Assessment of Control of Breathing, P0.1, CO2 Stimulation Test

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Assessment of Control of Breathing, P0.1, CO2
Stimulation Test

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Lecture Content

• Respiratory center physiology
• Respiratory center output chain
• P0.1 definition
• P0.1 technology
• Clinic application of P0.1
• Respiratory physiology, Pharmacology
• COPD
• MV adjustment
• Weaning

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Control of breathing, Important

• Gas exchange in the lung can be divided into
• Ventilation
• Diffusion
• Perfusion
• Control of breathing

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Control of Breathing, Passive lung

• Ventilation (of lung) is a passive behavior
• There is no rhythm generator (pace maker) nor
  respiratory muscle in the lung
• All respiratory muscle are striated muscle which
  controlled by nerve, the striated muscle without
  autonomic activity in the usual

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Respiratory Center

• Sensor input
• Central, peripheral
• Chemorecepotrs (O2, CO2, pH? ), stretch receptor,
  irritant receptors, J receptors, .
• Voluntary, involuntary
• Rhythm activation and integration
• Motor output

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Respiratory Central Network

• Respiratory center is not a single cell, not a
  single group of cells, but a network of many
  groups of neuron
• Respiratory rhythm is generated by a network of
  medullar neurons and transmitted by nerves to
  active respiratory muscle
• Rhythm generator
• On-switch and off-switch of inspiratory and
  expiratory activity
• Pattern generator
• Shapes the activity patterns of neuron

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Respiratory Center

• Central respiratory rhythm oscillating network
  in ventrolateral reticular formation of the
  brainstem, pre-Botzinger Complex
• Respiratory phase Inspiration, post inspiration
  (E-2), expiration (active exhalation), late
  expiration (passive expiration), ..
• Many neurons involved
• Pre-inspiratory, early-inspiratory,
  throughout-inspiratory, late-inspiratory,
  postinspiratory, expiratory,

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Respiratory Center Neuron Transmitter

• Neurons synaptic activation mediated by glutamate
• NMDA, AMPA,
• Most inhibitory mediated synaptic by GABA (Cl
  channel)
• Early- and postinspiratory is glycinergic

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Respiratory Center Neuron Activity

• Both excitation and inhibition
• Inspiration starts when early- and
  throughout-inspiratory neurons are released from
  postsynaptic inhibition
• The inspiratory ramp activity is also transmitted
  to late-inspiratory neurons
• The discharge of late-inspiratory neurons inhibit
  early-inspiratory neuron

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Control of Breath CNS and Output
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Respiratory Drive Index

• Tidal volume, respiratory frequency
• Minute ventilation marked variation, lung
  mechanism dependent
• Measurement of nerve or muscle electrical
  activity
• Mean inspiratory flow rate (MIF, VT/Ti)
• Inspiratory time fraction (Ti/Ttot)
• Mouth occlusion pressure

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Measurement of Respiratory Neuron Output

• CNS electrode Too invasive
• Phrenic N activity Invasive,
• Difficult to compare
• Diaphragm muscle Noise, Complicate
• activity Difficult to compare
• Ventilation Simple to measurement Indirect method
• Noninvasive Affected by chest
• Measure total output mechanism and muscle
• O2 cost of Noninvasive Indirect method
• breathing Measure total output Difficult to
  measure accurate

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Respiratory pattern generation

• Classically, breathing pattern is analyzed by
  respiratory frequency (f) and tidal volume (VT)
• Animal studies suggests the respiratory center
  output is controlled by driving (force) and duty
  cycle
• Ventilation Flow (amplitude) Time
• VE VT x f (VT/Ti) (Ti/Ttot) 60 (l/min)
• Ti/Ttot inspiratory duty ratio
• VT/Ti mean inspiratory flow rate, an index of
  the intensity of the driving
• VT/Ti and Ti/Ttot is interpreted as drive and
  timing components of ventilation which are
  somewhat controlled independently.

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Time Control versus Flow Control

• Time Ti, Ti/Ttot
• Flow MIF

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Correlation Between Nerve Activity and Muscle
Power
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Mouth Occlusion Pressure

• Occluded mouth (airway) pressure change after 100
  msec initial inspiration
• P0.1
• Assume mouth pressure equal to alveolar pressure
  in zero flow condition, by occluded airway
• Although negative in nature, P0.1 values are
  usually reported in positive units (cmH2O)
• It presents as the force output of respiratory
  center

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Termination of P0.1

• Mouth occlusion pressure
• Airway occlusion pressure
• P0.1 , P100

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Other express of occlusion pressure

• Maximal rate of change in mouth pressure dP/dtmax
• Maximal rate of change in mouth pressure in first
  100msce
• P0.1eso
• Peso max in non-occlusion method

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Characteristics of P0.1 (I)

• Respiratory muscle contraction in occluded airway
  (no flow, iso-volume, isometric constriction)
• Under isometric condition the force produced by a
  muscle changes proportionally to its electrical
  activity
• Less influenced by lung mechanism changes
• Correlate to respiratory center activity, phrenic
  nerve electrical activity and diaphragm force
  output

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Characteristics of P0.1 (II)

• No pressure loss due to resistance or elastance
• Index of respiratory center output
• Relatively regardless of the subject's lung
  condition
• Till severe respiratory muscle weakness, P0.1 is
  little changed with muscle weakness
• Before subject recognizes the occlusion and
  reacts to it (100 msec), less conscious dependent

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Normal value

• P0.1 (non stress) 0.98 /- 0.48 usually less
  than 2
• P0.1/PCO2 slope 0.6 (SEE 0.11)

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Tips of P0.1 measurement

• The tester unknowns the occlusion (occlusion time
  less than 0.2sec, without conscious interference)
• Airway rapid occluded before inspiration
• Adequate occlusion time
• Complete occlusion
• The lung volume (FRC, EELV) are not significant
  changed during testing

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Factors Influencing Measurement of Occlusion
Pressure

• Alteration in end-expiratory lung volume
• Time constant of the respiratory system
• Alteration in muscle length and velocity
• Chest wall distortion
• Expiratory muscle activity
• Shape of the driving pressure wave
• Pressure-flow phase lag

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Factors Influencing Measurement of Occlusion
Pressure

• Alternation in end-expiratory lung volume
• Time constant of respiratory system
• Alteration in muscle length and velocity
• Chest wall distortion
• Expiratory muscle activity
• Shape of the driving pressure wave
• Pressure-flow phase lags
• Expiratory pause
• P0.1 measure the onset of mechanic but not neural
  inspiration

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Airway Occlusion Recording
No flow
No -Occlusion
Occlusion
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Occlusion Time
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P0.1 and Borg Score
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Correlation between P0.1 and MIF
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Correlation of P0.1 to Work
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Effects of Muscle Weakness to Respiratory Drive
Estimate
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Poor Correlation of VE in Severe Muscle Weakness
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Effects of Muscle Weakness to Respiratory Drive
Estimate
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P0.1 versus PACO2
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CO2 Threshold
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Application of P0.1

• Central respiratory driving physiologic study
• Assess the effect of drugs to respiratory center
• Assess the effect of diseases to respiratory
  center
• Adjusting mechanical ventilation setting
• Predict the weaning outcome

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Conditions Influence P0.1

• P0.1 increase in
• Increase ventilatory load
• Asthma
• Breathing viscous gas mixture
• Even blood gas is held constant
• Respiratory center stimulant, anxiety
• P0.1 depressed by
• Tranquilizers
• Alcohol
• Central nerve system hypoxia

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Beta2-agonist Increase CO2 Respiratory Drive
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Beta2-agonist Increase O2 Respiratory Drive
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Bronchodilator Improve Borg Score and P0.1
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P0.1 in Pregnancy
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P0.1 and Progestgerone
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LVRS Decrease Respiratory Drive (Dyspnea)
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Respiration Change during HD
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P0.1 and COPD (I)

• Ventilation (tidal volume, minute ventilation) is
  significantly influenced by flow resistance,
  compliance and respiratory muscle strength
• Measurement of diaphragmatic EMG, oxygen cost of
  breathing and inspiratory mechanical work rate
  have been used but they are technically complex,
  time consumption and nonstandardized

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P0.1 and COPD (II)

• P0.1 at rest are either normal or increased in
  chronic muscle weakness (Begin, ARRD 1982)
• In COPD, high values and electromyographic sign
  indicate impending diaphragmatic fatigue
• No correlation between P0.1 and ABG
• In normal healthy individuals p0.1 values of 6-8
  cmH2O can only be obtained with a maximal
  voluntary ventilation (MVV) between 50 - 70 l/m

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Airway Occlusion Pressure in COPD Patients

• Irrespective of CO2 level, baseline central drive
  is increased in patients with COPD compared with
  control subjects
• Occlusion pressure responding to CO2 stimulation
  is intact in COPD patients

Eur Respir J 1998 12 666-671
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Increase Respiratory Drive in COPD
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Airway Occlusion Pressure in COPD
Eur Respir J 1998 12 666-671
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Tension Time index in COPD
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Airway Occlusion Pressure in Pressure Support
Ventilation
Thorax 199954119-123
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Pressure Support Decrease P0.1
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Titrate PEEP in COPD
Anesthesiology 2000 9381-90
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WOB and P0.1 COPD
Anesthesiology 2000 9381-90
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PEEPi and PO.1 in COPD
Anesthesiology 2000 9381-90
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P0.1 in Weaning
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P0.1 in Respiratory Failure
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Patients Characteristics Determinate Weaning
Parameters Predicting Accuracy
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Po.1 and Weaning
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Improve P0.1 in Success Weaning Patients
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P0.1 to Predict Weaning
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P0.1 Change in Weaning
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Predict the Weaning Outcome by P0.1

• P0.1 less than 4.2 can predict success weaning
  (Herrera, Int Care Med 1985)
• P0.1 (after T-tube for 5 min) more than 6 (mean
  8) predict weaning failure in COPD (Sassoon, ARRD
  1987)
• Decrease P0.1 (from 7.4 to 3.9 after 5 to 9 days
  treatment) predict success weaning in COPD
  (failure group from 6.6 to 6.5) (Murciano, Ann
  Int Med 1988)
• CO2 stimulate P0.1 by 3 CO2, success group
  increase P0.1 2 times failure group only 1.17
  times (Montgomery, Chest 1987)

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P0.1 in Weaning (Success)
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P0.1 in Weaning (Failure)
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Airway Occlusion Pressure for Extubation Failure
Intensive Care Med(2004) 30234-240
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Airway Occlusion Pressure for Extubation Failure
Intensive Care Med(2004) 30234-240
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Airway Occlusion Pressure in COPD After Extubation
Intensive Care Med (1998) 241277-1282
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Airway Occlusion Pressure in Respiratory Failure

• Normal person has P0.1 between 6-8 cmH2O when
  maximal voluntary ventilation(MVV) 50-70 l/m, but
  cannot maintain for a long time, may progress to
  fatigue
• P0.1 above 4.2cmH2O is uncomfortable to maintain
  spontaneous breathing, also difficult to weaning

Intensive Care Med (1985) 11134-139
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Respiratory Parameters at Start of the ATC
1 Success, 2 failure (CHEST 2002
122980984)
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Respiratory Parameters at End of the ATC
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Predict Weaning at ATC
2 min ATC
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Predict Weaning at ATC
All the evaluated indexes are useful but poor
predictors of weaning outcome in a general
intensive care unit population.
Intensive Care Med (2004) 30830836
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Airway Occlusion Pressure, Summery

• An index of neuromuscular drive, not influenced
  by resistance or compliance
• P0.1 increased in COPD patient, and the response
  to CO2 change is as well as normal person
• A good indicator in adjusting ventilator support,
  for example for adjust pressure support level or
  PEEP
• P0.1 as predictor of weaning is still
  controversial

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Thanks
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Correlation of Respiratory Drive by Mean
Inspiratory Flow Rate and Occlusion Pressure by
Different Methods

• MIF Paw0.1 Pawmax Peso0.1 Pesmax
• MIF 1 0.6 0.6 0.5 0.5
• Paw0.1 0.6 1 1.0 0.9 0.9
• Pawmax 0.6 1.0 1 0.9 0.9
• Peso0.1 0.5 0.9 0.9 1 0.98
• Pesomax 0.5 0.9 0.9 0.98 1
• Correlation is significant at the 0.05 level
  (2-tailed).

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Estimation of Occlusion Pressure During Assisted
Ventilation in Patients with Intrinsic PEEP

• Giorgio Conti, Gilda Cinnella, Enrico Barboni,
  Francois Lemaire, Alain Harf and Laurent Brochard
• Am J Respir Crit Care Med 1996 154907-12
• Reliable measurements of inspiratory drive
  can be obtained easily, on breath-by-breath
  basis, from airway pressure tracings during
  pressure-support ventilation in patients with
  variable levels of PEEPi

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Maximum Rate of Change in Oesophageal Pressure
Assessed from Unoccluded Breaths an Option where
Mouth Occlusion Pressure is Impractical

• C-H Hamnegard, MI Polkey, D Kyroussis, GH Mills,
  M Green. B Bake, J Moxham
• The maximum rate of change in oesophageal
  pressure measured form unoccluded breaths could
  be an alternative in circumstances where it is
  not feasible to used measurements of the mouth
  occlusion pressure 100ms after onset of
  inspiration

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Correlation between P0.1 Trigger and Occlusion
Method
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Special Consideration of P0.1 Measurement in
Ventilated Patients

• Trigger mode
• Trigger sensitivity
• Airway occlusion
• Time constant change due to tube circuit

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Correlation between P0.1 Trigger and Esophagus
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Correlation between P0.1max-eso to P0.1 Occlusion
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Auto-PEEP to P0.1 Trigger
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