Respiratory Module - Lecture Notes (PDF)

Respiratory module Session 3: Lecture 1: Mechanics of Breathing Ass. Lecturer Ali Jaafar Mohammed M.Sc. Medical Physiology 1 Intended learning outcomes By the end of this session, the student should be able to: 1. describe the mechanical s...

Respiratory module Session 3: Lecture 1: Mechanics of Breathing Ass. Lecturer Ali Jaafar Mohammed M.Sc. Medical Physiology 1 Intended learning outcomes By the end of this session, the student should be able to: 1. describe the mechanical system of the lungs and thorax 2.define the term 'compliance' of the lungs and state how, in principle, it is measured 3.describe the factors which affect the compliance of the lungs, including the role of surfactant 4.describe the factors which influence airway resistance in the normal lung and how airway resistance changes over the breathing cycle 2 Objective number 1 Describe the mechanical system of the lungs and thorax 3 Lecture 1: Mechanics of Breathing Inspiration is an active process. The space between the lungs and thoracic wall - the pleural space - is normally filled with a few milliliters of fluid, which forms a pleural seal holding the outer surface of the lungs to the inner surface of the thoracic wall. If, therefore the volume of the thorax cage changes so will the volume of the lungs. 4  Pleura Pleural fluid produced by pleural membranes – Acts as lubricant – Helps hold parietal and visceral pleural membranes together  7 The resting expiratory level? inward force of the elastic recoil of the lungs is balanced by the outward recoil of the chest wall Pleural pressures?? 8 9 Muscles of Inspiration In quiet breathing: The Diaphragm External intercostal In forced inspiration These are the sternocleidomastoid and scalene muscles of the neck, and serratus anterior and pectoralis major muscles. 10  I- Inspiration On DEEP inspiration there will be: 1. More contraction of the diaphragm (7 cm descent) and the external intercostal. 2. Contraction of the accessory muscles of inspiration : - Sternocleidomastoid: that elevates the sternum. - Serratus anterior: that elevates many ribs more. - Scaleni muscles: that elevates first rib. Lungs follow passively the movements of the chest wall due to presence of a thin layer of fluid between the parietal and the visceral pleurae. So, the two layers of pleura slide on each other but resist separation. The diaphragm is responsible for 75 % of inspiration, yet , when it is paralysed the external intercostal alone can produce inspiration needed for moderate activity. The resting expiratory level In the absence of muscular activity (when the respiratory muscles are relaxed) - there is an equilibrium position, when the inward force of the elastic recoil of the lungs is balanced by the outward recoil of the chest wall. This corresponds to the state of the lungs at the end of a normal quiet expiration. Breathing out involves passive recoil of the lungs in quiet expiration and contraction of the abdominal muscles and the internal intercostal muscles in forced expiration. 12 Muscles of expiration In quiet breathing, expiration is passive due to the elastic recoil of the lungs. In forced expiration, accessory muscles of expiration are used. These are the internal intercostal muscles & the abdominal wall muscles (external & internal oblique muscles and the rectus abdominis muscles) 13  14 Muscles of expiration These are the internal intercostal muscles & the abdominal wall muscles (internal oblique muscles and the rectus abdominis muscles). 15  II- Expiration Now expiration will be caused by contraction of: 1- Abdominal muscles : that will increase the pressure inside the abdominal cavity pushing the diaphragm upward. 2- Internal intercostal muscles : that causes “lowering” of the ribs leading to decreased transverse & A-P chest diameters. Respiratory Rate : normally it is about 12- 16 cycles /min. Respiratory cycle : is composed of : 1-Short inspiration (I) 2- Longer expiration (E) 3-Expiratory pause (during which the glottis is “closed”). Objective 2 Define the term 'compliance' of the lungs and state how, in principle, it is measured 18 Compliance The stretchiness of the lungs is known as compliance. Compliance is defined as the volume change per unit pressure change. Volume change per unit pressure change Starting volume of lung 19 Figure: Compliance, - normal, increased & decreased 20  There are 2 different curves according to different phases of respiration.  The curves are called :  Inspiratory compliance curve  Expiratory compliance curve  Shows the capacity of lungs to “adapt” to small changes of transpulmonary pressure.  compliance is seen at low volumes (because of difficulty with initial lung inflation) and at high volumes (because of the limit of chest wall expansion)  The total work of breathing of the cycle is the area contained in the loop. Objective 3 Describe the factors which affect the compliance of the lungs, including the role of surfactant 22 The elastic properties of the lungs arise from two sources:  Elastic tissues in the lungs  Surface tension forces of the fluid lining the alveoli 23 Compliance of lungs occurs due to elastic forces. A. Elastic forces of the lung tissue itself B. Elastic forces of the fluid that lines the inside walls of alveoli and other lung air passages Elastin + Collagen fibres Is provided by the substance called surfactant that is present inside walls of alveoli. Compliance is reduced when (1) The pulmonary venous pressure is increased and the lung becomes engorged with blood (2) There is alveolar edema due to insufficiency of alveolar inflation (3) The lung remains unventilated for a while e.g. atelectasis and (4) Because of diseases causing fibrosis of the lung e.g. chronic restrictive lung diseases. On the contrary in chronic obstructive pulmonary disease (COPD, e.g. emphysema) the alveolar walls progressively degenerate, which increases the compliance. In asthma (hyperactive airway smooth muscle) the lung compliance is usually normal Surface Tension The airways and alveoli of the lungs are lined with a film of fluid which is increased in area as the lungs expand. 26 Surface tension of the alveolar fluid varies with the surface area of the alveolus As an alveolus expands, its surface area increases and the surfactant molecules are spread further apart, making them less efficient in reducing surface tension. Hence, as the alveolus expands the surface tension of the fluid lining it increases. As an alveolus shrinks, the surfactant molecules come closer together increasing their concentration on the surface and act more efficiently to reduce the surface tension. Hence, the effect of surfactant is to reduce surface tension forces greatly as area of the alveolus decreases. The force required to expand small alveoli is therefore less than that required to expand large ones. 27 This property of Surfactant also serves to stabilise the lungs by preventing small alveoli collapsing into big ones. The alveoli are, in effect, an interconnected series of bubbles. The pressure within a bubble is determined by the Law of Laplace: P = 2T/r p= pressure in the alveolus, T = surface tension r= radius of alveolus. Thus, if ‘T’ is constant, smaller bubbles (with a smaller radius ‘r ‘) would have higher pressures (P) within it. Therefore if two bubbles are connected by an airway the smaller bubble which has a higher pressure (P) within it will empty into the larger bubble which has a lower pressure. The effect of this would be that the larger bubbles will collect air from the smaller, bubbles which would collapse. 28 Alveoli vary in size, so if the surface tension (‘T’) was constant, the alveoli would collapse to form a few huge air filled spaces (known as bullae). This would be drastically reduce the surface area available for gas exchange, because the combined surface area of a few large bulla would be much less than the combined surface area of thousands of small alveoli. But this does not happen in the normal lung, because, as the alveolus expands increasing its radius ‘r’, the surfactant molecules are spread further apart, making them less efficient, thereby increasing the surface tension ‘T’. 29 Thus: As the alveolus expands the ‘r’ & ‘T’ both increase. As the alveolus shrinks the ‘r’ & ‘T’ both decrease. Therefore, different sized alveoli can have the same pressure within them. This stabilizes the lungs by preventing small alveoli collapsing into big ones. Lung surfactant is absent from alveoli of a fetus younger than about 25 weeks and is occasionally absent from full term babies, producing 'Respiratory Distress Syndrome'. 30 Surfactant: 1. It increases lung compliance by decreasing surface tension 2. It stabilises the lungs, by preventing small alveoli collapsing into big ones 3. It prevents the surface tension in alveoli creating a suction force tending to cause transudation fluid from pulmonary capillaries 31  Surfactant Phospholipid produced by alveolar type II cells. Lowers surface tension. Reduces attractive forces of hydrogen bonding by becoming interspersed between H20 molecules. As alveoli radius decreases, surfactant’s ability to lower surface tension increases. Disorder: Acute respiratory distress syndrome ARDS. 34  36 Surface tension of the alveolar fluid varies with the surface area of the alveolus as the alveolus expands the surface tension of the fluid lining it increases. As an alveolus shrinks, the surfactant molecules come closer together increasing their concentration on the surface and act more efficiently to reduce the surface tension. Hence, the effect of surfactant is to reduce surface tension forces greatly as area of the alveolus decreases. The alveoli are, in effect, an interconnected series of bubbles. The pressure within a bubble is determined by the Law of Laplace: P = 2T/r p= pressure in the alveolus, T = surface tension r= radius of alveolus 37  Surface Tension Law of Laplace: – Pressure in alveoli –directly proportional Insert fig. 16.11 to surface tension –inversely proportional to radius of alveoli – if surface tension were the same in all alveolus.... 38 39 Disorder: ARDS. Objective 4 describe the factors which influence airway resistance in the normal lung and how airway resistance changes over the breathing cycle 41  42 Airway Resistance The resistance of an airway to flow is determined by Poiseulles Law = Resistance = Pressure x viscosity of air x length of tube 8 Rate of flow P x (radius) 4  43 Resistance of a single tube increases sharply with falling radius. However, the combined resistance of the small airways is normally low because they are connected in parallel over a branching structure where the total resistance to flow in the downstream branches is less than the resistance of the upstream branch. Most of the resistance to breathing therefore resides in the upper respiratory tract, except when the small airways are compressed during forced expiration.  44 Overall: Work is done against the elastic recoil of lungs and thorax, greatest part of work being against more or less equally the elastic properties of lung tissues and surface tension forces in the alveoli. Resistance to flow through airways is of little significance to total work load of breathing in healthy subjects, though it can often be affected by disease.