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Seminar Exam 3 Flashcards

1
Q

define acute pancreatitis

A

pancreatic enzymes, which are normally inactive until reaching duodenum, are activated within pancreas

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2
Q

GI/hepatic changes in sepsis

A
  • bowel ischemia
  • stress ulcer
  • hepatic dysfunction
    • increased LFTs, jaundice
    • encephalopathy
  • w/o gut perfusion, lose protective mucosa
    • bacteria colonizes
    • bacterial translocation to blood stream
    • bacteremia
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3
Q

ACS and pancreatitis

A
  • ACS may be as high as 78% in acute pancreatitis
  • d/t inflammatory response syndrome
    • capillary fluid leak and edema in mesentary and bowel wall
    • leads to IAP
  • fluid resusc worsens
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4
Q

activation of coagulation system in SIRS

A
  • results in
    • clot formation in microvasculature (microemboli)
  • decreases cellular perfusion and causes cellular death
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5
Q

risk factors for ACS

A
  • diminished abd wall compliance
  • increased abd contents 2/2 air, blood, fluid sequestration
  • capillary leak from fluid resusc measures
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6
Q

damage control procedure on airway and bladder pressures

A
  • emergent laparotomy
  • abdominal compartment open and left open so organs can swell
  • decreaes airway and bladder pressures immediately
  • goal is immediate restoration of perfusion, reverse ischemia, prevent necrosis, and close back up
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7
Q

platelet aggregation and microclot formation in SIRS

A
  • clots can’t pass through capillary beds
  • clump
  • blockage
  • poor perfusion
  • in all oragns, not just periphery
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8
Q

ROSC

A
  • return of spontaneous circulation (ROSC)
  • pulse and blood pressure
  • abrupt sustained increase in PETCO (>40 mmHg)
  • spontaneous arterial pressure waves w/ intra-arterial monitoring
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9
Q

end result of SIRS response

A

decreased tissue perfusion resulting in cellular death and organ dysfunction

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10
Q

hyperventilation during resusc

A
  • correct vent rate is 10 breaths/min (q6sec)
  • tidal volume is: ideal body weight * 6-8 ml
    • don’t need entire bag!
  • risk of too much tidal volume = overdistention
    • barotrauma
    • rising lung bed pressures
    • less venous filling of SVC to heart
    • less room for heart expansion
      • no stretch, no squeeze
  • 30:2 w/ no artifical airway
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11
Q

“the person” in aseptic technique

A
  • perfection
  • thoughtful process
  • repetition
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12
Q

pharmacy in code

A

code drugs

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13
Q

systemic effects of intraabdominal hypertension (IAH)

A
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14
Q

how to keep patients safe with great outcomes

A
  • aseptic technique
  • hand hygiene
    • in & out of rooms
  • thoughtful culture usage
  • PPE use
    • never out of rooms
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15
Q

members of the code team

A
  • primary nurse
  • nurses on unit
  • anesthesia
  • CC/intensivist physician
  • nursing supervisor
  • resp therapist
  • pharmacy
  • transport
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16
Q

kill time

A

how long it takes for chemical to kill organisms after application to skin

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17
Q

characteristics of effective CPR

A
  • adequate CC
    • rate correlated w/ increased survival
    • depth correlated w/ increased survival and successful defib
  • CC 90-100/min (highest survival rate)
  • shocks more successful with 2-2.4 in compression depth
  • greater pre-shock pause = less successful shock
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18
Q

PCI and cooling

A
  • incidence of CAD in VF pts is high
  • STEMI - minimize delay to cath lab and initiation of cooling
    • can be used during angiography
      • surface or catheter
  • NSTEMI - initial streategy
    • early invasive approach with PCI (w/in 24-48 hrs) in patients with
      • recurrent angina or ischemia at rest
      • elevated biomarkers
      • new ST seg depression
      • other high-risk features
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19
Q

improving oxygenation in sepsis

A
  • ventilator therapy
  • oxygen conservation
  • improve delivery (hemoglobin)
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20
Q

anesthesia provider during code

A
  • except in surgical critical care environment
    • already there
  • manage airway
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21
Q

hemodynamic variables reflecting various shock mechanisms

A
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22
Q

neuro implications in ACS

A
  • decreased perfusion from poor outflow
  • high intrathoracic pressure may
    • compress jugular veins
    • obstruct cerebral outflow
    • increase ICP
      • d/t poor venous return vai jugulars
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23
Q

cardiac arrest epidemiology

A
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24
Q

patho of acute pancreatitis

A
  • autodigestion of pancreatic tissue
    • leading to inflammation and necrosis
  • amylase and lipase are really good at digesting protein, fat, and starch
    • which is what we are made of
  • interruprs normal endocrine and exocrine fxns of pancreas
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25
Q

chlorhexidine gluconate + alcohol

A
  • antimicrobial (not antifungal) skin prep
  • alcohol - 70% or higher isopropol
  • not for neonates < 32 weeks
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26
Q

calculate abdominal perfusion pressure (APP)

A
  • MAP - IAP
  • maintain APP > 60 to decrease morbidity, mortality
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27
Q

rapid response team members

A
  • critical care nurse
  • respiratory therapist
  • physicial (CC or hospitalist)
  • nursing supervisor (coordinators)
    • can get a pt a bed
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28
Q

three key points in SIRS

A
  • increased capillary permeability
    • 3rd spacing of fluids
  • activation of immune response
    • fever, tachycardia
  • activation of clotting cascade
    • microemboli
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29
Q

drug therapy for code

A
  • epi IV/IO: 1 mg q3-5 min
  • amiodarone IV/IO:
    • first dose 300 mg
    • second dose 150 mg
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30
Q

monitoring ACS

A
  • abd girth
  • bladder pressure - gold standard
    • q2-4 hr until abd pressure returned to normal
    • continu to monitor even during release of pressure via damage control procedure
      • until fascia closed and IAP normal
    • via specific manometer that utilizes needle or needle-free access to aspiration port of indwelling urinary cath
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31
Q

epidemiology of acute pancreatitis

A
  • 18 per 100,000
  • 3x more in AA than caucasian
  • males > females
  • 10-15% mortality in uncomplicated acute
  • 30% if mounting MODS reaction
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32
Q

stages of SIRS response

A
  • release of pro-inflammatory mediators
  • pro-inflammatory and anti-inflammatory mediators appear in systemic circulation
  • massive systemic inflammation
  • compensatory anti-inflammatory response occurs to try and suppress inflammation
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33
Q

severe sepsis

A
  • sepsis associated with
    • organ dysfxn
    • hypoperfusion (shock)
    • hypotension
  • other symptoms include:
    • lactic acidosis (lactate >2)
    • oliguria - poor renal perfusion, poor intravascular volume
    • acute alteration in mental status - poor cerebral perfusion
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34
Q

hematologic side effects of therapeutic hypothermia

A
  • coagulopathy, despite normal lab tests
  • decreased platelet function @ 35 C
  • decreased function of plasma proteins @ 34 C
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35
Q

prognosis of MODS

A
  • depends on length and severity of SIRS
  • unpredictable organ response
    • 1 organ <50% mortality
    • 2 organs 50-60%
    • 3 organs 60-100%
    • 4 organs 100%
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36
Q

concept of antimicrobial stewardship

A
  • provide support to healthcare workers
  • decrease inappropriate antimicrobial use
  • optimize selection, dose, and udration of antimicrobial therapy
  • streamline costs associated with antimicrobial use
  • decrease spread and emergence of antimicrobial resistance
  • improve patient outcomes
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37
Q

renal changes in sepsis

A
  • metabolic acidosis
  • decreased renal perfusion
  • acute renal failure (pre-renal)
  • kidneys lose ability to help body compensate for this d/t decreased renal perfusion
    • usually produce bicarb
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38
Q

not recommended during therapeutic hypothermia

A
  • focus on preventing fever or maintaining normothermia will not have same outcomes
    • not substantiated
  • prehospital cooling not recommended
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39
Q

causes of infection

A
  • central lines, foley, A-lines
  • trauma, surgery
  • translocation of gut bacteria
  • ventilators
  • diabetes
  • cancer, immune compromised
  • alcohol, malnourished
  • epithelial barrier
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40
Q

what happens when you cut your finger? (normal response)

A
  • bleeds - washes away bacteria and flow of blood brings WBCs
  • hyperemia - red and puffy (“too much blood”)
    • d/t inflammation leading to local cap dilation b/c WBC much larger than other blood components
  • clot - stops bleeding, forms foundation for regeneration of new tissue
  • swelling reduces, area heals over
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41
Q

maintaining therapeutic hypothermia

A
  • internal catheter or external cooling blanket
  • from time until patient hits target temp until re-warming begins
  • serial labs
  • patient testing
  • EEG monitor
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42
Q

neuro monitoring during therapeutic hypothermia

A
  • 80% of caridac arrest survivors comatose
  • seizures common - 44%
    • EEG most reliable way to detect
    • many are subclinical
    • NMB agents suppress convulsions but not seizures
  • rebound fevers common (41%) and can be associated with worse outcomes
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43
Q

renal implications in ACS

A
  • acute failure 2/2 renal vein obstruction
  • indirect failure 2/2 decreased intravascular volume
    • prerenal AKI
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44
Q

measuring intraabdominal pressure

A
  • directly via intra-abdominal catheter
  • more commonly indirectly via bladder pressure (special device on Foley)
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45
Q

1 way to prevent infection

A

hang hygiene

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46
Q

1st hit vs 2nd hit in SIRS

A
  • 1st hit - initial injury followed by SIRS response
  • 2nd hit - another injury on top results in increased SIRS response
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47
Q

antibiotics for sepsis

A
  • gram +
    • vanco, linezolid
  • gram -
    • gentamycin, levaquin, ticarcillin, cefepime
  • broad spectrum
    • imipenem
    • zosyn
    • augmentin
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48
Q

“helper” nurses during code

A
  • assist with families
  • maintain privacy
  • make necessary phone calls to chaplain, OR, radiology
  • obtains needed equipment/supplies for patient
  • watches other pts during this time
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49
Q

why would MODS patient need to be in ICU?

A
  • if failure of 1+ body system requiring support
    • cardiopulmonary - pressors and vent
    • neurologic - invasive ICT monitoring, frequent neuro checks
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50
Q

allowing chest recoil during CPR

A
  • perfuse coronary arteries
  • diastolic filling of heart
  • without recoil:
    • blood can’t get back into heart effectively
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51
Q

MODS

A
  • multiorgan dysfunction syndrome
  • presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention
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52
Q

circulating nurse in code

A
  • obtain & dispense supplies
  • supplies meds
  • access, prime IVs
  • send labs
  • set up equipment
  • dispense supplies
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53
Q

S/Sx of ACS

A
  • earlier
    • decrease CO/BP
    • change in mental status
    • increase in peak airway pressure
    • decrease in tidal volume
  • later
    • increase in abd girth
    • oliguria
    • systemic and dependent edema
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54
Q

secondary conditions causing IAH and ACS

A
  • severe intra-abd infection
  • large-volume fluid replacement
  • ascites
  • pancreatitis
  • ileus
  • sepsis
  • major burns
  • continuous ambulatory peritoneal dialysis
  • morbid obesity
  • pregnancy
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55
Q

integumentary side effects of therapeutic hypothermia

A

skin breakdown d/t decreased circulation

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56
Q

2010 therapeutic hypothermia guidelines

A
  • with ROSC after out-of-hospital VF, should be cooled to 32 to 34 for 12-24 hrs
  • with ROSC after in-hospital cardiac arrest of any initial rhythm or after out-of-hospital cardiac arrest with an initial rhythm of PEA or asystole
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57
Q

supportive measures for sepsis

A
  • fluid resuscitation
  • improve oxygenation
  • coag support
  • treat organ dysfxn/failure as needed
  • nutritional support
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58
Q

define abdominal compartment syndrome

A

increased pressure in closed anatomic space threatening viability of surrounding tissue

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59
Q

hands-only CPR

A
  • can work until rescue gets there
  • capacity of hbg molecular to carry up to 4 oxygen molecules
  • blood is oxygenated enough
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60
Q

cardiac implications in ACS

A
  • diaphragmatic elevation and increased intrathoracic pressure
    • compress heart
    • decrease venous return and contractile effectiveness
  • decrease in preload 2/2 IVC compression, inhibits venous return
    • decreased CO, more hypoperfusion
    • increased IAP inhibits venous emptying from abd viscera and organs (venous pooling)
    • venous pooling in lower extremities, overcoming oncotic pressure and forcing fluid to interstitium
    • afterload increased 2/2 abd aorta compression
      • decrease flow to abd, liver, kidneys
  • shock
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61
Q

increased cap permeability in SIRS

A
  • fluid leaks out of blood vessels and into interstitial space
    • loss of vessels’ normal response to stress
  • normal response - catecholamines release and vessels tighten up
  • results in
    • massive edema
    • intravascular fluid volume deficit
    • hypotension
  • distributive shock
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62
Q

site of injury in SIRS

A

vascular endothelium

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63
Q

IAH impact on hemodynamics

A
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64
Q

renal side effects of therapeutic hypothermia

A
  • diuresis
  • electrolyte imbalances
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65
Q

re-warming in therapeutic hypothermia

A
  • initiate 24 hr after target temp reached
  • set point 37 C moderate mode
    • increase set point 0.33 C q1h until tem reaches 37 C (~12 hr)
  • hold fluids w/ K+
  • maintain normothermia 48-72 hours post-rewarm
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66
Q

leaky capillary syndrome (SIRS)

A
  • fenestrations (opening) in capillaries allow for exchange of nutrients and oxygen btwn blood and tissue
  • inflammatory response causes dilation of capillaries and fenestrations enlarge
  • normally a balance between
    • oncotic pressure attracting fluid to intravascular space
    • hydrostatic pressure, cap filtration pressure pushing exchange of oxygen and fluid with tissues
  • when fenestrations enlarge, cap filtration pressure overwhelmes oncotic pressure, resulting in inappropriate fluid movement to interstitium (3rd spacing edema)
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67
Q

why are SIRS patients in metabolic acidosis?

A
  • anaerobic metabolism to overcome poor perfusion
  • results in high lactate (byproduct of anaerobic metabolism)
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68
Q

bactericidal vs bacteriostatic

A
  • bactericidal - killing bacteria
  • bacteriostatic - preventing further growth
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69
Q

integumentary implications in ACS

A
  • massive edema –> skin breakdown
    • dermis may separate from basement membrane
    • form large bolus lesions
      • infection risk if ruptured
    • risk for insensible fluid loss
70
Q

cardiovascular side effects of therapeutic hypothermia

A
  • bradycardia
  • hypovolemia
  • prolonged QT
71
Q

direct tissue injury/necrosis r/t SIRS

A
  • direct tissue injury
    • trauma
    • surgery
      • abdominal, cardiac, vascular
  • necrotic tissue
    • ischemic gut (very pro inflammatory)
    • ischemic extremity
72
Q

simultaneous pro and anti-inflammatory response in SIRS

73
Q

thoughtful bacterial culture usage

A
  • when is ordering a culture appropriate?
  • what are the implications for patient?
  • what are the implications for hospital?
74
Q

CNS side effects of therapeutic hypothermia

A
  • confusion
  • amnesia
75
Q

bystander CPR

A

improves survival rates to discharge

76
Q

invasion of microorganisms r/t SIRS

A
  • SIRS + infection = sepsis
  • gram +
  • gram -
  • fungus
  • virus
  • parasite
77
Q

what does SIRS stand for?

A
  • systemic
  • inflammatory
  • response
  • syndrome
78
Q

types of direct tissue injury leading to SIRS

A
  • obstetrical emergencies
    • abruptio placenta (tears away from uterine wall)
  • blood pump dyscrasias
    • cardio-pulm bypass
    • ECMO (extracorporeal membrane oxygenation)
79
Q

neuroprotective effects of therapeutic hypothermia

A
  • decreased neuro injury - decreased:
    • cerebral metabolism
    • oxygen consumption
    • inflammatory response
    • free radical release
    • cell damage, apoptosis
    • cerebral edema
  • cerebral metabolism decreases 6-10% every degree Celsius body temperature drops
80
Q

nursing management of hematologic fxn during therapeutic hypothermia

A
  • if bleeding, increase target temp to 34-35 C
  • treat as needed
81
Q

antibiotic stewardship

A
  • bactericidal vs bacteriostatic
  • effectiveness of drug
    • location of infection
    • ability for antibiotic to permeate area
    • ability of bacteria to resist/inactivate antibiotic
  • minimum inhibitory concentration (MIC)
    • level of abx associated with effective tx
    • lowest concentration to tx organism
    • lower MIC = better antimicrobial agent (also more expensive)
82
Q

pediatric SIRS criteria

A

at least 2 of the following, one of which is abnormal temp or leukocyte count

  • HR >2 st.dev above normal for age in absnece of stimuli
    • or unexplained elevation for > 30min - 4 hr
    • in infants: HR < 10th percentile for age in absence of stimuli OR unexplained depression for > 30 min
  • body temp < 36 or > 38.5
  • RR > 2 st.dev above normal for age or requiring methcanical ventilation not r/t neuromuscular disease or anesthesia
  • WBC eleated or depressed for age not r/t chemo OR >10% bands plus other immatuer forms
83
Q

CPR Quality

A
  • push hard (2-2.4 in) and fast (100-120/min)
  • allow complete chest recoil
  • minimize interruptions in compression
  • avoid excessive ventilation
  • rotate compressor q2 min
  • if no advanced airway: 30:2 compression-ventilation
84
Q

nursing management of infectious disease during therapeutic hypothermia

A
  • watch for fevers 48-72 hrs post event
    • treat with acetaminophen and/or cooling blanket
85
Q

supportive care for patient with open abdomen

A
  • tx causative process
  • invasive hemodynamic monitoring
  • careful I/O
  • vasoactive meds to support BP
  • ventilatory support
  • paralystics to decreas pressure and prevent evisceration
  • skin care
  • analgesia/sedation with paralytic
  • train of four (how many twitches of 4)
86
Q

lipase

A
  • most sensitive marker for pancreatitis
  • stays elevated for 14 days
  • amylase could be elvated for another reason
    • stone blocking salivary glands
    • also returns to normal w/in 72 hr
87
Q

pulmonary changes in sepsis

A
  • pulmonary edema - from third spacing
  • hypoxemia / shunting
  • atelectasis
  • initial respiraotry alkalosis, eventual acidosis
  • ARDS - acute respiratory distress syndrome
88
Q

treating sepsis

A
  • treat underlying cause
    • repair injury
    • remove necrotic tissue
    • immunosuppression for organ rejection
89
Q

fluid resuscitation in sepsis

A
  • crystalloid
  • blood products BP support
  • vasoconstrictors
    • levophed
    • dopamine
    • vasopressin
    • neosynephrine
90
Q

adult cardiac arrest - steps

91
Q

when will leukopenic responses occur during SIRS?

A
  • in elderly - can’t mount leukocytotic response
  • or fungal infections
92
Q

primary conditions causing IAH and ACS

A
  • blunt/penetrating trauma
  • liver transplant
  • ruptured abd aortic aneurysm
  • post op bleeding
  • retroperitoneal hemorrhage
  • mechanical intestinal obstruction
  • postop closure of abd under tension
  • bleeding pelvic fractures
93
Q

nursing management of musculoskeletal fxn during therapeutic hypothermia

A
  • sedate and paralyze prior to cooling
  • check skin under wraps
94
Q

exclusion criteria for therapeutic hypothermia

A
  • > 12 hrs since return of spontaneous circulation
  • glasgow motor score > 5
  • minimial premorbid cognitive status
  • other reason for coma
  • sepsis as cause of arrest (no longer exclusion)
  • DNR
  • significant trauma - d/t risk of bleeding
95
Q

nursing management of renal function during therapeutic hypothermia

A
  • follow electrolytes closely
    • esp during rewarming
  • stop all K+ fluids prior
96
Q

primary nurse during code

A
  • knows patient best - don’t leave room
  • communicate with code captain
    • what’s been happening during shift or recent days
    • events and assessment
  • coordinate care for pt
  • administer meds
  • assist with procedures
97
Q

hematologic changes in sepsis

A
  • leukocytosis
  • activation of clotting cascade (microemboli)
  • DIC
    thrombocytopenia
98
Q

define infection

A

host response to presence of microorganisms or tissue invasion by microorganisms

99
Q

endotoxin

A
  • substance found in cell walls of gram negative bacteria
  • aka lipopolysaccharide (LPS)
  • LPS activates cell mediator pathway
    • activates tumor necrosis factor
100
Q

pathophys of ACS

A
  • vicious cycle
    • rising abd pressures –> bowel ischemia –> tissue dysfxn/anaerobic metabolism
    • release of inflammatory mediators –> 3rd spacing 2/2 leaky capillary beds and decreased intravascular volume –> worsening hypoperfusion
  • increasing amounts of fluid in interstitial space
    • resulting edema rapidly increases pressure on abd
101
Q

musculoskeletal side effects of therapeutic hypothermia

A
  • shivering
    • increases metabolic demand and O2 consumption
102
Q

lower survival rates re: CPR

A
  • PEA and asystole
    • b/c less useful electrical and mechanical activity
    • can’t defib
103
Q

integumentary changes in sepsis

A
  • massive edema
  • skin breakdown
  • separation of skin from basement membrane
104
Q

ACLS secondary survey

A
  • airway
    • intubate if non-invasive breaths ineffective
  • breathing
    • confirm airway, ventilate
  • circulation
    • establish IV, administer meds
  • defib or differential diagnosis
    • find and treat cause
105
Q

biliary system

A

pancreatic enzymes normally travel to duodenum via pancreatic duct

106
Q

documentation in code

A
  • person identifies self as documenter
  • code form on code cart
  • document
    • time of meds
    • procedures
    • vital signs
    • events
  • obtain necessary signatures after code
107
Q

hallmarks of CPR

A
  • compress deep and fast
  • stay on chest while defib charging
  • 2 min CPR btwn each shock
    • then pulse check
  • minimize hands-free time
  • compressed heart = happy heart
108
Q

when the rapid response team arrives…

A

communication is key!

  • S - what’s happening now?
  • B - what were preceding events?
  • A - findings and what you think is happening
  • R - what do you want to be done?
109
Q

pulmonary implications in ACS

A
  • rising abdominal pressures mechanically elevate diaphraghm
    • (rising 2/2 compression from abd edema)
  • increases peak airway pressures and decrease in lung capacity
    • resulting atelectasis
  • also ARDS and direct tissue injury d/t pancreatic enzymes
110
Q

preventing sepsis

A
  • identify high risk patients
    • elderly
    • immunosuppressed
    • surgery, trauma, vents
    • all ICU patients
  • keep IV lines clean, dry, intact dressings
  • prevention of nosocomial infections
  • feed patient
  • handwashing
111
Q

nursing management of CNS during therapeutic hypothermia

A
  • if patient is not following commands, no cooling
  • GMS < 6
  • no neuroprognostication until 72 hrs after re-warming
112
Q

why not cool patients less than 32?

A
  • pro-arrhythmic properties
  • vtach and vfib become more refractory to successful defib at colder temps
113
Q

hand hygiene products

A
  • hand sanitizer
  • soap & water
  • antimicrobial soap
  • CHG
114
Q

coagulation abnormalities in SIRS

A
  • considered key to organ dysfunction / death
    • clots decrease perfusion, oxygen delivery
  • research to design therapies to combat this destruction
115
Q

SIRS criteria - diagnosing

A

2+ of following = SIRS

  • temp > 38.3/100.9 or <36/96.8
  • HR > 90
  • RR > 20 or PaCO2 < 32mmHg
  • WBC > 12,000, <4,000, or >10% bands
116
Q

inflammation/increased WBCs in SIRS

A
  • increases immune response
  • results in
    • fever
    • vasodilation
    • tachycardia
    • leukocytosis
117
Q

body’s response to SIRS

A
  • tissue hypoperfusion
    • = shock
  • systemic response - every cell affected
  • in response to 3 key points
    • cap permeability
    • immune response
    • clotting cascade
118
Q

CAB in BLS

A
  • circulation
    • feel for pulse - start compressions
    • 2-2.4 in, 100-120 bpm, chest recoil
  • airway
    • position head - tilt chin-lift
  • breathing
    • if not breathing, flatten head of bed
    • begin bag/valve mask
119
Q

treatment for ACS

A
  • improve abd wall compliance
    • analgesia, anxiolysis, +/- paralytics
  • proper body alignment
    • avoid hip flexion, HOB < 20 (increased ICP, aspiration)
  • evacuate abd contents
    • NGT/OGT, +/- drugs to increase gastric motility
  • correct positive fluid balance
    • restrict fluids, administer colloids
    • diuretic therapy
    • HD or CRRT to remove fluid
  • surgical decompression, damage control abdomen with open fascia, sterile dressing
120
Q

clinical parameters indicating need for rapid response

A
  • cardiovascular
    • HR >140 or <40
    • CP unrelieved by nitro
  • pulm
    • oxygen sat <90% w/ oxygen
    • inability to protect airway
  • neuro
    • acute change in mental status
    • seizure
  • urine output
    • <50 ml in 4 hrs
  • uncontrolled pain
  • staff or family member concerned about patient’s condition
121
Q

early goal directed therapy in sepsis

A
  • recognize patients via SIRS criteria
  • appropriate labs, tests
  • early abx targeted empirically
  • fluid resuscitation
122
Q

pediatric emergencies (re: code)

A
  • usually airway issues
  • pediatric bls
    • clear obstructed airway
    • resusc breathing
123
Q

SIRS overview

A
  • can affect any patient, especially acute care
  • often associated with infection (sepsis)
  • occurs in response to injury
    • may be result of multitude of causes
  • mostly d/t
    • direct tissue injury/necrosis
    • presence of foreign invaders
    • invasion of microorganisms
124
Q

cooling methods in therapeutic hypothermia

A
  • surface ooling
    • precooled surface cooling pad
    • water-circulating surface cooling pad
  • core cooling methods
    • cold IV fluids
    • catheter-based endosvascular device inserted in femoral vein
125
Q

timeline for therapeutic hypothermia

A
  • cool for 24 hours
  • rewarm gradually over 12 hrs
  • check neuro outcome 3 days later
126
Q

define syndrome

A
  • set of medical signs and symptoms that are correlated with each other and, often, with a specific disease
  • derived from Greek word “concurrence”
127
Q

bacterial sepsis

A
  • bacteria invade and release endotoxins
  • cell mediator pathway is initiated
128
Q

as code team arrives

A
  • documentation
  • bring code cart (CPR board on back of cart)
  • bring airway box
    • situate at head of bed for anesthesia to arrive
    • connect and test suction
  • apply leads on patient and defib pads if indicated
  • crowd control
129
Q

how does hypothermia protect from ischemic injury?

A
  • neuroexitatory processes slowed by stabilizing influx of calcium and glutamate
  • cerebral metabolism slowed –> decreased oxygen consumption
  • inflammatory response hampered –> decreased release of free radicals –> decreased cell damage and apoptosis
  • limits cell death, decreases disruptions in blood brain barrier, limits cerebral edema
130
Q

characteristics of hemorrhagic vs nonhemorrhagic acute pancreatitis

131
Q

cardiovascular changes in sepsis

A
  • tachy
  • increased CO in early phase
  • decreased SVR
  • hypotension
  • fluid shifts
132
Q

why is a SIRS patient tachypneic?

A

blowing off CO2 to combat metabolic acidosis through respiratory compensation

133
Q

non-bacterial sepsis

A
  • fungal
    • aspergillus, coccidiomycosis, histoplasma
  • yeast - candida
  • parasites
134
Q

endocrine side effects of therapeutic hypothermia

A
  • hyperglycemia
    • decreased insulin sensitivity and secretion
135
Q

advanced airway in code

A
  • supraglottic or ET
  • waveform capnography to confirm/monitor ET placement
  • 8-10 breaths/min with continuous chest compressions
136
Q

what is a rapid response?

A
  • when a patient demonstrates signs of imminent clinical deterioration, a team of providers is summoned to the bedside to immediately assess and treat the patient with the goal of preventing ICU transfer, cardiac arrest, or death
  • used as a system to recognize clinical deterioration before we reach need for a code
137
Q

nurses on unit during code

A
  • sometimes might have too many
  • may need to do crowd control
  • don’t forget about other patients
138
Q

immune/inflammatory response to therapeutic hypothermia

A
  • impaired
  • increased risk of pneumonia and infectious disease
139
Q

cell mediated activity r/t SIRS

A
  • damage to vascular endothelium causes release of cell mediators
  • cascade effect occurs resulting in:
    • increased cap permeability
      • 3rd spacing of fluids
    • activation of immune response
      • fever, tachycardia
    • activation of clotting cascade
      • microemboli
140
Q

leading cause(s) of acute pancreatitis

A
  • alcohol abuse
  • gallstones
  • ERCP
141
Q

transport in code

A

may need emergent teting or emergent surgical intervention

142
Q

shock energy in code

A
  • biphasic
    • initial 120-200 J
    • if unknown, use maximum available
    • second doses equivalent or higher
  • monphasic 360 J
143
Q

septic shock

A
  • subset of severe sepsis
  • severe tissue hypoperfusion, organ failure, hypotension, acidosis
  • sepsis induced hypotension despite adequate fluid resuscitation
    • post 30 ml/kg bolus
    • SBP <90, MAP <65 or lactate >4
144
Q

betadine

A
  • for mucosal areas
  • b/c alcohol is very drying and betadine isn’t
  • betadine + alcohol = duraprep (in OR)
145
Q

presence of anti-inflammatory mediators in SIRS response

A
  • released in response to the release of pro-inflammatory mediators
    • to protect areas not affected by SIRS response
  • normally come in to chill the body out after healing is done
  • presence of both pro and anti mediators confused body and creates negative result
146
Q

induction phase of therapeutic hypothermia

A
  • infuse 2L 0.9% NS over 30 min
  • continuous temp monitoring
  • goal temp 32-34 C asap (w/in 4 hrs)
    • sedation, paralytics, neuromuscular blocking agents
    • maintain goal temp for 24 hours from time target temp reached
147
Q

purpose of targeted temperature management

A

optimize neurological outcomes for survivors of cardiac arrest

148
Q

neurological changes in sepsis

A
  • decreased level of consciousness
  • decreased cerebral blood flow
149
Q

types of foreign invaders leading to SIRS

A
  • transplant organ rejection
    • acute/chronic rejection breaks through immune suppression and has tremendous inflammatory response to that foreign tissue
  • obstetrical
    • retained placental fragments
      • after vaginal delivery or spontaneous miscarriage
150
Q

when inflammatory response is not normal

A
  • inflammatory response to injury is usually normal, compensatory mechanism
  • SIRS increases exponentially and overwhelms body’s system
151
Q

gram negative sepsis

A
  • most common cause of sepsis/septic shock
  • “classic” sepsis
  • common organisms
    • enterobacter - e.coli, salmonella, serratia, proteus
    • pseudomonus, acinetobacter - tend to be HAI, require long-term care
    • H influenza
152
Q

mortality from cardiac arrest

153
Q

define bacteremia

A

presence of viable bacteria in circulating blood

154
Q

characteristics of ineffective CPR

A
  • w/o effective CC
    • oxygen to brain and heart stops
  • excessive pauses associated with
    • decreased survival, unsuccessful defib
  • hyperventilation = decreased survival
155
Q

gram positive bacteria

A
  • more prevalent in surgical population
  • also produce toxins (peptidoglycans) that activate cell mediator pathway
  • organisms
    • staph (skin flora), strep
    • bacillus
156
Q

what do we know about CPR?

A
  • quality of CPR is poor
  • time to defib is too long (goal is 2 min)
  • hyperventilation is rampant
  • pauses are long and frequent
157
Q

“the equipment” in aseptic technique

A
  • bundles
  • skin prep
  • sterile field
158
Q

what is a code?

A
  • pt requires immediate life-saving intervention
  • cardiac or resp in nature
  • if no intervention is performed, patient will not survive
159
Q

link btwn acute pancreatitis and ACS

A
  • IAH as early as day 1 of symptoms and up to 6 days
  • ACS initiated by inflammatory process
  • capillary leakage and fluid resusc worsens edema
  • paralytic ileus and upper GI tract obstrution by pancreatic collections can aggravate ACS
  • reduced abd wall compliance d/t edema
  • arterial/venous bleeding from necrotic/inflammed tissue
    • increase IAP
  • pancreatic perfusion affected by disease process itself
  • bacterial translocation
160
Q

how does local infection become systemic SIRS response?

A

bacteria doesn’t get into blood - toxins do

161
Q

GI implications in ACS

A
  • high abd pressure decreases perfusion of organ tissue
    • via compression of vasculature
  • resulting ischemia, acidosis, breakdown of intestinal epithelium
    • bacterial translocation
    • sepsis if not already occuring
162
Q

coagulation support in sepsis

A
  • blood products
  • xigris
    • synthetic protein C to control inflammation, coagulation and fibrinolysis
    • pulled from markets Oct 2011
163
Q

treating organ dysfunction/failure in sepsis

A
  • dialysis
  • ventilator (PEEP, PCV)
  • inotropes
164
Q

types of ACS

A
  • primary
    • disease process in abdomino-pelvic region
    • most frequent
  • secondary
    • conditions not originating in abdomino-pelvic region
    • most often after large volume resusc in burns, sepsis
  • recurrent
    • after treatment for prior ACS
165
Q

nursing management of respiration during therapeutic hypothermia

A
  • avoid hyperventilation
  • avoid high FiO2
166
Q

neuroprognostication re: therapeutic hypothermia

A
  • neuro exam impaired for days
  • associated w/ delay in recovery of motor response for 6+ days
  • neuro exam (esp motor) at day 3 is less certain
  • seizures may not have same implication on prognosis
  • certain CT scans may not have same implication on prognosis
  • should not neuroprognosticate until at least 72 hours after rewarming
    • maybe longer
167
Q

hypothermia mechanisms

168
Q

SIRS epidemiology

A
  • 10th leading cause of death
    • 500 patients/day
  • # 1 cause of death in non-coronary ICUs
  • 750,000 cases/year
  • mortality
    • gram negative 20-50% (like to share mechanisms for resistance)
    • septic shock 40-60%
169
Q

sepsis

A
  • systemic inflammatory response to infection
  • manifestations of sepsis are same as those for SIRS
170
Q

nursing management of endocrine function during therapeutic hypothermia

A
  • hyperglycemia - follow ICU protocol
  • watch for drug accumulation
    • train of four - paralytics
    • BIS - sedation
171
Q

IAP and ACS

A
  • normal IAP < 12 mmHg
  • persistent IAP > 12 mmHg = intra-abdominal hypertension (IAH)
  • IAP > 20 mmHg + new onset organ dysfxn = ACS

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