Ventilation of Patients with COPD and Asthma. Chronic lung diseases with airflow obstruction Asthma...

Ventilation of Patients with COPD and Asthma

Chronic lung diseases with airflow obstruction

Asthma Emphysema Bronchitis

COPD CXR

Near fatal asthma

Mechanical Venitlation ofCOPD & Asthma Exacerbations

Objectives Pathophysiology

- PaCO2 dederminants - Gas trapping

- Work of breathing - Auto-PEEP

NIPPV- IPAP- EPAP

Mechanical ventilation- FIO2 - PEEP

- VT

Pathohysiology ofAsthma/COPD Exacerbations

AirwayInflammation

Airwaynarrowing &obstruction

Shortenedmuscles,

curvature

FrictionalWOB

musclestrength VT

PaCO2

pH PaO2

Gastrapping

Auto-PEEP

VCO2

VE

ElasticWOB

VA

PEEP

IPAPMV?

Steroids

Abx?

MV?

IPAP

MV

BDs

Determinants of PaCO2

PaCO2 VCO2

VA

VCO2

Work- Agitation- Seizures- WOB

Metabolism- Fever- CHO- T4

VA

VE

- RR- VT

- VD (without VE)

Oxygen Cost of Breathing

Roussos, JCI 1959

PV Curve in COPD and Asthma(Stable)

Macklem and Becklake, 1963

-10 -20 -30 -40

2

4

6

Ptp (cm H2O)

VL (L)

VT

VT

Normal/Asthma

Emphysema

PV Curve in COPD & Asthma(Acute Exacerbtion)

-10 -20 -30 -40

2

4

6

Ptp (cm H2O)

VL (L)

VT

VT

Asthma

Emphysema

Implication

VT falls because FRC encroaches on TLC Limited ability to VT with MV/IPAP

Best way to PaCO2 is to VCO2

WOB (frictional and/or elastic) PaCO2 even if VT, VE and VA are constant

Work of Breathing

Work

of

Bre

ath

ing

RV FRC TLC

Total Work

Elastic Work

Frictional Work

Effect of VA/Q on PaCO2

(Normal)

VCO2 =100 ml/min

PcCO2

= 40

PaCO2

= 40

PcCO2

= 40

PvCO2

= 46PvCO2

= 46

DCO2 = 100 ml/min

DCO2 = 100 ml/min

PAO2 = 100PACO2 = 40

PAO2 = 100PACO2 = 40

VCO2 =100 ml/min


(Low VA/Q, Normal)

PcCO2

= 40

PaCO2

= 40

PcCO2

= 40

PvCO2

= 46

DCO2 = 50 ml/min

DCO2 = 150 ml/min

HPV

50% VE

VCO2 = 50 ml/min

50% VE

VCO2 = 150 ml/min

PvCO2

= 46

PAO2 = 50PACO2 = 40

PAO2 = 100PACO2 = 40


(Low VA/Q,, AECOPD)

PcCO2

= 44

PaCO2

= 42

PcCO2

= 40

PvCO2

= 46PvCO2

= 46

DCO2 = 50 ml/min

HPV

VE at max50% VE

VCO2 = 50 ml/min

VCO2 = 100 ml/min

DCO2 = 150 ml/min

PAO2 = 50PACO2 = 40

PAO2 = 100PACO2 = 40


(Low VA/Q,, AECOPD, FIO2)

PcCO2

= 44

PaCO2

= 44

PcCO2

= 44

PvCO2

= 46PvCO2

= 46

DCO2 = 100 ml/min

HPV

VE constant50% VE

VCO2 = 50 ml/min

VCO2 = 50 ml/min

DCO2 = 100 ml/min

FIO2PAO2 = 100PACO2 = 44

PAO2 = 100PACO2 = 44

Ventilation in COPD/Asthma

Which Patients with COPD benefit from NIV ?

NIPPV

Pathophysiology of AECOPD & Asthma is amenable to Rx with NIPPV

EPAP for auto-PEEP IPAP for inspiratory RawWill work of breathing

VCO2

At constant VA, PaCO2 and pH

May VA

May mortality and intubation rate

Which Patients with COPD benefit from NIV ?

Hospital Mortality

12%

2%

NNT 8

NIV in Severe Asthma

17 Episodes of ARF due to asthma 2 patients required intubation for worsening PaC02 Duration of NPPV was 16±21 h. All patients survived. Length of hospital stay was 5±4 days

Deterimental effects of hyperinflationDeterimental effects of hyperinflationExpiratory recoil of

the thoracic cage

Shortened muscle fibersDecreased curvature

Impaired blood supply

Decreased zone of apposition

Medial orientation of diaphragmatic fibers

Resistance

Pressure

Time

Pressure

Time

Compliance

Resistance

Peak Airway Pressure & Normal Plateau

Tidal ventilation

Lung volume

VT

FRC

VT

VEE

Time

VEI

I :E1:1

I : E1: 6

Air-trapping in Asthma/COPD Patients on Mechanical Ventilation

Assessment of Mechanics

Auto-PEEPRaw= Peak - Plateau

Obstructive Airway Disease

• Beware of auto-PEEP!

After the third breath, the airway was occluded at end-expiration using the end-expiratory hold function on the ventilator. During the period of zero flow, pressure in the alveoli and ventilator circuit equilibrate, and the plateau pressure reflects auto or intrinsic positive end-expiratory

pressure (PEEPi), indicated by the arrow.

Giving CPAP to a patient who has auto-PEEP

• The increased work of breathing associated with auto-PEEP can be offloaded by applying CPAP to the trachea/mouth, and splinting open the connecting airways.

• The use of external PEEP in the setting of auto-PEEP may be conceptualized by the

"waterfall over a dam" analogy. In this analogy, the presence of dynamic hyperinflation and 10 cmH20 of auto-PEEP is represented in the top panel by the reservoir of water trickling over the dam represented by the solid block. In the middle panel, as long as the external PEEP is less than or equal to the amount of auto-PEEP, the amount of water in the upstream reservoir, representing dynamic hyperinflation, does not increase. However, once the amount of water in the reservoir does increase (bottom panel), dynamic hyperinflation worsens.

Detrimental effects of autoPEEPDetrimental effects of autoPEEPTrigger with acute

exacerbation

Tachypnea (decreased I:E ratio)

Increased airway resistance

Increased work of breathing

Increased work of breathing

HyperinflationHyperinflation

autoPEEPautoPEEP

Decreased effectiveness of

inspiratory musclesIncreased oxygen cost of

breathingIncreased oxygen cost of

breathing

Respiratory muscle fatigueRespiratory

muscle fatigue

Excessive Inspiratory TimeExcessive Inspiratory Time

Inspiration

Expiration

NormalNormalPatientPatient

Time (sec)

Flo

w (

L/m

in)

Air TrappingAuto-PEEP

}

Increase WOB and “Fighting” of the ventilator

Pressure or Volume Mode?

Volume• Predictable TV• Peak-Plat gradient• Monitor Plat• Better acidosis

control

Pressure• Minimise over-

distension• Monitor Tidal

volume• Excess volumes as

airway resistance improves

Mechanical Ventilation ofCOPD & Asthma Exacerbations

Mode: AC vs IMV PS ? rest respiratory muscles: CMV Better sleep with AC vs. IMV-PS Ventilator-induced diaphragm changes

(?)Triggering: key issue with either mode PEEP to counter auto-PEEP Major cause of patient-ventilator

dissynchrony

Initial Ventilator Settings

• Inspiratory time 0.8 – 1.2 secs• RR 10-12• TV 6-8 ml/Kg• Pplat < 30 cm H2O• PEEP ??

Assessment of Hyperinflation

Reducing Hyperinflation

• Reduce rate• Reduce tidal volume• Increase expiratory time

– Increase inspiratory flow rate– Increased Peak Airway Pressure

• Monitor (Pplat)• Tolerate increased CO2

(minimise dead space)

I : E1: 6

I : E1: 2

COPD flow and frequency

• As flow increased from 30 to 60 and 90 L/min (from right to left), frequency increased from (18 to 23 and 26 breaths/min, respectively), Auto-PEEP decreased (from 15.6 to 14.4 and 13.3 cm H2O, respectively) and end-expiratory chest volume also fell. Increases in flow from 30 L/min to 60 and 90 L/min also led to decreases in the swings in Pes from 21.5 to 19.5 and 16.8 cm H2O.

Hypercapnia: How permissive?

• Defence of intracellular pH • Apnoeic oxygenation in dogs to pH 6.5 and

PaCO2 of 55kPa• Anaesthetic mishap with PaCO2 of > 300

mmHg (40 kPa) and pH of 6.6 survived without sequelae

Am J Respir Crit Care Med 1994; 150:1722-37

PplPpl

EPPEPP

Pel

PalvPalv

PaoPao

1010

10

+10

1010

10

00

Waterfall ConceptExternal & Internal PEEP

10

Effect of Auto-PEEP

Patm = 0PA = 0

Ppl =- 5

Normal airway resistance (end-exhalation)

Pel = 5

Ppl needed to initiate inhalation: - 1PA drops to - 1 relative to Patm

- 5

- 5Ptp = 5

Effect of Auto-PEEP

PA = 10

Airway narrowing causing auto-PEEP

Patm = 0Ppl = 2

Pel = 8

Ppl needed to initiate inhalation: - 11

2

2

Ptp = 8

Treatment of Auto-PEEP with PEEP or CPAP

Airway narrowing with auto-PEEP: Treatmentwith PEEP

PA = 10PEEP = 10Ppl 2

Pel = 8

Ppl needed to initiate inhalation: - 1The only thing PEEP does is work of breathing

2

2

Ptp = 8

Implication

PEEP, EPAP, CPAP No effect on VE, VT or VA

WOB (elastic)

- VCO2 (on next breath)

- PaCO2 (on next breath)

Treatment of Auto-PEEP with Vinsp

Longer time for exhalation, PA falls

PA = 6Ppl = 1

Pel = 6

Ppl needed to initiate inhalation: - 7

1

1

Ptp = 5

Patm = 0

External PEEP

• Reduce inspiratory muscle load• Improve ventilator triggering• 80% of PEEPi can be matched

without increase PEEP tot• Reduce hyperinflation by

improving expiration

Titrating PEEP to PEEPi

Heliox and Obstructive Airway Disease

• Low density high thermal conductivity • Reduce pressure gradient in turbulent flow• Administered in

– NIV– IPPV – Nebulisers

• Role in Asthma and COPD?

OutcomeOutcome

Gluck et al. Chest 1990; 98:693-98Gluck et al. Chest 1990; 98:693-98N2-O2 He-O2

6.8

6.97

7.17.2

7.37.4

7.5

N2-O2 He-O220

40

60

80

100

120N2-O2 He-O2

30405060708090

100110

Pt#1

Pt#2

Pt#3

Pt#4

Pt#5

Pt#6

Pt#7

Peak inspiratory pressure (cmH

2O)

PCO2

(mmHg)pH

2.5 min2.5 min

22.2 min22.2 min

Theophylline

Administration of Bronchodilators

Administration of Bronchodilators

• Nebuliser or MDI?• Lung deposition of radiolabelled drug*

– MDI 5.6% v Nebuliser 1.2%

• Urinary excretion**– MDI with spacer 38%– MDI in line 9%– Nebuliser 16%

• 4-10 puffs MDI effective in reducing RAW

* Chest 1999; 115:1653-1657**Am Rev Respir Dis 1990; 141:440–444

MDI adapters for use with MV circuits

Myopathy in Asthma

• Steroid myopathy

• Muscle relaxants

• Polyneuropathy of the critically ill

Myopathy in Asthma

Principles of managing the ventilated patient with obstructive lung disease

Ventilation of Patients with COPD and Asthma. Chronic lung diseases with airflow obstruction Asthma...

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