Ischemia + Shock Flashcards
(22 cards)
Heart + Baroreceptors + Brain
heart provides driving pressure
baroreceptors to signal medulla in brain
sympathethic + parasympathetic output balanced
blood pressure maintained
additionally = sodium + water vol. control within body
Variable Blood Distribution
blood flow needs to change with conditions = role of beta2 + alpha receptors
more flow to lungs, GIT, kidney + liver
large fraction of blood volume in venous system
Altered Blood Flow
increased inflow = hyperemia
decreased outflow = congestion
Hyperemia
increased inflow
stimuli = increased conc. of CO2, acids + other metabolites
ex = GIT after meal, tissue injury
Ischemia
altered tissue perfusion
inadequate perfusion of tissue, leading to metabolic insufficiencies
causes:
- local congestion
- local vascular obstruction
- decreased cardiac output
- prolonged art. vasoconstriction
many factors influence consequences
Consequences of Ischemia
brief ischemia -> possibly no major effect
protracted ischemia or sensitive tissue -> infarction
many factors influence outcome of infarction (similar to ischemia)
Infarction
gross appearance:
- dark red -> particularly at first
- may become pale with time
aftermath:
- inflammation
- followed by new BV formation + healing tissue
- dead tissue eventuallly replaced with fibrosis (scar tissue)
Reperfusion Injury
counterintuitively, restoration of blood flow can also endanger tissue
interstitial edema can prevent local venous return
clot formation within tissue d/t capillary rupture
influx of O2 reacts with accumulated substances during hypoxia
- ROS are generated
- result in additional cell damage
Shock
CV collapse d/t dysfunction
general causes:
- loss of circ. blood vol.
- reduced cardiac output from any cause
- inappropriate vascular resistance
diverse causes which can be categorized
similar effects ensue = impaired tissue perfusion, cellular hypoxia, cell degeneration, cell death
if persistent, becomes irreversible, leading to organism death
Clinical Features of Shock
hypotension
weak pulse
tachycardia
hyperventilation w/ pulmonary rales
reduced urine output
hypothermia
organ + system failure in later stages
Morphologic Features of Shock
vascular deterioration
pulmonary changes
cell damage + necrosis
Types of Shock
cardiogenic -> includes obstructive
hypovolemic
blood maldistribution
- septic
- anaphylactic
- neurogenic
Cardiogenic Shock
failure of heart to adequately pump blood
- arrythmias
- dilated/hypertrophic cardiomyopathy
- obstruction of blood flow away from heart (aka obstructive shock)
compensation = stimuli to increase heart rate, contractility, stroke volume, total cardiac output
variable success of compensatory mechanisms
Hypovolemic Shock
substantial decrease in circ. blood volume
compensatory mechanisms:
- peripheral vasoconstriction
- fluid shift from interstitium into plasma
- activation of RAAS
Blood Maldistribution
decreased peripheral vascular resistance
causes = systemic neural or cytokine induced vasodilation
subdivisions:
- septic
- anaphylactic
- neurogenic
Septic Shock
inductin of excessive vascular + inflammatory mediators by bacterial/fungal components
most common = endotoxin, LPS complex of gram neg bacterial cell wall
Activation of:
- endothelium (switch to procoagulant+antifibrinolytic state)
- coagulation system
- inflammatory cells
- complement cascade
Advanced effects:
- profound systemic vasodilation, hypotension, tissue hypoperfusion
- will progress to death if uncorrected
- coagulation within vessels activated
- further mechanisms to exacerbate vasodilation + hypotension
Anaphylactic Shock
generalized/system Type I hypersensitivity reaction
Neurogenic Shock
autonomic discharges stimulate peripheral vasodilation
causes include:
- trauma (esp. to CNS)
- electrocution
- extreme fear
- severe emotional stress
Stages + Progression of Shock
nonprogressive stage
progressive stage
irreversible stage
Nonprogressive Shock
compensatory mechanisms can control decreased blood volume + pressure
vasoconstriction
fluid shifting + retention
net effect is to increase heart rate, cardiac output, blood pressure
Progressive Shock
occurs when compensatory mechanisms are insufficient
insufficient ATP production
arteriolar relation + dilation
cell necrosis
Irreversible Shock
generally, can’t ID exact shift form progressive to irreversible
widespread innappropriate vasodilation
multiple organ dynsfunction (MODS)
end point = disseminated intravascular coagulation (DIC)
