ARDS Flashcards

1
Q

Causes of ARDS

A

Alveolar capillary interface becomes damaged and more permeable to intravascular fluid –alveoli fill with fluid

Sepsis
Pneumonia
Aspiration
Trauma
Massive transfusions
Pancreatitis
Shock states 

Inflammation!!

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2
Q

How do we define ARDS clinically

A

Acute onset
Bilateral infiltrates
Severe, refractory hypoxemia PaO2/FiO2 ratio

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3
Q

PaO2/FiO2 ratios and severity of ards

A

200-300 mild
100-200 moderate
<100 severe

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4
Q

Refractory hypoxemia results from & leads to..

A

Severe V/Q mismatch & shunting of pulmonary capillary blood

Unresponsive to increasing O2 concentrations

Lungs are less compliant
Increased airway pressures must be generated.

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5
Q

Exudative phase changes

A
Inflammatory
mediators
• Disruption of alveolar
capillary membrane
• Fluid in the alveoli
• V/Q mismatch
• Loss of
surfactant=alveolar
collapse
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6
Q

Manifestations of Exudative phase

A
Tachypnea and
tachycardia
• Mild hypoxemia and
respiratory alkalosis
caused by
hyperventilation
• Dyspnea, tachypnea,
cough, restlessness
• Chest auscultation may
be normal or may reveal
fine, scattered crackles
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7
Q

Proliferative phase changes

A
Inflammatory
mediators cross ACM =
damaged alveolar and
capillary epithelium =
diffusion defects
• V/Q worsens
• Pulmonary HTN due to
hypoxemic
vasoconstriction=R HF
• Fibrotic changes
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8
Q

Proliferative phase manifestations

A
Decreased lung
compliance=increased
work of
breathing=tachypnea
• Hypercarbia and
worsening refractory
hypoxemia
• Diaphoresis, decreased
LOC, cyanosis, and pallor
• Increased peak
inspiratory pressures
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9
Q

Fibrotic phase changes

A
Changes
• Diffuse scarring
• Worsening pulmonary
HTN
• Worsening V/Q
mismatch, diffusion
defects and shunting
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10
Q

Fibrotic phase manifestations

A
• R sided HF
• Decreased BP, CO
• Refractory hypoxemia
• Tissue hypoxia/lactic
acidosis
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11
Q

Diagnostic labs and testing for ARDS

A
• CXR – bilateral infiltrates
– Ground glass appearance
• Laboratory testing
– ABGs
– CBC with differential
– Cultures
– CMP
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12
Q

Treatment for ARDS

A
• Treat the Cause!
• Mechanical Ventilation with PEEP
• Diuresis
• Antibiotics
• Steroids - improve oxygenation, not survival
– use is controversial
• Hydration – maintain circulatory volume, decrease
viscosity of secretions
• Nutrition
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13
Q

Mechanical ventilation

A

– Low Tidal Volumes to reduce barotrauma
– High PEEP to aid in recruitment
– No mode proven to improve outcomes
– Requires advanced airway

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14
Q

Positive End Expiratory Pressure

PEEP

A

• Increase FRC and open up collapsed alveoli
• Higher levels of PEEP are often needed to maintain
Pa
O
2 at 60 mm Hg or greater
• High levels of PEEP can compromise venous return

↓ Preload, CO, and BP

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15
Q

Nursing O2 managment

A
Nursing
• Optimize O2 delivery
– Frequent assessment – hemodynamic and ventilatory
– Keep the airways clear
• Minimize O2 demand - Decrease O2 consumption
– Comfort
– Sedation
– Pain relief
– Neuromuscular blockade
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16
Q

• Positioning for ards

A

– Prone positioning
– Elevate HOB
– Frequent changes

17
Q

Risk factors for PE

A
DVT:Virchow’s triad
• Venous stasis/prolonged immobility
• Vessel wall damage
• Hypercoagulability
Smoking 
Obesity
Fractures (hip/leg)
Major surgery/trauma
Malignancy
18
Q

Types of PE

A
Blood clot
• Fat embolus
• Air embolus
• Amniotic fluid
• Tumor particles
19
Q

Pathophysiology of PE

A
Obstruction in
Pulmonary Artery  -->
Ventilation‐
Perfusion Mismatch
(high V/Q/dead
space ventilation)--->
Hypoxemia
Local
Vasoconstriction (pulmonary HTN R heart failure)
20
Q

Classification (massive PE)

A

– Profound hypotension
– R & L ventricular dysfunction
– Shock/cardiac arrest

21
Q

Classification: Submassive PE

A

– Normotensive
– R ventricular dysfunction
– Elevated cardiac markers

22
Q

Classification: Low risk PE

A

– Normotensive/No ventricular dysfunction or elevation in cardiac
markers
Pts can have PE w/o symptoms, may or may not need hospitalization

23
Q

Initial PE clinical manifestations

A
  • Dyspnea
  • Chest pain (most common, pleuretic chest pain)
  • Tachypnea
  • Tachycardia
24
Q

Submassive/Massive PE

clinical manifestation

A
• R heart failure with JVD
• Hypotension
• Anxious/restless/confused
• Hypoxia
• Poor peripheral perfusion
• Hemoptysis with pulmonary
infarction
25
Q

Diagnosis of PE (imagine/labs)

A
Primarily to R/o other causes 
-Imaging
– CXR
– CT scan (w/con)
• Laboratory testing
– D-dimer (key test) tells us if there are fibrin degradation products in the blood
– ABG (massive/submassive)
– Cardiac markers(massive/submassive)
26
Q

Medical management once PE diagnosed

A

Anticoagulation
• IVC filters - prevent recurrence
• Cautious fluid management (prevent R heart failure)
• Hemodynamically compromised
– Thrombolytics (break down the clot)
– Embolectomy (instrument will break down clot)
– Vasoactive/inotropic support

27
Q

Nursing assessments for PE

A
Oxygenation/Spo2
• Chest pain (better/worse?)
• VS
• Labs
– ABGs
– Lactate
– Coagulation studies
– Cardiac markers (damage in cardiac tissue)
• Urine output (CO)
28
Q

Nursing actions for PE

A
Provide O2
• Elevate HOB
• Medication Management
• Fluid management
• Bleeding precautions
29
Q

Nursing actions for PE

A
Provide O2
• Elevate HOB
• Medication Management
• Fluid management
• Bleeding precautions
30
Q

Pneumo/hemothroax

A

Collection of air/blood in the pleural
space

Reduction in the negative thoracic
pressure and poor lung expansion

Reduction of gas exchange at the
alveolar level resulting in hypoxemia

31
Q

Manifestations (Pneumo/hemothorax)

A
  • Decreased oxygenation
  • Tachypnea = Respiratory alkalosis
  • Later - respiratory acidosis
  • Pain (severe) ECG r/o MI
  • SOB
  • Agitation, anxiety
  • Later – Decreased LOC
32
Q

Chest tube types

A

Hooked up to drainage system can be water filled or dry/amount of suction to dial in pressure (common)

Pneumo - chest tube higher bc air rises
hemo- low because of gravity

33
Q

Assessment of chest tube

A
  • Monitor vital signs, SpO2, pain, SOB
  • Secure Connections
  • Observe tidaling
  • Observe for air leak (bubbling in water-seal chamber)
  • Monitor drainage
  • If break in system, place distal end in sterile water to maintain water-seal
  • Do NOT clamp!