ventilator waveforms are graphical representation of pulmonary physiology, mechanics and patient ventilator interaction. optimal patient ventilator interaction is needed to balance two goals of mechanical ventilation, safety and comfort.
1. PATIENT VENTILATOR INTERACTION
Dr. Ubaidur Rahaman
M.D. (General Medicine), EDIC
Senior Consultant Critical Care Medicine
Meenakshi Mission Hospital and Research Center
Madurai, Tamilnadu
2. “The world will ask you who you are,
and if you don’t know,
the world will tell you”
-Carl Gustav Jung
3. APPROACH
1. WHAT IS PATIENT VENTILATOR INTERACTION (PVI)
2. WHY IT IS IMPORTANT TO UNDERSTAND
3. HOW TO UNDERSTAND
1. READ VENTILATOR WAVEFORMS
1. IDENTIFY TAG (TAXONOMY ATTRIBUTE GROUPING) FOR MODE OF VENTILATION
2. BASIC PHYSIOLGY OF PATIENT VENTILATOR INTERACTION (PVI)
3. DIAGNOSE PATIENT VENTILATOR INTERACTION (PVI)
4. REVERSE TRIGGER
5. REAL PATIENT SCENARIOS
4. PATIENT VENTILATOR INTERACTION
Central controller
• Respiratory center
RESPIRATORY CONTROL APPERATUS
• ventilator
Input
• Sensors-
• PaO2, PaCO2, pH,
• sensation of stiffness,
irritation from lung/ chest
wall
• Effect of drugs
Effector pumps
• Respiratory muscle
• inspiratory muscle
• expiratory muscle
6. PATIENT VENTILATOR ASYNCHRONY (PVA)
CONSEQUENCE WHERE PVI IS NOT OPTIMAL
DELIVERY OF GAS BY VENITLATOR
• does not correspond in timing, quantity or pattern to what patient wants
INCIDENCE
• 25% patients on mechanical ventilation
• 80% patients on NIV
IT MAY BE
• innocuous in relation to safety and comfort of ventilation
• have disastrous consequence
SIGNS OF PVA MAY BE LESS OBVIOUS CLINICALLY BUT
• very obvious in ventilator graphics
7. • ineffective ventilation
• dynamic hyperinflation
• increased WoB
• Respiratory muscle dysfunction
• patient discomfort
• Confusion with respect to readiness for weaning
• overuse of sedatives and NMB agents
• Prolong mechanical ventilation
• distress for family members at bedside
• conflict among team members
PATIENT VENTILATOR ASYNCHRONY (PVA)- CONSEQUENCES
9. COMFORT
•optimal patient ventilator
interaction
SAFTETY
•optimal gas exchange
•Minimizing VILI/ PSILI
LIBERATION
•shorter duration of
mechanical ventilation and
minimizing complications
PATIENT CAN NOT BE MADE
• to conform to ventilator performance
RATHER VENTILATOR SHOULD MATCH PATIENT'S DEMAND
THUS, ONUS IS ON PHYSICIAN
• to optimize mechanical ventilation setting to reach a
consensus between SAFETY and COMFORT
WHAT IS THE SOLUTION?
AIM
Of
MV
PATIENT SHARED VENTILATOR
10. Who is the Boss?
WHAT IF VENTILATOR SETTING CAN NOT BE OPTIMIZED?
INCREASED VENTILATORY DEMAND:
• increased dead dead space,
• increased neurogenic drive,
• increased metabolic demand
DERANGED PULMONARY MECHANICS:
• ARDS,
• OAD, neuromechanical uncoupling,
HEMODYNAMIC COMPROMISE
• DHI, acute cor pulmonale
PATIENT SHARED VENTILATOR
Acute Phase
Recovery Phase
11. CALMING CENTRAL CONTROLLER- TO DO OR NOT TO DO
Central controller
• Respiratory center
inactive respiratory muscle
• VIDD- ventilator induced
diaphragmatic dysfunction
• oxidative stress
• Altered gene expression
• ultrastructural changes
• contractile dysfunction
• atrophy
• CONSEQUENCES OF NMB
• CINM
consequences of patient ventilator asynchrony
• ineffective ventilation
• dynamic hyperinflation
• increased WoB
• Respiratory muscle dysfunction- disease related,
use of NMB and steroid
• patient discomfort, fighting ventilator
• Confusion with respect to readiness for weaning
• overuse of sedatives and NMB agents
• Prolong mechanical ventilation
• distress for family members at bedside
• conflict among team members
PATIENT SHARED VENTILATOR
12. WHAT TO DO?
• IDENTIFY THE PROBLEM,
HOW TO IDENTIFY THE PROBLEM?
PATIENT VENTILATOR INTERACTION RECOGNITION IS BASED ON
• PATTERN RECOGNITION
• multiple trigger, double trigger, false/ pseudo double trigger
• ETIOLOGY
• reverse trigger, pseudo reverse trigger, flow asynchrony
• OUTCOME
• breath stacking,
NO STANDARD VOCABULARY TO DESCRIBE THIS
• Rather different names and definitions further confuse us.
13. HOW TO IDENTIFY THE PROBLEM?
• READ VENTILATOR WAVEFORM,
HOW TO READ VENTILATOR WAVEFORM?
• THIS IS WHAT WE GOING TO DISCUSS,
14.
15. READING VENTILATOR WAVEFORMS- 3 STEPS
1.Identify TAG (Taxonomy attribute grouping) for mode of ventilation
2. Understand Basic physiology of Patient Ventilator Interaction (PVI)
3. Diagnose Patient Ventilator Interaction (PVI)
17. IDENTIFY TAG FOR MODE OF VENTILATION
CONTROL VARIABLE
PRESSURE
VOLUME
BREATH SEQUENCE
CMV
CSV
IMV
VENTILATORY
PATTERN
PC-CMV
VC-CMV
PC-CSV
PC-IMV
VC-IMV
TARGETING SCHEMES
SET POINT
DUAL
BIO-VARIABLE
SERVO
ADAPTIVE
OPTIMAL
INTELLIGENT
VENTILATOR
MODE
18. IDENTIFY TAG FOR MODE OF VENTILATION
COMMON MODES
PC A/C
• PC-CMVs
VC-A/C
• VC-CMV:
• constant flow- set point or adaptive,
• de accelerating flow: set point
• In macquet servo I, constant flow set Point, flow is dual
targeted
PC- SIMV
• PC-IMVss
VC-SIMV WITH PS
• VC-IMVss
PRVC
• PC-CMVa
PRVC- SIMV
• PC-IMVas
20. BASIC PHYSIOLOGY OF PATIENT VENTILATOR INTERACTION
Pressure (P) delivered to the respiratory system at any given time is equal to
1. Elastic recoil pressure (product of tidal volume and elastance of respiratory system-VT×ERS)- Elastic load
2. Resistive pressure (product of airway resistance and inspiratory flow-RAW×F)- Resistive load and
3. Applied PEEP.
EQUATION OF MOTION
Pmus +Pvent = 𝑉𝑇 × 𝐸𝑅𝑆 + 𝑅𝐴𝑊 × 𝑉 + 𝑃𝐸𝐸𝑃
P = 𝑉𝑇 × 𝐸𝑅𝑆 + 𝑅𝐴𝑊 × 𝑉 + 𝑃𝐸𝐸𝑃
21. VC MODES
• 1. pressure is dependent variable, which is determined by
respiratory system mechanics (compliance and resistance).
Therefore PVI is seen in Pressure waveform,
• 3. Ventilators are excellent in controlling flow, so VT and flow
waveform configuration will be unaffected by Pmus for VC
set point targeting,
Pmus +Pvent = 𝑉𝑇 × 𝐸𝑅𝑆 + 𝑅𝐴𝑊 × 𝑉 + 𝑃𝐸𝐸𝑃
BASIC PHYSIOLOGY OF PATIENT VENTILATOR INTERACTION
VC MODE
• constant flow, set point targeting
• constant flow with flow adaptation
• De accelerating/ descending ramp flow with set point
targeting
22. PC MODES,
• 1. flow and tidal volume are dependent variable, determined
by respiratory system mechanics (C/R).
• Thus, PVI is visible in flow waveform,
• 3. As ventilators are poor in controlling pressure, compared
to flow, effect of Pmus (PVI) is also seen in pressure
waveform in PC modes.
Pmus +Pvent = 𝑉𝑇 × 𝐸𝑅𝑆 + 𝑅𝐴𝑊 × 𝑉 + 𝑃𝐸𝐸𝑃
BASIC PHYSIOLOGY OF PATIENT VENTILATOR INTERACTION
PC MODE
• set point targeting
• adaptive targeting- PRVC, autoflow
23. PRESSURE
FLOW
TIME
TIME
initial rapid rise in pressure is result of resistive load,
once tidal volume starts to be delivered
• pressure is function of both resistive and elastic load
once flow stops, resistive load becomes zero,
• therefore pressure drops as it overcomes elastic load
only
BASIC PHYSIOLOGY OF PATIENT VENTILATOR INTERACTION
VC- CMV, CONSTANT FLOW, SET POINT TARGETING
24. SLOPE OF PRESSURE RISE IS LINEAR, CONSIDERING CONSTANT ELASTANCE,
SLOPE OF PRESSURE WAVEFORM MAY BE CURVED BECAUSE OF
• PVI- patient effort (Pmus) or
• changing compliance (recruitable/ overdistention of ARDS lung- stress
index)
STRESS INDEX
• upward concavity- overdistention,
• downward concavity- recruitment,
PRESSURE
TIME
PRESSURE
TIME
PRESSURE
TIME
BASIC PHYSIOLOGY OF PATIENT VENTILATOR INTERACTION
VC- CMV, CONSTANT FLOW, SET POINT TARGETING
25. PRESSURE
FLOW
TIME
TIME
Pmus MAY ADD TO OR SUBTRACT FROM Pvent, AND
• deform pressure waveform
INSPIRATORY Pmus WILL
• deflect pressure waveform towards baseline (upward
concave), we will further explore in later slides
EXPIRATORY MUSCLE ACTIVITY-
• we will explore in later slides
BASIC PHYSIOLOGY OF PATIENT VENTILATOR INTERACTION
VC- CMV, CONSTANT FLOW, SET POINT TARGETING
26. PRESSURE
FLOW
TIME
TIME
INSPIRATORY Pmus WILL
• deflect pressure waveform towards baseline (upward
concave),
VENTILATORS ALLOWS EXTRA FLOW DESIRED BY PATIENT,
• flow waveform is deformed with upward convexity,
• Tidal volume also increases,
BASIC PHYSIOLOGY OF PATIENT VENTILATOR INTERACTION
VC- CMV, CONSTANT ADAPTIVE FLOW
27. PRESSURE
FLOW
TIME
TIME
VOLUME
TIME
INITIAL RAPID RISE IN PRESSURE IS RESULT OF RESISTIVE LOAD,
ONCE TIDAL VOLUME STARTS TO BE DELIVERED
• pressure is function of both resistive and elastic load
IF FLOW GOES TO ZERO BEFORE CYCLING,
• resistive load becomes zero, therefore pressure drops as it overcomes
elastic load only,
BASIC PHYSIOLOGY OF PATIENT VENTILATOR INTERACTION
VC- CMV, DESCENDING RAMP FLOW, SET POINT TARGETING
28. Pmus may add to or subtract from Pvent, and deform pressure waveform
inspiratory Pmus will deflect pressure waveform towards baseline (upward
concave)
BASIC PHYSIOLOGY OF PATIENT VENTILATOR INTERACTION
VC- CMV, DESCENDING RAMP FLOW, SET POINT TARGETING
FLOW
TIME
29. PRESSURE
FLOW
TIME
TIME
VOLUME
TIME
CONSTANT PRESSURE CREATES
• pressure difference between airway opening and alveoli,
• starting flow which decays exponentially a function of compliance and
resistance
RATE OF EXPONENTIAL DECAY IN FLOW IN BOTH INSPIRATION AND EXPIRATION IS
DETERMINED BY
• time constant of respiratory system,
TC= C × R
BASIC PHYSIOLOGY OF PATIENT VENTILATOR INTERACTION
PC- SET POINT TARGETING
30. Pmus THEORETICALLY DEFORMS ONLY FLOW WAVEFORM,
• but practically distorts pressure waveform also
INSPIRATORY FLOW MOVING AWAY FROM BASELINE (INCREASING FLOW),
• indicates inspiratory effort (Pmus)- flow index
• pressure waveform deflects towards baseline (upward concave)
INSPIRATORY FLOW MOVING TOWARDS BASELINE (DECREASING FLOW),
• indicates ventilator flow is more than patient's demand-
• we will explore in later slide- flow index
BASIC PHYSIOLOGY OF PATIENT VENTILATOR INTERACTION
PC- SET POINT TARGETING
31. EXPIRATORY PHASE
EXPIRATORY PHASE CAN DEMONSTRATE
• PVI (failed trigger and early cycle) and
• EXPIRATORY WORK
WILL DISCUSS IN LATER SLIDES
35. DIAGNOSE PATIENT VENTILATOR INTERACTION
SYNCHRONY
• a near zero phase difference between patient signal and ventilator response (beginning of flow/ cyling/
expiration)
ASYNCHRONY
• absence of ventilator response to a patient signal or vice versa
• Failed trigger, false trigger
DYSYNCHRONY
• a clinically important phase difference in timing between patient signal and ventilator response (beginning of
flow/ cycling/ expiration)
WORK SHIFTING
• when both Pvent and Pmus are active, portion of work shifted from ventilator to patient
36. PRESSURE
FLOW
TIME
TIME
DIAGNOSE PATIENT VENTILATOR INTRACTION
TRIGGER
TRIGGER DELAY
• PRESSURE TRIGGER
• Duration between drop in pressure below baseline (PEEP) to
return to baseline (PEEP) and beginning of inspiration (flow)
• FLOW TRIGGER
• Duration between rise in flow above base line (PEEP) and
beginning of inspiration (flow)
CLASSIFICATION
• NORMAL TRIGGER
• LATE TRIGGER
• EARLY TRIGGER
• FAILED TRIGGER
• FALSE TRIGGER
37. NORMAL TRIGGER (SYNCHRONY)
• clinically unimportant (near zero) trigger delay- less than 100 msec
LATE TRIGGER
• clinically important delay between patient trigger (Pmus) and beginning of inspiration (flow)- more than 100 msec
• delayed pressurization may mimic late trigger
• inappropriate slow inspiratory rise time does not matches patient effort
• Both late trigger and delayed pressurization increase WoB (work shifting)
• Causes- trigger threshold set too high, slow ventilator response time
EARLY TRIGGER
• machine triggered breath (mandatory breath) precedes patient trigger
• patient trigger may occur during inspiration or early expiration
• patient trigger (Pmus) is detected after start of inspiration (mandatory breath), patient trigger may or may not trigger
another breath
• defined as REVERSE TRIGGER as it is reverse of normal situation (machine breath-P vent is followed by Pmus)
• Causes- deep sedation, brain injury, pleural irritation
DIAGNOSE PATIENT VENTILATOR INTRACTION
TRIGGER
41. PATIENT VENTILATOR INTERACTION
TRIGGER
FALSE TRIGGER
• inspiration is trigger by non Pmus activity
• secretions in circuit/ endotracheal tube/ airway
• Cardiac oscillations
• Leak in patient circuit
• Hiccups
FAILED TRIGGER
• patient effort (Pmus) fails to initiate inspiration
• expiratory waveform deflection towards baseline that does not reach zero
• Causes
• Auto PEEP, DHI
• trigger threshold set to high
• In case of trigger threshold set to high, expiratory deflection towards baseline will reach zero but could not
trigger breath (initiate inspiration)
44. PATIENT VENTILATOR INTERACTION
INSPIRATION
WORK SHIFTING
• Presuming increased WoB should be dome by ventilator, portion of work shifted
from ventilator to patient, is defined as WORK SHIFTING,
PATTERN OF WORK SHIFTING IS AFFECTED BY MODE AND TARGETING SCHEME
• in VC and PC with adaptive targeting scheme, relationship of work shifting is
inverse
• more patient effort will shift more work from ventilator to patient (work shifting
increases)
• in PC with set point targeting, work output of ventilator remains constant
irrespective of patient effort, though total WoB increases proportionate to patient's
demand
• in servo targeting schemes, work shifting decreases in proportion to patient's effort
(Pmus)
Ventilator Patient
WoB WoB
45. PATIENT VENTILATOR INTERACTION
INSPIRATION: WORK SHIFTING AND MODES OF MV
Pmus
(Patient demand)
Pvent
(Patient
delivered)
Zero Highest
Highest
PC-CSVr (PAV, NAVA)
PC-CMVs (Pressure control)
PC-CSVs (Pressure support)
PC-IMVs,s (PC/PC)
VC-CMVs (Volume control)
PC-CMVa (PRVC, autoflow)
PC-CSVa (volume support)
46. VC with set point targeting- deflection in Pressure waveform
• as Pmus increases, inspiratory pressure waveform deflects towards baseline
with upward concavity
• total WoB remains constant, as VT and total pressure (Pmus+Pvent) remains
constant
• Work shifting occurs from ventilator to patient
• FLOW STARVATION- extreme case of work shifting, where patient generates
very high Pmus, Pvent decreases below baseline (PEEP)
• in this case patient is doing work on ventilator
Ventilator Patient
PATIENT VENTILATOR INTERACTION
INSPIRATION: WORK SHIFT
47. PRESSURE
FLOW
TIME
TIME
VC WITH SET POINT TARGETING- DEFLECTION IN PRESSURE WAVEFORM
FLOW STARVATION
(extreme work shifting)
VOLUME
PATIENT VENTILATOR INTERACTION
INSPIRATION: WORK SHIFT
48. PATIENT VENTILATOR INTERACTION
INSPIRATION: WORK SHIFT
PC with set point targeting- deflection in Flow waveform
• Patient effort (Pmus) increases inspiratory flow and tidal volume
• as total driving pressure (Pvent+Pmus) increases and tidal volume increases,
total WoB increases at the cost of WoB of patient (ventilator WoB is constant)
• increasing Pmus, flow deflects away from baseline (increasing flow)
• pressure waveform deflects towards baseline,
Ventilator Patient
WoB WoB
50. PC with adaptive targeting
• as Pmus increases, Pvent decreases, to maintain target VT
similar to VC- set point targeting
• but compared to VC with set point targeting, WoB in not
constant, as VT can be larger than set target
• with high Pmus patient may be breathing at PEEP level with
little assistance from ventilator and larger VT than target
• work shifting may be severe to deflect Pressure below
baseline
Ventilator Patient
PATIENT VENTILATOR INTERACTION
INSPIRATION: WORK SHIFT
52. PATIENT VENTILATOR INTERACTION
CYCLE
Synchrony between cycle and end of patient’s inspiratory effort (Pmus)
NORMAL CYCLE
LATE CYCLE
• neural Ti shorter than set ventilator Ti
• set Ti too long, flow cycle threshold set too low
EARLY CYCLE
• neural Ti longer than set ventilator Ti
• set Ti too short, flow cycle threshold set too high
FALSE CYCLE
• early cycle but not related to timing
• Pmax
FAILED CYCLE
• late cycle but not related to time, patient signal fail to cycle ventilator
• RUN AWAY PHENOMENON in PAV- ventilator continues to assist in spite of
patient terminating inspiratory effort due to ventilator's inaccurate estimation
of lung mechanics
53. PATIENT VENTILATOR INTERACTION
CYCLE
VC mode
• observe Pressure waveform and expiratory flow waveform
PC mode
• observe inspiratory flow waveform, expiratory flow waveform and pressure waveform
54. PATIENT VENTILATOR INTERACTION
CYCLE
NORMAL CYCLE
• inspiration ends within clinically acceptable time near Pmus peak
LATE CYCLE
• inspiration ends with clinically important delay after Pmus peak
• Late cycling becomes relevant when there is expiratory effort before cycling
• VC mode- upward (positive) deflection in pressure waveform
• PC mode-
• downward (towards baseline) deflection in flow waveform, reaching baseline or crossing into negative
flow (below baseline) before ventilator cycles
• Upward (positive) deflection in pressure waveform
58. PATIENT VENTILATOR INTERACTION
CYCLE: EARLY CYCLE
INSPIRATION END WITHIN CLINICALLY IMPORTANT TIME BEFORE Pmus PEAK (BEFORE PATIENT'S EFFORT CEASES)
INSPIRATORY FLOW MAY NOT COME TO ZERO IN PATIENT’S WITH LONG TC AT THE END OF INSPIRATION (OAD),
• but if there is no continued inspiratory effort, after cycling, it is not a synchrony problem
RELEVANT IF EVIDENCE OF INSPIRATORY EFFORT AFTER CYCLING
• Recognized in expiratory flow waveform in both PC and VC modes
• Distortion of peak expiratory flow and disruption of normal smooth exponential decay of expiratory flow
• Deflection of expiratory flow towards baseline
MAY ALSO OCCUR BECAUSE OF
• False cycling - safety feature (Pmax) setting
• erroneous setting like in CSV, flow cycle threshold reaching rapidly in short TC (low compliance)- high peak
followed by rapid decay in flow)
62. FLOW
TIME
EXPIRATORY FLOW IN VENTILATOR IS
• always pressure controlled with set point targeting (target being PEEP),
• irrespective of mode (PC or VC),
THAT IS DURING EXPIRATION
• ventilator controls the pressure, by operator set PEEP
AS EXPIRATION IS PASSIVE (NO Pmus)
• expiratory flow waveform and volume waveform displays smooth exponential decay
PATIENT VENTILATOR INTERACTION
EXPIRATORY PHASE
63. Expiratory phase can demonstrate
• Normal expiration- exponential decay of expiratory flow waveform
• EXPIRATORY WORK
• Patient's expiratory effort (exp Pmus) will deflect expiratory flow
waveform away from baseline (negative direction)
• may be normal, as during coughing or exercising
• may indicate high resistive load (obstructive airway disease),
acidosis, pain, anxiety
• PVI (failed trigger and early cycle)- distortion of PEF and or deflection
of expiratory flow towards baseline- inspiratory effort
PATIENT VENTILATOR INTERACTION
EXPIRATORY PHASE
Normal Expiration
Expiratory effort
Failed trigger
Early cycle
64. PATIENT VENTILATOR INTERACTION- CONFUSION
Flow dyssynchrony- inspiration PVI- work shifting
double trigger-early cycle,, inspiration PVI, reverse trigger
multiple trigger- false trigger, inspiration PVI, early cycle
breath stacking- consequence of double/ multiple trigger
reverse trigger- Trigger PVI- early trigger
65. PATIENT VENTILATOR INTERACTION- CONFUSION
double trigger: two consecutive breaths delivered by ventilator in response to
patient’s respiratory muscle effort
• Patient triggered breath followed by ventilator trigger breath
patient trigger breath may be preceded by ventilator trigger breath
• RT- false or pseudo double trigger
Double trigger- patient (DT-P): patient triggered breath followed by ventilator
triggered breath
Double trigger- Vent (DT-V): patient triggered breath preceded by ventilator
triggered breath: RT
Double trigger- auto (DT-A): patient triggered breath preceded by auto triggered
breath (false triggered breath)
66. PATIENT VENTILATOR INTERACTION- CONFUSION
DT-V
• REVERSE TRIGGER:
• due to entrainment
• PSEUDO REVERSE TRIGGER
• due to high ventilatory demand
Double trigger, Reverse triggering and pseudo-Reverse-Triggering, Jose Antonio Benitez Lozano, Jose Manuel serrano Simon, Arch Med Case Rep. 2020, vol 2, issue 1
67. PATIENT VENTILATOR INTERACTION- VOLUME WAVEFORM
AT THE BEGINNING OF BREATH (BOTH PATIENT TRIGGERED OR MACHINE TRIGGERED)
• ventilator resets volume waveform to zero so that inspiratory tidal volume displayed is accurate
IF THERE IS DIFFERENCE BETWEEN INSPIRATORY AND EXPIRATORY TIDAL VOLUME,
• volume waveform is displayed as a sharp drop (reset) prior to next breath- square root sign
THIS SQUARE ROOT SIGN HAS 4 CAUSES-
• LEAK FROM CIRCUIT, AIRWAY OR LUNG, airway or lung- leaked volume is falsely detected as flow trigger
and another breath is triggered
• ACTIVE EXPIRATION DURING INSPIRATION- some ventilators do not account for VT exhaled during
inspiration
• AIR TRAPPING- patient has not been able to exhale the inhaled VT and another breath is delivered
• FLOW SENSOR MALFUNCTION
71. PATIENT VENTILATOR INTERACTION- CONFUSION
DT-V: EARLY TRIGGER
• REVERSE TRIGGER:
• due to entrainment
• PSEUDO REVERSE TRIGGER
• due to high ventilatory demand, early cycle
Double trigger, Reverse triggering and pseudo-Reverse-Triggering, Jose Antonio Benitez Lozano, Jose Manuel serrano Simon, Arch Med Case Rep. 2020, vol 2, issue 1
72. accidental observation in a patient with a continuous oesophageal pressure (Pes) recording, inspiratory efforts
occurred near the end of each mechanical inspiration in a repetitive and consistent manner.
First description of respiratory entrainment in critically ill patient
2013; 143(4):927–938
REVERSE TRIGGER instead of patient triggering ventilator to deliver breath, time triggered ventilator
breath triggered neural effort (patient trigger)
muscular effort (diaphragmatic contraction lagged behind time triggered ventilator
breath
reversal of normal relationship between patient trigger and machine delivered breath
73. REVERSE TRIGGER
Entrainment was defined as a pattern in which the inspiratory efforts of the patient occurred over a specific and repetitive phase of
the ventilator cycle, therefore, with a minimal variability of their neural respiratory time (Ttot neu).
Ability of the brain stem to entrain the respiratory rhythm to periodic mechanical inflations is considered a normal phenomenon
steadily reproduced experimentally in vagally intact humans and animals.
It seems to reflect the ability of the central controller to adapt its output to afferent information. In addition, the positive impact of
wakefulness to 1:1 entrainment has been interpreted by Simon et al as an adaptive strategy to avoid discomfort during mechanical
ventilation.
On the other hand, respiratory entrainment indicates a loss of breathing variability. Preservation of breathing variability has been
linked to improvement of oxygenation and weaning success. Prospective studies are needed to investigate the prognostic
significance of entrainment in patients in the ICU.
The consequences of this asynchrony are potentially large. This may indeed continuously induce pliometric contractions of the
diaphragm. These contractions are associated with muscle cytokine release and muscle fiber damage. They also induce increased
respiratory muscle work and oxygen consumption, may contribute to cardiovascular instability, and make monitoring of the plateau
pressure very misleading. Moreover, reverse-triggered efforts may generate higher plateau pressure in VAC and large Vt and
transpulmonary pressure swings during pressure assist control. In a study by Papazian et al, the administration of neuromuscular
blocking agents early in the course of severe ARDS was associated with improved survival and more ventilator-free days.
CHEST / 143 / 4 / APRIL 2013
Mechanical Ventilation-Induced Reverse-Triggered Breaths A Frequently Unrecognized Form of Neuromechanical Coupling
Evangelia Akoumianaki , MD ; Aissam Lyazidi , PhD ; Nathalie Rey , MD ; Dimitrios Matamis , MD ; Nelly Perez-Martinez , MD ; Raphael Giraud , MD ;
Jordi Mancebo, MD; Laurent Brochard, MD; and Jean Christophe Marie Richard, MD, PhD
74.
75. RESPIRATORY ENTRAINMENT
Entrainment of respiratory rhythm to the ventilator rate implies a fixed, repetitive, temporal relationship
between the onset of respiratory muscle contraction and the onset of a mechanical breath.80–82 Human subjects
exhibit one- to-one entrainment over a considerable range above and below the spontaneous breathing
frequency.83,84 Cortical influences (learning or adaptation response) and the Hering-Breuer reflex are postulated
as the predominant mechanisms of entrainment. Theoretically, one-to-one entrainment should facilitate
patient–ventilator synchrony, but studies of the entrainment response in critically ill patients are lacking.
Georgopoulos D . Effects of Mechanical ventilation on control of breathing . In: Tobin MJ , ed.
Principles and Practice of Mechanical Ventilation . New York, NY : Mc Graw-Hill ; 2006 : 715 - 728 .
Entrainment was defined as a pattern in which the inspiratory efforts of the patient occurred over a specific
and repetitive phase of the ventilator cycle, therefore, with a minimal variability of their neural respiratory
time (Ttot neu).
76. ENTRAINMENT
INTERACTION OF TWO RHYTHMIC PROCESS
• adjustment and locking in common phase and or periodicity
DOMINANT PROCESS: ENTRAINING RHYTHM, RECESSIVE PROCESS: ENTRAINED RHYTHM
LOCKING IN PHASE: SYNCHRONOUS
LOCKING IN PERIODICITY: SYNCHRONOUS OR ASYNCHRONOUS
107. KEEP LEARNING, UNLEARNING AND RELEARNING…….
“A wise man once said that which is simple is rarely seen,
and that which is seen is seldom understood.
What to say about that which is complicated?”
In spontaneous breathing, respiration is controlled by respiratory control system which consists of central controller (respiratory center) which receives input from multiple sensors and gives output to two independent effector pumps (inspiratory and expiratory muscles). Central controller responds variably to a wide array of stimulating and depressing inputs including paO2, PaCO2, pH, sensation of stiffness and irritation from lung and chest wall as well as effect of drugs and responds differently depending upon whether patient is awake or sleep. Output of effector pumps modify sensory inputs which further modifies central controller’s command to effector pumps until it contends with outcome of effector pumps.
In mechanically ventilated patient, central controller must contend with 3 separate effector pumps, patient’s inspiratory and expiratory muscle and mechanical ventilator.
This is made further complicated by interaction between time and demand of patient’s desired breath and that delivered by the ventilator.
Interaction between respiratory control system and mechanical ventilator is called patient ventilator interaction
Ventilator output (delivery of gas) does not matches in timing (trigger and cycle), quantity (inspiratory flow, tidal volume) and pattern (inspiratory time rise, peak inspiratory flow rate, peak expiratory flow rate, expiratory flow), to what patient wants.
It may be due to increased metabolic demand of patient (fever, severe metabolic acidosis) or deranged pulmonary mechanics ( parenchymal/ pleural or airway disease) or vascular disease (pulmonary embolism).
Incidence- quoted from Robert Chatburn, 2019 year in review: patient ventilator synchrony, Res Car April 2020, 65:4
Artist’s depiction of a mechanically ventilated patient experiencing respiratory distress, indicating the characteristic physical signs associated with severe patient-ventilator asynchrony. Clinicians participating in ventilator management are all-too-familiar with this picture, stylized and exaggerated as it is in this cartoon. However, less dramatic patient-ventilator asynchrony may have less obvious signs and be difficult to detect by simple bedside observation.
Optimizing ventilator setting means balancing between comfort and safety,
if ventilator setting can not be optimized, one of pump (respiratory center or mechanical ventilator) has to be knocked out. Obviously respiratory center has to be calmed and ventilator is allowed to dictate,
By sedating and relaxing patient, optimizing pulmonary mechanics, prone ventilation, ECLS
Calming respiratory center will ameliorate PVA but it has its own consequences, as PVA itself,
given the importance of maintaining some respiratory muscle activity, control system needs to be active, so that dysfunction and atrophy do not develop, but not so active as to cause overt patient distress.
Ventilator waveforms provide continuous stream of information on both pulmonary mechanics and patient ventilator interactions. But most of us do not interpret these waveforms and fail to collect information relevant to basic aim of ventilation, that is safety, comfort and liberation.
Like electrical manifestation of heart’s activity in EKG provides us heart’s physiology and function, ventilator waveforms reveal physiology and function of respiratory system as well as how two independent systems (patient’s neural activity and ventilators mechanical activity) interact with each other.
Robert L. Chatburn and collegues have proposed standardized nomenclature and taxonomy along with method to read ventilator waveforms based on modes of mechanical ventilation, physiology of respiratory system and analysis of interaction of patient with ventilator
Pmus is detected by oesophageal pressure waveform (Pes), diaphragmatic electrical activity (Eadi) or ventilator waveforms (pressure trigger- dip in pressure waveform before beginning of inspiration, flow trigger- color in flow waveform)
based on Control variable, Breath sequence and Targeting schemes,
Control variable dictates which waveform (pressure or flow) should be read to identify load and PVI
Breath sequence determines where to read load or PVI
Targeting schemes affect how patient and ventilator are interacting with each other
Ventilator waveform are graphical representation of equation of motion,
In other words, during inspiration respiratory muscles and or ventilator generate pressure to overcomes elastic load and resistive load of patient’s respiratory system.
if Pmus is active (patient is making effort), elastic and resistive loads are shared between patient's inspiratory muscle (Pmus) and ventilator (Pvent).
identify dominant load- elastic or resistive
identify dominant load- elastic or resistive
PVI is matching of patient’s desired breath/ neural breath with ventilator delivered breath, in terms of timing, quantity and pattern,
PVI can be divided in synchrony and work shift,
Synchrony is matching of different phases of patient’s neural breath and ventilator breath,
Work shift is sharing of WoB between patient and ventilator,
PVI is diagnosed in terms of synchrony and work shifting,
we will define synchrony and work shifting in different breath phase and then diagnose PVI in different modes of ventilation
Work shift is seen in inspiratory phase of breath- work shifting is shifting of WoB from ventilator (Pvent) to patient (Pmus) when Pmus is active,
in presence of patient effort (Pmus), some portion of work is being done by ventilator and some by patient. In other words, some portion of work is shifted from ventilator to patient.
synchrony is timing of Pvent and Pmus in relation to each other, patient activity (Pmus is reference event), in other words, phase difference between patient signal and ventilator delivery
Pmus is detected by oesophageal pressure waveform (Pes), diaphragmatic electrical activity (Eadi) or ventilator waveforms (pressure trigger- dip in pressure waveform before beginning of inspiration, flow trigger- color in flow waveform)
Relationship between patient effort and ventilator delivered pressure and resultant work shifting according to mode of MV
In PC PC set point targeting irrespective of ventilatory pattern, ventilator bears set pressure (WoB) and patient’s WoB is proportionate to patient’s effort, ie work shifting is constant but patient’s WoB increases with patient’s demand, (better mode where patient’s demand is high- acute phase of disease, increased metabolic demand, but may further derange pulmonary mechanics by causing neruromechanical dissociation (OAD, severe ARDS) and cause more PVA,
In PC servo targeting, work shifting is constant as ventilator bears the set percentage of total WoB, irrespective of patients demand
In VC set point targeting and PC adaptive targeting, work shifting is inversely proportional to total WoB. If patient’s demand increases more work shifting occurs from Pvent to Pmus. (not a good mode where patient’s demand is high or fluctuating- lung disease in acute phase, severe metabolic acidosis, hyperthermia, raised ICP, anxiety, high dose vasopressors, poor LV function, but better mode during recovering phase of disease/ weaning period
As per equation of motion, as Pmus increases, Pvent decreases to maintain equality of equation.
When should work shifting becomes abnormal and needs correction?
As per equation of motion, as Pmus increases, Pvent decreases to maintain equality of equation.
When should work shifting becomes abnormal and needs correction?
Late cycle should be assessed according to clinical context- eg in IRV- APRV- if may be acceptable from patient’s safety and comfort point of view
Inspiratory flow reaching zero before cycle and end inspiratory rise in pressure (expiratory muscle activity),
End inspiratory rise in pressure may also be caused by inspiratory muscle relaxation,
End inspiratory rise in pressure (expiratory muscle activity),
End inspiratory rise in pressure may also be caused by inspiratory muscle relaxation,
Patient neural Ti and set Ti, neural Ti means inspiratory muscle activity- contraction to relaxation,
Inspiratory flow may not ceases before cycling, because of various reasons:
1. inspiratory muscle still contracting to continue inspiration, but ventilator cycle,
2. long TC: OAD
3. flow cycle criteria in CSV, is set to low:
If inspiratory muscle continue contracting after cycling, it will be seen in expiratory flow towards baseline in both VC and PC modes
Expiratory flow in ventilator is always pressure controlled irrespective of mode (PC or VC),
That is during expiration ventilator controls the pressure, by operator set PEEP
inspiratory and expiratory time constants may be different, as compliance and resistance may be different in two phases ( end inspiratory alveolar pressure, autoPEEP, peak expiratory flow)
Expiratory phase remains unaffected by patient effort (Pmus), therefore, expiratory flow waveform may be used to confirm inspiratory waveform finding or when Pmus is present
If there is discordant between inspiratory and expiratory waveform, look for variable obstruction, circuit problem or ventilator setting, eg. Normal inspiratory flow but prolong expiratory flow may be due to filter block or expiratory valve obstruction.
Expiratory flow in ventilator is always pressure controlled irrespective of mode (PC or VC),
That is during expiration ventilator controls the pressure, by operator set PEEP
inspiratory and expiratory time constants may be different, as compliance and resistance may be different in two phases ( end inspiratory alveolar pressure, autoPEEP, peak expiratory flow)
Expiratory phase remains unaffected by patient effort (Pmus), therefore, expiratory flow waveform may be used to confirm inspiratory waveform finding or when Pmus is present
If there is discordant between inspiratory and expiratory waveform, look for variable obstruction, circuit problem or ventilator setting, eg. Normal inspiratory flow but prolong expiratory flow may be due to filter block or expiratory valve obstruction.
A process where two rhythmic process interact with each other in such a way that
they adjust towards and eventually lock in to a common phase (timing) and/ or periodicity (frequency).
To entrain one of the process should be dominant over the other and
periodicity (frequency) of two processes processes should be close to each other
Dominant rhythm is called entraining rhythm and
adapted rhythm is called entrained rhythm
If two processes are locked in phase (timing), processes are synchronous
If two processes are locked in periodicity (frequency), phases may be synchronous or asynchronous
Relationship between phases of two rhythms are calculated by phase angle
Phase angle of zero means perfect synchrony, while phase angle of 180 denotes asynchrony
Two processes with nearly identical periodicity (frequency)
Frequency locking with phase locking with 1:1 entrainment and 2:1 entrainment
Synchronous phases
Frequency locking with phase locking with 1:1 entrainment and 2:1 entrainment
Synchronous phases
Phase synchrony or asynchrony
Frequency locking with phase locking with 1:1 entrainment and 2:1 entrainment
Synchronous phases
Frequency locking with phase lagging 1:1 and 2:1 entrainment
Asynchronous phase
Frequency locking with phase lagging 1:1 and 2:1 entrainment
Asynchronous phase
TAG- PC- set point targeting
LOAD- Inspiration- resistive (could be better in VC), expiration- resistive
PVI- trigger – normal
Inspiration- normal work shift
cycle- normal
Intervention-
TAG- VC- constant flow, set point targeting
LOAD- inspiration- resistive, expiration- resistive
PVI- Trigger- normal, evidence of failed trigger in expiration
Inspiration- moderate work shift
cycle- normal
Intervention-
TAG- VC- constant flow- set point targeting
LOAD- Inspiratory- Resistive- Ppeak- Pplat difference, expiratory- resistive- flow limitation- increased airway resistance
PVI- trigger- early- RT
Inspiration- no work shift
cycle- normal
How to differentiate RT from early cycle as a cause of double trigger?
TAG- VC- descending ramp flow- set point targeting
LOAD- inspiration- could not be commented, Expiration- resistive- expiratory flow limitation- increased airway resistance
PVI- trigger- early trigger – reverse trigger in early expiration where breath is delivered
inspiration- work shift- normal- as pressure waveform not deflected towards baseline
cycle- normal
This developed after patient was given bolus sedation
How to differentiate RT and early cycle as a cause of double trigger?
TAG- VC- constant flow, set point targeting
LOAD- could not commented as active Pmus
PVI- Trigger- normal
Inspiration- severe work shift (flow starvation)
cycle- normal
Intervention-
TAG- VC- constant flow, set point targeting
LOAD- could not be commented as active Pmus
PVI- Trigger- normal
Inspiration- severe work shift (flow starvation)
Cycle- normal
Intervention-
TAG- VC- constant flow, set point targeting
LOAD- could not be commented as active Pmus
PVI- Trigger- normal
Inspiration- severe work shift (flow starvation)
Cycle- normal
Intervention-
TAG- VC- constant flow, set point targeting
Load- inspiration- resistive- Ppeal- Pplat diference, expiration- resistive- flow limitation
PVI- no patient effort (Pmus)
Intervention- Total PEEP was 18, as PEEP was increased form 6 to 12, flow limitation improved gradually
TAG- VC-constant flow, set point targeting
LOAD- inspiration- could not be commented, expiration- resistive- (Ppeak- Pplat difference)- more of viscoelastic resistance, but no flow limitation
PVI- trigger- machine trigger, inspiration- normal work shift, cycle- early, expiratory flow waveform deflected to baseline
Intervention-
TAG- PC, set point targeting
LOAD- could not commented as active Pmus
PVI- Trigger- machine trigger
Inspiration- severe work shift- inspiratory flow waveform deflected away from baseline giving impression of constant flow waveform, pressure waveform deflected towards baseline- as pressure is set variable it will not show large deflection as seen in VC where pressure is derived variable (showing flow starvation)
cycle- early cycle- expiratory flow wav-eform deflected towards baseline
Intervention-
How to differentiate early cycling from failed trigger?
PRVC
Severe work shift
Late cycle
Neural respiratory rate is higher than set respiratory rate,
Failed trigger
Work shift
Late cycle
Macquet servo I VC is dual targeting scheme. each breath starts out in VC, but if the patient makes an inspiratory effort sufficient to decrease airway pressure by 3 cm H2O, the ventilator switches to PC within the breath. Depending on the intensity of the inspiratory effort, the ventilator may switch back to VC with a volume cycle criterion or end inspiration in PC with a flow cycle criterion, similar to a pressure support breath. In fact, the Servo-i operator's manual (V3.1, page 36) actually says “… if a pressure drop of 3 cm H2O is detected during inspiration, the ventilator cycles to Pressure Support with a resulting increase in inspiratory flow.”
Reverse trigger, double trigger, Patient biting tube, late cycle
Neural respiratory rate is higher than set respiratory rate,
Work shift
Late cycle
:PC-CMV,
Small TC: ARDS/ ILD
Neural respiratory rate is higher than set respiratory rate,
Failed trigger
Work shift
Late cycle
Macquet servo I VC is dual targeting scheme. each breath starts out in VC, but if the patient makes an inspiratory effort sufficient to decrease airway pressure by 3 cm H2O, the ventilator switches to PC within the breath. Depending on the intensity of the inspiratory effort, the ventilator may switch back to VC with a volume cycle criterion or end inspiration in PC with a flow cycle criterion, similar to a pressure support breath. In fact, the Servo-i operator's manual (V3.1, page 36) actually says “… if a pressure drop of 3 cm H2O is detected during inspiration, the ventilator cycles to Pressure Support with a resulting increase in inspiratory flow.”