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
what do you want to keep your pulse ox at with RF
- SpO2 >94
26
what care do you want to do with RF
- normalize ABG and Hgb
27
VQ mismatch
- 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
mild ARDS pf ratio
- > 200-300 with peep at > 5
29
moderate ARDS pf ration
- 100-<200 with peep at >5
30
Severe ARDS pf ratio
- <100 with PEEP > 5
31
pulmonary capillary wedge pressure normal (PCWP)
-4-12
32
In ARDS PCWP is...l
- normal or less than 18 = non cardiogenic pulmonary edema
33
PCWP greater than 18
- shows cardiogenic pulmonary edema
34
Cardiovascular complications
- hypotension - mottled skin and altered microcirculation - increased lactate levels (in septic shock) - altered echocardiography variables - decreased CO - decreased MAP - dysrhythmia
35
Hepatic complications
- increased bilirubin levels | - increased enzymes
36
renal complications
- oliguria - increased serum creatinine - increased blood urea nitrogen - increased biomarkers - AKI
37
neuro complications
- - altered mentation - confusion - disorientation - agitation - delirium - PICs
38
respiratory complications
- hypoxemia - decreased PaO2/FiO2 ratio - abnormal lung function - VAP - barotrauma/volutrauma - O2 toxicity - PE - endotracheal: laryngeal ulceration, tracheal in
39
hematological complications
- low platelets - DIC - Petechiae - VTE - Anemia - Thrombocytopenia
40
infection complications
- CAUTI, CLABSI, sepsis
41
GI complications
- stress ulceration - hemorrhage - ileus
42
Intervention: maintain adequate oxygenation:
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
Intervention: maintain adequate PERFUSION pressures:
- adequate BP, MAP, CO - CO, BP, SV, SVV > SV-stroke volume SVV stroke volume variance - monitor volume status - UOP, weight, I/Os - Labs
44
intervention: IV fluids:
- crystalloid, colloids, blood products
45
Intervention: medications:
- inotropic vasopressor drugs (dopamine, norepinephrine, vasopressin, dobutamine, milrinone) - corticosteroids - meds to reduce oxidative stress: vitamin C - nitric oxide, surfactant
46
Intervention: maintain adequate fluid
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
intervention: nutrition
- 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
Respiratory care:
Positive pressure ventilation: - non-invasive (NIVPP): partial support - invasive endotracheal intubation: artificial airway w/ mechanical ventilation, full respiratory support
49
Endotracheal Intubation: indications
- 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
What is the supportive care for ARDS?
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
What is prone positioning?
> 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
Interventions:
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
Goal of mechanical ventilation:
- maintain alveolar ventilation appropriate for pts metabolic needs - correct hypoxemia in order to maximize O2 transport