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
What is a downside of **mechanical ventillators?**
* Lungs are vulnerable to **postive pressure,** esp: * atelectic parts: can overstretch * alveoli can excessively close during expiration
26
What strategy is used to improve survival from **ARDS** and **prevent ventilator associated lung injury**?
**_Low tidal volume ventilation._**
27
What is used as a **rescue therapy** in patients with **_refractory_ hypoxemia?**
* **High-frequency oscillatory ventilation (HFOV)** * Has **high RR** with **very small tidal volumes**
28
What are nonventilatory strategies to treat ARDS?
* 1. **Conservative fluid management;** reduces number of days on ventalator and ICU * 2. No pharmcotherapy has been ID'd * 3. Corticosteroids are not benefit * 4. **Extracorporeal membrane oxygenation (ECMO) c**an help w hypoxemia w/o injurous ventilator
29
What preventative measures should be taken to prevent ICU-related complications in patients with **ARDS**?
* 1. **Prophalyxis** against stress ulcers, bleeding, DVT * 2. **Raise head 30 degrees** to prevent ventilatory-assx pneumonia * **3. Screen daily to free from ventilator**
30
What is the best predictor of outcome as we employ ventilator techniques?
**Berlin definition of hypoxia**
31
Patients that do not have lower O2 requirements by day 7 have what outcomes?
* **1. Longer time in ICU** * **2. Increase risk for long-term ventilator dependency** * **3. Longer recovery**
32
What are managment strategies of ARDS?
* 1. Low tidal volume (6 cc/kg tidal volume) * 2. Prone ventilation 16 hrs a day * 3. Manage fluids * 4. Central venous catheter directed fluid management Not corticosteroids or pulmonary artery catheterization.
33
Survival of ARDS depends on what
patient population and where investigation occured.
34
What are complications in those who survive ARDS?
* **Few respiratory system problems** * **Lung fx goes back to nL** * Most have **funtional limitation** d.t weak muscle and fatigue