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Patho > chapter 67: acute respiratory failure and acute respiratory distress syndrome > Flashcards

chapter 67: acute respiratory failure and acute respiratory distress syndrome Flashcards

1
Q

(ARF

A

-not a disease –> symptom
-not enough O2 or not enough ventilation
-can be hypoxemic or hypercapnic in nature(or both)

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2
Q

hypoxemic resp failure

A

PaO2 < 60 mm Hg when receiving inspired O2 concentration of 60% or more

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3
Q

hypercapnic resp failure

A

-“ventilatory failure”
-PaCO2 over 50 mm HG with acidemia

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4
Q

acute vs chronic resp failure

A

acute
-hemodynamic instability, increased WOB, decreased LOC
-urgent intervention

chronic
-develops slowly andd the body has time to compensate for bad changes

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5
Q

what causes hypoxemia in resp failure?

A

-V/Q mismatch
-shunt
-diffusion limitation
-alveolar hypoventilation

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6
Q

V/Q mismatch

A

-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

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7
Q

Shunt

A

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

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8
Q

Diffusion limitation

A
  • 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

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9
Q

Alveolar hypoventilation

A

-usually from CNS condition, chest wall disfunc, acute asthma, or restrictive lung diseases
-increases PaCO2

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10
Q

Results of hypoxemia

A

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

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11
Q

Hypercapnic resp failure

A

-usually lungs are fine, but body is having issues regulation CO2

Causes:
-CNS issues
-neuromuscular conditions
-chest wall abnormalities
-probs w/ airway or alveoli

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12
Q

CNS issues

A

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

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13
Q

Neuromuscular conditions

A

Guillain-Barre syndrome
multiple sclerosis
toxins which interfere with muscle innervation
muscle weakness

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14
Q

Chest wall abnormalities

A

flail chest, kyphosis, obesity

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15
Q

Probs with airway/alveoli

A

COPD, cystic fibrosis, asthma
-airflow obstruction and air trapping

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16
Q

Consequences of hypercapnia

A

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

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17
Q

system wide manifestations of low O2

A

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

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18
Q

What’s priority in ARF?

A
  1. Assess patient’s ability to breathe
  2. provide assistance if neededd
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19
Q

Things to look for when assessing patient’s ability to breathe

A

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

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20
Q

Diagnostic studies for ARF

A

-chest xray
-ABG analysis

you can do all the other ones too if you want/need

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21
Q

Oxygen therapy

A

-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

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22
Q

Mobilization of secretions

A

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

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23
Q

Positive Pressure Ventilation

A
  • 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

24
Q

Drug therapy goals for ARF

A

Reduce airway inflammation and Bronchospasms
Relieve Pulmonary congestion
Treat infection
Reduce anxiety/pain/restlessness

25
Q

Drugs to reduce inflammation and bronchospasms

-possible side effects

A

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

26
Q

Drugs to relieve pulmonary congestion

A

diuretics (Lasix, morphine, nitroglycerin)

CAUTION: HEART PROBS AND LOW BP

27
Q

drugs for anxiety, pain, and restlessness

A

Benzodiazepines and opioids

28
Q

what’s weird ab old ppl’s alveoli?

A

they’re bigger with more air space and less surface area

29
Q

ARDS

A

Sudden and progressive form of ARF where alveolar-capillary membrane is damaged and permeable to intravascular fluid

30
Q

Things that cause ARDS

A

-Sepsis is most common
-multiple organ dysfunction syndrome
-direct or indirect lung injury

31
Q

What are the phases of ARDS?

A
  1. Injury or exudative phase
  2. reparative or proliferative phase
  3. fibrotic or fibroproliferative phase
32
Q

Injury or exudative phase:
inflammatory response

A

-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

33
Q

heart and breathing response to hypoxemia in ARDS

A

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

34
Q

Injury/exudate phase: surfactant

A

can’t make it well anymore
atelectasis
necrotic cells, prot, and fibrin make hyalin membrane along alveoli –>fibrosis

35
Q

refractory hypoxemia

A

patients condition doesn’t improve, but continues to worsen despite receiving high levels of O2

36
Q

Reparative or proliferative phase

A

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

37
Q

Fibrotic/fibroproliferative phase

A

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

38
Q

Manifestations and diagnostic studies for ARDS

A

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

39
Q

Cause of death in most ARDS patients

A

MODS + sepsis

40
Q

COmpications of ARDS

A

Abnormal lung func
Ventilator assoc pneumonia
Barotrauma
Stress ulcers
Venous thromboembolism
AKI
Psych issues

41
Q

ARDS abnormal lung func

A

-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

42
Q

Ventilator assoc pneumonia

A

-impaired immunity
-aspiration of GI stuff
-prolonged time on ventilator

*helps to raise HOB to 30-45

43
Q

Barotrauma

A

bursting alveoli from aggressive ventilation

can cause:
-pulmonary interstitial emphysema
-pneumopericardium
-tension pneumothorax

44
Q

Stress ulcers

A

-blood is shunted from GI to resp system to try to oxygenate

*give anti ulcer drugs, mucosal protecting drugs, and early enteral nutrition

45
Q

VTE

A

Its a risk
compression socks and anticoagulating drugs
also early ambulation

46
Q

AKI

A

-happens bc of decreased perfusion or sepsis
CRRT is used due to hemodynamic instability
-bad prognosis if this happens though

47
Q

psych issues

A

might have ptsd for years afterward

48
Q

Steps for caring for ARDS patient

A
  1. oxygen administration
  2. mechanical ventilation
  3. low tidal volume ventilation
    4 permissive hypercapnia
  4. PEEP
  5. prone positioning
  6. extracorporeal membrane oxygenation (ECMO)
49
Q

Oxygen administration ARDS

A

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

50
Q

Mechanical ventilation ARDS

A

-usually a pressure control system to prevent alveoli rupturing

51
Q

Low tidal volume ventilation

A

4-8 ml/kg
prevents volutrauma

52
Q

Permissive hypercapnia

A

-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

53
Q

PEEP (positive end expiratory pressure)

A

-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

54
Q

Prone position ARDS

A

-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

55
Q

Extracorporeal membrane oxygenation (ECMO)

A

basically like dialysis but for oxygenation
-use catheter in internal jugular, femoral artery, or femoral vein
ECCO2R is the same, but requires less bloodflow

56
Q

CLRT and kinetic therapy

A

tilt patient left to riht to stimulate postural drainage
-may include vibrations to mobilize secretions too

57
Q

Analgesia and sedation

A

alleviate discomfort and ensure patients don’t breath out of sync with machine
-if continued asynchronous, may need neuromuscular blocking agent NMBA

Patho (44 decks)

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