Blood Vessels

BLOOD VESSEL IDENTIFICATION IS DONE IN LAB.

COMPARISON OF ARTERIES AND VEINS  (See p. 715, 7th ed.; p. 695, 8th ed.)
 

Internal, media and external tunics of artery - daigram.
Notice the blue layer of elastic tissue under the endothelium and the
purple layer under the smooth muscle (red) of the tunica media.
 

Characteristic      Arteries              Veins
 
Function carry blood away from the heart carry blood to the heart from the body
Lumen/wall size small lumen (hollow portion)/thick wall  larger lumen/thinner wall
Muscle more muscular (smooth muscle cells: non-striated by actins and myosins, contract slowly) less muscular (but have valves)
Elastic fibers more elastic fibers in interna, media layer less elastic fibers
 
Collagenous fibers (stiff) less in media and adventitia (outer layer) more in media and externa/adventitia
 
All vessels are lined with squamous epithelium (tile-like cells called endothelium). Veins
in arms and legs have valves. Striated/skeletal muscle (with stripes of actin and myosin
myofilaments) push against the vein walls and push blood upward. See the muscle pump
below.

Here are some generalities:
 

    Arteries - See p. 715, 7th ed.; p. 696, 8th ed.  

    1.  Arteries have to be flexible, they pulsate with the spurts of blood flow.
    The largest arteries like the aorta and carotids and elastic.  Their recoil helps
    to move blood forward towards tissues. The aorta is an elastic artery.

    2.  Medium arteries or muscular arteries control by vasoconstriction and
    vasodilation.

    3.  large and medium arteries carry blood at higher velocities and higher pressure than veins.

    4.  Arteries have 22% of all blood in the body in them at any time. See p. 701, 8th ed.

    Veins

    1.  Veins carry blood at low pressures and velocities.  Because of the
    decreased surface area and increased volume of the veins they contain 60%
    of all the blood at any time.  Venous blood flows at higher pressure and velocity
    than you would expect. See p. 722, 7th ed.; p. 700, 8th ed..

    2.  In order to move this slow-moving blood back to the heart, venous valves
    assist by preventing blood from staying in the legs, arms, and abdomen.
    The skeletal muscle pump sends blood through these valves.  See p. 726, 7th ed.; p. 705, 8th ed. The respiratory pump (breathing movements in the abdomen and thorax)
    sends blood back to the heart.  Explain this. Refer to the extra credit IP muscle cd assignment.

Three layers of vein
In this illustration, the blue layer is collagenous. Therefore,
note the absence of the elastic laminae. The smooth
muscle of the media is reduced (not adequately illustrated).


Valves in veins - diagram
Veins have valves.

 

CONTROL OF PERIPHERAL CIRCULATION

Arterioles are lined with smooth muscle cells, they control the blood volume circulated
to local areas in body tissues served by the capillaries.  By contracting (vasoconstriction),
they  lower blood volume delivered to that specific area; or by  relaxing (vasodilation),
they open and increase blood delivery to the capillary bed.  See p. 717, 7th ed.; p. 707, 8th ed.

Capillaries are only wide enough for one RBC to pass through at a time (two can't go
side-by-side), and capillary walls are not lined with smooth muscle cells.  Flowing out
of the capillary net/bed to tissue cells are nutrients, Oxygen, fluids and antibodies.
Capillaries may be continuous with the endothelial cells joined closely as in the brain.
They may be fenestrated and have little window-like openings.  These are found in
the kidney and choroid plexi of the brain ventricles. Sinusoidal capillaries are very porous because the endothelial basement membrane has openings. See p. 720, 7th ed.; p. 699, 8th ed.
.

Feeder arteriole, capillary bed and venule
Identify the precapillary sphinters and the thoroughfare channels. Which side
of the bed has higher hydrostatic pressure? See p. 721, 7th ed.; p. 700, 8th ed.

Generalized vasodilation (dilatation) lowers blood pressure in capillary beds and leads to shock.

CONTROL OF PERIPHERAL CIRCULATION

The Sympathetic Nervous System is sympathetic to Flight-Fight activities.
Control of circulation is illustrated by the activities of the Sympathetic nervous nystem
that has nerves and secretions that cause increased blood flow (vasodilation) to the
brain, heart, lungs and muscles, while at the same time decreasing blood flow by
vasoconstriction to the intestinal tract and skin. See p. 725-731, 7th ed.; 706, 8th ed.

Generalized vasoconstriction increases blood pressure.  The sympathetic vasomotor center
and cardiac accellerator center are both located in the medulla oblongata area called the
cardiovascular center. Arterioles are always in a moderate state of contraction - vasomotor tone.

The Parasympathetic Nervous System reacts the opposite way by slowing heart and
breathing rate, and increasing intestinal tract motility and vasodilation and skin vasodilation
by inhibiting sympathetic vasoconstriction.  The Vagus nerve X nucleus is also located in the
cardiovascular center.

If you ran across a mama Grizzly Bear with cubs in the woods, what would happen to
your speed of digestion and the amount of blood flowing to your digestive tract?

HEMODYNAMICS

Generalized vasoconstriction occurs to increase blood pressure.  Blood is moved from
the venous reservoirs to the heart, lungs, and tissues.  If blood loss occurs (below 15%
total volume), this mechanism will help restore blood pressure.  If blood loss above
25% occurs, tissue capillary beds, being starved for oxygen and nutrients and having
an excess of CO2, will auto-dilate and shock will deepen due to falling blood pressures.

Organ tissue capillary beds auto-constrict if oxygen, nutrients and pH are high and the
CO2 levels are low.  However, the reverse is true of capillary beds in lungs. Organ
tissue capillaries auto-dilate if CO2 is high and pH is low and vice versa for capillaries
of the pulmonary circulation.

VELOCITY OF FLOW

Generally speaking, velocity increases the nearer arterial blood is to the left ventricle.
Flow is 40cm/sec in the aorta and 0.1 cm/sec in capillaries.  Also blood velocity
increases when the blood enters the veins from capillary beds because veins have less surface area for friction with a large volume of blood.  See graph on p.735, 7th ed.; p. 705, 8th ed.

Standard blood pressure and pulse readings are taken at the brachial artery.
See below. Review

BP is greatest closer again to the left ventricle.  Notice that
the pulse disappears as blood enters the capillaries.  Polycythemia (too many
RBCs) can increase BP.  The smaller the vessel, the more surface area is
exposed to the small volume of blood.  Friction increases.

EXCHANGES OF MATERIALS BETWEEN THE BLOOD AND TISSUES
- See p.737, 7th ed.; p. 713, 8th ed.

If one examines the pressures which pull fluids into and out of capillaries, the blood
colloid pressures are the same on the arterial and venous sides of the capillary bed.
Similarly, interstitial fluid osmotic pressures are the same on both sides.  However,
blood hydrostatic pressure is higher on the arterial side.  This means that fluids are
forced out of the capillaries here on the arterial side of the bed.  A net flow of 10 mm
Hg pressure exists carrying fluids outward.  These interstitial fluids will bathe the tissue
cells with nutrients.  On the venous side of the capillary bed, a net force of -9 mm Hg
pressure carries 85%-95% of the fluids around the tissue cells, and back into the capillary
bed.  Wastes flow back to the blood this way.  What happens to the other 10-15%?
This fluid flows into lymph vessels, and thus back to the venous circulation after the
lymph has been cleaned by the immune system.
 

EDEMA

Abnormal increases (30%+ above normal) in interstitial fluid pressure occur in
swelling or edema. Any force that increases the movement of fluids from the blood to
the interstitial fluids or one that restricts fluid movement back into blood vessels from
the interstitial fuids, causes edema.

Causes of Edema

1.  Increased venous pressure - see left and right ventricular failure.

2.  Decreased plasma proteins - caused by burns, protein malnutrition, liver
or kidney disease, water flows from the blood to tissues.

3.  Allergic responses and infections elicit histamine release that causes vessels
to become leaky.  Fluid moves into tissues.

4.  Water retention may be due to salt retention or kidney failure.

5.  Blockage of lymphatic drainage by elephantiasis roundworm parasites
or removal of lymph vessels in radical mastectomies.

Varicose veins have weak, bulging walls because of defective valves.

Phlebitis is an inflammation of the leg veins; clots form easily there.
 

Review

Arteriosclerosis - hardening of the arteries, due to the build up of minerals,
 fatty plaque and collagen, is a natural outcome of long term high blood pressure.
What is the relationship between high salt levels in the blood and high blood
pressure? See more details below.

Why are arteries more flexible than veins?

Atherosclerosis (review)
Macrophages eat low density lipoproteins and
migrate into lesions (perhaps caused by the hydrogen cyanide or carbon monoxide of
cigarette smoke), in the internal layer of arteries. The  smooth muscle cells fill with fats and
cholesterol and die. Platelet clots or thrombi tend to form on the irregular surfaces. Heart
attacks occur when the Coronary Arteries serving heart muscle are blocked by fatty
plaque and/or platelet clots, and the muscle tissues become starved for oxygen and
nutrients (ischemia).

The first symptom of coronary vessel blockage may be chest pain called angina pectoris.
As the cardiac muscle cells die, the heart attack occurs. As cells rupture, free radicals
are released that perfuse through the myocardium and nodal conduction systems causing
further damage.

If the attack causes a loss of the regular heart contraction rhythm (by damaging conduction fibers),
ventricular twitching or fibrillation will occur and the patient dies. The dead tissue or infarct will
become a scar in time.

Coronary artery spasms can also block arteries. Why are spasms more likely if
atherosclerotic plaque is present? Ventricular fibrillation will kill the patient if CPR is
unsuccessful.

When blood sugar levels rise to high levels, 180mg/dl+, a carbohydrate layer forms on
the basement membrane that the capillary endothelial cells rest upon. Over time this
thickened layer prevents the movement of nutrients into the tissues. Therefore, progressive
amputations of the toes, feet and legs of long term sugar diabetics are common. The spinal
cord may also be damaged and reflexes inhibited. Arteriosclerosis, strokes and retinal
blindness also occur. Explain why. Think of osmosis!

Blood Pressure and Heart Sounds - review

The systolic pressure is the pressure read at the first sound heard in a stethoscope
when the blood pressure cuff, which has closed off arterial flow, is released and the
first spurt of blood comes through the artery below the cuff. The diastolic pressure
is read when the last sound is heard. The numbers, e.g., 120 systolic/80 diastolic,
means the systolic pressure over the diastolic pressure. A systolic pressure below 60
is insufficient to perfuse (force) nutrients into the tissue spaces between cells. During
ventricular contraction the atrio-ventricular valves make the "lubb" sound:
semilunar valves snap shut with a "dupp"sound.

Ateries in arm
 
 

Blood pressure cuff

 

Hypotension - Orthostatic hypotension is a dizziness when standing
suddenly caused by pooling of blood in the legs. See p. 732, 7th ed., p. 712, 8th ed.

Acute hypotension may be due to circulatory shock.

Chronic hypotension may be due to hypoalbuminemia due to liver disease
or protein malnutrition.

Hypertension -. See p. 732, 7th ed., p. 712, 8th ed.

A systolic blood pressure of above 160 or a diastolic pressure above 115 indicates severe
hypertension. Look at fig. 9.1 to determine the mild and moderate hypertension ranges.  The general hypertension numbers are >140 systolic and >100 diastolic.

Remember that prolonged hypertension leads to arteriosclerosis (hardening of the arteries).
Blood pressure medications focus on vasodilation (Ca2+ channel blockers), reducing blood volume (some diuretics),
or decreasing heart rate (beta blockers).

So, why should hypertensive patients stay on their medications constantly.

Primary hypertension (90% of all cases) is caused by diet, smoking, excessive
alcohol intake, obesity, stress, lack of exercise, and heredity. The underlying causes
of these conditions are obscure. Secondary hypertension has a known cause such
as uncontrolled hyperglycemia, hypersecretion of aldosterone as in some forms of
adrenal cortical hyperplasia, excessive secretion of renin by the kidney, and tumors of
the adrenal medulla. See the endocrine chapter and review the related hormones and
their actions. Fifty percent of hypertensive patients have trouble controlling their salt (NaCl) levels.
What do the levels of Na+ have to do with blood pressure? Explain!

Describe the actions of drugs used to control hypertension. Hint - beta receptor
blockers interfere with the action of the hormone Epinephrine (old=adrenalin) on heart
muscle.
 

Nurse taking blood pressure - cartoon          Physician taking very high blood pressure of old man - cartoon
      B.P. = 120/80                     B.P.=180/120
 

CARDIOVASCULAR CENTER OF THE MEDULLA - See p.727, 7th ed.; 707, 8th ed.

The CV center includes inputs from:

1.  Afferent neurons from the carotid and aortic baroceptors travelling by the
IX glossopharyngeal and X vagus nerves, respectively.  Remember Marey's Law
of the Heart and the right heart reflex?

2.  Carotid and aortic chemoreceptors detect changes in pH.  Acidosis occurs
if the pH is low, breathing speeds up, and CO2 is "blown off."  Why does
this raise blood pH?  Vasoconstriction also occurs as a result.  What causes
low blood pH?  Oxygen levels are also sensed to regulate breathing rate and
vasoconstriction.

3.  Parasympathetic Vagus (decelerator) center

4.  Sympathetic cardiac accelerator center

5.  Sympathetic vasomotor center.
 

HORMONES - See p.741, 7th ed.; p. 709, 8th ed.

1.  Epinephrine and norepinephrine (NE).  Review functions, please.

2.  ADH (also called vasopressin)

3.  Angiotensin II and Aldosterone

4.  Atrial natriuretic hormone - also vasodilator, causes Na+ excretion in
the urine.  What effects would result?

5.  The histamines liberated by mast cells (which develop from basophils) are vasodilators.

6. Cortisol is a vasoconstrictor.

7.  Some prostaglandins (thromboxane A2) are vasoconstrictors.

8. Vasodilators in tissues are nitric oxide, lactic acid, and low pH.

CIRCULATORY SHOCK

  1. Hypovolemic shock is caused by blood loss or dehydration, wounds, internal
    hemorrhage, excessive sweating, diarrhea, excessive urine production, and third
    degree burns.
  2. Toxic shock is caused by bacterial toxins that cause widespread vasodilation.
  3. Allergic shock or anaphylaxis occurs in many allergies such as penicillin allergy
    and insect bite or sting allergies. Mast cells release histamines all over the body.
  4. Cardiogenic shock - heart failure.

 

Stages of Hypovolemic Shock
    1. Compensated Shock - blood loss of up to 10% of total blood volume can be
    compensated for by increased heart rate, vasoconstriction and water and salt
    reclamation by the kidneys. The hormones Epinephrine or adrenalin, Norepinephrine,
    aldosterone, angiotensin II, renin, antidiuretic hormone, and aldosterone, contribute
    their effects increasing heartrate (Ep and NEp), causing generalized vasoconstriction
    (renin --> angiotensin II),and increasing blood volume (ADH and aldosterone) and
    blood pressure.

    2. Decompensated or progressive shock. If the blood volume drops more than 15-25%,
    vasodilation becomes more widespread as pH levels drop and hypoxia occurs in tissues.
    Positive feedback mechanisms result in depressed heart rate and activity of the
    cardiovascular center or the medulla. A mean systolic BP of below 60 is life threatening.
    As vasodilation occurs, morefluids enter tissue spaces. Intravascular clotting occurs.

     

        3. Irreversible, decompensated shock. Cells die. Acidosis shuts off the
        cardiovascular center. Heart output declines, ATP is depleted and the heart stops.
 

Specific blood vessels will be considered in the Lab!

Strokes - review.

Strokes are less commonly caused by hypertension-induced "blow outs" of cerebral aneurysms
(vessels with a weakened wall than balloons outward), and more commonly by clots
that lodge in and block cerebral blood vessels. Clots that form in one place, beak away
and are carried "downstream" to another, narrower blood vessel are called emboli.
Platelet clots/thrombi stay where they are formed.

How can one reduce the risk of stroke?

Study Questions

1. Compare and contrast arteriosclerosis and atherosclerosis on peripheral circulation.

2. Compare and contrast the structures of arteries and veins.

3. Describe the causes of edema. Why does right ventricular failure cause peripheral edema?
Left ventricular failure cause pulmonary edema?

3. Describe the stages of shock.
 

Letter image for emailjohn.aliff @ gpc.edu