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Hypertension (FL INITIAL Autonomous Practice - Pharmacology)

2 Contact Hours including 2 Pharmacology Hours
Only FL APRNs will receive credit for this course.
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This course is only applicable for Florida nurse practitioners who need to meet the autonomous practice initial licensure requirement.
This peer reviewed course is applicable for the following professions:
Advanced Practice Registered Nurse (APRN)
This course will be updated or discontinued on or before Thursday, June 5, 2025

Nationally Accredited

CEUFast, Inc. is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center's Commission on Accreditation. ANCC Provider number #P0274.


Outcomes

≥ 92% of participants will know the differences between the types of hypertension.

Objectives

Upon completion of this course, the participant will be able to meet the following objectives:

  1. Summarize the pathophysiology of hypertension (HTN).
  2. Differentiate between the types of HTN.
  3. Identify symptoms of HTN.
  4. Distinguish between the classes of antihypertensives.
  5. Outline the role of non-pharmacological treatments in the management of HTN.
CEUFast Inc. and the course planners for this educational activity do not have any relevant financial relationship(s) to disclose with ineligible companies whose primary business is producing, marketing, selling, re-selling, or distributing healthcare products used by or on patients.

Last Updated:
To earn of certificate of completion you have one of two options:
  1. Take test and pass with a score of at least 80%
  2. Reflect on practice impact by completing self-reflection, self-assessment and course evaluation.
    (NOTE: Some approval agencies and organizations require you to take a test and self reflection is NOT an option.)
Author:    Desiree Reinken (MSN, APRN, NP-C)

Introduction

High blood pressure (BP), also known as hypertension (HTN), is when BP is consistently higher than the recommended range (Desai, 2020). Unfortunately, HTN is a commonly diagnosed disease. Nearly half of all adults living in the United States (U.S.) have HTN (Centers for Disease Control and Prevention [CDC], 2023). Having HTN increases the risk of a heart attack or myocardial infarction (MI) and a patient's stroke risk. MI's and strokes are the second leading cause of death, so it is pertinent to control HTN to prevent further complications (CDC, 2023).

Unfortunately, only one in four individuals who have HTN are considered controlled. Even patients on antihypertensive medications may still struggle to keep their BP within normal ranges. Uncontrolled HTN may be asymptomatic, increasing the need for patient education and awareness.

HTN costs the U.S. over $130 billion annually (CDC, 2023). Costs accrue from regular patient office visits, medications to treat the disease, and production loss from premature mortality (CDC, 2022). Improvements in controlling BP would decrease healthcare costs and prevent early mortality from this disease.

The Basics of Blood Pressure

To understand HTN, it is essential first to understand what BP is. BP is the pressure or force of the blood pushing against artery walls. BP is measured using the systolic and diastolic pressures. Systolic BP (SBP) measures the exertion of the blood against arterial walls during contraction. Diastolic pressure (DBP) measures the same pressure or force while the heart is at rest between beats (CDC, 2023). BP is measured in millimeters of mercury, typically written as mmHg.

The minimum acceptable BP or standard is individualized and depends on how well the heart can adequately perfuse the vital organs without showing signs or symptoms of low BP or hypotension. Depending on a patient's health status and comorbid conditions, there is variation, but it is usually more than 90 mmHg SBP and 60 mmHg DBP (Brzezinski, 1990). Normal BP is ≤ 120/80 mmHg (American Heart Association, 2023). BP varies depending on the state and activity level of the patient. For example, SBP decreases with respirations, and SBP and DBP rise with exercise (Brzezinski, 1990). It is essential to monitor BP as it can indicate perfusion status to vital organs.

Pathophysiology of Hypertension

Several factors can cause HTN, and there are varying degrees and ranges of HTN. Spontaneous variations in our BP can be caused by emotions, such as anger, dietary causes, high salt intake, or exertional influences, such as running a marathon (Brzezinski, 1990). However, there are pathophysiologic contributors that should be discussed.

Cardiac Output

Normal levels of BP depend on an important balance between peripheral vascular resistance and cardiac output. Usually, peripheral vascular resistance is increased in patients with HTN, while cardiac output may be within normal limits. The small arterioles that contain smooth muscle cells aid in determining the level of peripheral resistance. The longer smooth muscles are contracted, the greater the likelihood of wall thickening and an irreversible rise in peripheral resistance (Beevers et al., 2001).

Renin-angiotensin System

It is thought that the renin-angiotensin system may be the most significant contributor to HTN. Renin, secreted from the kidney's juxtaglomerular apparatus, is released in response to decreased salt consumption (glomerular underperfusion) or sympathetic nervous system stimulation. Renin is essential as it converts angiotensin to angiotensin I. Angiotensin I is eventually converted to angiotensin II by a converting enzyme and is known to be a significant vasoconstrictor, contributing to a rise in BP (Beevers et al., 2001).

The Autonomic Nervous System

The autonomic and central nervous systems both play a pivotal role in HTN. Because the sympathetic nervous system causes constriction and dilation of the arterioles, the autonomic nervous system acts to maintain BP within normal range. The autonomic nervous system also aids in correcting acute and short-term rises in BP, such as with stress (Beevers et al., 2001).

Genetics

Research has shown that genetics may play a role in the development of HTN. It is twice as likely for someone with parents who have HTN to have the condition themselves. There are specific genetic mutations that can cause HTN. Genetic mutations and conditions that could contribute to this condition include congenital adrenal hyperplasia due to 17α-hydroxylase deficiency, the angiotensinogen gene, and glucocorticoid-remediable aldosteronism (Beevers et al., 2001).

Other Pathophysiologic Factors

Another pathophysiologic cause includes endothelial dysfunction involving peptide endothelin (vasoconstrictor) and nitric oxide (vasodilator). Vasoactive mechanisms and systems involving vascular tone and sodium transport also play a role in the development of HTN. Abnormalities of the vessel wall and blood, such as abnormal platelet activation, are often seen in patients with HTN (Beevers et al., 2001).

Risk Factors

There are modifiable and non-modifiable risk factors for developing HTN. Modifiable risk factors include:

  • Physical inactivity and a sedentary lifestyle
  • Increased/excessive sodium consumption
  • Increased intake of trans and saturated fats
  • Smoking (tobacco)
  • Excessive alcohol intake
  • Being overweight or obese (World Health Organization [WHO], 2023)
  • Obstructive sleep apnea
  • High cholesterol
  • Stress (AHA, 2017)

Non-modifiable risk factors include:

  • ≥ 65 years of age
  • Family history of HTN
  • Comorbid conditions, especially of the kidney and heart (WHO, 2023)
  • Gender- Men aged 64 or under are at a greater risk. However, women over 65 are more likely than men to have HTN
  • Race- African Americans are more likely to develop and have more severe cases of HTN (AHA, 2017)

Diagnosis

Next, the diagnosis of HTN will be discussed. Later in this module, specific forms of HTN, including their symptoms, will be reviewed. 

HTN is diagnosed by a BP screening using a sphygmomanometer. As mentioned above, ≤ 120/80 mmHg is ideal for a healthy individual. 

Stages of HTN are defined by the following levels:

  • Elevated- 120-129 mmHg systolic and < 80 mmHg diastolic
  • Stage 1- 130-139 systolic or 80-89 mmHg diastolic
  • Stage 2- ≥ 140/90 mmHg
  • Crises levels- ≥ 180/120 mmHg (Iqbal, A.M., & Jamal, 2022)

Graphic showing Hypertension Categories

Hypertension Categories

Other laboratory tests may be performed to look at potential causes of HTN and to see if there is target organ damage. Blood tests may include a blood count, a chemistry panel, and tests that examine cholesterol and specific electrolytes, such as sodium and potassium. An electrocardiogram (ECG) and a urinalysis may also be performed (Chen, 2022).

Types of Hypertension

There are different types of HTN based on causes and BP readings. Sometimes, it is difficult to differentiate between the types of HTN and what is causing an increase in BP.

Primary Hypertension

Primary HTN, also known as essential HTN, accounts for almost 90% of all cases. Primary HTN is characterized by SBP values of 130 mmHg or more and/or DBP of over 80 mmHg. Primary HTN can be idiopathic or without an identifiable cause (Carretero & Oparil, 2000). It is considered a heterozygous disorder where patients have casual factors causing their high BP. Previous research has identified that patients may be salt sensitive, leading to the development of HTN (Iqbal & Jamal, 2022).

Specific factors known to increase BP in primary HTN include:

  • Increased consumption of alcohol
  • Increased consumption of salt
  • Aging
  • Overweight/obesity
  • Stress
  • Low calcium and potassium intake (Carretero & Oparil, 2000)

Primary HTN may be asymptomatic; therefore, diagnoses may be based on BP screenings. If the HTN has been chronic, patients may present with symptoms of end-organ damage, such as encephalopathy or acute pulmonary edema.

If patients are symptomatic, they may experience:

  • Headaches
  • Nose bleeds
  • Chest pain
  • Dizziness
  • Hematuria
  • Fatigue (Cleveland Clinic, 2021)

Though the physical exam may appear unremarkable, healthcare providers should examine for aortic valve disease, polycystic kidney disease, coarctation of the aorta, thyroid disorders, and renovascular diseases. 

With examination, the patient should be seated for at least five minutes before taking BP. To diagnose primary HTN, the American College of Cardiology recommends that the BP be high on two office visits on separate dates. The European Society of Cardiology and European Society of Hypertension recommends recording the BP three times, at one to two minutes apart. Additional measurements may be warranted if the first two readings differ by > 10 mmHg. If not, BP is then recorded as an average of the readings. An ambulatory BP measurement, or a consistent measurement over 24 hours, has been noted to be the best method to diagnose HTN (Iqbal & Jamal, 2022).

The diagnosis and evaluation for primary HTN involve the following:

  • Labs- blood count, electrolytes, cholesterol levels, erythrocyte sedimentation rate (ESR), serum uric acid, creatinine, estimated glomerular filtration rate (eGFR), thyroid levels, hemoglobin A1C (HbA1C), and urine albumin-to-creatinine ratio.
  • 12-lead ECG- this will look at the rhythm and rate of the heart and if there is evidence of left ventricular hypertrophy.
  • Fundoscopy- this will review maculopathy or retinopathy of the eye.
  • Ankle-brachial pressure index (ABI)- to look for evidence of peripheral arterial disease.

Treatment for primary HTN consists of pharmacological and non-pharmacological interventions.

The Joint National Commission (JNC) has set treatment recommendations that include:

  • Patients with diabetes mellitus and chronic kidney disease (CKD) whose BP is ≥ 140/90 mmHg should be given pharmacologic therapy and have a target BP less than 140/90 mmHg.
  • Patients over the age of 60 with a BP of ≥ 150/90 mmHg should be given pharmacologic therapy and have a target BP of less than 150/90 mmHg.
  • Patients between the ages of 18-59 with an SBP ≥ 140 mmHg should be given pharmacologic therapy and have a target BP less than 140 mmHg.
  • Patients with diabetes who are African American should be treated with a thiazide diuretic and/or calcium channel blocker (CCB).
  • Patients who have CKD should be treated with an angiotensin receptor blocker (ARB) unless contraindicated (Iqbal & Jamal, 2022).

Specific pharmacological agents depend on the level of BP and the patient's condition. Stage 1 HTN can be treated with one medication, also called monotherapy. Angiotensin-converting enzyme (ACE) inhibitors, ARBs, CCBs, and thiazide diuretics are generally the first choices. When using two medications, they should be from different drug classes. Most commonly, an ACE inhibitor or ARB and a CCB are the top choice. These guidelines change with patients who have significant comorbid conditions (Mann & Flack, 2023).

Secondary Hypertension

Secondary HTN is elevated BP with an identifiable cause; it occurs in nearly 10% of adults. It is pertinent that healthcare providers identify the etiology of secondary HTN as it may guide therapy or eliminate the need for treatment altogether.

Patients exhibiting any of the following may have secondary HTN:

  • An acute rise in BP with no history of elevated pressures
  • Resistant HTN despite proper interventions and treatment
  • HTN associated with electrolyte disorders such as low potassium or metabolic alkalosis
  • HTN in patients before age 30 without any risk factors (family history, obesity, diet, etc.)
  • HTN before puberty
  • Patients with severe HTN and end-organ damage
  • Reverse dipping patterns while on a 24-hour ambulatory monitoring
  • Snoring and daytime sleepiness
  • Weight gain, fatigue, moon face
  • History of renal insufficiency
  • Palpitations, heat intolerance, tachycardia, tremors
  • Recurrent urinary tract infections/kidney stones
  • Decreased/delayed femoral pulses
  • Atherosclerotic cardiovascular disease ((Hegde et al., 2013)

Secondary HTN can be caused by the following:

  • Endocrine disorders- this can be an increase in hormone release. Specific hormone disorders include Cushing's disease, aldosteronism, pheochromocytoma, and thyroid disorders.
  • Vascular disorders- this may include coarctation of the aorta.
  • Renovascular disorders- this is a rare cause but includes stenosis of the renal arteries.
  • Renal parenchymal disease- this is the most common cause of secondary HTN. This group includes diabetic nephropathy, polycystic kidney disease, and glomerulonephritis.
  • Miscellaneous- obstructive sleep apnea, preeclampsia, and the intake of certain drugs (Hegde et al., 2013; Puar et al., 2016). 

A thorough history and physical should be taken to ensure the right underlying cause is found. The symptoms of secondary HTN may depend on what is causing the increase in BP. Symptomatic HTN may present with chest pain, dizziness, nose bleeds, fatigue, etc.

Treatment for secondary HTN is dependent on the underlying cause.

Resistant Hypertension

Resistant HTN is a form of high BP that does not readily respond to treatment and often requires many medications to achieve a BP within an acceptable range. Resistant HTN can present without an identifiable cause or may result from secondary HTN. Providers should recognize this disease as it can cause end-organ damage if not caught, and it may require non-traditional methods to control BP.

BP is said to be resistant when it remains above 140/90 mmHg despite using three antihypertensive medications, including a diuretic. Generally, resistant HTN is thought to be caused by a multitude of factors. These factors include genetics, altered salt and water handling due to a dysfunction in the renin-angiotensin-aldosterone system, and altered sympathetic nervous system activation (Yaxley & Thambar, 2015).

It should be noted that there is a difference between poor adherence and resistant HTN. When medication is not taken as prescribed, poor adherence can cause extremely high BP. Resistant HTN is when BP remains high, despite adhering to the prescribed medication regimen. 

There are a few specific causes or factors that may play a part in the development of resistant HTN and include the following:

  1. Genetics- Studies have shown that some patients diagnosed with resistant HTN have mutations of the β and γ subunits of the epithelial sodium channel.
  2. Obesity- obesity can cause elevated BP. Obesity-induced HTN is complex and involves multiple body systems.
  3. Salt intake- salt intake affects BP in different ways; it can increase and blunt the effect of BP, decreasing the effect of many antihypertensive medications. This is more commonly seen in African Americans, older adults, and those with CKD.
  4. Alcohol intake- not only does heavy consumptions cause an increase in BP, but it can also lead to treatment-resistant HTN.
  5. Drug-related causes- Some pharmacological agents may increase BP and make it more difficult to control.

Medications include:

  • Oral contraceptives
  • Sympathomimetic agents such as decongestants or diet pills
  • Stimulants, such as modafinil, amphetamine, or methylphenidate
  • Natural licorice
  • Cyclosporine
  • Erythropoietin
  • Ephedra

When the diagnosis of resistant HTN is made in older adults, usually, there is a secondary cause. More common causes include the following:

  • Renal artery stenosis
  • Obstructive sleep apnea
  • Primary aldosteronism
  • Renal parenchymal disease

Uncommon causes include the following:

  • Aortic coaction
  • Pheochromocytoma
  • Cushing's disease
  • Intracranial tumor (Calhoun et al., 2008)

A thorough history and physical should be completed. Beyond the typical examination, serum creatinine, a urine dipstick, and the eGFR should be checked (Yaxley & Thambar, 2015).

Pharmacological treatment for resistant HTN is often standardized and includes an ACE inhibitor or ARB, a CCB (usually amlodipine), and a thiazide-like diuretic (usually indapamide or chlorthalidone). Often, spironolactone is added as a fourth agent. Coupled with pharmacological treatments, additional non-pharmacological therapies are necessary to control this condition (Acelajado et al., 2019).

Hypertensive Urgency

Hypertensive urgency occurs when BP is severely elevated, but end-organ damage has not occurred (Naranjo et al., 2022). Cutoffs for hypertensive urgency have been proposed but sometimes overlap with hypertensive emergencies and malignant HTN. However, standards generally say a hypertensive urgency is defined by an SBP > 180 mmHg and a DBP > 110 mmHg. Because of a lack of precise cutoffs for this condition, healthcare providers denote the patient as having a hypertensive urgency if the patient has severely elevated BP and has risk factors for end-organ damage, such as kidney failure.

Acute elevations of BP resulting in a hypertensive urgency can be caused by thyroid dysfunction, medication noncompliance, or the use of sympathomimetics. Extreme pain and heightened anxiety may also cause a significant rise in BP. The treatment is dependent on the cause of the very elevated BP (Alley & Copelin, 2022).

The history and physical examination for this condition should focus on pinpointing if there is any end-organ damage. Symptoms to watch for include dizziness, chest pain, vision changes, shortness of breath, vomiting, and a headache. BP should be taken while sitting, lying, and in both upper extremities to assess if aortic dissection is present. Specific physical signs and symptoms indicative of a more significant problem include rales, jugular venous distention, and a gallop. Fundoscopy and cerebellar testing should be performed to check for extensive organ damage.

Specific diagnostic exams may include the following:

  • Tomography (of the brain)
  • Chest X-ray
  • ECG
  • Metabolic panels
  • Urinalysis- to identify hematuria or proteinuria and review the urine microscopy
  • Pregnancy screen
  • Toxicology screen (Alley & Copelin, 2022)

Sodium nitroprusside is commonly used to treat this condition because it is short-acting and can be titrated rapidly, depending on the patient's condition. Labetalol has also been used as it can be administered as a bolus dose or an IV infusion. Two other treatment options include fenoldopam or clevidipine (Alley & Copelin, 2022).

Malignant Hypertension

Malignant HTN is used to describe patients who have elevated BP, multiple complications, such as organ damage/failure, and who have a poor outlook or prognosis. Severe elevations of BP can be seen and are often called a hypertensive crises. SBP is usually ≥ 180 mmHg, and DBP is usually ≥ 120 mmHg.

Some of the more common causes of malignant HTN include:

  • Poor medication adherence
  • Amphetamines
  • Renal parenchymal disease
  • Renal artery stenosis
  • Endocrine dysfunction
  • Central nervous system disorders
  • Head injury
  • Coaction of the aorta
  • Medication withdrawal

With malignant HTN, there is an increase in systemic vascular resistance and increased vasoconstriction. End-organ damage results from ischemia and hypoperfusion. Commonly, anemia is seen because of the red blood cell destruction in the obstructed vessels (Naranjo et al., 2022).

Patients with malignant HTN may present with headaches, back pain, chest pain, nausea, difficulty breathing, and visual disturbances. Healthcare providers should discuss antihypertensive medication regimens, the time of the last dose, if any has been missed, and if the patient is taking nonprescription medications. A funduscopic exam is performed to look for papilledema and may also reveal exudates and hemorrhages. Other signs and symptoms that may be present include seizures, agitation, delirium, bruits, pulmonary edema, and heart murmurs.

Besides the history and physical, the examination may include the following:

  • Urinalysis
  • Chest X-ray
  • ECG
  • Blood work- creatinine and electrolytes
  • Toxicology screen
  • CT/MRI of the brain and chest

Standard treatment options include the following:

  • Nicardipine at 5 mg per hour, increasing by 2.5 mg per hour every 5 minutes to a maximum of 15 mg hourly.
  • Sodium nitroprusside, 0.3-0.5 mcg/kg/minute, increased by 0.5 mcg/kg per minute as needed to a maximum dose of 10 mcg/kg per minute.
  • Labetalol 10-20 mg followed by 20-80 mg bolus doses at 10-minute intervals. The maximum is a 300-mg cumulative dose.
  • Esmolol with an initial loading dose of 500 mcg/kg/minute over 1 minute, then 50 to 100 mcg/kg/minute. The maximum dose is 300 mcg/kg per minute (Naranjo et al., 2022).

Isolated Systolic Hypertension

Isolated systolic HTN is characterized by a SBP > 140 mmHg while the DBP remains < 90 mmHg. Isolated systolic HTN is often seen in older adults; in fact, 15% of adults over 60 years of age have a BP that falls into this diagnostic category. Non-Hispanic African Americans are at the greatest risk.

Reduced elasticity of the arterial system is often the causative factor behind isolated systolic HTN. Reduced compliance, increased thickening of the vascular system, and decreased lumen-to-wall ratio lead to stiffened arteries, increasing the SBP and decreasing the DBP. The chronic diseases discussed in other types of HTN are also contributing factors to this diagnosis (Tan & Thakur, 2023).

History and physical exam with isolated systolic HTN include the following:

  • Family history, including renal disease, HTN, and cardiovascular disease
  • Diet, including usual salt consumption, alcohol intake, and processed foods
  • Any risk factors, such as obesity, diabetes, and smoking
  • Symptoms of end-organ damage, such as headache, chest pain, claudication
  • Symptoms of secondary causes of isolated systolic HTN, such as tachycardia, depression, and loud snoring
  • Prescription drugs, such as steroids or estrogen

The healthcare provider should do a complete examination, including the following:

  • BP should be documented on two to three separate occasions. A home log detailing BP is acceptable evidence
  • General appearance, including flushing, sweating, and body mass index
  • The neck to look for carotid bruits and if the thyroid is enlarged
  • The lungs for rhonchi or rales
  • The heart for a heave, gallop, or distension
  • The abdomen for an enlarged kidney or any bruits
  • A neurologic exam for confusion or weakness
  • Extremities for edema and the presence of pulses
  • A fundoscopy for cotton wool spots, arteriolar narrowing, and arteriovenous nicking

Further evaluation should consist of diagnostic tests such as:

  • ECG
  • Urine analysis
  • Electrolytes
  • Creatinine
  • Renal ultrasound
  • ABI
  • HgbA1c (Tan & Thakur, 2023)

First-line agents for treating isolated systolic HTN include CCBs and thiazide diuretics (Angeli et al., 2020).

White Coat Syndrome

White coat effect refers to the phenomenon of an elevated BP seen with a health care provider in the clinic versus outside the clinic, such as at home. The difference is considered clinically significant if it exceeds 20/10 mmHg. White coat syndrome is the sustained effect of high BP when seeing a health care provider, but a quick resolution when at home or ambulatory outside the clinic. White coat syndrome is essential to understand as it is a risk factor for target organ damage, MI, stroke, and sustained HTN; it can also lead to atherosclerosis. A BP reading of ≥ 140/90 mmHg in-office with a mean BP reading of 130/80 mmHg outside the healthcare office suggests white coat syndrome. 

The cause of white coat syndrome is not clear. Risk factors such as anxiety and public speaking are linked to this syndrome. The pathophysiologic mechanisms behind white coat syndrome involve the endocrine and sympathetic nervous system. Unfortunately, white coat syndrome is an under-researched topic that deserves more attention to understand the pathophysiology and treatment interventions (Nuredini et al., 2020).

Preeclampsia and Eclampsia

Hypertensive disorders affect around 10% of pregnancies and are commonly called gestational HTN or preeclampsia. New onset of HTN after 20 weeks of gestation, with a BP of ≥ 140 mmHg systolic or ≥ 90 mmHg diastolic fits under the diagnosis of preeclampsia. Blood pressure measurements should be repeated to confirm the diagnosis; they should be taken at least four hours apart on two separate occasions. HTN during pregnancy has severe consequences on the mother and baby, including long-term HTN and significant cardiovascular events, such as MI or stroke. The fetus may experience preterm birth, distress, growth restriction, early placental abruption, or even death.

Risk factors for preeclampsia include the following:

  • ≥ 40 years old
  • BMI ≥ 35 kg/m
  • Multi-fetus pregnancy
  • Family history of preeclampsia
  • Polycystic ovarian syndrome
  • Sleep-disordered breathing
  • Helicobacter pylori
  • History of recurrent urinary tract infections
  • Raised mean arterial BP before 15 weeks gestation 

Besides an increase in BP, the mother must experience one of the following to be diagnosed:

  • Proteinuria- usually confirmed by a urine dipstick and then a 24-hour urine.
  • Uteroplacental disruption- this may include oxidative stress and systemic inflammation.
  • Organ (renal, liver, neurological) dysfunction- laboratory tests include hemoglobin, creatinine, liver enzymes, and uric acid (Fox et al., 2019).

Eclampsia is a significant condition that requires prompt attention. It can lead to liver failure, renal dysfunction, pulmonary edema, central nervous system abnormalities, and death. Tonic-clonic seizures mark the progression of preeclampsia to eclampsia. Other signs and symptoms may include agitation and unconsciousness. Before experiencing these symptoms, many women will experience headaches, swelling, vision changes, and gastrointestinal upset.

Specific signs of eclampsia include:

  • New onset headache that does not respond to medications
  • BP ≥ 160/110 mmHg
  • Serum creatinine > 1.1 mg/dl

Rapid clinical interventions are necessary to prevent eclampsia from progressing to the deadly hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome (Akre et al., 2022).

First-line therapy includes labetalol, nifedipine, or methyldopa (Odigboegwu et al., 2018).

Pharmacological Management of Hypertension

Management of HTN depends on the cause and the specific type of HTN. The common classes of medications used will be discussed more thoroughly.

Diuretics

Diuretics have been used as a first-line agent to treat HTN. Diuretics promote diuresis, increasing the excretion of salt and water. The diuretic class is further broken down into three categories.

  1. Thiazide diuretics- these diuretics block the sodium-chloride channel in the distal convoluted tubule. With these medications, a limited amount of sodium crosses the membrane, decreasing sodium and water passage. Chlorthalidone, hydrochlorothiazide, and indapamide are the most commonly used thiazide diuretics. Common adverse effects of thiazide diuretics include hypokalemia, hyponatremia, hyperglycemia, and hypercalcemia (Akbari et al., 2023).
  2. Loop diuretics- these medications increase urine production resulting in the excretion of more fluid. They compete with chloride to bind to the sodium potassium chloride cotransporter, inhibiting sodium and chloride's reabsorption. The most common loop diuretics include furosemide, butanamide, and torsemide. Adverse effects usually occur from electrolyte abnormalities (Huxel et al., 2022).
  3. Potassium-sparing diuretics- this type of diuretic has similar actions to the others, except it does not cause potassium loss with urination. It should be noted that this type of diuretic does not decrease BP as well as others. Common potassium-sparing diuretics include amiloride, triamterene, and spironolactone (Ellis, 2023).

Beta-blockers

Beta-blockers are a common medication for treating HTN and its associated side effects, such as tachycardia. Beta-blockers bind to the B1 and B2 receptors, which inhibit their effects. However, some beta-blockers also bind to alpha receptors. The inhibition of inotropic and chronotropic receptors results in a decreased heart rate. A reduction in cardiac output and a decrease in renin drops BP. Common adverse effects include hypotension and bradycardia. Other side effects include fatigue, nausea, and dizziness.

Commonly used beta blockers for treating HTN include propranolol, labetalol, carvedilol, atenolol, and metoprolol. Dosages depend on the specific medication and the level of HTN. However, they are often dosed twice daily (Farzam, 2022).

Angiotensin-converting Enzyme Inhibitors

ACE inhibitors lower the mean arterial BP, the SBP, and the DBP. They interfere with the renin-angiotensin-aldosterone system and block the conversion of angiotensin I to angiotensin II. A decrease in angiotensin II lowers the BP. Common ACE inhibitors include enalapril, lisinopril, benazepril, captopril, and fosinopril. All ACE inhibitors, except enalapril, are given orally. The most common adverse effect noted with these medications is a bothersome dry cough for which there is no treatment (Herman et al., 2023).

Angiotensin Receptor Antagonists

These are also called ARBs, and they inhibit and reduce the action of angiotensin II type 1 receptor (which increases BP). They are often used in patients who cannot tolerate ACE inhibitors. Side effects of ARBs are minimal, and the medications are usually well tolerated. However, they are contraindicated in patients with renal artery stenosis and some cases of heart failure. Common ARBs include irbesartan, valsartan, losartan and candesartan (Hill et al., 2022).

Calcium Channel Blockers

CCBs block calcium's movement by binding to the voltage-gated calcium channels. Their effects on the atrioventricular and sinoatrial nodes in the heart slow contractility and conduction, decreasing BP. CCBs may cause worsening cardiac output, bradycardia, headaches, and flushing. Common CCBs include amlodipine, verapamil, diltiazem, and nifedipine (McKeever & Hamilton, 2022).

Alpha-blockers

Alpha-blockers, which alter the sympathetic nervous system, fall into three categories:

  1. Nonselective alpha-blockers- cause vasodilation when they block both alpha-1 and alpha-2 receptors.
  2. Selective alpha-1 blockers- cause vasodilation as they prevent norepinephrine from activating the alpha-1 receptor.
  3. Selective alpha-2 blockers- stimulate the sympathetic nervous system by inhibiting negative feedback of norepinephrine.

Adverse effects include hypotension, tachycardia, weakness, and tremors. Common alpha-blockers include prazosin, terazosin, and doxazosin (Nachawati & Patel, 2022).

Other Medications

Another class of medications for HTN includes alpha-2 adrenergic receptor agonists, though they are less commonly used. Alpha-2 adrenergic receptor agonists cause neuromodulation resulting in a reduction in BP, vasodilation, and a decreased heart rate (Nguyen et al., 2017). Some of the more common medications under this class include clonidine, dexmedetomidine, and tizanidine. Common side effects include drowsiness, fatigue, headache, and irritability (Nguyen et al., 2017).

Direct vasodilators are also used for HTN. They allow the blood to flow easier due to the widening of the blood vessels. Minoxidil and hydralazine are examples of direct vasodilators. Common side effects include tachycardia, headache, vomiting, and fluid retention (Hariri & Patel, 2022).

Non-Pharmacological Treatments

There are many non-pharmacological treatment options that are used instead of pharmacological interventions or are coupled with pharmacological treatments.

Diet- Increased consumption of fruits, vegetables, and whole grains can decrease BP. Other diet recommendations include the consumption of low‐fat dairy products, legumes, fish, and nuts. Patients should reduce their intake of sugary beverages, sweets, and red meat (Verma et al., 2021).

Specifically, the Dietary Approaches to Stop Hypertension (DASH) diet is often employed to reduce HTN. The DASH diet increases the intake of lean meat and dairy, fruits and vegetables, and micronutrients and promotes reducing sodium intake to 1500 mg/day.

A typical serving guide for a patient following the DASH diet is as follows:

  • Fruits: 4-5 servings per day
  • Vegetables: 4-5 servings per day
  • Low-fat dairy products: 2-3 servings per day
  • Lean meat products, poultry, fish: ≤ 6 servings per day
  • Nuts and seeds: 4-5 servings per week (Challa et al., 2023)

Physical activity- Patients should participate in moderate to vigorous physical activity four times weekly. Patients should get at least 150 minutes of physical activity weekly. If the patient is overweight, a weight loss of 10 kg may reduce SBP by up to 20 mmHg (Verma et al., 2021).

Tobacco and alcohol- The cessation of tobacco will decrease BP, heart rate, and contractility. Alcohol, especially long-term heavy consumption, can cause a rise in BP. Many providers will warn against alcohol use with HTN.

Dietary supplements- Research has shown that cocoa and garlic can significantly reduce BP.

Relaxation techniques- Using stress-relieving techniques such as tai chi, mindfulness‐based stress‐reduction, and meditation (Verma et al., 2021).

Complications and Prevention

Uncontrolled HTN can result in the following complications:

  • Stroke- this is due to the thickening/hardening of the arteries
  • Renal failure- this is from narrowing and weakened vessels
  • Heart failure- this is from narrowing and weakened vessels
  • Coronary heart disease- this is from narrowing and weakened vessels
  • Heart attack- this is due to thickening/hardening of the arteries
  • Vision changes- narrowed vessels in the eye can result in vision loss
  • Peripheral arterial disease-- this is from narrowing and weakened vessels
  • Aneurysm- vessels weaken and bulge
  • Death (Iqbal, A.M., & Jamal, 2022)

graphic showing the main complications of hypertension in human body

Complications of HTN

There are prevention methods to keep BP within the normal range and prevent HTN from worsening. These methods include the following:

  • Eating a healthy diet or following the DASH diet
  • Maintaining a healthy weight or losing weight if overweight or obese
  • Getting regular physical exercise
  • Limiting alcohol and avoiding tobacco
  • Managing or decreasing exposure to stress (Carey et al., 2018)

Case Study

Jenna is a 41-year-old female who is 32 weeks pregnant. She is being seen today for a regularly scheduled OBGYN check-up. Her BP is 143/95. After 10 minutes of rest, her BP is retaken and has not changed. The nurse further reviews previous BP measurements at the last three appointments and notices all of the BP measurements have been over 140/90 mmHg. She reports the BP to the provider of care.

The provider decides that Jenna is fine, as she is not symptomatic and has no complaints. Two weeks later, Jenna presented to the emergency department with a new onset headache that had not been relieved with over-the-counter medications. When taking her vitals, Her BP is 165/115 mmHg, and she starts convulsing. After the emergency department attending speaks with the OBGYN, she realizes Jenna has eclampsia. She administers labetalol for the BP and magnesium sulfate for the seizures to prevent this condition from advancing.

After a couple of hours, the patient's BP is now 130/82 and still decreasing. Jenna has not had any more seizures, is alert, and no longer has a headache. Luckily, the emergency room attending could recognize the disorder before it became HELLP syndrome.

Unfortunately, the progression from preeclampsia to eclampsia may have been prevented if the OBGYN had recognized the increase in BP and listened to the nurse's concerns. The patient's age placed her at an increased risk of an elevated BP while pregnant. The elevation at the repeated office visits was enough to diagnose her with preeclampsia.

Conclusion

HTN is a common disease affecting millions that contribute to increased morbidity and mortality. HTN can be challenging to detect as it is often asymptomatic until BP is taken. There are different stages and types of HTN; each may be treated differently, depending on the severity, patient's clinical status, and comorbid conditions.

The treatment for HTN depends on the cause or underlying cause contributing to the increase in BP. Several medication classes can be used to treat HTN, including beta blockers, ACE inhibitors, and CCBs. Healthcare providers should be cautious about the side effects of the medications and if the medication use will cause any worsening of comorbid conditions, such as CKD.

BP measurement should occur when vitals are taken. Providers should ensure they review past histories/vital signs if the BP is elevated. A thorough physical exam should be performed to look for complications of HTN.

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Implicit Bias Statement

CEUFast, Inc. is committed to furthering diversity, equity, and inclusion (DEI). While reflecting on this course content, CEUFast, Inc. would like you to consider your individual perspective and question your own biases. Remember, implicit bias is a form of bias that impacts our practice as healthcare professionals. Implicit bias occurs when we have automatic prejudices, judgments, and/or a general attitude towards a person or a group of people based on associated stereotypes we have formed over time. These automatic thoughts occur without our conscious knowledge and without our intentional desire to discriminate. The concern with implicit bias is that this can impact our actions and decisions with our workplace leadership, colleagues, and even our patients. While it is our universal goal to treat everyone equally, our implicit biases can influence our interactions, assessments, communication, prioritization, and decision-making concerning patients, which can ultimately adversely impact health outcomes. It is important to keep this in mind in order to intentionally work to self-identify our own risk areas where our implicit biases might influence our behaviors. Together, we can cease perpetuating stereotypes and remind each other to remain mindful to help avoid reacting according to biases that are contrary to our conscious beliefs and values.

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