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NSCC 7320 > Sepsis > Flashcards

Sepsis Flashcards

1
Q

ABCCs of Sepsis

A

Is a framework to assist in understanding the pathophysiology of sepsis. A stands for
Arachidonic Acid, B for Bradykinin, C for Complement and C for Coagulation.

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2
Q

Arachidonic Acid

A

A highly reactive substance that contributes to:
organ dysfunction,
vascular permeability,
and prolongs inflammation.

The vascular permeability leads to third spacing of fluid and decreases in preload.

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3
Q

Bradykinin

A

Stimulates mast cells and release of histamine as
well as Arachidonic Acid.

This leads to vasodilatation and permeability.

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4
Q

Coagulation

A

In sepsis, the coagulation cascades become overstimulated resulting in the formation of micro-clotting in the vascular bed resulting in poor end organ perfusion.

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5
Q

Complement

A

proteins that stimulate phagocytosis, promote
immune and inflammatory responses

The release of complement proteins causes mast cells to be stimulated resulting in vasodilatation and promotion of the coagulation cascade.

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6
Q

Continuum of sepsis

A 
SIRS
Sepsis
severe sepsis
septic shock
MODS 
death
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7
Q

Early Goal Directed Therapy

A

increase supply of oxygen to the body, first through improvement of preload,
if fluid not effective vasoactive drugs such as levophed, blood products to increase carrying capacity and demand management via sedation, analgesics or NMB.
Parameters monitored for treatment effectiveness include MAP, ScV02 and Lactate.

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8
Q

Sepsis

A

Sepsis is a systemic inflammatory response to an infection.
Results in :
vasodilation,
third spacing of fluid.

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9
Q

Septic shock

A

This is a type of shock related sepsis. Patient experiences low perfusion, despite efforts at
fluid resuscitation and use of vasoactive drugs.

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10
Q

Shock

A

Shock is an acute and widespread process that results in massive organ dysfunction as the
result of poor perfusion. Causes are numerous but include hypovolemia, cardiogenic,
neurogenic, anaphylactic and sepsis

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11
Q

SIRS

A

Systemic Immune Response Syndrome is a whole body response to any insult. The insult
could be burns, infection or trauma. The immune system becomes hyperactive resulting in
vasodilation, increased vascular permeability and inappropriate clotting.

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12
Q

Vasopressin IV

A

A naturally occurring substance in the body also known as anti-diuretic hormone (ADH). It is
part of the RAAS compensatory mechanism. It is used in sepsis to support vascular tone and works synergistically with levophed to improve EOP.

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13
Q

Briefly describe the patho of sepsis

A

Bacteria in the blood causes release of endotoxins (gram neg) and exotoxins (gram pos) causing pro-inflammatory cytokines
Cytokines activate the (ABCC) complement and coagulation system, kinin system and arachadonic
causing vasodilation and vascular leaking

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14
Q

MECHANICAL VENTILATION-PROTECTIVE LUNG STRATEGIES RECOMMENDED

A

LOWER TIDAL VOLUMES (6CC/KG)
• HIGHER PEEP (AS NEEDED TO SUPPORT GAS EXCHANGE)
• LIMITING PLATEAU PRESSURE TO 30 CMH2O
• USE OF NEUROMUSCULAR BLOCKADE DRUGS TO FACILITATE MV, LIMITED TO <48 HOURS

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15
Q

Sepsis definition

A

a life threatening condition that arises when the body’s response to infection injures its own tissues and organs

Systemic inflammatory response + suspected or confirmed infection

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16
Q

sepsis continuum

A

Infection->sepsis->septic shock->multiple organ dysfunction syndrome->death

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17
Q

SIRS

A 
Temperature >38C or <36C
Heart Rate > 90bpm
Resp. Rate >20/min. or
PaCO2 <32 mmHg
WBC >12 or <4 or 10% band (immature
cells)
18
Q

Septic shock

A

hypotension despite adequate fluid resuscitation and Need for vasopressors

19
Q

Septic shock criteria

A
  1. Diagnosed with Sepsis
  2. Require vasopressor therapy to
    maintain MAP >65
  3. Lactate > 2mmol/L despite
    adequate fluid resuscitation
20
Q

Risk for sepsis

A 
• Age: <1 year, >65 years
• Immunocompromising
conditions and/or medications
• Multiple comorbidities
• Chronic diseases
• Obstructions (e.g. calcuous cholecystitis)
• Hospital acquired infection (e.g. VAP)
• Breaks in skin (trauma, invasive medical devices, wounds)
• Incomplete antibiotic regimes
• Surgery and diagnostic procedures
• Antibiotic resistant organisms
21
Q

VIPP

A

Overall goal is to keep injury/infection LOCALIZED and under CONTROL

VASCULAR RESPONSE
IMMUNE RESPONSE
PLATELETS
PLASMA PROTEIN RESPONSE

22
Q

VASCULAR RESPONSE to infection

A 
Vasodilation
Capillary Permeability
HISTAMINE
BRADYKININ
PROSTAGLANDINS
23
Q

IMMUNE RESPONSE to infection

A

Neutrophils
Monocytes /Macrophages
Antibody
Antigen

24
Q

PLATELETS response to infection

A

Coagulation

Fibrinolysis

25
Q

PLASMA PROTEIN RESPONSE to infection

A

Compliment cascade

26
Q

ABCCs of sepsis

A

Arachidonic
Bradykinin
Coagulation
Complement

27
Q

Arachidonic

A

Prostoglandins:
Vasodilation
Increase permeability

Tromboxane:
Promotes platelet aggregation

-Increased permeability: fluid shifting from the vascular space to the interstitial space
-Decreased preload
-Decreased ventilation and gas exchange
if the fluid shifts in the lungs

28
Q

Bradykinin

A

Mast Cell Degranulation
Histamine Release = Potent vasodilation

  • Vasodilator
  • Increased capillary permeability
  • Mast-cell->histamine->vasodilation
  • Mast cell->AA pathway->Further vasodilation and capillary permeability
  • Decreased preload
  • Decreased afterload
29
Q

Coagulation

A

Fibrin formation/Broken plasminogen pathway
Microemboli formation

  • Coagulation cascade becomes systemic
  • Anticoagulation pathway fails->Microemboli throughout the systemic circulation->blood flow impeded->decrease cellular oxygen supply->end organ dysfunction
  • AA pathway further triggered
  • Kinin cascade triggered
  • Complement pathway triggered
30
Q

Complement

A 
MAC
Intensify inflammation
Damage endothelium
Cell Adhesion
Cell Death/Lysis

Stimulation of phagocytosis

  • Promotion of immune response
  • Promotion of inflammatory response (increased permeability and vasodilation)
  • Stimulation of mast cells->histamine release ->vasodilation
31
Q

Primary outcomes of the dysregulated inflammatory response in sepsis (SIRS):

A 
Systemic vasodilation (hypotension)
Increased capillary permeability
 Inappropriate clotting in the microvasculature (through activation of coagulation system and failure of the fibrinolytic system)
Maldistribution of blood flow
Diminished myocardial contractility
Poor end-organ perfusion
Degreased cellular oxygenation
Organ dysfunction
32
Q

Medications which act on Arachidonic Acid pathway

A
  1. Steroids (Phospolipase release inhibition)
  2. NSAIDs (Non selective COX inhibitor)
  3. Celebrex (COX 2 Inhibitor)
  4. ASA (thromboxane inhibition)
  5. Asthma drugs (Leukotrienese inhibition)
33
Q

Where do the ABCC’s effect patients O2 Supply and Demand?

A

Vasodilation decreased afterload

Cap permeability decreases preload

34
Q

qSOFA

A

GCS <15
RR >22 bpm
SBP < 100mmHg

35
Q

1 HOUR BUNDLE

A
  1. Measure Lactate
  2. Obtain blood cultures prior to administration of antibiotics
  3. Administer broad spectrum antibiotics
  4. Administer 30ml/kg crystalloid for hypotension or
    lactate > 4mmol/L
  5. Apply vasopressors if patient is hypotensive during or
    after fluid resuscitation to maintain MAP >65mmHg
36
Q

INTERVENTIONS IN THE FIRST 6 HOURS

A
  • ATTAINING A MAP > 65MMHG
  • NORMALIZING LACTATE
  • ADEQUATE FLUID RESUSCITATION
  • PRELOAD ASSESSMENT
  • VASOPRESSOR THERAPY
37
Q

FLUID RESUSCITATION

A

CRYSTALLOID AND COLLOID IV FLUID THERAPY A BALANCE BETWEEN THE TWO

  • BEGIN WITH 30M/KG RECOMMENDATION, THEN ONGOING ASSESSMENT OF PRELOAD
  • 2L WITHIN FIRST HOUR
  • 2 WITHIN THE FIRST 6-8 HOURS
38
Q

FLUID RESPONSIVENESS

A

• INCREASE IN STROKE VOLUME
• INCREASE IN CARDIAC OUTPUT
• ‘PRELOAD RESERVE’ OR ‘ROOM FOR MORE PRELOAD’
• INCREASE IN MAP, DECREASE IN HR, CHANGE IN PULSE CONTOUR
• NOTICEABLE RESPONSE TO SMALL VOLUMES OF FLUID-ASCENDING PART OF THE STARLING
CURE
• NO RESPONSE-ON THE FLAT PART OF THE CURVE

39
Q

PASSIVE LEG RAISE

A
  • RAISING THE PATIENT’S LEG WHILE IN SUPINE
  • FACILITATES VENOUS RETURN
  • IMMEDIATE IMPROVEMENT IN PRESSURES->ROOM FOR MORE PRELOAD
40
Q

FLUID CHALLENGE

A
  • RAPID ADMINISTRATION OF 250-500 CC IV FLUID (NS)

* IMPROVEMENTS IN HEMODYNAMICS->ROOM FOR MORE PRELOAD

41
Q

When do we use VASOACTIVE DRUGS

A
  • NOT RESPONDING TO FLUID RESUSCITATION

* MAP <65MMHG IN THE PRESENCE OF ADEQUATE PRELOAD

42
Q

VASOACTIVE DRUGS of choice for sepsis

A

• LEVOPHED (NOREPINEPHRINE)

• VASOPRESSIN (0.03UNITS/MIN) WHEN NOT RESPONDING TO LEVO TO ATTAIN MAP GREATER
THAN OR EQUAL TO 65

• PERSISTENT HYPOPERFUSION DESPITE FLUIDS AND PRESSORS->DOBUTAMINE

NSCC 7320 (9 decks)

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