21.06.2013 Views

Ganong's Review of Medical Physiology, 23rd Edition

Ganong's Review of Medical Physiology, 23rd Edition

Ganong's Review of Medical Physiology, 23rd Edition

SHOW MORE
SHOW LESS

You also want an ePaper? Increase the reach of your titles

YUMPU automatically turns print PDFs into web optimized ePapers that Google loves.

686 SECTION VIII Renal <strong>Physiology</strong><br />

Additional graduations on the upper curved scale <strong>of</strong> the<br />

nomogram (Figure 40–7) are provided for measuring buffer<br />

base content; the point where the CO 2 calibration line <strong>of</strong> the<br />

arterial blood sample intersects this scale shows the mEq/L <strong>of</strong><br />

buffer base in the sample. The buffer base is equal to the total<br />

number <strong>of</strong> buffer anions (principally Prot – , HCO 3 – , and Hb – )<br />

that can accept hydrogen ions in the blood. The normal value<br />

in an individual with 15 g <strong>of</strong> hemoglobin per deciliter <strong>of</strong><br />

blood is 48 mEq/L.<br />

The point at which the CO 2 calibration line intersects the<br />

lower curved scale on the nomogram indicates the base<br />

excess. This value, which is positive in alkalosis and negative<br />

in acidosis, is the amount <strong>of</strong> acid or base that would restore 1<br />

L <strong>of</strong> blood to normal acid–base composition at a PCO 2 <strong>of</strong> 40<br />

mm Hg. It should be noted that a base deficiency cannot be<br />

completely corrected simply by calculating the difference<br />

between the normal standard bicarbonate (24 mEq/L) and the<br />

actual standard bicarbonate and administering this amount <strong>of</strong><br />

NaHCO 3 per liter <strong>of</strong> blood; some <strong>of</strong> the added HCO 3 – is converted<br />

to CO 2 and H 2 O, and the CO 2 is lost in the lungs. The<br />

actual amount that must be added is roughly 1.2 times the<br />

standard bicarbonate deficit, but the lower curved scale on the<br />

nomogram, which has been developed empirically by analyzing<br />

many blood samples, is more accurate.<br />

In treating acid–base disturbances, one must, <strong>of</strong> course, consider<br />

not only the blood but also all the body fluid compartments.<br />

The other fluid compartments have markedly different<br />

concentrations <strong>of</strong> buffers. It has been determined empirically<br />

that administration <strong>of</strong> an amount <strong>of</strong> acid (in alkalosis) or base<br />

(in acidosis) equal to 50% <strong>of</strong> the body weight in kilograms<br />

times the blood base excess per liter will correct the acid–base<br />

disturbance in the whole body. At least when the abnormality is<br />

severe, however, it is unwise to attempt such a large correction<br />

in a single step; instead, about half the indicated amount should<br />

be given and the arterial blood acid–base values determined<br />

again. The amount required for final correction can then be<br />

calculated and administered. It is also worth noting that, at least<br />

in lactic acidosis, NaHCO 3 decreases cardiac output and lowers<br />

blood pressure, so it should be used with caution.<br />

CHAPTER SUMMARY<br />

■ The cells <strong>of</strong> the proximal and distal tubules secrete hydrogen<br />

ions. Acidification also occurs in the collecting ducts. The reaction<br />

that is primarily responsible for H + secretion in the proximal<br />

tubules is Na + –H + exchange. Na is absorbed from the<br />

lumen <strong>of</strong> the tubule and H is excreted.<br />

■ The maximal H + gradient against which the transport mechanisms<br />

can secrete in humans corresponds to a urine pH <strong>of</strong> about<br />

4.5. However, three important reactions in the tubular fluid<br />

remove free H + , permitting more acid to be secreted. These are<br />

the reactions with HCO 3 – to form CO2 and H 2 O, with HPO 4 2–<br />

to form H 2 PO 4 – , and with NH3 to form NH 4 + .<br />

■ Carbonic anhydrase catalyzes the formation <strong>of</strong> H 2 CO 3 , and<br />

drugs that inhibit carbonic anhydrase depress secretion <strong>of</strong> acid<br />

by the proximal tubules.<br />

■ Renal acid secretion is altered by changes in the intracellular<br />

PCO 2, K + concentration, carbonic anhydrase level, and adrenocortical<br />

hormone concentration.<br />

MULTIPLE-CHOICE QUESTIONS<br />

For all questions, select the single best answer unless otherwise directed.<br />

1. Which <strong>of</strong> the following is the principal buffer in interstitial fluid?<br />

A) hemoglobin<br />

B) other proteins<br />

C) carbonic acid<br />

D) H 2 PO 4<br />

E) compounds containing histidine<br />

2. Increasing alveolar ventilation increases the blood pH because<br />

A) it activates neural mechanisms that remove acid from the<br />

blood.<br />

B) it makes hemoglobin a stronger acid.<br />

C) it increases the PO 2 <strong>of</strong> the blood.<br />

D) it decreases the PCO 2 in the alveoli.<br />

E) the increased muscle work <strong>of</strong> increased breathing generates<br />

more CO 2.<br />

3. In uncompensated metabolic alkalosis<br />

A) the plasma pH, the plasma HCO 3 – concentration, and the<br />

arterial PCO 2 are all low.<br />

B) the plasma pH is high and the plasma HCO 3 – concentration<br />

and arterial PCO 2 are low.<br />

C) the plasma pH and the plasma HCO 3 – concentration are low<br />

and the arterial PCO 2 is normal.<br />

D) the plasma pH and the plasma HCO 3 – concentration are<br />

high and the arterial PCO 2 is normal.<br />

E) the plasma pH is low, the plasma HCO 3 – concentration is<br />

high, and the arterial PCO 2 is normal.<br />

4. In a patient with a plasma pH <strong>of</strong> 7.10, the [HCO 3 – ]/[H2 CO 3 ]<br />

ratio in plasma is<br />

A) 20.<br />

B) 10.<br />

C) 2.<br />

D) 1.<br />

E) 0.1.<br />

CHAPTER RESOURCES<br />

Adrogué HJ, Madius NE: Management <strong>of</strong> life-threatening acid–base<br />

disorders. N Engl J Med 1998;338:26.<br />

Brenner BM, Rector FC Jr. (editors): The Kidney, 6th ed. 2 vols.<br />

Saunders, 1999.<br />

Davenport HW: The ABC <strong>of</strong> Acid–Base Chemistry, 6th ed. University<br />

<strong>of</strong> Chicago Press, 1974.<br />

Halperin ML: Fluid, Electrolyte, and Acid–Base <strong>Physiology</strong>, 3rd ed.<br />

Saunders, 1998.<br />

Lemann J Jr., Bushinsky DA, Hamm LL: Bone buffering <strong>of</strong> acid and<br />

base in humans. Am J Physiol Renal Physiol 2003;285:F811.<br />

<strong>Review</strong>.<br />

Vize PD, Wolff AS, Bard JBL (editors): The Kidney: From Normal<br />

Development to Congenital Disease. Academic Press, 2003.

Hooray! Your file is uploaded and ready to be published.

Saved successfully!

Ooh no, something went wrong!