Safety and Management of Parturition (Childbirth/Labor)

1. What is Parturition?

1. Transformation of the myometrium from a quiescent to a highly contractile state
2. Cervical softening, effacement, and dilation
3. Rupture of fetal membranes
4. Expulsion of uterine contents
5. Return of the uterus to its prepregnant state

• Medical Physiology, p. 3464

2. Physiology of Labor - Hormonal Mechanisms

• Fetal cortisol: Near term, the fetal hypothalamic-pituitary-adrenal axis is activated, producing cortisol. This increases the estrogen/progesterone ratio, which increases uterine sensitivity to contractile stimuli. Estrogen increases contractility; progesterone decreases it.
• Prostaglandins (PGE2 and PGF2α): Stimulated by estrogen; they (1) increase intracellular calcium in uterine smooth muscle, (2) promote gap junction formation for synchronous contractions, and (3) cause cervical softening, effacement, and dilation.
• Oxytocin: A powerful stimulant of uterine contractions. Uterine oxytocin receptors are up-regulated near term; cervical dilation during labor further stimulates oxytocin secretion via a positive feedback loop.
• Gap junctions (connexin-43): Form electrochemical connections between myometrial cells to synchronize contractions across the entire uterus.
• Costanzo Physiology 7th Edition, p. 1515-1517; Guyton and Hall Textbook of Medical Physiology, p. 1423

3. Stages of Labor

• Tintinalli's Emergency Medicine, p. 2013-2014; Guyton and Hall, p. 1427-1429

4. True vs. False Labor

• Tintinalli's Emergency Medicine, p. 1928-1929

5. Assessment in Active Labor

• Vital signs and IV venous access
• IV hydration
• Maternal and fetal monitoring
• Rupture of membranes (ROM): Confirmed with nitrazine paper (amniotic fluid pH 7.0-7.4 turns paper dark blue; vaginal fluid pH 4.5-5.5 stays yellow) or ferning test (NaCl crystals visible on microscopy)
• Cervical dilation: 0-10 cm (10 cm = fully dilated); assess effacement (%) and fetal station relative to ischial spines

• Tintinalli's Emergency Medicine, p. 1916-1924

6. Normal Vaginal Delivery - Management Steps

1. Obtain IV access, provide hydration, initiate monitoring
2. Assess presentation: Palpate skull sutures and fontanelle or buttock/extremity - >95% of births are cephalic (vertex) presentation
3. Wait for full cervical dilation before pushing (to avoid cervical lacerations)
4. Perineal support: Gentle digital stretching of the inferior perineum aids delivery
5. Episiotomy: Not routine; indicated for fetal distress, shoulder dystocia, or operative delivery. Use 1% lidocaine. Mediolateral episiotomy (45 degrees) has lower risk of anal sphincter injury than midline
6. Deliver the infant: Place posterior hand under the axilla; grasp ankles firmly. Do not routinely suction the nose and mouth (can cause bradycardia/hypoxia)
7. Keep infant warm, provide gentle stimulation
8. Cord clamping: Can allow mother to hold infant while cord is cut if delivery uncomplicated
9. Apgar scores at 1 and 5 minutes (color, tone, heart rate, respiratory effort, reflexes)

• Tintinalli's Emergency Medicine, p. 2009-2025

7. Dysfunctional Labor Patterns and Management

Prolonged Latent Phase

• Nullipara: >20 hours; Multipara: >14 hours
• Causes: unripe cervix, false labor, sedation, uterine inertia
• Management: rest, observation, possibly oxytocin augmentation; therapeutic morphine for rest. Avoid amniotomy (risk of chorioamnionitis). NOT an indication for caesarean section alone.

Protracted Active Phase (Primary Dysfunctional Labor)

• Dilation <1.2 cm/hr (nullipara) or <1.5 cm/hr (multipara)
• Causes: fetal malposition (occiput posterior), cephalopelvic disproportion (CPD), inadequate contractions, anesthesia
• Management: active management with oxytocin; associated with increased risk of operative delivery

Secondary Arrest of Cervical Dilation

• Cessation of dilation for ≥2 hours after previously normal dilation
• Management: assess with intrauterine monitor; consider amniotomy, ambulation, oxytocin augmentation; high association with CPD - many require operative delivery

Second Stage Abnormalities

• Arrest of descent: unchanged fetal station
• Assess: adequacy of contractions, distended bladder, CPD, maternal exhaustion, conduction anesthesia
• Protracted descent: <1 cm/hr in nulliparas
• Textbook of Family Medicine 9e, p. 492-517

8. Specific Complications and Their Management

Shoulder Dystocia

• After delivery of the head, anterior shoulder fails to deliver
• McRoberts maneuver: Hyperflex maternal thighs onto abdomen (widens pelvic outlet)
• Suprapubic pressure: Press down on the suprapubic area to dislodge the anterior shoulder (do NOT fundal pressure)
• Gaskin maneuver: Place mother on all fours - widens pelvic outlet
• Rubin/Woods screw maneuver, deliberate episiotomy, or internal rotational maneuvers if above fail

Breech Presentation (3-4% of term deliveries)

• Risks: cord prolapse, trauma, hypoxia, fetal distress
• Caesarean section is recommended for term breech presentations
• Frank/complete breech: emergency vaginal delivery may proceed; footling/incomplete breech - unsafe for vaginal delivery
• During breech vaginal delivery: allow spontaneous delivery to umbilicus; do not apply traction; deliver arms with slight oblique rotation; deliver head with one hand on occiput (flexing pressure) and fingers of other hand on maxilla; assistant applies suprapubic pressure

Postpartum Hemorrhage (PPH)

• Primary PPH (within 24 hours): Uterine atony (most common), retained placental fragments, genital tract lacerations, uterine rupture, uterine inversion, coagulopathy
• Secondary PPH (24 hours to 6 weeks): Subinvolution, retained tissue, infection
• Defined as: 10% drop in hematocrit, need for PRBC transfusion, or hemodynamic compromise
• Management: uterine massage, uterotonics (oxytocin, ergometrine, misoprostol), manual placental removal if retained, surgical repair of lacerations, escalate to uterine tamponade, surgical or radiological intervention if needed
• Tintinalli's Emergency Medicine, p. 2109-2131

9. Preterm Labor (Before 37 Weeks)

• Definition: Uterine contractions before 37 weeks causing cervical change (≥2 cm dilation or ≥80% effacement, or documented progression)
• Risk factors: Prior preterm birth, multiple gestation, cervical anomalies, infections, uterine abnormalities
• Diagnosis tools: Transvaginal ultrasound for cervical length; fetal fibronectin test (high negative predictive value - if negative, delivery unlikely for 7-10 days)

• Textbook of Family Medicine 9e, p. 102-125

10. Key Safety Points

• Medical Physiology (Boron & Boulpaep) - Stages 0-3 of parturition, molecular mechanisms
• Guyton and Hall Textbook of Medical Physiology - Mechanics of parturition, labor pain
• Costanzo Physiology 7th Edition - Hormonal regulation of parturition
• Tintinalli's Emergency Medicine: A Comprehensive Study - Active labor management, delivery technique, complications
• Textbook of Family Medicine 9e - Dysfunctional labor, preterm labor management

Safety and Management of Perturbations During Cardiopulmonary Bypass (CPB)

What is CPB?

• Miller's Anesthesia, 10e, p. 7539

Major Physiological Perturbations During CPB and Their Management

1. HEMODYNAMIC PERTURBATIONS

Initiation Hypotension

• CPB initiation is almost universally associated with a drop in arterial blood pressure due to hemodilution of the pump prime, loss of pulsatile flow, and acute vasodilation.
• Management: Administer an α-agonist (e.g., phenylephrine) into the venous reservoir of the ECC circuit. Cerebral oximetry should be monitored; acutely reduced values may indicate poor SVC drainage or selective perfusion of a single aortic head vessel.

Target Perfusion Pressures During CPB

• Maintain mean arterial pressure (MAP) of 50-90 mm Hg with pump flow of 1.6-3.0 L/min/m² (commonly targeting ~2.4 L/min/m², i.e., 50-70 mL/kg).
• Arterial line pressure in the ECC circuit must remain <300 mmHg to prevent trauma to blood elements.
• Mixed venous O₂ saturation (SvO₂) should be maintained >65% as a marker of adequate global perfusion.

Hypotension During CPB

• If hypotension persists despite adequate flow and SvO₂:
  • Titrate vasoconstrictors (phenylephrine, norepinephrine) to increase SVR
  • Verify venous cannula position (if CVP/PAP don't fall to 0 mmHg, reposition cannula)
  • Check for sources of blood loss (surgical field, suction losses)

Hypertension During CPB

• If MAP is persistently elevated:
  • Titrate vasodilators to reduce SVR
  • Ensure adequate anesthetic depth (awareness prevention)

Pulsatility Loss

• CPB flow is inherently non-pulsatile, which impairs microcirculatory flow, especially in combination with hypothermia. This is one reason hemodilution is routinely used.
• Miller's Anesthesia, 10e, p. 7555-7556

2. TEMPERATURE PERTURBATIONS (HYPOTHERMIA / HYPERTHERMIA)

Hypothermia - Protective but Managed Carefully

Deep Hypothermic Circulatory Arrest (DHCA)

• Core temperature cooled to 15-22°C before completely stopping blood flow (used for aortic arch repairs).
• Cool to a target temperature and then continue cooling for 20-30 more minutes to allow brain parenchymal temperature to equilibrate with arterial blood temperature (a time lag exists).
• For 30-40 minute arrest periods: temperature of 18-20°C is generally adequate.
• EEG isoelectricity from hypothermia should be confirmed before commencing circulatory arrest.

Rewarming - Critical Safety Point

• Rewarming should be gradual and started early enough to achieve stable temperature before coming off CPB.
• Avoid aggressive rapid rewarming - this causes cerebral hyperthermia at the exact moment cerebral embolization risk is highest (during termination of CPB).
• Even 2°C elevation above normal is harmful: delays neuronal recovery, increases excitotoxins, free radicals, and BBB permeability.

Temperature Monitoring

• Brain temperature cannot be measured directly. Use surrogate sites: nasopharyngeal, tympanic, esophageal, rectal, bladder, jugular venous bulb.
• Jugular bulb temperature is considered the gold standard (proximity to carotid origins makes it closest to brain temperature).
• Monitor multiple temperature sites simultaneously during CPB to observe trends.
• Miller's Anesthesia, 10e, p. 7563-7565

3. HEMODILUTION

Why It Occurs

Why Hemodilution is Used

• Reduces blood viscosity during hypothermia (viscosity increases 3-4x at 18°C for hematocrit of 30-35%)
• Improves microcirculatory flow - hypothermia plus non-pulsatile flow causes blood sludging, small vessel occlusion, and tissue hypoperfusion

Safe Hematocrit Targets

• For standard CPB: maintain hematocrit approximately 25-30% to optimize O₂ delivery to vital organs (especially brain)
• For DHCA procedures: hematocrit closer to 18-20% (for anticipated temperatures) but never below 10% (causes inadequate O₂ delivery)
• RBCs serve as the primary O₂ reservoir during circulatory arrest, especially during rewarming, so hematocrit values closer to 30% are preferred when DHCA is contemplated.
• In neonates/infants: add packed RBCs to the pump prime to achieve target hematocrit (use formula: Added RBCs = (BVpt + TPV)(Hct desired) - (BVpt)(Hctpt))

Risks of Hemodilution

• Reduces O₂-carrying capacity of blood
• Reduces perfusion pressure
• Increases cerebral blood flow → potentially increases microembolic load to brain
• Miller's Anesthesia, 10e, p. 10778-10779

4. ANTICOAGULATION MANAGEMENT

Heparin Dosing

• Heparin is mandatory during CPB to prevent clotting in the circuit.
• Standard dose: 300-400 units/kg (weight-based), or guided by dose-response curve.
• Target plasma heparin concentration: 1.5-3.0 units/mL.

Monitoring: Activated Clotting Time (ACT)

• ACT is the standard bedside monitor of heparin adequacy.
• ACT >480 seconds (some protocols >400 seconds) is required before initiating CPB.
• ACT requires normothermia, normal platelet count, and normal coagulation proteins (including antithrombin III) for accuracy.
• Limitation in pediatrics: In neonates and infants, ACT does not correlate well with plasma heparin concentration; children show ongoing thrombin generation even at very high ACT values.

Antithrombin III

• Heparin works by accelerating the reaction between thrombin and antithrombin III (AT-III).
• Neonates have low AT-III levels (reach adult levels at 3 months). Children with congenital heart disease have ~50% functional AT-III activity.
• Low AT-III = low heparin sensitivity → monitor carefully.

Heparin Reversal

• Neutralized with protamine: 2-4 mg/kg, dosed according to total heparin administered or body weight.

Heparin-Induced Complications

• Patients who cannot receive heparin (heparin-induced thrombocytopenia, HIT): alternative anticoagulants (bivalirudin) may be used.
• Miller's Anesthesia, 10e, p. 10780-10781

5. BLOOD GAS / ACID-BASE MANAGEMENT

• During DHCA in adults: α-stat is standard.
• During DHCA in pediatric/neonatal patients: pH-stat is preferred because it increases cerebral blood flow during cooling, ensuring more uniform brain cooling before circulatory arrest.
• During rewarming: blood gas management transitions back toward α-stat.
• Miller's Anesthesia, 10e, p. 7517

6. EMBOLIC PERTURBATIONS (MACRO- AND MICRO-EMBOLI)

• CPB generates particulate and gaseous microemboli from the circuit, aortic manipulation, pump sucker blood, and air entrainment.
• Air entrainment is especially dangerous with vacuum-assisted venous drainage: reservoir vacuum pressure should be maintained at minimum necessary and entrainment of air from the surgical field must not be permitted. Reservoir pressures below -60 mm H₂O pose risks.
• The arterial line filter removes particles and air before blood returns to the patient.
• Aggressive rewarming increases cerebral metabolic rate at the time of highest embolic risk → avoid.
• Hemodilution (by reducing viscosity) paradoxically increases cerebral blood flow and may increase microembolic delivery to the brain - a key safety trade-off.

7. SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS) DURING CPB

• Complement activation, cytokine release (IL-1, IL-6, TNF-α), neutrophil activation
• Manifests as: capillary leak, vasodilation, pulmonary dysfunction, end-organ injury

• Biocompatible coated tubing: Modern polyvinyl chloride tubing with surface coatings reduces plasma markers of subclinical coagulation, attenuates cytokine release, and shortens intubation times compared to uncoated tubing.
• Volatile anesthetic agents (isoflurane, sevoflurane, desflurane): Anti-inflammatory effects; trigger ischemic preconditioning cascade; mitigate reperfusion injury. Used throughout pre-bypass, bypass, and post-bypass periods.
• Corticosteroids (methylprednisolone, dexamethasone): Used in some centers to reduce the inflammatory response; evidence is mixed.
• Ketamine: Meta-analysis of 14 studies suggests ketamine significantly reduces the IL-6 response to surgery.
• Miniaturized circuits and off-pump techniques can reduce SIRS trigger.
• Miller's Anesthesia, 10e, p. 7575

8. AORTIC MANIPULATION AND CANNULATION

• Arterial cannulation site: usually the ascending aorta (for standard CABG/valve surgery) or femoral artery.
• Venous cannulation: right atrium for most procedures; bicaval (SVC + IVC) for mitral/tricuspid valve surgery requiring bloodless right heart.
• Femoral venous cannula extends through the IVC into the right atrium (useful for minimal access surgery).
• Aortic cross-clamp causes global myocardial ischemia → cardioplegia solution delivered (anterograde via aortic root or retrograde via coronary sinus) to arrest and protect the heart.

9. CEREBRAL PROTECTION STRATEGIES

Summary of Key Safety Rules During CPB

• Miller's Anesthesia, 2-Volume Set, 10e - Management of CPB, DHCA, Anticoagulation during CPB, Hemodilution, Temperature management, Cerebral protection
• Tintinalli's Emergency Medicine: A Comprehensive Study - Macrovascular hemolysis and CPB
• Goldman-Cecil Medicine - Prolonged CPB and arrhythmia/cardiomyopathy