neuraxial req reduced by 40% at term
- Epidural veins distended
- Volume of epidural fat increases
- → increases size of epidural space/volume of CSF in SA space → more spread
Considerations for fetal heart rate monitoring? tachycardia? Bradycardia?
- Follow:
- Baseline HR (120-160 bpm)
- beat to beat variability
- FHR pattern
- Baseline
- Normal varies between 120 -160 BPM
-
Fetal Tachycardia- fetal distress
- > 160 BPM
- Fetal hypoxia
- maternal fever
- sympathomimetic drugs
- fetal anemia
- fetal cardiac anomalies
- > 160 BPM
-
Fetal Bradycardia (more ominous)
- < 100 BPM
- Fetal head compression
- umbilical cord compression
- sympatholytic drugs
- prolonged hypoxia
- fetal cardiac anomalies
- < 100 BPM
What are some various fetal heart rate patterns?
- A. Early Decelerations
- Fetal head compression → baroreceptor activation
- Uniform in nature – mirrors contraction
- ~ 10 – 40 beat/min –NOT associated w/ fetal distress
- B. Late Decelerations
- Uteroplacental insufficiency
- Decrease FHR at or following peak of uterine contraction
- Decrease varies b/t 10 – 20 beats/min
- Gradual and smooth return to baseline
- can be concerning
- C. Variable Decelerations
- Most common fetal pattern
- Variable in onset, duration, and magnitude
- > 30 BPM
- Variable in onset, duration, and magnitude
- R/t cord compression
- Associated with: FETAL HYPOXIA
- FHR declines < 60 BPM
- lasts > 60 seconds
- persists > 30 minutes
- Most common fetal pattern
- Late decels and ominous variable decels → emergent c/s
Category I, II, III FHR intepretation system?
Catergory 1:
- All of the following:
- Baseline rate 110-160 bpm
- Baseline FHR variability moderate
- Late or variable decels- absent
- early decel present or absent
- accelerations: present or absent
Catergory 3:
- Absent baseline FHR varaibility and any of the following:
- recurrent late decels
- recurrent varaibile decels
- bradycardia
- sinusoidal pattern
- concerning and need to go to OR
Catergory 2: all FHR tracings not categorized as I or III.
Preop considerations for elective c-section (from coexist)
- Preoperatively
- History/Physical
- Airway evaluation
- Informed Consent
- LUD (left uterine displacement)
- > 20 weeks – Aortic Caval Syndrome
- IV access (free flowing 18-16 gauge)
- Hydration (minimal 500 mL)
- Aspiration prophylaxis (bicitra, metoclopramide, ranitidine)
- Supplemental O2
- Anesthetic plan/ postoperative analgesia plan
- History/Physical
- Choice of anesthetic depends on
- Indications for surgery
- Degree of urgency
- Maternal status
- Condition of fetus
- Desires of the patient
- Sometimes too emergent → put to sleep
Anesthetic plan for preop/induction emergent c-section? (coexist)
- Preop assessment of airway
- Large bore IV
- Aspiration prophylaxis (Non-particulate antacid, H2-blocker, Reglan)
- Monitors/suction/ emergency airway cart
- Optimal airway positioning/ LUD
- Preoxygenate! (3 min or longer)
- Prep + drape –surgeon ready
- RSI w/cricoid (10 N while awake; inc to 30 N after LOC) → start putting force before even asleep
- Agents available
- Ketamine (used with maternal hypotensive crisis) 1 mg/kg
- Etomidate 0.3 mg/kg
- Propofol 2-2.5 mg/kg
- Succinylcholine 1-1.5 mg/kg
- Preferred muscle relaxant
- Smaller ETT- 6.0, 6.5
- Glidescope
Intubation considerations for emergent c-section? What happens immediately following intubation?
- Intubate
- Expect difficult intubation
- Proper positioning
- Short handled laryngoscope (Datta) recommended
- Use minimal amount of time; first attempt best attempt
- Smaller ETT 6.0 or 6.5
- Use caution…friable tissues and decreased airway size
- Verify placement of ETT → tell surgeon!
- Then…Surgeon makes skin incision (after tube placement verified)
- Ventilate with 50% O2/50% N2O & VA (~1 MAC) → overpressure!
- Don’t forget to turn on gas! Tremendous recall
- Secure ETT, tape eyes, OGT
- ****Critical interval of 3 minutes between uterine incision and delivery of fetus
- Tremendous recall risk → medications waring down and youre busy (mom remembers)
- Delivery of baby
- PCA pump (bc didn’t do spinal)
- As soon as baby is delivered→ can give Versed, Fent, etc.
What happens after delivery in emergent c-section (coexist)
-
AFTER DELIVERY:
-
Reduce VA (.75 MAC) → may increase N2O to 70%, and give opioids and benzodiazepine
- Reduce MAC → don’t want to vasodilate & bleed out
-
Reduce VA (.75 MAC) → may increase N2O to 70%, and give opioids and benzodiazepine
- Possible NDMR
- Delivery of placenta
- Then can add oxytocin to IV → start contracting of uterus so that mom doesn’t hemorrhage
- At end:
- Suction OGT
- Reverse NDMR if necessary
- Extubate AWAKE
- Emergence and recovery is a critical period for anesthesia-related deaths from airway factors!
What is gestational hypertension?
- Most frequent cause of HTN during pregnancy
- Incidence:
- ~ 7% parturients
- Characterizations:
- BP > 140/90 AFTER 20 wks gestation after previously normal BP
- Without proteinuria
- Most cases develop > 37 weeks’ gestation
- Self-limiting: Resolves by 12 weeks postpartum
- ~ ¼ will develop preeclampsia
- True diagnosis only made after delivery when chronic hypertension can be ruled out
What is chronic hypertension of pregnancy?
- Systolic BP > 140 and/or diastolic BP > 90
- Starts before pregnancy or PRIOR to 20 weeks
- Elevated blood pressure that fails to resolve after delivery
- Consequences:
- Develops into preeclampsia ~ 1/5- ¼ affected patients
- Still an important risk factor for unfavorable maternal and fetal pregnancy outcomes
Describe the pathophysiological process assicated with developing preeclampsia
-
Unknown Exact pathogenic mechanism
- Hypothesis: Immune maladaptation → leads to inflammation
- Focus on the placenta
- Delivery of placenta resolves preeclampsia
- Can occur in absence of a fetus (molar pregnancy)
-
2 stage disorder
- 1st stage = asymptomatic
- 2nd stage = symptomatic
-
1st stage
- Impaired remodeling of spiral arteries
- End branch of uterine artery that supplies placenta
-
Normally
- Cytotrophoblasts invade the spiral arteries changing them to low resistance and high flow vessels
- Adrenergic denervation
- Cytotrophoblasts invade the spiral arteries changing them to low resistance and high flow vessels
-
Preeclampsia
- Invasion is incomplete leaving small and constricted vessels that are responsive to adrenergic stimuli
- Not undergo necessary remodeling →
- Leaves high pressure system
- Responsive to adrenergic stimuli
- Not undergo necessary remodeling →
- Invasion is incomplete leaving small and constricted vessels that are responsive to adrenergic stimuli
- Impaired remodeling of spiral arteries
-
2nd Stage
- Widespread endothelial damage/dysfunction causing
- plt aggregation, thrombocytopenia, hemolytic anemia, increase liver enzymes → HELLP
- HTN from:
- Decrease production/sensitivity of vasodilatory substances → increase SVR → HTN
- Increase sensitivity to vasocontrictor substances (Angiotensin, NE) –> vasospasm → dec GFR → dec aldosterone escape/Na & H20 retention → HTN
- Increase glomerular cap permeability and proteinuria → EDEMA
- Insufficient placental BF → leads to placental hypoxia→ IUGR
- Increased production of free radicals and lipid peroxides
- Imbalances
- Vasoconstrictors: (thromboxane A2 = ⇧)
- Vasodilators (prostacyclin’s = ⇩)
- Hypoxia →
- increase antiangiogenic factors (sFlt-1 and soluble endoglin) factors → decrease vascular endothelial growth factors & placental growth factors.
- Widespread endothelial damage/dysfunction causing
What are diagnostic criteria for mild vs severe pre-eclampsia? Risk factors associated?
Mild:
- BP > 140/90 after 20 wks gestation
- Proteinuria
- 300 mg/24 hours
- 1+ on dipstick
- protein/creatine ratio > 0.3
Severe:
- BP > 160/110
- Proteinuria
- > 5g/24 hours
- >3+ on dipstick)
- Thrombocytopenia
- platelet < 100,000
- Serum creatinine
- > 1.1 mg/dl (or 2x’s baseline)
- Pulmonary edema
- New onset cerebral or visual disturbances
- Impaired liver function
- Epigastric pain
- Intrauterine growth restriction
Coexisting diseases that increase r/f pre-e
- Chronic renal disease
- Lupus
- Protein S deficiency
- Increased pulse pressure during 1st trimester
Obstetric Factors
- African American
- Nulliparity
- Advanced age (> 40)
- Smoking
- Obesity
- Diabetes
- Multiple gestation
- History of pre-eclampsia
Pathologic alterations/complications per system in preeclampsia?
- Neurological
- Headache, Visual disturbances
- Hyperreflexia
- Seizures (*eclampsia)
- Cerebral edema
- Cardiovascular
- Increased BP
- Decreased intravascular volume (d/t contraction of vascular space)
- Increased arteriolar resistance
- Heart failure
- Respiratory
- Pharyngeal and laryngeal edema → airway management difficult
- Potentially WORSE d/t Na/H2O retention
- Pulmonary edema
- Pharyngeal and laryngeal edema → airway management difficult
- Hepatic:
- impaired fx/elevated enzymes
- Hematomas/Ruptures
- Renal:
- Proteinuria
- Na retention
- GFR decrease
- increase serum uric acid
- Heme:
-
Coagulopathy
- Thrombocytopenia (both)
- Quantitative: number
- Qualitative: function
- Platelet dysfunction
- Prolonged PTT
- *risk of cerebral hemorrhage → so need to tx HTN
- Tx: (SBP >160) w/ labetolol, Hydralazine, nifedipine
- *risk of cerebral hemorrhage → so need to tx HTN
- Thrombocytopenia (both)
-
Coagulopathy
General managmenet of preeclampsia?
- Lots of overlap between obstetricians and anesthesia
- General Overview (4)
- Timing of delivery
- R/o regional technique d/t coagulopathy?
- Fetal and maternal surveillance
- Treatment of hypertension
- Seizure prophylaxis
- Timing of delivery
Timing of Delivery for Preeclampsia
-
Timing of delivery
-
Delivery only cure
-
> 37 weeks
- Induction of labor
- > 34 weeks with severe symptoms
-
< 34 weeks
- Expectant management
- Delay delivery for 24 – 48 hours
- Administer steroids to facilitate fetal lung function
- Ex: betamethasone- mature fetal lungs
- Should be undertaken at facilities with neonatal and maternal intensive care resources
-
> 37 weeks
-
Delivery only cure
What does surveillance of Preeclampsia involve?
*Preop testing for patient with preeclampsia*
- Ex: renal, liver
- Laboratory
- CBC
- PLT count (most important)
- > 100,000
- < 100,000 – additional tests
- PT/PTT/INR
- Chemistry
- Urine protein/creatinine
- LFTs
- Uric acid testing – conflicting evidence
- CBC
What are some guidelines for treatment of HTN in preeclampsia?
1st line and 2nd line therapies?
-
Control BP- important
-
Considerations:
- Rapid maternal perfusion pressure changes can adversely affect uteroplacental perfusion pressure
- → uteroplacental perfusion pressure form arteries are already maximally dilated
- *If drop BP rapidly → negatively affect perfusion to placenta
- Rapid maternal perfusion pressure changes can adversely affect uteroplacental perfusion pressure
-
Considerations:
-
Targets:
- 15 – 25% reduction BP
- Initial BP > 160 (labetalol, Hydralazine, nifedipine)
- Systolic: 120 – 160 mmHg
- Diastolic: 80 – 105 mmHg
- 15 – 25% reduction BP
- 1st line agents:
-
Labetalol
- Crosses placenta but does NOT cause fetal bradycardia
- B:A of 7:1
-
Dose:
- 1st: 20 mg IV
-
2nd: 40 mg q10min
- Max: 220 mg
-
Hydralazine
- MOA: Potent direct vasodilator
- decreases MAP and SVR
- increasing HR and CO
-
Dose: 5 mg IV q20 minutes
- Max: 20 mg
- MOA: Potent direct vasodilator
-
Labetalol
- 2nd Line Agents:
-
Nifedipine
-
Dose: 10 mg PO q20 min
- Max: 50 mg
-
Dose: 10 mg PO q20 min
-
Nicardipine
- Dose: 1– 6 mg/hr
-
CAUTION:
- Combo Ca+ blockers + Mg
- profound hypoTN
- myocardial depression
- Combo Ca+ blockers + Mg
-
Nifedipine
What meds should you use with caution in patients with preeclampsia?
- Methergine- any form of HTN in peripartum period
- Lead to HTN crisis
- Sensitive to exogenous and endogenous catecholamines (adrenergic agents)
- Magnesium- utilized for preeclampsia
- Leads to uterine atony → increased PP bleeding