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Chapter 5 Respiration. When you can not breath, nothing else matters Slogan of the American Lung Association. Respiration is the process by which the body takes in and utilizes oxygen (O 2 ) and gets rid of carbon dioxide (CO 2 ). An Overview of Key Steps in Respiration.
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Chapter 5 Respiration When you can not breath, nothing else matters Slogan of the American Lung Association
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 • Metabolism: Synthesize and metabolize different compounds (Nonrespiratory Function of the Lung)
Ventilation • 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
Pleural fluid produced by pleural membranes • Acts as lubricant • Helps hold parietal and visceral pleural membranes together
Conducting Airways Lungs Gas Exchange Pleural Cavity Very small space Maintained at negative pressure Transmits pressure changes Allows lung and ribs to slide Chest Wall (muscle, ribs) Diaphragm (muscle) Pleural CavityImaginary Space between Lungs and chest wall Principles of Breathing Functional Unit: Chest Wall and Lung Follows Boyle’s Law:Pressure (P) x Volume (V) = Constant
CW Principle of Breathing Follows Boyle’s Law: PV= C At Rest with mouth open Pb = Pi = 0 Pb Airway Open A Pi PS D 1
Principle of Breathing 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 PS CW D 2
Principle of Breathing 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
Principle of Breathing 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
Principle of Breathing 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
Principle of Breathing 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
Rib Cage Contract IntercostalsContractto Lift Spine Rib Diaphragm Volume Volume Ribs Mechanisms of Breathing: How do we change the volume of the rib cage ? • To Inhale is an ACTIVE process • Diaphragm • External Intercostal Muscles Both actions occur simultaneously – otherwise not effective
II Resistance of the Ventilation • Elastic Resistance • Inelastic Resistance
1. Elastic Resistance • A lung is an elastic sac. • The thoracic wall is also an elastic element. • So during inspiration • the inspiratory muscles must expand the thoracic cage • which are together with the elastic resistance.
The elastic forces can be divided into two parts: • Caused by the elastic tissue of the lung and the thoracic wall • 2) 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 (表面张力): a measure of the attraction force of the surface molecules per unit length of the material to which they are attached
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.
At surface Unbalanced forces Generate Tension Within Fluid All forces balance What is Surface Tension ?
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
AirFlow Expand Collapse Effect of Surface Tension on Alveoli size
Surfactant (表面活性物质) • 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.
Low S/unit Area Slider - Change Surface Area Increase Area DecreaseArea Surfactant High S/unit Area Area Saline Saline Tension Area dependence of Surfactant action
Normal (with surfactant) Saline Filled Volume L 6 3 Without surfactant RV Pleural Pressure 0 0 - 15 - 30 cm H2O Volume-pressure curves of lungs filled with saline and with air (with or without surfactant)
Physiology Importance of Surfactant • Reduce the work of breathing • Stabilize alveoli • Prevent collapse and sticking of alveoli • Maintain the dryness of the alveoli • Prevent the edema of the alveoli
Compliance • Distensibility (Stretchability, Elasticity): • 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. • Specific compliance (比顺应性, CL): the compliance per unit volume • CL = pulmonary compliance/residual volume
2. Inelastic Resistance • The inelastic resistance comprises • airway resistance (friction) • 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 : • internal friction between gas molecules • 2) friction between gas molecules and the walls of the airways
Laminar flow • … is when concentric layers of gas flow parallel to the wall of the tube. • The velocity profile obeys Poiseuille’s Law
Poiseuille and Resistance • Airway Radius or diameter is KEY. • radius by 1/2 resistance by 16 FOLD - think bronchodilator here!!
The gas flow in the larger airways (nose, mouth, glottis, and bronchi) is turbulent • Gas flow in the smaller airway is laminar • Breath sounds heard with a stethoscope reflect the turbulent airflow • Laminar flow is silent
Airway Resistance • 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 (哮喘), parasympathetic stimulation, etc. • Emphysema (肺气肿), which decreases small airway diameter during forced expiration • Increase of the density and viscosity of the inspired gas also increase the airway resistance
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 • Local factors • histamine binds to H1 receptors-constriction • histamine binds to H2 receptors-dilation • slow reactive substance of anaphylaxis (过敏反应)- constriction-allergic response to pollen • Prostaglandins (前列腺速) E series - dilation • Prostaglandins (前列腺素)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
Pulmonary Volumes • Tidal volume (潮气量) • Volume of air inspired or expired during a normal inspiration or expiration (400 – 500 ml) • Inspiratory reserve volume (补吸气量) • Amount of air inspired forcefully after inspiration of normal tidal volume (1500 – 2000 ml) • Expiratory reserve volume (补呼气量) • Amount of air forcefully expired after expiration of normal tidal volume (900 – 1200 ml) • Residual volume (残气量,RV) • Volume of air remaining in respiratory passages and lungs after the most forceful expiration (1500 ml in male and 1000 ml in female)