The cardiovascular system in systemic disease Medical Assignment Help

Systemic hypertension

Blood pressure within a population has a skewed distribution, i.e. there is a single peak frequency of blood pressure and there are more individuals with high pressures than low pressures. Different populations have different levels of blood pressure, with those of African origin tending to have higher pressure than Caucasians, i.e. the whole distribution is shifted to the left. The distribution curves for systolic and diastolic blood pressure are similar. Risk of mortality and morbidity rises continuously with increasing blood pressure throughout the range. The rise of risk is not linear, however, being steeper at higher pressures.

Cardiac involvement in some systemic disorders.

Cardiac involvement in some systemic disorders.

The level of blood pressure can be said to be abnormal when it is associated with a clear increase in morbidity and mortality. This level varies with age, sex, race and country. For life insurance reasons and for simple clinical purposes, a diastolic blood pressure in a young adult above 100 mmHg and/or 160 mmHg systolic is taken as definitely hypertensive and a diastolic pressure above 95 mmHg is regarded as probably hypertensive. The World Health Organization have used a definition of 160/95 mmHg, and in Framingham (a small town in Massachusetts, USA), where a very detailed population study is being carried out, 160/95 mmHg was deemed abnormal and 140/90 to 160/95 mmHg was regarded as borderline. The significance of a single elevated reading is unclear and for a firm diagnosis the blood pressure should be elevated on more than one examination. In a proportion of patients the blood pressure increases due to the presence of a doctor (‘white coat hypertension’). In patients without probable target organ damage, some weeks or months can be taken to be sure that the blood pressure is elevated. The blood pressure should be taken twice with the patient in the sitting position and this should be repeated three or four times over several months. When target organ damage is present or the blood pressure reading is very high, a more urgent assessment is needed.

If there is any doubt about the validity of blood pressure measurements taken in the clinic, ambulatory blood pressure monitoring offers a non-invasive assessment during normal daily activities and largely circumvents the problem of ‘white coat hypertension’.


In the large majority of cases no cause can be identified, and this form of hypertension is known as primary or essential. A cause of hypertension can be discovered in less than 10% of patients; such cases are known as secondary hypertension.

Essential hypertension

No single factor has been found to explain essential hypertension; many factors are probably responsible. The blood pressure is determined by the product of the cardiac output and the peripheral vascular resistance. In the early stages of essential hypertension the increase of blood pressure is due to a small increase in cardiac output. This could be due to sympathetic overactivity. Later in the disease, the cardiac output is normal but the peripheral resistance is increased. It is possible that the initial increase in cardiac output induces vascular changes that then sustain and increase the blood pressure. The baroreceptor reflexes operate at a higher pressure in hypertension. An increased blood pressure should stimulate a bradycardia via the carotid sinus baroreceptor mechanism. This does not happen in essential hypertension. This abnormal reflex may be due to the hypertension rather than being its cause.
The causes of essential hypertension include the following.
GENETIC FACTORS. Racial and familial tendencies to high blood pressure are found.
ENVIRONMENTAL FACTORS. Numerous factors have been related to the development of hypertension but only the following appear to be important.
OBESITY. Blood pressure rises with increasing obesity. This relationship persists even when errors of blood pressure measurement in obese subjects (cuff artefact,) are taken into account.
ALCOHOL INTAKE. Ingestion of alcohol acutely raises blood pressure and alcohol intake tends to be higher in individuals with higher pressures. Reduction or withdrawal of regular alcohol intake reduces blood pressure 5-10 mmHg.
SALT INTAKE. There is much controversy about the role of salt in hypertension. There is some evidence of a relationship between the salt intake of an individual and the level of the blood pressure within populations. Similar, but weaker relationships are found between populations. There is less convincing evidence that a moderate reduction of salt intake will reduce blood pressure. Salt intake may increase intravascular volume in the initial stages of the genesis of hypertension, but once peripheral vascular resistance becomes raised, alterations of salt intake may play little part in the regulation of blood pressure.
HUMORAL FACTORS have been implicated in the genesis of hypertension including catecholamines, the reninangiotensin system, and atrial natriuretic peptide. Convincing evidence is lacking that any of these are involved.

Secondary hypertension

This should always be considered in patients with hypertension.In particular, a careful search should be made in hypertensive patients presenting under the age of 35 years. The causes of secondary hypertension can be divided into the following.
RENAL CAUSES. Renal diseases are the most common causes of secondary hypertension, accounting for over 80% of cases. Chronic glomerulonephritis, chronic atrophic pyelonephritis and congenital polycystic kidneys are the conditions usually involved. It may be difficult to determine whether renal disease has caused hypertension or whether the hypertension has produced the renal disease.
The mechanism by which renal disease causes hypertension is probably related to salt and water retention. Occasionally, renal artery stenosis due to fibromuscular hyperplasia or atheroma may cause hypertension (renovascular hypertension) owing to excess renin production.
These include:
• Conn’s syndrome
• Adrenal hyperplasia
• Phaeochromocytoma
• Cushing’s syndrome
• Acromegaly
CARDIOVASCULAR CAUSES. Renovascular hypertension is discussed above.
Coarctation of the aorta (see p. 608) should be considered in young patients with hypertension and a late systolic murmur.
PREGNANCY. Hypertension in the early stages of pregnancy is usually essential hypertension or due to renal disease.
Pre-eclampsia or toxaemia of pregnancy is diagnosed when hypertension develops in the last 3 months of pregnancy and is associated with oedema and proteinuria. The cause of pre-eclampsia is unknown.
Pre-eclampsia may worsen, with the development of severe hypertension, nausea, vomiting, pulmonary oedema and fits. This condition, known as eclampsia, needs urgent treatment.
DRUGS. Oestrogen-containing contraceptives, other steroids, carbenoxolone, liquorice and vasopressin may all cause hypertension. Paroxysms of severe hypertension may occur in patients taking monoamine oxidase inhibitors who eat cheese or other tyramine-containing foods and those who drink wines.


An increase in vascular tone initially accounts for the increased peripheral vascular resistance. As the disease progresses, the walls of small arteries thicken and atheroma develops in larger arteries. Malignant hypertension is characterized by fibrinoid necrosis of the vascular wall. The increased peripheral vascular resistance leads to a greater impedance to left ventricular emptying. Consequently, left ventricular hypertrophy develops. A reduction in renal perfusion pressure can occur, leading to decreased glomerular filtration and reduced sodium and water excretion. The renal changes are described in more detail. The decreased renal perfusion leads to the production of renin, which converts angiotensinogen to angiotensin I. This is changed to angiotensin II, which stimulates the secretion of aldosterone and further contributes to salt and water retention.
Secondary aldosteronism, which occurs with severe or accelerated hypertension and with the use of diuretics, is characterized by high serum levels of aldosterone and renin. In primary aldosteronism (Conn’s syndrome), only the aldosterone is raised. About 10% of patients with essential hypertension have a high plasma renin level, and 25% have a low renin level.
In some cases the pressure rises rapidly and these patients are said to have ‘malignant’ hypertension. Without treatment death occurs within 1-2 years. The accelerated rise in blood pressure produces cerebral oedema, left ventricular failure and severe renal impairment, with proteinuria and microscopic haernaturia Retinal haemorrhages, exudates and papilloedema are also seen and are diagnostic of malignant hypertension.


Hypertension is a risk factor for developing atheroma and patients may therefore develop thrombotic cerebral vascular disease, coronary artery disease and peripheral vascular disease. The increased pressure in the circulation can result in heart failure, cerebral haemorrhage, renal disease and dissecting aortic aneurysms.


The possible causes and consequences of hypertension are assessed. In uncomplicated or essential hypertension, apart from the high blood pressure there are usually no signs, symptoms or abnormal investigations.

The patie!J.t with mild hypertension is usually asymptomatic. Nose bleeds and headaches have been traditionally regarded as possible symptoms, but are probably no commoner than in the general population. There may be a past history of renal disease or a family history of hypertension. Secondary causes of hypertension are suggested by a specific history, such as attacks of sweating and tachycardia in phaeochromocytoma.
Angina may occur either because of associated coronary artery disease or because of the high oxygen demand from hypertrophied muscle. If cardiac failure develops, breathlessness occurs.
Accelerated or malignant hypertension presents with visual impairment, nausea and vomiting, fits, transient paralysis, severe headaches, impairment of consciousness, or symptoms of acute cardiac failure.


In the majority of patients the only sign is the high blood pressure, but in others features of the cause of hypertension may be noted. For example, there may be abdominal bruit due to renovascular obstruction, or delayed femoral pulses due to coarctation of the aorta. Hypertensive heart disease presents with a loud aortic second sound, a prominent left ventricular apical heave and a fourth heart sound. Sinus tachycardia and a third heart sound develop if cardiac failure occurs. Examination of the retina may reveal various abnormalities which are known as Keith-Wagener retinal changes. They are graded as follows:
GRADE I-increased tortuosity of retinal arteries and increased reflectiveness (silver wiring)
GRADE 2 -grade 1 plus the appearance of arteriovenous nipping produced when thickened retinal arteries pass over the retinal veins
GRADE 3 -grade 2 plus flame-shaped haemorrhages and soft ‘cotton wool’ exudates
GRADE 4-grade 3 plus papilloedema (bulging and blurring of the edges of the optic disc)
The presence of haemorrhages, exudates or papilloedema is diagnostic of malignant hypertension which requires urgent treatment.


Routine investigation of a hypertensive patient should always include:
• Chest X-ray
• Echocardiogram
• Urinalysis
• Fasting blood lipids
• Urea, creatinine and electrolytes
If the urea or the creatinine level is abnormal, creatinine clearance, intravenous excretion urography, renal ultrasound and other tests of renal function are necessary. If the tests of renal function or an abnormal bruit suggest a renovascular cause, full renal investigation is essential. If coarctation of the aorta is suspected, digital vascular imaging with intravenous contrast injection or MRI will usually demonstrate the lesion.
If the patient is not taking diuretics, a low serum potassium should suggest an endocrine problem, and aldosterone, cortisol and renin measurements should be performed. A history suggestive of phaeochromocytoma can be investigated with measurement of serum catecholamines or urinary catecholamine metabolites. The chest X-ray may show a large heart and pulmonary congestion if heart failure has developed, or rib notching in coarctation of the aorta. The ECG may show left ventricular hypertrophy or signs of myocardial infarction or ischaemia. Very rarely, ECG features of hyperkalaemia (e.g. with renal failure) or hypokalaemia may be detected.

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