Acid-Base Flashcards
The role of H+ concentration in the body
what is the normal pH of the serum
what are some ways that the acid-base concentration in the bdody can be altered
- the amount of H+ in the body plays a role in the ability of bodily functions to occur –> H+ concentration impacts the cells a lot (impacts enzymes function and process)
- acids: solutions with a high H+ concentration
Normal pH : 7.35-7.45
(arterial = 7.4, venous 7.35 (carrying CO2))
Balance of Acid-Base affected by…
1. respiratory contribution: CO2 levels (volitile because it will become a gas)
2. metabolic contribtuion: (non-volitile- freely form gas) lactic acid, phosphoric acie, sulfuric acid, aecoacetic acic, etc. (these will disassociate in the blood, release H+ and impact pH)
The role of CO2 within the blood
- how does it travel (what form)
- what does it become to exhale
the role of Carbonic Acid within the blood
- where does it come from
CO2: approx. 20,000 milimols due to oxidative metabolism
- CO2 majority of it travels within the blood as HCO3-
- when it reaches the lungs: converted back into H2O & CO2
- then expelled in expiration
Carbonic Acid: made from the conversion of H2O and CO2
H2O + CO2 = H2CO3 = H+ + HCO3-
- when H2O + CO2 combine, brief formation of carbonic acid but it is quickly dissassoicated into H+ and HCO3-
- the H+ is buffere by Hgb & proteins
- the HCO3- and the carbonic acid are “elimated” via Co2 exhaled
- HCO3- used as a buffer within the body
so then, whats the role of HCO3- if its not buffering the H+ from the carbonic acid???
what are these metabolic contributors (non-carbonic acids) and where do they come from
HCO3- is responsible for buffering the other metabolic contributors of pH within the body –
the metabolic acids which are prodcued from other bodily functions
- metabolic (non-volitile) acids are produced –> they dissassociated and form H+ ions floating
- the H+ ions are buffered by the HCO3- in the blood
Non-Carbonic Acids (strong acids which need the kidney to buffer via HCO3-)
- lactic acid: from anerobic metabolism
- acetoacetic & beta hydrobutratic: from DKA
- phosphoric acid & sulfuric acid: from metabolism
- urice acid: DNA/RNA breakdown
- acetic acid: metabolism
so then, whats the role of HCO3- if its not buffering the H+ from the carbonic acid???
what are these metabolic contributors (non-carbonic acids) and where do they come from
HCO3- is responsible for buffering the other metabolic contributors of pH within the body –
the metabolic acids which are prodcued from other bodily functions
- metabolic (non-volitile) acids are produced –> they dissassociated and form H+ ions floating
- the H+ ions are buffered by the HCO3- in the blood
Non-Carbonic Acids (strong acids which need the kidney to buffer via HCO3-)
- lactic acid: from anerobic metabolism
- acetoacetic & beta hydrobutratic: from DKA
- phosphoric acid & sulfuric acid: from metabolism
- urice acid: DNA/RNA breakdown
- acetic acid: metabolism
What are the buffers of the body (briefly)
tissue buffers
blood buffers
renal buffers
HCO3- (bicarb) = short -term
ammonia = longer-term
Tissue Buffers
- cellular proteins and phosphates
Bone & Muscle Buffers
- bicarbonate does this
- responosible for neutralizing 5x as much as the blood does
Blood Buffers
- within the RBC and outside in the plasma
1. bicarb: responsible for buffering the H+ which come from acids which arent carbonic acid
2. hemoglobin: which buffers the h+ which comes from carbonic acid
- phosphate also plays a buffering role, but minimal avalibility
Renal Buffers
- bicarb
- phosphate
- ammonia (most important)
specifics of the blood buffers
- bicarb
- hemoglobin
Hemoglobin (Hgb)
- buffer for the H+ which comes from the carbonic acid breakdown (HCO4+ –> HCO3- + H+)
- the response of hemoglobin is proportional to the amount of O2 released (increased need for O2 in the blood dumps it from the Hgb, and therefore there is more avalibel to uptake the h+)
Bicarbonate Buffer
- handles 75% of the non-carbonic acid dumped into the plasma
- its not very powerful: doesnt get all the H+
- but due to HOW MUCH HCO3- there is – it works well
- relationship with respiratory and renal
normal PCO2 = 33-45
nromal bicarb = 22-28
thus, in metabolic acidotic situations – the main player is bicarb to buffer , with a minial amount of help from the respiratory system to elimate some of the H+ as CO2
- respiraroy: release CO2
- secretion of H+ via urine in the nephrons helps
- regeneration of the bicarb via reserves
what is the alkali reserve/buffer capacity?
the overall avalibility of the buffer to do its job ; to buffer!
the kidney regerates the buffereing capcity
regeneration of buffer assoicated with the secretion of H+
the secretion of H+ into the urine needs a urinary buffer system
- filtered bicarbonate (from the body that is filtered through glomerulus)
- filterated phosphate (from the body that is filtered through the glomerulus)
- ammonia buffer (helps to excrete the non-volitile acids)
within the PCT: there is a net gain of HCO3- back into the blood = regenration of HCO3-
DCT/CT is where H+ secretion occurs (via phosphate and ammonia)
- diphosphate + h+ = monophosphate = excrete
- throughout this process of buffering an H+ via phosphate – a bicarb is produced
- glutamine –> ammonium (NH4+) + HCO3- made = NH4+ excreted, HCO3- made
- NH3 (ammonia) (urea in its stable form) + H+ = NH4+ = excreted
Acidemia
Acidosis
Alkalmeia
Alkalosis
Acidemia: the blood pH < 7.35
Acidosis: any process which causes an increase in H+ or a decrease in HCO3-
Alkalemia: the blood pH > 7.45
Alkalosis: any process which causes a decrease in H+ or an increase in HCO3-
Metabolic Acidosis
normal gap causes
increase gap causes
clinical signs of metabolic acidosis
Normal Anion Gap Acidosis
- bicarb loss due to diarrhea
- failure to regenerate bicarb in the PCT, DCT/CT (think diueretics)
Increased Anion Gap Acidosis
- a reduction in the ability to excrete the acids (urea, etc. due to renal failure)
- an accumulation of orangic acids (lactic acidosis, DKA)
Clincial Signs
- accumulatee H+ in blood
- decreased plasma HCO3-
- increased ventilation to try to “blow off” the CO2
- a low pCO2 (compensatory mechanism)
Metabolic alkalosis
- causes
- clinical signs
Causes
- ingestion of alkali (for ucler treatemtn – too many tums)
- diuretics which increaed H+ secretion too much
Clinical signs
- a drop in H+ concentration in the blood
- increase in serum bicarb ( > 28) & seeing dumping of bicarb in the urine
- increased blood pH
- ventilation slow: trying to hold ont the CO2
- kidneys no regenerating HCO3-
- HCO3- remianes high despite the drop in pH due to increased ventilation and drop in CO2
Respiratory Acidosis
- causes
- clinical signs
Causes
- anything causing a decrease in the ability to ventilate
- CNS depression of ventilation center in medulla
- drug depression of breathing drive
- obstructed pasageway (PE)
- pneumonia
- decrease ventilation surface (COPD)
Clinical SIgns
- respiration is blocked
- CO2 retention and increased levels
- pH decreases
- H+ increased
- HCO3- increase (compensatory)
Respiratory Alkalosis
- causes
- clinical signs
Causes
- high altitude: low pO2 causes an increase in respiratory rate and a loss of CO2 as a result
- hyperventilation (anxiety)
Clinical Signs
- pH is high
- decrease pCO2 and H+ concentration
- HCO3- is lowered as a compensatory process
- kidneys attempt to adjust via…
1. not regenerating HCO3- , dump into urine
2. decreae making NH3 (which would bind to H+ to release)
3. increase their rentention to H+
