CHAPTER 19RESPIRATORY SYSTEM

RESPIRATORY SYSTEM

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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

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SINUSES

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

VOICE BOX

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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 = ?

TRACHEA

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ALVEOLI

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ALVEOLI

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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