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complex care 2 > ARDS- sarah > Flashcards

ARDS- sarah Flashcards

1
Q

what is ARDS

A
  • capillary membrane that surrounds the alveoli sac leaks fluid into the sac
  • decreased gas exchange
  • collapse of alveoli from being overfilled with fluid
  • hypoxemia (low o2 in the blood)

=all causing organs to suffer

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2
Q

what does ARDS develop from

A

-systemic inflammation that is either direct or indirect

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3
Q

direct causes

A
  • things that affect the lungs directly
  • PNA
  • aspiration
  • inhalation injury
  • near drowning
  • embolism
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4
Q

indirect causes

A
  • things that don’t affect the lungs
  • sepsis
  • burns
  • blood transfusions
  • inflammation of pancreas
  • drug overdose
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5
Q

3 phases of ARDS

A
  1. exudative
  2. proliferation
  3. fibrotic
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6
Q

exudative phase timing

A

-24 hours after injury

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7
Q

exudative phase pathO

A

-damaged capillary membrane –> fluid leaks in
(its protein rich).
- fluid then enters the intsretisium and then the sac = pulmonary edema
- surfactant cells are damaged causing the sac to not be stable and it will collapse with exhale = ATELECTASIS
- hyaline membrane will develop = less elastic lung = decreased lung compliance = VQ mismatch

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8
Q

hallmark sign of ARDS

A
  • refractory hypoxemia

- no matter how much 02 giving oxygen never improves

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9
Q

proliferation timing

A
  • 14 days after insult
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10
Q

proliferation phase

A
  • influx of neutrophils, monocytes, lymphocytes, fibroblasts causing increased vascular resistance and pulmonary hypertension all causing even more decreased lung compliance from the fibrosis
  • all causing decreased lung compliance and hypoxemia worsening
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11
Q

fibrotic time

A
  • 3 weeks after the insult
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12
Q

fibrotic phase

A
  • lung tissue is remodeled and fibrous= decreased compliance (hypoxemia, hypercapnia) causing systemic dysfunction from the decreased ventilation and oxygenation
  • pulmonary hypetension
  • will need mechanical ventilation and have poor prognosis
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13
Q

DX of ARDS

A
  • CXR- white out bilaterally
  • ABG
  • Serum lactate will be increased
  • CBC for less than 4 or over 10-12
  • sputum and blood cultures
  • coags
  • electrolytes
  • liver function tests
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14
Q

early signs of ARDS

A
  • hard to notice
  • normal to random crackles
  • difference in breathing “air hunger”
  • hyperventilation (increased RR) = decreased CO2, increased ph = respiratory alkalosis
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15
Q

late signs of ARDS

A
  • refractory hypoxemia
  • cyanosis
  • change in mental status
  • increased HR
  • retractions
  • crackles throughout
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16
Q

what is respiratory failure

A
  • failure in gas exchange

- either oxygenation or ventilation (co2 removal)

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17
Q

what is ARDS

A
  • caused by direct or indirect lung injury that causes progressive hypoxemia, infiltration, and fibrosis of lung tissue
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18
Q

hypoxemic RF

A
  • PaO2 < 60 and normal pac02
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19
Q

hypercapnic RF

A

respiratory acidosis; Paco2 > 50 and ph less than 7.35

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20
Q

hypercapnia RF signs

A
  • HA, confusion, decreased LOC, tachycardia, tachypnea, flushed skin
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21
Q

hypoxemia RF signs

A
  • increased HR, RR, BP
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22
Q

early signs of RF

A
  • tachycardia
  • increased BP
  • dyspnea
  • restlessness
  • anxiety
  • fatigue
23
Q

late signs of RF

A
  • cyanosis
  • decreased BP
  • agonal respiration
  • coma
24
Q

RF dx

A
  • abg
  • CHEMISTRY
  • CBC
  • coags
  • cxr
  • chest ct
  • sputum culture
  • History and physical
25
Q

what do you want to keep your pulse ox at with RF

A
  • SpO2 >94
26
Q

what care do you want to do with RF

A
  • normalize ABG and Hgb
27
Q

VQ mismatch

A
  • ventilation-perfusion mismatch
  • normally, the volume of blood perfusing the lungs and the amount of gas reaching the avleoli are almost identical
  • d/t secretions or mucus plug: this will either block blood flow or block air flow.
  • low V/Q mismatch: d/t shunt and alveoli is perfused but not ventilated
  • high V/Q mismatch: d/t dead space and alveoli are ventilated, but not perfused
28
Q

mild ARDS pf ratio

A
  • > 200-300 with peep at > 5
29
Q

moderate ARDS pf ration

A
  • 100-<200 with peep at >5
30
Q

Severe ARDS pf ratio

A
  • <100 with PEEP > 5
31
Q

pulmonary capillary wedge pressure normal (PCWP)

A

-4-12

32
Q

In ARDS PCWP is…l

A
  • normal or less than 18 = non cardiogenic pulmonary edema
33
Q

PCWP greater than 18

A
  • shows cardiogenic pulmonary edema
34
Q

Cardiovascular complications

A
  • hypotension
  • mottled skin and altered microcirculation
  • increased lactate levels (in septic shock)
  • altered echocardiography variables
  • decreased CO
  • decreased MAP
  • dysrhythmia
35
Q

Hepatic complications

A
  • increased bilirubin levels

- increased enzymes

36
Q

renal complications

A
  • oliguria
  • increased serum creatinine
  • increased blood urea nitrogen
  • increased biomarkers
  • AKI
37
Q

neuro complications

A
    • altered mentation
  • confusion
  • disorientation
  • agitation
  • delirium
  • PICs
38
Q

respiratory complications

A
  • hypoxemia
  • decreased PaO2/FiO2 ratio
  • abnormal lung function
  • VAP
  • barotrauma/volutrauma
  • O2 toxicity
  • PE
  • endotracheal: laryngeal ulceration, tracheal in
39
Q

hematological complications

A
  • low platelets
  • DIC
  • Petechiae
  • VTE
  • Anemia
  • Thrombocytopenia
40
Q

infection complications

A
  • CAUTI, CLABSI, sepsis
41
Q

GI complications

A
  • stress ulceration
  • hemorrhage
  • ileus
42
Q

Intervention: maintain adequate oxygenation:

A

Goal: PaO2 of 60mmHg; FiO2 less than 60%
Goal: adequate ventilation-maintain normal pH
Goal: SaO2 saturation greater than 90%
- Mechanical ventilation almost always necessary
- ECMO or ECCO as necessary
- PRBC transfusion if needed
- HgB as low as 7 before transfusion

43
Q

Intervention: maintain adequate PERFUSION pressures:

A
  • adequate BP, MAP, CO
  • CO, BP, SV, SVV
    > SV-stroke volume SVV stroke volume variance
  • monitor volume status
  • UOP, weight, I/Os
  • Labs
44
Q

intervention: IV fluids:

A
  • crystalloid, colloids, blood products
45
Q

Intervention: medications:

A
  • inotropic vasopressor drugs (dopamine, norepinephrine, vasopressin, dobutamine, milrinone)
  • corticosteroids
  • meds to reduce oxidative stress: vitamin C
  • nitric oxide, surfactant
46
Q

Intervention: maintain adequate fluid

A

Monitor fluid status:

  • fluid balance is difficult d/t “leaky” pulmonary capillaries and third spacing
  • crystalloids, diuretics used depending on fluid status
  • use of colloids controversial d/t leakage into the pulmonary interstitium
47
Q

intervention: nutrition

A
  • maintain protein and energy stores: loss of muscle mass can prolong mechanical ventilation, decrease mobility and set pt up for pressure ulcers, VTE, increase LOS
  • enteral feeding
  • parenteral feeding
48
Q

Respiratory care:

A

Positive pressure ventilation:

  • non-invasive (NIVPP): partial support
  • invasive endotracheal intubation: artificial airway w/ mechanical ventilation, full respiratory support
49
Q

Endotracheal Intubation: indications

A
  • acute respiratory or ventilatory failure
  • PaCO2 greater than 50mmHg
  • pH: 7.3
  • respiratory less than 8 or greater than 40
  • diminished or absent breath sounds
  • unprotected airway
50
Q

What is the supportive care for ARDS?

A

Identify and treat the underlying cause:

  • infection-sepsis (Pan culture, causative rx: antibiotics)
  • corticosteroids (treat the inflammation-treat the inflammatory cells that are affecting the alveoli capillary membrane)
  • hydration
  • hemodynamic monitoring
  • nutritional therapy (within 24-72 hours of ventilator)
  • no specific treatment or drug
  • identify those at risk for ARDs
  • culture: suspicious wounds, secretions
51
Q

What is prone positioning?

A

> early phases of ARDs, fluid moves freely throughout the lung
bc of gravity the fluid pools in the dependent regions of the lung
as a result, some alveoli are fluid filled (depdent areas), while others are air filled (nondepedent areas)
when pt is supine, the heart and mediastinal contents place added pressure on the lungs, which predisposes pts to atelectasis
prone positioning is option for pts with refractory hypoxemia who do not respond to other strategies to increase PaO2
by turning the pt prone, perfusion may be better matched to ventilation
air-filled alveoli in the anterior part of the lung become dependent
alveoli in the posterior part of the lungs are recruited (given the opportunity to re-expand), improving oxygenation.

52
Q

Interventions:

A
  1. O2 administration- supplemental oxygenation
    > goal is to correct hypoxemia
  2. **Ventilation
    > PPV w/ PEEP
    > lung protective strategies: permissive hypercapnia, low vT
  3. low vT ventilation (too high vT into stiff lungs is associated w/ volutrauma and barotrauma, so keep low to reduce risk)
  4. permissive hypercapnia: (d/t low vT, PaCO2 levels will slowly rise above normal limits, body is able to compensate slowly)
  5. PEEP
  6. prone positioning
  7. extracorporeal membrane oxygenation (ECMO): a large vessel is cannulated and a catheter is inserted-allows the blood to exit the pt and pass across a gas-exchanging membrane outside the body and oxygenated blood is returned back to the pt
53
Q

Goal of mechanical ventilation:

A
  • maintain alveolar ventilation appropriate for pts metabolic needs
  • correct hypoxemia in order to maximize O2 transport

complex care 2 (8 decks)

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