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RESPIRATORY SYSTEM http://kidshealth.org/kid/htbw/lungs.html MARIA WILL YOU GO TO THE PROM WITH ME? DREW VENTILATION EXTERNAL RESPIRATION TRANSPORT INTERNAL RESPIRATION CELLULAR RESPIRATION TO GET OXYGEN FOR AEROBIC CELLLULAR RESPIRATION: FORM ATP TO GET RID OF CO2 CO2 +H2O= CARBONIC ACID: MAINTAINS PORPER pH UPPER RESPIRATORY TRACT NOSE, NASAL CAVITY, SINUSES, PHARYNX LOWER RESPIRATORY TRACT LARYNX, TRACHEA, BRONCHIAL TREES, LUNGS www.emc.maricopa.edu www.emc.maricopa.edu 2 NOSTRILS HAIRS TO REMOVE LARGE PARTICLES 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? 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 SINUSES PASSAGEWAY FOR FOOD AND AIR AIDS IN FORMING SOUNDS SUBDIVISIONS: CHAPTER 17 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 VOCAL CHORDS OF MUSCLE AND CONNECTIVE TISSUE WITH MUCOUS MEMBRANE FALSE VOCAL CHORDS TRUE VOCAL CHORDS UPPER FOLDS NO SOUND CLOSE TRACHEA DURING SWALLOWING 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 VOICE BOX en.wikipedia.org 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? 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 = ? TRACHEA en.wikipedia.org library.thinkquest.org/ www.emc.maricopa.edu en.wikipedia.org www.siumed.edu/ http://www.niehs.nih.gov/oc/factsheets/ozone/ithurts.htm 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 ALVEOLI = INCREASE SURFACE AREA INCREASED DIFFUSION 300 MILLION ALVEOLI = SURFACE AREA OF ½ TENNIS OCURT EXCHANGE CO2 AND O2 www.emc.maricopa.edu 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 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, EXPIRATION PASSIVE ELASTIC RECOIL OF LUNGS, ABDOMINAL ORGANS, RIBS PRESSURE INCREASES FORCEFUL EXPIRATION BY CONTRACTION OF INTERNAL INTERCOSTALS AND AB MUSCLES PUSH DIAPHRAGM UP HIGHER COLLAPSED LUNG www.emc.maricopa.edu people.eku.edu people.eku.edu 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 VOLUME OF NEW AIR MOVED IN EVERY MINUTE TIDAL VOLUME – PHYSIOLOGIC DEAD SPACE x BREATHING RATE AFFECTS CONCENTRATION OF O2 AND CO2 CLEAR AIR PASSAGEWAYS EMOTIONS COUGHING, SNEEZING COUGH: AIR FORCED THROUGH CLOSED GLOTTIS SNEEZE: CLEARS UPPER TRACT, FORCED OUT BY AIR THROUGH GLOTTIS BY IRRITATION LAUGHING, CRYING HICCUP SUDDEN INSPIRATION FROM SPASMODIC CONTRACTION YAWNING: PURPOSE? CONTAGIOUS? 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 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 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 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+ STRETCH RECEPTORS STIMULATED AS LUNGS EXPAND VAGUS NERVE IMIPULSE TO PONTINE RESPIRATORY CENTER SHORTENS INFLATION PREVENTS OVERINFLATION ALSO AFFECTED BY EMOTIONS, COLD, VOLUNTARILY HOLDING BREATH: CO2 H+ INCREASE AND EVENTUALLY NEED TO BREATHE HYPERVENTILATION DECREASES CO2 PASS OUT ALVEOLAR PORES CAN ALLOW AIR TO PASS TO OTHER ALVEOLI: ALLOWS AIR TO BY-PASS SOME BLOCKAGES ALVEOLAR PHAGOCYTES IN ALVEOLI AND PORES ? TYPE 2 CELLS: SECRETE SURFACTANT MOST: TYPE I: SIMPLE SQUAMOUS CAPILLARIES OUTSIDE ALVEOLI BASEMENT MEMBRANE HOLDS ALVEOLI AND CAPILLARIES TOGETHER GAS MOVES THROUGH 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 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 PICKED UP FROM CELLS ? DISSOLVED (7%); CARBAMINOHEMOGLOBIN (1525%); 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 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 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 ALVEOLI @ 8 YEARS, SAME AMOUNT BUT DEPTH DECREASES BY 40 = 3 SQ FT PER YEAR OXYGEN TRANSOPRT IS LESS EFFICIENT BREATHING ABILITY DECREASES