Blood flow Flashcards
Hyperemia
Increased flow can be physiologic or pathologic
Congestion
Decreased flow blood still in the vessel passive accumulation that can be generalized or localized
Physiologic hyperemia
-heat loss in skin
-Increased GI flow after meal
Pathologic hyperemia
-Inflammation
Morphology of hyperemia
Bright red and warm
Histologic morphology of hyperemia
Blood vessel looks engorged
Causes of localized congestion
-Venous thrombi can cause total venous obstruction
-External pressure can occur form inflammation or neoplastic masses, organ displacement or localized fibrosis
Causes of generalized congestion
Right or left sided heart failure. Once one side fails the other side will soon follow
Morphology of congestion
Vessels dark red and engorged
Pulmonary congestion
Edema concurrent due to increased hydrostatic pressure. See RBC pop out and the macrophages eat the RBC and they are left with the iron (heart failure cells)
Hepatic congestion
Centrilobular sinusoids are initially affected. Have a nutmeg appearance
Significance of congestion
-Hypoxia and ischemia
-Often get edema
-Tissues cool because it is stagnant
Ischemia
WHen perfusion becomes inadequate to meet metabolic needs of the tissue
Tissue perfusion
Have adequate flow in tissues based on their need
Causes of ischemia
-Arterial lumenal blockage
-Prolonged arteriolar vasoconstriction
-Venous intralumenal occlusion or external pressure
-Capillary intralumenal occlulsion or external pressure
What dictates severity of ischemia
-Vascular anatomy (collateral circulation)
-Extent of decreased perfusion
-Rate of decreased perfusion (rapid more damaging than slow)
-Tissue type (brain and heart)
Outcome of ischemia
-return to normal (usually after brief)
-Reperfusion injury (from prolonged)
Reperfusion injury
Affected vessels are leaky and move fluid to interstitial
-Damaged tissue releases tissue factor to activate coagulation
-ATP converted to adenosine and combines with O2 and creates O2 radicals and cause additional damage
Infarction
Local area of peracute ischemia that undergoes coagulative necrosis or liquefactive in nervous tissue. Usually caused by thrombus
Highly susceptible tissues to infarction
-Myocardium
-Brain
-Renal tubules
-Epithelium
Low susceptibility to infarction
CT
Influencing factors of infaction
-susceptibility of tissue
-Vascular anatomy
-Decreased cardiovascular function
-Anemia
Characteristics of infarction
-Type and siaze (artery which is immediate vs vein which is slower and causes congestion; large or small vessel)
-Tissue affected (susceptibility, anatomy)
-Duration
-Status of tissue prior to infarct
Infarction morphology
Depends on vessel occuled and tissue affected
-White (anemic)
-Red (hemorrhagic)
Red infarcts
Infarct and get hemorrhage into damaged cells. Cells swell and undergo necrosis, once it degrades blood flows back in and looks red
White infarts
Occurs in solid tissues with minimal anastomosis like the heart. See zone of inflammation around. Because it is solid blood can’t seep back into the tissue
Reasons for red infarct
-Venous stasis or obstruction
-Arterial obstruction in loose tissues
-Tissues with dual blood supply or anastomoses
-Reperfused necrotic tissues
Infarction significane
-Vital organs can be fatal and serious
-Non vital organs better tolerated
-Want to know what the cause was though that could be important
Shock
Circulatory dyshomeostasis where circulating blood volume and volume of circulatory system that needs to be filled are disporportionate. Get widespread tissue hypoxia and altered metabolism
Cardiogenic shock
BLood flow is reduced due to failure of central pump
-Myocardial infarction or arrhythmias
-Pulmonary embolism
-Cardiomyopathy
Hypovolemic shock
Not enough blood in circulation. Decrease in vascular pressure see compensatory peripheral vasoconstriction and fluid movement. See porblems when you lose 35-45% loss
-Severe hemorrhage
-Vomiting
-Diarrhea
-Burns
Blood maldistribution
Systemic vasodilation of periphery and get bleed pooling in peripheral tissues
Three categories of blood maldistribution
-anaphylactic shock
-neurogenic shock
-septic shock
Anaphylactic shock
Generalized type I hypersensitivity leading to systemic vasodilation from histamine and get increased permeability, decreased pressure and tissue hypoperfusion. IgE based reaction
Neurogenic shock
Autonomic nervous discharges resut in peripheral vasodilation
Causes of neurogenic shock
-Trauma
-Electrocution
-Fear or stress
Septic shock
Excessive release of vsaoactive and pro inflammatory mediators resulting in vasodilation. Bacteria and fungus are the normal causes
LPS and septic shocl
Activates endothelium and leukocytes
-Decreases anticoagulant properties
-Activates the complement pathways
-Activate Factor XIIa-related pathways
-enhanced leukocyte adhesions
-TNF and IL- release (procoagulant and proinflammatory)
3 stages of shock
- Compensation
- Progressive stage
- Irreversible stage
Compensation
Reflex mechanisms
-Increase heart rate
-Peripheral vasoconstriction
-ADH and ANG II increase blood volume
-Diversion of blood to vital tissues
-If mild can return to normal here
Progression
Compensatory mechanisms are inadequate and tissue hypoperfusion occurs
-Metabolism shifts to anaerobic
-Acidosis
-Host mediators accumulate
-Peripheral vasoconstriction turns to dilation as hypoxia occurs and get pooling of blood
Irreversible stage
Hypoperfusion, tissue hypoxia, and hemodynamic dysfunction leads to cell damage
-Cell energy stores depleted, and membranes deteriorate
-Disseminated intravascular coagulation
-organ failure
Morphology of shock
Depends on stage
-Hemorrhage and edema
-Microthrombosis
-Necrosis
-Multiorgan
Significance of shock
Life threatening
-Hypotension and weak pulse
- Tachycardia and hyperventilation
-Cool extremities and cyanosis
-Multi organ failure
