HEMODYNAMIC DISODER

The health and well being of cells and tissue depends not only on intact circulation to deliver oxygen,
also on normal fluid homeostasis.
Abnormalities in either blood supply or fluid balance are result in morbidity/mortality.
The pathologies include edema, vascular congestion, hemorrhage, thrombosis, embolism, infarction
and shock.
A. Edema
Edema signifies increased fluid in the interstitial tissue space.
Edema caused by increased hydrostatic pressure or reduced plasma protein is typically a
protein-poor fluid called a transudate. Edema fluid of this type is seen in patients
suffering from heart failure, renal failure, hepatic failure, and certain forms of
malnutrition.
In contrast, inflammatory edema is a protein-rich exudate that is a result of increased
vascular permeability.
Causeof edema:

Increased Hydrostatic Pressure.

Reduced Plasma Osmotic Pressure.
Sodium and Water Retention.
Lymphatic Obstruction.

B. HYPEREMIA AND CONGESTION

Indicate a local increase volume of blood in particular tissue.
Hyperemia is an active process in which arteriolar dilation (e.g., at sites of
inflammation or in skeletal muscle during exercise) leads to increased blood flow.
Affected tissues turn red (erythema) because of the engorgement of vessels with
oxygenated blood.
Congestion is a passive process resulting from reduced outflow of blood from a
tissue. It can be systemic, as in cardiac failure, or local, as in isolated venous
obstruction. Congested tissues take on a dusky reddish-blue color (cyanosis) due to
the accumulation of deoxygenated hemoglobin. As a result of the increased volumes
and pressures, congestion commonly leads to edema.
C. HEMMORAGE
Indicate extravasation of blood because of vessel rupture.
Rupture of a large artery or vein, is almost due to vascular injury, including trauma,
atherosclerosis, inflammatory and neoplastic erosion of the vessel wall.
The referred accumulation known as hematoma.
i. Petechiae: 1-2 mm into skin, mucous membranes or serosal surface
ii. > 3mm called purpura.
iii. > 1 to 2 cm called ecchymosis.
Depending on the location, Large accumulations : hemothorax, hemopericardium,
hemoperitoneum, and hemarthrosis.
Clinical significance of hemorrhage depends on the volume & rate of blood loss

D. HEMOSTASIS AND THROMBOSIS

Normal hemostasis accomplish two important functions :
(1) maintain blood in a fluid and
(2) rapid and localized hemostasis plug at a site of vascular injury.
Both hemostasis and thrombosis depend on : vascular wall, platelets and the
coagulation cascade.
Normal Hemostasis:
i. Vasoconstriction
Injury reflex neurogenic mechanism and local secretion endothelin factor
vasoconstrictor.
ii. Primary Hemostasis
Exposes highly thrombogenic subendothelial extracellular matrix
activated platelets secretory granules hemostatic plug.
iii. Secondary Hemostasis
Exposes tissue factors conjunction with platelet factors activate
coagulation cascade. Thrombin convert fibrinogen to insoluble fibrin
deposition fibrin platelet plug enlargement.
iv. Thrombus and Antithrombotic Events
Polimerized fibrin and platelet agregates permanent plug to prevent any
further hemorrhage.

Thrombosis
i. Endothelial injury is dominant and can cause thrombosis. Thrombosis result
from exposed subendothelial ECM & tissue factor, adherence platelets &
depletion of prostaglandin I2 and PAIs
ii. Alteration in normal blood flow can cause thrombosis. Normal blood flow is
laminar, disrupt of this flow bring platelets into contact with the
endothelium
iii. Hypercoagulability contributes less frequently to thrombotic states but is
important in certain states

E. EMBOLI
Is a detached intravascular solid, liquid or gaseous that is carried by the blood to a
site distant from its point of origin.
Caused disturbance vessel passage partial/complete vascular occlusion
ischemic necrosis distal tissue/infarction.
Type of Embolism:
i. Pulmonary Thromboembolism
ii. Systemic Thromboembolism
iii. Fat Embolism
iv. Air Embolism
v. Amniotic Fluid Embolism
F. INFARCTION
an area ischemic necrosis caused by occlusion of either the arterial supply or the
nervous drainage in a particular tissue.
Classified on the basis of their color :
i. Red infarcts (hemorrhagic) : venous occlusions
ii. White infarcts (anemia) : arterial occlusion
Factors that influence development of an Infarct
i. The nature of the vascular supply.
ii. Rate of development of the occlusion.
iii. Vulnerability of a given tissue to hypoxia
iv. Oxygen content of the blood.
G. SHOCK
Shock or cardiovascular collapse, is the final common pathway for a number of
potentially lethal clinical events.
Constitutes systemic hypoperfusion owing to reduction either in cardiac out put or
in the effective circulating blood volume.
End result : hypotension, impaired tissue perfusion and cellular hypoxia/anoxia.
Neurogenic shock, e.g. in the setting of anesthetic accident or spinal cord injury.
Loss of vascular tone and peripheral pooling of blood.
Anaphylactic shock, initiated by a gene-ralized IgE-mediated hypersensitivity
response, is associated with systemic vasodilatation and increase vascular
permeability.

Stages of Shock
i. An initial nonprogressive phase during which reflex compensatory
mechanisms are activated and perfusion of vital organs is maintained.
ii. A progressive stage characterized by tissue hypoperfusion and onset of
worsening circulatory and metabolic imbalances including acidosis.
iii. An irreversible stage that sets in after the body has incurred cellular and
tissue injury so severe that even if the hemodynamic defects are corrected,
survival is not possible.