Introduction to Acid-Base Physiology
I. Definitions
A. Acid - can donate a hydrogen ion
B. Base - can accept a hydrogen ion
C. Strong acid - completely or almost completely dissociates into a hydrogen ion and its conjugate base in aqueous solution; a weak acid is only slightly ionized in aqueous solution. A strong acid usually has a weak conjugate base and a weak acid usually has a strong conjugate base. Do not confuse the strength of an acid or base with its concentration.
D. Buffer - mixture of substances in aqueous solution, usually a combination of a weak acid and its conjugate base, that can resist changes in [H+] when strong acids or bases are added.
II. Quantification of Acidity
A. pH = -log [H+]
B. pH of 7.10 is [H+] of 80 nM/L
C. pH of 7.30 is [H+] of 50 nM/L
pH of 7.40 is [H+] of 40 nM/L
pH of 7.50 is [H+] of 32 nM/L
pH of 7.70 is [H+] of 20 nM/L
D. Note that as [H+] increases, pH decreases. An increase of 0.3 pH units indicates that [H+] is cut in half; a decrease of 0.3 pH units indicates that [H+] is doubled.
E. By convention:
1. Arterial pH< 7.35 is acidemia
2. Arterial pH >7.45 is alkalemia
3. Acidosis and alkalosis are underlying disorders
III. Sources of Acids in the Body
A. CO2 + H2O 
H2CO3 ( a volatile acid)
Lungs remove about 15,000 - 25,000 mmol of carbon dioxide per day.
B. Fixed acids produced as a result of metabolism. About 70 mEq of H+'s is removed mainly by the kidneys (a minor portion is removed by the G.I. tract) each day. Fixed acids normally represent only about 0.2% of the total body acid production. May be much higher - e.g. in diabetic ketoacidosis.
IV. Buffer systems of the human body - Isohydric principle - all buffer pairs in a homogenous solution are in equilibrium with the same hydrogen ions.
A. Bicarbonate:
1. Open system: CO2 removed in lungs
2. CO2 dissolved in plasma (in mM/L) is equal to 0.03 x Pco2
3. CO2 + H2O H2CO3; but in equilibrium, so both dissolved CO2 and H2CO3 are considered part of [HA].
The ratio of dissolved CO2 to carbonic acid is about 1,000 to 1.
4. Note that "total CO2" = dissolved CO2 + H2CO3 + HCO-3
5. Henderson-Hasselbalch equation:
pH = pK' + log 
But the H2CO-3 is negligible,
so:pH = pK' + log
The pK' of this system at physiological pH's and at 38°C is 6.1.
Therefore, at pHa of 7.40 and PaCO2 of 40 torr:
7.40 = 6.1 + log 
6. The [HCO-3] is therefore normally about 24 mM/L because the log of 20 is about 1.3.
7. The buffer value of plasma in the presence of Hb is 4-5 times that of plasma separated from erythrocytes. (Buffer value = H+'s in mEq/L that can be added to or removed from a solution with a resultant change of one pH unit).
B. Phosphate:
; pK is about 6.8. Other organic phosphates have pK's near 7.0: Glucose - 1-P, ATP,
etc.
C. Proteins
Imidazole groups of histidine residues have pK's ranging from 5.5 to 8.5
1. Main protein: Hb. DeoxyHb is a weaker acid than is oxyHb. This allows CO2 loading in the tissues as deoxyHb can accept H+'s from the dissociation of H2CO3 and from carbamino compounds (see Levitzky, Chapter 7); and unloading in the lungs.
2. Other plasma proteins may also act as buffers.
D. Buffers of the interstitial fluid:
1. Mainly bicarbonate; some phosphate.
2. Note that the volume of interstitial fluid is much larger than that of the plasma, so the ISF may play an important role in buffering.
E. Bone:
Much calcium and phosphate in bone. Chronic acidosis may lead to bone demineralization.
F. Intracellular buffering: Intracellular proteins and organic phosphates. Note that Hb is an intracellular buffer.
V. Acidosis and Alkalosis: use of the Davenport Diagram (Levitzky Fig. 8-1)
A. Respiratory acidosis:
pHa
Causes: Impairment of 
A (Levitzky Table 8-1)
B. Respiratory Alkalosis:
pHa
Causes: Hyperventilation (Levitzky Table 8-2)
C. Metabolic Acidosis
pHa
Causes: ingestion, infusion or production of fixed acids; decreased renal H+excretion; loss of HCO-3 etc. e.g. diarrhea, diabetic ketoacidosis, lactic acidosis (Levitzky Table 8-3)
D. Metabolic Alkalosis
pHa
Causes: Loss of fixed acids; ingestion, infusion, or excessive reabsorption of bases. e.g. vomiting; excess antacids (Levitzky Table 8-4)
VI. Compensatory Mechanisms
A. Respiratory: H+'s stimulate arterial chemoreceptors; compensation takes minutes
B. Renal: excretion of fixed acids; reabsorption of base; compensation takes hours or days. Mechanisms:
1. Secretion of H+ by tubular cells into lumen (inverse relationship with K+secretion) and reabsorption of filtered HCO-3. 90% of all HCO-3 is "reabsorbed" either directly or by carbonic acid dissociation in the proximal tubule.
2. Phosphate
3. Ammonia
4. In alkalosis the kidney decreases H+ secretion and decreases HCO-3 reabsorption. Kidney tends to reabsorb almost all filtered HCO-3 until [HCO-3]p reaches about 27-28 mEq/L.
C. Summary of Acid-Base Disorders (Levitzky Table 8-5):
pHa = a constant +
VII. Base excess (or Deficit): The number of mEq of acid or base needed to titrate one liter of blood to a pHa of 7.40 at 37°C, if the Paco2 were held constant at 40 torr.
VIII. Anion gap = [Na+] - ([Cl-] + [HCO-3]); should be 12+ 4 mEq/L High anion gap (>16 mEq/L ) in metabolic acidosis suggests presence of anions that are not usually measured. Causes of high Anion Gap: (Levitzky Table 8-6)
IX. Disorders that can cause of tissue hypoxia (Levitzky Table 8-7)
Copyright 2000 M. G. LEVITZKY
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