Acid-Base Homeostasis Flashcards
pH
-log[H] (no units)
[CO2]
(0.0301 mM/ mm Hg) x PCO2
units of mM OR mmol/L
strong acid
completely dissociated at physiologic pH
HCl -> H+ + Cl-
strong cations
completely dissociated
ex: Na+, K+, Mg2+ and Ca2+
strong anions
completely dissociated
ex: Cl-, SO4(2-)
weak acid
exists in both dissociated and undissociated forms
-> act as buffers
buffer
molecule or molecular system that resists changes in [H+]
acid dissociation constant
Ka = [products]/[reactants]
*[H20] concentration can be ignored because it’s concentration in the body is generally constant
equilibrium expression for bicarbonate buffer
Ka’ = [H+][HCO3-]/[CO2] = 800 x 10^-9M
equilibrium constant for bicarbonate buffer
800 x 10^-9M
800 nM
normal values in arterial blood for H+, HCO3- and CO2 concentrations
[H+] = 40 nM (40 x 10^-9M) [HCO3-] = 24 mM (24 x 10^-3M) [CO2] = 1.2 mM (1.2 x 10^-3M)
*carbonic acid occurs 1:320 to CO2 -> 4 uM
So,
[H+] < [H2CO3] < [CO2] < [HCO3-]
hyperchloremia
bicarbonate anion is replaced by the chloride anion
HCl + HCO3- = CO2 + H2O + Cl-
closed system
retains CO2
large change in pH with each addition of acid
open system
elimination of CO2
small change in pH with each addition of acid
PCO2 isobar
In an open system, dissolved [CO2] remains constant. So the pH-bicarbonate diagram illustrates the relationship that forms a line called the PCO2 isobar
Henderson-Hasselbalch equation
mathematical rearrangement of the equilibrium expression for CO2-bicarbonate
-> generates family of PCO2 isobars by choosing various [HCO3-] for given
pH = 6.1 + log ([HCO3-]/(.0301 x PCO2))
CO2-bicarbonate system
effectively buffers hydrogen ions from non-carbonic acids
-cannot buffer itself
isohydric principle
pH can be known if [CO2] (or PCO2) AND [HCO3-] are both known
CO2-bicarbonate rxn
CO2 + H20 H+ + HCO3-
futile cycle of buffering bc the CO2 that is added is regenerated
THUS the body requires other buffers to remove free H+ without regenerating CO2
*not good for respiratory (carbonic acid) challenge
buffer line
formed by pH-bicarbonate values
flat is undesirable, ex: increasing PCO2 -> no change in bicarbonate and pH drops
steep is desirable- large amounts of bicarbonate formed with little change in pH
metabolic acidosis
increase in non-carbonic acid
respiratory acidosis
increase in PCO2 (hypoventilation)
advantages of other buffers
1) buffer H+ produced by CO2
2) transport added CO2 as HCO3- not as dissolved CO2
other buffers
1) plasm and interstitial phosphate
2) plasma and interstitial protein
3) red cell
4) intracellular buffering
5) bone
plasm and interstitial phosphate
H+ + HPO4(2-) H2PO4-
plasma and interstitial protein
H+ + (protein) (protein-H+)
red cell buffer
a) dissolve CO2 crosses cell membrane
b) some remains dissolved, some becomes carbamino compound on hemoglobin
c) rest catalyzed by carbonic anhydrase -> H+ and HCO3-
d) H+ is buffered by hemoglobin, cannot rapidly diffuse across membrane
e) HCO3- diffuses out of cell and is exchanged for Cl- (chloride shift)
*not metabolic acid challenge
intracellular buffering
H+ enters cell and then either:
a) Cl- follows
b) Na+ or K+ leaves (could lead to hyperkalemia)
bone buffering
may lose calcium carbonate -> lose bone density
Renal System
compensation and correction of acid-base homeostasis
time course of buffering
ECF:
millisec- plasma and hemoglobin in rbc
10-30min- interstitial fluid compartment
ICF:
2-4hrs- intracellular buffering
several days- renal system
minutes-years- bone
buffer value
= d(HCO3-)/d(pH)
units = slykes (sl) or mmol/L per pH
ability of all boady buffer systems other than CO2-bicarbonate to buffer a change in [H+] caused by changes of PCO2 ie how effective can they turn CO2 into HCO3-
high value is preferred
-> can indicate relationships on pH-bicarb diagram
plasma (4sl) < ECF (11sl) < blood (25sl)
individual variation of buffer values
base excess
amount of strong acid to return blood to pH of 7.4
represent increase in bicarbonate cause by:
1) intracellular/bone buffering and renal compensation for chronic respiratory acidosis
2) metabolic alkalosis
3) administration of sodium bicarbonate
base defecit
amount of strong base to return blood to pH of 7.41)
represent decrease in bicarbonate cause by:
1)intracellular/bone buffering and renal compensation for chronic respiratory alkalosis
2) metabolic acidosis
metabolic acidosis
caused by
a) bicarbonate loss due to renal or diarrheal disease
b) bicarbonate loss due to buffering of metabolic acids (lactic acid and ketoacids increase H+ load)
c) gain of non-carbonic acid (“metabolic” or “non-volitle”)
d) inability to excrete H+ thus bicarbonate is consumed- renal disease
dx: < 22mM
compensation: hyperventilation PCO2, 35 mmHg
correction: increasing plasma HCO3-
a) administer NaHCO3 (dangerous)
b) kidney restores bicarbonate by excreting H+
ABG
arterial blood gases
pH 7.35-7.45
Pa(CO2) 35-45 mmHg
HCO3- 22-26mM
acid-base disorder
- respiratory and/or renal abnormality
- acid-base load exceeds capacity of these systems to handle it (ex: diarrhea)
respiratory acidosis
- abnormal PCO2 from hypoventilation
compensation: renal creation and retention of bicarbonate
correction: treating respiratory problem if possible
dx: PCO > 45 mm Hg, pH < 7.35, normal or above HCO3-
causes:
a) depressed ventilation (drug overdose)
b) obstructive lung disease (COPD and pulmonary fibrosis)
c) chest wall/ muscle disorders
d) pulmonary fibrosis
respiratory alkalosis
- abnormal PCO2 from hyperventilation
compensation: renal secretion of bicarbonate
correction: treating respiratory problem
dx: PCO2 < 35mm Hg, pH > 7.45, normal or below HCO3-
causes:
1) hypoxia -> hypoxic drive
2) pain/ anxiety -> psychogenic hyperventilation
3) dyspnea
4) mechanical overventilation
metabolic alkalosis
- loss of non-carbonic acid
- gain of bicarbonate
dx: >7.45pH and HCO3- > 26mM
compensation: hypoventilation (PCO2 > 45 mmHg)
causes:
a) GI loss of H+ due to vomiting bc pancreas secretes bicarbonate
b) hypokalemia (K+ leaves cell, H+ enters so ECF becomes alkaline)
c) contraction alkalosis (from diuretics -> loss of NaCl->H2O follows salt-> ECF volume decreases -> [HCO3-] increases
stages:
1) initiation
2) maintenance
compensation
physiologic adjustment when acid-base homeostasis is disturbed to restore pH
->PCO2 or bicarbonate will become abnormal bc pH is priority
correction
resolution or cure when acid-base homeostasis is disturbed to restore pH
plasma anion gap
= [Na+] - ([HCO3-] + [Cl-])
normal range is 8-16mM
