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7320 > Sepsis > Flashcards

Sepsis Flashcards

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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

Study These Flashcards
A

vasodilation, increased permeability and pain

19
Q

effects of leukotrienes produced by one AA pathway include?

20
Q

main effects of prostaglandins

Study These Flashcards
A

vasodilation and increased capillary permeability

21
Q

AA pathway reflects what of the determinants of CO

Study These Flashcards
A

decreased preload, decreased afterload and decreased contractility

22
Q

Bradykinin is?

Study These Flashcards
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

Study These Flashcards
A
  • decreased preload and afterload
24
Q

systemic effects of bradykinin include?

Study These Flashcards
A
  • profound vasodilation, increased capillary permeability
  • amplification of the AA pathway effects
  • loss of preload and hypotension
25
what is included in normal coag process
- 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
In sepsis (and in SIRS), which of the following occurs in the coagulation system
- 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
complement cascade acts through three pathways to?
- activate formation of membrane attack complex and cell lysis - enhance phagocytosis - promote chemotaxis
28
the systemic effects if the cell-derived and plasma-derived inflam cascades during sepsis (and SIRS) include
- 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
qSOFA
quick sequential organ failure assessment | score of > or = 2 should prompt clinicians to further assess
30
qSOFA screening
RR > or = 22 altered mentation GCS < 15 systolic hypotension < or = 100
31
How does the Arachidonic Acid path effect O2 sup and dem?
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
How does the Bradykinin path effect O2 sup and dem?
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
How does the coagulation path effect O2 sup and dem?
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
How does the compliment path effect O2 sup and dem?
- 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
what part of sepsis effects contractility?
MDF- myocardial depressant factor triggered by - from ischemic pancreas - cytokines, prostanoids, nitric oxide...
36
cardiogenic shock pre, AL, contract
P- increased AL- increased (SNS and RAAS) cont- decreased
37
hypovolemic shock Pre, AL, cont?
P- decreased AL- increased (SNS and RAAS) cont- decreased (preload)
38
Sepsis (early) | Pre, AL, cont?
P- decreased AL- decreased (SNS and RAAS overdriven) cont- decreased (MDF and preload)
39
EOP of Sepsis CVS, RESP, GI, GU, HEME, Hepatic, Global
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
1 hour bundle
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
If you gave fluids to increase preload, what do you do next?
- 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
what do you do before 1 hr bundle?
Check qSOFA. IF > 2 OR lactate > 4 then start bundle.
43
ABCD of Sepsis Treatment:
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

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