chapter 67: acute respiratory failure and acute respiratory distress syndrome Flashcards
(ARF
-not a disease –> symptom
-not enough O2 or not enough ventilation
-can be hypoxemic or hypercapnic in nature(or both)
hypoxemic resp failure
PaO2 < 60 mm Hg when receiving inspired O2 concentration of 60% or more
hypercapnic resp failure
-“ventilatory failure”
-PaCO2 over 50 mm HG with acidemia
acute vs chronic resp failure
acute
-hemodynamic instability, increased WOB, decreased LOC
-urgent intervention
chronic
-develops slowly andd the body has time to compensate for bad changes
what causes hypoxemia in resp failure?
-V/Q mismatch
-shunt
-diffusion limitation
-alveolar hypoventilation
V/Q mismatch
-a little bit always exists: higher at apex; lower at base
-caused by COPD, pneumonia, asthma, atelectasis, PE, and pain
Not only does pain cause less lung expansion, but it activates stress response, leading to a greater O2 consumption and CO2 production rate
O2 therapy is appropriate first step
Shunt
blood exits heart w/o having done gas exchange –> extreme V/Q mismatch
Anatomic shunt
-blood passes through channel in heart
Intrapulmonary shunt
-blood goes thru lungs w/o doing gas exchange
-usually bc fluid filled alveoli
Need mech ventilation with high FIO2
Diffusion limitation
- issues with alveolar membrane or pulmonary capillaries
-pulmonary fibrosis, interstitial lung disease, ARDS
-also fluid OUTSIDE the alveoli –> pulmonary edema
Usually manifests as hypoxemia during exercise, but not rest
Alveolar hypoventilation
-usually from CNS condition, chest wall disfunc, acute asthma, or restrictive lung diseases
-increases PaCO2
Results of hypoxemia
hypoxia
-cells switch from aerobic to anaerobic respiration
-not efficient
-more energy needed
-byproduct is lactic acid which requires Na bicarbonate to expel
-w/o Na bicarb, metabolic acidosis and eventually cell death
Hypercapnic resp failure
-usually lungs are fine, but body is having issues regulation CO2
Causes:
-CNS issues
-neuromuscular conditions
-chest wall abnormalities
-probs w/ airway or alveoli
CNS issues
opioids, brain injury (infarction) w/ or w/o LOC, or high spinal cord injury messes with medulla
-body doesn’t stimulate breathing in response to hypercapnia
Neuromuscular conditions
Guillain-Barre syndrome
multiple sclerosis
toxins which interfere with muscle innervation
muscle weakness
Chest wall abnormalities
flail chest, kyphosis, obesity
Probs with airway/alveoli
COPD, cystic fibrosis, asthma
-airflow obstruction and air trapping
Consequences of hypercapnia
honestly, the body can usually handle it
kidneys adapt and retain bicarbonate to manage pH levels
may have morning headache, decreased LOC, and slow RR
system wide manifestations of low O2
neuro
-restlessness, agitation, decreased LOC
GI
-tissue ischemia and increased intestinal wall permeability
kidney
-sodium/water retention and AKI
cardiopulmonary
-tachycardia, tachypnea, mild hypertension
cyanosis
What’s priority in ARF?
- Assess patient’s ability to breathe
- provide assistance if neededd
Things to look for when assessing patient’s ability to breathe
position: see if they need to be upright/tripod to breathe
RR: if changes from rapid to slower –> resp muscle fatigue
can they talk?
pursed lips
retraction and use of accessory muscles –> paradoxical breathing if severe
breath sounds
Diagnostic studies for ARF
-chest xray
-ABG analysis
you can do all the other ones too if you want/need
Oxygen therapy
-Set to lowest possible FIO2
-Keep patients PaO2 above 60 and SaO2 above 90%
Risks
-inflammation (and eventual fibrosis) from o2 radicals
-absorption atelectasis when O2 replaces N
-increased pulmonary capillary permeability
-Prob if body relies on low O2 signals to instigate breathing
Mobilization of secretions
Positioning
-at least 30 degrees –> v/q will be best at base
-side lying if aspiration risk
-If one lung is affected, lie on side with good lung down
Coughing
-Huff
-augmented coughing –> push from provider
-staged cough = 3-4 breaths then cough while leaning over pillow
CPT
-postural drainage, percussion, vibration
-don’t do if TBI, spinal injury, or hemoptysis
Suction
Humidification
-saline or mucolytic drugs –> watch for irritation though
Hydration
-to thin mucus
Positive Pressure Ventilation
- mask
-good for chronic resp failure w/ chest or neuromusc probs
-bad if low LOC, high O2 needs, facial trauma, hemolytic instability, or excessive secretions
CPAP = constant pressure
BiPAP = changing pressure on inhale vs exhale –> best option
Drug therapy goals for ARF
Reduce airway inflammation and Bronchospasms
Relieve Pulmonary congestion
Treat infection
Reduce anxiety/pain/restlessness
Drugs to reduce inflammation and bronchospasms
-possible side effects
corticosteroids e.g. methylprednisone
-IV, not inhaled –> inhalation takes 4-5 days
Short acting bronchodilators (e.g. albuterol)
-every 15 to 30 mins in acute bronchospasm
-use hand-held nebulizer or MDI w/ spacer
side effects:
-tachyccardia and htn
-if prolonged use, dysrhythmias and cardiac ischemia
-MONITOR VITAL SIGNS AND ECG
Drugs to relieve pulmonary congestion
diuretics (Lasix, morphine, nitroglycerin)
CAUTION: HEART PROBS AND LOW BP
drugs for anxiety, pain, and restlessness
Benzodiazepines and opioids
what’s weird ab old ppl’s alveoli?
they’re bigger with more air space and less surface area
ARDS
Sudden and progressive form of ARF where alveolar-capillary membrane is damaged and permeable to intravascular fluid
Things that cause ARDS
-Sepsis is most common
-multiple organ dysfunction syndrome
-direct or indirect lung injury
What are the phases of ARDS?
- Injury or exudative phase
- reparative or proliferative phase
- fibrotic or fibroproliferative phase
Injury or exudative phase:
inflammatory response
-happens 1-3 days after insult and lasts a week
-peribronchial and perivascular interstitial spaced engorge leading to interstitial edema
-fluid in lung parenchyma enters alveolar space –> V/Q mismatch, pulmonary shunt, no gas exchange
the membrane damage is prob caused by neutrophils releasing stuff
heart and breathing response to hypoxemia in ARDS
J reflex initially causes rapid shallow breaths –> alkalosis
Cardiac output increases to try to increase pulmonary bloodflow
When this fails, hypoventilation, decreased cardiac output, and decreased tissue oxygenation occur
Injury/exudate phase: surfactant
can’t make it well anymore
atelectasis
necrotic cells, prot, and fibrin make hyalin membrane along alveoli –>fibrosis
refractory hypoxemia
patients condition doesn’t improve, but continues to worsen despite receiving high levels of O2
Reparative or proliferative phase
1-2 weeks after onset
-still influx of inflammatory shit
-pulmonary vascular resistance and HTN bc fibroblasts destroy pulmonary vasculature
-fibrosis worsens
-airway resistance due to secretions
Fibrotic/fibroproliferative phase
2-3 weeks after onset
-complete remodeling of lung with collagen and fibrous tissues
-scarring
-not enough surface area for gas exchange
-hypoxemia and pulmonary htn
**some ppl recover before entering this stage
Manifestations and diagnostic studies for ARDS
chest xray shows infiltrates
tachypnea, tachycardia, accessory muscles, cyanosis, mental changes
lung crackles
messed up ABGs
P/F ratio (should be at least 400) dips
*start out alkalotic, but become acidotic as you tire from WOB
Cause of death in most ARDS patients
MODS + sepsis
COmpications of ARDS
Abnormal lung func
Ventilator assoc pneumonia
Barotrauma
Stress ulcers
Venous thromboembolism
AKI
Psych issues
ARDS abnormal lung func
-most ppl recover in 6 mo, but some don’t
-abnormal lung func can persist for years
-severity of scarring is a factor, as is time spent on ventilator
Ventilator assoc pneumonia
-impaired immunity
-aspiration of GI stuff
-prolonged time on ventilator
*helps to raise HOB to 30-45
Barotrauma
bursting alveoli from aggressive ventilation
can cause:
-pulmonary interstitial emphysema
-pneumopericardium
-tension pneumothorax
Stress ulcers
-blood is shunted from GI to resp system to try to oxygenate
*give anti ulcer drugs, mucosal protecting drugs, and early enteral nutrition
VTE
Its a risk
compression socks and anticoagulating drugs
also early ambulation
AKI
-happens bc of decreased perfusion or sepsis
CRRT is used due to hemodynamic instability
-bad prognosis if this happens though
psych issues
might have ptsd for years afterward
Steps for caring for ARDS patient
- oxygen administration
- mechanical ventilation
- low tidal volume ventilation
4 permissive hypercapnia - PEEP
- prone positioning
- extracorporeal membrane oxygenation (ECMO)
Oxygen administration ARDS
Good first step, but often not enough (even w/ BiPAP and high O2 pressure)
Even with mech ventilation, patients may need an FIO2 of 70-80% higher to keep PaO2 at least 60 mm Hg
Mechanical ventilation ARDS
-usually a pressure control system to prevent alveoli rupturing
Low tidal volume ventilation
4-8 ml/kg
prevents volutrauma
Permissive hypercapnia
-PaCO2 rises bc of low tidal volume administration
-its ok as long as PaCO2 stays below 60 mm Hg
watch ABGs closely
administer analgesics and sedation
Don’t use this method if TBI or increased ICP
PEEP (positive end expiratory pressure)
-increases functional residual capacity and helps open up collapsed alveoli
-apply in 3-5 cm H2O increments –> prob need more for ARDS ppl
Caution: may compromise venous return –> decrease preload, CO, and BP
***also beware of barotrauma
Prone position ARDS
-supine makes heart crush lungs and predisposes ppl to atelectasis
-prone allows posterior alveoli to open up –> should be side lying
-need ICU intensivist, RT, and 3-4 nurses when placing in prone
Caution: more secretions to suction and possible hemodynamic instability
Extracorporeal membrane oxygenation (ECMO)
basically like dialysis but for oxygenation
-use catheter in internal jugular, femoral artery, or femoral vein
ECCO2R is the same, but requires less bloodflow
CLRT and kinetic therapy
tilt patient left to riht to stimulate postural drainage
-may include vibrations to mobilize secretions too
Analgesia and sedation
alleviate discomfort and ensure patients don’t breath out of sync with machine
-if continued asynchronous, may need neuromuscular blocking agent NMBA
