Hypertension


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What is Hypertension?

Hypertension, or high blood pressure, in general usage applies to blood pressure measured in muscular arteries in systemic circulation supplied by blood pumped from the heart. It is defined as persistent systolic blood pressure at least 130 mm Hg or diastolic blood pressure at least 80 mm Hg. It is estimated at least a billion adult persons worldwide have hypertension. (Carey et al, 2022)

There are many possible causes for systemic arterial hypertension. In most cases when high blood pressure is discovered, a specific cause is not identifiable, and has been called "essential" hypertension. Regardless of the cause, lowering blood pressure decreases morbidity and mortality. Persons with essential hypertension often have other cardiovascular risk factors: aging, being overweight, having insulin resistance (including diabetes mellitus), and having high blood lipids. When hypertension is not treated, there is increased risk for stroke, heart disease, and kidney failure. (Messerli et al, 2007)

Two measurements define blood pressure. The systolic pressure results from contraction of the left ventricle of the heart, forcing blood into the aorta and out into its branches that form the systemic arterial circulation. The pressure wave of this contraction is measured peripherally, typically in the arm. The diastolic pressure results from relaxation of the left ventricle of the heart, and the pressure diminishes to a level sustained by the residual pressure retained by the elasticity of muscular arteries.

The average healthy adult blood pressure is desirable at less than 120/80 mmHg, as measured by a sphygmomanometer with blood pressure cuff around the upper arm while sitting. Elevated pressures can be categorized as follows: (Whelton et al, 2018)

  • Sustained systolic pressure of 120 - 129 mm Hg defines an elevated blood pressure

  • Sustained systolic pressure of 130 - 139 and diastolic of 80 - 89 mmHg defines hypertension at stage 1

  • Sustained systolic pressure exceeding 140 mm Hg and diastolic above 90 mm Hg defines Stage 2

A hypertensive crisis (hypertensive emergency) is defined with systolic pressure ≥180 and/or diastolic pressure ≥120 mmHg, and signs of acute or ongoing end-organ damage such as brain damage from encephalopathy, reduced or lost vision from retinal hemorrhage, papilledema, or renal failure with acute/subacute kidney injury are typically present. Hypertensive emergency may occur de novo or complicate long-standing, asymptomatic "essential" hypertension. (American Heart Association, 2022)

Young persons may have a blood pressure of 90/60 mm Hg, and as long as that can be maintained, the better one's overall health will be. However, sustained increases in blood pressure above 115/75 mm Hg can increase morbidity.

Hypertension is a silent disease. It is insidious and relentless. The only reliable way to detect hypertension is to regularly check blood pressure. This should be done as part of a physical exam on every adult.

If hypertension is not treated, there will be organ damage, particularly to kidneys, heart, and brain, which is generally not reversible. Death in persons with hypertension most often occurs from heart failure, chronic renal failure, and stroke. (Law et al, 2009)

Regulation of Blood Pressure

Blood pressure is maintained by the force generated by a pump (the heart), the resistance in the distribution system (the arteries), and the amount of intravascular fluid. Resistance is related to the size of the arterial bed. At the arteriole level, opening and dilating arterioles reduces pressure.

The system requires pressure monitors. The kidney contains mechanisms to control blood pressure. When the glomerular filtration rate (GFR) drops, the stretch receptors in the macula densa signal cells of the juxtaglomerular apparatus to secrete renin into circulation. The renin is converted to angiotensin, which effects vasoconstriction, mainly in peripheral arterioles, which increases peripheral vascular resistance, thereby elevating blood pressure. In addition, renin stimulates release of aldosterone by adrenal cortical cells in the zona glomerulosa. Aldosterone exerts an effect on the distal renal tubules, causing them to increase sodium reabsorption while secreting potassium. Retention of sodium increases fluid within the vascular system to maintain pressure. (Manrique et al, 2009)

Another factor in blood pressure control is natriuretic factor (measured as b-type natriuretic factor, or BNP) released from myocardium, which senses filling of blood. Increased blood volume, and subsequent increased heart filling, results in release of more BNP into circulation, which then acts to inhibit sodium reabsorption at the distal renal tubule, so sodium and vascular fluid volume are lowered to reduce blood pressure.

Causes for Hypertension

Over 90% of the time, a specific identifiable cause for hypertension cannot be found. This is known as "primary" or "essential" hypertension. The term "essential" arose from a belief long ago that an increased pressure was essential to maintain blood perfusion through an abnormal arterial system. Autoregulation of blood pressure is based upon vascular changes, and dietary sodium may also play a major role in this process. Increased sodium intake leads to increased intravascular fluid volume with resultant increased cardiac output that leads to increased peripheral resistance and an increase in blood pressure. Elevated blood pressure then increases renal perfusion pressure that should trigger increased excretion of sodium with water. In essential hypertension the process of sodium excretion is impaired, probably due to multigenic influences. (Sacks and Campos, 2010)

The onset of essential hypertension is typically in middle age. Some factors that may contribute to primary hypertension include: (Padwal et al, 2008)

  • Genetics: persons whose parents had hypertension are more likely to be hypertensive themselves.

  • Diet: more salt (sodium chloride) in the diet promotes increasing blood pressure.

  • Stress: native peoples of the world are far less likely to develop hypertension than persons living in cities of developed nations.

  • Vascular alteration: over time, hypertension results in thickening of small muscular arteries and arterioles, which makes them less responsive to vasodilators.

Less than 10% of the time, hypertension has an identfiable underlying cause, though this does not necessarily mean that recognition will provide a cure for hypertension. Specific causes for hypertension may include:

  1. Renal Diseases: just about any renal disease leading potentially to renal failure can result in hypertension. Such diseases can include:

    • Diabetic nephropathy

    • Glomerulonephritis

    • Renal vascular diseases (renal artery stenosis, fibromuscular dysplasia, vasculitis)

    • Polycystic kidney diseases

    • Renal cell carcinoma

  2. Endocrine Diseases:

    • Cushing syndrome with increased cortisol

    • Pheochromocytoma, with increased catecholamines (tends to be episodic)

    • Aldosterone secreting neoplasm (adrenal cortical adenoma)

  3. Neurogenic Causes: such as increased intracranial pressure (tends to be of sudden onset)

  4. Arterial Vascular Diseases:

    • Aortic coarctation

    • Vasculitis (such as polyarteritis nodosa)

Consequences of Hypertension

  1. Renal Disease: the renal vasculature shows changes with hypertension.

    • "Benign" nephrosclerosis: modest elevations in blood pressure over the years result in thickening of small renal arteries and arterioles, known as hyaline arteriolosclerosis. This vascular disease leads to formation of small cortical scars, with reduction in renal size.

    • Hyperplastic "Malignant" nephrosclerosis: in a small number of persons with previously mild hypertension, or as the initial event, there is a marked rise in blood pressure. Diastolic pressure may exceed 120 to 150 mm Hg. The changes seen in arterioles may include:

  2. Heart Disease: the pressure load placed on the left ventricle results in left ventricular hypertrophy. The heart enlarges and dilates, with hypertrophy more marked than dilation, until the left heart begins to fail, particularly when the heart reaches 500 gm in size. Congestive heart failure and cardiac arrhythmias may result from the failing heart.

  3. CNS Disease: the effect of hypertension on small arteries and arterioles in the brain is to cause thickening and loss of resilience. This hypertensive hyalinization may produce occlusion with resultant small lacunar infarcts, or "lacunes" that appear most commonly in the region of the basal ganglia, internal capsule, thalamus, basis pontis, and hemispheric white matter. This arteriolar sclerosis also results in in vessels that are more prone to rupture. The most common site for rupture is the region of the basal ganglia. The hypertensive hemorrhage that results from rupture is one of the causes for a "stroke".

Treatment of Hypertension

Treatment of hypertension depends upon severity and response to interventions. Mild hypertension may respond to lifetyle changes with diet and exercise. Dietary changes include reducing intake of sodium and increasing intake of fruits and vegetables. Weight reduction to a BMI of <25 is beneficial. (Aaron and Sanders, 2013) (Whelton et al, 2018)

High sodium intake, above 2 grams per day, is implicated in many cardiovascular deaths worldwide. Reducing dietary sodium would save many lives. (Kontis et al, 2019)

For milder hypertension with blood pressures above 140 mm Hg systolic and/or 90 mm Hg diastolic, if lifestyle changes are not followed or not effective, then phamacologic therapy can be instituted, One may begin with a single antihypertensive agent. If that doesn't work, the medication can be continued longer to determine if there is an effect, the dose may be increased, or another agent added. (Chobanian, 2009)

For more severe hypertension with systolic pressures above 160 mm Hg or diastolic above 100 mm Hg, pharmacologic therapy is instituted with two antihypertensive agents. If that doesn't work, another agent is added. (Whelton et al, 2018) (Carey et al, 2022)

References

Aaron KJ, Sanders PW. Role of dietary salt and potassium intake in cardiovascular health and disease: a review of the evidence. Mayo Clin Proc. 2013;88(9):987-95. doi: 10.1016/j.mayocp.2013.06.005.

American Heart Association, https://www.heart.org/en/health-topics/high-blood-pressure/understanding-blood-pressure-readings#.WmtDNyOfnRY (accessed June 14, 2022).

Carey RM, Moran AE, Whelton PK. Treatment of Hypertension: A Review. JAMA. 2022 Nov 8;328(18):1849-1861. doi: 10.1001/jama.2022.19590.

Chobanian AV. The Hypertension Paradox - More Uncontrolled Disease despite Improved Therapy. N Engl J Med 2009;361:878-887

Kontis V, Cobb LK, Mathers CD, Frieden TR, Ezzati M, Danaei G. Three Public Health Interventions Could Save 94 Million Lives in 25 Years. Circulation. 2019 Aug 27;140(9):715-725. doi: 10.1161/CIRCULATIONAHA.118.038160.

Law MR, Morris JK, Wald NJ. Use of blood pressure lowering drugs in the prevention of cardiovascular disease: meta-analysis of 147 randomised trials in the context of expectations from prospective epidemiological studies. BMJ 2009;338:b1665.

Manrique C, Lastra G, Gardner M, Sowers JR. The renin angiotensin aldosterone system in hypertension: roles of insulin resistance and oxidative stress. Med Clin North Am. 2009 May;93:569-582.

Messerli FH, Williams B, Ritz E. Essential hypertension. Lancet. 2007;370(9587):591-603. doi: 10.1016/S0140-6736(07)61299-9.

Padwal RS, Hemmelgarn BR, Khan NA, et al. The 2008 Canadian Hypertension Education Program recommendations for the management of hypertension: Part 1 - blood pressure measurement, diagnosis and assessment of risk. Can J Cardiol. 2008;24:455-463.

Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2018 May 15;71(19):e127-e248. doi: 10.1016/j.jacc.2017.11.006.


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