13. HYPERTENSION IN CARDIOVASCULAR DISEASES

Question 1

1. Coarctation of aorta?

Answer 1

It is an inborn narrowing of the aortic isthmus, i.e. of the section
between the ostia of the subclavian artery and the attachment of the ductus arteriosus. In broader
sense of the coarctation of aorta its stenosis might be localized along the whole aorta, proximal and
distal from the isthmus itself. In aortic coarctation the adequate blood flow and pressure in the lower
half of the body is obtained via three mechanisms:
* by increasing the systolic blood pressure in the proximal segment of the aorta
* by arteriolar vasoconstriction that maintains a high diastolic blood pressure
* by a collateral circulation and possibly by the opening of ductus arteriosus. The blood
pressure measured in the upper limbs shows an increased systolic, diastolic, and mean arterial blood
pressure, while the systolic blood pressure is measured in the lower limbs it is in all cases low, and
the diastolic pressure is increased. The mean arterial blood pressure in the lower limbs is always low,
however it is kept at the value around 50 mm Hg (6,6 kPa), what is the minimal pressure needed for
adequate function of the kidneys.

Question 2

2. Aortic valve insufficiency?

Answer 2

It will cause a raise in the systolic blood pressure, by the fact that a
part of the systolic cardiac output flows back into the left ventricle at the beginning of the systole
and hence increases its diastolic filling. The left ventricular systolic volume gets larger as the
regurgitation volume increases. The diastolic blood pressure becomes lower due to the faster blood
flow from the aorta. The total peripheral resistance is lower as a result of the adaptation to the
increased cardiac output.

Question 3

3. Large arteriovenous fistula (congenital or acquired)?

Answer 3

They cause the increase of the systolic
blood pressure what is the result of the increased cardiac output. The blood flow passes by the
arterioles and the capillaries and that is why the diastolic blood pressure decreases. As an example of
this is the systolic hypertension in cases of multiple arterio-venous aneurysms in the skeleton as it is
in Pagets disease.

Question 4

4. Increase of the minute cardiac output and tachycardia at hyperkinetic syndrome?

Answer 4

It occurs at
dysfunction of the vegetative nervous system which is due to an increased sensitivity of the cardiac
or blood vessels beta adrenoreceptors. The positive effect of beta blockers strengthens this
hypothesis. We consider a hyperkinetic circulation also states with an increased cardiac output at
rest and they are accompanied by a normal blood pressure (e.g. anemia). In cases of juvenile
hypertension and also in early stages of the essential hypertension the peripheral vascular resistance
is not able to adapt itself to this high blood flow and so the blood pressure increases. So the
hypertension here does not start as a generalized vasoconstriction, rather as an inadequate ability of
the peripheral vascular bed produce effective dilatation. This is considered to be so called relatively
increased peripheral vascular resistance.

Question 5

5. Decrease of elasticity of the large arteries with a restriction of aortic elasticity?

Answer 5

The systolic blood pressure is usually slightly
increased. The rigid arteries do not expand during systole. The diastolic blood pressure is normal or
lower than normal, because the impedance strength which pushes the blood to the periphery during
diastole cannot be applied. This type of hypertension is called elasticity hypertension.

Question 6

OTHER CAUSES?

Answer 6

1.Obstructive sleep apnea is another fairly common cause of hypertension. The cause of obstructive
sleep apnea is a critical narrowing of the upper airway that occurs when the resistance of the upper
airway musculature fails against the negative pressure generated by inspiration. In most patients,
this is a result of a reduced airway size that is congenital or perhaps complicated by obesity. These
patients frequently become hypoxic and hypercarbic multiple times during sleep, which, among
other things, eventually can lead to systemic vasoconstriction, systolic hypertension, and pulmonary
hypertension.
2.From the toxic effects hypertension can be caused by acute porphyria, lead, thallium, carbon
monoxide, mercury poisoning, and experimentally cadmium poisoning. The pathogenic mechanism is
probably a centrally conditioned stimulation of adrenergic activity.
3.Post radiation hypertension. Occur in those patients treated by radiotherapy. Those are patients with
abdominal tumors probably due to the occurrence of so known radiation nephritis. This hypertension
might inquire a malignant character.

Question 7

EXOGENOUS CAUSES?

Answer 7

Several medications can elevate blood pressure. For example, oral contraceptives may cause
secondary hypertension in some women. The mechanism is likely related to increased activity of the
renin–angiotensin system. Estrogens increase the hepatic synthesis of angiotensinogen, leading to
greater production of angiotensin II. Angiotensin II raises blood pressure by several mechanisms,
most notably by direct vasoconstriction and by stimulating the adrenal release of aldosterone. The
latter hormone causes renal sodium retention and therefore increased intravascular volume. Other
medications that can raise blood pressure include glucocorticoids, cyclosporine (an antirejection drug
used in patients with organ transplants), erythropoietin (a hormone that increases bone marrow red
blood cell formation and elevates blood pressure by increasing blood viscosity and reversing local
hypoxic vasodilatation), and sympathomimetic drugs (which are common in over-the-counter cold
remedies). Nonsteroidal anti-inflammatory drugs can contribute to hypertension through doserelated augmentation of sodium and water retention by the kidneys. Two other substances that may
contribute to hypertension are ethanol (i.e., chronic excessive consumption) and cocaine. Both of
these are associated with increased sympathetic nervous system activity.