physiological changes in pregnancy moderator: prof. dr. surinder singh presented by: dr.chittra


Post on 17-Dec-2015




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  • CAUSES Hormonal factors Mechanical effects of the gravid uterus Increased metabolic and oxygen requirements Demands of the fetoplacental unit Hemodynamics of placental circulation.
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  • CARDIOVASCULAR SYSTEM Physiologic changes in CVS begin in the first trimester CARDIAC OUTPUT Increases from 5th week of pregnancy reaches its maximum levels at around 32 weeks, after which there is a slight increase til labor, delivery, and the postpartum period in stroke volume and heart rate Stroke volume 20% to 50% at term Heart rate 20% by 4th week
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  • BLOOD PRESSURE Systemic arterial pressure is never increased during normal gestation Mid pregnancy, slight decrease in diastolic pressure Pulmonary arterial pressure maintains a constant level. Vascular tone is more dependent upon sympathetic control than in the nonpregnant state, hypotension develops more readily and more markedly consequent to sympathetic blockade following spinal or extradural anaesthesia. Central venous and brachial venous pressures remain unchanged during pregnancy, but femoral venous pressure is progressively increased due to mechanical factors
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  • Supine hypotension syndrome At term decrease in cardiac output due to obstruction of the inferior vena cava by the gravid uterus, which did not occur when women are placed in the lateral position. Despite the increase in blood volume and cardiac output, at term chances of hypotension, especially when in the supine position. 10% pregnant patients at term show signs of severe hypotension when assuming the supine position
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  • Aortocaval Compression. From mid-pregnancy, the enlarged uterus compresses both the inferior vena cava and the lower aorta when the patient lies supine. Obstruction of the inferior vena cava reduces venous return to the heart leading to a fall in cardiac output by 24% towards term. In the unanaesthetised state, most women are capable of compensating for the resultant decrease in stroke volume by increasing SVR and HR
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  • During anesthesia these compensatory mechanisms are reduced or abolished so that significant hypotension may rapidly develop Obstruction of the lower aorta and its branches causes diminished blood flow to kidneys, uteroplacental unit and lower extremities. During the last trimester, maternal kidney function is markedly lower in the supine than in the lateral position.
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  • ParameterChangeAmount (%) Heart rateIncreased20-30 Stroke volumeIncreased20-50 Cardiac outputIncreased30-50 ContractilityVariable10 Central venous pressure Unchanged Pulmonary capillary wedge pressure Unchanged Systemic vascular resistance Decreased20 Systemic blood pressureSlight decrease Midtrimester 10- 15 mm Hg, then rises Pulmonary vascular resistance Decreased30
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  • Investigation Findings Chest radiography Apparent cardiomegaly Enlarged left atrium Increased vascular markings Straightening of left-sided heart border Postpartum pleural effusion Electrocardiography Right-axis deviation Right bundle branch block ST-segment depression of 1 mm on left precordial leads Q waves in lead III T-wave inversion in leads III, V 2, and V 3 Small decrease in PR and QT interval Rotation 15 degrees (QRS axis)
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  • HEMATOLOGICAL SYSTEM Blood volume begins to increase early in pregnancy as a result of changes in osmoregulation and the renin-angiotensin system By term blood volume increases by up to 45% red cell volume increases by only 30%.This differential increase leads to the physiologic anemia of pregnancy with an average hemoglobin and hematocrit of 11.6 g/dL and 35.5% respectively. Oxygen transport is not impaired mother's body compensates for it by increased cardiac output, increased Pa O 2, and a rightward shift in the oxyhemoglobin dissociation curve.
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  • Factor Change II- Unchanged VII- Increased +++ VIII, IX, X, XII- Increased XI- Reduced Fibrinogen- Increased +++ Platelets- Stable
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  • Hypercoagulability exists in pregnancy, with increased levels of most coagulation factors Fibrinogen and factor VII are markedly increased other factors increase to a lesser extent. Protective adaptation to lessen the risks associated with the acute hemorrhage that occurs at delivery. The platelet count remains unchanged throughout most of pregnancy The platelet count increases in the postpartum period because of activation of hemostasis at the time of delivery The incidence of low platelet counts in normal pregnancy is approximately 8%.
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  • Previously the cutoff for initiation of neuraxial blocks was considered 100,000 10 9 /L but now in regional technique with platelet counts it is above 75,000 10 9 /L and with counts between 50,000 and 75,000 if the level is stable and clinical laboratory abnormalities or signs of a coagulopathic state are absent.
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  • RESPIRATORY SYSTEM Respiratory Tract. Hormonal changes to the mucosal vasculature of the respiratory tract lead to capillary engorgement and swelling of the lining in the nose, oropharynx, larynx, and trachea These symptoms can be exacerbated by fluid overload or oedema associated with pregnancy- induced hypertension or pre-eclampsia In such cases manipulation of the airway can result in profuse bleeding from the nose or oropharynx endotracheal intubation can be difficult only a smaller than usual endotracheal tube may fit through the larynx. Airway resistance is reduced due to the progesterone-mediated relaxation of the bronchial musculature
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  • Lung Volumes. Upward displacement by the gravid uterus causes a 4 cm elevation of the diaphragm, but TLC decreases only slightly because of compensatory increases in the transverse and antero-posterior diameters of the chest, and flaring of the ribs Diaphragm moves with greater excursions during breathing in the pregnant than in the non-pregnant state,breathing is more diaphragmatic than thoracic during gestation an advantage during supine positioning and high regional blockade.
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  • From middle of the second trimester, expiratory reserve volume, residual volume and functional residual volume are progressively decreased, by approximately 20% at term. Lung compliance is relatively unaffected, but chest wall compliance is reduced, especially in the lithotomy position.
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  • Ventilation and Respiratory Gases. Increase in minute ventilation starts soon after conception and peaks at 50% above normal levels around the second trimester. It is effected by a 40% rise in tidal volume and a 15% rise in respiratory rate Alveolar ventilation is about 70% higher at the end of gestation Arterial and alveolar carbon dioxide tensions are decreased by the increased ventilation An average PaCO 2 of 32 mmHg and arterial oxygen tension of 105 mmHg persist during most of gestation
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  • During labour, ventilation may be further accentuated, either voluntarily or involuntarily in response to pain and anxiety. Such excessive hyperventilation results in marked hypocarbia and severe alkalosis, which can lead to cerebral and uteroplacental vasoconstricton and a left shift of the oxygen dissociation curve The latter reduces the release of oxygen from haemoglobin with consequent decreased maternal tissue oxygenation as well as reduced oxygen transfer to the fetus.
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  • Increased oxygen consumption and the decreased reserve due to the reduced functional residual capacity, may result in rapid falls in arterial oxygen tension despite careful maternal positioning and preoxygenation Even with short periods of apnea, whether from obstruction of the airway or inhalation of a hypoxic mixture of gas, little defense against the development of hypoxia The increased minute ventilation combined with decreased functional residual capacity hastens inhalation induction or changes in depth of anaesthesia when breathing spontaneously
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  • GASTROINTESTINAL SYSTEM Mechanical Changes. Enlarging uterus causes a gradual cephalad displacement of stomach and intestines. At term the stomach has attained a vertical position rather than its normal horizontal one These mechanical forces lead to increased intragastric pressures as well as a change in the angle of the gastroesophageal junction, which in turn tends toward greater oesophageal reflux
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  • Progesterone relaxes smooth muscle consequently, it impairs esophageal and intestinal motility during pregnancy Whether gastric emptying is delayed during pregnancy is controversial Risk of pulmonary aspiration of gastric contents is there especially when undergoing an emergency cesarean delivery under general anesthesia. Established labor and the administration of parenteral opioids delay gastric emptying
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  • Epidural analgesia using local anesthetics without opioids does not affect gastric emptying The pain of labor may delay gastric emptying and promote emesis These changes may be caused by the effects of placentally derived gastrin
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  • RENAL SYSTEM Renal vasodilatation increases renal blood flow early during pregnancy but autoregulation is preserved Increased renin and aldosterone levels promote sodium retention Renal plasma flow and the GFR 50% durin