
High blood pressure — a silent killer
Hypertension means an increase in blood pressure (BP); it affects up to 20% of the population in developed countries and is also common in developing countries. It is important to understand this topic as hypertension leads to a lot of pathology if unmanaged but when recognised it is usually eminently preventable or treatable.
Normal physiology
Blood pressure simply describes the pressure of blood on the vessel walls in which it is contained. The venous system is described as a low-pressure system and the pressures generated by the right ventricle in the pulmonary arteries is usually about 25/8 mmHg. The term blood pressure as commonly used refers to systemic arterial pressure and this can be defined as cardiac output multiplied by systemic peripheral resistance. Cardiac output is the volume of blood pumped out by the left ventricle in a one minute period and is equal to heart rate multiplied by stroke volume (stroke volume is the volume of blood pumped out of the left ventricle per cardiac contraction). However, cardiac output and systemic peripheral resistance are both influenced by renal function and sodium homeostasis. Hypertension results from an imbalance between these factors. Systolic blood pressure (SBP) is the highest pressure in the arterial system during cardiac contraction, i.e. during systole. Diastolic blood pressure (DBP) is the lowest pressure occurring in the systemic arteries during a cardiac cycle and occurs during diastole. Sixty percent of mean arterial pressure is determined by diastolic and 40% by systolic pressure. This is because arterial BP remains closer to the diastolic pressure than the systolic for more of the cardiac cycle.
Definition of hypertension
There is no clear agreement on what constitutes hypertension. The World Health Organisation has defined hypertension as a systolic BP over 160 mmHg and a diastolic BP above 90, or both. The International Society of Hypertension of the WHO goes on to define a systolic pressure of 130–139 mmHg and a diastolic of 8589 mmHg as being ‘high normal’ BP. Others define hypertension as a consistent systolic of over 140 mmHg or a diastolic of over 90 mmHg. The British Hypertension Society considers an optimal BP to be a systolic of less than 120 and a diastolic of less than 80 mmHg. As the risk of hypertensive complications rises progressively with increasing systolic and diastolic pressures, perhaps the best definition of hypertension is ‘that level of blood pressure above which investigation and treatment do more good than harm’.
Hypertension may be essential or secondary. In essential hypertension, it is not possible to discover a cause of the problem, there is a primary elevation of BP. However, despite there being no clear cause, many factors are known to influence BP and some of these are open to modification. Conversely, acquired or secondary hypertension has an identifiable underlying disorder which causes the elevation in BP. Malignant or accelerated hypertension describes a rapid development of very high blood pressures associated with significant development of complications. Without treatment, these patients have a short term high mortality from stroke, heart or renal failure.
Causes and prevention of essential hypertension
Genetic factors
A genetic factor is important in most cases of essential hypertension. No specific gene has been identified for essential hypertension and the genetic component is probably polygenic, i.e. caused by several different interacting genes. Children of hypertensive parents have an increased risk and hypertension tends to run in families. While this is likely to have a genetic explanation, it is always worth considering that a family may have shared environmental risk factors.
Congenital factors
Low birth weight babies are more likely to become hypertensive as adults. This may be caused by fetal under nutrition affecting the development of the vascular system. This is sometimes referred to as the ‘bad start’ problem. Future cases of this problem can be reduced by good maternal nutrition and prenatal care.
Race
In Europe and the US hypertension is more common in people of African extraction compared to traditional European populations. It has been suggested that African populations, used to high temperatures and hence higher levels of sweating, have a ‘salt thrifty gene’ that allows them to conserve salt. This is supported by the observation that African people are generally more salt sensitive than European populations. In salt sensitive individuals blood pressure is increased when salt is eaten. This means it is particularly important for such high risk groups to eat less salt.
Obesity
Obese people generally have higher BPs than thin people and it is likely that obesity causes hypertension. Central obesity is a greater risk factor for hypertension than fat on the buttocks and legs. This may be because abdominal fat is more insulin resistant. This is why it is particularly important to advise people to have a relatively thin waist. If individuals who are obese lose weight, their blood pressure will be reduced.
Alcohol
Doses of alcohol over 21 units per week are associated with increased BP. All forms of alcoholic drinks may contribute to hypertension, with the systolic BP being affected more than the diastolic. BP readings are higher during a ‘hangover’ due to increased sympathetic activity. Reduction of alcohol intake should therefore, be recommended. Some people may need to stop drinking altogether if they find it difficult to cut down. While small doses of alcohol may lower BP slightly we should not advise people to start drinking. In addition, all alcohol consumption is calorific and so will contribute to obesity.
Sodium and potassium
Populations who have a high sodium intake have a tendency to have higher BP compared to low sodium consumers. While individual sensitivity to sodium varies, there are clear positive correlations between salt intake and systolic and diastolic BP. Many people in developed countries consume much more than the recommended maximum of 6g per day. Most dietary salt comes from processed and manufactured foods. It is unfortunate that food manufacturers add so much salt to many of their products. We should advise people to avoid manufactured foods with a high salt content. Also, we should advise adding less salt to food in general. Once the palate becomes accustomed to low salt content foods they taste just as good. Conversely, high potassium intake will slightly lower BP. This seems partly to be due to a direct effect of the potassium but also because high potassium intake encourages sodium excretion. Fruit and tea are both sources of potassium.
Physical inactivity
Lack of physical exercise leads to increases in BP. People who are physically active have relatively lower BPs than their more sedentary counterparts. Exercise is also a factor in the prevention and correction of obesity. People should be advised to take regular aerobic exercise up to their individual advisable levels. Physical inactivity also contributes to the development of metabolic syndrome.
Metabolic (insulin resistance) syndrome
Metabolic syndrome (also called insulin resistance syndrome) is a collection of metabolic risk factors which promote the development of atherosclerosis with subsequent cardiovascular and cerebrovascular disease. Dyslipidemia, hypertension, central (abdominal) obesity and hyperglycemia caused by insulin resistance are the most widely recognised components of the syndrome. While it is unclear exactly how one component of metabolic syndrome inter-relates with the others, it is generally agreed that the underlying causative problems are central obesity and insulin resistance. One possible mechanism is that insulin resistance leads to hyperglycemia which in turn stimulates hyperinsulinemia. It is possible that high insulin levels stimulate the sympathetic nervous system in an attempt to use up excess glucose present in the blood. While this increased sympathetic activity will increase metabolic demand it also increases blood pressure, probably by stimulating vasoconstriction.
Smoking
Smokers typically have a slightly lower BP than average when they are not smoking, however when they are smoking BP is increased. This means in heavy smokers the BP may be increased for much of the day. Also hypertensive patients who smoke are more likely to develop accelerated or malignant hypertension in comparison to their non-smoking counterparts. Smoking is also a synergistic risk factor for ischaemic heart disease in the presence of hypertension, diabetes mellitus or hypercholesterolemia. Clearly it is important for hypertensive patients not to smoke.
Psychological stress
It is certainly true that acute pain, anxiety or stress can significantly increase BP in the short term. However, there is very little evidence to suggest that psychological stress leads to the development of essential hypertension.
Other factors
It is normal for BP to fall during the night when a person sleeps. It may be that failure of the BP to fall overnight is a significant factor in the development of end organ complications. Oral contraceptive drugs may cause a mild increase in BP and in some predisposed women may cause a more significant increase. The prevalence of hypertension generally increases with age.
Clinical features of hypertension
It is important to know that essential hypertension does not usually generate clinical features, it is asymptomatic. Clinical features which do present are typically a result of the long term complications of hypertension. This means a diagnosis is made on the basis of recording blood pressure levels. As BP may vary significantly from time to time, a diagnosis should only be made if the BP is elevated on several occasions. Recordings should be made in a seated patient who has rested for five minutes and is feeling relaxed. The arm should be supported on a table at the same level as the heart. SBP should be recorded when the first sound is heard and DBP at the last sound that is audible. The British Hypertension Society advises that everyone should have their BP measured at least every 5 years up to the age of 80. Individuals with readings which are high or in the ‘high normal’ ranges (i.e. SBP of 130–139 or a DBP of 85–89) should be reassessed annually. All hypertensive people should be monitored and treated for life.
‘White coat’ hypertension
Unfortunately, the presence of nurses and doctors often leads to anxiety in our patients. This is counter-therapeutic. As part of our philosophy of doing no harm, our presence should relax and reassure patients, not frighten them. This means we need to examine how we interrelate with our patients and to empathise strongly with them. We should not put up barriers between ‘us’ and ‘them’, we are all people together and one is certainly not better or worse than the other.
In white coat hypertension, the blood pressure increases via an alarm response. This makes hypertension very hard to diagnose because every time we take the patients BP it will be elevated. Sometimes the BP will drop when the patient becomes more relaxed after several recordings, over several visits. It may befound that readings are lower when taken by relatives or friends at home. Another approach is to use a 24-hour ambulatory monitoring device. This will record the BP automatically throughout the patient’s normal day. This syndrome of course challenges us as health care workers, can we metaphorically ‘take off our white coats’?
Orthostatic or postural hypotension
This occurs when there is an excessive drop in BP when a person stands up. Blood tends to pool in the lower parts of the body with resultant hypoperfusion of the brain. This causes dizziness with possible fainting (i.e. syncope). Posturalhypotension is particularly noticeable when getting out of a hot bath. The heatleads to vasodilation and so further lowers BP. Pathological causes of postural hypotension include reduced blood volume and disorders of the endocrine or autonomic nervous system function. Hypotension may be a particular problemwhen patients start to take hypotensive medication to treat hypertension. However, this problem usually resolves once the correct doses are titrated and over time the baroreceptors adapt to the new lower blood pressure. Postural hypotension is also more common after prolonged bed rest and in the elderly.
Treatment principles
The first line of treatment for essential hypertension is lifestyle modification. Lifestyle changes such as those discussed above can lower SBP and DBP and significantly reduce the risk of morbidity and mortality. For many individuals these changes can bring BP down to acceptable levels. In the absence of other disease states, the aim of treatment is to achieve SBP below 140 and the DBP below 90. If lifestyle modification is not sufficiently effective, drugs may be used. It is important to realise drugs should be given in combination with a healthy lifestyle, i.e. drugs are ‘as well as, not instead of’.
In chronic essential hypertension the principle factor increasing the blood pressure is increased peripheral resistance caused by vasoconstriction of the small muscular arteries and arterioles. This is why BP will drop rapidly in persons with hypertension when given vasodilators. Several drugs may be used to control hypertension and will need to be taken on an ongoing basis. Therapy should be titrated with BP remembering hypotension may be a possible side effect of BP lowering medications.
Thiazide-type diuretics, such as bendroflumethiazide, may be effective in relatively low doses. They promote a moderate diuresis which will have the initial effect of reducing total plasma volume; this will lower cardiac output and therefore lower blood pressure. However, when thiazide diuretics are given over time the blood volume will return to normal. Despite this the hypotensive effect persists indicating their principle mode of action is peripheral vasodilation lowering peripheral systemic resistance. At the time of writing the U.K. National Institute for Health and Care Excellence (NICE) guidelines advise that in hypertensive patients aged 55 or over, or black patients of any age, the first choice for initial therapy should be either a calcium-channel blocker or a thiazide-type diuretic.
ACE inhibitors, such as enalapril, captopril and lisinopril, inhibit the conversion of angiotensin I to angiotensin II by blocking the action of angiotensin converting enzyme. As angiotensin II is a potent vasoconstricting agent this effect is reduced allowing more vasodilation. ACE inhibitors also suppress aldosterone secretion thereby reducing blood sodium levels. They also increase renal blood flow so promoting urine formation. NICE currently advises that in white hypertensive patients younger than 55, the first choice for initial therapy should be an ACE inhibitor. ACE inhibitors must not be used in pregnancy. If the use of one drug does not bring the blood pressure down to desired levels a second hypotensive drug should be added in combination. Therefore, NICE further recommend that if initial therapy was with a calcium-channel blocker or a thiazide-type diuretic and a second drug is required, add an ACE inhibitor. If initial therapy was with an ACE inhibitor, add a calcium channel blocker or a thiazide-type diuretic.
Beta-blocking drugs such as propranolol, atenolol and nebivolol still have a place in some hypotensive treatments but are no longer recommended as a first line option. Other drugs used in hypertension may include angiotensin II receptor antagonists, alpha blockers and vasodilators such as hydralazine or minoxidil.
