Respiratory physiology

Respiration is the process by which the body takes in and utilizes oxygen (O2) and gets rid of carbon dioxide (CO2).

Respiration can be divided into four major functional events Ventilation: Movement of air into and out of lungs Gas exchange between air in lungs and blood Transport of oxygen and carbon dioxide in the blood Internal respiration: Gas exchange between the blood and tissues

Respiratory System Functions Gas exchange: Oxygen enters blood and carbon dioxide leaves Regulation of blood pH: Altered by changing blood carbon dioxide levels Voice production: Movement of air past vocal folds makes sound and speech Olfaction: Smell occurs when airborne molecules drawn into nasal cavity Protection: Against microorganisms by preventing entry and removing them

Section 1 Pulmonary Ventilation Pulmonary ventilation means the inflow and outflow of air between the atmosphere and the lung alveoli, which is determined by the activity of the airways, the alveolus and the thoracic cage.

I Functions of the Respiratory Passageways

Respiratory System Divisions Upper tract Nose, pharynx and associated structures Lower tract Larynx, trachea, bronchi, lungs

Conducting Zone All the structures air passes through before reaching the respiratory zone. Cartilage holds tube system open and smooth muscle controls tube diameter Warms and humidifies inspired air. Filters and cleans: Insert fig. 16.5

Respiratory Zone Region of gas exchange between air and blood. Includes respiratory bronchioles and alveolar sacs.

Airway branching

Bronchioles and Alveoli

Thoracic Walls and Muscles of Respiration

Breathing Occurs because the thoracic cavity changes volume Insipiration uses external intercostals and diaphragm Expiration is passive at rest, but uses internal intercostals and abdominals during severe respiratory load Breathing rate is 10-20 breaths / minute at rest, 40 - 45 at maximum exercise in adults

Thoracic Volume

Pleura

Pleural fluid produced by pleural membranes Acts as lubricant Helps hold parietal and visceral pleural membranes together

Ventilation Movement of air into and out of lungs Air moves from area of higher pressure to area of lower pressure Pressure is inversely related to volume

Alveolar Pressure Changes During Respiration

Principles of Breathing Functional Unit: Chest Wall and Lung Conducting Airways Follows Boyle’s Law: Pressure (P) x Volume (V) = Constant Pleural Cavity Imaginary Space between Lungs and chest wall Pleural Cavity Very small space Maintained at negative pressure Transmits pressure changes Allows lung and ribs to slide Chest Wall (muscle, ribs) Lungs Gas Exchange Diaphragm (muscle)

Pb Pi Principle of Breathing At Rest with mouth open Pb = Pi = 0 Follows Boyle’s Law: PV= C At Rest with mouth open Pb = Pi = 0 Pb Airway Open A CW Pi PS D 1

Pb Pi Principle of Breathing At Rest with mouth open Pb = Pi = 0 Follows Boyle’s Law: PV= C At Rest with mouth open Pb = Pi = 0 Inhalation: Increase Volume of Rib cage Decrease the pleural cavity pressure - Decrease in Pressure inside (Pi) lungs Pb Airway Open A Pi CW PS D 2

Pb Pi Principle of Breathing At Rest with mouth open Pb = Pi = 0 Follows Boyle’s Law: PV= C At Rest with mouth open Pb = Pi = 0 Inhalation: Pb outside is now greater than Pi - Air flows down pressure gradient Until Pi = Pb Pb Airway Open A Pi CW PS D 3

Pb Pi Principle of Breathing At Rest with mouth open Pb = Pi = 0 Follows Boyle’s Law: PV= C At Rest with mouth open Pb = Pi = 0 Exhalation: Opposite Process Decrease Rib Cage Volume Pb Airway Open A Pi CW PS D 4

Pb Pi Principle of Breathing At Rest with mouth open Pb = Pi = 0 Follows Boyle’s Law: PV= C At Rest with mouth open Pb = Pi = 0 Exhalation: Opposite Process Decrease Rib Cage Volume Increase in pleural cavity pressure - Increase Pi Pb Airway Open A Pi CW PS D 5

Pb Pi Principle of Breathing At Rest with mouth open Pb = Pi = 0 Follows Boyle’s Law: PV= C At Rest with mouth open Pb = Pi = 0 Exhalation: Opposite Process Decrease Rib Cage Volume Increase Pi Pi is greater than Pb Air flows down pressure gradient Until Pi = Pb again Pb Airway Open A Pi CW PS D 6

Mechanisms of Breathing: How do we change the volume of the rib cage ? To Inhale is an ACTIVE process Diaphragm External Intercostal Muscles Intercostals Contract to Lift Rib Spine Ribs Volume Rib Cage Contract Diaphragm Volume Both actions occur simultaneously – otherwise not effective

II Respiratory Resistance Including Elastic Resistance and Inelastic resistance

Elastic Resistance A lung may be considered as an elastic sac. The thoracic wall also can be considered as an elastic element. So during inspiration the inspiratory muscles must expand the thoracic cage which are together with the elastic resistance.

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.

Compliance Distensibility (stretchability): Ease with which the lungs can expand. The compliance is inversely proportional to elastic resistance Change in lung volume per change in transpulmonary pressure. DV/DP 100 x more distensible than a balloon.

Static lung compliance C = DV/DP 100 deflation Lung volume (%TLC) 50 normal breathing inflation Transpulmonary pressure (cmH2O) 30

The elastic forces can be divided into two parts: the elastic forces of the lung tissue itself 2) the elastic forces caused by surface tension of the fluid that lines the inside wall of the alveoli. The elastic forces caused by surface tension are much more complex. Surface tension accounts for about two thirds of the total elastic forces in a normal lungs.

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

What is Surface Tension ? At surface Unbalanced forces Generate Tension Within Fluid All forces balance

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. Insert fig. 16.11

Effect of Surface Tension on Alveoli size Air Flow Expand Collapse

Surfactant Phospholipid produced by alveolar type II cells. Lowers surface tension. Reduces attractive forces of hydrogen bonding by becoming interspersed between H20 molecules. Surface tension in alveoli is reduced. As alveoli radius decreases, surfactant’s ability to lower surface tension increases.

Area dependence of Surfactant action Low S/unit Area Saline Decrease Area Saline Slider - Change Surface Area Increase Area High S/unit Area Tension Area Surfactant

Surfactant prevents alveolar collapse

Factors Contributing to Compliance - Hysteresis Volume L 6 Saline Filled Normal (with surfactant) 3 Without surfactant RV - 30 cm H2O Pleural Pressure - 15

Inelastic Resistance The inelastic resistance comprises the airway resistance (friction) and pulmonary tissue resistance (viscosity, and inertia). Of these the airway resistance is by far the more important both in health and disease. It account for 80%-90% of the inelastic resistance.

Airway Resistance Airway resistance is the resistance to flow of air in the airways and is due to : 1) internal friction between gas molecules 2) friction between gas molecules and the walls of the airways

Types of Flow

Laminar flow … is when concentric layers of gas flow parallel to the wall of the tube. The velocity profile obeys Poiseuille’s Law (pg 43:11)

Poiseuille and Resistance Airway Radius or diameter is KEY.  radius by 1/2  resistance by 16 FOLD - think bronchodilator here!!

Airway resistance increase Any factor that decreases airway diameter, or increases turbulence will increase airway resistance, eg: Rapid breathing: because air velocity and hence turbulence increases Narrowing airways as in asthma, parasympathetic stimulation, etc. Emphysema, which decreases small airway diameter during forced expiration

Control of Airway Smooth Muscle Neural control Adrenergic beta receptors causing dilatation Parasympathetic-muscarinic receptors causing constriction NANC nerves (non-adrenergic, non-cholinergic) Inhibitory release VIP and NO  bronchodilitation Stimulatory  bronchoconstriction, mucous secretion, vascular hyperpermeability, cough, vasodilation “neurogenic inflammation”

Control of Airway Smooth Muscle (cont.) Local factors histamine binds to H1 receptors-constriction histamine binds to H2 receptors-dilation slow reactive substance of anaphylaxsis-constriction-allergic response to pollen Prostaglandins E series- dilation Prostaglandins F series- constriction

Control of Airway Smooth Muscle (cont) Environmental pollution smoke, dust, sulfur dioxide, some acidic elements in smog elicit constriction of airways mediated by: parasympathetic reflex local constrictor responses

III Pulmonary Volume and Capacity

Pulmonary Volumes Tidal volume Inspiratory reserve volume Volume of air inspired or expired during a normal inspiration or expiration (400 – 500 ml) Inspiratory reserve volume Amount of air inspired forcefully after inspiration of normal tidal volume (1500 – 2000 ml) Expiratory reserve volume Amount of air forcefully expired after expiration of normal tidal volume (900 – 1200 ml) Residual volume Volume of air remaining in respiratory passages and lungs after the most forceful expiration (1500 ml in male and 1000 ml in female)

Pulmonary Capacities Inspiratory capacity Functional residual capacity Tidal volume plus inspiratory reserve volume Functional residual capacity Expiratory reserve volume plus the residual volume Vital capacity Sum of inspiratory reserve volume, tidal volume, and expiratory reserve volume Total lung capacity Sum of inspiratory and expiratory reserve volumes plus the tidal volume and residual volume

Minute and Alveolar Ventilation Minute ventilation: Total amount of air moved into and out of respiratory system per minute Respiratory rate or frequency: Number of breaths taken per minute Anatomic dead space: Part of respiratory system where gas exchange does not take place Alveolar ventilation: How much air per minute enters the parts of the respiratory system in which gas exchange takes place

Dead Space Area where gas exchange cannot occur Includes most of airway volume Anatomical dead space (=150 ml) Airways Physiological dead space = anatomical + non functional alveoli

DEAD SPACE Basic Structure of the Lung VD VA NO GAS EXCHANGE A tube = Airway (Trachea – Bronchi – Bronchioles) NO GAS EXCHANGE DEAD SPACE A thin walled Sac = Alveolus Blood Vessels GAS EXCHANGE OCCURS HERE VA Formula: Total Ventilation = Dead Space + Alveolar Space VT = VD + VA

Similar Concept: Physiological Dead Space Healthy Lungs: Anatomical Dead Space = Airways (constant) VA VD Diseased lungs: Physiological = Anatomical Dead Space Dead Space + Blocked Vessel Additional Dead Space

FVC - forced vital capacity defines maximum volume of exchangeable air in lung (vital capacity) forced expiratory breathing maneuver requires muscular effort and some patient training initial (healthy) FVC values approx 4 liters slowly diminishes with normal aging significantly reduced FVC suggests damage to lung parenchyma restrictive lung disease (fibrosis) constructive lung disease loss of functional alveolar tissue (atelectasis) FVC volume reduction trend over time (years) is key indicator intra-subject variability factors age sex height ethnicity

FEV1 - forced expiratory volume (1 second) defines maximum air flow rate out of lung in initial 1 second interval forced expiratory breathing maneuver requires muscular effort and some patient training FEV1/FVC ratio normal FEV1 about 3 liters FEV1 needs to be normalized to individual’s vital capacity (FVC) typical normal FEV1/FVC ratio = 3 liters/ 4 liters = 0.75 standard screening measure for obstructive lung disease (COPD) FEV1/FVC reduction trend over time (years) is key indicator calculate % predicted FEV1/FVC (age and height normalized) reduced FEV1/FVC suggests obstructive damage to lung airways episodic, reversible by bronchodilator drugs probably asthma continual, irreversible by bronchodilator drugs probably COPD

Spirometry 1 sec Total Lung Capacity Forced Vital Capacity - FVC Volume (litres) Time (sec) Forced Expiratory Volume in 1 sec - FEV1 Residual Volume

Lung Volume in Restrictive Disease Assessment of RESTRICTIVE Lung Diseases These are diseases that reduce the effective surface area available for gas exchange Normal Lung Volume Lung Volume in Restrictive Disease eg fibrosis / pulmonary oedema

RESTRICTIVE lung disease Volume (litres) Time (sec) Vital Capacity Total Lung Capacity Residual Volume Spirometry RESTRICTIVE lung disease REDUCED

Assessment of OBSTRUCTIVE Lung Diseases These are diseases that reduce the diameter of the airways and increase airway resistance - remember Resistance increases with 1/radius 4 Normal Airway Calibre Airway Calibre in Obstructive Disease eg asthma / bronchitis

FEV1 > 80% of FVC is Normal Forced Vital Capacity - FVC or in words - you should be able to forcibly expire more than 80% of your vital capacity in 1 sec. Forced Expiratory Volume in 1 sec - FEV1

OBSTRUCTIVE lung disease Volume (litres) Time (sec) Total Lung Capacity Residual Volume Spirometry 1 sec OBSTRUCTIVE lung disease Forced Vital Capacity - FVC Forced Expiratory Volume in 1 sec - FEV1 FEV1 < 80% of FVC