Understanding Hypertension: Risks and Statistics

Hypertension (HTN) Overview

• Approximately 1.28 billion adults (30-79 years old) worldwide have HTN.
• In the US, 1 in 3 adults has HTN where 2/3 live in low- and middle-income countries.
• 46% of adults with HTN are unaware of their condition, and only about 1 in 5 adults have it under control.
• HTN is more prevalent in men than women (not dramatically different).
• Non-Hispanic Black adults (57.2%) are more likely to have HTN than non-Hispanic White (42.6%) or Hispanic (43.7%) adults.
• HTN is an attributable risk factor in 41% of all cardiovascular disease (CVD) deaths from myocardial infarction (MI), heart failure, and stroke.
• Blood pressure (BP) increase of 20 mmHg (systolic) or 10 mmHg (diastolic) is associated with doubling the risk of CVD death regardless of age.
• Middle-age patients with HTN have a known increase in developing chronic kidney disease and dementia later.
• Globally the HTN prevalence is 39%

Blood Pressure

• Blood pressure is defined as the pressure of blood pushing against the walls of arteries as it carries blood.
• Systolic pressure is the pressure in the arteries when the heart beats, i.e., contracts.
• Diastolic pressure is the pressure in the arteries when the heart is at rest, i.e., between beats or refilling.
• Normal BP is considered to be 120/80 mmHg.
• The non-Hispanic African-American ethnicity is more likely to have HTN than Caucasians, Asians, or Hispanic people.
• HTN affects 22.4% of adults between 18 to 39.
• HTN affects 54.5% of adults between 40 to 59.
• HTN affects 74.5% of adults above 60.

American College of Cardiology/American Heart Association (ACC/AHA) Guidelines

• BP readings as per ACC/AHA include
• Normal BP: <120/<80 mmHg, with recommendation to promote a healthy lifestyle and reassess BP annually.
• Elevated BP: 120-129/<80 mmHg, start with nonpharmacologic therapy, reassess BP in 3-6 months.
• Stage 1 Hypertension: 130-139/80-89 mmHg, follow different recommendations based on the atherosclerotic cardiovascular disease (ASCVD) risk score.
• Stage 2 Hypertension: ≥140/≥90 mmHg, start with both nonpharmacologic and pharmacologic therapy and reassess BP in 1 month.

ASCVD Risk Estimator

• Atherosclerotic Cardiovascular Disease (ASCVD) Risk Estimator is a tool to calculate a patient's 10-year risk for developing atherosclerotic cardiovascular disease (*developed and endorsed by ACC and AHA).
• Factors include age, gender, ethnicity, cholesterol levels, blood pressure, and smoking status.
• Calculator risk levels provide guideline treatment decisions on starting a statin based on a patient's calculated risk level.
• Risk categories include
• Low-risk (<5%)
• Borderline risk (5% to 7.4%)
• Intermediate risk (7.5% to 19.9%)
• High risk (≥20%)

JNC-8 Classification of Blood Pressure

• BP Classification as per JNC-8
• Normal: Systolic <120 and Diastolic <80(mmHg)
• Prehypertension: Systolic 120-139 or Diastolic 80-89(mmHg)
• Stage 1 HTN: Systolic 140-159 or Diastolic 90-99(mmHg)
• Stage 2 HTN: Systolic >=160 or Diastolic >=100(mmHg)

Hypertensive Crisis

• Hypertensive crisis occurs when systolic BP is >180 mmHg and/or diastolic BP is >120 mmHg.
• Subcategories of hypertensive crisis are:
• Hypertensive emergencies, characterized by severe BP elevation associated with new onset or worsening organ damage.
• Hypertensive urgencies, characterized by elevation in blood pressure values without clinical, laboratory, or instrumental evidence of acute hypertensive organ damage.
• Symptoms of a hypertensive emergency can include dizziness, headache, vision problems, nausea, vomiting, trouble breathing, and chest pain.

Hypertension Symptoms

• As HTN continues to progress, untreated patients can experience HA (headaches), blurry vision, or dizziness.
• Severely elevated BP can cause acute, severe, and life-threatening complications such as papilledema, stroke, encephalopathy, acute kidney injury, and heart failure.

Blood Pressure Assessment

• Measuring blood pressure accurately is crucial for diagnosing and managing hypertension, including:
• Preparing a quiet room with comfortable temperature.
• Avoiding smoking, caffeine, and exercise for 30 minutes before measurement, emptying the bladder, and remaining seated and relaxed for 3-5 minutes.
• Avoiding talking by the personnel/pt before, during, and between measurements.
• Measurements with arm resting on table at heart level, back supported on chair, legs uncrossed, and feet flat on floor.
• Validated electronic (oscillometric) upper-arm cuff device is used.
• Size of cuff is appropriate for the individual's arm circumference.
• Three measurements are taken one minute apart, with the average of the last two measurements used.
• At each visit, take three measurements with 1 min between them, calculating the average of the last 2 measurements; BP of the first reading is <130/85 mm Hg, no further measurement is required.
• Blood pressure of 2-3 office visits ≥140/90 mm Hg indicates hypertension.
• Inappropriate cuff size will result in inaccurate measurements.
• The bladder of the cuff must cover 75%-100% of the individual's arm circumference for manual auscultatory devices.
• Following an elevated blood pressure reading
• Recheck BP after 5 minutes
• Assess patient's overall health status for any history of MI, angina, stroke, renal disease, or other systemic concerns.
• Document, provide patient education and advise patient to recheck at home and contact PCP if necessary for Stage 1.
• Stage II, proceed as above, and consider consulting with the patient's primary care physician.
• White coat hypertension is a condition where a patient's blood pressure spikes in medical settings due to anxiety.

Primary Hypertension

• Primary hypertension is most likely due to multiple factors (95%).
• It is multi-factorial and does not have one distinct cause.
  • Age
  • Diet
  • Excess caffeine/sodium intake
  • Family history
  • Obesity
  • Alcoholism
  • Sedentary lifestyle
• Primary HTN develops gradually over time, and patients can be asymptomatic.
• Smoking, alcohol intake in access, not enough physical activity, poor diet and genetic factors are considered risk factors for HTN
• Arterial stiffening/hardening occurs due to loss of elastin fibers and buildup of stiffer collagen fibers with age where isolated systolic HTN is seen in 80% are over 65yo

Secondary Hypertension

• Secondary hypertension is when there is an identified cause.
  • Kidney disease
  • Endocrine disorders
  • Certain medications
  • Changes to blood vessels (aorta/kidney arteries
• Typically happens at a younger age with some underlying disease.
• Common causes include
  • Renal disease. Symptoms: early onset HTN, resistant to treatment, and increased urea excretion
  • Endocrine disorders (Thyroid), adrenal gland (Conn's syndrome, Pheochromocytoma)
  • Neurological disease (Cushing's Triad)
  • Aortic disease: Coarctation of the aorta

Mean Arterial Pressure

• Governing factors in determining blood pressure include mean arterial pressure (MAP), cardiac output, and peripheral resistance.
• MAP = the average arterial blood pressure over an entire cardiac cycle.
  • Calculated as Cardiac Output (CO) * Total Peripheral Resistance (TPR)
• Cardiac output is the product of heart rate times stroke volume.

Peripheral Resistance

• Increase in blood pressure may result from arterial tone changes due to increased alpha-adrenergic stimulation and vessel wall elasticity reduced by vascular smooth muscle contraction.
• Atherosclerosis and Arteriosclerosis can contribute to increased peripheral resistance.

Sympathetic Nervous System (SNS)

• The SNS manages the "fight-or-flight response".
• Regulates blood pressure, influencing the vasculature, kidneys, and heart
• SNS is activated by the hypothalamus by sending signals to the adrenal glands, which release epinephrine into the bloodstream.
• Causes increased heart rate, contractility, vasoconstriction, and blood pressure
• Affecting the beta-1-adrenergic receptors, located in the SA node and cardiac muscles
• Less effect on the alpha-adrenergic receptors in the heart (coronary blood vessel constriction)

Renin-Angiotensin-Aldosterone System (RAAS)

• A hormonal system in the body (kidneys) primarily regulates blood pressure by controlling fluid and electrolyte balance through the action of different hormones:
  • Renin
  • Angiotensin II
  • Aldosterone
• When blood pressure drops, the kidneys release renin, which leads to a cascade of reactions that lead to vasoconstriction and increased sodium absorption, leading to blood pressure elevation.
• Main function of RAAS - maintain BP is regulating blood volume and vascular tone.
• Hormones being released are: Renin: enzyme secreted by the kidneys when blood pressure drops. Angiotensinogen: a protein produced by the liver converts to Angiotensin I by renin. Angiotensin Converting Enzyme (ACE): enzyme converts Angiotensin 1 to active hormone, Angiotensin II. Angiotensin II: causes blood vessels to constrict and stimulates the adrenal glands to release aldosterone. Also causes release of antidiuretic hormone from the pituitary gland. Causes the kidneys to retain water from the urine, which increases blood volume and blood pressure. Aldosterone: causes kidneys to retain sodium and water, which increases blood pressure.
• Drugs act on the RAAS (ACE inhibitors and Angiotensin receptor blockers).
• These are commonly used to treat high blood pressure by blocking the conversion of Angiotensin I to Angiotensin II or by blocking the Angiotensin II receptor.
• Kidneys release enzyme "renin" in bloodstream when blood pressure falls. At the same time, the liver makes & releases a protein, called angiotensinogen.
• Renin converts angiotensinogen to hormone angiotensin I. - Bloodstream Angiotensin I gets converted by angiotensin-converting
• Enzyme" in lungs and bloodstream kidneys into angiotensin I.
• Angiotensin 1 then causes small arteries (arterioles) to constrict/narrow, which raises blood pressure.
• Angiotensin I also triggers adrenal glands to release
• Aldosterone and your pituitary gland to release antidiuretic hormone (ADH, or vasopressin).-
• Lastly, aldosterone and ADH both cause kidneys to retain sodium. -Aldosterone causes kidneys to release (excrete) potassium in urine.

Kidneys

• Kidneys / Juxtaglomerular Apparatus.
• Located in the kidneys at the junction of the afferent arteriole and the distal convoluted tubule.
• Glomerulus filters blood to remove waste products, excess fluid, and solutes which is collected by Bowman's capsule.
• In the nephron, each kidney 1 million nephrons, which filters to produce urine.
• Retinal vein thrombosis cause formation of a clot in a vein to the kidney

Juxtaglomerular (JG) Cells

• Juxtaglomerular (JG) cells contains renin. *activating the RAAS
• Are smooth muscle cells responsible as mechanoreceptors to sense blood pressure.

Macula Densa Cells

• The Macula Densa cells specialized cells which function as chemoreceptors that sense changes to solute concentration and flow rate (filtration).
• Specialized cells of the distal convoluted tubule (DCT) at the point of contact with the afferent arterioles.
• If there is reduced osmolality or diminished flow rate, there is vasodilation of the afferent arteriole that stimulate JG cells to release renin, Increasing glomerular filtration rate.
• Conversely, if there is increased osmolality, there is vasoconstriction of the afferent arteriole, decreasing glomerular filtration rate.

Renal Tubules

• Renal tubule filtrate passes kidneys which ends at the collecting duct: include the proximal convoluted tubule, loop of Henle, distal convoluted tubule, and collecting duct.

Arteriosclerosis vs. Atherosclerosis

• Arteriosclerosis is a general term for hardening and thickening of the arteries and caused by Age ,HTN, DM and smoking or loss of elasticity and flexibility in the arteries.
• Atherosclerosis is a particular type of arteriosclerosis.
• It involves the formation on inner arterial walls caused by buildup of fatty deposits (plaque).

Arteriosclerosis

• There is a elastic decrease happens with function that affect the arteries with age that also increase in BP. In this case. Vessels become thicken/stiffen.
• This Can clinically manifest in different ways:
  • Coronary Artery Disease: plaque buildup inside a coronary artery
  • Peripheral Artery Disease: artery narrowing in the legs, arms or pelvis Peripheral Artery Disease)
  • Carotid disease: Artery narrowing (Caused by plaque buildup) is more common and the Carotid Artery carry blood throughout aorta, including at the HEAD . Peripheral Artery Disease: Artery narrowing in the legs, arms or pelvis
• Treatment is include eating a healthy diet, exercise, stopping, proper sleep stress and smoking managements

Atherosclerosis

• atherosclerosis is a condition when the patient plaque is build up for a prolonged period of time
  • This are caused with a diet with lots of lipids, diabetes patient are to consider, cigarette, hypertension, and to note genetic are abnormalities. -Atherosclerosis are changes in the arterial endothelial permeability.

Hypertensive Retinopathy

• Vascular differences between the retina, the choroid, and the optic nerve is linked with different responses to hypertension.
• Often asymptomatic and presents bilaterally, tends to come earlier in african american patients.
• Second Most common retinal vascular disease
• Initially, see vasoconstriction as a presence of vasoplasm increase (Clinically Appears).
• Hypertensive changes can cause Gunn's sign = A.V nicking along with vascular changes, with copper red to dark wiring leading to blindness, Retinopathy
• Classifications are:
• Grades I and II are typically chronic for hypertension retinopathy.
• Grades III and IV are typically acute findings for hypertension retinopathy with increasing higher risk of clinical stroke.

Hypertension Choroidopathy

• In younger patients this often find it when they are malignant
• Ischemic changes is present as acute, at acute focal lesion of RPE that involves Choriocapillaris and overlying RPE result in
• Elschnig Spots and Siegrest Streaks will happens within this situation.

Medication

• Medications: A.B.C.D
• A's : Ace angiotensin agents inhibitors and Agiotensin 2 Diminishes RAAS system.
• Reductions with B (beta blockers) for peripheral resistance and both reduction of cardiac output
• Reduction Vasocontriction ( Calcium CB’')

Alpha Blockers

• Alpha blockers /Alpha antagonist , it reduce stimulation, it reduces prostate hypertension.
• Alpha blocker might cause hypotentiaons which are increased incidence and might cause Chf.
• Beta Blockers may cause Fatigue and dry eyes and dysfunction in sexual activity.
• Diuretics could increased hypotension or increased dyhdration.