| Arrow
4 |
|
basic
concepts |
|
|
|
| basic
concepts |
|
Cardiac
output is the product of heart rate and stroke volume. Stroke volume in
turn depends on pre-load, myocardial contractility, and after-load or impedance
to flow. Patients with secondary hypertension whose initial derangement
is an increased cardiac output generally do not have hypertension secondary
to increased heart rate. They tend to have increased stroke volume from
an increased pre-load. The increased pre-load is a consequence of renal
sodium retention, either caused by renal parenchymal disease or secondary
renal sodium retention signaled by hormonal disturbances (Note
1). The hormones causing renal sodium retention are termed mineralo-corticoids,
aldosterone being the prototype. |
| |
|
|
| Note
1 |
|
One
type of blood pressure elevation of uncertain origin: hypertension in women
on oral contraceptives, may be a consequence of increased cardiac output.
Although estrogens increase the hepatic synthesis of the renin substrate
angiotensinogen, and subsequently, levels of angiotensin II become elevated,
the likeliest cause of hypertension is renal sodium retention caused by
angiotensin II -mediated decreased renal perfusion. |
| |
|
top |
| |
|
|
| |
|
|
| |
|
|
| |
|
|
| |
|
|
| |
|
|
| |
|
|
| |
|
|
| |
|
|
| |
|
|
| |
|
|
|
|
|
|
