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CHAPTER 19RESPIRATORY SYSTEM
RESPIRATORY SYSTEM
http://kidshealth.org/kid/htbw/lungs.html
MARIA WILL YOU GO TO THE PROM
WITH ME?
DREW
RESPIRATION
VENTILATION EXTERNAL RESPIRATION TRANSPORT INTERNAL RESPIRATION CELLULAR RESPIRATION
WHY?
TO GET OXYGEN FOR AEROBIC CELLLULAR RESPIRATION:FORM ATP
TO GET RID OF CO2CO2 +H2O= CARBONIC ACID: MAINTAINS PORPER pH
ORGANS
UPPER RESPIRATORY TRACTNOSE, NASAL CAVITY, SINUSES, PHARYNX
LOWER RESPIRATORY TRACTLARYNX, TRACHEA, BRONCHIAL TREES, LUNGS
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NOSE
2 NOSTRILS HAIRS TO REMOVE LARGE
PARTICLES
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?
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
PHARYNX
PASSAGEWAY FOR FOOD AND AIR AIDS IN FORMING SOUNDS SUBDIVISIONS: CHAPTER 17
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
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
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?
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 = ?
ALVEOLI
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ALVEOLI
http://www.niehs.nih.gov/oc/factsheets/ozone/ithurts.htm
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
FUNCTIONS
ALVEOLI = INCREASE SURFACE AREA INCREASED DIFFUSION
300 MILLION ALVEOLI = SURFACE AREA OF ½ TENNIS OCURT
EXCHANGE CO2 AND O2
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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
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 BREATHCOMPLIANCE= 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
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BREATHING
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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 SIZEANATOMICAL DEAD SPACE:
AIR THAT IN PASSAGEWAY: NOT EXCHANGEDALVEOLAR DEAD SPACE
AIR IN ALVEOLI THAT AREN’T WORKINGPHYSIOLOGIC DEAD SPACE
ANATOMIC AND ALVEOLAR DEAD SPACEIN NORMAL LUNG BOTH THE SAME (ANATOMIC AND PHYSIOLOGIC)CHECKS FOR DISEASES
ALVEOLAR VENTILATION
VOLUME OF NEW AIR MOVED IN EVERY MINUTE
TIDAL VOLUME – PHYSIOLOGIC DEAD SPACE x BREATHING RATE
AFFECTS CONCENTRATION OF O2 AND CO2
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?
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
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
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
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+
HERING-BREUER REFLEX
STRETCH RECEPTORS STIMULATED AS LUNGS EXPAND
VAGUS NERVE IMIPULSE TO PONTINE RESPIRATORY CENTER
SHORTENS INFLATION PREVENTS OVERINFLATION
BREATHING RATE
ALSO AFFECTED BY EMOTIONS, COLD, VOLUNTARILY
HOLDING BREATH: CO2 H+ INCREASE AND EVENTUALLY NEED TO BREATHE
HYPERVENTILATION DECREASES CO2 PASS OUT
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 ?
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
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
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
CO2 TRANSPORT
PICKED UP FROM CELLS ? 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
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
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