Summer 2013 Risk Factors Age – under 17 over 35 Gravida and Parity Socioeconomic status Psychological well-being Predisposing chronic illness – diabetes, heart conditions, renal Pregnancy related conditions – hyperemesis gravidarum, gestational hypertension Goals of Care for High Risk Pregnancy © Provide optimum care for the mother and the fetus © Assist the client and her family to understand and cope through education Abortions Termination of pregnancy at any time before the fetus has reached the age of viability Either: spontaneous – occurring naturally induced – artificial Types of Abortions Threatened Imminent Complete Incomplete Missed Recurrent/Habitual Question??? What are two main complications related to a missed abortion? 1. 2. Cerclage procedure -- purse-string suture placed around the internal os to hold the cervix in a normal state Nursing Care post cerclage Bedrest in a slight trendelenberg position Teach Assess for leakage Assess for contractions Assess fetal movement and report decrease movement Assess temperature for elevation Key Concepts Related to Bleeding Disorders If a woman is Rh-, RhoGam is given within 72 hours of abortion Provide emotional support. Feelings of shock or disbelief are normal Encourage to talk about their feelings. It begins the grief process Ectopic Pregnancy Implantation of the blastocyst in ANY site other than the endometrial lining of the uterus ovary (5) Cervical Early: Assessment Ectopic Pregnancy • Missed menstruation followed by vaginal bleeding (scant to profuse) • Unilateral pelvic pain, sharp abdominal pain • Referred shoulder pain • Cul-de-sac mass Acute: • • • • Shock – blood loss poor indicator Cullen’s sign -- bluish discoloration around umbilicus Nausea, Vomiting Faintness Treatment Options / Nursing Care Combat shock / stabilize cardiovascular • Type and cross match • Administer blood replacement • IV access and fluids Laparotomy Psychological support Linear salpingostomy Methotrexate – used prior to rupture. Destroys fast growing cells Gestational Trophoblastic Disease Hydatiform Molar Pregnancy A DEVELOPMENTAL ANOMALY OF THE PLACENTA WITH DEGENERATION OF THE CHORIONIC VILLI As cells degenerate, they become filled with fluid and appear as fluid filled grapesize vessicles. Assessment: Vaginal Bleeding -- scant to profuse, brownish in color (prune juice) Possible anemia due to blood loss Enlargement of the uterus out of proportion to the duration of the pregnancy Vaginal discharge of grape-like vesicles May display signs of pre-eclampsia early Hyperemesis gravidarium No Fetal heart tone or Quickening Abnormally elevated level of HCG Question 6 Interventions and Follow-Up Empty the Uterus by D & C or Hysterotomy Extensive Follow-Up for One Year • Assess for the development of choriocarcinoma • Blood tests for levels of HCG frequently • Chest X-rays • Placed on oral contraceptives • If the levels rise, then chemotherapy started usually Methotrexate Critical Thinking Exercise A woman who just had an evacuation of a hydatiform mole tells the nurse that she doesn’t believe in birth control and does not intend to take the oral contraceptives that were prescribed for her. How should the nurse respond? Placenta Previa Low implantation of the placenta in the uterus Etiology • Usually due to reduced vascularity in the upper uterine segment from an old cesarean scar or fibroid tumors Three Major Types: • Low or Marginal • Partial • Complete Question 8 Interventions and Nursing Care Placenta Previa Bed-rest Assessment of bleeding Electronic fetal monitoring If it is low lying, then may allow to deliver vaginally Cesarean delivery for All other types of previa Abruptio Placenta Premature separation of the placenta from the implantation site in the uterus Etiology: ª Chronic Maternal Hypertension ª Short umbilical cord ª Trauma ª History of previous delivery with separation ª Smoking / Caffeine / Cocaine ª Vascular problems such as with diabetes ª Multigravida status ª Defined as marginal, partial or complete Treatment and Nursing Care Abruptio Placenta Cesarean delivery immediately Combat shock – blood replacement / fluid replacement Blood work – assessment for complication of DIC Placenta Previa • PAINLESS vaginal bleeding Abruptio Placenta Bleeding accompanied by • Bright red bleeding • First episode of bleeding is slight then becomes profuse Signs of blood loss comparable to extent of bleeding Uterus soft, non-tender Fetal parts palpable; FHT’s countable and uterus is not hypertonic Blood clotting defect absent • • • • PAIN Dark red bleeding First episode of bleeding usually profuse Signs of blood loss out of proportion to visible amount Uterus board-like, painful and low back pain Fetal parts non-palpable, FHT’s non-countable and high uterine resting tone (noted with IUPC) Blood clotting defect (DIC) likely Signs of Concealed Hemorrhage Increase in fundal height Hard, board-like abdomen High uterine baseline tone on electronic fetal monitoring Persistent abdominal pain and low back pain Systemic signs of hemorrhage Critical Thinking Mrs. A., G3 P2, 38 weeks gestation is admitted to L & D with scant amount of dark red bleeding. What is the priority nursing intervention at this time? A. Assess the fundal height for a decrease B. Place a hand on the abdomen to assess if hard, board-like, tetanic C. Place a clean pad under the patient to assess the amount of bleeding D. Prepare for an emergency cesarean delivery Disseminated Intravascular Coagulation (DIC) Anti-coagulation and Pro-coagulation effects existing at the same time. Etiology Defect in the Clotting Cascade An abnormal overstimulation of the coagulation process Activation of Coagulation with release of thromboplastin into maternal bloodstream Thrombin (powerful coagulant) is produced Fibrinogen fibrin which enhances platelet aggregation and clot formation Widespread fibrin and platelet deposition in capillaries and arterioles Etiology continued Resulting in Thrombosis (multiple small clots) Excessive clotting activates the fibrinolytic system Lysis of the new formed clots create fibrin split products These products have anticoagulant properties and inhibit normal blood clotting A stable clot cannot be formed at injury sites Hemorrhage occurs Ischemia of organs from vascular occlusion of numerous fibrin thrombi Multisite hemorrhage results in shock and can result in death Assessment & Intervention Precipitating factors Abruption PIH/HELLP syndrome Sepsis Anaphylactoid Syndrome Labs to review PT, PTT, Platelets, D-Dimer, FSP Interventions Remove the cause Replace fluids (Blood or blood products) Meds Assessment/Signs and Symptoms Spontaneous bleeding – from gums and nose (epistaxis, injection and IV sites, incisions) Excessive bleeding – Petechiae and ecchymosis at site of blood pressure cuff, pulse points Tachycardia, diaphoresis, restlessness, hypotension Hematuria, oliguria, occult blood in stool Altered LOC if cerebral circulation is decreased or cerebral bleed Diagnostic Tests Lab work reveals: PT – Prothrombin time is prolonged PTT – Partial thromboplastin time increased D-Dimer – increased, product that results from fibrin degradation. More specific marker of the degree of fibrinolysis Platelets – decreased, thrombocytopenia Fibrin Split Product – increased An increase in both FSP and D-dimer are indicative of DIC Assessment Persistent nausea and vomiting Weight loss from 5 - 20 pounds May become severely dehydrated with oliguria AEB increased specific gravity, and dry skin Depletion of essential electrolytes Metabolic alkalosis -- Metabolic acidosis Starvation Nursing Care / Interventions Hyperemesis Gravidarium Control vomiting Maintain adequate nutrition and electrolyte balance Allow patient to eat whatever she wants If unable to eat – Total Parenteral Nutrition Combat emotional component – provide emotional support and outlet for sharing feelings Mouth care Weigh daily Check urine for output, ketones Classification of HTN in Pregnancy Gestational HTN = BP > or equal to 140/90 after 20 weeks (replaces term of PIH), protein negative or trace Pre-eclampsia = BP > or equal to 140/90 after 20 weeks, proteinuria, edema considered nonspecific Eclampsia = Progression of pre-eclampsia to generalized seizures not attributable to other causes Chronic HTN = BP > or equal to 140/90 that was known to exist before pregnancy or develops prior to 20 weeks gestation or does not resolve after 6 weeks after delivery Predisposing Factors Primigravida Multiple gestation pregnancy Vascular Disease Age >35 Obesity Hydatiform Molar Pregnancy Family History Lower SES (poor nutrition,/decreased protein intake, inadequate prenatal care) PATHOLOGICAL CHANGES Gestational Hypertension due to: GENERALIZED ARTERIOLAR CYCLIC VASOSPASMS (decrease in diameter of blood vessel) INCREASED PERIPHERAL RESISTANCE; IMPEDED BLOOD FLOW ( in blood pressure) Endothelial CELL DAMAGE Intravascular Fluid Redistribution Decreased Organ Perfusion Multi-system failure Disease 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 Increased blood viscosity = Increased hematocrit Key Point to Remember ! HEMOCONCENTRATION develops because: Vessels became narrowed forcing fluid to shift out of the vascular space Fluid leaves the intravascular space and moves to extravascular spaces Now the blood viscosity is increased (Hematocrit is increased) **Very difficult to circulate thick blood Proteinuria With renal vasospasms, narrowing of glomerular capillaries which leads to decreased renal perfusion and decreased glomerular filtration rate PROTEINURIA 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 The Nurse Must Know The difference between dependent edema and generalized edema is important. The patient with pre-eclampsia has generalized edema because fluid is in all tissues. Placenta Due to Vasospasms and Vasoconstriction of the vessels in the placenta. Decreased Placental Perfusion and Placental Aging Positive CST / __________Decelerations With Prolonged decreased Placental Perfusion: Fetal Growth is retarded - IUGR, SGA Oliguria – 100ml/4 hrs or less than 30 ml. / 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 LOC 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 Mild Pre-eclampsia Systolic> or = to 140/90 but <160 mm Hg Diastolic > or = to 90 but < 110 mm Hg Protein > or = to 0.3 g but < 2 g in 24 hr specimen (1-2+ dipstick) Creatinine , serum normal Platelets normal ALT/AST normal or minimal increase Urine output normal No HA Absent RUQ pain/ no N/V Absent to minimal visual changes No pulmonary edema or heart failure Normal fetal growth Severe Pre-eclampsia > or = to 160 mm Hg 2 readings 6 hrs apart on bedrest > or = to 110mm Hg Protein > or = to 5 g in 24 hr specimen (3+ or higher dipstick) Creatinine elevated > 1.2 mg/ dL Platelets decreased < 100, 000 cells/mm3 ALT/AST Elevated levels Oliguria common, often <500 ml/day HA Often present N&V, epigastric pain may be present, often precedes seizures Visual disturbances common May be present IUGR, reduced amniotic fluid 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, creatinine, uric acid Liver studies -- AST, ALT, 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. Vasodilator-- Apresoline (hydralazine) 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; < 12 is critical 2. Assess for hyporeflexia -- D/C if hyporefexia 3. Measure Urinary Output >100ml in 4 hrs. 4. Measure Magnesium levels – normal is 1.5-2.5 mg/dl per hr 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 Control Blood Pressure Check B / P frequently. Give Antihypertensive Drugs Hydralazine Labetalol Nifedipine Check Hematocrit •Do NOT want to decrease the B/P too low or too rapidly. Best to keep diastolic ~90. •WHY? Promote Diuresis **Don’t give Diuretic, masks the symptoms of Gestational Hypertension Bed rest in left or right lateral position Check hourly output -- foley catheter with urimeter Dipstick for Protein Weigh daily -- same time, same scale Monitor Fetal Well-Being FETAL MONITORING-- assessing for late decelerations. NST -- Non-stress test CST –contraction stress test BPP –biophysical profile If all else fails ---- Deliver the baby!! HELLP Syndrome A multisystem condition that is life threatening and complicates 10% of pregnancies in women with severe HTN and may occur during PP period H = hemolysis of RBC EL = elevated liver enzymes LP = low platelets <100,000mm3 (thrombocytopenia) Etiology of HELLP Hemolysis occurs from fragmentation and destruction of erythrocytes leading to anemia Release of bilirubin R/T liver impairment and hemolysis of erythrocytes causing hyperbilirubinemia 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 Syndrome Assessment: 1. Prominent symptom is right upper quadrant pain, lower chest or epigastric 2. Nausea and vomiting 3. Severe edema 4. Flu like symptoms 5. Avoid traumatizing the liver, restrict palpation of abdomen 6. This patient needs to be managed in a critical care setting due to severity of condition HELLP Intervention: 1. Bedrest – any trauma or increase in intraabdominal pressure could lead to rupture of the liver capsule hematoma. 2. Volume expanders 3. Antithrombic medications 4. Includes all care directed at management of pre- eclampsia and eclampsia T O R C H A Infections T = Toxoplasmosis O = Other Syphilis, Gonorrhea, Chlamydia,Hepatitis A or B R = Rubella C = Cytomegalovirus H = Herpes A = Aids Urinary Tract Infection Most common infection complicating Pregnancy Etiology Pressure on ureters and bladder causing Stasis with compression of ureters Reflux Hormonal effects cause decrease tone of bladder Assessment Dysuria, frequency, urgency lower abdominal pain; costal vertebral pain fever Group B Streptoccocus Infection (GBS) Leading cause of life-threatening perinatal infections Gram positive bacteria colonizes the rectum, vagina, cervix and urethra of pregnant and non-pregnant women Associated with PROM and preterm birth 60% chance of transmission to NB Fetal effects Sepsis Pneumonia Meningitis Therapeutic Management Routine culture for all pregnant women between 35-37 weeks gestation PCN drug of choice to decrease risk of transmission to fetus Risk for transmission to fetus is at time of labor so no treatment until patient presents in labor Administer PCN IV every 4 hours until delivery Toxoplasmosis Etiology Protozoan infection. Raw meat and cat litter Maternal and Fetal Effects Mom - flu-like symptoms, lymphadenopathy Fetus – stillborn, premature birth, microcephaly; mental retardation * Instruct to cook meat thoroughly * Avoid changing cat litter * Advise to wear gloves when working in the garden Treatment: Sulfa drugs Syphilis Etiology • Spirochete – Treponema Pallium Maternal and Fetal Effects May pass across the placenta to fetus causing spontaneous abortion. Major cause of late, second trimester abortion Infant born with congenital anomalies Syphilis Intervention: • 1. Penicillin • 2. Advise to return for prenatal visits monthly to assess for re-infection • 3. Advise that if treated early, fetus may not be infected Gonorrhea Etiology – Neisseria Gonorrhoeae Maternal and Fetal Effects: May get infected during vaginal delivery causing Ophthalmia neonatorium (blindness) in the infant Mom will experience dysuria, frequency, urgency Major cause Pelvic Inflammatory Disease which leads to infertility. Treated with Rocephin Spectinomycin Treat partner!! Chlamydia Three times more common than gonorrhea. Etiology - Chlamydia trachomatis Maternal and Fetal Effects Mom – pelvic inflammatory disease, dysuria, abortions, pre-term labor Fetus -- Stillbirth, Chylamydial pneumonia Interventions Erythromycin, doxycycline, zithromax Advise treatment of both partners is very important Hepatitis A or B Highly contagious when transmitted by direct contact with blood or body fluids Maternal and Fetal Effects: • All moms should be tested for Hep B during pregnancy • Fetus may be born with low birth weight and liver changes • May be infected through placenta, at time of birth, or breast milk Intervention: • Recommend Hepatitis B vaccination to both mother and baby after delivery. Rubella Etiology Spread by droplet infection or through direct contact with articles contaminated with nasopharyngeal secretions. Crosses placenta Maternal and Fetal Effects Mom– fever, general malaise, rash Most serious problem is to the fetus--causes many congenital anomalies (cataracts, heart defects) Intervention Determine immune status of mother. If titer is low, vaccine given in early postpartum period CYTOMEGALOVIRUS Etiology -- Member of the Herpes virus • Crosses the placenta to the fetus or contracted during delivery. Cannot breast feed because transmitted through breast milk Effects on Mom and Fetus • Mom – no symptoms, not know until after birth of the baby Fetus -- Severe brain damage; Eye damage • Intervention No drug available at this time Teach mom should not breast feed baby Isolate baby after birth Herpes Simplex Type 2 Maternal and Fetal Effects Painful lesions, blisters that may rupture and leave shallow lesions that crust over and disappear in 2-6 weeks Culture lesions to detect if Herpes, No cure If mom has an outbreak close to delivery, then cannot deliver vaginally. Must deliver by Cesarean birth *Virus is lethal to fetus if inoculated at birth Intervention: Zovirax HIV/AIDS Etiology: Human Immunodeficiency Virus, HIV Transmission of HIV to the fetus occurs through: The placenta; birth canal Through breast milk **The virus must enter the baby’s bloodstream to produce infection. Diagnosis: ELISA test – identifies antibodies specific to HIV. If positive = person has been exposed and formed antibodies Western Blot – used to confirm seropositivity when ELISA is positive. Viral load - measures HIV RNA in plasma. It is used to predict severity – lower the load the longer survival. CD4 cell count – markers found on lymphocytes to indicate helper T4 cells. HIV kills CD4 cells which results in impaired immune system. Goal: reduce viral load to below 50 copies /ml. and increase the CD4 cell count. Nursing Care: **Provide Emotional Support **Teach measures to promote wellness AZT oral during pregnancy IV during labor liquid to newborn for 6 weeks. **Provide information about resources Fetal Demise/ Intrauterine Fetal Death 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 Diabetes in Pregnancy Diabetes creates special problems which affect pregnancy in a variety of ways. Successful delivery requires work of the entire health care team Endocrine Changes During Pregnancy There is an increase in activity of maternal pancreatic islets which result in increase production of insulin. Counterbalanced by: a. Placenta’s production of Human Chorionic Somatomammotropin (HCS) b. Increased levels of progesterone and estrogen--antagonistic to insulin c. Human placenta lactogen – reduces effectiveness of circulating insulin d. Placenta enzyme-- insulinase Gestational Diabetes Diabetes diagnosed during pregnancy, but unidentifable in non-pregnant woman Known as Type III Diabetes - intolerance to glucose during pregnancy with return to normal glucose tolerance within 24 hours after delivery Glucose tolerance test: 1 hr oral GTT – if elevated, do 3 hour GTT Gestational diabetes if: Fasting – 95 mg / dl 1 hour - 180 mg/ dl 2 hour - 155 mg/ dl 3 hour – 140mg/dl Treatment Controlled mainly by diet May use insulin No use of oral hypoglycemics Effects of Diabetes on the Pregnancy MATERNAL Increase incidence of INFECTION Fourfold greater incidence of Preeclampsia Increase incidence of Polyhydramnios Dystocia – large babies Rapid Aging of Placenta FETAL increase morbidity Increase Congenital Anomalies neural tube defect (AFP) Cardiac anomalies Spontaneous Abortions Large for Gestation Baby, LGA Increase risk of RDS Effects of Pregnancy on the Diabetic Insulin Requirements are Altered First Trimester--may drop slightly Second Trimester-- Rise in the requirements Third Trimester-- double to quadruple by the end of pregnancy Fluctuations harder to control; more prone to DKA Possible acceleration of vascular diseases Interventions/ Nursing Care Diet Therapy Insulin Regulation Blood Glucose Monitoring Exercise Monitor Fetal Well Being Heart Disease in Pregnancy Cardiac Response in All Pregnancies Every Pregnancy affects the cardiovascular system ¤ Increase in Cardiac Output 30% - 50% ¤ Expanded Plasma Volume ¤ Increase in Blood (Intravascular) Volume 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 Restricted Fetus Spontaneous Abortion Premature Labor and Delivery Effects of Pregnancy on A Diseased Heart 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 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 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 decompensation Assess for Signs of CHF 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 Education Diet high in iron, protein low in sodium and calories ( fat ) Weight gain Medications Supplemental iron Heparin, not coumadin – monitor lab work Diuretics – very careful monitoring Antiarrhythmics –Digoxin, quinidine, procainamide. *Beta-blockers are associated with fetal defects. Reinforce physicians care Nursing Care: During Labor • Labor in an upright or side lying position • Restrict fluids • On O2 per mask throughout labor and cardiac monitoring. • Sedation / epidural given early • Report fetal distress or cardiac failure • Stage 2 - gentle pushing, high forceps delivery Nursing Care Postpartum The immediate post delivery period is the MOST significant and dangerous for the mom with cardiac problems because: Following delivery, fluid shifts from extravascular spaces into the blood stream for excretion Cardiac output increases, blood volume increases Strain on the heart! Watch for cardiac failure Test Yourself ! Mrs. B. has mitral valve prolapse. During the second trimester of pregnancy, she reports fatigue and palpitations during routine housework. As a cardiac patient, what would her functional classification be at this time? a. Class I b. Class II c. Class III d. Class IV