*** A&p Ch. 23 Respiratory System - Physiology

Front 1

Video of gas exchange

Back 1

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Front 2

List the 4 pressures in the thoracic cavity

Back 2

- atmospheric pressure: P exerted by air surrounding body

- intrapulmonary (intra-alveolar) pressure: P in alveoli. P inside lung decreases as lung V increases during inspiration; P increases during expiration.

- intrapleural pressure: P in the plural cavity (always -) pleural cavity P becomes more negative as chest wall expands during inspiration. Returns to intial value as chest wall recoils.

- transpulmonary pressure: P that keeps lung spaces open, keeping lungs from collapsing. Greater the TP, larger lungs will be. (-TP must be maintained to keep lungs inflated)

- volume of breath (not a pressure): during each breath, the P gradients move 0.5 L of air into and out of the lungs.

Front 3

What is atelectasis?

Back 3

Lung collapse due to; plugged bronchioles, which cause collapse of alveoli or pneumothorax

Front 4

What is a pneumothorax?

Back 4

Air in the pleural cavity.

Can occur from wound in parietal pleura or rupture of visceral pleura

- ex. Stab wound

Front 5

Explains main 2 mechanical processes involved in pulmonary ventilation

Back 5

- inspiration and expiration: movement of air into lungs; depend on volume changes in thoracic cavity.

- volume changes = pressure changes (Boyle)

- pressure changes = gases flow to equalize pressure

- inspiration: involving inspiratory muscles: DIAPHRAM and INTERCOSTAL MUSCLES. Sequence of events:

1. Inspiratory muscles contract, diaphram descends, rib cage rises.

2. Thoracic cavity V increases

3. Lungs stretch, intrapulmonary V increases

4. Intrapulmonary P drops

5. Air (gases) flows into lungs down its pressure gradient until intrapulmonary P is 0 (= to atmospheric pressure)

- expiration: quiet breathing, inspratory muscles relax, lungs recoil. Forced expiration uses ollblique & transverse abdominal muscles, as well as internal intercostal muscles. Events:

1. Inspiratory muscles relax, diaphram rises, rib cage descends due to recoil of costal carrilages

2. Thoracic cavity V decreases.

3. Elastic lungs recoil passively, intrapulmonary V decreases

4. Intrapulmonary P rises

5. Air (gases) flows out of lungs down its pressure gradient until intrapulmonary pressure is 0

Front 6

What are the accessory respiratory muscles?

Back 6

- valsalva maneuver: taking deep breath, holding it by closing the glottis, then contracting abdominal muscles to raise abdominal P and pushing organ contents out. (Childbirth, urination, defecation, vomiting)

- nonrespiratory air movements: (coughing, sneezing, crying, laughing, hiccups, yawns)

Front 7

What are the 3 gas laws in ventilation (BCD)? What law consists of gas mixtures, not law of ventilation

Back 7

- Boyle's law: Relationship between pressure and volume of a gas. - P inversely proportional to V: P1V1=P2V2. If lung V increases, P inside lungs drops. If lung V decreases, P inside lungs rises. - relationship between F, P and R =F = P/R (similar to BF in the cardiovascular system)

- Charles law: V of gas directly proportional to temperature: PV=nRT. Air must be warmed on it's way into the lungs, warm air takes up more space than cooled air.

- Dalton's law: each component of a gas mixture has it's own pressure, total pressures exerted by mixture of gases= sum of pressures exerted by each gas.

partial pressure: P exerted by each gas in mixture, directly proportional to its % in mixture.

Nitogen= ~78.6% of air

O2= 20.9%

CO2= 0.04%

- Henry's law: consists of gas mixtures in contact with liquid. Each gas dissolves in proportion to its partial P. Amount of each gas that will dissolve depends on: solubility (CO2 20x more soluble in water than O2, little N2 dissolves in water) and temperature (as temp. rises, solubility decreases)

Ex. Hyperbaric chambers.

Front 8

What are 3 factors influencing pulmonary ventilation?

Back 8

1. airway resistance (diameter of bronchioles): BRONCHODIALATION: increase in diameter of a bronchus or bronchiole. Stimulated by Epinephrine and sympathetic stimulation, increases air flow. BRONCHOCONSTRICTION: decrease in diameter of a bronchus or bronchiole. Stimulated by histamine, parasympathetic nerves, cold air & chemical irritants.

2. Pulmonary compliance: the ease with which the lungs can expand. Measure of change in lung V that occurs with given change in transpulmonary P. Higher lung compliance = easier to expand. Normally high due to distensibilty of lung tissue and surfactant which decreases alveolar surface tension.

3. Surface tension of the alveoli and distal bronchioles. Surfactant- reduces surface tension of fluid and discourages alveolar collapse. "Soapy like" lipid and protein complex produced from type II alveolar cells. Insufficient quantity in premature infants.

Front 9

What is infant respiratory distress syndrome? What causes it?

Back 9

In premature infants- Alveoli collapse after each breath, caused by insufficient quantity of surfactant: reduces surface tension of fluid and discourages alveolar collapse.

Front 10

List the respiratory volumes

Back 10

- tidal volume (TV): V of air inhaled and exhaled in one cycle during quiet breathing. (500ml)

- inspiratory reserve volume (IRV): air in excess of tidal volume that can be inhaled with maximum effort (3000ml)

- expiratory reserve volume (ERV): air in excess of todal volume that can be exhaled with maximum effort. (1200ml)

- residual volume (RV): air remaining in lungs after maximum expiration. (1300ml).

Front 11

List the respiratory capacities

Back 11

- vital capacity (VC): total amount of air that can be inhaled and then exhaled with maximum effort. Important measure in pulmonary health.

VC= ERV+TV+IRV (4700ml)

- inspiratory capacity (IC): maximum amount of air that can be inhaled after a normal tidal expiration.

IC= TV+IRV (3500ml)

- functional residual capacity (FRC): amount of air remaining in the lungs after a normal tidal expiration.

FRC= RV+ERV (2500ml)

- total lung capacity (TLC): maximum amount of air the lungs can contain

TLC= RV+VC (6000ml)

Front 12

What is a spirometer?

Back 12

Measurement of ventilation: instrument for measuring respiratory volumes and capacities. Recaptures expired breath and records such variables such as rate and depth of breathing, speed of expiration, and rate of O2 consumption.

Pulmonary function tests: spirometry can distinguish between:

- obstructive pulmonary disease: increased airway resistance (ex.bronchitis) TLC, FRC, RV may increase because of hyperinflation of lungs.

- restrictive disorders: reduced TLC due to disease (ex. tuberculosis or fibrosis) VC, TLC, FRC, RV declines because lung expansion is compromised.

Pulmonary function tests can measure rate of gas movement:

- forced vital capacity (FVC): amount of gas forcibly expelled after taking a deep breath.

- forced expiratory volume (FEV): amount of gas expelled during specific time interval of FVC.

FEV1: amount of air expelled in 1st second. Healthy= 80%

Front 13

What is the alveolar ventilation rate and what is minute ventilation?

Back 13

- alveolar ventilation rate (AVR): flow of gases into and out of alveoli during particular time. Better indicator of effective ventilation.

- minute ventilation: total amount of gas that flows into or out of respiratory tract in 1 minute.

Normal at rest= ~6L/min.

Normal with exercise= up to 200 L/min

Only enough estimate of respiratory efficiency.

- normal rate and depth: 70% effective ventilation

- slow, deep breathing: 85%

- rapid, shallow breathing: 40%

Front 14

What are the mechanisms for mass transfer across the alveolar membrane and into the blood?

Back 14

Perfusion/respiration- transfer of air from lungs to blood? Internal and external respiration?

Front 15

Perfusion/ gas exchanges between blood, lungs and tissues (2 mechanisms)

Back 15

- internal respiration: diffusion of gases between blood and tissues. Involves capillary gas exchange in body's tissues. Partial P and diffusion gradients are reversed compared to external respiration.

Tissue Po2 is always lower than in arterial blood Po2 (40 vs 100mmhg), so o2 moves from blood to tissues.

Tissue Pco2 is always higher than arterial blood Pco2 (45 vs 40mmhg), so Co2 moves from tissues to blood.

- external respiration: diffusion of gases between blood and lungs. Involves exchange of O2 and CO2 across respiratory membrane. Influenced by 1. thickness and surface area of respiratory membrane. Respiratory membranes are very thin (0.5 to 1um thick). Large total surface area of the alveoli is 40x the surface area of the skin. 2. Partial P gradients and gas solubilities. Steep partial P gradient for O2 exists between blood and lungs: venous blood po2 = 40mmhg and alveolar po2 = 104mmhg. Drives O2 flow into blood. Partial P gradient for Co2 is less steep: venous blood pco2 = 45mmhg and alveolar pco2 = 40mmhg. Though gradient is not as steep, co2 still diffuses in equal amounts with O2 because CO2 is 20x more soluble in plasma and alveolar fluid than O2. 3. Ventilation-perfusion coupling; perfusion: BF reaching alveoli, changes in po2 in alveoli changes in diameters of arterioles. Where alveolar o2 is high, arterioles dilate, where alveolar O2 is low, arterioles contract. Directs most blood where alveolar O2 is high. ventilation: amount of gas reaching alveoli, changes in pco2 in alveoli cause changes in diameters of bronchioles. Where alveolar co2 is high, bronchioles dilate, where alveolar CO2 is low, bronchioles constrict. Allows elimination of co2 more rapidly.

Rates for both must be matched for optimal, efficient gas exchange. Both are controlled by local auto regulatory mechanisms: po2 controls perfusion by changing arteriolar diameter and pco2 controls ventilation by changing bronchiolar diameter.

- opposite mechanism seen in systemic arterioles that dilate when O2 is low and constrict when high. Balancing ventilation and person. Changing diameters of local arteries and bronchioles synchronizes ventilation-perfusion. Ventilation-perfusion is never balanced for all alveoli because regional variations may be present, due to effect of gravity on blood and air flow. Occasionally, alveolar ducts plugged with mucus cause unventilated areas.

* both involve physical properties of gases and composition of alveolar gas.

Front 16

Homeostatic imbalance

Back 16

- Breathing O2 gas at 2atm is not a problem for short periods; however, O2 toxicity develops rapidly when Po2 is greater than 2.5-3atm.

- excessively high O2 concentrations generate huge amounts of harmful free radicals.

- results in CNS disturbances, coma and even death.

Front 17

Homeostatic imbalances

Back 17

- effective thickness of respiratory membrane increases dramatically if the lungs become waterlogged and edematous. Seen in pneumonia or left heart failure.

- the 0.75 seconds that RBCs spend in transit through pulmonary capillaries may not be enough for adequate gas exchange.

- result: body tissues suffer from O2 deprivation.

- certain pulmonary diseases drastically reduce alveolar surface area.

- ex. Emphysema, walls of adjacent alveoli break down, and alveolar chambers enlarge.

- tumors, mucus, or inflammatory material also can reduce surface area by blocking gas flow into alveoli.

Front 18

When ventilation is less than perfusion and when ventilation is greater than perfusion

Back 18

- When ventilation is less than perfusion: pulmonary arterioles serving these alveoli constrict. Match of ventilation and perfusion= decreased ventilation and decreased perfusion.

- When ventilation is greater than perfusion: pulmonary arterioles serving these alveoli dilate. Match of ventilation and perfusion= increased ventilation and increased perfusion.

Front 19

O2 transport

Back 19

- molecular o2 carried in blood. 1.5% dissolved in plasma and 98.5% loosely bound to each Fe of hemoglobin (Hb) in RBCs (unloading of O2 facilitated by change in shape of Hb) 4 O2 per Hb.

- Oxyhemoglobin (HbO2): hemoglobin-O2 combination.

- reduced hemoglobin (deoxyhemoglobin) (HHb): hemoglobin that has released O2.

- HHb + O2 to HbO2 + H+ (between lungs and tissues)

Front 20

Unloading of O2

Back 20

- rate of loading and unloading of O2 is regulated to ensure adequate O2 delivery to cells.

- factors that influence hemoglobin saturation: po2

- other factors such as: temp., blood Ph, pco2, concentration of BPG.

- venous reserve: o2 remaining in venous blood that can still be used (Hb is still 75% saturated)

Front 21

What is hypoxia?

Back 21

Inadequate O2 delivery to tissues, can result in cyanosis.

Hypoxia is based on cause:

- anemic hypoxia: too few RBCs or abnormal or too little Hb.

- ischemic hypoxia: impaired or blocked circulation.

- hypoxemic hypoxia: cells unable to use O2 as in metabolic poisons.

- carbon monoxide poisoning: especially from fire. HB has 200x greater affinity for carbon monoxide than oxygen

Front 22

CO2 transport

Back 22

CO2 transported in blood in 3 forms:

- 7-10% dissolved in plasma

- 20% bound to globin of hemoglobin (carbaminohemoglin).

- 70% transported as bicarbonate ions (HCO3-) in plasma (formation of bicarbonate involves CO2 combining with water to form carbonic acid (H2CO3), which quickly dissociates into bicarbonate and H+)

Influence of CO2 on blood Ph:

- Carbonic acid-bicarbonate buffer system: helps blood resist changes in Ph.

- If H+ concentration in blood rises H+ is removed by combining with HCO3- to form H2CO3, which dissociates into CO2 and H2O.

- If H+ concentration begins to drop, H2CO3 dissociates, releasing H+.

- HCO3- is considered the alkaline reverse of carbonic acid-bicarbonate buffer system.

Rapid, deep breathing causes a decrease in CO2 in blood, resulting in a rise in ph.

Changes in respiratory rate and depth affect blood ph: slow, shallow breathing cause in increase in CO2 in blood, resulting in a drop in Ph. Rapid, deep breathing causes a decrease in CO2 in blood, resulting in a rise in ph. - changes in ventilation can help adjust Ph when disturbances are caused by metabolic factors. Breathing plays major role in acid-base balance of body.

- changes in ventilation can help adjust Ph when disturbances are caused by metabolic factors. Breathing plays major role in acid-base balance of body.

Front 23

Transport and exchange of CO2

Back 23

- CO2 combines with water to form carbonic acid (H2CO3) which quickly dissociates.

CO2 (carbon dioxide)

+ H2O (water) =

H2CO3 (carbonic acid) =

H+ (hydrogen ion)

+ HCO3- (bicarbonate ion)

- occurs primarily in RBCs, where carbonic anhydrase reversibly and rapidly catalyzes reaction.

- in systemic capillaries, after HCO3- is created, it quickly diffuses from RBCs into plasma: outrush of HCO3- from RBCs is balanced as CI- moves into RBCs from plasma= chloride shift occurs.

- in pulmonary capillaries, the processes occur in reverse (H+ + HCO3- to H2CO3 to H2O + CO2; diffuse into alveoli.

Front 24

Tidal volume (TV):

Volume of air moved in or out of lungs with each breath in normal breathing.

Back 24

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Front 25

Expiratory reserve volume (ERV):

Amount of air that can be forcibly exhaled from lungs after normal quiet expiration.

Back 25

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Front 26

Inspiratory reserve volume (IRV):

Amount of air that can be forcibly inhaled after normal quiet expiration.

- IRV= VC - (TV + ERV)

Back 26

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Front 27

Vital capacity (VC):

TV + ERV + IRV

- The greatest volume of air that can be expelled from the lungs after taking the deepest possible breath.

Back 27

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Front 28

Residual volume (RV):

Amount of air left in lungs after forceful expiration.

Back 28

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Front 29

Spirometer:

Instrument used to measure respiratory VOLUMES.

Back 29

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Front 30

What drives respiration?

- blood CO2 levels (NOT O2 levels)

Back 30

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Front 31

Does inspiration increase or decrease as CO2 goes up?

- inspiration increases as CO2 increases.

- inspiration decreases as CO2 decreases

Back 31

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Front 32

After hyperventilating in fresh air, blood CO2 content increases or decreases?

- decreases

(This helps swimmers hold their breath longer)

Back 32

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Front 33

A decrease in CO2 increases or decreases respiration?

- decreases

Back 33

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Front 34

What is a method of rebreathing?

- hyperventilation into a paper bag

Back 34

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Front 35

Hyperventilation into a paper bag (rebreathing), causes CO2 content to increase or decrease?

- increase

Back 35

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Front 36

An increase of CO2 will be followed by a increase or decrease in in the rate and depth if respiration?

- increase

Back 36

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Front 37

The subject was able to hold their breath longer when they did or did not hyperventilate first (without a paper bag)?

- did

Back 37

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Front 38

Hyperventilation decreases the ____ content of blood so it takes longer for it to accumulate high enough to stimulate respiration.

- CO2

Back 38

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Front 39

The rate and depth of respiration are inversely or directly related to CO2 levels?

- directly

Back 39

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Front 40

Normally, when CO2 levels increase, rate of respiration increases or decreases?

- increases

Back 40

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Front 41

Hyperventilation: breathing deeply

Apnea: no breathing

Back 41

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Front 42

Control of respiration

Back 42

- involves higher brain centers, chemoreceptors, and other reflexes.

Neural controls/mechanisms: neurons in medulla and pons.

Medullary respiratory centers:

- VENTRAL RESPIRATORY GROUP (VRG): rhythm generating and integrative center. Sets up eupnea (12-15 breaths/min)- normal respiratory rate and rhythm. Its inspiratory neurons excite inspiratory muscles via phrenic (diaphram) and intercostal nerves (external intercostals). Expiratory neurons inhibit inspiratory neurons.

- DORSAL RESPIRATORY GROUP (DRG): Near root of cranial nerve IX. Integrates input from peripheral stretch and chemoreceptors; send information to VRG.

Pontine respiratory centers:

Neurons in this center influence and modify activity of VRG only. Act to smooth out transition between inspiration and expiration and vice versa. Transmit impulses to VRG that modify and fine tune breathing rhythms during vocalization, sleep, exercise. Lesions in this area of brain lead to apneustic breathing, where patient takes prolonged inspirations.

Front 43

Influence of CO2 on blood pH

Back 43

Changes in respiratory rate and depth affect blood pH.

- slow, shallow breathing leads to increased CO2 leading to drop in pH.

- rapid, deep breathing leads to decreased CO2 leading to a rise in pH.

Changes in ventilation can adjust pH when disturbed by metabolic factors.

Front 44

Define hyperventilation

Back 44

Increased depth and rate of breathing that exceeds body's need to remove CO2. (Can be caused by anxiety attacks, leads to hypocapnia: decreased CO2 levels) which causes cerebral vasoconstriction and cerebral ischemia, resulting in dizziness, fainting. Early symptoms include tingling and involuntary muscle spasms in hands and face. Treatment= breathing into paper bag which increases CO2 levels being inspired.

Front 45

Define acidosis, alkalosis, hypocapnia, and hypercapnia.

Back 45

Acidosis: blood pH lower than 7.35

Alkalosis: blood pH higher than 7.45

Hypocapnia: pCO2 less than 37mmHg (normal= 37-43mmHg) this is the most common cause of ALKALOSIS.

Hypercapnia: pCO2 greater than 43mmHg. This is the most common cause of ACIDOSIS.

Front 46

What is the most common form of an upper respiratory tract infection? What are the 4 types?

Back 46

1. Strep throat:

- primary bacterial infection

- caused by Streptococcus pyogenes

- can lead to a generalized upper respiratory infection

2. Sinusitis

3. Tonsillitis

4. Laryngitis

* viral infections can lead to secondary bacterial infections

Front 47

What is sinusitis?

Back 47

Infection of the cranial sinuses.

- develops when nasal congestion blocks openings to the sinuses.

- symptoms include postnasal discharge and facial pain.

- treatment depends on restoring proper drainage of the sinuses. (Frontal, ethmoid and maxillary)

Front 48

What is tonsillitis? And laryngitis?

Back 48

Tonsillitis: inflamed and enlarged tonsils. Tonsillectomy- surgical removal of tonsils.

Laryngitis: inflammation of the larynx. Hoarseness leads to the inability to talk in an audible voice. Causes: upper respiratory infection and overuse.

Front 49

What are the types of lower respiratory infections?

Back 49

Bronchitis: bacterial infection of the primary and secondary bronchi. Usually preceded by a viral URI.

Pneumonia: viral or bacterial infection of the lungs. Bronchi and alveoli fill with thick fluid. May be localized in specific lobules of the lungs. Advanced age, weakened immune system, smoking and being immobilized.

Front 50

Tuberculosis

Back 50

Caused by the tubercle bacillus bacterium. Lung tissue develops tubercles around the invading pathogens. TB skin test can detect if a person has been exposed to the bacteria.

Front 51

Restrictive pulmonary disorders

Back 51

- vital capacity is reduced.

- lungs have lost their elasticity.

- pulmonary fibrosis (fibrous connective tissue buildup on the lungs. Can be caused by: silica, coal dust, asbestos, clay, cement, flour or fiberglass)

Front 52

Obstructive pulmonary disorders

Back 52

- air does not flow freely on the airways

- maximal inhalation or exhalation time is greatly increased

- COPD: develop slowly, over a long period of time, recurrent, chronic bronchitis (airways are inflamed and filled with mucous, bronchi have undergone degenerative changes) smoking.

Front 53

Emphysema

Back 53

Incurable disorder, alveoli are destended, alveolar walls have been damaged and the surface area available for gas exchange has been reduced, often preceded by chronic bronchitis, lungs have lost their elasticity, exhaling is difficult and residual volume increases, less O2 reaches the heart and brain.

Front 54

Asthma

Back 54

Acute obstructive disorder.

Disease of the bronchi and bronchioles. Marked by: wheezing, breathlessness, sometimes a cough and expectoration of mucous. Airways are sensitive to irritants, is not curable but is treatable.

Front 55

Lung cancer

Back 55

Linked to smoking, progressive steps in the development of lung cancer:

- thickening and callusing of the cells lining in primary bronchi.

- cells with atypical nuclea appear in the callused lining.

- cells break loose and penetrate other tissues (metastasis)

Front 56

Oxygen excess

Back 56

Oxygen toxicity: pure O2 breathed at 2.5atm or greater. Safe to breathe 100% O2 at 1atm for a few hours. Generates free radicals and H2O2, destroys enzymes, damages nervous tissue, leads to seizures, come and death.

Hyperbaric oxygen: formerly used to treat premature infants, caused retinal damage, was discontinued.

Front 57

Tracheostomy

Back 57

To make a temporary opening in the trachea inferior to the larynx and insert a tube to allow airflow.

- prevents asphyxiation, inhaled air bypasses the nasal cavity and is not humidified, promotes infection

Front 58

Pneumothorax

Back 58

Presence of air in the pleural cavity.

Thoracic wall is punctured, inspiration sucks air through the wound into the pleural cavity, potential space becomes an air filled cavity, loss of negative intrapleual pressure allows lungs to recoil and collapse.

Atelectasis: collapse of part or all of lung. Can also result from an airway obstruction.

Front 59

Variations in respiratory rhythm

Back 59

Eupnea: relaxed quiet breathing (TV= 500ml, RR= 12-15 bpm)

Apnea: temporary cessation of breathing.

Respiratory arrest: permanent cessation of breathing.

Dyspnea: labored, gasping breathing, shortness of breath.

Hyperpnea: increased rate and depth of breathing in response to exercise, pain or other conditions.

Hyperventilation: increased pulmonary ventilation in excess of metabolic demand.

Hypoventilation: reduced pulmonary ventilation.

Kussmaul respiration: deep, rapid breathing often induced by acidosis.

Orthopnea: dyspnea that occurs when a person in lying down.

Tachypnea: accelerated respiration