18 - Respiratory Failure & ARDS Flashcards

1
Q

What is the onset of acute vs. chronic respiratory failure? Which one is more serious?

A

Acute - rapid onset, life-threatening

Chronic - weeks-years

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2
Q

What are the physiologic responses to hypoxemia and hypercarbia from acute respiratory failure?

A

Hypoxemia

  • increased catecholamines –> tachycardia
  • increased carotid body stimulation –> tachypnea and hyperventilation

Hypercarbia

  • decreased pH and increased intracranial pressure –> CO2 narcosis
  • increased PaCO2 –> cerebral vasodilation
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3
Q

What is the equation for O2 delivery?

A

DO2 = CO * CaO2

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4
Q

What are the physiologic responses to hypoxemia and hypercarbia from chronic respiratory failure?

A

Hypoxemia
- increased erythropoietin –> increased hemoglobin

Hypercarbia
- increased bicarbonate –> less severe acidosis

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5
Q

How does pulse oximetry work?

A

2 wavelengths of light due to different absorption by reduced and oxygenated hemoglobin –> allows us to calculate the percentage of oxyhemoglobin

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6
Q

What are the complications of oxygen therapy?

A
  • reactive O2 species are cytotoxic
  • blindness or bronchopulmonary dysplasia in children
  • decreased mucuciliary clearance
  • tracheitis
  • acute lung injury
  • absorptive atelectasis (removing N2 from air will create a much stronger gradient, causing instantaneous alveolar collapse as gas quickly diffuses out of alveoli)
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7
Q

What are the nonspecific and specific therapies for respiratory failure?

A

Nonspecific

  • hypoxemia –> supplemental oxygen (ineffective if hypoxemia is due to shunt)
  • hypercapnia –> avoid/correct

Disease specific

  • pneumonia: antibiotics, secretion clearance
  • atelectasis: remove secretions
  • COPD/asthma: bronchodilators, steroids
  • drug overdose: antidote
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8
Q

What are the indications for mechanical ventilation? What are the complications?

A

Hypoxemic failure

  • shunt
  • inadequate lung expansion due to atelectasis

Hypercapnic failure

  • elevated work of breathing
  • respiratory muscle weakness
  • insufficient respiratory drive
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9
Q

What are the advantages, disadvantages, and indications for non-invasive ventilation?

A

Advantages

  • avoid endotracheal tube
  • less sedation
  • care can be given outside of ICU

Disadvantages

  • may not tolerate mask or pressure
  • no access to airway to remove secretions

Indications

  • respiratory failure that can get better in a day or two
  • chronic respiratory failure (neuromuscular disease, OHS)
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10
Q

What is the pathogenesis of acute respiratory distress syndrome?

A

Inflammatory injury to alveoli –> increased alveolar-capillary permeability –> non-cardiogenic pulmonary edema –> reduced compliance and increased shunt –> hypoxemia

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11
Q

What are the common pulmonary and extra-pulmonary causes of acute respiratory distress syndrome?

A

Pulmonary

  • pneumonia
  • gastric aspiration
  • inhalation
  • near drowning
  • toxic gas inhalation
  • thoracic trauma (pulmonary contusion)

Extra-pulmonary

  • sepsis
  • pancreatitis
  • non-thoracic trauma
  • fat embolism
  • massive transfusion
  • drugs (heroin)
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12
Q

Heterogeneity injury to the lung with areas of poor ventilation and areas of better ventilation is suggestive of ___.

A

acute respiratory distress syndrome

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13
Q

What is the pathogenesis of acute respiratory distress syndrome?

A
  • Injured alveolar and capillary endothelium –> increased permeability –> fluid leaks into interstitium then alveolar space –> fluid filled alveoli have decreased compliance and cause a shunt
  • injury causes significant inflammation and leaking of protein into alveolar space
  • type II cells are injured –> reduction in surfactant
  • existing surfactant is inhibited by inflammatory cells, oxidation, and proteolytic enzymes –> decreased compliance, alveolar collapse, and alveolar flooding
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14
Q

How is pulmonary circulation affected in acute respiratory distress syndrome? What causes it?

A
  • abnormal
  • increased pulmonary arterial pressure
  • increased pulmonary vascular resistance
  • increased dead space fraction

Results from:

  • vasoconstriction
  • microthrombi
  • compression of vessels by edema
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15
Q

What are the complications of placing someone with ARDS on a ventilator with normal settings? How should ventilator settings be modified?

A

Normal settings –> all or much of volume will go to better-ventilated areas of lung, leading to:

  • barotrauma (disruption of lung with air leaking into pleural space, causing pneumothorax)
  • volutrauma (injury to alveolar/capillary interface –> inflammatory process)
  • atelectrauma - alveolar injury from opening and closing of alveoli
  • biotrauma (increase in cytokines, causing systemic dysfunction)

Modified settings:

  • low tidal volumes (to avoid overdistension)
  • PEEP (to keep alveoli from completely collapsing at end of expiration)
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16
Q

What treatment will improve ARDS survival? What is an acceptable side effect of this treatment?

A

low tidal volume ventilation (increase respiratory rate to make up for lowered TV)

results in mild-moderate hypercapnia, which is okay

17
Q

What is the prognosis for ARDS?

A
  • 30-40% mortality
  • those who survive –> generally no or minimal lung dysfunction
  • long term side effects: fatigue, weakness, cognitive deficits, PTSD
18
Q

What is neonatal respiratory distress syndome? How can it be prevented?

A

Hypoxemic respiratory failure in neonates born at 26-28 weeks due to insufficient quantities of surfactant

Administer corticosteroids prior to birth, administer surfactant after birth

19
Q

Surfactant administration is beneficial in [neonatal respiratory distress syndrome/acute respiratory syndrome/both]. Why?

A

Neonatal respiratory distress syndrome only - primarily due to a lack of surfactant

ARDS involves the breakdown of surfactant in addition to a lack of production –> added surfactant will be broken down

20
Q

What are the two types of respiratory failure? How do you differentiate between them?

A

Type I - due to hypoxemia (PaO2 < 60 mmHg)
Type II - due to hypercapnia (PaCO2 > 45 mmHg)

Have to get an arterial blood gas

21
Q

What are the most common mechanisms for hypoxic respiratory failure?

A
  • shunt

- V/Q mismatch

22
Q

What two types of ILD can cause acute hypoxemic respiratory failure if severe enough?

A
  • cryptogenic organizing pneumonia

- acute interstitial pneumonia

23
Q

What are the common pulmonary and extra-pulmonary causes of chronic hypoxemic respiratory failure?

A
  • COPD
  • pulmonary fibrosis
  • pulmonary hypertension
  • intracardiac shunt
  • pulmonary arteriovenous malformation
  • hepatopulmonary syndrome
24
Q

What are the common pulmonary and extra-pulmonary causes of acute hypoxemic respiratory failure?

A
  • pneumonia
  • acute respiratory distress syndrome (noncardiogenic pulmonary edema)
  • cardiac pulmonary edema
  • lobar collapse
  • pulmonary embolism
  • pneumothorax
  • severe acute ILD (cryptogenic organizing pneumonia or acute interstitial pneumonia)
25
Q

What are the common pulmonary and extra-pulmonary causes of acute hypercapnic respiratory failure?

A
  • drug overdose
  • acute spinal cord injury
  • acute neuromuscular disease
  • COPD exacerbation
  • status asthmaticus
26
Q

What are the common pulmonary and extra-pulmonary causes of chronic hypercapnic respiratory failure?

A
  • chronic neuromuscular disease
  • thoracic cage problem
  • abnormal control of breathing (OHS)
  • COPD
27
Q

What is the definition of acute respiratory distress syndrome?

A

All must be present:

  • acute onset (within one week of known clinical insult)
  • abnormal CXR or CT (bilateral opacities with pulmonary edema) not fully explained by other processes
  • respiratory failure (hypoxemic or hypercapnic) not fully explained by fluid overload or CHF
  • hypoxemia: PaO2/FiO2 < 300
28
Q

What is the approach to treat ARDS?

A
  • mechanical ventilation
  • supportive care (avoid excessive fluids, provide adequate nutrition, etc.)
  • drug therapy if indicated
29
Q

What does PEEP stand for? What does it do?

A

PEEP = positive end-expiratory pressure (setting used with ventilation)

  • keeps alveolar pressure above atmospheric pressure at end-expiration to prevent alveolar collapse
  • recruits atelectic lung and keeps alveoli open
  • improves oxygenation, FRC, and lung compliance