Exam (elaborations) NR 507 PATHOPHYSIOLOGY WEEK 3 TD2 Vascular, Cellular and Hematologic Disorders Discussion Part Two.pdf

Exam (elaborations) NR 507 PATHOPHYSIOLOGY WEEK 3 TD2 Vascular, Cellular and Hematologic Disorders Discussion Part T This week's graded topics relate to the following Course Outcomes (COs). 1 Analyze pathophysiologic mechanisms associated with selected disease states. (PO 1) 2 Differentiate the epidemiology, etiology, developmental considerations, pathogenesis, and clinical and laboratory manifestations of specific disease processes. (PO 1) 3 Examine the way in which homeostatic, adaptive, and compensatory physiological mechanisms can be supported and/or altered through specific therapeutic interventions. (PO 1, 7) 4 Distinguish risk factors associated with selected disease states. (PO 1) 5 Describe outcomes of disruptive or alterations in specific physiologic processes. (PO 1) 6 Distinguish risk factors associated with selected disease states. (PO 1) 7 Explore age-specific and developmental alterations in physiologic and disease states. (PO 1, 4) Discussion Discussion Part Two (graded) 0 Responses Lorna Durfee 5/16/2016 9:26:22 PM Discussion Part 2 Discussion Part Two (graded) Jesse is a 57-year-old male who presents with gradual onset of dyspnea on exertion and fatigue. He also complains of frequent dyspepsia with nausea and occasional epigastric pain. He states that at night he has trouble breathing especially while lying on his back. This is relieved by him sitting up. His vitals are 180/110, P = 88, T = 98.0 C, R = 20. Subjective: 57-year-old male who presents with gradual onset of dyspnea on exertion and fatigue. He also complains of frequent dyspepsia with nausea and occasional epigastric pain. The patient states that he has trouble breathing at night especially while lying on his back. This condition is relieved when he sits up. Objective: His vitals are 180/110, P = 88, T = 98.0 C, R = 20. Write a differential in this case and explain how each item in your differential fits and how it might not fit. Doctor Brown and Class: This patient, according to Gould and Dyer (2011) is exhibiting signs of paroxysmal nocturnal dyspnea and the presence of acute pulmonary edema. When sleeping, the patient has increased blood volume in the lungs leading to fluid in the alveoli. The fluid will interfere with diffusion of oxygen and therefore lung expansion (Gould & Dyer, 2011, p. 300). This condition leads to pulmonary edema and can be caused by left-sided heart failure. 0 0 DIFFERENTIAL: CONGESTIVE HEART FAILURE: Gould and Dyer (2011) state that congestive heart failure (CHF) occurs when the heart can no longer pump the necessary blood to meet all the demands of the body metabolically. Congestive heart failure can happen as a result of infarction or valve defect. It can arise from increased demands placed on the heart, such as hypertension or disease of the lung. One side of the heart fails first then the other. Infarction of the left ventricle or hypertension affects the left ventricle first. Pulmonary valve stenosis can affect the right ventricle. It is important to decipher which side it is. It is leftsided or right-sided CHF (Gould & Dyer, 2011, p. 297). There is a reduced flow of blood into the systemic circulation, and then the kidneys. These conditions lead to the secretion of increased renin and aldosterone. The result is vasoconstriction and an increased afterload and increased blood volume or preload which adds more work for the heart (Gould & Dyer, 2011, p. 298). The sympathetic nervous system then increases heart rate and peripheral resistance. There is a decrease in the efficiency of the heart. The heart change dilates, and the cardiac muscle then hypertrophies. The wall of the heart ventricle becomes thick. This condition leads to increased demand for blood supply to the myometrium. The myocardial cells die and are replaced with fibrous tissue (Gould & Dyer, 2011, p. 299). This item may fit: Dyspnea on exertion - Wahls (2012) relates that chemoreceptors in the brain and vascular system, as well as mechanoreceptors in the chest wall as well as the diaphragm and vagal receptors, regulate breathing. The cortical and cerebral pathways allow appraisal of the status of the lungs. When a patient has dyspnea it can be respiratory, neurogenic or cardiac in origin (Wahls, 2012, p. 173). Shortness of breath can be related to myocardial ischemia and congestive failure as well as COPD, lung disease and pneumonia and disorders that are psychogenic. He states that cardiac and pulmonary etiology dominates in most of the cases (Wahls, 2012, p.173). The description of the exacerbation of heart failure is a sensation of shortness of breath on exertion (Wahls, 2012, p. 174). This item may not fit: Because the patient could have another condition that may be causing the dyspnea on both exertion and at night. Schwartzstein (2015) confirms that dyspnea is acute when it develops over hours to days and chronic if more than four to eight weeks. The cause of dyspnea could be a new problem or a worsening underlying disease (e.g., asthma, COPD, or heart failure) (Schwartzstein, 2016). This may fit: Fatigue – The American Heart Association (2015) relates tiredness and fatigue are part of the signs and symptoms of heart failure. The heart cannot pump enough blood to meet the demands of the body. The body then sends the blood from less vital organs, the muscles in the limbs, and sends it to the heart and brain. The result is fatigue (The American Heart Association, 2015). This item may not fit: Because fatigue can happen for various reasons. Further evaluation is warranted. This item may fit: Dyspepsia and epigastric pain – This condition could be caused by angina. The National Heart, Lung, and Blood Institute (2011) remind us that symptoms of pressure, burning and tightness in the chest are signs of angina. It starts behind the breastbone. Also, there can be a pain in the arms, neck, jaw, throat or back. Sometimes it is hard to describe where the pain is coming from (The National Heart, Lung and Blood Institute, 2011). Angina is related to Coronary Heart Disease. Patients that I have cared for sometimes have had excess fluid in the body, and it can cause congestion, and this can be from congestive heart failure. This item may not fit: We do not know what other medical issues are present. There needs to be an evaluation of this patient with testing and further physical examination. This may fit: Nocturnal Dyspnea - When sleeping the patient has increased blood volume in the lungs, and this leads to fluid in the alveoli, and that will interfere with diffusion of oxygen and therefore lung expansion (Gould & Dyer, 2011, p. 300). This condition could lead to nocturnal dyspnea and could be a sign that the heart is not functioning properly. This item may not fit: However, there could be another problem such as COPD or pulmonary function issues. Testing is needed. This may fit: Blood Pressure: 180/110 - The systolic and diastolic pressures are both elevated. With left-sided heart failure, the heart moves oxygen-rich blood from the left to the left atrium and then to the left ventricle. With left-sided heart failure, there can be an inability of the left ventricle to contract normally. It cannot push enough of the blood into circulation. The left ventricle loses its ability to relax because the muscle is stiff. The heart cannot fill with blood properly with resting in between beats (The American Heart Association, 2015). This item may not fit: The high blood pressure can be from hypertension and needs to be ruled out. We need to identify what type of hypertension exists. What tests would you order? What immediate treatment would you consider giving this patient and what treatment when he went home? Assume your first differential is definitive. Tests to order and Treatment: Colucci (2015) states that heart failure is complex syndrome clinically. It can result in any disorder that impairs the heart and ventricle to fill with or eject blood. There are specific symptoms: such as dyspnea and fatigue, and signs relating to fluid retention. The ways to assess cardiac function is numerous. There needs to be a careful history and physical (Colucci, 2016). Arnold (2013) informs us that heart failure is a syndrome of ventricular dysfunction. With left ventricular failure, there is shortness of breath and fatigue. With right failure, it causes peripheral and abdominal fluid accumulation. The ventricles are involved either together or separately. The basis of the initial diagnosis is on clinical findings. The support of this diagnosis can be by chest x-ray, echocardiography and obtaining levels of plasma natriuretic peptides. He suggests as a treatment to start with patient education, diuretic medication, ACE inhibitors, angiotensin II receptor blockers, beta-blockers, and other medications. Also the use of digitalis and pacemakers and to definitively find the underlying disorder (Arnold, 2013). Now, he comes back to your clinic 3 months later and both his ankles are slightly swollen. What possible explanations are there for this observation? If this patient has congestive heart failure, swelling in both ankles is another sign. This condition means that the patient is retaining fluid. Sterns (2016) relates that edema in the ankles is called peripheral edema. He could now have pulmonary edema and worsening heart failure. He needs an evaluation for chronic venous disease, deep vein thrombosis, heart failure and a review of his medications (Sterns, 2016). References Arnold, M. O. (2013). Heart failure. In Merck Manual online. Retrieved from failure/heart-failure#Treatment Colucci, W. S. (2016). In T. W. Post (Ed.), UpToDate. Evaluation of the patient with suspected heart failure. Retrieved from Gould, B. E., & Dyer, R. M. (2011). Cardiovascular disorders. In Pathophysiology for the health professions (4th ed., pp. 297 - 300). St. Louis, MO: Saunders/Elsevier. The National Heart, Lung and Blood Institute. (2011). What Are the Signs and Symptoms of Angina? Retrieved from Schwartzstein, R. M. (2016). In T. W. Post (Ed.), UpToDate. Approach to the patient with dyspnea. Retrieved from Sterns, R. H. (2016). In T. W. Post (Ed.), UpToDate. Edema (swelling). Retrieved from The American Heart Association. (2015). Types of Heart Failure. Retrieved from The American Heart Association. (2015). Warning Signs of Heart Failure. Retrieved from Wahls, S. A. (2012). Causes and evaluation of chronic dyspnea. American Family Physician, 86(2), 173-182. Jennifer Roth reply to Lorna Durfee 5/19/2016 11:27:21 AM RE: Discussion Part 2 Hi Lorna, What a great and thorough post. Obtaining the values of electrolytes is imperative in heart failure. Sodium and potassium are two vital values which affect heart arrhythmias as well as fluid congestion. Sodium tends to follow water so the value can give a provider a sense of how severe the heart failure is. Potassium is another key value due to the arrhythmias that can occur due to too low or too high of a value. Creatinine will demonstrate kidney function. Kidneys filter out excess fluid and if they are not working properly, then the excess fluid will present as edema in the lower extremities (AHA, 2015). An EKG will also be beneficial in that it will give information on the heart rhythm the patient is currently in and can be compared to a previous EKG if one is available. This will demonstrate the worsening of heart failure or if a new issue is arising. There are so many options to evaluate the appropriate course of diagnosing and treating heart failure. Each individual is different so there is not one way which is correct compared to another. Underlying medical conditions and non-compliance affect the outcomes for patients with heart failure. A you had previously mentioned, patient education is probably the most important intervention provided to patients with heart failure. There are changes patients can make in their daily lives to improve outcomes as well as complying with medical interventions. Jennifer Roth Reference Heart failure. (2015). Retreived from: Failure_UCM__SubHomeP Liberty Neoh 5/17/2016 8:16:10 PM Discussion Part Two Dr. Brown and Class, Write a differential in this case and explain how each item in your differential fits and how it might not fit. This patient is showing signs of Heart Failure (HF). Patients with heart failure are likely to present, exertional dyspnea, fatigue, orthopnea, exercise intolerance, and fluid retention which can lead to peripheral edema. Hypertension may be the single most important modifiable risk factor for HF in the United States. Hypertensive men and women have a substantially greater risk for developing HF than normotensive men and women Elevated levels of diastolic and especially systolic blood pressure are major risk factors for the development of HF (Yancy et al, 2013). What tests would you order? In ambulatory patients with dyspnea, measurement of BNP or N-terminal pro-B-type natriuretic peptide (NT-proBNP) is useful to support clinical decision making regarding the diagnosis of HF, especially in the setting of clinical uncertainty. According to Yancy and colleagues (2013), “BNP or its amino-terminal cleavage equivalent (NT-proBNP) is derived from a common 108- amino acid precursor peptide (proBNP108) that is generated by cardiomyocytes in the context of numerous triggers, most notably myocardial stretch. Following several steps of processing, BNP and NT-proBNP are released from the cardiomyocyte, along with variable amounts of proBNP108, the latter of which is detected by all assays that measure either “BNP” or “NT-proBNP.” (Yancy et al, 2013). What immediate treatment would you consider giving this patient and what treatment when he went home? Diuretic-based antihypertensive therapy has repeatedly been shown to prevent HF in a wide range of patients; ACE inhibitors, ARBs, and beta blockers are also effective. Data are less clear for calcium antagonists and alpha blockers in reducing the risk for incident HF (Yancy et al, 2013). Now, he comes back to your clinic 3 months later and both his ankles are slightly swollen. What possible explanations are there for this observation? If patient’s symptoms are not improving and now the patient has swollen ankles, I need to investigate whether the patient complies with the pharmacologic management. If Jesse is following the treatments and taking his medications, it would mean that the current treatment plan is not working. Reference Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey, D. E., Drazner, M. H.,…Wilkoff, B. L. (2013). 2013 ACCF/AHA guideline for the management of heart failure. Journal of the American College of Cardiology, 62(16). doi: 10.1016/.2013.05.019 Rechel DelAntar reply to Liberty Neoh 5/18/2016 6:59:02 PM RE: Discussion Part Two Hello Liberty and class, It is important to assess not just for the effectiveness of the treatment but also patient compliance. This is sometimes often bypassed assuming patients will always follow the regimen. Studies show that in the United States alone, nonadherence to medications causes 125,000 deaths annually and accounts for 10% to 25% of hospital and nursing home admissions. This makes nonadherence to medications one of the largest and most expensive disease categories. Moreover, patient nonadherence is not limited to medications alone. It can also take many other forms; these include the failure to keep appointments, to follow recommended dietary or other lifestyle changes, and to follow other aspects of treatment or recommended preventive health practices.Therefore, actual implications of nonadherence goes far beyond the financial aspect of medication compliance (American College of Preventative Medicine, 2016). I agree with you that part of follow up should not just be the effects of the medication but is the patient following the regimen and if not why. References: American College of Preventative Medicine. (2016). Medication Adherence Time Tool: Improving Health Outcomes A Resource from the American College of Preventive Medicine. Retrieved from Lanre Abawonse reply to Liberty Neoh 5/21/2016 4:15:01 PM RE: Discussion Part Two Great Job on pointing out the impact of hypertension on heart failure. Hypertension is one of those diseases that are often ignored by many people over a long period of time because they are unaware they have it. Yarmolinsky, Gon, and Edwards (2015) stated that hypertension is the leading risk factor for disease globally. Hypertension can do significant damage to the heart by affecting the performance of the arteries. Normally, arteries expand and contract effortlessly with each heartbeat. With sustained hypertension, the arterial walls become thickened, inelastic, and resistant to blood flow. This process injures arterial linings and accelerates plaque formation, thus causing the left ventricle to pick up the slack of nonfunctioning blocked vessels. Reference Yarmolinsky, J., Gon, G., & Edwards, P. (2015). Effect of tea on blood pressure for secondary prevention of cardiovascular disease: a systematic review and meta-analysis of randomized controlled trials. Nutrition Reviews, 73(4), p. doi:nutrit/nuv001 Rechel DelAntar 5/17/2016 9:44:24 PM Differential Diagnoses Hello Professor and Class, Differential Diagnoses This is a case of a 57-year-old gentleman complaining of gradual onset of dyspnea on exertion and fatigue. Also complains of occasional epigastric pain, dyspepsia and nausea. The patient expresses difficulty breathing at night when he is lying on his back. Noted elevated BP at 180/100, PR=88 R=20 and afebrile at 98C. Based on this presentation, the following diagnoses the patient is most likely having: 1. Heart Failure = often referred to as congestive heart failure (CHF), occurs when the heart is unable to pump sufficiently to maintain blood flow to meet the body's needs. Heart failure is a physiological state in which cardiac output is insufficient to meet the needs of the body and lungs. The term "congestive heart failure" is often used, as one of the common symptoms is congestion, that is, build-up of too much fluid in tissues and veins (McCance, K.L., ., 2013). Specifically, congestion takes the form of water retention and swelling (edema), both as peripheral edema (causing swollen limbs and feet) and as pulmonary edema(causing breathing difficulty), as well as ascites (swollen abdomen) and dyspepsia. Another sign of heart failure is Paroxysmal nocturnal dyspnea manifested as shortness of breath while sleeping at night or in a reclining position, which is due to the lung’s air sacs filling up with fluid or pulmonary edema. Ischemic heart disease and hypertension are the most important predisposing risk factors (McDonagh, T., 2011). The patient symptoms fit the profile of heart failure. 2. Acute Coronary Syndrome = Coronary obstruction caused by thrombus formation over a ruptured or ulcerated atherosclerotic plaque. Unstable angina is the result of reversible myocardial ischemia and is a predictor of impending infarction while Myocardial infarction (MI) is the prolonged ischemia of the heart causing irreversible damage to the heart muscle (McCance, K.L., et. al, 2013). The classic symptom is chest pain due to ischemia of the heart muscles known as angina pectoris. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and upper abdomen, where it may mimic heartburn accompanied by dyspnea, weakness and fatigue (American heart Association, 2014). Although some of the symptoms fit the patient description, the patient is not experiencing chest pain, which is a classic sign of an MI or ischemia. 3. Pulmonary Hypertension = is a type of high blood pressure that affects the arteries in your lungs and the right side of your heart. Tiny arteries in your lungs, called pulmonary arterioles, and capillaries become narrowed, blocked or destroyed. This makes it harder for blood to flow through your lungs, and raises pressure within your lungs' arteries. As the pressure builds, your heart's lower right chamber (right ventricle) must work harder to pump blood through your lungs, eventually causing your heart muscle to weaken and fail. Elevated pressures in the heart and lungs as well as the back flow of blood to the liver and kidneys produce symptoms of shortness of breath, tiredness, chest pain, elevated heart rate (Mayo clinic, 2016). Although some of the symptoms fit, the patient is not exhibiting chest pain and elevated heart rate present in PHN 4. GERD = Gastro-esophageal Reflex Disease is a chronic condition of mucosal damage caused by stomach acid coming up from the stomach into the esophagus (chronic reflux). Occasional reflux causes heartburn, but chronic reflux leads to reflux esophagitis, GERD, and sometimes Barrett's esophagus. GERD is usually caused by changes in the junction between the stomach and the esophagus, including abnormal relaxation of the lower esophageal sphincter, which normally holds the top of the stomach closed, impaired expulsion of gastric reflux from the esophagus, or a hiatal hernia. Sign and symptoms are similar to cardiac symptoms of chest pain, dyspepsia, coughing as well as night time GERD Reflux. Night time reflux is associated with a more aggressive for of GERD (International Foundation for Functional Gastrointestinal Disorders, 2016) . Although the symptoms of this disease may be similar to what the patient is experiencing, it does not cause hypertension such as the one the patient is experiencing. 5. Pernicious Anemia = Anemia is a condition in which the body does not have enough healthy red blood cells. Pernicious anemia is a decrease in red blood cells that occurs when the intestines cannot properly absorb vitamin B12. The principal disorder in PA is an absence of intrinsic factor (IF), a transporter required for absorption of dietary vitamin B , which is essential for nuclear maturation and DNA synthesis in erythrocytes. Symptoms develop slowly but the once the disease progresses; it will later include neurologic complication. Classic symptoms of anemia—weakness, fatigue, parenthesis of the feet and fingers, difficulty in walking, loss of appetite, abdominal pains, weight loss, and a sore tongue that is smooth and beefy red secondary to atrophic glossitis (McCance, K.L., 2013). This diagnosis does not fit the symptomatology of the patient because the patient is not experiencing glossitis and parenthesis. Also PA does not exhibit signs of shortness of breath at night while in bed. In the case of this patient suspected of having Heart Failure, some of the tests that could be ordered would be labs such as a complete blood count, complete metabolic panel, Cardiac function panel and BNP. Also it is important to get an EKG to identify heart rhythm or conduction abnormalities. An echocardiogram is also needed to assess heart function. A chest x-ray can be ordered in conjunction with the ECHO to assess cardiomegaly. Treatment is focused on improving symptoms and stopping disease progression. Assess their functional status to provide guidance to their treatment (NY Heart Class I-IV). Start with managing his uncontrolled BP, as hypertension is one of the predisposing factors for heart failure. Suggest using an ACE inhibitors, calcium channel blockers or ARB to control blood pressure and add a diuretics to remove fluids and decrease cardiac workload (McDonagh, T., 2011). Education counseling in cardiac diet such as limiting salt intake and to keep a blood pressure log. Patient comes back to clinic and noted bilateral pedal edema. Assess the degree of pedal edema and check for pulmonary congestion. Ask if symptoms have improved or not and check patient’s BP log to see BP trends. IF the patient expresses improvement, assess current meds that may be causing pedal edema. Check labs to assess effects of treatment and kidney function from diuretic use. May consider increasing diuretic therapy to unload fluid from the body. Also may consider coronary angiogram to assess patency of coronary arteries. If symptoms are worse, may consider hospital admission for advance heart failure therapies. References: American Heart Association. (2014). Heart Attack or sudden cardiac arrest: How are they different? Retrieved from Conditions/More/MyHeartandStrokeNews/Heart-Attack-or- Sudden-Cardiac-Arrest-How-Are-They Different_UCM__A#.VzvJXpMrJo4. International Foundation for Functional Gastrointestinal Disorder. (2016). GERD: Signs and Symptoms. Retrieved from Mayo Clinic. (2016). Pulmonary Hypertension. Retrieved from hypertension/home/ovc-. McCance, K.L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2013). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis, MO: Mosby. McDonagh, T. (2011). Oxford Textbook of heart failure. Oxford: Oxford University Press. [4] 12 Lanre Abawonse 5/17/2016 11:14:55 PM Discussion Part Two Heart Failure (HF) occurs when the heart is unable to pump sufficient blood to meet the metabolic need of the body. The result of inadequate cardiac output is poor organ perfusion and vascular congestion in the pulmonary or systemic circulation. HF can be classified as systolic or diastolic, left sides(ventricle unable to produce a CO sufficient to prevent pulmonary congestion) or right sided(ventricle is unable to maintain an adequate cardiac output, and systemic congestion occurs), acute or chronic (Nicholson, 2014).HF may be described as backward or forward failure, high or low output failure. For backward failure, the ventricles fail to eject its content, which result in pulmonary edema on the left side of the heart and systemic congestion on the right. Forward failure causes inadequate CO which lead to decreased organ perfusion. Low output failure occurs when the ventricle is unable to generate enough CO to meet the metabolic demand of the body maintain an adequate cardiac output, and systemic congestion. In HF with preserved ejection fraction there is a compliance abnormality where relaxation of the ventricle is impaired (Shih & DeNofrio, 2016). Dyspnea or breathlessness, occurs early in the progression of left-sided heart failure and may be considered the cardinal symptom (Copstead & Banasik, 2013). Most of breathleness starts as exertional breathlessness and can manifest as paroxysmal nocturnal dyspnea, orthopnea or breathlessness at rest and blood volume from excessive salt or fluid intake (Thackwray& Walton, 2011). Orthopnea and paroxysmal nocturnal dyspnea are due in part when the individual lies down. The failing of the left ventricle is unable to effectively pump extra volume and pulmonary congestion is worsened. Thus the severity of orthopnea may be quantified by the degree of head elevation example is how many pillows use to relieve dyspnea. Hypertension is a persistent or intermittent elevation of systolic blood pressure above 140 or diastolic pressure above 90 (Copstead & Banasik, 2013). If untreated, hypertension can contribute to complication of end organ damage such as heart failure. Increased fluid volume increases both preload, and the volume of blood returned to the heart and afterload, the resistance against which the heart pumps (Whitlock, & MacInnes, 2010) What tests would you order? What immediate treatment would you consider giving this patient and what treatment when he went home? Assume your first differential is definitive. With this patient condition it will be helpful to have the patient undergo echocardiography as this would measure the chamber size of the heart, take a look at the valvular structure and function, estimate the ventricular wall motion, and estimated ejection fraction. Multigated blood pool imaging would be consider to assess the cardiac volume both during systole and diastole, which would determine the ejection fraction, this value are sometime depressed in low output failure. The use of BNP has being useful, being a major source of plasma BNP, is the cardiac ventricle. The level increases when major HF failure symptoms are worsen and decreases when the condition stabilizes. Troponin levels should be checked on all patients complaining of chest pain to confirm if the patient has experienced an acute coronary event (Whitlock, & MacInnes, 2010). Chest x-ray may be used to detect, cardiomegaly, pulmonary vascular congestion, alveolar or interstial edema, or pleural effusion. Serum electrolytes, BUN/creatine, colorflow mapping and cardiac angiogram are some of the other use test that can be order to find other associated problem. Treatment should focus on reducing the current symptomatic problems. This patient received an immediate respiratory relieve, which the administration of diuretics would be of great benefit. Thus, it helps to control fluid and sodium retention, oxygen therapy is very vital. Beta-blockers to help reduce afterload and increase myocardial perfusion (Nicholson, 2014). Vasodialators can be added to reduce arterial and venous vasoconstriction due to activation of adrenergic and reninangiotensin system, thereby reducing the vasoconstriction, reduce afterload and enhancing myocardial performance and decreasing preload and ventricular filling presure and cardiac consult (Whitlock, & MacInnes, 2010). Now, he comes back to your clinic 3 months later and both his ankles are slightly swollen. What possible explanations are there for this observation? Patients with dyspnea or breathlessness that present with swelling lower extremities are typical patient with congestive heart failure. In this patient there is impaired ability of myocardial fibers to contract (systolic failure) and relax (diastolic failure) or both (Copstead & Banasik, 2013). There is complex mechanism that involve in this situation, one of such is the sympathetic constriction of arterioles which helps to maintain blood pressure when cardiac output is reduced. This patient heart is unable to pump sufficient amount of oxygenated blood to supply the body needs. In some cases the liver and the kidney function is disrupted. Since the heart fail to pump adequately, it causes increased pressure in the circulatory system, allowing fluid to escape from the bloodstream and accumulate in tissues and organs. With failure occurring in the right side of the heart, it means the right side is not keeping pace with the left side and the blood accumulates in the vessels leading to the heart. The most common place for the excess fluid is at peripheral edema which occurs in the lower legs, feet, and ankles. . In HF, reduced renal perfusion results in the activation of the renin-angiotensin-aldosterone system which increases salt and water re-absorption with the aim of increasing blood volume, but this response exacerbates fluid retention (Whitlock, & MacInnes, 2010). Reference Copstead, L. C., & Banasik, J. L. (2013). Pathophysiology (5 th ed.). St. Louis, MO: Mosby. Nicholson, C. (2014). Chronic heart failure: pathophysiology, diagnosis and treatment. Nursing Older People, 26(7), 29-38 10p. doi:10.7748/nop.26.7.29.e584 Shih, J. & DeNorfrio, D. (2016) Congestive heart failure: Differential diagnosis. In F. J. Domino (Ed.), The 5-minute clinical consult 2016 (24th ed., pp. A-29). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. Thackwray, J., & Walton, A. (2011). Clinical assessment of a patient with stable heart failure. British Journal Of Cardiac Nursing, 6(3), 110-117 8p. Whitlock, A., & MacInnes, J. (2010). Acute heart failure: Patient assessment and management. British Journal Of Cardiac Nursing, 5(11), p. Jonathan Bidey 5/18/2016 12:13:46 PM Discussion Part 2 Dr. Brown and Class, The patient is exhibiting signs and symptoms typical of heart failure. This is most likely his diagnosis, but we must further analyze and review other possible diagnoses. 1. Heart Failure: Heart failure can present gradually with frequent episodes of shortness of breath and fatigue. This is caused by the heart’s inability to properly expel blood. Due to injury or chronic disease, the heart experiences hypertrophy as it meets resistance against a compensated, increased pulmonary pressure. Re-architecture of the muscle then occurs, and the heart is no longer able to appropriately mobilize blood. The result is often excesses of fluid in the thorax and abdomen. This is experienced as shortness of breath, fatigue, dyspepsia, nausea, abdominal pain, and paroxysmal nocturnal dyspnea (McCance & Huether, 2014). The patient is experiencing all of these symptoms and is likely experiencing heart failure. However, additional testing must be completed to verify this diagnosis. 2. Gastroesophageal Reflux Disease (GERD): GERD could cause the patient to experience frequent dyspepsia, nausea, epigastric pain, and paroxysmal nocturnal dyspnea. Although, unless severely painful, GERD is not likely to raise the patient’s blood pressure to such an extreme or cause such frequent shortness of breath. 3. Chronic Obstructive Pulmonary Disease (COPD): The patient could be experiencing COPD. Hypercapnia from prolonged elevated levels of carbon dioxide could cause hypertension, and COPD would certainly result in shortness of breath and paroxysmal nocturnal dyspnea. COPD would not likely cause epigastric pain or dyspepsia. 4. Hypertension: The patient is significantly hypertensive. Hypertension could contribute to fatigue and nausea, depending on the patient’s sensitivity to a hypertensive state. However, hypertension is not likely to cause epigastric pain, dyspepsia, or paroxysmal nocturnal dyspnea. It is most likely that another health issue is causing the patient’s symptoms. 5. Obstructive Sleep Apnea (OSA): Untreated OSA can result in elevated blood pressure, paroxysmal nocturnal dyspnea, and daytime fatigue. However, it does not typically manifest with dyspnea on exertion, nausea, or epigastric pain. Testing: There are many tests which must be considered if we are to evaluate the patient for heart failure. These tests would include labs and imaging. Bloodwork would include a complete blood count, comprehensive metabolic panel, and a b-type natriuretic peptide (BNP). The BNP is significant, because high levels of BNP are seen as a result of pressure changes in the heart (Pellicori & Cleland, 2014). The level of BNP can be indicative of the level of severity of the patient’s heart failure. Imaging should include a chest x-ray, ECG, and echocardiogram with Doppler study. This should be done to evaluate for fluid buildup in the chest, as well as cardiac blood flow, and ejection fraction (Pellicori & Cleland, 2014). Also a cardiac stress test should be completed. Treatment: Initial treatment must include a way to get the patient’s blood pressure under control, as it is dangerously high. This can be achieved through a beta-blocker. The patient should be started on something with a positive inotropic effect to help improve the function of the cardiac muscle, such as Digoxin. Also the patient should augment salt and free water intake, as well as begin use of a diuretic. Follow Up: When the patient returns to clinic with bilateral lower extremity edema, this can be explained by revisiting the pathophysiology of heart failure. The heart is unable to adequately eject. To compensate, preload and afterload are increased. Eventually the cardiac muscle experiences hypertrophy from prolonged resistance against increased pulmonary pressure and the heart is no longer able to appropriately mobilize blood. The result is often excesses of fluid in the thorax and abdomen. As the disease progresses, peripheral circulation also becomes effected. Blood cannot be ejected and congestion is experienced in the peripheral circulation. Excess fluid becomes unable to be mobilized and sits within the vessels of peripheral extremities. Gravity causes the fluid to pool and manifests as dependent edema (McCance & Huether, 2014). -Jonathan References: McCance, K. L., & Huether, S. E. (2014). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis, MO: Elsevier-Mosby. Pellicori, P., & Cleland, J. G. (2014). Heart failure with preserved ejection fraction. Clinical Medicine, 14, 22-28. Retrieved from pdfviewer?sid=3ddbd6f4-69c5-44ee-a465-68db3e61c164%40sessionmgr103&vid=7&hid=103 Lorna Durfee reply to Jonathan Bidey 5/19/2016 7:53:54 AM RE: Discussion Part 2 Jonathan: I totally agree with your post about hypertension and control of heart failure. Kaplan (2016) states that hypertension is the most modifiable risk factor for any further development of heart failure. Hypertension increases the work of the heart which leads to left ventricular hypertrophy. We know that hypertension is a risk factor for coronary heart disease. Kaplan (2016) also explains that the incidence of HF varies by population and follow-up. He informs the reader that treatment of hypertension in patients with HF must take into account the type of HF that is present. He states that patients can have an impairment with systolic dysfunction and cardiac contractility as the primary abnormality, or diastolic dysfunction, where there is a limitation to filling in diastole thus in forward output due to increased ventricular stiffness. References Kaplan, N. M. (2016). T In T. W. Post (Ed.), UpToDate. Treatment of hypertension in patients with heart failure. Retrieved from Instructor Brown reply to Jonathan Bidey 5/19/2016 8:15:14 PM RE: Discussion Part 2 Explain from a patho process how heart failure causes fatigue? Jonathan Bidey reply to Instructor Brown 5/22/2016 3:45:02 PM RE: Discussion Part 2 Dr. Brown, Heart failure related fatigue can be caused by disturbed cardiac function. As I have discussed, heart failure results in poor cardiac output. This lack of proper blood ejection causes a decrease in available oxygen in peripheral blood (Conley, Feder, & Redeker, 2015). This causes poor systemic tissue profusion, manifesting as fatigue. Also, heart failure patients have significant levels of excess fluid. This can collect around the lungs, or in extremities. This causes the person to need to work much harder to fulfill activities of daily living without become overwhelmed with breathlessness and fatigue. Reference: Conley, S., Feder, S., & Redeker, N. S. (2015). The relationship between pain, fatigue, depression and functional performance in stable heart failure. Heart & Lung, 44(2), 107-112. g.2014.07.008 Sarah Boulware 5/18/2016 2:52:31 PM Part Two Dr. Brown and Class, Heart Failure Heart failure (HF) occurs due to depressed cardiac function. This can be a result of coronary artery disease, valvular dysfunction, cardiac arrhythmias or hypertension. In left-sided HF, the left ventricle becomes unable to pump at a normal stroke volume, which leads to tissue hypoperfusion and inadequate oxygen delivery. Fluid may back up into the pulmonary system resulting in pulmonary edema. Clinical manifestations may include fatigue, dyspnea, cough, and angina at rest or with physical exertion, and possibly tachycardia or hypertension (AuCoin, 2011). Jesse appears to be very hypertensive as well as experiencing orthopnea. His epigastric discomfort could be caused by fluid build up related to HF. Jesse’s fatigue and dyspnea on exertion are also signs of HF. Tests that should be ordered to evaluate Jesse for HF include: electrocardiogram (ECG), serum troponin to evaluate for acute ischemia, serum B-type natriuretic peptide (BNP) levels, a chest x-ray to evaluate heart size and pulmonary congestion, and an echocardiography to determine cardiac output. BNP provides valuable information for the diagnosis HF. Elevated BNP levels tend to predict adverse reactions of HF (Oktay & Shah, 2015). Treatment involves managing and preventing symptoms associated with HF. Oxygen, nitrates, and morphine administration immediately improves oxygenation. ACE inhibitors and beta-blockers are effective drugs at reducing mortality by reducing preload and afterload. Salt restrictions, diuretics, and aldosterone-blockers effectively reduce preload and improve outcomes. The primary feature of HF is congestion; diuretics are routinely prescribed to help prevent this complication (Guglin, 2011). When Jesse presents three months later with swelling in his ankles I would be concerned his HF has progressed to congestive heart failure (CHF) that is poorly maintained. If Jesse is not adhering to his treatment regimen, and not maintaining a low salt diet and taking his diuretics and other medications as prescribed it could easily result in the worsening of his HF, progression to CHF, and swelling in his feet and ankles (Guglin, 2011). Abdominal Aortic Aneurysm Abdominal Aortic Aneurysms (AAAs) are often caused from atherosclerosis, which weakens the elastin fibers of the smooth muscle of the aorta resulting in a weakened muscle wall. The weakened wall leads to remodeling and enlargement of the aorta wall and lumen. Older men are more prone to AAAs. Common symptoms include back pain, feeling full between meals, nausea that is increased at night, abdominal pulsation, weak or absent peripheral pulses, and a 15 mmHg or more difference between the left and right arm. Many people with aortic aneurysms also have hypertension, coronary artery disease (CAD), and peripheral vascular disease (PVD). Jesse is experiencing epigastric discomfort and orthopnea which could possible be caused by an AAA. A pulsating mass in the abdomen and a difference in blood pressure along with weak peripheral pulses would provide a more definitive diagnosis of AAA (Woodrow, 2011). Pulmonary Arterial Hypertension (PAH) PAH is a disease that affects the small pulmonary arteries. Vascular obstruction leads to vascular resistance. Right ventricular afterload is increased and results in right ventricular failure. Dyspnea on exertion is the most common and frequent symptom, which Jesse is experiencing. Fatigue and weakness are also symptoms. Signs of right heart failure are evidence in severe PAH. Jesse is exhibiting some symptoms of PAH but further testing is needed to make a definitive diagnosis. An ECG and chest x-ray can help to determine the presence of PAH (Montani et al., 2013). Peptic Ulcer Disease This is a non-fatal disease that primarily presents with symptoms of epigastric pain. Symptoms tend to come and go at times. Abdominal pain is the most common symptom along with feelings of fullness, mild nausea, pain or discomfort in the upper abdomen, pain in the abdomen that wakes you up at night. Less common signs and symptoms include chest pain and fatigue (Graham, 2014). Jesse is experiencing a lot of abdominal symptoms that could be related to an ulcer. Further testing is needed. His dyspnea on exertion and orthopnea also need to be addressed. Gastroesophageal Reflux Disease (GERD) GERD is a condition that develops when the reflux of the stomach contents into the esophagus causes symptoms and/or injury. Heartburn and acid regurgitation that may be accompanied by chest pain is a common symptom. GERD could be responsible for some of Jesse’s symptoms including fullness, epigastric pain, and nausea (Subramanian & Triadafilopoulos, 2015). References AuCoin, A. (2012). Management of a patient with congestive heart failure and acute pulmonary edema – a case study. Canadian Journal of Respiratory Therapy, 47(1), 12-17. Graham, D. (2014). History of Helicobacter pylori, duodenal ulcer, gastric ulcer and gastric cancer. World Journal of Gastroenterology, 20(18), 5191- 5204. doi: 10.3748/wjg.v20.i18.5191 Guglin, M. (2011). Diuretics as pathogenetic treatment for heart failure. International Journal of General Medicine, 4, 91-98. doi: 10.2147/ijgm.s16635 Montani, D., Gunther, S., Dorfmuller, P., Perros, F., Girerd, B., Garcia, G.,…& Sitbon, O. (2013). Pulmonary arterial hypertention. Orphanet Journal of Rare Diseases, 8(97), 1-28. doi: 10.1186/ Oktay, A. & Shah, S. (2015). Diagnosis and management of heart failure with preserved ejection fraction: 10 key lessons. Current Cardiology Reviews, 11(1), 42-52. doi: 10.2174/x Subramanian, C. & Triadafilopoulos, G. (2015). Refractory gastroesophageal reflux disease. Gastroenterology Report, 3(10), 41-53. doi: 10.1093/gastro/gou061 Woodrow, P. (2012). Abdominal aortic aneurysms: clinical features, treatment and care. Nursing Standard, 25(50), 50-58. Instructor Brown reply to Sarah Boulware 5/19/2016 8:17:40 PM RE: Part Two How does GERD cause chest pain? Explain the patho process. Sarah Boulware reply to Instructor Brown 5/21/2016 9:31:08 AM RE: Part Two Dr. Brown, Gastroesophageal reflux disease (GERD) develops when the reflux of gastric contents causes symptoms or complications. It usually is classified as an upper gastrointestinal and esophageal condition. Reflux may be acidotic or alkaline. The frequency, duration, and location of the reflux are what determine GERD. The lower esophageal sphincter (LES) may become relaxed and promote reflux. Pressure changes in the LES may also promote reflux. Peristaltic dysfunction of the esophagus causes prolonged esophageal clearance, which increases the chance of reflux. High fat foods often cause delayed gastric emptying. Acidic foods may trigger symptoms. Sleeping supine or consumption of a specific food right before sleep may trigger nocturnal awakening form symptoms. Symptoms include heartburn, acid regurgitation, chest pain, epigastric pain, or sleep disturbance (Lee & Goldstein, 2015). Non-cardiac chest pain is the term used to describe chest pain that persists after a cardiac source has been eliminated. Esophageal chest pain (ECP) is common and can greatly affect quality of life. It is essential to identify the underlying causes and mechanisms of chest pain for successful management to occur. GERD is often the cause of ECP. Approximately 46 percent of patients with non-cardiac chest pain were found to have acid reflux. Acid reflux has been found to be the direct cause of ECP. Fass and Achem (2011) found that there is an association between GERD and ECP but the association does not confer casualty. GERD can be determined the cause of the chest pain when symptoms resolve in response to the treatment of anti-reflux medications. The mechanism by which GERD causes ECP is still poorly understood but confirmed by the resolution of symptoms upon treatment. References Coss-Adame, E. & Rao, S. (2015). A review of esophageal chest pain. Gastroenterology & Heppatology, 11(11), 759-766. Fass, R. & Achem, S. (2011). Noncardiac chest pain: epidemiology, natural course and pathogenesis. Journal of Neurogastroenterology, 17(2), 110-123. doi: 10.5056/jnm.2011.17.2.110 Lee, A. & Goldstein, R. (2015). Gastroesophageal reflux disease in COPD: links and risks. International Journal of COPD, . doi: 10.2147/COPD.S77562 Jennifer Roth 5/19/2016 10:48:09 AM Part 2 Hello Dr. Brown and Classmates, Heart Failure (HF) is a condition of heart where it is unable to pump effectively enough to support physiological function properly. HF is caused by structural or functional abnormalities of the heart (Gilmour, Strong, Hawkins, Broadbent, & Huntington, 2013). HF is a complex disease with multiple symptoms which can impact on quality of life. Dyspnea, orthopnea, pain, fatigue, anxiety, nausea, and edema are the most common symptoms present (Gilmour, Strong, Hawkins, Broadbent, & Huntington, 2013). Dyspnea on exertion is progressive or an individual may have dyspnea at rest depending on the severity of HF. Dyspnea occurs due to blood backing up in the pulmonary veins because the heart is unable to efficiently pump blood to the rest of the tissues (American Heart Association, 2015). This causes fluid to build up and leak into the lungs which decreases the available space in the lungs for alveoli to exchange gases. Orthopnea occurs for the same reasons. When the individual is supine, the fluid continues to impair gas exchange resulting in orthopnea. When the individual sits up, gravity takes affect and pulls the fluid to the bottom of the lungs instead of being spread out. In other words, the surface area the fluid is able to cover is decreased when the patient is vertical. Fatigue occurs due to the lack of oxygen to the body’s tissues. The body diverts blood away from less vital organs and sends it to the heart and brain (AHA, 2015). When the oxygen available is less than the demand, fatigue occurs. Nausea and abdominal pain present due to the body diverting blood to the vital organs. This means that digestion is occurring at a slow pace and food may sit in the stomach for a while longer than usual causing nausea and abdominal pain. Tachycardia is typically present due to a compensatory mechanism within the body. To compensate for the loss in pumping capacity, the heart beats faster (AHA, 2015). Hypertension (HTN) occurs due to baroreceptors located within the arteries. The baroreceptors recognize that the heart is not pumping blood efficiently which is causing low blood pressure. Blood vessels are constricted so the force to push the blood must increase. This results in hypertension. The only symptom that is unexplained is dyspepsia. Although, some individuals can mistake chest pain and dyspepsia. Chest pain can be a result of wheezing or a cough that may be present or if a pleural effusion is present. Tests for heart failure include: CBC; CMP which includes electrolytes, albumin, and creatinine; serum troponin to determine acute ischemia, and serum BNP to determine the severity of HF; an EKG to determine if any arrhythmias are present and degree of ischemia; a chest x-ray to see the size of the heart and if pulmonary congestion is present; and an echocardiography to show the thickness of the heart muscle as well as how well the heart is pumping (AHA, 2015). Treatments to be administered immediately would include oxygen, nitrates, and morphine if necessary. All three of these options improve myocardial oxygenation (Gilmour, Strong, Hawkins, Broadbent, & Huntington, 2013). ACE inhibitors are useful to decrease preload and afterload. Beta blockers are used to decrease myocardial demand. Diuretics should also be given to decrease the preload. Possible treatments to be used after discharge would include: ACE inhibitors, angiotensin II receptor blockers, angiotensin-receptor neprilysin inhibitors, beta blockers, aldosterone antagonists, and diuretics (AHA, 2015). After three months the patient returns with slightly swollen ankles. This may be explained by the decreased blood flow out of the heart causes the blood to back up in the veins, which in turn causes the fluid to leak out of the veins and into the surrounding tissue. The kidneys are less able to dispose of sodium and water, also causing fluid retention in the tissues (AHA, 2015). The fluid tends to accumulate in the lower extremities due to gravity. Individual spend most of their time in an erect vertical position which forces the fluids to the lower extremities. References Gilmour, J., Strong, A., Hawkins, M., Broadbent, R., & Huntington, A. (2013). Nurses and heart failure education in medical wards. Nursing Praxis in New Zealand, 29(3), 5-17. Heart failure. (2015). Retrieved from: Instructor Brown reply to Jennifer Roth 5/19/2016 8:18:40 PM RE: Part 2 How do nitrates effect this process? What patho process is involved? Matthew Dove reply to Instructor Brown 5/22/2016 11:53:46 AM RE: Part 2 The rudimentary pathophysiology of nitrates Jennifer and Dr. Brown, are that they are vasodilating agents (and have other applications such industrial explosives) that alleviate tension on vascular smooth muscle stressed during Major Adverse Cardiac Events (MACE)—and subsequently expanding peripheral veins and arteries. This process is the culmination of Guanosine monophosphate (cyclic GMP) increasing in smooth muscle (through a decrease in intracellular calcium) by stimulating guanylate cyclase through formation of free radical nitric oxide. This activity results in dephosphorylation of the myosin light chain, which improves the contractile state in smooth muscle achieving vasovenodilation effect. This results in a decrease in preload returning to heart, afterload, and wall tension against cardiac tissue--allowing a decreased systemic drop in blood pressure and reduction in oxygen demand to cardiac tissue to function (Porth, 2014). O’Gara et al. suggest in the American College of Cardiology Foundation/American Heart Association Task Force Practice Guidelines for specific nitrate therapies in MACE. As follows: Congestive heart failure - Myocardial infarction with complication · IV: non-polyvinylchloride tubing, 5 mcg/min, initial titration should be in 5 mcg/min increments at intervals of 3 to 5 minutes guided by patient response; if no response at 20 mcg/min, incremental increases of 10 and 20 mcg/min may be used; polyvinylchloride tubing, initial dose 25 mcg/min IV Hypertension, Perioperative · IV: 5 mcg/min, initial titration should be in 5 mcg/min increments at intervals of 3 to 5 minutes guided by patient response; if no response at 20 mcg/min, incremental increases of 10 and 20 mcg/min may be used Hypotension, induction and maintenance, Intraoperative · IV: initial, 5 mcg/min using nonabsorptive tubing, titrate 5 mcg/min every 3 to 5 min to response; if no response at 20 mcg/min, incremental increases of 10 and 20 mcg/min may be used; starting dose of 25 mcg/min has been used in clinical studies using polyvinylchloride tubing Myocardial infarction · initial, 10 mcg/min IV; titrate to desired blood pressure · 0.4 mg SL every 5 minutes up to 3 doses (O’Gara et al., 2012). It should be noted in patients receiving nitrates regularly that tolerance could developed and if patients exhibit symptoms of tachyphylaxis, a minimum of 8 hour drug holiday is recommended for nitrates to regain efficacy (O’Gara et al., 2012). Reference O'Gara, P.T., Kushner, F.G., Ascheim, D.D., Casey, D.E., Chung, M.K., de Lemos, J.A., Ettinger, S.M., Fang, J.C., Fesmire, F.M., Franklin, B.A., Granger, C.B., Krumholz, H.M., Linderbaum, J.A., Morrow, D.A., Newby, L.K., Ornato, J.P., Ou, N., Radford, M.J., Tamis-Holland, J.E., Tommaso, C.L., Tracy, C.M., Woo, Y.J., Zhao, D.X., Anderson, J.L., Jacobs, A.K., Halperin, J.L., Albert, N.M., Brindis, R.G., Creager, M.A., DeMets, D., Guyton, R.A., Hochman, J.S., Kovacs, R.J., Kushner, F.G., Ohman, E.M., Stevenson, W.G., Yancy, C.W. (2012) ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal American of College of Cardiology, 61(4) DOI: 10.1016/.2012.11.019. Porth, C.M. (2014). Essentials of Pathophysiology: Concepts of Altered Health States (4 Ed.) Philadelphia, PA: Lippincott Williams & Wilkins. th Brittany Heller CHF My first consideration would be heart failure considering all the symptoms this patient is presenting with. Heart failure: “Heart failure is a complex clinical syndrome that can result from any structural or functional cardiovascular disorder causing systematic perfusion inadequate to meet the body’s metabolic demands without excessively increasing left ventricular filling pressures” (Colucci, 2016, p. 1). Some of the classic symptoms of presentation of this disease are dyspnea and fatigue and signs that would be caused by fluid retention (Colucci, 2016, p. 1). The causes that are associated with this disorder are disease that affect the pericardium, myocardium, endocardium, cardiac valves, vasculature or metabolism (Colucci, 2016, p. 2). The patient is presenting with dyspnea on exertion, fatigue, and epigastric pain. All these signs could be associated with heart failure. Due to the increased fluid retention the patient would exhibit all the reported symptoms. Systolic dysfunction (systolic heart failure) is associated with a reduced ejection fraction, which is a left ventricular EF of less than or equal to 40% (Colucci, 2016, p. 2). The second portion of this disease is also characterized the inability to generate an adequate cardiac output to perfuse vital tissues (McCance & Huther, 2014, p. 1175). Cardiac output is determined by the stroke volume and heart rate (McCance & Huether, 2014, p. 1175). Stroke volume is affected by three factors: contractility, preload, and afterload. (McCance & Huther, 2014, p. 1175). The most common causes related to systolic heart failure are ischemic coronary atery disease, idiopathic dilated cardiomyopathy, hypertension, and valvular disease (Colucci, 2016, p. 2). Management of systolic dysfunction should include effective therapy for hypertension. All these disorders can affect the contractility of the heart. When the contractility of the heart decreases, stroke volume falls, and the left ventricular end-diastolic volume increases (McCance & Huether, 2014, p. 1175). Systolic congestive heart failure also has complex neurohumoral, inflammatory, and metabolic process. The first test I would consider is an EKG to see if there were any changes from the previous one. I would specifically look to see if there were any ischemic heart disease changes noted from the previous. The second test would be lab work specifically looking at a BNP and troponins. “BNP is a substance secreted from the ventricles or lower chambers of the heart in response to changes in pressure that occur when heart failure develops and worsens (Cleveland Clinic, 2016, p. 1). An echocardiogram is an ultrasound of the heart and is able to provide information about ventricular size and function (Colucci, 2016, p. 5). An echo would provide thean ejection fraction. Management and treatment for heart failure is geared towards increasing the contractility and reducing preload and afterload (McCance & Huehter, 2014, p. 1179). The first medication to consider is an ACE inhibitor. “ACE inhibitors reduce preload and afterload and have shown significantly reduce mortality in chronic left heart failure” (McCance & Huether, 2014, p. 1179). Cleveland Clinic. (2016). B-type Natriuetic Peptide (BNP) Blood Test. Retrieved at: Colucci, W. (2016) Determining etiology and severity of heart failure or cardiomyopathy. UpToD. Retrieved at: McCance, K. & Huether, S. (2014) Pathophysiology: The Biologic Basis for Disease in Adults and Children(7 ed). St. Lois: Elsevier. th Brittany Heller 5/19/2016 11:26:05 AM CHF My first consideration would be heart failure considering all the symptoms this patient is presenting with. Heart failure: “Heart failure is a complex clinical syndrome that can result from any structural or functional cardiovascular disorder causing systematic perfusion inadequate to meet the body’s metabolic demands without excessively increasing left ventricular filling pressures” (Colucci, 2016, p. 1). Some of the classic symptoms of presentation of this disease are dyspnea and fatigue and signs that would be caused by fluid retention (Colucci, 2016, p. 1). The causes that are associated with this disorder are disease that affect the pericardium, myocardium, endocardium, cardiac valves, vasculature or metabolism (Colucci, 2016, p. 2). The patient is presenting with dyspnea on exertion, fatigue, and epigastric pain. All these signs could be associated with heart failure. Due to the increased fluid retention the patient would exhibit all the reported symptoms. Systolic dysfunction (systolic heart failure) is associated with a reduced ejection fraction, which is a left ventricular EF of less than or equal to 40% (Colucci, 2016, p. 2). The second portion of this disease is also characterized the inability to generate an adequate cardiac output to perfuse vital tissues (McCance & Huther, 2014, p. 1175). Cardiac output is determined by the stroke volume and heart rate (McCance & Huether, 2014, p. 1175). Stroke volume is affected by three factors: contractility, preload, and afterload. (McCance & Huther, 2014, p. 1175). The most common causes related to systolic heart failure are ischemic coronary atery disease, idiopathic dilated cardiomyopathy, hypertension, and valvular disease (Colucci, 2016, p. 2). Management of systolic dysfunction should include effective therapy for hypertension. All these disorders can affect the contractility of the heart. When the contractility of the heart decreases, stroke volume falls, and the left ventricular end-diastolic volume increases (McCance & Huether, 2014, p. 1175). Systolic congestive heart failure also has complex neurohumoral, inflammatory, and metabolic process. The first test I would consider is an EKG to see if there were any changes from the previous one. I would specifically look to see if there were any ischemic heart disease changes noted from the previous. The second test would be lab work specifically looking at a BNP and troponins. “BNP is a substance secreted from the ventricles or lower chambers of the heart in response to changes in pressure that occur when heart failure develops and worsens (Cleveland Clinic, 2016, p. 1). An echocardiogram is an ultrasound of the heart and is able to provide information about ventricular size and function (Colucci, 2016, p. 5). An echo would provide thean ejection fraction. Management and treatment for heart failure is geared towards increasing the contractility and reducing preload and afterload (McCance & Huehter, 2014, p. 1179). The first medication to consider is an ACE inhibitor. “ACE inhibitors reduce preload and afterload and have shown significantly reduce mortality in chronic left heart failure” (McCance & Huether, 2014, p. 1179) Other treatments and medications to consider with patients that have heart failure are beta-blockers, salt restriction, loop diuretics, and aldosterone-blockers (McCance & Huether, 2014, p. 1179). My immediate treatment would be adding an ACE inhibitor such as Lisinopril. If the patient returned complaining of swelling in his ankles I would consider a low dose diuretic to decrease the amount of edema present. The patient may be having a worsening exacerbation of symptoms possibility due to blood pressure or an increased salt intake as well. Cleveland Clinic. (2016). B-type Natriuetic Peptide (BNP) Blood Test. Retrieved at: Colucci, W. (2016) Determining etiology and severity of heart failure or cardiomyopathy. UpToD. Retrieved at: McCance, K. & Huether, S. (2014) Pathophysiology: The Biologic Basis for Disease in Adults and Children(7 ed). St. Lois: Elsevier. th Brittany Heller reply to Brittany Heller 5/19/2016 11:26:57 AM RE: CHF sorry for posting this twice but when I tried to post it the first time and went back to look at it, half the paper looked like it didn't show up. Joleen Jimenez 5/19/2016 12:25:30 PM Part two Dr. Brown and class, In the case study presented a 57-year old male patient complains of dyspnea on exertion, fatigue, dyspepsia, nausea, epigastric pain, and orthopnea. He presents with hypertension but otherwise normal vital signs and no further assessment findings are noted. Based on this information provided, the writer would conclude this patient is suffering from heart failure. Heart failure is defined as an abnormality of cardiac structure or function that leads to failure to provide adequate oxygen systemically at a rate that is required for metabolizing tissues (McMurray, 2012). Diagnosis of this disease can be difficult because symptoms experienced by the patient can be vague and masking. Typically, the symptoms are a result of sodium and water retention. Heart failure is most commonly caused by myocardial disease resulting from systolic ventricular or diastolic dysfuntion, cardiac valves, pericardium, endocardium, heart rhythm, or electrical conduction failure (McMurray, 2012). Common symptoms include breathlessness, edema, fatigue, loss of appetite, depression, palpitations, reduced exercise intolerance, nocturnal cough, wheezing, weight gain greater than two pounds in a week, bloating, confusion, and orthopnea. Common signs include: elevated jugular venous pressure, pulmonary crackles, displaced apex beat, hepatojugular reflex, cardiac murmur, gallop rhythm, peripheral edema, pulmonary crepitus, t