Blood pressure can be defined as the lateral pressure exerted by the moving column of blood on the wall of arteries. The normal blood pressure is about 120/80 mm of Hg.

What is blood pressure?

Pressure is highest during ‘systole‘ when the ventricles are contracting (systolic pressure) and lowest during ‘diastole‘ when the ventricles are relaxing and refilling (diastolic pressure). Keeping blood pressure within normal limits is very important. If it becomes too high, blood vessels can be damaged, causing clots or bleeding from sites of blood vessel ruptures. If it falls too low, blood flow through tissue beds may be inadequate. That is particularly dangerous for essential organs like the heart, brain, or kidneys.

Systolic blood pressure

It is the maximum pressure exerted in the arteries during the heart’s systole.

Normal SBP = 110-140 mm Hg

Diastlic blood pressure

It is the maximum pressure exerted in the arteries during the diastole of the heart.

Normal DBP = 60-80 mm Hg

Pulse pressure

The difference between SBP and DBP.

Normal pulse pressure = 40 mm Hg

Mean arterial pressure

Average pressure existing in the arteries. It is not the arithmetic mean of systolic and diastolic pressure.

MAP = DBP + 1/3 PP

MEASUREMENT OF BLOOD PRESSURE

There are two methods of recording:

Direct method: mainly in animals, the artery is exposed and the cannula introduced, the other end is connected to a manometer. Either end pressure or lateral pressure can be recorded. This method is used in humans during cardiac catheterization.

Indirect method: Used in humans, lateral pressure is recorded.

Principle: It is balancing air pressure against blood pressure in the brachial artery and then estimating the air pressure using a mercury or anaeroid manometer or a digital BP recording device.

methods

Oscillometric method
Palpatory method
Auscultatory method

HOW IT OCCURS

When the left ventricle contracts and pushes blood into the aorta, the pressure produced within the arterial system is called systolic blood pressure. In adults, it is about 120 mmHg or 16 kPa.

When complete cardiac diastole occurs and, the heart is resting following the ejection of blood, the pressure within the arteries is much lower and is called diastolic blood pressure. In an adult, this is about 80 mmHg or 11 kPa. The difference between systolic and diastolic blood pressure is pulse pressure.

Blood pressure varies according to the time of day, posture, gender, and age of the individual. During bedrest at night, the blood pressure tends to be lower. It increases with age and is usually higher in women than in men.

Arterial blood pressure is measured with a sphygmo-manometer and is usually expressed with the systolic pressure written above the diastolic pressure.

BP = 120/80 mm of Hg or BP = 16/11 kPa

FACTORS MAINTAINING BLOOD PRESSURE

Central factors:
A. Cardiac output – Directly proportional
B. Heart rate – No effect
2. Peripheral factors:
A. Peripheral resistance- Directly proportional
B. Blood volume – Directly proportional
C. Venous return – Directly proportional
D. Elasticity of blood vessels – Inversely proportional
E. Diameter of blood vessels – Inversely proportional
F. Velocity of blood flow – Directly proportional
G. Viscosity of blood – Directly proportional

HIGH BLOOD PRESSURE( HYPERTENSION)

DEFINITION OF HYPERTENSION

Hypertension is an increase in either systolic or diastolic pressure or both conditions. In adults, the reading exceeds 140/90 mm Hg.

High blood pressure is the elevation of arterial blood pressure above the normal range expected in a particular age group. It describes a level of blood pressure that, taking all other cardiovascular risk factors into account, would benefit the patient if reduced. A measurement above 140/90 mmHg is considered higher than ‘normal’. It tends to rise naturally with age.

TYPES

1. PRIMARY HYPERTENSION

It means hypertension of unknown cause, may be due to heredity. It accounts for 95% of all cases and is subdivided according to the rate at which the disease progresses.

CHRONIC (BENIGN) HYPERTENSION

The rise of blood pressure is usually slight to moderate and continues to rise slowly over many years. Sometimes complications, such as heart failure cerebrovascular accident, or myocardial infarction is the first indication of hypertension. Still, the condition is often symptomless and only discovered during a routine examination.

Risk factors for hypertension include obesity, diabetes mellitus, family history, cigarette smoking, a sedentary lifestyle, and high intakes of salt or alcohol. Stress may increase blood pressure, and there is a well-documented link between low birth weight and the incidence of hypertension in later life.

ACCELERATED (MALIGNANT) HYPERTENSION

It stands for a rapid and aggressive acceleration of hypertension disease. Diastolic pressure above 120 mmHg is familiar. The effects are severe and quickly become apparent ex- it exudes into the retina, papilloedema (edema around the optic disc) encephalopathy (cerebral edema), and progressive renal disease, leading to cardiac failure.

2. SECONDARY HYPERTENSION

Hypertension resulting from other diseases accounts for 5% of all cases.

A–KIDNEY DISEASE

Raised blood pressure is a complication of many kidney diseases. There is salt and water retention in kidney disease, sometimes with excessive renin activity.

B–ENDOCRINE DISORDERS

ADRENAL CORTEX. Secretion of excess aldosterone and cortisol stimulates the retention of excess sodium and water in the kidneys, raising the blood volume and pressure. Over secretion of aldosterone (conn’s syndrome) is due to a hormone-secreting tumor. Over secretion of cortisol may be due to overstimulation of the gland by an adrenocorticotrophic hormone secreted by the pituitary gland or to a hormone-secreting tumor.
ADRENAL MEDULLA. Secretion of excess adrenaline (epinephrine) and noradrenaline raises blood pressure, ex. pheochromocytoma.

CONSTRICTION OF THE AORTA

Hypertension develops in branching arteries proximal to the site of a stricture, ex—congenital coarctation

CAUSES/AETIOLOGY

Predisposing factors

Family history ( history of stroke, and coronary heart disease )
Obesity
high salt intake
A diet high in fat and low in fruits and vegetables
Stress
Excess alcohol intake
Smoking
Exercise
Sexual function

Secondary causes

Anatomical causes
Endocrine causes
Renal causes

SIGNS AND SYMPTOMS

Constant headache
Irritation
Vomiting without any reason
Visual disturbance
Dizziness
Palpitation
Possibility of sleep apnea

Investigations

Ambulatory blood pressure monitoring is desirable if available and acceptable to the patient.
Full blood count
Blood chemistry ( including sodium, potassium, urea, creatinine, and urate )
Fasting glucose and lipids
Urine analysis for glucose, blood, and protein
ECG ( for arrhythmia, previous myocardial infarction, and left ventricular hypertrophy )
Echocardiogram
If available, ankle-brachial blood pressure index, pulse wave velocity, and carotid ultrasound help assess the vasculature.

Treatments for high blood pressure

1- A. Non-pharmacological treatment

Reduction of salt intake
Smoking cessation
Weight reduction
Removal of excessive alcohol intake
Physical exercise
Increase in fruit and vegetable intake and decrease in saturated and total fat intake

B. Novel non-pharmacological treatment

Vaccination against angiotensin
Renal sympathetic denervation procedure
Baroreceptor device

2- Pharmacological treatment

Alpha-adrenergic receptor blockers ( alpha-blockers )
Angiotensin-converting enzyme inhibitors (ACEIs)
Angiotensin II receptor blockers (ARBs)
Beta-adrenergic receptor blockers ( beta-blockers)
Calcium channel blockers (CCBs)
Diuretics: thiazides

Hypertension may be a side effect of some drugs, ex: corticosteroids and oral contraceptives.

LOW BLOOD PRESSURE (HYPOTENSION)

It usually occurs as a complication of other conditions, such as shock or Addison’s disease. Low blood pressure leads to inadequate blood supply to the brain. Depending on the cause, unconsciousness may be brief (fainting) or more prolonged, possibly causing death.

Postural hypotension syncope (fainting) is due to a sudden reduction in blood pressure on standing up quickly from a sitting or lying position. It occurs most commonly in the elderly. That may be caused by a delay in response of the baroreceptors in the carotid sinuses to the gravitational effects of standing up. It may also occur when treating patients with antihypertensive drugs, especially when the most appropriate dose is standing inaugurated.

TYPES

1. Primary/idiopathic – cause not known

2. Secondary hypotension-

Due to any bleeding, MI, heart failure, hypothyroidism, or postural/orthostatic hypotension: The sudden fall in BP on standing, below the critical level, which is not corrected by a neural mechanism within the physiological range.

REGULATION OF BLOOD PRESSURE

It is maintained within this range by various regulatory mechanisms, some of which are long-term and some short-term.

These mechanisms are:-

Neural
Renal
Hormonal
Chemical
Stress relaxation phenomenon
The capillary fluid shift mechanism

1- Neural mechanisms (short-term regulation)

The cardiovascular center (CVC) is a collection of interconnected neurons in the medulla and pons of the brainstem. The CVC receives, integrates, and coordinates input from:

Baroreceptor reflex (Marey’s reflex)
Chemoreceptor reflex
Cushing’s reflex

Baroreceptor reflex

These receptors are located in the carotid sinus and aortic arch, which respond to the stretch. They act by decreasing or raising the sympathetic and vagal tone through the vasomotor and cardioinhibitory centers. Their action can be demonstrated in two different situations, i.e. either BP is increased or decreased.

Chemoreceptor reflex

These are nerve endings situated in the carotid and aortic bodies and are primarily involved in the control of respiration. They are sensitive to changes in the levels of carbon dioxide, oxygen, and the PH of the blood: rising blood CO2, falling blood O2 levels, or falling tissue perfusion. When the chemoreceptors detect these changes, they send signals to the CVC, increasing the sympathetic drive to the heart and blood vessels, and pushing blood pressure up to improve tissue blood supply. Because respiratory effort is also stimulated, blood oxygen levels rise as well.

Cushing’s reflex

Input to the CVC from the higher centers is affected by emotional states such as fear, anxiety, pain, and anger that may stimulate changes in blood pressure.

Cushing’s reflex, likewise known as last ditch effort, comes into play when BP is below 40 mm Hg and is due to brain ischemia or increased intracranial pressure.

2- Renal regulation (long-term regulation)

The kidney plays a significant role in the long-term regulation of blood pressure. The mechanisms by which the kidney regulates BP are:

I. Renin-angiotensin system

ii. Prostaglandins E2 and I2 and bradykinin

iii. Renal body fluid mechanisms

I. Renin-angiotensin system consists of three hormones: Renin, angiotensin II, and III. It is angiotensin II and III, which regulate the BP. Renin helps in the synthesis of angiotensin.

Renin is a glycoprotein produced by the juxtaglomerular cells of the kidney in an inactive form called prorenin whenever there is a fall in BP thus reducing the blood supply to the kidney. This is converted to active renin by the action of kallikreins.

Angiotensin II and III increase peripheral resistance, blood volume, cardiac output, and thus blood pressure by:

Vasoconstriction
ADH secretion
Aldosterone secretion
potentiates the effect of catecholamines on blood vessels
Stimulation of thirst center

II. Prostaglandins and bradykinins– PGE2 and I2 are released from the renal medulla in response to increases in the blood volume, and BP produces vasodilation and Na+ excretion in the urine hence the BP falls.

Bradykinin is produced from kininogen released by the renal medulla by elevated BP and delivers similar effects to reduce BP.

III. Renal body fluid mechanism– Whenever there is a rise in ECF volume blood volume, the kidney increases urine output till the BP returns to normal.

In brief, all the renal mechanisms interact to maintain the BP in an acceptable range in the long run.

3- Hormonal mechanism

Catecholamines, Norepinephrine, Epinephrine
Glucocorticoids
Mineralocorticoids
Thyroid hormones
Angiotensin II
ADH
Serotonin
Histamine
Atrial natriuretic factor
Nitric oxide

4- Chemical mechanisms

Increased PO2, increased PCO2, and raised H+ act via the aortic body or carotid body or directly on the vasomotor center, stimulating it to increase the BP. They can reduce BP by straight-acting on vascular smooth muscle and relaxing them.

5- Stress relaxation phenomenon

According to it, the smooth muscle undergoes relaxation after prolonged stretching.

Increased BP – stretched blood vessels – stress relaxation – decreased influential blood – decreased volume decreased BP vice versa occurs in the case of BP and is called reverse stress relaxation.

6- Capillary fluid shift phenomenon

The excess fluid is filtered into the interstitial space to bring it back to normal in case of elevated BP. The reverse occurs in the case of reduced BP.

All these mechanisms interact to play an essential role in the regulation of BP though some for the short term and some for the prolonged phase.

Summary

The pressure of blood against the walls of the main arteries. Blood Pressure is measured in (millimeters of mercury) using a sphygmomanometer at the brachial artery of the arm, where the pressure is most similar to that of blood leaving the heart. The normal range varies with age, but a young adult would be expected to have a systolic pressure of around 120 mm and a diastolic pressure of 80 mm. These are recorded as 120/80.

References

Hung-Fat-Tse, Gregory Y. H. Lip, Andrew J. Stewart Coats. OXFORD DESK REFERENCE CARDIOLOGY.

M. Chandrasekar. Exam-oriented review in physiology

Ross and Wilson, Anatomy and physiology.