Clinical Development Nurse PICU BRHFC - UH … · Clinical Development Nurse PICU BRHFC Respiratory Anatomy Function of the Respiratory System - In conjunction with the cardiovascular

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Respiratory Anatomy and Physiology

Michaela Dixon Clinical Development Nurse

PICU BRHFC

Respiratory Anatomy

Function of the Respiratory System

- In conjunction with the cardiovascular system, to supply oxygen to the cells

of the body and remove by-products of cellular metabolism (carbon dioxide)

Additionally the lungs play a major role in –

Maintaining homeostasis

Mounting a host defence response to potentially threatening organisms

Development of the Respiratory System

The development of the respiratory system in the

foetus is divided into five distinct phases

Embryonic period

Pseudoglandular period

Canalicular period

Saccular period

Alveolar period

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Embryonic Period

Ventral out-pouching from the foregut occurs between days 26 and 52

Foregut divides to form the oesophagus and trachea

Lung buds appear from the trachea

Primary bronchial buds split to form the main bronchi and the lung

lobes

Blood supply from the Pulmonary Artery


Pseudoglandular Period

Occurs from day 56 – week 16 of gestation

All major conducting airways including the terminal bronchioles are

formed

Arterial blood supply increases

Diaphragm is derived from the fusion of pleuro-peritoneal fields

(normally between 8 -10 weeks)


Canalicular Period

Occurs week 16 – 26 of gestation

Development of the respiratory bronchioles each of which ends in a

small dilated bulge (primitive alveoli)

Continued development of the pulmonary vascular beds

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Saccular Period

Occurs week 24 – 38 of gestation

Lung vascularisation intensifies

Development of elastic fibres

Close contact between air spaces and capillaries develops

True alveoli present by week 34 of gestation

Gas exchange is possible throughout this period but not optimal


Alveolar Period

Occurs week 36 onwards (to term)

Further refinement of terminal sacs and walls of true alveoli

Development of columnar cells into two types

Type One – alveolar surface area

Type Two – surfactant production

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Respiratory System Physiology

Pressure changes associated with respiration

Before inspiration (diaphragm relaxed)

Atmospheric pressure = Alveolar pressure

760mmHg = 760mmHg

No air movement

Inspiration (diaphragm contracting)

Atmospheric pressure > Alveolar pressure

760mmHg > 758mmHg

Air moves into the lungs


Pressure changes associated with respiration:

Inspiration (diaphragm contracting)

Atmospheric pressure > Alveolar pressure

760mmHg > 758mmHg

Air moves into the lungs

Expiration (diaphragm relaxing)

Atmospheric pressure < Alveolar pressure

760mmHg < 762mmHg

Air is expelled by the lungs


Pulmonary Volumes and Capacities

Tidal Volume (TV or Vt)

The volume of air entering and leaving the lungs in a single breath in the resting

state

Tidal volume is constant throughout life at between 6 – 8mls/kg

Infant of 3kgs: TV = 18 - 24mls (6 / 8 x 3)

Adult of 70kgs: TV = 420 – 560mls (6 /8 x 70)

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Inspiratory Reserve Volume (IRV)

The amount of air that can be inspired over and above the resting tidal volume

Expiratory Reserve Volume (ERV)

The volume of air remaining in the lungs at the end of normal expiration which

may be exhaled by active contraction of the expiratory muscles



Residual Volume (RV)

The amount of air remaining in the lungs after maximal expiration – presence of

this prevents the lungs from emptying completely

Vital Capacity (VC)

The sum of normal tidal volume, inspiratory reserve volume and expiratory

reserve volume

Infants: 33 – 40ml/kg

Adults: 52ml/kg



Functional Residual Capacity (FRC)

The amount of air remaining in the lungs at the end of normal expiration

In the presence of atelectasis FRC falls as the number of alveoli participating in

gas exchange decreases

SO WHAT?

Airway closure (complete collapse) occurs in areas of the lungs that have low

volumes – this is known as the closing volume or capacity

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Importance

In adults – closing capacity is usually at residual volume

(amount of air remaining in the lungs after maximal expiration)

In infants – closing capacity is at FRC due to the reduced elasticity of lung tissue,

therefore closing capacity may be present during normal tidal breathing



Functional Residual Capacity (2)

Any pulmonary disease which affects the relationship between tidal volume, FRC

and closing capacity will contribute significantly to ventilation – perfusion

mismatching and hypoxia

Chronic Lung Disease (infants)

Cystic Fibrosis

Asthma

Bronchiolitis

Pneumonia



Dead Space

Anatomic dead space – the volume of conducting air that fills the nose, mouth,

pharynx, larynx, trachea, bronchi and distal bronchial branches which does not

participate in gas exchange

Normal anatomic dead space is 2ml/kg

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Dead Space

Alveolar dead space – the volume of gas which fills alveoli whose perfusion is

either reduced or absent

Contributing Factors:

Hypotension

Compression of the alveolar capillary bed

Pulmonary embolism



Physiologic Dead Space

The sum of both anatomic and alveolar dead space

Dead Space Ventilation

The amount of gas ventilating physiologic dead space per minute. It is expressed

as a fraction of TV

Normal ratio is 0.3 (30%) which means that 30% of the volume of each breath

does not participate in gas exchange


Surfactant

Pulmonary surfactant is a mixture of

Phospholipids produced by -

Type II alveolar Pneumocytes

Function of surfactant is to

Lower surface tension

Increase compliance

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Surfactant: How does it work? Each alveoli is lined with a water containing fluid film Due to the polarity of the water molecules they act as weak magnets, pulling towards each other. This force also pulls the alveoli walls inwards causing them to collapse increasing the surface tension The presence of surfactant acts as a barrier against these forces preventing the collapse of the alveoli (Smaller alveoli generate greater forces – clinical implication for infants)

Gas Laws

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The total pressure of a gas is the

sum of all the partial pressure of

the gases within the mixture -

Normal atmospheric air consists

of:

Oxygen

Nitrogen

Carbon Dioxide

Water

Atmospheric pressure is 760mmHg


Gas Laws – Boyles Law

The volume of a gas varies inversely with pressure assuming constant

temperature

In order for inspiration to occur the lungs expand, reducing the pressure

within – this facilitates the movement of gas along the pressure gradient

When expiration occurs the lungs recoil, increasing pressure within -

consequently reducing the volume of air present


Gas Laws – Charles Law

The volume of a gas is directly proportional to temperature assuming

pressure is constant

When a gas is heated, the molecules move faster – the force exerted by the

molecules causes expansion of the gas volume

When gases enter the warmer lungs, gases expand increasing lung volumes

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Gas Laws – Henrys Law

The quantity of a gas that will dissolve in a liquid is proportional to the partial

pressure and its solubility coefficient (physical attraction to water) when

temperature is constant

The higher the partial pressure of a gas over a liquid the more gas will stay in

solution



Example:

78% of room air is Nitrogen but little dissolves in the plasma because it has a

low solubility coefficient

In compressed air used by divers, nitrogen dissolves in plasma because of

altered partial pressures - if a diver returns to the surface too quickly

nitrogen bubbles remain in the blood stream causing the ‘Bends’



Clinical Application –

Solubility co-efficient of CO2 is high but O2 is low and N2 is very low therefore

a reduction in haemoglobin will significantly impact on oxygen carrying

capacity and delivery as there is no real alternative transport system

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Gas Laws – Ficks Law

Diffusion through tissue is proportional to the partial pressure of the gas and

the difference in the partial pressures on the two sides

It is inversely proportional to the thickness of the tissue


Gas Laws – Ficks Law

Clinical Application –

Children with chronic lung conditions such as CF or CLD post prematurity will

have decreased capacity for effective gas exchange if they have developed

fibrotic changes in their lung parenchyma.

These children are at greater risk of respiratory failure secondary to infection

than those with normal healthy lungs

Gas Exchange

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Gas Exchange

All organ systems depend to varying degrees on the delivery of oxygen to

maintain normal cellular metabolism

The primary function of the respiratory system is to move O2 from the air

to the blood and CO2 from the blood to the air



Gas Exchange

This process of gas exchange involves three stages

Pulmonary ventilation

External respiration

Internal respiration

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Pulmonary ventilation

Movement of air is between the lungs and the atmosphere is

dependent on the existence of a pressure gradient and lung

compliance

Compliance is a measure which reflects the ease with which the lungs and thoracic wall expand

Compliance is dependent upon elasticity (elastic recoil) and

surface tension

Decreased compliance = poor chest wall movement


External Respiration

Exchange of O2 and CO2 between the alveoli and the pulmonary

capillaries

Conversion of deoxygenated blood to oxygenated blood

O2 and CO2 exchange occur through diffusion (Ficks Law applies)

This process is aided by several anatomical features


External Respiration

Total thickness of the alveolar-capillary membrane is only 0.5

micrometres

Lungs have an enormous surface area – up to 70m2 / 753ft2 by

adulthood

Multiple capillaries lying over each alveoli allow 100ml of blood to

participate in gas exchange at any one time

Structure of the pulmonary capillaries is designed to give maximum

exposure to facilitate gas exchange

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Internal Respiration

Oxygenated blood (transported by the circulatory system) leaves the

lungs and is delivered to the tissue cells

Exchange of O2 and CO2 occurs again at this point through diffusion

and the presence of a concentration gradient

At rest only 25% of available O2 is extracted by the cells to meet their

metabolic demands

Ventilation – Perfusion Mismatch

Gas exchange becomes optimal when both ventilation and pulmonary blood

flow are equally matched

Under normal conditions the ventilation – perfusion ratio (V/Q) is less than 1.0

This is because gravitational forces create regional differences in intra-pleural

pressure and pulmonary pressures


Intrapulmonary shunting is the major cause of clinical hypoxaemia A shunt refers to venous blood that travels from the right to left side of the circulation without ever coming into contact with ventilated lung Anatomic shunt Capillary shunt - occurs when the alveolar-capillary blood flow comes into contact with non ventilating alveoli

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Venous blood passing non-functioning alveoli creates an admixture of venous

and arterial blood which decreases the PaO2

Venous admixture represents the ratio of shunted blood (Qs) to total

pulmonary blood flow (Qt)

Normal Qs/Qt is 3-7%

Changes of more than 5% are considered significant

Work of breathing significantly increases when the Qs/Qt is greater than 15%

Oxygenation Index

Oxygenation Index (OI)

OI = Mean Airway Pressure x FiO2 (%)

PaO2 (mmHg)

OI < 5 = Normal

OI > 10 = Severe oxygenation problem

OI > 20 = Extreme oxygenation problem

Transportation of Gases

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Oxygen Transportation

Almost all of the oxygen transported in systemic arterial blood is chemically

bound to haemoglobin - approx 98.5% (1.5% is dissolved in plasma)

Normal haemoglobin consists of 4 O2 binding sites

Because so much oxygen is trapped inside red cells through binding, there are

a number of factors which influence the ease with which it binds or

dissociates from haemoglobin


OXYHAEMOGLOBIN DISSOCIATION CURVE

Reflects the relationship between the % saturation of

haemoglobin and oxygen partial pressure


The OHDC can move either to the right or to the left

A right shift means that oxygen will be released by haemoglobin easily but it is more difficult for it to bind

A left shift means that oxygen will bind easily with haemoglobin but it is more difficult for it to be released

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Factors affecting Oxygen binding / release

Partial pressure of oxygen

Acidity (blood pH)

Carbon Dioxide

Temperature

BPG (2,3 bisphosphoglycerate)


The most important factor which determines how much O2 binds to haemoglobin is the Partial Pressure of oxygen

When PO2 is high – haemoglobin binds with large amounts of oxygen and is almost 100% saturated

Therefore in the pulmonary capillaries where the PO2 is high (because PO2 in

atmospheric air is higher) a lot of oxygen binds with haemoglobin


In the tissue capillaries where PO2 is lower – haemoglobin does not hold as much oxygen therefore oxygen is released for use by the tissues through diffusion

At a PO2 of 40mmHg (5.4kPa) which is tissue capillary PO2 haemoglobin is still 75% saturated

WHY?

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Acidity (Blood pH)

As acidity increases the pH of blood will decrease

As pH decreases the affinity of haemoglobin for O2 decreases and more O2

becomes available for the tissues

This is reflected in a shift in the OHDC to the right and at any given PO2

haemoglobin will be less saturated with O2 – known as the Bohr effect


Acidity (Blood pH)

Clinical Relevance:

Haemoglobin can act as a buffer for acids (H+ ions) in the blood to maintain

blood pH within normal limits

The process of binding hydrogen ions to the amino acids in haemoglobin

causes a slight change in the structure of haemoglobin, decreasing its O2

carrying capacity


Carbon Dioxide

Acts in a similar way to acidity – as PCO2 increases blood pH decreases and

the OHDC shifts to the right

Consequently O2 is released by haemoglobin more easily

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BPG (2,3 bisphosphoglycerate)

Decreases the affinity of haemoglobin for O2 therefore making it more available

to the tissues

BPG is produced by the red cells when they metabolise glucose to produce ATP

(energy)

Increased energy demands from cells cause an increase in BPG levels

OHDC shifts to the right


Temperature

As temperature increases the OHDC moves to the right and more oxygen is

released to the tissues

Heat is a by-product of the metabolic activity in the cells – the heat of contracting muscle fibres tends to raise body temperature

Metabolically active cells require more O2 to maintain anaerobic metabolism – a by-product of increased metabolism is the production of acids

Control of Respiration

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Breathing is an involuntary process that is controlled by the medulla and pons

of the brain stem.

The frequency of normal, involuntary breathing is controlled by three groups

of neurons or brain stem centres;

the medullary respiratory centre

the apneustic centre

the pneumotaxic centre


Central Chemoreceptors The central chemoreceptors located in the brain stem, are the most important for the minute-to-minute control of respiration These chemoreceptors are located on the ventral surface of the medulla, near the point of exit of the Glossopharyngeal and Vagus nerves and only a short distance from the medullary inspiratory centre Central chemoreceptors communicate directly with the inspiratory centre

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The brain stem chemoreceptors are exquisitely sensitive to changes in the Ph

of cerebrospinal fluid (CSF)

Decreases in the pH of CSF produce increases in respiratory rate (hyperventilation)

Increases in the pH of CSF produce decreases in respiratory rate (hypoventilation)


Peripheral Chemoreceptors

There are peripheral chemoreceptors for O2, CO2 and H+ in the carotid bodies

located at the bifurcation of the common carotid arteries and in the aortic

bodies above and below the aortic arch

Information about PaO2 / PaCO2 and pH is relayed to the medullary inspiratory

centre which orchestrates an appropriate change in breathing rate



Decreases in PaO2 are the most important responsibility of the peripheral

chemoreceptors

BUT

Peripheral chemoreceptors are relatively insensitive to changes until PaO2 reaches

60mmHg or less (< 8kPa)

Once in this range of PaO2 the chemoreceptors are exquisitely sensitive to O2

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Decreases in arterial pH cause an increase in ventilation mediated by peripheral

chemoreceptors for H+

This effect is independent of changes in the PaCO2 and is mediated only by

chemoreceptors in the carotid bodies (not by those in the aortic bodies)

Thus, in metabolic acidosis, in which there is decreased arterial pH, the

peripheral chemoreceptors are stimulated directly to increase the ventilation

rate



The peripheral chemoreceptors also detect increases in PaCO2 but the effect is

less important than their response to decreases in PaO2

Detection of changes in PaCO2 by the peripheral chemoreceptor is also less

important than detection of changes in PaCO2 by the central chemoreceptors


Lung stretch receptors

Mechanoreceptors are present in the smooth muscle of the airways. When

stimulated by distention of the lungs and airways, mechanoreceptors initiate a

reflex decrease in breathing rate called the Hering-Breuer reflex. The reflex

decreases breathing rate by prolonging expiratory time

Joint and muscle receptors

Mechanoreceptors located in the joints and muscles detect the movement of

limbs and instruct the inspiratory centre to increase the breathing rate.

Information from the joints and muscles is important in the early (anticipatory)

ventilatory response to exercise

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Irritant receptors

Irritant receptors for noxious chemicals and particles are located between

epithelial cells lining the airways. Information from these receptors travels to

the medulla and causes a reflex constriction of bronchial smooth muscle and an

increase in breathing rate

J receptors

Juxtacapillary (J) receptors are located in the alveolar walls and therefore, are

near the capillaries. Engorgement of pulmonary capillaries with blood and

increases in interstitial fluid volume may activate these receptors and produce

an increase in the breathing rate

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Clinical Development Nurse PICU BRHFC - UH … · Clinical Development Nurse PICU BRHFC Respiratory Anatomy Function of the Respiratory System - In conjunction with the cardiovascular