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22-1 Chapter 22 Lecture Outline See PowerPoint Image Slides for all figures and tables pre-inserted into PowerPoint without notes. Copyright (c) The McGraw-Hill.

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Presentation on theme: "22-1 Chapter 22 Lecture Outline See PowerPoint Image Slides for all figures and tables pre-inserted into PowerPoint without notes. Copyright (c) The McGraw-Hill."— Presentation transcript:

1 22-1 Chapter 22 Lecture Outline See PowerPoint Image Slides for all figures and tables pre-inserted into PowerPoint without notes. Copyright (c) The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

2 22-2 Respiratory System Anatomy of the Respiratory System Pulmonary Ventilation Gas Exchange and Transport Respiratory Disorders

3 22-3 Organs of Respiratory System Nose, pharynx, larynx, trachea, bronchi, lungs

4 22-4 General Aspects Airflow in lungs –bronchi bronchioles alveoli Conducting division –passages for airflow, nostrils to bronchioles Respiratory division –distal gas-exchange regions, alveoli Upper respiratory tract –organs in head and neck, nose through larynx Lower respiratory tract –organs of thorax, trachea through lungs

5 22-5 Nose Functions –warms, cleanses, humidifies inhaled air –detects odors –resonating chamber that amplifies the voice Bony and cartilaginous supports –superior half: nasal bones medially and maxillae laterally –inferior half: lateral and alar cartilages –ala nasi: flared portion shaped by dense CT, forms lateral wall of each nostril

6 22-6 Anatomy of Nasal Region

7 22-7 Anatomy of Nasal Region

8 22-8 Nasal Cavity Extends from nostrils to posterior nares Vestibule: dilated chamber inside ala nasi –stratified squamous epithelium, vibrissae (guard hairs) Nasal septum divides cavity into right and left chambers called nasal fossae

9 22-9 Upper Respiratory Tract

10 22-10 Upper Respiratory Tract

11 22-11 Nasal Cavity - Conchae and Meatuses Superior, middle and inferior nasal conchae –3 folds of tissue on lateral wall of nasal fossa –mucous membranes supported by thin scroll- like turbinate bones Meatuses –narrow air passage beneath each conchae –narrowness and turbulence ensures air contacts mucous membranes

12 22-12 Nasal Cavity - Mucosa Olfactory mucosa –lines roof of nasal fossa Respiratory mucosa –lines rest of nasal cavity with ciliated pseudostratified epithelium Defensive role of mucosa –mucus (from goblet cells) traps inhaled particles bacteria destroyed by lysozyme

13 22-13 Nasal Cavity - Cilia and Erectile Tissue Function of cilia of respiratory epithelium –sweep debris-laden mucus into pharynx to be swallowed Erectile tissue of inferior concha –venous plexus that rhythmically engorges with blood and shifts flow of air from one side of fossa to the other once or twice an hour to prevent drying Spontaneous epistaxis (nosebleed) –most common site is inferior concha

14 22-14 Regions of Pharynx

15 22-15 Pharynx Nasopharynx (pseudostratified epithelium) –posterior to choanae, dorsal to soft palate –receives auditory tubes and contains pharyngeal tonsil –90 downward turn traps large particles (>10 m) Oropharynx (stratified squamous epithelium) –space between soft palate and root of tongue, inferiorly as far as hyoid bone, contains palatine and lingual tonsils Laryngopharynx (stratified squamous) –hyoid bone to level of cricoid cartilage

16 22-16 Larynx Glottis – vocal cords and opening between Epiglottis –flap of tissue that guards glottis, directs food and drink to esophagus Infant larynx –higher in throat, forms a continuous airway from nasal cavity that allows breathing while swallowing –by age 2, more muscular tongue, forces larynx down

17 22-17 Views of Larynx

18 22-18 Nine Cartilages of Larynx Epiglottic cartilage - most superior Thyroid cartilage – largest; laryngeal prominence Cricoid cartilage - connects larynx to trachea Arytenoid cartilages (2) - posterior to thyroid cartilage Corniculate cartilages (2) - attached to arytenoid cartilages like a pair of little horns Cuneiform cartilages (2) - support soft tissue between arytenoids and epiglottis

19 22-19 Walls of Larynx Interior wall has 2 folds on each side, from thyroid to arytenoid cartilages –vestibular folds: superior pair, close glottis during swallowing –vocal cords: produce sound Intrinsic muscles - rotate corniculate and arytenoid cartilages –adducts (tightens: high pitch sound) or abducts (loosens: low pitch sound) vocal cords Extrinsic muscles - connect larynx to hyoid bone, elevate larynx during swallowing

20 22-20 Action of Vocal Cords

21 22-21 Trachea Rigid tube 4.5 in. long and 2.5 in. diameter, anterior to esophagus Supported by 16 to 20 C-shaped cartilaginous rings –opening in rings faces posteriorly towards esophagus –trachealis spans opening in rings, adjusts airflow by expanding or contracting Larynx and trachea lined with ciliated pseudostratified epithelium which functions as mucociliary escalator

22 22-22 Lower Respiratory Tract

23 22-23 Lungs - Surface Anatomy

24 22-24 Thorax - Cross Section

25 22-25 Bronchial Tree Primary bronchi (C-shaped rings) –from trachea; after 2-3 cm enter hilum of lungs –right bronchus slightly wider and more vertical (aspiration) Secondary (lobar) bronchi (overlapping plates) –one secondary bronchus for each lobe of lung Tertiary (segmental) bronchi (overlapping plates) –10 right, 8 left –bronchopulmonary segment: portion of lung supplied by each

26 22-26 Bronchial Tree Bronchioles (lack cartilage) –layer of smooth muscle –pulmonary lobule portion ventilated by one bronchiole –divides into terminal bronchioles ciliated; end of conducting division –respiratory bronchioles divide into 2-10 alveolar ducts; end in alveolar sacs Alveoli - bud from respiratory bronchioles, alveolar ducts and alveolar sacs –main site for gas exchange

27 22-27 Lung Tissue

28 22-28 Alveolar Blood Supply

29 22-29 Alveolus Fig b and c

30 22-30 Pleurae and Pleural Fluid Visceral (on lungs) and parietal (lines rib cage) pleurae Pleural cavity - space between pleurae, lubricated with fluid Functions –reduce friction –create pressure gradient lower pressure assists lung inflation –compartmentalization prevents spread of infection

31 22-31 Pulmonary Ventilation Breathing (pulmonary ventilation) – one cycle of inspiration and expiration –quiet respiration – at rest –forced respiration – during exercise Flow of air in and out of lung requires a pressure difference between air pressure within lungs and outside body

32 22-32 Respiratory Muscles Diaphragm (dome shaped) –contraction flattens diaphragm Scalenes - hold first pair of ribs stationary External and internal intercostals –stiffen thoracic cage; increases diameter Pectoralis minor, sternocleidomastoid and erector spinae muscles –used in forced inspiration Abdominals and latissimus dorsi –forced expiration (to sing, cough, sneeze)

33 22-33 Respiratory Muscles

34 22-34 Neural Control of Breathing Breathing depends on repetitive stimuli from brain Neurons in medulla oblongata and pons control unconscious breathing Voluntary control provided by motor cortex Inspiratory neurons: fire during inspiration Expiratory neurons: fire during forced expiration Fibers of phrenic nerve go to diaphragm; intercostal nerves to intercostal muscles

35 22-35 Respiratory Control Centers Respiratory nuclei in medulla –inspiratory center (dorsal respiratory group) frequent signals, you inhale deeply signals of longer duration, breath is prolonged –expiratory center (ventral respiratory group) involved in forced expiration Pons –pneumotaxic center sends continual inhibitory impulses to inspiratory center, as impulse frequency rises, breathe faster and shallower –apneustic center prolongs inspiration, breathe slower and deeper

36 22-36 Respiratory Control Centers

37 22-37 Input to Respiratory Centers From limbic system and hypothalamus –respiratory effects of pain and emotion From airways and lungs –irritant receptors in respiratory mucosa stimulate vagal afferents to medulla, results in bronchoconstriction or coughing –stretch receptors in airways - inflation reflex excessive inflation triggers reflex stops inspiration From chemoreceptors –monitor blood pH, CO 2 and O 2 levels

38 22-38 Chemoreceptors Peripheral chemoreceptors –found in major blood vessels aortic bodies –signals medulla by vagus nerves carotid bodies –signals medulla by glossopharyngeal nerves Central chemoreceptors –in medulla primarily monitor pH of CSF

39 22-39 Peripheral Chemoreceptor Paths

40 22-40 Voluntary Control Neural pathways –motor cortex of frontal lobe of cerebrum sends impulses down corticospinal tracts to respiratory neurons in spinal cord, bypassing brainstem Limitations on voluntary control –blood CO 2 and O 2 limits cause automatic respiration

41 22-41 Pressure and Flow Atmospheric pressure drives respiration –1 atmosphere (atm) = 760 mmHg Intrapulmonary pressure and lung volume –pressure is inversely proportional to volume for a given amount of gas, as volume, pressure and as volume, pressure Pressure gradients –difference between atmospheric and intrapulmonary pressure –created by changes in volume thoracic cavity

42 22-42 Inspiration - Pressure Changes intrapleural pressure –as volume of thoracic cavity, visceral pleura clings to parietal pleura intrapulmonary pressure –lungs expand with visceral pleura Transpulmonary pressure –intrapleural minus intrapulmonary pressure (not all pressure change in the pleural cavity is transferred to the lungs) Inflation aided by warming of inhaled air 500 ml of air flows with a quiet breath

43 22-43 Respiratory Cycle

44 22-44 Passive Expiration During quiet breathing, expiration achieved by elasticity of lungs and thoracic cage As volume of thoracic cavity, intrapulmonary pressure and air is expelled After inspiration, phrenic nerves continue to stimulate diaphragm to produce a braking action to elastic recoil

45 22-45 Forced Expiration Internal intercostal muscles –depress the ribs Contract abdominal muscles – intra-abdominal pressure forces diaphragm upward – pressure on thoracic cavity

46 22-46 Pneumothorax Presence of air in pleural cavity –loss of negative intrapleural pressure allows lungs to recoil and collapse Collapse of lung (or part of lung) is called atelectasis

47 22-47 Resistance to Airflow Pulmonary compliance –distensibility of lungs; change in lung volume relative to a change in transpulmonary pressure Bronchiolar diameter –primary control over resistance to airflow –bronchoconstriction triggered by airborne irritants, cold air, parasympathetic stimulation, histamine –bronchodilation sympathetic nerves, epinephrine

48 22-48 Alveolar Surface Tension Thin film of water needed for gas exchange –creates surface tension that acts to collapse alveoli and distal bronchioles Pulmonary surfactant (great alveolar cells) –decreases surface tension Premature infants that lack surfactant suffer from respiratory distress syndrome

49 22-49 Alveolar Ventilation Dead air –fills conducting division of airway, cannot exchange gases Anatomic dead space –conducting division of airway Physiologic dead space –sum of anatomic dead space and any pathological alveolar dead space Alveolar ventilation rate –air that ventilates alveoli X respiratory rate –directly relevant to ability to exchange gases

50 22-50 Measurements of Ventilation Spirometer - measures ventilation Respiratory volumes –tidal volume: volume of air in one quiet breath –inspiratory reserve volume air in excess of tidal inspiration that can be inhaled with maximum effort –expiratory reserve volume air in excess of tidal expiration that can be exhaled with maximum effort –residual volume ( keeps alveoli inflated) air remaining in lungs after maximum expiration

51 22-51 Lung Volumes and Capacities

52 22-52 Vital capacity –total amount of air that can be exhaled with effort after maximum inspiration assesses strength of thoracic muscles and pulmonary function Inspiratory capacity –maximum amount of air that can be inhaled after a normal tidal expiration Functional residual capacity –amount of air in lungs after a normal tidal expiration Respiratory Capacities

53 22-53 Respiratory Capacities Total lung capacity –maximum amount of air lungs can hold Forced expiratory volume (FEV) –% of vital capacity exhaled/ time –healthy adult - 75 to 85% in 1 sec Peak flow –maximum speed of exhalation Minute respiratory volume (MRV) –TV x respiratory rate, at rest 500 x 12 = 6 L/min –maximum: 125 to 170 L/min

54 22-54 Respiratory Volumes and Capacities Age - lung compliance, respiratory muscles weaken Exercise - maintains strength of respiratory muscles Body size - proportional, big body/large lungs Restrictive disorders – compliance and vital capacity Obstructive disorders –interfere with airflow, expiration requires more effort or less complete

55 22-55 Composition of Air Mixture of gases; each contributes its partial pressure –at sea level 1 atm. of pressure = 760 mmHg –nitrogen constitutes 78.6% of the atmosphere so P N 2 = 78.6% x 760 mmHg = 597 mmHg P O 2 = 159 P H 2 O = 3.7 P CO 2 = P N 2 + P O 2 + P H 2 O + P CO 2 = 760 mmHg

56 22-56 Composition of Air Partial pressures (as well as solubility of gas) –determine rate of diffusion of each gas and gas exchange between blood and alveolus Alveolar air –humidified, exchanges gases with blood, mixes with residual air –contains: P N 2 = 569 P O 2 = 104 P H 2 O = 47 P CO 2 = 40 mmHg

57 22-57 Air-Water Interface Important for gas exchange between air in lungs and blood in capillaries Gases diffuse down their concentration gradients Henrys law –amount of gas that dissolves in water is determined by its solubility in water and its partial pressure in air

58 22-58 Alveolar Gas Exchange

59 22-59 Alveolar Gas Exchange Time required for gases to equilibrate = 0.25 sec RBC transit time at rest = 0.75 sec to pass through alveolar capillary RBC transit time with vigorous exercise = 0.3 sec

60 22-60 Factors Affecting Gas Exchange Concentration gradients of gases –P O 2 = 104 in alveolar air versus 40 in blood –P CO 2 = 46 in blood arriving versus 40 in alveolar air Gas solubility –CO 2 20 times as soluble as O 2 O 2 has conc. gradient, CO 2 has solubility

61 22-61 Factors Affecting Gas Exchange Membrane thickness - only 0.5 m thick Membrane surface area ml blood in alveolar capillaries, spread over 70 m 2 Ventilation-perfusion coupling - areas of good ventilation need good perfusion (vasodilation)

62 22-62 Concentration Gradients of Gases

63 22-63 Ambient Pressure and Concentration Gradients

64 22-64 Lung Disease Affects Gas Exchange

65 22-65 Perfusion Adjustments

66 22-66 Ventilation Adjustments

67 22-67 Oxygen Transport Concentration in arterial blood –20 ml/dl 98.5% bound to hemoglobin 1.5% dissolved Binding to hemoglobin –each heme group of 4 globin chains may bind O 2 –oxyhemoglobin (HbO 2 ) –deoxyhemoglobin (HHb)

68 22-68 Oxygen Transport Oxyhemoglobin dissociation curve –relationship between hemoglobin saturation and P O 2 is not a simple linear one –after binding with O 2, hemoglobin changes shape to facilitate further uptake (positive feedback cycle)

69 22-69 Oxyhemoglobin Dissociation Curve

70 22-70 Carbon Dioxide Transport As carbonic acid - 90% –CO 2 + H 2 O H 2 CO 3 HCO H + As carbaminohemoglobin (HbCO 2 )- 5% binds to amino groups of Hb (and plasma proteins) As dissolved gas - 5% Alveolar exchange of CO 2 –carbonic acid - 70% –carbaminohemoglobin - 23% –dissolved gas - 7%

71 22-71 Systemic Gas Exchange CO 2 loading –carbonic anhydrase in RBC catalyzes CO 2 + H 2 O H 2 CO 3 HCO H + –chloride shift keeps reaction proceeding, exchanges HCO 3 - for Cl - (H + binds to hemoglobin) O 2 unloading –H + binding to HbO 2 its affinity for O 2 Hb arrives 97% saturated, leaves 75% saturated - venous reserve –utilization coefficient amount of oxygen Hb has released 22%

72 22-72 Systemic Gas Exchange

73 22-73 Alveolar Gas Exchange Revisited Reactions are reverse of systemic gas exchange CO 2 unloading –as Hb loads O 2 its affinity for H + decreases, H + dissociates from Hb and bind with HCO 3 - CO 2 + H 2 O H 2 CO 3 HCO H + –reverse chloride shift HCO 3 - diffuses back into RBC in exchange for Cl -, free CO 2 generated diffuses into alveolus to be exhaled

74 22-74 Alveolar Gas Exchange

75 22-75 Factors Affect O 2 Unloading Active tissues need oxygen! –ambient P O 2 : active tissue has P O 2 ; O 2 is released –temperature: active tissue has temp; O 2 is released –Bohr effect: active tissue has CO 2, which lowers pH (muscle burn); O 2 is released –bisphosphoglycerate (BPG): RBCs produce BPG which binds to Hb; O 2 is released body temp (fever), TH, GH, testosterone, and epinephrine all raise BPG and cause O 2 unloading ( metabolic rate requires oxygen)

76 22-76 Oxygen Dissociation and Temperature

77 22-77 Oxygen Dissociation and pH Bohr effect: release of O 2 in response to low pH

78 22-78 Haldane effect –low level of HbO 2 (as in active tissue) enables blood to transport more CO 2 –HbO 2 does not bind CO 2 as well as deoxyhemoglobin (HHb) –HHb binds more H + than HbO 2 as H + is removed this shifts the CO 2 + H 2 O HCO H + reaction to the right Factors Affecting CO 2 Loading

79 22-79 Blood Chemistry and Respiratory Rhythm Rate and depth of breathing adjusted to maintain levels of: –pH –P CO 2 –PO2–PO2 Lets look at their effects on respiration:

80 22-80 Effects of Hydrogen Ions pH of CSF (most powerful respiratory stimulus) Respiratory acidosis (pH < 7.35) caused by failure of pulmonary ventilation –hypercapnia: P CO 2 > 43 mmHg CO 2 easily crosses blood-brain barrier in CSF the CO 2 reacts with water and releases H + central chemoreceptors strongly stimulate inspiratory center –blowing off CO 2 pushes reaction to the left CO 2 (expired) + H 2 O H 2 CO 3 HCO H + –so hyperventilation reduces H + (reduces acid)

81 22-81 Effects of Hydrogen Ions Respiratory alkalosis (pH > 7.45) –hypocapnia: P CO 2 < 37 mmHg –Hypoventilation ( CO 2 ), pushes reaction to the right CO 2 + H 2 O H 2 CO 3 HCO H + – H + (increases acid), lowers pH to normal pH imbalances can have metabolic causes –uncontrolled diabetes mellitus fat oxidation causes ketoacidosis, may be compensated for by Kussmaul respiration (deep rapid breathing)

82 22-82 Effects of Carbon Dioxide Indirect effects on respiration –through pH as seen previously Direct effects – CO 2 may directly stimulate peripheral chemoreceptors and trigger ventilation more quickly than central chemoreceptors

83 22-83 Effects of Oxygen Usually little effect Chronic hypoxemia, P O 2 < 60 mmHg, can significantly stimulate ventilation –emphysema, pneumonia –high altitudes after several days

84 22-84 Hypoxia Causes: –hypoxemic hypoxia - usually due to inadequate pulmonary gas exchange high altitudes, drowning, aspiration, respiratory arrest, degenerative lung diseases, CO poisoning –ischemic hypoxia - inadequate circulation –anemic hypoxia - anemia –histotoxic hypoxia - metabolic poison (cyanide ) Signs: cyanosis - blueness of skin Primary effect: tissue necrosis, organs with high metabolic demands affected first

85 22-85 Oxygen Excess Oxygen toxicity: pure O 2 breathed at 2.5 atm or greater –generates free radicals and H 2 O 2 –destroys enzymes –damages nervous tissue –leads to seizures, coma, death Hyperbaric oxygen –formerly used to treat premature infants, caused retinal damage, discontinued

86 22-86 Chronic Obstructive Pulmonary Disease Asthma –allergen triggers histamine release –intense bronchoconstriction (blocks air flow) Other COPDs usually associated with smoking –chronic bronchitis –emphysema

87 22-87 Chronic Obstructive Pulmonary Disease Chronic bronchitis –cilia immobilized and in number –goblet cells enlarge and produce excess mucus –sputum formed (mucus and cellular debris) ideal growth media for bacteria –leads to chronic infection and bronchial inflammation

88 22-88 Chronic Obstructive Pulmonary Disease Emphysema –alveolar walls break down much less respiratory membrane for gas exchange –healthy lungs are like a sponge; in emphysema, lungs are more like a rigid balloon –lungs fibrotic and less elastic –air passages collapse obstruct outflow of air air trapped in lungs

89 22-89 Effects of COPD pulmonary compliance and vital capacity Hypoxemia, hypercapnia, respiratory acidosis –hypoxemia stimulates erythropoietin release and leads to polycythemia cor pulmonale –hypertrophy and potential failure of right heart due to obstruction of pulmonary circulation

90 22-90 Smoking and Lung Cancer Lung cancer accounts for more deaths than any other form of cancer –most important cause is smoking (15 carcinogens) Squamous-cell carcinoma (most common) –begins with transformation of bronchial epithelium into stratified squamous –dividing cells invade bronchial wall, cause bleeding lesions –dense swirls of keratin replace functional respiratory tissue

91 22-91 Lung Cancer Adenocarcinoma –originates in mucous glands of lamina propria Small-cell (oat cell) carcinoma –least common, most dangerous –originates in primary bronchi, invades mediastinum, metastasizes quickly

92 22-92 Progression of Lung Cancer 90% originate in primary bronchi Tumor invades bronchial wall, compresses airway; may cause atelectasis Often first sign is coughing up blood Metastasis is rapid; usually occurs by time of diagnosis –common sites: pericardium, heart, bones, liver, lymph nodes and brain Prognosis poor after diagnosis –only 7% of patients survive 5 years

93 22-93 Healthy Lung/Smokers Lung- Carcinoma

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