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Cardiovascular and Lymphatic Systems Unit 8

Cardiovascular and Lymphatic Systems Unit 8. Heather, Merissa and Tammy. Case Study 1. Mr. H has come to see you because his brother has just had a ‘heart attack’ and he wants to know if this is going to happen to him. Question.

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Cardiovascular and Lymphatic Systems Unit 8

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  1. Cardiovascular and Lymphatic SystemsUnit 8 Heather, Merissa and Tammy

  2. Case Study 1 Mr. H has come to see you because his brother has just had a ‘heart attack’ and he wants to know if this is going to happen to him

  3. Question Mr. H. says someone told him he could have atherosclerosis and could have a blood clot and die. He wants to know, first, if this is true and second, if true, what is atherosclerosis and what happens to the heart to make a person have a ‘heart attack’.

  4. Atherosclerosis • Occurs when the vessels of the heart thicken and harden as a result of accumulation of lipid-laden macrophages within the arterial wall which forms plague lesions (McCane & Huether, 2006) • It is the leading contributor to coronary artery and cerebrovascular disease (McCane & Huether, 2006) • Atherosclerosis is a form of arteriosclerosis, and is an inflammatory condition caused by the accumulation of lipid-laden macrophages in the arterial walls (McCane & Huether, 2006) • Atherosclerosis is a progressive disease process that can be described as follows: Low density lipoproteins (the bad cholesterol) enter the vessel and are oxidized into proinflammatory lipids. The oxidized LDL adheres to the vessel wall allowing monocytes and T lymphocytes to cross into the epithelium. Monocytes differentiate into macrophages that consume the LDL, transforming into foam cells. These foam cells then release cytokines that encourage atherosclerosis (McCance & Huether, 2006).

  5. Atherosclerosis Atherosclerosis is a process that occurs in several phases: • Damaged endothelium – Platelets attach to an injured site • Fatty Streak – Platelets attach to endothelium • Fibrous Plague – Lipids pool and form a fissure in plague • Complicated Lesion – A thrombus forms McCane & Huether, 2006

  6. Link to Animation of Atherosclerosis Below is a link to a video on atherosclerosis that discusses and demonstrates the phases of the disease http://www.youtube.com/watch?v=fLonh7ZesKs

  7. Answer Yes, Mr. H could have atherosclerosis. • He requires a detailed health history, physical examine and blood work to determine his risk factors for the disease. • Family history is a strong predictor of atherosclerosis and coronary artery disease (CAD). It would also be important to ask Mr. H about other risk factors for atherosclerosis including his age, the last time his lipids were checked and the results, whether or not he smokes, his level of physical activity, obesity, diet, and whether he was been screened for diabetes (McCance & Huether, 2006; National Heart, Lung, and Blood Institute, 2007; The Heart and Stroke Foundation of Canada, 2007).

  8. Pathophysiology of a “Heart Attack” • As a result of atherosclerosis many plagues that form in the arteries are ‘unstable’ and rupture • When these plaques rupture, platelet adhesion and thrombus formation results, causing complete vessel obstruction and cardiac ischemia and infarction (American Heart Association, 2009; McCance & Huether, 2006). • The thrombus may occlude the vessel resulting in ischemia and infarction (McCane & Huether, 2006)

  9. What happens to the Heart during a “Heart Attack” • During a ‘heart attack’ or MI (myocardial infarction) blood flow is occluded in the coronary arteries, causing hypoxia and ischemia (McCane & Huether, 2006) • Cardiac cells begin to die, and after 30-60 seconds of hypoxia ECG changes are noted (McCane & Huether, 2006) • The coronaryartery primarily affected in an MI describes the region of an MI in the heart. These include anterior, inferior, posterior or lateral (McCane & Huether, 2006) • These locations also determine the type of treatment required in an MI

  10. Mr. H. returns for a follow up visit after having the “tests” you advised. You review the results with him. The only abnormality to date is ECG evidence of left ventricular hypertrophy (LVH). You are not surprised, as last visit you checked Mr. H.’s blood pressure and it was 180/100. When you take his BP at this visit, it is the same. You tell him this and he shrugs and tells you it has been high for a while. About a year ago he was started on “BP med” but hadn’t felt unwell and felt no different when he was taking it so he stopped taking it.

  11. Hypertension • Hypertension is caused by any factors that increase cardiac output or total peripheral resistance, or a combination of the two (Breen, 2008; Mayoclinic.com, 2008; McCance & Huether, 2006) • Increased cardiac output is caused by increased heart rate and stroke volume whereas increased resistance is caused by increased blood viscosity or decreased blood vessel diameter • Primary (or essential) hypertension can be caused by genetic predisposition, specifically genetic factors influencing renal sodium excretion, insulin sensitivity, activity of the renin-angiotensin-aldosterone system, cell membrane sodium and calcium transport, and the systemic response to neurogenic hormones (Breen, 2006; McCance & Huether, 2006). • Secondary hypertension results from altered hemodynamics due to a primary disease, such as renal dysfunction or congenital heart defects (Mayoclinic.com, 2008; McCance & Huether, 2006).

  12. Causes of Hypertension There are several causes of hypertension, some modifiable and others that can not be changed. Causes include: • family history • Age (45 and over for men and 55 and over for women) • Ethnicity • Gender • smoking • being overweight • being physically inactive • excessive alcohol consumption • diet • Diabetes • High Cholesterol • Stress • Renal Disease • high sodium intake Ministry of Health, 2009

  13. Mr. H. You discuss with Mr. H. the damage to his heart. You want to impress upon him the other end organ damage that occurs with untreated hypertension.

  14. Clinical Signs and Symptoms of Untreated Hypertension • Hypertension is diagnosed when the systolic BP is greater than 140, or the diastolic BP is greater than 90 on with two different blood pressure readings on different occasions (McCance & Huether, 2006). • Sustained uncontrolled hypertension can lead to cardiac disease, renal insufficiency, transient ischemic attacks, strokes, and retinopathy, among others (Breen, 2008; McCance & Huether, 2006) • If symptoms of hypertension are present, they may include headaches, dizzy spells, and nose bleeds (Mayoclinic.com, 2008)

  15. Clinical Signs and Symptoms of Untreated Hypertension • Enlarged heart. High blood pressure puts extra demand on the heart. Over time, the heart grows bigger to compensate for the extra work and, ultimately,weakens. • Kidney damage. Over time, uncontrolled high blood pressure can cause narrowing of the arteries supplying the kidneys. High blood pressure also damages the kidneys directly and may lead to kidney failure. Kidney damage, in turn, raises blood pressure even more. • Stroke. High blood pressure can cause narrowing of the arteries that supply the brain. If a blood clot forms and block a vessel, the subsequent lack of oxygen to the brain can cause a stroke. High blood pressure can also cause arteries in the brain to burst. The resulting bleeding into the brain produces a different kind of stroke. • Heart attack. The coronary arteries carry blood that delivers oxygen to the heart. If these vessels become blocked, a heart attack can occur (National Institute of Health, 2003) • Hypertensive Retinopathy: In untreated hypertension, the small vessels in the eyes become damaged, causing thickening, bulging and leakage (Wikipedia.com, 2009).  Signs and symptoms would include headache and visual disturbances. • Hypertensive (valvular) cardiomyopathy:Occurs because of the continual increased resistance to ventricular ejection seen in HTN. Diastolic and Systolic dysfunction eventually occur (McCance & Huether, 2006).  Signs and symptoms would coincide with the severity of heart failure (and if left, right or both).

  16. References American Heart Association (2009). Atherosclerosis. Retrieved February 22, 2009 from http://www.americanheart.org/presenter.jhtml?identifier=4440 Breen, J. (2008). An introduction to causes, detection, and management of hypertension. Nursing Standard, 23 (14), 42-46. Retrieved February 22, 2009 from ProQuest Nursing & Allied Health Source database. Mayoclinic.com (2008). High blood pressure (Hypertension). Retrieved February 22, 2009 from http://www.mayoclinic.com/health/high-blood-pressure/DS00100/DSECTION=causes McCane, K. & Huether, S. (2006). Pathophysiology: The biologic basis for disease in adults and children. (5th ed.). St. Louis, MI: Elsevier Mosby. Ministry of Health. (2009). Chronic Disease Management. Retrieved February 21, 2009 from: http://www.health.gov.bc.ca/cdm/patients/hyperten/index.html#causes National Heart, Lung, and Blood Institute (2007). What is atherosclerosis? Retrieved February 22, 2009 from http://www.nhlbi.nih.gov/health/dci/Diseases/Atherosclerosis/Atherosclerosis_WhatIs.html

  17. References National Institute of Health. (2003). Complications of Untreated Hypertension. Retrieved February 22, 2009 from: http://www.healthatoz.com/healthatoz/Atoz/common/standard/transform.jsp?requestURI=/healthatoz/Atoz/dc/caz/card/hypr/hypercomp.jsp The Heart and Stroke Foundation of Canada (2007). Atherosclerosis. Retrieved February 22, 2009 from http://www.heartandstroke.com/site/c.ikIQLcMWJtE/b.3484059/k.9F8E/Atherosclerosis.htm The Heart and Stroke Foundation of Canada (2007). Heart disease prevention. Retrieved February 22, 2009 from http://www.heartandstroke.com/site/c.ikIQLcMWJtE/b.3483919/k.78DE/Prevention_of_Risk_Factors.htm Wikipedia.com. ( 2009). Hypertension. Retrieved February 22, 2009, from  http://en.wikipedia.org/wiki/Hypertensive_retinopathy

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