Respiratory Failure & NIV: Prior to session read & think about the case

in the next 10 slides

Ken Whyte,

Respiratory Physician

67 yr old male smoker: July 2001

• Forklift driver, heavy smoker (60 pack years) with exertional dyspnoea for 3+yrs

• Heavy alcohol intake (6+ cans of beer/day)

• No relevant past medical history

• Only regular medication: Combivent inhaler

67 yr old male smoker: July 2001

• 3/52 history of cough (initial response to antibiotic) then increasing SOB for 1/52.

On Examination:– cyanosed, respiratory rate 30/min, SpO2:85%;– in respiratory distress with widespread wheeze and

scattered crackles, tired ++.– Clinically hyperinflated;

ABG on 2l/min O2: PaO2-7.6kPa (58mmHg);

PaCO2-11.5kPa (87mmHg); HCO3--34; pH-7.22

CXR on admission

67 yr old male smoker:July 2001

• Commenced on nebulised ipratropium and IV beta agonist + aminophylline; oral prednisone and antibiotic;

• Repeat blood gas marginally better but still acidotic (pH - 7.27) and respiratory rate remains >30/min. Tired++

• Commenced on mask ventilation at 2+hrs;

Sequential blood gas measurements

On O28.09.07.3510:1527/07

Off NIV+O25.69.77.3308:5027/07

weaning10.46.27.4020:3023/07

No change9.67.57.3503:4522/07

IPAP 6.99.67.3221:5521/07

NIV started9.511.37.2719:4021/07

CommentPaO2PaCO2pHTimeDate

67 yr old male smoker: July 2001

• Mask ventilation weaned off over first 48hrs;

• Mobilised in ward, smoking cessation;

• Discharged home after 9 days, weaning off oral steroids;

• Continued to smoke & returned to work

67 yr old male smoker: August

• Readmitted 31/8/01: increasing dyspnoea for ?3/52 and sputum darker (grey/green):– pyrexial; respiratory rate 26/min, not

distressed;– widespread wheeze;

– pH: 7.35; PaO2:7.4kPa; PaCO2:8.5;HCO3

-:35;

• Rx: low flow oxygen, antibiotics, nebulisers and increased prednisone, PaCO2:7.4kPa.

• Discharged at 8 days, FEV1: 0.86l (27%);

67 yr old male smoker: October

• Admitted on 20/10/01:– 24 hr history of increasing SOB with purulent

sputum;– respiratory distress, respiratory rate 36/min;

– cyanosed on O2 (24%); SpO2:55%;

– IV aminophylline, nebulised ipratropium & β2 ;

– after 4-5 hrs deteriorating and transferred to DCCM for CPAP;

67 yr old male smoker: October

• CPAP not tolerated;

• pH: 7.1-7.2; PaCO2: 11-14kPa;

• IV salbutamol added; [theophylline] normal;

• trial of bi-level pressure support ventilation via mask: struggled to cope: abandoned;

• sedated with boluses of IV morphine (5mg in total) - increasingly comatose but PaCO2 fell!

67 yr old male smoker• Transferred to Respiratory Medicine: Day 3

– re-commenced on mask ventilation; increased inspiratory pressure and changed to nasal mask;

– other therapy continued;– respiratory rate fell from 40/min to 32/min;– well oxygenated on 4l/min;– gradual improvement;– NIV only at night on day 6, home at day 10;

Respiratory Failure & NIV

Ken Whyte,Respiratory PhysicianGreenlane Respiratory

Service

Oxygen cascade

DaO2 = CaO2 x CO

SaO2 x Hb x 1.34 SV x HR

Pulmonaryfailure

Heart failure

Oxygen Delivery depends on intact cardiorespiratory system

Hypoxia versus Hypoxemia

Oxygen content equation

CaO2 = (SaO2 x Hb x 1.34) + .003(PaO2)

ie: normal blood carries between 160-220mls per litre

e.g. Hb: 150 then CaO2: 200mls/litre

Hb: 100 then CaO2: 133mls/litre

63 yr old male: ex-smoker• Known severe lower lobe bronchiectasis +/-

CORD (uses inhalers)• Recently returned from living in Australia• Found “in extremis” by daughter – no clear history

available• On Exam:

– hypotensive and shutdown– Respiratory distress– GCS 12/15– No wheeze or crackles

63 yr old male: ex-smoker

• Cyanosed: SpO2: 73% on air• Respiratory rate 40/min• HR: 140/min, sinus, BP 90/55• No urine on catheterisation• CXR: extensive bilateral lower lobe change

& hyperinflation

What test next?

Arterial blood gas on admission

• PaO2: 6.2kPa (47mmHg)

• PaCO2: 11.1kPa (83mmHg)

• pH 7.13

• HCO3 (-) 25

What type of respiratory failure is this?

Types of respiratory failure

Type I

Lung failure

Type II

Pump failure

PaO2 Low (< 60 mmHg) Low

PaCO2 Normal High (>45 mmHg)

Mechanism 1. Ventilation-perfusion inequality

2. Diffusion abnormality

3. Shunt

alveolar ventilation

Disorders • Asthma, ILD, COPD

• Cardiac septal defect

COPD, OSA, 1o hypoventilation

Chest wall disorder incl. respiratory muscle weakness

Rx O2, CPAP (?) NIV

Respiratory Failure

Definitions:

Type I Respiratory Failure:

PaO2 < 8.0kPa; PaCO2 <6.0kPa

Type II Respiratory Failure:

PaO2 < 8.0KPa; Pa CO2 > 6.0kPa

The Respiratory System

Lungs Respiratory pump

Pulmonary Failure

• PaO2

• PaCO2 N/

Ventilatory Failure

• PaO2

• PaCO2

Hypoxic Respiratory

Failure

Hypercapnic Respiratory

Failure

Types of respiratory failure

Normal range

Respiratory failure

Type I

(Hypoxaemic)

Type II

(Hypercapnic)

Acute Chronic Acute on chronic

pH 7.35-7.45 Normal < 7.35 Normal < 7.35

PaO2, mmHg 80-100 < 60 < 80 < 80 < 80

PaCO2, mmHg 35-45 Normal > 45 > 45 > 45

HCO3,mM/L 22-28 Normal Normal > 28 > 28

Arterial blood gas on admission• PaO2: 6.2kPa (47mmHg)• PaCO2: 11.1kPa (83mmHg)• pH 7.13• HCO3

(-) 25

Hypercapnic hypoxic respiratory failure

What is his A-aO2 gradient?

What other tests would you order based on these results?

On Admission

Further investigation?• Lactate: 10 mmol/L• Creatinine: 245• Mixed acidosis:

– Renal failure (?dehydration)

– Poor tissue oxygenation – lactic acidosis

– ?all acute respiratory acidosis or acute on chronic respiratory acidosis?

Not possible to determine with certainty but if this was pure acute respiratory acidosis plus metabolic acidosis he should be even more acidotic?

On Admission

?starting point

Is it important to distinguish?

• Essential to have an aim of therapy?– Does he have a normal CO2 drive?– If not then ventilating him down to

normocapnia will not be wise!– If he is normally hypoxic then restoring

normoxia with active therapy may not be wise!

Effect of chronic hypercapnia on CO2 drive

Ventilatory response to CO2: effect of hypoxia

Ventilatory response to hypoxia

Raised Pa CO2

Is it important to distinguish?

• Essential to have an aim of therapy?– Does he have a normal CO2 drive?– If not then ventilating him down to

normocapnia will not be wise!– If he is normally hypoxic then restoring

normoxia with active therapy may not be wise!

What is your next step in writing down an action plan in this man?

Hypoxia versus hypercapnia

What is the mechanism of hypercapnia in airways disease?

Determinants of PaCO2

Alveolar Ventilation (V’A)CO2 output (V’CO2)

PaCO240

45

50

35

30

PaCO2 = k V’CO2 / V’A

Determinants of alveolar ventilation

AlveolarVentilation

Work of breathingRespiratory muscles

LoadsElastic

Resistive

Energy supply Blood flowArterial O2

Nutrition

ActivationNeural drive

NM transmission

Muscle functionStrengthEfficiency

Acute and acute-on-chronic respiratory failure in COPD

Airway infection

TTOT, TI, and TE

Dynamic hyperinflation

PEEPi

respiratory muscle efficiency

Raw and EL,dyn

work of breathing

O2 cost of breathing

Respiratory muscle fatigue

Roussos & Koutsoukou ERJ 2003

FB

V’/Q’ inequality expiratory flow limitation

Work of breathing

• To maintain a normal V’A and PaCO2, respiratory muscles must maintain a power output (work rate) to overcome respiratory loads.

• Work of breathing es in proportion to 1. V’E2. Inspiratory pressure3. Inspiratory duration4. Inspiratory flow

• High work of breathing – respiratory muscle fiber injury (membrane damage and

sarcomere disruption) (Zhu et al. AJRCCM 1997; Orozco-Levi et al. AJRCCM 2001).

– fatigue (“reversible weakness”): peripheral or central

Tension time index (TTI)

• Reduced compliance at high lung volumes

• Intrinsic PEEP– >50% of the in WOB in COPD

(Coussa et al. JAP 1993)

P = 0P =

+3cmH2O

Airway

Alveolus

NORMAL COPD

END-EXPIRATION

Increased elastic loads in COPD

Respiratory failure in COPD: effect of hyperinflation on resp. muscles

Healthy Emphysema

1. muscle length2. distorted geometry of diaphragm mechanical disadvantage: conversion of

tension to pressure (Laplace law) and displacement; action on lower rib cage.3. energy supply during sustained muscle contractions

predisposition to respiratory muscle fatigue.

Consequences of reduced respiratory muscle length in COPD

Altering deadspace: work of breathing

Respiratory muscle fatigue

Diaphragm fatigues at • PI > 60% max at FRC and • PI > 30% max during hyperinflation

( FRC + 50% IC)

Roussos et al. JAP 1979 Bellemare & Grassino JAP 1982

Diaphragm fatigues at tension time index (TTI) > 0.15

Effect of fatiguing respiratory loads on pattern of breathing

• Rapid shallow breathing FB, VT, constant or slightly V’E.

• May be a behavioural response to dyspnoea es load on muscle by

PI developed and – respiratory muscles work at a more optimal length – may postpone or prevent fatigue.

• But inefficient in terms of gas exchange VD/VT leading to PaCO2.

Ventilatory failure in COPD/emphysema

AlveolarVentilation

Work of breathing Resp. muscle reserve

Elastic • PEEPi• Hyperinflation

Resistive

Energy supply Blood flow (sustained forceful contractions)Arterial O2 Nutrition

ActivationNeural drive NM transmission

Muscle functionStrength (steroids, fatigue)Efficiency (reduced length,

mechanical disadvantage)

Hypercapnic respiratory failure in COPD: Aims of therapy

• Not to restore either “normal” PaO2 or PaCO2:– avoid death by either hypoxia or acute on chronic

respiratory acidosis;

• Stop the slide into increasing acidosis and support the pump whilst “standard” medical therapy restores the status quo (i.e. chronic respiratory failure);

Aim: pH>7.35 and SpO2>88-92% (>85% acceptable?)

Treatment of Respiratory Failure

• Maximise remaining respiratory function;

• Minimise work of breathing;

• Monitor closely: Oximetry is not enough!

Repeated ABGs are essential!

Effect of alveolar ventilation on alveolar gas tensions

Lumb 2000

Simple Acid Base chart

Treatment of Respiratory Failure

• Maximise remaining respiratory function;• Minimise work of breathing;• Monitor closely: Oximetry is not enough!

• Intervene to support the respiratory pump before exhaustion, biochemical/metabolic deterioration and severe distress supervene and prevent salvage.

Repeated ABGs are essential!

63 yr old: Appropriate ceiling of care?

• He is likely to fail maximal medical therapy• Next step in hypercapnic hypoxic

respiratory failure is non-invasive ventilation:– Acceptable with this mental state?– Acceptable with renal failure?– Acceptable with hypotension?– If the ceiling of care is NIV then these are only

relative contraindications.

Typical pressure support ventilator: VPAP™

What does it do? Principle is simple!

• Via a tight fitting nasal or full face mask it will generate pressure in the airway (PAP):

– Inspiratory PAP (IPAP) - if you always blow into a balloon with the same force (pressure) it always expands to the same size (= same tidal volume).

– Expiratory PAP (EPAP) - not essential, helps to splint open airways & alveoli thus increasing FRC, decreasing shunt and may decrease work of breathing.

Selection of available masks:the year before last!

Newer interfaces

Determinants of PaCO2

Alveolar Ventilation (V’A)CO2 output (V’CO2)

PaCO240

45

50

35

30

PaCO2 = k V’CO2 / V’A

What does non-invasive ventilation do?

Assists the failing pump (remember the central drive is high) by:

– increasing tidal volume;– increasing effective alveolar ventilation;– decreasing respiratory rate;– decreasing work of breathing;

NIV: effect on work of breathing in acute COPD

Hypercapnic respiratory failure in COPD: Aims of therapy

• Not to restore either “normal” PaO2 or PaCO2:– avoid death by either hypoxia or acute on chronic

respiratory acidosis;

• Stop the slide into increasing acidosis and support the pump whilst “standard” medical therapy restores the status quo (i.e. chronic respiratory failure);

Aim: pH>7.35 and SpO2>88% (>85% acceptable?)

Non-invasive ventilation in COPD

Advantages:

• Avoids sedation;

• patient can eat, drink and talk;

• decreased risk of noscomial pneumonia (cf ICU & intubation)

• Not continuous!

Disadvantages:• Claustrophobic mask;• skin damage;• gastric distension;• large leaks possible

resulting in ineffective therapy;

• bronchial toilet difficult;

NIV in COPD:Algorithim(Plant et al, Lancet 2000;355:1931)

• VPAP + 2 facemasks & 2 nasal masks

• EPAP @ 4cmH2O• IPAP @ 10cmH2O 15 20cmH2O

(or max tolerated over one hour)

• O2 entrained to keep SpO2 between 85-90%

• Maximum possible day 1; then 16 hrs day 2 then 12 hrs day 3 and off on day 4;

NIV in COPD:Results

P lan t e t a l, L ance t 2000 ; 355 ; 1931-1935

2 4 d ied9 4 su rvived

fro m the 1 18 ra n do m ised

3 2 m e t crite ria fo r in tu ba tion 8 6 success fu lly trea ted

1 1 8 a llo ca te d s tan d ard th e ra py

1 8 m e t crite ria fo r in tu ba tion

1 2 d ied1 0 6 su rvived

fro m the 1 18 ra n do m ised

1 0 0 su ccess fu lly tre a ted

1 1 8 a lloca te d no n -in vas ive ven tila t ion

2 3 6 ra nd o m ised

Acute exacerbation of COPDInstitute standard medical therapy:

Inc. O2 via Venturi or NC at 24 or 28%

AIM FOR SpO2 88-92%

Repeat ABG

pH< 7.20

NIV very strongly advisedWith NIV 50% will need ET tube

but better hospital outcomes

pH<7.30

NIV strongly advisedWithout NIV 50% will die

or need ET tube

pH<7.35RR>23

Pa CO2>6.0kPa

NIV advisedWithout NIV 80% will

recover but NNT to save one ET tube/death is 10

After two hours

NIV in COPD: Long term survival(Plant et al, Thorax 2001;56:708-712)

NIV in Respiratory failure in COPD

• Grade I evidence of benefit with non-invasive ventilation:

– decreased intubation rates;– decreased mortality;– decreased length of stay;– decreased use of ICU resource;

Take home messages for COPD treatment?

• If hypoxic and increasing acidosis?

– Do not turn down the oxygen (unless poisoned)!

– Think non-invasive ventilation!• Reduced GCS is not

contraindication

• If they fail mask ventilation ( + DCCM not interested) then keep comfortable, dying of dyspnoea is very unpleasant.

Survival in chronic respiratory failure: Brompton Hospital.

NIV in Asthma

• Two randomised studies showing reduced intubation rates;

• Very difficult to predict who will respond and avoid intubation;

• No study outside the ICU/HDU setting;Worthwhile in exhausting asthmatics but only

in ICU setting:

Never in Medical wards etc.

Cardiogenic pulmonary edema

Pneumonia

pulmonary ARDS

extra pulmonary ARDS

Atelectasis

Post surgery changes

Aspiration

Trauma

Infiltrates inimmunsuppression

Hypoxic

Respiratory

Failure Pulmonaryfibrosis

The respiratory System

Lungs Respiratory pump

Pulmonary Failure

• PaO2

• PaCO2 N/

Ventilatory Failure

• PaO2

• PaCO2

Hypoxic Respiratory

Failure

Hypercapnic Respiratory

Failure

Respiratory Failure• Type I or hypoxic respiratory failure:

Defined as PaO2 < 8kPa (60mmHg)

PO 2 (mmHg)

%O

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O 2 IN PHYSICAL SOLUTION (ml/liter)

T=37°C;pH=7.40;PCO 2=40 mmHg

PO 2 (mmHg)

%O

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tura

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of H

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O 2 IN PHYSICAL SOLUTION (ml/liter)

T=37°C;pH=7.40;PCO 2=40 mmHg

Hypoxaemia

• Mechanisms of hypoxaemia (low PaO2):

– Low FiO2

– Shunt

– V/Q mismatch

HYPOTENSION

D

E

H

Y

D

R

A

T

I

O

N

V/Q: infinite possibilities

• V/Q =1 is “normal” or “ideal”

• V/Q =0 defines “shunt”

• V/Q =∞ defines “dead space” or “wasted ventilation”

0 ∞1

Why does “V/Q mismatch” cause hypoxemia?

• Low V/Q units contribute to hypoxemia

• High V/Q units cannot compensate for the low V/Q units

• Reason being the shape of the oxygen dissociation curve which is not linear

Hypoxic respiratory failure• Gas exchange failure

• Respiratory drive responds

• Increased drive to breathe– Increased respiratory rate– Altered Vd/Vt (increased dead space etc)– Often stiff lungs (oedema, pneumonia etc)

Increased load on the respiratory pump which can push it into fatigue and precipitate

secondary pump failure and hypercapnia

Aim of therapy?• SpO2 at least over 95%

• Minimise work of breathing:– To avoid exhaustion and/or pump failure– To improve gas exchange

• To avoid mechanical ventilation if possible

• To avoid emergency intubation (high death rate) and thus recognise deterioration early and intervene in controlled manner

Is there a role for CPAP?

• Potentially increases FRC by providing PEEP:– This may decrease work of breathing by:

• Altering pressure/volume point

• Improving gas exchange by decreasing amount of atelectasis (ie less shunt and low V/Q units)

BUT

• if airways disease then may lead to hyperinflation

• If very stiff lung could potentially decrease V/Q

SAFE OUTWITH ICU/HDU? UNPROVEN

Is there a role for NIV?• No proven role!

• NIV supports a failing pump by decreasing WOB

• Per se it does not improve gas exchange

• In the exhausting, deteriorating patient with a problem likely to respond quickly to therapy (e.g. pulmonary oedema) ?role

NIV should not be given for hypoxic respiratory failure outside an

ICU/HDU environment

Any Questions?