NORMAL ACID–BASE HOMEOSTASIS

through three

main processes: (1) “reabsorption” of filtered HCO3

The kidneys regulate plasma HCO3

(2) formation of titratable acid, and (3) excretion of

NH4

Systemic arterial pH is maintained between 7.35 and

7.45 by extracellular and intracellular chemical buffering

together with respiratory and renal regulatory mechanisms.

The control of arterial CO2 tension (PaCO2

in the urine. The kidney filters ~4000 mmol of

HCO3

the renal tubules must therefore secrete 4000 mmol of

hydrogen ions. Between 80 and 90% of HCO3

per day.To reabsorb the filtered load of HCO3

) by

the central nervous system (CNS) and respiratory system

and the control

of the plasma bicarbonate by

the

kidneys
stabilize the arterial

pH by

excretion

or retention

of acid or alkali.

The metabolic and respiratory

components that regulate systemic pH are described by

the Henderson-Hasselbalch equation:

is reabsorbed

in the proximal

tubule.

The distal nephron reabsorbs

the remainder

and secretes

protons,

as generated

from metabolism, to defend systemic pH. Although this

quantity of protons, 40–60 mmol/d, is small, it must be

secreted to prevent chronic positive H

balance and

metabolic acidosis. This quantity of secreted protons is

represented in the urine as titratable acid and NH4

HCO3

pH = 6.1 + log

Metabolic acidosis in the face of normal renal function

increases NH4

PaCO2

× 0.0301

production and excretion. NH4

Under most circumstances, CO2 production and excretion

are

matched,

and the usual steady-state PaCO2

production

and excretion

are

impaired

in chronic

renal

failure,

hyperkalemia, and renal tubular acidosis.

In sum, these regulatory responses, including chemical

buffering, the regulation of PaCO2

is maintained

at 40 mmHg.

Underexcretion of CO2 produces

hypercapnia, and overexcretion causes hypocapnia. Nevertheless,

production and excretion are again matched at a

new steady-state PaCO2

by the respiratory system,

and the regulation of HCO3

−
is regulated

primarily by neural respiratory factors (Chap. 22) and is

not subject to regulation by the rate of CO2 production.

Hypercapnia is usually the result of hypoventilation rather

than of increased CO2 production. Increases or decreases

in PaCO2

. Therefore, the PaCO2

by the kidneys, act in concert

to maintain a systemic arterial pH between 7.35 and 7.45.

DIAGNOSIS OF GENERAL TYPES

OF DISTURBANCES

represent derangements of neural respiratory

control or are caused by compensatory changes in

The most common clinical disturbances are simple

response to a primary alteration in the plasma [HCO3

acid–base disorders (i.e., metabolic acidosis or alkalosis

].

410

411

TABLE 40-1

PREDICTION OF COMPENSATORY RESPONSES ON SIMPLE ACID–BASE

DISTURBANCES AND PATTERN OF CHANGES

Acidosis and Alkalosis

CHAPTER 40

RANGE OF VALUES

DISORDER

PREDICTION OF COMPENSATION

pH
HCO3

PaCO

Metabolic PaCO

= (1.5 × HCO3

)+8±2

Low

Low

Low

acidosis

or

will ↓ 1.25 mmHg per

PaCO

mmol/L ↓ in HCO3

or

PaCO

= HCO3

+ 15

Metabolic PaCO

will ↑ 0.75 mmHg per

High
High

High

alkalosis

mmol/L ↑ in HCO3

or

will ↑ 6 mmHg per

PaCO

10 mmol/L ↑ in HCO3

or

PaCO

= HCO3

+ 15

Respiratory High

Low

Low

alkalosis

Acute

HCO3

will ↓ 0.2 mmol/L

per mmHg ↓ in PaCO

Chronic

−
HCO3

will ↓ 0.4 mmol/L

per mmHg ↓ in PaCO

Respiratory Low

High

High

acidosis

Acute

HCO3

will ↑ 0.1 mmol/L

per mmHg ↑ in PaCO

Chronic

HCO3

will ↑ 0.4 mmol/L

per mmHg ↑ in PaCO

or respiratory acidosis or alkalosis). Because compensation

is not complete, the pH is abnormal in simple disturbances.

More complicated clinical situations can give

rise to mixed acid–base disturbances.

respiratory compensation expected in a simple form of

metabolic acidosis can be predicted from the relationship:

PaCO2

= (1.5 × HCO3

−
) + 8 ± 2, i.e., the PaCO2

is expected

to decrease 1.25 mmHg for each mmol per liter decrease

in HCO3

. Thus, a patient with metabolic acidosis and

HCO3

SIMPLE ACID–BASE DISORDERS

of 12 mmol/L would be expected to have a PaCO2

Primary respiratory disturbances (primary changes in

PaCO2

) invoke compensatory metabolic responses (secondary

changes in HCO3

between 24 and 28 mmHg. Values for PaCO2

<24 or >28

mmHg define a mixed disturbance (metabolic acidosis and

respiratory alkalosis or metabolic alkalosis and respiratory

acidosis, respectively). Another way to judge the appropriateness

of the response

in HCO3

), and primary metabolic disturbances

elicit predictable

compensatory

respiratory

responses.

Physiologic compensation can be predicted

from the relationships displayed in Table 40-1. Metabolic

acidosis caused by

an increase

in endogenous

acids

(e.g.,

ketoacidosis) lowers extracellular fluid (ECF)

HCO3

is to use an

acid–base nomogram (Fig. 40-1). Although the shaded

areas of the nomogram show the 95% confidence limits

for normal compensation in simple disturbances, finding

acid–base values within the shaded area does not necessarily

rule

out a mixed

disturbance.

Imposition of one

disorder over another may result in values lying within

the area of a third.Thus, the nomogram, although conve-

or PaCO2

and decreases extracellular pH. This stimulates

the medullary chemoreceptors to increase ventilation

and to return the ratio of HCO3

to PaCO2

, and thus pH,

toward normal, although not to normal. The degree of

nient, is not a substitute for the equations in Table 40-1.