Page 218 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Hypertension
Hypertension (H.), used as a term by itself, nism). Similarly, an increase in sympathetic ac-
refers to an abnormally high arterial pressure tivity of central nervous system origin and/or
in the systemic circulation (for pulmonary raised responsiveness to catecholamines (e.g.,
hypertension, → p. 214). In the industrialized caused by cortisol or thyroid hormone) can
countries it affects about 20% of the popula- cause an increase in cardiac output (→ A, left).
tion. As H. almost always begins insidiously, Resistance hypertension is caused mainly
yet can be treated effectively, the upper limit by abnormally high peripheral vasoconstriction
of normal blood pressure needs to be deter- (arterioles) or some other narrowing of pe-
mined. The World Health Organisation (WHO) ripheral vessels (→ A, right), but may also be
has proposed the following values for all age due to an increased blood viscosity (increased
groups (mmHg/7.5 = kPa): Threshold Hyper- hematocrit). Vasoconstriction mainly results
from increased sympathetic activity (of nervous
Heart and Circulation diastolic pressure < 140 tension sion siveness to catecholamines (see above), or an
normal
or adrenal medullary origin), raised respon-
ten-
hyper-
increased concentration of angiotensin II. Auto-
regulatory mechanisms also include vasocon-
> 95
< 90
90–95
(P D [mmHg])
striction. If, for example, blood pressure is in-
creased by a rise in cardiac output (see above),
140–160
> 160
systolic pressure
tract) “protect” themselves against this high
Cases of alternating normal and elevated levels
pressure (→ A, middle). This is responsible for
7 (P S [mmHg]) various organs (e.g., kidneys, gastrointestinal
(labile H.) are included in the column ‘Thresh- the frequently present vasoconstrictor compo-
old hypertension’. Patients with a labile H. of- nent in hyperdynamic H. that may then be
transformed into resistance H. (→ A). Addi-
ten develop fixed H. later (→ p. 207 D). As P S
regularly rises with age (→ p. 207 C), the upper tionally, there will be hypertrophy of the vaso-
limit of P S in adults has been widely set at constrictor musculature. Finally, H. will cause
150 mmHg for those aged 40–60 years and at vascular damage that will increase TPR (fixa-
160 mmHg for those aged over 60 years (P D at tion of the H.).
90 mmHg for both adult groups). Lower values Some of the causes of hypertension are
have been set for children. Assessment of blood known (e.g., renal or hormonal abnormalities;
pressure should be based on the mean values → B2,3), but these forms make up only about
of at least 3 readings on two days (see also 5–10% of all cases. In all others the diagnosis
p. 206). by exclusion is primary or essential hyperten-
The product of cardiac output (= stroke vol- sion (→ B1). Apart from a genetic component,
ume [SV] · heart rate) and total peripheral re- more women than men and more urbanites
sistance (TPR) determines blood pressure than country dwellers are affected by primary
(Ohm’s law). H. thus develops after an increase H. In addition, chronic psychological stress, be
in cardiac output or TPR, or both (→ A). In the it job-related (pilot, bus driver) or personal-
former case one speaks of hyperdynamic H. or ity-based (e.g., “frustrated fighter” type), can
cardiac output H., with the increase in P S being induce hypertension. Especially in “salt-sensi-
tive” people (ca. ⁄3 of patients with primary H.;
1
much greater than that in P D . In resistance H., P S
and P D are either both increased by the same increased incidence when there is a family his-
amount or (more frequently) P D more than P S . tory) the high NaCl intake (ca. 10–15 g/
The latter is the case when the increased TPR d = 170–250 mmol/d) in the western indus-
delays ejection of the stroke volume. trialized countries might play an important
The increase of cardiac output in hyperdy- role. While the organism is well protected
+
namic hypertension is due to an increase in ei- against Na loss (or diminished extracellular
ther heart rate or extracellular volume, leading volume) through an increase in aldosterone,
208 to an increased venous return and thus an in- those with an increased salt sensitivity are ap-
creased stroke volume (Frank–Starling mecha- parently relatively unprotected against a high
"
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
All rights reserved. Usage subject to terms and conditions of license.