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Hypertension by Mind Map: Hypertension

1. Treatment: Normal BP (Systolic <120mmHg, Diastolic <80mmHg): Prevention - Promote optimal lifestyle habits Elevated BP (SBP 120-129mmHg, DBP <80mmHg): Nonpharmacologic therapy; Drug therapy is not needed Hypertension Stage 1 (SBP 130-139mmHg, DBP 80-89mmHg): Presence of ASCVD or 10-year CVD risk >10%? Possible drug therapy Hypertension Stage 2 (SBP >140mmHg, DBP >90mmHg): BP Lowering drug therapy All Patients: Follow-up and on-going care with PCP, follow medication and lifestyle adherence when necessary

2. Diagnosis: The best way to diagnose hypertension is to take a series of blood pressure readings. They readings have to be high over a period of time and the patient’s health history needs to back up this diagnosis. The provider will take the blood pressure twice or more in one appointment and a second appointment to make sure it isn’t a false high. The patient may also take their blood pressure at home and keep track of reading. The patient can be diagnosed if they have a consistent systolic reading of over 140 mm Hg and a diastolic reading of over 90 mm Hg. A whole health history and physical exam must be performed as well. The patient might have big risk factors such as family history, eating habits, exercise habits, race, sex, and age. Other diagnostic tests may be performed to rule out other diseases that may be the cause of hypertension (High Blood Pressure, 2018).

3. Clinical Manifestations: Hypertension is known as the “silent killer” because it is an asymptomatic disorder. In advanced stages of this disease, central nervous system changes occur such as headache, fatigue, new onset blurred vision, weakness, confusion, vomiting, mental status changes and nausea. There are also clinical manifestations that are related to the long term effects of hypertension that affects target organs such as the heart, brain, eyes, kidneys and blood vessels. Heart complications include left ventricular hypertrophy, which is caused by the increased workload and increased pressure of the left ventricle. Other heart complications that may occur are angina, myocardial infarction, prior coronary revascularization, atherosclerosis and congestive heart failure. Brain related complications include stroke, transient ischemic attack and cerebral aneurysm. Kidney complications include chronic kidney failure and nephrosclerosis. Blood vessel complications include peripheral vascular disease. Eye complications include retinopathy, caused by arteriolar damage (Grossman & Porth, 2014, p. 776).

4. Pathogenesis: Hypertension depends on the interrelationship between cardiac output, peripheral vascular resistance, sympathetic overactivity, blood volume, blood viscosity, and arterial elasticity. An increase in heart rate, heart muscle contractility, or blood volume increases cardiac output. As cardiac output increases, a greater amount of blood is pumped against the arterial walls, raising blood pressure. Blood pressure depends on a balance between cardiac output and peripheral vascular resistance. The smooth muscle around the arteries and arterioles typically contract or relax to control and direct blood flow throughout the body. Vessel elasticity decreases with age and disorders such as atherosclerosis, and fibrous tissue replaces smooth muscle within the vessel walls. Hypertension is characterized by a thickening and loss of elasticity in the arterial walls. This increased peripheral vascular resistance forces the heart to pump against a greater resistance, reducing blood flow to organs throughout the body. Systemic pressure rises as blood forces though rigid arterial walls. When smooth muscle contraction is prolonged, the arteriolar vessel walls thicken, causing an irreversible rise in peripheral resistance. (Potter & Perry, 2009, p. 1230) This forces the heart to work harder to pump blood through the vessels, increasing blood pressure (Beevers et al., 2001). The renin-angiotensin system influences hypertension because when renin is secreted from the kidney in response to sympathetic stimulation, angiotensin 1 converts to angiotensin 2. Angiotensin 2 is a vasoconstrictor and stimulates aldosterone release which increases sodium and water retention, both consequences result in increased blood pressure. Increased blood volume forces blood pressure to rise. When blood viscosity increases, like when hematocrit levels rise, blood flow slows down; which forces the heart to contract more forcefully, resulting in hypertension (Beevers et al., 2001).

5. Etiology/Risk Factors: Hypertension is a condition caused by long-term increased pressure of blood against the walls of arteries. If the pressure is high enough that it can cause other health problems. There are factors that can put an individual at risk for developing hypertension. Age – Risk of hypertension increases with age due to the thickening and stiffening of blood vessels. Additionally, recently young kids and teenagers have been developing high blood pressure which has been linked to obesity and sedentary lifestyle. Family History/Genetics – Hypertension has been linked to genetics and also family history. There is a gene that is associated with small increase in risk of development. This gene can be passed down through different generations. Also, sensitivity to sodium, which increases risk, can run in the family. Certain DNA changes during fetal development can increase risk of development later in life. Unhealthy Lifestyle Habits – eating patterns, such as too much salt, can increase risk of high blood pressure. Additionally, too much alcohol and smoking could pose a threat. Being physically inactive puts individuals at risk. Race/Ethnicity– High blood pressure is more common in African Americans than in Caucasian, Hispanic, or Asian individuals. African Americans have a higher average blood pressure earlier in life. Sex – Before the age of 55, men are more at risk for hypertension. Women are more at risk after age 55 (High Blood Pressure, 2018).

6. By: Kristie Houlihan, Deanna Scopaz, Micah Bardell, Taylor Pastorok, Karen Lu, Enyoman Cudjoe