Page 196 - Cardiac Nursing

LWBK340-c07_p153-176.qxd 6/29/09 10:14 PM Page 172 Aptara Inc.

172 PA R T II / Physiologic and Pathologic Responses

Table 7-22 ■ MIXED ACID–BASE IMBALANCES
Concurrent Primary
Acid–Base Imbalances Effect on pH Clinical Examples Blood Gas Values
Respiratory acidosis plus Opposing effect on pH Person with type B COPD (chronic bronchitis) pH possibly near normal
metabolic alkalosis develops repeated emesis Pa CO2 increased
–
HCO 3 increased
Respiratory alkalosis plus Opposing effect on pH Person with encephalitis develops circulatory shock pH possibly near normal
metabolic acidosis Pa CO2 decreased
–
HCO 3 decreased
Metabolic acidosis plus Opposing effect on pH Person with chronic renal failure develops Vary, depending on severity and
metabolic alkalosis repeated emesis duration of imbalances
Respiratory acidosis and Same effect on pH Person with type B COPD (chronic bronchitis) pH greatly decreased
metabolic acidosis develops prolonged diarrhea Pa CO2 increased
–
HCO 3 decreased
Two different types of Same effect on pH Person with diabetic ketoacidosis becomes pH greatly decreased
metabolic acidosis dehydrated and develops lactic acidosis from Pa CO2 likely decreased (compensation)
–
poor tissue perfusion HCO 3 greatly decreased
Metabolic alkalosis and Same effect on pH Person who received massive blood transfusion pH greatly increased
respiratory alkalosis hyperventilates from pain and fear Pa CO2 decreased
–
HCO 3 increased

A basic understanding of acid–base imbalances facilitates dif- types of coexisting alkalosis) can create a pH that rapidly ap-
ferentiating between primary and compensatory respiratory im- proaches the fatal limit. Examples of mixed acid–base imbalances
balances. If the individual has primary respiratory acidosis, then the are presented in Table 7-22.
pH would be expected to be below 7.40. A compensatory respira-
tory acidosis would occur in response to a metabolic alkalosis, so
the pH would be above 7.40. SUMMARY OF ACID-BASE
The third laboratory value to consider is the bicarbonate ion
concentration. 171 If it is above the normal range, the individual Cellular metabolism generates carbonic acid, which the lungs
has metabolic alkalosis, which may be the primary problem or excrete, and metabolic acids, which the kidneys excrete. Respiratory
may be compensatory. If the bicarbonate ion concentration is be- acid–base imbalances are disorders of too much or too little car-
low the normal range, then the individual has primary or com- bonic acid (carbon dioxide and water). Their laboratory marker is
pensatory metabolic acidosis. A bicarbonate ion concentration an altered Pa CO2 . The body compensates for an ongoing respira-
within the normal range indicates no metabolic acid–base disor- tory acid–base disorder by excreting more or fewer metabolic
der. The differentiation between primary and compensatory im- acids in the urine to normalize the pH.
balances is made by considering the pH. An individual who has a Metabolic acid–base imbalances are disorders of too many or
primary metabolic acidosis would be expected to have a pH below too few metabolic acids. Their laboratory marker is an altered
7.40. A compensatory metabolic acidosis would be a response to a bicarbonate ion concentration. The body compensates for meta-
primary respiratory alkalosis, so the pH would be above 7.40. Fol- bolic acid–base disorders by adjusting alveolar ventilation to ex-
lowing similar logic, with a primary metabolic alkalosis, the pH crete more or less carbonic acid to normalize the pH. In addi-
would be above 7.40; with a compensatory metabolic alkalosis, the tion to their other effects, acid–base imbalances alter cardiac
pH would be below that value. contractility and may cause cardiac arrhythmias. They influence
Once the three values have been examined, the final step in in- the degree of vasoconstriction in various vascular beds. Thus, an
terpreting arterial blood gas values is to compare the interpreta- understanding of acid–base balance and imbalances is important
tion with the individual’s history and condition to verify that it in the care of people who have heart failure and other cardiovas-
makes sense. The principles of laboratory value interpretation pre- cular pathophysiologies.
sented in this section apply to people who have only one primary
acid–base imbalance. Mixed acid–base imbalances (more than one REFE R E NC ES
concurrent primary imbalance) are presented briefly in the next
section. 1. Felver, L. (2010). Fluid and electrolyte homeostasis and imbalances. In
L. Copstead & J. Banasik (Eds.), Pathophysiology (4th ed.) (pp. 592–614).
St Louis: Elsevier Saunders.
Mixed Acid–Base Imbalances 2. Blackburn, S. (2003). Maternal, fetal and neonatal physiology. Philadel-
phia: WB Saunders.
Occasionally, an individual may have more than one primary 3. Rose, B. (2009). Clinical physiology of acid-base and electrolyte disorders.
acid–base imbalance at the same time. In this circumstance, coex- New York: McGraw-Hill.
isting primary acidosis and alkalosis may somewhat neutralize 4. Johnson, A. K. (2007). The sensory psychobiology of thirst and salt ap-
petite. Medicine and Science in Sports and Exercise, 39, 1388–1400.
each other so that the pH is near normal while the Pa CO2 and bi- 5. Selektor, Y., & Weber, K. T. (2008). The salt-avid state of congestive
carbonate ion concentration are grossly abnormal. Alternatively, heart failure revisited. American Journal of Medical Science, 335,
two primary disorders that cause the same pH alteration (e.g., 209–218.