About this course:
This learning activity aims to increase the nurse's knowledge of hypertensive disorders and the risk factors, prevalence, diagnostic criteria, classifications, and treatment of hypertension (HTN).
Hypertension Diagnosis and Management for Nurses (RNs and LPNs)
This learning activity aims to increase the nurse's knowledge of hypertensive disorders and the risk factors, prevalence, diagnostic criteria, classifications, and treatment of hypertension (HTN).
Upon completion of this activity, the learner should be able to:
- identify the appropriate terms and definitions related to HTN
- formulate an understanding of the pathophysiology of HTN
- identify various risk factors for HTN and methods for prevention
- reference applicable guidelines used to diagnose and manage HTN
- develop a basic understanding of various nonpharmacological and pharmacological interventions used to treat and prevent HTN
- consider the management of HTN in specialty populations
Hypertension (HTN) is primary care's most common chronic health issue. Due to its prevalence and effects, HTN has been one of the most studied health topics. HTN is a significant comorbidity in the development of stroke, cardiovascular disease (CVD), myocardial infarction (MI), heart failure (HF), and end-stage renal disease (ESRD). HTN is cited as the leading cause of CVD and stroke, two of the leading causes of death in the US. In the US, HTN accounts for more CVD deaths than any other modifiable risk factor and is second to smoking as a leading preventable cause of death. The American Heart Association (AHA) defines HTN as “the silent killer” as people typically have no apparent symptoms, and detection often occurs during routine blood pressure (BP) assessment. It is also considered the first domino to drop, leading to the development of various other disorders (AHA, 2019; Ignatavicius et al., 2018; Iqbal & Jamal, 2022).
Nearly half (47% or 116 million) of the US population are diagnosed with HTN. This number is likely an underrepresentation of adults with HTN, as 1 in 5 individuals with high BP is unaware. Lifestyle modifications only are recommended for 1 in 5 adults (24.3 million) diagnosed with HTN, and lifestyle modifications in conjunction with medication management are recommended for the other 4 out of 5 adults (91.7 million). Of those diagnosed with HTN, 92.1 million do not have their BP controlled, including 100% of the 24.3 million individuals who were recommended lifestyle modifications alone and 67.8 million individuals who were recommended lifestyle modifications with medication management. Approximately half (45% or 37 million) of adults in the US with uncontrolled HTN have a baseline BP greater than 140/90 mmHg (Centers for Disease Control and Prevention [CDC], 2021, 2023a).
The effects of uncontrolled HTN are costly to the individual and the US healthcare system. The total medical costs, including healthcare services and medications, are between $131 and $198 billion annually, and this number is projected to exceed $220 billion by 2035. The overall cost of healthcare for the individual with HTN is $2,500 more than the average cost for the individual without HTN; this amount increases to $4,000 more annually for people with a comorbidity such as diabetes. The overall cost of HTN medication management is low compared to the costs of treating the diseases that can occur due to uncontrolled HTN. Many first-line treatment drugs are widely available with a low-cost generic option, averaging $350 annually to be paid by the individual and insurance company. However, since approximately 650 million prescriptions are filled for antihypertensive medications each year, the overall cost is estimated at $29 billion, including $3.4 billion in out-of-pocket costs paid by individuals (US Department of Health and Human Services [HHS], 2020).
Types of Hypertension
The most common type of HTN is idiopathic, primary, or essential HTN, which is not caused by an existing health condition. The development of primary HTN is often related to lifestyle choices (i.e., dietary and exercise habits) and genetic factors. It is thought that approximately 50% to 60% of individuals with primary HTN have a genetic predisposition to salt sensitivity, increasing the risk of HTN development (Iqbal & Jamal, 2022).
Secondary HTN is caused by certain disease states or drugs that can increase BP. Kidney disease is the most common cause of secondary HTN. Renal artery stenosis (RAS), the narrowing of one or more of the main arteries carrying blood to the kidneys, can lead to HTN. These patients may benefit from dilation of these arteries through angioplasty and stent placement. Adrenal medulla or cortex dysfunction can cause secondary HTN. Excess aldosterone, cortisol, epinephrine, and norepinephrine can result in adrenal-mediated HTN. Excess aldosterone, caused by primary aldosteronism, can result in HTN and hypokalemia. This usually arises from benign adenomas of the adrenal cortex. Primary aldosteronism is one of the most frequent causes of secondary HTN (5% to 10%) and resistant HTN (20%). Benign tumors in the adrenal medulla called pheochromocytomas can cause life-threatening HTN. These tumors secrete excess epinephrine and norepinephrine, or catecholamines. Cushing’s syndrome is an excess of glucocorticoids that can result in HTN and is usually caused by adrenocortical hyperplasia or adrenocortical adenoma. Medications that may cause secondary HTN include glucocorticoids (prednisone [Deltasone], dexamethasone [Decadron]), mineralocorticoids (fludrocortisone [Florinef], spironolactone [Aldactone]), sympathomimetics, cyclosporine (Neoral), non-steroidal anti-inflammatories (NSAIDs), erythropoietin (Epogen), and estrogen-containing oral contraceptives (norethindrone and ethinyl estradiol [Ovcon50]; Ignatavicius et al., 2018; Whelton et al., 2018).
Malignant HTN or hypertensive crisis is a severe form of HTN where the BP elevates rapidly. This condition may present with morning headaches, blurred vision, dyspnea, or symptoms of uremia (the accumulation of urea and nitrogenous waste products in the blood that would typically be eliminated in the urine). These patients are often in their 30s-50s with systolic blood pressure (SBP) above 200 mmHg. According to the AHA, the defining characteristic is an SBP above 180 mmHg and diastolic blood pressure (DBP) above 120 mmHg in a stable patient with the development of target organ damage (TOD). Immediate intervention is required, or the condition could progress to a stroke, left ventricular heart failure, or kidney failure (AHA, 2019; Ignatavicius et al., 2018).
Pathophysiology of Hypertension
BP is the force that blood exerts on the walls of blood vessels. This pressure is highest in large arterial blood vessels and lower in the capillaries. BP is determined by cardiac output (CO; the amount of blood pumped out of the left ventricle each minute) and total peripheral vascular resistance (PVR). Cardiac output is calculated by multiplying the stroke volume (SV) by the heart rate (HR). Since BP depends on CO and PVR, anything that increases the PVR or CO (HR or SV increase) increases the BP. Conversely, anything that decreases PVR or CO (HR or SV decrease) lowers BP. Typically BP is maintained at a relatively constant level with minimal but expected changes based on the time of day. Mechanisms within the body stabilize and regulate BP to avoid circulatory collapse (Ignatavicius et al., 2018). These regulatory mechanisms include:
- the autonomic nervous system (ANS), which acts on the sympathetic nervous system in response to impulses received from peripheral chemo and baroreceptors
- the kidneys which control the renin-angiotensin-aldosterone pathway based on vascular volume and flow rate
- the endocrine system releases hor
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BP is affected by the amount of fluid circulating in the vascular space. If there is an increase in sodium or water in the body, BP will rise. If the kidneys are properly functioning, a rise in BP will trigger diuresis, consequently bringing the BP back down by reducing sodium and/or water in the body. Various pathologic conditions can change the pressure threshold causing the kidneys to excrete excess sodium and water, altering the BP. Vascular autoregulation is poorly understood, but this process maintains tissue perfusion in the body at a constant rate but can also lead to elevated BP. The renin-angiotensin-aldosterone system regulates BP through a complex mechanism of action. The kidneys produce renin, an enzyme that acts on angiotensin to produce angiotensin I, which is converted to angiotensin II. Angiotensin II causes vasoconstriction of the blood vessels, which triggers the release of aldosterone. Aldosterone causes the collecting tubes in the kidneys to reabsorb sodium, which causes fluid retention, increasing blood volume and BP. Arterial baroreceptors are primarily found in the walls of the left ventricle, the aorta, and the carotid sinus. The baroreceptors are stimulated when the arterial walls are stretched, indicating increased BP. Once the baroreceptors are stimulated, they send impulses that inhibit the vasomotor center of the brain (pons and medulla), which results in vagally mediated cardiac slowing and vasodilation with a decreased sympathetic tone. This action controls the circulation and causes systemic arterial pressure to increase and decrease as needed. The failure of the baroreceptors to adjust BP in those with HTN is not entirely understood (Ignatavicius et al., 2018).
Risk Factors and Methods for Prevention
While an existing health problem does not cause primary HTN, it can be influenced by modifiable and unmodifiable risk factors. Patients need to understand their role in HTN and how their behaviors and actions can change the course of the disease (Ignatavicius et al., 2018; Whelton et al., 2018). Modifiable risk factors that can increase an individual's risk of developing HTN include:
- hyperlipidemia or hypercholesterolemia
- smoking or chronic exposure to second-hand smoke
- excess caffeine or sodium intake
- obesity or overweight
- lack of physical activity
- excess alcohol intake
- insufficient magnesium, potassium, or calcium intake (especially from vegetables)
- excess stress (Ignatavicius et al., 2018; Whelton et al., 2018)
Nonmodifiable risk factors include:
- family history
- non-Hispanic black individuals (have the highest rate of HTN)
- age (postmenopausal or over age 60)
- male sex
- low socioeconomic/educational status
- premature birth and low birth weight (Ignatavicius et al., 2018; Whelton et al., 2018)
While many of the risk factors for HTN are nonmodifiable, many can be avoided. Knowledge is power in changing the outcomes. Educating the individual on their risk factors, determining where modifications can occur, and developing a personalized care plan can provide a foundation for a healthier BP. Patients should be well educated in their role in reducing their BP. A minimal reduction in SBP or DBP can significantly decrease their overall health risks. A 10 mmHg reduction in SBP can reduce a patient's risk of coronary heart disease by 17%, stroke by 27%, and HF by 28%. Nurses can educate patients on monitoring their BP at home and using online resources like the AHA’s Check. Change. Control. Calculator to track their progress. This resource helps patients self-monitor their BP readings at home to maintain a healthy heart (AHA, n.d., 2019).
Healthy People 2030 includes preventing heart disease and stroke and improving cardiovascular health. As a part of this, the US Healthy People 2030 campaign focuses on HTN with several objectives that attempt to decrease cardiovascular mortality and morbidity through prevention (Office of Disease Prevention and Health Promotion, n.d.). The following objectives focus on HTN and reducing BP:
- HDS-04: Reduce the proportion of adults with high BP
- HDS-05: Increase control of high BP in adults
- HDS-06: Reduce cholesterol in adults
- HDS-07: Increase cholesterol treatment in adults
- HDS-D07: Increase the proportion of adults whose risk for atherosclerotic cardiovascular disease (ASCVD) was assessed
- CKD-06: Reduce the proportion of adults with chronic kidney disease who have elevated BP (Office of Disease Prevention and Health Promotion, n.d.).
Although HTN often has no apparent symptoms, there may be indications of HTN present on physical examination. Patient evaluation should focus on identifying TOD and possible secondary causes of HTN. Correctly identifying the underlying cause of HTN can aid in planning an effective treatment regime. Patient history, including changes in BP measurement over time, should be considered focusing on potential features that may differentiate between primary and secondary HTN. BP changes associated with decreased physical activity, weight gain, stress, dietary changes, alcohol consumption, tobacco use, or advancing age with a family history of HTN can indicate the presence of primary HTN. Some causes of secondary HTN can be detected with a physical assessment. A difference between BP readings in each arm or an upper and lower extremity greater than 20 mmHg may indicate the presence of coarctation of the aorta. When auscultating heart sounds, a 4th heart sound or a systolic ejection murmur may indicate aortic valve disease. A renal or carotid bruit can indicate the presence of renovascular disease or fibromuscular dysplasia (FMD). Upon palpation, enlarged kidneys may indicate polycystic kidney disease (PKD). The presence of thin skin, hyperglycemia, and patient reports of bruising easily may suggest an endocrine disorder. When assessing the neck, the presence of an enlarged, palpable thyroid that is tender to the touch may indicate the presence of a thyroid disorder, a common cause of secondary HTN (Iqbal & Jamal, 2022; Whelton et al., 2018).
Herbals (i.e., ginseng), over-the-counter (OTC) medications (i.e., pseudoephedrine), and some food substances (i.e., convenience foods high in sodium) can increase BP. Drug-drug interactions can increase the BP or cause a patient currently taking an antihypertensive to have an increase in their BP. A careful history can identify some of these substances and elicit information about changes in OTC drug use, illicit drugs, or herbal products (Whelton et al., 2018). Table 1 outlines the clinical indications and diagnostic testing for common causes of secondary HTN.
Diagnostics for Common Causes of Secondary Hypertension
Resistant HTN; abrupt onset HTN; early-onset HTN in women
Abdominal S/D bruit; bruits over the carotid artery
Renal duplex Doppler ultrasound; MRA; abdominal CT
Resistant HTN; HTN with hypokalemia; HTN and OSA; HTN and family history of early-onset HTN or stroke
Arrhythmias with hypokalemia, particularly A-fib
Plasma aldosterone/renin ratio under standardized conditions.
Resistant HTN; snoring; fitful sleep; breathing pauses during sleep; daytime sleepiness
Berlin Questionnaire; Epworth Sleepiness Sore; overnight oximetry
Alcohol or drug-induced
Sodium-containing antacids; caffeine; nicotine; alcohol; NSAIDs; oral contraceptives; sympathomimetics; cocaine; amphetamines or illicit drugs; herbal agents such as ephedra
Tachycardia; sweating; acute abdominal pain; fine tremors
Urinary drug screen (illicit drugs)
(Whelton et al., 2018)
Uncommon diagnostics that may be considered are plasma thyroid levels for hypo- or hyperthyroidism, 24-hour urine for metanephrines with pheochromocytomas, overnight dexamethasone suppression test for Cushing’s syndrome, echocardiogram for suspected aortic coarctation, serum calcium for suspected primary hyperparathyroidism, or serum growth hormone for suspected acromegaly (Whelton et al., 2018).
The HCP will determine the patient’s goals and risk tolerance for therapy. Older patients may have multiple chronic conditions, weakness, or frailty, and prognosis should be considered. A physical examination should include accurate BP measurements in the office and a review of self-administered BP readings. Often, the most precise BP measurements occur outside the office and can help identify those individuals with white coat syndrome or masked HTN. Due to this, teaching the patient how to assess their BP correctly is extremely important (Iqbal & Jamal, 2022; Whelton et al., 2018).
The criteria for diagnosing HTN require accurate BP measurements. BP measurements that are elevated enough to classify as any form of HTN should be repeated. However, there should be at least a 10-minute refractory period between measurements. Instructing the patient on proper positioning when obtaining BP is essential for accuracy. The patient should be seated with uncrossed legs, feet planted on the floor, and their back supported. Ideally, the patient should sit for at least 5 minutes before assessing BP. Neither the patient nor the HCP obtaining the BP should speak during the assessment. Improper positioning can lead to an elevated result. To eliminate falsely elevated readings, the patient should not have ingested caffeine, nicotine, or other stimulants in the 30 minutes before the BP assessment. The right arm is preferred when measuring BP unless contraindicated due to another medical condition (Muntner et al., 2019; Whelton et al., 2018). Table 2 contains a detailed outline for accurately performing a BP measurement.
Checklist for Accurate Measurement of Blood Pressure
Step 1: Properly prepare the patient.
Step 2: Use proper technique for BP measurements.
Step 3: Take the proper measurements needed for diagnosis and treatment of elevated BP/HTN
Step 4: Properly document accurate BP readings.
Step 5: Average the readings
Step 6: Provide BP readings to the patient.
(Muntner et al., 2019; Whelton et al., 2018)
The most common error when measuring BP is choosing the wrong cuff size, known as miscuffing. It is essential to use a cuff that is the appropriate size for the patient. A cuff that is not the proper size can affect the BP reading. A cuff that is too small can artificially elevate the BP, while a cuff that is too large can show a falsely reduced BP. Using a cuff that is too small for larger arms accounts for 84% of all miscuffings. When choosing cuff size, ensure the cuff has a length that is 1.5 times the circumference of the upper arm, the bladder length of the cuff should be at least 80% of the arm circumference, and the bladder width should be 37% to 50% of the arm circumference (a 2:1 ratio). When measuring arm circumference, the tape measure should be placed mid-arm between the acromion and olecranon around the patient's bicep (Muntner et al., 2019; Whelton et al., 2018). Table 3 lists the appropriate cuff size based on arm circumference.
Estimated BP Cuff Size for Accuracy
Arm Circumference, cm (inches)
Bladder Dimension, cm (width x length)
Usual Cuff Size
12 x 22
16 x 30
16 x 36
16 x 42
Extra-large adult (thigh)
(AHA, 2019; Muntner et al., 2019)
Categories for Blood Pressure Classification
In 2017 the American College of Cardiology (ACC)/AHA released their most updated HTN diagnostic guidelines. In 2018 the European Society of Cardiology (ESC)/European Society of Hypertension (ESH) released their most recent clinical practice guidelines for diagnosing and treating HTN (Whelton et al., 2022).
The ACC/AHA recommends averaging the BP results of at least two separate readings on at least two separate occasions utilizing the same BP monitoring device. BP measurements outside the provider's office setting should confirm any elevation in BP. The ESC/ESH recommends three separate in-office readings with additional measurement required if the difference between the first two readings is greater than 10 mmHg. BP results are documented as an average of the last two readings. Both guidelines agree that out-of-office BP measurements should be used to recognize masked or white-coat HTN. Based on BP measurements following the above standards, the ACC/AHA categorizes BP as normal, elevated, HTN stage 1, or HTN stage 2. The new 2017 recommendations released by the ACC/AHA lowered the cutoff BP for diagnosis of HTN stage 1 from greater than 140/90 to an SBP greater than 130 mmHg and DBP greater than 80 mmHg (Whelton et al., 2018, 2022). See Table 4 for ACC/AHA BP classifications.
ACC/AHA Blood Pressure Classifications
Systolic Blood Pressure (mmHg)
Diastolic Blood Pressure (mmHg)
120 - 129
Hypertension, stage 1
130 - 139
80 - 89
Hypertension, stage 2
(Whelton et al., 2018, 2022)
For patients that meet the criteria of stage 1 HTN (SBP 130-139/ DBP 80-90), the HCP will determine their 10-year risk of ASCVD to develop the most appropriate treatment plan (AHA, 2018a).
As described above, the HCP will typically screen for white-coat HTN or masked HTN. Due to these conditions, as many as 10% of the population could either be over-treated or under-treated for HTN. White-coat HTN increases the patient’s BP in the office setting due to fear and anxiety when entering the healthcare environment. Management for white-coat HTN should begin with lifestyle modification for 3 months. The patient should be counseled to check their BP daily at home, and if it remains above 130/80, continue with lifestyle modifications and initiate antihypertensive drug therapy. If the BP is consistently below 130/80 at home, continue lifestyle modifications with annual BP checks, and diagnose as white coat HTN. Masked HTN is characterized by an SBP between 120-129 and DBP between 75-79 consistently in the office but higher BP readings elsewhere. Similar to the above, masked HTN management should include a 3-month trial of lifestyle modification and home BP monitoring. If home BP readings are consistently above 130/80, consider masked HTN and continue with lifestyle modifications, and start antihypertensive drug therapy. If the BP is consistently below 130/80 at home, continue with lifestyle modifications, annual, and home BP monitoring (AHA, 2019; Whelton et al., 2018).
Although primary HTN can be diagnosed through history and physical and home and in-office BP monitoring, additional testing may be completed to provide a complete patient picture, determine CVD risk, and establish baseline values before medication initiation. Initial basic testing includes fasting glucose, complete blood count (CBC), lipid profile, serum creatinine, serum electrolytes (sodium, potassium, and calcium), thyroid-stimulating hormone (TSH), urinalysis, and electrocardiogram. Additional optional testing that can be completed as indicated is an echocardiogram, uric acid level, and urinary albumin to creatinine ratio. This testing can also provide information about TOD (Whelton et al., 2018).
HTN during pregnancy can bring unique complications. Not only is the pregnant individual’s health compromised, but also the fetus’s. HTN in pregnancy is caused by four different disorders collectively known as hypertensive disorders of pregnancy (HDP). HDP consists of chronic HTN, gestational HTN, preeclampsia, and preeclampsia superimposed over chronic HTN. Globally, chronic HTN affects 1% to 2% of pregnancies, gestational HTN affects 5% to 6% of pregnancies, and preeclampsia affects 2% to 4% of pregnancies. Individuals who have already been diagnosed with chronic HTN and begin to have preeclampsia symptoms after 20 weeks are considered to have preeclampsia superimposed over chronic HTN. In the US, the prevalence of gestational HTN increased from 10.8% in 2017 to 13% in 2019. During that same period, the rate of chronic HTN increased from 2% to 3% (Ford et al., 2022; Garovic et al., 2022; Magee & von Dadelszen, 2021).
HDP affects 10% of pregnancies and causes 14% of maternal and perinatal deaths worldwide, second only to maternal hemorrhage. Preeclampsia and eclampsia are responsible for approximately 10% of maternal deaths worldwide. This equates to over 50,000 deaths, with a death occurring every 7 minutes. HDP is a common pregnancy complication in the US and the leading maternal mortality cause (American College of Obstetricians and Gynecologists [ACOG] 2020; Ford et al., 2022; Lowdermilk et al., 2016; UNICEF, 2021.
Hypertension induced by pregnancy is classified as SBP above 140 mmHg, DBP above 90 mmHg, or a combination of elevated SBP and DBP that occurs after 20 weeks of gestation. Typically, BP readings must be elevated on two separate readings at least 4 hours apart. In cases where the readings are extremely elevated (SBP ≥ 160 or DBP ≥ 110), a shorter interval between readings is indicated to expedite treatment (ACOG, 2019).
Individuals with gestational HTN or preeclampsia during pregnancy have an increased risk of CVD, stroke, peripheral artery disease, and cardiovascular mortality later in life. Their risk is nearly doubled compared to individuals who did not have HTN during pregnancy. For individuals with recurrent preeclampsia in subsequent pregnancies or early onset preeclampsia, this risk increases to 4 to 8 times higher than those who remained normotensive during pregnancy. Due to this increased risk, follow-up monitoring of BP and weight should occur 6 to 8 weeks after pregnancy and then again 6 to 12 months after pregnancy. Assessments of BP, cholesterol levels, fasting glucose, and hemoglobin A1C should be completed annually until the age of 50 to monitor for the development of cardiovascular complications (ACOG, 2020; Benschop et al., 2019). See Table 5 for an HTN screening tool for women related to previous pregnancy risks. This tool was created in 2010 by two cardiologists to determine cardiovascular risks based on a woman's pregnancy history (Gongora et al., 2018).
Female Pregnancy Risk Screening Tool
(Gongora et al., 2018)
Management of Hypertension
The goal of HTN management is to improve patient health outcomes. Treatment also emphasizes reducing the patient's risk of experiencing future adverse cardiovascular events such as MI or stroke. Patient comorbidities, stage of HTN, race and ethnicity, age, and risk of future cardiovascular events dictate the intensity and choice of treatment. Treatment may include nonpharmacological interventions alone or in conjunction with pharmacological management (Whelton et al., 2018).
The AHA has developed a clinical algorithm to guide the treatment of HTN. The basic premise is that patients with normal BP (under 120/80 mmHg) should be instructed to continue with primary prevention techniques and lifestyle choices, such as a healthy diet, regular physical activity, tobacco cessation (if applicable), weight loss (if applicable), and moderation of alcohol intake. Their BP should be reassessed annually. Those with elevated BP (SBP 120-129, DBP < 80 mmHg) should be counseled on nonpharmacological treatment options (below) and reassessed every 3-6 months. Those categorized as stage 1 (BP 130-139/80-89 mmHg) should be stratified based on cardiovascular risk. Nonpharmacological treatment options and follow-up in 3-6 months are recommended in those with a 10-year risk below 10%. Nonpharmacological treatment options, medication, and follow-up in 1 month are recommended in those with stage 1 disease and cardiovascular risk > 10% or stage 2 disease (BP ³ 140/90 mmHg). Once their BP goals have been met, those with higher-risk stage I or stage 2 disease can be reassessed every 3-6 months (AHA, 2018b).
There are both modifiable and nonmodifiable risk factors associated with HTN. Modifiable risk factors can be addressed through nonpharmacological interventions and lifestyle changes. These interventions can be implemented alone to prevent the development of HTN in those with high-risk or elevated BP (120-129 SBP and DBP < 80 mmHg) or as the primary treatment option for those individuals with stage 1 HTN with no atherosclerotic cardiovascular disease (ASCVD) and a 10-year CVD risk less than 10%. Those with stage 2 HTN also benefit from nonpharmacologic interventions in conjunction with pharmacological treatment (Goetsch et al., 2021; Whelton et al., 2018). The most proven nonpharmacological interventions for the prevention and treatment of HTN include:
- smoking cessation
- diabetes management
- dietary changes
- weight loss
- increased physical activity
- decreased alcohol consumption
Tobacco cessation is encouraged, and supportive resources should be shared with the patient. The CDC offers resources to support patients' journey toward a tobacco-free life. A hotline called Quitline offers 24/7 access to coaches to support individuals quitting smoking or tobacco use. In addition to coaching, the Quitline can provide the individual with resources within their geographical area, including support groups. Patient information is available in several languages for the most significant level of support to those trying to quit smoking. Other tools available through the CDC include a quitSTART mobile app, free texts to support quitting, and guidance on making a quit plan (CDC, 2023b).
Patients with co-existing type 2 diabetes can decrease their risk of HTN-related complications with lifestyle changes. Type 2 diabetes is a factor that can be modifiable through control of blood glucose levels (HbA1c below 6%), tobacco cessation, weight loss, dietary changes, and engaging in moderate-intensity physical activity. The benefits of controlling blood glucose levels and decreasing cardiovascular risk are related. Diabetes is a strong risk factor for ASCVD and is incorporated in the 10-year ASCVD calculator. Diabetes also increases an individual's risk of developing other microvascular complications, including renal disease. Controlling diabetes can directly influence BP control, decreasing mortality and morbidity from ASCVD and subsequent heart failure (ElSayed et al., 2023).
Research has shown that increased lipoprotein levels can contribute to cardiovascular risk in those patients with HTN. Lipids can be controlled through a healthy diet low in saturated fats and avoiding trans-fatty acids. Dyslipidemia is a condition that includes elevated levels of low-density lipoprotein (LDL) and triglycerides within the blood. Those with high levels of lipids are at a higher risk of coronary artery disease (CAD) and vessel damage, thus increasing BP. Those with diabetic dyslipidemia have high levels of LDL and triglycerides but also a decrease in high-density lipoprotein (HDL), leading to poor cardiovascular outcomes. Dyslipidemia is treated like HTN with lifestyle modifications and pharmacological interventions. To improve LDL, a diet focusing on the intake of vegetables, fruits, legumes, nuts, and whole grains is recommended, with no more than 35% of daily calories coming from total fats and no more than 7% from saturated fats. Trans fats should be avoided entirely. Exercise and glycemic control will further improve cholesterol levels and decrease vascular damage. It is recommended that individuals engage in 150 minutes of moderate-intensity or 75 minutes of vigorous-intensity activity weekly. When lifestyle changes are not enough, statins, niacin, and fish oil may be integrated into the treatment regime (Arnett et al., 2019).
Weight loss and weight management are the optimal nonpharmacological intervention for lowering BP. This can be achieved through decreased caloric intake, increased physical activity, and dietary changes. A 1 kg (2.2 lbs) decrease in body weight can lower BP by 1 mmHg. Dietary changes that improve HTN and can help facilitate weight loss include The Dietary Approaches to Stop Hypertension (DASH) or the Mediterranean diet (described in Table 6). The DASH diet was explicitly designed to reduce BP and is considered the most effective diet for lowering BP. The DASH diet is associated with a 20% decrease in CVD risk and a reduction in BP by 11 mmHg. Due to the increased consumption of fruits, vegetables, and low-fat dairy options, this change in diet can lead to an increase in potassium, calcium, magnesium, and fiber intake. It is recommended that an individual consumes 3500-5000 mg of potassium per day. Although supplementation with potassium chloride can be effective, dietary intake of increased potassium is more beneficial. This amount can decrease BP by 4 to 5 mmHg or even twice that in individuals that consume a high-sodium diet. There is also a correlation between alcohol consumption and BP, especially in those individuals that consume more than three alcoholic drinks per day (equivalent to more than 36 ounces of beer, 15 ounces of wine, or 4.5 ounces of distilled spirits). Reducing alcohol intake to no more than two drinks per day for men and one for women can decrease BP by 4 mmHg (Benson & Hayes, 2020; Whelton et al., 2018). Providers should be cognizant of the challenges many patients face when trying to incorporate lifestyle changes, such as a lack of social support and limited access to healthy food choices and locations to engage in physical activity (Whelton et al., 2018).
Overview of the DASH and Mediterranean Diets
6 oz/day (at least 3 oz whole grains)
2-3 servings/day (low-fat dairy)
Nuts, seeds, legumes
5 oz/week of nuts and seeds; 0.5 cups/week of legumes
Fats and oils
27 grams/day (2 Tbsp); extra virgin oil preferred
Meat, eggs, fish
6.5 oz/day; 15 oz/week fish, 26 oz/week meat and eggs
≤ 5 servings/week
< 13% of calories (approximately 260 calories)
< 1,500 mg/day for those with HTN
Encourage the use of herbs and spices instead of added salt
Men: <2 drinks/day
Women: < 1 drink/day
Wine (preferably red) allowed during meals
(Benson & Hayes, 2020)
Increased physical activity can lead to weight loss, reduced BP, and improved cardiovascular health. Different types of exercise can decrease BP, including aerobic, dynamic resistance, and isometric resistance. Studies have demonstrated that both high and low-intensity workouts that are continuous or utilize an interval format can lead to BP reduction. The ACC/AHA recommends engaging in 90 to 150 minutes of aerobic exercise per week, and following this recommendation can decrease BP by 5 to 8 mmHg. Completing dynamic resistance exercises 90 to 150 minutes per week can reduce BP by 4 mmHg. Adding isometric resistance exercises thrice weekly can decrease BP by 5 mmHg (Whelton et al., 2018).
Obstructive sleep apnea (OSA) is recognized as a secondary cause of HTN and produces surges in both SBP and DBP that cause continued HTN during the day and the night. Treatment of OSA through nasal continuous positive airway pressure (CPAP) prevents apneic episodes and can slightly improve BP by 2 to 3 mmHg when used regularly (Whelton et al., 2018).
Pharmacologic treatment is based on BP and the patient's risk of CVD. Individuals with stage 1 HTN (BP of 130-139/80-89 mmHg) in addition to ASCVD or a 10-year CVD risk at least 10% should have pharmacological and nonpharmacological treatment initiated at the time of diagnosis. Patients diagnosed with stage 2 HTN (BP above 140/90 mmHg) should be treated with nonpharmacological and pharmacological management. The HCP may initiate at least two antihypertensive medications from different drug classes for patients with stage 2 HTN. If the patient presents with a BP greater than 160/100 mmHg, treatment will be initiated promptly with close monitoring and dosage adjustments (Whelton et al., 2018).
Individualized therapy should consider age, comorbidities, concurrent medication use and potential interactions, BP history, out-of-pocket costs, and the ability of the patient to adhere to the recommended treatment and follow-up plan. Setting BP goals and choosing an antihypertensive agent should be a collaboration between the prescriber and the patient. Once-daily dosing is preferred for medication compliance, particularly for older patients, due to the decrease in compliance that polypharmacy can cause. There are many antihypertensive drugs available (Whelton et al., 2018). Classes that have been shown to reduce BP and the risk of cardiovascular events are preferential. The ACC/AHA recommends the following categories of medications as first-line agents for the treatment of HTN (see Table 7):
- thiazide or thiazide-type diuretics
- angiotensin-converting enzyme (ACE) inhibitors
- angiotensin receptor blockers (ARBs)
- calcium-channel blockers (CCBs; Whelton et al., 2018)
Primary Agents Used in HTN
Thiazide or thiazide-type diuretics
Metolazone (Mykrox, Zaroxolyn)
Electrolyte imbalance (especially potassium), elevated cholesterol, hypercalcemia, hyperglycemia, photosensitivity
Lisinopril (Prinivil, Zestril)
Dry cough, dysgeusia, fatigue, headaches, hyperkalemia, hypotension, proteinuria, rash, tachycardia, angioedema of the face and limbs
May cause severe anaphylactoid reactions
Dizziness, fatigue, headaches, peripheral edema, angina, sinusitis, abdominal pain, diarrhea, nausea, vomiting, albuminuria, back pain, bronchitis, upper respiratory infection, angioedema
Nicardipine SR (Cardene SR)
Nifedipine LA (Procardia XL)
Headaches, fatigue, dizziness, somnolence, edema, nausea, abdominal pain, flushing, palpitations, dyspnea, pruritis, rash
Associated with dose-related pedal edema
Avoid taking them with a high-fat meal
Diltiazem ER (Dilacor XR)
Verapamil IR (Calan)
Verapamil SR (Calan SR)
Verapamil-delayed onset ER (Verelan PM)
Headaches, dizziness, somnolence, edema, arrhythmia, AV block, bradycardia, hypotension, flushing, nausea, constipation, hepatic injury
(Whelton et al., 2018; Woods, 2023)
Although other medications are effective in reducing BP, these medications are not used as a first-line treatment due to less effective reduction in cardiovascular risk, poor tolerability, or safety concerns and contraindications (Whelton et al., 2018). The following six classes of medications are recommended as second-line agents for the treatment of HTN (see Table 8):
- diuretics, including loop, potassium-sparing, and aldosterone antagonists
- beta-blockers, including cardioselective, vasodilatory, non-cardioselective, intrinsic sympathomimetic activity, and combined alpha- and beta-receptors
- direct renin inhibitors
- alpha-1 blockers
- central alpha-2 agonists
- direct vasodilators (Whelton et al., 2018)
Secondary Agents Used in HTN
Hypokalemia, hyperuricemia, hypomagnesemia, hypovolemia, vertigo, orthostatic hypotension, dehydration, photosensitivity; can cause hearing loss and tinnitus following rapid parenteral administration
Hyperkalemia, nausea, vomiting, headaches, weakness, fatigue, cough, and dyspnea
Aldosterone antagonist diuretics
Headaches, drowsiness, confusion, ataxia, diarrhea, ulceration, nausea, vomiting, gastritis, renal failure, erectile dysfunction, menstrual disturbances, hyperkalemia, hypovolemia, gout, Stevens-Johnson syndrome
Metoprolol succinate (Toprol XL)
Metoprolol tartrate (Lopressor)
Dizziness, fatigue, lethargy, vertigo, fever, light-headedness, orthostatic hypotension, bradycardia, heart block, intermittent claudication, atrial fibrillation, bronchospasm, dyspnea, wheezing, nausea, diarrhea, supraventricular tachycardia
Should not be discontinued abruptly
Apical pulse should be evaluated before administration
Propranolol IR (Inderal)
Propranolol LA (Inderal LA)
Fatigue, lethargy, vivid dreams, agitation, hallucinations, dizziness, insomnia, hypotension, bradycardia, heart failure, abdominal cramping, constipation, diarrhea, vomiting, nausea, bronchospasm, peripheral vascular insufficiency
Should not be discontinued abruptly
Combined alpha- and beta-receptor beta blockers
Dizziness, fatigue, headaches, fever, vertigo, somnolence, insomnia, paresthesia, hypotension, bradycardia, AV block, syncope, angina, hypovolemia, edema, blurred vision, diarrhea, vomiting, nausea, melena, erectile dysfunction, albuminuria, hematuria, hyperkalemia, hypoglycemia, cough
Should not be discontinued abruptly
Direct renin inhibitor
Headaches, dizziness, fatigue, seizures, hypotension, abdominal pain, diarrhea, gastroesophageal reflux, cough, upper respiratory infection, rash, angioedema, hyperkalemia
Should not be taken with a high-fat meal
Dizziness, headaches, vertigo, somnolence, drowsiness, orthostatic hypotension, edema, tachycardia, abdominal pain, nausea, vomiting, dry mouth, blurred vision, erectile dysfunction, rash, pruritus, dyspnea
May cause orthostatic hypotension, particularly in individuals over 65
Centrally acting alpha-2 adrenergic agonists
Clonidine oral (Catapres)
Clonidine patch (Catapres-TTS-1)
Drowsiness, dizziness, sedation, weakness, fatigue, agitation, depression, bradycardia, orthostatic hypotension, severe rebound HTN, constipation, dry mouth, anorexia, nausea, vomiting, erectile dysfunction, weight gain, urinary retention;
the use of clonidine transdermal patch may cause pruritus and dermatitis; methyldopa (Aldomet) can cause decreased mental acuity, parkinsonism, Bell's palsy, nightmares, involuntary movements, black tongue, breast enlargement, and salivary gland inflammation
Should not be discontinued abruptly due to the risk of hypertensive crisis
Anxiety, headaches, depression, increased intracranial pressure, angina, tachycardia, orthostatic hypotension, nausea, vomiting, diarrhea, anorexia, urinary retention, diaphoresis, neutropenia, thrombocytopenia, anemia, leukopenia, agranulocytosis, dyspnea
May cause a drug-induced lupus-like syndrome
Should be taken with food to increase absorption
Minoxidil (Loniten) may cause fluid retention, pericarditis, pericardial effusion and tamponade, hypertrichosis, thrombocytopenia, nausea, vomiting, hirsutism
(Whelton et al., 2018; Woods, 2023)
Initial treatment is based on patient presentation and the presence of comorbidities, ASCVD, and 10-year CVD risk. Patients with stage 2 HTN are typically started on two antihypertensive drugs from different classes. Many individuals initially treated with monotherapy will eventually require at least two medications to control BP. The second medication is often from another drug class and has a complementary mechanism of action that can offset the body's compensatory response to the initial antihypertensive drug. Many combination medications are available to provide multiple medications in a single pill, which is preferred over free equivalents (medications provided in individual formulations). Utilizing combination pills can increase compliance and lead to better BP control and quicker goal attainment. Once an effective dosage is reached, the patient will be switched to the single-pill combination formulation (Mann & Flack, 2023; Whelton et al., 2018).
There have been discrepancies among HCPs regarding morning versus evening dosing of antihypertensive medications. The Treatment in Morning versus Evening (TIME) study aimed to determine if the time of administration impacts medication effectiveness and patient outcomes. The TIME study included 21,104 individuals randomly assigned to morning and evening administration groups over 7 years from 2011 to 2018. This study determined no differences in cardiovascular outcomes based on the timing of once-daily medication administration. Based on this data, patients can be advised to take their once-daily antihypertensive medications at a time that is convenient for their lifestyle. These recommendations do not apply to diuretics, which should be administered upon waking to minimize sleep disruptions due to increased urination (Mackenzie et al., 2022).
Further considerations should be given to the role of concomitant medications prescribed for other conditions, such as those used to treat diabetes. For instance, insulin stimulates the sympathetic nervous system, promoting renal sodium retention and vascular smooth muscle hypertrophy, which can increase BP. Sodium-glucose cotransport 2 inhibitors(SGLT2i) such as canagliflozin (Invokana), dapagliflozin (Farxiga), and empagliflozin (Jardiance) cause weight loss, have a mild diuretic effect, improve arterial stiffness, reduce sympathetic activity, and suppress the renin-angiotensin cycle which can result in a reduction of SBP by 3-6 mmHg and DBP by 1-2 mmHg. Glucagon-like peptide 1 receptor agonists such as liraglutide (Victoza) or dulaglutide (Trulicity) are also associated with a reduction in SBP of 2-3 mmHg and DBP of 0-1 mmHg (Li et al., 2022).
Patients with resistant HTN who do not meet BP targets on conventional drug therapy with three drugs, including a diuretic, are typically referred to a hypertension specialist. Before diagnosing resistant HTN, the nurse should confirm that medication compliance is not a contributing factor. Common causes for noncompliance include medication cost, side effects, or polypharmacy. Aldosterone antagonist diuretics can be effective in patients with resistant HTN and type 2 diabetes who are already on an ACE/ARB, a diuretic, and a CCB. An increased risk for hyperkalemia should be discussed and screened for regularly (Whelton et al., 2018).
Treating HTN in patients with diabetes at risk for kidney disease can be challenging. An ACE inhibitor or ARB is considered the first-line treatment in patients with diabetes and albuminuria. These drugs slow the progression of renal disease in comparison to other classes of antihypertensives. When multi-drug treatment is required, combining an ACE inhibitor with an ARB or direct renin inhibitor is not recommended due to the risk of hyperkalemia, syncope, and acute kidney injury (AKI). Thiazide-like diuretics such as HCTZ (Hydrodiuril) can be effective in reducing volume as well as reducing systemic potassium levels. With advanced renal disease and an eGFR of 30 mL/min/1.73 m2 or less, a long-acting loop diuretic is preferred, such as torsemide (Demadex; ElSayed et al., 2022; Whelton et al., 2018).
Pregnant individuals who are not taking antihypertensive medications before pregnancy, or are not taking an effective regimen, may be started on labetalol (Trandate) or nifedipine (Procardia) as indicated. These medications have been used extensively during pregnancy and have well-documented safety profiles for this patient population. The risks versus benefits of continuing that regimen must be determined based on the individual patient and clinical presentation for patients who become pregnant while already following an effective medication regimen. ACE inhibitors and ARBs have been associated with fetal malformations and neonatal complications, including intrauterine growth restriction (IUGR) and kidney failure. Therefore, women of childbearing age taking ACE inhibitors and ARBs should be counseled on the risks of becoming pregnant while taking these medications. Before pregnancy, these medications should be discontinued, and the treatment regimen should be adjusted whenever possible. Aldosterone antagonists, including spironolactone (Aldactone) and eplerenone (Inspra), should also be avoided during pregnancy, as they can cause a male fetus to develop feminine features (Chandrasekaran et al., 2022; Friel, 2022).
Due to the increased risk of HTN for non-Hispanic Blacks, meticulous screening, aggressive management with specific medications, and education are crucial. Lifestyle modifications are essential in this patient population. The pharmacological management of HTN in non-Hispanic Black individuals follows similar guidelines to those outlined above; however, in this patient population, thiazide-type diuretics and CCBs are more effective at controlling BP, and the use of two or more antihypertensive drugs may be required to achieve goal BP (Whelton et al., 2018).
There are age-related considerations in the treatment of HTN. SBP and DBP increase in the 5th and 6th decade of life due to age-related cardiovascular system changes. Additional treatment considerations in this population include comorbidities, frailty, cognitive function, polypharmacy, and life expectancy. For patients considered in good health with few comorbidities, the treatment regime is similar to adult patients under 65. Individuals that experience frequent falls, have advanced cognitive impairment, or have multiple comorbidities may experience adverse effects from intensive BP lowering; therefore, a higher SBP goal should be considered in these patients. Individuals with a limited life expectancy should be treated based on patient preference and clinical judgment related to the risks versus benefits of treatment (Whelton et al., 2018).
Follow-up visits to the primary provider for the reassessment of BP and to monitor for adherence and response to the medication regime are recommended based on the patient's baseline BP and stage of HTN. Those with normal BP should be monitored annually at routine office visits. Those with an elevated BP (120-129/<80 mmHg) or stage 1 HTN without ASCVD or a 10-year CVD risk of less than 10% should be monitored every 3 to 6 months. Patients with stage 1 HTN with ASCVD or a 10-year CVD risk greater than 10% or stage 2 HTN on pharmacological treatment should be reassessed in 1 month. If the established BP goal is met, a reassessment should occur every 3 to 6 months (Whelton et al., 2018).
For more information on hypertension during pregnancy, see the NursingCE course Maternal Hypertension.
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