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Mechanics of respiration By Dr. M.B.Bhat. Mechanics of Respiration • Ventilation –Breathing in & out of air from lungs • Inspiration –Taking in of air –Active process • Expiration –Given out of air –Passive process (normally) –Active process in forced expiration • Normal respiration by • Negative pressure breathing – • Advantage –increase venous return Normal Respiration • During inspiration – • By operation of respiratory pump (Muscle Force)—Thorax expand –along with Lungs also expand– • Decreases pressure in thoracic cavity • By over-coming resistance • Rushing of air from atmosphere through the respiratory tract into lungs • Till intra-pulmonary & atmospheric pressure equals • During expiration – (cessation of inspiratory activity) • By elastic recoiling – Thorax assumes its original position –Lungs get compressed – • Thoracic cavity pressure rises – • Air goes out (through the same routes) –till the air pressure between intra-pulmonary & atmospheric are equal • Hence normal expiration is apassive process Mechanism of respiration • Involves 3 processes • Creation of Force (for operation of respiratory pump) –by respiratory muscles • Pressure changes (in the thoracic cavities) • Resistance to over come (for air movements) Respiratory muscles –Inspiratory & Expiratory muscles • Inspiratory muscles – • Chief inspiratory muscles (operate during quite respiration) –Diaphragm & External inter-costal muscles • Expiratory muscles –(operate only during forceful expiration) –Internal inter-costal muscles; Abdominal muscles • Accessory respiratory muscles (operate only in forceful respiration) –Scaleni, Sternocledomastoid, Anterior Serati, Extensor muscles of vertebral columns Diaphragm –Chief inspiratory muscle • Nerve supply –Phrenic nerve (C3,4&5) • Contraction of diaphragm flatten it towards abdomen by 1.5cm (during quite respiration) & up to 7cm (during forceful respiration) • Result –increase in vertical dimension of thoracic cavity • Account for 75% change in intrathoracic volume during quite respiration (2/3rd of Tidal volume) • Though important for respiration not absolute necessity External inter-costal muscles • Origin –From the lower border of one rib to -• Insertion— upper border of the rib below • Course –From origin pass obliquely forwards & downwards to the lower rib • Nerve supply –Nerve to inter-costal muscles (T1 to T12) • Contraction –leads to upward & forward movements of ribs Thoracic cavity • Thoracic lid –made up of 1st pair of ribs jointed between vertebral column & manubrium sterni –moves very little (in hyperpnea manubrium moves upwards –thereby increase antero-posterior diameter) • Upper costal area –2nd to 6th ribs –slope obliquely downward & forward from posterior to anterior • Lower costal area –7th to 10th ribs – swing outward & upwards • As Thoracic lid is immovable – • Contraction external inter-costal muscles pull the lower ribs causing upward & outward movements • Upward movements push manubrium upwards –increase antero-posterior diameter –Pump-handle movement • Outward movements –by virtue of the bowed mid-part of ribs –increase transverse diameter –Buckethandle movement • By the contraction of diaphragm— • Vertical dimension of thoracic cavity increases – to about • 1.5cm during quite respiration & • 7cm during forceful respiration • By the action of inter-costal muscles & accessory muscles – • Circumference of chest increases by – • 1cm in quite respiration • 5 to 11cm in forced respiration • Expiration isa quiet passivemotion • Cessation of inspiratory muscle activity – • Due to elastic recoiling tendency of lungs & chest –expiration takes place • For forceful expiration – • Internal inter-costal muscles (arrangement of which is quiet opposite to external inter-costal muscles) draws the ribs inwards & downwards • Abdominal muscles –increase intra abdominal pressure and abdominal contents push diaphragm upwards; & draws the lower ribs downwards & medially thereby decrease thoracic dimension Pressures of the thoracic cage • Two types of pressures 1. Intra-Pleural pressure (Or) Intra-Thoracic pressure (Pressure between two pleura) 2Intra-Alveolar pressure (Or) Intra-Pulmonary pressure (Pressure in the lungs –alveoli) Pressures in the thoracic cage Intra pleural pressure (or) Intra thoracic pressure – • Normal value—During quite respiration • At the beginning of inspiration= –3 cm H2O (–2mm Hg) • At the end of inspiration= –7.5 cm H2O (–6mmg) • Max. in forced inspiration = –20 mm Hg • Ma. In forced expiration = +40 mm Hg Measurement of intra pleural pressure • Direct-• Indirect– Principle --pressure at lower 3rd of esophagus beneath the lungs is same as intra thoracic pressure –as esophagus also present in the thoracic cavity. • Procedure - Catheter tipped with a balloon is swallowed & kept at lower 3rd of esophagus and inflate & connect the catheter with manometer. • Reasons for negative pressure (explain) Significance of intra pleural pressure • Always negative (sub-atmospheric) in normal respiration • Prevents collapse of alveoli • Prevents collapse of small air ways • Aids in venous return (Respiratory pump) • In Pneumothorax it becomes equal to atmospheric pressure –alveoli collapse Intra alveolar pressure (or) Intra pulmonary pressure • At the beginning of inspiration & at the end of expiration –it is zero • During inspiration= minus 1to 4 mm Hg • During expiration – Plus 1to 4 mm Hg • During forced inspiration – minus 20 mm Hg • During forced expiration – plus 40 mm Hg • Measurement – “Mouth pressure” Trans-pulmonary pressure • Difference between intra thoracic pressure & intra pulmonary pressure • Pressure operating inner & outer wall of the alveoli • Measure the elastic forces in the lungs Resistances • • 1. 2. Elastic resistance & Non-elastic resistances –are; Air-way resistance Non-elastic tissue resistance Elastic resistance • Resistance due to elastic nature of lungs & thoracic cage • Reciprocal of elastic resistance is compliance Compliance • Compliance is the measure of stretch ability or elasticity • StaCompliance is change in volume by unit change in pressure (∆V/∆P) – L/cm H2O • Specific compliance – Compliance/FRC (in L per cm H2O per L) Types of compliances • As both lungs & thoracic cage has elastic nature –in the respiratory system the various compliances are; • Lung compliance (L.C) • Thoracic compliance (Th.C) • Total compliance (T.C) -- (both L.C & Th.C) • Compliance is measured in static condition Lung compliance • Volume of lung expansion for each unit increase in intra pleural pressure • Normal value –0.22L / cm H2O • (range – 0.09 to 0.26 / cm H2O) • In infant – 0.005 / cm H2O Factors affecting lung compliance • Size • Phases of Respiratory cycle – Deflation & Inflation • Gravity –less at apices • Factors Compliance -• Emphysema & Old age • Factors Compliance -• Pul. Congestion, Pul. edema & fibrosis -- Total compliance • Normal value – 0.11L / Cm H2O • Measurement -- ∆V / ∆P (Airway pressure –Intra pulmonary Pressure) Thoracic compliance • • • • Is due to Sterno-costal joints Normal value – 0.22L / cm H2O Cannot measure directly Calculate by using the equation- Factors determining lung compliance 1. Elastic nature of pulmonary tissue (contribute 1/3rd) 2. Surface tension (contribute 2/3rd) Elastic nature of pulmonary tissue • Inter woven of elastin & collagen fibers like nylon stocking arrangement • In emphysema –degradation of elastin & collagen frame work –leads to increase distensiblity • In old age –change in physicochemical properties of elastin & collagen –increase distensibility • In pul.fibrosis –increase in interstitial tissue –stiffness – distensibility Surface tension • Of pure water =70dynes/cm • Of Alveolar fluid without surfactant =50dynes/cm • Of Alveolar fluid with surfactant =5 dynes/cm • Laplace law – P = 2T/r • Average size alveoli (100µm) – the collapsing pressure Or distending pressure (P)-• with surfactant; P= 4cm H2O (3 mm Hg) • Without surfactant; P = 18cm H2O Surfactant • • • • • • • • • • Surface tension lowering agent Secreted from Type II cells Contains – Dipalmitoyl phosphatidyl choline (DPPC) (Dipalmitoyl lecithin) – 62% Phosphatidly glycerol –5% Other phospholipids –10% Neutral lipids –13% Protein – 8% Carbohydrate – 2% And calcium ions Mechanism of action of Surfactant • Surfactant consist of mainly of– Phospholipids • Phospholipids have hydrophilic (phosphate portion) & hydrophobic (lipid portion) ends • The hydrophilic end dissolves into the alveolar fluid; while the hydrophobic end facing the exterior. • As the hydrophobic portion (lipid) has attraction towards gas, the inward attraction of the molecules of the surface area can be minimized & thereby lowering the surface tension. Significance of surfactant • Surface tension (by 1/12th –1/2) • Compliance • Respiratory work load is • Helps in stability of alveoli of unequal size • Prevent collapse of alveoli during expiration • Prevent bursting of alveoli during inspiration • Keeps the alveoli dry (prevent pul. Congestion) Factors affecting surfactant • Factors surfactant – 1. Occlusion of main bronchus 2. Occlusion of pulmonary artery 3. Long-term inhalation of 100% O2 4. Cutting of both vagi 5. Cigarette smoking Factors surfactant – 1. Thyroid hormone -- production 2. Glucocorticoids – accelerate maturation Clinical significance of surfactant • (Infant) Respiratory distress syndrome (IRDS) or • Hyaline membrane disease (due to deficiency of surfactant in fetal life) Pulmonary Resistance 1. Non-elastic tissue resistance (Viscous resistance) 2. Air-way resistance Resistance are measured during dynamic condition R = ∆P/ V (flow) in liter/sec Pulmonary resistance (Total resistance) • Air way resistance + viscous resistance • Obtained by using intra pleural pressure • 3.5cm H2O per liter per second Air way resistance • Due to friction between molecules of flowing gas & also with walls of the tube • Raw = (Pmouth – Palv) / V in L/sec • Normal value = 0.6 to 2.4 cm H2O per Liter per second • LFTs used in determine Raw are – • PEFR; MVV; FEV • Raw --Increases in obstructive type respiratory diseases Factors determining air way resistance • • • • • • • Factors air way resistance Decrease lung volume Decrease in diameter Total cross sectional area Increase in Density & viscosity Types of flow -Dynamic compression of air ways Non-elastic tissue resistance • Resistance offered by the nonelastic tissue of the thoracic cavity – Lungs, rib-cage, diaphragm & abdominal content • Responsible for the Hysteresis (closed loop) type of pressurevolume relation of respiratory cycle • Account for 20% of total pulmonary resistance • Itis increased greatly in Emphysema Thoracic resistance • Pulmonary resistance (Airway resistance + viscous resistance) + chest wall resistance • Thoracic cage resistance –no measurement developed so far Work done of breathing • Work done = Pressure x volume • Normal value of total work done = 0.3 to 0.8 kg m/min • Elastic work –65% • Non-elastic work –35%; out of this • Airway resistance work –28% • Viscous resistance work (Inertia work)–7% • Work of breathing increases in – • Emphysema, asthma, congestive cardiac failure with dyspnea & orthopnea • During heavy breathing – air way work is more • In obstructive –airway work increases • In fibrosis –elastic & nonelastic tissue work increase • In pulmonary diseases all types of work are increased • Work of breathing can be calculated from relaxation pressure curve • During respiration, work done not only to overcome elastic resistance, but alsofor frictional airway & non-elastic resistance, the respiratory curve is hysteresis loop Efficiency of respiratory muscle • Efficiency = work done per unit oxygen consumption • = Useful work X 100/ Total energy expended (O2 cost) • O2 cost is 0.5 to 1ml/L of pulmonary ventilation • Mechanical efficiency is 8% • Voluntary hyper ventilation it is — 30% • In exercise though total work rises; the energy cost still represents <3% of total energy expanded. 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