Respiratory atef

Acute respiratory failure

Topics

Definition of acute respiratory failure Basic respiratory physiology Pathophysiology Respiratory monitoring Treatment

Definitions

acute respiratory failure occurs when:– pulmonary system is no longer able to meet

the metabolic demands of the body hypoxaemic respiratory failure:

– PaO2 60 mmHg when breathing room air

hypercapnic respiratory failure:– PaCO2 50 mmHg

Basic respiratory physiology

O2CO2

Pulmonary Ventilation and pressures

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Oxygen in

• Depends on– PAO2

– Diffusing capacity– Perfusion– Ventilation-perfusion matching

2A2A2A2A NPOHPCOPOPpressureAlveolar

Nitrogen

Water vapour

Carbon dioxide

Oxygen

PAO2= (PB-PH2O)FIO2 – CO2/0.8

PAO2= (760-47)0.21 -40/0.8=100

Alveolar Oxygen tension

How much oxygen is in the blood

PaO2

SaO2

Oxygen content (CaO2)

How much oxygen is in the blood

PaO2• The amount of dissolved oxygen in the plasma phase --

and hence the PaO2 -- is determined by alveolar PO2 and lung architecture only

SaO2• The percentage of hemoglobin molecule bounded with

oxygen.

Oxygen Content CaO2• CaO2 = Hb (gm/dl) x 1.34 ml O2/gm Hb x SaO2 + PaO2 x

(.003 ml O2/mm Hg/dl)

Oxygen dessociation Curve

Oxygen in

• Depends on– PAO2

• FIO2

• PACO2

• Ventilation• Alveolar pressure

– Ventilation-perfusion matching– Perfusion– Diffusing capacity

Carbon dioxide out

Largely dependent on alveolar ventilation

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

)V-(V xRR nventilatio Alveolar DT

Carbon dioxide out

• Patient Vt f Ve Description– A (400) (20) = 8.0 L/min slow and

deep– B (200) (40) = 8.o L/min fast/shallow

• Patient Va-Vd f Va Description – A (400-150)(20) = 5.0 L/min slow and deep– B (200-150)(40) = 2.0 L/min fast/shallow

Increase PaCO2

Increase work of breathing

Muscle fatigue

Shallow breathing followed by increase in RR

Acute Lung Compromise

Carbon dioxide out

Respiratory rate

Tidal volume

Ventilation-perfusion matching

Ventilation-perfusion matching

Dead space

Shunt

Pathophysiology

Pathophysiology

• Low inspired Po2

• Hypoventilation• Ventilation-perfusion mismatch

– Shunting– Dead space ventilation

• Diffusion abnormality

PAO2=105 mmHg PACO2=37 mmHg

75% 100%

Pathophysiology

• Low inspired oxygen concentration• Hypoventilation• Shunting• Dead space ventilation• Diffusion abnormality

FIO2

Ventilation without

perfusion(deadspace ventilation)

Diffusion abnormality

Perfusion without

ventilation

(shunting)

Hypoventilation

Normal

BrainstemSpinal cordNerve root

Airway

Nerve

Neuromuscular junction

Respiratory muscle

Lung

Pleura

Chest wall

Sites at which disease may cause ventilatory disturbance

Causes of respiratory failure

Respiratory Center in BrainBrain


Respiratory Center in Brain Neuromuscular Connections

(peripheral nervous system)

Brain

Nerves


Respiratory Center in Brain Neuromuscular Connections Thoracic Bellows

(intact rib cage and chest wall musculature)

Brain

Nerves

Bellows


Respiratory Center in Brain Neuromuscular Connections Thoracic Bellows Airways (upper & lower)

Brain

Nerves

Bellows

Airways


Respiratory Center in Brain Neuromuscular Connections Thoracic Bellows Airways (upper & lower) Alveoli

Brain

Nerves

Bellows

AirwaysAlveoli

All the links are disrupted !

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

Respiratory monitoring

Clinical

• Respiratory compensation• Sympathetic stimulation• Tissue hypoxia• Haemoglobin desaturation

Clinical

• Respiratory compensation– Tachypnoea– Accessory muscles– Recesssion– Nasal flaring

• Sympathetic stimulation• Tissue hypoxia• Haemoglobin desaturation

Clinical

• Respiratory compensation• Sympathetic stimulation

– HR– BP (early)– sweating

• Tissue hypoxia• Haemoglobin desaturation

Clinical

• Respiratory compensation• Sympathetic stimulation• Tissue hypoxia

– Altered mental state– HR and BP (late)

• Haemoglobin desaturation

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

Treatment

Treatment

• Treat the cause• Supportive treatment

– Oxygen therapy– CPAP– Mechanical ventilation

Oxygen therapy

• Fixed performance devices

• Variable performance devices

Variable performance device

Time

Flow

30

0

6 l/min O2

6

100% O2

Variable performance device

Time

Flow

30

0

6

6 l/min O2

37% O2

24 l/min air

Fixed performance device

Time

Flow

30

0

100% O2 15 l/min

15 l/min air

60% O2 60% O2 30 l/min

Venturi mask

Other devices

•Reservoir face mask•Bag valve resuscitator

CPAP

• reduces shunt by recruiting partially collapsed alveoli

Mechanical ventilation

• Decision to ventilate– Complex– Multifactorial– No simple rules

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

Ventilate?

• 43 year old male• Community acquired pneumonia• Day 1 of antibiotics• PaO2 60 mmHg, PaCO2 30 mmHg, pH

7.15 on 15 l/min via reservoir facemask• Respiratory rate 35/min• Agitated

No Yes

Yes



Yes



Yes



Yes

• 43 year old male• Community acquired pneumonia• Day 1 of antibiotics• PaO2 60 mmHg, PaCO2 30 mmHg, pH 7.15

on 15 l/min via reservoir facemask• Respiratory rate 35/min• Agitated

Yes



Ventilate?• 24 year old woman• Presents to ER with acute asthma

– SOB for 2 days• Salbutamol inhaler, no steroids• PFR 60 L/min, HR 105/min• pH 7.25 PaCO2 51 mmHg, PaO2 315 mmHg on

FiO2 0.6• RR 35/min• Alert

No Yes

No

• 24 year old woman• Presents to A&E with acute asthma



No




No




No




No




No




Thank you

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