Acute Resp Failure (ARF) Flashcards
resp failure def
system fail in one or both major function
- gas exchange (oxygenation)
- ventilation (eliminate CO2)
diagnose ARF?
ABGs
PAO2< 60
PaCO2 > 45
pH < 7.35 (for Pts with chronic elevated CO2)
Type 1 resp failure
acute hypoxemic resp failure
- low PaO2
- prob gas exchange**
ex: CHF, atelectasis, fibrosis, pneumonia, decreased CO, hypotension, PE, shock
Type 2 resp failure
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,
mixed/combined resp failure
hypoxemic/hypercapnic
- diff to determine primary cause
- if either type left too long, will result in both
type 1 resp fail impaired by?
- 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
What do you want for PaO2?
60-65 is aprx = SaO2 90%
what happens when PaO2< 60
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
type 2 resp failure impaired by?
- ventilation moving air in and out of lungs
- when lungs cant clear CO2**
what do we see in hypercapnic resp failure?
- 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
ETCO2 monitor
Continuoue end tidal CO2 monitor
- can have small deviation of 0-5mmHg normal
- ***look at trend
- measure CO2 at end expire
compensatory mechanisms
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
diagnose ARF
- clinic presentation
- Hx
- ABG
- CXR/CT
- V/Q scan (PE)
- Cand S samples
- CBC
PT admitted with asthma. sedated on vent ACV: TV 650, RR 10, FiO2 30 %, PEEP 0
Why?
the longer I:E ration decreases air trapping and auto peep improving
classification of pneumonia
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
- staph/strep
ABX start…. then….
start broad spectrum and send cultures
then: narrow by gram stain - or + (24 hrs)
then: narrow culture and sensitivity (48hrs)
promoting gas exchange
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
promoting ventilation
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
when do you use CPAP
only with O2 issues. same pressure the entire cycle
When to use BiPAP
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
NIPPV
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
assess PTs on NIPPV
- 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
Hyperglycemia in critical illness
- glucose >10 twice in 24 hrs
- weakens the immune defense system
- contributes to abnormal inflammatory responses to infection
- induces elevated lactate levels
intubation
- compromised airway
- cough,gag, secretions, vomit, GI bleed, upper airway edema, obstruction, decrease LOC, - Severe Oxygenation issue:
- rapid shallow breathing
- tachycardia, diaphoresis
- ABG= hypoxemia, poss resp alkalosis - Severe vent issue
- rapid, shallow breathing or apnea (drug OD)
- tachy, diaphoresis
- HX: COPD, decresed LOC, pneumonia,)
- ABG = resp acidosis - Anticipated clinical course
- PT likely get worse
- PT with little reserve to compensate (loss resp muscles from long admit, chronic ill)
7 P’s of RSI
rapid sequence intubation
- prep
- pro-oxygenate- tight non-rebreather, or bvm ambubag with jaw thrust
- up to 3-5 min to wash out nitrogen - pre-treat
- paralysis with induction
- give analgesia/sedation and then paralytic
- push IV direct
- closed loop communication - 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 - placement with proof
- post-intubation manage
Gluconeogenesis
process of generating glucose from sorces other than carb, occurs mainly in the liver as a method of maintaining adequate glucose levels
glucogenolysis
breaks down glycogen to glucose to provide energy for muscle contraction. Takes place in the cell of the muscle and liver tissue
hyperglycemia occurs bc
- SNS response
- elevated cortisol levels
- insulin resistance
malnutrition in CC is caused by?
- frequesnt pausing of enteral feeds
- SNS response and inhibition of digestive organs
- hypermetabolic state
