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7320 > Sepsis > Flashcards

Sepsis Flashcards

1
Q

SIRS

A

systemic inflammatory response syndrome

  • when normal inflam response goes out of control
  • can magnify and self-perpetuate, and not be local, instead effect whole body
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2
Q

2013 SIRS clinical criteria

A
  1. Temp > 39 or < 36
  2. HR > 90
  3. RR > 20 or PaCO2 < 32
  4. WBC > 12,000 or < 4000 or > 10% band cells
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3
Q

sepsis 2016 and 2013

A

life-threatening organ dysfunction caused by dysregulated host response to infection

SIRS + suspected or confirmed infection

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4
Q

Septic shock 2016 and 2013

A

2016- subset of sepsis in which circulatory, cellular and metabolic alterations are associated with a higher mortality rate than sepsis alone

2013- sepsis induced hypotension (SBP < 90 or MAP < 70) persisting despite adequate fluid replacement

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5
Q

MODS

A

Multiple organ dysfunction syndrome

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6
Q

what does dysregulated mean?

A

having an excessive inflam response to infection
- normal response gets out of control and exerts its effects systemically. The response disrupts normal physiology and often results in organ dysfunction

  • life threatening organ dysfunction caused by dysregulated host response to infection
  • response to whole body
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7
Q

septic shock

A

subset of sepsis “circulatory, cellular and metabolic alterations are associated with a higher mortality rate than sepsis alone.

-sepsis with hypotension despite fluids and lactate > or = to 2.o and need vasopressors to keep MAP >65

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8
Q

MODS

A

sepsis and shock can = MODS

  • can occur when noninfectious processes trigger dysregulated host response (SIRS in association with pancreatitis can lead to MODS)
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9
Q

what is VIPP

A

Normal Local inflam response

  • vascular response
  • immune response
  • platelets
  • plasma/protein response
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10
Q

4 main responses in normal inflam response

A
  • platelets
  • immune
  • vascular
  • plasma protein cascades
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11
Q

immune response in normal inflam response incluse

A
  • monocytes/macrophages and neutrophils

- antibodies and antigens

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12
Q

in acute inflam response, vascular response include

A

vasodilation and increased cap permeability

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13
Q

neutrophils can…

A
  • form the first wave of an acute inflam response
  • engage in phagocytosis
  • can leave the vascular space (extravasion)
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14
Q

monocytes

A

become macrophages when they leave vascular space

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15
Q

mast cells

A

release histamine when they degranulate

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16
Q

cytokines

A

are chemical messengers or mediators

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17
Q

cytokines are released and trigger arachidonic acid, coagulation, kinin and complement cascades

A

True

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18
Q

Arachidonis acid pathways more prominent effects are

A

vasodilation, increased permeability and pain

19
Q

effects of leukotrienes produced by one AA pathway include?

A

bronchospasm

20
Q

main effects of prostaglandins

A

vasodilation and increased capillary permeability

21
Q

AA pathway reflects what of the determinants of CO

A

decreased preload, decreased afterload and decreased contractility

22
Q

Bradykinin is?

A
  • part of the kinin cascade
  • is a potent vasodilator
  • creates increased capillary permeability
  • stimulates the arachidonic acid pathway
23
Q

bradykinin impacts what determianent of CO

A
  • decreased preload and afterload
24
Q

systemic effects of bradykinin include?

A
  • profound vasodilation, increased capillary permeability
  • amplification of the AA pathway effects
  • loss of preload and hypotension
25
Q

what is included in normal coag process

A
  • intrinsic pathway is triggered by proenzymes (Hagerman factor)
  • Extrinsic pathway is triggered by tissue factor released by injury
  • thrombin converts fibrinogen to fibrin in the common pathway
  • platelets aggregate at injury and join with fibrin mesh form clot
26
Q

In sepsis (and in SIRS), which of the following occurs in the coagulation system

A
  • microemboli result in maldistribution of blood flow and lack of adequate cellular oxygenation
  • the procoagulant pathways are sustained while fibrinolytic pathways fail
  • widespread microemboli form in systemic circulation impeding blood flow
27
Q

complement cascade acts through three pathways to?

A
  • activate formation of membrane attack complex and cell lysis
  • enhance phagocytosis
  • promote chemotaxis
28
Q

the systemic effects if the cell-derived and plasma-derived inflam cascades during sepsis (and SIRS) include

A
  • vasodilate and increased cap permeability
  • widespread clotting in the microvasculature and maldistribution of blood flow
  • decreased cellular oxygenation and oxygen supply and demand imbalance
29
Q

qSOFA

A

quick sequential organ failure assessment

score of > or = 2 should prompt clinicians to further assess

30
Q

qSOFA screening

A

RR > or = 22
altered mentation GCS < 15
systolic hypotension < or = 100

31
Q

How does the Arachidonic Acid path effect O2 sup and dem?

A

Prostaglandins:
- vasodilates. Decreases Afterload (BP, MAP, wide PP, low diastolic, strong pedal pulse

  • Increases Permeability: decreased Preload (leaky capillaries, fluid shift, third spacing, edema) = decreased CO. Fluid shift in lungs = vent and gas exchange issues

Thromboxane: Promotes platelet aggregation to stop bleeding. But making microclots everywhere = decreased EOP to many places

= organ dysfunction, pro inflammatory
= MODS

32
Q

How does the Bradykinin path effect O2 sup and dem?

A

Potent vasodilator (Mast cells): (wide PP, low DBP, strong pulses, MAP

Mast cells: also stimulate AA as well

= decreased Preload and Afterload
vent/gas exchange issues

+ MODS

33
Q

How does the coagulation path effect O2 sup and dem?

A

Microemboli: Low plt, low Hgb, coag abnormalities

fibrin to fibrinogen to make clots, but disrupts plasminogen to plasmin and inhibits break down of clots.

= impedes blood flow = decreased O2 supply and creates organ dysfunction

= MODS

34
Q

How does the compliment path effect O2 sup and dem?

A
  • intensifies inflammation effects in other systems (increased vasodilation and permeability),
  • damages the endothelium,
  • cellular adhesion and
  • cell death (phagocytosis of good and bad cells)

= MODS

35
Q

what part of sepsis effects contractility?

A

MDF- myocardial depressant factor triggered by - from ischemic pancreas

  • cytokines, prostanoids, nitric oxide…
36
Q

cardiogenic shock pre, AL, contract

A

P- increased
AL- increased (SNS and RAAS)
cont- decreased

37
Q

hypovolemic shock Pre, AL, cont?

A

P- decreased
AL- increased (SNS and RAAS)
cont- decreased (preload)

38
Q

Sepsis (early)

Pre, AL, cont?

A

P- decreased
AL- decreased (SNS and RAAS overdriven)
cont- decreased (MDF and preload)

39
Q

EOP of Sepsis CVS, RESP, GI, GU, HEME, Hepatic, Global

A

CVS- GCS, decreased LOc, confusion

RESP- PaO2/FiO2 ratio, tachy, increased WOB, hypoxemia, mech vent?, RR

GI- absent BS, decreased gastric resid, N/V

GU- low urine O/P, increased BUN/ CR

HEME- low, Hgb, thrombocytopenia, decresed clotting factors, decreased plt

Hepatic: abnorm LFTs, jaundice

Global: lactate, metabolic acidosis, decreased ScVO2

40
Q

1 hour bundle

A
  1. measure the lactate level
  2. obtain blood cultures before admin ABX
  3. begin broad spectrum ABX
  4. begin rapid admin crystalloids (unless low HGB) 30ml/kg for hypotension OR lactate >/= 4
  5. apply vasopressors if hypotensive during or after fluid resuscitation to mntn MAP >/= 65
41
Q

If you gave fluids to increase preload, what do you do next?

A
  • check MAP. If < 65 still then reassess Preload (CVP, POCUS, passive leg raise, ScvO2)
  • Adequate Preload - give vasopressor Levophed (increases Afterload)
  • Inadequate Preload - adequate perfusion/MAP? no: decreased O2 demand. Then give Inotrope to increase contractility (Dobutamine)–> based on last ScvO2 and Lactate >4
42
Q

what do you do before 1 hr bundle?

A

Check qSOFA. IF > 2 OR lactate > 4 then start bundle.

43
Q

ABCD of Sepsis Treatment:

A

A: Airway and Antibiotics (fast and fitted)
B: breathing
A+B = improve vent and gas exchange (mech vent, increase PEEP, position

C: cardiac output

  • Preload- fluids (CVP 8-12)
  • Afterload- MAP > 65 : Vasopressor (Levo)
  • Contract- If ScvO2 < 70 Inotropes (Dobutamine)

D: decrease demand, drugs, dinner

7320 (8 decks)

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