Lecture 18: Assisted Breathing Methods Flashcards
What is the main inspiratory muscle and what muscle fibres does it consist of?
- diaphragm
- fatigue resistance slow-twitch type I and fast twitch II a myofibres
List some central and peripheral causes of loss of control of one or both hemidiaphragms
Central causes:
* brain or brainstem stroke, ALS
* spinal cord injury, syringomyelia, polio
* autoimmune (MS, Guillain-Barré)
Peripheral causes:
* phrenic nerve trauma from surgery,
radiation, tumor
* phrenic neuropathy, viral or bacterial
infections, unknown etiology (idiopathic)
What % is the diaphragm active during breathing
duty cycle: active 30-40% of the time
Since they’re busy all the time, they’re susceptible to inactivity or disuse
Describe early negative pressure mechanical ventilation
aka Iron Lung or Cuirass ventilators
sealed pressurized vessel, only thing that came out was the person’s head. machine is snug around neck
vacuum in the chamber causes the chest to expand, allowing airflow into the lungs
pressurize chamber, chest to deflate, allowing for exhalation
Describe early positive pressure mechanical ventilation - why was it created?
During the 1952 polio epidemic, iron lung ventilators were in short supply.
Anesthetist discovered bellows to provide positive pressure can keep polio patients alive
Hired teams of volunteers (medical students), to keep people alive by squeezing the bag.
central apnea
a sleep disorder that causes breathing to repeatedly stop and start during sleep
somewhat related to positioning
baby suddenly stops breathing
obstructive sleep apnea
overweight. tongue falls back and is an obstacle to breathing
Positive Pressure Ventilation - Fundamentals
Pressurized air is forced in, either through dialing the applied pressure (pressure control) or the supplied volume (volume control).
The ventilator can
* Provide a mandatory breath,
* Assist a patient who can initiate a breath, or
* do combinations of the above.
Patients can vary between being deeply comatose
to alert and interactive.
List 4 harms of positive pressure ventilation
- Ventilator-induced lung injury – VILI (or VALI). Has 3 aspects to it:
- Volutrauma/Barotrauma
- Atelectotrauma
- Biotrauma
- Ventilator-associated pneumonia – VAP
- Ventilator-induced diaphragmatic dysfunction (or atrophy/due to atrophy) – VIDD
- Ventilator-associated brain injury - VABI
Describe 3 types of Ventilator-induced lung injury – VILI (or VALI)
volutrauma/biotrauma
too much end-inspiratory volume
* direct lung damage and inflammation
* increases epithelial and microvascular permeability allowing fluid filtration into the alveoli
* leads to pulmonary edema
barotrauma
too much high positive airway pressure
* causes lung overdistension with gross tissue injury
* causes transfer of air into interstitial tissues at the proximal airways
* pneumothorax
atelectasis: a complete or partial collapse of a lung or a lobe that develops when
alveoli within the lung become deflated
Positive pressure ventilation yields inhomogeneous pressure distribution and parts of the lung collapse due to extrinsic weight (chest wall) and intrinsic compression (superior portions of the lung, mediastinal contents)
* Cyclical collapse and re-opening of terminal lung units induces inflammation and damage through recurrent shear stress and alterations in local surfactant
* villi can permanently collapse. can result in insufficient lung capactiy after being taken off the vent. occurs if on the ventilator for a long time
- more pressure on top of lung than rest of lung; wrong distribution of air
can lead to Acute respiratory distress syndrome (ARDS)
Slide 10: components of lung protective ventilation to reduce ventilator associated lung injury and decrease incidence of ARDS
keep range of tidal volume to a narrow 6-8mL/kg of predicted body weight
stay within these limits:
Positive end-expiratory pressure set to limit atelectasis and shunt (PEEP table); the remaining pressure when you exhale. be careful of going lower than this to prevent vili collapse
pleateau pressure: <30 cm H2O
minimize FiO2
Slide 11: Lung Protective Ventilation cannot eliminate VILI
No matter how you fiddle with these parameters, something in the lung will be suboptimal.
Ventilation with low VT and low PEEP: higher amounts
of atelectasis are present at end-expiration and end-
inspiration with minimal areas of overinflation
Ventilation with high VT and low PEEP: less atelectasis
is present at end-expiration and end-inspiration, with
increased areas of overinflation at end-inspiration.
Furthermore, a higher amount of tissue collapsing
and de-collapsing during breathing is present.
Ventilation with low VT and higher PEEP: less
atelectasis is present. However, higher overinflation
occurs at end-inspiration and end- expiration.
Ventilator-associated pneumonia (VAP)
- Exogeneus sources
- mechanism
- length of time to develop
- problem with VAP
- how does VAP differ from community acquired pneumonia
- hands of healthcare worker, ventilator circuit, biofilm of endotracheal tube
- pneumonia occurs when colonized secretions are inhaled into the lungs through the endotracheal tue
- VAP develops 48+ hours after MV is given via an endotracheal tube or tracheostom
- VAP causes increased lengths of ICU stay and up to 20-30% higher death rates. Several bacteria (referred to as multidrug resistant) are particularly important causes of VAP.
- The microbiologic flora responsible for VAP is different from that of the more common
community-acquired pneumonia (CAP).
Describe the clinical manifestations of ventilator associated brain injury
- delirium
- coma
- disability
- impaired quality of life
- long-term cognitive impairment
Work in multiple animal models showed a significant
reduction of _______ that was
proportional to duration of mechanical ventilation.
diaphragmatic force-generating capacity
