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(size of RBC)82-98 fL/cell |
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(weight of Hgb) 27-33 g/dL |
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(size variation) 11-14.5% |
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Blood loss Nutritional Iron deficiency Vitamin B12 deficiency Folic acid deficiency Hemolytic Sickle cell Thalassemia Bone marrow depression Aplastic anemia |
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Primary Idiopathic
Secondary Erythropoietin-secreting tumors Renal diseases Cushing’s syndrome Prolonged hypoxemia |
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Hgb 10-14 g/dl Palpitations, dyspnea on exertion |
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Severity of Anemia Moderate |
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Hgb 6-10 g/dl Increased symptoms, “roaring” in ears |
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Hgb <6 g/dl Pallor, blurred vision, tachycardia, systolic murmur, headache, dyspnea at rest, organomegaly, sore mouth, difficulty swallowing, bone pain, sensitivity to cold, weight loss, lethargy |
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Total amt of Hgb and volume of RBCs |
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Immature RBCs--measures bone marrow ability to make RBCs |
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70% of iron in body is found in RBCs |
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Measures proteins available for binding Fe |
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Reactant protein—has inverse relationship to inflammation or chronic disease, malignancy |
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30% of body’s iron that is stored |
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Measures liver’s ability to metabolize RBC breakdown |
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Blood loss 20-30% symptoms |
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tachycardia with exercise, sl postural hypotension |
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hypotension, cardiac output down, rapid & thready pulse, cool & clammy skin |
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Dietary deficiency, malabsorption Blood loss Hemolysis |
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Pallor Glossitis or burning sensation of tongue Cheilitis Headache Paresthesis |
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Autosomal recessive gene causing inadequate production of normal Hgb Heterozygous—thalassemia minor (trait, mild form) Homozygous—thalassemia major (severe disease) is a problem with the globin protein |
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Vitamin is needed for DNA synthesis, especially in proliferating RBCs deficiency produces RBCs that are macrocytic, have thin membranes, are oval shaped Causes malabsorption from gut (pernicious anemia) is most common cause lack of intrinsic factor gastrectomy dietary deficiency |
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Vitamin B12 Deficiency sxs |
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Symptoms (develop gradually) pallor or slight jaundice weakness paresthesia in extremities smooth, red, sore tongue diarrhea |
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Needed for DNA synthesis Most likely to occur in people who are chronically undernourished or those whose metabolic requirements are increased older adults, alcoholics, drug addicts, TPN pregnant women, infants, teens Characterized by fragile megaloblastic cells |
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Folic Acid Deficiency sxs |
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pallor progressive weakness and fatigue SOB palpitations glossitis and cheilosis diarrhea paresthesias and altered proprioception |
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Anemia of Chronic Disease |
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Due to chronic inflammatory, autoimmune, infectious, or malignant disease Underproduction of RBCs and a shortening of the RBC lifespan Distinguished from iron deficiency anemia by elevated serum ferritin and increased iron stores Treatment aimed at underlying cause |
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Anemia of Chronic Disease Dx |
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Elevated serum ferritin and increased iron stores in macrophages distinguish this type of anemia from iron-deficiency anemia; normal folate and cobalamin levels |
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Anemia of Chronic Disease Tx |
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Correction of underlying problem Erythropoietin in the presence of chronic renal disease If severe, blood transfusion |
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Bone marrow fails to produce RBCs Causes genetic or idiopathic exposure to certain chemical substances some antibiotics and chemotherapy drugs viral infections mono, HIV, hepatitis C Characterized by pancytopenia RBCs are normocytic and normochromic |
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Symptoms can occur at any age fatigue, exertional dyspnea pallor of skin and mucous membranes progressive weakness headache tachycardia and CHF platelet deficiency may cause bleeding problem |
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Treatment Remove the underlying cause Blood transfusion therapy Bone marrow transplant Complete recovery may take months |
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Symptoms Pain Fatigue Grayish color Jaundice Gallstones Priapism |
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Treatment (symptomatic) Pain management Oxygen Vasodilators Rest Fluids & lytes Hydroxyureia (anti-sickling agent) Bone marrow transplant is only tx available that can cure some patients |
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Two types Primary, also called polycythemia vera, a neoplastic stem cell disorder Secondary, hypoxia-driven or hypoxia-independ. r/t renal tumors Excessive number of circulating RBCs Relatively rare but most common in Caucasian men of European Jewish ancestry Gradual onset, begins between age 40-60 yr |
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Often asymptomatic hypervolemia, hypertension, hypermetabolism, distended blood vessels, splenomegaly HA, blurred vision tinnitus, dizziness bruising, GI bleeding, ulcers, epistaxis severe pruritus pain in fingers and toes |
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focus is on reducing blood viscosity and volume initial phlebotomy of 300-500 ml blood 2-5 x/wk to keep Hct <45% may need Fe supplement symptomatic relief for PV, radioactive phosphorus or chemotherapy can be used to suppress bone marrow function, however the danger is risk of developing leukemia |
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Malignant condition of WBCs and blood-forming tissues Characterized by replacement of bone marrow with malignant immature WBCs Most often diagnosed in children but growing problem in adults number of adults is 10 times that of children |
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Acute Manifestations of Leukemia |
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Integument ecchymosis, petechiae open lesion pallor of conjunctiva, nail beds, palmar creases, around mouth GI bleeding gums anorexia, wt loss organomegaly Renal hematuria CV tachycardia, palpitations orthostatic hypotension Respiratory exertional SOB Neuro fatigue, HA, fever MSK joint swelling, bone pain |
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Named according to the predominant type of abnormal cell involved and according to the acuity or chronicity of the condition Terms acute and chronic r/t cell maturity and nature of disease onset |
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Most common types of leukemia in adults |
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acute myelogenous leukemia (85%) chronic lymphocytic leukemia |
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Acute Myelogenous Leukemia |
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Uncontrolled proliferation of myeloblasts (granulocyte precursors) with hyperplasia of spleen and bone marrow Onset abrupt and dramatic Sx: fatigue, headache, pallor, exertional dyspnea, fever, mouth sores, infection, bleeding lab findings: myeloblasts in marrow; low RBCs & platelets, H&H Tx is chemotherapy, possible bone marrow transplant |
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Chronic Lymphocytic Leukemia |
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Proliferation of abnormal B-lymphocytes in the bone marrow; infiltrate spleen, liver, bone marrow Slow onset, often diagnosed on routine PE Sx are vague weakness, malaise, enlarged lymph nodes, infection lab findings: anemia, reduced platelet and erythrocyte counts, total WBCs >100,000, lymphocytes in marrow Tx chemo, radiation (survival rate ~7 yr) |
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lymphatic cancer occurs ages 15-35 and over 50, men>women 2:1 high cure rate if discovered early malignant cells attack any body area, sx vary characteristic finding is Reed-Sternberg cells from node biopsy or bone marrow secrete cytokines, tumor necrosis factor-alpha, colony-stimulating factor that attract inflammatory cells to tumor site |
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Manifestations of Hodgkin’s |
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Early enlarged lymph nodes persistent fever night sweats fatigue weight loss malaise pruritus anemia Later edema of face and neck jaundice nerve pain enlargement of retroperitoneal nodes nodular infiltration of spleen, bones, liver bone pain |
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Stage I single node region Stage II two or more regions on same side of diaphragm Stage III regions on both sides of diaphragm Stage IV disseminated disease |
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Malignant disorder of lymph tissues but no hallmark diagnostic feature, can originate outside the lymph nodes Cause unknown suspect viral illnesses, ionizing radiation, toxic chemicals, immunosuppressive medications Begins as single node and spreads throughout lymphatic system, unpredictable can involve bone, CNS, GI tract |
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Manifestations of Lymphoma |
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Early sign may be enlarged lymph node Other GI symptoms, jaundice, abdominal cramping, bowel obstruction compression of the spinal cord hemolytic anemia (late) Diagnosis made by node biopsy Staging Low-grade, intermediate (aggressive), high-grade (very aggressive) |
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Neoplastic plasma cells infiltrate bone marrow and destroy bone Men 2:1 women, develops after age 40 Afr Amer more common than whites Prognosis—2 year survival |
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Slow onset so sx not initially noticed Diffuse osteoporosis develops, pathologic fractures Skeletal pain Hypercalcemia Renal, GI, neuro, cardiac problems Anemia, thrombocytopenia, granulocytopenia |
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is a decrease in total WBCs Total count <4000/μl |
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Neutropenia is a decrease in neutrophils |
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Defined as a count of <1000-1500/μl (nl 4000-11,000) |
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Most common cause of neutropenia |
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is iatrogenic Chemo, immunosuppressants, autoimmune diseases |
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Diagnostics WBC count w/diff If neutrophil count 500-1000, pt at moderate risk for infection. If <500, risk is severe. Peripheral blood smear Hct Platelet count Bone marrow aspiration |
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ID cause Antibiotic therapy Hematopoietic growth factors Isolation, HEPA filtration Monitor for S/S infection |
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Formed in the bone marrow, controlled by thrombopoietin 30-40% stored in spleen before release into circulation Life span 8-10 days Role in clot formation |
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Defined as platelet count <150,000/µl Condition is generally acquired rather than inherited Antibodies attack platelets destroying them Usual mechanism is drug-dependent antibodies that bind to platelet surface protein Causes Foods, herbs, drugs, bone marrow suppression or failure |
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Immune thrombocytopenic purpura (ITP) |
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Autoimmune condition destroying platelets Platelets coated with antibodies, have normal function but when they reach the spleen they are recognized as “foreign” and are destroyed Survive only 1-3 days |
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Thrombotic thrombocytopenic purpura (TTP) |
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Combo of hemolytic anemia, thrombocytopenia, fever w/o infection, neuro and renal abnormalities Platelet agglutination, forms microthrombi |
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Extravasation of blood into tissues Many may be asymptomatic Most common sx is bleeding Multiple sites possible Petechiae, purpura, ecchymoses Does not blanch Major complication is hemorrhage |
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Diagnostics Platelet count low If below 20,000 /μl is life-threatening PT, aPTT H & H Fibrin products Bone marrow biopsy Treatment Steroids Danazol may increase CD4 T cells Immunoglobulin Immunosuppressants Platelet transfusion for life-threatening hemorrhage Splenectomy |
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Sex-linked recessive genetic disorder causing defective coagulation |
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Hemophilia A most common (80%) Factor VIII deficiency Hemophilia B (Christmas disease) Factor IX deficiency |
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Deficiency in VonWillebrand coagulation protein (vWF) |
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Diagnosis Factor assays deficiencies in VIII, IX, XI, XII, or vWF PT, thrombin time, platelet count not involved PTT and bleeding prolonged Treatment Stop bleeding Replace clotting factors Desmopressin (DDAVP) to stimulate increases in factor VIII and vWF Antifibrinolytics to stabilize clots Treat symptoms Gene therapy is experimental Cell removal and modification |
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Disseminated Intravascular Coagulation (DIC) |
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Is not a disease but rather an abnormal clotting cascade response from a disease or other condition is a generalized response to injury or sepsis injury to blood cells, leads to platelet aggregation and decreased blood flow fibrin clots form throughout microcirculation, slows circulation further and stimulates excess fibrinolysis simultaneous bleeding and clotting, eventually clotting factors are depleted, result is generalized hemorrhage often have MODS |
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Conditions That May Cause DIC |
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Widespread tissue damage trauma OB complications neoplasms Hemolysis drugs, toxins transfusion reactions uremic syndrome acute pancreatitis Hypotension hypovolemic shock sepsis Hypoxia and circulatory stasis sickle cell MI, cardiac arrest PE, ARDS, near drowning (fresh water) Metabolic acidosis |
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CV hypotension tachycardia Respiratory tachypnea decreased breath sounds ARDS Urinary oliguria or anuria hematuria GI occult blood abdominal distention CNS increased ICP anxiety, confusion to stupor and coma seizures Integument petechiae, purpura, ecchymosis, bleeding cyanosis, gangrene |
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Increased bleeding time, platelet count, fibrinogen levels, PT, PTT, aPTT Increased fibrin degradation products Elevated D-dimer Decreased clotting factors II, V, VII, X |
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ID underlying problem IVs FFP, cryo, platelet concentrates Heparin (controversial) and antithrombin III Monitor VS, pulse ox, mental status Maintain urine output Pain management Bedrest, position change q2h, TCDB Emotional support |
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Nursing Care for Bleeding Disorders |
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Assess for and control topical bleeding Administer coag factors Rest bleeding joints, apply ice Analgesics (no ASA) for pain Teaching safety and recognition of disease-related problems Oral hygiene without trauma |
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Nursing diagnoses for Bleeding Disorders |
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activity intolerance altered oral mucous membranes self-care deficit risk for insufficient cardiac output |
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Circulating endotoxins from gram negative or gram positive microorganisms (septicemia) leads to inflammatory response bacteria gain entry, rapid growth, damages body by a combination of factors bacterial endotoxins leaking into plasma that damage endothelial linings of blood vessels increased vessel permeability, fluid shifts altered oxygenation of tissues and cellular death leads to systemic shock 60% mortality rate despite treatment |
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Oxygen and respiratory support Fluid replacement, vasodilators Hemodynamic monitoring Blood cultures Broad spectrum antibiotics Vasopressors if BP not maintained by IVs Enteral nutrition Environmental controls, skin care |
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Hypodynamic (“cold shock”, sudden deterioration)—compensation failing clotting factors are used up so hypovolemic, MODS dramatic decrease in CO and BP, tachycardia, may have dysrhythmia respirations rapid, shallow, dyspneic subnormal temperature, cold clammy skin, pale oliguric to anuric altered mentation sx resemble late stages of shock |
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Compensatory staeg of sepsis |
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Hyperdynamic (“warm shock”, hrs to days) vasodilation, increased CO, normal or elevated BP thready pulse respirations rapid and deep (Kussmaul) normal urine output n/v/d, impaired GI motility dry skin, tissue hypoxia (change to anaerobic metabolism ) but color normal, fever/chills peripheral edema, weakness platelet aggregation, DIC, inflammatory reaction alert, oriented, anxious |
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May have no outward signs Metabolism changes from aerobic to anaerobic, lactic acid begins to accumulate Lactic acid needs to be removed but process requires oxygen which is unavailable to tissues |
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LV loses ability to generate pressure to eject blood into aorta Hallmark is decreased EF |
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Inability of ventricles to fill during diastole Result is venous engorgement in pulmonary and systemic circulation |
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Mixed (biventricular) failure |
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Poor CO further compromised by enlarged heart |
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Pump failure leads to fall in cardiac output Decrease SV and EF stimulates baroreceptors which stimulate sympathetic nervous system Increased HR increases workload of compromised myocardium Decreased renal perfusion activates renin-angiotensin-aldosterone system Result is vasoconstriction, water retention, increase in vascular volume and venous return |
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Ht chambers and muscle adapts to increased volume and incomplete emptying Hypertrophy of cells in myocardium Overstretching and loss of effective contraction Contributes to deterioration of ht function Eventual thinning and degeneration of myocardium Less coronary blood flow results in ischemia |
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LV often affected because of high workload and oxygen demand Results from muscle damage or volume overloading Increased ventricular pressures due to overfilling and incomplete emptying Increased pressure results in higher pressures in pulmonary vasculature Fluid moves from blood vessels into interstitial tissues and alveoli |
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Effects of Left-Sided Failure |
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Definition
Pulmonary congestion Dyspnea, SOB, dry cough, orthopnea Cyanosis Inspiratory crackles S3 and S4 gallop Tachycardia, palpitations Fatigue, activity intolerance decreased PaO2 and increased PaCO2 Decreased urine output, nocturia |
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Definition
Primary cause is L ventricular failure Also caused by pulmonary hypertension, cor pulmonale, or R ventricular infarct Distention of RA and RV Blood accumulates in venous system resulting in engorgement and anasarca |
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Effects of Right-Sided Failure |
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Definition
Elevated central venous pressure, JVD Peripheral edema Congestion in abdominal organs Liver engorgement, hepato-jugular reflux Splenomegaly Ascites, abdominal distention Anorexia, nausea Fatigue Dysrhythmias, murmurs, RV heaves |
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Both ventricles affected Symptoms of both R and L failure Paroxysmal nocturnal dyspnea S3 and S4 present Heart’s compensatory mechanisms fail Can lead to impaired organ function Risk of sudden death is high |
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New York Heart Association Functional Classification of Persons with Cardiac Disease |
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Class 1 No limitation of physical activities, activity does not cause fatigue, dyspnea, palpitations, or angina Class 2 Slight limitation of activity, no sx at rest Class 3 Marked limitation of activity, uncomfortable at rest Class 4 Inability to carry on any activity without discomfort, sx of angina present even at rest |
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Definition
Lab Electrolytes Serum osmolarity LFTs ABGs BNP MI markers CPK CK-MB LDH Troponins CRP Diagnostic Imaging CXR EKG Echocardiography Cardiac cath Nuclear imaging |
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Improve LV function Decrease intravascular volume Decrease preload and afterload Improve gas exchange and oxygenation Increase CO Reduce anxiety |
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ACE inhibitors (-pril drugs) Diuretics Inotropes Sympathomimetic agents Phosphodiesterase inhibitors Direct vasodilators Beta-blockers Antidysrhythmic drugs |
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Monitor VS, heart and lung sounds, hemodynamic pressures, gas exchange Rest—physical and emotional Plan activities to preserve energy Elevate HOB to 45o Strict I&O, weigh daily, measure abd girth Med administration, watch for SEs Patient and family teaching |
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Definition
Decreased CO with evidence of tissue hypoxia in the presence of adequate circulating volume
Precipitating factors (see table p. 1797) MI most common cause
Hemodynamic parameters: BP < 90 for at least 30 min and reduced cardiac index <2.2 L/min |
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Signs/Symptoms cardiogenic shock |
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Definition
Hypotension, narrowed pulse pressure Tachycardia, thready pulse, JVD Tachypnea, labored respirations, crackles, wheezes, pulmonary edema Skin pale, peripheral cyanosis, clammy Oliguria to anuria Dependent edema Dysrhythmias Anxiety, confusion, agitation |
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Cardiogenic shock Diagnosis: |
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Definition
Early RBCs, H & H normal Cardiac enzymes may be elevated if MI BUN/Cr increased Lytes– glu Na, K increased Urine sp gr increased Respiratory alkalosis Other tests include CXR, CT, EKG, echocardiogram Late RBCs, H & H decreased if hemorrhage LFTs increased Lytes—glu, Na, K decreased Urine sp gr fixed at 1.010 if renal failure Metabolic acidosis |
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Treatment for cardiogenic shock |
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Definition
Life-threatening emergency Oxygen therapy PASG contraindicated Fluid replacement—judicious Pharmacology Vasoactive drugs, diuretics Antidysrhythmic agents Digitalis |
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Nursing Care cardiogenic shock |
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Definition
Oxygenation Monitor cardiovascular function BP, HR, rhythm, pulse ox, peripheral pulses, hemodynamic monitoring Strict I & O Monitor urine output (keep >30 ml/hr) Monitor for CP, cyanosis, dyspnea, restlessness, anxiety Bedrest, provide calm environment Emotional support |
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Definition
Accumulation of fluid in lung—pt is “drowning” Cardiac causes Volume overload, valvular disease, MI Noncardiac causes ARDS, trauma, sepsis, drug OD, neuro |
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Definition
Cardiogenic Inadequate LV contractility Rise in end-diastolic volume and pressure Hydrostatic pressure in pulm vessels>osmotic pressure, fluid leaks into alveoli S/S Dyspnea, SOB Cough, frothy, pink sputum Tachypnea, orthopnea Hypotension Cyanosis Hypoxemia Restlessness, anxiety Feeling of doom |
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Definition
Focus on improving oxygenation, reducing fluid volume, and emotional support Airway management, oxygen by CPAP, pulse ox Monitor heart and lung sounds Strict I & O, foley, IV Rotating tourniquets may be ordered Reassurance, explain all procedures, maintain contact with family |
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Definition
Most common type Cause: idiopathic but most often follows myocarditis Dilated chambers, impairs LV function Can present with sx R and L sided failure S3 and S4 present Dysrhythmias common Poor prognosis—most die within 2 yr of sx onset Tx rhythm control |
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Term
Hypertrophic cardiomyopathy |
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Definition
Cause: hereditary, may be due to chronic hypertension, men > women LVH, impaired relaxation, aortic outflow obstructed Sx associated with increased oxygen demand and increased contractility, double apical pulse, S4 present Ventricular or atrial dysrhythmias common Often asymptomatic, sudden cardiac death may be first sign |
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Term
Restrictive cardiomyopathy |
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Definition
Cause: fibrotic rigidity of ventricular walls, least common type Decreased ventricular compliance, decreased size of ventricular chambers, elevated pressures Contractility unaffected Sx biventricular failure S3 and S4 present Prognosis poor—most die in 3 years |
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Term
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Definition
EKG Echo CXR shows cardiomegaly, pulmonary congestion Nuclear scans Cardiac cath Endomyocardial biopsy |
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Term
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Definition
Pharmacology ACE inhibitors, diuretics, dig, vasodilators, anticoagulants, antidysrhythmics Beta-blockers to reduce anginal symptoms Surgery Transplant Ventricular assist devices in the interim Dual chamber pacing, AICD Myotomy and/or myectomy |
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Term
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Definition
50% are patients with cardiomyopathy, 40% are those with inoperable CAD Indications and contraindications (see table, p. 857) Donor and recipient tissue must match Once heart harvested, must transplant within 4-6 hr Lifelong immunosuppressive drugs |
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