Clinic BP measurement
Category
Systolic
Diastolic
Optimal
<120
<80
Normal
120–129
80–84
High-normal
130–139
85–89
Stage 1 hypertension
140–159
90–99
Stage 2 hypertension
160–179
100–109
Severe hypertension
≥180
≥110
Accelerated hypertension
≥210
≥130
Malignant hypertension
As above with papilloedema
Measuring BP
Conventional BP Measurements
Blood pressure can be measured indirectly with a manual (mercury or anaeroid) or automated sphygmomanometer. Errors in measurement can arise from technique and also use of un-validated or poorly maintained equipment. It is important to ensure the correct cuff size is used, and that the inflatable bladder covers at least 80 % of the arm circumference. If the cuff is too small it may underestimate BP.
It is recommended that BP measurement should be performed in a standardised environment to allow for inherent variation in BP. Systolic BP can be altered by up to 20 mmHg by factors such as time of day, posture, emotion, exercise, meals, drugs and temperature. Ensure that the patient is relaxed, seated and rested in a temperate setting and has the arm outstretched and supported in midline of sternum. The correct sized cuff should be applied (arm circumference should be noted on the outside of the cuff) and BP measured with a manual or automated device. It is recommended that patients with atrial fibrillation (AF) have their BP measured manually as current automatic devices are inaccurate when the pulse is irregular.
NICE has issued guidance on optimally obtaining a manual blood pressure reading. The environment should be standardised as above with the correct cuff size applied. Then:
Palpate the brachial pulse in antecubital fossa
Rapidly inflate the cuff to 20 mmHg above where the brachial pulse disappears
Deflate the cuff and note where the pulse reappears. This is an approximation of the systolic pressure
Re-inflate the cuff until 20 mmHg above where the brachial pulse disappears
Place the stethoscope over the brachial artery ensuring complete skin contact
Deflate the cuff at 2–3 mmHg per second listening for Korotokoff sounds. Phase 1 indicates systolic BP and phase 5 diastolic. In some patients (pregnant, children, anaemic and elderly patients) phase 5 is present until 0 mmHg, so phase 4 sounds should be used.
Korotokoff Sounds
Phase 1: First appearance of faint tapping sounds increasing in intensity lasting for at least 2 consecutive beats.
Phase 2: Auscultatory Gap – sounds soften, swish or disappear for a brief period
Phase 3: Return of sharper sounds
Phase 4: Abrupt muffling of sounds that become soft and blowing in quality
Phase 5: All sounds disappear completely
Ambulatory BP Monitoring (ABPM) and Home BP Monitoring (HBPM)
It is now recommended that patients with possible hypertension based on clinic measurements, borderline readings, or white coat hypertension should be offered ambulatory BP monitoring (ABPM) or home BP monitoring (HBMP). ABPM measures the BP twice per hour during the usual waking hours of the patient. A minimum of 14 readings are needed to make a diagnosis of hypertension. HBPM requires the patient to make 2 BP readings per day while seated, with 2 consecutive readings taken 1 min apart. The HBPM should continue for a minimum of 4 days, ideally 7 before a diagnosis of hypertension is made. Averages of these readings can be used to determine need for medical therapy according to ABPM/HBPM thresholds (see Table 5.1).
Target Organ Damage and Cardiovascular Risk
Assessing target organ damage will aid further cardiovascular risk calculation. For instance, LVH and microalbuminuria are independent risk factors of adverse outcome in patients with hypertension and their presence may prompt more aggressive treatment. Conversely, the presence of acute complications may help define the presence of acute, urgent or malignant hypertension, for which immediate treatment is warranted (Table 5.2).
Table 5.2
Acute and chronic target organ damage
Organ | Chronic complications | Acute complications |
|---|---|---|
Cardiac | LVH on ECG/echo, CAD from history or ECG, CCF | MI, pulmonary oedema |
Cerebrovascular | TIA, stroke | Intracerebral bleeding, TIA, stroke, posterior reversible encephalopathy syndrome (PRES) (seizure, confusion, coma) |
Renal | Microalbuminuria, proteinuria, CKD | Haematuria |
Retinal | Hypertensive retinopathy grade 1–4 | Papilloedema, haemorrhages |
Large vessels | Accelerated atherosclerosis, peripheral vascular disease, aneurysms dilatation | Aortic dissection |
Aetiology
Over 90 % of patients with hypertension have essential or primary hypertension. The remainder have an underlying cause such as renal disease, endocrine disease, obstructive sleep apnoea, co-arctation of the aorta or genetic diseases of the adrenal-renal axis causing salt retention. In such cases, hypertension may improve when the underlying disease process is corrected.
Essential Hypertension
Studies estimate that up to 90–95 % of hypertension cases are idiopathic. Physiologically, blood pressure is proportional to cardiac output and peripheral resistance. As such, it is hypothesised that the cause of essential hypertension is a complex interaction of genetic polymorphisms controlling blood volume and vascular resistance with environment and patient’s lifestyle (such as raised BMI, smoking status, salt intake and levels of physical activity) combining to cause hypertension.
Secondary Hypertension
Secondary causes of hypertension are rare, but patients may present at a younger age with a more accelerated disease process with or without signs and symptoms of an underlying disease.
Renal disease is the most common cause of secondary hypertension. This includes renal parenchymal disease, glomerulonephritis, chronic pyelonephritis or polycystic kidneys and renovascular disease (renal artery stenosis or fibromuscular dysplasia).
Endocrine disease affecting the adrenal glands is a relatively common cause of secondary hypertension. Aldosterone is a mineralocorticoid and excess will cause active reabsorption of sodium (with passive reabsorption of water) causing blood volume expansion. Causes of mineralocorticoid excess include Conn’s syndrome (adrenal ademona), bilateral/congenital adrenal hyperplasia, renin-secreting tumours and glucocorticoid-remediable aldosteronism and may also contribute to hypertension in patients with renal artery stenosis. Corticosteroid excess as seen in Cushing’s syndrome and with patients prescribed steroid therapy causes hypertension in a variety of ways, including activation of the renin-angiotensin system, upregulation of vasoactive substances and intrinsic mineralocorticoid activity. Phaeochromocytomas can cause hypertension by episodic excretion of catecholamines, adrenaline and noradrenaline, increasing cardiac output and peripheral resistance. Other endocrine causes include acromegaly, hypo and hyperthyroidism.
Alterations in Aldosterone Metabolism
Glucocorticoid-remediable aldosteronism: This is an autosomal dominant gain of function mutation resulting from unequal cross-over and fusion of the regulatory gene for 11-hydroxylase (which is normally under physiological control by ACTH) to the coding region of aldosterone synthase. As a consequence, aldosterone synthase is sensitive to ACTH and suppressed by treatment with exogenous glucocorticoids.
Congenital adrenal hyperplasia: Thisa is an autosomal recessive disorder of 11β-hydroxylase or 17α-hydroxylase deficiency causing an excess of mineralocorticoids (and deficiency of glucocorticoids)
Apparent mineralocorticoid excess (AME): autosomal recessive disorder causing inactivation of 11β-hydroxysteroid dehydrogenase type 2. This enzyme usually deactivates cortisol present in the renal tissue to minimise the effect of cortisol on mineralocorticoid receptors. Thus, with the mutation, impaired inactivation of cortisol leads to cortisol receptor intoxication and AME.< div class='tao-gold-member'>Only gold members can continue reading. Log In or Register to continue
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