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Hypertensive Disorders with Pregnancy Professor Zouhair O Amarin MD MSc (Med. Sci) MSc (Med. Edu) FRCOG Department of Obstetrics and Gynaecology Jordan University of Science and Technology Hypertensive Disorders in Pregnancy Hypertensive disorders are some of the most common complications of pregnancy They complicate 7-10% of all pregnancies. Pregnancy Induced Hypertension - 70% Chronic Hypertension - 30% Up to 13% of PE patients well have chronic or essential hypertension Pregnancy can: Induce hypertension in women with no preexisting history Aggravate an already existing hypertensive disorder Generalized edema and Proteinuria Epigastric pain and visual or respiratory problems Eclamptic convulsions and coma Death In Jordan, hypertensive disease during pregnancy is a major cause of maternal deaths. It is associated with 6.7% of maternal mortality (5/76) National Maternal Mortality Study, Jordan, 2007-2008. Amarin et al. Classification A- Pregnancy Induced Hypertension 1. Gestational hypertension 2. Pre-eclampsia 3. Eclampsia B- Pregnancy Aggravated Hypertension Superimposed pre-eclampsia and eclampsia (on top of chronic hypertension) C- Chronic Hypertension with Pregnancy Definitions Gestational Hypertension BP reading 140/90 mmHg for the first time after 20 weeks of pregnancy No proteinuria BP returns to normal within 12 weeks postpartum (if the BP elevation persists, the woman is diagnosed as having chronic hypertension) Final diagnosis is only made postpartum May even be associated with an increased birth weight Definitions (cont.) Pre-eclampsia Mild pre-eclampsia BP 140/90 mmHg after 20 weeks gestation Proteinuria 1+ by urine dipstick or a total protein level 300 mg/24 hours - Pre-eclampsia can develop before the 20 week of mole and in the presence of hydatidiformgestation in lupus anticoagulant Definitions (cont.) Severe pre-eclampsia BP 160 mmHg systolic or 110 mmHg diastolic Proteinuria 2+ by urine dipstick or a total protein level of 2 gm/24 hours Definitions (cont.) Eclampsia Central nervous system (CNS) involvement with the occurrence of convulsions that cannot be attributed to other causes Superimposed PE or eclampsia Development of PE or eclampsia in pre-existing hypertension detected by a further increase of 30 mmHg in SBP or 15 mmHg in DBP or of 300 mg/24 hours in proteinuriaNew onset proteinuriahypertensive women but with no before 20 weeks gestation or or a drop in proteinuriaA sudden increase in with 3platelet count to 35 Parity: PG have double incidence Lower socio-economic status Genetic predisposition, recessive trait Obstetric complications: multiple and molar pregnancy, fetal hemolytic diseases (hydrops fetalis), polyhydramnios Existing medical conditions: chr BP, ren D, DM, SLE, antiphospholipid AS, Previous PE. The recurrence rate for PE with the same male partner is 20%, and usually becomes apparent at later gestation than in the first pregnancy Obesity: 4.3% for a women with a body mass index 35 kg/m2 Conditions that appear to decrease PE incidence Prolonged exposure to paternal antigen Smoking, but if PE occurs then perinatal mortality triples Placenta previa Pre-existing (chronic) hypertension: Hypertension is present before pregnancy or detected before 20 weeks Or Hypertension first diagnosed after 20 weeks gestation and persisted after 12 weeks postpartum The cause of pre-eclampsia is unknown The placenta appears to be incriminated Delivery of the placenta is the only known cure The disorder is more frequent with large placental mass, e.g. twins or abnormal placentae A proposed cause is the release of a toxic factor from the placenta which alters maternal endothelial cell functions. This hypothesis has not been proven Theories Defective trophoblastic invasion of the spiral (I) arteries (II) Immunologic factor (III) Increased pressor responses (IV) Prostaglandins imbalance (V) Genetic predisposition (VI) Inflammatory factors Many investigators feel that uteroplacental insufficiency is necessary for the development of the disease. - Ischemia could be due to: Underlying vascular changes (hypertensive disease or failure of the normal physiologic changes in the spiral arteries of the uterus) Increased myometrial resistance of the myometrial vessels, which could be related to a heightened myometrial tension produced by the large fetus in a primiparous women, by twins, or by polyhydramnios The poorly perfused trophoblast release “factor X” which enters maternal circulation and causes endothelial dysfunction (serum of women with PET is able to activate and damage vascular endothelial tissue in vitro) imbalance between different causesEndothelial dysfunction classes of locally produced vasoconstrictor and vasodilators Immunologic factor Stimulation of the maternal immune system by the early conceptus is essential for production of blocking antibodies to antigenic sites on the placenta, thus preventing the rejection of the fetus and placenta. Hypoimmune response results in damage of the placenta and subsequent PE PE is less common in previously stimulated immunity conditions as in: Previous pregnancy Consanguineous marriages Increased maternal anti-HLA antibodies Pathophysiology IIAngiotensin Serotonin Endothelin Prostacyclin Nitric oxide Platelet activation Thrombocytopenia Reduced production of anti-thrombin III Vasospasm Intravascular coagulation Plasma volume constriction Patho-physiologic changes in pre-eclampsia Vasospasm Intravascular coagulation Plasma volume constriction Patho-physiologic Changes in Pre-eclampsia (cont.) Vasospasm Excess production/sensitivity to vasoconstrictors: Angiotensin II Serotonin Endothelin Decreased production/sensitivity to vasodilators: Prostacyclin Nitric oxide Patho-physiologic Changes in Pre-eclampsia (cont.) Intravascular coagulation: Platelet activation Thrombocytopenia Reduced production of anti-thrombin III Patho-physiologic Changes in Pre-eclampsia (cont.) Plasma volume contraction Redistribution of fluid from the intra-vascular to interstitial fluid spaces so that total extra cellular fluid volume remains unaltered This is an important consideration as intravascular volume correction may result in pulmonary edema when capillary permeability is high and plasma oncotic pressure low Organ hypoperfusion Kidney: GFR, proteinuria, hyperuricaemia, oliguria Liver: SGOT, SGPT, epigastric pain Brain: visual scotomata due to occipital lobe ischemia, headache, convulsions (eclampsia) Placenta: IUGR, placental abruption Diagnosis History Personal history Past history Menstrual history Obstetric history Complaints and history of present pregnancy Diagnosis (cont.) Physical Examination Hypertension Edema Obstetric examination Diagnosis (cont.) Investigations PCV and thrombocytopenia CBC: SGOT, SGPT: Elevated liver enzymes Creatinine clearance, serum creatinine, uric acid, total protein in urine, and blood urea: impaired PT, PTT, clot. and bleed. time in DIC. Fibrinogen and Coagulation profile: FDP to diagnose DIC Fetal Surveillance Diagnosis (cont.) Indicators of severity of pre-eclampsia Presence of symptoms Persistent headache or other cerebral or visual disturbances Persistent epigastric pain Diastolic BP 110 mmHg Proteinuria of 2+ or more by urine dipstick or a total protein level of 2 gm/liter in a 24-hour urine sampling Diagnosis (cont.) Abnormal laboratory findings Obvious fetal growth restriction Neurological effects: Scotomata, hyperreflexia Eclamptic convulsions Indications to terminate pregnancy in pre-eclampsia Maternal Indications Completed 37 weeks Abnormal liver/ renal functions Severe preeclampsia/ eclampsia regardless of the gestational age In selected cases of severe PET, where the expertise and equipment are available, expectant management may be undertaken for fetal indications Indications to terminate pregnancy in pre-eclampsia (cont.) Fetal Indications Obvious IUGR Oligohydramnios, IUFD The presence of congenital fetal malformations incompatible with life Management of pre-eclampsia Convulsion prophylaxis Treatment of hypertension Timing of delivery Fluid management Supportive care for various end organ complications Management of Mild Pre-eclampsia Completed 37 weeks gestation: Termination of pregnancy yields better fetal and maternal outcomes 3437 weeks: Expectant management Gestation Antihypertensive therapy is recommended when SBP 105-110, as such treatment 160-170 and DBP decreases the maternal cerebral and cardiovascular complications In acute control of sever hypertension, the objective of reduction of blood pressure to a gradual therapy is a mmHg140-150 / 90-100level of about Blood pressure should be assessed every 15 minutes initially, once the blood pressure is stabilized the interval can be lengthened to 30 minutes Lowering the blood pressure rapidly over minutes may be associated with abrupt and profound decrease cardiac decrease in blood pressure output to the uterus with possible fetal hypoxia continuous fetal heart rate monitoring should be performed during initial therapy to detect such effect and allow early remedial action Hydralazine, nifedipine and labetalol are the most commonly used drugs. There is no convincing evidence that one is particularly better than another , Atenolol should be avoided in asthma. Labetalol should be avoideddiureicsACE inhibitor, ARB and is a vasodilatorHydralazine (Apresoline) a bolus may 5-10 mg I.V given slowly (Loading dose have a dramatic hypotensive effect so it is necessary to )be given slowly different regimens:Maintenance dose l Syringe pump with 100 mg hydralazine / 50 mL N.S run at 2-20 mg/hr (1-10 mL/h). The rate is determined by titration against the blood pressure response l 2.5-5 mg as an I.V boluses with dosage interval not closer than every 20 minutes until BP is controlled l 40 mg hydralazine / 1000 ml N.S. The rate is determined by titration against the blood pressure response Chronic Hypertension: Management Antihypertensive treatment: Alpha methyldopa: Centrally acting drug Dose: 13 gm/day Beta blockers: Atenolol: 50-200 mg/day Labetalol: 2002000 mg/day Nifedipine: Calcium channel blocker Dose: 3090 mg/day orally Chronic Hypertension: Management (cont.) Diuretics are not recommended Angiotensin converting enzyme inhibitors are contraindicated with pregnancy Termination if: Fetal maturity reached Fetal distress and severe IUGR Additional complications occur (severe preeclampsia, abruptio placentae) Screening At the present time, there are no screening tests for PE that are reliable and valid Roll-over test A positive roll-over test is defined as a 20 mmHg or more increase in DBP when measured 5 minutes after the gravid woman is asked to assume a supine position after lying laterally recumbent between 28 and 32 weeks gestation The positive predictive value is 33% 24 hours urinary calcium excretion Is lower in women with PE than normotensive pregnant women. the sensitivity of 24 hours urinary calcium excretion measured between 10 and 24 weeks in predicting PE was 88% and the positive predictive value was 32% (Ramos 1991) Plasma urate Uric acid value of 5.9 mg/dL determined at 24 weeks of gestation has a positive predictive value of 33% Angiotensin II sensitivity A normal pregnant patient requires a mean angiotensin II dose of 13.5 14.9 ng/kg/min to increase her DBP by 20 mmHg angiotensin II is infused in a In angiotensin II test stepwise fashion until there is a 20-mmHg rise in DBP. About 90% of women requiring 8 ng/kg/min angiotensin II remained normotensive throughout pregnancy. Conversely 90% of women who respond with 80% of women who will subsequently develop PE and with a false +ve of only 5%. If diagnosed before 24 week the false +ve will be higher Others Increase fibronectin , factor VIII Ag Leptin begin to decline as much as 13 Antithrombin III weeks prior to the development of clinical manifestations of PE Increase ALP , HCG Inhibin A and activin A appear to be particularly promising in the search for early pregnancy markers for the development of PE Prevention 1. Low dose aspirin: Inhibits the enzyme cyclooxygenase which is essential for the synthesis of prostaglandins Inhibits the AII binding sites on platelets A low dose (60-80 mg daily) was found to selectively inhibits thromboxane A2 synthesis. However two large studies have failed to show any significant benefit of aspirin therapy in preventing PET There is no recommendation to use aspirin as routine for prevention of PE, but it is recommended in certain cases where patient is thought to gain benefit like in anticardiolipin syndrome Aspirin It decreases PE PNM Preterm birth No effect on the weight, placental abruption 2 receptor seretonin: selective Ketanserin antagonist 2. Antioxidants Antioxidants are a diverse family of components that function to prevent overproduction of and damage caused by noxious free radicals Vitamin E (alpha tocopherol) Vitamin C (ascorbic acid) Beta-carotene A total of 283 women at risk for PET were randomized at 18-22 weeks gestation to treatment with antioxidant or placebo. Antioxidant therapy significantly reduced endothelial cell activation, suggesting that such therapy might be beneficial in the prevention of PE. A larger trial must be performed before concluding that such therapy prevents PE (Chappell 1999) 3. Dietary manipulation Dietary supplementation in areas of Ca+ deficiency Research showed that low Ca+ lead to increase parathyroid hormone activity and an increase in cytosolic Ca+, resulting in increased smooth vascular reactivity At least 14 randomized trial and resultant meta-analysis showed that Ca+ supplementation during pregnancy significantly lowered SBP and DBP as well as the incidence of PE. However, Levin (1997) performed a randomized trial, in which 4589 healthy nulliparous women were randomly administered either 2 g of supplemental calcium or placebo. Supplemental calcium didnt prevent any of the hypertensive disorder due to pregnancy including gestational hypertension or PE At the present time, Ca+ supplementation (1.5-2 g / day) should be considered in women who are likely to have a relatively low dietary Ca+ intake (e.g. teenagers and women with low pre-pregnancy body mass index) Other dietary manipulation that have been tested to prevent PET includes: Sodium restricted diet Administering 4-9 capsules containing fish oil each day Both are proven to be ineffective in preventing PET 4. Prophylactic administration of antihypertensive medication Prophylactic administration of antihypertensive medication has not been shown to prevent the development of PE Meta-analysis of randomized studies examining given to chronically hypertensive antihypertensives women didnt influence the incidence of superimposed PE Recommendation for measuring BP Time of Measurements For diagnosing hypertension, multiple readings should be taken at various times throughout the waking hours of the patient Extraneous variables that can influence the blood pressure should be avoided in the 60 minutes prior to evaluation. This include food intake, strenuous exercise, smoking and the ingestion of caffeine Smoker person who stopped smoking for more than 30 minutes before measurement is made - Caffeine intake can raise the BP acutely, primarily in non- habitual coffee drinkers. - Taking the BP in a cool room - Neither the patient nor the observer should talk during the measurement (while talking the measured value can raise by as much as 8 to 15 mmHg). - The stethoscope should be placed lightly over the brachial artery, since the use of excessive pressure can increase the diastolic pressure reading up to 10 to 15 mmHg. - The cuff should be deflated slowly at a rate of 2 to 3 mmHg per heartbeat. - The BP should be measured initially in bo