pO2 Is Too Low (i.e., < 60)
AC/SIMV: increase PEEP or FiO2
APRV: increase PHigh, THigh, or FiO2
HFOV: increase mean airway pressure or FiO2
pCO2 Is Too High (i.e., > ??)
VCAC/SIMV: increase RR or TV
PCAC/SIMV: increase RR or driving pressure
APRV: increase the gradient between PHigh and PLow; decrease the THigh; increase TLow
HFOV: decrease the frequency, increase amplitude, increase Ti%, allow a 5 cm cuff leak
pCO2 Too Low (i.e. < 35)
VC-AC/SIMV: decrease RR or TV
PC-AC/SIMV: decrease RR or driving pressure
APRV: increase THigh, lower PHigh, decrease TLow
HFOV: increase the frequency, decrease the amplitude, decrease Ti%
High Peak Pressures (PIPs or Paws)
perform an inspiratory pause & obtain a Pplat
Pplat represents the portion of PIP actually applied to the small airways & alveoli during inspiration
difference between PIP & Pplat: pressure due to airway resistance
difference between Pplat & PEEP: pressure due to lung compliance
↑ PIP & ↓ Pplat: problem is ↑ airway resistance
kinked ET tube (unkink the tube)
mucus plugging (pass a suction catheter)
bronchospasm (inhaled bronchodilators)
too narrow of an ETT (change the tube)
↑ PIP & ↑ Pplat: problem is ↑ lung compliance
mainstem intubation (retract ETT)
atelectasis (chest percussion, or broncho to open airway)
pulmonary edema (diuresis or inotropes)
ARDS (decrease TV, increase PEEP, paralyze, prone)
PTX (chest tube)
Dynamic Hyperinflation (Auto-PEEP)
PEEP is the alveolar pressure above atmospheric pressure that exists at the end of expiration, and there are 2 types
Extrinsic PEEP (or applied PEEP): PEEP provided by the mechanical ventilator to mitigate end-expiratory alveolar collapse
Intrinsic PEEP (or auto-PEEP): PEEP secondary to incomplete expiration, leading to progressive air trapping (i.e., dynamic hyperinflation); usually due to inadequate time for exhalation, & is exacerbated by high airway resistance (i.e., bronchospasm, COPD, mucus plugging)
potential sequelae
hypotension esp. if hypovolemic (↑ intra-thoracic pressure → ↓ VR → ↓ CO)
VILI (i.e., volutrauma, barotrauma)
patient-ventilator asynchrony (due to ↑ WOB)
therapy incl.
lower RR to 10-14
shorten Ti to keep I:E ratio 1:3 to 1:5
keep TV 6-8 mL/kg
if air hungry, increase inspiratory flow to 60-80 LPM
narcotic sedation can blunt tachypneic response
treat bronchospasm w/inhaled bronchodilators & systemic steroids
Sudden Drop in SpO2
disconnect pt from ventilator & BVM
re-confirm ETT / trach placement
obtain an ABG & chest XR
consider PE as the cause
if unilateral absent breath sounds, pull ETT back a few cm
if still absent, consider PTX or mucus plugging w/complete atelectasis
consider tension PTX if absent breath sounds & pt is hypotensive
Fighting the Ventilator
before sedating and/or paralyzing the pt, always check TSS
T: tube (confirm placement & not obstructed)
S: sounds (present & equal bilaterally)
S: sats (ensure pt is not hypoxemic)
other things to consider incl.
dynamic hyperinflation
untreated pain esp. in trauma / surgery pts
ensure the RR and TV are adequate
switch to AC if the pt is getting fatigued
consider other causes of distress (cardiac ischemia, fever, abdominal distention, neurologic deterioration, etc.)
Change in EtCO2
confirm the EtCO2 waveform is present; if not present, it means one of three things
tube is not in the trachea (emergency)
tube is occluded (emergency)
EtCO2 sensor is faulty (diagnosis of exclusion)
if the waveform is present, obtain an ABG for the paCO2
↑ EtCO2 & ↑ paCO2: either ↑ CO2 production or alveolar hypoventilation due to
fever
malignant hyperthermia
thyrotoxicosis
suppressed respiratory drive w/o sufficient ventilation
↓ EtCO2 & ↑ paCO2 (or unchanged): the widening between the two suggests an increase in dead space ventilation from
PE
↓ CO (cardiogenic, hypovolemic shock)
dynamic hyperinflation (auto-PEEP)
↓ EtCO2 & ↓ paCO2: there is an increase in alveolar ventilation
pain
agitation
fever
sepsis
Abbreviations