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CPR Exam 2 > ASRD DSA > Flashcards

ASRD DSA Flashcards

1
Q

What measures can be taken to prevent the progression of ARDS and prevent morbidity and mortality?

A
    1. Transferring to high level of care (ICU) sooner
    1. ID predisposing syndromes
    1. Initiate ICU measures.
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2
Q

Acute respiratory distress syndrome can be distinguished from other causes of respiratory distress by a(n) __________

A

Inciting event

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3
Q

The Berlin Definition of Acute Respiratory Distress Syndromes (ARDS)

  • Timing
  • Chest imaging
  • Oxygenation
    • Mild
    • Moderate
    • Secere
A

Timing: within 7 days of precipitating cause or onset of new/worsening respiratory symptoms

Chest imaging: Bilateral diffuse airway infiltrates that cannot be explained by anything else (cardiac failure or volume overload). If predisposing cause is not present, run echo to exclude hydrostatic edema

Oxygenation:

  • Mild: PaO2 (less than or equal to 300) with PEEP or CPAP greater than or equal to 5cm H20
  • Moderate: PaO2 (less than or equal to 200) with PEEP greater than or equal to 5cm H20
  • Severe: PaO2 (less than or equal to 100) with PEEP greater than or equal to 5cm H20
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4
Q

The hypoxia that occurs in the acute respiratory distress syndrome (ARDS) is a result of

A

Ventilation-perfusion mismatch

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5
Q

What are the most common causes of ARDS?

A

Pulmonary and nonpulmonary sepsis

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6
Q

How do we differentiate ARDS from other causes of respiratory diseases that cause hypoexemia?

A

ID inciting event.

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7
Q

How long does it take from for the inciting event to cause ARDS?

A

3-5 days

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8
Q

What can patients with ARDS experience that is EXTREMLY worrisome and if noticed, needs medical attention.

A
  • Hypercapnia (high CO2) in the face of tachypnea.
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9
Q

What are common predispoing causes of ARDS that involve DIRECT injury to the lungs?

A
  • 1. Pneumonia
  • 2. Gastric aspiration
  • 3. Chest trauma/lung contusion
  • 4. Inhalation injury
  • 5. Near drowning
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10
Q

What are common predispoing causes of ARDS that involve INDIRECT injury to the lungs?

A
  1. Nonpulmonary sepsis
  2. Acute pancreatitis
  3. Severe nonchest trauma
  4. Blood transfusions
  5. Surface burns
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11
Q

In ARDS, as hypoxemia requires higher amounts of inspired supplimental O2, what does this suggest?

A

Evolving acute lung injury with worsening ventilation-perfusion (V/Q) mismatching and worsening shunt physiology.

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12
Q

When should we give a patient with ARDS endotracheal intubation?

A
  1. Altered mental status
  2. Hypercapnia
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13
Q

As ARDS worsens, what changes do we see on chest radiography?

A

Patchy infiltrates become more confluent

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14
Q

In general, how does ARDS cause acute respiratory failure?

A
    1. Increase in permeability d/t direct injury or inflammation
    1. Decrease lung compliance that fucks up gas exchange.
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15
Q

If we think the patient has coexistant or predomina,nt HF what tests should we run to rule other causes and confirm diagnosis of ARDS?

A
  • 1. Echo
  • 2. CT
  • 3. Pulmonary artery catherization
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16
Q

The pathophysiology of ARDS involves 2 stages: exudative stage and proliferative stage. Describe the exudative stage.

A
  • Exudative stage: Predisposing injury damages the aveolar-capillary barrier, causing it to loose its ability to limit fluid, proteins and debris from vascular space,
    • Type 1 pneumocytes support alveoli and fluid/solute transport through aquaporin 5 protein.
    • Type 2 pneumocytes can differentiate into type 1 and make surfactant
  • Injury to type 1 disrupts barrier in acute exudative phase.
  • Injury to type 2 => atelectasis and worse compliance.
  • Forms a proteinaceous edema by moving fluid from plasma space => institial sub-compartment.
    • Worsening V/Q mismatch
    • Physiologic shunt
17
Q

In the early phase of ARDS, what dominates the clinical picture?

A
  • 1. Shunting
  • 2. Hypoxemia
18
Q

How does atelectasis affect the lungs in ARDS?

A

Requires higher pressures to maintain alveoli so that we can breathe.

19
Q

What worsens dead space ventilation?

A
    1. Increase in pulmonary arterial pressure d/t hypoexmia causing pulmonary a vasoconstriction
    1. Decrease in pulmonary circulation d/t microthrombi
  • Both worsen dead space ventilation and cause increase work of breathing.
20
Q

The pathophysiology of ARDS involves 2 stages: exudative stage and proliferative stage. Describe the proliferative stage.

A
  • Proliferative stage: Type 2 pneumocytes regnerate surfactant and type 1 rebuild epithelium.
    • If repair goes well: recover from ARDS in 7-21 days.
    • If procollagen 3 is depostited in interstitial space + fibrosis => increase risk for morbidity and mortality => pt needs prolonged mechanical ventiliation.
  • -As vascular changes that occur in phase 1 becomes irreversible => pulmonary HTN occurs.
21
Q

How do we diagnose ARDS?

A

Based on clinical criteria and exlusion of other diseases.

22
Q

What can our differentials be for a patient that presents with ARDS?

A

Acute infectious pneumonias. like:

  1. Pneumocytis jivoveci pneumonia
  2. Community acquired bacterial pneumonia

Similar CXR and refractory hyoxemia, but without cellular toxicity.

These can also cause ARDS

23
Q

Patients with ARDS have to work harder to breathe and ventilate.

How do we often fix hypoxemia?

A
  • Invasive mechanical ventilation.
  • Non-invase methods only fix the problem temporarily.
24
Q

How does mechanical ventilation work?

A
  • Makes it easier to breath by easing resp muscles and improving effective minute ventilation.
    • ​CO2 decreases and acid-base levels are restored.
25
Q

What is a downside of mechanical ventillators?

A
  • Lungs are vulnerable to postive pressure, esp:
    • atelectic parts: can overstretch
    • alveoli can excessively close during expiration
26
Q

What strategy is used to improve survival from ARDS and prevent ventilator associated lung injury?

A

Low tidal volume ventilation.

27
Q

What is used as a rescue therapy in patients with refractory hypoxemia?

A
  • High-frequency oscillatory ventilation (HFOV)
    • Has high RR with very small tidal volumes
28
Q

What are nonventilatory strategies to treat ARDS?

A
    1. Conservative fluid management; reduces number of days on ventalator and ICU
    1. No pharmcotherapy has been ID’d
    1. Corticosteroids are not benefit
    1. Extracorporeal membrane oxygenation (ECMO) can help w hypoxemia w/o injurous ventilator
29
Q

What preventative measures should be taken to prevent ICU-related complications in patients with ARDS?

A
    1. Prophalyxis against stress ulcers, bleeding, DVT
    1. Raise head 30 degrees to prevent ventilatory-assx pneumonia
  • 3. Screen daily to free from ventilator
30
Q

What is the best predictor of outcome as we employ ventilator techniques?

A

Berlin definition of hypoxia

31
Q

Patients that do not have lower O2 requirements by day 7 have what outcomes?

A
  • 1. Longer time in ICU
  • 2. Increase risk for long-term ventilator dependency
  • 3. Longer recovery
32
Q

What are managment strategies of ARDS?

A
    1. Low tidal volume (6 cc/kg tidal volume)
    1. Prone ventilation 16 hrs a day
    1. Manage fluids
    1. Central venous catheter directed fluid management

Not corticosteroids or pulmonary artery catheterization.

33
Q

Survival of ARDS depends on what

A

patient population and where investigation occured.

34
Q

What are complications in those who survive ARDS?

A
  • Few respiratory system problems
  • Lung fx goes back to nL
  • Most have funtional limitation d.t weak muscle and fatigue

CPR Exam 2 (29 decks)

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