The Respiratory System

Front 1

Define the terms ventilation, external respiration, and internal respiration.

Back 1

Ventilation - breathing; ensures continuous refreshing of the gas in the alveoli of the lungs
Gas exchange:
External respiration - takes place in pulmonary capillaries, the blood takes on O2 and gives up CO2
Internal respiration - takes place in the systemic capillaries; blood gives up O2 and takes on CO2

Front 2

Distinguish between the conducting zone and the respiratory zone of the respiratory center.

Back 2

- Organization of the respiratory system when organized functionally
Conducting - structures that are conduits for air passage (nostrils, nasal cavity, pharynx, larynx, all structures from the trachia to the terminal bronchioles)
Respiratory - where gas exchange occurs (respiratory bronchiles, alveolar ducts which are indistinct structures, alveoli)

Front 3

What are the general functions of the nostrils and nasal cavity? What structural features support these functions?

Back 3

Functions: filter, warm and humidify incoming air, home to smell receptors
Mucus - nasal cavity lined with ciliated pseudostratified columnar ET with scattered goblet cells to secrete mucus; ET rests on lamina propria (richly supplied with mucus secreting and serous glands)
Warmth - rich plexus of capillaries/small veins underneath nasal ET; blood warms air
Turbulence - created to filter; created by superior, middle and inferior nasal conchae and meatuses - inc. number of particles that hit the walls of the nasal cavity and get trapped by the mucus

Front 4

Name and describe the location of the three levels of the pharynx.

Back 4

Nasopharynx - posterior to nasal cavity, inferior to sphenoid bone, superior to level of soft palate; continuous with nasal cavity; L + R auditory tubes open into it just lateral to pharyngeal tonsil
Oropharynx - posterior to oral cavity, continuous with it; palatine and lingual tonsils found here
Laryngopharynx - directly posterior to upright epiglottis and extends the the larynx, where respiratory and digestive pathways converge; surrounds opening of esophagus and Larynx

Front 5

How does the epithelial lining change from one level of the pharynx to another?

Back 5

- Nasopharynx - lined with ciliated pseudostratified columnar ET that contains coblet cells
- Oropharynxs - transition between pseudostratified columnar ET of the nasopharynx to the stratified squamous ET in the laryngopharynx
- Laryngopharynx - lined with stratified squamous ET

Front 6

What are the functions of the larynx? What special features support these functions?

Back 6

Functions:
Provides open/patient airways - the ventricular or vestibular folds narrow the opening through the larynx and help prevent large objects from entering the glottis,
Switching mechanism to properly route air instead of food through canals - epiglottis attatches to edge of thyroid cartilage (projects upward when air is coming out of larynx, larynx pulled upward to cover opening when swallowing food
Making sounds/speaking - the arytenoid, cuneiform and corniculate cartilages pivot on the coricoid cartilladge and abduct the vocal folds during speaking breathing and coughing; vocal folds and glottis

Front 7

Describe the general location and function of each of the following: thyroid cartilage, coricoid cartilage.

Back 7

- Thyroid cartilage - one of 9 cartillage peices in the larynx; hyaline cartilage; the adam's apple
Location: anchored to the hyoid bone via the thyrohyoid membrane
Function:the epiglottis is attatched to it's superio-arterial edge
Coricoid cartilage: made of hyaline cartilate
Location - ring shaped and inferior to thyroid cartilage in the larynx
Function - anchors the trachea to the larynx (and is the landmark for a tracheostomy)

Front 8

Describe the general location and function of each of the following: epiglottis, glottis.

Back 8

Epiglottis: made of elastic cartilage; spoon shaped, covered by mucosa with some scattered taste buds
Location - attatches to superio-anterior rim of the thyroid cartilage and extends upward toward the tongue
Function: points upward when air is flowing in/out of larunx (airway open); swallowing: larynx pulled up and epiglottis tips to cover opening to larynx
Glottis:
Location - the opening between the vocal cords (which attratch to the arytenoid and thyroid cartilage)
Function - air passing through the glottis vibrates the local folds and produces sound saves

Front 9

Describe the general location and function of each of the following:arytenoid cartilage, ventricular folds (false vocal cords, vocal folds (true vocal cords).

Back 9

Arytenoid cartilage:
Location - part of lateral and posterior wall of larynx; articulates with superior border of coricoid cartilage
Function: works with cuneiform and corniculate cartilages to pivot on coricoid cartilage and abduct/adduct the vocal folds during speaking/breathing/coughing
Ventricular folds:
Location - superior pair of folds/pairs of ligaments that extend across the larynx, attaching to the arytenoid and thyroid cartilage
Function - fibrous; move passively; narrow opening through larynx to prevent large objects from entering the glottis
Vocal folds:
Location - inferior pair of folds/pairs of ligaments that extend across the larynx, attaching to the arytenoid and thyroid cartilage
Function - air passes through glottis and vibrates the ligaments and produces sound

Front 10

Of what type of cartilage are the thyroid cartilages composed?

Back 10

- hyaline cartilage makes up the adams apple
- most of the 9 cartilage pieces in the larynx are hyaline; except epiglottis, which is elastic cartilage

Front 11

Identify and describe the three layers of the tracheal wall.

Back 11

Mucosa - ciliated pseudostratified columnar ET; scattered goblet cells secrete mucus; cilia beat upward/sweep mucus on apical surface up towards thoat to swallow it; smoking destroys cillia, so they cough for the same purpose (why cough suppressants are bad for them)
Submucosa - loose CT; contains seromucus glands (that open onto the surface of mucosa); secrete more mucus
Adventitia; dense tough CT reinforced by incomplete c-shaped hyaline cartilage rings that keep trachea from collapsing; elastic Ct/smooth muscle fibers (trachialis musc.) attatch to open end of rings. C shaped w/open end posterior to allow for stretching of esophagus as bolus passes down it; SNS stimulation = relaxation of trachialis

Front 12

Name the branches of the bronchial tree, beginning with the tubes formed by the branching of the trachea.

Back 12

- Trachea - branches in mediastinum at T5
- R + L primary bronchi - pass through media stinum into lung; enters lung at root/hillus (right usually shorter/bigger diameter, so objects usually lodge in this side)
- Secondary bronchi ("lobar bronchi") - supply lobes of lungs; 3 on R, 2 on L
- Tertiary bronchi("segmental bronchi") - supply a bronchopulmonary segment
- Bronchiles - call tree a bronchus until <1 mm diameter, then a bronchiole
- Terminal bronchioles - smallest tube in conducting zone of airways
- Respiratory bronchioles - 1st branches in respiratory zone
- alveolar ducts
- alveolar sacs

Front 13

How does the structure of the bronchial tubes change as the tubes branch and become smaller?

Back 13

- Mucosa characteristics: Cilliated pseudostratafied columnar Et @ first, thins as diameter dec.; becomes cilliated columnar in larger bronchi, then simple cuboidal ET; @ small bronchioles becomes non-cilliated ET, so can't sweep mucus up/out
- Cartilage and supportive structure - cartilage rings become irregular cartilage plates, and then disappear entirely @ bronchiole level; elastic fibers of adventitia present/supportive all the way down; bronchioles can colapse
- Smooth muscle - smaller diameter = more smooth muscle, down to bronchioles which have spiraling bundles of s. musc that completely encircle them; contraction can dramatically inc. resistance to airflow; inervated by S+P parts of ANS (dilation - SNS, epinepherine, constriction = parasymp w/ACH + histamine)

Front 14

Which of the respiratory system structures are considered part of the conducting zone? the respiratory zone?

Back 14

Conducting - trachea, primary bronchi, secondary bronchi, tertiary bronchi, bronchioles, terminal bronchioles
Respiratory - respiratory bronchioles, alveolar ducts, alveolar sacs

Front 15

In what three ways to the upper respiratory system structures "condition" air before it reaches the lungs?

Back 15

Warm - the rich plexus of capillaries/small veins under the ET warms the air
Humidify
Cleanse - the cillia and mucus

Front 16

Identify and describe the location of the pleural membranes and pleural cavity.

Back 16

Pleural membranes:
Parietal pleura - fused to iner surface of thoracic cavity; made of a thin serous membrane
Visceral plura - inner, fused to outer surface of lungs; reflects back to form parietal pleura
Pleural cavity - potential space b/w parietal pleura (outer) and visceral pleura (inner); filled with pleural fluid secreted by the membranes

Front 17

Identify the two major functions of pleural fluid.

Back 17

- Reduce friction - visceral and parietal membranes can slide past eachother
- Surface tension - parietal pleura associates closely/is "stuck to" the visceral pleura; when the thoracic cavity or diaphragm expands, it pulls the lungs out with it; when the elastic fibers in the lungs recoil in exhalation, it pulls the thoracic cavity and diaphragm back with it

Front 18

Describe the structure of an alveolus.

Back 18

- thin waled sac made up of type I cells (simple squamous ET; also the source of angiotensin converting enzyme: antiogensin I to antiogensin II), surrounded by thin basal lamina
- Type II alveolar cells/septal cells secrete surfactant (proteins/phospholipids that coat inner alveolar surface and dec. surface tension; (decreases desire of H2O to assocate w/itself and not the things around it/when it beads up.; inc. sufrace tension would cause water in membrane to come together and collapse the alveoli)
- Mobile alveolar macrophages/"dust cells" - gradually moved up into conducting zone and swallowed
- surrounded by dense cap. network
- supported by elastic fiber network responsible for quiet exhalation w/o work b/c of their recoil

Front 19

What is the function of type II alveolar cells? of alveolar macrophages?

Back 19

- Type II alveolar cells/septal cells secrete surfactant (proteins/phospholipids that coat inner alveolar surface and dec. surface tension; (decreases desire of H2O to assocate w/itself and not the things around it/when it beads up on the surface of a car it is showing high surface tension.; inc. sufrace tension would cause water in membrane to come together and collapse the alveoli)
- Mobile alveolar macrophages/"dust cells" - gradually moved up into conducting zone and swallowed

Front 20

What is the structure and function of the respiratory membrane?

Back 20

- it's the conposite structure across which gas exchange occurs (the endothelium of the capillary, the epithelium of the alveoli and their fused basal lamina); very thin
- rapid gas exchange b/c: diffusion is effective over thort distances (very thin membrane) and b/c with millions of alveoli in the lungs, there is a HUGE surface area

Front 21

Describe the phenomenon of ventilation perfusion coupling.

Back 21

- blood flow is controlled locally so that capillary blood flow will go past ventilated alveoli
- high PCO2 and low PO2 autoregulates the arteriole diameter to cause vasoconstriction; and visa versa
- opposite of what happens in the tissues, where hypoxia triggers vasodilation
- PO2 is the main regulator, although PCO2 also plays a role

Front 22

How does ventilation-perfusion coupling enhance respiratory efficiency?

Back 22

- the vasoconstriction/vasodilation is coordinating with the ventilated alveoli
- blood flows past the alveoli with fresh air, where they can pick up more O2 and get rid of more CO2, just based on the conc. gradients

Front 23

hilus

Back 23

- where blood vessels and bronchus enter and leave the lungs
- on the medial surface
- also called the root

Front 24

root (of the lung)

Back 24

- where blood vessels and bronchus enter and leave the lungs
- on the medial surface
- also called the hilus

Front 25

Describe the mechanics of inspiration and expiration (i.e., how do we move air into and out of our lungs?).

Back 25

- intrapulmonary pressure (Palv or Ppul) within the alveoli must be less than the Patm for gas to move into the lungs
- atmospheric pressure = 760 mm Hg at sea level (all pressures are described reletive to Patm)
- change Palv by changing the volume (because of boyles law - P1V1 = P2V2)

Front 26

What is intrapleural pressure?

Back 26

- pressure within the pleural cavity between the visceral and parietal pleura
- always 4-6 mm Hg less than Patm
- caused by 2 forces: the recoil tendency of the lungs and surface tension of alveolar fluid (minimized by surfactant) vs.the pull of the thorax out, but they are held together by the surface tension of the pleural fluid

Front 27

How is intrapleural pressure created?

Back 27

- caused by 2 forces: the recoil tendency of the lungs and surface tension of alveolar fluid vs.the pull of the thorax out, but they are held together by the surface tension of the pleural fluid
- the pressure is always negative 4-6

Front 28

Describe the fluctuations in intrapleural pressure during inspiration and expiration.

Back 28

- inspiration - parietal pleura of thorax pulls outwards as diaphragm and external intercostals contract
- expiration - visceral pleura pulls inwards as muscles relax; due to the recoil tendency of the elastic tissue in lungs and surface tension of alveolar fluid as it tries to bead up

Front 29

What is Boyle's Law?

Back 29

P1V1 = P2V2
- at a constant temperature, the pressure of a gas varies inversely with its volume
- basically, a change in the volume = a change in the pressure = a change in the gas flow (into or out of lungs)

Front 30

How does Boyle's Law relate to the mechanics of pulmonary ventilation?

Back 30

P1V1 = P2V2
- basically, a change in the volume = a change in the pressure = a change in the gas flow (into or out of lungs)
- the volume of the lungs can be changed by increasing or decreasing their dimensions (diaphragm and ribs)

Front 31

Is alveolar (i.e. intrapulmonary) pressure higher or lower than atmospheric during inspiration? during expiration?

Back 31

inspiration - alveolar pressure is lower/negative
expiration - alveolar pressure is higher/positive

Front 32

What effects do changes in thoracic volume have on intrapulmonary pressure?

Back 32

- Boyles law P1V1 = P2V2
- volume of the lungs increasing makes the alveolar pressure decrease during inspiration

Front 33

What muscles are involved in quiet inspiration? What nerve innervates the diaphragm?

Back 33

- diaphragm and external intercostals
- the phrenic nerve (C3, C4, C5... keep the diaphragm alive)

Front 34

What phase of quiet breathing is a passive process?

Back 34

- normal expiration
- because it depends primarily on the elastic recoil of the lungs

Front 35

What forces are constantly acting to collapse the lungs? Which of these forces is normally most responsible for quiet exhalation?

Back 35

- Both the recoil tendency of the lungs and the surface tension of the alveolar fluid (the water that wants to bead up and collapse the alveoli)
- the recoil/elasticity of the lungs is primarily responsible

Front 36

What muscles are involved in forceful inspiration? expiration?

Back 36

- inspiration - sternocleidomastoid, scalenes in neck, pectoralis minor, erector spinae, serratus posterior; also the diaphragm and the intercostals
exhalation - muscles of abdominal wall, internal intercostals

Front 37

Identify the three main physical factors that influcence pulmonary ventilation.

Back 37

- resistance in the respiratory passageways (bronchoconstriction and dilation); also resistance falls as we go deeper into lungs b/c gasses are diffusing not flowing
- alveolar surface tension - where the epithelial walls of the alveoli have water that wants to collapse and bead up
- lung compliance - how easy it is to expand the lungs and the thoracic wall (we don't want it completely compliant, b/c we need the recoil ability)
- they can affect the energy that it requires to breathe

Front 38

What is the effect of bronchodilation on airway resistance and gas flow? of bronchoconstriction?

Back 38

- Dilation - reduces resistance, so their will be more gas flow; caused by SNS and epinepherine
- Constriction - increased resistance and less gas flow; caused by PNS releasing Ach and by inflammatory chem. like histamine; also by asthma, cystic fibrosis(mucus), Chronic Obstructive Pulmonary Disorder (narrowing/collapse of airways), tumors, infectious materials

Front 39

What effect do the following neural and chemical factors have on airway resistance: sympathetic activation; parasympathetic activation; epinephrine; histamine.

Back 39

SNS - bronchodilation
PNS - bronchoconstriction
Epiniphrine - bronchodilation
Histamine - bronchoconstriction

Front 40

Explain the relationship between the following: lung conpliance, lung elasticity, alveolar surface tension.

Back 40

- lung compliance - determined by surface tension in alveoli (esp. @ beg. of breath, when H2O mol are closest to eachother) and elacticity of lung tissue
- less compliance = more energy spent breathing

Front 41

What is the effect of changes in lung compliance on pulmonary ventilation?

Back 41

- pulmonary ventilation becomes much more difficult in a less compliant lung (like one stiff with fibrous tissue of TB, or with pheumonia or chronic bronchitis)
- C = change in V/change in P (transpulmonary press)

Front 42

What is the function of surfactant?

Back 42

- minimizes surface tension in the lungs
- secreted by type II cells of alveoli walls, so that less energy is needed to expand the lungs
- infant respiratory distress syndrome - primie doesn't have much surfactant at all

Front 43

Define the following: tidal volume; inspiratory reserve volume; espiratory reserve volume; residual volume.

Back 43

- Tidal volume - vol. inspired/expired with each breath during quiet breathing (500 mL)
- IRV - vol. that can be forcefully inhaled after a normal tidal volume inspiration (2100-3200 mL)
- ERV - vol. that can be forcefuly exhailed after a normal tidal volume expiration (1000-2000 mL)
- RV - vol. remaining in lungs after forced expiration (1200 mL); loose it = wind knocked out of you; important to keep surface tension low enough and to keep a constant gas exchange occurring

Front 44

Define the following: inspiratory capacity; functional residual capacity; vital capacity; total lung capacity.

Back 44

- IC - vol. that can be inspired after tidal expiration (IC = Tidal volume + inspiratory reserve volume)
- FRC - vol remaining in lungs after tidal expression (FRC = expiratory reserve volume + reserve volume)
- VC - total vol. of exchangeable air (VC = inspiratory reserve volume + tidal volume + expiratory reserve volume) or ( VC = total lung capacity - residual volume)
- TLC - total vol in lungs after max inspiration; sum of all lung volumes; (6000 mL)

Front 45

Define the FEV1 and tell its clinical significance.

Back 45

- Forced Expiratory Volume
- amt of air expelled during a specific time interval of the FVC (forced vital capacity) test
- forced expiratory vol in first sec; should be about 80% of lungs
- obstructive pulmonary disorders cause a lot less than 80% to come out in the first sec
- restrictive diseases can exhale 80% of their lung capacity, but that capacity has just shrunk overall

Front 46

Define the following: anatomical dead space; alveolar dead space; total dead space.

Back 46

- Anatomical - volume of conducting space; not part of gas exchange (about 150 mL)
- Alveolar - if alveoli cease to act in gas exchange b/c of collapse or mucus
- Total - anatomical + alveolar dead space; "non useful volumes"

Front 47

Define minute respiratory volume (MRV) and alveolar ventillation rate (AVR).

Back 47

- MRV - total amt. of gas that flows in and out of resp. tract in 1 min (6 L/min) (in exercise can be up to 200 l/min)
- AVR - frequency X (tidal volume - dead space)

Front 48

Which provides the best assessment of effective ventilation - MRV (minute respiratory volume) or AVR (alveolar ventilation rate)?

Back 48

- AVR - because that's calculating the area/rate where the gas exchange is actually occuring
- MRV is just a rough estimate to help you

Front 49

Explain the law of partial pressures of gases (i.e. Dalton's Law).

Back 49

- total press. exerted by a mix of gases equals the sum of the press. exerted by each individual gas in the mixture
- partial press = press exerted by a specific gas (ex. PO2 = 160 mmHg)
- as a result, each gas in a mix tends to diffuse independently down their own gradient

Front 50

How does the partial pressure of a gas influence its diffusion?

Back 50

- each gas in a mixture diffuses independently down its own gradient

Front 51

What is Henry's law? How does this law relate to the process of respiratory gas exchange?

Back 51

- when a mixture of gases is in contace with a liquid, the conc. of each gas dissolved in the liquid is proportional to the partial pressure of the gas
- because the gases are diffusing from the air in the lungs into the blood directly in some cases (unless they aren't very soluble and need a carrier)

Front 52

What is Graham's law? How does this law relate to the process of respiratory gas exchange?

Back 52

- the diffusion rate is directly propotrional to the solubility coefficient of the gas (an index of how soluble the gas is in a liquid)
- the amount of a gas dissolved = solubility coeficient (s) x Partial pressure gradient of that gas
[O2]diss. = s x PO2

Front 53

Rank the solubility in water (or plasma) of the following gases: oxygen, carbon dioxide, nitrogen.

Back 53

- CO2 - most soluble (20x more than O2)
- O2
- N2 - 1/2 as soluble as O2

Front 54

Rank the pO2 of the following sites: air in the alveoli; arterial blood; venous blood; interstitial fluid; intracellular fluid.

Back 54

Highest pO2:
- air in atmosphere (160 mm Hg)
- air in alveoli (104 mm Hg; lower b/c of inhales water/humidity)
- pulmonary veins (100 mm Hg)
- arteries (100 mm Hg)
- Interstitial fluid
- Intracellular fluid (< 40 mm Hg)
- Venous blood (40 mm Hg)

Front 55

Rank the pCO2 of the following sites: : air in the alveoli; arterial blood; venous blood; interstitial fluid; intracellular fluid.

Back 55

Highest:
- intracellular fluid (>45 mm Hg)
- Interstitial fluid
- Venous blood (45 mm Hg)
- air in alveoli (40 mm Hg b/c air in alveoli has bee in here for 2 breaths by the time it gets past the dead zone and into the alveoli)
- arterial blood (40 mm Hg)
- air in the atmosphere (.3 mm Hg)

Front 56

Identify the main factors that influence the rate of pulmonary and systemic gas exchange.

Back 56

- the diffusion rate if proportional to the solubility coefficient (so it depends on the gas itself)
- depends on the partial pressure gradient of the gas

Front 57

How is O2 transported in the blood?

Back 57

- dissolved in the plasma - 1.5-2% of the transport
- Hb - the rest; hemoglobin made up of 2 alpha and 2 beta chains with a heme group each; the heme group has ferrous that binds to O2 reversibly

Front 58

Compare and contrast adult hemoglobin (HbA), fetal hemoglobin (HbF), and sickle cell hemoglobin (HbS).

Back 58

- HbA - made up of 2 alpha and 2 beta chains with a heme group each; the heme group has ferrous that binds to O2 reversibly
- HbF - for polypeptide chains it has 2 alpha and 2 gamma; makes it have more affinity fo O2 than adult Hb
- HbS - 2 normal alpha chains; beta chains have a single amino acid substitution; deoxygenated HbS aggregates and forms rigid rods that deform the cell and creates anemia etc.

Front 59

Why is oxygen-hemoglobin binding called cooperative binding?

Back 59

- the first O2 is the hardest to bind, then gets progressively easier with 2nd, 3rd, 4th b/c O2 affinity increasese with the saturation
- causes saturation and/or release to occur very quickly

Front 60

How many O2 molecules are bound to Hb that is fully saturated?

Back 60

- four

Front 61

Define the term percent saturation of hemoglobin.

Back 61

- the percentage of the blood that is full of HbO2 as opposed to HHb (deoxyhemoglobin)
- in arteries at 100 mm Hg it's 97.5% saturate
- in tissues at 40 mm Hg its 75 % saturated

Front 62

Describe the oxygen-hemoglobin dissociation curve.

Back 62

- as the PO2 increases, the percent Hb saturation also increases
- PO2 is the most important factor in determining how much O2 combines with Hb
- has a steep region that reflects the cooperative binding properties (since small change in PO2 creates big change in Hb saturation)

Front 63

How does an increase in O2-Hb affinity effect O2 unloading in the tissues? a decrease in affinity?

Back 63

- affinity increase - makes it harder to unload O2 in metabolically active tissues
- occurs when the oxygen-hemoglobin dissociation curve shifts down/to the right
- decrease - makes it easier to unload O2 in the tissues

Front 64

- what effect does each of teh following have on O2-Hb affinity: pCO2; body temperature; pH; 2,3-BPG.

Back 64

- inc pCO2 - occurs when more met. active, wants more O2, so decrease Hb affinity
- inc body temp - occurs when more met. active, wants more O2, so decrease Hb affinity
- inc H ions (so dec pH) - caused by lactic acid, which occurs in metabolically active tissues, so decreased Hb affinity to release more O2
- inc 2,3-BPG - a metabolite in anaeroblic glycolysis in rbcs; builds up when cells are hypoxic; need more oxygen; dec in Hb affinity

Front 65

What direction does the oxygen-hemoglobin dissociation curve shift when the affinity between Hb and O2 increases? decreases?

Back 65

- increases - shifts up to the left
- decreases - shifts down and to the right

Front 66

What is the Bohr effect?

Back 66

- effect is on the oxygen-hemoglobin dissociation curve
- decreases the Hb-O2 affinity
- caused by increased blood H (decreased pH) from lactic acid in metabolically active tissues
- makes it easier for rbcs to unload O2 @ tissue

Front 67

What are the three forms of CO2 in the blood?

Back 67

- CO2 dissolved in the blood (7-8%)
- HbCO2 in rbcs; bound to the globin portion; carbaminohemoglobin (25%)
- HCO3- in plasma (70%); transformed in blood; CO2 + H2O = H2CO3 = H+ + HCO3-

Front 68

What reversible reaction is catalyzed by carbonic anhydrase?

Back 68

- CO2 + H2O = H2CO3 = H+ + HCO3-
- Carbonic acid dissociates inside the rbc and then H+ is buffered by the Hb so pH doesn't increase
- HCO3- diffuses out of rbcs into plasma, in exchange for one Cl- going inside

Front 69

Is carbonic anhydrase present in the plasma? inside red blood cells?

Back 69

- not in plasma
- found in rbcs
- catalyzes formation of carbonic acid (H2CO3) from CO2 and H2O

Front 70

Identify each of the molecules/ions in the following equation: CO2 + H2O = H2CO3 = H+ + HCO3-

Back 70

- CO2 - carbon dioxide
- H2O - water
- H2CO3 - carbonic aid
- H+ - hydrogen ion; buffered by Hb, would decrease the pH
- HCO3- bicarbonate

Front 71

What happens to the HCO3-(bicarbonate) formed in red blood cells through the dissociation of H2CO3 (carbonic acid)?

Back 71

- the hydrogen ion from the dissociation is buffered by Hb
- the bicarbonate diffuses out of rbc in exchange for one Cl- going in
- stays in blood (about 70% of CO2 transported this way)
- when it gets to the lungs, the opposite happens: it is converted back to carbonic acid in the rbd and then to CO2 and water to exit the lungs in exhalation

Front 72

Explain the chain of reactions that occur as pCO2 (i.e. the amount of CO2) increases inside red blood cells.

Back 72

- as the amount of CO2 increases, (coming in from interstitial fluid/tissues), some becomes carbaminohemoglobin
- more CO2 comes in and binds to the water, and then makes carbonic acid, which dissociates into a hydroben ion and bicarbonate
- the bicarbonate diffuses out into the plasma, in exchange for one Cl- that enters the rbc
- the hydrogen ion is buffered by the Hb in the rbc
- at lungs, CO2 in rbc decreases, so rxn reverses

Front 73

What is the Haldane effect?

Back 73

- the effect of changes in oxyhemoglobin saturation on CO2 saturation at a given pCO2
- when O2 binds to Hb, it tends to displace CO2, so saturated Hb will have much less CO2
- allows for greatly increased pick- up of CO2 in the systemic capillaries (we could probably carry much more CO2 except that even after the tissues, the Hb is still 70% saturated)
- opposite (ish) of the bohr effect, but has a much bigger effect in the body

Front 74

Identify the location of the neuron groups making up the respiratory center.

Back 74

- 4 respiratory centers in the pons and medulla oblongata
- inspiratory center/dorsal respiratory group - dorsal medulla
- expiratory area/ventral respiratory group - in medulla
- pneumotaxic area - in pons
- apneustic center - in pons

Front 75

What is the function of the dorsal respiratory group (i.e. inspiratory center)?

Back 75

- generates basic respiratory rhythm (12-15 breaths/min)
- abrupt increase in DRG neuron firing at onset of inspiration; then ramp-like increase in firing; abrupt decrease at end of inspiration

Front 76

What is the role of the ventral respiratory group (i.e. expiratory center)?

Back 76

- forceful expiration - stimulates internal intercostal and abdominal muscles
- activated by inspiratory center when rate/depth of breathing increases above a threshold

Front 77

Which of the centers (the dorsal respiratory group or the ventral respiratory group) plays a major role in regulating the rate and depth of quiet breathing

Back 77

- the DRG
- generates basic respiratory rhythm
- stimulates phrenic nerve to diaphragm and intercostal nerves to external intercostals
- on for 2 sec, exhale for 3-4 sec
- needed for every type of breathing; w/o it breathing doesn't happen @ all

Front 78

What are the muscles of quiet inspiration?

Back 78

- the diaphragm (stimulated by phrenic n.)
- the external intercostals (stimulated by intercostal nerves)

Front 79

Which of the respiratory centers (the dorsal respiratory group or the ventral respiratory group) is only active during forceful breathing? How is this center activated?

Back 79

- ventral respiratory group (VRG)/expiratory area
- stimulates internal intercostal and abdominal muscles
- neurons activated by DRG when rate/depth of breathing increases above critical threshold
- found in medulla

Front 80

What is the general function of the pneumotaxic center? What effect does increased output from this center have on respiration rate?

Back 80

- "fine tunes" inspiratory center activity
- limit length of inspiration: w/o it, the DRG would send ramped APs for 7 sec
- increased output = faster shallower breathing
- without it, you have very deep slow breathing
- found in pons

Front 81

What is the role of the apneustic center?

Back 81

- found in pons
- exact role not certain
- seems to be involved in stimulating DRG on same side of brain stem

Front 82

What chemical factors influence respiration?

Back 82

- pCO2 - most powerful stimulant; stimulates central chemoreceptors by dec. pH in CSF
- pO2 - effects peripheral chemoreceptors in carotid bodies; only activated when pO2 <60 mmHg (like in chronic lung conditions)
- arterial pH - affects peripheral chemoreceptors

Front 83

Identify the location of the central and peripheral chemoreceptors.

Back 83

- Central - in medula oblongata bilaterally, under blood-brain barrier; primary role in responding to pCO2 of arterial blood; doesn't respond directly to changes in arterial blood chemistry (responds to the decrease in pH caused in the CSF)
- Peripheral - in carotid bodies near where common carotid splits into external/internal; in aortic bodies in arch of aorta; monitors changes of pO2, pCO2, pH in arterial blood

Front 84

Specifically, what changes are monitored by the central and peripheral chemoreceptors?

Back 84

- central - monitors blood pCO2; the most powerful stimulant for respiration; it decreases the pH of the CSF, which is what the chemorec. monitor
- peripheral - monitor changes of pO2, pCO2, pH in arterial blood

Front 85

What chemical factor exerts the most powerful influence on respiration?

Back 85

- blood pCO2
- it affects the central chemoreceptors in the medulla
- very sensitive

Front 86

Explain the indirect effect that increase arterial pCO2 exerts on the central chemoreceptors.

Back 86

- inc CO2 (arterial) causes..
- inc CO2 (in CSF)
- H+ and HCO3- formed
- dec pH in CSF
- Central chemoreceptors stimulated
- inc. rate/depth of breathing
- CO2 exhaled
- dec. arterial CO2
- dec CO2 in CSF

Front 87

Explain why only the peripheral chemoreceptors (and not the central chemoreceptors) are sensitive to changes in arterial pH.

Back 87

- the periperal receptors are outside the blood-brain barrier

Front 88

Under what circumstances might you see a decrease in pH of arterial blood while pCO2 and pO2 are normal?

Back 88

- lactic acid formation
- ketones (from starvation or diabetes etc)
- high iron conc in blood

Front 89

hypercapnia

Back 89

- decreased pH of DSF due to inc blood CO2
- it is the pH/H+ ions that stimulate the central chemoreceptors
- through the equation CO2 +H2O = H2CO3 = H+ + HCO3-

Front 90

Hering-Breuer reflex

Back 90

- aka. inflation relfex
- activation of stretch receptors in lungs; send APs to DRG and apneustic center to limit inspiration
- thought to be a protective mechanism; only induced in certain diseases
- found in alveoli, pleural membranes, walls of bronchioles

Front 91

chloride shift

Back 91

- HCO3- diffuses out of rbcs; one in exchange for one Cl- going in
- occurs when carbonic acid (H2CO3) dissociates for form H+ and HCO3-;
- prevents a negative charge from building up across the membrane
- part of the HCO3- transport of CO2 in the plasma (70% of total transport)

Front 92

hypoxia

Back 92

- oxygen deprivation in tissues
types: hypoxemic (from defective loading of O2 onto Hb in lungs, most common), anemic (from reduced O2 carrying capacity/reduced Hb), ischemic (from a vascular disease that prevents blood from flowing to a part of the body)

Front 93

oxyhemoglobin

Back 93

HbO2
- HHb + O2 = HbO2 + H+

Front 94

deoxyhemoglobin

Back 94

- reduced Hb
- HHb
- HHb + O2 = HbO2 + H+

Front 95

pneumothorax

Back 95

- air in the pleural cavity
- air disrupts surface tension in pleural cavity
- allows a lung to collapse
- breaking a rib can cause it

Front 96

pleurisy

Back 96

- inflammation of teh pleura
- can make less pleural fluid = friction = pain w/breathing

Front 97

pleural effusion

Back 97

- caused by long inflamation/pleurisy
- too much pleural fluid made
- impinges on lungs prevents proper in/out ventillation

Front 98

cardiac notch

Back 98

- on the L lung, where the stroma of lung has to form itself around the pericardium to make room for the heart

Front 99

terminal bronchiole

Back 99

- smallest tube/passage in the conducting zone of airways (where gas passes in/out of lungs)

Front 100

respiratory bronchiole

Back 100

- 1st branches in respiratory zone
- right after terminal bronchiole

Front 101

trachialis muscle

Back 101

- found in cartillage rings of the trachea b/w the two ends of the horseshoe shape
- it contracts to diminish the diamiter of the trachea
- touches esophagus; trachea is horseshoe shape to accomodate boluses trabeling down the esophagus

Front 102

eupnea

Back 102

Easy, free respiration, as is observed normally under resting conditions

Front 103

dyspnea

Back 103

Difficulty in breathing, often associated with lung or heart disease and resulting in shortness of breath

Front 104

hyperpnea

Back 104

energetic (deep and rapid) respiration that occurs normally after exercise or abnormally with fever or various disorders

Front 105

hyperventilation

Back 105

an increased depth and rate of breathing greater than demanded by the body needs; can cause dizziness and tingling of the fingers and toes

Front 106

carbaminohemoglobin

Back 106

- HbCO2
- the form that CO2 takes when bound to Hb
- 25% of total CO2 transport
- loading and unloading of this CO2 determined by pCO2 in tissues and % Hb saturation with O2

Front 107

Distinguish between the following levels of lung organization: lobe, bronchopulmonary segment, and lobule.

Back 107

- lobe - Left divided into 2 (superior and inferior; split by oblique fissure); right divided into 3 (superior, middle and inferior; divided by oblique and horizontal fissures)
- broncho. segment - contained w/in lobe; pyramid shaped, separated by connective tissue septa; each served by an artery, vein, and gets air from a segmental bronchus (10 in R, 8-9 in L); disease often contained to one
- Lobule - hexagons; each served by a large bronchiole and its branches; smalles subdivisions visible to naked eye

Front 108

Using the figure on p 833, explain the chemical reactions that occur during gas exchange in both the pulmonary and systemic capillaries.

Back 108

TISSUES:
- CO2 dissolves into plasma
- CO2 + H20 = H2CO3 = HCO3- + H+ (this occus slowly in the plasma, and quickly in rbcs, due to carbonic anhydrase; in rbcs)
- in rbcs, the H+ is buffered by the free Hb left when the O2 disattatches, forming HHb and the HCO3- diffuses out, exchanged for Cl-
- CO2 + Hb = HbCO2 (carbaminohemoglobin)
- HbO2 = O2 + Hb (which joins with the free H+ to form HHb)
- O2 dissolved in plasma diffuses into ISF and into tissue cells
REVERSE OCCURS IN LUNGS