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CHAPTER 19 RESPIRATORY SYSTEM.

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Presentation on theme: "CHAPTER 19 RESPIRATORY SYSTEM."— Presentation transcript:

1 CHAPTER 19 RESPIRATORY SYSTEM

2 RESPIRATORY SYSTEM

3 MARIA WILL YOU GO TO THE PROM WITH ME? DREW

4 VENTILATION EXTERNAL RESPIRATION TRANSPORT INTERNAL RESPIRATION
CELLULAR RESPIRATION

5 TO GET OXYGEN FOR AEROBIC CELLLULAR RESPIRATION:
WHY? TO GET OXYGEN FOR AEROBIC CELLLULAR RESPIRATION: FORM ATP TO GET RID OF CO2 CO2 +H2O= CARBONIC ACID: MAINTAINS PORPER pH

6 ORGANS UPPER RESPIRATORY TRACT NOSE, NASAL CAVITY, SINUSES, PHARYNX
LOWER RESPIRATORY TRACT LARYNX, TRACHEA, BRONCHIAL TREES, LUNGS

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9 HAIRS TO REMOVE LARGE PARTICLES
NOSE 2 NOSTRILS HAIRS TO REMOVE LARGE PARTICLES

10 NASAL CAVITY NASAL SEPTUM NASAL CONCHAE
FORM PASSAGEWAYS: SUPERIOR, MIDDLE, INFERIOR MEATUSES ? UPPER POSTERIOR PORTION: OLFACTORY RECEPTORS PSEUDOSTRATIFIED COLUMNAR EPITHELIUM WITH GOBLET CELLS MANY BLOOD VESSELS ? WATER FROM MUCOUS MEMBRANE EVAPORATES TO MOISTEN AIR MUCUS ? CILIA MOVES MUCUS TO PHARYNX TO BE SWALLOWED?

11 SINUSES AIR FILLED IN FRONTAL, SPHENOID, ETHMOID AND MAXILLARY BONES
OPEN INTO NASAL CAVITY WITH MUCOUS MEMBRANE DRAIN TO NASAL CAVITY SINUSITIS= HEADACHE WHY PRESENT ? RESONANCE

12 SINUSES en.wikipedia.org

13 PHARYNX PASSAGEWAY FOR FOOD AND AIR AIDS IN FORMING SOUNDS
SUBDIVISIONS: CHAPTER 17

14 LARYNX LETS AIR IN, KEEP OBJECTS OUT, HOUSE VOCAL CHORDS
MUSCLE AND BONE AND CARTILAGE HELD BY ELASTIC TISSUE THYROID CARTILAGE= ADAM’S APPLE EPIGLOTTIC CARTILAGE: ONLY ELASTIC CARTILAGE (HYALINE FOR REST); SUPPORTS EPIGLOTTIS: BLOCKS TRACHEA WHEN SWALLOWING (CHAPTER 17) CORNICULATE CARTILAGE: MUSCLE ATTACHMENTS REGULATE TENSION ON VOCAL CHORDS FOR SPEECH

15 VOCAL CHORDS OF MUSCLE AND CONNECTIVE TISSUE WITH MUCOUS MEMBRANE
FALSE VOCAL CHORDS UPPER FOLDS NO SOUND CLOSE TRACHEA DURING SWALLOWING TRUE VOCAL CHORDS ELASTIC FIBERS FOR MAKING SOUND SPEECH: VOCAL CHORDS VIBRATE= SOUND WAVES, WORDS FORMED BY: PHARYNX, ORAL CAVITY, TONGUE AND LIPS CHANGING TENSION OF LARYNGEAL MUSCLES CHANGES PITCH INTENSITY (LOUDNESS) FROM FORCE OF AIR

16 VOICE BOX en.wikipedia.org

17 TRACHEA 2.5cm DIAMETER, 12.5 cm LONG, INFRONT OF ESOPHAGUS
RIGHT AND LEFT BRONCHI CILIATED MUCOUS MEMBRANE, GOBLET CELLS TRAPS PARTICLES AND MOVES UP TO SWALLOW C SHAPED HYALINE CARTILAGE WHY?

18 BRONCHIAL TREE TRACHEA PRIMARY BRONCHI (2)  SECONDARY (LOBAR) BRONCHI (2 LEFT; 3 RIGHT) TERTIARY (SEGMENTAL) BRONCHI (8 LEFT; 10 RIGHT)  INTRALOBULAR BRONCHIOLES (INTO LOBULES)  TERMINAL LOBULES (50-80 IN EACH LOBULE)  RESPIRATORY BRONCHIOLES (A FEW ALVEOLI)  ALVEOLAR DUCTS  ALVEOLAR SACS (OUTPOUCHING OF DUCT)  ALVEOLI CARINA AIR SLOWS AS IT PASSES THROUGH BRANCHES = ?

19 TRACHEA en.wikipedia.org

20 ALVEOLI library.thinkquest.org/

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22 ALVEOLI en.wikipedia.org

23 ALVEOLI

24 ALVEOLI

25 STRUCTURE COMPLETE CARTILAGE RINGS BECONME THINNER TILL GONE, REPLACED BY SMOOTH MUSCLE ELASTIC FIBERS PSEUDOSTRATIFIED, CILIATED COLUMNAR EPITHELIUM  CUBOIDAL  SIMPLE SQUAMOUS GOBLET CELLS DECREASE IN NUMBER TILL NONE CILIA LESSEN AND DISAPPEAR MUCOUS MEMBRANE THINS TILL GONE

26 FUNCTIONS ALVEOLI = INCREASE SURFACE AREA  INCREASED DIFFUSION
300 MILLION ALVEOLI = SURFACE AREA OF ½ TENNIS OCURT EXCHANGE CO2 AND O2

27

28 LUNGS BRONCI AND BLOOD VESSELS ENTER/EXIT AT HILUM
VISCERAL PLEURA FOLDS TO BECOME PARIETAL PLEURA PLEURAL CAVITY = FILM OF SEROUS FLUID ? RIGHT HAS 3 LOBES (SUPERIOR, MIDDLE INFERIOR LOBES), LARGER WHY? LOBES SUBDIVIDE INTO LOBULES

29 BREATHING MECHANISM INSPIRATION EXSPIRATION INSPIRATION:
DIAPHRAGM CONTRACTS: INCREASES CHEST CAVITY SIZE THEREBY DECREASING ATMOSPHERIC PRESSURE BY 2mm Hg EXTERNAL INTERCOSTAL MUSCLES AND SOME THORACIC MUSCLES MAY ALSO CONTRACT PLEURAL MEMBRANE HELD TO THORACIC CAVITY WALL BY DECREASED PRESSURE, WATER, SURFACE TENSION SURFACTANT RELEASED BY ALVEOLAR CELLS WHICH KEEP ALVEOLI FROM STICKING TOGETHER AIR DIFFUSES IN MUSCLES CONTRACT MORE AND MORE MUSCLES ARE USED TO TAKE A DEEPER BREATH COMPLIANCE= EASE WITH WHICH THE LUNGS EXPAND DECREASES AS LUNGS EXPAND; ALSO DUE TO OBSTRUCTIONS, DAMAGED LUNG TISSUE,

30 EXPIRATION PASSIVE ELASTIC RECOIL COLLAPSED LUNG
OF LUNGS, ABDOMINAL ORGANS, RIBS PRESSURE INCREASES FORCEFUL EXPIRATION BY CONTRACTION OF INTERNAL INTERCOSTALS AND AB MUSCLES PUSH DIAPHRAGM UP HIGHER COLLAPSED LUNG

31

32 BREATHING people.eku.edu

33 people.eku.edu

34 AIR VOLUMES SPIROMETRY
RESPIRATORY CYCLE: ONE INSPIRATION AND ONE EXPIRATION RESTING TIDAL VOLUME NORMAL BREATH: ~500mL INSPIRATORY RESERVE VOLUME EXTRA AIR ENTERING DURING A MAXIMUM BREATH: ~3,000mL EXPIRATORY RESERVE VOLUME EXTRA AIR EXITING DURING A MAXIMUM EXHALE: ~1,100mL RESIDUAL VOLUME AIR LEFT IN LUNGS AFTER MAXIMUM EXHALATION: ~1200mL VITAL CAPACITY MAXIMUM AIR EXHALED AFTER A MAXIMUM INHALATION: ~4,600mL INSPIRATORY CAPACITY TIDAL VOLUME + INSPIRATORY RESERVE: ~3,500mL FUNCTIONAL RESIDUAL CAPACITY RESPIRATORY RESERVE + RESIDUAL VOLUME: ~2,300mL TOTAL LUNG CAPACITY VITAL CAPACITY PLUS RESIDUAL VOLUME: 5,800mL VARIES WITH AGE, GENDER, BODY SIZE ANATOMICAL DEAD SPACE: AIR THAT IN PASSAGEWAY: NOT EXCHANGED ALVEOLAR DEAD SPACE AIR IN ALVEOLI THAT AREN’T WORKING PHYSIOLOGIC DEAD SPACE ANATOMIC AND ALVEOLAR DEAD SPACE IN NORMAL LUNG BOTH THE SAME (ANATOMIC AND PHYSIOLOGIC) CHECKS FOR DISEASES

35 ALVEOLAR VENTILATION VOLUME OF NEW AIR MOVED IN EVERY MINUTE
TIDAL VOLUME – PHYSIOLOGIC DEAD SPACE x BREATHING RATE AFFECTS CONCENTRATION OF O2 AND CO2

36 NONRESPIRATORY AIR MOVEMENTS
CLEAR AIR PASSAGEWAYS COUGHING, SNEEZING COUGH: AIR FORCED THROUGH CLOSED GLOTTIS SNEEZE: CLEARS UPPER TRACT, FORCED OUT BY AIR THROUGH GLOTTIS BY IRRITATION EMOTIONS LAUGHING, CRYING HICCUP SUDDEN INSPIRATION FROM SPASMODIC CONTRACTION YAWNING: PURPOSE? CONTAGIOUS?

37 CONTROL INVOLUNTARY BUT CAN BE VOLUNTARY SOMEWHAT
RESPIRATORY AREAS IN BRAINSTEM CONTROL INSPIRATION AND EXPIRATION, ADJUST RATE AND DEPTH OF BREATHING RESPIRATORY CENTER OF BRAINSTEM MEDULLARY RESPIRATORY CENTER VENTRAL RESPIRATORY GROUP BASIC RHYTHM 2 DIFFERENT GROUPS TO CONTROL INSPIRATION AND EXPIRATION DORSAL RESPIRATORY INSPIRATORY MUSCLES (ESPECIALLY DIAPHRAGM) MORE FORCEFUL HELPS PROCESS THE SENSORY INFO PONTINE RESPIRATORY : PNEUMOTAXIC LIMITS INSPIRATION AFFECTS RHYTHM

38 FACTORS AFFECTING BREATHING
PARTIAL PRESSURE: PROPORTIONAL TO GAS’ CONCENTRATION (O2=21%/160Hg) BREATHING AFFECTED BY PARTIAL PRESSURE IN BODY FLUIDS, LUNG TISSUE STRETCH, EMOTIONS, PHYSICAL ACTIVITY RECEPTORS: MECHANORECEPTORS (STRETCH); CENTRAL AND PERIPHERAL CHEMORECEPTORS

39 CENTRAL CHEMORECEPTORS
IN VENTRAL MEDULLA NEAR VAGUS NERVE INDIRECTLY TO CHANGES IN BLOOD pH H+ CANNOT PASS BLOOD-BRAIN BARRIER CO2 + H20  H2CO3 H2CO3  H+ + HCO3- HIGHER CO2 INCREASES BREATHING RATE AND TIDAL VOLUME MORE CO2 EXHALED AND H+ DECREASES LOW O2 HAS LITTLE EFFECT

40 PERIPHERAL CHEMORECEPTORS
PICK UP CHANGES IN PARTIAL PRESSURE OF O2 IN CAROTID AND AORTIC BODIES (WALLS) LOW 02 (BELOW 50%) IMPULSE TO RESPIRATORY CENTER  INCREASE ALVEOLAR VENTILATION CAN BE AFFECTED SOME BY CO2 AND H+

41 HERING-BREUER REFLEX STRETCH RECEPTORS STIMULATED AS LUNGS EXPAND
VAGUS NERVE IMIPULSE TO PONTINE RESPIRATORY CENTER SHORTENS INFLATION PREVENTS OVERINFLATION

42 BREATHING RATE ALSO AFFECTED BY EMOTIONS, COLD, VOLUNTARILY
HOLDING BREATH: CO2 H+ INCREASE AND EVENTUALLY NEED TO BREATHE HYPERVENTILATION  DECREASES CO2  PASS OUT

43 ALVEOLAR GAS EXCHANGE ALVEOLAR PORES CAN ALLOW AIR TO PASS TO OTHER ALVEOLI: ALLOWS AIR TO BY-PASS SOME BLOCKAGES ALVEOLAR PHAGOCYTES IN ALVEOLI AND PORES ?

44 RESPIRATORY MEMBRANE TYPE 2 CELLS: SECRETE SURFACTANT
MOST: TYPE I: SIMPLE SQUAMOUS CAPILLARIES OUTSIDE ALVEOLI BASEMENT MEMBRANE HOLDS ALVEOLI AND CAPILLARIES TOGETHER GAS MOVES THROUGH

45 DIFFUSION THRU MEMBRANE
DIFFUSION: FROM HIGHER PARTIAL PRESSURE TO LOWER CO2: PRESSURE IN CAPILLARIES = mm45Hg AND ALVEOLI = mm 40Hg DIFFUSES ? O2 40mm Hg IN CAPPILARIES AND 104 mm Hg IN ALVEOLI (DIFFUSES?) DISEASE: HARMS RESPIRATORY MEMBRANE OR REDUCES SURFACE AREA DECREASES DIFFUSION SINCE RESPIRATORY MEMBRANE IS THIN OTHER CHEMICALS CAN DIFFUSE: ALCOHOL

46 OXYGEN TRANSPORT 98%  HEMOGLOBIN OF RBC: OXYHEMOGLOBIN
HIGHER THE PARTIAL PRESSURE OF O2 MORE BINDS TILL SATURATION UNSTABLE BOND: BREAKS WHEN PRESSURE DECREASES HIGHER CO2 CONCENTRATION, ACIDITY, AND TEMPERATURE RELEASES MORE O2 WHY MORE ACTIVE CELLS RECEIVE MORE O2

47 CO2 TRANSPORT PICKED UP FROM CELLS ? BONDS TO AMINE GROUP IMPORTANCE?
DISSOLVED (7%); CARBAMINOHEMOGLOBIN (15-25%); BICARBONATE (~70%) BONDS TO AMINE GROUP IMPORTANCE? RBC CONTAINS CARBONIC ANHYDRASE (?) TURNS CO2 + H20 TO CARBONIC ACID DISSOCIATES TO BICARBONATE + H+ H+ BUFFERED BY DEOXYHEMOGLOBIN CHLORIDE SHIFT: BICARBONATE LEAVES RBC + CHLORIDE ENTERS TO MAINTAIN IONIC BALANCE AFTER CO2 DIFFUSES OUT, CARBONIC ACID REFORMS CO2 + H2O

48 LIFE SPAN CHANGES POLLUTED AIR/SMOKING = BRONCHITIS, EMPHYSEMS, CANCER, DAMAGED CELLS CILIATED EPITHELIUM AND CILIA DECREASE MUCUS THICKENS, SWALLOWING, GAGGING, COUGHING REFLEXES SLOW TO STOP MACROPHAGES DON’T WORK AS WELL =MORE SUSCEPTIBLE TO RESPIRATORY INFECTIONS

49 SHAPE OF THORACIC CAVITY CHANGES
CARTILAGE STIFFENS MORE FIBEROUS CONNECTIVE TISSUE = LESS FLEXIBILITY VITAL CAPACITY DECREASES ~-1/3 BY 70 BRONCHIOLES THIN AND DON’T STAY AS OPEN MORE DEAD SPACE BY 80 MAXIMUM VENTILATION DROPS BY 50% 300 MILLION 8 YEARS, SAME AMOUNT BUT DEPTH DECREASES BY 40 = 3 SQ FT PER YEAR

50 OXYGEN TRANSOPRT IS LESS EFFICIENT
BREATHING ABILITY DECREASES


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