Hypertension is the leading preventable risk factor for cardiovascular disease (CVD) and all-cause mortality worldwide. The prevalence of hypertension is rising globally owing to the aging of the population and increases in exposure to lifestyle risk factors including unhealthy diets and lack of physical activity. Due to the associated morbidity and mortality and cost to society, preventing and treating hypertension is an important public health challenge.
High blood pressure or hypertension is defined by two levels by the 2017 American College of Cardiology/American Heart Association (ACC/AHA) guidelines: (1) elevated BP, with systolic pressure between 120 and 129 mm Hg and diastolic pressure less than 80 mm Hg, and (2) stage 1 hypertension, with a systolic BP of 130 to 139 mm Hg or a diastolic BP of 80 to 89 mm Hg. However, defining abnormally high blood pressure is extremely difficult and arbitrary. A level for high BP must be agreed upon in clinical practice for screening clients diagnosed with hypertension and for instituting diagnostic evaluation and initiating therapy. Because the risk to an individual client may correlate with the severity of hypertension, a classification system is essential for making decisions about the aggressiveness of treatment or therapeutic interventions.
The 2017 guideline classifies BP into four categories: normal, elevated, and stage 1 and 2 hypertension. The greatest departures from the JNC 7 are the elimination of prehypertension, the addition of a new definition for elevated BP, and the reclassification of the stages of hypertension (DePalma et al., 2018). Based on the recommendations of the Joint National Committee (JNC) 8, the classification of BP for adults aged 18 years or older is as follows:
- Normal: Normal blood pressure is characterized by systolic BP of <120 mm Hg and diastolic BP of <80 mm Hg.
- Elevated: An elevated BP is measured as systolic BP between 120 and 129 mm Hg and diastolic BP of less than 80 mm Hg.
- Stage 1 hypertension: This stage is characterized by a systolic BP of 130 to 139 mm Hg or a diastolic BP of 80 to 89 mm Hg.
- Stage 2 hypertension: Stage 2 refers to a systolic BP between 140 to 159 mm Hg, even higher than 160 mm Hg, and a diastolic BP of 90 to 99 mm Hg or greater than 100 mm Hg.
From another perspective, hypertension may be categorized as either essential or secondary.
- Essential hypertension. Primary, or essential, hypertension is diagnosed in the absence of an identifiable secondary cause. Approximately 90 to 95% of adults diagnosed with hypertension have primary hypertension. One of the described factors for the development of essential hypertension is the client’s genetic ability to the salt response. It has long been suggested that an increase in salt intake increases the risk of developing hypertension.
- Secondary hypertension. Secondary hypertension is elevated BP secondary to an identifiable cause. Secondary forms of hypertension account for 20% of resistant hypertension. Resistant hypertension refers to hypertension in which BP is >140/90 mm Hg despite the use of medications from three or more drug classes.
Hypertensive crises are defined as BP of more than 180/120 mm Hg and may be further categorized as hypertensive emergencies or urgencies. Hypertensive emergencies are characterized by impending or progressive target organ dysfunction, whereas hypertensive urgencies are those situations without progressive target organ dysfunction.
The risk factors for hypertension can be divided into two: modifiable and non-modifiable risk factors.
Modifiable risk factors. The modifiable risk factors include diet, physical activity, alcohol consumption, tobacco smoking, and obesity or overweight.
- Unhealthy diet. In addition to sodium and potassium, several macronutrients are associated with BP, including dietary fiber, protein, and fat. In the DASH-Sodium trial, 412 people with an average systolic BP of 120 to 159 mm Hg and diastolic BP of 80 to 95 mm Hg were randomly assigned to high sodium, intermediate sodium, and lower sodium diets for 30 days. The results showed that reducing sodium intake from a high to an intermediate level lowered systolic BP by 2.1 mm Hg during consumption of the usual American control diet.
- Physical inactivity. Epidemiological studies have reported an inverse relationship between physical activity (such as walking to work) are associated with a decrease in the risk of incident hypertension.
- Excessive alcohol consumption. Ingesting too much alcohol also raises blood pressure. Women should have no more than one drink a day, while men should have no more than two drinks per day.
- Obesity. Obesity refers to excess fat in the body. Obesity increases the workload of the heart. Over time, this can add stress to the heart and blood vessels. Obesity is also linked to the prevalence of heart disease and diabetes.
- Tobacco use. Tobacco use increases the risk of hypertension. Nicotine increases blood pressure, and breathing in carbon monoxide- which is produced from smoking tobacco, reduces the amount of oxygen that the blood can carry.
Non-modifiable risk factors. Non-modifiable risk factors include a family history of hypertension, age >65 years, and the presence of comorbidities.
- Family history. Genetics likely play some role in hypertension, heart disease, and other related conditions. It is also likely that people with a family history of hypertension share common environments and other potential risks.
- Age >65 years. Because blood pressure tends to raise as one gets older, the risk for hypertension increases with age. About 9 or 10 Americans will develop high blood pressure during their lifetime.
- Gender. Men have higher BP at younger ages than women, but BP increase per decade is higher in women than in men. By the age of 60 years, women have a higher mean BP and hypertension prevalence than men.
- Race and ethnicity. A study that analyzed the National Health and Nutrition Examination Survey 2015-2016 data for 4,821 adults aged >20 years reported a significantly higher age-standardized prevalence of hypertension in non-Hispanic Black individuals than in non-Hispanic white individuals.
- Presence of comorbidities. The associations between high blood pressure and having diabetes, having chronic kidney disease (CKD), and exhibiting elevated non-HDL cholesterol are complex. Diabetes and hypertension commonly coexist. More than half of clients diagnosed with diabetes also have hypertension, and people with elevated blood pressure are nearly 2.5 times more likely to develop diabetes. In contrast, CKD was associated with a greater RR of hypertension among women, independent of diabetes, whereas this was not the case for men.
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.
- Environmental/genetic causes. Hypertension develops secondary to environmental factors, as well as multiple genes, whose inheritance appears to be complex. Furthermore, obesity, diabetes, and heart disease also have genetic components and contribute to hypertension.
- Renal causes. Renal causes (2.5 to 6%) of hypertension include renal parenchyma diseases and renal vascular diseases. Renovascular hypertension (RVHT) causes 0.2% to 4% of cases. The coexistence of renal arterial vascular disease and hypertension roughly defines this type of nonessential hypertension.
- Vascular causes. Vascular causes include coarctation of the aorta, vasculitis, and collagen vascular disease. Coarctation obstructs blood flow from the heart to the lower part of the body. Blood pressure increases above the constriction. The blood pressure is much higher than normal in the left ventricle and the heart must work harder to pump blood through the constriction in the aorta.
- Endocrine causes. Endocrine causes account for 1 to 2% and include exogenous or endogenous hormonal imbalances. Exogenous causes include the administration of steroids. Another common endocrine cause is oral contraceptive use. Activation of the renin-angiotensin-aldosterone system (RAAS) is the likely mechanism because the hepatic synthesis of angiotensin is induced by the estrogen component of oral contraceptives Endogenous causes include primary hyperaldosteronism, Cushing syndrome, pheochromocytoma, and congenital adrenal hyperplasia.
- Obstructive sleep apnea (OSA). 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 per hour, which leads to excessive daytime sleepiness. Approximately half of the individuals with hypertension have OSA, and approximately half with OSA have hypertension.
Having hypertension puts clients at risk for heart disease and stroke, which are the leading causes of death in the United States.
- In 2020, more than 670,000 deaths in the U.S. had hypertension as a primary or contributing cause.
- Nearly half the adults in the U.S. (47% or 116 million) have hypertension, defined as systolic blood pressure greater than 130 mm Hg or diastolic blood pressure greater than 8- mm Hg, or are taking medication for hypertension.
- Only about 1 in 4 adults (24%) diagnosed with hypertension have their condition under control.
- About half of adults (45%) diagnosed with uncontrolled hypertension have a blood pressure of 140/90 mm Hg or higher. This includes 37 million U.S. adults.
- A greater percentage of men (50%) have a high blood pressure than women (44%).
- High blood pressure is more common in non-Hispanic black adults than in non-Hispanic white adults, non-Hispanic Asian adults, or Hispanic adults.
- 2017 data from the CDC National Center for Health Statistics (NCHS) spanning 2015 to 2016 show a hypertension prevalence of 29% among those aged 18 and older.
- Overall, hypertension affects US men and women nearly equally, affecting an estimated 40.8 million men and 44.9 million women.
- Globally, an estimated 26% of the world’s population (972 million) has hypertension, and the prevalence is expected to increase to 29% by 2025, driven largely by increases in economically developing nations.
Hypertension is a state of the vascular system where the whole vasculature is set at a particular level for a particular person. Hypertension is said to be caused by increased cardiac output and/or increased peripheral resistance. Cardiac output is determined by stroke volume and heart rate; stroke volume is related to myocardial contractility and to the size of the vascular compartment. Peripheral resistance is determined by functional and anatomic changes is small arteries and arterioles.
Overt increase in sympathetic activity is associated with increased heart rate, cardiac output, peripheral resistance, plasma, and urinary noradrenaline levels, regional noradrenaline spillover, and peripheral postganglionic sympathetic nerve discharge. Both central and peripheral mechanisms are involved in increased sympathetic activity. Emotional and physical stress activates sympathoadrenal activity and raises BP.
According to renal mechanisms, the basic defect in hypertension is the kidney’s inability to excrete the excess sodium load imposed by a high salt diet. Excess sodium intake causes hypertension by increasing fluid volume and preload, thus increasing cardiac output. Renal sodium retention also contributes to increased cardiac output.
According to hormonal mechanisms or the RAAS, renin is a circulating enzyme that participates in maintaining extracellular volume and arterial vasoconstriction. Renin breaks down angiotensinogen into angiotensin I. angiotensin-converting enzyme breaks down angiotensin I into angiotensin II, the most vasoactive peptide and a potent constrictor of all blood vessels. It acts on the musculature of arteries, raises peripheral resistance, and elevates BP. Angiotensin II also results in the release of aldosterone through adrenal glands, which stimulates the epithelial cells of the kidneys to increase the reabsorption of salt and water, leading to raised blood volume and raised BP.
Accurate measurement of blood pressure is the key to diagnosis. Several determinations should be made over a period of several weeks. At any given visit, an average of three blood pressure readings taken two minutes apart using a mercury manometer is preferable. On the first visit, blood pressure should be checked in both arms and in one leg to avoid missing the diagnosis of coarctation of the aorta or subclavian artery stenosis.
Most clients with hypertension have no symptoms, even if the blood pressure readings reach dangerously high levels. When symptoms do occur, they can include the following:
- Early morning headaches
- Irregular heart rhythms
- Vision changes
- Buzzing in the ears
In general, the evaluation of hypertension primarily involves accurately measuring the client’s blood pressure, performing a focused medical history and physical examination, and obtaining results of routine laboratory studies. A 12-lead electrocardiogram should also be obtained.
Initial laboratory tests may include:
- Urinalysis. Proteinuria can be a feature of renal parenchymal disease. A 24-hour urine specimen should be collected for sodium and potassium measurement. If the urine sodium level is more than 100 mmol/L and urine potassium is less than 30 mmol/L, hyperaldosteronism is unlikely.
- Fasting blood glucose (FBS). FBS levels are widely used to assess the condition of diabetes. Low insulin insensitivity or insulin resistance has been found to cause hypertension through multiple mechanisms, including increased renal sodium reabsorption, sympathetic nervous system activation of transmembrane ion transport, and hypertrophy of resistance vessels. According to data collected and analyzed in a study, higher FBS levels in nondiabetic individuals act as a risk factor for hypertension.
- Basic metabolic panel (BMP). Hypokalemia presents in primary hyperaldosteronism and Cushing syndrome. Also seen on the BMP in primary aldosteronism, are metabolic alkalosis and hypernatremia. Blood urea nitrogen and creatinine become elevated in renal parenchymal disease.
- Complete blood count (CBC). Polycythemia can be present in obstructive sleep apnea.
- Lipid profile following a 9 to 12-hour fast. Elevated BP often coexists with lipid disorders and is an additional factor that increases cardiovascular risk. HDL small subfractions can also increase the risk of CV events.
Effective management and treatment of hypertension requires clinicians and clients to work together to balance pharmacologic and non-pharmacologic interventions and prevent target organ damage.
- BP thresholds and targets. After the publication of the Systolic blood PRessure Intervention Trial (SPRINT) conducted a study with participants randomly assigned to a standard systolic BP target of <140 mm Hg or an intensive systolic BP target of <120 mm Hg.
- First-line hypertensive medications. Typically, antihypertensive pharmacotherapy begins with first-line antihypertensive medications either in monotherapy or in combination. Combination therapy may be preferable in clients with higher levels of pretreatment BP. First-line antihypertensive medications include:
- Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers. ACE inhibitors and angiotensin II receptor blockers have improved outcomes in clients diagnosed with heart failure with reduced left ventricular ejection fraction or with diabetic nephropathy, making them particularly good choices in these populations. Both classes appear to be comparable in reducing CVD risk and also tend to improve glucose metabolism and, therefore, could be preferable in younger clients and in clients with conditions predisposing to type 2 diabetes mellitus, including obesity and metabolic syndrome.
- Calcium channel blockers. Dihydropyridine calcium channel blockers elicit vasodilation by blocking vascular smooth muscle L-type calcium channels. They are effective antihypertensive drugs with extensive experience in large clinical trials. A practical advantage of this drug class is that it can be combined with all other first-line antihypertensives. Non-dihydropyridine calcium channel blockers, especially verapamil, also inhibit cardiac calcium channels, which can reduce heart rate and cardiac contractility.
- Thiazide diuretics. Thiazide-type diuretics have a benzothiadiazine ring, whereas thiazide-like diuretics lack the benzothiadiazine structure. Both subclasses of thiazide diuretics inhibit Na+ and CI- co-transporters in renal tubules, thereby promoting natriuresis, and have been an important component of pharmacological hypertension management ever since the first trials showing morbidity benefits of antihypertensive therapy.
- Beta-blockers. Beta-blockers lower BP reducing cardiac output, heart rate, renin release, and adrenergic control nervous system effects. They improve outcomes following acute myocardial infarction and in clients diagnosed with heart failure with reduced left ventricular ejection fraction.
- Device-based treatments. Device-based treatments have been primarily developed for clients with severe resistant hypertension whose BP cannot be controlled with antihypertensive drugs. Catheter-based renal nerve ablation, electrical carotid sinus stimulation, modulation of baroreflex transduction with a dedicated carotid stent, carotid body denervation, and deep brain stimulation are thought to lower BP through SNS inhibition. The creation of a defined arteriovenous stent with a coupler device lowers BP by reducing peripheral vascular resistance. These treatments are in various stages of clinical development, with the most extensive data available on renal nerve ablation and electrical carotid sinus stimulation.
Lifestyle advice is recommended for all clients diagnosed with hypertension. Over the years, the role of nurses in BP management has changed significantly. There has been a move away from nurses simply measuring, monitoring, and charting BP to specialist hypertension nurses who are trained to lead and manage all aspects of BP care for clients, including detection, referral, and prescribing and managing medications.
- A sedentary lifestyle
- Weakness or fatigue
- Shortness of breath
- History of elevated BP
- Episodes of palpitations
- Multiple stress factors such as relationships, financial, or job-related problems
- Past history of kidney disease
- High-calorie, high-salt, high-fat, and high-cholesterol diet
- Weight changes
- Throbbing, suboccipital headaches
- Visual disturbances
- Stiffness of the neck
- Smoking history
- Episodes of numbness
- Light-headedness with position changes
- Familial risk factors such as hypertension, atherosclerosis, heart disease, diabetes mellitus, cerebrovascular disease, or kidney disease
- Use of birth control pills or hormone replacement therapy
- Changes in heart rhythm
- Dyspnea with exertion
- Bounding carotid pulses
- Heart murmurs
- Slow capillary refill
- Moodiness, irritability
- Normal weight or obesity
- Presence of edema
- Jugular vein distention
- Decreased strength and reflexes
- Mild sclerosis, arterial narrowing
- Avoidance of bright lights and noise
- Impaired coordination or gait
- Risk for Decreased Cardiac Output
- Activity Intolerance
- Acute Pain
- Imbalanced Nutrition: More than Body Requirements
- Ineffective Coping
- Deficient Knowledge
- Ineffective Self Health Management
- Risk for Sexual Dysfunction
- Readiness for Enhanced Family Coping
Nursing Desired Outcomes
- The client will maintain BP within individually acceptable limits.
- The client will demonstrate stable cardiac rhythm and rate within the normal range.
- The client will participate in activities that can reduce BP and cardiac workload.
- The client will demonstrate a decrease in physiological signs of intolerance.
- The client will report pain or discomfort from headaches and neck stiffness are relieved or controlled.
- The client will demonstrate changes in eating patterns and initiate appropriate exercise programs.
- The client will identify coping behaviors and utilize them.
- The client will adhere to the pharmacologic therapy religiously.
- Promote reduced salt intake. For metabolic balance, the amount of salt consumed must equal that lost. Under normal living conditions and physical activity levels, an intake of 5 g salt/day is considered sufficient, in line with the WHO recommendation of <5 g per day. The current recommendations of the American Heart Association and American Society of Hypertension are stricter than the European guidelines, recommending lowering salt intake to 3.8 g per day. Reduced sodium intake can also prevent hypertension, improve hypertension control, and possibly reduce the need for antihypertensive medication.
- Educate about the DASH diet. Randomized controlled trials carried out in persons diagnosed with hypertension have consistently shown that reduced sodium intake is associated with a reduction in BP. The most convincing evidence is provided by the Dietary Approaches to Stop Hypertension (DASH-sodium) trial, in which the effects of three different sodium intakes were tested separately in combination with two diets: the DASH diet, rich in fruit, vegetables, low-fat dairy products and reduced in saturated fat and cholesterol, and a control diet consisting of what many people in the United States typically eat. Reduction of sodium intake by 0.9 g per day induced a greater BP reduction when the starting sodium intake was <2.3 g per day.
- Encourage increased intake of potassium. Increased potassium intake is associated with reduced BP in individuals with low as well as high baseline potassium intake. The effect of potassium on BP is dependent on salt intake. There is greater BP reduction with increased potassium intake in the context of lower salt intake. The preferred strategy to increase potassium intake is to increase the consumption of fruits and vegetables that are rich in potassium rather than using supplements.
- Encourage moderate alcohol consumption. Keeping alcohol intake <2 standard drinks per day for men and <1 standard drink per day for women can also contribute to a 2-4 mm Hg BP reduction.
- Promote participation in physical activity. Regular physical activity reduces BP in individuals diagnosed with hypertension. Endurance training reduces BP more in persons diagnosed with hypertension than in individuals with normal BP. Sessions lasting 40-60 minutes performed at least three times a week had the greatest effect on BP.
- Educate about the importance of weight loss. Excess adiposity generally raises BP in susceptible individuals, and clients diagnosed with hypertension who also have obesity require more antihypertensive medications to control their BP and are more likely to be treatment resistant. In a recent meta-analysis, any reduction in body weight lowered systolic BP by on an average of 2.69 mm Hg and in diastolic BP by on an average of 1.34 mm Hg. However, the response varies substantially between individuals.
- The client exhibited BP within individually acceptable limits.
- The client’s cardiovascular and systemic complications were prevented or minimized.
- The client understood the disease process, prognosis, and therapeutic regimens.
- The client initiated necessary lifestyle and behavioral changes.
- The client adhered to the plan in place to meet needs after discharge.
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