What is Hypertension?
Hypertension is increased blood pressure. Two measurements indicate what the blood pressure is. 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. 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 the arteial system.
There can be considerable variation in blood pressure between persons. The average adult blood pressure is around 120/80 mmHg, as measured by a sphygmomanometer with blood pressure cuff around the upper arm while sitting. In general, a sustained diastolic pressure >90 mmHg and a sustained systolic pressure >140 mmHg define hypertension. However, lower is better. 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. (Sacks and Campos, 2010)
The European Society of Hypertension and the European Society of Cardiology (ESH-ESC) guidelines for the management of arterial hypertension define a prehypertensive state in two categories: (1) normal blood pressure with systolic blood pressure of 120 to 129 mm Hg or diastolic blood pressure of 80 to 84 mmHg; and (2) high-normal blood pressure with systolic blood pressure of 130 to 139 mm Hg or diastolic blood pressure of 85 to 89 mm Hg. The Joint National Committee 7 from the USA has combined the normal and high-normal blood pressure categories into a single entity termed 'prehypertension'. Persons with prehypertension are at increased risk for cardiovascular diseases. (Kokubo and Kamide, 2009)
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 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.
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 glomerulosa. Aldosterone exerts an effect on the distal renal tubules, causing them to increase sodium reabsorption while secreting potassium. Retention of sodium increases fluid in the vascular system to maintain pressure. (Manrique et al, 2009)
Another factor in blood pressure control is natriuretic factor released from the atria of the heart, which senses filling of blood. Increased volume, and subsequent increased filling, results in release of this factor, which inhibits sodium reabsorption at the distal renal tubule.
Causes for Hypertension
Over 90% of the time, an 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 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. This increased 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 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. Causes for hypertension may include:
Renal Diseases: just about any renal disease leading potentially to renal failure can result in hypertension. Such diseases can include:
Renal vascular diseases (renal artery stenosis, fibromuscular dysplasia, vasculitis)
Dominant polycystic kidney disease
Renal cell carcinoma
Cushing's syndrome with increased cortisol
Pheochromocytoma, with increased catecholamines (tends to be episodic)
Aldosterone secreting neoplasm (adrenal cortical adenoma)
Neurogenic Causes: such as increased intracranial pressure (tends to be of sudden onset)
Consequences of Hypertension
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.
"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 mmHg. The changes seen in arterioles may include:
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.
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. (Sacks and Campos, 2010)
High sodium intake, above 2 grams per day, is implicated in 1.65 million cardiovascular deaths worldwide in 2010. During that year, the mean level of sodium consumption per person on earth was estimated to be almost 4 grams per day. (Mozaffarian et al, 2014)
A reduction in dietary salt intake by 9.5%, which has been achieved in the United Kingdom over the past 5 years, could prevent a million deaths from stroke and myocardial infarction, and reduce health care costs by over 32 billion dollars, among the current U.S. adult population aged 40 to 85 years. (Smith-Spangler et al, 2010)
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. (Frank, 2008)
Chobanian AV. The Hypertension Paradox - More Uncontrolled Disease despite Improved Therapy. N Engl J Med 2009;361:878-887
Frank J. Managing hypertension using combination therapy. Am Fam Physician. 2008;77:1279-1286.
Kokubo Y, Kamide K. High-normal blood pressure and the risk of cardiovascular disease. Circ J. 2009;73:1381-1385.
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.
Mozaffarian D, Fahimi S, Singh GM, et al. Global Sodium Consumption and Death from Cardiovascular Causes. N Engl J Med 2014;371:624-634.
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.
Sacks FM, Campos H. Dietary therapy in hypertension. N Engl J Med. 2010;362:2102-2112.
Smith-Spangler CM, Juusola JL, Enns EA, Owens DK, Garber AM. Population strategies to decrease sodium intake and the burden of cardiovascular disease. Ann Intern Med. Ann Intern Med. 2010;152:481-487.