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NURS 3512 - Class 7-12 > Week 8 - Septic Shock > Flashcards

Week 8 - Septic Shock Flashcards

1
Q

what is inflammation

A

part of the process by which the immune system defends the body from harmful agents

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2
Q

what are the 4 stages of the inflammatory response

A
  1. vascular response –> seals the injury via fibrin clots and mobilization of leukocytes
  2. cellular response –> sends help
  3. formation of exudate –> form circ to injruy
  4. healing –> regen and repair
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3
Q

describe the relationship between the inflammatory response and infection

A
  • inflammation does not = infection

- infection = inflammation

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4
Q

describe how the inflammatory response changes w different agents

A
  • it is the same regardless of the agent that causes cell injury
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5
Q

what is shock

A
  • a syndrome characterized by decreased tissue perfsuion and impaired cellular metabolism
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6
Q

what is an infection

A
  • an invasion of the body by a pathogen with resulting S*S
  • can be local or systemic
  • is usually bacterial
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7
Q

what is sepsis

A
  • systemic inflammatory response to an overwhelming infection
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8
Q

what are some examples of things that can cause sepsis (3)

A
  • uti
  • wound
  • indwelling lines
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9
Q

what is severe sepsis

A
  • sepsis w organ dysfunction –> hypoperfusion and hypotension
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10
Q

what is imperative to survival w septic shock? why?

A
  • early identification and intervention

- longer in shock & unstable = worse their condition gets = higher mortality

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11
Q

what is septic shock

A
  • shock due to an overwhelming infection , causing hypotension that cannot be reserved by fluid resus and tissue perfusion abnormalities are present
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12
Q

what are the primary organisms that cause sepsis?

A
  • gram + and gram - bacteria
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13
Q

what are risk factors for septic shock (12)

A
  • very young pts
  • very old pts
  • immunosuppressed/immunocompromised pts
  • malnourishment
  • debilitated pts
  • DM
  • cancer
  • CKD
  • HIV
  • HF
  • invasive procedures
  • indwelling devices
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14
Q

as a nurse, it is important to know ?? r/t septic shock (3)

A
  • source of pathogen (ex. indwelling cath)
  • causative agent (bacteria type, C&S)
  • stages of shock
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15
Q

what is imp to know about the pt r/t septic shock (5)

A
  • any diseases they may have (ex. liver disease)
  • regular meds used
  • age (v old or v young)
  • baseline organ function
  • any indewlling lines/tubes, wound/incisions (entry points)
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16
Q

describe the impact that liver disease has on septic shoxck

A
  • causes the pt to move thru the stages of septic shock quicker –> lactic acid is produced during septic shock, which is usually broken down by the liver
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17
Q

why is it imp to know any regular meds the pts used r/t septic shock

A
  • determine if any interactions between their reg meds and the rescue meds
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18
Q

what should you do if you suspect sepsis (3)

A
  • act fast!
  • if pt is high risk and are experiencing S&S, notify physician
  • consider nursing protocol
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19
Q

what should be done while you are notifying the physician if you suspect sepsis (4)

A
  • have a buddy ensure large bore IV access
  • apply O2 (d/t increased CO that is seen at first = increased demand for O2)
  • put pt in high fowlers
  • take vitals
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20
Q

why is it imp to check nursing protocol is you suspect sepsis

A
  • check if there is anything you can do or get started without a dr’s order
    ex. blood cultures?
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21
Q

describe the clinical presentation of sepsis

A
  • complex

- no single symptom or group of symptoms

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22
Q

what is usually initially experienced by pts in septic shock (3)

A
  • hyperdynamic state
  • increased CO
  • decreased SVR
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23
Q

as the inflammatory response becomes overwhelmed in spetic shock, the result is.. (4)

A
  • peripheral dilation
  • increased cap permeability
  • micro-emboli formation (decreased fibrinolysis)
  • maldistribution of blood flow thru relative hypovolemia (d/t third spacing)
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24
Q

what are the general symptoms we will see in septic shock (stage dependent) (12)

A
  • low BP (d/t vasodilation & fluid shift)
  • increased HR and CO (in beginning)
  • tachypnea (to try and compensate)
  • crackles (d/t third spacing)
  • changes to LOC
  • decreased urine output
  • GI dysfunction
  • edema
  • warm & flushed skin in early stages
  • later, cold & clammy skin
  • pain (chest pain d/t increased O2 demand)
  • discomfort & anxiety
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25
what GI signs may occur during septic shock (2)
- GI bleeding | - paralytic ileus
26
what is included in nursing care for septic shock (12)
- ensure airway is patent and assess ABCs - optimize O2 - insert 2 large bore IVs --> fluid resus (need to reperfuse organs) - vasopressors - locate the source of infection - send cultures - abx therapy - neurochecks q15 min - VS - monitor I&O --> foley cath - assess perfusion (cap refill, peripheral pulses) q15 min - stress ulcer prophylaxis(H2RB) - DVT prophylaxis
27
how can we optimize O2 during treatment of septic shock (4)
- decrease demands (position changes, etc.) - admin of O2 to keep at 90% or higher - admin high flow O2 (100%) by non-breather mask - anticipate need for intubation and mechanical ventilation
28
what is the cornerstone of therapy for septic shock
- volume expansion and restoration of perfusion w admin of the appropriate fluid
29
what type of fluids are used for fluid resus in septic shock (2)
isotonic fluids : - NS - LR
30
when should LR not be used for treatment of septic shock
- if pt has liver failure --> cannot convert lactate to bicarb
31
how can we monitor the pt's response to fluid resus (2)
- BP | - insert indwelling cath to monitor I&O
32
what are 2 complications that can occur w the insertion of lrg amounts of fluids
- hypothermia | - coagulopathy
33
how can hypothermia during fluid resus be avoided
- warm the fluids
34
how cancoagulopathy be avoided during fluid resus
- replace clotting factors on the basis of the clinical situation and results of blood studies
35
at what point can vasopressors be used to help increase BP
- used if perfusion cannot be restored w fluid resus | - only after adequate fluid resus (if still low fluid vol, vasoconstriction would only worsen perfusion)
36
when should cultures be sent?
- before broad spectrum antibiotic therapy
37
what lab values should be monitored w septic shock (6)
- lactic acid lvl - liver enzymes - kidney function - glucose (glycogen dumped into bloodstream) - Na (increased) - K (decreased)
38
what should be done within the 1st hour of septic shock and for at least 6 hrs (^6)
1. give 100% oxygen 2. take blood cultures to help determine abx therapy 3. give IV abx 4. give IV fluid therapy 5. measure lactate and hemoglobin 6. insert catheter, monitor UO
39
what are some ways to prevent septic shock (4)
- prevent infection - decreased # of indwelling catheters - use aseptic technique - strict attention to handwashing
40
what should be assessed during acute intervention of septic shock (8)
- neuro status - CVS status - resp status - renal status - body temp & skin changes - GI status - personal hygeine - emotional support
41
why is it imp to monitor neuro status w septic shock
- neuro status is the best indicator of cerebral blood flow
42
describe assessment of CVS during acute intervention of septic shock (4)
- assess BP and HR q15 min if unstable - EKG monitoring continuously - assess pt's response to fluid and med admin q10-15 min - assess perfusion
43
how often is resp status assessed during acute intervention of septic shock
- q15-30 min
44
describe resp assessment during acute intervention of septic shock (5)
- assess rate, depth, freq, and rhythmn of resps - continuous pulse ox - monitor ABGs - many pts w shock are intubated & on mechanical ventilation - maintain airway patency
45
describe assessment of renal status during acute intervention of septic shock (3)
- hourly measurements of urine output - insert indwelling cath - monitor BUN and creatinine
46
describe assessment of body temp & skin changes during acute intervention of septic shock (5)
- monitor temp - keep pt comfortably warm w light covers and control of external enviro temp - if has fever, use NSAIDs, tylenol, or remove covers as Tx - monitor cap refill for perfusion - monitor pts skin color & warmth
47
describe assessment of GI status during acute intervention of septic shock (4)
- auscultate BS q4hr - assess for abdominal distension - monitor for occult blood in stools - monitor for signs of GI bleeds
48
describe mngmt of personal hygeine during acute intervention of septic shock (7)
- monitor for skin breakdown - prevent infections - oral care imp d/t dry and fragile mucous membranes r/t volume depletion - consider priorities of care r/t bathing d/t increased demands for O2 - apply water-soluble lubricant to lips to prevent drying and cracking - ROM 3-4x/day - turn q2h
49
what are the stages of shock
- compensatory - progressive - refractory
50
what changes occur at the cellular level during shock
- metabolism changes from aerobic to anaerobic = lactic acid buildup
51
how is lactic acid removed from the body? how does this change w septic shock
- lactic acid = waste product - must be removed by the liver - however, no o2 to remove lactic acid d/t decreased perfusion
52
what is the compensatory stage of shock
- involves the body activating neural, hormonal, and biochemical compensatory mechanisms to attempt to overcome the anaerobic metabolism & maintain homeostasis
53
what signs are seen during the compensatory stage of shock (9)
- decreased BP - decreased CO - elevated HR - body shunts blood to vital organs (heart and brain) - skin warm and flushed (d/t hyperdynamic state) - restless & confusion - hyperdynamic state - decreased GI motility - tachypnea (to attempt to compensate)
54
describe the prognosis of the compensatory stage of shock
- may survive w aggressive treatment
55
what is the progressive stage of shcok
- stage that begins as the compensatory mechanisms fail and aggressive treatment is required to prevent MODS
56
what signs are present during the progressive stage of shock (16)
- edema (d/t increased cap permeability) - tachypnea - crackles - increased WOB - decreased BP and CO - bradycardia - changes in mental status - weak peripheral pulses - ischemia of distal extremities - dysrhytmias - myocardial ischemia, potentially MI - renal tubular ischemia - decreased urine output - increased BUN and creatinine - r/o GI ulcers & bleeding (d/t ischemia to the protective mucosal barrier) - failure of liver to metabolize drugs and waste products - cold, clammy skin
57
what symptoms does failure of the liver to metabolize during the progressive stage of shock cause (4)
- increased ammonia - increased lactate - jaundice - elevated liver enzymes
58
what is the refractory stage of shock
- final stage - everything is more profound - decreased perfusion from peripheral vasoconstriction and decreased CO exacerbate anaerobic metabolism - organs are in failure, body's compensatory mechanisms are overwhelmed
59
what signs are seen during the refractory phase of shock (8)
- cold, clammy skin - mottled skin - profound hypotension - bradycardia - lactate increase = acidosis - anuria - profound hypoexmia - failure of the liver, lungs, and kidneys = accumulation of waste products
60
describe the prognosis in the progressive and refractory stage of septic shock
- will likely not survive
61
what is SIRS
- systemic inflammatory response syndrome | - sysytemic inflammatory response to a variety of insults, such as infection, ischemia, infarction, and injury
62
what is SIRS characterized by: (6)
at least two of the following: - fever - edema - hypotension - tachycardia - imapired oxygenation - elevated WBC
63
describe the relationship between SIRS and septic shock
- can have SIRS not be septic | - or can be septic and have SIRS
64
what happens if organs are not perfused d/t the inflammatory response seen in sepsis or SIRS and it is not treated quickly?
- MODS
65
what is MODS (4)
- multiple organ dysfunction syndrome - failure of 2 or more organ systems - a progression from SIRS and septic shock - high mortality rate
66
what is included in shock mngmt? (15)
- monitor VS - monitor neuro status - monitor UO - monitor trends in hemodynamic paremeters - admin crystalloid or colloid IV fluids - monitor lab values - monitor determinants of tissue O2 delivery (PaO2, SaO2, hgb) - monitor for symptoms resp failure - monitor fluid status - monitor renal function - admin O2 and/or mechanical ventilation - monitor serum BG and treat abnormal lvls - admin DVT and stress ulcer prophylaxis - initiate early admin of antimicrobial agents - admin vasopressors
67
what is included in shock mngmt r/t the CVS (4)
- monitor for inadequate coronary artery perfusion (EKG, cardiac enzymes, angina) - promote adequate organ system perfusion (w fluid resus and/or vasopressors) - promote afterload reduction (vasodilators, ACEI, aortic balloon pumping) - promote optimal preload while minimizing afterload
68
what is included in shcok mngmt r/t vasogenic (6)
- monitor for physiological changes r/t loss of vascular tone (decreased BP, bradycardia, tachypnea) - place pt in supine position w legs elevated to increased preload - maintain 2 large bore IV access - admin isotonic crystalloid as bolus doses --> keep systolic above 90 - admin abx - admin sympathomimetic drugs
69
what is included in shock mngmt r/t volume (7)
- monitor for sudden loss of blood - monitor for dehydration - check secretions for frank or occult blood - monitor for S&S of hypovolemic shock - admin blood products - monitor hgb and hct - admin IV fluids

NURS 3512 - Class 7-12 (49 decks)

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