Hypertension also called high blood pressure (HBP) is an important risk factor for the future development of cardiovascular disease. It may be defined as a disturbance in the circulatory function associated with a persistent elevation of diastolic and systolic blood pressure to a level likely to lead to adverse consequences and where clinical benefit will be obtained from blood pressure (BP) lowering. Whatever may be the cause, the arteries are narrowed and the heart has to pump blood through these narrow vascular beds resulting in increased resistance to blood flow.
Blood pressure is continuously distributed in the population, and there is no clear cut-off point between hypertensive and normotensive patients, although a figure of systolic/diastolic blood pressure of 140/90 mmHg is considered the upper limit of ‘normal’. Hypertension has therefore been arbitrarily defined as a systolic blood pressure above 140 mmHg or a diastolic blood pressure above 90 mmHg, or both.
Types of hypertension
There are two broad classifications of hypertension based on aetiology
- Primary or essential hypertension
- Secondary hypertension
Other types of hypertension include
- White-coat hypertension
- Resistant hypertension
- Isolated systolic hypertension
- Hypertensive crisis
- Hypertensive urgency
- Hypertensive emergency
1. Primary or essential hypertension
Primary or essential hypertension occurs when there is no identifiable cause for a patient’s chronically elevated blood BP. 90 – 95 % of patients with hypertension have essential hypertension. Although the cause is unknown, some factors that may contribute to development of primary hypertension include:
- Humoral abnormalities involving the renin-angiotensin-aldosterone system (RAAS) or natriuretic hormone;
- Disturbance in the central nervous system (CNS), autonomic nerve fibres, adrenergic receptors, or baroreceptors;
- Abnormalities in renal or tissue autoregulatory processes for sodium excretion, plasma volume, and arteriolar constriction;
- Deficiency in synthesis of vasodilating substances in vascular endothelium (prostacyclin, bradykinin, and nitric oxide) or excess vasoconstricting substances (angiotensin II, endothelin I); and
- High sodium intake or lack of dietary calcium
2. Secondary hypertension
Patients with secondary hypertension have identifiable pathology responsible for their chronically elevated BP. Although only 5% to 10% of those among the hypertensive population have causes that are purely secondary, further diagnostic evaluation should occur if physical or laboratory findings suggest the possibility of a secondary cause. Such causes include chronic kidney disease (CKD), renovascular disease, coarctation of the aorta, pheochromocytoma, primary aldosteronism, sleep apnea, hyperparathyroidism, hyperthyroidism and Cushing syndrome. Other cardiovascular risk factors include smoking, alcoholism and some drugs (e.g., nonsteroidal anti-inflammatory drugs, amphetamines, antidepressants, anabolic steroids, calcineurin inhibitors etc.).
3. White-coat hypertension
This describes patients who have consistently elevated blood pressure values measured in a clinical environment in the presence of a health care professional (e.g., physician’s office), yet when measured elsewhere or with 24-hour ambulatory monitoring, blood pressure is not elevated. The commonly used definition is a persistently elevated average office BP of greater than 140/90 mm Hg and an average awake ambulatory reading of less than 135/85 mm Hg.
White-coat hypertension applies only to patients without target-organ disease who are not on antihypertensive therapy. The decision to treat or not treat white-coat hypertension is controversial.
4. Resistant hypertension
Patients with resistant hypertension have blood pressure that remains above goal in spite of concurrent use of three antihypertensive agents from different classes, prescribed at optimal doses, one of which is ideally a diuretic. Also, patients whose blood pressure is controlled by four or more antihypertensive drugs are considered to have resistant hypertension.
Important risk factors for the development of resistant hypertension include older age, obesity, chronic kidney disease, diabetes, obstructive sleep apnea, consumption of a high-salt diet, African-American race, and female gender.
5. Isolated systolic hypertension
Isolated systolic hypertension is diastolic blood pressure values less than 90 mm Hg and systolic blood pressure values of 140 mm Hg or more. This type of hypertension is most common in people over the age of 65 and is caused by the loss of elasticity in the arteries.
6. Hypertensive crisis
Hypertensive crises are acute, severe elevations in blood pressure that may or may not be associated with end-organ dysfunction. Hypertensive crisis may be categorized as hypertensive urgency or hypertensive emergency.
a. Hypertensive urgency
Hypertensive urgency occurs when a patient comes to medical attention with severe hypertension (systolic blood pressure ≥180 mm Hg or a diastolic blood pressure ≥120 mm Hg) without symptoms or evidence of acute end-organ damage. There are limited data describing the presentation and characteristics of patients with hypertensive urgency.
Hypertensive urgency is not an immediately life-threatening situation; a reduction in BP to a safe level can occur more slowly in the next 24 to 48 hours. Hypertensive urgency can be treated with oral antihypertensive agents including clonidine, labetalol, or captopril. Caution must be taken to prevent rapid reductions in blood pressure.
b. Hypertensive emergency
The term hypertensive emergency describes a clinical situation in which the elevated blood pressure is immediately life-threatening and needs to be lowered to a safe level (not necessarily to normal) within a matter of minutes to hours using parenteral antihypertensive medications.
Symptoms associated with hypertensive emergency are highly variable and reflect the degree of damage to specific organ systems. The organs primarily affected as a result of a hypertensive emergency are the central nervous system, eyes, heart, and kidneys. Whether treatment can completely reverse end-organ damage is related to two factors:
- how soon treatment is initiated and
- the extent of damage at the initiation of therapy.
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