Alterations of Blood Flow Flashcards
1
Q
Hyperemia
A
- An active, increased flow of blood into the microvasculature with normal outflow
2
Q
Physiologic hyperemia
A
- Increased flow to the skin for heat loss
- Increased GI flow following a meal
3
Q
Pathologic hyperemia
A
- Inflammation
- initial vascular response
4
Q
Hyperemia Morphology and Significance
A
- Blood vessels are bright red and engorged
- Affected areas are warmer than normal
5
Q
Congestion
A
- A passive accumulation of blood in a vessel usually due to decreased outflow, with normal inflow
- Can be localized or generalized
- localized congestion occurs due to acute or chronic occlusion of a vein
- Generalized is usually due to heart failure
6
Q
Localized Congestion
A
- Localized Congestion can be due to either intralumenal blockage or occlusion due to external pressure
- Venous thrombi can cause total venous obstruction
- External pressure can occur from inflammatory or neoplastic masses, organ displacement, or localized fibrosis
7
Q
Generalized Congestion: Heart Failure
A
- Right Sided Heart Failure:
- Liver and abdominal vasculature are primarily congested
- Left Sided Heart Failure:
- Pulmonary circulation is primarily congested
- Once one side of the heart fails, the other side will follow soon after
8
Q
Congestion Morphology
A
- Vessels are dark red and engorged
- Pulmonary congestion:
- Edema occurs concurrently (due to increased intravascular hydrostatic pressure)
- Red cells lost to alveoli are phagocytosed resulting in “heart failure cells” hemosiderin-laden macrophages)
- Edema occurs concurrently (due to increased intravascular hydrostatic pressure)
- Hepatic Congestion:
- Centrilobular sinusoids are initially affected resulting in a “nutmeg” appearance
9
Q
Congestion Significance
A
- Congested tissue is usually hypoxic
- if prolonged, can result in tissue injury
- Increased hydrostatic pressure associated with congestion often results in edema
- Congested tissue is usually cool
10
Q
Tissue perfusion
A
- Normal homeostatic mechanisms maintain adequate flow and perfusion to tissues based on their need
- Ischemia occurs when perfusion becomes inadequate to meet the metabolic needs of the tissue
11
Q
Ischemia Causes
A
- Usually involves some form of vascular occlusion
- Atrial lumenal blockage (thrombus or emboli)
- Prolonged arteriolar vasoconstriction
- Venous intralumenal occlusion (thrombus) or external pressure
- Capillary intralumenal occlusion or external pressure
12
Q
Ischemia Characteristics
A
- Severity determined by:
- Local vascular anatomy
- degree of anastomoses, collateral circulation and number of capillaries
- Extent of the decreased perfusion
- Rate of decreased perfusion
- rapid is more damaging than slow, progressive
- Metabolic needs
- Brain and heart are most susceptible
- Organs receiving large amounts of blood flow are relatively resistant (lungs, liver, kidneys)
- Local vascular anatomy
13
Q
Ischemia Outcome
A
- Return to Normal:
- Most common
- ATP of ischemic tissue is degraded to adenosine, a potent vasodilator
- Reperfusion injury
- After prolonged ischemia, return of blood flow can produce additional detrimental effects
14
Q
Cardiogenic Shock
A
- Reduced cardiac output most commonly due to cardiac disease
- failure of the central pump
- Predisposing problems include:
- Myocardial infarction
- myocardial arrhythmia
- pulmonary embolism
- Cardiomyopathy
- Decrease in both stroke volume and cardiac output
- Compensatory mechanisms attempt to increase SV, contractility, HR, and total output
- success depends on the nature of the problem
15
Q
Reperfusion Injury
A
-
HyTissue damaged by ischemia doesn’t function properly
- affected vessels are leaky
- increased interstitial hydrostatic pressure and and additional vessel compression
- Damaged tissue releases tissue factor to activate coagulation
- Ischemic cells produce hypoxanthine from ATP
- When combined with O2 hypoxanthine is converted into urates and O2 radicals (H2O2 and superoxide anions)
- O2 radicals can produce additional damage to the already compromised tissue
- affected vessels are leaky
16
Q
Infarction
A
- A local area of peracute ischemia that undergoes coagulative necrosis (liquefactive in nervous tissue)
- Caused by sudden reduction in blood and O2 supply to the tissue
- Could be caused by obstruction of arterial flow, or reduction in venous flow
- Usually the result of thrombosis
17
Q
Influencing Factors of Infarction
A
- Susceptibility of the tissue to ischemia
- High susceptibility: Myocardium, brain renal tubular epithelium
- Low susceptibility: connective tissues
- Vascular acatomy
- Functional end arteries
- Parallel vascular supply
- Dual blood supply
- Decreased cardiovascular function
- Anemia
18
Q
Infarction Characteristic
A
- Variable
- Based on
- Type and size of the occluded vessel
- Tissue affected
- Duration of the occlusion
- Status and vitality of the tissue prior to the infarct
- pre-existing damage/disease increase likelihood of ischemia progressing to infarction
19
Q
How does type and size of the occluded vessel affect the characteristics of Infarction?
A
- Arterial vs venous
- Complete arterial obstruction results in immediate infarction
- Venous obstruction usually preceded by venous congestion and edema
- Large vs small
- Obstruction of larger vessels generally affects more tissue
20
Q
How does the type of tissue affect the characteristics of Infarction
A
- Tissues with minimal anastomoses (brain, heart, kidney) are more predisposed to infarction
- Tissue with parallel blood supplies with numerous anastomoses (skeletal muscle, GIT) are relatively resistant to infarction
- Tissues with dual blood supplies (liver, lung) are relatively resistant to infarction
21
Q
Infarction Morphology
A
- Appearance mainly depends on type of vessel occluded and the tissue affected
- White (anemic)
- Red (hemorrhagic)
- Other factors, like age of infarct, affect appearance
- Most are red soon after occurance due to hemorrhage into the damaged tissue
- cells swell and undergo necrosis, some blood is forced out
- As healing occurs, infarcts become pale, contracted scars
22
Q
White Infarcts Morphology
A
- Occur most commonly with arterial thrombi/emboli in solid tissues with minimal anastomoses
- Solidity of the tissue limits the amount of blood that can seep back into the necrotic area
- There is general a red zone of hemorrhage, and later inflammation that surrounds the necrotic tissue
23
Q
Red Infarct Morphology
A
- These occur in a variety of situation:
- Venous stasis or obstruction
- Arterial obstruction in loose tissues
- Tissues with dual blood supply or extensive anastomoses
- Reperfused necrotic tissues
24
Q
Infarction Significance
A
- Clinical significance depends on location and size
- Infarcts involving vital organs can be serious
- Infarcts in non-vital tissues or tissues with large functional reserves are better tolerated
25
Shock
* A circulatory dyshomeostasis
* Circulating blood volume and the volume of of the circulatory system that needs to be filled are disproportionate
* systemic vascular collapse
* May be a loss of circulating blood volume, reduced cardiac output or inappropriate peripheral vascular resistance
* Failure leads to widespread tissue hypoxia and altered metabolism due to decreased delivery of nutrients and removal of waste products
* initially reversible, but rapidly become progressive and irreversible
26
Types of Shock
* Cardiogenic
* Hypovolemic
* Peripheral pooling (blood maldistribution)
27
Hypovolemic Shock
* Not enough blood in circulation
* Predisposing factors include fluid loss due to:
* severe hemorrhage
* Vomiting
* Diarrhea
* Burns
* Decreased vascular pressure, and decreased tissue perfusion
* Compensation includes peripheral vasoconstriction and fluid movement into the plasma to increase vascular pressure
* Vascular pressure can be maintained with loss of 10% of blood volume
* Losses of 35-45% of blood volume can result in dramatic decreases in vascular pressure
* Blood flow to critical tissues is prioritized
28
Blood Maldistribution
* Decreased peripheral resistance results in pooling of blood in peripheral tissues
* Cased by neural or cytokine-induced systemic vasodilation
* More capillary beds are open than can be filled
* Blood volume is normal, but the amount of vasculature needing to be filled is increased
* There are 3 categories of blood maldistribution
* Anaphylactic shock
* Neurogenic shock
* Septic shock
29
Anaphylactic shock
* Generalized Type 1 hypersensitivity
* Mast cell degranulation results in systemic release of histamine and other vasoactive mediators
* Systemic vasodilation nd increased permeability result in decreased vascular pressure and tissue hypoperfusion
* Causes Include:
* Allergens (plants and insect products)
* Drugs and vaccines
30
Neurogenic shock
* Autonomic nervous discharges result in peripheral vasodilation
* cytokines do not mediate this
* Causes include:
* Trauma
* Electrocution
* Fear or distress
31
Septic Shock
* Excessive release of vasoactive and pro-inflammatory mediators result in systemi vasodilation
* This is he most common type of blood maldistrbution syndrome
* Bacterial/fungal products are the most common cause
* Endotoxin (LPS)
* Peptidoglycans
* Lipoteichoic acid
32
LPS in Septic Shock
* LPS activates
* Cells (endothelium, leukocytes)
* cell activation includes interaction of LPS-binding protein, CD14 and Toll-like receptor-4
* Protein pathways (complement)
* Endothelial activation results in decreased production of anticoagulant substances
33
Effects of LPS
* Activation of Factor Xlla-related pathways
* Intrinsic coagulation, kinins, fibrinolysis, complement
* Activation of complement pathways
* C3a and C5a
* Decreased endothelial production of anticoagulants and enhanced expression of leukocyte adhesion molecules
* TNF and IL-1 released leukocytes
* Secondary effects of TNF and IL-1 include activation of extrinsic coagulation (TF release), PAF release, endothelial activation, production of arachidonic acid products
34
Shock Pathogenesis
1. Compensation (non-progressive) stage
2. Progressive stage
3. irreversible stage
35
Compensation Stage
* Reflex mechanisms are activated to maintain adequate circulating blood volume and pressure
* HR increases
* Peripheral Vasoconstriction
* ADH and angiotensin II release to increase blood volume
* Diversion of blood flow to vital tissues
* If the initiating cause is mild, compensation usually increases vascular pressure and there is a return to normal
36
Shock: Progression Stage
* Compensatory mechanisms are inadequate and tissue hypoperfusion occurs
* Metabolism shifts to anaerobic
* Cellular and systemic acidosis
* Host mediators accumulate (Cytokines & other inflammatory.coagulant substances
* Peripheral vasoconstriction gives way to vasodilation as local hypoxia occurs
* Blood pools and stagnates in the capillary beds
37
Shock: Irreversible
* Hypoperfusion, tissue hypoxia, and hemodynamic dysfunction result in irreversible cell damage
* cell energy stores are depleted
* Cell membrances deteriorate
* There is systemic activation of platelets and coagulation factors
* Disseminated intravascular coagulation
* Multiple organ failure occurs
* Failure of one system contributes to failure o another
38
Shock: Morphology
* Changes observed with shock depend on it's underlying cause and stage
* Basic changes include:
* Hemorrhage and edema
* Microtromosis
* Necrosis
* Major tissues affected:
* Heart, lungs, liver, kidney, brain, intestines, adrenal glands, pancreas
39
Shock: Significance
* Shock can be rapidly progressive and life-threatening
* Rapid and ggressive therapy is needed to prevent progression
* Clinical features include:
* Hypotension and weak pulse
* Tachycardia and hyperventilation
* Cool extremities and cyanosis
* In later stages, multi-system organ failure
