Respiration. Functions Anatomy

Transcription

1 Respiration Functions Anatomy

2 Major Functions Gas exchange: absorb O 2, eject CO 2 Regulate blood ph: Alters CO 2 levels Voice production: air movement past vocal cords Olfaction: in nasal cavity Innate immunity: physical protection with mucus & stratified ET. Specific immunity: tonsils are home to White blood cells (leucocytes)

3 Requirements & adaptations Thin gas exchange surface: minimize T d d 2 Mechanism for gas binding & delivery Specialized gas carrying molecules Specialized gas storage molecules

4 Anatomy Common passageway for respiratory & digestive tracts

5 Protective functions: Nasopharynx Pressure equalization; Auditory tubes empty here Immune functions: Pharyngeal tonsils & mucus Nasal turbinates (conchae); humidify incoming dry air keeps lungs moist Separation of respiratory and digestive tubes; Floor of nasopharynx = Soft palate; posterior portion = uvula Elevates (closes) when we swallow & remains open when we sneeze

6 Oropharynx & Laryngopharynx Oro extends from uvula to epiglottis Oral cavity opens into oropharynx Lined with stratified epithelium (protects against abrasion) Lingual & palatine tonsils Laryngo extends from epiglottis to esophagus Food and drink

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8 Larynx Complex assortment of articulating cartilages: Structural support of air tube Voice production Allow us to hold breath Closes air tube when we swallow to prevent food from entering trachea

9 Elastic Cartilage

10 Trachea = windpipe Trachea & Bronchi Pseudostratified, columnar ciliated ET over CT & smooth muscle, supported by hyaline cartilage Bronchi Cartilage maintains an open airway; smooth muscle constricts airway Effect of smoking: Destroys ciliated cells; mucous collects; microorganisms are not ejected Symmetrical branches from trachea Extensions with same tissue types

11 Protection of respiratory passage Pseudostratified, ciliated ET Lots of goblet cells (mucus) Produce a mucus escalator that traps & removes debris & invaders

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13 Lungs Divided into lobes (R=3, L=2), divided by septa Trachea -> 1 (main) Bronchi -> 2 bronchi -> bronchioles -> terminal bronchi -> alveolar ducts > alveolar sacs > alveoli (an individual chamber for gas exchange). As bronchi & bronchioles divide, cartilage decreases & smooth muscle increases During exercise alveolar duct diameter increases During asthma attack, diameter decreases

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15 Bronchi, alveolar duct, alveolar sac

16 Alveolar sac with many alveoli Simple squamous ET Macrophages: immunity Pneumocytes: produce surfactant, reduces surface tension; makes inhalation easy High capillary density

17 Ventilation Inspiration and expiration Caused by changes in thoracic volume, which produce changes in air pressure in lungs Muscles of expiration: abdominals, internal intercostals Muscles of inspiration: diaphragm, external intercostals, pectoralis minor, scalenes, sternocleidomastoid

18 Inspiration & expiration Induced by changes in thoracic volume, which changes air pressure in lungs Diaphragm is mainly responsible Others are recruited during exercise or stress Muscles of Inspiration Muscles of expiration

19 Pressure changes & Airflow At end of expiration: P atm = P alv No air flow

20 Pressure changes & Airflow At end of expiration: P atm = P alv No air flow

21 Pressure changes & Airflow During inspiration: increased thoracic volume decreases P alv P atm > P alv Air flows into alveoli

22 Pressure changes & Airflow End of inspiration: P atm = P alv No air flow

23 Pressure changes & Airflow During expiration: Decreased thoracic volume = increased pressure in side alveoli P atm < P alv Air flows out of lungs

24 Passive expiration Passive expiration occurs due to lung recoil: Lung recoil has two causes: Elastic fibers in CT of lung Surface tension (caused by H-bonding) of H 2 O molecules pull on alveolar walls, encouraging collapse. P = 2T/r What happens as r decreases? Surfactant opposes lung recoil Secreted by pneumocytes of alveolar epithelium Consists of lipoproteins which interfere with surface tension (H-bonds) produced by water

25 Lung volumes Tidal Volume ml Inspiratory Reserve Volume ml What you can forcefully inspire after TV Expiratory Reserve Volume ml What you can forcefully expire after TV Residual Volume ml Air remaining in lungs & respiratory passage after max expiration = anatomical dead space

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27 Vital Capacity Sum of Tidal, Inspiratory, Expiratory Reserve volumes Maximum amount of air one can forcefully inspire and expire Influenced by age, sex, body size, and training Trained athlete may have 40% higher VC than untrained Clinical importance - used to assess resistance to airflow; high resistance may indicate fluid build-up, inflammation, alveolar collapse, smooth muscle constriction, etc. Emphysema patients, asthmatics, chronic bronchitis:

28 What makes gas exchange efficient? Short distances for diffusion SA T is large Substantial differences in PP of gases across respiratory membrane Gases are lipid soluble Coordinated blood flow & air flow

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30 Respiratory membrane Characterized by extreme thinness = distance Thin fluid layer lines alveolus Alveolar epithelium = simple squamous Interstitial space = THIN Capillary epithelium = simple squamous

31 Gas Exchange: where and why Across respiratory membranes of alveoli (mainly) some in alveolar ducts & respiratory bronchioles; remainder = functional dead space THIN - gas exchange occurs quickly minimize T d d 2 ANY increase in thickness decreases gas exchange rate Ex: pulmonary edema = increased fluid layer in alveoli; rate of gas exchange plummets; O 2 diffusion is disproportionately affected

32 Surface Area (SA) Total SA of respiratory epithelium = 70 m 2 Why so large? During strenuous exercise, ANY reduction in SA severely affects gas exchange Other examples: surgical removal of lung tissue; destruction by cancer or emphysema (alveoli expand but capillaries deteriorate); reduced production of surfactant (premature infants may not have enough yet)

33 Partial Pressure (PP) PP = pressure exerted by ONE gas in a mixture of gases Total pressure = 760 mm Hg (sea level) & 21% is O 2 PO 2 = (760 mm Hg x 0.21) = 160 mm Hg PO 2 in alveoli = 100 mm Hg At liquid/air interface, gasses diffuse so that PP of each gas is equal in both media

34 Sites of Gas Diffusion At respiratory surface of lungs: In pulmonary capillaries: PO 2 is LOW & PCO 2 is HIGH In alveolar sacs: the reverse is true This leads to O 2 diffusing into capillaries and CO 2 diffusing into alveoli At tissues: In interstitial fluid: PO 2 is LOW & PCO 2 is HIGH Inside cells, reverse is true O 2 diffuses into cells and CO 2 diffuses into interstitial fluid

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36 O 2 Transport 98.5% of O 2 in blood is bound to hemoglobin (iron-containing protein) O 2 binds reversibly with hemoglobin O 2 movement depends on PO 2 in neighboring areas Hemoglobin releases O 2 at tissues, where PO 2 is LOW, it binds O 2 at alveoli, where PO 2 is HIGH

37 CO 2 Transport 7% as dissolved CO 2 23% attached to hemoglobin 70% as bicarbonate ions Carbonic anhydrase (enzyme) converts CO 2 to carbonic acid; these dissociate into bicarbonate ions Carbonic anhydrase exists on surface of capillary epithelia and inside RBCs

38 CO 2 Transport In lungs: the reverse reaction occurs, converting bicarbonate ions to CO 2 and allowing diffusion into alveoli

39 PO 2 effects binding to Hb As PO 2 increases, so does binding to Hb on RBC s Virtually ALL Hb is saturated with O 2 when it leaves the lungs On Mt. Everest, air pressure ~ 253 mm Hg PO 2 = 253 * 0.21 = 53 mm Hg Exercising tissues Resting tissues Lungs

40 Temp & ph changes shift this saturation curve As ph declines Hb saturation decreases As temp. increases Hb saturation decreases

41 Physiologic regulation of respiration Reflexes Exercise Emotion & Intention

42 Ventilation rates Normal adult rate = cycles/min Children = cycles/min Primary control of rate at MO Neurons stimulate muscles of respiration Deeper, more rapid breathing results from stimulating more muscle fibers more frequently. More APs & increased frequency of APs

43 Respiratory Areas 2 paired medullary centers (MO) Dorsal nuclei (DRG) contract diaphragm during all types of breathing Ventral nuclei (VRG) are active during forced breathing; expiratory & inhibitory centers Internal intercostals & abdominals stimulated during exhalation external intercostals & others stimulated during inspiration 1 pontine center regulates depth & rate of respiration

44 Respiration Cycle Basic Rythmicity: DRG & VRG set pace. Integrate info (baroreceptors, chemoreceptors, stretch receptors & voluntary inputs) & fire when threshold is reached modifiers: apneustic center stimulates DRG. Pneumotaxic center inhibits apneustic. Stimulate pneumotaxic, inhibits apneustic = increases respiratory rate (limiting inhalation) Inhibit pneumotaxic, releases apneustic = reduces respiratory rate & increases respiratory depth.

45 Modification of Ventilation Nervous control and feedback Higher brain centers: speech, breath holding, sobbing & gasping (limbic system) Reflexes: Sneeze, cough, Hering-Breuer H-B limits extent of inspiration; prevents overventilation in infants & in adults during heavy exercise Touch, thermal pain receptors in skin cause rapid inspiration

46 Modification of Ventilation Chemical control (chemoreceptors) MO monitors ph level of blood (proxy for CO 2 levels) Increases in CO 2 = decrease in ph Hypercapnia = high CO 2 concentration Carotid artery & aorta monitors O 2 level Hypoxia = low O 2 levels excitation Emphysema, high altitude, asphyxiation reduce O 2, leaving CO 2 unchanged

47 Excitatory Inhibitory

48 Immediate Effect of Exercise Abrupt increase in ventilation rate Induced by collateral motor neurons that activate skeletal muscle Increased by sensory feedback from collateral fibers reporting joint movement Learned through training to match respiration rate to level of activity Gradual increase Levels off 4-6 min after onset

49 Immediate Effect of Exercise If exercise remains aerobic, average arterial O 2, CO 2 and ph levels remain close to resting levels At anaerobic threshold the ability to exercise indefinitely ends, due to accumulation of lactic acid and H + ions and reduction of bicarbonate (ph changes), so ventilation rate increases

50 Adaptations to Exercise Increased efficiency of cardiovascular function: O 2 delivery and CO 2 expulsion (i. e. ventilation is not the rate limiting step) Tiny increase in VC & decrease in RV TV during exercise increases lots Respiratory rate & ventilation rate increase lots

51 Changes with age and smoking