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+ presentHR gt 90RR gt 20 -or- PaCO2 lt 32T lt 36 -or- gt 38leuk- WBC lt 4k -or- gt 12k- OR gt 10% immature neutrophilsin high risk pts that can’t be explained by other causes

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3
Q

SIRSinsult → pathophysiology x4

A

peripheral vasodilationcapillary permeabilitymicrovascular clottingcellular activation

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4
Q

what is shock?

A

broad categoryinitiated 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 shockcompensatory mechanisms: moderately effectivecause:- rapidly corrected = minimal residual effects- not corrected → uncompensated

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6
Q

what is MODS? x3

A

uncompensated shock worsens → MODSinvolves 2+ organ systems (that weren’t previously failing)altered organ function in acutely ill patientsorgan system homeostasis cannot be achieved without interventioncompensatory 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 emptyingend 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 arteriescauses ↓ ventricular emptying → obstructive shock

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16
Q

cardiogenic shock is

A

occurs when heart fails as a pump↓ contractility → ↓ SVwhich 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 toneresults: 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 mediatorsresults: 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 SHOCKmust 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 mediatorsto injured area

26
Q

inflammatory response: goal of microvascular permeability

A

increase availability of - nutrients- cells- mediatorsto 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

neutrophilsmacrophagesmast cellsendothelial cellsplatelets

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 mediatorsinflammatory cellsplasma protein systems