Download 10- Hypertension, heart failure and regulation of blood flow

10- Hypertension, heart failure and
regulation of blood flow.
Hypertension:
It is a sustained elevation of the systemic arterial pressure. The
increased pressure leads to damage the heart and other organs because of
the added stress to the blood vessels. The British Hypertension Society
has defined range of blood pressure which falls within the normal range
and those that indicate hypertension (table 4).
Table (4): The BP in normal person and hypertension.
Type
SBP (mmHg)
DBP (mmHg).
Optimal
< 120
< 80
Normal
< 130
< 85
High normal
130 – 139
85 – 90
Mild hypertension
140 – 159
90 – 99
Moderate
160 – 179
100 – 109
hypertension
Sever hypertension
≥ 180
≥ 110
SBP = Systolic blood pressure.
DBP = Diastolic blood pressure.
There are two types of hypertension:
1- Essential hypertension: The cause of this type is unknown. More
than 90 % of all cases of hypertension are essential hypertension. It has a
strong hereditary tendency.
2- Secondary hypertension: The cause of this type is known.
1- Renal disease (e.g. polycystic kidney disease, glomerulonephritis, and
renal artery stenosis).
2-Endocrine dysfunction (e.g. Cushing's syndrome, acromegaly).
3-Drugs (e.g. oral contraceptives, anabolic steroids, corticosteroids and
sympathomimetic agents).
4- Coarctation of the aorta.
Pulmonary hypertension occurs when pulmonary vascular resistance
increases. Pulmonary hypertension is commonly associated with
pulmonary disease.
During pregnancy, many patients develop hypertension (toxemia of
pregnancy), in which, there is thickening of the kidney glomerular
membranes (autoimmune process), reduce rate of fluid filtration from
glomeruli into renal tubules.
Effect of hypertension:
1- Left ventricular failure.
2- Renal failure.
3- Rupture a major blood vessel.
4- Retinal damage.
Even moderate elevation of the arterial pressure for long time leads
to shortened life expectancy. In severe high pressure, a person can
expect to live no more than a few more years unless appropriately
treated.
Treatment of essential hypertension:
1- General measurement:
a- Correction of obesity & alcohol intake.
b- Restricting salt intake.
c- Regular physical exercise.
d- Increase consumption of fruit and vegetable.
e- Stop smoking and saturated fat may reduction of cardiovascular
diseases risk.
2- Drugs:
A- Drugs that increase renal blood flow (vasodilator drugs).
B- Drugs that decrease tubular reabsorption of salt and water (diuretics).
Response to an increase in arterial pressure:
The baroreceptors in the carotid sinus and the aortic arch are
stimulated; informations are transmitted through glossopharyngeal
nerve (CN IX) and vagus nerve (CN X) to nucleus tractus solitarus of
medulla (VMC). Cardiovascular center is stimulated to reduce arterial
pressure back to normal; these responses include an increase in
parasympathetic outflow to the heart to reduce heart rate and decrease
the sympathetic outflow to the heart and blood vessels.
Heart failure (HF):
Pathogenesis: The heart failure (HF) is due to:
1-Chronic hypertension.
2-Myocardial infarction.
3-Arteriovenous fistula.
4- Thyrotoxicosis and thiamin deficiency.
The heart fails to putout adequate amount of blood and fails to handle
all the blood return to it. The ejection fraction becomes low as 20%
instead normal value of 65 %. Diastolic dysfunction reduces ventricular
filling in diastole, causing venous congestion. At first cardiac output is
an inadequate only during exercise but later it is an inadequate at rest.
The inadequate filling of the arterial system triggers baroreceptormediated to increase sympathetic activity with renal vasoconstriction
and increased secretion of rennin and aldosterone. Aldosterone causes
marked Na and water retention, which add to venous congested and
edema.
Manifestation:
The manifestations of HF range from sudden death due to ventricular
fibrillation or air embolism to chronic congestive HF.
The terms forward and backward failure are used to refer
manifestations produced by systolic and diastolic dysfunction
respectively. The manifestations of heart failure are illustrated in table
5:
Table (5): Summary of the signs, symptoms and pathogenesis of heart
failure.
Abnormality
Causes
Weakness
Ankle and sacral edema.
Forward failure, COP inadequate to perfuse muscles.
Backward failure of right ventricle, increased venous pressure,
increased fluid transudation.
Increased venous pressure, increased resistance to portal flow.
Backward failure of left ventricle, increased pulmonary venous
pressure, pulmonary venous distention and transudation of
fluid into air spaces.
Failure of left ventricle output to rise during exercise,
increased pulmonary venous pressure.
Probably sudden failure of left heart output to keep up with
right heart output, acute rise in pulmonary venous and
capillary pressure transudation of fluid into air space.
Normal pooling of blood in lung in supine position added to
already congested pulmonary vascular system, increased
venous return, not putout by left ventricle (relieved by sitting
up, raising head of bed, lying on extra pillows.
Greater ventricular end-diastolic volume.
Hepatomegaly
Pulmonary congestion
Dyspnea on exertion
Paroxysmal dyspnea,
pulmonary edema
Orthopnea
Cardiac dilatation
Treatment:
1-To improving cardiac contractility.
2- Inhibition of the production of angiotensin II with angiotensinconverting enzyme inhibitors.
3- To reduce the circulating aldosterone level.
4- Reducing venous tone with nitrates, to reduce the amount of blood
return to the heart (lowering the preload).
5- Diuretics are used to reduce the fluid overload.
Regulation of blood flow
1- Local mechanism (intrinsic control):
Autoregulation is the capacity of tissue to regulate their own blood
flow. Blood flow to an organ remains constant over a wide range of
perfusion pressures. The capacity is well developed in the kidneys, but it
has been observed in the mesentery, skeletal muscles, brain, liver and
myocardium.
A- It is probability due to in part to intrinsic contractile pressure of
smooth muscle to stretch (myogenic theory) of autoregulation. As
pressure rises, the blood vessels are distended and vascular smooth
muscle fibers that surround the vessels contract.
B- Vasodilator substances tend to accumulate in active tissue and these
metabolites also contribute to autoregulation (metabolic theory).
When blood flows decrease the blood vessels dilate due to
accumulation of vasodilator substances. When blood flow increase,
the vasodilator substances are tend to be washed away, They include
decrease in O2 tension and pH which lead to relax of arterioles and
precapillary sphincters. Increase in CO2 which have direct dilatation
in skin and brain. Rise in temperature exerts vasodilation effect due
to the increase metabolism. K+ ions have dilator activity secondary to
hyperpolarization of vascular smooth muscle cells. Adenosine may
play a vasodilator role in cardiac vessels but not in skeletal muscle
vessels due to inhibit the release of norepiphedrin. Lactate may also
contributes to dilatation. In the injured tissue histamine release from
damaged cells which increase capillary permeability.
Active hyperemia:
Blood flow to an organ is proportional to its metabolic activity.
Reactive hyperemia:
It means increase in BF to an organ after a period of occlusion of
blood flow. The longer period of occlusion, greater increase in blood
flows.
A drop in tissue temperature causes vasoconstriction and this local
response to cold plays a part in temperature regulation. Injured arteries
and arterioles constrict strongly. The constriction appears to be due in
part the local liberation of serotonin from platelets that stick to the vessel
wall in the injured area.
II- Systemic mechanism (extrinsic control):
1-Nervous system: It regulates blood flow via vasomotor center
(VMC) figurer 46 through:
A- Sympathetic discharge to small arteries and arterioles
(vasoconstriction) for
changing the rate of blood flow.
B- Sympathetic discharge to adrenal gland to secrete both epinephrine
and Norepinephrine into circulation. These two hormones act directly on the
blood vessels
to cause vasoconstriction and decrease blood flow.
C- Parasympathetic discharge and inhibition the tonic discharge of
sympathetic
nerves produce vasodilation to increase blood flow.
Figure (46):Vasomotor center (VMC)
2- Humoral system:
Many circulating hormones affect the vascular system:
A- Vasoconstrictor agents such as Epinephrine, nor-epinephrine,
angiotensin II and vasopressin (ADH).
B- Vasodilator agents such as histamine, kinin, vasoactive intestinal
peptide (VIP), and atrial natriuretric peptide (ANP).
Endothelial cells:
They play a major role in the control of blood flow in many organs.
They release vasodilator substances such as bradykinin, Endotheliumderived relaxing factor that is now known nitric oxide (NO). It Also
they release vasoconstriction substances such as endothelin, and
prostaglandin. Endothelin-1 is the most potent vasoconstrictor agent.