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Anesthetic Considerations of Physiological Changes During Pregnancy. Presented by: Mona Abdelsamie Assistant lecturer of Anesthesiology Under Supervision of: Prof. Dr. Hoda Omar Professor of Anesthesiology & Intensive care Anesthesiology Department Ain Shams University. OBJECTIVES.
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Anesthetic Considerations of Physiological Changes During Pregnancy Presented by: Mona Abdelsamie Assistant lecturer of Anesthesiology Under Supervision of: Prof. Dr. Hoda Omar Professor of Anesthesiology & Intensive care Anesthesiology Department Ain Shams University
OBJECTIVES • Maternal physiology during pregnancy. • Uteroplacental circulation. • Placental transfer of anesthetic agents. • Effect of labor on maternal physiology.
Anaesthesia for parturient What is the difference? 2 Patients are cared For simultaneously Physiological changes Mother Fetus Alter the usual response to anaesthesia
Maternal Physiology during Pregnancy CNS 1) Progressive MAC. by 40% at term Returns to normal by 3rd day postpartum. Progesterone increases 20 times normal level at term β- endorphin surge during labor & delivery
Hormonally Mediated 2) ↑ Sensitivity to Local Anesthetics. LA requirements during RA ↓ by 30%. ↓CSF Volume Engorged Epidural Venous Plexus ↓Volume of Epidural Space ↑Epidural space Pressure
↑Oxygen consumption 20 – 40% ٌRespiratory system Progesterone ↑ CO2 Production ↑Minute Ventilation 40 – 50% ↑↑ VT & ↑ RR & ↑P50 (30 mmHg)↑PaO2 ↓ PaCo2 (28-32 mmHg) Compensatory ↓ HCo3ˉ
Volumes Capacities Lung volumes & capacities at term gestation in absolute volumes & as the percentage change from non-pregnant Values.
↓ FRC + ↑O2 Consumption = Rapid desaturation during periods of apnea. ☼Pre-oxygenation prior to GA is mandatory. ☼Parturient Should not lie flat without supplemental oxygen. ☼ ↑Uptake of Inhalational Anesthetics. ↓FRC & ↑MV
Capillary engorgement of respiratory tract mucosa Hormonal Changes 1) ↑ Incidence of difficult intubation. 2) Trauma and bleeding during endotracheal intubation. ☼ Use a small ETT (6 – 7 mm) during GA
I : ↑ Blood Volume ( up to 90ml/ Kg) ↑ by 1000 – 1500 ml at term. Returns to normal 1 – 2 weeks postpartum. Hematological Changes + ↑ Plasma Volume > ↑ RBC mass = Dilutional anemia & ↓ blood viscosity Facilitates maternal & fetal exchange of respiratory gases, nutrients & metabolites ↓ Impact of maternal blood loss at delivery
II : Hypercoagulable state ↑ Fibrinogen, factors VII, VIII, IX, X & XII ↓Factor XI Risk Of DVT One of the leading causes of maternal mortality III : Other changes: * Leucocytosis up to 21,ooo/µL. * 10-20% ↓ in platelet count. * Marked ↓ cell mediated immunity→ ↑susceptibility to viral infection.
↑ COP by 40% at term CVS ↑ HR 15 – 30% ↑ SV 30% Returns to normal 2 weeks postpartum. ↓ SVR → ↓ SBP & ↓↓ DBP, the response to adrenergic and vasoconstrictor agents is decreased. CVP, PAP, PAWP → unchanged.
Supine Hypotension syndrome COP ↓ in supine position after 28th week of gestation. Occurs in 20% of women at term. Aortocaval compression Compression of IVC Compression of lower aorta ↓ VR → ↓ COP by 24% at term. ↓ blood flow to kidneys, uteroplacental circulation & lower extremeties
Compensatory mechanisms in unanaesthetised Women Venous Collaterals ↑ SVR & HR Reduced during general or regional anesthesia. Paravertebral Venous plexus Abdominal wall Severe Hypotension Profound Fetal Hypoxia
No woman in late pregnancy should lie supine without shifting the uterus off the great abdomino-pelvic vessels. Left lateral decubitus Rigid wedge under The right hip Tilting the table Left side down Fluid preloading before neuroaxial anesthesia It does not completely avoid maternal hypotension but it↑ maternal COP → preserve uteroplacental blood flow.
The parturient should be considered a full stomach patient during most of gestation GIT ☼ Upward displacement of the stomach by the uterus → Incompetence of gastroesophageal sphincter → Gastroesophageal reflux & esophagitis. ☼ ↑ Progesterone → ↓ tone of gastroesophageal sphincter. ☼ Placental Gastrin → Hypersecretion of gastric acid. ☼ Gastric emptying → Delayed with labor.
For GA: Pharmacological prophylaxis against aspiration. No positive pressure ventilation before intubation Rapid sequence induction. Sellick’s maneouvre
♦ RBF & GFR ↑ by 50% at 1st trimester but returns to normal in 3rd trimester. Renal System ♦↑ Renin & Aldosterone → Na+ retention. ♦ Sr. Creatinine & BUN may ↓ to 0.5 – 0.6mg/dL & 8 – 9 mg/dL respectively. ♦↓ Renal tubular threshold for glucose & amino acids → mild glycosuria (1-10g/d) & proteinuria (< 300mg/d). ♦ Plasma osmolality ↓ by 8 – 10 mosm/Kg.
♦Hepatic function & hepatic blood flow→ unchanged. Hepatic Effects ♦Minor ↑ in Sr. Transaminases & LDH in 3rd trimester. ♦↑ Sr. Alkaline phosphatase (placental). ♦ Mild ↓ in Sr. albumin (dilutional). ♦ 25 – 30% ↓ in pseudocholine estrase activity. ♦↑ Progesterone levels→ inhibit release of cholecystokinin→ incomplete emptying of gall bladder→ altered bile acid composition→ formation of cholesterol stones.
Pregnancy is Diabetogenic Metabolic Effects Human Placental lactogen→ relative insulin resistance. Starvation like state ↓ Blood Glucose & Amino Acid levels. ↑ Free Fatty Acids, Ketones & triglycerides. ↑ Estrogen levels→Thyroid gland hypertrohy→ ↑ T3 & T4 ↑ TBG → Free T3, T4 & TSH remain normal
Uteroplacental Circulation At term: uterine blood flow is 10% of COP ≈ 600 – 700 ml/min. 80% to placenta
Maximally dilated uterine vasculature with absent autoregulation. Directly proportional to difference between uterine arterial and venous pressure. Uterine Blood Flow Inversely proportional to uterine vascular resistance. Abundant α-adrenergic & some β-adrenergic receptors. Previously , vasoconstrictor agents with predominant β-adrenergic activity (e.g. Ephedrine) were of choice for hypotension during pregnancy. Recent studies show that α-adrenengic drugs (e.g.Phenylephrine) have better effects.
3 major factors ↓ uterine blood flow during pregnancy Uterine Vasoconstriction Systemic Hypotension Uterine Contractions ♦ Aortocaval compression. ♦ stress-induced endogenous Catecholamines during labor. ♦ Labor. ♦ Hypovolemia. ♦ Oxytocin infusions. ♦ α-adrenergic agonists. ♦ Sympathetic block with regional anesthesia. ♦ Local anesthetic agents. ♦ Hypertensive disorders → generalized vasoconstriction. ♦ Barbiturates & Propofol. ♦ Extreme hypocapnia PaCO2 < 20 mmhg.
Placental transfer of anesthetic agents Placental transfer of drugs depends on: 1: Molecular weight : < 500 Da cross easily. 2: Protein binding. 3: Lipid solubility: Highly ionized substances have poor lipid solubility. 4: Maternal & fetal pH : affect ionization of the drug. 5: Maternal drug concentration: affected by dose given and route of administration. 6: Timing of administration.
Local anesthetics → Placental transfer depends on: 1: pKa. 2: Maternal & fetal pH : Fetal acidosis → higher fetal to maternal drug ratios . Binding of hydrogen ions to the nonionized form → trapping of local anesthetic in fetal circulation 3: Degree of protein binding : highly protein bound agents diffuse poorly across the placenta. Chloroprocaine has the least placental transfer as it is rapidly broken down by plasma cholinestrase in the maternal circulation.
Most of anesthetic agents show significant placental transfer Fetal effects of drugs administered to parturient depend on: 1:Maturity of fetal organs, substantial fetal hepatic uptake of many drugs. 2: Dilution of the umbilical venous blood by venous blood from lower half of fetal body → modify fetal drug distribution.
Effect of labor on maternal physiology Stages of labor 1st stage 2nd stage 3rd stage Starts with full cervical dilation, fetal descent occurs, ends with complete delivery of fetus. Starts with true labor pains, ends by full cervical dilation. Extends from birth of the baby to delivery of the placenta. Latent phase Active phase 8 – 12 h in nulliparous 5 – 8 h in multiparous. Contractions are 1.5- 2 min apart, last 1 – 1.5 min 15 – 30 min. Progressive cervical effacement & minor dilataton (2 – 4 cm). Progressive cervical dilatation up to 10 cm. 15 – 120 min.
Intense painful contractions Maternal hyperventilation MV ↑ up to 300%. ↑ O2 consumption 60% above 3rd trimester values PCo2 < 20 mmHg Uterine VC → Fetal acidosis + Periods of hypoventilation → transient maternal & fetal hypoxemia in between Contractions.
Each contraction Displaces 300 – 500ml blood from uterus to central circulation. COP ↑ 45% above 3rd trimesteric value. Maximum strain on the heart occurs immediately after delivery. Uterine intense involution→ sudden relieve of IVC → ↑ COP 80% above prelabor values.
Fetal blood concentrations of lidocaine following maternal administration would be higher than expected: X • If administered during uterine contraction. • In the presence of umbilical cord compression. • In the presence of maternal acidosis. • In the presence of fetal acidosis. • In the presence of increased maternal metabolism. X X √ X
During pregnancy: √ √ • Total peripheral resistance decreases. • Hb concentration decreases. • Plasma cholinestrase concentration increases. • Blood glucose concentration increases. • Functional residual capacity increases. X X X
The dose of bupivacaine required for spinal anesthesia is reduced in the pregnant patient at term because of decreased : √ • CSF volume. • Spinal cord blood flow. • Metabolism of bupivacaine. • CSF pressure. • Turnover of CSF. X X X X
Maternal hyperventilation produces a decrease in: X X • Maternal arterial pH. • Fetal cerebral blood flow. • Maternal cerebral blood flow. • Maternal uterine artery flow. • Fetal arterial PO2. √ X √
The following substances transfer freely across the placenta: √ • Neostigmine. • Insulin. • Pancuronium. • Atropine. • glycopyrolate. X X √ X