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7320 > Acute Resp Failure (ARF) > Flashcards

Acute Resp Failure (ARF) Flashcards

1
Q

resp failure def

A

system fail in one or both major function

  • gas exchange (oxygenation)
  • ventilation (eliminate CO2)
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2
Q

diagnose ARF?

A

ABGs

PAO2< 60
PaCO2 > 45
pH < 7.35 (for Pts with chronic elevated CO2)

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3
Q

Type 1 resp failure

A

acute hypoxemic resp failure

  • low PaO2
  • prob gas exchange**
    ex: CHF, atelectasis, fibrosis, pneumonia, decreased CO, hypotension, PE, shock
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4
Q

Type 2 resp failure

A

acute hypercapnia/hypercarbic resp failure

  • high PaCO2
  • primary issue ventilation** impacting elimination of CO2
    ex. COPD, Guillian Barre, Drug OD, pleural effusions. chest trauma, MS, muscluar dystrophy, asthma, trach obstruction, massive obese,
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5
Q

mixed/combined resp failure

A

hypoxemic/hypercapnic

  • diff to determine primary cause
  • if either type left too long, will result in both
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6
Q

type 1 resp fail impaired by?

A
  • diffusion or V/Q mismatch
  • most common V/Q mismatch - alveoli collapsed or fluid filled
  • O2 supply/demand imbalance = tissue hypoxia = impaired perfusion = develop lactic acidosis and MODS
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7
Q

What do you want for PaO2?

A

60-65 is aprx = SaO2 90%

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8
Q

what happens when PaO2< 60

A

chemoreceptors sense and trigers resp center to increase ventilation

early ABG=   later=
pH 7.33           7.37
PaO2 58          50
PaCO2 30       40
HCO2 24         24

without intervention fatigue sets in

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9
Q

type 2 resp failure impaired by?

A
  • ventilation moving air in and out of lungs

- when lungs cant clear CO2**

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10
Q

what do we see in hypercapnic resp failure?

A
  • PaCO2 changes

Initial ABG: Later: chronic
pH 7.50 7.45 partial or full comp
PaO2 75 75
PaCO2 50 50
HCO3 24 30 compensation

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11
Q

ETCO2 monitor

A

Continuoue end tidal CO2 monitor

  • can have small deviation of 0-5mmHg normal
  • ***look at trend
  • measure CO2 at end expire
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12
Q

compensatory mechanisms

A

central chemoreceptors

  • medulla (resp center): increased CO2 = increased RR and TV
  • periph aortic arch and baroreceptors increased CO2 = increase RR and TV

SNS- responds to hypoxemia to increase HR = increased supply

Vasodilation

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13
Q

diagnose ARF

A
  • clinic presentation
  • Hx
  • ABG
  • CXR/CT
  • V/Q scan (PE)
  • Cand S samples
  • CBC
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14
Q

PT admitted with asthma. sedated on vent ACV: TV 650, RR 10, FiO2 30 %, PEEP 0

Why?

A

the longer I:E ration decreases air trapping and auto peep improving

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15
Q

classification of pneumonia

A 
1. site of acquisition**
CAP
-- gram +
-- strep/ staph 
-- < 48 hrs from admission
-- thin watery sputum
HAP
-- gram - 
-- h. influ, e. coli
-- > 48 hrs from admit 
-- thick yellow sputum

Aspiration Pneumonia

VAP

    • 64%
    • staph/strep
      2. causal agent
      3. severity
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16
Q

ABX start…. then….

A

start broad spectrum and send cultures

then: narrow by gram stain - or + (24 hrs)
then: narrow culture and sensitivity (48hrs)

17
Q

promoting gas exchange

A

diffusion:

  • CPAP, EPAP, PEEP
  • recruitment maneuvers
  • FiO2
  • Lasix/minimize IV fluids
  • ABX

V/Q mismatch:

  • position HOB, good lung down, prone
  • suctioning
  • PEEP
  • optimize CO
  • vasopressors, heparin
18
Q

promoting ventilation

A

WOB:

  • BiPAP, CPAP
  • frqnt SBT
  • nutrition - resp muscle function
  • mobilize
  • suction
  • bronchodilators/ABX

Volumes and rate:

  • increase set TV and RR
  • increase pressure support
  • sedatives/analgesics
  • paralytics
19
Q

when do you use CPAP

A

only with O2 issues. same pressure the entire cycle

20
Q

When to use BiPAP

A

for vent and gas exchange issues
- senses inspire and delivers high flow air/O2 mix and maintains the whole cycle

IPAP - for vent

  • 10-20
  • boost of air each breath
  • adds TV
  • monitor PaCO2

EPAP/FiO2 - for gas exchange

  • 5-10
  • prevents alveoli from complete empty
  • monitor PaO2
  • PT needs to be awake and protect own airway
  • if not success then mech vent
21
Q

NIPPV

A

non-invasive + pressure vent

  • CPAP or BIPAP
  • uncomfortable = anxiety
  • major aspiration risk
  • can put air into stomach
  • need to be able to remove on own
  • NPO
  • short term
22
Q

assess PTs on NIPPV

A
  • WOB, TV, RR, SpO2, ETCO2 , hemodynamics, LOC
  • check ABG 30 min after starting or change in settings
  • improve should be within 1 hr, if not in 2 may need to be intubated
23
Q

Hyperglycemia in critical illness

A
  • glucose >10 twice in 24 hrs
  • weakens the immune defense system
  • contributes to abnormal inflammatory responses to infection
  • induces elevated lactate levels
24
Q

intubation

A
  1. compromised airway
    - cough,gag, secretions, vomit, GI bleed, upper airway edema, obstruction, decrease LOC,
  2. Severe Oxygenation issue:
    - rapid shallow breathing
    - tachycardia, diaphoresis
    - ABG= hypoxemia, poss resp alkalosis
  3. Severe vent issue
    - rapid, shallow breathing or apnea (drug OD)
    - tachy, diaphoresis
    - HX: COPD, decresed LOC, pneumonia,)
    - ABG = resp acidosis
  4. Anticipated clinical course
    - PT likely get worse
    - PT with little reserve to compensate (loss resp muscles from long admit, chronic ill)
25
Q

7 P’s of RSI

A

rapid sequence intubation

  1. prep
  2. pro-oxygenate- tight non-rebreather, or bvm ambubag with jaw thrust
    - up to 3-5 min to wash out nitrogen
  3. pre-treat
  4. paralysis with induction
    - give analgesia/sedation and then paralytic
    - push IV direct
    - closed loop communication
  5. positioning
    - sniff position
    - attempts limit to 30 sec
    - cuff inflate, tied, attach to vent, RN insert OG tube
    - CXR ETT/OG
    - document size/placement
    - ABG 15-30 min post
    - cont IV sedation until paralytic wears off (propofol 1-2 hrs until roc wears off)
    - entral feeds GI cont suction
  6. placement with proof
  7. post-intubation manage
26
Q

Gluconeogenesis

A

process of generating glucose from sorces other than carb, occurs mainly in the liver as a method of maintaining adequate glucose levels

27
Q

glucogenolysis

A

breaks down glycogen to glucose to provide energy for muscle contraction. Takes place in the cell of the muscle and liver tissue

28
Q

hyperglycemia occurs bc

A
  • SNS response
  • elevated cortisol levels
  • insulin resistance
29
Q

malnutrition in CC is caused by?

A
  • frequesnt pausing of enteral feeds
  • SNS response and inhibition of digestive organs
  • hypermetabolic state

7320 (8 decks)

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