Blood pressure

Blood pressure (BP) is the pressure exerted by circulating blood upon the walls of blood vessels, and is
one of the principal vital signs. During each heartbeat, BP varies between a maximum (systolic) and a
minimum (diastolic) pressure.[1] The mean BP, due to pumping by the heart and resistance to flow in
blood vessels, decreases as the circulating blood moves away from the heart through arteries. Blood
pressure drops most rapidly along the small arteries and arterioles, and continues to decrease as the
blood moves through the capillaries and back to the heart through veins.[2] Gravity, valves in veins, and
pumping from contraction of skeletal muscles, are some other influences on BP at various places in the
body.

The term blood pressure usually refers to the pressure measured at a person's upper arm. It is measured
on the inside of an elbow at the brachial artery, which is the upper arm's major blood vessel that carries
blood away from the heart. A person's BP is usually expressed in terms of the systolic pressure over
diastolic pressure (mmHg), for example 140/90

Pathophysiology

There are many physical factors that influence arterial pressure. Each of these may in turn be influenced
by physiological factors, such as diet, exercise, disease, drugs or alcohol, stress, obesity, and so-forth.
[16]

Some physical factors are:

Rate of pumping. In the circulatory system, this rate is called heart rate, the rate at which blood (the
fluid) is pumped by the heart. The volume of blood flow from the heart is called the cardiac output
which is the heart rate (the rate of contraction) multiplied by the stroke volume (the amount of blood
pumped out from the heart with each contraction). The higher the heart rate, the higher the arterial
pressure, assuming no reduction in stroke volume.[citation needed]

Volume of fluid or blood volume, the amount of blood that is present in the body. The more blood
present in the body, the higher the rate of blood return to the heart and the resulting cardiac output.
There is some relationship between dietary salt intake and increased blood volume, potentially resulting
in higher arterial pressure, though this varies with the individual and is highly dependent on autonomic
nervous system response and the renin-angiotensin system.[citation needed]

Resistance. In the circulatory system, this is the resistance of the blood vessels. The higher the
resistance, the higher the arterial pressure upstream from the resistance to blood flow. Resistance is
related to vessel radius (the larger the radius, the lower the resistance), vessel length (the longer the
vessel, the higher the resistance), blood viscosity, as well as the smoothness of the blood vessel walls.
Smoothness is reduced by the build up of fatty deposits on the arterial walls. Substances called
vasoconstrictors can reduce the size of blood vessels, thereby increasing BP. Vasodilators (such as
nitroglycerin) increase the size of blood vessels, thereby decreasing arterial pressure. Resistance, and its
relation to volumetric flow rate (Q) and pressure difference between the two ends of a vessel are
described by Poiseuille's Law.

Viscosity, or thickness of the fluid. If the blood gets thicker, the result is an increase in arterial pressure.
Certain medical conditions can change the viscosity of the blood. For instance, low red blood cell
concentration, anemia, reduces viscosity, whereas increased red blood cell concentration increases
viscosity. It had been thought that aspirin and related "blood thinner" drugs decreased the viscosity of
blood, but studies found[17] that they act by reducing the tendency of the blood to clot instead.

In practice, each individual's autonomic nervous system responds to and regulates all these interacting
factors so that, although the above issues are important, the actual arterial pressure response of a given
individual varies widely because of both split-second and slow-moving responses of the nervous system
and end organs. These responses are very effective in changing the variables and resulting BP from
moment to moment.

Moreover, blood pressure is the result of cardiac output increased by peripheral resistance: blood
pressure = cardiac output X peripheral resistance. As a result, an abnormal change in blood pressure is
often an indication of a problem affecting the heart's output, the blood vessels' resistance, or both.
Thus, knowing the patient's blood pressure is critical to assess any pathology related to output and
resistance.

Regulation

The endogenous regulation of arterial pressure is not completely understood. Currently, three
mechanisms of regulating arterial pressure have been well-characterized:

Baroreceptor reflex: Baroreceptors detect changes in arterial pressure and send signals ultimately to the
medulla of the brain stem, RVLM to be precise. 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 total peripheral resistance. The most important arterial baroreceptors are located in the left
and right carotid sinuses and in the aortic arch.[24]

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
angiotensin II or high serum potassium levels. Aldosterone stimulates sodium retention and potassium
excretion by the kidneys. Since sodium is the main ion that determines the amount of fluid in the blood
vessels by osmosis, aldosterone will increase fluid retention, and indirectly, arterial pressure.

These different mechanisms are not necessarily independent of each other, as indicated by the link
between the RAS and aldosterone release. Currently, the RAS is targeted pharmacologically by ACE
inhibitors and angiotensin II receptor antagonists. 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 suffer from orthostatic
hypotension and fainting
Some factors which affect blood pressure

Baroreceptors are important for minimizing changes in blood pressure: animal studies have shown that
blood pressure is much more variable if the influence of baroreceptors is removed. However, they do
not prevent all fluctuations from occurring. Continuous 24-hour recordings have been made in healthy
volunteers and have shown variations of 30-80 mm Hg in systolic pressure and of 10-80 mm Hg in
diastolic pressure. Blood pressure is particularly low during sleep, and high during physical activity or
emotional stress.

Physical exercise causes very major effects on the circulation. Due to the enormously increased blood
flow through the exercising muscle, the amount of blood pumped by the heart may increase four-fold,
or in elite athletes as much as six-fold. The increased volume of blood ejected at each heart beat causes
systolic blood pressure to increase, perhaps to 180 mm Hg. However, because blood flows very rapidly
out of the arteries, particularly to the working muscle where the resistance vessels are widely dilated,
diastolic pressure remains relatively unchanged or may even decrease. Isometric exercise has quite a
different effect. Here there is a much smaller effect on the total amount of blood pumped by the heart,
but reflexes, particularly those arising from the contracting muscle itself, cause blood vessels elsewhere
to constrict, and consequently both systolic and diastolic blood pressure rise sharply. This response may
also be augmented by a straining effect (see below).

Emotional stress can cause quite large increases in blood pressure. Prominent amongst the physiological
responses to stress is an increase in activity in the sympathetic nerves. Sympathetic overactivity
increases heart rate and force, and constricts resistance blood vessels (Fig. 1). All these effects increase
both systolic and diastolic blood pressure and are augmented by increased secretion into the blood of
adrenaline and noradrenaline.

Postural changes exert stresses on the cardiovascular system requiring effective reflex responses to
constrict arteries and veins and stimulate the heart, to control blood pressure, maintain brain blood
flow, and prevent loss of consciousness. The upright position means that blood vessels below the level
of the heart are subjected to increased distending pressures due to the effects of gravity. Veins are
particularly susceptible to gravitational stress due to their distensibility, and blood ‘pools’ in dependent
veins when we stand. Because of this, less blood flows back to the heart and, were it not for effective
reflexes, involving baroreceptors, blood pressure would fall catastrophically, particularly in the brain,
resulting in insufficient brain blood flow and consequent loss of consciousness. Blood pressure
frequently falls transiently when we stand. This is particularly noticeable if we stand suddenly when
warm, for example on getting out of a hot bath, because the resistance blood vessels initially will be
dilated. In some people blood pressure control may be inadequate to counter the stress of postural
changes and the result is that they faint.

Straining (the Valsalva manoeuvre) induces large and complex variations in blood pressure. The sort of
stresses that induce these changes include blowing against a resistance, lifting heavy objects, and
straining at stool. The effects on the circulation are illustrated in Fig. 2. The primary change is caused by
an increase in pressure within the chest (intrathoracic pressure) and within the abdomen. Normally,
intrathoracic pressure is lower than atmospheric, due to the tendency of lungs to collapse and their
prevention from so doing by the chest wall. This negative intrathoracic pressure aids the flow of blood to
the heart from the peripheral veins. Straining causes the pressure in both the chest and the abdomen to
become positive. Initially the compression of the heart and large arteries causes an increase in blood
pressure. Then, the high pressure in the chest impedes the inflow of blood from peripheral veins (veins
in the neck can be seen to distend), so the cardiac output decreases and blood pressure falls.
Baroreceptors detect this fall and initiate constriction of blood vessels and an increase in heart rate, so
that mean blood pressure is restored. At the end of the strain there is a transient fall in pressure before
blood rushes back to the heart, causing an overshoot and often a transient slowing of the heart. In
people with some autonomic nerve disorders these responses may be deficient: blood pressure falls
continuously, and the overshoot is absent.
Fig. 2 The Valsalva manoeuvre. The subject blows against a fixed resistance to generate a pressure in the
mouth(MP) of 40 mm Hg. This causes 4 phases of blood pressure change. Phase 1: blood pressure (BP)
rises due to the pressure transmitted to the arteries. Phase 2: BP falls and pulse pressure (difference
between systolic and diastolic pressures) particularly falls due to the reduced filling, and therefore
pumping, of the heart. Pressure subsequently recovers due to the reflex changes. Note also the reflex
increase in heart rate. Phase 3: BP falls as the pressure is taken off the arteries in the chest and
abdomen. Phase 4: there is an overshoot as the 'dammed back' blood rushes into the heart and is
pumped into a constricted circulation

Treatment

Lifestyle modifications

The first line of treatment for hypertension is the same as the recommended preventative lifestyle
changes[53] such as:

dietary changes,

physical exercise and

weight loss
which have all been shown to significantly reduce blood pressure in people with hypertension.[60] If
hypertension is high enough to justify immediate use of medications, lifestyle changes are still
recommended in conjunction with medication. Drug prescription should take into account the patient's
absolute cardiovascular risk (including risk of myocardial infarction and stroke) as well as blood pressure
readings, in order to gain a more accurate picture of the patient's cardiovascular profile.[4] Different
programs aimed to reduce psychological stress such as biofeedback, relaxation or meditation are
advertised to reduce hypertension. However, in general claims of efficacy are not supported by scientific
studies, which have been in general of low quality.[61][62][63]

Regarding dietary changes, a low sodium diet is beneficial; A Cochrane review published in 2008
concluded that a long term (more than 4 weeks) low sodium diet in Caucasians has a useful effect to
reduce blood pressure, both in people with hypertension and in people with normal blood pressure.[64]
Also, the DASH diet (Dietary Approaches to Stop Hypertension) is a diet promoted by the National Heart,
Lung, and Blood Institute (part of the NIH, a United States government organization) to control
hypertension. A major feature of the plan is limiting intake of sodium,[65] and it also generally
encourages the consumption of nuts, whole grains, fish, poultry, fruits and vegetables while lowering
the consumption of red meats, sweets, and sugar. It is also "rich in potassium, magnesium, and calcium,
as well as protein".

Medications

Several classes of medications, collectively referred to as antihypertensive drugs, are currently available
for treating hypertension. Reduction of the blood pressure by 5 mmHg can decrease the risk of stroke by
34%, of ischaemic heart disease by 21%, and reduce the likelihood of dementia, heart failure, and
mortality from cardiovascular disease.[66] The aim of treatment should be reduce blood pressure to
<140/90 mmHg for most individuals, and lower for individuals with diabetes or kidney disease (some
medical professionals recommend keeping levels below 120/80 mmHg).[67] If the blood pressure goal is
not met, a change in treatment should be made as therapeutic inertia is a clear impediment to blood
pressure control.[68] Comorbidity also plays a role in determining target blood pressure, with lower BP
targets applying to patients with end-organ damage or proteinuria.[4]

The first line antihypertensive supported by the best evidence is a low dose thiazides diuretic.[69]

Often multiple medications in combined are needed to achieve the goal blood pressure. Commonly used
prescription drugs include:[70]ACE inhibitors, alpha blockers, angiotensin II receptor antagonists , beta
blockers , calcium channel blockers, diuretics (e.g. hydrochlorothiazide), direct renin inhibitors.

Some examples of common combined prescription drug treatments include:

A fixed combination of an ACE inhibitor and a calcium channel blocker. One example of this is the
combination of perindopril and amlodipine, the efficacy of which has been demonstrated in individuals
with glucose intolerance or metabolic syndrome.[71]
A fixed combination of a diuretic and an ARB.

Combinations of an ACE inhibitor or angiotensin II–receptor antagonist, a diuretic and an NSAID

Epidemiology

In the year 2000 it is estimated that nearly one billion people or ~26% of the adult population had
hypertension worldwide.[85] It was common in both developed (333 million ) and undeveloped (639
million) countries.[85] However rates vary markedly in different regions with rates as low as 3.4% (men)
and 6.8% (women) in rural India and as high as 68.9% (men) and 72.5% (women) in Poland.[86]

In 1995 it is estimated that 43 million people in the United States had hypertension or were taking
antihypertensive medication, almost 24% of the adult population.[87] The prevalence of hypertension in
the United States is increasing and reached 29% in 2004.[88][89] It is more common in blacks and native
Americans and less in whites and Mexican Americans, rates increase with age, and is greater in the
southeastern United States. Hypertension is more prevalent in men (though menopause tends to
decrease this difference) and those of low socioeconomic status.[1]

Over 90–95% of adult hypertension is essential hypertension.[1] The most common cause of secondary
hypertension is primary aldosteronism.[42] The incidence of exercise hypertension is reported to range
from 1–10%.[10]

Special precautions of quinolones

The status of the patient’s renal function and hepatic function must also be taken into consideration to
avoid an accumulation that may lead to an overdose and the development of toxicity. Ciprofloxacin is
eliminated primarily by renal excretion. However, the drug is also metabolized and partially cleared
through the liver and the intestines. Modification of the dosage is recommended using the table found
within the package insert for those with impaired liver or kidney function. However, since the drug is
known to be substantially excreted by the kidneys, the risk of toxic reactions to this drug may be greater
in patients with impaired renal function. The duration of treatment depends upon the severity of
infection and is usually 7 to 14 days.[24]