acid-base balance Flashcards
proton regulation
must be tightly regulated because very reactive
ECF levels kept al low levels, 4nEq/L
should be 3-5nEq/L
pH of ECF
7.4
acidosis
process
acidaemia
state
<7.35
alkalosis
process
alkalaemia
state
>7.45
venous blood compared to arterial blood
more acidic
higher partial pressure of carbon dioxide
interstitial fluid
usually same an venous blood pH
pH effects of metabolism
practically every step of every metabolic process is pH dependant
deviate from optimal pH causes decrease in reaction efficiency, especially due to compromised enzyme activity
acidosis affect on neuromuscular system
inhibitory
alkalosis affect of neuromuscular system
excitatory
why does pH affect neuromuscular system
plasma Ca2+ binding to albumin is pH dependant
acidosis increases free Ca2_
bathmotropy - calcium blocks Na channels, raises AP threshold
bathmotropy
when free calcium interacts with Na channels and switches them off, which raises the AP threshold
potassium balance in pH
acidosis - more serum [K]
alkalosis - less serum K
consequences of acidosis
headaches, confusion, lethargy, tremors, sleepiness, cerebral dysfunction,
come
hyperventilation
consequences of alkalosis
muscular weakness, pain, cramps, spasms, (smooth and skeletal muscle), tetany
hypoventilation
most acid comes from
CHO/fat metabolism (CO2)
acids produced in the body
- metabolic activities continuously add H to the body
- glycolytic metabolism - lactic acid
- oxidative metabolism - CO2/carbonic acid
- FA/AA metabolism - ketoacids
- inorganic acids produced from intermediary metabolism
- stomach acid production loads HCO3 - blood
- pancreatic HCO3 production loads H+ - blood
vomiting causes
alkalosis
buffers
HCO3- in ECF
proteins, haemoglobin, phosphates in cells
phosphates, ammonia in urine
chemical buffering
- solutions preventing change in pH
- intracellular and extracellular buffers provide an immediate response to acid-base disturbances
- bonde also buffers acid loads
- immediate but exhaustible
pulmonary regulation
- PCO2 is regulated by changes in tidal volume and respiratory rate
- CO2 is exhaled - blood pH increases
- can only removed acid
renal regulation
- kidneys control adjust the amount of HCO3- and/or H+ that is excreted
- excreting HCO3- causes decrease in blood pH
- excreting H + causes increase in blood pH
buffer power
- determined by the pH appropriateness of the system
- pKa should patch pH
capacity of buffer determined by
total [buffer]
relative [HB] and [B]
chemical buffer systems
HCO3- (ECF buffer)
NH3 (renal tubular fluid)
PO42- (ICF)
proteins (ICF, Hb n RBCs)
ventilation
ventilation rates control pH balance
- increased ventilation removes CO2
hyperventilation causes
increase pH
decrease [H]
hypoventilation causes
increase [H]
decrease pH
renal control
kidneys constantly remove HCO3- from blood
to maintain balance, we must re absorb HCO3- back into the blood
kidneys can’t do that
first it has to be converted
conversion of HCO3- for reabsorption
HCO3- + H+ > H2CO3 > H2O + CO2
to do this, kidney must secrete H+ at a 1:1 ration with HCO3-
if H secretion = HCO3- filtration
no change in pH
if H secretion > HCO3- filtration
acid loss
if H secretion < HCO3- filtration
base loss
how is HCO3- reabsorbed
2nd degree active transport
- CO2 diffuses into cells
- carbonic anhydrase inside the cell forms CO2 into H2CO3 which becomes HCO3- and H+
- the H+ then leaves the cell again
1st degree active transport
- H+ pumped directly put into the lumen
acid being secreted as ammonium
ammonium is produced by removing amine group from amino acids
amine group is actively transported out of the cells as ammonium via counter transportation for Na
2 direct mechanisms
- Na/K ATPase - alkalosis causes a shift of K+ from the plasma > ICF
- electronuetrality - K+ will be passively secreted as an obligate cation partner to HCO3-
why do states of alkalosis cause hypokalaemia
because K+ ions are being secreted with the HCO3- ions to maintain electronuetrality
arterial blood gas analysis
PCO2 - reflect respiratory component
HCO3- - reflects the metabolic component
AB disorders
- may be metabolic or respiratory
- metabolic - due to production, ingestion or loss of acids/bases
- respiratory - due to hyper/hypoventilation
riased HCO3-
alkalosis
raised pCO2
acidosis
respiratory disorder leads to
metabolic compensation
metabolic disorder
respiratory compensation
subtypes of metabolic acidosis
[Na+] is greater than [HCO3-] + [Cl-]
difference between the two issues the anion gap
usually 12 mEq/L
major increase in anion gap implies existence of an organic acidosis (poisoning)
plasma anion gap exists because
- gap exists because there must be elctronuetrality
increased anion gap
organic acidosis
diabetic/sstarvation ketoacidosis, lactic acidosis, poisoning sulphates, methanol, ethylene glycol, os salicylates (aspirin)
normal anion gap acidosis
diarrhoea (HCO3- loss)
carbonic anhydrase-inhibitors
