High blood pressure (BP), or hypertension, is defined by two levels by 2017 American College of Cardiology/American Heart Association (ACC/AHA) guidelines [1, 2] : (1) elevated BP, with a systolic pressure (SBP) between 120 and 129 mm Hg and diastolic pressure (DBP) less than 80 mm Hg, and (2) stage 1 hypertension, with an SBP of 130 to 139 mm Hg or a DBP of 80 to 89 mm Hg. Show
Hypertension is the most common primary diagnosis in the United States. [3] It affects approximately 86 million adults (≥20 years) in the United States [4] and is a major risk factor for stroke, myocardial infarction, vascular disease, and chronic kidney disease. See the image below.  View Media Gallery Signs and symptoms of hypertensionHypertension is defined as a systolic blood pressure (SBP) of 140 mm Hg or more, or a diastolic blood pressure (DBP) of 90 mm Hg or more, or taking antihypertensive medication. [5] Based on recommendations of the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), the classification of BP for adults aged 18 years or older has been as follows [5] :
The 2017 ACC/AHA guidelines eliminate the classification of prehypertension and divides it into two levels [1, 2] :
Hypertension may be primary, which may develop as a result of environmental or genetic causes, or secondary, which has multiple etiologies, including renal, vascular, and endocrine causes. Primary or essential hypertension accounts for 90-95% of adult cases, and secondary hypertension accounts for 2-10% of cases. See Presentation for more detail. Diagnosis of hypertensionThe evaluation of hypertension involves accurately measuring the patient’s blood pressure, performing a focused medical history and physical examination, and obtaining results of routine laboratory studies. [5, 6] A 12-lead electrocardiogram should also be obtained. These steps can help determine the following [5, 6, 7] :
Other studies may be obtained on the basis of clinical findings or in individuals with suspected secondary hypertension and/or evidence of target-organ disease, such as CBC, chest radiograph, uric acid, and urine microalbumin. [5] See Workup for more detail. Management of hypertensionMany guidelines exist for the management of hypertension. Most groups, including the JNC, the American Diabetes Associate (ADA), and the American Heart Association/American Stroke Association (AHA/ASA) recommend lifestyle modification as the first step in managing hypertension. Lifestyle modifications JNC 7 recommendations to lower BP and decrease cardiovascular disease risk include the following, with greater results achieved when 2 or more lifestyle modifications are combined [5] :
The AHA/ASA recommends a diet that is low in sodium, is high in potassium, and promotes the consumption of fruits, vegetables, and low-fat dairy products for reducing BP and lowering the risk of stroke. Other recommendations include increasing physical activity (30 minutes or more of moderate intensity activity on a daily basis) and losing weight (for overweight and obese persons). The 2018 European Society of Cardiology (ESC) and the European Society of Hypertension (ESH) guidelines recommend a low-sodium diet (limited to 2 g per day) as well as reducing body-mass index (BMI) to 20-25 kg/m2 and waist circumference (to < 94 cm in men and < 80 cm in women). [9] Pharmacologic therapy If lifestyle modifications are insufficient to achieve the goal BP, there are several drug options for treating and managing hypertension. Thiazide diuretics, an angiotensin-converting enzyme inhibitor (ACEI) /angiotensin receptor blocker (ARB), or calcium channel blocker (CCB) are the preferred agents in nonblack populations, whereas CCBs or thiazide diuretics are favored in black hypertensive populations. [10] These recommendations do not exclude the use of ACE inhibitors or ARBs in treatment of black patients, or CCBs or diuretics in non-black persons. Often, patients require several antihypertensive agents to achieve adequate BP control. Compelling indications for specific agents include comorbidities such as heart failure, ischemic heart disease, chronic kidney disease, and diabetes. Drug intolerability or contraindications may also be factors. [5] The following are drug class recommendations for compelling indications based on various clinical trials [5] :
See Treatment and Medication for more detail. Next: BackgroundHigh blood pressure, or hypertension, is the most common primary diagnosis in the United States, [3] and it is one of the most common worldwide diseases afflicting humans and is a major risk factor for stroke, myocardial infarction, vascular disease, and chronic kidney disease. Despite extensive research over the past several decades, the etiology of most cases of adult hypertension is still unknown, and control of blood pressure is suboptimal in the general population. Due to the associated morbidity and mortality and cost to society, preventing and treating hypertension is an important public health challenge. Fortunately, recent advances and trials in hypertension research are leading to an increased understanding of the pathophysiology of hypertension and the promise for novel pharmacologic and interventional treatments for this widespread disease. According to the American Heart Association (AHA), approximately 86 million adults (34%) in the United States are affected by hypertension, which is defined as a systolic blood pressure (SBP) of 140 mm Hg or more or a diastolic blood pressure (DBP) of 90 mm Hg or more, taking antihypertensive medication, or having been told by clinicians on at least 2 occasions as having hypertension. [4] Substantial improvements have been made with regard to enhancing awareness and treatment of hypertension. However, a National Health Examination Survey (NHANES) spanning 2011-2014 revealed that 34% of US adults aged 20 years and older are hypertensive and NHANES 2013-2014 data showed that 15.9% of these hypertensive adults are unaware they are hypertensive; these data have increased from NHANES 2005-2006 data that showed 29% of US adults aged 18 years and older were hypertensive and that 7% of these hypertensive adults had never been told that they had hypertension. [4] Furthermore, of those with high blood pressure (BP), 78% were aware they were hypertensive, 68% were being treated with antihypertensive agents, and only 64% of treated individuals had controlled hypertension. [4] In addition, previous data from NHANES estimated that 52.6% (NHANES 2009-2010) to 55.8% (NHANES 1999-2000) of adults aged 20 years and older have prehypertension, defined as an untreated SBP of 120-139 mm Hg or untreated DBP of 80-89 mmHg. [4] (See Epidemiology.) Data from the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), which was released in 2003, were relatively similar to the NHANES data. The JNC 7 noted that approximately 30% of adults were unaware of their hypertension; up to 40% of people with hypertension were not receiving treatment; and, of those treated, up to 67% did not have their BP controlled to less than 140/90 mm Hg. [5] Hypertension is the most important modifiable risk factor for coronary heart disease (the leading cause of death in North America), stroke (the third leading cause), congestive heart failure, end-stage renal disease, and peripheral vascular disease. Therefore, health care professionals must not only identify and treat patients with hypertension but also promote a healthy lifestyle and preventive strategies to decrease the prevalence of hypertension in the general population. (See Treatment.) Definition and classificationDefining abnormally high blood pressure (BP) is extremely difficult and arbitrary. Furthermore, the relationship between systemic arterial pressure and morbidity appears to be quantitative rather than qualitative. A level for high BP must be agreed upon in clinical practice for screening patients with hypertension and for instituting diagnostic evaluation and initiating therapy. Because the risk to an individual patient may correlate with the severity of hypertension, a classification system is essential for making decisions about aggressiveness of treatment or therapeutic interventions. (See Presentation.) Based on recommendations of the JNC 7, the classification of BP (expressed in mm Hg) for adults aged 18 years or older is as follows [5] :
The classification above is based on the average of 2 or more readings taken at each of 2 or more visits after initial screening. [5, 7] Normal BP with respect to cardiovascular risk is less than 120/80 mm Hg. However, unusually low readings should be evaluated for clinical significance. Prehypertension, a new category designated in the JNC 7 report, emphasizes that patients with prehypertension are at risk for progression to hypertension and that lifestyle modifications are important preventive strategies. However, the 2017 ACC/AHA guidelines eliminate the classification of prehypertension and divides it into two levels [1, 2] : (1) elevated BP, with a systolic pressure (SBP) between 120 and 129 mm Hg and diastolic pressure (DBP) less than 80 mm Hg, and (2) stage 1 hypertension, with an SBP of 130 to 139 mm Hg or a DBP of 80 to 89 mm Hg. From another perspective, hypertension may be categorized as either essential or secondary. Primary (essential) hypertension is diagnosed in the absence of an identifiable secondary cause. Approximately 90-95% of adults with hypertension have primary hypertension, whereas secondary hypertension accounts for around 5-10% of the cases. [11] However, secondary forms of hypertension, such as primary hyperaldosteronism, account for 20% of resistant hypertension (hypertension in which BP is >140/90 mm Hg despite the use of medications from 3 or more drug classes, 1 of which is a thiazide diuretic). Especially severe cases of hypertension, or hypertensive crises, are defined as a BP of more than 180/120 mm Hg and may be further categorized as hypertensive emergencies or urgencies. Hypertensive emergencies are characterized by evidence of impending or progressive target organ dysfunction, whereas hypertensive urgencies are those situations without progressive target organ dysfunction. [5] In hypertensive emergencies, the BP should be aggressively lowered within minutes to an hour by no more than 25%, and then lowered to 160/100-110 mm Hg within the next 2-6 hours. [5] Acute end-organ damage in the setting of a hypertensive emergency may include the following [12] :
With the advent of antihypertensives, the incidence of hypertensive emergencies has declined from 7% to approximately 1%. [13] In addition, the 1-year survival rate associated with this condition has increased from only 20% (prior to 1950) to more than 90% with appropriate medical treatment. [14] (See Medication.) Previous Next: PathophysiologyThe pathogenesis of essential hypertension is multifactorial and complex. [15] Multiple factors modulate the blood pressure (BP) including humoral mediators, vascular reactivity, circulating blood volume, vascular caliber, blood viscosity, cardiac output, blood vessel elasticity, and neural stimulation. A possible pathogenesis of essential hypertension has been proposed in which multiple factors, including genetic predisposition, excess dietary salt intake, and adrenergic tone, may interact to produce hypertension. Although genetics appears to contribute, the exact mechanisms underlying essential hypertension have not been established. Investigations into the pathophysiology of hypertension, both in animals and humans, have revealed that hypertension may have an immunological basis. Studies have revealed that hypertension is associated with renal infiltration of immune cells and that pharmacologic immunosuppression (such as with the drug mycophenolate mofetil) or pathologic immunosuppression (such as occurs with HIV) results in reduced blood pressure in animals and humans. Evidence suggests that T lymphocytes and T-cell derived cytokines (eg, interleukin 17, tumor necrosis factor alpha) play an important role in hypertension. [16, 17] One hypothesis is that prehypertension results in oxidation of lipids such as arachidonic acid that leads to the formation of isoketals or isolevuglandins, which function as neoantigens, which are then presented to T cells, leading to T-cell activation and infiltration of critical organs (eg, kidney, vasculature). [18] This results in persistent or severe hypertension and end organ damage. Sympathetic nervous system activation and noradrenergic stimuli have also been shown to promote T-lymphocyte activation and infiltration and contribute to the pathophysiology of hypertension. [19, 20, 21] The natural history of essential hypertension evolves from occasional to established hypertension. After a long invariable asymptomatic period, persistent hypertension develops into complicated hypertension, in which end-organ damage to the aorta and small arteries, heart, kidneys, retina, and central nervous system is evident. The progression of essential hypertension is as follows:
As evident from the above, younger individuals may present with hypertension associated with an elevated cardiac output (high-output hypertension). High-output hypertension results from volume and sodium retention by the kidney, leading to increased stroke volume and, often, with cardiac stimulation by adrenergic hyperactivity. Systemic vascular resistance is generally not increased at such earlier stages of hypertension. As hypertension is sustained, however, vascular adaptations including remodeling, vasoconstriction, and vascular rarefaction occur, leading to increased systemic vascular resistance. In this situation, cardiac output is generally normal or slightly reduced, and circulating blood volume is normal. Cortisol reactivity, an index of hypothalamic-pituitary-adrenal function, may be another mechanism by which psychosocial stress is associated with future hypertension. [22] In a prospective sub-study of the Whitehall II cohort, with 3 years follow-up of an occupational cohort in previously healthy patients, investigators reported 15.9% of the patient sample developed hypertension in response to laboratory-induced mental stressors and found an association between cortisol stress reactivity and incident hypertension. [22] Previous Next: EtiologyHypertension may be primary, which may develop as a result of environmental or genetic causes, or secondary, which has multiple etiologies, including renal, vascular, and endocrine causes. Primary or essential hypertension accounts for 90-95% of adult cases, and a small percentage of patients (2-10%) have a secondary cause. Hypertensive emergencies are most often precipitated by inadequate medication or poor compliance. Environmental and genetic/epigenetic causesHypertension develops secondary to environmental factors, as well as multiple genes, whose inheritance appears to be complex. [14, 23] Furthermore, obesity, diabetes, and heart disease also have genetic components and contribute to hypertension. Epidemiologic studies using twin data and data from Framingham Heart Study families reveal that BP has a substantial heritable component, ranging from 33-57%. [24, 25, 26] In an attempt to elucidate the genetic components of hypertension, multiple genome wide association studies (GWAS) have been conducted, revealing multiple gene loci in known pathways of hypertension as well as some novel genes with no known link to hypertension as of yet. [27] Further research into these novel genes, some of which are immune-related, will likely increase the understanding of hypertension's pathophysiology, allowing for increased risk stratification and individualized treatment. Epigenetic phenomena, such as DNA methylation and histone modification, have also been implicated in the pathogenesis of hypertension. For example, a high-salt diet appears to unmask nephron development caused by methylation. Maternal water deprivation and protein restriction during pregnancy increase renin-angiotensin expression in the fetus. Mental stress induces a DNA methylase, which enhances autonomic responsiveness. The pattern of serine protease inhibitor gene methylation predicts preeclampsia in pregnant women. [28] Despite these genetic findings, targeted genetic therapy seems to have little impact on hypertension. In the general population, not only does it appear that individual and joint genetic mutations have very small effects on BP levels, but it has not been shown that any of these genetic abnormalities are responsible for any applicable percentage of cases of hypertension in the general population. [29] Secondary causes of hypertension related to single genes are very rare. They include Liddle syndrome, glucocorticoid-remediable hyperaldosteronism, 11 beta-hydroxylase and 17 alpha-hydroxylase deficiencies, the syndrome of apparent mineralocorticoid excess, and pseudohypoaldosteronism type II. [5] Causes of secondary hypertensionRenal causes (2.5-6%) of hypertension include the renal parenchymal diseases and renal vascular diseases, as follows:
Renovascular hypertension (RVHT) causes 0.2-4% of cases. Since the seminal experiment in 1934 by Goldblatt et al, [30] RVHT has become increasingly recognized as an important cause of clinically atypical hypertension and chronic kidney disease—the latter by virtue of renal ischemia. The coexistence of renal arterial vascular (ie, renovascular) disease and hypertension roughly defines this type of nonessential hypertension. More specific diagnoses are made retrospectively when hypertension is improved after intravascular intervention. Vascular causes include the following:
Endocrine causes account for 1-2% and include exogenous or endogenous hormonal imbalances. Exogenous causes include administration of steroids. The most common form of secondary hypertension is a renal cause (although the true prevalence of hyperaldosteronism is not clear). Another common endocrine cause is oral contraceptive use. Activation of the renin-angiotensin-aldosterone system (RAAS) is the likely mechanism, because hepatic synthesis of angiotensinogen is induced by the estrogen component of oral contraceptives. Approximately 5% of women taking oral contraceptives may develop hypertension, which abates within 6 months after discontinuation. The risk factors for oral contraceptive–associated hypertension include mild renal disease, familial history of essential hypertension, age older than 35 years, and obesity. It would be better to group oral contraceptives and steroids with drug-induced hypertension. Exogenous administration of the other steroids used for therapeutic purposes also increases blood pressure (BP), especially in susceptible individuals, mainly by volume expansion. Nonsteroidal anti-inflammatory drugs (NSAIDs) may also have adverse effects on BP. NSAIDs block both cyclooxygenase-1 (COX-1) and COX-2 enzymes. The inhibition of COX-2 can inhibit its natriuretic effect, which, in turn, increases sodium retention. NSAIDs also inhibit the vasodilating effects of prostaglandins and the production of vasoconstricting factors—namely, endothelin-1. These effects can contribute to the induction of hypertension in a normotensive or controlled hypertensive patient. Endogenous hormonal causes include the following:
Neurogenic causes include the following:
Drugs and toxins that cause hypertension include the following:
Other causes include the following:
Obstructive sleep apnea (OSA) is a common but frequently undiagnosed sleep-related breathing disorder defined as an average of at least 10 apneic and hypopenic episodes per sleep hour, which leads to excessive daytime sleepiness. Multiple studies have shown OSA to be an independent risk factor for the development of essential hypertension, even after adjusting for age, gender, and degree of obesity. Approximately half of individuals with hypertension have OSA, and approximately half with OSA have hypertension. Ambulatory BP monitoring normally reveals a "dip" in BP of at least 10% during sleep. However, if a patient is a "nondipper," the chances that the patient has OSA is increased. Nondipping is thought to be caused by frequent apneic/hypopneic episodes that end with arousals associated with marked spikes in BP that last for several seconds. Apneic episodes are associated with striking increases in sympathetic nerve activity and enormous elevations of BP. Individuals with sleep apnea have increased cardiovascular mortality, in part likely related to the high incidence of hypertension. Although treatment of sleep apnea with continuous airway positive pressure (CPAP) would logically seem to improve CV outcomes and hypertension, studies evaluating this mode of therapy have been disappointing. A 2016 review of several studies indicated that CPAP either had no effect or a modest BP-lowering effect. [31] Findings from the SAVE study showed no effect of CPAP therapy on BP above usual care. [32] It is likely that patients with sleep apnea have other etiologies of hypertension, including obesity, hyperaldosteronism, increased sympathetic drive, and activation of the renin/angiotensin system that contribute to their hypertension. Although CPAP remains an effective therapy for other aspects of sleep apnea, it should not be expected to normalize BP in the majority of patients. Causes of hypertensive emergenciesThe most common hypertensive emergency is a rapid unexplained rise in BP in patients with chronic essential hypertension. Most patients who develop hypertensive emergencies have a history of inadequate hypertensive treatment or an abrupt discontinuation of their medications. [33, 34] Other causes of hypertensive emergencies include the use of recreational drugs, abrupt clonidine withdrawal, post pheochromocytoma removal, and systemic sclerosis, as well as the following:
Previous Next: EpidemiologyHypertension is a worldwide epidemic; accordingly, its epidemiology has been well studied. Data from National Health and Nutrition Examination Survey (NHANES) spanning 2011-2014 in the United States found that in the population aged 20 years or older, an estimated 86 million adults had hypertension, with a prevalence of 34%. [4] 2017 Data from the Centers for Disease Control and Prevention's (CDC) National Center for Health Statistics (NCHS) spanning 2015-2016 show a hypertension prevalence of 29.0% among those aged 18 and older (see the following image). [36] The following image shows prevalence of hypertension among adults aged 18 and over, by sex and age: United States, 2015–2016.
View Media Gallery There was an increasing trend of hypertension in adults between 1999-2000 and 2009-2010, and 2013-2014, with mild falls in 2011-2012 and 2015-2016 (see the image below). [36] The image below shows the age-adjusted trends in hypertension and controlled hypertension among adults aged 18 and over: United States, 1999–2016. View Media Gallery Overall, hypertension affects US men and women nearly equally, affecting an estimated 40.8 million men and 44.9 million women. [4] Globally, an estimated 26% of the world’s population (972 million people) has hypertension, and the prevalence is expected to increase to 29% by 2025, driven largely by increases in economically developing nations. [37] The high prevalence of hypertension exacts a tremendous public health burden. As a primary contributor to heart disease and stroke, the first and third leading causes of death worldwide, respectively, high blood pressure was the top modifiable risk factor for disability adjusted life-years lost worldwide in 2013. [38, 39] Between 2006 and 2011, there was a 25% increase in the number of people visiting US emergency rooms for essential hypertension, according to an analysis of data from the Nationwide Emergency Department Sample in 2014. [40] The reason for the increase, however, remained uncertain. The rate of emergency department visits also increased significantly, according to the study, rising from 190.1 visits per 100,000 population in 2006 to 238.5 visits per 100,000 population in 2011. Over the same period, however, admission rates decreased, from 10.47% in 2006 to 8.85% in 2011. [40] Emergency department visits for hypertension with complications and secondary hypertension also rose, from 71.2 per 100,000 population in 2006 to 84.7 per 100,000 population in 2011, while again, admission rates fell, dropping from 77.79% in 2006 to 68.75% in 2011. The in-hospital mortality rate for admitted patients dropped as well, from 1.95% in 2006 to 1.25% in 2011. [40] Hypertension and sex- and age-related statisticsUntil age 45 years, a higher percentage of men than women have hypertension; from age 45 to 64 years, the percentages are nearly equal between men and women. Beyond age 64 years, a higher percentage of women have hypertension than men. [41] (See the image below.) View Media Gallery Hypertension in black adultsGlobally, black adults have among the highest rates of hypertension, with an increasing prevalence. Although white adults also have an increasing incidence of high BP, they develop this condition later in life than black adults and have much lower average BPs. In fact, compared to hypertensive white persons, hypertensive black individuals have a 1.3-fold higher rate of nonfatal stroke, a 1.8-fold higher rate of fatal stroke, a 1.5-fold higher mortality rate due to heart disease, and a 4.2-fold higher rate of end-stage renal disease (ESRD). [41] Table 2, below, summarizes age-adjusted prevalence estimates from the National Health Interview Survey (NHIS) and the NCHS according to racial/ethnic groups and diagnosed conditions in individuals 18 years of age and older. Table 2. NHIS/NCHS Age-Adjusted Prevalence Estimates in Individuals Aged 18 Years and Older in 2015. (Open Table in a new window) Race/Ethnic Group Have Hypertension, % Have Heart Disease, % Have Coronary Heart Disease, % Have Had a Stroke, % White only 23.8 11.3 5.6 2.4 Black/African American 34.4 9.5 5.4 3.7 Hispanic/Latino 23.0 8.2 5.1 2.4 Asian 20.6 7.1 3.7 1.4 American Indian/Alaska Native 28.4 13.7 9.3 2.2 (this number is considered unreliable) Source: Summary health statistics: National Health Interview Survey, 2015. Available at: https://ftp.cdc.gov/pub/Health_Statistics/NCHS/NHIS/SHS/2015_SHS_Table_A-1.pdf. Accessed: November 14, 2016.
NCHS = National Center for Health Statistics; NHIS = National Health Interview Survey. Previous Next: PrognosisMost individuals diagnosed with hypertension will have increasing blood pressure (BP) as they age. Untreated hypertension is notorious for increasing the risk of mortality and is often described as a silent killer. Mild to moderate hypertension, if left untreated, may be associated with a risk of atherosclerotic disease in 30% of people and organ damage in 50% of people within 8-10 years after onset. Patients with resistant hypertension are also at higher risk for poor outcomes, particularly those with certain comorbidities (eg, chronic kidney disease, ischemic heart disease). [42] Patients with resistant hypertension who have lower BP appear to have a reduced risk for some cardiovascular events (eg, incident stroke, coronary heart disease, or heart failure). [42] Death from ischemic heart disease or stroke increases progressively as BP increases. For every 20 mm Hg systolic or 10 mm Hg diastolic increase in BP above 115/75 mm Hg, the mortality rate for both ischemic heart disease and stroke doubles. [5] Hypertensive retinopathy was associated with an increased long-term risk of stroke, even in patients with well-controlled BP, in a report of 2907 adults with hypertension participating in the Atherosclerosis Risk in Communities (ARIC) study. [43, 44] Increasing severity of hypertensive retinopathy was associated with an increased risk of stroke; the stroke risk was 1.35 in the mild retinopathy group and 2.37 in the moderate/severe group. In a meta-analysis of pooled data from 19 prospective cohort studies involving 762,393 patients, Huang et al reported that, after adjustment for multiple cardiovascular risk factors, prehypertension was associated with a 66% increased risk for stroke, compared with an optimal blood pressure (< 120/80 mm Hg). [45, 46] Patients in the high range of prehypertension (130-139/85-89 mm Hg) had a 95% increased risk of stroke, compared with a 44% increased risk for those in the low range of prehypertension (120-129/80-84 mm Hg). [45, 46] The morbidity and mortality of hypertensive emergencies depend on the extent of end-organ dysfunction on presentation and the degree to which BP is controlled subsequently. With BP control and medication compliance, the 10-year survival rate of patients with hypertensive crises approaches 70%. [47] In the Framingham Heart Study, the age-adjusted risk of congestive heart failure was 2.3 times higher in men and 3 times higher in women when the highest BP was compared to the lowest BP. [48] Multiple Risk Factor Intervention Trial (MRFIT) data showed that the relative risk for coronary artery disease mortality was 2.3 to 6.9 times higher for persons with mild to severe hypertension than it was for persons with normal BP. [49] The relative risk for stroke ranged from 3.6 to 19.2. The population-attributable risk percentage for coronary artery disease varied from 2.3 to 25.6%, whereas the population-attributable risk for stroke ranged from 6.8-40%. The Framingham Heart Study found a 72% increase in the risk of all-cause death and a 57% increase in the risk of any cardiovascular event in patients with hypertension who were also diagnosed with diabetes mellitus. [50] Nephrosclerosis is one of the possible complications of long-standing hypertension. The risk of hypertension-induced end-stage renal disease is higher in black patients, even when blood pressure is under good control. Furthermore, patients with diabetic nephropathy who are hypertensive are also at high risk for developing end-stage renal disease. Comparative data from the NHANES I and III showed a decrease in mortality over time in hypertensive adults, but the mortality gap between hypertensive and normotensive adults remained high. [51] Clinical trials have demonstrated the following benefits with antihypertensive therapy [5] :
Moreover, it is estimated that 1 death is prevented per 11 patients treated for stage 1 hypertension and other cardiovascular risk factors when a sustained reduction of 12 mm Hg in systolic BP over 10 years is achieved. [5] However, for the same reduction is systolic BP reduction, it is estimated that 1 death is prevented per 9 patients treated when cardiovascular disease or end-organ damage is present. [5] Previous Next: Patient EducationHypertension is a lifelong disorder. For optimal control, a long-term commitment to lifestyle modifications and pharmacologic therapy is required. Therefore, repeated in-depth patient education and counseling not only improve compliance with medical therapy but also reduce cardiovascular risk factors. Various strategies to decrease cardiovascular disease risk include the following:
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References
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Table 2. NHIS/NCHS Age-Adjusted Prevalence Estimates in Individuals Aged 18 Years and Older in 2015. Race/Ethnic Group Have Hypertension, % Have Heart Disease, % Have Coronary Heart Disease, % Have Had a Stroke, % White only 23.8 11.3 5.6 2.4 Black/African American 34.4 9.5 5.4 3.7 Hispanic/Latino 23.0 8.2 5.1 2.4 Asian 20.6 7.1 3.7 1.4 American Indian/Alaska Native 28.4 13.7 9.3 2.2 (this number is considered unreliable) Source: Summary health statistics: National Health Interview Survey, 2015. Available at: https://ftp.cdc.gov/pub/Health_Statistics/NCHS/NHIS/SHS/2015_SHS_Table_A-1.pdf. Accessed: November 14, 2016.
NCHS = National Center for Health Statistics; NHIS = National Health Interview Survey. Table 2. Identifiable Hypertension and Screening Tests Condition Screening Test Chronic kidney disease Estimated glomerular filtration rate Coarctation of the aorta Computed tomography angiography Cushing syndrome; other states of glucocorticoid excess (eg, chronic steroid therapy Dexamethasone suppression test Drug-induced/drug-related hypertension* Drug screening Pheochromocytoma 24-hour urinary metanephrine and normetanephrine Primary aldosteronism, other states of mineralocorticoid excess Plasma aldosterone to renin activity ratio (ARR). If abnormal, refer for further evaluation such as saline infusion to determine if aldosterone levels can be suppressed, 24-hour urinary aldosterone level, and specific mineralocorticoid tests Renovascular hypertension Doppler flow ultrasonography, magnetic resonance angiography, computed tomography angiography Sleep apnea Sleep study with oxygen saturation (screening would also include the Epworth Sleepiness Scale [ESS]) Thyroid/parathyroid disease Thyroid stimulating hormone level, serum parathyroid hormone level Adapted from: Chobanian AV, Bakris GL, Black HR, et al, and the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program Coordinating Committee. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. Dec 2003;42(6):1206-52. [5] * Some examples of agents that induce hypertension include nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 (COX-2) inhibitors; illicit drugs; sympathomimetic agents; oral contraceptive or adrenal steroid hormones; cyclosporine and tacrolimus; licorice; erythropoietin; and certain over-the-counter dietary supplements and medicines, such as ephedra, ma huang, and bitter orange. Drug-related causes of hypertension may be due to nonadherence, inadequate doses, and inappropriate combinations. Table 3. Hypertensive Disorders in Pregnancy Classification Characteristics Chronic hypertension Prepregnancy or before 20 weeks’ gestation; SBP =140 mm Hg or DBP 90 mm Hg that persists >12 weeks postpartum Preeclampsia After 20 weeks’ gestation; SBP =140 mm Hg or DBP 90 mm Hg with proteinuria (>300 mg/24 h) Can progress to eclampsia More common in nulliparous women, multiple gestation, women with hypertension =4 years, family history of preeclampsia, previous hypertension in pregnancy, and renal disease Chronic hypertension with superimposed preeclampsia New-onset proteinuria after 20 weeks in hypertensive woman In a woman with hypertension and proteinuria before 20 weeks’ gestation Sudden 2- to 3-fold increase in proteinuria Sudden increase in BP Thrombocytopenia Elevated AST or ALT levels Gestational hypertension Temporary diagnosis Hypertension without proteinuria after 20 weeks’ gestation May be a preproteinuric phase of preeclampsia or a recurrence of chronic hypertension that abated in mid-pregnancy May lead to preeclampsia Severe cases may cause higher rates of premature delivery and growth retardation relative to mild preeclampsia Transient hypertension Diagnosis made retrospectively BP returns to normal by 12 weeks’ postpartum May recur in subsequent pregnancies Predictive of future primary hypertension ALT = alanine aminotransferase; AST = aspartate aminotransferase; BP = blood pressure; DBP = diastolic BP; SBP = systolic BP. Adapted from: Chobanian AV, Bakris GL, Black HR, et al, and the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program Coordinating Committee. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. Dec 2003;42(6):1206-52. [5] Table 4. Guidelines for Blood Pressure Screening in Adults Issuing Organization Year Screening Populations Screening Measurement Screening Interval European Society of Cardiology/ European Society of Hypertension (ESC/ESH) [9] 2018 All adults Office measurement At regular intervals on the basis of the blood pressure level:
US Preventive Services Task Force (USPSTF) [127] 2015 Adults ≥18 years without known hypertension Measurements outside of the clinical setting should be obtained for diagnostic confirmation before starting treatment. No evidence was found for a single gold standard protocol for HBPM or ABPM. However, both may be used in conjunction with proper office measurement to make a diagnosis and guide management and treatment options. Annually for adults age ≥40 and those at increased risk for high blood pressure including those who have high-normal blood pressure (130–139/85–89 mm Hg), are overweight or obese, or are African American. Adults ages ≥18 to < 40 years with normal blood pressure (≤130/85mm Hg) with no known risk factors should be screened every 3-5 years Seventh Report of the Prevention, Detection, Evaluation, and Treatment of the Joint National Committee on High Blood Pressure (JNC 7) [5] 2003 Adults ages ≥18 years Diagnosis based on average of 2 or more seated blood pressure readings on each of two or more office visits At least once every 2 years in adults with blood pressure less than 120/80 mm Hg and every year in those with levels of 120–139/80–89 mm Hg. American College of Obstetricians and Gynecologists (ACOG) [128] 2013 All females ages ≥13 years Office measurement Annually as part of routine well-woman care Department of Veterans Affairs/Department of Defense (VA/DoD) [129] 2014 All adults Office measurement; Diagnosis based on 2 readings at 2 separate visits; For patients where diagnosis remains uncertain, home blood pressure monitoring (2-3 times a day for 7 days) or 24 hour ambulatory monitoring to confirm diagnosis Periodic, preferably annually, at time of routine preventative care or health assessment; European Society of Hypertension /European Society of Cardiology (ESH/ESC) [126] 2013 All adults Office measurement; Diagnosis based on at least 2 readings at 2 separate visits; Consider home blood pressure monitoring or 24 hour ambulatory monitoring to confirm diagnosis At time of routine preventative care or health assessment Table 5. Target Blood Pressure Recommendations Issuing Organization Year Population Target Blood Pressure Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) [5] 2003 All adults except those with diabetes or chronic kidney disease Adults with diabetes or chronic kidney disease < 140/90 mm Hg
< 130/80 mm Hg Eighth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 8) [88] 2014 Adults age < 60 years and those >18 with diabetes or chronic kidney disease
Adults age ≥60 years < 140/90 mm Hg
< 150/90 mm Hg European Society of Hypertension/European Society of Cardiology (ESH/ECS) [126] 2013 All adults except those with diabetes
Adults with diabetes 140-150 mm Hg systolic; consider < 140 mm Hg if the patient is fit and healthy; for ages ≥80 years, the patient's mental capacity and physical heath should also be considered if targeting to < 140 mm Hg
< 85 mm Hg diastolic BP American Heart Association/American College of Cardiology/American Society of Hypertension (AHA/ACC/ASH) [130] 2015 Adults ages >80 years
Adults with CAD, except as noted below
Adults with MI, stroke, TIA, carotid artery disease, peripheral artery disease or abdominal aortic aneurysm
< 150/90 mm Hg
< 140/90 mm Hg
< 130/80 mm Hg
American Heart Association/American College of Cardiology (ACC)/Centers for Disease Control and Prevention (AHA/ACC/CDC) [131] 2014 All adults < 140/90 mm Hg American College of Cardiology/American Heart Association (ACC/AHA) [1] 2017 All adults < 130/80 mm Hg American Society of Hypertension/International Society of Hypertension (ASH/ISH) [132] 2014 Adults ages 18-79 years
Adults ages ≥80 years < 140/90 mm Hg; < 130/80 mm Hg BP target may be considered in younger adults < 150/90 mm Hg Department of Veterans Affairs/Department of Defense (VA/DoD) [129] 2014 All adults Adults with diabetes < 150/90 mm Hg < 150/85 mm Hg American Diabetes Association (ADA) [71] 2016 Adults with diabetes < 140/90 mm Hg; < 130/80 mm Hg target may be appropriate in younger adults American Diabetes Association (ADA) [83] 2017 Adults with diabetes < 140/90 mm Hg; < 130/80 mm Hg target may be appropriate for those at high risk of cardiovascular disease (if achievable without undue treatment burden) CAD = coronary artery disease; MI = myocardial infarction; TIA = transient ischemic attack. Table 6. American Society of Hypertension/International Society of Hypertension Treatment Recommendations Patients Without Other Major Medical Condition First-line Drugs Added 2nd Drug (if needed to reach BP target) Added 3rd Drug (if needed to reach BP target) African ancestry CCB or thiazide diuretic ARB or ACEI Combination of CCB plus ACEI or ARB plus thiazide diuretic White and other non-African ancestry ages < 60 years ARB or ACEI CCB or thiazide diuretic Combination of CCB plus ACEI or ARB plus thiazide diuretic White and other non-African ancestry ages ≥60 years CCB or thiazide diuretic; ARB or ACEI also effective ARB or ACEI; CCB or thiazide diuretic if ARB or ACEI used first Combination of CCB plus ACEI or ARB plus thiazide diuretic Major medical condition Diabetes (white and other non-African ancestry) ARB or ACEI CCB or thiazide diuretic Alternative 2nd drug (CCB or thiazide diuretic) Diabetes (African ancestry) CCB or thiazide diuretic ARB or ACEI Alternative 1st drug (CCB or thiazide diuretic) Chronic kidney disease ARB or ACEI CCB or thiazide diuretic Alternative 2nd drug (CCB or thiazide diuretic) Coronary artery disease Beta-blocker plus ARB or ACEI CCB or thiazide diuretic Alternative 2nd drug (CCB or thiazide diuretic) Stroke ACEI or ARB CCB or thiazide diuretic Alternative 2nd drug (CCB or thiazide diuretic) Symptomatic heart failure Beta-blocker plus ARB or ACEI plus diuretic plus spironolactone regardless of BP; CCB can be added if needed for BP control ACEI = angiotensin-converting enzyme inhibitor; ARB = angiotensin receptor blocker; BP = blood pressure; CCB = calcium channel blocker. Table 7. JNC 7 Classification of Hypertensive Disorders in Pregnancy Classification Characteristics Chronic hypertension SBP ≥140 mm Hg or DBP ≥90 mm Hg, present pre-pregnancy or before 20 weeks’ gestation and persisting >12 weeks postpartum Preeclampsia SBP ≥140 mm Hg or DBP ≥90 mm Hg with proteinuria (>300 mg/24 h) that develops >20 weeks’ gestation; Can progress to eclampsia More common in nulliparous women, multiple gestation, women with hypertension ≥4 years, family history of preeclampsia, previous hypertension in pregnancy, and renal disease Chronic hypertension with superimposed preeclampsia New-onset proteinuria after 20 weeks’ gestation in a hypertensive woman or In a woman with hypertension and proteinuria before 20 weeks’ gestation: • Sudden 2- to 3-fold increase in proteinuria • Sudden increase in BP • Thrombocytopenia • Elevated AST or ALT levels Gestational hypertension Temporary diagnosis Hypertension without proteinuria after 20 weeks’ gestation May be a preproteinuric phase of preeclampsia or a recurrence of chronic hypertension that abated in mid-pregnancy May lead to preeclampsia Severe cases may cause higher rates of premature delivery and growth retardation relative to mild preeclampsia Transient hypertension Diagnosis made retrospectively BP returns to normal by 12 weeks postpartum May recur in subsequent pregnancies Predictive of future primary hypertension ALT = alanine aminotransferase; AST = aspartate aminotransferase; BP = blood pressure; DBP = diastolic BP; SBP = systolic BP Back to List Contributor Information and Disclosures Author Matthew R Alexander, MD, PhD Fellow, Division of Cardiovascular Medicine, Department of Internal Medicine, Physician Scientist Training Program, Vanderbilt University School of Medicine Coauthor(s) Meena S Madhur, MD, PhD Assistant Professor, Department of Medicine, Divisions of Clinical Pharmacology and Cardiology, Vanderbilt University School of Medicine David G Harrison, MD Betty and Jack Bailey Professor of Medicine and Pharmacology, Director of Clinical Pharmacology, Vanderbilt University School of Medicine Albert W Dreisbach, MD Associate Professor of Medicine, Division of Nephrology, University of Mississippi Medical Center Kamran Riaz, MD Clinical Assistant Professor, Department of Internal Medicine, Section of Cardiology, Wright State University, Boonshoft School of Medicine Specialty Editor Board Gary Edward Sander, MD, PhD, FACC, FAHA, FACP, FASH Professor of Medicine, Director of CME Programs, Team Leader, Root Cause Analysis, Tulane University Heart and Vascular Institute; Director of In-Patient Cardiology, Tulane Service, University Hospital; Visiting Physician, Medical Center of Louisiana at New Orleans; Faculty, Pennington Biomedical Research Institute, Louisiana State University; Professor, Tulane University School of Medicine Chief Editor Eric H Yang, MD Associate Professor of Medicine, Director of Cardiac Catherization Laboratory and Interventional Cardiology, Mayo Clinic ArizonA Acknowledgements George R Aronoff, MD Director, Professor, Departments of Internal Medicine and Pharmacology, Section of Nephrology, Kidney Disease Program, University of Louisville School of Medicine George R Aronoff, MD is a member of the following medical societies: American Federation for Medical Research, American Society of Nephrology, Kentucky Medical Association, and National Kidney Foundation Disclosure: Nothing to disclose. Michael S Beeson, MD, MBA, FACEP Professor of Emergency Medicine, Northeastern Ohio Universities College of Medicine and Pharmacy; Attending Faculty, Akron General Medical Center Michael S Beeson, MD, MBA, FACEP is a member of the following medical societies: American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, National Association of EMS Physicians, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Pamela L Dyne, MD Professor of Clinical Medicine/Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine; Attending Physician, Department of Emergency Medicine, Olive View-UCLA Medical Center Pamela L Dyne, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Mert Erogul, MD Assistant Professor of Emergency Medicine, University Hospital of Brooklyn: Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center Mert Erogul, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Allysia M Guy, MD Staff Physician, Department of Emergency Medicine, State University of New York Downstate Medical Center Disclosure: Nothing to disclose. Dawn C Jung, MD Staff Physician, Department of Emergency Medicine, Suny Downstate Medical Center, Kings County Hospital Center Dawn C Jung, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Claude Kortas, MD, MEd, FRCP(C) Program Director, Associate Professor, Department of Medicine, University of Western Ontario, Canada Claude Kortas, MD, Med, FRCP(C) is a member of the following medical societies: American Society of Nephrology, College of Physicians and Surgeons of Ontario, Ontario Medical Association, and Royal College of Physicians and Surgeons of Canada Disclosure: Nothing to disclose. Stephen C Morris, MD Resident, Section of Emergency Medicine, Department of Surgery, Yale New Haven Hospital Stephen C Morris, MD is a member of the following medical societies: American College of Emergency Physicians and American Medical Association Disclosure: Nothing to disclose. L Michael Prisant, MD, FACC, FAHA Cardiologist, Emeritus Professor of Medicine, Medical College of Georgia L Michael Prisant, MD, FACC, FAHA is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Clinical Pharmacology, American College of Forensic Examiners, American College of Physicians, American Heart Association, and American Medical Association Disclosure: Boehringer-Ingelheim Honoraria Speaking and teaching Assaad J Sayah, MD Chief, Department of Emergency Medicine, Cambridge Health Alliance Assaad J Sayah, MD is a member of the following medical societies: National Association of EMS Physicians Disclosure: Nothing to disclose. Zina Semenovskaya, MD Resident Physician, Department of Emergency Medicine, Kings County Hospital, State University of New York Downstate Medical Center College of Medicine Disclosure: Nothing to disclose. Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association Disclosure: Nothing to disclose. Mark A Silverberg, MD, MMB, FACEP Assistant Professor, Associate Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate Medical Center Mark A Silverberg, MD, MMB, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment Mark Zwanger, MD, MBA Assistant Professor, Department of Emergency Medicine, Jefferson Medical College of Thomas Jefferson University Mark Zwanger, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and American Medical Association Which of the following are functions of the blood?Blood Basics. transporting oxygen and nutrients to the lungs and tissues.. forming blood clots to prevent excess blood loss.. carrying cells and antibodies that fight infection.. bringing waste products to the kidneys and liver, which filter and clean the blood.. regulating body temperature.. Which of the following is a function of the blood EMT quizlet?It transports gases along with nutrients, aids in excretion, and provides protection and regulation.
What are the 5 functions of blood quizlet?Define Blood. ... . 5 functions of Blood? ... . Transporting Dissolved Gases, Nutrients, Hormones, and Metabolic wastes. ... . Blood Clot or Clotting. ... . Defending against Toxins and Pathogens. ... . Stabilizing Body Temperature. ... . What is Normal Blood Temperature? ... . What is the Average pH level of Blood?. What are the 4 main functions blood does for your body quizlet?blood carries oxygen from your lungs and to all your body cells. and carbon dioxide from your body cells.. Blood carries waste products from your cells. to your kidneys to be removed.. Blood transports nutrients and. other substances to your body cells.. cellsand molecules in blood. fight infection and help heal wounds.. |
Which of the following is a function of the blood Quizlet
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