Hypertension: Key Concepts and Guidelines

Hypertension (HTN) Overview

• Approximately 1.28 billion adults aged 30-79 worldwide have hypertension (HTN).
• In the US, 1 in 3 adults has HTN, with 2/3 of those living in low and middle-income countries.
• 46% of adults with HTN are unaware of their condition.
• Only about 1 in 5 adults have their HTN under control.
• HTN is more prevalent in men than women.
• Non-Hispanic Black adults have a higher prevalence (57.2%) compared to non-Hispanic White (42.6%) or Hispanic (43.7%) adults.
• Based on the ACC/AHA, hypertension is defined as a blood pressure ≥ 130/≥ 80 mmHg.
• HTN is an attributable risk factor in 41% of all cardiovascular deaths from MI, heart failure, and stroke.
• An increase in BP of 20 mmHg (systolic) or 10 mmHg (diastolic) is associated with a doubling of cardiovascular death risk, regardless of age.
• Middle-aged patients with HTN have a higher risk of developing chronic kidney disease and dementia later in life.
• The global prevalence of HTN is 39%.

Who Gets Hypertension

• Hypertension is more common in men than in women in younger age groups, but becomes less pronounced with age.
• Non-Hispanic African-Americans are more likely to have HTN other ethnicities.
• By age:
  • 22.4% of adults aged 18 to 39 have this
  • 54.5% of adults aged 40-59 have this
  • 74.5% of adults over 60 have this

Understanding Blood Pressure

• Blood pressure measures the force of blood pushing against artery walls.
• Systolic pressure is the pressure in arteries when the heart beats (contracts).
• Diastolic pressure is the pressure in arteries when the heart is at rest (between beats/refilling).
• "Normal" blood pressure is considered 120/80 mmHg.
• Organizations such as the JNC and ACC/AHA have issued guidelines for screening/treating HTN.

ACC/AHA Guidelines for Blood Pressure Management

• Normal BP: <120/<80 mmHg is managed with healthy lifestyle promotion and annual BP reassessment.
• Elevated BP: 120-129/<80 mmHg is managed with nonpharmacologic therapy and BP reassessment in 3-6 months.
• Stage 1 Hypertension: 130-139/80-89 mmHg, management depends on ASCVD or 10-year CVD risk:
  • ≥10%: Start with both nonpharmacologic and pharmacologic therapy, reassess BP in 1 month, and every 3-6 months if at goal.
  • <10%: Start with nonpharmacologic therapy, reassess BP in 3-6 months, and consider pharmacologic therapy if not at goal.
• Stage 2 Hypertension: ≥140/≥90 mmHg treatment includes nonpharmacologic and pharmacologic therapy.

Atherosclerotic Cardiovascular Disease (ASCVD) Risk Estimator

• It is used to calculate a patient's 10-year risk of developing atherosclerotic cardiovascular disease.
• Risk is calculated based on factors like age, gender, ethnicity, cholesterol levels, blood pressure, and smoking status.
• The calculator guides treatment decisions, including if to start a statin based on a patient's calculated risk level.
• 10-year risk for ASCVD is categorized as low (<5%), borderline (5% to 7.4%), intermediate (7.5% to 19.9%), or high (≥20%).

JNC 8 Classification of BP

• This classification is for adults aged ≥18 years
• Normal BP is classified as <120 mmHg systolic AND <80mmHg diastolic
• Prehypertension is classified as 120-139 mmHg systolic OR 80-89mmHg diastolic
• Stage 1 HTN is classified as 140-159mmHg systolic OR 90-99mmHg diastolic
• Stage 2 HTN is classified as ≥160 mmHg systolic OR ≥100mmHg diastolic

Hypertensive Crisis and Subcategories

• Hypertensive crisis is defined as systolic blood pressure above 180 mmHg and/or diastolic blood pressure above 120 mmHg.
• There are two subcategories:
  • Hypertensive Emergency: Severe BP elevation with new onset or worsening organ damage.
  • Hypertensive Urgency: Elevated BP without clinical, laboratory, or instrumental evidence of acute hypertensive organ damage.
• Symptoms of this can include:
  • Dizziness
  • Severe Headache
  • Vision Problems
  • Nausea and Vomitting
  • Trouble Breathing
  • Chest Pain

Hypertension Symptoms

• Mild/moderate HTN rarely exhibits symptoms.
• Untreated, elevated blood pressure can lead to vague symptoms such as headache, blurry vision, or dizziness.
• Severely elevated BP may result in more severe symptoms due to acute, severe, and life-threatening complications, including papilledema, stroke, encephalopathy, acute kidney injury, and heart failure.
• Proper technique is vital when assessing HTN.

Blood Pressure Assessment Conditions

• Use a quiet room with comfortable temperature.
• Avoid smoking, caffeine, and exercise 30 minutes prior; empty bladder; remain seated and relaxed for 3–5 minutes prior.
• Neither the patient nor staff should talk before/during/between measurements.

Blood Assessment Positions

• Patient is sitting with arm resting on a table at heart level, back supported on chair, legs uncrossed, and feet flat on floor.

Blood Pressure Assessment Device

• Using a validated electronic (oscillometric) upper-arm cuff device.
• Calibrated auscultatory device (aneroid or hybrid).

Assessing Cuff Size

• Size is dependent upon individual arm circumference.
• Smaller cuffs overestimate blood pressure, larger cuffs underestimate it.
• Inflate the bladder of the cuff to cover 75%-100% of the individual's arm circumference for manual auscultatory devices and use cuffs according to instructions for electronic devices.

Blood Pressure Assessment Protocol and Interpretation

• At each visit, take 3 measurements with 1 minute between each.
• Take the average of the last two measurements, if BP of the first reading is <130/85 mm Hg no further measurement is required.
• Blood pressure exceeding 140/90 mm Hg during 2-3 office visits indicates hypertension.

Errors in Blood Pressure Measurement

• Inappropriate cuff size:
  • Too small increases the reading by 5-10 mmHg.
  • Too large decreases the reading by 5-10 mmHg.
• Poor cuff placement:
  • Cuff too loose or improperly placed results in false high readings.
  • Deflation of the cuff too slow (false high) or too fast (false low).

Blood Pressure Recommendations Based on ACC/AHA Classification

• Stage I (130-139/80-89):
  • Recheck BP in 5 minutes
  • Assess patient's overall health status
  • Document and provide patient education.
  • Advise to recheck at home and contact PCP if necessary.
• Stage II (>140/>90):
  • Follow the same steps as with Stage I.
  • Consider consulting with pt's PCP office.

White Coat Hypertension

• White coat hypertension is a condition where blood pressure spikes in medical settings due to anxiety.
• It is not uncommon.
• It indicates potential blood pressure increases in other stressful sitations.
• Patients should monitor their blood pressure at home, keep a record of the readings, and share the information with doctors to determine if treatment is necessary.

Primary Hypertension

• Primary Hypertension, accounting for 95% of cases, is often due to multiple factors and lacks a single distinct cause.
  • These multi-factoral causes include: Age, diet, excess caffeine or sodium intake, family history, obesity, alcoholism, and sedentary lifestyle
• Governing factors in determining blood pressure include mean arterial pressure (MAP), cardiac output and peripheral resistance.

Cardiac Output and Mean Arterial Pressure

• Cardiac output (CO) is the product of heart rate times stroke volume ejected with each beat.
• MAP is the average arterial blood pressure, and it’s the product of CO and total peripheral resistance.

Secondary HTN

• Secondary Hypertension, involves an identified cause suchs as:
  • Kidney disease
  • Endocrine disorders
  • Medications
  • Changes to blood vessels (Aorta or kidney arteries)
• The cardiovascular system's main goal is to maintain a constant flow of blood to the vital organs (homeostasis).

HTN and Peripheral Resistance

• Increases in blood pressure can result from changes in arterial tone due to enhanced alpha-adrenergic stimulation and reduced vessel wall elasticity from smooth muscle contraction.
• Atherosclerosis and Arteriosclerosis can contribute to increased peripheral resistance.
• Sympathetic stimulation from exercise, psychological stress, and pharmacological triggers can result in increased peripheral resistance,
• A transient rise in blood pressure because of exercise is very benficial for maintaining arterial elasticity.
• Chronic sympathetic stimulation from individuals in high stress, illicit drugs, living in fear can be harmful because it incerases blood pressure and muscle tone.

Cardiac Output in HTN

• Cardiac Output (Heart Rate x Stroke Volume) is elevated in younger patients.
• Total Peripheral Resistance (Systemic Vascular Resistance) and stiffness of the vasculature play a larger role in older patients (arteriosclerosis).
• Primary & Secondary HTN can co-exist, if there is an acute worsening of BP, a new secondary cause should be considered.

Primary/Essential HTN Risk Factors

• Primary/Essential HTN develops gradually - patients can be asymptomatic.
• Risk factors include:
  • Age, especially after 45 in men, and after 65 in women
  • Smoking
  • Alcohol Intake (in excess)
  • Obesity
  • Lack of physical activity
  • High Sodium Diet
  • Genetics (non-modifiable risk factor)

Age and HTN

• Increased arterial stiffening or hardening from loss of elastin fibers in large arteries and buildup of stiffer collagen fibers.
• Isolated systolic hypertension (80% are over 65 years old), elevated even if diastolic in range.
• This elevated blood pressure increases vessel wall load to the left ventricle impacting blood flow to the left ventricle, potentially creating ventricular hypertrophy and coronary failure.

Smoking and HTN

• Nicotine constricts blood vessels, leading to elevated blood pressure.
• Carbon monoxide in tobacco products damages the lining of the blood vessels, making them less elastic.
• Oxidative stress damages the blood vessels and leads to inflammation.
• Increased alcohol intake causes vasoconstriction which makes the heart work harder to pump blood.

Obesity and HTN

• Obesity is assessed by calculating BMI (>30).
• Obese individuals are 2-3xs more likely to develop HTN.
• Increased sympathetic nervous system activity.
• Increase in insulin resistance.
• Increased sodium retention caused by activation of the RAAS.
• Increased blood pressure.

Diet and HTN

• Sedentary lifestyles and prolonged sitting correlate with elevated blood pressure, since metabolism decreases and impacts impact blood flow.
• Increased sodium and a low potassium diet can lead to elevated blood pressure.
• High sodium intake causes the kidneys to work harder to remove sodium, leading to water retention and increased blood volume returning to the heart.
• Increases the "pre-load" and the stroke volume, which leads to increased Cardiac Output (CO).
• Increasing potassium intake (fruits/vegetables) can help improve blood pressure.
• Higher intake of saturated fats and sugar contribute to HTN risk.

Genetics and Primary/Essential HTN

• Patients with two parents with HTN have a 2.4x increased risk in developing HTN.
• Genetics have more impact on HTN in women.
• A genetic factor is more commonly seen factor in younger patients who develop HTN.

Sympathetic Nervous System

• Manages the "fight-or-flight" response.
• It regulates blood pressure by influencing the vasculature, kidneys, and heart.
• SNS is activated by the hypothalamus by sending signals to the adrenal glands to release epinephrine into the bloodstream.
• This causes increased heart rate, contractility, vasoconstriction, and blood pressure.
• It affects beta-1-adrenergic receptors, located in the SA node and cardiac muscles.
• It has less effect on alpha-adrenergic receptors in the heart, since they coronary blood vessel constriction.

Renin-Angiotensin-Aldosterone System (RAAS)

• This hormonal system in the body maintains blood pressure by controlling fluid and electrolyte balance.
• It is done using renin, angiotensin II, and aldosterone.
• When blood pressure decreases, the kidneys release renin, leading to vasoconstriction and increased sodium absorption (elevation of blood pressure).
• The primary function of RAAS = regulating blood volume and vascular tone to maintain BP.
• Hormones are released:
  • Renin, which is an enzyme secreted by the kidneys when blood pressure drops.
  • Angiotensinogen, which is a protein released by the liver that is converted to angiotensin 1 by renin.
  • Angiotensin Converting Enzyme, which converts angiotensin 1 to the active angiotensin 2.
  • Angiotensin II, which constricts blood vessels and aids the adrenal glands to release aldosterone.
    • It also causes the release of Anti-diuretic hormone from the pituitary gland and causes the kidneys to retain water, which increases blood volume and blood pressure.
  • Aldosterone, which causes the kidneys to retain sodium and water and thus increases blood pressure.
• RAAS is essential because drugs inhibit the RAAS and reduce HTN.

Basic summary - RAAS

1. Kidneys release renin when blood pressure falls.
2. Renin converts angiotensinogen (protein made & released by liver) into angiotensin I.
3. Angiotensin I is converted by angiotensin-converting enzyme (ACE) into angiotensin II (lungs and kidneys).
4. Angiotensin II constricts muscular walls in small arteries (arterioles), increasing pressure and triggers the adrenal glands and pituitary gland to release aldosterone and antidiuretic hormone (ADH)/vasopressin.
5. Aldosterone retains sodium and potassium (kidneys retain sodium in the urine).
6. Rising levels = water retention that increases blood volume and pressure (completes the system).
7. Juxtaglomerular (JG) cells in kidneys which filter waste from blood (nephrons produce urine).
8. Located in the kidneys at the junction of the afferent arteriole and the distal convoluted tubule
9. When blood pressure is reduced, the JG cells release renin (*activating the RAAS).
10. Blood pressure is impacted if something happens to the kidneys, since waste is removed waste and the JG is responsible for blood pressure via the aformentioned process.
11. The Macula Densa cells are specialized cells of the DCT at the point of contact with the afferent arterioles and function as as chemoreceptors.

• If there is reduced osmolality or low flow rate, there is vasodilation of the afferent arteriole and stimulation of the JG cells to release renin. Increasing the glomerular filtration rate.
• if there is increased osmolality or increased flow rate, there is vasoconstriction of the afferent arteriole to decreases filtration.

Glomerulus

• The glomerules has 120ml of blood is filtered / minute or 180 Liters/day. and 1.8 liters are removed daily though pee
• Rest is Absorbed through the peritubular capillaries (filtrate) and maintains balance of ions, amino acids, glucose, urea
• Damage can lead to glomerulonephritis, which can cause proteinuria, hematuria, and kidney failure

Renal tubules

• The continious structure contains fluid and ends at the collecting duct.
• Proximal convoluted tubules lie in the cortex (outer) and are lined by simple cuboidal epithelium with microvilli (brush borders)
• Blood from the efferent arterioles moves into the peritubular capillaries (surrounds the tubules) and form an efferent venule which combines with other efferent venules to form the renal vein.
• Distal Convoluted tubule is where diuretics inhibit absorption and leads to sodium release

Kidneys

• Is a key location where HTN and blood pressure are regulated
• Consists of a collecting tubule and filteration system to mainting homeostasis

Secondary HTN (Kidney/Renal Disease-Related)

• These are NOT very common and accounts for only 5% of patients
• The majority consists of a younger patient with some underlying disease
• These can include renal diease, endocrine disorders, nueroogical disorders etc
• Renal artery stenosis (RAS): Narrowing or blockage of an artery to the kidneys = kidney failure and HTN happens (Smoking, high cholesterol, high triglycerides, DM, obesity.) Early onset and increased urea excretion.
• Renal artery thrombosis: Clot forms in a renal artery = kidney failure risk factors (Atrial fibrillation, plaque formation, and complications from trauma/surgery), or pain.
• Retinal vein thrombosis: Risk factors: trauma/surgery, prolonged bed rest, & certain medications (BCP, HRT..), plus can cause some other issues.
• Renal artery aneurysm: Bulging/weakened area of vessels and kidney pain.

Secondary HTN (E - Endocrine)

• Thyroid dysfuntion
• Overactive and underactive tyroid conditions can result
• Can result in Elevated T3 & T4 (Cardiac output to increases with systolic blood pressure) or Low T3 & T4 (Total peripheral resistance and Diastolic Hypertension)
• Adrenal gland (Causes HTN by producing excess aldosterone, which causes the body to retain sodium and water plus increased blood pressure.
  • Conn's Syndrome
  • Pheochromocytoma: rare tumor in the adrenal glands that causes excess production of epinephrine and norepinephrine. and Cushing's Syndrome (overproduction of cortisol causes increased sympathetic activity)

Secondary HTN (N - Neurological Disease related)

• Can present as Cushing's Triad (Bradycardia/HTN/Irregular breathing) and as clinical sign that indicates intracranial pressure
• It can be caused by brain tumor, stroke, traumatic brain injury, subarachnoid hemorrhage, or intracranial infection

Causes by Aortic Disease

Mainly see in young patients who have a congenital defect. plus show Symptoms like chest pain dizziness and shortness of breath or aortic aneurysms.

Secondary HTN (L - Little People / Pregnancy)

Can lead to Pre-eclampsia vs Eclampsia (Mother experiences seizures) plus be characterized by HTN, protein, pain and discomfort. It can also can be impacted as the result of "substances" consumed though diet or drugs

Arteriosclerosis

The hardening of the arteries from age and calcium deficieny.

Atherosclerosis

• Dyslipidemia, diabetes, cigarette smoking, and hypertension.
• hypercholesterolemia
• Results in endothelioal permiability that allows lipids to fill the arterial space leading to clots

Impact of Hypertension in the eyes

• Vascular differences between the retina, the choroid, and the optic nerve allow for the different responses to hypertension in addition to arteriolar narrowing as and alter light reflex.

General Complications

• Lead to intimal thickening, hyperplasia of the medial wall, & hyaline degeneration Can cause increased or decreased ocular blood pressure, arterial occlsuions

Main Retinopathy Retinal Signs and Classifications

• Original classification by Keith et al (Keith-Wagener-Barker)
• Scheie developed a classification scale that took into account arteriosclerotic changes.
• 1- Arteriole Signs, 2 Av change 3- CWS hemorage and exodates 4 disc edemia with macular signs Studies also have shown
• The Wong-Mitchell grades are based on a detectable scale but correlate strongly to underlying conditions.
• Grade III/Moderate HTN Retinopathy had an increased risk, Grade 1 / Mild HTN had 2-6x's higher likliehood

Referral Recomendation

-Grade I or II = Non urgent -Grades III =More uregent -Grade IV = Send to ER

Treatment Options

• Lifestyle Changes (Diet, excersize stress)
• Vaspoasms
• Medical Treatment (A through D)
• Side effects exist, Alpha blockers cause hypotention Beta blockers =fatigue, dry eyes, and sexual dysfunction