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NUR283 Study Guide Exam 2 Chapter 8 Functions of the Skin: • Acts as the first line of defense • Prevents excess fluid loss • Controls body temperature • Active in sensory perception • Synthesizes vitamin D Pruritus: • Itching o Allergic responses, Type I sensitivity o Chemical irritation caused by insect bites o Parasite infestations Pruritus Causes: • Release of histamine in a hypersensitivity response Effects of Pruritus: • Redness and itching – inflammation • Risk of infection due to scratching Causes of Contact Dermatitis: • Allergic contact dermatitis o Exposure to an antigen o Sensitization occurs on first exposure ▪ Type IV cell-mediated hypersensitivity o Pruritic rash develops at site a few hours after exposure • Irritant Contact Dermatitis o Inflammatory because of direct exposure o Does not involve immune response o Removal of irritant o Reduction of inflammation with topical glucocorticoids Urticaria (hives) Causes: • Ingestion of substances, release histamine • Examples: shellfish, drugs, certain fruits • Result of type I hypersensitivity Urticaria Effects: • Eruption of hard, raised erythematous lesion • Often scattered all over the body • Highly pruritic • Check for pharyngeal mucosa and check airway o Administer EpiPen or other first aid required Psoriasis Causes: • Chronic inflammatory skin disorder o Onset usually in the teenage years o Psoriasis results from abnormal T cell activation • Psoriasis results from abnormal T cell activation o The rate of cellular proliferation is increased o Thickening of the dermis and epidermis Effects of Psoriasis: • A silvery plaque while the base remains erythematous • Lesions on face, scalp, elbows, knees • Itching or burning sensations Treatment of Psoriasis: • Glucocorticoids, tar preparations, antimetabolites Cellulitis (erysipelas): • Infection of the dermis and subcutaneous tissue Cellulitis Causes: • Secondary to an injury • Staphylococcus aureus or streptococcus Effects of Cellulitis: • Frequently in lower trunks and legs • Area becomes red, swollen and painful • Red streaks may develop; running along lymph vessels proximal to infected area Herpes Simplex Type 1: • Oral herpes o Cold sores or fever blisters Effects of HSV-1: • Painful oral ulcer Herpes Simplex Type 2: • Genital herpes Effects of HSV-2: • Genital vesical ulcer Herpes Simplex Virus: • Virus remains latent in sensory ganglia • Recurrence may be triggered by o Common cold, sun exposure, stress Treatment of Kaposi’s Sarcoma: • Combination of radiation, chemotherapy, surgery, biological therapy Diagnostic Tests for Skin Lesions: • Culture and staining • Biopsy • Blood test • Skin testing o Patch or scratch method Chapter Thirteen Functions of the Respiratory System: • Transport oxygen from air to blood o O2 important for cellular metabolism • Removal of CO2 from the blood o CO2 is a waste product from metabolism • Upper respiratory tract o Respiratory mucosa • Lower respiratory tract o Sterile Ventilation: • Process of inspiration and expiration • Air always moves from high pressure area to low pressure area o Inspiration ▪ Moves air from atmosphere to lungs ▪ Atmospheric pressure higher than pressure in alveoli o Expiration ▪ Air moves from lungs into atmosphere ▪ Pressure in alveoli higher than in atmosphere Tidal Volume: • Amount of air entering lungs with each normal breath Residual Volume: • Amount of air remaining in the lungs after forced expiration Vital Capacity: • Maximal amount of air expired following a maximal inspiration Primary Control: • Centers for breathing • Located in the medulla and pons Chemical Factors: • In respiratory control • Chemoreceptors detect changes in CO2 level, hydrogen ion and O2 levels in blood or cerebrospinal fluid • Hypoxic drive: chemoreceptors respond to hypoxemia • Hyperventilation: chemoreceptors respond to hypercapnia Gas Exchange: • Flow of gases between the alveolar air and blood Diffusion: • Gas exchange depends on the relative concentrations (partial pressures) of the gases • PO2: partial pressure of oxygen • PCO2: partial pressure of carbon dioxide Factors Affecting Diffusion of Gases: • Partial pressure gradient • Fluid accumulation in alveoli or interstitial tissue • Total surface area available for diffusion • Thickness of the alveolar membranes • Ventilation o Perfusion ration o Ventilation (air flow) and perfusion (blood flow) need to match for maximum gas exchange Transport of Oxygen: • Most is bound (reversibly) to hemoglobin • Binding and release of oxygen to hemoglobin depend on o PO2 and PCO2, temperature and plasma pH Transport of Carbon Dioxide: • Waste product from cellular metabolism • Most diffuses into red blood cells Sneezing: • Reflex response • Assists in removing irritant Coughing: • Protective reflex • Constant dry or nonproductive is fatiguing Sputum: • Normal secretions are relatively thin, clear and colorless or cream color • Abnormal sputum o Yellow-green, thick tenacious mucus, hemoptysis Eupnea: • Normal rate (10-18 inspirations per minute) Tachypnea: • Rapid superficial breathing Bradypnea: • Slow respiratory rate Apnea: • Cessation of breathing Kussmaul Respirations: • Labored respiration or prolonged inspiration or expiration Wheezing or Whistling Sounds: • Obstruction in small airways Stridor: • High-pitched crowing noise • Usually indicates upper airway obstruction Rales: • Light bubbly or crackling sounds with serous secretions Ronchi: • Deeper or harsher sounds from thicker mucous Absence: • Nonaeration or collapse of lungs Dyspnea: • Subjective feeling of discomfort o Feels unable to inhale enough air • Short of breath either on exertion or at rest • Severe dyspnea indicative of respiratory distress o Flaring of nostrils o Use of accessory respiratory muscles o Retraction of muscles between or above ribs Orthopnea: • Exudate contains fibrin and forms a consolidated mass • Exudate produces rusty sputum Pleurisy: • Pleuritic pain Hypoxia • May develop respiratory acidosis Pneumonia Manifestations: • Sudden onset • Systemic signs • Dyspnea, tachypnea, tachycardia – oxygen defecit • Pleural pain • Rales • Productive cough • Confusion or disorientation Tuberculosis: • Caused by mycobacterium tuberculosis • Mycobacterium is acid fast, aerobic, slow growing bacillus Tuberculosis Occurs In: • People living in crowded conditions • Immunodeficiency • Others: HIV infection, homeless area, malnutrition, etc… Primary Tuberculosis Infection: • When organism first enters the lungs Latent Infection: • The individual has been exposed to the bacillus and infected but does not have active disease and is asymptomatic Secondary or Re-Infection of Tuberculosis: • Reactivated – due to decrease host resistance Active TB (primary or secondary): • Organisms multiply, forming large areas of necrosis – cavitation • Cough, positive sputum, radiograph shows cavitation • Cavitation promotes spread to other parts of the lung Signs and Symptoms of Tuberculosis: • Weight loss, low grade fever, night sweat, cough anorexia Tuberculosis Diagnostic Tests: • Skin test results o Type IV cell mediated hypersensitivity reaction – mantoux test • Active infections o Acid-fast sputum test o Chest x-ray o Sputum culture and sensitivity Cystic Fibrosis: • Inherited (genetic) disorder • Thick secretion, tenacious mucus from the exocrine glands • Primary effects seen in lungs and pancreas Cystic Fibrosis in the Lungs: • Mucus obstructs airflow in bronchioles and small bronchi • Permanent damage to bronchiole walls • Infections are common due to o Stagnant mucus o Commonly caused by pseudomonas aeruginosa and staphylococcus aureus Digestive Tract Cystic Fibrosis: • Meconium ileus in newborns o Small intestine of neonate is blocked by mucous at birth, preventing the excretion of meconium • Blockage of pancreatic and bile ducts o Malabsorption and malnutrition Sweat Glands Cystic Fibrosis: • Sweat has high sodium chloride content • Most conclusive test for diagnosis Signs and Symptoms of Cystic Fibrosis: • Meconium ileus may occur at birth • Salty skin: skin test • Signs of malabsorption: steatorrhea, abdominal distention • Chronic cough and frequent respiratory infections • Failure to meet normal growth milestones Diagnosis of Cystic Fibrosis: • Sweat test • Genetic testing • Stool test o Fat content and trypsin • Radiography, pulmonary function test • Blood gas analysis Aspiration: • Passage of food, fluids, emesis, other foreign material into trachea and lungs • Common problem in young children or individuals laying down when eating or drinking Etiology of Aspiration: • Swallowing or gag reflex is depressed • Coma or neurologic damage • Postoperatively from the effects of anesthetic drugs Result of Aspiration: • Airway obstruction • Inflammation and swelling • Predisposition to pneumonia Potential Complications of Aspiration: • Aspiration pneumonia • Respiratory distress syndrome Signs and Symptoms of Aspiration: • Coughing and choking • Loss of voice • Stridor/hoarsness • Wheezing • Tachycardia and tachypnea • Nasal flaring, chest retractions, hypoxia – severe respiratory distress • Cardiac or respiratory arrest Obstructive Sleep Apnea: • Result of pharyngeal tissue collapse during sleep • Leads to repeated and momentary cessation of breathing • Men are affected more often than women • Obesity and aging are common predisposing factors Treatment of Sleep Apnea: • Continuous positive airway pressure pump (CPAP) • Oral appliances that reduce collapse of pharyngeal tissue Asthma: • Bronchial obstruction • Occurs in persons with hypersensitive or hyperresponsive airways Extrinsic Asthma: • Acute episodes triggered by type 1 hypersensitivity reactions • Antigen react with immunoglobulin E (IgE) • Inflammation in lungs is present • Plasma protein levels are low • Pulmonary hypertension develops S&S of Pulmonary Edema: • Cough, orthopnea, rales – in mild cases • Hemoptysis o Frothy, blood-tinged sputum Pulmonary Embolus: • Blood clot or mass that obstructs pulmonary artery or any of its branches • Large emboli may cause sudden death • 90% of pulmonary emboli originate from DVT in legs; are preventable Etiology of Pulmonary Embolus: • Virchow triad: vessel wall damage, venous stasis, hypercoagubility S&S of Pulmonary Embolus: • Chest pain, dyspnea, cough, tachypnea • Hypoxia, SNS stimulation • Massive emobli: severe chest pain, low BP, rapid weak pulse, loss of consciousness • Can develop acute respiratory distress Atelectasis: • Nonaeration or collapse of lung or part of a lung leading to deceased gas exchange and hypoxia • Alveoli become airless o Both ventilation and perfusion are altered o Affects oxygen diffusion Etiology of Atelectasis: • Obstructive or resorption atelectasis • Compression atelectasis • Increase surface tension in alveoli • Fibrotic tissue • Postoperative atelectasis S&S of Atelectasis: • Small areas are asymptomatic • Large areas: dyspnea, increased heat and respiratory rates and chest pain Pleural Effusion: • Presence of excessive fluid in the pleural cavity • Limiting lung expansion Etiology of Pleural Effusion: • Exudative effusions: result from inflammation • Hydrothorax: result from increased hydrostatic pressure or decreased osmotic pressure in blood vessels • Hemothorax: result from trauma, cancer or surgery S&S of Pleural Effusion: • Dyspnea • Chest pain • Increased respiratory and heart rates Pneumothorax: • Air in pleural cavity Closed Pneumothorax: • Air can enter pleural cavity from internal airways – no opening in chest wall Open Pneumothorax: • Atmospheric air enters the pleural cavity through an opening in the chest wall Tension Pneumothorax: • Most serious form of medical emergency • Air entry into pleural cavity on inspiration but hole closes on expiration • Severe hypoxia and respiratory distress develop quickly • Pressure increases on the affected side eventually push the mediastinal contents against the other lung Adult Respiratory Distress Syndrome: • Results from injury to the alveolar wall and capillary membrane o Multitude of predisposing conditions S&S of Adult Respiratory Distress Syndrome: • Marked sign: dyspnea • Restlessness • Rapid, shallow respirations • Increased HR • Combination of respiratory and metabolic acidosis Acute Respiratory Failure: • End result of pulmonary disorders • Severe hypoxia o Pao2 is less than 50 mmHg • Hypercapnia o PaCO2 is greater than 50 mmHg • Serum pH is decreasing Spirometry: • Pulmonary function test • Tests pulmonary volumes and airflow times Arterial Blood Gas Determination: • Checks oxygen, carbon dioxide, bicarbonate, serum Ph Oximetry: • Measures O2 saturation Exercise Tolerance Testing: • For patients with chronic pulmonary disease Radiography: • Helpful in evaluating tumors and infections Bronchoscopy: • Perform biopsy • Check site of lesion or bleeding Culture and Sensitivity Tests: • Sputum testing for presence of pathogens • Determine antimicrobial sensitivity of pathogen Chapter Ten Circulatory System: • Consists of the cardiovascular system and lymphatic system • Blood vessels Arteries: • Arterioles • Transport blood away from the heart Veins: • Venules • Return blood back to heart Capillaries: • Microcirculation within tissues Systemic Circulation: • Exchange of gases, nutrients and wastes in tissues Pulmonary Circulation: Pernicious Anemia (B12 Deficiency): • Basic problem is lack of intrinsic factor o Intrinsic factor secreted by gastric mucosa, required for intestinal absorption of Vitamin B12 • Characterized by very large, immature, nucleated erythrocytes • B12 is needed for the function and maintenance of neurons Etiology of B12 Anemia: • Dietary insufficiency • Malabsorption o Chronic gastritis, common in alcoholics and causes atrophy of the gastric mucosa or inflammation condition • Surgery, such as gastrectomy B12 Deficiency Anemia S&S: • General signs of anemia • Tongue is typically enlarged, red, sore and shiny • Digestive discomfort, often with nausea and diarrhea • Feeling of pins and needles, tingling in limbs Aplastic Anemia: • Impairment or failure of bone marrow leading to loss of stem cells and pancytopenia o Pancytopenia: decreased numbers of erythrocytes, leukocytes and platelets in the blood Etiology of Aplastic Anemia: • Myelotoxins: radiation, industrial chemicals, drugs • Others: genetic abnormalities, hepatitis C, SLE, etc… S&S Aplastic Anemia: • Blood counts indicate pancytopenia • Anemia signs • Leukopenia (recurrent infection) • Thrombocytopenia (petechiae) Cause of Sickle Cell Anemia: • Genetic condition o Autosomal recessive disorder o More common in individuals of African Sickle Cell Anemia: • Abnormal hemoglobin • Sickle cell crisis occurs when O2 levels are lowered o Lung infection or dehydration • Sickle-shaped cells have shorter lifespan • Sickle cell hemoglobin leads to multiple infarctions S&S of Sickle Cell Anemia: • General sign of anemia • Severe pain because of ischemia of tissues and infarction • Jaundice – hyperbilirubinemia • Acute symptom of vaso-occlusive/painful crisis Primary Polycythemia: • Increased production of erythrocytes and other cells in the bone marrow • Neoplastic disorder • Serum erythropoietin levels are low Secondary Polycythemia: • Increase in RBCs in response to prolonged hypoxia • Increased erythropoietin secretion • Compensation mechanism to provide increased oxygen transport S&S Polycythemia: • Plethoric and cyanotic o Deep bluish-red tone of skin and mucosa resulting from the engorged blood vessels and sluggish blood flow • Hepatomegaly • Increased blood pressure • Thromboses and infarctions • CHF can develop Blood Clotting Disorder: • Spontaneous bleeding or excessive bleeding flowing minor tissue trauma often indicates a blood- clotting disorder Blood Clotting Disorder Warning Signs: • Persistent bleeding from the gums, petechiae, bruises, ecchymosis, etc… Complication of Blood Clotting Disorder: • Risk for hemorrhage – invasive procedure Hemophilia A: • Classic hemophilia: deficit or abnormality of factor VIII o X-linked recessive trait o Manifested in men, carried by women S&S of Hemophilia A: • Prolonged bleeding after minor tissue trauma • Spontaneous bleeding into the joints • Possible hematuria or blood in feces Leukemia: • Group of neoplastic disorders involving white blood cells • Undifferentiated, immature, nonfunctional cells that multiply uncontrollably Acute Leukemia: • High proportion of immature nonfunctional cells • Onset usually abrupt, marked signs of complications • Occurs primarily in children and younger adults Chronic Leukemia: • Higher proportion of mature cells with reduced function • Insidious onset • Common in older adults S&S of Leukemia: • Frequent or uncontrolled infections • Weight loss, fatigue, possible fever Diagnostic Leukemia Tests: • CBC o RBC, WBC, and platelets o Leukocytosis (increased WBC) o Leukopenia (decreased WBC) o Increased eosinophils ▪ Common in allergic responses • Differential count for WBCs • Morphology o Observed with blood smears o Shows size, shape, uniformity, maturity of cells ▪ Different types of anemia can be distinguished • Hematocrit o Percent by volume of cellular elements in blood • Hemoglobin o Amount of hemoglobin per unit volume of blood • Mean corpuscular volume (MCV) o Indicates the oxygen-carrying capacity of blood • Reticulocyte count o Assessment of bone marrow function • Chemical analysis o Determines serum levels of components, such as iron, vitamin B12, folic acid, cholesterol, urea, glucose • Bleeding time o Measures platelet function • Prothrombin time (PT) and partial thromboplastin time (PTT) o Measures function of various factors in coagulation process o International normalized ratio (INR) is a standardized version o Variant angina: vasospasm occurs at rest o Unstable angina: prolonged pain at rest – may precede myocardial infarction Etiology of Angina Pectoris: • Insufficient myocardial blood supply o Atherosclerosis, arteriosclerosis, vasospasm and myocardial hypertrophy o Severe anemias and respiratory disease • Increased demands o Tachycardia, hypertension, etc… • Precipitating factors of angina attacks o Activities such as running and getting angry o Respiratory infection with fever o Exposure to weather extremes or pollution or eating a large meal Angina Pectoris S&S: • Recurrent, intermittent brief episodes of substernal chest pain • Triggered by physical or emotional stress • Attacks vary in severity and duration but become more frequent and longer as disease progresses • Relieved by rest and administration of coronary vasodilators (nitroglycerin) Myocardial Infarction: • Occurs when a coronary artery is totally obstructed, leading to prolonged ischemia and cell death, or infarction, of the heart wall Pathophysiology of MI: • Common cause: atherosclerosis • The heart muscle becomes necrotic, and an area of injury, inflammation, and scar formation • Specific enzymes (troponin) appear in the blood • Myocardial contractility and conduction are lost quickly as oxygen supplies are depleted. If the blood can be restored in the first 20 to 30 minutes Myocardial Infarction S&S: • Pain: sudden substernal chest pain that radiates to the left arm, shoulder, jaw or neck • Pallor and diaphoresis, nausea, dizziness and weakness, dyspnea • Marked anxiety and fear • Hypotension o Pulse is rapid and weak as cardiac output decreases and shock develops • Low-grade fever MI Complications: • Sudden death: cardiac dysrhythmias • Cardiogenic shock • Congestive heart failure Cardiac Dysrhythmias: • Deviations from normal cardiac rate or rhythm o Caused by electrolyte abnormalities, fever, hypoxia, stress, infection, drug toxicity o ECG: detects abnormalities • Reduction of the efficiency of the hearts pumping cycle o Many types of abnormal conduction patterns exist Sinus Node Abnormalities: • Bradycardia • Tachycardia • Atrial conduction abnormalities • Heart blocks • Ventricular conduction abnormalities Bradycardia: • Rate regular but slow than 60/minute Tachycardia: • Rate regular but faster 100-160/min Atrial Conduction Abnormalities: • Premature atrial contractions or beats • Atrial flutter • Atrial fibrillation Ventricular Conduction Abnormalities: • Ventricular tachycardia • Ventricular fibrillation: cardiac standstill – CARDIAC EMERGENCY • Others: PVC Heart blocks: • Conduction excessively delayed or stopped at AV node or bundle of His Cardiac Arrest: • Cessation of all heart activity o No conduction of impulses o Flat ECG Effects of Cardiac Arrest: • Loss of consciousness • Respiration ceases • No pulse Congestive Heart Failure: • Heart is unable to pump sufficient blood to meet metabolic demands of the body • Compensation mechanisms maintain cardiac output – may aggravate the condition o Increase renin aldosterone secretion o CNS response o Chamber of heart tend to dilate and cardiac muscles becomes hypertrophied Pathophysiology of CHF: • Cardiac output or stroke volume decreases o Less blood reaches the various organs o Decreased cell function o Fatigue and lethargy o Mild acidosis develops • Backup and congestion develop • Output from ventricle is less than the inflow of blood Etiology of CHF: • Infarction • CAD, hypertension • Pulmonary disease S&S CHF: • Forward effects o Decreased blood supply to tissues, general hypoxia o Fatigue and weakness o Dyspnea and SOB • Compensation mechanisms o Tachycardia, cutaneous and visceral vasoconstriction, daytime oliguria Left Side CHF S&S: • Left ventricle doesn’t empty, backup effects of left-sided failure, pulmonary congestion o Dyspnea and orthopnea ▪ Develop as fluid accumulates in lungs o Cough ▪ Associated with fluid irritating the respiratory passages o Paroxysmal nocturnal dyspnea ▪ Indicates the presence of acute pulmonary edema ▪ Usually develops during sleep ▪ Excess fluid in lungs frequently leads to infections Right Side CHF S&S: • Right ventricle weakens – systemic backup • Dependent edema in feet, legs, buttocks • Increased pressure in jugular veins leads to distention • Hepatomegaly and splenomegaly • Ascites • No early stage symptoms o Initial signs vague and nonspecific: tired, malaise, morning occipital headache Peripheral Vascular Disease: • Includes a range of arterial symptoms that are caused by atherosclerosis obstruction of the lower-extremity arteries • Increased incidence with diabetes • Most common sites: abdominal aorta, carotid arteries, femoral and iliac arteries S&S of PVD: • Intermittent claudication (leg pain) o Associated with exercise caused by muscle ischemia • Weak peripheral distal pulses • Sensory impairment • Increasing fatigue, weakness in the legs • Pallor or cyanosis, dry skin and hairless, toenails thick Diagnostic Tests PVD: • Doppler, arteriography • Plethysmography measures the size of libs and blood volume in tissues or organs Aortic Aneurysm: • Dilation or weakening of arterial wall • Develops from a defect in the medial layer Etiology of Aortic Aneurysm: • Atherosclerosis, trauma, HTM • Syphilis and congenital defects S&S of Aortic Aneurysm: • Frequently asymptomatic until rupture • Rupture may lead to moderate bleeding usually causes severe hemorrhage and death • Bruit may be heard on auscultation • Abdominal aneurysm are sometimes detected as palpable pulsating masses with bruits (abnormal sounds) Varicose Veins: • Irregular, dilated, tortuous areas of superficial veins • In the legs o May develop from defect or weakness in vein walls o Long period of standing o Appear as irregular, purplish, bulging structures • Predisposes to thrombus formation Etiology of Varicose Veins: • Familial tendency • Vein damaged by trauma • Long standing, crossing legs, wearing tight clothing, pregnancy Thrombophelbitis: • Thrombus developed in inflamed vein (IV site) Plebothrombosis (DVT): • Thrombus forms spontaneously without prior inflammation, attached loosely Factors for Thrombus Development: • Venous stasis • Venous endothelial damage • Hypercoagulable states S&S of Thrombophlebitis and Phlebothrombosis: • Often unnoticed • Aching, burning, tenderness, edema in affected legs and positive homans sign • Systemic signs – fever, malaise, leukocytosis Complication of Thrombophlebitis and Phlebothrombosis: • Deep venous thrombosis may lead to pulmonary embolism and cause pulmonary and cardiovascular complications Shock: • Result from a decreased circulating blood volume, leading to decreased tissue perfusion and general hypoxia Hypovolemic Shock: • Loss of circulating blood volume Cardiogenic Shock: • Inability of heart to maintain cardiac output to circulation Distributive, Vasogenic, Neurogenic, Septic, Anaphylactic Shock: • Changes in peripheral resistance leading to pooling of blood in the periphery Obstructive Shock: • Interfere blood flow to heart Shock S&S: • Anxiety • Tachycardia • Pallor • Light-headedness • Syncope • Sweating • Oliguria Shock Compensation Mechanisms: • SNS and adrenal medulla stimulated – increase HR, force of contraction, systemic vasoconstriction • Renin secretion increases • Increased ADH secretion • Secretion of glucocorticoids • Acidosis stimulates increased respiration Complications of Shock: • Decompensated metabolic acidosis • Acute renal failure • Acute respiratory distress • Acute liver failure Diagnostic Tests for Cardiovascular Function: • Electrocardiography o Useful in diagnosis and monitoring of dysrhythmias, myocardial infarction, infection, pericarditis • Auscultation o Determination of valvular abnormalities or abnormal shunts of blood that cause murmurs o Detected by listening • Echocardiography o Used to record hear valve movements, blood flow and cardiac output • Exercise stress tests o Used to assess general cardiovascular function • Chest x-ray o Used to show shape and size of heart • Cardiac catheterization o Measures pressure and assess valve and heart function o Determines central venous pressure and pulmonary capillary wedge pressure • Angiography o Visualization of blood flow in the coronary arteries • Doppler studies o Assess blood flow in peripheral vessels o Records sounds of blood flow or obstruction • Blood tests o Assess levels of serum triglycerides, cholesterol, sodium, potassium, calcium, other electrolytes • Arterial blood gas determination o Checks the current oxygen level and acid-base balance Dietary Modifications: • To decrease total fat intake • General weight reduction