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Hypertension: Pathophysiology and Treatment: Article
Hypertension: Pathophysiology and Treatment: Article
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Arterial hypertension is a major cause of risk of stroke and a reduction in the risk of
morbidity and mortality because of its associ- dementia.
Key points
ation with coronary heart disease, cerebro- The hypertension optimal treatment (HOT)
vascular disease and renal disease. The extent study indicates that the treatment goal is to Hypertension is a cause of
of target organ involvement (i.e. heart, brain reduce blood pressure to 140/85 mm Hg. It is morbidity and mortality.
and kidneys) determines outcome. North alsoestablishedthathighnormalbloodpressure In general practice, the level of
American studies have shown that hyperten- (130–139/85–89 mm Hg) progresses to Stage 1 blood pressure above which
sion is a major contributor to 500 000 strokes hypertension (>140/>90 mm Hg) in >37% of treatment of hypertension is
indicated is now set at
DOI 10.1093/bjaceaccp/mkh020 Continuing Education in Anaesthesia, Critical Care & Pain | Volume 4 Number 3 2004
ª The Board of Management and Trustees of the British Journal of Anaesthesia 2004 71
Hypertension: pathophysiology and treatment
converted into an active octapeptide, angiotensin II by the endothelin-1 may be accentuated by reduced generation of nitric
angiotensin-converting enzyme (ACE). Though the renin– oxide caused by hypertensive endothelial dysfunction.
angiotensin system is widespread in the body, the main source
of renin is the juxtaglomerular apparatus of the kidney. This Adrenal steroids
apparatus senses the renal perfusion pressure and the sodium
concentration in the distal tubular fluid. In addition, renin release Mineralo- and glucocorticoids increase blood pressure. This effect
is stimulated by b- and decreased by a-adrenoceptor stimulation. is mediated by sodium and water retention (mineralocorticoids) or
High angiotensin II concentrations suppress renin secretion via a increased vascular reactivity (glucocorticoids). In addition, gluco-
negative feedback loop. Angiotensin II acts on specific angiotensin corticoids and mineralocorticoids increase vascular tone by upregu-
AT1 and AT2 receptors causing smooth muscle contraction and lating the receptors of pressor hormones such as angiotensin II.
the release of aldosterone, prostacyclin, and catecholamines. The
renin–angiotensin–aldosterone system plays an important role in Renomedullary vasodepression
the control of arterial pressure including the sodium balance. Renomedullary interstitial cells, located mainly in the renal
papilla, secrete an inactive substance medullipin I. This lipid is
72 Continuing Education in Anaesthesia, Critical Care & Pain | Volume 4 Number 3 2004
Hypertension: pathophysiology and treatment
occur mainly after the end of systole, thus increasing pressure Table 1 Stages of hypertension (Joint National Committee VI Guideline)
during the early part of diastole and improving coronary perfu-
Stage Systolic Diastolic
sion. With ageing, stiffening of the aorta and elastic arteries
increases the pulse pressure. Reflected waves move from early Optimal <120 <80
Normal 120–129 80–84
diastole to late systole. This results in an increase in left ventricular High-normal 130–139 85–89
afterload, and contributes to left ventricular hypertrophy. The HT stage 1 140–159 90–99
widening of the pulse pressure with ageing is a strong predictor HT stage 2 160–179 100–109
HT stage 3 >180 >110
of coronary heart disease.
The autonomic nervous system plays an important role in the Systolic and diastolic pressures given in mm Hg.
HT, hypertension.
control of blood pressure. In hypertensive patients, both increased
release of, and enhanced peripheral sensitivity to, norepinephrine
can be found. In addition, there is increased responsiveness to Heart failure is a consequence of chronic pressure overload. It
stressful stimuli. Another feature of arterial hypertension is a may start as diastolic dysfunction and progresses to overt systolic
resetting of the baroreflexes and decreased baroreceptor sensitiv- failure with cardiac congestion. Strokes are major complications
Continuing Education in Anaesthesia, Critical Care & Pain | Volume 4 Number 3 2004 73
Hypertension: pathophysiology and treatment
addition of a diuretic or a calcium channel blocker is often bene- antihypertensive drugs. Losartan, valsartan and candesartan
ficial. However, b-blockade therapy is associated with symptoms are effective and cause less coughing than ACE inhibitors.
of depression, fatigue, and sexual dysfunction. These side-effects The LIFE study is the most recent landmark trial in hyperten-
have to be taken into consideration in the evaluation of the benefits sion. More than 9000 patients were randomized to receive either
of treatment. the angiotensin receptor antagonist losartan or a b-blocker
Over the past few years b-blockers have been used increasingly (atenolol). Patients in the losartan arm exhibited better reduction
frequently in the management of heart failure, a known complica- of mortality and morbidity, owing to greater reduction in strokes.
tion of arterial hypertension. They are effective but their introduc- Losartan was also more effective in reducing left ventricular
tion in the presence of heart failure has to be very cautious, starting hypertrophy, an independent powerful risk factor for adverse out-
with very low doses to avoid an initial worsening of heart failure. come. In patients with isolated systolic hypertension, the superi-
ority of losartan over atenolol was even more pronounced than in
Calcium channel blockers those with systolic and diastolic hypertension. These favourable
Calcium channel blockers can be divided into dihydropyridines results led to an editorial entitled: ‘Angiotensin blockade in hyper-
(e.g. nifedipine, nimodipine, amlodipine) and non-dihydropyridines tension: a promise fulfilled’. It must be noted that the comparator
74 Continuing Education in Anaesthesia, Critical Care & Pain | Volume 4 Number 3 2004
Hypertension: pathophysiology and treatment
occurring peptides more effective, thereby reducing vascular resist- Key references
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Continuing Education in Anaesthesia, Critical Care & Pain | Volume 4 Number 3 2004 75