Respiratory failure Flashcards

1
Q

Define respiratory failure

A
  • failure of respiratory system to maintain normal blood gases
  • hypoxemic (PaO2 50 mmHg)

• acute vs. chronic (compensatory mechanisms activated)

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2
Q

Px of hypoxemia

A

restlessness, confusion, cyanosis, coma, cor pulmonale

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3
Q

Px of hypercapnia

A

headache, dyspnea, drowsiness, asterixis, warm periphery, plethora, increased ICP (secondary to vasodilatation)

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4
Q

Define type 1 & type 2 RF

A

Type 1: hypoxaemic
PaO2 decreased, PaCO2 normal or decreased
V/Q mismatch problem & involves hyperventilation (hence normal/low CO2)

Type 2: hypercapnic
• PaCO2 increased, PaO2 decreased
Fatigue, lack of respiration problem. (hence low O2, high CO2)

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5
Q

Describe relationship b/w H+ & K+

A
Acidosis = hyperkalaemia
Alkalosis = hypokalaemia

H+ and K+ swap places (H+ into cell, K+ out of cell if too much H+. hence more K+ detected)

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6
Q

Rx of T1 RF

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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7
Q

Should you give O2 in RF?

A

Yes - T1 RF

No but Yes - T2 RF (decrease hypoxic drive to breathe but still need to give O2 if hypoxic)

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8
Q

Should you give O2 in COPD?

A

Yes - provide suppl O2 to achieve target SaO2 from 88-92%

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9
Q

Causes of hypercapnia

A
  • high inspired CO2
  • low total vent (e.g. brainstem stroke, myasthenia gravis, Guillain-Barre, muscle fatigue)
  • high deadspace vent
  • high CO2 production (e.g. fever, sepsis, seizure, acidosis)
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10
Q

Rx of T2 RF

A

• reverse the underlying pathology
• if PaCO2 >50 mmHg and pH is acidemic 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

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11
Q

Define ARDS

A

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

Defined by:
• Hypoxaemia PaO2/FiO2

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12
Q

What criteria do you use for ARDS and what does it consist of?

A

The Berlin criteria

    - 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
- an objective assessment (e.g. echocardiogram) should be performed if no clear risk factors
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13
Q

What are the risk factors for ARDS?

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)
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14
Q

What is the pathophysiology of ARDS?

A

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

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15
Q

Cx of ARDS

A

Fibrotic lung changes
• sequelae of ARDS include residual pulmonary impairment, severe debilitation, polyneuropathy and psychologic difficulties, which gradually improve over time

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16
Q

Rx of ARDS

A
  • treat underlying disorder (e.g. antibiotics if infection present)
  • mechanical ventilation using low tidal volumes (