Hypertension Overview and Definitions

Hypertension Overview

• Hypertension is a condition characterized by persistently high blood pressure
• Elevated blood pressure is a significant risk factor for cardiovascular diseases.

Hypertension Defined

• Optimal blood pressure is under 120/80 mmHg.
• Prehypertension is between 120-139 systolic or 80-89 diastolic mmHg
• Stage 1 hypertension is between 130-139 systolic or 80-89 diastolic mmHg
• Stage 2 hypertension is 140 or higher systolic or 90 or higher diastolic mmHg
• Hypertension is defined as a systolic pressure greater than 140 mmHg or a diastolic pressure greater than 90 mmHg, or both.
• The definition is based on the Sixth Joint National Committee (JNC 6) on the Detection, Evaluation, and Treatment of High Blood Pressure.
• Hypertension is determined using at least three consecutive blood pressure measurements.

Working Definitions

• Hypertension is defined as an arterial pressure of over 130/80 mmHg in adults.
• Prehypertension is identified in individuals with arterial blood pressure between 120-139 mmHg systolic OR 60-80 mmHg diastolic mmHg

Categories of Hypertension

• Primary or Essential Hypertension
  • Benign (Primary) Hypertension
  • Malignant (Primary) Hypertension
• Secondary Hypertension

Primary (Essential) Hypertension Defined

• Hypertension caused by an underlying pathophysiological mechanism with unknown etiology

Benign Primary Hypertension

• A form of primary hypertension characterized by a gradual onset and slow progression over a long duration, often without noticeable symptoms

Malignant Hypertension

• A form of primary hypertension with an abrupt onset and rapid progression.
• Acute symptoms often lead to acute kidney failure and/or cerebral hemorrhage

Secondary Hypertension

• Hypertension that arises from a specific cause, frequently outside the cardiovascular system.
• Instances where the cause is identified, treatments are sometimes available for a permanent cure.

Estimated Frequency of Hypertension Types

• Essential (primary) hypertension: 93% of the hypertensive population
• Benign hypertension: 88.0% of the hypertensive population
• Malignant hypertension: 5.0% of the hypertensive population
• Secondary hypertension: 7% of the hypertensive population
• Renal hypertension: 5.0% of the hypertensive population
• Endocrine hypertension: 1.7% of the hypertensive population
• Miscellaneous causes: 0.3% of hypertensive population

Cause of Hypertension

• The precise cause of primary hypertension is unknown.
• No specific generalized pathology is directly associated to hypertension.
• The mechanisms that control blood pressure likely have irregularities.

Control of Blood Pressure

• Blood pressure is a product of cardiac output and systemic vascular resistance to blood flow

Cardiac Output

• Stroke volume
• End diastolic volume
• End systolic volume
• Rate of contraction of the heart

Stroke Volume

• End diastolic volume
• Filling time
• Venous return
• Venous end restriction
• Skeletal muscle activity (as pumps)
• Blood volume
• Changes in peripheral circulation

Stroke Volume (Continued)

• End systolic volume
• Preload, which is end diastolic volume
• Contractility, affected by hormones and autonomic innervation
• After load, influenced by peripheral circulation

Cardiac Rate

• Hormones (e.g., adrenergic transmitter substances)
• Autonomic innervation
  • Carotid sinus baroreceptors
  • Chemoreceptors of carotid and aortic bodies
  • Atrial reflexes through baroreceptors

Cardiac Output Rate (Baroreceptors)

• Baroreceptors located in the carotid sinuses that detect vascular pressure
• High vascular pressure triggers baroreceptors' discharge and stimulates the vasomotor center in the brain.
• The vasomotor center then signals the heart via the vagus nerve to slow down heart rate.

Cardiac Output Rate (Baroreceptors - Low Pressure)

• Located in the atria and pulmonary arteries
• Reduced pressure stimulates the hypothalamus to release antidiuretic hormone (vasopressin)
• Vasopressin increases water reabsorption in kidneys, leading to increased blood volume
• Atrial receptors via the vagus nerve increase heart rate (Bainbridge reflex)

Cardiac Output Rate (Chemoreceptors)

• Located in carotid and aortic bodies
• Accumulation of CO2 and H+ trigger signal transmission via carotid sinus and vagus nerve to the vasomotor center of the brain
• The signal prompts the vasomotor center to increase heart rate

Systemic Vascular Resistance

• State of contraction of the vasculature
• Volume of blood

Systemic Vascular Resistance (Factors Affecting Dilation)

• Local factors: increased CO2, K+, adenosine, lactate, decreased O2, decrease in local pH, increase in local temperature, endothelial cell products, nitric oxide
• Hormones: vasoactive intestinal peptide, CBRPa, histamine, kinins, substance P, natriuretic peptides, epinephrine in skeletal muscle and liver
• Neural control: cholinergic dilator fibers to skeletal muscle, decrease discharge of noradrenergic vasomotor neurons

Systemic Vascular Resistance (Factors Affecting Constriction)

• Local factors: decrease in local temperature, autoregulation, locally released platelet serotonin
• Endothelial cell products: endothelin-1
• Hormones: norepinephrine, epinephrine, arginine vasopressin, angiotensin II, circulating NA+−K ATPase inhibitor, neuropeptide
• Neural control

Hypertension and Atherosclerosis

• Atherosclerosis, a disorder of large arteries, may cause changes to the vasculature, potentially leading to:
  • Narrowing of arteries
  • Reduced elasticity of blood vessels
• Wide-spread changes could lead to a permanent change in blood pressure.

Hypertension and Atherosclerosis (Atherosclerosis)

• Changes associated with atherosclerosis are not universally observed.
• The changes in individuals with atherosclerosis do not necessarily explain the elevated blood pressure in all cases.

Possible Mechanisms of Hypertension

• Hypertension is likely caused by a combination of alterations in mechanisms that regulate blood pressure.
• In most cases, the changes are not associated with any demonstrable pathology.
• Several potential mechanisms are postulated to account for the increase in blood pressure.

Mechanisms of Hypertension (Neural Component)

• Pathological disturbances in neural components responsible for modulating arterial blood pressure can lead to sustained elevated blood pressure.
• A primary defect in any of four components (CNS, ANS, adrenergic receptors, baroreceptors) may be responsible for hypertension's cause, potentially alone or in combination.

Mechanisms of Hypertension (Autoregulatory Component)

• Defects in blood volume autoregulation lead to a persistent increase in peripheral resistance causing vascular hypertrophy resulting in chronic elevated blood pressure

Mechanisms of Hypertension (Humoral Mechanism I: RAS System)

• Disturbances in the renin-angiotensin-aldosterone system lead to increased blood volume causing increased cardiac output and hypertension

Mechanisms of Hypertension (Humoral Mechanism II: Natriuretic Hormone)

• Over-secretion of natriuretic hormone due to sodium retention may increase blood volume, cardiac output, and peripheral resistance, thus leading to hypertension.

Genetics Links to Hypertension

• Hypertension is partly linked to genetics, and several autosomal inherited forms exist.
• An increased frequency of hypertension is observed in some families, although such observations may be coincidental.
• Atherosclerosis, frequently associated with hypertension, may have genetic causes.

Genetics Links to Hypertension (Genetic Alterations)

• Glucocorticoid-remediable aldosteronism (a genetic disorder)
  • An autosomal dominant condition
  • A hybrid gene in the adrenal gland zona fasciculata
  • The hybrid gene allows the release of excessive aldosterone in response to ACTH.
  • Hyperaldosteronism (overproduction of aldosterone) causes hypertension.
• Apparent mineralocorticoid excess
  • An autosomal recessive condition with a deficiency in 11β-hydroxysteroid dehydrogenase.
  • This enzyme transforms cortisol to cortisone.
  • Loss of the enzyme increases cortisol levels.
  • Elevated cortisol can enhance aldosterone receptor binding, further increasing aldosterone and causing hypertension
• Liddle syndrome
  • Autosomal dominant form of hypertension.
  • Exhibiting low levels of mineralocorticoids.
  • Possessing constitutively activated sodium channels in renal tubules.
  • Increased sodium uptake causes water retention, resulting in elevated blood pressure/hypertension.

This quiz covers the basics of hypertension, including its definition, stages, and risk factors associated with high blood pressure. Understand the significance of blood pressure measurements and the criteria used to classify hypertension. Perfect for those looking to gain a foundational knowledge of cardiovascular health.