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Patho Exam 4 > Shock > Flashcards

Shock Flashcards

1
Q

Shock

A

generalized inadequacy of blood flow throughout the body, to the extent the the tissues are damaged d/t inadequate cardiac output

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2
Q

Stages of Shock

A

Compensated
Progressive
Irreversible

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3
Q

Compensated Stage

A

Deficient perfusion; but not to the degree that CV system begins to deteriorate

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4
Q

Progressive

A

Circulatory system begins to deteriorate - cycle can end in death

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5
Q

Irreversible

A

All forms of therapy are inadequate to save the person’s life

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6
Q

Hypovolemic Shock

A

Loss of whole blood or plasma/Loss of ECF

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7
Q

Causes of hypovolemic shock

A

HEMORRHAGE
Severe hydration/burns
Excess loss of fluid by the kidneys
Adrenal insufficiency

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8
Q

S/Sx of hypovolemic shock

A 
Hypotension (know baseline) & Orthostatic hypotension
Decreased Urinary Output
Pale/clammy moist skin
Metabolic Alkalosis -->Metabolic Acidosis
Poor capillary refill
Anxiety/Impending Doom
Decreased pulse pressure
Brief Rise in BP/HR --> sustained low BP
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9
Q

Tx of Hypovolemic Shock

A

Replacement of Fluids:
Blood (whole/packed RBCs)
Dextran solutions/salt poor albumin (to increase plasma osmotic pressure=retains fluid in vascular spaces)
NS (restore volume
Lactated Ringers (correct metabolic acidosis)
Elevate legs to 45 degrees (NOT TRENDELENBURG)
Keep covered/ but not too warm

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10
Q

Neurogenic Shock

A

Normal amount of blood, but extensive dilation of the blood vessels d/t loss of sympathetic tone (SNS not constricting well)

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11
Q

Causes of Neurogenic Shock

A

Deep General/Spinal anesthesia
Brain damage
Spinal Cord Injury
Severe Hypoglycemia

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12
Q

FAINTING is NOT_______, but rather a massive ________ response

A

neurogenic shock

parasympathetic response

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13
Q

Anaphylactic Shock

A

Increase in size and permeability of the vascular bed (whole body is vasodilating)

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14
Q

Type I Anaphylactic Schock

A

BIG fluid shifts = hypersensitivity response releases vasodilating histamine and SRS-A which increases capillary permeability = huge fluid shifts into the tissues

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15
Q

Type I symptoms

A

Wheezing, sniffing, laryngeal edema, bronchial edema, suffocation

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16
Q

Treatment for Type I anaphylactic shock

A

**want BP to go back up
Epinephrine (increases vasoconstriction)
Corticosteriods (decreases capillary permeability/ stabalizes membranes)

17
Q

Septic Shock

A

gram - bacteria and their endotoxins
E.coli
Pseudomonas
Proteus

18
Q

Risk factors for septic shock

A

Age 65
DM, ETOH, Cancer, Liver, UTI
Cholecystitis - inflamed gallbladder
Ruptured Appendix

19
Q

SIRS (Systemic Inflammatory Response Syndrome) aka preseptic shock

A

Bacteria enter blood and are destroyed by macrophages, immune cells, and complement = Release endotoxins and Release chemical mediators
Vasodilation occurs and increases vascular permeability
**dangerous because this is occurring systemically

20
Q

Stages if Warm Septic Shock

A

Increased CO and low peripheral vascular resistance
Vasodilation effects histamine, bradykinins, and seratonin = making you look more flushed
Fluid shifts into tissues and 3rd spacing

Fever d/t pyrogens from WBCs

Profound diuresis= excessively urinating d/t dead bacteria and phagocytes/ waste products of cell metabolism

Increased Respiratory Rate

Activation of clotting - petechiae and mottling below knees (darkened appearance)

Decreased cerebral perfusion - endorphins released to help keep person comfortable

21
Q

Stages of Cold Septic Shock

A

Hypodynamic = decreased CO (6-72 hours after warm shock starts) DIC releases MDF from pancreas and endorphins depress myocardium

Subnormal body temp = cold clammy pail skiing

ABGs = hypoxemia/acidosis
ARDS = “wet lungs –>respiratory failure
ARF

22
Q

Tx of Septic Shock

A

IV fluids
Swan-Ganz monitoring - catheter inserted that measures pressure in L. Atrium and a good for measuring total circulating volume
Antibiotics
Steroids

23
Q

Why can death of bacteria make a person worse in septic shock

A

after tx with antibiotics the endotoxins are still released = will get worse before they actually get better

24
Q

What types of IV fluids do you give for septic shock

A 
NE = vasoconstriction
Dopamine = dilates splanchnic and renal vessels
25
Q

What are the 3 types of dopamine

A

Low / Renal = helps maintain blood flow to kidneys
Intermediate/ Cardiac =maintains/increases CO
High/Pressor = vasoconstricts and increases BP

26
Q

How do steroids tx septic shock

A

Stabilize capillary membrans = Decrease the release of myocardial depressant factor and decrease complement activation

27
Q

Why do we use Benadryl in septic shock

A

it’s an antihistamine/blocks histamine release

28
Q

Cardiogenic Shock Causes

A

Heart fails as a pump d/t decreased contractility (decreased coronary circulation, further myocardium damage, pump failure)
**Same event that occurs in late stages of other types of circulatory shock

29
Q

Tx of cardiogenic shock

A

Swan Ganz catheter
Inta-aortic balloon pump (takes over to help the heart pump)
Dopamine (increases CO) and Dobutamine

30
Q

What are some Complications of Shock

A

ARDS
ARF
GI problems
Disseminated Intravascular Coagulation (DIC)
Multiple Organ Dysfunction Syndrome (MODS)

31
Q

ARDS and shock

A

Lethal respiratory failure (>50% mortality)
develops 24-48 hours after injury
ABG: hypoxemia and hypercapnia (too much CO2)
V/Q mismatch

Though to result from: endothelial injury = leakage of fluid and plasma proteins into the interstitum/ alveolar spaces or abnormalities in production, composition, and function of surfactant

STIFF LUNGS AND HARD TO INFLATE

32
Q

ARF AND SHOCK

A

Late cause of death in severe shock; typically d/t septic shock or trauma
Degree of renal damage r/t severity and duration of shock
Damage of the tubules = necrosis (infrarenal) and may take months to restore

33
Q

When screening for ARF and shock what are some things you want to monitor

A

Urine output during shock

Serum creatinine and BUN

34
Q

GI Complications and Shock

A

GI = vulnerable to ischemia and decreased mucosal perfusion (d/t constriction of blood vessels that supply the GI tract)
Mucosal lesions in stomach
Bleeding from ulceration (2-10days)
Portal of entry for bacteria = leading to further sepsis and shock

35
Q

DIS and shock

A

Widespread activation of coagulation system (fibrin clot formation/occlusion of vessels) = ischemic damage and organ failure
Increased risk for bleeding d/t depletion of PLTs
***presence of DIC is an predictor of MORTALITY

36
Q

MODS and Shock

A

altered organ function = cannot maintain homeostasis
Common organs = kidneys, lungs, liver, brain, and heart
MOST FREQUENT CAUSE OF DEATH IN NON CORONARY ICUs

37
Q

Risk factors for the development of MODS

A

sepsis, shock, prolonged periods of Hypotension, hepatic dysfunction trauma, infarcted bowel, advanced age, and ETOH

Patho Exam 4 (7 decks)

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