Blood pressure

Systemic arterial pressure

The risk of cardiovascular disease increases progressively above 115/75 mmHg,^[8] below this level there is limited evidence.^[9]

Observational studies demonstrate that people who maintain arterial pressures at the low end of these pressure ranges have much better long-term cardiovascular health. There is an ongoing medical debate over what is the optimal level of blood pressure to target when using drugs to lower blood pressure with hypertension, particularly in older people.^[10]

The table shows the 2018 classification of office (or clinic) blood pressure by The Task Force for the management of arterial hypertension of the European Society of Cardiology (ESC) and the European Society of Hypertension (ESH).^[11] Similar thresholds had been adopted by the American Heart Association for adults who are 18 years and older,^[12] but in November 2017 the American Heart Association announced revised definitions for blood pressure categories that increased the number of people considered to have high blood pressure.^[13]

Blood pressure fluctuates from minute to minute and normally shows a circadian rhythm over a 24-hour period,^[14] with highest readings in the early morning and evenings and lowest readings at night.^[15][16] Loss of the normal fall in blood pressure at night is associated with a greater future risk of cardiovascular disease and there is evidence that night-time blood pressure is a stronger predictor of cardiovascular events than day-time blood pressure.^[17] Blood pressure varies over longer time periods (months to years) and this variability predicts adverse outcomes.^[18] Blood pressure also changes in response to temperature, noise, emotional stress, consumption of food or liquid, dietary factors, physical activity, changes in posture (such as standing-up), drugs, and disease.^[19] The variability in blood pressure and the better predictive value of ambulatory blood pressure measurements has led some authorities, such as the National Institute for Health and Care Excellence (NICE) in the UK, to advocate for the use of ambulatory blood pressure as the preferred method for diagnosis of hypertension.^[20]

A digital sphygmomanometer used for measuring blood pressure

Various other factors, such as age and sex, also influence a person's blood pressure. Differences between left-arm and right-arm blood pressure measurements tend to be small. However, occasionally there is a consistent difference greater than 10 mmHg which may need further investigation, e.g. for peripheral arterial disease or obstructive arterial disease.^{[21][22][23][24]}

There is no accepted diagnostic standard for hypotension, although pressures less than 90/60 are commonly regarded as hypotensive.^[25] In practice blood pressure is considered too low only if symptoms are present.^[26]

Systemic arterial pressure and age

High blood pressure

Overview of main complications of persistent high blood pressure

Arterial hypertension can be an indicator of other problems and may have long-term adverse effects. Sometimes it can be an acute problem, for example hypertensive emergency.

Levels of arterial pressure put mechanical stress on the arterial walls. Higher pressures increase heart workload and progression of unhealthy tissue growth (atheroma) that develops within the walls of arteries. The higher the pressure, the more stress that is present and the more atheroma tend to progress and the heart muscle tends to thicken, enlarge and become weaker over time.

Persistent hypertension is one of the risk factors for strokes, heart attacks, heart failure, and arterial aneurysms, and is the leading cause of chronic kidney failure. Even moderate elevation of arterial pressure leads to shortened life expectancy. At severely high pressures, mean arterial pressures 50% or more above average, a person can expect to live no more than a few years unless appropriately treated.^[44]

In the past, most attention was paid to diastolic pressure; but nowadays it is recognized that both high systolic pressure and high pulse pressure (the numerical difference between systolic and diastolic pressures) are also risk factors. In some cases, it appears that a decrease in excessive diastolic pressure can actually increase risk, probably due to the increased difference between systolic and diastolic pressures. If systolic blood pressure is elevated (>140 mmHg) with a normal diastolic blood pressure (<90 mmHg), it is called isolated systolic hypertension and may present a health concern.^[45][46] According to the 2017 ^[47]American College of Cardiology/American Heart Association Blood Pressure Guidelines, "an {systolic blood pressure] of 130 mm Hg is now considered hypertensive at all ages." This will lead to more diagnoses of hypertension among all ages.

For those with heart valve regurgitation, a change in its severity may be associated with a change in diastolic pressure. In a study of people with heart valve regurgitation that compared measurements two weeks apart for each person, there was an increased severity of aortic and mitral regurgitation when diastolic blood pressure increased, whereas when diastolic blood pressure decreased, there was a decreased severity.^[48]

Low blood pressure

Blood pressure that is too low is known as hypotension. This is a medical concern if it causes signs or symptoms, such as dizziness, fainting, or in extreme cases, circulatory shock.^[49]

Causes of low arterial pressure include:^[50]

• Sepsis
• Hemorrhage – blood loss
• Cardiogenic shock
• Neurally mediated hypotension (or reflex syncope)
• Toxins including toxic doses of blood pressure medicine
• Hormonal abnormalities, such as Addison's disease
• Eating disorders, particularly anorexia nervosa and bulimia

Variable or fluctuating blood pressure

Some fluctuation or variation in blood pressure is normal. Variations in pressure that are significantly greater than the norm are associated with increased risk of cardiovascular disease^[53] brain small vessel disease,^[54] and dementia^[55] independent of the average blood pressure level. Recent evidence from clinical trials has also linked variation in blood pressure to mortality,^[56][57] stroke,^[58] heart failure,^[59] and cardiac changes that may give rise to heart failure.^[60] These data have prompted discussion of whether excessive variation in blood pressure should be treated, even among normotensive older adults.^[61] Older individuals and those who had received blood pressure medications are more likely to exhibit larger fluctuations in pressure,^[62] and there is some evidence that different antihypertensive agents have different effects on blood pressure variability;^[55] whether these differences translate to benefits in outcome is uncertain.^[55]

Hemodynamics

A simple view of the hemodynamics of systemic arterial pressure is based around mean arterial pressure (MAP) and pulse pressure. Most influences on blood pressure can be understood in terms of their effect on cardiac output,^[67] systemic vascular resistance, or arterial stiffness (the inverse of arterial compliance). Cardiac output is the product of stroke volume and heart rate. Stroke volume is influenced by 1) the end diastolic volume or filling pressure of the ventricle acting via the Frank Starling mechanism—this is influenced by blood volume; 2) cardiac contractility; and 3) afterload, the impedance to blood flow presented by the circulation.^[68] In the short-term, the greater the blood volume, the higher the cardiac output. This has been proposed as an explanation of the relationship between high dietary salt intake and increased blood pressure; however, responses to increased dietary sodium intake vary between individuals and are highly dependent on autonomic nervous system responses and the renin–angiotensin system,^[69][70][71] changes in plasma osmolarity may also be important.^[72] In the longer-term the relationship between volume and blood pressure is more complex.^[73] In simple terms, systemic vascular resistance is mainly determined by the caliber of small arteries and arterioles. The resistance attributable to a blood vessel depends on its radius as described by the Hagen-Poiseuille's equation (resistance∝1/radius⁴). Hence, the smaller the radius, the higher the resistance. Other physical factors that affect resistance include: vessel length (the longer the vessel, the higher the resistance), blood viscosity (the higher the viscosity, the higher the resistance)^[74] and the number of vessels, particularly the smaller numerous, arterioles and capillaries. The presence of a severe arterial stenosis increases resistance to flow, however this increase in resistance rarely increases systemic blood pressure because its contribution to total systemic resistance is small, although it may profoundly decrease downstream flow.^[75] Substances called vasoconstrictors reduce the caliber of blood vessels, thereby increasing blood pressure. Vasodilators (such as nitroglycerin) increase the caliber of blood vessels, thereby decreasing arterial pressure. In the longer term a process termed remodeling also contributes to changing the caliber of small blood vessels and influencing resistance and reactivity to vasoactive agents.^[76][77] Reductions in capillary density, termed capillary rarefaction, may also contribute to increased resistance in some circumstances.^[78]

In practice, each individual's autonomic nervous system and other systems regulating blood pressure, notably the kidney,^[79] respond to and regulate all these factors so that, although the above issues are important, they rarely act in isolation and the actual arterial pressure response of a given individual can vary widely in the short and long term.

Mean arterial pressure

MAP is the average of blood pressure over a cardiac cycle and is determined by the cardiac output (CO), systemic vascular resistance (SVR), and central venous pressure (CVP):^[80][81][82]

${\displaystyle \!{\text{MAP}}=({\text{CO}}\cdot {\text{SVR}})+{\text{CVP}}}$

In practice, the contribution of CVP (which is small) is generally ignored and so

${\displaystyle \!{\text{MAP}}={\text{CO}}\cdot {\text{SVR}}}$

MAP is often estimated from measurements of the systolic pressure, ${\displaystyle \!P_{\text{sys}}}$ and the diastolic pressure, ${\displaystyle \!P_{\text{dias}}}$ ^[82] using the equation:

${\displaystyle \!{\text{MAP}}\approxeq P_{\text{dias}}+k(P_{\text{sys}}-P_{\text{dias}})}$

where k = 0.333 although other values for k have been advocated.^[83][84]

Pulse pressure

A schematic representation of the arterial pressure waveform over one cardiac cycle. The notch in the curve is associated with closing of the aortic valve.

The pulse pressure is the difference between the measured systolic and diastolic pressures,^[85]

${\displaystyle \!P_{\text{pulse}}=P_{\text{sys}}-P_{\text{dias}}.}$

The pulse pressure is a consequence of the pulsatile nature of the cardiac output, i.e. the heartbeat. The magnitude of the pulse pressure is usually attributed to the interaction of the stroke volume of the heart, the compliance (ability to expand) of the arterial system—largely attributable to the aorta and large elastic arteries—and the resistance to flow in the arterial tree.^[85]

Regulation of blood pressure

The endogenous, homeostatic regulation of arterial pressure is not completely understood, but the following mechanisms of regulating arterial pressure have been well-characterized:

• Baroreceptor reflex: Baroreceptors in the high pressure receptor zones detect changes in arterial pressure. These baroreceptors send signals ultimately to the medulla of the brain stem, specifically to the rostral ventrolateral medulla (RVLM). The medulla, by way of the autonomic nervous system, adjusts the mean arterial pressure by altering both the force and speed of the heart's contractions, as well as the systemic vascular resistance. The most important arterial baroreceptors are located in the left and right carotid sinuses and in the aortic arch.^[86]
• Renin–angiotensin system (RAS): This system is generally known for its long-term adjustment of arterial pressure. This system allows the kidney to compensate for loss in blood volume or drops in arterial pressure by activating an endogenous vasoconstrictor known as angiotensin II.
• Aldosterone release: This steroid hormone is released from the adrenal cortex in response to activation of the renin-angiotensin system, high serum potassium levels, or elevated adrenocorticotropic hormone (ACTH). Renin converts angiotensinogen to angiotensin I, which is converted by angiotensin converting enzyme to angiotensin II. Angiotensin II then signals to the adrenal cortex to release aldosterone.^[87] Aldosterone stimulates sodium retention and potassium excretion by the kidneys and the consequent salt and water retention increases plasma volume, and indirectly, arterial pressure. Aldosterone may also exert direct pressor effects on vascular smooth muscle and central effects on sympathetic nervous system activity.^[88]
• Baroreceptors in low pressure receptor zones (mainly in the venae cavae and the pulmonary veins, and in the atria) result in feedback by regulating the secretion of antidiuretic hormone (ADH/Vasopressin), renin and aldosterone. The resultant increase in blood volume results in an increased cardiac output by the Frank–Starling law of the heart, in turn increasing arterial blood pressure.

These different mechanisms are not necessarily independent of each other, as indicated by the link between the RAS and aldosterone release. When blood pressure falls many physiological cascades commence in order to return the blood pressure to a more appropriate level.

1. The blood pressure fall is detected by a decrease in blood flow and thus a decrease in glomerular filtration rate (GFR).
2. Decrease in GFR is sensed as a decrease in Na⁺ levels by the macula densa.
3. The macula densa causes an increase in Na⁺ reabsorption, which causes water to follow in via osmosis and leads to an ultimate increase in plasma volume. Further, the macula densa releases adenosine which causes constriction of the afferent arterioles.
4. At the same time, the juxtaglomerular cells sense the decrease in blood pressure and release renin.
5. Renin converts angiotensinogen (inactive form) to angiotensin I (active form).
6. Angiotensin I flows in the bloodstream until it reaches the capillaries of the lungs where angiotensin-converting enzyme (ACE) acts on it to convert it into angiotensin II.
7. Angiotensin II is a vasoconstrictor that will increase blood flow to the heart and subsequently the preload, ultimately increasing the cardiac output.
8. Angiotensin II also causes an increase in the release of aldosterone from the adrenal glands.
9. Aldosterone further increases the Na⁺ and H₂O reabsorption in the distal convoluted tubule of the nephron.

Currently, the RAS is targeted pharmacologically by ACE inhibitors and angiotensin II receptor antagonists, also known as angiotensin receptor blockers (ARBs). The aldosterone system is directly targeted by spironolactone, an aldosterone antagonist. The fluid retention may be targeted by diuretics; the antihypertensive effect of diuretics is due to its effect on blood volume. Generally, the baroreceptor reflex is not targeted in hypertension because if blocked, individuals may experience orthostatic hypotension and fainting.

Taking blood pressure with a sphygmomanometer

Hypertension in cats and dogs

Hypertension in cats and dogs is generally diagnosed if the blood pressure is greater than 150^[103] mm Hg (systolic), although sight hounds have higher blood pressures than most other dog breeds; a systolic pressure greater than 180 mmHg is considered abnormal in these dogs.^[104]