Acid-Base Balance Flashcards
Buffer
combination of a weak acid or weak base and its salt
resists pH changes
Acidosis
pH < 7.35
describes the process that leads to an decreased blood pH
Acidemia
describes the state of low blood pH
compensation vs correction
compensation, a metabolic or respiratory change outside of the normal range to compensate for acidosis or alkalosis
correction is intervening action to return the blood pH to the proper range
Oxidative Metabolism
uses O2 at the mitochondrial level to metabolize nutrients and turn them into ATP & waste products
normal blood range pH
7.34- 7.44
If H+ was not regulated the acid environment would damage:
metabolic processes
alter consciousness
increase neuromuscular irritability
coma, death
Buffer systems (4)
bicarbonate-carbonic acid buffer
hemoglobin buffer system
proteins as buffers of H+ (usually only in cells)
phophate buffer - only for the kidneys
Major organs involved in acid-base maintenance
Kidney & Lungs
Bicarb-Carbonic Acid Buffer general characteristics
h2co3 dissociates into co2 & h20 allowing co2 to be eliminated by lungs & H+ to leave as water through the kidneys
correction to bicarb-carbonic acid system
changes in co2 modify the ventilation rate of the lungs
compensation of bicarb-carbonic acid system
hco3- concentration can be altered by the kidneys
this system also binds H+ when it appears
Bicarbonate- carbonic acid buffer system equation
co2 + h2o h2co3 H+ + hco3-
reaction is reversible
formula to calculate carbonic acid
pCO2 x 0.0307
tCO2 component
carbonic acid + bicarbonate (90%)
carbonic acid molecular formula
H2CO3
bicarbonate ion molecular formula
HCO3-
pH calculation
pKa + log salt/acid pKa - always use 6.1 during these calculations acid- carbonic acid salt - bicarbonate normal ratio is around 20/1
pCO2 range interpretation
respiratory associated
range 35-45 mmHg
lower than range = alkaline
higher than range = acidosis
tCO2 range interpretation
metabolic associated
range 23-29 mmol/L
lower than range = acidosis (loss of bicarb ion)
higher than range = alkaline (increase of bicarb ion)
Lung involvement
exhale co2, inhale o2
1st line of defense for acid-base disorders
quick effect on acid-base
Kidney involvement
reclaims hco3-
produces more hco3- if needed & takes several days to correct a hco3- deficiency
long term compensation
factors affecting increased levels hco3-
when hco3- is increased we excrete hco3-
retain it when compensating lung disease & when cl- loss exceeds what is needed for electrical neutrality
factors affecting decreased levels of hco3-
diuretics
reduced absorption when there is loss of cations
when kidney is not functioning (nephritis, infections)
Acid-base disorders
respiratory acidosis
respiratory alkalosis
metabolic acidosis
metabolic alkalosis
metabolic acidosis (non respiratory )
decreased hco3- ( bicarb ion)
increase in acids= ketoacidosis
decrease in acid excretion= renal tubular acidosis, diarrhea, loss of bicarb ion
respiratory acidosis
increased pCO2 ( increase in carbonic acid bc lungs cant get rid of co2) COPD: chronic obstructive pulmonary disease, hypoventilation CHF
most common causes of metabolic acidosis
ketoacidosis, shock, severe diarrhea, impaired kidney function
metabolic alkalosis
increased hco3- (bicarb ion)
ingestion of bicarb producing salts
disease: diuretic therapy, vomiting, nasogastric suction
respiratory alkalosis
decreased pCO2
more common
missing H+
hypoxia from drugs like salicylates or increased temp due to fever, hysteria, pulmonary embolism, pulmonary fibrosis
breathing into paper bag to correct - increase lvl of carbonic acid by breathing co2 rich air
Oxygen transport
transported by hemoglobin
sigmoidal curve due to affinity of o2 & hem
after 1 o2 attaches, the affinity for other o2 is increased & same in the reverse
see release of o2 when po2 is 60 mmHg or less
oxygen at lung level is influenced by :
alveolar destruction pulmonary edema airway blockages inadequate blood supply rate of diffusion of co2 from blood & diffusion rate of o2 out of lung
oxygen transport in hemoglobin is influenced by :
[co] pH temp of blood [pco2] 2,3 DPG in RBC presence of non-functioning hemoglobin
left shift in o2 saturation curve
^ o2 saturation & v pco2
^ pH ( v H+), v 2,3 DPG, v temp
right shift in o2 saturation curve
v o2 saturation % ^pco2
^ pH (^H+), ^ 2,3 DPG, ^ temp
if a sample is not on ice what will be increased?
pCO2
if a sample is correctly & anaerobically collected but is not processed immediately what will be abnormal?
incrased p02 from the leching of hemoglobin
low end of pco2
respiratory alkaline
loss of carbonic acid
v h2co3
high end of pco2
respiratory acidosis
increase carbonic acid
^ h2co3
low end of tco2
metabolic acidosis
loss of bicarb ion
v hco3-
high end of tco2
metabolic alkalosis
increase of bicarb ion
^ hco3-
Measurements of blood gases
pH potentiometric
pCO2: modified pH electrode thatm easures dissolved co2
pO2: amperometrical electrode
Errors in electrode measurements
protein build up on the ISE membrane **
bacterial contamination of inner electrode solutions
incorrect calibration of the ISE
Calibration of blood gas analyzers
always 37 C temp
2 different pH buffer solutions to calibrate
2 gas mixtures to calibrate pCO2 & pO2
Specimens for blood gases
collected in heparin* placed on ice* collected anaerobically* processed immediately ** otherwise metabolism will continute to occur in the tube & will generate additional H+ & p02
