Respiratory Physiology Flashcards
respiratory pigments
- oxygen transport pigments
- serve to bind O2 at respiratory surface and transport it through blood to tissues, and to remove CO2
- some also used as storage (ex: myoglobin in tissues)
- reversible combination with oxygen (pick up O2 at lungs, release at tissue)
inc the amount of O2 that can be carried by unit volume of blood
facultative diffusion
accepts O2 from hemoglobin and stores it in tissues until muscle need it
hemoglobin
- acid-base buffers
- participate in blood CO2 transport and O2 transport
- each contains 4 iron porphyrin prosthetic groups (hemes)
- contains 2 copies of alpha globin and 2 copies of beta globin
- each 4 polypeptide chains contain a heme molecule which is site for O2 binding
heme
associated non-covalently with protein globulin
- each heme binds 1 oxygen (4 hemes)
- 4 units=4 O2 molecules
globins
- proteinaceous
- subunits are different
human fetal hemoglobin
gamma and epsilon chains
oxygenated
hemoglobin combined with O2
deoxygenated
hemoglobin released O2
differences in Hb are due to differences in…
- amino acids in proteins
- alpha globin genes from chromosome 16
- beta and fetal genes from chromosome 11
where is hemoglobin found?
inside RBC (except with some insects)
myoglobin
- muscle hemoglobin
- 1 heme
- concentrated in muscle (cytoplasm of muscle fibers)
- hemoglobin unloads oxygen to myoglobin
- myoglobin has greater oxygen affinity than hemoglobin
chlorocruorin
- “green hemoglobin”
- 80 hemes per molecule
- green, found in 4 families marine annelids
- free floating, not specialized cells (dissolved in blood plasma)
- contains Fe and heme
- binds 1 O2 molecule per heme
hemerythrin
- 8 subunits
- no heme
- contain Fe directly to protein (each O2 binding site has 2 iron atoms)
- found in polychaetas
- sound in blood cells
hemocyanin
- copper containing pigment bound directly to protein (each O2 binding site has 2 copper atoms– 1 O2 per 2 Cu)
- no heme, no iron
- blue with oxygen
- high mw keeps down osmolarity
- not found in blood cells
- found in non-insect arthropods
- reverse Bohr effect (dec pH-> inc affinity)
never in muscle/solid tissue)
cytochromes
- have heme structure
- involved in electron transport and oxidative phosphorylation in mitochondria
Affinity for Oxygen
- affinity= how readily combine with O2
- respiratory pigments combine reversibly with oxygen over a range of partial pressures of O2
- thus serving as O2 carriers by loading at the respiratory surface and unloading at the tissues
saturated
O2 partial pressure is high enough for all O2 binding sites to be oxygenated
% saturation
percentage of binding sites that are oxygenated
Hb-O2 saturation curve
shows the relation between the percentage of binding sites that are oxygenated and the O2 partial pressure
P50
- when Hb is 50% saturated
- partial pressure of O2 at 50% saturation of hemoglobin
- measure of affinity of a particular Hb for O2
as P50 inc-> affinity dec
low affinity
pigments that need high O2 partial pressure for full loading and unload substantial amounts of O2 at high partial pressures
high affinity
pigments that load fully at low partial pressure and require low partial pressure for unloading
a shift to the right means…
O2 affinity
the O2 partial pressure needed to saturate is higher and the P50 is higher, thus… O2 affinity is lower
(lowering O2 affinity shifts to the right, raising affinity shifts to the left)
When hemoglobin molecule binds 1 O2…
this increases affinity of the molecule to bind more O2
- if 4 hemes bind O2 = 100% saturated
- the affinity of Hb must be turned to specific needs of the organism (ie: animals need to bind Hb at the lungs and unload it at the tissues; partial pressure of O2 differs at these two sites)
best strategy
- animals try to have 90-95% saturation at lungs, while still being able to unload at tissues, where there’s low PO2 at capillaries
- hemoglobin with high affinity are saturated at low partial pressures of O2 (es: myoglobin)
- hemoglobin with great O2 affinities facilitates movement of O2 into blood from the environment because O2 is bound to hemoglobin at low PO2
- since tissues have low PO2, you don’t want to have great affinity here, because you want hemoglobin to release oxygen at tissues
- hemoglobin is nearly saturated at O2 partial pressures maintained in lungs by breathing
what types of respiratory pigments have greater oxygen affinity than hemoglobin
- myoglobin has greater oxygen affinity then hemoglobin
- fetal hemoglobin has greater oxygen affinity than adult hemoglobin
- in both cases, this facilitates hemoglobin unloading oxygen to myoglobin/fetal hemoglobin
- with lower affinity it won’t bind O2 at low PO2 (at tissue), so hemoglobin unloads more to these other pigments
- hemoglobin with greater O2 affinity will not release O2 to tissues until PO2 is very low
fish P50
lesser P50, greater affinities than mammals, so it can uptake O2 in more oxygen deprived environments
bird P50
- have greater P50, lesser affinities than mammals so it can unload more
- with high MR, they need great O2 at tissues
- p50= 40-60 mmHg
main point about hemoglobin
- hemoglobin with great O2 affinity favors uptake of O2 by blood
- hemoglobin with less O2 affinity favors release of O2 to tissues
**Hemoglobin should have great affinity at respiratory surface and low affinity at tissues
bicarb equation
CO2 + H2O <-> H2CO3 <-> H+ + HCO3-
- high CO2 shifts equation to right-> high H+, low pH
- increase in H+ shifts equation below to left-> dec O2 affinity
- deoxyHHb <-> H+ + Hb
HHb+ + O2 <->HbO2 (oxyHb) + H+
Bohr effect
- inc CO2-> dec affinity by dec pH
- H+ complexing with Hb and releasing O2
- also CO2 complexes with Hb and releases O2
- shifts Hb dissociation curve to right
- at low pH and high PCO2-> dec affinity and dec P50
- normally occurs when blood enters capillaries because of increased pCO2
at tissues…
pH, pCO2, affinity, P50
- low pH, high pCO2, low affinity, high P50
- low pH and high PCO2 allows hemoglobin to unload more O2
stagnant water
low pH and high pCO2 causes problems with animals loading at respiratory surfaces
inc in CO2 partial pressure
causes pH decrease
inc in H+ concentration
inc in combination os Hb with H+-> favors dissociation of O2
what is responsible for Bohr effect?
- Proteins come from:
1) COOH terminal of the beta chain has a histidine (N+) imidazole group
2) amino terminal of the alpha chain has NH3 - some fish won’t show Bohr effect
Reverse Bohr effect
- animals with hemocyanin have a reverse Bohr effect
- ie: dec pH-> inc affinity
- good for animals that live in stagnant waters
- also back up hemoglobins found
- fishhave Hb with a Bohr effect (facilitates unloading at tissues) and also one without a Bohr effect (facilitates loading at the respiratory surface)
Root Effect
- inc in CO2 partial pressure/dec in pH causes Bohr effect AND reduces amount of O2 the respiratory pigments bind when saturated
- dec pH-> dec amount of O2 bound to Hb (dec in O2 capacity
- root effect at low pH: blood can’t bind O2 at respiratory surface
- acidification forces O2 bound to hemoglobin to dissociate by change og pH
2,3 DPG
- in RBC
- Inc in 2,3 DPG-> dec affinity, inc P50, facilitates O2 unloading
- IHP in birds
- ATP in fish and some amphibians
temperature and Hb
- increased temperature shifts Hb-O2 dissociation curve to the right
(dec affinity=inc P50, low temp=inc affinity) - O2 affinity of respiratory pigments is inversely dependent on temperature
what do P50 values depend on
- pH, pCO2, 2,3 BPG, and temperature
in general with mammals…
P50/affinity trend
small mammals have greater P50s than large ones
- with greater MR, they need more O2 to tissues
O2 affinity of blood hemoglobin tends to decrease as body size decreases
- need lowest affinity possible so its just saturated at respiratory surface and can unload at tissues
P50 values
- normal range: 20-45
- adult human: 30 (2 alpha, 2 beta)
- fetus: 20 (fetal Hb has greater affinity; 2 alpha, 2 gamma–> allows fetal Hb to take up O2 from mother because O2 leaves lower affinity hemoglobin of mom to go to higher affinity hemoglobin of fetus)
Reptile P50
- great diversity, meets needs of organism
- P50- 20-50
amphibian P50
- tadpoles: low P50s, high affinity because of water
- Adults: higher P50s
fish affinity
fast swimmers, stagnant warer, low O2
- fast swimmersL from water with high Po2 and low temp; usually have Hb-O2 curves to right of other fish (lower affinity helps unload O2, thy don’t need high affinity in high O2 tension water)
- stagnant water fish: low P50s
- species that live in low O2 environment have evolved respiratory pigments with higher O2 affinities than related species in high O2 environments
Invertebrate P50s
- respiratory pigments in blood of some invertebrates probably functions as O2 stores
- very high O2 affinity (do not unload under routine conditions)
- unload when face severe O2 shortages
effect of temperature on Hb (fish)
1) increased temp-> dec O2 concentration of water
- elevated temps create O2 stress
2) high temp-> inc MR of poikilotherms (require more O2 at elevated temp; may also result in inc PCO2 levels and lower pH-> dec affinity and higher P50s)
3) high temp-> inc P50, dec affinity, dec amount absorbed at respiratory surface
means of compensation
1) inc ventilation (ie: inc respiratory rate to get more O2, also may inc loss of CO2-> inc pH and inc affinity; yet inc muscle activity and energy costs)
2) inc blood flow across respiratory surface to maintain high O2 gradient
3) increased Hb concentration and/or number of RBC (more RBC in oxygen poor environment; in environment without O2-> 20x increase in Hb concentration)
4) change in type of Hb (ex: summer Hb has higher affinity; synthesizing different molecular forms(diff globulin-> different O2 affinity)
5) some sort of modulation with Hb
6) back up Hb
several invertebrates and some vertebrates lack respiratory pigments
- no O2 transport by blood hemoglobin
- no Hb, clear blood, only serum
- Active fish, MR high
- high rate os blood circulation, high CO, high blood volume
- large hearts circulate blood rapidly
- very high respiratory surface area where O2 can diffuse
- important that cold water has greatest O2 tension
Air vs water respiratory systems
- less O2 per liter in water than air
- h=water is 100x more viscous
- water is 10^3 higher density than air
- diffusion rates are 3 million times higher in air
- its easier to breather in air; more energy involved in water breathing
problem with water breathing
- desiccation
- respiratory surface must be kept wet
evolutionary tendencies of respiratory systems
1) increased surface area of respiratory surface to facilitate diffusion (high surface area= lungs densely filled with branching airways)
2) increased mechanisms for ventilation of respiratory surface (inc rate of respiratory medium across respiratory surface)
3) increased circulation to respiratory surface (greater blood flow; greater number of capillaries or greater perfusion of existing capillaries)
4) decreased diffusion distance (reduced area between blood and air; thinner epithelium of surface; faster diffusion rates)
5) decreased size of alveoli (small areas in lungs where gas exchange occurs)
- increased internal septation (inc number of alveoli/unit vol of lung, trend to inc surface area per unit vol of lung, inc SA with inc body weight and O2 uptake)
integument repiratory system
- skin
- well vascularized
- protozoans, eggs, annelids
- some verts (certain fish, amphibians)
- modifications that render skin poorly permeable to water make it poorly permeable to O2/CO2
external gills
- amphibians, fish larvae, invertebrates
- fern like feather like, high surface area
- well vascularized (great blood flow)
- not a good system (fragile, problems with ventilation, also problems with predation)
internal gills
- gill consists of 4 gill arches
- each gill arch contains 2 rows of gill filaments (at 90 degree angle)
- filaments of adjacent rows touch
- also has operculum to help ventilate gills and provide protection for fragile gills
gill arches
run dorsal ventrally between gill slits on each side of the head, provide support for gills
operculum
protective external flap that covers the set of gills on each side of the head
gill slits
lateral pharyngeal openings; gills arrayed across these openings
secondary lamellae
- on each gill filament
- run perpendicular to long axis of the filament
- flaps that project up and down from the filament
- actual respiratory surface where gas is exchanged (capillary beds in secondary lamellae is where gas exchange occurs)
- blood flows up the arch; across the filaments and through the capillary beds of lamellae)
- richly perfused with blood and thin walled
blood flow across lamellae
- in opposite direction to that of water
- countercurrent system which maximizes O2 taken from water
adaptations in fish gills
- fish can adjust flow to each arch and to each lamellae in each filament
- inc flow to lamellae-> inc O2 uptake
- inc flow to other portions–> inc ion regulation via Cl- cells
- vasotocin: will decrease blood flow to lamellae, inc it to Cl- cells
- gills innervated by sympathetic fibers (epi and NE-> inc blood flow to lamellae)
- and parasympathetic fibers (Ach-> dec blood flow to lamellae)
ventilation in fish
- water is forced through a meshwork of secondary lamellae
- water-> mouth-> gills-> operculum-> outside
- dual pump mechanism: process of gill ventilation (buccal pump in cavity of mouth, operculum pump)
dual pump mechanism
- two pumps are arranged so theres a continuous flow of O2 across gills
- maintains high O2 gradient across gills
buccal pump
develops positive pressure in buccal cavity and forces water from buccal cavity through gill array into opercular cavity
- opens mouth: water flows in (ups vol), operculum closed
- mouth closes, forces water back (lowers vol), operculum opens
operculum pump
- develops negative pressure in opercular cavity-> sucks water from buccal cavity into opercular cavity
- as operculum moves out it increases volume across gills, as it move in (closes) it dec volume
mechanisms for air breathing fish
1) breathe across skin, some areas highly vascularized
2) specialized gills that are rigid
3) specially designed areas, Pharyngeal epithelium, highly vascularized
4) pharyngeal or opercular lungs
5) gastrointestinal tract
6) air or swim bladder (lungs of lungfish)
diffusion lungs
- no ventilation
- ex: book lungs- spiders, pulmonated snails
- can’t maintain high concentration gradient
ventilation lungs
- actively being ventilated (ie: forcing air back and forth)
- lungfish: evolutionary prototypes, similar to amphibians
alveoli
small areas where gas exchange occurs
- dec size of alveoli-> greater number per unit space
- increase surface area
- increase internal septation
- all for increased gas exchange
- thin walls
- surrounded by capillary beds
ventilation mechanism for amphibians
- buccal force pump
- air through nostrils opens into buccal cavity in mouth
- this then shunts air via glottis into lungs by raising buccal floor
- also lungs release air to buccal cavity (lungs = simple, well vascularized sacs)
- this air can be returned to lungs
glottis
closed by muscular contraction after inhalation
- when glottis is opened, air is exhaled
reptile ventilation
- don’t possess a diaphragm
- still inc SA
- inc internal septations
- dec size of alveoli
- ventilation mechanism similar to higher verts (thoraco-abdominal pump)
- with a breath, thoracic cage increases, pressure decreases and blood flows to heart
- lungs take up essentially all O2 and eliminate essentially all CO2
- skin does not readily allow respiratory gases to pass through
mammals lungs
greatest surface area compares with amphibians and reptiles
- also greatest internatl septation
- for greatest amount of gas exchange
anatomy of mammal lungs
- trachea bifurcates into bronchi
- bronchi branch repeatedly into bronchioles
- these branch into terminal bronchioles -
- these into respiratory bronchioles
acinus
respiratory portion of lungs
- respiratory bronchioles
- alveolar duct, alveolar sac and alveoli
alveolar duct
final bronchioles; ends blindly
alveolar sac
walls composed of outpocketings (alveoli)
- form blind ends of tidally ventilated airways that are never fully emptied
conducting airways
not involved in much gas exchange
- trachea, bronchi, most bronchioles
respiratory airways
where gas exchange between air and blood occurs
- respiratory bronchioles, alveolar ducts, alveolar sacs)
- has smooth muscle and is innervated by sympathetic and parasympathetic fibers
small vs large mammals
- small mammals have even a greater surface area than large mammals due to the greater O2 demand
- another reason why their Hb-O2 affinity can be less
surfactant
- interior surface of lungs is coated with a lipoprotein “surfactant”
- dec surface tension in lungs which prevents lungs from collapsing
- alveoli gas exchange surfaces are coated with an exceedingly thin water layer
- phospholipids associate with water layer and reduce surface tension properties of water-> prevents collapse
law of La Place
- pressure difference between inside and outside of bubble is proportional to 2Y/R
- Y= wall tension
- R= radius
- so increased wall tension or decreased radius-> inc pressure-> collapse
tidal volume (TV)
- normal breathing
- volume of air inhaled and exhaled per breath
inspiratory reserve (IR)
- forceful inhalation
- IRV: air inspired above normal
- max volume of air that can be inhaled beyond resting inspiratory level
expiratory reserve (ER)
- forceful exhale
- ERV: air exhaled above normal
- max volume of air an individual can expel beyond the resting expiratory level
residual volume (RV)
air remaining
vital cpacity (VC)
IRV + TV + ERV
- max tidal volume; achieved by using both reserves
physiological dead space (PDS)
volume of lung minus alveoli
anatomical dead space (ADS)
normally = PDS
diaphragm
- a sheet of muscular and connective tissue that completely separates the thoracic and abdominal cavities
- contraction of disphragm pulls center away from thorax toward abdomen-> expands lungs-> air inflow
alveolar ventilation (AV)
amount of air moving in and out of alveolar sac
- depends on breathing rate, TV and ADS
AV(l/min) = (TV x RR) - (ADS x RR)
- (TV x RR)= MRV; minute respiratory volume
MRV
total amount of new air moved into respiratory passages each minute
- MVV = max ventilation volume = MRV for max effort
inspiratory muscles
A) diaphragm
B) external intercostal muscles (contracts, pulls pib cage and enlarges thoracic cage; innervated by neurons from inspiratory center in medulla)
expiratory muscles
- internal intercostal muscles: pulls back on rib cage, reducing volume of thoracic cage
- innervated by expiratory center in medulla, inhibited by inspiratory center
inhalation vs exhalation
- during inhalation, the lungs are expanded to greater that their relaxation volume-> entails muscular effort (active)
- exhalation= lung volume returns elastically to its passive equilibrium state (relaxation volume)
- expiring is a passive process normally
- due to compliance or elasticity of the thoracic muscles; they snap back
regulation of ventilation
- in mammals, all influences on ventilation are integrates by neurons in the medulla respiratory center
- respiratory center in medulla (inspiratory and expiratory center)
- apneustic center in pons
- pneumotaxic center in pons
neural reverberating circuits
- originating in respiratory center
- stretch receptors in lung feedback to respiratory center
- Hering-Breur Reflex
- chemoreceptors in brain
Hering-Breur Reflex
- mechanosensory responses
- inflation os lungs yield via vagus a decrease frequency of breathing
- signals for inhalation are inhibited by lung expansion and excited by lung compressions
chemoreceptors in brain
- more strengthful and sensitive, also in aorta and carotids
- blood-brain barrier: increase CO2, lower pH= inc RR
- CSF: inc in CO2 will override vagus and inc inspiration
- these receptors sense pCO2 inc and feedback to respiratory center
- CO2 inc leads to inc H+ which is sensed by medulla-> inc ventilation= more CO2 exhalation
bird lungs
- high metabolic rates (especially during flight)
- smaller surface area than even reptiles
- trachea-> two primary bronchus that enter lungs (passes through= mesobronchus)-> secondary bronchi (arise from mesobronchus)-> parabronchi
- air sace located outside lungs (little role in gas exchange)
parabronchi in birds
- gas exchange surface
- central lumen of each parabronchi gives off finely branching air capillaries that are surrounded by blood capillaries and are sites of gas exchange
functions of air sacs in birds
1) involved in respiration: NO (gas isn’t exchanged across here, only parabronchi)
2) buoyancy: NO (makes density less, lighter for flights)
3) acts as bellow: YES (air pump for respiration, arrangement of air sace with parabronchi is important)
Anterior and posterior air sacs with parabronchi
- air flows posterior-> anterior
1) air enters the posterior sac= respiration 1 (valves prevent air from going into others)
2) when breathe out, posterior sac is squeezed so air goes through parabronchi expiration 1 (not exhaled at this time)
3) second inspiration drives into anterior sac
4) second inspiration-> out
bird flow through system
- 2 breaths for air to be taken in and expelled
- every time they breathe, theres a fresh pulse of air
- maintains high concentration gradient
- always high O2 uptake because air is high in O2, low in CO2
- no residual volume
- can get by with low Hb-O2 affinity
respiratory system of insects
- gas exchange surface itself is close to every cell in the body-> insects get O2 directly from breathing system and circulating system plays little/no role in O2 transport
- use tracheal system
- hemolymph isn’t used for O2 carrying
- tracheoles: smallest branches (blind endings and poke between and within cells; gets gas right next to cells; tip is fluid filled)
insect tracheal system
- tracheoles are principal site of gas exchange
- trachea= gas filled tubes; penetrate into body from each spiracle and branch repeatedly, reaching all parts of animal
- tracheal system: system of air passages which open to outside through spiracles
- gases diffuse through trachea to tissues
- ventilation by contraction of body wall
- spiracles not open all the time, usually this is regulated to prevent dessication
- requires passive diffusion, consequently limits size of the organism
Acid-base balance
- important to maintain proper pH
- enzyme activity is sensitive to pH; permeability of membranes
- levels of Na+/K+ impacted by pH
- protein structure
- noncovalent, weak bonding, hydrophobic interactions, importance in binding O2 to hemoglobin
what is pH
- expresses concentration of H+
- pH= log1/[H+]= -log[H+]
- a change in pH from 6 to 7 involves a 10 fold change in H+ concentration
- neutral pH at 25C=7
- neutral pH varies with temperature (higher at lower temps)
normal pH of blood
7.4
pH of blood in acidosis
less than 7.4
pH of blood in alkalosis
greater than 7.4
normal pH range in mammals
7-7.7
sources of acid
- addition of acid= reduction of alkaline
1) diet: protein, AA degradation-> acidosis
2) CO2: inability of animal to get rid of CO2-> acidosis
3) Exercise: increased CO2 levels; build up of lactic acid
how can respiration help maintain acid base balance
- compensatory response to inc acid= inc lung ventilation (lowering CO2 PP-> lower H+)
- slowing ventilation helps when too alkaline-> inc CO2-> more H+
CO2 + H20<-> H2CO3<-> H+ + HCO3-
- high CO2 shift equation to right-> high H+, low pH
- inc in H+ shifts equation to left-> dec O2 affinity
- major extracellular buffer system
- when H+ is low, HCO3- is high
- H+ is high, HCO3- is low
sources of alkalosis
- addition of alkaline= removal of acid
1) diet: mostly inc salts (ammonia)
2) excess vomiting (elimination of HCl)
3) hyperventilation: rids body of excess CO2
blood buffers
- under conditions when concentration of H+ is driven upward, they are able to restrain the rise in concentration by removing free H+ ions from solution
1) hemoglobin, 35% buffering
2) Phosphate buffers, inorganic 2% and organic 3%
3) serum proteins, 7%
4) Bicarbonate system, 53% (35% in plasma, 18% in RBC; major system mostly because its an open system) - if buffers are effective, most H+ is removed as it is formed-> H+ will stay low, HCO3- will build up
what causes departure from normal pH
respiratory causes
respiratory causes: brough about by changes in rate of CO2 elimination by lungs/gills
Respiratory acidosis
- inability to get rid of CO2
- occurs hen CO2 exhalation is too slow to void CO2 at rate it is produced, causing CO@ to accumulate in body
- high pCO2-> high bicarb, equation shifts to right
- build up of bicarb and H+ ion-> lower pH
respiratory acidosis compensation
- corrects for pH with bicarb further elevated
1) mostly via renal compensation - kidney inc secretion of H+, however this results in a net reabsorption of HCO3-, so elevated bicarb levels more
- urine buffers: bicarb system, inorganic phosphate, ammonia
2) some respiratory compensation might occur - inc pCO2 sensed by resp chemoreceptors-> leads to inc ventilation
- if respiratory acidosis was due to inability to get rid of CO2, major correction will be renal compensation, which is fairly slow, hrs to days
respiratory alkalosis
- arises when exhalation of CO2 is inc-> PP of CO2 decreases below level to maintain normal pH
- due to hyperventilation-> low pCO2, shifts equation to left-> inc pH and dec bicarb
- primary compensation is renal, to dec H+ secretion, but this further dec bicarb reabsorption
- correction is to dec pH
metabolic acidosis
- can occur during chronic diarrhea because of excessive loss of HCO3- in evacuated gastrointestinal fluids
- accumulation of H+ in body fluids beause of production of lactic acid during exercise-> lowers HCO3- concentration
- pCO2 normal
- inc H+, dec pH
- shifts equation to left (caused by diet or less H+ being secreted; dec bicarb, causing it to form H2CO3)
compensation for metabolic acidosis
- primarily respiratory: inc ventilation, inc loss of CO2, this inc pH, more bicarb loss
- some renal compensation too: inc elimination of H+ which will also raise bicarb levels, time factor
metabolic alkalosis
- caused by dec H+ which shifts equation to the right-> inc bicarb
- due to inc H+ secretion or additional alkaline
- pCO2 normal
compensation for metabolic alkalosis
- primarily respiratory: dec ventilation-> inc pCO2 levels which further inc bicarb, but lowers pH
- some renal compensation to dec H+ secretion yet this reduces bicarb levels
