Hypertension: Risks, Screening, and Types

• BP is high enough to be a danger to well-bring of the individual.
• Hypertension is a major risk factor for coronary artery disease, stroke, heart failure, renal disease, and peripheral vascular disease.
• Elevated BP is usually asymptomatic until an acute cardiovascular event.
• Screening for hypertension is critical for preventative medicine.
• In ~90% of affected patients the etiology of BP elevation is unknown, termed primary or essential hypertension (EH).
• High BP attributed to a definable cause is termed secondary hypertension.
• Conditions that cause secondary hypertension can be curable and may carry excess risk beyond elevated BP.
• BP values vary widely in the population and tend to rise with age
• Normal BP is <120 mm Hg systolic and <80 mm Hg
• A systolic BP ≥ 120 mm Hg is considered elevated
• A systolic BP ≥130 mm Hg or diastolic BP ≥80 mm Hg is stage 1 hypertension
• More severe stage 2 hypertension is present if the systolic BP is ≥140 mm Hg or diastolic BP is ≥90 mm Hg
• Elevating both systolic and diastolic BP contributes significantly to cardiovascular risk.
• BP is the product of cardiac output (CO) and total peripheral resistance (TPR).
• BP = CO × TPR
• CO is the product of cardiac stroke volume (SV) and heart rate (HR).
• CO = SV × HR
• Four systems are directly responsible for BP regulation: the heart, the blood vessel tone, kidney, and hormones.
• Renal excretion can return BP to normal by reducing intravascular volume.
• Cardiovascular system has feedback mechanisms that continuously monitor arterial pressure.
• One such mechanism for maintaining homeostasis is the baroreceptor reflex.
• Baroreceptors constantly reset themselves.
• After a day or two of exposure to higher-than-baseline pressures, the baroreceptor firing rate slows back.

Essential Hypertension

• Approximately 90% of hypertensive patients have BPs that are elevated for no readily definable reason and are considered to have EH.
• Genetics and epidemiology provide insights.
• EH likely results from multiple defects of BP regulation that interact with environmental stressors.
• First-degree relatives of hypertensive patients have a higher rate of elevated BP than the general population.
• The genes regulating the renin-angiotensin-aldosterone axis have been most thoroughly studied because of the central role of this system in determining intravascular volume and vascular tone.
• Hypertension has been epidemiologically linked to dietary and exercise patterns, poor access to health care, low socioeconomic status, and comorbid medical conditions.
• The heart can contribute to a high CO-based hypertension owing to sympathetic overactivity.
• The blood vessels may contribute to peripheral vascular resistance-based hypertension by constricting in response to increased sympathetic activity.
• The kidney can induce volume-based hypertension by retaining excessive sodium and water.
• Renin levels in EH patients compared with normal are subnormal in 25%, normal in ~60%, and high in 10%-15%.
• Vascular smooth muscle cell hypertrophy may be caused by a direct mitogenic effect of insulin, or through enhanced sensitivity to platelet-derived growth factor.
• Possible explanations for Obesity being associated with hypertension includes the release of angiotensinogen from adipocytes as substrate for the renin-angiotensin system.

Natural History

• EH characteristically arises after young adulthood.
• Its prevalence increases with age.
• More than 60% of Americans older than 60 years are hypertensive.
• The systolic pressure increases throughout adult life, while the diastolic pressure increases until about the age of 50 and then declines slightly thereafter.
• Diastolic hypertension is more common in young people, while a substantial number of hypertensive patients over age 50 have isolated systolic hypertension with normal diastolic values.
• In younger persons with hypertension, elevated BP tends to be driven by high CO.
• With advancing age, however, the effect of CO declines.
• EH is a syndrome that may arise from many potential abnormalities, but it exhibits a characteristic hemodynamic profile and natural history.

Secondary Hypertension

• A defined structural or hormonal cause for hypertension may be found in a subset of patients.
• If secondary hypertension is left uncontrolled, cardiovascular adaptations may develop that could cause the elevated pressures to persist, even after the underlying cause is corrected.
• Important clues include Age, Severity, Onset, Associated signs and symptoms.
• Several medications can elevate BP, e.g. oral contraceptives.
• Renal disease contributes to two causes of secondary hypertension: renal parenchymal disease and renovascular hypertension (renal arterial stenosis).
• Parenchymal damage to the kidney can result from diverse pathologic processes, that leads to elevated BPis through increased intravascular volume.
• Stenosis of one or both renal arteries leads to hypertension.
• Elevated BP in RH arises from reduced renal blood flow to the affected kidney, stimulating the Renin-Angiotensin System, increasing BP.
• Coarctation is an infrequently occurring congenital narrowing of the aorta
• Clinical clues to the presence of coarctation include symptoms of inadequate blood flow to legs or left arm, and a Midsystolic murmur associated with the stenotic segment of the aorta may be auscultated.
• Adrenocortical Hormone, Excess of either of these can result in hypertension.
• Mineralocorticoids, primarily aldosterone, increase blood volume.

Consequences of Hypertension

• High BP is itself generally asymptomatic, but can result in devastating effects on many organs.