Ischemia + Shock

Question 1

Heart + Baroreceptors + Brain

Answer 1

heart provides driving pressure

baroreceptors to signal medulla in brain

sympathethic + parasympathetic output balanced

blood pressure maintained

additionally = sodium + water vol. control within body

Question 2

Variable Blood Distribution

Answer 2

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

Question 3

Altered Blood Flow

Answer 3

increased inflow = hyperemia

decreased outflow = congestion

Question 4

Hyperemia

increased inflow

Answer 4

stimuli = increased conc. of CO2, acids + other metabolites

ex = GIT after meal, tissue injury

Question 5

Ischemia

altered tissue perfusion

Answer 5

inadequate perfusion of tissue, leading to metabolic insufficiencies

causes:
- local congestion
- local vascular obstruction
- decreased cardiac output
- prolonged art. vasoconstriction

many factors influence consequences

Question 6

Consequences of Ischemia

Answer 6

brief ischemia -> possibly no major effect

protracted ischemia or sensitive tissue -> infarction

many factors influence outcome of infarction (similar to ischemia)

Question 7

Infarction

Answer 7

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)

Question 8

Reperfusion Injury

Answer 8

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

Question 9

Shock

Answer 9

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

Question 10

Clinical Features of Shock

Answer 10

hypotension
weak pulse
tachycardia
hyperventilation w/ pulmonary rales
reduced urine output
hypothermia
organ + system failure in later stages

Question 11

Morphologic Features of Shock

Answer 11

vascular deterioration
pulmonary changes
cell damage + necrosis

Question 12

Types of Shock

Answer 12

cardiogenic -> includes obstructive

hypovolemic

blood maldistribution
- septic
- anaphylactic
- neurogenic

Question 13

Cardiogenic Shock

Answer 13

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

Question 14

Hypovolemic Shock

Answer 14

substantial decrease in circ. blood volume

compensatory mechanisms:
- peripheral vasoconstriction
- fluid shift from interstitium into plasma
- activation of RAAS

Question 15

Blood Maldistribution

Answer 15

decreased peripheral vascular resistance

causes = systemic neural or cytokine induced vasodilation

subdivisions:
- septic
- anaphylactic
- neurogenic

Question 16

Septic Shock

Answer 16

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

Question 17

Anaphylactic Shock

Answer 17

generalized/system Type I hypersensitivity reaction

Question 18

Neurogenic Shock

Answer 18

autonomic discharges stimulate peripheral vasodilation

causes include:
- trauma (esp. to CNS)
- electrocution
- extreme fear
- severe emotional stress

Question 19

Stages + Progression of Shock

Answer 19

nonprogressive stage
progressive stage
irreversible stage

Question 20

Nonprogressive Shock

Answer 20

compensatory mechanisms can control decreased blood volume + pressure

vasoconstriction

fluid shifting + retention

net effect is to increase heart rate, cardiac output, blood pressure

Question 21

Progressive Shock

Answer 21

occurs when compensatory mechanisms are insufficient

insufficient ATP production

arteriolar relation + dilation

cell necrosis

Question 22

Irreversible Shock

Answer 22

generally, can’t ID exact shift form progressive to irreversible

widespread innappropriate vasodilation

multiple organ dynsfunction (MODS)

end point = disseminated intravascular coagulation (DIC)