Lecture 9 Flashcards

1
Q

What is weaning?

A

Refers to the reduction in the amount of ventilatory support (eg. IMV to SIMV to PSV) - pump and O2 support (O2 can be delivered other ways besides MV - nasal prongs, mask etc)

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2
Q

When is the patient ready to be weaned?

A
  1. Cause of RF has been reversed
  2. Can spontaneously breathe
  3. Low PEEP and FiO2 requirements
  4. CV is stable
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3
Q

What are 3 methods of weaning?

A
  1. Step down assistance (SIMV - PSV - CPAP)
  2. T piece (easy transition between MV and non vent; can be off the entire day and put on vent at night)
  3. NIV post extubation
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4
Q

What are the factors that affect weaning?

A
Energy supply (reduced)
- nutrition, O2 supply (cardiac dysfunction affecting Q, or pulmonary edema affecting O2 diffusion), O2 utilisation, stealing theory (high O2 use by resp mm's)

Energy demand (increased)

  • reduced pump efficiency
  • increased resp load (airway resistance, chest and lung compliance)

Neuromm competence

  • reduced resp drive
  • mm weakness
  • impaired neuromm transmission - permanent or reversible (spinal cord injury vs GBS)
  • psychogenic (pt has come to rely on intubation esp if previous extubation hasn’t been successful)
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5
Q

What percentage of pt’s fail to wean and what are prognostic factors?

A

20% fail to wean

Worse outcome likely with:

  • age
  • COPD dx
  • prolonged MV
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6
Q

What’s the role of the physio in the weaning process?

A

Basically:

  • reduce the load
  • improve the pump
  • optimise O2 movement
  • prevent deconditioning

RRASP N

Respiratory mm mechanics
Reassure
Atelectasis
Secretion clearance assistance
Peripheral deconditioning minimization

NIV/Tracheostomy

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7
Q

What is a flail segment?

A

4 consecutive rib #s in 2 or more places

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8
Q

What is the effect of a sternal and rib fracture/flail segment on O2 movement, CO2 movement, secretion movement?

A
  1. Reduced CO2 movement (so increased PaCO2)
    - increased load and reduced ability to cope with load
    - reduced pump efficiency
  2. Reduced O2 movement (so increased PaO2)
    - generalized bc of pain driven smaller tidal volumes
    - localized bc of lung contusion
  3. Reduced secretion movement
    - reduced cough effectiveness d/t pain

*acute changes also include pain and reduced movement of ribs (or paradoxical movement)

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9
Q

What is a pulmonary contusion

A

Bruising of the lung NOT confined to anatomical segmients; gets worse over 48 hrs; can get contusion without rib # if the ribs are springy

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10
Q

What are the effects of pulmonary contusion?

A
  1. Coagulation cascade
    - blood clots/fibrin - means that part of the lung can’t participate in gas exchange and the lung gets stiffer
  2. Reduced O2 movement
    - d/t reduced SA for gas exchange
  3. Reduced CO2 movement
    - d/t reduced lung compliance (from coagulation cascade and edema) - therefore increased LOAD
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11
Q

What is the physio management for pt’s with pulmonary contusion/rib fractures?

A
  1. Pain management
  2. Positioning
  3. Mobilisation
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12
Q

What is ARDS?

A
  • non cardiogenic pulmonary edema
  • bilateral + diffuse alveolar damage
  • follows from an acute insult
  • d/t endothelial damage/inflammation and increased microvascular permeability
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13
Q

What are the KEY features for dx with ARDS?

A
  1. Acute hypoxaemic RF (PaO2 < 60 no responding to increasing levels of FiO2)
  2. Bilat + diffuse infiltrate on CXR
  3. No evidence of heart or lung disease, or fluid overload
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14
Q

What are the severity levels for ARDS - what are the

on?

A

Severe - <100 PaO2
Moderate 100-200 PaO2
Mild 200-300 PaO2

*for ALL the above - PEEP > 5cmH2O

(Normal PaO2 = 450)

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15
Q

What are the 3 phases of ARDS? Explain them

A
  1. Exudative phase
    > Damage to alveolar-capillary layer
    - increased permeability
    - damaged pulmonary capillary endothelium
    - remember this is NON CARDIOGENIC
    > Inflammatory infiltrates
    > Surfactant dysfunction - changes in composition of surfactant predisposes to further collapse
  2. Proliferative+fibrotic phase
    - thickening (endothelium, interstitium, epithelium)
    - interstitial fibrosis (affect lung compliance)
    - vascular occlusion
    - emphysematous type changes
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16
Q

What is the pathophysiology of O2 and CO2 movement impairment in ARDS?

A

O2 movement impairment:
- reduced SA for gas exchange d/t pulmonary edema (exudative phase)

CO2 movement impairment:

  • reduced lung compliance d/t pulm edema and fibrosis (later stages); also increased airway resistance from emphysematous changes
  • reduced PUMP efficiency d/t increased RR - fatigued resp mm’s
17
Q

What are protective ventilator strategies to prevent barotraum and volutrauma?

A
  1. Pressure controlled ventilation
  2. High frequency ventilation (>4x normal rate)
  3. Inhaled NO (better VQ matching)
  4. Extra Corporeal Life Support/Extra Corporeal Membrane Oxygenation (like a bypass machine - venous blood oxygenated outside the body through a machine)
18
Q

What is the mechanism of action of prone lying in improving SA for gas exchange in ARDS?

A

Prone lying - reinflation of dorsal posterior lung - improves VQ matching

  • take care of lines/drains
  • take care of body alignment in heavily sedated/paralysed pts to prevent 2º joint/mm issues
19
Q

What is the physio management for ARDS?

A
  1. Positioning
  2. Suctioning/manual techniques (percs/vibes)
  3. MHI - but be careful to not overinflate- monitor pressures (<30); dont use with high PEEP
  4. Exercise/mobilisation