Seminar Exam 3 Flashcards

(171 cards)

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
chlorhexidine gluconate + alcohol
* antimicrobial (not antifungal) skin prep * alcohol - 70% or higher isopropol * not for neonates \< 32 weeks
26
calculate abdominal perfusion pressure (APP)
* MAP - IAP * maintain APP \> 60 to decrease morbidity, mortality
27
rapid response team members
* critical care nurse * respiratory therapist * physicial (CC or hospitalist) * nursing supervisor (coordinators) * can get a pt a bed
28
three key points in SIRS
* increased capillary permeability * 3rd spacing of fluids * activation of immune response * fever, tachycardia * activation of clotting cascade * microemboli
29
drug therapy for code
* epi IV/IO: 1 mg q3-5 min * amiodarone IV/IO: * first dose 300 mg * second dose 150 mg
30
monitoring ACS
* 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
31
epidemiology of acute pancreatitis
* 18 per 100,000 * 3x more in AA than caucasian * males \> females * 10-15% mortality in uncomplicated acute * 30% if mounting MODS reaction
32
stages of SIRS response
* 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
33
severe sepsis
* 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
34
hematologic side effects of therapeutic hypothermia
* coagulopathy, despite normal lab tests * decreased platelet function @ 35 C * decreased function of plasma proteins @ 34 C
35
prognosis of MODS
* 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%
36
concept of antimicrobial stewardship
* 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
37
renal changes in sepsis
* 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
38
not recommended during therapeutic hypothermia
* focus on preventing fever or maintaining normothermia will not have same outcomes * not substantiated * prehospital cooling not recommended
39
causes of infection
* central lines, foley, A-lines * trauma, surgery * translocation of gut bacteria * ventilators * diabetes * cancer, immune compromised * alcohol, malnourished * epithelial barrier
40
what happens when you cut your finger? (normal response)
* 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
41
maintaining therapeutic hypothermia
* internal catheter or external cooling blanket * from time until patient hits target temp until re-warming begins * serial labs * patient testing * EEG monitor
42
neuro monitoring during therapeutic hypothermia
* 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
43
renal implications in ACS
* acute failure 2/2 renal vein obstruction * indirect failure 2/2 decreased intravascular volume * prerenal AKI
44
measuring intraabdominal pressure
* directly via intra-abdominal catheter * more commonly indirectly via bladder pressure (special device on Foley)
45
#1 way to prevent infection
hang hygiene
46
1st hit vs 2nd hit in SIRS
* 1st hit - initial injury followed by SIRS response * 2nd hit - another injury on top results in increased SIRS response
47
antibiotics for sepsis
* gram + * vanco, linezolid * gram - * gentamycin, levaquin, ticarcillin, cefepime * broad spectrum * imipenem * zosyn * augmentin
48
"helper" nurses during code
* 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
49
why would MODS patient need to be in ICU?
* if failure of 1+ body system requiring support * cardiopulmonary - pressors and vent * neurologic - invasive ICT monitoring, frequent neuro checks
50
allowing chest recoil during CPR
* perfuse coronary arteries * diastolic filling of heart * without recoil: * blood can't get back into heart effectively
51
MODS
* multiorgan dysfunction syndrome * presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention
52
circulating nurse in code
* obtain & dispense supplies * supplies meds * access, prime IVs * send labs * set up equipment * dispense supplies
53
S/Sx of ACS
* 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
54
secondary conditions causing IAH and ACS
* severe intra-abd infection * large-volume fluid replacement * ascites * pancreatitis * ileus * sepsis * major burns * continuous ambulatory peritoneal dialysis * morbid obesity * pregnancy
55
integumentary side effects of therapeutic hypothermia
skin breakdown d/t decreased circulation
56
2010 therapeutic hypothermia guidelines
* 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
57
supportive measures for sepsis
* fluid resuscitation * improve oxygenation * coag support * treat organ dysfxn/failure as needed * nutritional support
58
define abdominal compartment syndrome
increased pressure in closed anatomic space threatening viability of surrounding tissue
59
hands-only CPR
* can work until rescue gets there * capacity of hbg molecular to carry up to 4 oxygen molecules * blood is oxygenated enough
60
cardiac implications in ACS
* 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
61
increased cap permeability in SIRS
* 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
62
site of injury in SIRS
vascular endothelium
63
IAH impact on hemodynamics
64
renal side effects of therapeutic hypothermia
* diuresis * electrolyte imbalances
65
re-warming in therapeutic hypothermia
* 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
66
leaky capillary syndrome (SIRS)
* 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)
67
why are SIRS patients in metabolic acidosis?
* anaerobic metabolism to overcome poor perfusion * results in high lactate (byproduct of anaerobic metabolism)
68
bactericidal vs bacteriostatic
* bactericidal - killing bacteria * bacteriostatic - preventing further growth
69
integumentary implications in ACS
* massive edema --\> skin breakdown * dermis may separate from basement membrane * form large bolus lesions * infection risk if ruptured * risk for insensible fluid loss
70
cardiovascular side effects of therapeutic hypothermia
* bradycardia * hypovolemia * prolonged QT
71
direct tissue injury/necrosis r/t SIRS
* direct tissue injury * trauma * surgery * abdominal, cardiac, vascular * necrotic tissue * ischemic gut (very pro inflammatory) * ischemic extremity
72
simultaneous pro and anti-inflammatory response in SIRS
73
thoughtful bacterial culture usage
* when is ordering a culture appropriate? * what are the implications for patient? * what are the implications for hospital?
74
CNS side effects of therapeutic hypothermia
* confusion * amnesia
75
bystander CPR
improves survival rates to discharge
76
invasion of microorganisms r/t SIRS
* SIRS + infection = sepsis * gram + * gram - * fungus * virus * parasite
77
what does SIRS stand for?
* systemic * inflammatory * response * syndrome
78
types of direct tissue injury leading to SIRS
* obstetrical emergencies * abruptio placenta (tears away from uterine wall) * blood pump dyscrasias * cardio-pulm bypass * ECMO (extracorporeal membrane oxygenation)
79
neuroprotective effects of therapeutic hypothermia
* 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
nursing management of hematologic fxn during therapeutic hypothermia
* if bleeding, increase target temp to 34-35 C * treat as needed
81
antibiotic stewardship
* 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
pediatric SIRS criteria
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
CPR Quality
* 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
nursing management of infectious disease during therapeutic hypothermia
* watch for fevers 48-72 hrs post event * treat with acetaminophen and/or cooling blanket
85
supportive care for patient with open abdomen
* 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
lipase
* 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
pulmonary changes in sepsis
* pulmonary edema - from third spacing * hypoxemia / shunting * atelectasis * initial respiraotry alkalosis, eventual acidosis * ARDS - acute respiratory distress syndrome
88
treating sepsis
* treat underlying cause * repair injury * remove necrotic tissue * immunosuppression for organ rejection
89
fluid resuscitation in sepsis
* crystalloid * blood products BP support * vasoconstrictors * levophed * dopamine * vasopressin * neosynephrine
90
adult cardiac arrest - steps
91
when will leukopenic responses occur during SIRS?
* in elderly - can't mount leukocytotic response * or fungal infections
92
primary conditions causing IAH and ACS
* 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
nursing management of musculoskeletal fxn during therapeutic hypothermia
* sedate and paralyze prior to cooling * check skin under wraps
94
exclusion criteria for therapeutic hypothermia
* \> 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
nursing management of renal function during therapeutic hypothermia
* follow electrolytes closely * esp during rewarming * stop all K+ fluids prior
96
primary nurse during code
* 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
hematologic changes in sepsis
* leukocytosis * activation of clotting cascade (microemboli) * DIC thrombocytopenia
98
define infection
host response to presence of microorganisms or tissue invasion by microorganisms
99
endotoxin
* substance found in cell walls of gram negative bacteria * aka lipopolysaccharide (LPS) * LPS activates cell mediator pathway * activates tumor necrosis factor
100
pathophys of ACS
* 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
musculoskeletal side effects of therapeutic hypothermia
* shivering * increases metabolic demand and O2 consumption
102
lower survival rates re: CPR
* PEA and asystole * b/c less useful electrical and mechanical activity * can't defib
103
integumentary changes in sepsis
* massive edema * skin breakdown * separation of skin from basement membrane
104
ACLS secondary survey
* 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
biliary system
pancreatic enzymes normally travel to duodenum via pancreatic duct
106
documentation in code
* person identifies self as documenter * code form on code cart * document * time of meds * procedures * vital signs * events * obtain necessary signatures after code
107
hallmarks of CPR
* 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
when the rapid response team arrives...
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
pulmonary implications in ACS
* 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
preventing sepsis
* 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
nursing management of CNS during therapeutic hypothermia
* if patient is not following commands, no cooling * GMS \< 6 * no neuroprognostication until 72 hrs after re-warming
112
why not cool patients less than 32?
* pro-arrhythmic properties * vtach and vfib become more refractory to successful defib at colder temps
113
hand hygiene products
* hand sanitizer * soap & water * antimicrobial soap * CHG
114
coagulation abnormalities in SIRS
* considered key to organ dysfunction / death * clots decrease perfusion, oxygen delivery * research to design therapies to combat this destruction
115
SIRS criteria - diagnosing
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
inflammation/increased WBCs in SIRS
* increases immune response * results in * fever * vasodilation * tachycardia * leukocytosis
117
body's response to SIRS
* tissue hypoperfusion * = shock * systemic response - every cell affected * in response to 3 key points * cap permeability * immune response * clotting cascade
118
CAB in BLS
* 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
treatment for ACS
* 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
clinical parameters indicating need for rapid response
* 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
early goal directed therapy in sepsis
* recognize patients via SIRS criteria * appropriate labs, tests * early abx targeted empirically * fluid resuscitation
122
pediatric emergencies (re: code)
* usually airway issues * pediatric bls * clear obstructed airway * resusc breathing
123
SIRS overview
* 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
cooling methods in therapeutic hypothermia
* 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
timeline for therapeutic hypothermia
* cool for 24 hours * rewarm gradually over 12 hrs * check neuro outcome 3 days later
126
define syndrome
* set of medical signs and symptoms that are correlated with each other and, often, with a specific disease * derived from Greek word "concurrence"
127
bacterial sepsis
* bacteria invade and release endotoxins * cell mediator pathway is initiated
128
as code team arrives
* 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
how does hypothermia protect from ischemic injury?
* 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
characteristics of hemorrhagic vs nonhemorrhagic acute pancreatitis
131
cardiovascular changes in sepsis
* tachy * increased CO in early phase * decreased SVR * hypotension * fluid shifts
132
why is a SIRS patient tachypneic?
blowing off CO2 to combat metabolic acidosis through respiratory compensation
133
non-bacterial sepsis
* fungal * aspergillus, coccidiomycosis, histoplasma * yeast - candida * parasites
134
endocrine side effects of therapeutic hypothermia
* hyperglycemia * decreased insulin sensitivity and secretion
135
advanced airway in code
* supraglottic or ET * waveform capnography to confirm/monitor ET placement * 8-10 breaths/min with continuous chest compressions
136
what is a rapid response?
* 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
nurses on unit during code
* sometimes might have too many * may need to do crowd control * don't forget about other patients
138
immune/inflammatory response to therapeutic hypothermia
* impaired * increased risk of pneumonia and infectious disease
139
cell mediated activity r/t SIRS
* 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
leading cause(s) of acute pancreatitis
* **alcohol abuse** * gallstones * ERCP
141
transport in code
may need emergent teting or emergent surgical intervention
142
shock energy in code
* biphasic * initial 120-200 J * if unknown, use maximum available * second doses equivalent or higher * monphasic 360 J
143
septic shock
* 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
betadine
* for mucosal areas * b/c alcohol is very drying and betadine isn't * betadine + alcohol = duraprep (in OR)
145
presence of anti-inflammatory mediators in SIRS response
* 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
induction phase of therapeutic hypothermia
* 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
purpose of targeted temperature management
optimize neurological outcomes for survivors of cardiac arrest
148
neurological changes in sepsis
* decreased level of consciousness * decreased cerebral blood flow
149
types of foreign invaders leading to SIRS
* 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
when inflammatory response is not normal
* inflammatory response to injury is usually normal, compensatory mechanism * SIRS increases exponentially and overwhelms body's system
151
gram negative sepsis
* 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
mortality from cardiac arrest
153
define bacteremia
presence of viable bacteria in circulating blood
154
characteristics of ineffective CPR
* w/o effective CC * oxygen to brain and heart stops * excessive pauses associated with * decreased survival, unsuccessful defib * hyperventilation = decreased survival
155
gram positive bacteria
* more prevalent in surgical population * also produce toxins (peptidoglycans) that activate cell mediator pathway * organisms * staph (skin flora), strep * bacillus
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what do we know about CPR?
* quality of CPR is poor * time to defib is too long (goal is 2 min) * hyperventilation is rampant * pauses are long and frequent
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"the equipment" in aseptic technique
* bundles * skin prep * sterile field
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what is a code?
* pt requires immediate life-saving intervention * cardiac or resp in nature * if no intervention is performed, patient will not survive
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link btwn acute pancreatitis and ACS
* 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
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how does local infection become systemic SIRS response?
bacteria doesn't get into blood - toxins do
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GI implications in ACS
* 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
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coagulation support in sepsis
* blood products * xigris * synthetic protein C to control inflammation, coagulation and fibrinolysis * pulled from markets Oct 2011
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treating organ dysfunction/failure in sepsis
* dialysis * ventilator (PEEP, PCV) * inotropes
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types of ACS
* 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
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nursing management of respiration during therapeutic hypothermia
* avoid hyperventilation * avoid high FiO2
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neuroprognostication re: therapeutic hypothermia
* 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
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hypothermia mechanisms
168
SIRS epidemiology
* 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%
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sepsis
* systemic inflammatory response to infection * manifestations of sepsis are same as those for SIRS
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nursing management of endocrine function during therapeutic hypothermia
* hyperglycemia - follow ICU protocol * watch for drug accumulation * train of four - paralytics * BIS - sedation
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IAP and ACS
* normal IAP \< 12 mmHg * persistent IAP \> 12 mmHg = intra-abdominal hypertension (IAH) * IAP \> 20 mmHg + new onset organ dysfxn = ACS