shock Flashcards

1
Q

define shock

A

failure of the circulatory system to adequately perfuse vital organs

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2
Q

describe what happens to tissues during shock

A

tissue perfusion and oxygen delivery are insufficient to meet the basal metabolic demands of tissues

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3
Q

what is characterized by shock?

A

low blood flow that is usually accompanied by low blood pressure (hypotension)

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4
Q

what is compensated shock?

A

compensatory mechanism that may maintain viability of vital organs and sustain the life of the patient

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5
Q

what is uncompensated shock?

A

ensues where progressive circulatory collapse leads to increasingly severe disruption of critical cellular metabolic pathways and death

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6
Q

what is the primary goal of therapy for shock?

A

rapid restoration of systemic blood flow by replacement of intravascular fluid and the use of drugs that increase vascular tone and support cardiac function

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7
Q

how is shock initiated?

A

anything that severely and usually relatively suddenly decreases cardiac output, blood volume, and/or peripheral vascular resistance

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8
Q

what is the cause of cardiogenic shock?

A

by insults that negatively affect cardiac output (inhibit the heart’s ability to pump blood)

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9
Q

what is the the formula for anything affecting heart rate or contractility can decrease cardiac output or cardiogenic shock?

A

Cardiac output = heart rate x stroke volume

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10
Q

what might occur with myocardial degeneration?

A

vitamin E/selenium deficiency in pigs (mulberry heart disease), monensin toxicity in horses, or myocardial infarcts (which occur much more commonly in humans than in domestic animals), can cause heart failure and cardiogenic shock

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11
Q

what are infarcts

A

areas where the blood supply has been compromised

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12
Q

how does cardiac tamponade cause acute heart failure resulting cardiogenic shock?

A

fluid (usually blood) accumulates rapidly in the pericardial space and impinges on the ability of the cardiac ventricles to dilate and fill with blood

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13
Q

what is an example of electrolyte imbalances that negatively affect heart rate leading to heart failure and cardiogenic shock?

A

hyperkalemia in uremic animals

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14
Q

what is hypovolemic shock caused by?

A

sudden severe loss of blood volume

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15
Q

what are the causes of hypovolemic shock?

A
  • acute hemorrhage involving loss of greater than 1/4 to 1/3 of total blood volume. The blood may be lost externally or into internal spaces such as the peritoneal cavity or the alimentary tract.
  • loss of fluid (intravascular and extravascular), which may occur with water deprivation, vomiting, diarrhea, etc.
  • increased vascular permeability leading to loss of intravascular fluid, proteins, and sometimes blood cells
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16
Q

what injures the vessels when there is increased vascular permeability? specific examples?

A

infections, toxicities, and immune reactions that injure vessels

Specific examples include equine viral arteritis, African swine fever, hog cholera, and the hemorrhagic fevers (e.g., simian hemorrhagic fever, Ebola virus infection)

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17
Q

what causes distributive (or vasogenic) shock?

A

sudden severe decrease in peripheral vascular resistance that causes extensive pooling of blood within the venous system and subsequent decreased venous return to the heart.

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18
Q

what is the cause of septic shock?

A

bacterial infection (localized or systemic) in which large quantities of endotoxin are released into circulation

19
Q

what are endotoxins?

A

complex components of the cell wall of gram-negative bacteria and then can really do a number on the body, and especially on the vasculature

20
Q

why are endotoxins sometimes called lipopolysaccharide?

A

most toxic part of the complex is this type of molecule

21
Q

what is the pathogenesis of endotoxic/septic shock?

A

Endotoxin binds to serum protein → resulting complex binds to macrophage/monocyte → TNFα secreted into circulation → marked capillary dilation → severe pooling of venocapillary blood → decreased cardiac venous return and cardiovascular collapse

22
Q

what is the pathogenesis of anaphylactic shock?

A

Exposure to allergens → activation of mast cells or other effector cells → massive release of histamine and other chemical mediators
→ marked venocapillary dilation

23
Q

what is anaphylactic shock?

A

systemic manifestation of an acute hypersensitivity (allergic) response

24
Q

how does the idiosyncratic reaction of anaphylactic shock occur?

A

predisposed individuals upon exposure to certain antigens (substances, usually proteins, to which the individual is allergic) such as insect stings, foods, medicines, etc.

25
Q

upon exposure to allergens, histamine and other chemicals are released from what cells?

A

mast

26
Q

what is the result of histamine binding to receptors?

A

vasodilation and increased vascular permeability with loss of intravascular fluid

27
Q

how can neurogenic shock happen?

A

severe trauma, severe pain, or occasionally following restraint.

28
Q

what is the pathogenesis of neurogenic shock?

A

massive autonomic nervous system discharge which disrupts vasomotor control and there is extensive venocapillary pooling of blood so it doesn’t get moved to vital organs

29
Q

true or false: the consequence of shock is that oxygen doesn’t get to cells

A

true

30
Q

what does anoxic injury to endothelial cells lead to?

A

increased vascular permeability and further loss of intravascular fluid, aggravating the hypovolemia and anoxia

31
Q

what is the result of insufficient renal and muscular perfusion?

A

metabolic acidosis, which further suppresses cardiac output

32
Q

what does insufficient myocardial perfusion cause?

A

anoxic injury to myocytes, further decreasing cardiac output.

33
Q

how does the body respond to shock?

A

by attempting to increase cardiac output and by shunting blood flow to vital organs such as brain, heart and kidneys and away from tissues such as the gastrointestinal tract, skeletal muscle, and skin

34
Q

how does the secretion of norepinephrine and epinephrine by the adrenal medulla support cardiac function?

A

increases heart rate.

35
Q

how does the production of aldosterone by the adrenal cortex support cardiac function?

A

stimulates retention of sodium and water, thus increasing blood volume

36
Q

how does the secretion of norepinephrine and epinephrine by the adrenal medulla support vascular changes?

A

stimulates vasoconstriction

37
Q

how does the renin-angiostensin system support vascular changes?

A

results in the eventual production of angiotensin II, which is a potent vasoconstrictor

38
Q

the lesions of shock are of what?

A

a. the various initiating causes (e.g., hemorrhages, burns, cardiac tampanode, etc.)
b. changes that reflect edema and venocapillary pooling of blood
c. degenerative changes in tissues subjected to anoxia.

39
Q

lesions of shock will cause severe organ congestion where?

A

liver, gastrointestinal tract, kidneys, and adrenal glands

40
Q

hemorrhage into the lumen of the GI tract follows congestion and anoxic necrosis of what?

A

superficial mucosa

41
Q

why is the lung considered a “shock organ”?

A

because of the frequent occurrence of severe edema, thrombosis, and degenerative changes associated with shock

42
Q

in horses, why is the large colon considered the shock organ?

A

because of the tremendous submucosal colonic edema that occurs with endotoxemia

43
Q

what type of response does shock elicit?

A

systemic

involving generalized cardiovascular collapse