increased hydrostatic pressure

decreased plasma colloid osmotic pressure

sodium and water retention

lymphatic obstruction

increased vascular permeability

local: isolated venous constriction

systemic: cardiac failure

vascular congestion: passive provess that results from impaired outflow caused by increased hydrostatic pressure causing vasodilation

hyperemia: an active process that is caused by vasodilation typically due to inflammation

rate and volume of blood loss

site of bleeding

loss of iron

hemotasis: normal, maintains blood in a fluid state and vascular integrity

thrombosis: pathologic, inappropriate activation of normal hemostatic processes in uninjured vasculature

-vascular injury

-vasoconstriction

-primary hemostasis, platelet function

-secondary hemostasis, tissue factors act with platelets to activate coagulation cascade, production of thrombin which converts fibrinogen to fibrin, fibrin deposits at injury site

-permanent plug formation

ulcerated artherosclerotic plaque

aneurysm

myocardial infarction

mitral valve stenosis

hyperviscosity syndromes

sickle cell anemia

thrombotic or embolitic events

arterial occlusions

nature of the vascular supply

rate of development of occlusion

vulnerability of a tissue to hypoxia

oxygen content of blood

cardiogenic: low cardiact output due to myocardial pump failure

hypovolemic: low cardiac output due to inadequate blood or plase volume

distributive: vasidilation causes a state of hypovolemia

petichia associated with increased intravscular pressure, low platelet counts, defective platelet function, clotting factor deficiencies

purpura associated with same as petichia and also trauma, vasculities, and increased vascular fragility

ecchymoses associated with trauma

origin: leg vein

destination: carried through right side of heart into pulmonary vasculature

effects: clinically asymptomatic, sudden death, infarction

origin: intracardiac, forms in the heart

destination: lower extremities, brain

effects: infarction

nonprogressive: compenastion occurs, perfusion of vital organs is maintained

progressive: hypotension as compensatory mechanism starts to fail, reduced stroke volume, weak pulse caused by decreased cardiac output, shallow respirations, reduced urine output cold and clammy skin

irreversible: cell injury is widespread causing reduced perfusion which damages cell membranes, multiple system organ failure

cardiogenic: increased heart rate, strengthen myocardial contractions, promote sodium and water retention

hypovolemic: hemorrhage, fluid loss, ascites, hemothorax

septic: gram negative bacteria, gram positive septicemia, fungal sepsis

initial threat: precipitating event

subsequent threat: changes to organs, electrolyte disturbances, metabolic acidosis, renal insufficiency

petichiae: 1 - 2mm hemorrhages into skin, muscous membranes, serosal surfaces

purpura: > 3mm

eccymoses > 10 - 12cm

accumulation of blood in body cavities:

hemothorax: chest

hemopericardium: heart

hemoperitoneum: abdomen

hemoarthrosis: joints

poor venous circulation and resultant fluid accumulation

localized: impaired venous outflow; emboli

systemic: congestive heart failure, constrictive pericarditis, ascites

protein concentration in blood is lower than in the interstitial tissue

fluid leaves the plasma and causes a reduced intravascular volume and renal hypoperfusion occurs

increased salt intake with renal insufficiency and increased tubular reabsorption of sodim

causes increased hydrostatic pressure and diminished vascular colloid osmotic pressure