Sepsis & Shock Flashcards

1
Q

Sepsis:

A

Systemic response to infection

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2
Q

Severe Sepsis:

A

Sepsis with organ dysfunction

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3
Q

Septic Shock:

A

Sepsis with marked hypotension despite adequate fluid resuscitation

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4
Q

SIRS

A

Widespread systemic inflammatory response

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5
Q

SIRS Triggers

A

-Microbial invasion: bacteria, viruses, fungi
-Endotoxin release: gram-negative bacteria
-Global perfusion deficits: post cardiac resuscitation, shock states
-Regional perfusion deficits: distal perfusion deficits

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6
Q

SIRS Associated disorders

A

 Infection
 Trauma
 Shock
 Pancreatitis
 Ischemia

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7
Q

SIRS Criteria & S/S

A

-High Temperature 100.4 (38) or Low Temperature 96.8 (36)
-Heart Rate greater than 90bpm
-Respiratory Rate greater than 20
-WBC less than 4k or greater than 12k
-BG greater then 140 in non-diabetic patient

*Must meet 2 of these criteria and have a known source of infection to be septic

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8
Q

Initial Sepsis One hour bundle

A

 Measure Lactate
-Greater than 4 is critical
 Obtain Blood Cultures
-X2 sites, 2 bottles per site (anaerobic and aerobic)
 Initial fluid resuscitation: 30ml/kg (run it wide open)
 Begin broad spectrum antibiotics
-Zosyn and Levaquin are common
 Closely monitor hemodynamics
-B/P Q10-15min,
 Repeat Lactate at 2 hour mark
-Lactate should go down

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9
Q

Sepsis Monitoring Labs

A

Redraw Lactate q4 hours

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10
Q

Sepsis Monitoring Meds

A

Vasopressors for hypotension persisting after fluids
-Titrate to maintain MAP above 65

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11
Q

Sepsis Monitoring

A

Place CVC & A-line with monitoring
-Keep CVP between 8 and 12 (12 to 15 if vented)
-Keep SCVO2 above 70%
-A-line continuous B/P monitoring & ABG’s

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12
Q

Sepsis Urine Monitoring

A

Keep urine output greater than 0.5ml/kg/hr

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13
Q

Sepsis Vented Monitoring

A

-ensure Vt at 6ml/kg of IBW
-monitor FiO2/PaO2 ratio
-assess for ARDS
-assess for abdominal compartment syndrome (3rd spacing)

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14
Q

How often to assess for sepsis

A

-At least once per shift
-Ideally twice per shift

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15
Q

Who to test for sepsis

A

Everyone

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16
Q

Shock

A

A clinical syndrome
-Life-threatening response to alterations in circulation
-Inadequate tissue perfusion
-Imbalance between cellular oxygen supply and demand

-Impacts all body systems

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17
Q

Shock patho

A

Shock begins with cardiovascular system failure

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18
Q

Shock Alterations

A

Alterations in at least one of four components:
Blood volume
Myocardial contractility
Blood flow
Vascular resistance

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19
Q

Classifications of Shock

A

Hypovolemic
-Absolute (hemmorhage) and Relative (vasodialation)
Cardiogenic
Obstructive
Distributive
-Anaphylactic (allergen)
-Neurogenic Assault on neuro system/directly related to trauma
-septic

20
Q

4 stages of shock

A

Initial
Compensatory
Progressive
Refractory

21
Q

Initial Shock

A

-Hypoperfusion: inadequate delivery or extraction of oxygen
-Lactic acid begins to build up
-No obvious clinical signs
-Early, reversible

22
Q

Compensatory Shock

A

Sustained reduction in tissue perfusion
Initiation of compensatory mechanisms in an attempt to overcome consequences of anaerobic metabolism
-Neural: baroreceptors and chemoreceptors
-Improve cardiac output – BUT increased myocardial O2 demand, so RR goes up
Hormonal: ACTH and ADH
-Increased BG and reduces OU to increase intravascular volume
BioChemical
-Hyperventilation leads to respiratory alkalosis which causes vasoconstriction of cerebral arteries and a decreased CP

23
Q

Progressive Shock

A

-shock begins as compensatory mechanisms fail
-Changes in the patient’s mental status are important findings in this stage.

24
Q

Progressive Shock UPDATE!!

A

Failure of compensatory mechanisms
Profound cardiovascular effects
Hypoperfusion
Widespread Vasoconstriction
-Extremity ischemia
-Cellular hypoxia
-Anaerobic metabolism
-Lactic acid production (metabolic acidosis)
-Failure Na+/K+ pump

25
Refractory Shock
Prolonged inadequate tissue perfusion -Unresponsive to therapy -Dysrhythmias -Pulmonary edema -Respiratory Distress Syndrome (RDS) -Cerebral changes -Renal decreased GFR -Contributes to multiple organ dysfunction and death
26
Shock assessment findings Central nervous system
 Most sensitive to early changes  Initial stage -Anxiety/restlessness  Late stage -Coma
27
Shock assessment findings Cardiovascular system
Blood pressure -Initial compensatory stages -Slightly elevated -Narrow pulse pressure  Late stages -Very low Pulses -Progressively become weaker
28
Shock assessment findings Pulmonary system
Early stages  Rapid, deep respirations Late stages  Shallow respirations  Poor gas exchange
29
Shock assessment findings Renal system
Decreased glomerular filtration Activated renin-angiotensin-aldosterone system  Sodium retention  Water reabsorption  Oliguria
30
Shock assessment findings Gastrointestinal system
Slowing intestinal activity  Decreased bowel sounds, distension, nausea, and constipation
31
Shock assessment findings Hepatic System
Altered liver enzymes Clotting disorders Increased susceptibility to infection
32
Shock assessment findings Hematological System
Consumptive coagulopathy (DIC)  Enhanced clotting/inhibited fibrinolysis  Depletion of clotting factors  Clotting in the microcirculation
33
Shock assessment findings Integumentary System
Skin color, temperature, texture, and turgor  Most will present pale and cool  Septic shock will be warm and flushed  Cyanosis-late/unreliable sign
34
General management of shock
Treat underlying cause Reverse altered circulatory component -Maintain circulatory volume Combination therapy  Fluid  Pharmacotherapy  Mechanical therapy Minimize oxygen consumption
35
Hypovolemic shock
Inadequate intravascular blood/fluid volume
36
Cardiogenic shock
Heart fails to act as an effective pump
37
Obstructive shock
Physical impairment to adequate circulating blood flow
38
Distributive shock
Widespread vasodilation and decreased vascular tone resulting in a relative hypovolemia -Neurogenic -Anaphylactic -Septic
39
Hypovolemic Shock Management
40
Hypovolemic Shock Findings
41
Hypovolemic Shock Treatment
42
Cardiogenic Shock Management Pharmacological
Decrease preload -Diuretics, venous vasodilators Increase cardiac output -Positive inotropes Decrease afterload -Arterial vasodilators
43
Cardiogenic Shock Management Mechanical
-IABP – Intra aortic Balloon Pump -VAD – Ventricle Assistive Device
44
Cardiogenic Shock Findings
-Tachycardia -low BP -narrow pulse pressure -high RR -pulmonary edema Decreased cardiac output; impaired perfusion
45
Cardiogenic Shock Treatment
46
Septic Shock