Acute respiratory failure

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10/2/2012 1

ACUTE RESPIRATORY FAILURE

Ihab B Abdalrahman, MBBS, MD, ABIM, SSBB Ihab Tarawa Consultant of Acute Care Medicine, Soba University Hospital

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BASIC RESPIRATORY PHYSIOLOGY

Respiratory system made ridiculously easy

It is as simple as moving the air in and out.

Allowing gas exchange.

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O2 CO2

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1,2,3

Bottom line of the respiratory system is to

Let oxygen in,

And carbon dioxide out.

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Definitions

acute respiratory failure occurs when:

pulmonary system is no longer able to meet the metabolic demands of the body

hypoxaemic respiratory failure:

PaO2 8 kPa when breathing room air

hypercapnic respiratory failure:

PaCO2 6.7 kPa

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Oxygen in Depends on Ventilation

PAO2

Perfusion

Ventilation-perfusion matching

Diffusing capacity

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PAO2

The alveolar pressure is equal to the sum of the partial pressures of the gases within the alveolus.

The partial pressure of each gas is proportional to the concentration of the gas.

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2A2A2A2A NPOHPCOPOPpressure Alveolar

Nitrogen

Water vapour

Carbon dioxide

Oxygen

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Nitrogen

Water vapour

Carbon dioxide

Oxygen

2A2A2A2A NPOHPCOPOPpressure Alveolar

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Nitrogen

Water vapour

Carbon dioxide

Oxygen

2A2A2A2A NPOHPCOPOPpressure Alveolar

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Oxygen in

Depends on PAO2

FIO2

Alveolar pressure

PACO2

Ventilation

Ventilation-perfusion matching

Perfusion

Diffusing capacity

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Ventilation-perfusion matching

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Carbon dioxide out

Largely dependent on alveolar ventilation

Anatomical dead space constant but physiological dead space depends on ventilation-perfusion matching

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)V-(V xRR nventilatio Alveolar DT

Carbon dioxide out

Respiratory rate

Tidal volume

Ventilation-perfusion matching

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PATHOPHYSIOLOGY

PAO2=14.74 kPa PACO2=5 kPa

75% 100%

Normal

ventilation &

perfusion

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Pathophysiology

Low inspired Po2

Although, in theory, acute respiratory failure may result from a low inspired PO2 this is rarely a problem in Intensive Care except in locations at high altitude.

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Pathophysiology

Low inspired oxygen concentration

Hypoventilation

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Nitrogen

Water vapour

Carbon dioxide

Oxygen

2A2A2A2A NPOHPCOPOPpressure Alveolar

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PAO2=9.74 kPa PACO2=10 kPa

75% 92%

Hypoventilation

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Brainstem

Spinal cord

Nerve root Airway

Nerve

Neuromuscular junction

Respiratory muscle

Lung

Pleura

Chest wall

Sites at which disease may cause hypoventilation 10/2/2012 Ihab Tarawa 22

Brainstem

Spinal cord

Nerve root Airway

Nerve

Neuromuscular junction

Respiratory muscle

Lung

Pleura

Chest wall

Sites at which disease may cause hypoventilation 10/2/2012 Ihab Tarawa 23

Pathophysiology

Low inspired oxygen concentration

Hypoventilation

Shunting

Dead space ventilation

Diffusion abnormality

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Shunt

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75% 75%

100% 75%

87.5%

oxygen therapy

has relatively

little effect on

hypoxia due to

shunting.

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75% 75%

100% 75%

90%

hypoxic vasoconstriction

↓perfusion to non-ventilated alveoli

↑perfusion to ventilated alveoli,

↓ magnitude of the shunt

↑and increasing the arterial saturation

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Shunting

Intra-pulmonary Pneumonia

Pulmonary oedema

Atelectasis

Collapse

Pulmonary haemorrhage or contusion

Intra-cardiac Any cause of right to left shunt eg Fallot’s, Eisenmenger,

Pulmonary hypertension with patent foramen ovale

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Pathophysiology

Low inspired oxygen concentration

Hypoventilation

Shunting

Dead space ventilation

Diffusion abnormality

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Dead space ventilated but not perfused

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Pathophysiology

Low inspired oxygen concentration

Hypoventilation

Shunting

Dead space ventilation

Diffusion abnormality

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Diffusion abnormalities.

These can result from a failure of diffusion across the alveolar membrane

or a reduction in the number of alveoli resulting in a reduction in the alveolar surface area.

Causes include ARDS and fibrotic lung disease

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RESPIRATORY MONITORING

Clinical

Respiratory compensation

Sympathetic stimulation

Tissue hypoxia

Haemoglobin desaturation

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Bottom line of the respiratory system is to let oxygen in and CO2 out.

Some sensors will go off

Hypoxia

Acidosis

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Clinical

Respiratory compensation Tachypnoea

Accessory muscles

Recession

Nasal flaring

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Clinical

Sympathetic stimulation

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Clinical

Sympathetic stimulation

HR

BP (early)

sweating

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Point of making a difference

Coming for help

Or coming with a coffin

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Clinical

Tissue hypoxia

Altered mental state

HR and BP (late)

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Clinical

Haemoglobin desaturation

cyanosis

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If we wait for the patient to become cyanosed

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PaO2 (kPa)

Hb s

atu

rati

on (

%)

8

90

Pulse oximetry, notice the sigmoid curve

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The oxygen content of blood is mainly dependent on:

the haemoglobin saturation,

with the a very small contribution from dissolved oxygen.

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Oxygen delivery

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222

2 2

PaO0.0031.37Hbsaturation O content O

10contentOoutput CardiacdeliveryO

Monitoring

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123

80 40

87% HR=95

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Sources of error

Poor peripheral perfusion

Poorly adherent/positioned probe

False nails or nail varnish

Lipaemia

Bright ambient light

Excessive motion

Carboxyhaemoglobin or methaemoglobin

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Thing to remember

Saturation is not a measure of

ventilation

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Summary

worry if RR > 30/min (or < 8/min) unable to speak 1/2 sentence without pausing agitated, confused or comatose cyanosed or SpO2 < 90% deteriorating despite therapy

remember normal SpO2 does not mean severe ventilatory problems are not

present

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TREATMENT

Treatment

Treat the cause Supportive treatment

Oxygen therapy

CPAP

Mechanical ventilation

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Oxygen therapy

Fixed performance devices

Variable performance devices

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Nasal canula

Simpler mask

Other

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Other devices

Reservoir face mask

Bag valve resuscitator

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CPAP

reduces shunt by recruiting partially collapsed alveoli

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Pressure

Volu

me

Lung compliance and FRC

reduces work of breathing

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Mechanical ventilation

Decision to ventilate

Complex

Multifactorial

No simple rules

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Ventilate?

Severity of respiratory failure

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Ventilate?

Severity of respiratory failure

Cardiopulmonary reserve

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Ventilate?

Severity of respiratory failure

Cardiopulmonary reserve

Adequacy of compensation

Ventilatory requirement

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Ventilate?

Severity of respiratory failure

Cardiopulmonary reserve

Adequacy of compensation

Ventilatory requirement

Expected speed of response

Underlying disease

Treatment already given

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Ventilate?

Severity of respiratory failure

Cardiopulmonary reserve

Adequacy of compensation Ventilatory requirement

Expected speed of response Underlying disease

Treatment already given

Risks of mechanical ventilation

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Ventilate?

Severity of respiratory failure

Cardiopulmonary reserve

Adequacy of compensation Ventilatory requirement

Expected speed of response Underlying disease

Treatment already given

Risks of mechanical ventilation

Non-respiratory indication for intubation

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Ventilate?

43 year old male

Community acquired pneumonia

Day 1 of antibiotics

PaO2 8 kPa (60 mmHg), PaCO2 4 kPa (30 mmHg), pH 7.15 on 15 l/min O2 via reservoir facemask

Respiratory rate 35/min

Agitated

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Yes

43 year old male

Community acquired pneumonia

Day 1 of antibiotics

PaO2 8 kPa (60 mmHg), PaCO2 4 kPa (30 mmHg), pH 7.15 on 15 l/min O2 via reservoir facemask

Respiratory rate 35/min

Agitated

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Yes

43 year old male

Community acquired pneumonia

Day 1 of antibiotics

PaO2 8 kPa (60 mmHg), PaCO2 4 kPa (30 mmHg), pH 7.15 on 15 l/min O2 via reservoir facemask

Respiratory rate 35/min

Agitated

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O2

O2

Yes

43 year old male

Community acquired pneumonia

Day 1 of antibiotics

PaO2 8 kPa (60 mmHg), PaCO2 4 kPa (30 mmHg), pH 7.15 on 15 l/min O2 via reservoir facemask

Respiratory rate 35/min

Agitated

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Yes

43 year old male

Community acquired pneumonia

Day 1 of antibiotics

PaO2 8 kPa (60 mmHg), PaCO2 4 kPa (30 mmHg), pH 7.15 on 15 l/min O2 via reservoir facemask

Respiratory rate 35/min

Agitated

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Yes

43 year old male

Community acquired pneumonia

Day 1 of antibiotics

PaO2 8 kPa (60 mmHg), PaCO2 4 kPa (30 mmHg), pH 7.15 on 15 l/min O2 via reservoir facemask

Respiratory rate 35/min

Agitated

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Ventilate?

24 year old woman

Presents to A&E with acute asthma SOB for 2 days

Salbutamol inhaler, no steroids

PFR 60 L/min, HR 105/min

pH 7.25 PaCO2 6.8 kPa (51 mmHg), PaO2 42 kPa (315 mmHg) on FiO2 0.6

RR 35/min

Alert

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No

24 year old woman

Presents to A&E with acute asthma SOB for 2 days

Salbutamol inhaler, no steroids

PFR 60 L/min, HR 105/min

pH 7.25 PaCO2 6.8 kPa (51 mmHg), PaO2 42 kPa (315 mmHg) on FiO2 0.6

RR 35/min

Alert

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No

24 year old woman

Presents to A&E with acute asthma SOB for 2 days

Salbutamol inhaler, no steroids

PFR 60 L/min, HR 105/min

pH 7.25 PaCO2 6.8 kPa (51 mmHg), PaO2 42 kPa (315 mmHg) on FiO2 0.6

RR 35/min

Alert

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No

24 year old woman

Presents to A&E with acute asthma SOB for 2 days

Salbutamol inhaler, no steroids

PFR 60 L/min, HR 105/min

pH 7.25 PaCO2 6.8 kPa (51 mmHg), PaO2 42 kPa (315 mmHg) on FiO2 0.6

RR 35/min

Alert

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No

24 year old woman

Presents to A&E with acute asthma SOB for 2 days

Salbutamol inhaler, no steroids

PFR 60 L/min, HR 105/min

pH 7.25 PaCO2 6.8 kPa (51 mmHg), PaO2 42 kPa (315 mmHg) on FiO2 0.6

RR 35/min

Alert

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No

24 year old woman

Presents to A&E with acute asthma SOB for 2 days

Salbutamol inhaler, no steroids

PFR 60 L/min, HR 105/min

pH 7.25 PaCO2 6.8 kPa (51 mmHg), PaO2 42 kPa (315 mmHg) on FiO2 0.6

RR 35/min

Alert

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No

24 year old woman

Presents to A&E with acute asthma SOB for 2 days

Salbutamol inhaler, no steroids

PFR 60 L/min, HR 105/min

pH 7.25 PaCO2 6.8 kPa (51 mmHg), PaO2 42 kPa (315 mmHg) on FiO2 0.6

RR 35/min

Alert

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Pathway

Airway patent

Secure airway

Patient breathing

Ventilat

Is he hypoxic

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Hypoxic

Yes No

Acidosis

Shock

PE

Asthma

Pumonary edema

Anxiety

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Hypoxic

Pco2

High /normal Low Pco2

pneumonia

ARDS

Pulmonary edema

Aspiration

PE

pneumothorax

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Hypoxic

Pco2

High /normal

Normal A-a gradient

Breathing hard

Asthma

COPD

PE

Breathing normally

CND

Drugs

High A-a gradient

Fatigue from hypoxia

Acute on chronic

Low Pco2

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QUESTIONS?

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