Chapter 4: hemodynamic disorders, Thromboembolism, and shock
Capillary regulation:
At arterial end the pressure is in the pressure in
the lumen pushes out small molecules while
retaining the proteins in the vessels.
In the capillary bed the protein concentration
relatively rises because water goes out.
At the end in the venous part the water will be
sucked in again, restoring the amount of
circulating fluid. Not everything goes back in the
capillary, and the remaining goes back into the
subclavian vein via the venous system.
Colloid osmotic pressure = the proteins attract water back into the vessels.
Hyperemia = increased from at the arterial end, mostly due to exercise or inflammation.
Congestion = decreased outflow, due to local construction or heart failure.
The distribution of blood is done to parts where its needs to be (some brain parts get more
blood then others).
Edema: can occur because of:
Increased egress of water at the capillary level via:
1. Increased pressure at the venous end (cardiac failure or
blockades)
2. Increased permeability (inflammation or neurogenic due
to injury in the NS)
3. Increased pressure arterial end > almost never!!
Decreased return of fluid from interstitial > a decrease in colloid
osmotic pressure
Blocked flow of lymph, iatrogenic (problem caused by doctor) or tumor
Consequences and risks of Edema: it occurs frequently and usually locally. In most cases
risks are limited. Sometimes big risk, brain (due to the skull) and larynx (airway obstruction).
Generalised Edema is dangerous, because insufficient circulation, and can cause shock.
Haemorrhage: from small to big:
Petechiae (thrombopenia) > purpura (vascular malformations) > ecchymoses (trauma) and
hematoma (trauma)
Haemostasis:
1. After injury: vasoconstriction
2. Primary haemostasis: platelet changes shape and recruit more platelet to the place
on injury. Formation of platelet plug
3. Secondary haemostasis: fibrinogen to fibrin to glue to platelets to each other. This
platelet coagulated because of the coagulation factor thrombin.
4. Antithrombotic counter regulation: EC expressed fibrinolysis
Drugs can interfere and blocking the mediators, results in change of blood flow. Example is
aspirin.
EC mostly inhibits thrombosis. Upon trauma can favour thrombosis. The P-selectin contains
vWF to let the platelets adhere better to the surface of the EC. Deficiency in Gplb = not good
adherence of platelet to surface.
Capillary regulation:
At arterial end the pressure is in the pressure in
the lumen pushes out small molecules while
retaining the proteins in the vessels.
In the capillary bed the protein concentration
relatively rises because water goes out.
At the end in the venous part the water will be
sucked in again, restoring the amount of
circulating fluid. Not everything goes back in the
capillary, and the remaining goes back into the
subclavian vein via the venous system.
Colloid osmotic pressure = the proteins attract water back into the vessels.
Hyperemia = increased from at the arterial end, mostly due to exercise or inflammation.
Congestion = decreased outflow, due to local construction or heart failure.
The distribution of blood is done to parts where its needs to be (some brain parts get more
blood then others).
Edema: can occur because of:
Increased egress of water at the capillary level via:
1. Increased pressure at the venous end (cardiac failure or
blockades)
2. Increased permeability (inflammation or neurogenic due
to injury in the NS)
3. Increased pressure arterial end > almost never!!
Decreased return of fluid from interstitial > a decrease in colloid
osmotic pressure
Blocked flow of lymph, iatrogenic (problem caused by doctor) or tumor
Consequences and risks of Edema: it occurs frequently and usually locally. In most cases
risks are limited. Sometimes big risk, brain (due to the skull) and larynx (airway obstruction).
Generalised Edema is dangerous, because insufficient circulation, and can cause shock.
Haemorrhage: from small to big:
Petechiae (thrombopenia) > purpura (vascular malformations) > ecchymoses (trauma) and
hematoma (trauma)
Haemostasis:
1. After injury: vasoconstriction
2. Primary haemostasis: platelet changes shape and recruit more platelet to the place
on injury. Formation of platelet plug
3. Secondary haemostasis: fibrinogen to fibrin to glue to platelets to each other. This
platelet coagulated because of the coagulation factor thrombin.
4. Antithrombotic counter regulation: EC expressed fibrinolysis
Drugs can interfere and blocking the mediators, results in change of blood flow. Example is
aspirin.
EC mostly inhibits thrombosis. Upon trauma can favour thrombosis. The P-selectin contains
vWF to let the platelets adhere better to the surface of the EC. Deficiency in Gplb = not good
adherence of platelet to surface.
