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Acid-base balance (concept definition)
The process of regulating the pH, bicarbonate concentration, and partial pressure of carbon dioxide of body fluids.
Acid
A substance that releases hydrogen ions (H+).
Base
A substance that takes up hydrogen ions (H+). The most important base in the body is bicarbonate (HCO3−).
pH (meaning)
A measure of a solution's acidity. Low pH = acidic (high H+); high pH = basic/alkaline (low H+).
pH (technical definition)
The negative logarithm of the H+ concentration. Scale runs 1-14; 7 is neutral.
Three processes of acid-base balance
Acid production (or intake), acid buffering, and acid excretion.
Acid intake
Entry into the body of acids or acid precursors (substances the body converts to acid).
Acid buffering
The process by which body fluids resist large pH changes when acids or bases are added or removed.
Acid excretion
Removal of acid from the body (lungs for carbonic acid, kidneys for metabolic acid).
Acidemia vs. alkalemia
Acidemia: blood pH below normal (acidotic), even if still above 7.0. Alkalemia: blood pH above normal (alkalotic).
Two main categories of acid-base imbalance and their subtypes
Acidosis (too much acid) and alkalosis (too little acid); each is either respiratory or metabolic.
Normal arterial blood pH (adult)
7.35-7.45 (slightly alkaline). Lower range in neonates and infants.
Normal PaCO2 (adult)
35-45 mm Hg (4.7-6.0 kPa). Lower in infants.
Normal serum HCO3− (adult)
22-26 mEq/L (22-26 mmol/L). Lower in infants.
Normal base excess
−2 to +2 mmol/L
Bicarbonate-to-carbonic acid ratio for normal pH
20:1
Two kinds of acid made by cellular metabolism
Carbonic acid (H2CO3) and metabolic acids.
Effect of increased cellular metabolism on acid
More carbonic and metabolic acids are produced.
Carbonic acid equation
CO2 + H2O ⇌ H2CO3 ⇌ HCO3− + H+
Carbonic anhydrase
Enzyme in red blood cells and other cells that converts CO2 + H2O to carbonic acid and back, depending on location.
What happens to carbonic acid in the lungs?
CO2 diffuses into the alveoli; carbonic anhydrase converts H2CO3 back to CO2 and H2O, which are exhaled.
Weak acid
An acid that only partially dissociates into H+ and its anion in solution (e.g., carbonic acid, metabolic acids).
Metabolic acid
General term for all acids except carbonic acid; symbol HA (A = anion). Examples: citric, pyruvic, lactic acid.
Example of an abnormal metabolic acid
Ketoacids such as β-hydroxybutyric acid, produced when metabolism is disrupted or incomplete.
Buffer
A pair of chemicals (a weak acid and its base) in equilibrium that take up or release H+ to keep pH normal.
Most important ECF buffer system
Bicarbonate buffer system: carbonic acid (weak acid) + bicarbonate (its base).
How bicarbonate buffers metabolic acid
HCO3− combines with H+ from metabolic acid to form carbonic acid: H+ + HCO3− ⇌ H2CO3. The lungs then exhale the carbonic acid as CO2 and water.
Can bicarbonate buffer carbonic acid?
No. Carbonic acid is part of the buffer itself; bicarbonate mainly buffers metabolic acid.
Too much metabolic acid → plasma HCO3−?
Decreases below normal, because bicarbonate is used up in buffering.
Too little metabolic acid → plasma HCO3−?
Increases above normal, because carbonic acid releases H+ and forms more bicarbonate.
Plasma HCO3− is an indicator of...
Metabolic acid status in the blood.
Organ that excretes carbonic acid
The lungs (as CO2 and H2O). They cannot excrete metabolic acid because it can't become a gas.
Organ that excretes metabolic acid
The kidneys. They cannot excrete carbonic acid.
Hyperventilation vs. hypoventilation
Hyperventilation (↑ rate and depth) excretes more carbonic acid; hypoventilation (↓ rate and depth) excretes less.
Chemoreceptors
Sense blood CO2, H+, and sometimes O2, and adjust respiratory rate and depth.
Correction
Fixing the problem so blood values return to normal (e.g., lungs adjusting for a carbonic acid problem).
Compensation
Moving pH toward normal by making other blood values abnormal (e.g., hyperventilating to offset excess metabolic acid).
Respiratory response to too much metabolic acid
Chemoreceptors trigger hyperventilation (compensation); this lowers carbonic acid but does not remove metabolic acid.
Respiratory response to too little metabolic acid
Hypoventilation (compensation), letting carbonic acid build up to balance the deficit.
How the proximal tubules excrete metabolic acid
They secrete H+ from blood into tubular fluid while moving HCO3− back into the blood; A− also enters tubular fluid.
Titratable acid
Secreted H+ in urine that is buffered, mostly by phosphate buffers filtered at the glomerulus.
Role of ammonia (NH3) in acid excretion
Distal tubular cells make NH3; it binds H+ to form ammonium (NH4+), which is excreted in urine and doesn't affect pH.
Kidney response to too much metabolic acid (correction)
Increase H+ secretion and make more NH3, removing acid and raising blood HCO3−.
Kidney response to too little metabolic acid (correction)
Decrease H+ secretion and make less NH3; more HCO3− is excreted in urine.
Kidney response to too much carbonic acid (compensation)
Excrete more metabolic acid than usual (↑ H+ secretion, ↑ NH3), leaving too little metabolic acid to offset the excess.
Kidney response to too little carbonic acid (compensation)
Secrete less H+ and make less NH3, so metabolic acid rises to offset the deficit.
Respiratory acidosis
Too much carbonic acid; shown by elevated PaCO2.
Metabolic acidosis
Too much metabolic acid (or loss of bicarbonate); shown by decreased HCO3−.
Respiratory alkalosis
Too little carbonic acid; shown by decreased PaCO2.
Metabolic alkalosis
Too little metabolic acid (or excess bicarbonate); shown by increased HCO3−.
Respiratory acidosis: cause and correction (Table 7.1)
Cause: hypoventilation. Correction: hyperventilation. Renal compensation: ↑ H+ secretion, ↑ NH3.
Respiratory alkalosis: cause and correction (Table 7.1)
Cause: hyperventilation. Correction: hypoventilation. Renal compensation: ↓ H+ secretion, ↓ NH3.
Metabolic acidosis: cause and correction (Table 7.1)
Cause: more metabolic acid than kidneys can excrete. Correction: ↑ renal H+ secretion, ↑ NH3. Respiratory compensation: hyperventilation.
Metabolic alkalosis: cause and correction (Table 7.1)
Cause: more bicarbonate than kidneys can excrete. Correction: ↓ renal H+ secretion, ↓ NH3. Respiratory compensation: hypoventilation.
Three levels of compensation
Uncompensated, partially compensated, fully compensated.
How long does renal compensation take?
Several days to become clinically significant, so a short-lived respiratory imbalance won't be compensated.
How fast does respiratory compensation start?
Within a few minutes, so metabolic imbalances usually show some compensation.
Why is metabolic alkalosis rarely fully compensated?
Compensatory hypoventilation is limited by the respiratory drive for oxygen.
Do compensatory mechanisms always normalize pH?
No, but they keep the pH from becoming more abnormal.
Compensatory respiratory acidosis develops with...
Primary metabolic alkalosis.
Compensatory respiratory alkalosis develops with...
Primary metabolic acidosis.
Compensatory metabolic acidosis develops with...
Primary respiratory alkalosis lasting at least several days.
Compensatory metabolic alkalosis develops with...
Primary respiratory acidosis lasting at least several days.
Which imbalances cause more neurologic signs: respiratory or metabolic?
Respiratory, because CO2 crosses the blood-brain barrier easily and quickly changes CSF pH. Metabolic acid and HCO3− cross slowly.
Effect of acidosis on LOC
Decreased level of consciousness.
Effect of alkalosis on LOC
Initial excitation, followed by decreased LOC if severe.
Cardiac effect of acid-base imbalance
Cardiac dysrhythmias (from cell dysfunction and associated potassium imbalances).
Respiratory acidosis signs
Headache, decreased LOC, hypoventilation (the cause), dysrhythmias, hypotension if severe.
Metabolic acidosis signs
Decreased LOC, hyperventilation (compensation), abdominal pain, nausea and vomiting, dysrhythmias.
Respiratory alkalosis signs
Excitation, belligerence, lightheadedness, unusual behavior, then decreased LOC if severe; perioral and digital paresthesias, carpopedal spasm, tetany, diaphoresis, hyperventilation (the cause), dysrhythmias.
Metabolic alkalosis signs
Excitation then decreased LOC if severe, perioral and digital paresthesias, carpopedal spasm, hypoventilation (compensation), signs of volume depletion or hypokalemia if present.
Why do acid-base signs often go unnoticed?
They are nonspecific and usually overshadowed by the underlying condition unless the imbalance is severe.
Definitive diagnostic test for acid-base balance
Arterial blood gas (ABG). Venous blood gas is sometimes used instead.
ABG values used for acid-base status
pH, PaCO2, HCO3−, and base excess. (PaO2 and SaO2 measure oxygenation.)
PaCO2 indicates...
How well the lungs are excreting carbonic acid.
Increased PaCO2 means...
Too much carbonic acid from primary or compensatory hypoventilation.
Decreased PaCO2 means...
Too little carbonic acid from primary or compensatory hyperventilation.
HCO3− indicates...
How well the kidneys are excreting metabolic acid.
Increased vs. decreased HCO3−
Increased = too little metabolic acid. Decreased = too much metabolic acid.
Base excess indicates...
How well buffers are managing metabolic acid. Below −2 = too much metabolic acid; above +2 = too little.
Anion gap and osmolal gap
Calculated values used to help identify the specific cause of metabolic acidosis.
ABG pattern: respiratory acidosis
pH ↓ (or low-normal if fully compensated), PaCO2 ↑, HCO3− ↑ if compensating.
ABG pattern: metabolic acidosis
pH ↓ (or low-normal if fully compensated), HCO3− ↓, PaCO2 ↓ from compensation.
ABG pattern: respiratory alkalosis
pH ↑, PaCO2 ↓, HCO3− ↓ if compensating.
ABG pattern: metabolic alkalosis
pH ↑, HCO3− ↑, PaCO2 ↑ from compensation.
Practice: pH 7.20, PaCO2 21, HCO3− 8
Metabolic acidosis with partial respiratory compensation (Kevin's DKA case).
Four individual risk factors for acid-base imbalance
Excess production or intake of metabolic acid; altered buffering from loss or gain of HCO3−; altered acid excretion; abnormal shift of H+ into cells.
Causes of respiratory acidosis
Alveolar hypoventilation (type B COPD, end-stage emphysema, severe asthma, pneumonia, pulmonary edema), ineffective respiratory pump (Guillain-Barré), central suppression (opioid overdose).
Causes of metabolic acidosis
Excess acid (DKA, starvation or alcohol ketoacidosis, lactic acidosis, thyroid storm), decreased excretion (oliguria), HCO3− loss (prolonged diarrhea, intestinal/pancreatic fistula).
Causes of respiratory alkalosis
Hyperventilation from acute hypoxia, acute pain, anxiety or emotional distress, or central stimulation (head injury, meningitis).
Causes of metabolic alkalosis
Base gain (NaHCO3 intake/infusion, massive transfusion, diuretics/contraction alkalosis) or excess acid loss (repeated vomiting, mineralocorticoid excess).
Diabetic ketoacidosis (DKA)
Metabolic acidosis in which lack of insulin causes ketoacids to be made faster than the kidneys can excrete them; most common in type 1 diabetes.
Social determinants that raise DKA risk
Economic instability and food insecurity, which can lead to insulin rationing or poor food intake.
Acid or acid-precursor ingestions that cause metabolic acidosis
Boric acid (ant poison), methanol, hand sanitizer (isopropanol, possibly methanol), antifreeze.
Why is decreased acid production not a risk factor?
Cells cannot stop producing metabolic acid.
Prolonged diarrhea causes...
Metabolic acidosis (loss of bicarbonate).
Repeated vomiting causes...
Metabolic alkalosis (loss of hydrochloric acid plus renal bicarbonate retention).
Baking soda as an antacid can cause...
Metabolic alkalosis (bicarbonate gain).
Hypokalemia and acid-base
K+ leaves cells and H+ enters cells to balance charge, leaving too little acid in the blood: metabolic alkalosis.
Large rapid infusion of IV isotonic saline can cause...
Metabolic acidosis, partly from dilution of bicarbonate.