Perfusion Flashcards
What is hyperemia
Vasodilation
Where are the body’s main baroreceptors and what do they do
Aortic arch, carotid sinus
Signal medulla to balance SNS/PSNS control of blood pressure
Which receptors regulate blood volume and pressue
Left atrial volume receptors
Osmoreceptors in hypothalamus
Signal ADH release/RAA
Which organs receive more blood than neccessary for their metabolic needs and why
Organs that recondition blood:
- Lungs (oxygenate blood)
- GI (nutrient processing)
- Kidneys (remove waste, balance electrolytes)
Where are B2 receptors most prevalent
Cardiac and skeletal muscle
Are alpha receptors present in brain
No!
What is congestion
Decreased outflow of blood causing passive engorgement of vascular bed
What physiological processes cause hyperemia
Heat dissipation
Increased metabolic activity in GI after meal
Whats the main pathological cause of hyperemia
Inflammation (due to prostaglandins, histamine)
Where does acute passive venous congestion occur
Liver and lungs —> heart failure
Spleen –> euthanasia (smooth muscle relaxation and dilation of vasculature)
How would liver appear in acute passive venous congestion
Dark, engorged. Due to blood being unable to return to heart, so it engorges in liver
Right sided heart failure
Pulmonary congestion is caused by
Left sided heart failure
Hepatic congestion is caused by
Right sided heart failure
What causes chronic passive congestion
Obstruction of venous outflow from:
1) neoplastic mass
2) inflammatory mass
3) organ displacement
4) fibrosis of healed injury
The liver appears nutmeg colored. Whats happening
Chronic congestion due to fibrosis
Portal hypertension causes
Ascites, hydroperitoneum
The liver is dark red. Whats going on
Acute congestion (due to right sided heart failure)
The lungs are yellow-brown, firm. Whats going on
Chronic congestion. Due to macrophage induce fibroplasia. They contain iron so it makes lungs appear yellow
Pulmonary hypertension causes
Pleural effusion
Pulmonary edema
The kidney appears red, swollen and theres a bulge in the capsule. Whats likely happening
Vessel occlusion resulting in acute infarction
What causes venous infarction
Congestion due to volvulus, twisting of organs etc
Which organs are most sensitive to oxygen deprivation
Heart and brain
Which organs are less susceptible to oxygen deprivation
Lungs
GI
Kidneys
Skin
Pathogenesis of reperfusion injury (5)
1) During prolonged ischemia, ATP is degraded to Adenosine (potent vasodilator)
2) When blood returns, fluid moves into interstitium
3) High pressure leads to compression of veins, inhibiting blood return
4) Blood vessels hemorrahge
5) TF released —> secondary hemostasis
You can ALSO get release of reactive oxygen species from ATP breakdown. These damage cells.
Whats a tan infarct
More chronic infaction. Cells swell and tissue becoming necrotic – lysing of RBCs
Are cellular effects of shock reversible?
Initially
Persistent shock leads to irreversible damage to cells and tissues
CV collapse leads to
- Decreased volume
- Reduced CO
- Hypotension (reduced peripheral resistance)
4 things that hypotension elads to
1) Hypoperfusion
2) Cellular hyoxia
3) Anaerobic metabolism
4) Cellular degeneration/death
Types of shock
Cardiogenic
Hypovolemia
Blood maldistribution
Types of blood maldistribution shock
Anaphylactic shock
Neurogenic shcok
Septic shock
What is blood maldistribution shock
Pooling of blood in peripheral circulation due to neural or cytokine mediated vasodilation
Pathogenesis of anaphylactic shock
1) Exposure of antigen to sensitized mast cells
2) Degranulation –> release of histamine and other vasoactive mediators
- ———> vasodilation, pooling of blood, hypotension, hypoperfusion
3) Increased vascular permeability
- —> hypotension, hypoperfusion, leaking of fluid into interstitium or lung alveoli
4) Smooth muscle contraction —> constricts broncioles, difficult breathing
Pathogenesis of neurogenic shock
Electroshock —> lightening strike, emotional distress
1) Autonomic discharge, causing vasodilation
2) Venous pooling
- —> hypotension, tissue hypoperfusion
Pathogenesis of septic shock
1) Exposure to infectious pathogens (endotoxin, proteoglycans etc)
2) Leukocytes and endothelium activated
3) Macs release IL-1, TNF
A) activate platelet activating factor
B) activate nitric oxide –> vasodilation
C) neutrophil migration to tissues
4) Endothelium release anti-coagulants
- –> activates contact pathway of coagulation
What is involved in non-progressive shock
Barorecptors: E/NE release
—> Increased CO, increased BP
Left atrial volume and hypothalamic osmoreceptors RAAS, ADH
—> increased blood volume and CO
Vasoconstriction (endothelin)
Shift of fluid from interstitium to plasma
What is progressive shcok
Damage to heart results in decreased CO, blood pooling, tissue hypoperfusion
Mechanism of progressive shock
1) Lack of perfusion, lack of oxygen in tissues
2) Metabolism switches to anerobic
3) Decreased ATP, acidosis
4) Metabolic waste leads to increased osmolality, local hypoxia, increased CO2
5) Cell death, releasse of systemic cytokines
- –> inflammation, coagulation, fibrinolysis
Mechanism of irreversible shock
Anerobic metabolism inhibits cellular enzymes for energy
Vasodilatory substances accumulate, override compensatory mechanisms
Further drop in BP
MULTIORGAN FAILURE
Morphological changes of shcok
o Generalized congestion, pooling of blood (liver, intestine) o Edema (lung) o Hemorrhage (petechial and ecchymotic) o Microthrombosis o Centrilobular hepatic necrosis o Renal tubular necrosis o Intestinal mucosal necrosis o Myocardial fiber degeneration
Morphological changes of shcok
o Generalized congestion, pooling of blood (liver, intestine) o Edema (lung) o Hemorrhage (petechial and ecchymotic) o Microthrombosis o Centrilobular hepatic necrosis o Renal tubular necrosis o Intestinal mucosal necrosis o Myocardial fiber degeneration o Cerebral edema and ischema (necrosis)
