Septic Shock Flashcards

1
Q

The 4 key components of normal/effective immune response and their main functions

A

VIPP - Very Inflammatory Plasma Parts

  1. Vascular response - localized vasodilation and capillary membrane permeability
    - designed to increase blood flow to area and bring in WBC. inc perm allows big WBC to leave vascular space and enter tissues to fight infxn agents. Mediated by Bradykinin, Histamine, Prostaglandins
  2. Immune response - WBC (macrophages, monocytes, neutrophils), antigens, antibodies
  3. Platelets - Coagulation and fibrinolysis - stops local bleed and spread of toxins
  4. Plasma Protein Response - Complimentary system - broad area attack when targeted phagocytic response is inadequate. Good at local site, bad when its broad/systemic
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2
Q

SIRS definition and Criteria

A
  • Generalized Systemic inflammatory response to infection, trauma, shock, surgery, burns
  • The inflammatory response is now causing more damage that the causative agent, in organs and systems remote from the site of insult. Systemic

Criteria: 2 or more of the following

  • Temp <36, >38
  • HR >90
  • RR >20 or PaCO2 >32
  • WBC <4 or >12
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3
Q

Definition of Sepsis

A

Two SIRS criteria + confirmed or suspected infection

-Inflammatory response is systemic, compensatory mechanisms on

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4
Q

Definition of Severe Sepsis

A

SIRS + Sepsis + One organ dysfunction (usually kidneys) as a result of organ perfusion problem from O2S/D imbalance resulting from inflammatory response
-Compensatory mechanisms are maintaining hemodynamic stability, but CO is insufficient to perfuse all organs

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5
Q

Definition of Septic Shock

A

SIRS + Severe sepsis + Hypotension
-Compensatory mechanisms are failing to maintain hemodynamic stability, organ systems are hypoperfused, now we need preload and afterload supports in ICU

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6
Q

Definition of MODS

A

Multiple Organ Dysfunction Syndrome

Septic Shock + 2 or more organ system failure resulting from lack of adequate perfusion from inflammatory response.

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7
Q

Who’s at greatest risk for worst outcomes of sepsis

A
  • Immune compromised
  • young
  • old
  • big open wounds (burns, trauma)
  • addicts
  • lots of invasive procedures/exams (chronically ill)
  • abx use
  • resistant bacteria hospital acquired
  • multiple comorbiities
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8
Q

What do the ABCC of sepsis stand for

A

The chemical agents which active the VIPP system of inflammation
A - Arachidonic Acid pathway - Stimulated by mast cells to cause vasodilation, vascular permeability, promotion of platelet aggregation (agents: prostaglandin, thromboxane, leukotrienes)
B - Bradykinin - mast cells release histamine, cause vasodilation
C - Coagulation Pathways (the platelets part of VIPP) - clotting pathways activate to clot bleeds and isolate infection - in sepsis this happens inappropriately and plasminogen pathways (fibrinolysis) work less effectively - forms clots and causes organ ischemia in sepsis
C - Complimentary systems (the plasma protein response in VIPP) - Via Classical, alternative and Lectin pathways, pathogens are marked for phagocytosis (opsonization, chemotaxis), Membrane attack complex (MAC) form to lyse pathogen cells (and systemic cells in sepsis), and inflammation is perpetuated
-in sepsis this causes intensified inflammation, damage to vessel endothelium, cell adhesion and cell death

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9
Q

3 Hour Sepsis Bundle

A

1) Measure lactate level.
2) Obtain blood cultures prior to administration of antibiotics (if reasonable <45mins).
3) Administer broad spectrum antibiotics.
4) Administer 30 ml/kg crystalloid for hypotension or lactate ≥4mmol/L. Target CVP 8-12 reassess lactate in 2-4h if lactate >4

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10
Q

6 Hour Sepsis Bundle

A

5) Apply vasopressors (for hypotension that does not respond to initial fluid resuscitation) to maintain a mean arterial pressure (MAP) ≥65 mm Hg.
6) Persistent hypotension after initial fluid administration (MAP < 65 mm Hg) or if initial lactate was ≥4 mmol/L, re-assess volume status and tissue perfusion and document findings according to Table 1 (Below)
- Treat with inotrope. dobutamine
- decrease demand w/ sedation, mechanical ventilation
7. Re-measure lactate if initial lactate elevated.

EITHER:
• Repeat focused exam (after initial uid resuscitation) including vital signs, cardiopulmonary, capillary refill, pulse, and skin findings.
OR TWO OF THE FOLLOWING:
• Measure CVP.
• Measure ScvO2 should be >70
• Perform bedside cardiovascular ultrasound.
• Perform dynamic assessment of fluid responsiveness with passive leg raise or fluid challenge.

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11
Q

ABCD of treating septic shock

A

A- Airway - ensure patent airway, ABX - ASAP fitted to suspected organism, started within 1h esp if lactate >4
B- Breathing - optimize gas exchange with MV, targeting tv 6ml/kg ideal body weight, plateau pressure limit of 30cm H2O
C- Cardiac output. optimize preload, afterload, contractility to ensure tissue perfusion
-CVP goal 8-12(non vent)12-15 for MV - fluids (start with fluid challenge 30cc/kg), passive leg raise to check impact of preload on hemodynamics
-Vasopressor support MAP >65 once preload is supported - 1st line: levophed, dopamine(but has higher incidence of dysrhythmias). 2nd line if 1st ineffective: epinephrine. Only after all that, try: phenylephrine (no inotropic effects), vasopressin0.03-0.04u/min (only really effective used as adjunct to levo)
-Contractility if above done but ScVO2 <70 - dobutamine, esp in suspected or confirm cardiomyopathy
D- Decrease Demand - sedation, MV, pain control
Drugs - insulin for glycemic control BG 4-7, corticosteroids only considered in refractory shock unresponsive to catecholamine therapy/pressors

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