Younsuck Koh, MD, PhD, FCCM

Dept. of Pulmonary & CCM

Asan Medical Center,

Univ. of Ulsan College of Medicine

Seoul, Korea

Patient-Ventilator Asynchrony:

How to fix it

2 Systems

• Comfort

• Stable hemodynamics

• Less injury

Patient-Ventilator Synchrony

Outcome

Definition of Dyssynchrony

Analysis of Complaints

during MV after cardiac surgery

From Kunming Medical Univ.

Wang Y, et al. J Cardiothoracic Vasc Anesth 2015

Patient-Ventilator Asynchrony during assisted MV

15 of 62 pts (24%) had an asynchrony index > 10% of respiratory

effect

6

7.5

(3-20)*

25.5

(9.5-42.5)

0

5

10

15

20

25

30

< 10% > 10%

TVT

* interquartile

Thille AW, et al. Intensive Care Med 2006;32:1515-22

Outcome – A Significant Impact on the Duration of Mechanical Ventilation

8

Ventilator Asynchrony vs. Outcome

Blanch L, et al. Intensive Care Med 2015;41:633-642

Case 1

78/M with COPD

Home O2 with 1.5 L of Nasal Prongs

Transferred to ER due to respiratory difficulty with mental change

• ABGA:

7.322 - 101.6 - 23.9 –

19.2 - 51.4 - 34.2

• Hospital Course

1st Day: PCV with sedation

2nd Day: decreased VT and increased f with PSV trial using accessory respiratory muscles

During Stable With distress

12

Q1. How to approach?

Causes of Asynchrony

Patient-related causes

• resp. pump related

• complications; embolism..

• agitation

Ventilator-related causes

Time (sec)

Airway Pressure (cm H2O)

Asynchrony in each breath phase

-Triggering - Flow

demand

Time (sec)

Airway Pressure (cm H2O)

- Delayed expiration

- Auto-PEEP

16

Q2. What do you think first?

Auto-PEEP

elastic pressure remaining in alveoli at end-expiration

Physiologic Consequences of Hyperinflation

Respiratory

• increased work of breathing

• resp. pump efficiency

– Portion of diaphragm contacting with the inner surface of the ribcage (no lung in between)

– 55 % of total diaphragm surface at FRC

DH as a cause of Diaphragm Dysfunction: Zone of Apposition for Diaphragm Movement

Normal

COPD

Diaphragm dysfunction by Lung Hyperinflation in

COPD

FRC in normal

FRC in COPD

Mechanical disadvantages of flattened diaphragm:

• Length-tension relationship

• Laplace’s law (P = 2T/radius)

Comparison of work of breathing

(WOB) and pressure-time product

(PIP) between patients with (■)

and without (■) auto-PEEP

Comparison of expiratory airway

resistance (RAWe) and mean airway

resistance (RAWm) between patients

with (■) and without (■) auto-PEEP

JY Chin, et al. Tuberculosis and Respiratory Disease 1996: 43; 201

N = 20

Increased Work of Breathing:

Comparison of P0.1 between patients with (■) and

without (■) auto-PEEP JY Chin, et al. Tuberculosis and Respiratory Disease 1996: 43; 201

20 ARF patients

“Auto-PEEP may be associated with ineffective triggering.”

Hemodynamics

• hypotension

• misinterpretation of volume status

and pressures (CVP, BP)

Physiologic consequences of DPH

Case: COPD on MV: PC 20 cm H2O

BP 90/60 mm Hg

CO 2.6 L/min

PAOP 22 cmH2O

Auto-PEEP 12 cm H2O

Ventilator-off

BP 135/80 mm Hg

CO 4.4 L/min

PAOP 11 cm H2O

Pepe & Marini. 1982

27

Q3. How to detect Auto-PEEP?

Time (sec)

Airway Pressure (cm H2O)

Fig. 1. Flow and esophageal pressure waveforms showing dynamic auto-PEEP. Arrow

indicates the beginning of inspiratory effort. Dotted line shows the beginning of the

inspiratory flow after overcoming the auto-PEEP.

29

Q4. How to solve?

• MV resetting - VT -I:E -External PEEP

• Correct underlying causes - Bronchodilator/steroid - Anxiety control; sedation

Solutions

Ppl

Triggering

sensitivity

Insp flow

10

6

0

-2

cm H2O

Koh Y. Crit Care Clin 2007;23:169-81

Case: 71M, asthma on MV 8th day

with 8 cm H2O of auto-PEEP auto-PEEP

external PEEP, cm H2O

0 2 4 6 8 10

0.8

0.9

1.0

1.1

1.2

1.3

1.4

1.5

Pp

ea

k, cm

H2

O

20

22

24

26

PaC

O2

, m

m H

g

60

65

70

75

VE

I, lit

er

Synchrony: Panic Cycle

ANXIETY

INCREASED VENTILATION

HYPERINFLATION

AUTO PEEP HEMODYNAMIC COMPROMISE

MUSCLE WEAKNESS

INCREASED WORK OF BREATHING

DISCOORDINATE BREATHING

Marini JJ. Ventilatory management in severe airflow obstruction. In: Acute

Respiratory Failure in Chronic Obstructive Pulmonary Disease.

Marcel Dekker, 1996:761.

M/85, COPD with RF

MV : PCV 13 cm H2O

FiO2 0.4

PEEP 5 cm H2O

f 14/min

Sedation : Midazolam 2 mg/h iv

+ morphine 4 mg iv

Sedatives

BP

&

PR

100

Under sedation

Case 2

Flow-Time Curve

After awakening

37

Q4. What is the difference?

P.-Time Wave

Flow-Time Wave

2 waves in Pressure 1 wave in Flow Not double triggering

P.-Time Wave

Flow-Time Wave

2 waves in Pressure 2 waves in Flow Double triggering

P.-Time Wave

Flow-Time Wave

Q5. How to correct #2 by #3?

3

#2 P.-Time Wave

Flow-Time Wave

#2 P.-Time Wave

Flow-Time Wave

By increasing pressure delivery in PCV mode

A B

Better Breath-Stacking Index Improvement through Ventilator Setting

Effective measures: Increase in insp. Time PSV

Changques G, et al. Crit Care Med 2013; 41:2177-87

Case 3

Breast ca. with lung metastasis. Sudden respiratory distress: Insp. VT 650 mL Exp. VT 39 mL F: 41 MV 1.4 L

44

Q6 What could be a cause of the distress?

Distress resolved after A-node insertion Cuff p. 25 mmHg

Observe airway: Suction injury

Case 4

Postop due to aortic aneurysm. Sudden respiratory pattern change to Deep & Rapid tidal breath at CPAP

48

Q7 What could be a cause of the change?

Initial With breath change

M/61 Pn. with ARDS Prone

positioning Weaning: Tachypnea

Case 5

51

Q8 What could be a cause of the tachypnea?

Ventilator synchrony is getting better after improved ileus.

M/75, pn with ARDS

On Ad. Weaning trial 16 cmH2O of PSV

Case 6: Respiratory Difficulty with mode change

54

Q9 What could be a cause of the distress?

Critical Illness Polyneuropathy

• Definition: acute generalized dysfunction of nerve axon

Bolton et al. J. Neurol Neurosurg Psychiatry 47: 1223-1231,1984

• A cause of unexplained difficult weaning from ventilator

• Occurred in 70% of MODS patients Witt NJ et al. Chest. 99: 176-184, 1991

Causes of Diaphragm Dysfunction in ICU

– Shock

– Sepsis

– Drugs: NM blockade, antibiotics (aminoglycosides, polymyxins, beta blockers, calcium channel blockades, diuretics, steroids)

– ICU-acquired weakness

– Dynamic hyperinflation

– Prolonged MV

MV D27

Rt diaphragm dysfunction Normal Lt diaphragm

PKP Rt.AVIPKP Lt.AVI

Case 7 F/35, ARDS with IRAB pn., Sudden Respiratory Distress

Colistin inhalation, VT 350-400 ml 120-150 ml

59

Q10. What could be a cause of the distress?

Filter clogging

• Initiation phase: clinical deterioration

• Maintenance phase: heavy sedation

• Weaning phase: weaning delay

Summary: Clinical Impact of Patient-Ventilator Asynchrony

Detection of Patient-Ventilator Asynchrony

• Observe patient synchrony with MV

• Detect accessory resp. m use

• Observe MV monitor: flow-time curve

Summary: how to approach

Disconnect MV with Pt

Airway patency

Ambu bagging: observe pt’s condition

Acute Clinical Deterioration

Suspect pneumothorax, PE…

Auto-PEEP, pain, CIP..

+ -

Careful Paralysis & Sedation