Respiration Flashcards
1
Q
what is respiration
A
uses o2 and releases co2
2
Q
what is ficks law
A
- the rate of diffusion Q
3
Q
what should you do to maximize Q
A
- larger concentration gradient
- large surface area
- small coefficient
- small surface area
4
Q
what do you need to consider with animals of specialized surfaces
A
- holding environment - moisture level and temp
- hnadling can cause damage to the skin (should you wear gloves )
- watch you dont change skin properties
5
Q
what is the conducting zone
A
- gas transport, covered in mucus
6
Q
why is there mucus
A
- purifies air from dust and pathogens
7
Q
what is the pleural cavity and what does it contain
A
- visceral pleura - layer stuck to lungs
- parietal pleura - stuck to the ribs
- pleural cavity - the space between the layers
8
Q
what adaptations do obligate nasal breathers
A
- the palate pushes further back and the epiglottis rests on soft palate sealing the trachea from the oral cavity
- they can chew their food and smell for predators
9
Q
what muscles are used for inspiration (requires energy)
A
- costs ATP to breath in
- diaphragm = primary muscle of inspiration
- innervated by phrenic nerve
- external intercostal muscles - rib breathing (pulls ribs out and up)
- accessory muscles in neck for deep breath
10
Q
what muscles are used for expiration (usually passive)
A
- relaxed muscles and negative chest pressure pulls air out
- abdominal muscles - increases abdominal pressure push diaphram up
- internal intercostal muscles pulls ribs in and down
11
Q
what are the 7 non-respiratory functions of the respiratory system
A
- redulation of water and heat exchange = turbinates warm air as it goes in
- circulation = move from high and low pressure
- acid-base balance
- defence = mucus coating, trapping dust and pathogens
- removal (in-) activated of materials = as soon as they get to the lungs they are deactivated
- olfaction = neurons from nasa cavity to olfactory bulb that allows for smell (when you are sick it gets blocked)
- sound production = can be effected by mucus
12
Q
what assists with defending the respiratory system
A
- mucociliary escalator = goes from down to up, bringing the mucus up to trap pathogens
- alveolar macrophages = swollow whatever is there, can be inhibited by stress and corticosteroid hormones
- leads to respiratory diseases
- environmental conditions can affect immunity = smoke paralyzes cilia
13
Q
what are prostoglandins
A
- chemical messangers that are released in numerous tissues to mediate local response
- PGs are inactivated when they go through the lungs, preventing systemic effects
- lungs generates angiotensin II (hormone regulated blood pressure )
14
Q
when does the total ventilation depends on 2 factors
A
- tital volume (L/breath)
- respiratory rate ( breath/min)
- pulmonary ventilation = tidal volume X resp rate
15
Q
what is anatomic dead space
A
- air remaining in the conduction airways ( 30% of tidal volume)
16
Q
what is physiological dead space
A
- anatomical dead space + alveolar air with no blood supply
17
Q
what is equipment dead space
A
- anything that increases repsiratory tract volume
18
Q
Obstruction lung disease
A
long time moving out or exhaling
- asthma, emphysema, chronic bronchitis, cystic fibrosis
- patients cannot exhale easily
- damage to the lung, narrowing of airways makes iar come out more slowly
19
Q
restrictive lung disease
A
- much lower volume
- pulmonary fibrosis, obesity, muscular dystrophy
- often caused by stiffness of the lung (lack of compliance ), or anything that restricts lung expansion
20
Q
what is negative pressure breathing
A
- air is pulled into the lungs, not pushed
- air travels from a place of high pressure to a place of lower pressure
21
Q
lung movement
A
- lung sticks to thoracic wall via 2 forces
- intrapleural fluids cohesiveness
- water on the 2 pleural surfaces makes them super resitant to pulling
- transmural pressure gradient
- as the lung recoils, lower pressure in intrapleural cavity
but : thorax is rigid, so not caving in - lungs sticks to thoracic wall
22
Q
steps in inspiration
A
- repiratory muscles contracts (diaphragm)
- thoracic cavity expands (increases its volume) - intrapleural pressure decreases (756-754)
- lung volume increases
- alveolar pressure drops (760-759)
- air moves from high pressure (760) to low pressure (759) area
23
Q
expiration steps
A
- respiratory muscles relax
- thoracic cavity decreases its volume passively
- lung volume decreases (intrapleural pressure increases)
- alveolar pressure increases (760-761)
- air moves from high pressure (761) to low pressure area (760)
24
Q
what are the consequences of sub atmospheris intrapleural pressure
A
- prevents lung from collapsing like deflated balloons at expiration
- lower pressure in mediastinum helps venous return
- blood is pulled into the vena cava at inspiration
- venous valves prevent back flow at expiration
25
Q
dog is hit by a car and is pneumothorax
A
- collapsed lung/ air in the pleural cavity
26
Q
how does pneumothorax affect respiratory function
A
- lungs will strink under the air pressure
must be released to prevent lungs from getting crushed
27
Q
what diagnosed pneumothorax
A
- caused by hole in chest or lung
- loss of sub atmospheric pressure in the pleural cavity
- lungs dont stick to the thorax and collapse
- lungs dont expand on inspiration so no air flow
- diagnosed with an X ray
28
Q
lung elasticity
A
- refers to how easily the lung recoils after being stretched
1. elastin fibres: rubber like proteins that form a meshwork in lung connective tissue, amplifying g their stretching capacity
2. alveolar surface tension : surface tension pushes liquid to adopt the smallest surface area possible - water lining each alveolus pushes the the alveolus to reach the smallest surface area possible
29
Q
what problem can arise with water surface tension
A
- water surface tension is so powerful that is would collapse the lung
- it has a much greatwe pressure than the transmural pressure gradient
- would take a great effort to breath
30
Q
what is a solution for water surface tension
A
- surfactant = weakens water and decreases the pool, collapsing the pressure
- soap like mixture of lipids and proteins interspersed between water molecules
- reduces surface tension but maintains weak recoil
- increases pulmonary compliance
31
Q
what is the law of LaPLace
A
- pressure is the nagative pressure of radious
- small alveoli will tend to collapse more than larger ones
32
Q
when is surfactant more densily packed
A
- in small alveoli
- helps equalizing collapsing pressure among alveoli
32
Q
A
33
Q
A
34
Q
what is compliance
A
- how much effort is required to stretch the lungs by a given amount
35
Q
what is the difference between low and high compliance
A
low - stiff lungs = requires more energy during inspiration
high - requires more effort during expiration
36
Q
what can happen with low compliance and low surfactant
A
infant respiratory distress syndrome (IRDS)
37
Q
what is IRDS
A
infant respiratory distress syndrome
- leading cause of death in preterm infants
- there is a lack surfactant, so the pressure from surface tension starts to collapse the lungs
38
Q
how do you treat IRDS
A
- O2, positive pressure ventilation, addition of surfactants (synthetic or from animal lungs)
39
Q
why is synthetic surfactants not used in production animals
A
expensive!
40
Q
what is pulmonary fibrosis
A
- elastin fibers are replaced by scar tissue - non reversable
- no cure, lung transplant is necessary
41
Q
what is emphysema
A
- poor elastic recoil of the lungs = no problem inhaling, but difficulty exhaling
- chronic chemical irritants cause an increase in immune cells in the lungs - enzymes released by macrophages (trypsin) breaks down lung tissues
- small airways collapse due to lack of structural support, decreasing airway radious
42
Q
how do you measure airflow
A
- pressure gradient/airway resistance
- to maximize airflow = high pressure gradient and low airwat resistance (R)
- small decrease in radious leads to large increase of resistance
43
Q
what can affect airway radius
A
- bronchioles surrounded by smooth muscles
- contractions causes bronchoconstriction (decrease in radius)
- due to the vagal nerve (parasympathetic)
- relaxation of causes bronchodilation (increase in radius) - via sympathetic nerve
- not under conscious control
44
Q
what else can cause decrease in airway radius
A
- asthma
- treatment = long term= corticosteroids to reduce inflammation
- short term = beta 2 agonist to relax smooth muscles (force relaxation)
45
Q
what is COPD
A
- chronic obstructive pulmonary disorder
- chronic lung disorder that results in blocked airflow to the lungs ( and eventually leads to respiratory failure)
3rd leading cause of death worldwide - no cure
- includes chronic bronchitis and emphysema
46
Q
chronic bronchitis
A
- exposure to environment irritant
- smoking
- accumulation of mucus in vocal cords
47
Q
necrotic laryngitis (calf diptheria )
A
- larynx inflamed, radius od airways is decreased
48
Q
tracheal collapse
A
- dogs and horse
- genetic condition
- reduction of the airway - honking coughing and wheezing
49
Q
laryngeal paralysis
A
- horses
- prevents max opening of the trachea
- reduction of airway
50
Q
brachycephalic syndrome
A
- stenotic nares (narrow airways)
- elongated soft palate (partially blocks trachea at the back of the throat)
- hypoplastic trachea (small diameter)
- everted laryngeal saccules
- restricted air flow causes respiratory distress
- open mouth breathing, wheezing, exercise/stress/heat intolerance, change in posture to help airflow (head and neck entended , chin up)
- increased lung workload can often cause COPD
51
Q
cost of respiration
A
- 3-5% of resting metabolic rate is for respiration
- during exercise:
- muscles need more O2
- more ventilation is required (higher rate and depth)
- proportionally the same
52
Q
animals with respiratory disease
A
- compensate decreased airflow by increasing inspiratory effort
- more emergy required to breath
- decrease feed efficiency.
53
Q
what are type 1 alveolar cell
A
- forms the alveolar wall
54
Q
what are type 2 alveolar cells
A
- secretes surfactant
55
Q
alveolar macrophages
A
- dust cells destroys foreign material (dust or bacteria)
56
Q
gas partial pressure
A
- the pressure exerted by a particular gas is directly promotional to the percentage of gas in the total air mixture
- the pressure is not related to the size of the molecule
57
Q
gas partial pressure during inspiration
A
- air gets saturated with water - PP h2O goes up and other gases go down
- fresh air gets mixed in with old; less than 15% of inspired air in alveoli is fresh air
58
Q
Ficks law during exercise and increased diffusion
A
- P gets larger as P 02 can be as low as 30 mm Hg, ventilation is increases to compensate
- A ( surface area for exchange) increases, since some capillaries, otherwise closed off due to lower pressure, open up as blood pressure rises
X (thickness of memebrane) is reduced since larger tidal volumes (deeper breathing) stretch alveolar more than normal - D (diffusion) is increased a bit as body temperature increases
59
Q
thickness of membrane can be increased by
A
- pathologies
- pulmonary edema (fluid accumulation between alveoli and capillaries ) inflammation and left sided heart failure
- pulmonary fibrosis - thickened the alveoli walls
- ## pneumonia ; accumulation of fluid in the alveoli
60
Q
what is the deal with O2
A
- at rest our cells need 250 mL O2/min
- O2 has very poor solubility with water
- at 37C and P 02 of 100 mmHg 3mL O2 dissolved /L blood
- need 83 L pumped every minute
- our heart pumps 5L blood per minute
61
Q
O2 transfer
A
- respiratory pigment to transport O2 is very common throughout the animal kingdom
mammals: tetrameric hemoglobin (Hb)
globin: highly folded poly peptide chain
62
Q
why is mammalian blood called a2b2
A
because the tetramer has 2 a units and 2 B units ( fish has isomeric variants)
-m each iron atom can bind (reversibly) to one molecule of O2
- PP gas only exerted by gas molecules that are dissolved, gas molecules that are bound do not count
63
Q
blood colour
A
- arterial blood: bright red from Hb saturated
- venous blood : dark red/maroon - deoxygenated
64
Q
concentrations of hemoglobin in the blood can change
A
- seasonally (winter vs summer )
- activity ( spleen producing more Hb )
- high altitude (low O2 leads to higher (Hb) )
- stress ( stress hormones can lead to anemia) (Hb)
65
Q
myoglobin
A
- not supposed to be in the blood
- only in some muscles
- monomeric pigment, related to Hb
- found in high concentration in type 1 muscle cells (slow oxidative cells and heart )
- helps provide o2 for muscles
- only presented in the blood after muscle damage (including heart attacks)
66
Q
law of mass action
A
at location where o2 is high (lung), o2 will be loaded
at location where o2 is low (tissue) o2 will be released
67
Q
r state in conformational change
A
- relaxed
- high affinity to o2
- easy to load
68
Q
t state conformational change
A
- tense
- low affinity to o2
- easy to unload o2
69
Q
role of myoglobin
A
- Mb facilitates the diffusion of o2 from the blood into the muscles the same way Hb facilitates the diffusion of o2 from the alveoli to the blood
- because of its high affinity for o2 Mb binds o2 even at low po2 kepping it low inside the cell as well and favouring the diffusion of o2 from the blood into the cells
- if the cell ever reaches a critical low po2 level during exercise mb would relase its o2 allowing the cell to conitnue
70
Q
pH
A
when pH drops, H ions change the conformation of Hb and decreases its affinity to o2 (easier to unload)
71
Q
temperature dissociation curves
A
- when temp increases, Hb has a lower affinity for o2 ( easier to unload)
- where would temp normally be high?
- active muscle
72
Q
organic phosphate and dissociation curves
A
- inside red blood cells
- decrease affinity for o2, even at the lung
- where would DGP normally be high
- muscle conc o2 is lower - high altitude training
- chronic low o2 delivery leads to an up regulation of DGP production in RBC
73
Q
how about a left shift
A
- carbon monoxide
- Hb - affinity fo CO 200 x greater then for o2
- forms carboxyhemoglobin increases affinity to o2 (forced Hb to keep r formation )
- at high concentration, co binds to all sites (preferentially to o2 ) and o2 cannot be delivered
74
Q
anemia
A
- decreased o2 carrying capacity of blood
- decrease in red blood cell number or Hb
75
Q
what are the three main causes of anemia
A
- impaired red blood cell (RBC) production (iron deficiency)
- increase RBC destruction (hemolytic anemia (jaundice) )
- blood loss ( hemorrhaging), ulcers, paracites and surgery
76
Q
Co2 Transport
A
- CO2 has to go from tissues to alveoli
76
Q
what are the three main ways of transportation
A
- co2 dissolved in blood (5-10%, more soluable than O2)
- CO2 bound to Hb (25-30%, bound to the globin to form HbCO2 (carbamino - Hb)
- turned into biocarbonate HCO3- 60-70% (either naturally (slow and via carbonic acid H2CO3) directly via carbonic anhydrase
76
Q
Co2 transport in tissues
A
- carbonic anhydrase: CO2 -> HCO3 + H+ pH drops
- low pH favours the release of O2 (bohr effect)
- release of O2 forms deoxy Hb, which can pick up Co2 and H+ from tissue (haldane effect)
- bohr amd haldane work together in synchrony to facilitate gas exchange
76
Q
cyanide posioning
A
- prussic acid (hydrocyanic acid) from sorghum plants
- pesticides and insecticides, cig smokes and fumes burning polyurethane or vinyl (house fire)
- inhibits cellular aerobic respiration enzyme (cytochrome c oxydase)
- o2 cannot be used by cells, so Po2 in tissue is high
- o2 not released from Hb -> bright red venous blood
77
Q
nitrate poisoning
A
- ruminants comsuming feed with high nitrates: to much nitrogen fertilization, low temp, not enough water
- nitrate - nitrite - ammonia - amino acid and protein
- too much nitrates leads to accumulation of nitrites no2
- this tuens Hb to methHb (iron heme goes from Fe2 to Fe3 ) which cant carry O2
- little O2 results in chocolate coloured blood
77
Q
what is the treatment for cyanide poisoning
A
- chemicals that bind with cyanide (nitrites )
78
Q
treatment for nitrate posioning
A
- methylene blue (methHb - Hb)
79
Q
control of respiration
A
- respiration muscles controlled by the phrenic nerve (diaphragm) and intercostal nerves, with bodies located in the spinal cord.
- controlled by neurons located in the medullar center
- when they fire = inspiration
- when inactive = passive expiration
80
Q
Medulla
A
- dorsal respiratory group
- ventral respiratory group
81
Q
DRG
A
- dorsal respiratory group (closes to the spine)
- inspiratory neurons for quiet breathing (fire for inspiration, but not for passive expiration)
- reflex that tells body to stop breathing in
82
Q
VRG
A
- ventral respiratory group (closest to belly)
- inspiratory and expiratory neurons (inactive during quiet breating, works when DRG needs help) for anything other then quiet breathing
- expiratory neurons firing during forced expiration only
- firing to motor neurons controlling abdominal and internal intercostal muscles
83
Q
3 main components of respiration control
A
- pattern generator ( inspiration/expiration)
- control magnitude of respiration (fine tuning) ( frequency and depth of breathing
- factors that modify respiratory activity for other functions (vocalizing, holding breath, or reflexes like coughing or sneezing)
84
Q
pre - bötzinger complex
A
- the pattern generator
- neurons with pace maker activities
- stimulate DRG
85
Q
respiratory centers in the pons has control over the medullary center
A
- fine tuning
- pneumotaxic center
- abneustic center
86
Q
pneumotaxic center
A
- tells DRG to switch off inspiraory neurons
- makes you exhale, limiting inspiration time
87
Q
abneustic center
A
- prevents inspiratory neurons from being switched off
- makes you inhale more
88
Q
voluntary control of respiration
A
- hold breath, deep breath talk : activities with control over breathing
- cerebral cortex via voluntary connections to motor neurons innervating the respiratory muscles in the spinal cord
chemoreceptor reflex can override it
89
Q
hering - breuer reflex
A
- receptors in the smooth muscle of airways repsond to excessive stretching
- send AP through vagus nerve to inhibit inspiratory cener (VRG and apneustic center) and activate the pneumotaxic
90
Q
feedback
A
- Po2 and Pco2 are relatively constant in blood no matter what happens (rest or activity )
- tightly regulated
[H+] also influences respiratory activities - want to watch influence of Pco2 because the smallest change will be detected faster then oxygen
91
Q
input provided by receptors
A
- peripheral chemoreceptors
- central chemoreceptors
92
Q
peripheral chemoreceptors
A
- carotid bodies (to brain)
- aortic bodies ( to heart)
- sensors can detect hypoxia (Po2) quick (fresh out of the heart)
- aldo respond to H+
- activated when po2 in arterial blood falls below 60 mmHg
- sensory neurons relay information to respiratory center (increases respiration to increase Po2)
- prevents life threatening drop in Po2 which could depress the respiratory center
92
Q
central chemoreceptors
A
located near the medulla
- respond to Po2, Pco2 and H through arterial H+ cant penetrate the blood/ brain barrior
93
Q
what is the problem with peripheral chemoreceptors
A
- receptors dont fire until Po2 is critical
- only measure Po2 not HbO2 - so it wouldnt respond to Hb saturation
- CO poisnioning
- detect changes in the brain (not blood)
- indirect way to measure CO2:
- co2 diffuses through the blood brain barrier
- converted to H+ ia carbonic anhydrase
- H+ in blood cannot diffuse through the barrier
- only activated by respiratory acidoses
94
Q
what is the response of H+ increasing in arteria blood
A
- increased respiration
- blow off CO2 that leads to H in blood (carbonic anhydrase)
- respiratory compensation for systemic acidosis or metabolic
95
Q
what happens to the central chemoreceptors if H+ in blood is too high
A
- chentral chemoreceptors are activated ‘- ventilation is increased
- more Co2 is echaled - and it returns to normal
96
Q
what happens to the central chemoreceptors if the H in the brain is too low
A
- central chemoreceptors are activated
- ventilation is reduced
- less co2 is exhaled - return to normal
97
Q
how is respiration controlled
A
- small changes in CO2 elicits a response
- a large change in O2 is required before response is elicited
98
Q
blood supply to the lungs
A
bronchial circulation
pulmonary circulation
99
Q
bronchial circulation
A
- oxygenated blood from left ventrical and aorta
- supplies o2 to bronchial smooth muscles and connective tissue
- small percentage of cardiac output
100
Q
pulmonary circulation
A
deoxygenated blood from right ventricle and pulmoary artery
- large volume of blood, low pressure, low resistance
- all for gas exchange 9uptake of O2 and release of Co2
101
Q
distribution of blood flow
A
- dorsal/upper lung regions receive less perfusion, but more ventilation (air light, blood heavy)
- ventral/lower lung region receive more blood (gravity) but less ventilation (opposite of dorsal region
102
Q
V/Q ratio
A
- ventilation and perfusion should be evenly matched:
- enough blood to pick up all the available O2
- enough o2 to saturate the Hb of available blood
- when air is brought in - something needs to be there to collect O2 - needs to saturate, enough blood needs to be presetn
target : V/Q = 1
103
Q
is V/Q> 1
A
- usually because Q is too low
- ventialtion is normal, but there is not enough blood to pick up o2 - pressure is too low, effecting rate of exchange
- emboli pulmoary vessels
- low blood pressure (bleeding )
- co2 decreases - bronchiolar smooth muscels contract (bronchoconstriction) - decreases ventilation - V/Q -1
- O2 increases - arterial smooth muscle relax (vasodilation) more perfusion - V/Q -1
104
Q
if V/Q <1
A
- usually because V is too low
- not enough airflow to oxygenate the blood in pulmonary vessels
- Ex. obstruction of small airways by fluid or mucous or tissue break - down (emphaysema)
- Co2 increase - bronchiolar smooth musccles relax (bronchodilation) - more ventilation - V/Q - 1
- O2 decreases - arteriolar smooth muscles contract (vasoconstriction - less perfusion (not enough air = decrease blood flow)
105
Q
in tissues
A
- the partial pressure opposite effect in tissues compared to the lungs:
- decrease in Po2 in tissues casues vasodilation: increase blood perfusion to area that needs o2
- increase in Po2 in tissues casues vasoconstriction: tissue has enough o2 already, so oxygenated blood should go elsewhere
106
Q
birds
A
- have two lungs that are ridgid
- lungs are devided into bronchi and parabronchi that open up onto capillaries (not alveoli)
- they also have sacs connected tot he respiratory system
- some air sacs extend all the way into the bones ( very light to fly, get rasp infections through bones)
107
Q
bird respiration is much more efficient than mammalian respiration
A
- air is continously flowing passed the capillaries (no unused air from inspiration/expiration)
- gas gets transferred from air to blood via a cross current exchange
- the air blood barrier is at least 30-40% thinner than for mammals (0.5uM in mammals to 0.3 uM in birds)
- the capillary blood volume per gram of body weight is 20% greater in birds than mammals
- the exchange area per gram body weight is about 10X that of mammals (increased efficiency is necessary becasue birds have a higher metabolic rate than mammals
108
Q
mechanics of bird respiration
A
- inspiration and expiration both require muscle contraction and air moves in via changes in pressure
- inspiration: sternum is lowered and expands chest. lower pressure causes air to fill sacs( remeber the lungs are quite rigid)
- posterior sacs oull in air into trachea, bronchi and lung
- anterior sacs pull air from lungs
- expiration : sternum moves backwards and up, reduces the volume of the thoracic cavity, sacs are compressed, air moves out of those sacs
- air from posterior sacs moves into the lungs
- air from the anterior sacs moves into trachea and out
109
Q
birds in coal mines
A
- increase respiratory efficiency means that birds are more susceptible to inhale toxins
canaries were used as animal sentinels in coal mines because they would die from co posioning before miners
110
Q
water respires have a greater challenge due to
A
- viscosity: water is 850 x more viscous that air - it is more costly to move air
- solubility : Co2 is more soluable, but o2 is not. thus making it more difficult to extract
- diffusion: diffusion rate is 10 000 x slower in water
- temperature : diffusion rate with high temp is good
- salinity : less of in saline water
111
Q
fish
A
- gills are the main site of gas exchange
- gills are made up of a gill arch that anchors pairs of gill filaments. small ultra thin lamellae protrude from the filaments
- lamellae are well perfused, very thin (low ) and numeras (high A)
112
Q
bony fishes
A
- operculum hard bondy flap covers all the gills and is used in breathing. bony fish usually have 8 gill arches (4 on each side)
- gill rakers - protect the gills by removing large particles (sand and rocks that are sucked in)
113
Q
breathing pump
A
- respiration in fishes is not tidal (inspiration/expiration) but flow through
- water enters by mouth and exits through the opercular cavity
- both entry and exit are active processes
114
Q
water enters
A
- mouth is opened, opercular cavity is sealed bottom of the buccal cavity is lowered - decreases pressure in the buccal cavity - water enters through mouth
115
Q
water exits
A
- mouth is closed, opercular cavity is opened bottom of the buccal cavity is raied - increased pressure on the buccal cavity - water exits through the opercular opening
116
Q
ram ventilation
A
- flow through motion of water can be achieve by the fishs own movement
- swimming with mouth and opercula slighty open also provide a water current for gas exchange
- some fish depend on ram ventilation (tunas) most fish are facultative ram ventilators = need to swim to breath
117
Q
cartilaginous fishes
A
- sharks and rays are more primitive than bony fishes, they lack an operculum and rather have gills for each gill arch
- most sharks have 5 gill arches on each side, and hence 5 gill slits on each side
- the breathing pumo works just the same, as the gill slits can close to prevent back flow
- most sharks will use ram ventilation - moving all the time, mouth open swimming
118
Q
spitacle
A
- most cartilaginous fishes have a spitacle, which is derived from a modified first gill slit
- is it a hole behind their eye that can serve for water entry, when their mouth is closed
- skates and rays (bottom feeders) have exaggerated spiracles because they need it to breath in clean water rather then sand
119
Q
temperature will effect HB carrying o2
A
- fish adapted to cold water cannot survive in warm water becasue their Hb cannot pick up enough o2 (shift right - decrease affinity of Hb for o2)
- they sufficate
120
Q
the Hb of some active fishes (tunas, some sharks) are not sensitive to temperature changes
A
- blood may increase more than 10C as it travels from the gills to the warm swimming muscles (countercurrent heat exchange)
- if Hb were not thermally stable, arterial blood might unload its o2 as it warmed in the counter current heat exchange resulting in o2 loss to the venous blood
- many fish have two or more types of Hb circulating in their blood
121
Q
physiological considerations
A
- species living in low o2 environment will have Hb that loads at low o2 and has a steep uploading curve, at a po2 just below the loading po2
- fish adapted to high o2 water load at high po2 and unload at a high po2
- they miantain higher o2 in thei tissues but loose ability to extract o2 from water poor in o2
122
Q
gills
A
- are the site of other functions such as acid base balance, excretion, nutrient uptake and osmoregulation
- their exposure to the environment makes them susceptible to diseases (environment gill disease) and paracites
- injury to the gills will cause suffication
