{"id":"1953","type":{"id":"30","name":"Pathophysiologic Disorders","urlId":"pathophysiologic-disorder","subtypes":[],"schema":"http:\/\/schema.org\/Article","numTerms":0},"subtype":{"id":"22","name":"Cardiovascular Disorders","urlId":"cardiovascular-disorder"},"urlId":"hypertension","role":"term","course":{"id":"38","urlId":"pathology","name":"Clinical Pathology"},"children":[],"name":"Hypertension","demo":0,"description":"\u003E ### **Hypertension Definitions**\n\n## Overview:\n\nHypertension is characterized by sustained elevated [blood pressure](\/term\/physiology\/blood-pressure-profile).  \n\nHypertension is common worldwide, and, according to updated guidelines, approximately 46% of Americans 20 years and older have hypertension.\nMany of these individuals are unaware of their status, which is why hypertension is sometimes referred to as a \u0022silent killer.\u0022\n\nHypertension predisposes patients to **cardiovascular disease,** which is one of the most common causes of death in both men and women worldwide.\n\n**Review of blood pressure and its determinants:**\n[Review Cardiac Cycle](\/term\/physiology\/cardiac-cycle)\n\n**Systolic pressure** is the highest arterial pressure, reached after blood is ejected from the left ventricle.\n\u2013 120 mmHg\n\n**Diastolic blood pressure** is the lowest arterial pressure, reached during ventricular relaxation.\n- 80 mmHg\n\n**Mean arterial pressure** is determined by Cardiac Output and Total Peripheral Resistance. \n- 93 mmHg\n\n[Cardiac output](\/term\/physiology\/cardiac-output) refers to the amount of blood ejected by the left ventricle in in one minute\n\n[Total Peripheral Resistance](\/term\/physiology\/vascular-resistance) refers to the resistance of the systemic arteries to blood flow (total peripheral resistance is also referred to as systemic vascular resistance, SVR).\n\n**Hypertension** occurs when the cardiac output and\/or total peripheral resistance increases.\n\n**Classification of Hypertension:**\n2017 guidelines by the American College of Cardiologists and American Heart Association.\n\n**Healthy\/normotensive**: Systolic blood pressure less than 120 mmHg, and diastolic pressure less than 80 mmHg.  \n\n**Elevated**: Systolic blood pressures between 120 and 129 mmHg, and diastolic pressures less than 80 mmHg. \n\n**Stage 1 hypertension**: Systolic pressures between 130 and 139 mmHg, OR diastolic pressures between 80 and 89 mmHg.\n\n**Stage 2 hypertension**: Systolic pressures above 140 mmHg, OR diastolic pressures above 90 mmHg.\n\nThe higher value determines the stage of hypertension if the systolic and diastolic values fall in different categories. \n- For example, if a patient\u0027s systolic pressure is 135 mmHg and but diastolic pressure is 75 mmHg, it would be classified as Stage 1 hypertension. \n\nBlood pressure fluctuates throughout the day and in response to various situations, so multiple measurements need to be taken in and out of the health clinic, and during waking and sleeping.\n\nOne frustrating aspect of measuring blood pressure is that the presence of a health care professional can affect the blood pressure! This may be due to sympathetic activation in response to anxiety or other factors.\n**\u0022White coat hypertension\u0022** occurs when an untreated patient has high blood pressure in the presence of a medical professional, but is otherwise normotensive.\n\n\u0022**White coat *effect***\u0022 is the same phenomenon, but in patients who are under ***treatment*** for high blood pressure.\n\n**\u0022Masked hypertension\u0022** is when an untreated patient is normotensive in the presence of a medical professional but is hypertensive otherwise;\n\n**\u0022Masked *uncontrolled* hypertension\u0022** is the same phenomenon, except in patients who are being ***treated*** for hypertension. \n\t\n\u003E ### **Primary Hypertension**\n\nPrimary hypertension accounts for ***90-95%*** of all adult cases of hypertension.\n\nIn primary hypertension, there is no single identifiable cause.\n\nInstead, one or more of the following factors contribute to high blood pressure:\n**Genetic and epigenetic** factors can contribute to development of high blood pressure.\n\n**Obesity** contributes to hypertension via various direct and indirect mechanisms; for example, some propose that dysfunction in the sympathetic nervous system and kidneys contribute to high blood pressure in obese patients.  \n\n**Sedentary lifestyles** which are common in societies where we spend several hours per day at our desks.\n- Increasing physical activity confers multiple protective effects on the cardiovascular system. \n\n**Diet** is a significant predictor of hypertension\n- Particularly salt intake and salt sensitivity. Salt sensitivity refers to how efficiently individuals excrete salt and, therefore, avoid elevations in blood pressure. Exactly what determines salt sensitivity is uncertain, but African-Americans, the elderly, and post-menopausal women seem to be particularly susceptible to elevations in blood pressure due to lower rates of salt excretion.  \n\n- Inadequate intake of other nutrients, including calcium, potassium, vegetable proteins, and fiber may also contribute to hypertension.\n\n**Alcohol** as well as electronic and tobacco cigarettes are associated with hypertension due to their effects on the sympathetic nervous system and other regulators of blood pressure.\n\n**Chronic stress,** including psychosocial stress, also contributes to hypertension; this may be due to activation of the sympathetic nervous system and\/or other physiological reactions to stress.\n\n**Population differences**\nHypertension prevalence varies by population, and are likely due to differences in both genetic and environmental factors. \nThere are dramatic differences in the prevalence of hypertension in United States subpopulations, due to both genetic and environmental differences. \n- Hypertension prevalence is highest in non-Hispanic African Americans, American Indians, and Native Alaskans as compared to non-Hispanic Caucasian Americans and Hispanic Americans. \n\n**Age and sex**\nIn general, hypertension prevalence increases with age.\n**Premenopausal women** typically have lower blood pressures than do age-matched men or post-menopausal women.\n**Post-menopausal women*** have blood pressures equal to or higher than their age-matched male peers.\nTo illustrate this, we draw a simple graph that shows that, as men and women age, blood pressure increases; after menopause, women\u0027s blood pressure levels exceed that of men\u0027s. \n\nNote that some of these variables are modifiable, and many are interrelated.\n\n\u003E ### **Secondary Hypertension**\n\nSecondary hypertension accounts for 5-10% of adult hypertension. \n\nIn secondary hypertension, an underlying condition causes the elevation in blood pressure. \n\n## Causes include:\n\n**Renovascular hypertension** occurs when [renal artery stenosis](\/term\/pathology\/renal-vascular-diseases) prevents blood from reaching the kidneys; in response to low oxygen levels, the kidneys release hormones that increase blood pressure. \n- Notice that the adaptive physiological response to low oxygen levels is, in this case, contributing to pathology. \n- Two key causes of renal artery stenosis and renovascular hypertension are atherosclerosis and fibromuscular dysplasia.\n\n**Obstructive sleep apnea**\n\n**Primary aldosteronism](\/term\/physiology\/aldosterone-physiology-hyperaldosteronism)** is characterized by adrenal glands that release excess [aldosterone](\/term\/physiology\/gfr-regulation-extrinsic), which leads to increased sodium and fluid retention, and, therefore, increased blood volume and pressure. \n- Two key causes of primary [aldosteronism](\/term\/physiology\/aldosterone-physiology-hyperaldosteronism) and hypertension are aldosterone-producing adenomas and bilateral idiopathic hyperaldosteronism. \n\n**Renal parenchymal diseases** also lead to hypertension due to inadequate blood volume regulation by damaged renal tissue. \n\n**Drugs**\n- Examples: caffeine, NSAIDS, hormonal contraceptives (especially those with synthetic estrogen), decongestants, cocaine, amphetamines, and some herbal agents. \n\n**Pregnancy**:pregnant women can develop gestational hypertension, which can lead to [pre-eclampsia](\/term\/physiology\/pregnancy-terms-clinical-considerations) (aka, toxemia). \n- Hypertension is a significant cause of morbidity and mortality in both mothers and their neonates, and women who are hypertensive prior to pregnancy require special attention. \n\n**Additional Causes of Secondary Hypertension**\n- Pheochromocytoma\n- Coarctation of aorta (children)\n- [Cushing syndrome](\/term\/endocrine-system\/cortisol-physiology-cushing-s-syndrome)\n- [Hyperparathyroidism](\/term\/pathology\/parathyroid-hormone-calcium-disorders)\n","keywords":[],"images":[{"id":"4059","url":"term\/images\/hypertension-definitions-4059.png","title":"Hypertension definitions","demo":false},{"id":"4058","url":"term\/images\/hypertension-definitions-and-cutoffs-4058.png","title":"Hypertension definitions and cutoffs","demo":false},{"id":"4060","url":"term\/images\/primary-hypertension-etiologies-4060.png","title":"primary hypertension etiologies","demo":false},{"id":"4061","url":"term\/images\/secondary-hypertension-etiologies-4061.png","title":"secondary hypertension etiologies","demo":false}],"radiographs":[],"curricula":[{"id":"38","level":"graduate","category":"individual","urlId":"pathology","name":"Clinical Pathology","subjectGroups":[{"id":"463","name":"Cardiovascular Diseases","urlId":"cardiovascular-pathologies","subjects":[{"id":"2857","urlId":"hypertension","name":"Hypertension \u0026 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