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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).
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Diagnosing and Managing Hypertension for Nurses
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 and the leading cause of death and disability in the world. 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 cardiovascular diseases (CVDs). HTN is cited as the leading cause of coronary artery disease (CAD), stroke, heart failure, atrial fibrillation, dementia, and chronic kidney disease. It is a more prevalent risk factor for premature CVD than any other modifiable risk factor, such as smoking, diabetes, or dyslipidemia. It also often coexists with these risk factors and others such as elevated body mass index (BMI), physical inactivity, and an unhealthy diet. HTN is called the "silent disease," as early stages of HTN have no clinical manifestation (other than the elevated BP). In 2025, the American College of Cardiology (ACC) and American Heart Association (AHA)Joint Committee released new HTN guidelines to replace those released in 2017 (Basile & Bloch, 2025; Jones et al., 2025; Rogers & Brashers, 2023, p. 1066).
Epidemiology
Nearly half (48.1% or 119.9 million) of adults in the US have HTN, while only about 25% (27 million) of these adults have their HTN under control. This number is likely an underrepresentation of adults with HTN, as 1 in 5 individuals with high blood pressure (BP) is unaware. In 2023, HTN contributed to 664,470 deaths in the US. Around 20% of deaths related to coronavirus disease of 2019 (COVID-19) were individuals with HTN. Additionally, approximately half (45% or 37 million) of adults in the US with uncontrolled HTN have a baseline BP greater than 140/90 mmHg. HTN is more common in some areas of the country, such as the southeast. It is almost more common in males than females, and more common in non-Hispanic Black adults (58%) than non-Hispanic white adults (49%), non-Hispanic Asian adults (45%), or Hispanic adults (39%; Centers for Disease Control and Prevention [CDC], 2025b).
The effects of uncontrolled HTN are costly to the individual and the US healthcare system, being one of the costliest health conditions in the country. The most recent data shows the annual costs linked to high BP in the US are estimated at $219 billion. The total medical costs in 2021, including healthcare services and medications, are $2,759 higher annually for individuals with HTN than for those without. Additionally, as HTN is the most common modifiable risk factor associated with CVD, it has another significant impact on healthcare costs. An estimated 1 in 8 dollars spent on health care is associated with CVD, and CVD also contributes to increased Medicare costs (CDC, 2025a). Among individuals who are privately insured, one study found that HTN was associated with an annual $328 higher out-of-pocket costs and $3272 higher inpatient expenditure costs (Kumar et al., 2024).
Types of Hypertension
The most common type of HTN is primary HTN (also referred to as idiopathic and essential HTN), which is not caused by an existing health condition or medication. The development of primary HTN is a result of environmental influences (i.e., diet and lifestyle) and genetic factors. Examples of genetic factors associated with primary HTN include impaired excretion of renal sodium and insulin sensitivity. Ninety to 95% of causes of HTN are primary, while the other 5 to 10% are secondary HTN (Rogers & Brashers, 2023, pp. 1062-1063).
Secondary HTN is caused by certain disease states or drugs that can increase BP. Renovascular is one of the most common causes of secondary HTN. Renal artery stenosis, the narrowing of one or more of the main arteries carrying blood to the kidneys, can lead to HTN. These patients may benefit from the dilation of these arteries through angioplasty and stent placement (Cohen, 2025; White, 2025). Other common causes include primary kidney disease, primary aldosteronism, and obstructive sleep apnea (OSA). 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. Less common causes of secondary HTN include oral contraceptive use, pheochromocytomas, Cushing's syndrome, coarctation of the aorta, hypothyroidism, and primary hyperparathyroidism. 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 (White, 2025). Medications that may cause secondary HTN include glucocorticoids, non-steroidal anti-inflammatories (NSAIDs), erythropoietin (Epogen), estrogen-containing oral contraceptives, antidepressants (tricyclic antidepressants, monoamine oxidase inhibitors, and selective serotonin reuptake inhibitors), decongestants, sodium-containing antacids, stimulants, atypical antipsychotics, angiogenesis inhibitors, and tyrosine kinase inhibitors (Basile & Bloch, 2025).
A hypertensive emergency is a severe form of HTN where the BP is elevated greater than 180/120 mm Hg, and there are signs of acute target organ damage. Conditions associated with target organ damage include acute HF/pulmonary edema, encephalopathy, intracranial hemorrhage, acute ischemic stroke, acute kidney injury, and aortic dissection. Immediate intervention is required for these patients to prevent further organ damage. Alternatively, for patients with severe HTN without signs of acute target organ damage (previously called hypertensive urgency), their BP should not be aggressively lowered in a short period of time due to concerns of vital organ hypoperfusion related to autoregulation. For these patients, oral antihypertensive medication in the...
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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 (the volume 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 by the heart rate. Since BP depends on cardiac output and PVR, anything that increases the PVR or cardiac output (heart rate or stroke volume increase) increases the BP. Conversely, anything that decreases PVR or cardiac output (heart rate or stroke volume 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. These regulatory mechanisms include:
- the autonomic nervous system, which acts on the sympathetic nervous system in response to impulses received from peripheral chemoreceptors and baroreceptors
- the kidneys, which control the renin-angiotensin-aldosterone system (RAAS) based on vascular volume and flow rate
- the endocrine system releases hormones (e.g., serotonin, histamine, catecholamine) to stimulate the sympathetic nervous system (Egan, 2026; Rogers & Brashers, 2023, pp. 1062-1065)
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 and can also lead to elevated BP. The RAAS 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, an indication of 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 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 (Egan, 2026; Rogers & Brashers, 2023, pp. 1062-1065).
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. Modifiable risk factors that can increase an individual's risk of developing HTN include:
- cigarette smoking
- elevated BMI and weight gain
- lack of physical activity
- heavy alcohol intake
- insufficient magnesium, potassium, or calcium intake
- high dietary sodium intake
- insufficient sleep
- increased stress
- noise and air pollution (Egan, 2026; Rogers & Brashers, 2023, p. 1063)
Non-modifiable risk factors include:
- family history
- Black race (highest rate of HTN)
- advancing age
- reduced nephron number (genetics)
- low socioeconomic/educational status
- history of gestational HTN or preeclampsia (Egan, 2026; Rogers & Brashers, 2023, p. 1063)
While many of the risk factors for HTN are non-modifiable, 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 systolic blood pressure (SBP) or diastolic blood pressure (DBP) can significantly decrease their overall health risks. Optimal control of BP reduces cardiovascular, cerebrovascular, and kidney problems, and associated mortality related to these conditions. Nurses should encourage patients to monitor their BP at home and use online resources like those through the AHA to track their progress. This resource helps patients self-monitor their BP readings at home to maintain a healthy heart (AHA, 2025; Egan, 2026).
Healthy People 2030 includes preventing heart disease and stroke and improving cardiovascular health. As a part of this, the campaign focuses on HTN with several objectives that attempt to decrease cardiovascular mortality and morbidity through prevention. 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.)
Diagnosis
Although HTN often has no apparent symptoms, there may be indications of HTN present on physical examination. Patient evaluation should focus on identifying target organ damage and possible secondary causes of HTN. Correctly identifying the underlying cause of HTN can aid in planning an effective treatment regimen. 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, 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 physical assessment. A difference between BP readings in each arm or an upper and lower extremity may indicate the presence of coarctation of the aorta. Elevated creatinine or abnormal urinalysis may indicate primary kidney disease. Loud snoring may suggest OSA. The presence of thin skin, hyperglycemia, and bruising may suggest an endocrine disorder. When assessing the neck, the presence of an enlarged, palpable thyroid may indicate the presence of a thyroid disorder, a cause of secondary HTN (Basile & Bloch, 2025; White, 2025).
Herbals (i.e., ginseng, bayberry, liquorice, and blue cohosh), over-the-counter (OTC) medications (i.e., decongestants), illegal substances (i.e., cocaine) 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 (Basile & Bloch, 2025; Saper, 2025). Table 1 outlines the clinical indications and diagnostic testing for common causes of secondary HTN.
Table 1
Diagnostics for Common Causes of Secondary Hypertension
Common Cause | Prevalence | Clinical Indications | Physical Examination | Screening Test |
Renovascular HTN | 0.1-5% | Resistant HTN; abrupt onset HTN; early-onset HTN | Abdominal S/D bruit; bruits over the carotid artery | Renal duplex Doppler ultrasound; abdominal CT |
Chronic kidney disease | 14% | Diabetes, hematuria, family history of polycystic kidney disease, increased serum creatinine, abnormal urinalysis | Palpable kidneys, abdominal mass, pallor | Electrolytes, serum creatinine, urinalysis, renal ultrasound, urine microalbumin, serum cystatin C |
Primary aldosteronism | 5-25% | 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. |
OSA | 25-50% | Resistant HTN; snoring; fitful sleep; breathing pauses during sleep; daytime sleepiness | Elevated BMI, increased waist circumference | Berlin Questionnaire; Epworth Sleepiness Score; overnight oximetry |
Alcohol or drug-induced | 2-20% | 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) |
(Basile & Bloch, 2025; Jones et al., 2025; White, 2025)
Uncommon diagnostics that may be considered are plasma thyroid hormone 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 (Jones et al., 2025; White, 2025).
Nurses should determine the patient’s goals and risk tolerance for therapy. Older adults may have multiple chronic conditions, weakness, or frailty, and the 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 (Thomas et al., 2026).
The criteria for diagnosing HTN require accurate BP measurements. Common errors in measurement technique that occur involve patient preparation and positioning, equipment, and the environment. BP measurements that are elevated enough to be classified as any form of HTN should be repeated on multiple occasions to make a diagnosis. 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 nurse 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 (Jones et al., 2025; Thomas et al., 2026). Table 2 contains a detailed outline for accurately performing a BP measurement.
Table 2
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 |
|
(Jones et al., 2025, Thomas et al., 2026)
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. A standard BP cuff is 12 x 23 cm, which would be appropriate to measure the BP of an individual with an arm circumference up to 28 cm. When choosing cuff size, the bladder length of the cuff should be at least 80% of the arm circumference, and the bladder width should be 40% 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. If the patient has a large arm circumference, a 16 cm wide cuff is recommended. However, if the individual has a large arm circumference but a short upper arm, a thigh cuff or a very long cuff may be needed. If the arm circumference is greater than 50 cm and a thigh cuff is not appropriate, then utilize a cuff around the forearm and keep the forearm at heart level, feeling for the radial pulse. For adults with a very small arm circumference, a pediatric cuff may be needed (Bickley et al., 2021, p. 222). Cuffless devices and smartwatches should not be used or recommended to measure BP until further reliability and precision can be studied (Jones et al., 2025).
Categories for Blood Pressure Classification
In 2025, the ACC/AHA Joint Committee released its most updated HTN diagnostic guidelines. Some of the new or substantially revised recommendations since the 2017 guidelines are included in Table 3.
Table 3
What is New in 2025 Guidelines
New or Revised Recommendation | 2025 Recommendation |
New terminology | Severe HTN replaced hypertensive urgency. |
New | Screen for primary aldosteronism regardless of the presence of hypokalemia in adults with resistant HTN. |
New | Continue most antihypertensive medications (except mineralocorticoid receptor antagonists) when screening for primary aldosteronism is indicated. |
New | Potassium-based salt substitutes may be used to treat or prevent HTN in individuals without CKD or individuals who are on medications that reduce potassium excretion. |
Revised | For adults with HTN who do not have clinical but have diabetes, CKD, or a 10-year CVD risk of 7.5% or higher (as determined by PREVENT), it is recommended to start BP-lowering medications when the average SBP is 130 mm Hg or higher, and the average DBP is 80 mm Hg or higher. |
Revised | For adults with HTN who do not have clinical CVD and have an estimated 10-year CVD risk of less than 7.5% according to PREVENT, it is recommended to start BP-lowering medications if, after a 3- to 6-month trial of lifestyle changes, the average SBP remains at or above 130 mm Hg or the average remains at or above 80 mm Hg. |
Revised | For adults with diabetes and HTN, it is recommended to use angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) if CKD is present, indicated by an estimated glomerular filtration rate (eGFR) of less than 60 mL/min/1.73 m² or albuminuria of 30 mg/g or higher. These medications should also be considered when mild albuminuria (less than 30 mg/g) is present to help slow the progression of diabetic kidney disease. |
Revised | For adults with HTN and CKD, identified by an eGFR of less than 60 mL/min/1.73 m² and albuminuria of 30 mg/g or higher, it is recommended to use RAAS inhibitors (RAASi), either an ACE inhibitor or an ARB, but not both. |
New | For adults with resistant HTN, conducting a thorough evaluation for secondary causes, including a careful review of all medications and eliminating those that adversely affect BP, is beneficial for lowering BP and simplifying treatment. |
New | For adults with severe HTN (over 180/120 mm Hg) who are hospitalized for non-cardiac conditions and show no signs of acute target organ damage, it is not recommended to use additional intravenous or oral antihypertensive medications intermittently to rapidly lower BP. |
(Jones et al., 2025)
Since individual BP measurements can fluctuate unpredictably or randomly, a single reading is insufficient for making clinical decisions. 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. Out-of-office BP measurements should be used to recognize masked or white-coat HTN (Jones et al., 2025).
The 2025 ACC/AHA HTN Guidelines categorize BP as normal, elevated, HTN stage 1, or HTN stage 2. The 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 a DBP greater than 80 mmHg. These categories remain consistent in the 2025 guidelines. Refer to Table 4 for ACC/AHA BP classifications.
Table 4
ACC/AHA Blood Pressure Classifications
Category | Systolic Blood Pressure (mmHg) | And/Or | Diastolic Blood Pressure (mmHg) |
Normal | < 120 | And | < 80 |
Elevated BP | 120 - 129 | And | < 80 |
HTN, stage 1 | 130 - 139 | Or | 80 - 89 |
HTN, stage 2 | ≥ 140 | Or | ≥ 90 |
(Jones et al., 2025; Whelton et al., 2018)
For individuals newly diagnosed with HTN, conducting a comprehensive medical history, physical examination, and routine laboratory tests is beneficial for establishing baseline CVD risk and guiding management decisions. Relevant laboratory tests should be repeated at least annually to monitor potential adverse effects of treatments, assess the development or progression of kidney disease, and track changes in predicted CVD risk (Jones et al., 2025).
The 2025 ACC/AHA HTN Guidelines recommend using the PREVENT calculator to estimate the 10-year CVD risk for adults with HTN who do not have clinical CVD, to determine the BP threshold for starting treatment. PREVENT assesses the risk of total CVD, including myocardial infarction, stroke, and heart failure, which is particularly relevant since studies on antihypertensive treatments and BP thresholds have concentrated on major adverse cardiovascular events as the primary outcome. PREVENT is applicable to adults aged 30 to 79 and considers statin therapy as a factor, making it more widely applicable for guiding preventive decisions about antihypertensive treatment. PREVENT also includes kidney function metrics and place-based social risk factors (Jones et al., 2025).
As described above, patients should be screened for white-coat HTN or masked HTN. The use of out-of-office BP monitoring allows for the classification of HTN into these clinically relevant categories based on the difference between in-office and out-of-office BP readings. Due to these conditions, individuals 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. There is limited data on the cardiovascular risks of not treating white-coat HTN and not intensifying treatment for the white-coat effect, as well as the benefits of treating masked HTN and intensifying treatment for masked uncontrolled HTN (Jones et al., 2025; Thomas et al., 2026).
Maternal Hypertension
HTN during pregnancy can bring unique complications. The health of the pregnant individual and that of the fetus are both compromised. Due to vascular and hemodynamic changes during pregnancy, BP typically decreases by 10% in early pregnancy, reaches its lowest point in the second trimester, and gradually returns to baseline by the end of the third trimester. HTN in pregnancy is caused by four different disorders collectively known as hypertensive disorders of pregnancy (HDP). These disorders are the number one cause of pregnancy-associated mortality. They impact 15.9% of deliveries in the US and are more prevalent among Black and Indigenous Peoples, individuals 35 years of age and older, and individuals with elevated BMI. HDP consists of chronic HTN, gestational HTN, preeclampsia, and preeclampsia superimposed over chronic HTN. Refer to Table 5 for further classification of each of these disorders.
Table 5
Classification of Hypertensive Disorders of Pregnancy
Category | Definition |
Chronic HTN | HTN diagnosed before pregnancy or at less than 20 weeks of gestation |
Gestational HTN | New-onset HTN at 20 weeks of gestation or later, without proteinuria or other indicators of preeclampsia |
Preeclampsia | Gestational HTN accompanied by proteinuria or other signs of maternal end-organ dysfunction |
Preeclampsia superimposed on chronic HTN | Preeclampsia that occurs in an individual who had HTN prior to pregnancy or before reaching 20 weeks of gestation |
(Jones et al., 2025)
The primary goals of antihypertensive treatment during pregnancy are to prevent severe HTN and preeclampsia and to optimize clinical outcomes for both the mother and the fetus/neonate. Unlike the diagnostic criteria for HTN in adults outlined in the 2025 ACC/AHA HTN Guidelines, the American College of Obstetricians and Gynecologists (ACOG) defines HTN in pregnancy as a SBP of 140 mm Hg or higher or a DBP of 90 mm Hg or higher on two occasions at least four hours apart. Severe-range HTN is defined as a sustained SBP of 160 mm Hg or higher or a DBP of 110 mm Hg or higher. In cases where the readings are extremely elevated (SBP ≥ 160 or DBP ≥ 110), a shorter interval between readings is indicated to expedite treatment. If severe HTN is left untreated, it can lead to maternal stroke, kidney insufficiency or failure, myocardial infarction, heart failure, placental abruption, preterm birth, fetal growth restriction, and maternal death due to intracerebral hemorrhage, as well as stillbirth or perinatal death (ACOG, 2019, 2020; Jones et al., 2025).
Individuals with gestational HTN or preeclampsia during pregnancy have an increased risk of CVD, stroke, peripheral artery disease, and cardiovascular mortality later in life. For individuals with recurrent preeclampsia in subsequent pregnancies or early-onset preeclampsia, this risk increases further. BP typically decreases immediately after childbirth and continues to drop for a few days before rising again three to five days postpartum, often when the patient is already at home. The initial decline is generally attributed to blood loss and the effects of analgesia, while the subsequent increase is likely due to the mobilization of extravascular fluid, leading to a rise in intravascular volume, as well as factors like pain. Due to this increased risk, it is recommended to have early postpartum visits for a BP check within 3 to 10 days after delivery or to engage in home BP monitoring once or twice daily, especially during the first two to three weeks postpartum. In cases of poorly controlled BP or when ongoing medication adjustments are necessary, more frequent visits for BP monitoring may be required, rather than following the standard schedule of two- to four-week intervals. (Jeyabalan & Larkin, 2025; Jones et al., 2025). There were four new recommendations included in the 2025 ACC/AHA HTN Guidelines regarding HTN and pregnancy. These include (Jones et al., 2025):
- Individuals who are pregnant with an SBP of 160 mm Hg or higher, or a DBP of 110 mm Hg or higher, confirmed by a repeat measurement within 15 minutes, should be given antihypertensive medication.
- Individuals who are pregnant with chronic HTN before 20 weeks of gestation should receive antihypertensive treatment to achieve BP levels below 140/90 mm Hg.
- Individuals with HTN who are planning to become pregnant or who are already pregnant should be advised about the benefits of taking low-dose aspirin to lower the risk of preeclampsia.
- Individuals with HTN who are planning to become pregnant or who are already pregnant should avoid treatment with atenolol (Tenormin), ACE inhibitors, ARBs, direct renin inhibitors, nitroprusside (Nipride, Nitropress), or mineralocorticoid receptor antagonists to prevent harm to the fetus.
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 myocardial infarction 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 (Jones et al., 2025; Mann & Flack, 2026).
Patients with a 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 or more often if indicated. 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 with close follow-up are recommended in those without clinical CVD. Nonpharmacological treatment options, medication, and close follow-up are recommended in those with stage 1 disease and clinical CVD. Medication should also be initiated in individuals with an SBP of 130 mmHg and higher or a DBP of 80 mmHg or higher without clinical CVD if they have diabetes, CKD, or increased short-term CVD risk. Among individuals without clinical CVD and lower short-term CVD risk, medication is recommended if SBP remains at or above 130 mmHg or DBP remains at or above 90 mmHg, despite 3 to 6 months of lifestyle interventions. In all adults, medication should be initiated if SBP is 140 mmHg or higher or DBP is 90 mmHg or higher (Jones et al., 2025).
Nonpharmacologic Interventions
As outlined above, there are both modifiable and non-modifiable risk factors associated with HTN. Modifiable risk factors can be addressed through nonpharmacological interventions and lifestyle changes. These interventions can be implemented to prevent the development of HTN in those with elevated BP or as the primary treatment option for those individuals with stage 1 HTN without clinical CVD and an estimated 10-year CVD risk less than 7.5% based on PREVENT. Those with stage 2 HTN also benefit from nonpharmacologic interventions in conjunction with pharmacological treatment. The most proven nonpharmacological interventions for the prevention and treatment of HTN include:
- smoking cessation (if applicable)
- dietary changes (e.g., healthy eating pattern, sodium restriction, potassium supplementation)
- weight loss (if BMI above 25)
- regular physical activity (exercise)
- decreased alcohol consumption
- stress reduction (Jones et al., 2025)
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. Pharmacotherapies may also be offered to patients who are ready to quit smoking. These include varenicline (Chantix), bupropion (Wellbutrin), and nicotine replacement therapies (i.e., patch, gum, lozenge; CDC, 2024; Rigotti, 2025).
Patients with co-existing type 2 diabetes mellitus can decrease their risk of HTN-related complications with lifestyle changes. Type 2 diabetes mellitus is a factor that can be modifiable through control of blood glucose levels (Hemoglobin A1c 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. 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 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 regimen (Arnett et al., 2019).
Weight loss and weight management are optimal nonpharmacological interventions for lowering BP. This can be achieved through decreased caloric intake, increased physical activity, and dietary changes. The 2025 ACC/AHA HTN Guidelines recommend at least 5% reduction in body weight for individuals with a BMI over 25 to prevent or treat elevated BP and HTN. 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; described in Table 6). The DASH diet was explicitly designed to reduce BP and is considered the most effective diet for lowering BP. The decrease in BP with this diet ranges from 1 to 13 mm Hg for SBP and from 1 to 10 mm Hg for DBP. Typically, the DASH eating plan leads to a more significant BP reduction in Black individuals, as well as in those with higher initial BP, individuals under 50 years of age, or those with a higher sodium intake at baseline exceeding 2400 mg per day. 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 consume 3500-5000 mg of potassium per day. Although supplementation with potassium chloride can be effective, increased dietary intake of potassium is more beneficial. On average, moderate potassium supplementation reduces BP by 6/4 mm Hg. These effects are more pronounced in individuals with HTN and those with higher sodium intake (4000 mg/day or more). There is also a correlation between alcohol consumption and BP, especially in those individuals who 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). Males should consume no more than two drinks per day and females no more than one drink per day. 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 (Forman, 2026; Jones et al., 2025).
Table 6
Overview of the DASH Diet
Food | DASH Diet |
Vegetables | 4-5 servings/day |
Fruit | 4-5 servings/day |
Grains | 6-8 servings/day |
Low-fat or fat-free dairy | 2-3 servings/day |
Nuts, seeds, legumes | 4-5 servings/week |
Fats and oils | 2-3 servings/day |
Meat, poultry, fish | 6 servings/day or less |
Sweets/sugar | ≤ 5 servings/week |
Sodium | < 1,500 mg/day for those with HTN |
(National Heart, Lung, and Blood Institute, 2026)
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. In adults with HTN, 90 to 150 minutes of aerobic exercise per week can decrease BP by 4 to 8 mmHg. Completing dynamic resistance exercises for 90 to 150 minutes per week can reduce BP by 2 to 7 mmHg. Adding isometric resistance exercises three times a week can decrease BP by 5 to 10 mmHg (Jones et al., 2025).
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. Weight loss combined with continuous positive airway pressure (CPAP) therapy can lower BP in adults with OSA and elevated BMI. CPAP can also reduce BP for adults with resistant HTN and moderate-to-severe OSA. Although CPAP is an effective treatment for OSA, current data do not support its use for preventing cardiovascular events or mortality in adults with moderate-to-severe OSA. The potential benefits of newer therapies for OSA, like hypoglossal nerve stimulation, have not yet been demonstrated for BP (Jones et al., 2025).
Pharmacologic Management
Pharmacologic treatment is based on BP and the patient's risk of CVD. All individuals with stage 2 HTN and individuals with stage 1 HTN and clinical CVD, diabetes, CKD, or increased short-term CVD risk should be initiated on pharmacologic management. Among individuals without clinical CVD and lower short-term CVD risk, medication is recommended if BP levels remain in the stage 1 HTN range, despite 3 to 6 months of lifestyle interventions. Two antihypertensive medications from different drug classes are recommended for patients with stage 2 HTN (ideally in a single-pill combination). A single first-line agent is recommended for those with stage 1 HTN, followed by dosage titration and additional therapy as needed to achieve optimal control. Patients with severe HTN (formerly called hypertensive urgency; greater than 180/120 mmHg) who do not show signs of acute target organ damage should not undergo rapid BP reduction or receive parenteral antihypertensive medications in the short term. Instead, they should undergo frequent monitoring using standing medications (Jones et al., 2025).
Classes that have been shown to reduce BP and the risk of cardiovascular events are preferred. The ACC/AHA recommends the following categories of medications as first-line agents for the treatment of HTN (refer to Table 7):
- thiazide-type diuretics
- ACE inhibitors
- ARBs
- calcium-channel blockers (CCBs; Jones et al., 2025)
Table 7
Primary Agents Used in HTN
Drug | Adverse Effects/Considerations |
Thiazide or thiazide-type diuretics | |
Chlorthalidone (Thalitone) | Electrolyte imbalance (especially potassium), elevated cholesterol, hypercalcemia, hyperglycemia, photosensitivity, sexual dysfunction and sleep disturbance |
Hydrochlorothiazide (Inzirqo) | |
Indapamide (Lozol) | |
Metolazone (Mykrox, Zaroxolyn) | |
ACE inhibitors | |
Captopril (Capoten) | Dry cough, dysgeusia, fatigue, headaches, hyperkalemia, hypotension, proteinuria, rash, tachycardia, angioedema of the face and limbs |
Enalapril (Vasotec) | |
Ramipril (Altace) | |
Lisinopril (Prinivil, Zestril) | |
ARBs | |
Candesartan (Atacand) | Dizziness, fatigue, headaches, peripheral edema, angina, sinusitis, abdominal pain, diarrhea, nausea, vomiting, albuminuria, back pain, bronchitis, upper respiratory infection, angioedema |
Losartan (Cozaar) | |
Valsartan (Diovan) | |
CCBs-dihydropyridines | |
Amlodipine (Norvasc) |
|
Felodipine (Plendil) | |
Nicardipine (Procardia) | |
Nifedipine LA (Procardia XL) | |
(Arcangelo et al., 2022, pp. 297-307; 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 (Jones et al., 2025). The following additional classes of medications are used in the treatment of HTN (refer to Table 8):
- diuretics, including loop, potassium-sparing, and aldosterone antagonists
- beta-blockers
- direct renin inhibitors
- alpha-1 blockers
- central alpha-2 agonists
- direct vasodilators (Arcangelo et al., 2022, pp. 297-307)
Table 8
Additional Agents Used in HTN
Drug | Adverse Effects/Considerations | |
Loop diuretics | ||
Bumetanide (Bumex) |
| |
Furosemide (Lasix) | ||
Torsemide (Demadex) | ||
Potassium-sparing diuretics | ||
Triamterene (Dyrenium) |
| |
Aldosterone antagonist diuretics | ||
Spironolactone (Aldactone) |
| |
Eplerenone (Inspra) | ||
Beta-1 selective beta blockers | ||
Atenolol (Tenormin) |
| |
Metoprolol succinate (Toprol XL) | ||
Metoprolol tartrate (Lopressor) | ||
Nonselective beta blockers | ||
Carvedilol IR (Coreg) |
| |
Labetalol (Trandate) | ||
Direct renin inhibitor | ||
Aliskiren (Tekturna) |
| |
Alpha-1 blockers | ||
Doxazosin (Cardura) |
| |
Prazosin (Minipress) | ||
Terazosin (Hytrin) | ||
Centrally acting alpha-2 adrenergic agonists | ||
Clonidine oral (Catapres) |
| |
Clonidine patch (Catapres-TTS-1) | ||
Methyldopa (Aldomet) | ||
Guanfacine (Intuniv) | ||
Direct vasodilators | ||
Hydralazine (Apresoline) |
| |
Minoxidil (Loniten) |
| |
(Arcangelo et al., 2022, pp. 297-307; Jones et al., 2025; Woods, 2023)
Endothelin receptor antagonists may be used for resistant HTN. Aprocitentan (Tryvio) has been approved by the US Federal Drug Administration (FDA) to treat resistant HTN. It is contraindicated during pregnancy, and the most common adverse reactions are edema and fluid retention (UpToDate Lexidrug, n.d.). Aldosterone synthase inhibitors, such as baxdrostat (Baxfendy) and lorundrostat, are being studied for the management of HTN in patients who remain resistant despite being treated with several other medication classes. These are not yet approved by the FDA and have been associated with severe hyperkalemia (Brook & Townsend, 2026).
Initial treatment is based on patient presentation and the presence of comorbidities, clinical CVD, and 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 typically from another drug class and have 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 (Mann & Flack, 2026; Jones et al., 2025).
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, in most situations, patients can be advised to take their once-daily anti-hypertensive 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) can lead to 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).
Specialty Populations
Patients with resistant HTN who do not meet BP targets on conventional drug therapy with three drugs for six months or those with a specific secondary cause should be referred to an HTN specialist. Before diagnosing resistant HTN, the nurse should confirm that medication adherence is not a contributing factor. Common causes for nonadherence include medication cost, side effects, or polypharmacy. (Brook & Townsend, 2026; Mann & Flack, 2026).
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, CKD, and albuminuria, and those with diabetes and albuminuria without CKD. 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. Thiazide-type diuretics such as hydrochlorothiazide (HCTZ; Inzirqo) 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 often preferred, such as torsemide (Demadex; ElSayed et al., 2023; Jones et al., 2025).
Individuals who are pregnant and not taking antihypertensive medications before pregnancy, or are not taking an effective regimen, are typically 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. ACE inhibitors and ARBs have been associated with fetal malformations and neonatal complications, including intrauterine growth restriction (IUGR) and kidney failure. Therefore, patients capable of becoming pregnant taking ACE inhibitors and ARBs should be counseled on the risks of pregnancy while taking these medications. Before pregnancy, these medications should be discontinued, and the treatment regimen should be adjusted whenever possible. Additionally, individuals who are pregnant should not be treated with atenolol (Tenormin), direct renin inhibitors, nitroprusside (Nipride RTU), or mineralocorticoid receptor antagonists. 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; Jones et al., 2025).
Due to the increased risk of HTN for Black Americans, meticulous screening, aggressive pharmacological management, and education are crucial. Lifestyle modifications are essential in this patient population. The 2025 ACC/AHA HTN Guidelines no longer include race as a factor in pharmacological management choices. However, it is important to recognize that the Black population has a higher prevalence of not only overall HTN, but also masked HTN, HDPs, and resistant HTN. Their BP has also been shown to respond better to some interventions, such as the DASH diet (Jones et al., 2025).
There are age-related considerations in the treatment of HTN. SBP and DBP increase in the 5th and 6th decades 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 regimen is similar to that of adult patients under 65. Individuals who 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 (Jones et al., 2025).
Follow-Up Monitoring
Follow-up visits to the primary HCP for the reassessment of BP and to monitor for adherence and response to the medication regimen are recommended based on the patient's baseline BP, stage of HTN, medication use, and target organ damage. Those with BP under 120/80 mmHg should be monitored annually at routine office visits. Those with an elevated BP (120-129/<80 mmHg) or stage 1 HTN in the absence of diabetes, CKD, or increased short-term CVD risk initiated on lifestyle therapy should be re-assessed in 3 to 6 months. Patients with stage 1 HTN in the presence of diabetes, CKD, or increased short-term CVD risk should be initiated on lifestyle therapy and pharmacological treatment and reassessed in 1 month. If the established BP goal is met, a reassessment should occur every 3 to 6 months. All patients with stage 2 HTN should be started on pharmacological treatment and reassessed in 1 month. Similarly, if the BP goal is met, follow-up can extend to 3 to 6 months (Jones et al., 2025).
For more information on hypertension during pregnancy, refer to the NursingCE course Maternal Hypertension.
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