ARDS Flashcards

1
Q

How do you define respiratory failure? (include number values)

A
  • PaO2 < 50 (nl:80) on 50% oxygen
  • PaCo2 > 50 (nl:40)
  • acute resp failure: pH <7.25 (nl:7.4)
  • chornic resp failure: pH approaching 7.4 (compensatory)
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2
Q

Type 1 respiratory failure

A
  • hypoxemia
  • alveolar flooding –> shunting
  • ex: pulm edema (cardiogenic with CHF, or non-cardiogenic), pneumonia, alveolar hemorrhage,
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3
Q

Type 2 Respiratory failure

A
  • hypercapnic (cant get rid of CO2)
  • due to alveolar hypoventilation
  • treat underlying cause
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4
Q

3 “sources” of alveolar hypoventilation

A
  1. CNS (drugs, hypothyroidism, metabolic alkalosis, CNS lesion, idiopathic alveolar hypoventilation)
  2. Chest wall, neuromuscular system (kyphoscoliosis, Myasthenia Gravis, Guillain-Barre, ALS, Muscular dystrophy, Obesity, diaphragmatic fatigue, polymyositis, cervical cord injury)
  3. **Lung **(COPD, CHF, ARDS, Severe Asthma)
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5
Q

Type 3 Respiratory Failure

A
  • from atelectasis, “perioperative respiratory failure”
  • decreased FRC (after general anesthesia)
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6
Q

Type 4 Respiratory Failure

A
  • hypo-perfusion of respiratory muscles
  • occurs durign shock, multi organ system failure
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7
Q

Pulmonary Rules of Arterial Blood Gases

A

PaCo2:

ACUTE: for every 10 unit change in PaCO2, you have a 0.08 pH change

CHRONIC: for every 10 unit change in PaCO2, you have a 0.03 pH change (note: overcompensation never occurs)

PaO2:

AaDo2<25 normal lung/gas exchange unit

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8
Q

What is ARDS, how does it present

A

sudden onset of severe dyspnea from some diffuse lung injury

  • severe dyspnea
  • reapid onset
  • diffuse infiltrates in imaging
  • hypoxemia
  • leads to resp failure
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9
Q

Etiology of ARDS

A

Divided into direct and indirect lung injury

direct: pneumonia, aspiration of something, pulmonary contusion (bruise), drowning, toxic inhalation

indirect: sepsis, severe trauma (bone fractures, rail chest, head trauma, burns), multiple transfusions, drug OD, pancreatitis, postcardiopulmonary bypass

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10
Q

Pathophysiology of ARDS (4 steps)

A

key is to remember that inflammation takes place

  1. insunlt
  2. inflammation
  3. cytokine storm
  4. acute lung injury (increase capillary leak, lungs fill with fluid-interstitium first then alveoli) note: leakage causes proteins to leave vessel, and fluid follows. n ormally osmotic pressure keeps the fluid in the blood vessels, but you lose this with leakage
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11
Q

Clinical course of ARDS

A

Exudative stage:

  1. edema
  2. hyaline membrane (lung trying to repair itself)

Proliferative stage:

  1. interstitial inflammation
  2. interstitial fibrosis
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12
Q

Key cells and features in the pathophysiology of ARDS

A
  • shunting AND V/Q mismatch
  • secondary alterations in surfactant function
  • increased pulmonary vascular resistance
  • decreased pulmonary compliance
  • decreased FRC (lungs collapsing)
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13
Q

how do you rule out heart failure in ARDS?

A

wedge pressure (LAP) must be <18

if it were high, that would imply you have LHF and back up of blood and thus increased pressure in the LA

seeing a normal LAP tells us that its an isolated lung problem

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14
Q

treatment

A

ventilation to control RR,Tidal Vol, FiO2,

PEEP (to pop/stent open those collapsing alveoli)

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15
Q

Qualitative distinction between acute lung injury and ARDS

A

ALI: P/F less than or equal to 300

ARDS: P/F less than or equal to 200

P:F ratio is the ratio of arterial oxygen concentration to the fraction of inspired oxygen. It reflects how well the lungs absorb oxygen from expired air.

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