高血压英文ppt精品课件structural disorders fetal demise intrauterine fetal

,Structural Disorders Fetal Demise / Intrauterine Fetal Death,DEFINITION: Death of a fetus after the age of viability,Interventions and Nursing Care Allow patient to decide when she wants to deliver Most women go into labor on their own in 2 weeks, so may wait for labor to begin spontaneously Induce labor Prostaglandin (Prostin E) causes smooth muscles to contract: Side effects - nausea, vomiting, diarrhea Cytogel Provide with Emotional Support, allow to hold baby,Assessment: 1. First indication is usually NO fetal movement 2. NO fetal heart tones Confirmed by ultrasound 3. Decrease in the signs and symptoms of pregnancy,PREGNANCY INDUCED HYPERTENSION,A hypertensive disease of pregnancy. Known as pre-eclampsia and eclampsia. Pre-eclampsia = hypertension, proteinuria, edema Eclampsia = other signs plus convulsions It develops between the 20th and 24th week of gestation and disappears after the tenth day postpartum,PREDISPOSING FACTORS,PRIMIGRAVIDA,MULTIPLE PREGNANCY,VASCULAR DISEASE,UNDER 17 AND OVER 35,LOWER SOCIOECONOMIC STATUS,Severe malnutrition, decrease Protein intake,Inadequate or late prenatal care,FAMILY HISTORY,HYDATIFORM MOLE,Diabetes, renal,PATHOLOGICAL CHANGES,PIH is due to:,GENERALIZED,ARTERIOLAR CYCLIC VASOSPASMS,INCREASED PERIPHERAL RESISTANCE; IMPEDED BLOOD FLOW ( in blood pressure),Endothelial CELL DAMAGE,Intravascular Fluid Redistribution,(decrease in diameter of blood vessel),Decreased Organ Perfusion,Multi-system failure Disease,Clinical Manifestations Clinical Manifestation,HYPERTENSION,Earliest and The Most Dependable Indicator of PIH,Hypertension,B/P = 140 / 90 if have no baseline. 1. 30 mm. Hg. systolic increase or a 15 mm. Hg. diastolic increase (two occasions four to six hours apart) 2. Increase in MAP 20 mm.Hg over baseline or 105 mm. Hg. with no baseline,Positive Roll Over Test,Rationale for HYPERTENSION,The blood pressure rises due to: ARTERIOLAR VASOSPASMS AND VASOCONSTRICTION causing (Narrowing of the blood vessels) an increase in peripheral resistance fluid forced out of vessels HEMOCONCENTRATION Increase blood viscosity = Increased hematocrit,Key Point to Remember !,HEMOCONCENTRATION develops because: Vessels became narrowed forcing fluid to shift Fluid leaves the intracellular spaces and moves to extracellular spaces Now the blood viscosity is increased (Hemocrit is increased) *Very difficult to circulate thick blood,Test Yourself !,Which of these readings indicates hypertension in the patient whose blood pressure normally is 100 / 60 and MAP of 77? a. 120 / 76; MAP 96 b. 110 / 70; MAP 83 c. 130 / 80; MAP 98 d. 125 / 70; MAP 88,Proteinuria,With Renal vasospasms, narrowing of glomular capillaries which leads to decreased renal perfusion and decreased glomerular filtration rate (damage to glomeruli) PROTEINURIA Protein leaks across the membrane, tubules cannot reabsorb,The degree of PROTEINURIA reflects the severity of the disease Spilling of 1+ of protein is significant to begin treatment Oliguria and tubular necrosis may precipitate acute renal failure,Significant Lab Work Changes in Serum Chemistry,Decreased urine creatinine clearance (80-130 mL/ min) Increased BUN (12-30 mg./dl.) Increased serum creatinine (0.5 - 1.5 mg./dl) Increased serum uric acid (3.5 - 6 mg./dl.),Weight Gain and Edema,Clinical Manifestation: Edema may appear rapidly Begins in lower extremities and moves upward Pitting edema and facial edema are late signs Weight gain is directly related to accumulation of fluid,WEIGHT GAIN AND EDEMA,Rationale: Decreased blood flow to the kidneys causes a loss of plasma proteins and albumin This leads to a decreased colloid osmotic pressure. A in COP allows fluid to shift from from intravascular to extravascular. Now there is an accumulation of fluid in the tissues. Increased angiotensin and aldostersone triggers retention of sodium and water.,The difference between dependent edema and generalized edema is important. The patient with PIH has generalized edema because fluid is in all tissues.,The Nurse Must Know,Placenta,With Vasospasms and Vasoconstriction of the the vessels in the placenta. Decreased Placental Perfusion and Placental Aging,Fetal Growth is retarded - IUGR, SGA,Positive OCT / Late Decelerations,With Prolonged decreased Placental Perfusion:,Condition is Worsening,Oliguria 100ml./4 hrs or less than 30 cc. / hour Edema moves upward and becomes generalized (face, periorbital, sacral) Excessive weight gain greater than 2 pounds per week,Central Nervous System Changes,Cerebral edema - forcing of fluids to extracellular Headaches - severe, continuous Hyperreflexia Level of Consciousness changes changes in affect Convulsions / seizures,Visual Changes,Retinal Edema and spasms leads to: Blurred vision Double vision Retinal detachment Scotoma (areas of absent or depressed vision),Nausea and Vomiting Epigastric pain often sign of impending coma,Pre-Eclampsia Mild Severe,B/P 140/90 160/110 Protein 1+ 2+ 3+ 4+ Edema 1+, lower legs 3+ 4+ Weight 2lb. / week Reflexes 1+ 2+ brisk 3+ 4+ (Hyperreflexia) Clonus present Retina 0 Blurred vision, Scotoma Retinal detachment GI, Hepatic 0 N late decelerations,Interventions and Nursing Care,Home Management Decrease activities and promote bed rest Sedative drugs Lie in left lateral position Remain quiet and calm restrict visitors and phone calls Dietary modifications increase protein intake to 70 - 80 g/day maintain sodium intake Caffeine avoidance Weigh daily at the same time Keep record of fetal movement - kick counts Check urine for Protein,Hospitalization,If symptoms do not get better then the patient needs to be hospitalized in order to further evaluate her condition. Common lab studies: CBC, platelets; type and cross match Renal blood studies - BUN, creatitine, uric acid Liver studies - AST, LDH, Bilirubin DIC profile - platelets, fibrinogen, FSP, D-Dimer,Hospital Management Nursing Care Goal,1. Decrease CNS Irritability 2. Control Blood Pressure 3. Promote Diuresis 4. Monitor Fetal Well-Being 5. Deliver the Infant,Decrease CNS Irritability,Provide for a Quiet Environment and Rest 1. MONITOR EXTERNAL STIMULI Explain plans and provide Emotional Support Administer Medications 1. Anticonvulsant - Magnesium Sulfate 2. Sedative - Diazepam (Valium) 3. Apresoline Assess Reflexes Assess Subjective Symptoms Keep Emergency Supplies Available,Magnesium Sulfate,ACTION CNS Depressant, reduces CNS irritability Calcium channel blocker- inhibits cerebral neurotransmitter release ROUTE IV effect is immediate and lasts 30 min. IM onset in 1 hour and lasts 3-4 hours Prior to administration: Insert a foley catheter with urimeter for assessment of hourly output,Magnesium Sulfate,NURSING IMPLICATIONS 1. Monitor respirations 14-16; 100cc in 4 hrs. 4. Measure Magnesium levels normal is 1.5-2.5 mg/dl Therapeutic is 4-8mg/dl. Toxicity - 9mg/dl; Absence of reflexes is 10 mg/dl; Respiratory arrest is 12-15 mg/dl; cardiac arrest is 15 mg/dl. Have Calcium Gluconate available as antagonist,Test Yourself !,A Woman taking Magnesium Sulfate has a respiratory rate of 10. In addition to discontinuing the medication, the nurse should: a. Vigorously stimulate the woman b. Administer Calcium gluconate c. Instruct her to take deep breaths d. Increase her IV fluids,Nursing Care Hospital Management,1. Decrease CNS Irritability 2. Control Blood Pressure 3. Promote Diuresis 4. Monitor Fetal Well-Being 5. Deliver the Infant,Control Blood Pressure,Check B / P frequently. Give Antihypertensive Drugs Hydralzine ( apresoline) Labetalol Aldomet Procardia Check Hemocrit,* Do NOT want to decrease the B/P too low or too rapidly. Best to keep diastolic 90. Need to maintain uteroplacental perfusion!,Nursing Care Hospital Management,1. Decrease CNS Irritability 2. Control Blood Pressure 3. Promote Diuresis 4. Monitor Fetal Well-Being 5. Deliver the Infant,Promote Diuresis,*Dont give Diuretic, masks the symptoms of PIH Bed rest in left or right lateral position Check hourly output - foley cath with urimeter Dipstick for Protein Weigh daily - same time, same scale,Nursing Care Hospital Management,1. Decrease CNS Irritability 2. Control Blood Pressure 3. Promote Diuresis 4. Monitor Fetal Well-Being 5. Deliver the Infant,Monitor Fetal Well-Being,FETAL MONITORING- assessing for late decelerations. NST - Non-stress test OCT -oxytocin challenge test If all else fails - Deliver the baby,Key Point to Remember !,SEVERE COMPLICATIONS OF PIH: PLACENTAL SEPARATION - ABRUPTIO PLACENTA; DIC PULMONARY EDEMA RENAL FAILURE CARDIOVASCULAR ACCIDENT IUGR; FETAL DEATH HELLP SYNDROME,HELLP Syndrome,A multisystem condition that is a form of severe preeclampsia - eclampsia H = hemolysis of RBC EL = elevated liver enzymes LP = low platelets 100,000mm (thrombocytopenia),Etiology of HELLP,Hemolysis occurs from destruction of RBCs Release of bilirubin Elevated liver enzymes occur from blood flow that is obstructed in the liver due to fibrin deposits Vascular vasoconstriction endothelial damage platelet aggregation at the sites of damage low platelets.,HELLP,Assessment: 1. Right upper quadrant pain and tenderness 2. Nausea and vomiting 3. Edema Flu like symptoms Lab work reveals a. anemia low Hemoglobin b. thrombocytopenia low platelets. 20 u/L. - LDH when cells of the liver are lysed, they spill into the bloodstream and there is an increase in serum. 90 u/L/,HELLP,Intervention: 1. Bedrest any trauma or increase in intra- abdominal pressure could lead to rupture of the liver capsule hematoma. 2. Volume expanders 3. Antithrombic medications,Heart Disease in Pregnancy,Cardiac Response in All Pregnancies,Increase in Cardiac Output 30% - 50% Expanded Plasma Volume Increase in Blood (Intravascular) Volume,Every Pregnancy affects the cardiovascular system,A woman with a healthy heart can tolerate the stress of pregnancy, but a woman with a compromised heart is challenged Hemodynamically and will have complications,Effects of Heart Disease on Pregnancy,Growth Retarded Fetus Spontaneous Abortion Premature Labor and Delivery,Effects of Pregnancy on Heart Disease,The Stress of Pregnancy on an already weakened heart may lead to cardiac decompensation (failure). The effect may be varied depending upon the classification of the disease,Classification of Heart Disease,Class 1 Uncompromised No alteration in activity No anginal pain, no symptoms with activity Class 2 Slight limitation of physical activity Dyspnea, fatigue, palpitations on ordinary exertion comfortable at rest p. 669,Class 3 Marked limitation of physical activity Excessive fatigue and dyspnea on minimal exertion Anginal pain with less than ordinary exertion Class 4 Symptoms of cardiac insufficiency even at rest Inability to perform any activity without discomfort Anginal pain Maternal and fetal risks are high p. 669,Nursing Care - Antepartum,Decrease Stress Teach the importance of REST! watch weight assess for infections - stay away from crowds assess for anemia assess home responsibilities Teach signs of cardiac decompenstion,Key Point to Remember Signs of Congestive Heart Failure,Cough (frequent, productive, hemoptysis) Dyspnea, Shortness of breath, orthopnea Palpitations of the heart Generalized edema, pitting edema of legs and feet Moist rales in lower lobes, indicating pulmonary edema,Teach about diet high in iron, protein low in sodium and calories ( fat ) Watch