Presentation on theme: "Respiratory System Aim: Gas exchange: O2 to the cells & CO2 out of the body. Regulation of pH of extracellular fluid Respiration: the different processes."— Presentation transcript:
Respiratory System Aim: Gas exchange: O2 to the cells & CO2 out of the body. Regulation of pH of extracellular fluid Respiration: the different processes by which we finally obtain energy from different food stuffs
Respiration processes includes: 1- external respiration: a) pulmonary ventilation; gas exchange between lung & atmosphere b) pulmonary respiration; gas exchange between alveoli & blood 2- gas transport; O2 & CO2 transport in the blood & body fluids to & from the cells 3- internal respiration: a) gas exchange between cells & tissue fluids b) chemical reactions that end by release of energy
Mechanics of respiration The lungs are enclosed in an air tight compartment & the only connection with atmosphere is through the mouth & nose The lungs are surrounded by minute space called pleural space that contains a film of fluid to lubricate the movement of the lungs The pleural space is lying between 2 layers of pleura; visceral pleura, attached to the lungs & parietal pleura lining the inner surface of thoracic cage and diaphragm The chest wall is formed of muscles, ribs, vertebrae, skin & subcutaneous tissue
When external intercostal ms contract….. They raise the upper ribs & sternum…….. Increasing the antero-posterior diameter of the chest….. 23 – 30% of volume change and slightly the transverse diameter…1-2% When diaphragm contracts…….becomes less convex, pushes the abdominal viscera downwards…….. Increases the vertical diameter of the chest ….70% of the increase in volume
descent of diaphragm elevation of rib cage V1V1 V2V2 VaVa VbVb V 1 < V 2 V a < V b
Intra-alveolar pressure These changes in the intra alveolar pressure are caused by Changes in the Volume of the lungs. At the end of expiration with the glottis open, it is atmospheric During inspiration, the chest size increases, the pressure falls below atmospheric(-1), air will flow into the lungs During expiration, the lung recoils, the intra-alveolar pressure rises above atmospheric (+1), air flows out of the lungs.
The Intrapleural Pressure Def: It is the pressure inside the pleural sacs Value: It is always Negative. at the end of normal expiration: -2 at the end of normal inspiration: -6 to -8 --During forced inspiration: -30 to -70 --During forced expiration with the glottis closed +50 (Valsalva experiment) *Functions of the intra pleural pressure 1-It helps lung expansion. 2-It helps venous and lymphatic return. *Causes of negativity of intrapleural pressure: Tendency of the lung to recoil and tendency of the chest to expand. At equilibrium, these two opposing forces lead to the negativity of intrapleural pressure Causes of the tendency of the lung to recoil 1)Elastic tissues in the lungs 2)The surface tension of the fluid lining the alveoli. At the air water interface, the attractive forces between the water molecules make the water lining like a stretched balloon that tries to shrink. This force (Surface tension) is strong enough to collapse the alveoli. * If air is introduced into the pleural space: 1- the lung will collapse 2- the chest will expand 3- the intrapleural pressure increases, becomes atmospheric 4- venous return decreases
Mechanism of air flow between lungs and atmosphere Stimulation of the phrenic nerve, and the intercostal nerves… contraction of diaphragm & external intercostals…. Increasing the vertical & antero- posterior diameter of the chest….. Increase in chest volume …. Decrease intra-pleural pressure.. The lungs expands… decrease intra-alveolar pressure….the air flows into the lungs It is an active process (involving muscle contraction)
Inspiration The diaphragm and external intercostal muscles (inspiratory muscles) contract and the rib cage rises The lungs are stretched and intrapulmonary volume increases Intrapulmonary pressure drops below atmospheric pressure ( 1 mm Hg) Air flows into the lungs, down its pressure gradient, until intrapleural pressure = atmospheric pressure
Expiration When inspiration ends, the muscles relax…. Decrease in the diameters of the chest…. The thoracic wall recoils …. The intra-pleural pressure rises…the elastic lungs recoil… compressing the air… rising of the intra- alveolar pressure… air is forced out It is a passive process (relaxation of muscles & recoil of elastic fibers)
Accessory muscles of respiration During quiet breathing, only 1/10 of the external intercostal muscles & diaphragm are active & expiration is a passive process With more powerful respiration, all fibers of intercostal & diaphragm are active, this increases the pulmonary ventilation 10 folds More forced respiration, there is accessory ms of inspiration (sternomastoid, serratus anterior, scaleni) & expiration (internal intercostal, abdominal recti ms), these make respiration more deep & decrease airway resistance
Ventilation It is the movement of air between lungs & atmosphere
Lung volumes Lung volumes: 1- Tidal volume (TV or Vt): it is the volume of air inspired or expired each cycle during normal quiet breathing, it is 500 mL 2- Inspiratory reserve volume (IRV): it is the maximum volume of air can be inspired after normal inspiration, it is 3000 mL 3- Expiratory reserve volume (ERV) it is the maximum volume of air can be expired after normal expiration, it is 1100 mL 4- Residual volume (RV): it is the volume of air remaining in the lungs after maximal expiration, it can not be expired, it prevent lung collapse & aerates the blood between breaths, it is 1200 mL
Lung volumes Vital capacity (sum total of all except RV)
Lung capacities A capacity is two or more volumes added together 1- Inspiratory capacity (IC): it is the maximum volume of air can be inspired after normal expiration. IC= TV+ IRV= 3500mL 2- Functional residual capacity (FRC): it is the volume of air remained in the lung after normal expiration FRC=ERV+RV= 2300mL.
Lung capacities 3-Vital capacity: (VC) it is the maximum volume of air can be expired after maximal inspiration. VC=IRV+ERV+TV=4600mL Total lung capacity: (TLC) it is the volume of air contained in the lung after deep inspiration. TLC=IRV+ERV+TV+RV= 5800mL All lung capacities are 20-25% more in males than females, more in athletes, less in recumbent position
Work of Breathing Energy required during normal respiration is 2-3% of the total energy expenditure, it increases in heavy exercise, but the ratio to total energy expenditure remains nearly the same. Work is done only in inspiration, but normal expiration is a passive process depending on the elastic recoil of the lung and chest wall. *Contraction of expiratory muscles occurs when air way resistance or tissue resistance increases as in asthma. (expiration needs work) Energy required during normal respiration is 2-3% of the total energy expenditure, it increases in heavy exercise, but the ratio to total energy expenditure remains nearly the same. Work is done only in inspiration, but normal expiration is a passive process depending on the elastic recoil of the lung and chest wall. *Contraction of expiratory muscles occurs when air way resistance or tissue resistance increases as in asthma. (expiration needs work)
Work of breathing Energy are needed for contraction of respiratory muscles. Increase when accessory ms contracts in deep& forced breathing 1- overcome the viscosity of the expanding lung (non elastic tissue resistance) 2- stretch the thoracic & lung elastic fibers & overcome the surface tension in the alveoli. This energy increase if surfactant is deficient 3- overcome airway resistance. This increase in bronchial asthma or obstructive emphysema
Compliance It is the ability to expand or stretch It is the reciprocal of elasticity (recoil of stretched elastic fibers) It is a useful measurement for diagnosis of respiratory diseases It is the change in length or volume per unit change in stretching force. Normal compliance of lungs & thorax = 0.11L/cmH2O pressure Normal compliance of lungs alone = 0.2 L/cmH2O pressure
Compliance High compliance means a given change in pressure moves a larger volume of air in the lungs Low compliance in fibrosis, congestion, oedema, bronchial obstruction or in increased surface tension The compliance is small in newborn, increases gradually with age, decreases in old age The main factors affect compliance are: congestion, size, surface tension
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. H 2 0 molecules at the surface are attracted to other H 2 0 molecules by attractive forces. – Force is directed inward, raising pressure in alveoli.
Surfactant Def: It is the surface active agent Composition: Phospholipid (dipalmitoyl lecithin), protein and Carbohydrates Secretion: produced by alveolar type II cells. Action: Lowers surface tension. Functions of surfactant: 1)Facilitates lung expantion 2)Prevent lung collapse As alveoli radius decreases, surfactant’s ability to lower surface tension increases. 3)Prevent pulmonary oedema Surfactant Deficiency: RDS of the newborn. The lung is rigid and oedematous and the alveoli collapse
air What is surface tension ? How do we deal with surface tension??
Alveolar Ventilation The inspired air is distributed between: 1- The anatomical Dead Space: It is the part of the respiratory system where no gas exchange takes place. It extends from the mouth to the terminal bronchioles. Ventilation of dead space is said to be wasted ventilation.=1/3 of the resting tidal volume 2- the rest of air occupies the respiratory bronchioles, the alveolar ducts, alveoli and alveolar sacs, gas exchange takes place Minute Ventilation= VT (ml/breath) x Respiratory rate (breath/min) =500 x 12 =6000 ml/min. Alveolar ventilation= 2/3 x 500 x12 =4000 ml/min. Dead space ventilation= 1/3 x 500 x 12 = 2000ml/min.
Measurement of the dead space Bohr`s equation: Anatomical dead space= tidal volume x (alveolar CO2- expired CO2) Alveolar CO2
Physiological dead space The anatomical dead space + unperfused alveoli In Normal person the anatomical dead space= the physiological dead space In certain diseases the physiological dead space may be 10 times anatomical dead space or more.
Gas exchange Alveolar air contains less O2 & more CO2 than inspired air (mixed with air that was in the dead space) Expired air constitute a mixture of alveolar air and dead space (which is atmospheric) The exchange of oxygen & CO2 between alveoli & blood is passive by diffusion
Comparison between the respiratory gases Expired air Alveolar air atmospheric air 120mmHg104mmHg159mmHgO2 27mmHg40mmHg0.3mmHgCO2 47mmHg47mmHgvariableH2O 566mmHg569mmHg597mmHgN2 760mmHg760mmHg760mmHg Total pressure
Gas exchange O 2 of air is higher in the lungs than in the blood, O 2 diffuses from air to the blood. C0 2 moves from the blood to the air by diffusing down its concentration gradient. Gas exchange occurs entirely by diffusion. Diffusion is rapid because of the large surface area and the small diffusion distance.
Diffusion is determined by several factors : 1- Alveolar- capillary membrane: Semi-permeable: separates alveolar air from pulmonary capillary blood Layers: Fluid film lining the alveoli Alveolar membrane Interstitial fluid Capillary wall
Total AREA available for diffusion of gases is large in human 70 m 2 Diffusion PATH LENGTH is very small, =2µm Pulmonary Epithelium The respiratory membrane:
2- Partial pressure gradient of gases across the alveolar capillary membrane: The partial pressure of oxygen in mixed venous blood is 40mmHg The partial pressure of oxygen in alveolar air is 100mmHg O2 diffuses from the alveoli to the capillary blood along a partial pressure gradient of 60mmHg The partial pressure of CO2 in mixed venous blood is 46mmHg The partial pressure of CO2 in alveolar air 40 mmHg CO2 diffuses along pressure gradient of 6 mmHg
3- the physical properties of gases: Solubility: the more soluble the gas, the faster its diffusion (CO2 is 23 fold more soluble than O2) Molecular weight: the higher the molecular weight of the gas, the slower its diffusion The solubility of a gas & its MW determine diffusion coefficient (the rate of diffusion through a unit area of a given membrane per unit pressure difference. Diffusion coefficient = solubility / √ molecular size The diffusion coefficient of O2 = 1.0 The diffusion coefficient of CO2 = 20 CO2 can diffuse 20 times faster than O2 Diffusion failure affects O2 before affecting CO2 4- surface area of the alveolar capillary membrane: 70square meter When increased, gas exchange increases
5-Ventilation- blood flow ratio: Effective surface area means the functional alveoli in contact with functioning capillaries, where the alveolar air comes in contact with capillary blood Ventilation / perfusion ratio = alveolar ventilation/ pulmonary blood flow In a normal adult male at rest Alveolar ventilation is 4L/min Pulmonary blood flow is 5L/min Ventilation / perfusion ratio=0.8 Diseases that affects the alveolar capillary membrane will lower the diffusion capacity of O2 Fatal levels of O2 diffusion impairment is reached long before CO2 diffusion is affected
Exchange of gases Alveolar air Atmospheric air pressure%pressure% 40mmHg5.6%0.3mmHg0.04% CO 2 105mmHg14.8%159mmHg20.95% O2O2O2O2 568mmHg79.6%600mmHg79.00% N2N2N2N2
Gas Transport by The Blood Oxygen transport: O2 is transported in the blood in two forms: 1- Attached in loose combination with Hb Over 98% of arterial O2 is carried in the form of oxyhemoglobin. PO2 in systemic arterial blood is usually below 100mmHg eventhough it may be 100mmHg in the pulmonary capillary blood, because some venous blood mixes with arterial blood 2- Physically dissolved: less than 2% of O2 in the arterial blood. At PO2 100mmHg, about 0.3ml O2 dissolve in 100ml blood. In venous blood, PO2 is 40mmHg, about 0.12ml O2 /100ml blood is dissolved.
Oxyhaemoglobin Haemoglobin has great affinity for O2 It combines loosely & reversibly with O2 by process called oxygenation (not oxidation) The reaction is very fast, less than 10 msec The reaction increases with the increase in PO2 The relation between oxyHb formation and PO2 is studied in the Oxyhaemoglobin dissociation curve
Hemoglobin Each hemoglobin has 4 polypeptide chains and 4 hemes. In the center of each heme group is 1 atom of iron that can combine with 1 molecule 0 2. Fe remains in the ferrous form (Oxygenation and not oxidation) Hb carries 65 times as much as plasma at PO2 of 100mmHg Insert fig. 16.32 Figure 16.32
Hemoglobin dissociation curves: Def:It is a relationship between PO2 and %HbO2 saturation (and not content) Characteristics: 1-It is not linear, it is sigmoid (S shaped) with flat part and steep part. Causes of S shaped curve Hb is formed of 4 sub units which load or unload with different affinity. Oxygenation of one haem unit leads to configurational change in the Hb molecule, increasing affinity of the second, and oxygenation of the 2 nd, increasing affinity of the 3 rd,etc.. The dissociation curve starts slowly, but rapidly gained sigmoid shape 2-there is steep rise in the percentage saturation of Hb between PO2 0& 75mmHg 3- above 75mmHg, there is slow rise of the curve, becoming more or less flat at PO2 of 80mmHg
1gm of Hb binds up to 1.34ml O2 The partial pressure of O2 in the arterial blood is about 95mmHg,Hb is 97% saturated (Hb concentration is 150gm/L, O2 content is 195ml/l of blood) At PO2 40mmHg, Hb saturation is 75% saturated. At rest, Arterio-venous difference (O2 uptake by tissues) is about 40-45ml /L of blood During exercise, oxygen uptake by tissues increase, PO2 drops to 15 mmHg, % saturation 20%, O2 content=40ml During exercise, the arterio-venous O2 difference, 150ml/L Quantity of O2 carried in a volume of blood is dependent on PO2 & Hb concentration.
Factors which affect Oxy-Hb dissociation curve Shift to the right: (facilitate the release of O2 at tissues) → ↓ affinity of Hb for O2 → easier giving O2 to the tissues 1- ↑ PCO2: Bohr effect 2- ↓ pH :due to lactic acid during exercise, more CO2 production 3- ↑ temperature: active tissues during oxidative processes more heat is released, more O2 supply to the tissues 4- ↑ 2,3 DPG: found in RBCs & increases in cases of hypoxia & high altitudes
ml O 2 /100 ml blood 0 5 10 15 20 High affinity only Can’t release much O 2 to tissues Low affinity only Doesn’t hold on to But can’t pick up much O 2 at tissues much O 2 at lungs S-shaped hemoglobin curve Releases much Becomes saturated O2 at tissues with O 2 at lungs Advantages of “S-shaped” curve for Hb-O 2 association Active cell
Factors shift the curve to the left: (increases Hb affinity to O2, Easier picking up O2, Difficult release of O2) 1- ↓ PCO2 at lungs 2- ↑pH 3- ↓ temperature 4- foetal Hb: as it binds to 2,3 DPG less effectively
Dissolved O2: ↑ PO2….↑ dissolved O2 O2 is poorly soluble In 100ml blood, 0.003ml O2 dissolve /1mmHg PO2 In arterial blood, 0.3 ml/100ml In venous blood, 0.12 ml/100ml The dissolved O2 is at equilibrium with the O2 combined with Hb It is the dissolved O2 gets transferred to tissues & become replaced from O2 carried by Hb Although dissolved O2 is less than 2% of total O2 transport, it is essential for tissues that do not have blood supply, as cartilage & cornea which depend on O2 dissolved in tissue fluids ↑ dissolved O2 by breathing pure or hyperbaric O2 (this is the base of O2 therapy)
CO2 transport It is transported from tissues that produce CO2 to the lungs, where it is unloaded, removed to the atmosphere It is transported by plasma & RBCs
Transport of CO2 in the blood: 1- dissolves in the plasma & RBCs: 5%, it is important because it determines the tension (40mmHg in arterial blood & 46 mmHg in venous blood) & determine the direction of flow 2- chemically combined: 95% of CO2 a-carbamino compounds: carried by plasma proteins & hemoglobin b- bicarbonates: In the form of KHCO3 & NaHCO3 43ml/100ml in arterial blood 56ml/100ml in venous blood
Tidal CO2 transport It is the volume of CO2 added to each 100ml of arterial blood during its flow through the tissues CO2 produced by active cells as a result of metabolism Normally 4ml/100ml blood during rest (52-48) CO2 carried in 3 forms in plasma: 1- dissolves in the plasma 2- Bicarbonates: 3- Carbamino proteins:
CO 2 Tissues C.A. CO 2 + H 2 O H 2 CO 3 H + + HCO 3 - HCO 3 - slow HbO 2 Hb. H + O 2 + O2O2 How is CO 2 carried by the blood?? Plasma: dissolved HCO3- carbamino proteins RBCs: dissolved HCO3- Carbamino Hb Hb + CO 2 Hb. CO 2 (carbamino cmpd.)
Control of ventilation Mechanism of regulation involves: Nervous & chemical The respiratory centre: In the medulla & pons. Can be divided into 4 groups; 1- dorsal respiratory group: (Rhythmicity centre) In the medulla, they are inspiratory neurons, they discharge rhythmically during resting & forced inspiration 2- ventral respiratory group:( expiratory neurons) In the medulla, they are inactive during resting breathing Activated in forced ventilation as in exercise
3- Apneustic centre: In the pons It sends excitatory impulses to dorsal respiratory group, potentiates the inspiratory drive. Section to remove the apneustic impulses…. Gasping breathing( shallow inspiration followed by long expiration) Receives inhibitory impulses from vagus nerve during inflation of the lungs (Hering Breuer reflex) Receives inhibitory impulses from Pneumotaxic centre in the upper pons Section of vagus & abolishing the impulses from pneumotaxic centre, results in apneustic breathing (prolonged inspiration)
4-Pneumotaxic centre: in the upper pons It sends inhibitory impulses to apneustic center & to inspiratory areas to switch off respiration
Both inspiratory & expiratory areas are influenced by impulses from pneumotaxic & apneustic center & higher centers DRG are the integrating site for different inputs
Nervous control of ventilation The rhythmicity centre sends sends excitatory impulses via phrenic & intercostal nerves to diaphragm, external intercostal muscles The rhythmicity center receives impulses from higher brain centers, brain stem, special receptors Higher brain centers: 1- impulses from cerebral cortex: voluntary hyperventilation, voluntary apnea 2- impulses from cerebellum: coordinates breathing with other activities as swallowing, talking, coughing 3- Impulses from hypothalamus: centers of emotions & temperature regulation, breathing modified during emotional stress, changes of temperature, (panting of dogs)
Centers in the medulla & pons: 1- the rhythmicity center interconnected with the cardiac & vasomotor centers located in the medulla 2- apneustic center sends excitatory impulses to rhythmicity center to produce deep inspiration 3- pneumotaxic center to rhythmicity center to inhibit deep inspiration & to apneustic center
Special receptors: 1- sensory vagal fibers: when lung is inflated, stretch receptors are stimulated, send inhibitory impulses through vagus to inhibit the apneustic center (Hering Breuer inflation reflex) protects the lung from over- inflation. There is a weaker Hering Breuer deflation reflex 2- active & passive movement of joints & muscles: propioceptive stimulation stimulate breathing in exercise 3- skin receptors: noxious stimuli stimulate breathing 4- baroreceptors in aortic arch & carotid sinus modify breathing
Chemical control of ventilation Central & peripheral chemoreceptors: Peripheral chemoreceptors: Site: in the carotid & aortic bodies Stimuli: ↓ in arterial PO2, ↑PCO2, ↓pH Stimulation: send stimulatory impulses to rhythmicity center via glossopharyngeal & vagus nerves
Central chemoreceptors Central chemoreceptors: Site: medulla Stimuli: H+ ion concentration in the CSF H+ ion can not cross the blood brain barrier, but it increases in the CSF secondary to ↑PCO2 in the blood, which pass through BBB to the CSF It sends simulatory impulse to stimulates ventilation
BBB CSFPlasma CO 2 HCO 3 + H + CO 2 HCO 3 + H + Respiratory Alkalosis high pH CSF limits Hyperventilation When pH CNS returns to norm (HCO 3 pumped out) V E is less restrained
Chemoreceptors Monitor changes in blood P C0 2, P 0 2, and pH. Central: – Medulla. Peripheral: – Carotid and aortic bodies. Control breathing indirectly. Insert fig. 16.27 Figure 16.27
Hypoxia It means deficient O2 supply to the tissues Causes: 1- interference with O2 in the lungs 2- interference with O2 transport in blood 3- interference with O2 delivery to the tissues
Hypoxia Types: 1- hypoxic hypoxia: low PO2 in the arterial blood 2- anaemic hypoxia: lowering O2 carrying capacity of the blood 3- stagnant hypoxia: slow circulation 4- histotoxic hypoxia: disturbed uptake of O2 by tissues Treatment: O2 therapy, correcting underlying cause
Hypoxic hypoxia Causes: Any interference with normal oxygenation of the arterial blood leading to low PO2 as in: 1- low atmospheric PO2 as in high altitude 2- ventilation defects: as in paralysis of respiratory ms, airway obstruction, poisons that inhibits the respiratory center as morphine & barbiturates (high CO2) 2- interfere with normal O2 diffusion in the lung 3- mixing of arterial blood with venous blood as in veno- arterial shunts & congenital heart disease Low PO2, low % saturation of Hb, low O2 content in the arterial &venous blood
Anaemic hypoxia Causes: anaemia, abnormal hemoglobins, CO poisoning PO2 is normal in the arterial &venous blood % saturation is normal in the arterial &venous blood (except in CO poisoning) Low O2 content in the arterial &venous blood
Stagnant hypoxia Types: 1- localized: e.g. disturbed circulation in a limb 2- generalized as in heart failure normal arterial blood PO2, % saturation,O2 content ↓Venous blood PO2, ↓ % saturation, ↓Content of O2
Histotoxic hypoxia Disturbance of O2 uptake due to poisoning of cellular enzymes e.g. cyanide poisoning or tissue oedema normal arterial blood PO2, % saturation,O2 content ↑ Venous blood PO2, ↑ % saturation, ↑ Content of O2
Cyanosis Def: blue coloration of the skin & mucous membrane Cause: reduced Hb more than 5gm/100ml Types: Localized type: in the tips of fingers in cold Generalized: in veno-arterial shunts, severe hypoxia in the newborn, or at very high altitude It is more common seen in polycythemia it s very rare in anaemia (the person already has low Hb, so he cannot have 5gm reduced Hb)