Acute Respiratory Failure Flashcards

1
Q

Acute Respiratory Failure & types

A

syndrome in which either oxygenation or CO2 elimination fail

Type I: acute HYPOXEMIC RF (MC)
-pt can’t properly oxygenate blood
-PaO2 <60; PaCO2 is not elevated

Type II: acute HYPERCAPNIC RF
-pt has difficulty in removing CO2 from blood
-PaCO2 >45 (pH often acidic)
*can occur w/ OSA, COPD, asthma (obstructive lung dz)

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2
Q

Pathogenesis of hypoxemic RF

A

V/Q mismatch is MC cause:
-usu d/t atelectasis
-pneumonia, pneumothorax, PE

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3
Q

Pathogenesis of hypercapnic RF

A

-inability to move air in & out of lungs d/t shallow breathing or low RR
-stroke, ALC, spine injury, chest wall d/o, OD

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4
Q

Hypoxemia: S/S

A

-dyspnea
-drowsiness
-confusion
-cyanosis

Results of hypoxia on CNS: HA, somnolence, confusion, convulsions; permanent encephalopathy if severe hypoxia (aka anoxic insult)

Results of hypoxia on CV: (if mild) tachycardia & HTN as body tries to push O2 to organs; (if severe) bradycardia, hypotension - signs of shock

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5
Q

Hypercapnic: S/S

A

-same as hypoxemia (dyspnea, drowsy, confusion, cyanosis)
-acute elevation of CO2 –> confusion, HA, convulsions, coma, coarse tremor, coarse tremor, agitation, slurred speech, asterixis (activated muscles suddenly relax), papilledema

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6
Q

ARF workup (dx tests)

A

-take a good H&P
-assess for multiple etiologies
-CXR
-SpO2 (fast but not always reliable)
-EKG
-Bronchoscopy
-ECHO (if cardiac cause suspected, like cardiogenic pulmonary edema)

*remember ARF is failure to oxygenate, ventilate, or both

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7
Q

ARF workup (labs)

A

-ABG to assess for hypoxemia, hypercapnia, or both
-CBC (anemia can contribute to tissue hypoxia; polycythemia indicates chronic hypoxia)
-sputum, blood, urine culture
-blood electrolytes (K, Mg, Ph abnormalities can compound RF)
-thyroid panel (hyperthyroidism is a reversible cause of RF)

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8
Q

ARF: Possible findings on CXR

A

CXR often reveals the cause: pneumonia, cardiogenic pulm edema, ARDS, atelectasis

A clear CXR in pt w/ ARF may indicate: acute COPD, acute asthma, PE, NM dysfunction

*white, hazy appearance indicates fluid or infection
*normal lung should be black on XR

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9
Q

If there’s any suspicion of a PE what dx test should you order?

A

CTA of the chest

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10
Q

Bicarbonate Buffer System

A

CO2 + H2O <-> H2CO3 <-> HCO3- + H+

increase CO2 -> decreased pH (opposite direction)
increase HCO3- -> increased pH (same direction)

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11
Q

What is normal FIO2 and SpO2

A

Normal FIO2 (fraction of inspired O2 = [O2] in air): 21%
*room air = 21% O2 + 78% N + small amt of CO2, Ne, & H
*FIO2 tells us how much supplemental O2 the pt needs

Normal SpO2: >90%

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12
Q

What do you need to document to dx ARF w/ hypoxia

A

document “dyspnea”

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13
Q

“Rule of 4s” equation used to calculate FIO2

A

(Liters of O2 x 4) + 21% = FIO2
ex. (4 x 4) + 21 = 37%

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14
Q

Tx for hypoxic pt: non-rebreather mask vs. oxygen blender system

A

Non-rebreather mask: corrects hypoxia in pt who IS breathing

Oxygen blender system: medical device which mixes medical grade oxygen and medical air in a variable ratio (dial to calculated FIO2)

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15
Q

PaO2/FIO2 ratio

A

-used as a guide to see if there is sig RF or ARDS developing
(pt can be in RF and have a normal ABG)

400+ normal
<400 hypoxemia
<300 RF
<250 severe RF
<200 critical RF
**look at slide

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16
Q

Indications for mechanical ventilation

A

-failure of supplemental oxygen to increase PaO2
-apnea w/ respiratory arrest
-RR >30
-disturbed consciousness/coma
-hemodynamic instability
-hypercapnia w/ arterial pH <7.25
-ARDS

17
Q

Management of ARF

A
  1. Ensure airway patency (intubate & mech vent if needed)
  2. Restore PaO2 (50-70mmHg but aim for 80mmHg; SpO2 90-93%) (may increase FIO2 to accomplish this)

*remember ABCs (airway, breathing, circulation)

18
Q

Indications for Non-invasive Ventilation

A

-acute exacerbation of COPD***
-cardiogenic pulm edema
-post-extubation RF
-OSA & NM d/o

19
Q

Non-Invasive Ventilation: BiPAP

A

BiPAP (Bilevel Positive Airway Pressure) helps w/ oxygenation and ventilation (different pressures for inhale & exhale)

*CPAP only helps w/ oxygenation (Continuous Positive Airway Pressure = same pressure on inhale & exhale)

20
Q

when to consider intubation/invasive ventilation

A

-ARF
-inadequate oxygenation or ventilation
-airway protection/decreased mental status
-unconscious pts
-requiring surgery
-need for short term hyperventilation to manage increased intracranial pressure

21
Q

Ventilator modes: 2 main ways to ventilate

A
  1. Volume mode: set tidal volume w/ variable peak inspiratory pressure (monitor P)
  2. Pressure mode: set peak inspiratory pressure w/ variable tidal volume which depends on compliance
22
Q

Normal ventilation vs Ventilator

A

Normal ventilation:
-extra effort not applied
-NEGATIVE pressure

Ventilator:
-vol/breath
-POSITIVE pressure
-6-8 ml/kg target
-may affect PCO2 and O2

23
Q

PEEP

A

(Positive End Expiratory Pressure)
-SUPPORTS OXYGENATION
-pressure left at end of exhalation
-reflects FRC
-maintains airway pressure above atmospheric pressure
-keeps alveoli open for gas exchange
-start at 5-10 cm H2O

24
Q

Managing FIO2

A

-titrate to keep FIO2 >90% or >88% if COPD
-once >60%, will need to increase PEEP if still hypoxemic

25
Q

How to determine if the pt is breathing over the vent?

A

pt RR on the monitor will be higher than the set RR

26
Q

Pulmonary complications of mechanical ventilation

A

-endotracheal tube infection (burn/trauma pt at higher risk)
-alveolar overdistention (results in hypotension and barotrauma –> can cause tension pneumothorax)
-atelectasis

27
Q

what can endotracheal tube infection lead to?
MC cause of endotracheal tube infection (pathogens)?

A

-can lead to nosocomial pneumonia if aspiration occurs

in the first 48-72h it is typically d/t S. aureus, H. influenzae, or S. pneumoniae

after 72h, typical causes are P. aeruginosa, Acinetobacter, Enterobacter, & still S. aureus

28
Q

Other complications of mechanical ventilation include

A

-VTE (prevent w/ Lovenox & intermittent pneumatic compression stockings)
-GI bleeding d/t stress ulcer (prevent w/ H2 receptor antagonist or PPI)
-Pressure ulcers over bony prominences
-NM weakness (critical illness polyneuropathy (CIP) - diffuse, symmetric flaccid weakness)

29
Q

ARDS

A

-acute: w/in 7 days
-CXR shows pulmonary infiltrates, capillary endothelial injury alveolar damage
-PaO2/FIO2 <300
-Pulmonary consultation needed
-NM blocker in first 48h improves 98 day survival
-proning pt at least 8h/day shows benefit in 50-70% of pts (ant/post alveoli take turns working)