(From Dr. A’s handouts, by Brian Buschman)
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Nutrient arteries carry nutrients to the capillaries. Their size (i.e. level of vasoconstriction/vasodilatation) is a product of signals that include:
1) Nutrients
2) pH
3) Metabolic products
Capillaries have two types of pores to allow passage of material:
1) Intercellular clefts that allow free flow of small uncharged particles.
2) Plasma lemmal vesicles that allow for pinocytosis and exocytosis.
Starling’s law of the capillary:
Q=k[(PC+PI)-(PI+PC)]
Reflection Coefficient is a factor of how much protein passes through the membrane. If all the protein is reflected then the reflection coefficient is 1, if ˝ then it’s .5 and if no protein is reflected then the reflection coefficient is 0.
Blood flow can be controlled locally by mechanisms that serve and regulate according to tissue needs and O2/nutrient availability. Local control can occur actively by vasoconstriction and vasodilatation or it can occur by more long term mechanisms that regulate the number of blood vessels.
Acute control is regulated by:
1) O2 availability to tissues. Decreased O2 leads to vasodilatation. Signals for the vasodilatation include:
a. Adrine
b. CO2
c. Lactic Acid
d. Histamine
e. Increased H+
2) O2/nutrient demand. If there is a stronger need for nutrients somewhere else there may be vasoconstriction (mediated by glucose and vitamin B) to allow that other vasodilatation.
It is debated if local control of BP is based on regulation based on metabolic factors or based on vascular stretch.
Long term regulation is based on changes including angiogenesis, development of collateral circulations and of regulation of the blood volume.
Humoral regulation of circulation is done by vasoconstriction that is mediated by things like Epi, NE, angiotensin and ADH. Vasodilators include bradykinin, 5-HT, histamine and prostaglandin.
Sympathetics and parasympathetics working through centers in the pons and medulla function in vasodilatation and vasoconstriction. Part of the neural regulation is via the baroreceptor reflex with afferent fibers in CN IX and X and afferents in X.
When there is an increase in intracranial pressure it compresses cerebral arteries which causes decreased perfusion. This causes increase in PCO2 and decrease in pH. Medullary chemoreceptors respond by BOTH sympathetic and parasympathetic responses to increase TPR to increase atrial pressure and to decrease HR.
In any chamber of the heart blood flow to supply it is lowest during systole due to pressure that cuts of the circulation. The vessels in the endocardium are compressed to a greater extent because they are closer to the force of contraction. It is important to understand this because it can be seen that during systole the endocardium is more susceptible to infarction. Blood flow to the heart is primarily regulated through local mechanisms with a little bit of parasympathetic input.
During exercise blood flow to the heart is increased greatly. Such cardiac vasodilatation is stimulated by the pO2, adenosine, K+, CO2 and lactic acid accumulation. Note that those are mostly metabolic byproducts that need to be gotten rid of. The K+ should not be elevated in the interstitial fluid but is so in damaged tissues.
Skeletal muscle blood flow during exercise is regulated primarily by CNS signals.
Large arteries do not develop collaterals so of they become blocked that is VERY BAD. Five factors lead to death from sudden occlusion:
1) Cardiac shock from decreased pumping ability.
2) Peripheral tissue ischema due to decreased CO.
3) Venous congestion that causes problems with capillary flux.
4) V-fib from:
a. Increased extracellular K+ causing excitability.
b. An electrical current of injury.
c. Sympathetic activity increases.
d. Ventricle dilation
5) Large infracted areas may rupture.
Small infacts recover quickly with little permanent damage.
Large infacts have areas in the center with much damage that will mostly be replaced with scar tissue and other areas on the periphery that will be recover like in a small infacts.
IHD can be treated with vasodilators, angioplasty or coronary bypass.
Shock comes in three stages:
1) Nonprogressive shock can be easily corrected by the body’s natural homeostatic mechanisms.
2) Progressive shock has not caused irreversible damage but gets progressively worse until someone intervenes.
3) Irreversible shock is associated with tissue damage that makes death inevitable regardless of medical intervention.
I) Hypovolemic shock is associated with low blood volume that may result of any cause (dehydration, blood loss, burns, tissue trauma or whatever).
II) Neurogenic shock is associated with neural damage or anesthesia that causes depression of systems regulating the CV system.
III) Septic shock is a decreased CV function associated with an infection. It is the only shock associated with a fever.
IV) Anaphylactic shock is from an allergic reaction due to massive vasodilatation and increased vascular permeability.
Treat the shock with glucocorticoids to stabilize lysosomal membranes, administer O2 and treat the associated symptoms (i.e. transfusion, saline or plasma expanders if hypovolemic).
Cardiac failure results from:
1) Decreased coronary flow
2) Valvular defect.
3) Cardiac tamponade
4) Nutritional deficiencies (vit B especially)
5) Cardiac myopathies
In general increased right atrial pressure will not cause increase in CO. In hart failure increased RAP actually causes decreased CO.
When you get a cut the homeostatic response has five stages:
1) Vasoconstriction
2) Platelet plug formation
3) Coagulation with intrinsic and extrinsic pathways.
4) Clot retraction
5) Fibrinolysis with plasmin.
Most factors are synthesized in the liver and may require vitamin K for synthesis. That means anything that prevents fat soluble vitamin uptake will prevent factor formation. They are all synthesized in the liver except for:
May factors need to be bound to the endothelium and that is done in part by coordinating a Ca2+. Vitamin K is a cofactor in the reaction that modifies the AAs that will bind the Ca2+. If there is a vitamin K shortage the factors cannot be properly formed.
Dicumarol is one anticoagulant that functions by inhibiting that reaction being that it is a vitamin K analog.
The extrinsic pathway is activated by factor III which is released when the tissue is damaged. III then activated VII which works with IV to activate X.
The intrinsic pathway is activated when factors come into contact with the tunica media and release kininogen which functions with factor XIIa to activate XI to activate IX which activated X.
The common pathway is activated by X which works with V to activate prothrombin (II) which causes fibrinogen (I) to work. XIII helps make the clot stronger.
The clots are broken down by plasminogen which is stimulated by:
1) Tissue kinase
2) Urokinase
3) Streptokinase
We have three things that work as anticoagulants for us:
1) Antithrombin III which inhibits thrombin (II) and factor Xa.
2) Heparin (warfarin) which stimulates antithrombin III.
3) Plasminogen which is what naturally removes the clots.
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