CHAPTER 34: Structure and Function of the Pulmonary System

Background Information:

Structures of pulmonary system:

- Upper airway
o Structures
□ Nasal cavity
□ Pharynx
□ Nasopharynx
□ Oropharynx
□ Laryngopharynx
o All lines with ciliated mucosa which cleans, warms and humidifies
inspired air
o Larynx = connects upper and lower airways
□ Endolarynx = supraglottis and true vocal cords (slit between
cords = glottis)
- Two lungs
o Left v. right
□ Left lung (upper and lower lobe)
□ Right lung (upper, middle, and lower lobe)
o Each lobe divided into segments and lobules
o Mediastinum = space between lungs
□ Contains: bronchi = set of conducting airways that deliver air
to each section of the lung; supported by lung tissue that surrounds it to prevent distortion or collapse during ventilation
o Diaphragm = dome-shaped muscle that separates the thoracic and abdominal cavities and its involved in ventilation (contraction  diaphragm
move down to increase volume of pleural cavity)
- Lower airway
o Structures
□ Trachea = connects larynx to bronchi
□ Divides into two bronchi at the carina (v. sensitive; if stimulated  coughing and airway narrowing)
□ Bronchi = conducting airways of the lungs

1
□ Aspirated fluids enter right lung rather than left because the right mainstream bronchus is slightly larger and more vertical than the
left (20-30° vs 45°)
□ Bronchi enter at hila (root of lungs)
□ Bronchi  hila  lobar bronchi  segmental
bronchi  subsegmental bronchi (non-respiratory

then respiratory)  terminal bronchioles  alveoli

o As you go down, ↓ velocity of airflow
optimal gas diffusion
□ Bronchial wall layers (3)
o Epithelial lining
□ Goblet cells = mucus secreting
□ Ciliated cells
□ Submucosal glands = mucus contributes to the mucous blanket that covers the bronchial epithelium
□ *Ciliated cells and goblet cells more sparse, smooth muscle thin, connective tissue thins near terminal bronchioles
o Smooth muscle
o Connective tissue

2
 □ Cartilage

□ Gas-Exchange Airways
□ Acinus (participates in gas exchange)
rd
o Respiratory bronchioles (16th - 23 divisions)
o Alveolar ducts  alveolar sacs
o Alveoli (primary gas-exchange units)
□ Type I alveolar cells – provide structure
□ Type II alveolar cells – secrete surfactant = lipoprotein that coats the inner surface of the alveolus and facilitates its
expansion during inspiration, lowers alveolar surface tension at end-expiration  prevents lung collapse
o Alveolar macrophages = mononuclear phagocytes of the lungs; ingest foreign material that reaches the alveolus and
prepares it for removal via
lymphatics
- Blood vessel

Pulmonary and Bronchial circulation

- Pulmonary has lower pressure and resistance that systemic
circulation (pulmonary arteries have 1/5th the amount of
pressure and thinner muscle layer)
o Mean pulmonary artery pressure = 18 mmHg (compared
to 81 for systemic)
o 1/3 pulmonary arteries filled at any time  increased
delivery of blood ≠ increase pulmonary artery pressure
- Pulmonary artery
o Divides  enters lung at hilus  travels with main
bronchus  branches with bronchus at every division
(always has an accompanying artery/ arteriole 
division at terminal bronchiole to form pulmonary
capillaries (part of alveolar septa) around acinus
- Alveolocapillary membrane = alveolar and capillary wall; thin
membrane made up of alveolar epithelium, alveolar basement
membrane, IS space, capillary basement membrane and the
capillary endothelium | This is where gas exchange occurs
- Normal perfusion = ~100 ml blood spread thin across 140 m2 alveolar SA
- Pulmonary vein = drains pulmonary capillaries, dispersed randomly, leave lung at hila, enter LA, no valves

3
- Bronchial circulation = supplies conducting airways, nerves, lymph nodes, large pulmonary vessels, and membranes (pleurae) that surround the lungs and
moisten inspired air.
o Capillaries will drain in its own venous system as well as into the pulmonary vein  pulmonary admixture or right-to-left shunting
o Does not participate in gas exchange
- Pulmonary lymphatic capillaries = deep, superficial; begin at bronchioles (not in acinus); fluid and alveolar macrophages go from alveoli  terminal
bronchioles  enter lymphatic system  drained by superficial lymphatic capillaries  leave hilus via mediastinal lymph nodes

Control of the Pulmonary Circulation

- Important cause of pulmonary artery constriction is low alveolar PAO2
o Another cause = acidemia
- Hypoxic pulmonary vasoconstriction = vasoconstriction caused by alveolar and pulmonary venous hypoxia
o One section of the lung involves  arterioles to that segment constrict  shunts blood to other segments of the lung
o All sections of lung  vasoconstriction occurs throughout pulmonary vasculature  pulmonary hypertension results
o Reversible is PAO2 is resolved
o Chronic alveolar hypoxia  permanent pulmonary artery hypertension  cor pulmonale and HF

Chest Wall and Pleura

- Chest wall = skin, ribs, intercostal muscles
o Protects lungs from injury
o Muscles work with diaphragm  muscular WOB
- Mechanics of Breathing WOB – Capacity to take in air is affected by the muscles required to breath
o WOB determined by muscular effort required for ventilation
□ Normally low, unless disrupted by disease:
□ Pulmonary edema  decrease lung compliance
□ Spinal deformity/ obesity  decrease chest wall compliance
□ Obstructed airways by bronchospasm or mucous plugging (asthma and bronchitis)
□ Increase WOB  increase in O2 consumption and metabolic demand  increase morbidity
o Major and minor accessory muscles
□ Major muscles of inspiration
□ Diaphragm (separated abdominal and thoracic cavities; dome shaped)
o Contracts  flattens, increase volume of thoracic cavity  negative pressure draws gas into lungs via upper airways and
trachea
□ External intercostals
o Elevates the anterior portion of ribs  increase volume of thoracic cavity
o Increase AP diameter
□ Inspiration at rest is usually assisted by diaphragm alone

4
 □ Accessory muscles of inspiration
□ Sternocleidomastoid and scalene muscles
□ Enlarge thorax by increase AP (anteroposterior) diameter
□ Assist when minute volume is high (strenuous exercise or increased WOB due to disease)
□ Accessory muscles of expiration
□ Abdominal and internal intercostal muscles
o Abdominal muscle contacts  intra-abdominal pressure increases  diaphragm pushed up and decreased thorax volume
o Internal intercostal muscles pull down anterior ribs  decrease AP diameter in thorax
□ Assist expiration when minute volume is high, during coughing, or with an airway obstruction
o Elastic properties of lungs and chest walls
□ Elastic recoil = tendency of lungs to return to resting state after inspiration
□ Normal elastic reoil  passive expiration (no major muscles needed for expiration)
o Emphysema or blocked conducting airways  may need accessory muscles
□ Thorax opens  lungs collapse  negative intrapleural space
□ Compliance = measure of the lung and chest wall distensibility
□ Reciprocal of elasticity
□ ↑ compliance  lungs or chest wall is abnormally easy to inflate and lost some recoil
o i.e. emphysema
□ ↓ compliance  lungs lungs/ chest wall abnormally stiff or difficult to inflate
o I.e. ARDS, pneumonia, pulmonary edema, fibrosis
o Resistance to airflow through the conducting airways
□ Airway resistance = determined by length, radius, and cross-sectional area of airways; and by density, viscosity and velocity of gas
□ Normally very low
□ Very little resistance in conducting airways (large cross-section)
□ ↓ airways diameter  ↑resistance (vice versa)
□ Bronchoconstriction  increases airway resistance d/t irritants and inflammatory mediators
□ Bronchodilation = decrease resistance to airflow
□ Caused by B2-adrenergic receptor stimulation
□ Resistance also caused by edema of bronchial mucosa and airway obstructions (mucus, tumors, foreign bodies)
o Alveolar surface tension
□ Radius of alveolar is small  requiring more and more pressure in inflate it

5
 □ If lined with water-like fluid  breaths would be difficult
□ Alveolar ventilation possible by surfactant
□ Surfactant lowers surface tension
o Made of lipoproteins; produced from type II alveolar cells
o Surfactant proteins
□ Small hydrophobic molecules  separate liquid molecules  decrease surface tension
□ Collectins  inhibit foreign pathogens
o Reverses Laplace’s law (decrease size decrease
tension)
□ Lungs easier to inflate at low volumes than
high volumes
□ Lack of surfactant  alveolar surface tension increase
 alveolar collapse  decreased lung expansion 
increase WOB  severe exchange abnormalities
- Thoracic Cavity = chest wall and encases lungs
- Pleura = adheres to lungs and holds to attach to chest wall
o Visceral pleura = covers lungs
o Parietal pleura = lines thoracic cavity
o Pleural space/ cavity = space between
□ fluid lubricates this space, so they can slide past one another
without separating (negative pressure system)

Functions of Pulmonary System

- Ventilation: mechanical movement of gar or air into and out of the lungs –
inspiration and expiration
o Work of breathing (WOB)
o Carried out by the pulmonary system
o On a cellular level, the ventilation-perfusion ratio is relationship between ventilation and perfusion. This is known as the V/Q.
□ A normal V/Q ration is 0.8 (perfusion exceeds ventilation under normal conditions.
- Perfusion: the movement of blood into and out of capillary beds of the lungs to body organs and tissues
o Carried out by the cardiovascular system
o pumping of a fluid through (an organ or tissue) especially by way of blood vessel
- Diffusion: the movement of gases between air spaces in the lungs and the blood stream
o high concentration  low concentration (a concentration gradient is required for diffusion to work)

6
Control of Respiration/ Control of Breathing
o Medullary Center: primary inspiration and expiration
□ DRG (dorsal respiratory group) – inspiration; cluster of inspiratory nerve cells located in medulla  impulses to diaphragm
and inspiratory intercostal muscles
□ Receives impulses from peripheral chemoreceptors in carotid and aortic bodies (detects PaCO2 and PaO2 and H+)
□ VRG (ventral respiratory group) - contains inspiratory and expiratory neurons
□ Inactive during quiet respiration, active with required increased ventilation
o Pons – Secondary (do not generate primary rhythm, but modify inspiratory depth and rate established in medullary center)
□ Pneumotaxic: inhibits inspiratory time and increases breaths/ min
□ Pons control inspiration
□ Apneustic center
□ Inspiration and expiration
o Lung receptors
□ Stretch receptors = slowly adapting
□ In smooth muscles of airways
□ Sense increase size/ volume of lungs
□ Stimulation  decrease ventilatory rate and volume (Hering-Breuer expiratory reflex)
□ Active in newborns, for adults only active at high tidal volumes (exercise and mechanical ventilation)
□ Rapidly adapting receptors (RARs) – stretch receptors; important mediator of cough
□ Irritant Receptors = rapidly adapting
□ In epithelium of conducting airways
□ Noxious aerosols and particulate matter  cough reflex, bronchoconstriction, increase ventilatory rate
□ Located in proximal large airways, not distal (accumulation in distal w/o cough)
□ J receptors
□ Located near capillaries in alveolar septa
□ Sensitive to increase pulmonary capillary pressure  initiate rapid, shallow breathing, laryngeal constriction on expiration,
mucus secretion, hypotension, bradycardia
□ Lungs innervated by ANS
□ Parasympathetic  contract
□ Sympathetic  relax
o Chemoreceptors – detects CO2; ↑CO2  ↑respiratory rate
□ Central chemoreceptors = monitor arterial blood by sensing pH of CSF
□ Located in respiratory center of brain
□ Sensitive to H+ ions in CSF
□ PACO2 regulates ventilation through its effect on pH (H+ content) of the CSF

7
 □ ↓pH (↑H+)  ↑ depth and rate of breathing
o ↑ ventilation  PACO2 decrease < CSF  CO2 moves back to CSF  pH returns to normal
□ IN COPD, these receptors are insensitive to changes in PACO2 due to prolonged increase of PACO2
□ Peripheral receptors – blood vessels sense chemical concentration of CO2
□ Located in aortic bodies (aortic arch, carotid bodies, near baroreceptors)
□ Primarily responsive to arterial PAO2 (secondary sensitivity to PACO2 and pH)
□ Responsible for increase ventilation in response to arterial hypoxemia
□ ↓PAO2, ↓pH  ↑ven0la0on
□ PAO2 must drop to below normal (~60 mmHg) prior to ventilation adjustments
□ Important when central chemoreceptors are “reset” by chronic hypoventilation (COPD)
o Other
□ Pain
□ ↑pain  ↑respiration (r/t anxiety associated with pain)
□ Stress
□ Common cause for restless patients in decrease O2
□ Muscles
□ Joints

Gas Transport
- Delivery of oxygen to cells of the body and the removal of CO2
1. Ventilation of lungs
2. Diffusion of oxygen from alveoli into capillary blood
3. Perfusion of systemic capillaries with oxygenated blood
4. Diffusion of oxygen from systemic capillaries into cells
- Steps in the transport of CO2 occur in reverse order
1. Diffusion of CO2 from the cells into the systemic capillaries
2. Perfusion of the pulmonary capillary bed by venous blood
3. Diffusion of CO2 into alveoli
4. Removal of Cos from the lung by ventilation

Distribution of Ventilation and Perfusion

- Upright position
o Gravity pulls down on lungs toward diaphragm  compresses lower portions or bases
o Alveoli in apexes contain more residual gas volume, are larger, and are less numerous than those in bases
□ Increase in surface tension (due to larger alveoli)  upper portion of lungs more difficult to inflate (less compliant)

8
 o Most of tidal volume is distributes to bases of lungs (greater compliance)
o BP at apexes is lower than bases
□ Increase BP  better perfusion at bases
o Ventilation and perfusion greater in lower lobes
- Supine or side lying
o Areas of lungs most dependent  best ventilated/ perfused
- Alveolar pressure ???? p. 1240
o Alveolar pressure > capillary BP  capillary collapses and flow ceases
o Most likely to occur at apex

Oxygen Transport
- Blood in pulmonary vapillary for 0.75 second (only 0.25 required for oxygen concentration to equalize across alveolocapillary membrane)
- Increase PaO2 (partial pressure in arterial blood)  O2 moves from plasma to RBCS  binds hemoglobin

Oxygen-Hemoglobin Dissociation Curve

[Link]
- Air enters the resp. system in upper airways  conductive airway 
respiratory airways (bronchi  bronchioles  terminal bronchioles
 alveoli)
- Gas exchange between the lungs and the blood stream occurs are the level
of the alveoli (O2 and CO2)
- Heart will pump deoxygenated blood from RV to the lungs (↑CO2, ↓O2).
As blood travels through the capillaries associated with an alveolus, CO2
will exit and the blood will be re-oxygenated before it travels to the left
atrium  left ventricle  aorta  systemic circulation  tissues (to
create energy in the form of ATP, the tissues will form the byproduct CO2)
CO2 “exchanged” for O2  CO2 in blood travels back to heart
- O2 binds to hemoglobin (millions in each RBC) – in deoxygenated blood,
the structure of hemoglobin (or deoxyhemoglobin) is a tight structure
o Hemoglobin anatomy – protein made up of 4 subunits each which
contains a hemnoidty attached to a globin chain
o Each globin chain, contains Fe where O2 binds two – each 4 Fe
atoms can reversibly bind one O2 molecule
- Whey deoxyhemoglobin receives O2 it is rapid (< 0.01 s) – tight/ tense T-
bound hemoglobin reduces affinity for oxygen. When oxygen is first bound, the bond holding the globin are released, producing a relaxed configuration

9
 (R-configuration), which exposes more oxygen-binding states (increase O2 affinity)  this process is positive cooperativity  ends with
anoxyhemoglobin (in a relaxed structure)
- Partial Pressure (Deoxygenated)
o pO2 ~ 40
o pCO2 ~ 45
- Partial Pressure (Oxygenated)
o pO2 ~ 100%
o pCO2 ~40
- Hemoglobin Dissociation Curve: Oxygen Saturation of oxyhemoglobin, % (y-axis) vs Partial Pressure Oxygen, mmHg (x-axis)
o Oxygen-carrying power of hemoglobin to the partial pressure of oxygen
o The more oxygen bound to hemoglobin  higher oxyhemoglobin  higher saturation
o Sigmoid shape due to tense and relax configuration
o Plateau  ↑ pO2 does NOT cause ↑ SO2
□ PO2 at 100 already has a SO2 of 98 (not much change)
□ pO2 = 50  SO2 = 85% (dramatic change  small changes at low oxygen pressure leads to large changes in SI2)
□ a low pO2 (26) has already have an SO2 of 50%
□ Positive cooperativity = steep slope at left
o Shift in oxygenation dissociation curve
□ Right = reduced hemoglobin O2 affinity (occurs in tissues)  reduced in SO2
□ ↑CO2 = hypercapnia
□ ↓ pH (↑H+) = acidosis
□ ↑ Temp = hyperthermia
□ ↑ 2,3-DPG
□ Tissue = placenta (during exercise), placenta
□ Left = higher hemoglobin O2 affinity
□ ↓CO2 = hypocapnia
□ ↑ pH (↓H+) = alkalosis
□ ↓Temp = hypothermia
□ ↓ 2,3-DPG
□ Lungs

TEST OF PULMONARY FUNCTIONS

- Evaluated at rest and during exercise
- Spirometry
o Measures forced expiration (often affected by diffuse pulmonary disease)
o Can be used to detect restrictive or obstructive lung diseases

10
 o Measures volume and flow
o Spirogram produced = records ventilation in relation to time
□ FVC (forced residual capacity) = maximum amount of can that can be
displaced from a lung during forced expiration
□ FEV1 = forced expiratory volume in 1 second
□ FEV1/FVC = percent max inspiration that is expired in 1 second
(usually ~80% of FVC)
- Diffusion capacity = measure of the rate of gas diffusion across the alveolocapillary
membrane
o Carbon monoxide most commonly used (over O2)
o Amount of CO taken up by blood / pressure gradient across the
alveolocapillary membrane
- Residual volume
o Helium used
- Functional reserve capacity
o Helium used
- Total lung capacity
o Helium used
- Arterial blood gas analysis
o Pulmonary disease
o Analysis of pH and gas concentrations
o Acid-base status
□ Acidosis, alkalosis, ventilatory alteration, decrease PaO2 diagnosed
- Chest radiographs
o Most common examinations of the pulmonary systems
o Detects air trapping in the alveoli and airways (asthma or emphysema)
□ Consolidation of lung tissue (pneumonia or pulmonary edema)
□ Cavities (abscesses or TB)
□ Nodules (lung cancer)

AGING AND THE PULMONARY SYSTEM

- Normal alteration to age includes:
o Loss of elastic recoil – thickens, gas exchange is off, more resistance
o Stiffening of chest wall
□ d/t less-flexible ribs and stiffer joints  chest wall loses its ability to
expand

11
 □ Respiratory muscle strength and endurance decrease up to 20% by 70 in addition
o Alterations in gas exchange
□ Decrease ventilatory reserve  decrease ventilation-perfusion ratio
□ Older individuals have decreased compensation to hypercapnia and hypoxemia
□ Loss of alveolar SA
□ Increase ventilation-perfusion mismatch
o Increase flow resistance
- Influenced by environmental and sociocultural factors, nutritional status, respiratory disease, body size, gender, and race
- Vital capacity decrease, residual volume increase, total lung capacity unchanged

12