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Shock States Flashcards

1
Q

what is SIRS?

A

unchecked out of control systemic response of inflammatory/immune system

  • warning sign of what is to come
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2
Q

SIRS criteria

A

diagnosis: 2+ present

HR gt 90
RR gt 20 -or- PaCO2 lt 32
T lt 36 -or- gt 38
leuk
- WBC lt 4k -or- gt 12k
- OR gt 10% immature neutrophils

in high risk pts that can’t be explained by other causes

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3
Q

SIRS

insult → pathophysiology x4

A

peripheral vasodilation

capillary permeability

microvascular clotting

cellular activation

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4
Q

what is shock?

A

broad category

initiated by insult → inadequate tissue perfusion comp to cell metabo reqs → cellular hypoxia + end organ dysfxn

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5
Q

what is compensated shock?

A

relatively stable may see early s/s shock

compensatory mechanisms: moderately effective

cause:
- rapidly corrected = minimal residual effects

  • not corrected → uncompensated
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6
Q

what is MODS? x3

A

uncompensated shock worsens → MODS

involves 2+ organ systems (that weren’t previously failing)

altered organ function in acutely ill patients

organ system homeostasis cannot be achieved without intervention

compensatory mechanisms from compensated shock NO LONGER ADEQUATE

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7
Q

geriatric population & shock

A
  • progression rapid
  • reduced compensatory mechanisms
  • pre-existing comorbs (renal failure, lung disease, cardiomyopathy) INTERVENE STATE
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8
Q

present in every type of shock

A

inadequate tissue perfsuion & cellular hypoxia

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9
Q

hemodynamic goals of therapy for shock x7

A
  • MAP gt 60
  • CVP 8-12
  • CI gt 2.1
  • UOP gt 0.5 mg/kg/hr
  • SaO2 gt 92%
  • SVO2 gt 70
  • serum lactate lt 2 mmol/L
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10
Q

hypovolemic shock causes

A
  • ABL/ongoing hemorrhage
  • non-hemorrhage fluid depletion
    • GI (v/d)
    • burns
    • polyuria
    • aggressive pharm diuresis
    • insensible losses
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11
Q

can lose how much via insensible losses + how?

A

1L/day; diaphoresis, open burn wounds, vents

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12
Q

hypovolemic shock is

A

loss or redistribution of volume

… (blood, plasma, or other body fluids) which result in decreased intravascular volume

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13
Q

obstructive shock is

A

mechanical obstruction impacting the cardiovascular system
… that decreases ventricular filling and/or emptying

end result: ↓ CO, tissue perfusion, O2 delivery

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14
Q

obstructive shock causes

A

↓ ventricular filling =

  • cardiac tamponade
  • tension pneumothorax
  • vena cava compression/thrombus
  • atrial mass or thrombus

↓ ventricular emptying
- PE (saddle embolism = sitting across either/both arteries)

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15
Q

saddle embolism is

A

thrombus sitting across either/both arteries

causes ↓ ventricular emptying → obstructive shock

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16
Q

cardiogenic shock is

A

occurs when heart fails as a pump

↓ contractility → ↓ SV

which leads to ↓ CO, BP → ↓ tissue perfusion

17
Q

cardiogenic shock causes

A

MI !!!!!!!!

HFrEF exacerbation (ischemic v nonischemic)

dysrhythmias (poor O2 at first, can exacerbate cardiogenic shock states)

LV outflow tract obstruction (hypertrophic obstructive cardiomyopathy, muscle/tumor overgrowth is pretty uncommon)

18
Q

1 cause of cardiogenic shock

A

MI

19
Q

neurogenic shock is…

A

typically results from SCI w damaged symp pathways, usually seen in injuries T6 or higher

  • higher injury = greater symptoms
  • common in trauma or neuro patients

↓ symp of organs distal to injury = stimulated by PS tone

results: bradycardia, massive vasodilation, inability to regulate body temp (hypothermia)

EASIEST SHOCK TO SPOT

20
Q

anaphylactic shock is…

A

life threatening allergic reaction resulting in IgE mediated response or mast cell (non-IgE degranulation)

  • occurs following reexposure to specific antigen
  • immediate response causing release of histamines, prostaglandins, vasoactive mediators

results: massive vasodilation, capillary permeability, constriction of non-vascular smooth muscle (RESPIRATORY!!)
triggers: drugs, foods, other (see lecture)

s/s: see lecture

21
Q

*SEPSIS *

A

SIRS likely s/t infection; positive cultures add to validity but not required

22
Q

SEVERE SEPSIS

A

sepsis + at least 1 sign of hypoperfusion or organ dysfunction (new, not explained by other etiology)

23
Q

SEPTIC SHOCK

must know definition + pathophys/results

A

severe sepsis associated with refractory hypotension (BP lt 90/60) despite adequate fluid resus and/or serum lactate gt 4.0

release: endotoxins trigger overzealous release of inflammatory mediators (cytokines, interleukins, tumor necrosis factor, complement system)

results: systemic vasodilation, widespread endothelial injury, activation of coagulation cascade

24
Q

septic shock pathophys + results

A

release: endotoxins trigger overzealous release of inflammatory mediators (cytokines, interleukins, tumor necrosis factor, complement system)
results: systemic vasodilation, widespread endothelial injury, activation of coagulation cascade

25
Q

inflammatory response: goal of vasodilation

A

increase availability of

  • nutrients (O2, glucose)
  • neutrophils, macrophages, and their mediators

to injured area

26
Q

inflammatory response: goal of microvascular permeability

A

increase availability of

  • nutrients
  • cells
  • mediators

to injured area

27
Q

inflammatory response: goal of coagulation

A
  • minimize blood loss

- wall off injury

28
Q

inflammatory response: goal of cellular activation

A

WBCs –>

  • phagocytosis foreign debris + cells
  • wound microdebridement
29
Q

SIRS mediators: inflammatory cells

A 
neutrophils
macrophages
mast cells
endothelial cells
platelets
30
Q

SIRS mediators: biochemical mediators

A
  • tumor necrosis factor (TNF)
  • interleukins
  • platelet activating factor
  • arachidonic acid metabolites prostaglandins, leukotrienes, thromboxanes
  • toxic oxygen radicals
  • proteases
31
Q

SIRS mediators: plasma protein systems

A
  • complement system
  • kinin
  • coagulation
  • fibrinolysis
32
Q

organ dysfunction and SIRS

A

ORGAN DYSFUNCTION STARTS EARLY

33
Q

SIRS mediators x3

A

biochemical mediators
inflammatory cells
plasma protein systems

x 6113 (6 decks)

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