Hypertension – is very common (25% above 140/80), usually symptomless, with the potential of devastating effects. It is a major risk factor for coronary heart disease and stroke; it may lead to heart failure and to renal damage. Hypertension can be divided into 2 groups, primary and secondary. Primary hypertension is the commonest – 95% of patients with raised BP come in this category, for which there is no known cause, we only know the effects. Of the remaining 5% who have secondary hypertension, most are as a result of renal disease, the remainder are endocrine, vascular or neurogenic causes. Most hypertension is known as benign, in other words stable and is compatible with a long life, whilst 5% show a rapid rise in BP with a risk of death within a year or two – this is not surprisingly known as malignant hypertension.
Blood pressure control is dependent on cardiac output and the total peripheral resistance. The resistance is mainly dependent on the constriction of arterioles and the volume of blood. This is regulated by a ‘feed back mechanism’ of nerves and hormones that monitor the volume of blood and diameter of the blood vessels and force of the heartbeat.
Imagine that the cardiovascular system is like a balloon filled with water, the blood vessels are the walls of the balloon and the blood is like the water. So the pressure of the water inside depends on the amount of water and the elasticity of the balloon. Blood Pressure will depend on the strength of the pump, diameter of the vessels and the volume of the blood.
Anatomy and physiology recap of heart
The myocardium of the heart is made up of smooth muscle, arranged in layers, encircling the heart like a squeezing fist. The myocardium contains fibres that form a conducting system that initiates and spreads the heartbeat. The standard rate of the heart beat is 100, but it receives a nerve supply from both the sympathetic and parasympathetic system, the parasympathetic slows the rate of the heart down, whilst the sympathetic (vagus) speeds it up. So the pre-set rate is normally in ‘slow down mode’ to about 60 beats a minute. Contraction of the heart is triggered by depolarisation of the plasma membrane of the muscle cells, starting at the sinoatrial node in the Rt atrium to the atrioventricular node, down the bundle of His and along its two branches (Rt and Lt bundle branch) to the purkinje fibres. This stimulates the atria to contract first followed by the ventricles. (Sodium and Potassium involvement in the depolarisation, mediating the opening of calcium channels that allow Calcium to flow into the cells to constrict muscles).
- Contraction of the heart – systolic phase
- Relaxation of the heart – diastolic phase
The myocardium contains cells that secrete the hormone atrial natriuretic hormone (ANH) that has some control over reducing the re-absorption of sodium from the kidneys, it also inhibits the secretion of renin and aldosterone.
But major sensors are called barorecptors, they lie in the carotid sinus and aortic arch. These are stretch receptors that respond to altered pressure within the walls of vessels and send a message back to the pituitary. There are also other baroreceptors in the large veins, pulmonary vessels and walls of the heart. The feed back message acts on the sympathetic and parasympathetic nervous system to the muscles of the heart, arterioles and veins to alter their degree of constriction. These receptors can trigger the release of anti diuretic hormone (ADH), also known as vasopressin, which alters the excretion of salt and water from the kidneys and therefore affecting the total plasma volume. The baroreceptors also alter the generation of angiotensin II . These receptors can monitor change but at the same time can be ‘reset’ at a higher pressure within a couple of days and so get used a higher BP as the norm.
Like the muscular walls of the heart, the walls of the arteries and arterioles are also made up of smooth muscle and capable of relaxation and contraction, thus altering the diameter of the blood vessels. As they dilate, so the pressure drops.
The cardiac output is made up of the amount of blood returning to the heart, it is pumped into the heart the skeletal pump (such as the muscles of the legs), and the pumping action of when we breath in, by creating pressure on the abdominal veins, and as the diaphragm drops down, decreasing the pressure in the thorax, enhancing venous return to the Rt atrium of the heart.
However the rate of venous blood returning can be altered. The veins have thinner walls than arteries, but also contain smooth muscle innervated by the sympathetic nervous system therefore capable of some contraction. Venous return can also be increased by the skeletal pump – running and by the respiratory pump – breathing faster.
The volume of blood pumped out of the heart will then depend on the strength and rate of the heart pumping, which is controlled by the nervous and hormonal feed back system, which determines the output from the heart. However, the pressure in the arteries will also be determined by the resistance it meets in the arterioles.
So the formula for determining the mean arterial pressure is taken by multiplying the total peripheral resistance by the cardiac output.
There are other factors influencing blood pressure, there are various local controls.
- Increased levels of carbon dioxide, hydrogen ions, potassium, metabolites and a decrease in oxygen, will act as stimulants to alter the constriction of arterioles, either through local receptors or in the brain.
- Circulating prostaglandins will affect smooth muscle contraction and bradykinin will increase capillary permeability. The total blood volume, which can be reduced in haemorrhage, shock or dehydration, and also the viscosity of the blood will affect the total resistance within the arterioles, however a major effect on the resistance within the arterioles is brought about by the relaxation or contraction of the arterioles.
- Sympathetic nervous system – constriction & relaxation of arterioles Fright and flight. Largely the sympathetic, will increase heart rate and constrict arterioles (open airways) to increase the BP and allow flight. Norepinephrine released by neurones activate alpha receptors of smooth muscles, constriction of arterioles. (in heart, activate beta receptors).
- Action of norepinephrine on beta receptor of heart – opening of calcium channel, increased inflow of calcium – muscle contraction. (Calcium channel blockers ‘pine’) (Beta-blockers ‘olol’) both drugs act on same pathway, hence not used together. I have mentioned angiotensin in passing, but we need to go into how the kidneys effect some control of blood pressure Angiotensin; renin; aldosterone – overhead
- The kidneys influence both the peripheral resistance and blood volume. So it is no suprise that kidney disease is associated with hypertension. The renin- angiotensin system alters the BP by increasing peripheral resistance and blood volume. Angiotensin II causes arterioles to constrict and stimulates the production of aldersterone, which increases reabsorption of water at the distal tubules.
- A decrease in the BP reduces the stretch on the baroreceptors, which affects the release of renin. Arterioles in kidneys synthesise renin, which converts to angiotensin I, which in turn is converted to angiotensin II, by a converting enzyme, called angiotensin converting enzyme (found in lungs). (angiotensin converting enzyme inhibitor – ACEI – drug used to control BP, by blocking the action of the angiotensin converting enzyme). Angiotensin II stimulates aldosterone secretion from the adrenal cortex which stimulates sodium re-absorption (and water) from the distal tubules into the renal circulation .
- Increased renin secretion plays an important role in renal artery stenosis and malignant hypertension.
- Na and water secretion (diuretics)
- Extracellular fluid and therefore blood volume, is regulated mostly by total body sodium levels. The kidney is intimately involved in the complex process of sodium balance within the body. When the BP falls the glomerular filtration rate falls, this in turn leads to increased re-absorption of sodium by the proximal tubules in an attempt to conserve sodium and expand blood flow. Failure of this system is commonly found in patients with chronic renal failure, which leads to sodium retention.
- Salt or sodium balance has an important part in BP control, and the use of diuretics increases the output of sodium and water from the kidneys. Essential or Primary Hypertension – is the commonest form of hypertension (95%) although there is no known cause, it is believed that a combination of genetic and environmental factors together is responsible for the condition. Salt intake has been a controversial subject in hypertension, but it is believed that a high sodium diet in the genetically susceptible person may lead to hypertension. People living in remote areas, who have diets low in sodium, show little evidence of this type of hypertension, until they move into more affluent conditions.
- It is thought that a defect in sodium excretion may be part of the cause of primary hypertension. Other causes include – stress; obesity; smoking; oestrogens (O.C.)
Types of hypertension
- Primary or essential hypertension (90 – 95%)
- Secondary Hypertension (5 – 10%)
- Acute glomerulonephritis
- Chronic renal disease
- Renal artery stenosis
- Renal vasculitis
- Renin-producing tumours
- Adrenocortical hyperfunction (Cushing’s sydrome)
- Oral contraceptives
- Thyrotoxicosis (systolic)
- Coarction of aorta
- Polyarteritis A
- ortic insufficiency
- Increased cranial pressure
- Polyneuritis, bulbar poliomyelitis, others