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Respirology > Respiratory failure > Flashcards

Respiratory failure Flashcards

1
Q

What is the definition of respiratory failure

A
  • failure of respiratory system to maintain normal blood gases
  • hypoxemic (PaO2 <60 mmHg)
  • hypercapnic (PaCO2 >50 mmHg)
  • acute vs. chronic (compensatory mechanisms activated)
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2
Q

What are signs and symptoms of respiratory failure

A
  • signs of underlying disease
  • hypoxemia: restlessness, confusion, cyanosis, coma, cor pulmonale
  • hypercapnia: headache, dyspnea, drowsiness, asterixis, warm periphery, plethora, increased ICP (secondary to vasodilatation)
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3
Q

Respiratory failure investigations

A
  • serial ABGs

* CXR and/or CT, bronchoscopy to characterize underlying cause if unclear

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4
Q

Definition of hypoxemic respiratory failure

A

• PaO2 decreased, PaCO2 normal or decreased

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5
Q

Hypoxemic respiratory failure treatment

A
  • reverse the underlying pathology
  • oxygen therapy: maintain oxygenation (if shunt present, supplemental O2 is less effective)
  • ventilation, BiPAP, and PEEP/CPAP: positive pressure can recruit alveoli and redistribute lung fluid
  • improve cardiac output: ± hemodynamic support (fluids, vasopressors, inotropes), reduction of O2 requirements
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6
Q

What are different types of hypoxemia

A

Low FiO2

Hypoventialtion

Shunt (intrapulmonary)

Shunt (right to left)

Low mixed venous O2 content

V/Q mismatch

Diffusion impairment

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7
Q

What are the settings, PaCO2, A-aDO2, effect of oxygen therapy, effect of ventilation, BiPAP and PEEP and effect of improved cardiac output on low fiO2 hypoxemia

A

Post op, high altitude

Normal or decreased

Normal

Improves

No change

No change

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8
Q

What are the settings, PaCO2, A-aDO2, effect of oxygen therapy, effect of ventilation, BiPAP and PEEP and effect of improved cardiac output on Hypoventilation hypoxemia

A

Drug overdose

Increased

Normal

Improves

Improves with ventilation

No change

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9
Q

What are the settings, PaCO2, A-aDO2, effect of oxygen therapy, effect of ventilation, BiPAP and PEEP and effect of improved cardiac output on shunt (intrapulmonary) hypoxemia

A

ARDS, pneumonia

Normal or decreased

Increased

No change

Improves (except if one-sided)

Improves

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10
Q

What are the settings, PaCO2, A-aDO2, effect of oxygen therapy, effect of ventilation, BiPAP and PEEP and effect of improved cardiac output on shunt (right to left)

A

Pulmonary hypertension

Normal or decreased

Increased

No change

Worsens

Worsens

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11
Q

What are the settings, PaCO2, A-aDO2, effect of oxygen therapy, effect of ventilation, BiPAP and PEEP and effect of improved cardiac output on low mixed venous o2 content hypoxemia

A

Shock

Decreased

Increased

Improves or no change

Worsens

Improves

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12
Q

What are the settings, PaCO2, A-aDO2, effect of oxygen therapy, effect of ventilation, BiPAP and PEEP and effect of improved cardiac output on V/Q mismatch hypoxemia

A

COPD

Normal or increased

Increased

Improves (small amounts)

Often improves

Improves

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13
Q

What are the settings, PaCO2, A-aDO2, effect of oxygen therapy, effect of ventilation, BiPAP and PEEP and effect of improved cardiac output on diffusion impairment hypoxemia

A

ILD, emphysema

Normal

Increased

Improves

Improves with positive pressure

No change or worsens

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14
Q

What is dead space

A
  • Ventilation without perfusion

* The opposite of shunt

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15
Q

Causes of hypercapnia

A
  • High Inspired CO2
  • Low Total Ventilation
  • High Deadspace Ventilation
  • High CO2 Production
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16
Q

What is the definition of hypercapnic respiratory failure

A

• PaCO2 increased, PaO2 decreased

17
Q

What is the pathophysiology of hypercapnic respiratory failure

A

• increased CO2 production: fever sepsis, seizure, acidosis, carbohydrate load

• alveolar hypoventilation: COPD, asthma, CF, chest wall disorder, dead space ventilation (rapid shallow breathing)
■ inefficient gas exchange results in inadequate CO2 removal in spite of normal or increased minute volume

• hypoventilation
■ central: brainstem stroke, hypothyroidism, severe metabolic alkalosis, drugs (opiates, benzodiazepines)
■ neuromuscular: myasthenia gravis, Guillain-Barré, phrenic nerve injury, muscular dystrophy, polymyositis, kyphoscoliosis
■ muscle fatigue

18
Q

Should you provide oxygen in chronic hypercapnia

A

In chronic hypercapnia, supplemental O2 may decrease the hypoxic drive to breathe, but do not deny oxygen if the patient is hypoxic

19
Q

In COPD patients with chronic hypercapnia what should O2 sat target be

A

In COPD patients with chronic hypercapnia (“CO2 retainers”), provide supplemental oxygen to achieve target SaO2 from 88-92%

20
Q

Hypercapnic respiratory failure treatment

A
  • reverse the underlying pathology
  • if PaCO2 >50 mmHg and pH <7.35 consider noninvasive or mechanical ventilation

• correct exacerbating factors
■ NTT/ETT suction: clearance of secretions
■ bronchodilators: reduction of airway resistance
■ antibiotics: treatment of infections

  • maintain oxygenation (see above)
  • diet: increased carbohydrate can increase PaCO2 in those with mechanical or limited alveolar ventilation; high lipids decrease PaCO2
21
Q

What is the definition of acute respiratory distress syndrome

A

• clinical syndrome characterized by severe respiratory distress, hypoxemia, and noncardiogenic pulmonary edema

• The Berlin Criteria (JAMA 2012; 307:2526-2533) for ARDS
■ acute onset
◆ within 7 d of a defined event, such as sepsis, pneumonia, or patient noticing worsening of respiratory symptoms – usually occurs within 72 h of presumed trigger
◆ bilateral opacities consistent with pulmonary edema on either CT or CXR
◆ not fully explained by cardiac failure/fluid overload, but patient may have concurrent heart failure
◆ objective assessment of cardiac function (e.g. echocardiogram) should be performed even if no clear risk factors

22
Q

ALI vs ARDS

A

ALI vs. ARDS: Definition is the same,
except ALI is a PaO2/FiO2 ≤300,
while ARDS is a PaO2/ FiO2 ≤200

23
Q

Categorization of ARDS as Mild, Moderate or Severe – The Berlin Criteria

A

Mild
PaO2/FiO2 (mm Hg) 200-300
Mortality 27%

Moderate
PaO2/FiO2 (mm Hg) 100-200
Mortality 32%

Severe
PaO2/FiO2 (mm Hg) <100
Mortality 45%

24
Q

ARDS etiology

A
  • direct lung injury
  • airway: aspiration (gastric contents, drowning), pneumonia, inhalation injury (oxygen toxicity, nitrogen dioxide, smoke)
  • circulation: embolism (fat, amniotic fluid), reperfusion injury
  • indirect lung injury
  • circulation: sepsis, shock, trauma, blood transfusion, pancreatitis
  • neurogenic: head trauma, intracranial hemorrhage, drug overdose (narcotics, sedatives, TCAs)
25
Q

ARDS pathophysiology

A

• disruption of alveolar capillary membranes → leaky capillaries → interstitial and alveolar pulmonary edema → reduced compliance, V/Q mismatch, shunt, hypoxemia, pulmonary HTN

26
Q

ARDS clinical course

A

A. Exudative Phase
• first 7 d of illness after exposure to ARDS precipitant
• alveolar capillary endothelial cells and type I pneumocytes are injured, resulting in loss of normally tight alveolar barrier
• patients develop dyspnea, tachypnea, increased work of breathing
■ these result in respiratory fatigue and eventually respiratory failure

B. Fibroproliferative Phase
• after day 7
• may still experience dyspnea, tachypnea, fatigue, and hypoxemia
• most patients clinically improve and are able to wean off mechanical ventilation
• some patients develop fibrotic lung changes that may require long term support on supplemental oxygen or even mechanical ventilation
• if fibrosis present, associated with increased mortality

27
Q

Risk factors for aspiration pneumonia

A

Decreased level of consciousness (ex. Alcoholism)

Upper GI tract disorders (ex. Dysphagia, esophageal disorders)

Mechanical instrumentation (ex. Intubation, nasogastric tube, feeding tubes)

Neurologic conditions (ex. Dementia, Parkinson disease)

Others (ex. Protracted vomiting)

28
Q

Typical location of aspiration pneumonia

A

Lower lobes, specifically superior part of lower lobes (lowest part when lying down)

29
Q

ARDS treatment

A

• treat underlying disorder (e.g. antibiotics if infection present)

• mechanical ventilation using low tidal volumes (<6 mL/kg) to prevent barotrauma
■ use optimal amount of PEEP (positive end-expiratory pressure) to keep airways open and allow the use of lower FiO2
■ may consider using prone ventilation, ± inhaled nitric oxide, short term paralytics (<48 h) or ECMO (extracorpeal membrane oxygenation) if conventional treatment is failing

  • fluids and inotropic therapy (eg. dopamine, vasopressin) if cardiac output inadequate
  • pulmonary-arterial catheter now seldom used for monitoring hemodynamics
30
Q

Complications and prognosis of ARDS

A
  • mortality: 30-40%, usually due to non-pulmonary complications
  • sequelae of ARDS include residual pulmonary impairment, severe debilitation, polyneuropathy and psychologic difficulties, which gradually improve over time
  • most survivors eventually regain near-normal lung function, often with mildly reduced diffusion capacity

Respirology (4 decks)

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