Physiological changes in pregnancy include changes in the central nervous, respiratory, and cardiovascular systems. The minimum alveolar concentration of anesthetic gases decreases by up to 40% due to hormonal and endogenous changes. Oxygen consumption and minute ventilation increase while functional residual capacity decreases, increasing the risk of desaturation. Blood volume and plasma volume increase substantially, elevating cardiac output and stroke volume and decreasing systemic vascular resistance.
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Introduction to physiological changes during pregnancy, classified into anatomical, physiological, and biomechanical.
Pregnancy induces significant physiological changes, impacting anesthesia responses and care for both mother and fetus.
Discussion of neurologic physiological changes during pregnancy, including MAC reduction and local anesthesia requirements.
Detailed overview of respiratory changes in pregnancy, highlighting increases in oxygen consumption, ventilation, and impacts on anesthesia.
Key cardiovascular changes in pregnancy, including increased blood volume, cardiac output, and effects on anesthesia practice.
Renal function changes during labor, including increased GFR and implications for renal health in pregnancy.
Increased gastroesophageal reflux risk and delayed gastric emptying leading to aspiration concerns during pregnancy.
Hepatic effects during pregnancy include changes in enzyme levels and gallbladder function.
Changes in hematologic parameters during labor, including increased clotting factors leading to a hypercoagulable state.
Metabolic alterations resembling starvation due to pregnancy, including changes in glucose, insulin, and thyroid function.
Overview of uteroplacental circulation and factors affecting uterine blood flow during pregnancy.
Functional aspects of the placenta regarding gas exchange, nutrient transfer, and mechanisms of placental exchange.
Physiological effects of labor on the mother, including increased cardiac output and oxygen consumption.
Details on fetal blood flow and oxygenation during labor, emphasizing circulation patterns and adaptations.
Challenges faced by anesthetists in obstetric anesthesia, including emergencies and the need for a multidisciplinary team.
Closing remarks on the complexity of obstetric anesthesia and thanks to the audience.
Changes In PregnancyPregnancy brings about many physical changes. These changes can be divided into 3 area – Anatomical Physiological Biomechanical.
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Changes In PregnancyPregnancy brings about many physical changes. These changes can be divided into 3 area – Anatomical Physiological Biomechanical.
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Physiological Changes InPregnancy 1.Pregnancy produces profound physiological changes that alter the usual responses to Anesthesia 2.Unique challenges - two patients are cared for simultaneously 3.Failure to take care can be disastrous for one or both of them
Average maximum physiologicalchanges associated with Pregnancy Parameter Change Neurologic MAC (minimum alveolar concentration )
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Average maximum physiologicalchanges associated with Pregnancy Parameter Change Neurologic MAC (minimum alveolar concentration ) - 40% 1.(MAC) progressively decreases during pregnancy—at term, by as much as 40%—for all general anesthetic agents 2.MAC returns to normal by The third day after delivery.
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Neurologic Changes inmaternal hormonal and endogenous opiate levels have been impilcated. Progesterone,increases at term ↑ β -endorphin levels during labor &delivery . local anesthesia reduced’ as much as 30%.
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Central Nervous SystemLA requirements for subarachnoid or epidural anaesthesia are reduced in pregnancy (30%) Possible causes include: a. increased diffusion of LA to the receptor site b. increased sensitivity of nerve fibres to LA (Lower connection needed) c. ? raised CSF progesterone levels Spinal ligaments including ligament flavum ď‚®ď€ SOFT
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Central Nervous SystemValsalva manoeuvres during delivery may increase CSF and epidural pressures, markedly increasing the spinal spread of anaesthetia
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2. What areRespiratory physiological changes during labour ?
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Average maximum physiologicalchanges associated with Pregnancy Respiratory Oxygen consumption Minute ventilation Tidal volume Respiratory rate PaO 2 PaCO 2 HCO 3 FRC (functional residual capacity )
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Average maximum physiologicalchanges associated with Pregnancy Respiratory Oxygen consumption + 20 to 50% Minute ventilation Tidal volume Respiratory rate PaO 2 PaCO 2 HCO 3 FRC (functional residual capacity )
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Average maximum physiologicalchanges associated with Pregnancy Respiratory Oxygen consumption + 20 to 50% Minute ventilation + 50% Tidal volume Respiratory rate PaO 2 PaCO 2 HCO 3 FRC (functional residual capacity )
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Average maximum physiologicalchanges associated with Pregnancy Respiratory Oxygen consumption + 20 to 50% Minute ventilation + 50% Tidal volume + 40% Respiratory rate PaO 2 PaCO 2 HCO 3 FRC (functional residual capacity )
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Average maximum physiologicalchanges associated with Pregnancy Respiratory Oxygen consumption + 20 to 50% Minute ventilation + 50% Tidal volume + 40% Respiratory rate + 15% PaO 2 PaCO 2 HCO 3 FRC (functional residual capacity )
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Average maximum physiologicalchanges associated with Pregnancy Respiratory Oxygen consumption + 20 to 50% Minute ventilation + 50% Tidal volume + 40% Respiratory rate + 15% PaO 2 + 10% PaCO 2 HCO 3 FRC (functional residual capacity )
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Average maximum physiologicalchanges associated with Pregnancy Respiratory Oxygen consumption + 20 to 50% Minute ventilation + 50% Tidal volume + 40% Respiratory rate + 15% PaO 2 + 10% PaCO 2 - 15% HCO 3 FRC (functional residual capacity )
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Average maximum physiologicalchanges associated with Pregnancy Respiratory Oxygen consumption + 20 to 50% Minute ventilation + 50% Tidal volume + 40% Respiratory rate + 15% PaO 2 + 10% PaCO 2 - 15% HCO 3 - 15% FRC (functional residual capacity )
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Average maximum physiologicalchanges associated with Pregnancy Respiratory Oxygen consumption + 20 to 50% Minute ventilation + 50% Tidal volume + 40% Respiratory rate + 15% PaO 2 + 10% PaCO 2 - 15% HCO 3 - 15% FRC (functional residual capacity ) - 20%
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Respiratory Effects Oxygen consumption and minute ventilation progressively increase during pregnancy. Both tidal volume and, respiratory rate increase. By term, oxygen consumption has increased about 20—40%, while minute ventilation has increased 40—50%. Paco 2 decreases to 28—32 mm Hg; significant respiratory alkalosis is prevented by a compensatory ↓in p asma bicarbonate concentration.
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Respiratory Effects Hyperventilationmay also increase Pa02 Elevated levels o 2,3-di phosphoglycerate offset the effect hyperventilation on hemoglobin affinity for oxygen. The P-50 for hemoglobin increases from 27 to 30 mm Hg the combination of these factors with increase in cardiac output enhances oxygen delivery to tissues.
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Respiratory Effects Thematernal respiratory pattern changes as the uterus enlarges. In the third trimester, elevation of diaphragm is compensated by an increase in the AP diameter of the chest Thoracic breathing is favored over abdominal breathing. Both vital capacity and closing capacity are minimally affected. FRC decreases up t 20° at term; FRC returns to normal within 48 hours of delivery. Reduction in expiratory reserve volume .
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Respiratory Effects Flow-volumeloops are unaffected Airway resistance decrease. Physiologic dead space decreases but intrapulmonary shunting increases towards term. A chest film often shows prominent vascular markings due to increased pulmonary blood volume and an elevated diaphragm. Pulmonary vasodilataion prevents pulmonary pressures form rising.
Respiratory: Importance forAnaesthesia ++Decreased FRC and increased oxygen consumption promotes rapid oxygen desaturation during periods of apnea . Preoxygenation prior to induction of general anesthesia is therefore mandatory to avoid hypoxemia in pregnant patients.
Respiratory: Importance forAnaesthesia Closing volume exceeds FRC in up to half of all pregnant women when they are supine at term. atelectasis hypoxemia. Parturients should not lie flat without supplemental oxygen.
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Respiratory: Importance forAnaesthesia Rapid gaseous induction ↓ MAC (as much as 40% decreases at term return to normal on third day of delivery) The decrease in FRC coupled with the increase in minute ventilation accelerates the uptake of all inhalational anesthetics. ↓ FRC ® less dilution ↑ MV ® rapid d depth
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Respiratory: Importance forAnaesthesia Intubation Trauma - mucosal bleeding - difficult intubation Capillary engorgement of the respiratory mucosa during pregnancy predisposes the upper airways to trauma, bleeding, and obstruction. Gentle laryngoacopy and the use of small endotracheal tubes (6—7 mm) during general anesthesia.
Average maximum physiologicalchanges associated with Pregnancy Parameter Change Cardiovascular Blood volume Plasma volume Cardiac output Stroke volume Heart rate Peripheral resistance
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Average maximum physiologicalchanges associated with Pregnancy Parameter Change Cardiovascular Blood volume + 35% Plasma volume Cardiac output Stroke volume Heart rate Peripheral resistance
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Average maximum physiologicalchanges associated with Pregnancy Parameter Change Cardiovascular Blood volume + 35% Plasma volume + 45% Cardiac output Stroke volume Heart rate Peripheral resistance
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Average maximum physiologicalchanges associated with Pregnancy Parameter Change Cardiovascular Blood volume + 35% Plasma volume + 45% Cardiac output + 40% Stroke volume Heart rate Peripheral resistance
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Average maximum physiologicalchanges associated with Pregnancy Parameter Change Cardiovascular Blood volume + 35% Plasma volume + 45% Cardiac output + 40% Stroke volume + 30% Heart rate Peripheral resistance
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Average maximum physiologicalchanges associated with Pregnancy Parameter Change Cardiovascular Blood volume + 35% Plasma volume + 45% Cardiac output + 40% Stroke volume + 30% Heart rate + 15 to 30% Peripheral resistance
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Average maximum physiologicalchanges associated with Pregnancy Parameter Change Cardiovascular Blood volume + 35% Plasma volume + 45% Cardiac output + 40% Stroke volume + 30% Heart rate + 15 to 30% Peripheral resistance - 15%
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Cardiovascular Effects Cardiacoutput and blood volume increase to meet accelerated maternal and fetal metabolic demands. An increase in plasma volume in excess of an increase in red cell mass produces dilutional anemia and reduce blood viscosity. Hemoglobin concentration remains greater than11.1gIdL. ↓ in systemic vascular resistance by the second trimester decreases both diastolic and, to a lesser degree, systolic blood pressure. The response to adrenergic agents and vasoconstrictors is blunted.
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Cardiovascular Effects Atterm, maternal blood volume has increased by 1000—1500 mL in most women, allowing them to easily tolerate the blood loss associated with delivery. total blood volume reaches 90 mL/kg. Average blood loss during vaginal delivery is 400—500 mL cesarean section 800—1000 mL Blood volume does not return to normal until 1—2 weeks after delivery.
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Cardiovascular Effects ↑cardiac output (40% at term) is due to ↑ in HR(15—30%) + SV (30%). Cardiac chambers enlarge and myocardial hypertrophy is often noted on echocardiography. Pulmonary artery, central venous, and pulmonary artery wedge pressures remain unchanged. Most of these effects are observed in the first and, to a lesser extent, the second trimester.
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Cardiovascular Effects Inthe third trimester, cardiac output does not appreciably rise, except during labor. The greatest increases in cardiac output are seen during labor and immediately after delivery . Cardiac output often does not return to normal until 2 weeks after delivery.
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Blood Pressure a. ď‚ď€ CO ~ 50% b. ď‚Żď€ TPR - uterine AV shunt & decreased viscosity ď€ ď€ ď€ ď€ ď€ ď€ ď€ ď‚®ď€ slight decrease in MAP NB: a high BP in pregnancy, except during labour, is always abnormal CVP and PAOP remain normal during pregnancy CVP increases 4-6 cmH2O during contractions
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CVS: Importance forAnaesthesia Decreases in cardiac output can occur in the supine position after the 28th week of pregnancy. decreases of venous return to the heart as the enlarging uterus compresses the inferior vena cava. Up to 20% of women at term develop the supine hypotension syndrome. (hypotension associated with pallor, sweating, or nausea and vomiting).
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CVS: Importance forAnaesthesia It is due to complete or near-complete occlusion of the inferior cava by the gravid uterus. Turning the patient on her side typically restores venous return from the lower body and corrects the hypotension .
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CVS: Importance forAnaesthesia The gravid uterus also compresses the aorta in pareurients when they are supine. ↓ blood flow to the lower extremities and, more importantly, to the uteroplacental circulation.
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CVS: Importance forAnaesthesia When combined with the hypotensive effects of regional or general anesthesia, aortocaval compression can readily produce fetal asphyxia. Pareurients with a 28-week or longer gestation should not be placed supine without left uterine displacement. This maneuver is most readily accomplished by placing a wedge (> 15 degrees) under the right hip. Chronic partial caval obstruction in the third trimester predisposes to venous stasis, phlebitis, and edema in the lower extremities.
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Cardiovascular: Importance forAnaesthesia Patients undergoing spinal or epidural anaesthesia must, a. Be maintained in a lateral tilt position, with left uterine displacement b. Be adequately volume preloaded
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CVS: Importance forAnaesthesia Elevation of the diaphragm shifts the heart’s position in the chest, resulting in the appearance of an enlarged heart on a plain chest film left axis deviation and T wave changes on the ECG. Physical examination often reveals a systolic ejection flow murmur (grade I or II) exaggerated splitting of the1 ST heart sound (S1) third heart sound (S3) may be audible. A few patients develop small, asymptomaic pericardial effusions.
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What are thecriteria to diagnose cardiac disease during pregnancy ?
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Criteria to diagnosecardiac disease during pregnancy: 1.Presence of diastolic murmurs. 2.Systolic murmurs of severe intensity (grade 3). 3.Unequivocal enlargement of heart (X-ray). 4.Presence of severe arrythmias, atrial fibrillation or flutter
Renal Effects Renalvasodilatation increases renal blood flow early during pregnancy Autoregulation is preserved. The kidneys often enlarge. Increased renin and aldosterone levels promote sodium retention. Renal plasma flow and the glomerular filtration rate increase as much as 50% during the first trirnester
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Renal Effects glomerularfiltration declines toward normal in the third trimester. Serum creatinine and blood urea nitrogen decrease to 0.5—0.6 mg/dL and 8—9 mgldL decreased renal tubular threshold for glucose and amino acids results in : mild glycosuria (1—10 g/d) prneteinuria (< 300 mg/d). Plasma osmolality decreases by 8—10 mOsm/kg.
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5. What areGastrointestinal changes during labour ?
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Gastrointestinal changesGastroesophageal reflux esophagitis are common during pregnancy. Upward and anterior displacemenr of the stomach by the uterus promotes incompetence of the gastroesophageal sphincter. Elevated progesterone levels reduce the tone of the gastroesophageal sphincter . Placental gastrin secretion causes hypersecretion of gastric acid. Intragastric pressure is unchanged.
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Gastrointestinal changesincreased risk of severe aspiration pneumonitis Gastric PH ≤ 2.5 Gastric volumes graeter than 25 ml ≤60% . Delayed gastric emptying time Narcotics and anticholinergics reduce lower esophageal sphincter pressure
Hepatic effeccts hepaticfunction and blood flow are unchanged minor elevations in serum trarsaminases and lactic dehydrogenase levels in the third trimester. Elevations in serum alkalin phosphatase are due to its seccetion by placenta . A mild decrease in serum albumin is due to an expanded plasma volume Colloid osmotic pressure progressively decreases, parallel with the fall in serum albumin
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Hepatic effeccts A25—30% decrease in serum pseudocholinescerase activity is also present at term rarely produces significant prolongation of succinylcholine’s action. The breakdown of mivacurium and ester-type local anaesthesia. Pseudocholinesrerase activity may not return to normal until up to 6 weeks postpartum.
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Hepatic effeccts Highprogesterone levels appear to inhibit the release of cholecystokinin incomplete emptying of the gallbladder altered bile acid composition, can predispose to formation of cholesterol gallstones.
Average maximum physiologicalchanges associated with Pregnancy Parameter Change Hematologic Hemoglobin Platelets Clotting factors
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Average maximum physiologicalchanges associated with Pregnancy Parameter Change Hematologic Hemoglobin - 20% Platelets Clotting factors
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Average maximum physiologicalchanges associated with Pregnancy Parameter Change Hematologic Hemoglobin - 20% Platelets - 10 to 20% Clotting factors
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Average maximum physiologicalchanges associated with Pregnancy Parameter Change Hematologic Hemoglobin - 20% Platelets - 10 to 20% Clotting factors + 50 to 250%
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Pregnancy leads toa hypercoagulable state , due to, a. ď‚ď€ factors VII, VIII, X, XII (? IX) b. ď‚ď€ ď€ fibrinogen and FDP's c. ď‚Żď€ fibrinolytic activity - ď‚Żď€ levels of plasminogen activators d. ď‚Żď€ antithrombin III increased risk of thromboembolic disease e. W.B.C ď‚ď€ to 21000/cmm f. Platelets ď‚Żď€ by 10-20 %
Metabolic Changes Secretionof human chorionic gonadotropin and elevated levels of estrogens promote hypertrophy of the thyroid gland increase thyroid-binding globulin T4 and T3 levels are elevated, free T4, free T3 thyrotropin (thyroidstimulatiflg hormone) remain normal Serum calcium levels decrease ionized calcium concentration remains normal.
Uteroplacental Circulation 10% CO 600-700ml/min pregnancy (50ml/min non pregnant uterus) 80% of (10% or 600ml)normally supply the placenta 20% Myometrium Dilation of uterious vasculature(no auto regulation)
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Uterine Blood Flow (No auto regulation) Abundant a-adrenergic & b-receptors Not affected by resp. gas tension But extreme hypocapnia Pa CO2< 20mmHg Proportional to uterine arterial and venous pressures Inversely proportional uterine vascular resistance
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Uterine Blood Flow (No auto regulation) Factors affecting ↓UBF Systemic hypotension Uterine vasoconstriction Uterine contraction Aortocaval compression Hypovolemia
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Uterine Blood Flow (No auto regulation) Factors affecting Systemic blockade(local blocks) Stress of labour (endogenous catacholamines) Phenylphrine (a-agonist) N.B. Ephidrine mainly b-agonist (used in spinal and epi hypotension) Oxytocin & hypertonic contrations
Foetal functions Foetus depends on the placenta for 1.Gas exchange – Respiration 2. Nutrition 3. Waste product elimination
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PHYSIOLOGIC ANATOMY Theplacenta is composed of projections of fetal tissue (villi) that lie in maternal vascular spaces (intervillous spaces). As a result of this arrangement, the fetal capillaries within villi readily exchange substances with the maternal blood that bathes them.
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PHYSIOLOGIC ANATOMY Maternalblood in the intervillous spaces is derived from spiral branches of the uterine artery and drains into the uterine veins. Fetal blood within villi is derived from umbilical cord via two umbilical arteries and returns to the fetus via a single umbilical vein.
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PLACENTAL EXCHANGE Mechanssmsof Placental exchange: 1. DIFFUTION Respiratory gases and small ions are transported by diffusion. Most drugs used in anesthesia have molecular weights well under 1000 can diffuse across the placenta. 2.BULK FLOW Water moves across by bulk flow. 3.ACTIVE TRANSPORT Amino acids, vitamins, and some ions (calcium and iron) utilize this mechanism.
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PLACENTAL EXCHANGE Mechanssmsof Placental exchange: 4.PINOCYTOSIS large molecules, such as immunoglobulins, are transported by pinocytosis. 5.Breaks Breaks in the placental membrane and mixing of maternal and fetal blood are probably responsible Rh sensitisation.
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Respiratory Gas Exchangeoxygen has the lowest storage to utilization ratio. term, fetal consumption averages about 21 mL/min Fetal oxygen stores are normally 42 mL. The normal fetus at term can survive 10 minutes or longer .
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Respiratory Gas ExchangeTransfer of oxygen across the placenta is dependent on the ratio of maternal uterine blood flow to fetal umbilical blood flow. The reserve for oxygen transfer is small. PaO, of only 40 mm Hg. The fetal hemoglobin oxygen dissociation curve is shifted to the left such that fetal hemoglobin has greater affinity for oxygen than does maternal hemogloin
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Respiratory Gas Exchangefetal hemoglobin concentration is usually 15 g/dL (compared with approximately 12 g/d.L in the mother. Carbon dioxide readily diffuses across the placenta. Maternal hyperventilation increases the gradient for the transfer of carbon dioxide from the fetus into the maternal circulation. Fetal hemoglobin also appears to have less affinity for carbon dioxide than does maternal hemoglobin.
Effect of Laboron Maternal Physiology During intense painful contraction the minute ventilation increase up to 300%. Oxygen consumption increases 60% excessive hyperventilation, PaCO2 ↓ below 20 mm Hg. Excessive maternal hyperventilation reduces uterine blood flow and promotes fetal acidosis. analogous to an auto transfusion 300-500ml Cardiac output rises 45% over third trimester values. The greatest strain on the heart,occurs immediately after delivery, 80% above prelabor values.
FETAL PHYSIOLOGY (1)Well-oxygenated blood from the placenta (approximately 80% oxygen saturation) mixes with venous blood returning from the lower body(25% oxygen saturation) and flows via the inferior vena cava into the right atrium. 2. Right atrial anatomy preferentially directs blood flow from the inferior vena cava (67% oxygen saturation) through the foramen ovale into the left atrium. 3. Left aerial blood is then pumped by the left ventricle to the upper body (mainly the brain and the heart). 4. Poorly oxygenated blood from the upper body returns via the superior vena rays to the right atrium.
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FETAL PHYSIOLOGY 5.Right atrial anatomy preferentially directs flow from the superior vena cava into the right ventricle. 6. Right ventricular blood is pumped into the pulmonary artery. 7. Because of high pulmonary vascular resistance, 95% of the blood ejected from the right ventricle (60% oxygen saturation) is shunted across the ductus arteriosus, into the destending aorta, and back to the placenta and lower body.
Obstetric Anaesthesia andits Challenges for the Anaesthetist Obstetric anaesthetist must understand maternal adoption to pregnancy in order to manipulate physiological changes following general or regional anaesthesia and anaesthesia in such a way that the condition of the neonate at delivery is optimized Understanding Physiology of Pregnancy has enabled many more women with chronic diseases to achieve pregnancy Pharmokokinetics of anesthetic drugs during pregnancy Placental transfer of drugs
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Obstetric Anaesthesia andits Challenges for the Anaesthetist Stress of multiple pregnancy, hypertension, PET, ET is well known now to anaesthetist. Distress of mother or fetus gives no leave way for anaesthetist but to conduct anaesthesia at VERY short notice without optimizing the condition Mother may be handling full stomach, bleeding, hypotension. Cannot be deferred otherwise we either loose mother or fetus or both Odd hours, emergency surgery without senior cover or at times lack of expert help culminates into catastrophic complications Maternal resuscitation, antepartum, postpartum hemorrhage etc.
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Obstetric Anaesthesia andits Challenges for the Anaesthetist Neonatal resuscitation – another challenge for both anaesthetist and neontalogist Failure to intubation or ventilate and another night mare for anesthesia Sever bleeding intra-op with little or no help from blood bank in the form blood, platelets, factors may end into demise also Amniotic embolism an other dreaded complication of sudden collapse,DIC, and ARDS HELLP syndrome and associated organ problems in unplanned unforeseen patient could be too much demanding and stressful situation for the anesthetist
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Obstetric Anaesthesia andits Challenges for the Anaesthetist Awareness during obstetric anaesthesia incidence is more than any other type of anaesthesia Supine hypotensive syndrome Epidural/ spinal failure/ collapse or cardiac arrest after spinal are some dreaded complications of obstetric anaesthesia Post spinal/ epidural headaches, backaches, quade-equina syndrome
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Some Other Challengesin Obstetric Anaesthesia Anaesthesia during pregnancy for non-obstetric purpose e.g. appendectomy, cervical circulate, tocolytic therapy and its implication may end in abortion and pulmonary edema, ARDS, & CHF Fetal lung maturity in certain diseases - prematurity , diabetes etc Drug effects- induction at delivery time and placental transfer, fetal handling of drugs, implication on well being of the newborn Congenital anomalies – resuscitation or needing immediate surgery e.g. neural defects
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Some Other Challengesin Obstetric Anaesthesia Trauma in pregnancy - another challenge Sudden cardiac arrest and its management is quite different from other types of cardiac arrest Many challenging scenarios may happen - patient in lathotomy - head stuck - cervical tear - patient demoralized from bad conduct of labor & - an anesthetic called to help ??? Drug abuse in parturient – another havoc
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Obstetric Anaesthesia isa multidisciplinary team involving Obstetrician Obstetric Anaesthetist Midwife Health visitors Physicians Neonatalogist Therefore communication is of utmost importance and good record keeping is vital for obstetric anesthetist
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“ A Pregnant Lady Is Like A Ticking Bomb That Can Burst Into Fatality Any Moment” Channa A B