Physiologic changes associated with aging leads to an increase in systolic blood pressure, an increase in mean arterial pressure, increase in pulse pressure and a decreased ability to respond to abrupt hemodynamic changes.

The increase in blood pressure seen with aging is most likely related to arterial changes. Aging results in narrowing of the vessel lumen and stiffening of the vessel walls through a process known as atherosclerosis. Atherosclerosis leads to structural alterations including increased vascular calcification causing earlier reflected pressure waves during blood pressure wave propagation. The pressure wave arrives back from the aortic root during systole and contributes to the increase in systolic blood pressure. Diastolic blood pressure tends to increase up to the age of about 50 and the increase is due to the rise in arteriolar resistance. The large artery stiffening that occurs later in life contributes a wider pulse pressure including a decreased diastolic blood pressure. The increase in arteriolar resistance along with large artery stiffening leads to a significant increase in systolic blood pressure, pulse pressure and mean arterial pressure.

The decreased ability to appropriately respond to abrupt hemodynamic changes is rooted in many pathophysiological factors including a change in heart structure and function and a decrease in the autonomic regulation of blood pressure. Left ventricular hypertrophy and a decrease in left ventricle compliance correlates with a reduction in cardiac performance and in the ability to increase systolic blood pressure in response to stress. The autonomic system plays a key role in the maintenance of blood pressure through physiologic responses to standing, volume depletion, and increased cardiac output during stress. With a decrease in the autonomic regulation of blood pressure, there is a significant impact on physiologic adaption. One example includes the high prevalence of orthostatic hypotension among the elderly population.[2]

The arterial pressure waveform is a good indicator of arterial wall stiffening. The arterial pressure waveform is representative of arterial pressure throughout a cardiac cycle. The waveform can be broken up into two distinct phases, the systolic and diastolic phases. The systolic phase characteristically demonstratesy a rapid upstroke, caused by the opening of the aortic valve and left ventricular ejection, followed by a quick decline. The characteristic of the diastolic phase is a gradual decline of arterial pressure and run-off of blood flow into the peripheral circulation. The demarcation of these two phases is a dicrotic notch formed by the closing of the aortic valve.

The arterial pressure wave is formed by two different waves. A forward wave and a reflected wave. The forward wave represents the flow of blood from the left ventricle during contraction. The reflected or reverse wave is created by structures that cause impedance (ex. branch points, direction changes, etc.). The speed of the wave is known as the pulse wave velocity. In a young artery, the reflected wave is reflected to the aortic root during diastole. In an older, stiffened artery, the reflected wave is reflected to the aortic root during systole because it has an increased pulse wave velocity, allowing it to contribute to the forward wave resulting in an increased peak forward wave. A pulse wave velocity greater than 10 to 12 m/sec, depending on the device used, is indicative of arterial wall stiffening.[3]

Other test modalities for increased arterial pressure include but are not limited to: regular blood pressure checks with a sphygmomanometer, ankle-brachial index, angiography, and stress testing.

Aging is associated with changes to the vascular system, heart, and autonomic system.

Stiffening of the arteries is one of the hallmarks of aging. In younger individuals, the peripheral arterial system is stiffer relative to the central arterial system. With time, this finding reverses; older individuals have greater central artery stiffness compared to peripheral arteries. This reversal and increased stiffening of the larger, central arteries is multifactorial in etiology. Changes in structural components, increased reactive oxygen species, inflammatory changes, and endothelial dysfunction are among some of the causes leading to the change in arterial structure and function seen with aging.[4]

Increased elastin degradation and collagen deposition are two characteristic changes seen with aging. The ratio of collagen to elastin increases with age leading to an increase in arterial stiffness. This change may also be present in ventricular smooth muscle cells. In the ventricle wall, the decrease in elastin results in an increase in diastolic filling pressure as the heart wall becomes less compliant. The exact cause of this structural change is unknown, and there are many hypotheses for why this change occurs in older populations including material fatigue and various signaling pathways leading to the destruction of elastin and increased deposition of collagen. Recent studies have shown that Ang II along with the activation of TGF-B1 and matrix metalloproteinases are some of the signaling molecules that may be involved.[4]

An increase in the levels of inflammatory mediators seen with aging leads to the production of reactive oxygen species that then lead to endothelial damage predisposing the vascular system to atherosclerosis.[5] Atherosclerosis presents with endothelial injury or dysfunction. It is a slow process by which large-to-medium-sized arteries (examples include: abdominal aorta, popliteal artery, carotid artery, coronary artery, etc.) undergo thickening of the intimal layer of blood vessel walls, leading to less compliant arteries. The process initiates by endothelial damage in an artery permitting lipids to get through the innermost layer of arteries, the intima, into the lumen of the vessels. These lipids are then oxidized and consumed by macrophages resulting in the formation of foam cells and fatty streaks. Following this, an inflammation and healing process ensues. An increase in a variety of growth factors then causes the recruitment and proliferation of smooth muscle cells. The resultant is a fibrous cap created by smooth muscle cells with a lipid core.

Reduced left ventricular compliance, and cardiac reserve are hallmarks in the aging population. Factors affecting left ventricular function include preload, afterload, and contractility. With age, cardiac myocytes tend to hypertrophy and decrease in number.  The left ventricle becomes stiffer and therefore its compliance decreases. Ventricular stiffening is the result of many processes including alteration in structural proteins, increases in inflammatory mediators, and increases in glycation end products. Another notable change to the left ventricle is prolonged isovolumetric relaxation time. This increase in relaxation time is associated with alterations in calcium signaling. Healthy, older adult hearts have less cardiac sarcoplasmic reticulum ATPase resulting in lower calcium content; this causes an increased dependency on L-type calcium channels, which explains the efficacy of medications used to block these channels in older populations.

With aging, there is a decrease in chronotropic, lusitropic, and inotropic responses. A reduced response to atropine due to increased parasympathetic vagal tone and decreased sympathetic tone is a typical finding. These changes may be a direct result of suppressed cAMP production, decreased beta receptor function and number, and increased G protein activity. Due to these changes, older adults present with elevated production and levels of circulating catecholamines and stress-stimulated levels of epinephrine and norepinephrine.[5]

These changes in blood pressure seen among the older population may lead to varying end-organ damage presentations. Early detection and treatment of hypertension may prevent or slow end-organ damage while it is in a reversible stage. When encountering a patient with hypertension, many factors come into play when choosing what treatment option is best. Healthy lifestyle changes (diet, physical activity, quitting smoking, managing stress are a few examples) are the first line options. If on follow-up, the patient continues to be hypertensive after implementing these changes, medical management is an appropriate option.