bio22.txt

• provides oxygen and carbon dioxide exchange between blood and air
• serves for speech and vocalization
• sense of smell
• pH regulation (via CO2)
• aids in angiotensin II synthesis (blood pressure)
• Assists CV system - respiratory pumps (venous/lymph return)
• dissolves blood clots

• nose
• pharynx
• larynx

• trachea
• bronchi
• alveoli

• fxn: warms, cleanses, and humidifies inhaled air, detects odors, serves as a resonating chamber that amplifies the voice, guard hairs/mucous traps tiny particles
• the nasal concha: creates turbulent air flow

• perpendicular plate (ethmoid bone)
• septal cartilage
• vomer

• nasopharynx: receives air only
• oropharynx: passes air, food and drink
• laryngopharynx: passes air, food, and drink

the respiratroy and digestive system share the oropharynx and laryngopharynx

• voice box, keeps food and drink of out of the airway
• epiglottis: closes the airway and directs food and drink into the esophagus
• thyroid cartilage: shieldlike, adam's apple
• cricoid cartilage: ringlike, connects layrnx to trachea
• hyoid bone
• vestibular folds: no role in speech, close larynx during swallowing
• vocal cords: produces sounds as air passes between them
• glottis: the vocal cords and the opening between them

• produce longer/thicker vocal cords
• vibrate slower and lower pitch
• taut cords: produce higher pitch
• looser cords: produce low pitch

speech is produced by pharynx, tounge, mouth and lips

• windpipe
• 16-20 C shaped rings, reinforce the trachea and keep it from collapsing when you inhale
• mucocililary escalator: debris removal, mucus traps particles, upward beating of cilia drives debris laden mucus toward pharynx, then swallowed, 10-20 beats/second

*smoking/pollution kills cillia

• apex
• mediastinal surface: faces medially
• hilum: how the lung receives the main bronchus, blood vessels, and nerves
• main bronchi: 1st degree
• superior lobar, middle lobar, inferior lobe bronchus: 2nd degree
• asymmetrical: R lung shorter, liver interfers so 3 lobes, L lung, heart interferes so 2 lobes

conducting zone: air flow only - nasal cavity, pharynx, trachea, main bronchus, lobar bronchus, segmental bronchus, bronchiole, smooth muscle and cartilage

*

• cillary elevator stops in between
• *
• reapiratory zone: gas exchange, no cartilage, includes, terminal broonchioles, respiratory bronchioles, alveloar ducts (8 x 10⁸)

• low blood pressure
• ensures only absorption of fluid, not filtiraion, so no pulmonary edema
• capillary networks around alveoli

• Squamous (type I) alveolar cell: covers about 95% of alveolar surface area, thin, layer provides rapid gas exchange
• great (type II) avleolar cell: 5% of surface, repair squamous (type I) cells when damaged, secrete surfactant
• alveolar macrophages: most abundant, phagocytize dust, debris, bacteria,

• fxn: reduces friction, when breathing, creates a negative pressure that keeps the lungs inflated, cmpartmentalization of each lung
• intrapuleural fluid: only a few mL
• parietal pleura: attached to the throacic wall, mediastinmum, inner surface of rib cage, superior diaphragm
• visceral plurea: covers the surface of the lung, serous membrane

diaphragm and intercostal muscles

boyles law

apnea

the pressure inside the lungs is less than the atmosphereic pressure

pulmonary compliance

dilaing the pumonary arteries near well-ventilated alveoli

bound to hemoglobine; bicarbonate

95 mmHg; 46 mmHg

acidosis; hyperventilates

true

• breathing
• respiratory cycle

• refers to relaxed, unconscious, automatic breathing
• external intercoastals ( elevates ribs 2-12)
• diaphragm (descends: impacts 2/3 airflow)

• refers to deep, rapid breathing, as in excerise, singing, plays instruments, coughing, sneezing
• sternoclediomastoid (elevates sternum)
• scalenes ( elevates ribs 1 - 2)
• pectoralis minor (elevates ribs 3-5)
• external intercoastals
• diaphragm

• passive, elastic recoil of lungs
• no muscles

• internal intercoastals (depress ribs)
• diaphragm (acends)
• abdominals ( compress abdominal cavity, push diaphragm upwards)

• pontine respiratory group (PRG): modulators of respiratory rhythm, receives input from hypothalamus, limbic system, cerebral cortex, adapts breathing to sleep, excerise, speech, emotions, under voluntary control
• dorsal respiratory group (DRG): intergrator, inputs from PRG, hypothalamus, medulla oblongata, chemorecptors ( CO2/pH), stretch and irriant receptors, outputs to the VRG
• ventral respiratory group (VRG): primary involunatary generatory in meduall oblongata, output to muscles, inspriatory neurons 2 sec., expiratory neurons 3 sec. = 12 breaths/min., pattern generator to spinal cord/muscles of respiration

Boyles law: the pressure of a given quantithy of gas is inversly proportional to its volume. If the lungs contain a quantity of gas and lung volume increases, their internal pressure (intrapulmonary pressure) falls.

• inspiration: P alveoli (low ) < P atm (high)
• expiration: P alveoli (high) > P atm (low)
• Airflow: high P to low P
• no flow: P atm = P alveoli

How does P change? volume

• at rest: pressure relavitve to atmospheric pressure; chest wants to expand outward, lung elasticity wants to recoil inward; no flow- P atm = P alveoli; pleura stuck together by intrapleural (IP) fluid; negative IP pressure (slight vaccum) - IP pressure = -4mmHg, holds lungs open
• inspiration: muscles contract; increases the volume in the throacic cavity - increase lung volume; increase lung volume - decrease pressure, so air flows in: P atm > P alveoli (0> - 3), until P atm = P alveoli
• expiration: muscles relax; decrease volume in throacic cavity - decrease lung volume, air flows out; P alveoli > P atm (3 > 0) until P alveoli = P atm
• pnemothroax: air in chest; P (IP) goes from -4 to 0, since nothing holds lungs open , then inwards recoil and collapse, atelectasis- collapsed lung or partial breath

• bronchodilation: an increase in the diameter of a bronchus or bronchiole, an increase in radius leads to a decrease in resistance; epinephrine and the SNS stimulate bronchodilation and increase airflow
• bronchoconstriction: a reduction in diameter; decrease in radius leads to an increase in resistance; internal stimulants - PSNS, ACh, histamines, interleukins, external stimulants - cold air, chemical irritants, asthema

asthema/inflammation- bronchonconstriction, treatment is bronchodilation/anti-inflammatory drugs

• pulmonary compliance: the ease with with the lungs expand or stretchability; expansion based on pressure changes - change in lung volume relative to a given pressure change
• increased compliance: floppy lungs, easy to inhale, hard to exhale; emphysema; "spent" ballon
• decreased compliance: stiff lungs; shallow breathing, expand less; TB, black lung disease; throacic expands normally, but lungs expand little

• alveoli have a slight moisture lining
• H-bonds attract water molecules to each other, creating surface tension, which leads to increase collapse
• fix: surfactant ; "detergent like";contains amphiphilic proteins and phospholipids - partially hydrophobic, so spread out over the surface of the water film *** reduces surface tension***; increased by type II cells
• Newborn respriatory diestress syndrom: no surfactant; decrease compliance; increased work breathing - alveloar collapse

• air that actually enters the alveoli becomes available for gas exchange, but not all inhaled air gets that far
• anatomical dead space: this air cannot exchange gases with blood; fills the conducting division of the airway; left over from preceeding breath; inspired air (TV) 500 mL - left over air (dead space) 150 mL = 350 mL ventilates into the alveoli
• *must account for dead space when calculating alveolar ventilation
• alveolar ventilation rate: most directly relevant to the body's ability to get oxygen to the tissues and dispose of carbon dioxide; respiratory rate X (TV - dead space) = AVR - the amount of fresh air moved/minute 4.2L/min
• minute ventilation rate: the amount of air inhaled per minute; respiratory rate X TV = mvr - amount of air moved per minute, 6L/min

• how does change rate and depth affect ventilation
• MVR: same - example; respiration rate (24) x TV (250) = 6000 mL/min
• AVR: fast shallow breaths example; respriation rate (24) X TV- dead space (250 - 150) = 2400 mL/min; *not effective ventilation, exchange rate decreases
• AVR: slow deep breaths example; respiration rate (6) X TV- dead space (1000 - 150) = 5100mL/min; * more effective than normal

*** depth is more important than rate**


unusable is constant, hyperventilation (increased rate) vs. excerise (increased rate and increased depth)

• tidal volume: the amout of air inhaled and exhaled in one cycle during quite breathing
• normal value: 500 mL

• inspriatory reserve volume: the amount of air in excess of tidal volume that can be inhaled with maximum effort; during forced inspiration
• normal value: 3,000 mL

• expiratory reserve volume: the amount of air in excess of tidal volume that can be exhaled with maximum effort; during forced expiration
• normal value: 1,200 mL

• residual volume: the amount of air remaining in the lungs after maximum expiration ( foreced expiration); the amount that can never be volunatrily exhaled
• normal value: 1,300 mL

• FRC: the amount of air remaining in the lungs after a normal tidal expiration
• normal value: 2,500 mL
• how to calculate: RV+ ERV

• IC: the maximum amount of air that can be inhaled after a normal tidal expiration
• normal value: 3,500 mL
• how to calculate: IC = TV + IRV

• VC: the amout of air that can be inhaled and exhaled with maximum effort; the deepest breath possible
• normal value: 4,700 mL
• how to calculate: VC= ERV + TV + IRV

• TLC: maximum amount of air the lungs can contain
• normal value: 6,000 mL
• how to calculate: TLC= RV + VC

• FEV: % of vital capacity exhaled over a given time
• normal value: 75-85%/1 second

• restricitve disorders
• reduce pulmonary compliance, thus limiting the amount to which the lungs can be inflated.
• hard to inflate
• decreased vital capacity
• example: black lung disease, TB

• obstructive disorders
• interfere with airflow by narrowing or blocking airway
• decreased FEV
• decreased airway radius
• can't get air out fast
• example: asthma and chronic bronchitis (COPD)

• decrease cilia - leads to increase mucos
• decrease macrophages activity - leads to increase bacteria, chronic cough and infection
• cig smoke as 15 carcinogens
• causes one of the more deadly cancers

• the total atmospheric pressure is a sum of the contributions of these individual gases
• 1. it is humidifed by contact with the mucous membrane, so its PH2O is more than 10x higher than the inhaled air
• 2. freshly inhaled air mixes wiht residual air left from previous respiratory cycle, so its O2 is diluited and it is enriched with CO2
• 3. alveolar air exchanges O2 and CO2 with the blood so the PO2 of alveolar air is about 65% of that inhaled air, and its PCO2 is more than 130 times higher

• **via diffusion: high concentration to low concentration
• *for external respiration

• the amount of gas that dissolves in the water is determined by its solubility in water and its partial pressure in the air.
• a. the PO2 of alveolar air is initially higher thatn the PO2 of the blood arriving at an alveolous. O2 diffuses into the blood until the two are in equilibrium
• b. the PCO2 of the arriving blood is initially higher than the PCO2 of teh alveolar air. CO2 diffuses into the alevolus until the two are at equilibrium.
• it takes about 0.25 second for both gases to reach equilibrium

• diffusion conditions
• gases diffused from high (parital pressure) to low PP; higher pressure - more gases dissolved
• each gas behaives independently
• constant temperature

• * CO2 is 20x more soluble than O2
• *RBC transit time = 0.75 -0.3 seconds

• arterial blood
• PO2 is 95 mmHg
• PCO2 is 40 mmHg

• venous blood
• PO2 = 40 mmHg
• PCO2 = 46 mmHg

• the PO2 is about 104 mmHg in alveolar air and 40mmHg in blood arriving at the alveolus, so O2 diffuses from the air into the blood
• the PCO2 is about 46 mmgh in blood arriving at teh alveolous and 40mmgh in alveolar air, so CO2 diffuses from the blood into alveoli

hyperbaric oxygen therapy: treatment with oxygen at greater than 1 atm of pressure, treates gangrene and caronbon monoxidea poisoning

• respiratory membrane between blood and alveoalr air is only 0.5 micorliters thick, presents little obstacles for diffusion, plently of equilibrium time
• diseased lung: respiratory membranes become edematous and thick, gases have farther to travel b/w blood and air and cannot equilibrate fast enough, so blood leaving lungs ( to rest of body) has high PCO2 and low PO2

congestive heart failure, pneumonia, cystic fibrosis

• healthy lung: 70m2 of respiratory membrane available for gas exchange, blood is spread very thinly
• diseased lung: elastic tissue breaks down, decrease surface area, decrease gas exchange, leads to low blood PO2

examples: emphysema, lung cancer, and TB

refers to physicological responses that match airflow to blood flow and vice versa

poor ventilation leads to a low PO2 (decreased pressure in blood vessels) in that region of the lung, this stimulates local vasoconstriction, rerouting the blood to better-ventilated areas of the lung.

increased ventilation (increased air flow) raises PO2 and stimulates vasodilation, increasing blood flow to that region to take advantage of the oxygen availability

• for CO2
• decreased blood flow leads to reduced PCO2 inthe alveoli, so constriction of the broncioles, leads to decreased airflow, could lead to a blood clot

increased blood flow leads to elevated PCO2 in alveoli, so dilitation of bronchioles, increased air flow, redirected blood flow

gas transport: the process of carrying gases fromthe alveoli to the systemic tissues and vice versa

• oxygen
• ~1.5% dissolved in blood
• ~98.5% is bound to hemoglobin (4O2/Hgb)
• arterial blood: ~98% saturated, (4O2/Hgb), bright red
• venous blood: ~75% saturated, 3O2/Hgb, dark red

• 02 Hgb dissocation
• the relationship between hemoglobin saturation and PO2
• at low PO2 there is a rapid increase in oxygen loading as PO2 rises further
• at high PO2 levels, Hgb approaches 100% saturation and cannot load much more oxygen
• 75%- cells can obtain more if needed
• exercise - 50% steepness, easy to load/unload, systemic tissues

• carbon monoxide
• ~210x affinity for Hgb than O2
• 0.1% CO (closed garage) binds to 50% of Hgb

• transported in 3 forms: carbonic acid, carbamino compounds, dissolved gas
• about 5% finds to the amino groups of plasma
• CO2 + H2o > H2CO3 > HCO3 + H+

• 5% of CO2 is carried in the blood as dissolved gas
• 70% of exchanged CO2 comes from carbonic acid
• 23% of schanged CO2 comes from carbamino compounds
• 7% from the dissolved gas

the unloading of O2 and the loading of CO2 at the systemic capillaries

• carbon dioxide loading
• typically a CO2 gradient of 46 - 40 mmHg from tissue fluid to blood.
• CO2 diffuses into bloodstream
• reacts with water to produce bicarbonate (HCO3-) and hydorgen (H+)
• most of the HCO3- is pumped out of the RBC in exchange for Cl- from blood plasma, called the chloride shift
• most of the H+ binds to hemoglobin or oxyhemoglobin, which buffers the intreacelluar pH

• Oxygen unloading
• when H+ binds to oxyhemglobin it reduces the afinity fo hemoglobin for O2
• PO2 of tissue fluid is low, pressure gradient of 95 > 40 mmHg from arterial blood to tissue fluid
• O2 unloads in tissues

• the rate of CO2 loading is adjusted to varying needs of the tissues, low level oxyhemoglobin enables the blood to transport more CO2
• 1. oxyhemoglobin does not bind to CO2 as well as deoxyhemoglobin does
• 2. deoxyghemoglobin binds more hydrogen ions than oxyhemoglobin by removing H+ from the solution
• shifts the carbonic rxn H20 + CO2 > HCO3- + H+ to the right, thus allows more CO2 to be transported

O2 binds to Hgb, has decreased affinity for CO2

• temperature: increased temperature ( active tissues) promotes O2 unloading, the curve shfits to the right("releasing") // decrease temperature > O2 loading, curve shifts to the left (''loading")
• borh effect: (acidity)active tissues generate extra CO2 which raises the H+ concentration, lowers pH. hydrogen ions weaken the bond b/w hemoglobin and oxygen and promote oxygen unloading
• drop in pH shifts the curve to the right (''releasing")

increased acid (decreaed pH) or acidosis, increase O2 loading

• unloads more oxygen at higher temps
• unloads more oxygen at lower pH

• Normal arterial blood values: PO2 - 95 mmHg, PCO2 - 40 mmHg, pH = 7.40
• breathing is ajusted to maintain -
• CO2+ H20 > H2Co3 - < - > HCO3 - + H+
• CO2 directly relates to pH, increases CO2 > increased H+ > decreased pH

• central chemoreceptors: near DRG receptors
• in blood brain barrier: Co2 easily crosses, H+ does NOT easily cross BBB, increases the central chemorecptor firing

peripheral receptors: less sensitive, stimulated by increased CO2, increased pH, decreased O2 (lower than 60 mmHg), causes increased ventilation

ablood pH lower than 7.35

blood pH greater than 7.45

a PCO2 less than 37 mmHg

a PCO2 greater than 43mmHg

increased pulmonary ventilation in excess of metabolic demand, frequently associated with anxitey; expels CO2 faster than it is produced, thus lowering the blood CO2 concentration and raising the blood pH

reduced pulmonary ventilation; leads to an increase in blood CO2 concentration if ventialtion is insuffient to expel CO2 as fast as it is produced

• A respiratory crisis triggered by allergens in pollen, mold, food, dust
• Allergens stimulate plasma cells to secrete IgE, which binds to mast cells of the respiratory mucosa, causes mast cells to release inflammatory chemicals , which trigger intense airway inflammation.

Respiratory membranes ( alveolar walls) are thick with edema, and the alveoli contain fluid and blood cells

The cilia are immobilized and reduced in number, while goblet cells enlarge and produce excess mucus

Alveolar walls break down and the lung exhibits larger but fewer alveoli, so there is much less respiratory membrane available for exchange.

The presences of air in the pleural cavity;without the negative intrapleural pressure to keep the lungs inflated, the lungs recoil and collapse

A deficiency of pulmonary surfactant and then experience great difficulty breathing; treated with artificial surfacant

Occurs when the rate of alveolar ventilation fails to keep pace with the body's rate of CO2 production

Results from hyperventilation, in which CO2 is eliminated faster than it is produced.

synthesizes and secretes vitamin B12

B. the bronchi and bronchioles contain smooth muscle

C. the same as

A. external intercostals

A. as volume increases, pressure decreases

D. ventral respiratory group

D. pressure inside the lungs increases

B. causes bronchodilation

A. when air gets into the pleural space causing the lungs to collapse

D. both B and C

B. a reduction of surfactant

C. 8000/3000

D. smoking increases the number of cilia along the respiratory tract.

A. 95 mmHg

A. deoxygenated hemoglobin has a higher affinity for CO2 than oxygenated hemoglobin

B. bound to hemoglobin; bicarbonate

C. increased; decreased

E. an increased in ventilation faster than the rate of CO2 production

B. increased H+

A. decreased blood pH