Blood Pressure

Blood pressure is the pressure exerted by the blood perpendicular to the walls of the
blood vessels. Unless indicated otherwise, blood pressure refers to systemic arterial
blood pressure, i.e., the pressure in the large arteries delivering blood to body parts other
than the lungs, such as the brachial artery (in the arm). The pressure of the blood in other
vessels is lower than the arterial pressure. Blood pressure values are universally stated in
millimetres of mercury (mmHg). The systolic pressure is defined as the peak pressure in
the arteries during the cardiac cycle; the diastolic pressure is the lowest pressure (at the
resting phase of the card cardiac cycle). The mean arterial pressure and pulse pressure are
other important quantities. Blood pressure is continually changing depending on activity,
temperature, diet, emotional state, posture, physical state, and medication use. n adults,
the systolic pressure should be less than 120 mmHg and the diastolic pressure should be
less than 80 mmHg.

Hypertension (high blood pressure) is when your blood pressure frequently goes over
140/90 mm Hg.

A patient is considered "pre-hypertensive" if the top (systolic) number of the blood

pressure reading is 120-139 mm Hg and if the bottom (diastolic) number is over 80-89
mm Hg on most measurements.

Low blood pressure (hypotension):

• Top number reading lower than 90 or pressure 25 mmHg lower than usual

Blood pressure readings may be affected by many different conditions, including:

• Cardiovascular disorders
• Neurological conditions
• Kidney and urological disorders
• Pre-eclampsia in pregnant women
• Psychological factors such as stress, anger, or fear
 • Various medications
• "White coat hypertension" may occur if the medical visit itself produces extreme
anxiety

Regulation

The endogenous regulation of blood pressure is not completely understood. Currently,

three mechanisms of regulating blood pressure have been well-characterized:

Baroreceptor reflex: Baroreceptors are specialized receptors that monitor the degree of
stretch in the walls of expandable organs. The baroreceptors involved with cardiovascular
regulation are located in the walls of the carotid sinuses, (expanded chambers near the
bases of the internal carotid arteries of the neck), the aortic sinuses, (pockets in the walls
of the ascending aorta adjacent to the heart), and the wall of the right atrium. These
receptors are components of the baroreceptor reflexes, which adjust cardiac output and
peripheral resistance to maintain normal arterial pressures.

Diagram showing baroreceptor reflex to a change in blood prssure

• Renin-angiotensin system (RAS): This system is generally known for its long-
term adjustment of blood pressure. This system allows the kidney to compensate
for loss in blood volume or drops in blood 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, blood pressure.

The rennin angiotensin system

These different mechanisms are not necessarily independent of each other. Currently, the
RAS system 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; however, the
antihypertensive effect of diuretics is not 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 suffer from fainting.
 Right And Left Ventricular Failure
In heart failure, the heart is unable to produce an adequate cardiac output (CO) to perfuse
the tissues, or can do so only with an elevated filling pressure. Initially adaptive
mechanisms may compensate and so maintain CO at rest, although they may not be
sufficient to allow normal increases in output during exercise. In spite of these
mechanisms cardiac function eventually declines, and heart failure becomes severe
(decompensated heart failure). Heart failure can be precipitated by other acute diseases or
stresses. Systolic failure is a defect in systolic function that impairs ejection, whereas
diastolic failure is a defect in ventricular filling. Systolic and diastolic failure often
coexists, particularly in ischaemic heart disease.

Underlying causes of heart failure

Primary defect Examples

Myocardial dysfunction Ischaemic heart disease, pregnancy, congenital

cardiomyopathies, myocardial disease, e.g. amyloidosis

Volume overload Aortic or Mitral valve regurgitation

Pressure overload Aortic stenosis, hypertension

Impaired filling Constrictive pericaritis: rheumatic heart disease

Cardiac tamponade: excess fluid pressure in pericardial space

Arrhythmias Atrial fibrillation

High output Thyrotoxicosis, arteriovenous shunts, anaemia

Clinical Manifestations
• dyspnoea( initially only during exercise)
• weakness
• fatigue
• peripheral oedema
• enlarged heart and liver
• high venous pressure pressure distends the jugular veins
• reduced ejection fraction( proportion of EDV ejected per beat)

Pathophysiology of Chronic Heart Failure

Many conditions may lead to heart failure. The most common cause is dysfunction of
cardiac muscle (myocardium) due to ischaemic heart disease. Coronary blood flow and
oxygen delivery are insufficient for the needs of the myocardium, leading to dysfunction.
The force developed for any degree of stretch (contractility) is reduced, and the
ventricular function curve is depressed. In mild failure, acceptable output can only be
obtained at rest with an increased end-diastolic pressure (EDP). In exercise the increase in
contractility is small because sympathetic tone is already high. In severe failure normal
resting output cannot be obtained even with substantial increases in EDP.

Left ventricular failure

Ischaemic heart disease most commonly affects the left ventricle. In left ventricular
failure (LVF) decreased output leads to an increased left ventricular EDP and pulmonary
venous pressure. This results in pulmonary congestion, fluid accumulation in the
interstitium of the lungs and pleural spaces(pleural effusion), and thus dyspnoea.
Dyspnoea may occur only when the patient lies down (orthopnea) or at night (paroxysmal
dyspnoea), when redistribution of body fluids allows fluid to collect in the lungs. If
severe, fluid enters the alveoli (pulmonary oedeme), this causes extreme dyspnoea, and
can drown the patient by reducing gas exchange. in severe pulmonary oedema the patient
is always breathless and hypoxaemic, and very occasionally produces pinkish foam lips
Right ventricular failure

Right ventricular failure occurs in chronic lung disease (cor pulmonale), pulmonary
hypertension or embolism, and valve disease of the right heart. Central venous pressure is
greatly increased with consequent distention of the jugular veins, enlarged heart, and
peripheral oedema, fluid accumulation in the peritoneum and tenderness and enlargement
of the liver (hepetomegaly). Ambulatory patients show pitting oedema of the ankles (a
depression is left following compression with a finger) which is relieved on lying down.

Left heart failure can cause subsequent failure of the right heart due to the greatly
increased pulmonary vascular pressure. the right ventricle will initially develop
hypertrophy against the increased afterload, but eventually it fails due to pressure
overload. This is known as congestive heart failure

This is shown below

Coronary Artery Disease

Coronary artery disease (CAD) is a narrowing of the small blood vessels that supply
blood and oxygen to the heart. CAD is also called coronary heart disease (CHD).

Coronary heart disease usually results from the build-up of fatty material and plaque, a
condition called atherosclerosis. As the coronary arteries narrow, the flow of blood to the
heart can slow or stop, causing chest pain (stable angina), shortness of breath, heart
attack, or other symptoms.

g
Narrowing of arteries due to plaque deposit

Coronary heart disease (CHD) is the leading cause of death in the United States for men
and women. According to the American Heart Association, some one in the United States
has a CHD-related event about every 29 seconds. Every minute someone dies from one.
Risk factors include:

• Family history of coronary heart disease (especially before age 50)

• Male gender
• Age (65 and greater)
• Tobacco smoking
• High blood pressure
• Diabetes
 • High cholesterol levels (specifically, high LDL cholesterol and low HDL
cholesterol)
• Lack of physical activity or exercise
• Obesity
• Higher-than-normal markers of inflammation
• High blood homocysteine levels
• Menopause

Symptoms

The symptoms associated with coronary heart disease may be pronounced, but the disease
can also exist without noticeable symptoms.

Chest pain (angina) is the most common symptom. It results from the heart not getting
enough blood or oxygen. The intensity of the pain varies from person to person. Chest
pain may be typical or atypical. Typical chest pain is felt under the sternum (breast bone)
and feels heavy or squeezing. It usually occurs with activity (exertion) or emotion, and it
goes away with rest or nitroglycerin.

Atypical chest pain can be felt in the left chest, abdomen, back, or arm. It is often fleeting
or sharp. Atypical chest pain is unrelated to exercise and is not relieved by rest or
nitroglycerin. Atypical chest pain is more common in women.

Adults with typical chest pain have a higher risk of CHD than those with atypical chest
pain.

Other symptoms include:

• Shortness of breath. This may be a symptom of congestive heart failure. The heart
is weak because of a long-term lack of blood and oxygen or because of a recent or
past heart attack. If the heart is not pumping enough blood to the body, shortness
of breath may be accompanied by swollen feet and ankles.
• Heart attack. In some cases, the first sign of CHD is a heart attack. The heart
attack occurs when atherosclerotic plaque or a blood clot blocks the blood flow of
 the coronary artery to the heart. The coronary artery was likely already narrowed
from CHD. The pain associated with a heart attack is usually severe, lasts longer
than the chest pain described above, and is not relieved with rest or nitroglycerin.

The treatment for CHD depends on your symptoms and the severity of disease. General
treatments involve lifestyle changes, medications, and medical procedures, including
surgery.

Cardiovascular Response to Hemorrhaging

When haemostasis fails to prevent a significant blood loss, the entire cardiovascular
system makes adjustments to maintain blood pressure and restore blood volume. The
immediate problem is the maintenance of adequate blood pressure and peripheral blood
flow. The long-term problem is the restoration of normal blood volume.

Short-Term Elevation of Blood Pressure

Almost as soon as the pressures start to decline, short-term responses appear. The steps
include the following:

• The initial neural response occurs as carotid and aortic reflexes increase cardiac
output and cause peripheral vasoconstriction. With the blood volume reduced,
cardiac output is maintained by increasing the heart rate, typically to 180-200
bpm.
• The combination of stress and anxiety stimulates the sympathetic nervous system
headquarters in the hypothalamus, which in turn triggers a further increase in
vasomotor tone, constricting the arterioles and elevating blood pressure. At the
same time, venoconstriction mobilizes the venous reserve and quickly improves
venous return.
• Short-term hormonal effects also occur. For instance, sympathetic activation
causes the secretion of E and NE by the adrenal medulla, increasing cardiac output
and extending peripheral vasoconstriction. In addition, the release of ADH by the
posterior lobe of the pituitary gland and the production of angiotensin II enhance
vasoconstriction while participating in the long-term response.

This combination of short-term responses elevates blood pressure and improves

peripheral blood flow, often restoring normal arterial pressures and peripheral circulation
after blood losses of up to 20 percent of the total blood volume. Such adjustments are
more than sufficient to compensate for the blood loss experienced when you donate
blood. (Most blood banks collect 500 ml of whole blood, roughly 10 percent of your total
blood volume.)

Long-Term Restoration of Blood Volume

Short-term responses temporarily compensate for a reduction in blood volume. Long-term
responses are geared to restoring normal blood volume, a process that can take several
days after a serious hemorrhage. The steps include the following:

• The decline in capillary blood pressure triggers a recall of fluids from the
interstitial spaces.
• Aldosterone and ADH promote fluid retention and reabsorption at the kidneys,
preventing further reductions in blood volume.
• Thirst increases, and additional water is obtained by absorption across the
digestive tract. This intake of fluid elevates the plasma volume and ultimately
replaces the interstitial fluids "borrowed" at the capillaries.

Erythropoietin targets the bone marrow, stimulating the maturation of red blood cells,
which increase blood volume and improve oxygen delivery to peripheral tissues.
Cardiovascular Responses to Hemorrhaging and Blood Loss
Reference
1. Principles of anatomy and physiology; Tortora Gerard; 3rd edition; New York.
John Wiley, 2003

2. Fundamentals of Anatomy and Physiology; Martini F; USA; Benjamin

Cummings; 2004

3. Textbook of medical physiology; Guyton & Hall; 11th edition; Elsevier

4. blood pressure; Wikipedia the free encyclopedia [online] March 2007; Available
at http://en.wikipedia.org/wiki/pressure