Alterations in Blood Flow Flashcards
(40 cards)
1
Q
Alterations in blood flow:
Intravascular events
A
- Increase flow
- hyperemia
- Decreased Flow
- congestion
2
Q
Alterations in Blood Flow:
Hyperemia
A
- An active, increased flow of blood into the microvasculature with normal outflow
- Physiologic Hyperemia
- increased flow to the skin for heat loss
- Increased GI flow following a meal
- Pathologic Hyperemia
- Inflammation, initial vascular response
3
Q
Hyperemia:
Morphology and Significance
A
Blood vessels are bright red and engorged
Affected areas are warmer than normal
4
Q
Alterations in Blood Flow:
Congestion
A
- Congestion is a passive accumulation of blood in a vessel usually due to decreased outflow, with normal inflow
- COngestion can be localized or generalized
- localized congestion occurs due to acute or chronic occlusion of a vein
- Generalized is usually due to heart failure
5
Q
Disturbances if blood Flow:
Localized congestion
A
- Can be due to either intralumenal blockage or occlusion due to external pressure
- venous thrombi can cause total venous obstruction
- External presure can occur form inflammatory or neoplastic masses, organ displacement, or localized fibrosis
6
Q
Generalized congestion:
Heart Failure
A
- Right Sided heart failure:
- the 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
7
Q
Congestion:
Morphology
A
- Vessels are dark red and engorged
- Pulmonary congestions
- edema occurs concurrently
- Hepatic Congestion
- centrilobular sinusoids are initially affected resultsin in a “nutmeg” appearance
8
Q
Congestion:
Significance:
A
Congested tissue is usually hypoxic
Increased hydrostatic pressure associated with congestion often results in edema
Congested tissue is usually cool
9
Q
Tissue Perfusion
A
- Normal Homeostatic mechanisms maintains adequate flow and perfusion to tissues based on their need
- Ischemia occurs when perfusion becomes inadequate to meet the metabolic needs of the tissue
10
Q
Ischemia:
Causes:
A
- Usually involves soem form of vascular occlusion
- Arterial lumenal blockage
- Prolonged arteriolar vasoconstriction
- Venous intralumenal occlusion or external pressure
- Capillary intralumenal occlusion or external pressure
11
Q
Ischemia:
Characteristics
A
- Severity is determined by:
- local vascular anatomy
- degree of anastomoses, collateral circulation, and number of capillaries
- Extent of hte decreased perfusion
- The rate of decreased perfusion
- rapid occlusion is more damaging than slow, progressive occlusion
- Metabolic needs of the tissues
- brain and heart are most susceptible
- Organs already receiving large amounts of blood flow are relatively resistant (lungs, liver, kidney)
- local vascular anatomy
12
Q
Ischemia:
Outcome
A
- Returm to normal:
- this is most common after brief ischemia
- ATP of ischemic tissue is degraded to adenosine, a potent vasodilator
- Reperfusion Injury:
- After prolonged ischemia, the return of blood flow can produce additional detrimental effects
13
Q
Ischemai:
Reperfusion Injury
A
- Tissue damaged by ischemia doesn’t function properly
- affected vessels are leaky and fluid moves to the interstitium
- increased interstitium hydrostatic pressure which increases vessel compression
- Damaged tissue releases tissue factor to activate coagulation
- Ischemic cells produce hypoxanthine from ATP
- When combined with O2 converted into urates and O2 radicals.
- O2 radicals can produce additional damage to the already compromised tissue
- affected vessels are leaky and fluid moves to the interstitium
14
Q
Decreased Tissue Perfusion:
Infaction
A
- In a local area of peracute ischemia tha under goes coagulative necrosis
- caused by sudden reduction in blood flow and O2 supply to the tissue
- This could be caused by obstruction of incoming flow, or reduction in the outgoing flow
- Usually the result of thormbosis
15
Q
Infarction:
Influencing Factors
A
- Susceptibility of the tissue is ischemia
- high susceptibility: Myocardium, brain, renal tubular epithelium
- Low susceptibility:
- connective tissue
- Vascular anatomy
- funcitonal end arteries
- Parallel vascular supply
- Dual blood supply
- Decreased cardiovascular function
- Anemia
16
Q
Infarction:
Characteristics:
Aterial Obstruction
A
- Complete arterial obstruction usually results in immediates infarction
17
Q
Infarction:
Characteristics:
Venous
A
Venous obstruction is usually preceded by venous congestion and edema
18
Q
Infarction:
Characteristics:
Small vs. Large
A
obstruction of larger vessels generally affects more tissues
19
Q
Infarction:
Characteristics:
Tissue Affected
A
- Tissues with minimal anastomoses are more predisposed to infarction
- Tissues with parallel blood supplies with numerous anastomoses are relatively resistnant to infarction
- Tissues with dual blood supplies are relatively resistant to infarction
20
Q
Infarction:
Characteristics
A
Variable based on:
Duration of the occlusion
Status and vitality of the tissue prior to the infarct
21
Q
Infarction:
Morphology
A
- The appearance of an infarct depends mainly on the type of vessel occluded and the tissues affected
- white (anemic)
- Red (hemorrhagic)
- Other factors, such as age of the infarct, also affect appearance
- Most infarcts are red soon after occurrence due to hemorrhage into the damged tissue
- As healing occurs infarcts become pale, contracted scars
22
Q
White Infarcts:
Morphology
A
- These 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 generally a red zone of hemorrhage, and later inflammation that surrounds the necrotic tissue
23
Q
Red infarcts:
Morphology
A
- These occur in a variety of situations:
- venouse stasis (congestion) or obstruction
- Arterial obstruction in loose tissues
- Tissues with dual blood supply or extensive anastomoses
- Reperfuced necrotic tissues
*
24
Q
Infarct:
Significance
A
- Clinical significance of infarction depends on its location and size
- infarcts involving vital organs can be serious
- brain, heart
- Infarcts in non-vital tissues or tissues with large functional reserves are better tolerated
- spleen, kidney
- infarcts involving vital organs can be serious
25
Alterations in Blood Flow:
Shock
Is a circulatory dyshomeostasis where the circulating blood volume and the volume of the circulatory system htat needs to be filled are disproportionate
There may be loss of circulating blooe volume, reduced cardiac output, or inappropriate peripheral vascular resistance
Failure of the circulatory system leads to widespread tissue hypoxia and altered metabolism due to decreased delivery of nutrients and removal of waste products
26
Shock:
Types
* Cardiogenic
* reduced cardiac output most commonly die to cardiac disease
* Hypovolemic
* decreased blood volume due to blood or fluid loss
* Peripheral Pooling
* decreased peripheral resistance due to vasomotor dysfunction
27
Cardiogenic Shock
* Blood flow to tissues is reduced due to failure of the central pump
* Predisposing problems include:
* myocardial infarction
* Myocardial arrhythmia
* Pulmonary embolism
* Cardiomyopathy
* tThere is a decrease in both stroke volume and cardiac output
* Compensatory mechanisms attempt to increase stroke volume, contractility, heart rate, and total output
* the success of compensation depends of the nature of hte cardiac problem
28
Hypovolemic Shock
* There is not enough blood withing the circulation
* Predisposing factors include fluid loss due to :
* severe hemorrhage
* Vomiting
* Diarrhea
* Burns
* THere is decreased vascular pressure, and decreased tissue perfusion
* Compensation included 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
29
Blood maldistribution
* Decreased peripheral resistance results in pooling of blood in peripheral tissues
* this is caused by neural or cytokine-induced systemic vasodilation
* More capillary beds are open than can be filled
* Blood volume is normal, but the amount of vasculater needing filled is increased
* There are three categories of blood maldistribution
* Anaphylactic shock
* Neurogenic shock
* Septic shock
30
Anaphylactic Shock
* This is a generalized Type 1 Hypersensitivity:
* Mast cell degranulation results in systemic release of histamine and other vasoactive mediators
* Systemic vasodilation and increased permeability results in decreased vascular pressure and tissue hypofusion
* Causes include:
* Allergens
* Drugs and vaccines
31
Neurogenic Shock
* Autonomic nervous discharges results in peripheral vasodilation
* cytokines do not mediate this
* Caused by:
* trauma
* Electrocution
* Fear or distress
32
Septic Shock
* Excessive release of vasoactive and pro-inflammatory mediators results in systemic vasodilation
* THis is the most common type of blood maldistribution syndrome
* Bacterial/fungal products are the most common cause:
* Endotoxin (LPS)
* Peptidoglycans
* Lipoteichoic acid
33
Septic Shock:
LPS Activates
* Cells
* cell acivation includes interactions of LPS-binding protein, CD14 and Toll-like receptor-4
* Protein pathways(complement)
* Endothelial activation results in decreased production of anticoagulant substances
34
Septic Shock:
Effects of LPS
* Activation of Facotr XIIa-related pathways
* intrinsic coagulation, kinnis, fibrinolysis,
* Activation of complement pathways
* C3a and C5a
* Decreased endothelial production of anticoagulants and enhanced expression of leukocyte adhesion molecules
* TNF and IL-1 released by leukocytes
* secondary effects of TNF and IL-1 include activation of extrinsic coagulation, PAF release, Endothelial activation, production of arachidonic acid products
35
Shock: Pathogenesis
Shock can be divided into 3 stages
1. Compensation
2. Progressive stage
3. Irreversible stage
36
Shock:
Compensation
* Reflex mechanisms are activated to maintain adequate circulating blood volume and pressure
* heart rate increased
* Peripheral vasoconstriction
* ADH and angiotensin II released 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
37
Shock:
Progression
* Compesatory mechanisms are inadequate and tissue hypoperfusion occurs
* metabolism shifts to anaerobic
* cellular and systemic acidosis
* Host mediators accumulate and other inflammatory/coagulant substances
* Peripheral vasoconstriction gives way to vasodilation as loval hypoxia occurs
* blood pools and stagnates in the capillary beds
38
Shock:
Irreversible
* Hypoperfusion, tissue hypoxia and hemodynamic dysfunction results in irreversible cell damage
* cell energy stores are depleted
* Cell membranes deteriorate
* There is systemic activation of platelets and coagulation factors
* DIC
* Multiple organ fialure occurs
* failure of one system contributes to failure of another
39
Shock:
Morphology
* The changes observed with shock depend on its underlying cause and stage
* hemorrhage and edema
* microthrombosis
* Necrosis
* Major tissues affected include:
* heart, lungs, liver, kidneys, brain, intestines, adrenal glands and pancreas
40
Shock:
Significance
* Shock can be rapidly progressive and life-threatening
* rapid and aggresive therapy is needed ot prevent progression
* Clinical Features include:
* Hypotension and weak pulse
* Tachycardia and hyperventilation
* Cool extremities and cyanosis
* In later stages, multi-system organ failure
