Objectives

To understand the physiologic anatomy of the respiratory system

List the passages through which air passes from the exterior to the alveoli List the major muscles in respiration and state the role of each Describe the chemical composition and function of surfactant Describe the pulmonary circulation and differentiate with systemic circulation Describe basic lung defense and metabolic functions

RESPIRATION
Ventilation: Movement of air into and out of lungs External respiration: - Gas exchange between air in lungs and blood - Transport of oxygen and carbon dioxide in the blood - Gas exchange between the blood and tissues
Internal respiration: (Cellular) - The use of O2 to produce ATP via Glycolysis, TCA cycle, & ETS, and production of CO2 wthin the tissue cells

RESPIRATORY SYSTEM FUNCTIONS

Gas exchange: Oxygen enters blood and carbon dioxide leaves Regulation of blood pH: Altered by changing blood carbon dioxide levels Carbonic acid Buffer system Sound production: Movement of air past vocal folds makes sound and speech Olfaction: Smell occurs when airborne molecules drawn into nasal cavity Thermoregulation: Heating and cooling of body Protection: Against microorganisms by preventing entry and removing them

Lungs

Two lungs: Principal organs of respiration

Right lung: Three lobes Left lung: Two lobes

Divisions
Lobes, bronchopulmonary segments, lobules

Pleura
Pneumothorax- a collection of air or gas in the pleural cavity of the chest between the lung and the chest wall

Pleural effusion- is excess fluid that accumulates in the pleura

Empyema- a collection of pus within the cavity

RESPIRATORY SYSTEM DIVISIONS

Upper airway
Nose, pharynx and associated structures

Lower airway
Larynx, trachea bronchi, lungs

Respiratory Passages Pharynx

Nasal Cavity - ciliated columnar
epithelium/ goblet cells - highly vascular - warms/ moistens the air - nasal hair filters off impurities - mucosal lining traps particles and bacteria, large particles up to 6 um - sedimentation in larynx 15 um

- nasopharynx - oropharynx - laryngopharynx - common opening for digestive and respiratory systems - abductor muscles in the larynx contracts during inspiration - adductor muscles contracts during swallowing

Trachea
Windpipe Divides to form
Primary bronchi Carina: Cough reflex

Insert Fig 23.5 all but b

Tracheobronchial Tree

Anatomical dead space: no exchange of gases occurs here Elastic tissue- responsible for the recoil of bronchial tree during expiration Cartilagenous rings ensure patency of the tubes

Conducting Zone
Trachea to terminal bronchioles which is ciliated for removal of debris, mucus lined
Insert fig. 16.5

Passageway for air movement controlled by smooth muscle at end of terminal bronchioles
Cartilage holds tube system open and smooth muscle controls tube diameter

No exchange of gases in this zone

Conducting Zone

Warms and humidifies until inspired air becomes: 37 degrees Saturated with water vapor Filters and cleans: Mucus secreted to trap particles Mucus/particles moved by cilia to be expectorated.

Respiratory Zone
Region of gas exchange between air and blood.
Respiratory bronchiole 5 or 6 alveolar ducts 3 to 6 air sacs alveoli Respiratory unit - respiratory bronchiole - alveolar ducts - alveolar sacs

Respiratory Zone
ALVEOLI Air sacs Honeycomb-like clusters ~ 300 million. Large surface area (6080 m2). Each alveolus: only 1 thin cell layer.

Alveolus and Respiratory Membrane

The area where gas exchange between air and blood occurs

Fused basement membrane

CELLS OF THE AIRWAY

ALVEOLAR CELLS type I - thin squamous epithelial cells - forms 90% of alveolar surface - gas exchange occurs ALVEOLAR CELLS type II - produces surfactant - regenerative capacity

Surfactant

Functions: Thin film lining the 1. lowers surface tension alveolar surface anti-stick property 2. promotes stability Phospholipid produced among alveoli of different by alveolar type II cells sizes by decreasing tendency of small alveoli Main component: to collapse (interdepence) dipalmitoylphosphatidylch oline (DPPC) 3. Reduces capillary filtration forces Production starts at 24 weeks AOG

 As alveoli radius decreases, surfactants ability to lower surface tension increases

Disorders: IRDS ARDS

Formation and metabolism of surfactant

Surface Tension
Force exerted by fluid in alveoli to resist distension.
Lungs secrete and absorb fluid, leaving a very thin film of fluid.

This film of fluid causes surface tension. Fluid absorption is driven (osmosis) by Na+ active transport. Fluid secretion is driven by the active transport of Clout of the alveolar epithelial cells.

H20 molecules at the surface are attracted to other H20 molecules by attractive forces.
Force is directed inward, raising pressure in alveoli.

Surface Tension
Law of Laplace:
Pressure in alveoli is directly proportional to surface tension; and inversely proportional to radius of alveoli.
Pressure in smaller alveolus would be greater than in larger alveolus, if surface tension were the same in both.

In the presence of surfactant, causes a decrease in T and results to a decrease in P, thus a lower tendency to collapse

Abnormalities:
Respiratory distress syndrome (IRDS) of newborn - also known as hyaline membrane disease - due to abnormal formation of surfactant because of immaturity of lungs - babies have inadequate gas exchange Atelectasis - alveolar collapse Adult respiratory distress syndrome (ARDS) - abnormal surfactant function caused by schock, infection and trauma

BLOOD SUPPLY
1. Pulmonary Circulation - deoxygenated blood from the RV passes via the pulmonary artery to the pulmonary capillary bed, where it is oxygenated and returned to the left atrium via the pulmonary veins 2. Bronchial Circulation - blood supply to the conducting airways, also supplies the pleura and hilar lymph nodes

 The pulmonary arteries branch into increasingly smaller arteries and travel with the bronchi toward the respiratory zones. The smallest arteries divide into arterioles and then into pulmonary capillaries, which form dense networks (capillary baskets) around the alveoli

 there are anastomoses between the bronchial capillaries and the pulmonary capillaries and veins, and although some of the bronchial blood enters the bronchial veins, some enters the pulmonary capillaries and veins, bypassing the right ventricle

Pulmonary Circulation
Rate of blood flow through the pulmonary circulation is = flow rate through the systemic circulation Driving pressure is about 10 mm Hg. Pulmonary vascular resistance is low Low pressure pathway produces less net filtration than produced in the systemic capillaries. Avoids pulmonary edema.

Pulmonary Circulation
In a fetus: Pulmonary circulation has a higher vascular resistance, because the lungs are partially collapsed After birth, vascular resistance decreases: Opening the vessels as a result of subatmospheric intrapulmonary pressure Physical stretching of the lungs Dilation of pulmonary arterioles in response to increased alveolar P02.

Pulmonary Blood Flow

On standing, blood flow is lowest at the apex of the lungs and highest at the base. (Gravitational effect) In supine position, the gravitational effects disappear

Regulation of Pulmonary Blood Flow

Regulated by altering the resistance of pulmonary arterioles Changes in in pulmonary arteriolar resistance are controlled by local factors in PaO2 causes hypoxic vasoconstriction

Matches ventilation/ perfusion ratio

Pulmonary and systemic circulation differences:

Thinned wall arteries Contain less elastin and smooth muscle than systemic vessels, making pulmonary circulation highly compliant Capillaries form a dense capillary bed, each alveoli sits on a capillary basket. High flow, high compliance Low resistance, low pressure system

Pulmonary lymphatics
Supplied by the superficial and deep lymphatic vessels which exits from the hilus

No lymphatics drain the alveoli

Remove plasma filtrate, particular matter absorbed from alveoli, and escaped protien from the vascular system

Help maintain negative interstitial pressure which pulls alveolar epithelium against capillary epithelium

Innervation of the Respiratory System

1. Autonomic nervous control - sympathetic control - activation of B2 adrenergic receptors bronchodilatation; bronchial secretion - parasymphatetic control - activation of muscarinic receptors bronchoconstriction

Vasoactive intestinal peptide (VIP) - a noncholinergic, nonadrenergic innervation of bronchioles bronchodilatation

Innervation of the Respiratory System

2. Local control - exerted by substances released in the lungs by mast cells: Histamine: binds to H1 receptor constriction binds to H2 receptor dilatation SRS- A: allergic response to pollen constriction Prostaglandin E dilatation Prostaglandin F constriction

Thoracic Walls Muscles of Respiration

Muscles of Inspiration Diaphragm

Movement of the diaphragm accounts for 75% of the change in intrathoracic volume during quiet inspiration Innervated by phrenic nerve (C3, C4, C5) The distance it moves ranges from 1.5 cm to as much as 7 cm with deep inspiration

Muscles of Inspiration Diaphragm

During inspiration - contraction of the diaphragm pulls the lower surfaces of the lungs downward
During expiration - by relaxation of the diaphragm and elastic recoil of the lungs, chest wall, and abdominal structures compresses the lungs

Muscles of Inspiration External Intercostals

External intercostals - lifts 2nd to 6th rib - ribs move like a bucket handle - sternum moves like a water pump

Muscle of Expiration
In quiet respiration - expiration is purely passive - accomplished when muscles of inspiration relax and by lung recoil In forced expiration - Expiratory muscles are used during exercise or when airway resistance is increased because of disease (asthma) 1. Abdominal muscles (rectus abdominus)- compress the abdominal cavity, push the diaphragm up, and push air out of the lungs. 2. Internal intercostal muscles- pull the ribs downward and inward.

PROTECTIVE MECHANISMS
Mucociliary clearance system - also known as mucociliary elevator - Mucus continually secreted by goblet cells that traps particles and debris - IgA protects against bacteria and viruses - impaired by toxins from cigarette smoking

PROTECTIVE MECHANISMS
Sneeze reflex - function to dislodge foreign substances from nasal cavity - Afferent impulses pass in CN V to the medulla - during the reflex, uvula and soft palate are depressed so that rapidly flowing air from lungs is directed through the nasal passages

PROTECTIVE MECHANISMS
Cough Reflex - afferent impulses pass in CN X to the medulla - Steps: 1. about 2.5 L of air is inspired 2. epiglottis closes and vocal cords shut tightly 3. muscles of expiration contract forcefully which causes pressure in lungs to rise to 100 mmHg 4. vocal cords and epiglottis suddenly open widely explosive outpouring of air at speed of 75 to 100 miles/hour

Objectives
To understand the mechanics of breathing
Know the different lung volume and capacities Understand the elastic properties of the lungs Describe volume changes in the lungs Relate volume changes to pressure changes Understand airflow dynamics Describe normal breathing cycle

Pulmonary Volumes:
Tidal volume (TV= 500 ml) - volume of gas inspired or expired in an unforced breathing cycle Inspiratory reserve volume (IRV= 3000 ml) - maximum volume of gas that can be inspired during forced breathing in addition to TV Expiratory reserve volume (ERV= 1200 ml) - maximum volume of gas that can be expired during forced breathing in addition to TV Residual volume (RV= 1200 ml) - maximum volume of gas remaining in the lungs after a maximum expiration

Pulmonary Capacities
Total lung capacity (TLC) - total amount of gas in lungs after a maximum inspiration Vital capacity (VC) - total amount of gas that can be expired after a maximum inspiration Inspiratory capacity (IC) - maximum amount of gas that can be inspired after a normal tidal expiration Functional residual capacity (FRC) - amount of gas remaining in the lungs after a normal tidal expiration

Vital capacity is affected by: Age- decreases with age Sex- adult females is 20-25% < males Height Body built: thin persons > overweight Trained athletes: 30-40% > untrained

Inspiratory Reserve Volume

Inspiratory Capacity
Vital Capacity

Tidal Volume
Expiratory Reserve Volume

Functional Residual Capacity

Residual Volume

Many of the lung volumes are measured by having the patient breathe through a mouthpiece and tubing that are connected to a spirometer. The subject is first asked to breathe normally, and the volume of air (the tidal volume) that is moved with each quiet breath is recorded. Then he is asked to inhale maximally and then exhale fully and completely. The total volume of exhaled air, from a maximal inspiration to a maximal exhalation is the vital capacity (VC). The air remaining in the lung after a complete exhalation is the residual volume (RV). The total lung capacity therefore is the sum of the VC and the RV. The functional residual capacity (FRC) is the volume of air in the lung at the end of exhalation during quiet breathing. The FRC is called the resting volume of the lung and is composed of the RV and the expiratory reserve volume (ERV), which is the volume of air that can be exhaled from FRC to RV. The inspiratory reserve volume (IRV) is the volume of air that can be inhaled from a tidal breath. The IRV and the Tidal volume (VT) comprises the inspiratory capacity.

Abnormalities:
Obstructive pulmonary diseases - associated with increased airway resistance - RV - FRC - TLC Restrictive pulmonary diseases - difficulty in lung expansion - TLC - VC

Obstructive disorder:Rate of expiration is reduced. Lungs are fine, but passageways are obstructed. Increase airway resistance, makes it harder to expire causing trapped air..

Restrictive disorder:Vital capacity is reduced. Less air in lungs.

Physical Properties of the Lungs

Ventilation occurs as a result of pressure differences induced by changes in lung volume

Physical properties that affect lung function: Compliance. Elasticity. Surface tension.

Compliance
Distensibility (stretchability): Ease with which the lungs can expand. Inversely correlated with elasticity Change in lung volume per change in transpulmonary pressure. DV/DP = 200 ml/cmH20

100 x more distensible than a balloon. Compliance is reduced by factors that produce resistance to distension.

Compliance
The greater the compliance, the easier it is for a change in pressure to cause expansion - emphysema , there is loss of elastic fibers A lower compliance means the lungs and thorax are harder to expand - fibrosis, stiffening of lung tissues

Hysteresis
Expiration

Inspiration

Transpulmonary pressure = Palv - Pip

Hysteresis
2 reasons : Surfactant Collapse of small airways

Static Compliance Curves

Emphysema (high compliance)

Lung Volume

Normal VT FRCE VT FRCN FRCF

2 0 -2 -4 -6 -8 -10 -12 -14 -16 -18

Fibrosis (low compliance) VT

Pleural Pressure, Ppl (cm H2O)

Elasticity
Tendency to return to initial size after distension High content of elastin proteins Very elastic and resist distension Recoil ability Elastic tension increases during inspiration and is reduced by recoil during expiration

Surface Tension
Force exerted by fluid in alveoli to resist distension

Lungs secrete and absorb fluid, leaving a very thin film of fluid. This film of fluid causes surface tension. Force is directed inward, raising pressure in alveoli.

Surface Tension
Law of Laplace:
Pressure in alveoli is Insert fig. 16.11 directly proportional to surface tension; and inversely proportional to radius of alveoli. A surfactant increases lung compliance and decreases work of breathing Pressure in smaller alveolus would be greater than in larger alveolus, if surface tension were the same in both.

Air Flow
is driven by, and is directly proportional to the pressure difference between the mouth (or nose) and the alveoli is inversely proportional to airway resistance Q = D P/D R
where: Q = airflow (mL/min or L/min) P = pressure gradient (cm H2O) R = airway resistance (cm H2O/L/min)

Airway Resistance
From trachea to alveolar ducts, total cross sectional area of airway progressively increases Velocity of airflow decreases rapidly In trachea and main bronchi, airflow is turbulent Major site of airway resistance is the medium-sized bronchi In small airways airflow is laminar

Airway Resistance
Airway radius is the most important determinant of resistance. is described by Poiseuille's law

R = nl r Smaller airway means/higher resistance for any flow rate

where: R = resistance = viscosity of the inspired gas l = length of the airway r = radius of the airway

Factors that change airway resistance

1. Contraction or relaxation of bronchial smooth muscle - changes airway resistance by altering the radius of the airways - sympathetic control - activation of B2 adrenergic receptors bronchodilatation; radius, resistance - parasymphatetic control - activation of muscarinic receptors bronchoconstriction; radius; resistance SRS-A bronchoconstriction VIP bronchodilatation

Factors that change airway resistance

2. Lung volume - alters airway resistance because of the radial traction exerted on the airways by surrounding lung tissue High lung volume - more traction and decreased airway resistance Low lung volume - less traction and increased airway resistance

Factors that change airway resistance

3. Viscosity or density of inspired gas

- changes the resistance to airflow. - During a deep-sea dive, both air density and resistance to airflow are increased - Breathing a low-density gas, such as helium, reduces the resistance to airflow

Neurohumoral Regulation of Airway Resistance

Increase airway resistance - stimulation of efferent vagal nerve fibers - smoke inhalation, dust particles, cold air - histamine, Ach, thromboxane A2, prostaglandin F2, leukotrienes

Decrease airway resistance - sympathetic stimulation - epinephrine

Common Uses of Pulmonary Function Tests

Screening for the presence of obstructive and restrictive diseases Evaluating the patient's condition for weaning from a ventilator

Documenting the effectiveness of therapeutic intervention Pre- OP evaluation

Pulmonary Function Test

Forced Vital Capacity (FVC) - maximum volume inhalation followed by exhalation as fast as possible - a low FVC indicates a restrictive pulmonary disorder Forced Expiratory Volume (FEV) - percentage of FVC that can be exhaled within a certain time frame - FEV1 = percent of FVC that can be exhaled within one second

Pulmonary Function Test

Normal FEV1/FVC = 80% - if FVC = 4000 ml, should expire 3200 ml in 1 sec - FEV1/FVC <80% indicates obstructive pulmonary disorder - FEV1 is used to quantitate severity of obstruction

Spirometric Patterns of Abnormalities

Measurement
FVC FEV1
FEV1/FVC TLC

Obstructive Pattern
Decreased or normal Decreased
Decreased Normal or increased

Restrictive Pattern
Decreased Decreased or normal
Normal Decreased

FEV1/FVC decreased ?
No
Restrictive or Normal pattern Yes Obstructive pattern

Is FVC decreased ?
No

Quantitate obstruction using FEV1 Is FVC decreased ? No Pure Obstruction

No Pure obstruction Yes Mixed

Yes Restrictive pattern

TLC low ?

Normal spirometry

Yes
TLC low ?
NK
Possible Mixed or Pure Obstruction

No

Yes Quantitate using TLC

NK Quantitate using FVC

Normal test

Flow volume profile for obstructive and restrictive respiratory disorders

Common Restrictive and Obstructive Lung Diseases

Common Obstructive Lung Diseases
Asthma Asthmatic bronchitis Chronic obstructive bronchitis COPD Cystic fibrosis Emphysema

Common Restrictive Lung Diseases

Idiopathic pulmonary fibrosis Interstitial pneumonitis Infectious inflammation (eg, histoplasmosis, mycobacterium infection) Sarcoidosis/beryllium disease Thoracic deformities Congestive heart failure Neuromuscular diseases

Work of Breathing
Compliance work (elastic work)- 65% - work required to expand the lungs against its elastic forces Tissue resistance work 7% - work required to overcome (inelastic tissues)viscosity of the lung and chest wall structures Airway resistance work- 28% - work required to overcome airway resistance during air movement into the lungs

Work of Breathing
Total work of quiet breathing is estimated to be at the range of 0.3 to 0.8 kg-m/min. Only 3 to 5% of the total work energy expended by the body is required Increases 50 fold during a heavy exercise WOB is greatly increased in cases of emphysema, asthma and CHF

MECHANICS OF BREATHING
Refers to the factors that participate in moving of the lungs and of the chest wall along the respiratory cycle

Atmospheric Pressure (Patm)

760 mmHg at sea level decreases in high altitude Increases under water

Intra- alveolar Pressure (Palv)

Also known as intrapulmonary pressure Pressure in the alveoli Varies with phase of respiration - during inspiration = negative - during expiration = positive - at rest, it equalizes with Patm Difference between Palv and Patm drives ventilation

Intrapleural Pressure (Pip)

Pressure in the intrapleural space Pressure is negative due to opposing forces of the lungs trying to collapse and chest wall trying to expand Always less than Palv and Patm At rest, -4 mmHg Any condition that equalizes Pip to Patm causes immediate lung collapse

Transpulmonary Pressure
Pressure difference across the wall of the lung. Palv - Pip Keeps the lungs against the chest wall and prevents collapse Peaks at the end of inspiration

Boyles Law
Relationship between the pressure and volume of gases As volume of a chamber increases, gas pressure wtihin it decreases As volume of a chamber decreases, gas pressure within it increases

P1V1 = P2V2
General Gas Law: at constant temperature, an increase in thoracic volume leads to a decrease in pleural pressure

Pressure-Flow Relationships

Resting Phase of Respiration

Inspiratory Phase

Expiratory Phase