Presentation on theme: "Respiratory System Aim:"— Presentation transcript:
1 Respiratory System Aim: Gas exchange: O2 to the cells & CO2 out of the body.Regulation of pH of extracellular fluidRespiration: the different processes by which we finally obtain energy from different food stuffs
2 Respiration processes includes: 1- external respiration:a) pulmonary ventilation; gas exchange between lung & atmosphereb) pulmonary respiration; gas exchange between alveoli & blood2- gas transport; O2 & CO2 transport in the blood & body fluids to & from the cells3- internal respiration:a) gas exchange between cells & tissue fluidsb) chemical reactions that end by release of energy
5 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
11 When external intercostal ms contract… 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
12 V2 V1 V1 < V2 Vb Va Va < Vb descent of diaphragm elevation of rib cageV1V2VaVbV1 < V2Va < Vb
14 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 atmosphericDuring inspiration, the chest size increases, the pressure falls below atmospheric(-1), air will flow into the lungsDuring expiration, the lung recoils, the intra-alveolar pressure rises above atmospheric (+1), air flows out of the lungs.
16 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 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
21 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 lungsIt is an active process (involving muscle contraction)
22 InspirationThe diaphragm and external intercostal muscles (inspiratory muscles) contract and the rib cage risesThe lungs are stretched and intrapulmonary volume increasesIntrapulmonary pressure drops below atmospheric pressure (1 mm Hg)Air flows into the lungs, down its pressure gradient, until intrapleural pressure = atmospheric pressure
25 ExpirationWhen 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 outIt is a passive process (relaxation of muscles & recoil of elastic fibers)
28 Accessory muscles of respiration During quiet breathing, only 1/10 of the external intercostal muscles & diaphragm are active & expiration is a passive processWith more powerful respiration, all fibers of intercostal & diaphragm are active, this increases the pulmonary ventilation 10 foldsMore 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
29 VentilationIt is the movement of air between lungs & atmosphere
30 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 mL2- Inspiratory reserve volume (IRV): it is the maximum volume of air can be inspired after normal inspiration, it is 3000 mL3- Expiratory reserve volume (ERV) it is the maximum volume of air can be expired after normal expiration, it is 1100 mL4- 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
33 Lung volumesVital capacity (sum total of all except RV)
34 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= 3500mL2- Functional residual capacity (FRC): it is the volume of air remained in the lung after normal expirationFRC=ERV+RV= 2300mL.
35 Lung capacities3-Vital capacity: (VC) it is the maximum volume of air can be expired after maximal inspiration.VC=IRV+ERV+TV=4600mLTotal lung capacity: (TLC) it is the volume of air contained in the lung after deep inspiration.TLC=IRV+ERV+TV+RV= 5800mLAll lung capacities are 20-25% more in males than females, more in athletes, less in recumbent position
36 Work of BreathingEnergy 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)
37 Work of breathingEnergy are needed for contraction of respiratory muscles. Increase when accessory ms contracts in deep& forced breathing1- 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 deficient3- overcome airway resistance. This increase in bronchial asthma or obstructive emphysema
38 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 diseasesIt is the change in length or volume per unit change in stretching force.Normal compliance of lungs & thorax = 0.11L/cmH2O pressureNormal compliance of lungs alone = 0.2 L/cmH2O pressure
39 ComplianceHigh compliance means a given change in pressure moves a larger volume of air in the lungsLow compliance in fibrosis, congestion, oedema, bronchial obstruction or in increased surface tensionThe compliance is small in newborn, increases gradually with age, decreases in old ageThe main factors affect compliance are: congestion, size, surface tension
40 Surface TensionForce 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.
41 Surfactant Def: It is the surface active agent Composition: Phospholipid (dipalmitoyl lecithin), protein and CarbohydratesSecretion: produced by alveolar type II cells.Action: Lowers surface tension.Functions of surfactant:Facilitates lung expantionPrevent lung collapse As alveoli radius decreases, surfactant’s ability to lower surface tension increases.Prevent pulmonary oedemaSurfactant Deficiency:RDS of the newborn. The lung is rigid and oedematous and the alveoli collapse
43 What is surface tension? airWhat is surface tension?How do we deal with surface tension??
44 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 volume2- the rest of air occupies the respiratory bronchioles, the alveolar ducts, alveoli and alveolar sacs, gas exchange takes placeMinute 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.
47 Measurement of the dead space Bohr`s equation:Anatomical dead space= tidal volume x (alveolar CO2- expired CO2)Alveolar CO2
48 Physiological dead space The anatomical dead space + unperfused alveoliIn Normal person the anatomical dead space= the physiological dead spaceIn certain diseases the physiological dead space may be 10 times anatomical dead space or more.
49 Gas exchangeAlveolar 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
50 Comparison between the respiratory gases Expired airAlveolar airatmospheric air120mmHg104mmHg159mmHgO227mmHg40mmHg0.3mmHgCO247mmHgvariableH2O566mmHg569mmHg597mmHgN2760mmHgTotal pressure
51 Gas exchangeO2 of air is higher in the lungs than in the blood, O2 diffuses from air to the blood.C02 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.
54 Diffusion is determined by several factors: 1- Alveolar- capillary membrane:Semi-permeable: separates alveolar air from pulmonary capillary bloodLayers:Fluid film lining the alveoliAlveolar membraneInterstitial fluidCapillary wall
55 Total AREA available for diffusion of gases is large The respiratory membrane:Total AREA available for diffusion of gases is largein human 70 m2Diffusion PATH LENGTH is very small, =2µmPulmonary Epithelium
56 2- Partial pressure gradient of gases across the alveolar capillary membrane: The partial pressure of oxygen in mixed venous blood is 40mmHgThe partial pressure of oxygen in alveolar air is 100mmHgO2 diffuses from the alveoli to the capillary blood along a partial pressure gradient of 60mmHgThe partial pressure of CO2 in mixed venous blood is 46mmHgThe partial pressure of CO2 in alveolar air 40 mmHgCO2 diffuses along pressure gradient of 6 mmHg
57 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 diffusionThe 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 sizeThe diffusion coefficient of O2 = 1.0The diffusion coefficient of CO2 = 20CO2 can diffuse 20 times faster than O2Diffusion failure affects O2 before affecting CO24- surface area of the alveolar capillary membrane: 70square meterWhen increased, gas exchange increases
58 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 bloodVentilation / perfusion ratio = alveolar ventilation/ pulmonary blood flowIn a normal adult male at restAlveolar ventilation is 4L/minPulmonary blood flow is 5L/minVentilation / perfusion ratio=0.8Diseases that affects the alveolar capillary membrane will lower the diffusion capacity of O2Fatal levels of O2 diffusion impairment is reached long before CO2 diffusion is affected
59 Exchange of gases Alveolar air Atmospheric air pressure % 40mmHg 5.6% 0.04%CO2105mmHg14.8%159mmHg20.95%O2568mmHg79.6%600mmHg79.00%N2
61 Gas Transport by The Blood Oxygen transport:O2 is transported in the blood in two forms:1- Attached in loose combination with HbOver 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 blood2- 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.
62 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 msecThe reaction increases with the increase in PO2The relation between oxyHb formation and PO2 is studied in the Oxyhaemoglobin dissociation curve
63 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 02.Fe remains in the ferrous form (Oxygenation and not oxidation)Hb carries 65 times as much as plasma at PO2 of 100mmHgInsert figFigure 16.32
64 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 curveHb 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 2nd , increasing affinity of the 3rd ,etc..The dissociation curve starts slowly, but rapidly gained sigmoid shape2-there is steep rise in the percentage saturation of Hb between PO2 0& 75mmHg3- above 75mmHg, there is slow rise of the curve, becoming more or less flat at PO2 of 80mmHg
67 1gm of Hb binds up to 1.34ml O2The 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 bloodDuring exercise, oxygen uptake by tissues increase, PO2 drops to 15 mmHg, % saturation 20%, O2 content=40mlDuring exercise, the arterio-venous O2 difference, 150ml/LQuantity of O2 carried in a volume of blood is dependent on PO2 & Hb concentration.
69 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 tissues1- ↑ PCO2: Bohr effect2-↓ pH :due to lactic acid during exercise, more CO2 production3-↑ temperature: active tissues during oxidative processes more heat is released, more O2 supply to the tissues4- ↑ 2,3 DPG: found in RBCs & increases in cases of hypoxia & high altitudes
70 S-shaped hemoglobin curve Advantages of “S-shaped” curve for Hb-O2 association20High affinity onlyCan’t release muchO2 to tissues15S-shaped hemoglobin curveReleases much Becomes saturatedO2 at tissues with O2 at lungsml O2/100 ml blood10Low affinity onlyDoesn’t hold on to But can’t pick upmuch O2 at tissues much O2 at lungs5Active cell
72 Factors shift the curve to the left: (increases Hb affinity to O2, Easier picking up O2, Difficult release of O2)1- ↓ PCO2 at lungs2- ↑pH3- ↓ temperature4- foetal Hb: as it binds to 2,3 DPG less effectively
73 Dissolved O2:↑ PO2….↑ dissolved O2O2 is poorly solubleIn 100ml blood, 0.003ml O2 dissolve /1mmHg PO2In arterial blood, 0.3 ml/100mlIn venous blood, 0.12 ml/100mlThe dissolved O2 is at equilibrium with the O2 combined with HbIt is the dissolved O2 gets transferred to tissues & become replaced from O2 carried by HbAlthough 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)
74 CO2 transportIt is transported from tissues that produce CO2 to the lungs, where it is unloaded, removed to the atmosphereIt is transported by plasma & RBCs
75 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 flow2- chemically combined: 95% of CO2a-carbamino compounds: carried by plasma proteins & hemoglobinb- bicarbonates:In the form of KHCO3 & NaHCO343ml/100ml in arterial blood56ml/100ml in venous blood
76 Tidal CO2 transportIt is the volume of CO2 added to each 100ml of arterial blood during its flow through the tissuesCO2 produced by active cells as a result of metabolismNormally 4ml/100ml blood during rest (52-48)CO2 carried in 3 forms in plasma:1- dissolves in the plasma2- Bicarbonates:3- Carbamino proteins:
77 How is CO2 carried by the blood?? Plasma: dissolved HCO3- TissuesCO2HbO2 Hb.H + O2+C.A.slowCO2 + H2O H2CO3 H+ + HCO3-O2HCO3-Hb + CO2 Hb.CO2 (carbamino cmpd.)How is CO2 carried by the blood??Plasma: dissolvedHCO3-carbamino proteinsRBCs: dissolvedCarbamino Hb
78 Control of ventilation Mechanism of regulation involves:Nervous & chemicalThe 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 inspiration2- ventral respiratory group:( expiratory neurons)In the medulla, they are inactive during resting breathingActivated in forced ventilation as in exercise
79 3- Apneustic centre:In the ponsIt 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 ponsSection of vagus & abolishing the impulses from pneumotaxic centre, results in apneustic breathing (prolonged inspiration)
80 4-Pneumotaxic centre: in the upper pons It sends inhibitory impulses to apneustic center & to inspiratory areas to switch off respiration
82 Both inspiratory & expiratory areas are influenced by impulses from pneumotaxic & apneustic center & higher centersDRG are the integrating site for different inputs
83 Nervous control of ventilation The rhythmicity centre sends sends excitatory impulses via phrenic & intercostal nerves to diaphragm, external intercostal musclesThe rhythmicity center receives impulses from higher brain centers, brain stem, special receptorsHigher brain centers:1- impulses from cerebral cortex: voluntary hyperventilation, voluntary apnea2- impulses from cerebellum: coordinates breathing with other activities as swallowing, talking, coughing3- Impulses from hypothalamus: centers of emotions & temperature regulation, breathing modified during emotional stress, changes of temperature, (panting of dogs)
84 Centers in the medulla & pons: 1- the rhythmicity center interconnected with the cardiac & vasomotor centers located in the medulla2- apneustic center sends excitatory impulses to rhythmicity center to produce deep inspiration3- pneumotaxic center to rhythmicity center to inhibit deep inspiration & to apneustic center
85 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 reflex2- active & passive movement of joints & muscles: propioceptive stimulation stimulate breathing in exercise3- skin receptors: noxious stimuli stimulate breathing4- baroreceptors in aortic arch & carotid sinus modify breathing
86 Chemical control of ventilation Central & peripheral chemoreceptors:Peripheral chemoreceptors:Site: in the carotid & aortic bodiesStimuli: ↓ in arterial PO2, ↑PCO2, ↓pHStimulation: send stimulatory impulses to rhythmicity center via glossopharyngeal & vagus nerves
87 Central chemoreceptors Site: medullaStimuli: H+ ion concentration in the CSFH+ 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 CSFIt sends simulatory impulse to stimulates ventilation
88 Plasma BBB CSF CO2 HCO3 + H+ CO2 HCO3 + H+ When pHCNS returns to norm(HCO3 pumped out)VE is less restrainedRespiratoryAlkalosishigh pHCSF limitsHyperventilation
89 Chemoreceptors Monitor changes in blood PC02, P02, and pH. Central: Medulla.Peripheral:Carotid and aortic bodies.Control breathing indirectly.Insert figFigure 16.27
90 Hypoxia It means deficient O2 supply to the tissues Causes: 1- interference with O2 in the lungs2- interference with O2 transport in blood3- interference with O2 delivery to the tissues
91 Hypoxia Types: 1- hypoxic hypoxia: low PO2 in the arterial blood 2- anaemic hypoxia: lowering O2 carrying capacity of the blood3- stagnant hypoxia: slow circulation4- histotoxic hypoxia: disturbed uptake of O2 by tissuesTreatment:O2 therapy, correcting underlying cause
92 Hypoxic hypoxiaCauses: Any interference with normal oxygenation of the arterial blood leading to low PO2 as in:1- low atmospheric PO2 as in high altitude2- ventilation defects: as in paralysis of respiratory ms, airway obstruction, poisons that inhibits therespiratory center as morphine & barbiturates (high CO2)2- interfere with normal O2 diffusion in the lung3- mixing of arterial blood with venous blood as in veno-arterial shunts & congenital heart diseaseLow PO2, low % saturation of Hb, low O2 content in the arterial &venous blood
93 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
94 Stagnant hypoxia Types: 1- localized: e.g. disturbed circulation in a limb2- generalized as in heart failurenormal arterial blood PO2, % saturation,O2 content↓Venous blood PO2, ↓ % saturation, ↓Content of O2
95 Histotoxic hypoxiaDisturbance of O2 uptake due to poisoning of cellular enzymes e.g. cyanide poisoning or tissue oedemanormal arterial blood PO2, % saturation,O2 content↑Venous blood PO2, ↑% saturation, ↑Content of O2
97 Cyanosis Def: blue coloration of the skin & mucous membrane Cause: reduced Hb more than 5gm/100mlTypes:Localized type: in the tips of fingers in coldGeneralized: in veno-arterial shunts, severe hypoxia in the newborn, or at very high altitudeIt is more common seen in polycythemiait s very rare in anaemia (the person already has low Hb, so he cannot have 5gm reduced Hb)