Pathophysiology of Hypertension

Pathophysiology of Hypertension

• Hypertension is defined as 130/80 mmHg or higher.
• It's often called the "silent killer" because it usually has no symptoms until target organ damage occurs.
• Symptoms can include fatigue, reduced activity tolerance, dizziness, palpitations, angina, dyspnea, early morning headaches, blurred vision, spontaneous nosebleeds, and depression.
• Hypertension can result in damage to the cardiovascular system, including increased afterload, systolic dysfunction, diastolic dysfunction, and ultimately, heart failure.
• Damage can affect the coronary and cerebral vessels, leading to myocardial ischemia and infarction, and ischemic strokes.
• Hypertension can also contribute to arterial damage, weakened vessel walls, aneurysms, and dissections. Further, it can lead to conditions in the renal, ophthalmic, and cerebral vessels.

Objectives

• Define hemodynamic determinants of systemic hypertension.
• Recognize primary and secondary forms of hypertension.
• Illustrate the role of the kidney in systemic hypertension.
• Recognize the role of renin, angiotensin II, aldosterone, and the sympathetic nervous system in the pathogenesis of hypertension.
• Discuss risk factors and complications for hypertension.
• Implement the above objectives when evaluating various cases of hypertension.

Definition of Terms

• Blood Pressure (BP): Force per unit area exerted on blood vessel walls, measured in mmHg. Systemic arterial BP is measured in large arteries near the heart. The pressure gradient drives blood flow from high-pressure to low-pressure areas.
• Resistance (Peripheral Resistance): Opposition to blood flow, primarily in peripheral systemic circulation. This friction depends on blood viscosity, total blood vessel length, and blood vessel diameter.

BP Formula

• Blood pressure (BP) is dependent on cardiac output (CO) and systemic vascular resistance (SVR).
• BP = CO x SVR
• Cardiac output (CO) is dependent on heart rate (HR) and stroke volume (SV).
• CO = HR x SV
• SVR is the total resistance of arterioles to blood flow.
• SV is the amount of blood pumped by the heart in each cycle.

Major Determinants for Cardiac Output

• Contractility: The strength of cardiac muscle contractions.
• Heart Rate: The speed of cardiac contractions.
• Preload (EDV): The volume of blood in the ventricles before contraction.
• Afterload (Resistance): The pressure the ventricles must overcome to eject blood.

Causes of Hypertension through Cardiac Output Increase

• Increased contractility and heart rate (β-adrenergic stimulation)
• Increased preload from increased venous return (increased circulating blood volume, largely due to sodium and water retention).
• Venous vasoconstriction (α-adrenergic stimulation).

Factors Influencing Peripheral Resistance

• Blood Viscosity: The "stickiness" of blood, affected by formed elements and plasma proteins.
• Blood Vessel Length: Longer vessels create more resistance.
• Blood Vessel Diameter: Changes frequently and significantly impact peripheral resistance; resistance is inversely proportional to the fourth power of the vessel radius (doubling the radius reduces resistance by 16 times).

Relationship Between Blood Flow, Blood Pressure, and Resistance

• Blood flow (F) is directly proportional to the pressure gradient (ΔP). Increased ΔP increases blood flow.
• Blood flow is inversely proportional to peripheral resistance (R). Increased R decreases blood flow.
• Resistance is more pivotal to local blood flow than pressure gradient as it changes readily due to alterations in blood vessel diameter.

Poiseuille's Law

• Poiseuille's law demonstrates dramatic impact of changes in radius on flow. A small increase in radius can double flow, while a reduction can greatly reduce flow.

Blood Flow Examples

• Body uses vasodilation of arterioles to increase flow when needed; this is a more effective way than increasing blood pressure. A five-fold increase in flow can occur through a 50% dilation of the arterioles; these are easily controlled by the body.

Cardiac Output (CO)

• CO is determined by venous return and neural/hormonal controls.
• Venous return largely dictates stroke volume.
• Neural/hormonal controls are mediated by the brain, sympathetic, and parasympathetic responses, responding to blood pressure (BP) and epinephrine levels.

Control of Vascular Resistance

• Autoregulation (neural and hormonal/humoral) in two forms:
• Neural control (quick): autonomic nervous system
• Hormonal/humoral factors (slow): hormones and chemical signals
• Examples of vasoconstrictors and vasodilators

Autoregulation

• Local hypoxia results in release of vasodilating agents (H+, K+, adenosine, prostaglandins) and nitric oxide from endothelial cells. This decreases resistance and increases tissue perfusion.
• Increased tissue perfusion results in lower concentrations of vasodilating agents and more endothelin (a vasoconstrictor) leading to decreased tissue perfusion.

Blood Pressure Regulation Mechanisms

• Short-term regulation:
  • Baroreceptor reflexes (receptors in the aortic arch and carotid sinuses; sensitive to changes in blood pressure to decrease pressure).
  • Chemoreceptor reflexes (sensitive to oxygen, carbon dioxide, and H+ to increase pressure).
• Long-term regulation:
  • Renin-angiotensin-aldosterone system (RAAS): essential for regulating sodium retention and blood pressure.
  • Natriuretic peptides (produced by the atrium, ventricles, and brain; to counter the RAAS to regulate sodium, water balance, blood volume, and arterial pressure via vasodilator and renal effects).

Renin-Angiotensin System

• A crucial hormonal system to regulate sodium and water balance and blood pressure. Dropping blood pressure triggers renin release from the kidneys.
• Renin converts angiotensinogen to angiotensin I, which then converts to angiotensin II (vasoconstrictor) by ACE.
• Angiotensin II stimulates the adrenal glands to release aldosterone, increasing sodium reabsorption and water retention, further raising blood pressure.

Clinical Manifestations

• Hypertension is called the "silent killer" as it often has no noticeable symptoms until significant organ damage occurs.

Risk Factors

• Obesity, high sodium intake, alcohol consumption, lack of physical exercise, diabetes mellitus, dyslipidemia (high cholesterol), stress, and smoking are risk factors for hypertension.
• A decrease in calcium, magnesium, and potassium is associated with hypertension.

Measurement of Blood Pressure (BP)

• Detailed steps for measuring blood pressure, including cuff placement, and listening for Korotkoff sounds.

Blood Pressure Cuff Selection

• The width and length of a blood pressure cuff should ideally be 80% of the upper arm circumference and 40% respectively to ensure accurate measurements.

Where to Listen for Blood Pressure Sounds

• Precise location on the arm for listening to Korotkoff sounds (the sounds during blood pressure measurement) using the stethoscope.