RESPIRATORY SYSTEM

dr. Sri Lestari Sulistyo Rini, MSc

Respiratory System

Functions of the Respiratory System

Exchange O2

Air to blood Blood to cells

Exchange CO2 Cells to blood Blood to air

Regulate blood pH

Vocalizations Protect alveoli

Function of the Nose

The only externally visible part of the respiratory system that functions by: Providing an airway for respiration Moistening and warming the entering air Filtering inspired air and cleaning it of

foreign matter Serving as a resonating chamber for

speech Housing the olfactory receptors

Conducting Zone: Bronchi

The carina of the last tracheal cartilage marks the end of the trachea and the beginning of the right and left bronchi

Air reaching the bronchi is: Warm and cleansed of impurities Saturated with water vapor

Bronchi subdivide into secondary bronchi, each supplying a lobe of the lungs

Air passages undergo 23 orders of branching in the lungs

Respiratory Zone

Defined by the presence of alveoli; begins as terminal bronchioles feed into respiratory bronchioles

Respiratory bronchioles lead to alveolar ducts, then to terminal clusters of alveolar sacs composed of alveoli

Approximately 300 million alveoli: Account for most of the lungs’ volume Provide tremendous surface area for gas

exchange

Breathing (ventilation): air in to and out of lungs

External respiration: gas exchange between air and blood

Internal respiration: gas exchange between blood and tissues

Cellular respiration: oxygen use to produce ATP, carbon dioxide as waste

Four Respiration Processes

Lung Volumes: Spirometer Measurements

PULMONARY VOLUMES, CAPACITIES, AND RATES

SPIROGRAM

Volumes tidal volume (500 ml)

anatomical dead space (150 ml)alveolar ventilation (350 ml)physiological dead space

inspiratory reserve volume (3000 ml)expiratory reserve volume (1200 ml)residual volume (1300 ml)

Capacities total lung capacity (TV+IRV+ERV+RV)vital capacity (TV+IRV+ERV) (4700 ml)inspiratory capacity (TV+IRV)functional residual capacity (RV+ERV)

Ratesmaximum voluntary ventilation = TV x breaths/minutealveolar ventilation rate = alveolar ventilation x breaths/minute

IRV

ERV

TV

RVmaximum expiration

VC TLC

6000 ml

5000 ml

4000 ml

3000 ml

2000 ml

1000 ml

maximum inspiration

Lung Volumes: Spirometer Measurements

PHYSIOLOGY OF RESPIRATION

Concepts related to pulmonary ventilation (breathing)

- inspiration (inhalation) vs. expiration (exhalation)- atmospheric pressure- intrapulmonic pressure- pressure gradient

Boyle’s Law

Boyle’s law – the relationship between the pressure and volume of gases

P1V1 = P2V2

P = pressure of a gas in mm Hg V = volume of a gas in cubic millimeters Subscripts 1 and 2 represent the initial

and resulting conditions, respectively

Pressure Relationships in the Thoracic Cavity

Respiratory pressure is always described relative to atmospheric pressure

Atmospheric pressure (Patm) Pressure exerted by the air surrounding the

body Negative respiratory pressure is less than Patm Positive respiratory pressure is greater than Patm

Pressure Relationships in the Thoracic Cavity

Intrapulmonary pressure (Ppul) – pressure within the alveoli

Intrapleural pressure (Pip) – pressure within the pleural cavity

Pressures

Atmospheric pressure – 760 mm Hg, 630 mm Hg here

Intrapleural pressure – 756 mm Hg – pressure between pleural layers

Intrapulmonary pressure – varies, pressure inside lungs

Alveolar Pressure Changes

Inspiration

Begins with the contraction of the diaphragm and the external intercostals

This causes thoracic volume to Which causes lung volume to Which causes lung pressure to Now Palv is <Patm so air will flow

down its pressure gradient and enter the lungs.

Inspiration ends when Palv=Patm

Inspiration

The diaphragm and external intercostal muscles (inspiratory muscles) contract and the rib cage rises

The lungs are stretched and intrapulmonary volume increases

Intrapulmonary pressure drops below atmospheric pressure (1 mm Hg)

Air flows into the lungs, down its pressure gradient, until intrapleural pressure = atmospheric pressure

Pressure – Volume Relationships

As vol. , pressure As vol. , pressure This is given by Boyle’s

Law which says: P1V1 = P2V2

Why does this occur? Remember, pressure

equals force/areaP = Force/Area

So, in this equation as A gets larger P must get smaller

Active processBoyle’s Law

INSPIRATION

air molecule

decrease volume increase pressure

increase volume decrease pressure

FORCED INSPIRATIONRESTING INSPIRATION

external intercostals(11 pairs)

diaphragm

sternocleidomastoidscalenes

Inspiratory musclesPhrenic nerves (C3-5)Thoracic nerves (T1 – T11)

thoracic volume pleural volume intrapleural pressure lung volume intrapulmonic pressureair flow into the lungs

760 mmHg

760 mmHg

760 mmHg

758 mmHg

BEFORE INSPIRATION DURING INSPIRATION

Process

Expiration

Inspiratory muscles relax and the rib cage descends due to gravity

Thoracic cavity volume decreases Elastic lungs recoil passively and

intrapulmonary volume decreases Intrapulmonary pressure rises above

atmospheric pressure (+1 mm Hg) Gases flow out of the lungs down the

pressure gradient until intrapulmonary pressure is 0

Expiration

Quiet expiration is a passive process that is due to the elasticity of the lungs. What pressure and volume

changes occur during quiet expiration?

Forced expiration is an active process due to contraction of oblique and transverse abdominus muscles, internal intercostals, and the latissimus dorsi.

Passive process at rest

EXPIRATION

internal intercostals(11 pairs)

internal intercostals (11 pairs)rectus abdominisabdominal obliquestransversus abdominis

Forced expiration

thoracic volume pleural volume intrapleural pressure lung volume intrapulmonic pressureair flow of the lungs

Process

external abdominal oblique

internal abdominal oblique

transversus abdominis

rectus abdominis

760 mmHg

762 mmHg

elastic recoilsurface tension

Factors that influence pulmonary air flow

F = P/R Diameter of airways, esp.

bronchioles Sympathetic & Parasympathetic NS

Factors Affecting Ventilation Airway Resistance Diameter Mucous blockage Bronchoconstrictio

n Bronchodilation Alveolar

compliance Surfactants Surface tension

Alveolar elasticity

Airway Resistance

Due primarily to diameter of the conducting tubes.

How increased parasympathetic affect tube diameter? How would it affect airway resistance?

Histamine causes massive bronchoconstriction.

When might one experience massive histamine release? Why treat it with epinephrine?

Local accumulations of mucus, infectious materials or solid tumors are also sources of airway resistance.

DEAD SPACE Tidal volume NOT used in gas exchange Anatomical: conducting pathways

(150mls) Alveolar: gas reach alveoli, not enough blood supply due to: - Pulmonary embolism - Non vascular air space

Physiological dead space= anatomical + alveolar

Types of Dead Space

Anatomic dead space That contained in the conducting airways

Alveolar dead space That contained in the respiratory portion

of the lung Physiologic dead space

The anatomic dead space plus alveolar dead space

Efficiency of Breathing: Normal & High Demand

Total Pulmonary Ventilation(rate X tidal vol about 6 L/min)

Alveolar ventilation(– dead air space – 4.5 L/min)

Little variation [O2] & [CO2] Exercise- High Demand

Depth of breathing Use inspiratory reserve

Matching Ventilation with Alveolar Blood Flow (Perfusion)

Mostly local regulation Low [O2] in alveoli vasoconstriction of

arteriole Reduced blood flow at rest

(lung apex ) saves energy

High blood [CO2] bronchodilation

VENTILATON-PERFUSION MATCHING

Alveolar gas

V

Q Capillary flow

Matching Ventilation and Perfusion

Required for exchange of gases between the air in the alveoli and the blood in pulmonary capillaries

Two factors interfere with the process: Dead air space and shunt

The blood oxygen level reflects the mixing of blood from alveolar dead space and physiologic shunting areas as it moves into the pulmonary veins

Efficiency of Breathing: Normal & High Demand

Figure 17-2 g: Anatomy Summary

FICK’S LAW Rate of transfer of a gas through a

sheet of tissue is proportional to tissue area difference in gas partial pressure diffusion constant

inversely proportional to tissue thickness

ΔPjaringan tebal

kL.gasV

difusioefperm ..

Respiratory Membrane

This air-blood barrier is composed of: Alveolar and capillary walls Their fused basal laminas

Alveolar walls: Are a single layer of type I epithelial cells Permit gas exchange by simple diffusion Secrete angiotensin converting enzyme

(ACE) Type II cells secrete surfactant

Composition of the Alveolar Structures

Type I alveolar cells Flat squamous epithelial cells across

which gas exchange takes place Type II alveolar cells

Produce surfactant, a lipoprotein substance that decreases the surface tension in the alveoli and allows for greater ease of lung inflation

Respiratory Membrane

Factors Affecting Alveolar-Capillary Gas Exchange

Surface area available for diffusion Thickness of the alveolar-capacity

membrane Partial pressure of alveolar gases Solubility and molecular weight of

the gas

Lung Compliance

The ease with which lungs can be expanded

Specifically, the measure of the change in lung volume that occurs with a given change in transpulmonary pressure

Determined by two main factors Distensibility of the lung tissue and

surrounding thoracic cage Surface tension of the alveoli

Lung Compliance

Lung compliance (C) = (ΔV)/(ΔP) The change in lung volume (ΔV)

that can be accomplished with a given change in respiratory pressure (ΔP)

Compliance is the ease with which the lungs and thoracic wall can be expanded during inspiration.

COMPLIANCE

elasticitysurface tension

Related to two factors:

destroys lung tissue (emphysema)fills lungs with fluid (pneumonia)produces surfactant deficiency (premature birth, near-drowning)interferes with lung expansion (pneumothorax)

Compliance is decreased with any condition that:

Alveolar Surface Tension

Surface tension – the attraction of liquid molecules to one another at a liquid-gas interface

The liquid coating the alveolar surface is always acting to reduce the alveoli to the smallest possible size

Surfactant, a detergent-like complex, reduces surface tension and helps keep the alveoli from collapsing

Factors That Diminish Lung Compliance

Scar tissue or fibrosis that reduces the natural resilience of the lungs

Blockage of the smaller respiratory passages with mucus or fluid

Reduced production of surfactant Decreased flexibility of the thoracic

cage or its decreased ability to expand

Pons centers Influence and modify activity of the

medullary centers Smooth out inspiration and expiration

transitions and vice versa Pneumotaxic center – continuously

inhibits the inspiration center Apneustic center – continuously

stimulates the medullary inspiration center

Control of Respiration: Pons Respiratory Centers

Respiration Regulation In the pons, there are 2 more respiratory

centers: the pneumotaxic and the apneustic centers.

The apneustic center acts to prolong inspiration or cause breath holding in the inspiratory phase.

The pneumotaxic center inhibits the apneustic center and promotes exhalation

They both act to smooth the transition btwn inspiration and expiration.

Control of Breathing

Automatic regulation of ventilation Controlled by input from two types of

sensors or receptors: Chemoreceptors: monitor blood levels of

oxygen, carbon dioxide and adjust ventilation to meet the changing metabolic needs of the body

Lung receptors: monitor breathing patterns and lung function

What factors affect breathing?

Respiratory control centers are sensitive tocarbon dioxide and hydrogen levels

If those rise (in blood), breathing rate increasesLow blood oxygen can also be detected

Hyperventilation lowers blood carbon dioxidelevels; can lead to blood alkalosis(slows breathing rate)

Respiratory Reflexes Respiratory center activity is modified by:1. Chemoreceptors sensitive to the Pco2, pH,

or Po2 of the blood or CSF2. BP changes detected in the carotid or

aortic sinuses3. Lung stretch receptors (Hering-Breuer

Reflex)4. Irritating physical or chemical stimuli in

the respiratory tract5. Other sensations (pain, emotions)

Herring-Breuer Reflex

Limits the degree of inspiration and prevents overinflation of the lungs Infants

Reflex plays a role in regulating basic rhythm of breathing and preventing overinflation of lungs

Adults Reflex important only when tidal volume

large as in exercise

Respiration Regulation

There’s reciprocal inhibition btwn the inspiratory neurons and the expiratory neurons

During quiet respiration, the DRG is active for about 2 seconds (inspiration) and then is inactive for 3 seconds (expiration)

Respiration Regulation

During forced respiration, the level of DRG activity increases to where it activates VRG neurons.

Thus, we’ll have our normal inspiratory muscles plus our accessory inspiratory muscles activated.

At the end of the active inspiration, the VRG expiratory neurons initiate active expiration.

Depth and Rate of Breathing

Inspiratory depth is determined by how actively the respiratory center stimulates the respiratory muscles

Rate of respiration is determined by how long the inspiratory center is active

Respiratory centers in the pons and medulla are sensitive to both excitatory and inhibitory stimuli

Control of Respiration: Medullary Respiratory Centers

Depth and Rate of Breathing: Reflexes

Pulmonary irritant reflexes – irritants promote reflexive constriction of air passages

Inflation reflex (Hering-Breuer) – stretch receptors in the lungs are stimulated by lung inflation

Upon inflation, inhibitory signals are sent to the medullary inspiration center to end inhalation and allow expiration

Depth and Rate of Breathing: PCO2

Changing PCO2 levels are monitored by chemoreceptors of the brain stem

Carbon dioxide in the blood diffuses into the cerebrospinal fluid where it is hydrated

Depth and Rate of Breathing: PCO2

Resulting carbonic acid dissociates, releasing hydrogen ions

PCO2 levels rise (hypercapnia) resulting in increased depth and rate of breathing

Factors Affecting Breathing

Depth and Rate of Breathing: Higher Brain Centers

Hypothalamic controls – act through the limbic system to modify rate and depth of respiration Example: breath holding that occurs in anger

A rise in body temperature acts to increase respiratory rate

Cortical controls – direct signals from the cerebral motor cortex that bypass medullary controls Examples: voluntary breath holding, taking a

deep breath

NEGATIVE FEEDBACK CONTROL

CONTROLLED CONDITIONA stimulus or stress disrupts

homeostasis by causing a decrease in arterial oxygen or an increase in carbon

dioxide and/or hydrogen ions

RECEPTORChemosensitive neurons in medulla and

chemoreceptors in aortic and carotid bodies respond to changes and direct nerve impulses to the control center

CONTROL CENTERInspiratory neurons of medulla interpret

sensory input and generate nerve impulses that pass ultimately to effectors

EFFECTORSMuscles of inspiration contract more often

and more forcefully (hyperventilation)

RETURN TO HOMEOSTASISHyperventilation results in increase in

arterial oxygen and/or pH, and/or decrease in arterial carbon dioxide

Modifying Respiration

Depth and Rate of Breathing: PCO2

Hyperventilation – increased depth and rate of breathing that: Quickly flushes carbon dioxide from the blood Occurs in response to hypercapnia

Though a rise in CO2 acts as the original stimulus, control of breathing at rest is regulated by the hydrogen ion concentration in the brain

Hypoventilation – slow and shallow breathing due to abnormally low PCO2 levels Apnea (breathing cessation) may occur until

PCO2 levels rise

Pco2, Po2, and pH

Central and peripheral chemoreceptors The central are located on the medulla The peripheral are located in the carotid

sinus and aortic arch. The central respond to pH (indirectly to

CO2) and are the most important. There are peripheral receptors for pH,

Pco2 and Po2. Of these pH and Pco2 are more important (but

still less so than the central chemoreceptors)

High Pco2 = Hypercapnia

When Pco2 rises, it will activate peripheral Pco2 receptors, peripheral pH receptors, and central pH receptors.

All will respond by increasing respiration rate and depth.

Decrease in plasma pH independent of Pco2 changes will activate peripheral pH receptors but not central ones. Why?

CARBON DIOXIDE IN THE LUNGS

H+ + HCO3- H2CO3 H20 + CO2

carbonic anhydrase

HCO3-

CO2Cl-

CAPILLARY ENDOTHELIUM

4O2-HbH-HbO2

ALVEOLUS

diffusion

diffusion

1.5% O2

dissolved in plasma

98.5% O2

goes to Hb

CO2

Total7% from plasma23% from globin

70% from bicarbonate

Depth and Rate of Breathing: Arterial pH

Changes in arterial pH can modify respiratory rate even if carbon dioxide and oxygen levels are normal

Increased ventilation in response to falling pH is mediated by peripheral chemoreceptors

Acidosis may reflect: Carbon dioxide retention Accumulation of lactic acid Excess fatty acids in patients with diabetes

mellitus Respiratory system controls will attempt to raise

the pH by increasing respiratory rate and depth

Respiratory Adjustments: Exercise

As exercise begins: Ventilation increases abruptly, rises slowly,

and reaches a steady state When exercise stops:

Ventilation declines suddenly, then gradually decreases to normal

Neural factors bring about the above changes, including: Psychic stimuli Cortical motor activation Excitatory impulses from proprioceptors in

muscles

Diffusion Through Respiratory Membrane

Gases are exchanged between alveolar air and capillary blood because of differences in partial pressure

Oxygen-HemoglobinDissociation Curve at

Rest

Bohr effect:

Shifting the Curve

Regulation of Blood pH and Gases

TERIMA KASIH