Flashcards in Hemodynamic Disorders Deck (63):
local increase in blood volume. increased arterial inflow due to arteriolar dilation. well oxygenated blood flowing into tissue=bright red erythema. warm. ACTIVE process
examples of hyperemia
inflammation, exercise, blushing
cause of hyperemia
vasodilation of artery leading to locally increased blood flow
hyperemic border around necrosis
white necrosis due to arterial thrombi-occlusion or thromboembolism and subsequent acute inflammatory response dilates border vessels
local increase in blood volume due to decreased venous outflow from an organ. blue-red tissue=cyanosis from increased deoxygenated blood. PASSIVE process
cause of congestion
impaired venous outflow due to compression, constriction, or functional problem of heart
how does congestion cause edema
hydrostatic pressure at venule end increases and exceeds osmotic pressure so that fluid is driven out everywhere via Starling forces and lymphatics are overwhelmed
what typically accompanies congestion?
venous thrombosis and congestion
blocks blood from exiting tissue. initially there is congestion, which causes increased hydrostatic pressure in vessel and edema. but most tissues have multiple venous drainage pathways, so additional channels open and help bypass obstructed vein.
right heart failure
back up of blood into systemic veins (IVC/SVC), which commonly affects the liver.
left side heart failure
back up of blood into lungs, shortness of breath
where is liver congestion due to right sided heart failure found?
central vein (hepatic vein to IVC)
centrilobar congestion and periportal fatty change= chronic passive congestion of liver. impaired o2 delivery to hepatocytes which then accumulate fat
extravasation of blood due to vessel rupture
space occupying lesion of blood
tissue hemorrhages small to big
petechiae (1-2mm), purpura (>3mm), ecchymoses (>1-2cm)
pathologica hemostatic plug within a blood vessel that is composed of platelets, fibrin, and trapped RBCs
intravascular solid, liquid, or gas that is carried from site of origin to a distal site in the bloodstream. doesn't mix with aqueous portion of blood
detached thrombus that embolizes
how to identify thrombi
lines of zahn and adhesion to vessel wall
endothelial injury, hypercoaguability, abnormal blood flow all lead to thrombi
important factors leading to arterial thrombi
endothelial cell injury and turbulent flow. atherosclerosis, inflammation
characteristics of arterial thrombi
prominent lines of zahn, white appearance (more platelets/fibrin than RBCs)
where are arterial thrombi more likely to occur
small to medium arteries (coronary, cerebral, femoral). often occlusive and present risk of infarction. less common in aorta (present as mural thrombi that stick to wall but don't occlude. still risk embolization)
important factors leading to venous thrombi
stasis, hypercoagulative states due to increased concentration of activated coag factors and depletion of inhibitors
characteristics of venous thrombi
less prominent lines of zahn due to slow blood flow, red appearance due to trapped RBCs
common locations of venous thrombi
superficial and deep veins of legs and pevic veins
important factors of cardiac chamber (mural) thrombi
endocardial injury, stasis: enlarged chambers (poor contractibility=stasis), atrial fibrillation (local stasis), post myocardial infarction (stasis due to wall motion abnormality), abnormal valves. more RBCs
4 general fates of thrombi
resolution, propagation, embolization, organization/recanalization
where do venous thromboemboli travel?
when might venous thromboemboli travel to systemic circulation? PARADOXICAL EMBOLIZATION
if there is a patent foramen ovale, ventricular septal defect, or PDA (pulmonary artery to aorta)
where do arterial thromboemboli travel?
lodge distally in a smaller artery
where do aortic thromboemboli travel?
variable distal locations in smaller branch off aorta
where do right cardia chamber thrombi travel?
pulmonary arterial circulation
where do left cardiac chamber thromboemboli travel?
systemic arterial circulation
organization of thrombi
ingrowth of granulation tissue cells into the thrombus as mechanism of repair and gradual conversion to fibrous tissue. recanalization. followed by incorporation into vessel wall via fibrous plaques and bands
new vascular channels connecting end to end, allowing reestablishment of blood flow through the scar
what type of tissue is involved in thrombi repair?
clinical consequences of thrombi/thromboemboli
edema, congestion, embolization, infarction
consequences common to venous thrombi/thromboemboli
edema, congestion, embolization
consequences common to arterial thrombi/thromboemboli
ischemic necrosis of tissue due to occlusion of arterial blood supply or venous drainage (uncommon)
what factors do infarctions depend upon?
susceptibility of tissue to ischemic injury, rate of occlusion development (slow=collateral formation more likely), location of thrombus (more likely arterial), arterial blood supply (1v2), venous drainage
which tissues are most susceptible to infarction
white (anemic) infarcts
arterial, solid organs with one blood supply. generally wedge shaped due to blood flow pattern from hilum
red (hemorrhagic) infarct
venous with single drainage (0vary, testes), in organs with 2 blood supplies (lung, liver:must be secondary to impairment of other circulation like congestive heart failure or underlying lung disease), or from repercussion after white infarct since damaged vessels are leaky or via free radical injury
redder tissue (increased oxygenated blood). due to hyperemia
right sided heart failure leads to...
liver congestion (via IVC backup)
left sided heart failure leads to...
lung congestion (via pulmonary vein backup)
normal pressure differentiation along capillary (A to V)
intravascular hydrostatic pressure decreases (fluid exits artery end) and intravascular osmotic pressure increases (reabsorbed at venous end) longitudinally.
do venous thrombi result in congestion and edema?
might. but most of the time, collateral vessels take over so venous thrombi not usually associated with infarction
thrombosis and age
risk increases with increasing age
who is at a much greater risk for thrombosis in addition to the elderly?
why are hospitalized patients at a higher risk for thrombi?
cardiovascular disease and prolonged immobilization lead to stasis in the venous system and allows low levels of activated clotting factors to accumulate
risk factors for venous thromboembolism (VTE)
systemic diseases, inflammatory states, things that affect movement of blood through the systemic system
VTE prevention in hospital
mobilize patients as soon as possible, anticoagulation via heparin, mechanical compression in patients unable to tolerate anticoagulation
Disseminated Intravascular Coagulation (DIC)
response to an injury that causes activation of normal blood clotting and fibrinolytic mechanisms. but the stimulus for activation overwhelms normal control mechanisms. Clotting exceeds factor replacement so that bleeding occurs as well
clinical manifestations of DIC
patient may present with severe blessing, thrombosis, or both. acutely ill patients usually bleed, thrombosis is classically seen with cancer
DIC lab findings
increased PT/aPTT (used up factors), decreased platelet count (aggregated), microangiopathic hemolytic anemia (schistocytes due to fibrin RBC shearing), presence of D dimers
treatment of DIC
TREAT UNDERLYING CAUSE
most common cause of as symptomatic prolongation of PT/aPPT
antiphospholipid antibodies/lupus anticoagulants prolong aPPT in vitro but don't interfere with clotting in vivo
antiphospholipid antibody syndrome
presence of one or more types of antiphospholipid antibodies on at least 2 occasions 3 mos apart and thrombosis, pregnancy morbidity, possibly thrombocytopenia