What is hypertension?

Causes and Symptoms

Hypertension is a higher-than-normal blood pressure (either systolic or diastolic). Blood pressure is usually measured using a sphygmomanometer and a stethoscope. The stethoscope is used to hear when the air pressure within the cuff of the sphygmomanometer is equal to that in the artery. When taking a blood pressure, the cuff is pumped to inflate an air bladder secured around the arm; the pressure produced will collapse the blood vessels within. As cuff pressure decreases, a slight thump is heard as the artery snaps open to allow blood to flow. At this point, the cuff pressure equals the systolic blood pressure. As the cuff pressure continues to fall, the sound of blood being pumped will continue but become progressively softer. At the point where the last sound is heard, the cuff pressure equals the diastolic blood pressure.

In hypertension, both
systolic and diastolic blood pressures are usually elevated. Blood pressures are reported as the systolic pressure over the diastolic pressure, such as 130/80 millimeters of mercury. It is important to recognize there are degrees of seriousness for hypertension. The higher the blood pressure, the more rigorous the treatment may be. When systolic pressures are in the high normal range, the individual should be closely monitored with annual blood pressure checks. Persistently high blood pressures (greater than 140–159/90–99 millimeters of mercury) require closer monitoring and may result in a decision to treat the condition with medication or other types of intervention.

The blood pressure in an artery is determined by the relationship among three important controlling factors: the blood volume, the amount of blood pumped by the heart (cardiac output), and the contraction of smooth muscle within blood vessels (arterial tone). To illustrate the first point, if blood volume decreases, the result will be a fall in blood pressure. Conversely, the body cannot itself increase blood pressure by rapidly adding blood volume; fluid must be injected into the circulation to do so.

A second controlling factor of blood pressure is cardiac output (the volume of blood pumped by the heart in a given unit of time, usually reported as liters per minute). This output is determined by two factors: stroke volume (the volume of blood pumped with each heartbeat) and the heart rate (beats per minute). As heart rate increases, output generally increases, and blood pressure may rise as well. If blood volume is low, such as with excessive bleeding, the blood returning to the heart per beat is lower and could lead to decreased output. To compensate, the heart rate increases to prevent a drop in blood pressure. Therefore, as cardiac output changes, blood pressure does not necessarily change.

Last, a major controlling factor of blood pressure is arterial tone. Arteries are largely tubular, smooth muscles that can change their diameter based on the extent of contraction (tone). This contraction is largely under the control of a specialized branch of the nervous system called the sympathetic nervous system. An artery with high arterial tone (contracted) will squeeze the blood within and increase the pressure inside. There is also a relaxation phase that will allow expansion and a decrease in blood pressure. Along with relaxation, arteries are elastic to allow some stretching, which may further help reduce pressure or, more important, help prevent blood pressure from rising.

There are two general types of hypertension: essential and secondary. Secondary hypertension is attributable to some underlying identifiable cause, such as a tumor or kidney disease, while essential hypertension has no identifiable cause. Therefore, essential hypertension is a defect that results in excessive arterial pressure secondary to poor regulation by any one of the three controlling factors discussed above. Each factor can serve as a focal point for treatment with medications.

The negative consequences of hypertension are mainly manifested in the deteriorating effect that this condition has on coronary heart disease (CHD). Cardiovascular risk factors for CHD are described as two types, unmodifiable and modifiable. Unmodifiable risk factors cannot be changed. This group includes gender, race, advanced age, and a family history of heart disease (hypertensive traits can be inherited). The modifiable risk factors are cigarette smoking (or other forms of tobacco abuse), high blood cholesterol levels, control over diabetes, and perhaps other factors not yet discovered. For example, additional factors are now recognized for their adverse effects on hypertension, including obesity, a lack of physical activity, and psychological factors.

There is no definitive blood pressure level at which a person is no longer at risk for CHD. While any elevation above the normal range places the person at increased risk for CHD, what are considered high normal blood pressures were previously defined as normal. (Looking back at older data, researchers noted that persons able to maintain pressures at or below 139/89 millimeters of mercury had less severe CHD.) The definition of normal blood pressure may change again in the future as new information is discovered. There is a practical limit as to how low pressure can be while maintaining day-to-day function.

In coronary heart disease, the blood supply to the heart is reduced, and the heart cannot function well. The common term for arteriosclerosis, “hardening of the arteries,” indicates the symptom of reduced blood flow, which is a major component of CHD. When the heart cannot supply itself with the necessary amount of blood (a condition known as ischemia), a characteristic chest pain called angina may be produced. The hardening aspect of this disease is the result of cholesterol deposits in the vessel, which decrease elasticity and make the vessel wall stiff. This stiffness will force pressures in the vessel to increase if cardiac output rises. As pressures advance, the vessel may develop weak spots. These areas may rupture or lead to the development of small blood clots that may clog the vessel; either problem will disrupt blood flow, making the underlying CHD worse. Eventually, if the blood supply is significantly reduced, a myocardial infarction(heart attack) may occur. Where the blood supply to the heart muscle itself is functionally blocked, that part of the heart will die.

Besides contributing to an increased risk of heart attack and coronary heart disease, hypertension is a major risk for other vascular problems, such as stroke, kidney failure, heart failure, and visual disturbances secondary to the effects on the blood vessels within the eye. Hypertension is a major source of premature death in the United States. According to the Centers for Disease Control and Prevention in 2014, over 67 million Americans, or 1 in 3 adults, have hypertension. Over forty percent of all African Americans and over 60 percent of those over the age of sixty-five are affected. Public awareness of hypertension is increasing, yet less than half of all patients diagnosed are treated or report having their condition under control. This lack of control is of particular concern when one considers the organs influenced by hypertension, most notably the brain, eyes, kidneys, and heart.

Although causative factors of hypertension cannot be identified, many physiological factors contribute to hypertension. They include increased sympathetic nervous activity (part of the autonomic nervous system), which promotes arterial contraction; overproduction of an unidentified sodium-retaining hormone or chronic high sodium intake; inadequate dietary intake of potassium or calcium; an increased or inappropriate secretion of renin, a chemical made by the kidney; deficiencies of arterial dilators, such as prostaglandins; congenital abnormalities (birth defects) of resistance vessels; diabetes mellitus or resistance to the effects of insulin; obesity; increased activity of vascular growth factors; and altered cellular ion transport of electrolytes, such as potassium, sodium, chloride, and bicarbonate.

The kidneys are greatly responsible for blood pressure control. They have a key role in maintaining both blood volume and blood pressure. When kidney function declines, secondary to problems such as a decrease in renal blood flow, the kidney will release renin. High renin levels result in activation of the renin-angiotensin-aldosterone system. The resulting chemical cascade produces angiotensin II, a potent arterial constrictor. Another chemical released is aldosterone, an adrenal hormone which causes the kidney to retain water and sodium. These two actions add to blood volume and increase arterial tone, resulting in higher blood pressure. Normally, the renin-angiotensin-aldosterone system protects kidney function by raising blood pressure when it is low. In hypertensives, the controlling forces seem to be out of balance, so that the system does not respond appropriately. The renin-angiotensin-aldosterone system has a negative effect on bradykinin, a chemical that protects renal function by producing vasodilating prostaglandins that help maintain adequate renal blood flow. This protection is especially important in elderly individuals, who may depend on this system to maintain renal function. The system can be inhibited by medications such as aspirin or ibuprofen, resulting in a recurrence of hypertension or less control over the existing disease.

Arteries are largely smooth muscles under the control of the autonomic nervous system, which is responsible for organ function. Yet there is often no conscious control of organs; for example, one can tell the lungs to take a breath, but one cannot tell the heart to beat. The autonomic nervous system has two branches, sympathetic and parasympathetic, that essentially work against each other. The sympathetic system exerts much control over blood pressure. Many chemicals and medicines, such as caffeine, decongestants, and amphetamines, affect blood pressure by mimicking the effects of increased sympathetic stimulation of arteries.

Numerous factors associated with blood pressure elevations will affect one or more of the key determinants of blood pressure; they affect one another as well. An example will show the extent of their relationship. Sodium and water retention will increase blood volume returning to the heart. As this return increases, the heart will increase output (to a point) to prevent heart failure. This higher cardiac output may also raise blood pressure. If arterial vessels are constricted, pressures may be even higher. This elevated pressure (resistance) will force the heart to try to increase output to maintain blood flow to vital organs. Thus, a vicious cycle is started; hypertension can be perceived as a merry-go-round ride with no exit.

Treatment and Therapy

Blood pressure reduction has a protective effect against cardiovascular disease. Generally, as blood pressure decreases, arteries are less contracted and are able to deliver more blood to the tissues, maintaining their function. Furthermore, this decreased blood pressure will help reduce the risk of heart attack in the patient with heart disease. With lower pressures, the heart does not need to work as hard supplying blood to itself or the rest of the body. Therefore, the demand for cardiac output to supply blood flow is less. This reduced workload lowers the incidence of angina.

Treatment of hypertensive patients may involve using one to four different medications to achieve the goal of blood pressure reduction. There are many types of medications from which to choose: diuretics, sympatholytic agents (also known as antiadrenergic drugs), beta-blockers (along with one combined-action alpha-beta blocker), calcium-channel blockers, peripheral vasodilators, angiotensin-converting enzyme inhibitors, and the newest class, angiotension receptor inhibitors. The list of available drugs is extensive; for example, there are fourteen different thiazide-type diuretics and another six diuretics with different mechanisms of action.

Patients prone to sodium and water retention are treated with diuretics, agents that prevent the kidney from reabsorbing sodium and water from the urine. Diuretics are usually added to other medications to enhance those medications’ activity. Research into thiazide-type diuretics has shown that these agents possess mild calcium-channel blocking activity, aiding their ability to reduce hypertension.

Beta-blocking agents are used less often than when they were first developed. They work by decreasing cardiac output through reducing the heart rate. Although they are highly effective, the heart rate reduction tends to produce side effects. Most commonly, patients complain of fatigue, sleepiness, and reduced exercise tolerance (the heart rate cannot increase to adapt to the increasing demand for blood in tissues and the heart itself). These agents are still a good choice for hypertensive patients who have suffered a heart attack. Their benefit is that they reduce the risk of a second heart attack by preventing the heart from overworking.

Calcium-channel blockers were originally intended to treat angina. These agents act primarily by decreasing arterial smooth muscle contraction. Relaxed coronary blood vessels can carry more blood, helping prevent the pain of angina. When calcium ions enter the smooth muscle, a more sustained contraction is produced; therefore, blocking this effect will produce relaxation. Physicians noted that this relaxation also produced lower blood pressures. The distinct advantage to these agents is that they are well tolerated; however, some patients may require increasing their fiber intake to prevent some constipating effects.

Peripheral vasodilators have been a disappointment. Theoretically, they should be ideal since they work directly to cause arterial dilation. Unfortunately, blood pressure has many determinants, and patients seem to become immune to direct vasodilator effects. Peripheral vasodilators are useful, however, when added to other treatments such as beta-blockers or sympatholytic medications.

The sympatholytic agents are divided into two broad categories. The first group works within the brain to decrease the effects of nerves that would send signals to blood vessels to constrict (so-called constrict messages). They do this by increasing the relax signals coming out of the brain to offset the constrict messages. The net effect is that blood vessels dilate, reducing blood pressure. Many of these agents have fallen into disfavor because of adverse effects similar to those of beta-blockers. The second group of sympatholytics works directly at the nerve-muscle connection. These agents block the constrict messages of the nerve that would increase arterial smooth muscle tone. Overall, these agents are well tolerated. Some patients, especially the elderly, may be very susceptible to their effect and have problems with low blood pressure; this issue usually resolves itself shortly after the first dose.

The renin-angiotensin-aldosterone system is a key determinant of blood pressure. Angiotensin-converting enzyme inhibitors (ACE inhibitors) work by blocking angiotensin II and aldosterone and by preserving bradykinin. They have been found quite effective for reducing blood pressure and are usually well tolerated. Some patients will experience a first-dose effect, while others may develop a dry cough that can be corrected by dose reductions or discontinuation of the medication. The angiotension receptor inhibitors work, instead, by blocking the effects of this substance on the target cells of the arteries themselves. They are proving to be excellent substitutes for people who cannot tolerate the related class of ACE inhibitors.

Unfortunately, and contrary to popular belief, no one can reliably tell when his or her own blood pressure is elevated. Consequently, hypertension is called a “silent killer.” It is extremely important to have regular blood pressure evaluations and, if diagnosed with hypertension, to receive treatment.

From 1950 through 1987, as advances in understanding and treating hypertension were made, the United States population enjoyed a 40 percent reduction in coronary heart disease and a more than 65 percent reduction in stroke deaths. (By comparison, noncardiovascular deaths during the same period were reduced little more than 20 percent.)

It is evident that blood pressure can be reduced without medications. Research in the 1980s led to a nonpharmacologic approach in the initial management of hypertension. This strategy includes weight reduction, alcohol restriction, regular exercise, dietary sodium restriction, dietary potassium and calcium supplementation, stopping of tobacco use (in any form), and caffeine restriction. Often, these methods can produce benefits without medication being prescribed. Stress is another common contributor to hypertension; therefore, stress reduction and management is another strategy to reduce blood pressure. This may be achieved through lifestyle changes, meditation, relaxation techniques, and exercise. Using this approach, medication is added to the therapy if blood pressure remains elevated despite good efforts at nonpharmacologic control.

Other aspects of hypertension and hypertensive patients have been identified to help guide the clinician to the proper choice of medication. With this approach, the clinician can focus therapy at the most likely cause of the hypertension: sodium and water retention, high cardiac output, or high vascular resistance. This pathophysiological approach led to the abandonment of the rigid step-care approach described in many texts covering hypertension. The pathophysiological approach to hypertension management is based on a series of steps that are taken if inadequate responses are seen.

The best strategy for controlling hypertension is to be informed. Each person needs to be aware of his or her personal risk for developing hypertension. One should have regular blood pressure evaluations, avoid eating excessive salt and sodium, increase exercise, and reduce fats in the diet. Maintaining ideal body weight may be a key control factor. Studies have shown that patients who have been successful at losing weight will require less stringent treatment. The benefits could be a need for fewer medications, reduced doses of medications, or both.

Bibliography

Cruickshank, J. M. Essential (Primary) Hypertension. New York: McGraw-Hill Medical, 2013. Print.

Elliott, William J., and Henry R. Black. Hypertension: A Companion to Braunwald's Heart Disease. Philadelphia: Elsevier Saunders, 2013. Print.

"High Blood Pressure Facts." Centers for Disease Control and Prevention. CDC, 7 July 2014. Web. 21 Aug. 2014.

McGowan, Mary P., and Jo McGowan-Chopra. The Hypertension Sourcebook. Chicago: Contemporary, 2001. Print.

Messerli, Franz H., ed. Cardiovascular Disease in the Elderly. 3d ed. Boston: Kluwer, 1993. Print.

Mancia, Giuseppe, and Adel E. Berbari. Special Issues in Hypertension. Milano: Springer-Verlag, 2012. Print.

Matthes, Jan, and Christian Albus. "Improving Adherence with Medication: A Selective Literature Review Based on the Example of Hypertension Treatment." Dtsch. Arztebl Int 111.4 (2014): 41–47. Print.

Messerli, Franz H. The Heart and Hypertension. New York: Yorke Medical, 1987. Print.

Piscatella, Joseph, and Barry Franklin. Take a Load Off Your Heart: 109 Things You Can Do to Prevent or Reverse Heart Disease. New York: Workman, 2003. Print.

Portman, Ronald J., Julie R. Ingelfinger, Joseph T. Flynn. "Pediatric Hypertension." Clinical Hypertension and Vascular Disease. 3d ed. New York: Humana, 2013. Print.

Rowan, Robert L. Control High Blood Pressure Without Drugs: A Complete Hypertension Handbook. Rev. ed. New York: Fireside, 2001. Print.

Seeley, Rod R., Trent D. Stephens, and Philip Tate. Anatomy and Physiology. 7th ed. New York: McGraw-Hill, 2006. Print.

Tierney, Lawrence M., Stephen J. McPhee, and Maxine A. Papadakis, eds. Current Medical Diagnosis and Treatment 2007. New York: McGraw-Hill, 2006. Print.

Zanchetti, Alberto. "Challenges of Hypertension and Hypertension Treatment." Journal of Hypertension. Lippincott Williams & Wilkins, 20 Aug. 2014. Web. 24 Aug. 2014.