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Anesthetic Implications for the Physiological Changes in Pregnancy & Basic FHR Monitoring. J.E. Pellegrini, CRNA, PhD. Changes during the Puerperium. Changes to anatomy & physiology Most changes to physiology occur during the 1st trimester
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Anesthetic Implications for the Physiological Changes in Pregnancy & Basic FHR Monitoring J.E. Pellegrini, CRNA, PhD
Changes during the Puerperium • Changes to anatomy & physiology • Most changes to physiology occur during the 1st trimester • Most changes to anatomy occur during the 2nd and 3rd trimester • Many of the changes are beneficial • As an anesthetist you must have a good understanding of these changes and so that you can determine if they will have an impact on your your anesthetic management
Physiological Changes of Pregnancy Primarily we’ll discuss: • Respiratory Changes • Cardiovascular Changes • GI/Hepatic/Renal Changes • Changes in Neural network (metabolism)
Factors influencing the Respiratory Systemand endotracheal intubation • Weight gain • Breast enlargement • Vascularity of the respiratory tract mucosa • Possible edema of the oropharynx, nasopharyx, and vocal cords (**most prevalent in preeclampsia) • Progesterone-beneficial
Compensatory Respiratory SystemChanges • Chest Expansion-expands anteroposterior • FRC - decreased • FRC & CC differences underventilated aveoli • Airway closure - (-a DO2)occurs in 50% of all parturients but hypoxemia extremely rare secondary to increased vent & CO • Residual Volume and ERV tolerance for apnea • ABG Changes- reflect chronic hyperventilation • PACO2 32-34 mm Hg by 12 weeks gestation • Respiratory Alkalosis(7.44) HCO3, BE and buffer base • More prone to metabolic acidosis during prolonged labor secondary to pyruvate & lactic acid accumulation
Compensatory Respiratory SystemChanges • Ventilation (8-10 wks gestation) • MV 50% at term ( 40% TV and 15% RR) • Helps decrease dead space component • PaCo2 levels (respiratory alkalosis - 7.44) • Hypoxia & Hypercarbia -develop rapidly with obstruction, prolonged apnea or hypoxic gas mixture • PO2 can 80 mm Hg/min faster than non-pregnant • Due to O2 consumption, FRC, C.O. & tissue extraction of Oxygen • Airway Resistance • Effects of Progesterone • Chest wall but not lung compliance decreases
Compensatory Respiratory SystemChanges • Oxygen Consumption 20% • demands during labor where it is estimated that the avg. labor jogging 12 miles • Oxyhemoglobin dissociation curve to the right • (P50 Values from 26 to 28 mm Hg)
Clinical Implications of these Respiratory System Changes • Effects on Inhalation Anesthetics • Faster induction rate ( RR and C.O.) • MAC decreased by 30-40% • MAC noted as early as the 8th week gestation • Effects of Maternal Hyperventilation • Constriction of umbilical and uterine vessels • incidence of fetal acidosis • Can attenuate most responses with adequate analgesia • Studies indicate that adequate pain relief (i.e. CLE can normalize oxygenation & MV & O2 consumption)
Cardiovascular System • Blood Volume • 35% (plasma volume 50% & red cell mass 15%) • Blood loss usually well tolerated at delivery • See fall in Hct in Postpartum by approximately 5% secondary to diuresis • Normally only have to consider blood after 1500 ml EBL • Cardiac Output • 30-40% in 1st trimester and 40-45% during labor and 50-60% in immediate postpartum period • Prone to Aortocaval Compression
Aorto-Caval Syndrome • Hypotension • 20 weeks gestation • Gravid Uterus Weight • Can Decrease C.O. 30% • Management Plan • Pre-induction hydration • Left Uterine Displacement (or RUD) • Ephedrine/Phenylephrine • Venal Caval Compression • Distention of epidural venous plexus • Decrease LA dose 1/3 (>14 wks)
Anesthetic Significance of Cardiovascular Changes • Venodilation- increases accidental epidural vein puncture • Oxytocin with free H20 volume overload • Hgb levels > 14 indicates low volume status, HTN or diuresis • C.O. high in 4 hrs postpartum • B/P < 90 to 95 torr uterine blood flow • Hypotension occurs 75% with T4 level
Gastrointestinal Changes • Stomach displaced upward and 45 to the right & displaces the intra-abdominal segment of the esophagus into the thorax decreased tone of the lower esophagus incidence of pyrosis • Delayed gastric emptying incidence of full stomach
Gastrointestinal Changes • Obesity - associated 2-20 fold in mortality (PIH, IDDM) • Progesterone • Gastrointestinal motility & esophageal sphincter tone • Parturients beyond 18th week of gestation more prone to vomiting and regurgitation • Treat as full stomach at 12th week *put it all together and this spells trouble
Other Compensatory Changes • Renal System - GFR 60% at term • in aldosterone and plasma osmolarity (ADH resetting) • RBF Creatinine clearance & a BUN & Uric Acid levels (½ to 2/3 that of normal) • Hepatic System • Usually no significant changes except slight in level enzymes and 2-4 fold in alkaline phosphatase & cholesterol (from growing placenta) • Slight in plasma cholinesterase & serum albumin • Can see spider angiomata & palmar erythema (from estrogen levels)
Neuromuscular Changes • Endorphins • MAC by 40% • Sedative Effect from Progesterone • Changes in SNS • See down-regulation • Altered Response to Catecholamines
Altered Responses to Anesthesia • sensitivity of neural network • Probably secondary to levels of circulating progesterone • Possible influence from circulating endorphins • Applicable for both neuraxial and peripheral blockades • Applicable for parturients beyond 24th week gestation • Decrease local anesthetic dose by as much as 1/3
Summary • Multiple physiological changes in pregnancy have profound impact on your anesthetic management • The conservative approach is the best approach when dealing with the OB patient • Your principle patient is the parturient
Fetal Monitoring • No ideal way to assess fetal well-being • FHR one of the better methods • FHR influenced by Para and sympathetic outflow • FHR responds to Baro & Chemo receptors
Fetal Heart Rate • Normal Baseline between 110-160/min • Small square = 10 seconds • Large square = 1 minute • Baseline rate determined by rate between contractions
Three Primary Mechanisms that Uterine Contractions cause FHR Abnormalities
FHR Accelerations • The FHR will normally remain steady or accelerate with uterine contractions • Typically viewed as a reassuring phenomenon
Early Decelerations • Begins with onset of contraction & ends at the conclusion of contraction (with return to baseline) • Typically caused from Head Compression & routinely not viewed as a sign of fetal distress
Late Decelerations • Transitory Decreases in FHR caused by Utero-Placental deficiency (hypoxia) indicating the fetus is not able to withstand the uterine contractions • Persistent Late Decelerations are considered an ominous sign especially when associated with loss of short term variability
Nonreassuring Patterns • Nonreassuring, or "warning," patterns suggest decreasing fetal capacity to cope with the stress of labor. • Nonreassuring Patterns (Warning Signs) • ·Decrease in baseline variability • ·Progressive tachycardia (>160bpm) • ·Decrease in baseline FHR • ·Intermittent late decelerations with good variability • Ominouspatterns suggest possible fetal compromise.
Ominous Patterns • ·Persistent late decelerations, especially with • decreasing variability • ·Variable decelerations with loss of variability, • tachycardia, or late return to baseline • ·Absence of variability • ·Severe Bradycardia
So – In summary • If an ominous pattern appears to be present: • Have the mother lie on her left side or in a knee chest position immediately followed by: • Increase IV fluid. • Give her oxygen @ 10-12L to breathe by mask. • Discontinue or decrease any CLE infusion • Notify the obstetrical nursing staff & Obstetrician