Assessing and managing primary hypertension
Hypertension is a major risk factor for coronary heart disease, stroke and heart
failure; accurate blood pressure measurement is essential for correct diagnosis
In this article…
- Treatments for primary hypertension
- The value of lifestyle interventions
- The importance of accurate blood pressure measurement
Sophie O’Connell is clinical nurse specialist in cardiac rehabilitation at Princess Elizabeth Hospital, Guernsey.
O’Connell S (2014) Assessing and managing primary hypertension. Nursing Times; 110: 14, 12-14.
Hypertension is a major risk factor for coronary heart disease, stroke and heart failure. This article discusses treatments for primary hypertension, including lifestyle interventions and drug therapy, and highlights the importance of accurate blood pressure measurement.
- This article has been double-blind peer reviewed
- Figures and tables can be seen in the attached print-friendly PDF file of the complete article in the ‘Files’ section of this page
5 key points
- Hypertension is a primary modifiable risk factor for the development of cardiovascular disease
- Accurate blood pressure measurement is essential
- All patients diagnosed with hypertension should be offered lifestyle advice
- ACE inhibitors are the first drug of choice in most patients aged under 55 years
- Calcium channel blockers are the first drug of choice in patients of African or Caribbean origin
Hypertension (high blood pressure (BP)) is a primary modifiable risk factor for the development of coronary heart disease, heart failure, cerebrovascular disease, peripheral vascular disease and renal disease; its prevalence increases with age in both sexes (British Heart Foundation, 2012).
The development of hypertension is inevitable in most people as they age and, although the cause is often unknown (primary hypertension), genetic factors, foetal environment, obesity, inactivity, smoking, alcohol intake, age, gender, ethnicity and salt intake have been linked to it (Kaplan, 2001). The three stages of hypertension are defined as:
- Stage 1: clinic BP of ≥140/90 and subsequent ambulatory BP monitoring (ABPM) or home BP monitoring (HBPM) daytime average of ≥135/85
- Stage 2: clinic BP of ≥160/100 and subsequent ABPM or HBPM daytime average 0f ≥150/95
- Severe: clinic systolic BP of ≥180 or clinic diastolic BP of ≥110 (National Institute for Health and Care Excellence, 2011).
BP is the pressure exerted by blood on the arterial walls (Wilmore and Costil, 2008). Systolic BP is the pressure exerted after ventricular contraction and reflects the workload of the heart, while diastolic BP is exerted during ventricular relaxation and indicates peripheral resistance to blood flow in the blood vessels (McArdle et al, 2007).
BP is measured in millimetres of mercury (mmHg). Normal BP (normotension) is a systolic pressure of ≤120mmHg and diastolic of ≤80mmHg; hypertension is usually defined as systolic pressure >140mmHg and diastolic >90mmHg (Wood, 2005). However, Kaplan (2001) states the condition is defined by the risk of adverse clinical events, such as the presence of left-ventricular hypertrophy, retinopathy, stroke, coronary artery disease, heart failure, aortic dissection and renal failure.
Diagnosing hypertension is complicated by the phenomenon of “white coat syndrome”, in which BP is raised when measured in the GP surgery or hospital. NICE (2011) emphasises the importance of accurate recording of BP. Box 1 outlines key points for BP measurement.
Management of hypertension
Management of hypertension is aimed at preventing organ damage, including stroke and heart failure, and reducing cardiovascular risk. Lifestyle interventions and pharmacological treatment form the cornerstone of therapy; lifestyle modification has been shown to reduce BP by as much as 10mmHg (NICE, 2011).
A diet high in saturated fats and low in fruit and green vegetables has been linked to the development of obesity, cardiovascular disease and endothelial dysfunction (Lopez-Garcia et al, 2004).
The endothelium (blood vessel lining) plays an important role in the prevention of long-term conditions; endothelial damage has been linked with the development of atherosclerosis (thickening of the arterial walls) (Mensah, 2007).
Obesity may increase the risk of hypertension through overactivation of the sympathetic nervous system (Esler et al, 2006). Increased levels of the neurotransmitter noradrenaline reduce blood flow to the kidneys, leading to activation of the renin-angiotensin-aldosterone system, sodium retention and an increase in heart rate. Skeletal muscle circulation is reduced due to vasoconstriction, suggesting an increase in peripheral resistance; however, the heart rate is relatively unaffected (Esler et al, 2006). Obesity is also associated with raised inflammatory markers, in particular C-reactive protein, which can lead to endothelial dysfunction (Esler et al, 2006) and abnormal lipid profiles.
Halperin et al (2006) found high lipid levels were independently associated with a greater risk of hypertension and could be present for years before its onset. Abnormal lipids can damage the endothelium, leading to impaired production of nitric oxide, a potent vasodilator. This impairs a blood vessel’s ability to relax and contract, leading to a raised resting blood pressure (Halperin et al, 2006).
Dietary modification and other lifestyle interventions are crucial in the management of hypertension and prehypertension to improve endothelial function. It could be argued the benefits of dietary modification arise not only from weight loss but also from the antioxidant effects of fruit and vegetables, which may help to protect against endothelial dysfunction.
Dauchet et al (2007) found a diet high in fruit and vegetables was associated with a lower systolic and diastolic BP. The Dietary Approaches to Stop Hypertension (DASH) diet, which is low in fat and high in fruit and vegetables, has been found to significantly reduce BP in patients with stage 1 systolic hypertension (Moore et al, 2001) (Box 2). In Moore et al’s study, pre-hypertension was defined as a systolic BP of 140-159mmHg and diastolic BP of <90mmHg. Participants were randomised to one of three diets, which they agreed to eat for 11 weeks; although the numbers were low, the findings have been corroborated. For example, the PREMIER Trial, involving 399 participants, found the DASH diet was effective in reducing BP in people with metabolic syndrome (Lien et al, 2007).
The Diet, Exercise and Weight-Loss Intervention Trial (DEW-IT) also found lifestyle interventions could significantly reduce BP (Miller et al, 2002); although only 20 participants completed the intervention, the diet protocol was similar to the DASH diet, suggesting the findings could be applicable to the wider population. Participants were also prescribed 30-45 minutes of moderate-intensity supervised exercise such as a treadmill or track-walking three days a week. Those in the DEW-IT intervention group lost more weight than the controls (average 5.5kg compared with 0.6kg); however, those in Moore et al’s study did not lose weight.
While dietary modification is important in hypertension management, its benefits may be short lived if not undertaken in conjunction with regular exercise.
Hu et al (2004) found regular physical activity was associated with lower BP, regardless of body mass index. This may be explained by the beneficial effects of exercise on the sympathetic nervous system, inflammatory markers and lipid profile, leading to an improvement in endothelial function. Hambrecht et al (2003) found exercise resulted in a rise in endothelial nitric oxide synthase, which is associated with an improvement in endothelial function. Endothelial nitric oxide is a potent vasodilator, and reduced production is associated with endothelial dysfunction.
The DASH-Sodium Trial (Bray et al, 2004) found a positive link between salt intake and hypertension. Low salt intake may be one reason why the DASH diet (or any diet high in fruit and vegetables) is so effective in reducing BP.
Smoking is a major risk factor for CVD, and has been shown to increase levels of C-reactive protein. It is associated with an increase in ankle-to-arm systolic BP index (also known as ankle brachial pressure index, ABPI), which is an indicator of peripheral atherosclerosis (Cui et al, 2006).
Ankle brachial pressure index is calculated by dividing the systolic blood pressure in the ankle by the systolic blood pressure measured at the brachial artery.
While lifestyle interventions are used in the initial management of hypertension, many patients will need medication to prevent stroke and heart failure. NICE (2011) guidance on pharmacological management uses a step approach (Fig 1).
Angiotensin-converting enzyme inhibitors
The choice for the initial treatment of hypertension in people aged under 55 years should be an ACE inhibitor or a low-cost angiotensin II receptor blocker (ARB) if an ACE inhibitor is not tolerated.
ACE inhibitors inhibit the conversion of angiotensin I to angiotensin II by ACE (Greenstein and Gould, 2004a). This results in vasodilatation through an increase in levels of bradykinin, a peptide that causes blood vessels to dilate and BP to, therefore, fall. ACE inhibitors also affect the production of the hormone aldosterone, which regulates water and electrolyte balance, leading to an increase in sodium and water excretion and decrease in BP. In addition, they reduce stroke volume and cardiac output, leading to a lowering of BP.
In the Heart Outcomes Prevention Trial, administration of the ACE inhibitor ramipril reduced cardiovascular morbidity and mortality. A sub-study of the trial suggests this was achieved by reducing 24-hour ambulatory BP - and especially night-time BP - indicating that administration timing is important (Svensson et al, 2001). This has implications for nurses administering ramipril or advising patients on its timing, as Svensson et al’s findings suggest it is more effective if taken at bedtime. Ramipril has also been shown to reduce ventricular hypertrophy (enlargement) (Lièvre et al, 1995), which has been linked to an increased risk of death and the development of heart failure.
In patients aged over 55 or in those of African or Caribbean origin of any age, calcium channel blockers are the first drugs of choice. This is because lower levels of circulating rennin in patients of African or Caribbean origin are thought to make ACE inhibitors less effective in lowering blood pressure than in Caucasians.
Calcium channel blockers result in vasodilation and reduced peripheral vascular resistance by inhibiting the movement of calcium ions into the muscle cells of the arterial walls (Greenstein and Gould, 2004a). If a calcium channel blocker is not tolerated, a thiazide diuretic should be used; these are also recommended for resistant hypertension, used in combination with ACE inhibitors and calcium channel blockers. Thiazide diuretics reduce blood volume by preventing sodium absorption by the kidneys (Greenstein and Gould, 2004b); they also have a vasodilatory effect, thereby reducing peripheral vascular resistance and reducing BP.
Beta-blockers are no longer recommended as a first-line treatment for hypertension but may be considered in younger patients and women of childbearing age (NICE, 2011).
Pharmacological treatment of hypertension, which lowers BP by altering peripheral vascular resistance and cardiac output, is a key part of managing the condition but patients may need a combination of medications. Lifestyle modification is also just as important; a holistic approach is needed. Regular physical activity and a diet that is high in fruit and vegetables, and low in fat and sugar-sweetened food/drinks, improves endothelial function and lowers BP.
Both aspects of management involve working in partnership with the patient, using goal-setting and moving away from a paternalistic approach.
Bray GA et al (2004) A further subgroup analysis of the effects of the DASH diet and three dietary sodium levels on blood pressure: results of the DASH-Sodium Trial. American Journal of Cardiology; 94: 222-227.
British Heart Foundation (2012) Coronary Heart Disease Statistics. London: BHF.
Cui R et al (2006) Relationship of smoking and smoking cessation with ankle-to-arm blood pressure index in elderly Japanese men. European Journal of Cardiovascular Prevention and Rehabilitation; 13: 243-248.
Dauchet L et al (2007) Dietary patterns and blood pressure change over 5-y follow-up in the SU.VI.MAX cohort. American Journal Clinical Nutrition; 85: 1650-1656.
Dougherty L, Lister S (eds) (2011) Royal Marsden Manual of Clinical Nursing Procedures. London: Wiley.
Esler M et al (2006) Mechanism of sympathetic activation in obesity-related hypertension. Hypertension; 48: 787-796.
Greenstein B, Gould D (2004a) Drugs used for blood pressure In: Greenstein B, Gould D, Trounce’s Clinical Pharmacology for Nurses. London: Churchill Livingstone.
Greenstein B, Gould D (2004b) Drugs affecting the kidney and renal function. In: Greenstein B, Gould D (eds), Trounce’s Clinical Pharmacology for Nurses. London: Churchill Livingstone.
Halperin RO et al (2006) Dyslipidemia and the risk of incident hypertension in men. Hypertension; 47: 45-50.
Hambrecht R et al (2003) Regular physical activity improves endothelial function in patients with coronary artery disease by increasing phosphorylation of endothelial nitric oxide synthase. Circulation; 107: 3152-3158.
Hu G et al (2004) Relationship of physical activity and body mass index to the risk of hypertension: a prospective study in Finland. Hypertension; 43: 25-30.
Kaplan NM (2001) Systemic hypertension: mechanisms and diagnosis. In: Braunwald E et al (eds), Heart Disease: a Textbook of Cardiovascular Medicine. London: WB Saunders: 941 -971.
Lien LF et al (2007) Effects of PREMIER lifestyle modifications on participants with and without the metabolic syndrome. Hypertension; 50: 609-616.
Lièvre M et al (1995) Ramipril-induced regression of left ventricular hypertrophy in treated hypertensive individuals. HYCAR Study Group. Hypertension; 25, 1: 92-97.
Lopez-Garcia E et al (2004) Major dietary patterns are related to plasma concentrations of markers of inflammation and endothelial dysfunction American Journal of Clinical Nutrition; 80: 1029-1035.
McArdle WD et al (2007) The cardiovascular system. In: Exercise Physiology: Energy, Nutrition and Human Performance. Baltimore MA: Lippincott, Williams and Wilkins.
Mensah GA (2007) Healthy endothelium: the scientific basis for cardiovascular health promotion and chronic disease prevention. Vascular Pharmacology; 5: 310-314.
Miller ER 3rd et al ( 2002) Results of the diet, exercise, and weight loss intervention trial (DEW-IT). Hypertension; 40: 612-618.
Moore TJ et al (2001) DASH (Dietary Approaches to Stop Hypertension) diet is effective treatment for stage 1 isolated systolic hypertension. Hypertension; 38: 155-158.
National Institute for Health and Care Excellence (2014) Hypertension Overview. London: NICE.
National Institute for Health and Care Excellence (2011) Hypertension. London: NICE.
Svensson P et al (2001) Comparative effects of ramipril on ambulatory and office blood pressures: a HOPE substudy. Hypertension; 38: e28-32.
Wood D (2005) JBS 2: Joint British Societies’ guidelines on prevention of cardiovascular disease in clinical practice. Heart; 91: Supplement 5, v1-52.
Wilmore JH, Costil DL (2008) The cardiovascular system. In: Physiology of Sport and Exercise. Leeds: Human Kinetics.