Definition and epidemiology
The dividing line between normal and elevated blood pressure is not absolute, a fact that makes a precise definition of hypertension difficult. Studies indicate that the morbidity and mortality related to an elevation in blood pressure increase in direct proportion to the level of systolic and diastolic blood pressure, beginning at levels well below 140/90. However, a blood pressure in excess of 140/90 is generally considered the point at which a patient can be considered hypertensive, particularly if the elevation is reproduced on at least two occasions. Hypertension is typically classified as mild, moderate, or severe depending on the level of the diastolic blood pressure (Table 1). However, isolated systolic hypertension may occur and is defined as a systolic blood pressure greater than or equal to 160 mm Hg associated with a diastolic blood pressure less than 85 mm Hg. The blood pressure in healthy children and pregnant women is typically lower, so that readings in excess of 120/80 may indicate an abnormal elevation in blood pressure.
In the United States, approximately 15% of the adult white population and 25% of the adult black population can be considered hypertensive. Many factors affect the risk of developing hypertension in an individual patient. The incidence of the disease increases with age. Heredity plays a strong role, with approximately 80 per cent of hypertensive patients displaying a positive family history. Obesity and the dietary intake of sodium are two other variables that increase the risk of hypertension in susceptible individuals. Whereas heredity and age cannot be controlled, factors such as body weight and diet can be modified.
Table 1. Classification of hypertension
The pathophysiology of hypertension
A review of the physiological determinants of normal blood pressure provides a way of introducing the factors that play a role in the development of hypertension. The blood pressure is generated by cardiac contraction, which produces its maximal pressure, the systolic blood pressure, during ejection. This is followed by cardiac relaxation, which results in a fall in blood pressure to its nadir level, the diastolic blood pressure. The mean arterial blood pressure lies between the systolic and diastolic pressure and can be defined as a function of cardiac output and systemic vascular resistance (Figure 1). The mean arterial pressure is tightly regulated within a range that maintains tissue perfusion but minimizes vascular trauma. Multiple factors impact on the control of blood pressure by mechanisms that affect either cardiac output or systemic vascular resistance (Figure 1).
Figure 1. Determinants of blood pressure.
The first of these is the baroreceptor reﬂex, a virtually instantaneous response that regulates the blood pressure by controlling autonomic discharge from the brain stem. Fluctuations in the mean arterial pressure are detected by specialized receptors in the carotid sinus which relay information rapidly to the brain stem. Adrenergic outﬂow from the brain stem directly modiﬁes the heart rate, cardiac contractility, and systemic vascular resistance to restore the blood pressure toward its prior set point.
The second mechanism involves the renin-angiotensin system. The kidney produces renin, an enzyme that acts on a plasma protein, termed renin substrate to form angiotensin I, which is subsequently converted primarily in the lungs, to angiotensin II. Angiotensin II is a potent vasoconstricting hormone that raises systemic vascular resistance. Angiotensin II aim stimulates the adrenal gland to synthesize aldosterone a mineralocorticoid hormone that promotes the reabsorption of sodium and water by the kidney. Stimulation of the renin-angiotensin system, therefore, produces vasoconstriction and renal sodium and water retention. Multiple factors affect the release of renin from the juxtaglomerular cells of the kidney, including alterations in renal perfusion pressure, changes in the sodium content of the distal renal tubule, beta-adrenergic stimuli, and the inﬂuence of locally produced prostaglandins.
Third, the extracellular fluid volume affects the systemic arterial blood pressure. The kidney plays an important role in the regulation of extracellular volume at a level that allows for adequate tissue perfusion. In states of extracellular ﬂuid volume depletion, the kidney responds with avid reabsorption of sodium and water from the renal tubules. Conversely, if the blood pressure rises because of an increased plasma volume, the kidney undergoes a natriuresis in order to return plasma volume to its baseline.
Other factors including the sympathetic nervous system, vasodilating hormones such as the prostaglandins and kinins, and local auto-regulatory forces all impact on systemic vascular resistance and hence on the control of blood pressure.
Dr. Afsaneh Jeddi