Unit I - Respirology

Integrative Lecture:Week 7 – The Normal Airway &

Lung

Tom Kovesi MDPediatric Respirologist

Children’s Hospital of Eastern Ontario

• Understand how changes in muscle activity alter respiratory system pressures to create air flow, producing inspiration and expiration

• Understand the concept of work of breathing, and appreciate it’s components.

• Understand the causes of dynamic hyperinflation• Explain the effect that the presence of lung units

with different VA/Q ratios have on arterial PO2• Recognize the shape of a normal time-volume

curve

Objectives

[Unit name – Lecture title – Prof name]

Part 1 – “How Does Kate Breathe?”

http://www.olympics.org.uk/Beijing2008/AthleteProfile.aspx?id=6862

http://www.thisisbristol.co.uk/news/Olympic-runner-s-asthma-worries/article-238277-detail/article.html

Why Worry About Kate?

Kate at Rest

• What determines Kate’s resting lung volume?

http://news.bbc.co.uk/sport2/hi/olympics/athletics/7506976.stm

Mechanical Properties: Functional Residual Capacity

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FRC

•The pressures created by each are transmitted to, and influence each other, via the fluid in the pleural space. • If there’s no muscle activity acting on the respiratory system, the volume where the outward forces of the chest wall match the inward forces of the alveoli is the resting (or equilibrium) lung volume, known as FunctionalResidual Capacity (FRC).

Taking a Breath

• Kate, tired of all these media photographers, takes a long breath.

• How does she do it?

http://news.bbc.co.uk/sport2/hi/olympics/athletics/7506976.stm

Note frozen smile

The Respiratory Muscles:

• Inspiratory muscles:– Diaphragm– External intercostals– Assessory muscles

• Scalenes, • Sternocleidomastoid

• Inspiration active – Expiration passive

• Diaphragm does 75% of inspiratory work

• Tidal breathing: dome descends 1-2 cm.

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• Kate’s inspiratory muscles must generate enough negative intrapleural pressure to overcome the intrinsic elastic recoil of the lungs.

• They are assisted by the chest wall (which has an intrinsic outward recoil at this respiratory system volume).

•Once intra-alveolar pressure is negative relative to atmospheric, air flows into the lungs

Air travels from a region of high pressure to low pressure. If pressure in the respiratory system (airways & alveoli is negative relative to atmospheric, air will flow into the lungs.

Normal (Tidal Volume) Breathing: “Breathe in, please”

Pleural Pressure

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•During normal Expiration, respiratory muscles stop contracting.

•Intrinsic elastic recoil of the lungs then takes over, creating enough positive pressure to push air out of the lungs

•Diaphragm, chest wall follows passively, deflating (it’s connected to alveolar forces by pleural fluid)

Normal (Tidal Volume) Breathing: “Breathe out, please”

Pleural Pressure

Welcome to Beijing

Small particulate levels (PM10) 150 mcg/m3 (target < 50)

Starting the Race

• Kate starts the 10,000 m run, without her inhalers

• To keep up with her increased respiratory rate, she must exhale forcefully (or actively), to exhale fast enough

• How does she do this?

Forceful Expiration

• Expiratory muscles– Rectus abdominis– Internal intercostals– Internal and external

obliques– Transversus abdominis

• During active expiration, the abdominal muscles push the abdominal contents and thus diaphragm forcefully upwards, rapidly pushing air out of the lungs

EXPIRATION

Bigger Breaths

• Kate starts running faster, and starts taking deeper breaths. How does she increase her inspiratory volumes further?

• The descent of the diaphragm: – increases the vertical dimension of the thorax– Downward pressure by the diaphragm pushes the abdominal

contents downwards and forwards, further lifting the sternum forward, and expanding the rib cage

• The ribs are raised, sternum moves upward and forward (like a “pump handle”), increasing the anterior-posterior dimension of the thorax

• The ribs separate, increasing the lateral dimension of the thorax (like a “bucket handle”)

• During deep inspiration, the neck muscles (and sometimes even arm muscles) contract, raising the 1st rib & upper part of the thorax

– Visible accessory respiratory muscle activity indicates increased work of breathing

Breathing in Beijing

• Beijing’s smog starts to get to Kate. She starts to get an asthma attack.

• What normally keeps her airways open?• As she starts getting asthma, what happens to:

– Her Airways?– Her Airflow?– Her Time Constant?– Her Lung Volume?– Her Work of Breathing?

http://www.sportsister.com/?p=1063

What Keeps Bronchi Open (1)?

• Trachea and bronchi are surrounded by smooth muscle. These muscles are normally relaxed. In response to airway irritants (e.g. smoke, air pollution), the bronchial smooth muscles contract, narrowing the airways – In people with asthma, muscles are “hyper-

reactive,” narrowing in response to lower concentrations of irritants (e.g. air pollution) or substances that shouldn’t act as irritants (cold air, allergens, etc.)

– In response to irritants (especially in people with asthma), airway mucosa becomes inflamed and swollen, and bronchi hyper-secrete mucous, further narrowing the airways

• Narrowing of the airways increases airway resistance

What Keeps Bronchi Open (2)?

• Lung volume: – Alveoli act like little springs. – Expansion of alveoli pulls the airway

open, expanding the airway

Turbulent Flow

Laminar

Transitional

Turbulent

• In the presence of increased airflow speed (rapid breathing) and increased airway resistance (asthma), airflow becomes more transitional and turbulent

• Kate must use higher inspiratory and expiratory pressures to achieve the flow rates she needs to breathe quickly, and airway resistance will be further increased

An Olympic Time (Constant)

• Time Constant (τ) = Resistance x Compliance• With her increased airway resistance, Kate’s Time

Constant will increase• She’ll need more time to inflate or deflate the

lungs (especially deflate, since the airways are compressed more by positive pleural pressure during forced expiration)

Dynamic Hyperinflation

• Since her expiratory time will be shorter than her time constant, Kate’s lungs will inflate until alveoli are so overinflated and stiff that the time constant shortens

• Leads to elevation of FRC and hyperinflation

FRC

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Effects of Dynamic Hyperinflation

• Dynamic Hyperinflation will:– Increase her work of breathing

(inspiratory muscles need to generate more pressure to inflate her lungs)

– Reduce her airway resistance a little, as more-inflated alveoli will open her bronchi a little

FRC

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How can Kate reduce her Work of Breathing?

• During rapid breathing, flow rates are higher, and the viscous (dark green) work area is increased, as more work is needed to overcome tissue (tissue expansion) and airway resistance, more rapidly.

• Kate, given her airway obstruction, will need to expend more energy overcoming viscous resistance

• To avoid this, her coach will have taught her to try and breathe slower but deeper, since it takes less energy to overcome the additional elastic forces than would be needed to overcome her markedly increased viscous work

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FRC

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Hypoxia’s Bad for You (especially during an Olympic race)

http://www.telegraph.co.uk/sport/othersports/olympics/2566345/Kate-Reed-hits-out-after-flop-in-10000m---Olympics.html

Gas Exchange During an Asthma Attack

• During an asthma attack, different airways have different degrees of bronchoconstriction and airflow obstruction

• Total amount of air entering and leaving the lungs and total blood flow to the lungs doesn’t change (at least early on)

• So why would Kate’s arterial oxygen tension and saturation drop?

Ventilation 4.8 L/min

Ventilation 2.4 L/minVentilation 2.4 L/min

PAO2 101PACO2 40

PAO2 101PACO2 40

Perfusion 3 L/min Perfusion 3 L/min

PpaO2 40SpaO2 70PpaCO2 46

PaO2 101SaO2 98PaCO2 40

PpvO2 101SpvO2 98PpvCO2 40

PpvO2 101SpvO2 98PpvCO2 40

PpaO2 40SpaO2 70PpaCO2 46

Lt Atrium

LEGEND:

pa: Pulmonary Arterypv: Pulmonary vein

Values adapted from: Murray, “The Normal Lung” Saunders, 1986.

Regional Differences in Ventilation: Perfect V/Q Matching

Ventilation 4.8 L/min

Ventilation 1.2 L/minVentilation 3.6 L/min

PAO2 105PACO2 36

PAO2 77PACO2 45

Perfusion 3 L/min Perfusion 3 L/min

PpaO2 40SpaO2 70PpaCO2 46

PaO2 92SaO2 97PaCO2 39

PpvO2 105SpvO2 98PpvCO2 36

PpvO2 77SpvO2 95PpvCO2 45

PpaO2 40SpaO2 70PpaCO2 46

Lt Atrium

Regional Differences in Ventilation: Kate - V/Q Mismatch

Total Ventilation & Perfusion haven’t changed

Just VQ mismatch will reduce SaO2

Minimizing the Impact of V/Q Mismatch

• Kate’s lungs will attempt to minimize the effect of V/Q mismatch by vasoconstricting the pulmonary arteries supplying poorly ventilated areas of lung

• This will not fully compensate for the effects of V/Q mismatch as blood supplying poorly-ventilated regions will still emerge from the lung less-well oxygenated, reducing overall blood oxygen saturation in the LA

– However, the better the lungs can compensate, minimizing blood flow to poorly-ventilated lung regions, the lower the impact of poorly-oxygenated pulmonary venous blood will be on systemic arterial oxygen saturation

• Pulmonary arteries are able to sense alveolar PAO2, and vasoconstrict when alveolar PAO2 is low.

– This activity is mediated by Nitric Oxide (NO)

V/Q Mismatch – Clinical Correlates

• Our lungs attempt to V/Q mismatch all the time – when we’re slouching, lying on one side…

– This effect is even more important during any disease state affecting the airways (e.g. asthma), or the alveoli (e.g. pneumonia)

• V/Q mismatch is the main cause of hypoxemia in the great majority of lung diseases

• In severe, advanced lung disease, all the pulmonary arterioles sense that the alveoli they’re serving are hypoxic, and they all vasoconstrict (hoping to redirect blood to better functioning alveoli)

– If all the pulmonary arteries vasoconstrict at the same time, this raises main Pulmonary Artery Pressure

– This, in turn, raises RV pressure– The RV handles pressure loads poorly, and quickly fails. – This is the mechanism whereby hypoxia due to end-stage lung disease leads to

Pulmonary Hypertension, and Cor Pulmonale.

Ventilation/Perfusion Inequality

• Regional differences in ventilation leads to reduced PaO2 • In other words, V/Q mismatch alone will lead to hypoxia• Kate finishes a disappointing 23rd in her race

– (but actually mainly because of a calf injury)

.

Back to Bristol for a Check-up

• After her time breathing smoggy air in Beijing, Kate returns to Bristol and visits her asthma specialist for a check-up

• She has a PFT• What’s different about

airflow on a PFT, in someone with asthma?

Kate’s usual forced expiration and flow-volume curve in Bristol

EARLY LATE

+10

+10

+10

+10

+10

+10

+10

+10+5+20

+18+14

+12+10

+15

+12+10

FLOW

VOLUMEminmax

+5

NORMAL

+10

+10

+10

+10

+10+20

+18+14

+12+10

FLOW

+10

+10

+10

+10

+10+20

Kate’s forced expiration, and her flow-volume curve, after visiting Beijing!

OBSTRUCTED

VOLUMEminmax

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What About Kate’s Residual Volume?

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+2

+12

+10+11

+10

+4

+14

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Normal Small-airways disease(“Gas Trapping")

So What About All her Lung Volumes?

TLC

FRC

RV

VC

Usual Post-Beijing

TLC elevated because of dynamic hyperinflation

FRC elevated because of dynamic hyperinflation

RV elevated because of gas trapping

VC decreased a little because TLC is elevated

a little, and RV is elevated a lot

How can we tell how inflamed and irritable Kate’s lungs are?

• Measure bronchial response– Bronchodilator response: 12% increase in FEV1 after bronchodilator

• Re-check her Methacholine challenge– A few labs do this routinely, as a measure of bronchial inflammation

and reactivity• Checking Residual Volume assesses airway obstruction involving the very

small airways– Equal pressure point will be right near the mouths of the alveoli

Best Friends

• Kate makes two lifelong friends in Beijing, Elina and Alicia

• Elina’s very tall• Alicia’s very short• Both have normal lungs.• Which is more likely to

develop a spontaneous pneumothorax, sometime in her life?

• Why?

Elina Alicia

The Lungs in Space

• Lungs are attached to body at the hila, which are located fairly high up in the chest

• Lungs dangle within the chest, like a phone dangling on a coiled telephone cord

• With normal body motion, alveoli at top are stretched more than alveoli at the bottom (just like coils @ the top versus coils @ the bottom)

• Alveoli at the top get more wear and tear, and are more likely to rupture, causing a spontaneous pneumothorax

• This effect is exaggerated (and more likely to happen) in tall, thin people – sorry Elina!

Stretched

Not-so-stretched

Regional Differences in Ventilation

• Alveoli near top of lungs are more open, but also start inspiration closer to the top of their pressure-volume curves, so they don’t get much bigger (and therefore don’t receive much fresh air) during inspiration– These alveoli don’t ventilate very well

• Alveoli near bottom of the lungs are more compressed, but start inspiration near the bottom of their pressure-volume curves, so they inflate a lot (and therefore receive a lot of fresh air) during inspiration– These alveoli ventilate very well P

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Regional Differences in Perfusion

• Pulmonary arterial blood flow from the heart to the lungs follows the influence of gravity – so more blood flows to the lower lobes than to the apices

Amount of Blood Flow

Matching Ventilation and Perfusion

• Since there’s more ventilation to the lower lobes and more perfusion to the lower lobes, the body maintains ventilation-perfusion matching, optimizing oxygenation of arterial blood

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VENTILATION PERFUSION=

Ventilation-Perfusion Matching

• Minor differences in ventilation between lung units (such as different zones of the lung) will lead to ventilation-perfusion inequality and desaturation

• You generate some ventilation-perfusion inequality every time you slouch

• The lungs minimize this effect by design (apex gets less ventilation and perfusion) and V/Q matching by pulmonary arterioles

Elina’s Bad Day

• About a year later, Elina hears a particularly funny joke about the American Basketball Team

• During a fit of laughter, she develops sharp chest pain, complains of severe difficulty breathing, and turns a bit bluish

Elina’s X-ray

Elina’s X-ray

• What’s happened to her right lung?

• Why’s her chest so much larger on the right side?

Spontaneous Pneumothorax

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FRC

•Alveolar rupture allows air to fill pleural space

•Air prevents pressures generated by chest wall and lungs from interacting with each other

•Lungs naturally collapse

•Chest wall naturally recoils out

•Spontaneous rupture is much commoner at apex (where lung has more wear) & in tall, thin people, where effect is exaggerated Pleural Pressure

Questions?