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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
Q

what GI signs may occur during septic shock (2)

A
  • GI bleeding

- paralytic ileus

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26
Q

what is included in nursing care for septic shock (12)

A
  • 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
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27
Q

how can we optimize O2 during treatment of septic shock (4)

A
  • 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
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28
Q

what is the cornerstone of therapy for septic shock

A
  • volume expansion and restoration of perfusion w admin of the appropriate fluid
29
Q

what type of fluids are used for fluid resus in septic shock (2)

A

isotonic fluids :

  • NS
  • LR
30
Q

when should LR not be used for treatment of septic shock

A
  • if pt has liver failure –> cannot convert lactate to bicarb
31
Q

how can we monitor the pt’s response to fluid resus (2)

A
  • BP

- insert indwelling cath to monitor I&O

32
Q

what are 2 complications that can occur w the insertion of lrg amounts of fluids

A
  • hypothermia

- coagulopathy

33
Q

how can hypothermia during fluid resus be avoided

A
  • warm the fluids
34
Q

how cancoagulopathy be avoided during fluid resus

A
  • replace clotting factors on the basis of the clinical situation and results of blood studies
35
Q

at what point can vasopressors be used to help increase BP

A
  • 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
Q

when should cultures be sent?

A
  • before broad spectrum antibiotic therapy
37
Q

what lab values should be monitored w septic shock (6)

A
  • lactic acid lvl
  • liver enzymes
  • kidney function
  • glucose (glycogen dumped into bloodstream)
  • Na (increased)
  • K (decreased)
38
Q

what should be done within the 1st hour of septic shock and for at least 6 hrs (^6)

A
  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
Q

what are some ways to prevent septic shock (4)

A
  • prevent infection
  • decreased # of indwelling catheters
  • use aseptic technique
  • strict attention to handwashing
40
Q

what should be assessed during acute intervention of septic shock (8)

A
  • neuro status
  • CVS status
  • resp status
  • renal status
  • body temp & skin changes
  • GI status
  • personal hygeine
  • emotional support
41
Q

why is it imp to monitor neuro status w septic shock

A
  • neuro status is the best indicator of cerebral blood flow
42
Q

describe assessment of CVS during acute intervention of septic shock (4)

A
  • 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
Q

how often is resp status assessed during acute intervention of septic shock

A
  • q15-30 min
44
Q

describe resp assessment during acute intervention of septic shock (5)

A
  • 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
Q

describe assessment of renal status during acute intervention of septic shock (3)

A
  • hourly measurements of urine output
  • insert indwelling cath
  • monitor BUN and creatinine
46
Q

describe assessment of body temp & skin changes during acute intervention of septic shock (5)

A
  • 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
Q

describe assessment of GI status during acute intervention of septic shock (4)

A
  • auscultate BS q4hr
  • assess for abdominal distension
  • monitor for occult blood in stools
  • monitor for signs of GI bleeds
48
Q

describe mngmt of personal hygeine during acute intervention of septic shock (7)

A
  • 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
Q

what are the stages of shock

A
  • compensatory
  • progressive
  • refractory
50
Q

what changes occur at the cellular level during shock

A
  • metabolism changes from aerobic to anaerobic = lactic acid buildup
51
Q

how is lactic acid removed from the body? how does this change w septic shock

A
  • lactic acid = waste product
  • must be removed by the liver
  • however, no o2 to remove lactic acid d/t decreased perfusion
52
Q

what is the compensatory stage of shock

A
  • involves the body activating neural, hormonal, and biochemical compensatory mechanisms to attempt to overcome the anaerobic metabolism & maintain homeostasis
53
Q

what signs are seen during the compensatory stage of shock (9)

A
  • 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
Q

describe the prognosis of the compensatory stage of shock

A
  • may survive w aggressive treatment
55
Q

what is the progressive stage of shcok

A
  • stage that begins as the compensatory mechanisms fail and aggressive treatment is required to prevent MODS
56
Q

what signs are present during the progressive stage of shock (16)

A
  • 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
Q

what symptoms does failure of the liver to metabolize during the progressive stage of shock cause (4)

A
  • increased ammonia
  • increased lactate
  • jaundice
  • elevated liver enzymes
58
Q

what is the refractory stage of shock

A
  • 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
Q

what signs are seen during the refractory phase of shock (8)

A
  • 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
Q

describe the prognosis in the progressive and refractory stage of septic shock

A
  • will likely not survive
61
Q

what is SIRS

A
  • systemic inflammatory response syndrome

- sysytemic inflammatory response to a variety of insults, such as infection, ischemia, infarction, and injury

62
Q

what is SIRS characterized by: (6)

A

at least two of the following:

  • fever
  • edema
  • hypotension
  • tachycardia
  • imapired oxygenation
  • elevated WBC
63
Q

describe the relationship between SIRS and septic shock

A
  • can have SIRS not be septic

- or can be septic and have SIRS

64
Q

what happens if organs are not perfused d/t the inflammatory response seen in sepsis or SIRS and it is not treated quickly?

A
  • MODS
65
Q

what is MODS (4)

A
  • multiple organ dysfunction syndrome
  • failure of 2 or more organ systems
  • a progression from SIRS and septic shock
  • high mortality rate
66
Q

what is included in shock mngmt? (15)

A
  • 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
Q

what is included in shock mngmt r/t the CVS (4)

A
  • 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
Q

what is included in shcok mngmt r/t vasogenic (6)

A
  • 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
Q

what is included in shock mngmt r/t volume (7)

A
  • 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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