Page 192 - Cardiac Nursing

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168 PA R T II / Physiologic and Pathologic Responses

Table 7-16 ■ SUMMARY OF PHYSIOLOGIC RESPONSES THAT MAINTAIN ACID–BASE BALANCE
Physiological Response to Increased pH (too much
Mechanism Response to Decreased pH (too much acid in blood) bicarbonate in blood)
Buffers Accept hydrogen ions Release hydrogen ions
Respiratory system Excretes carbonic acid by increasing rate and depth of respiration Retains carbonic acid in the body by decreasing rate and
depth of respiration
Kidneys Excrete more metabolic acid by increasing secretion of H
Excrete less metabolic acid by decreasing secretion of

into renal tubular fluid, increasing reabsorption of bicarbonate, H into renal tubular fluid, decreasing reabsorption
and increasing production of NH 3 of bicarbonate, and decreasing production of NH 3

is characterized by abnormal pH, Pa CO2 , and plasma bicarbonate and pH that is decreased (partially compensated) or normal (fully
ion concentration. However, the pH is not as abnormal as it was compensated).
before the partial compensation. When an acid–base imbalance In respiratory acidosis, excess CO 2 diffuses into cardiac cells.
d
d
is fully compensated, the pH is in the normal range, but the Pa CO2 Although intracellular buffering of carbonic acid may protect in-
and plasma bicarbonate ion concentration both are abnormal. By tracellular pH in cardiac cells more effectively than in many other
moving the pH toward normal, compensation for an acid–base types of cells, the intracellular pH in cardiac cells does decrease. 141
imbalance helps to protect cells from death. Respiratory acidosis depresses cardiac contractility. 142 The nega-
tive effects of decreased myocardial cell contractility in respiratory
Acidosis acidosis are offset partially by increased sympathetic neural dis-
charge and increased catecholamine levels. 143 Tachycardia and
An individual who has acidosis has processes that tend to decrease cardiac arrhythmias in individuals who have respiratory acidosis
the pH of the blood below normal by creating a relative excess of may be caused by the increased circulating catecholamines.
acid. The resulting acidemia may persist or may be lessened by the Respiratory acidosis also affects blood vessels, altering both pe-
body’s compensatory response. A pH below 6.9 usually is fatal. ripheral vascular resistance and distribution of blood flow. Periph-
Acidosis is classified as respiratory or metabolic, depending on eral vasodilation decreases the peripheral vascular resistance. 144 and
what type of acid initially is relatively excessive. coronary vasodilation also occurs. 145 The peripheral vasculature be-
comes less sensitive to - and -adrenergic stimulation. Decreased
Respiratory Acidosis
Respiratory acidosis occurs when too much carbonic acid accu-
mulates in the blood. Clinically, the increase of carbonic acid is Table 7-17 ■ CAUSES OF RESPIRATORY ACIDOSIS
measured as an increased Pa CO2 . Carbonic acid normally is ex-
creted by the lungs. Thus, any factor that decreases ventilation Category Clinical Examples
can cause respiratory acidosis (Table 7-17). People in whom Decreased gaseous exchange Decreased alveolar ventilation for any
pulmonary heart disease (cor pulmonale) develops because (problem in the airways reason
of chronic lung disease commonly have chronic respiratory or alveoli of lungs) Acute airway obstruction by foreign body
acidosis. Severe asthma
Sleep apnea (obstructive type)
Carbon dioxide diffuses readily through membranes. 135 Thus, Chronic obstructive pulmonary disease
the pH of CSF decreases when respiratory acidosis occurs. As ex- (COPD) type A (emphysema) in
cess CO 2 enters brain cells, intracellular acidosis alters enzyme ac- end-stage
tivity and central nervous system (CNS) depression results. Clin- Chronic obstructive pulmonary disease
(COPD) type B (chronic bronchitis)
ical manifestations of respiratory acidosis are CNS depression Atelectasis
(disorientation, lethargy, somnolence), headache, blurred vision, Pneumonia
tachycardia, and cardiac arrhythmias. Adult respiratory distress syndrome (ARDS)
Respiratory acidosis can be corrected only by restoring lung Pulmonary edema
function because the lungs are the only route of excretion of car- Impaired neuromuscular Hypoventilation with mechanical ventilator
Chest injury
bonic acid. If the respiratory acidosis lasts long enough, the kid- function of chest (problem Surgical incision in chest or upper abdomen
neys compensate by excreting more than the usual amount of in the chest muscles or (pain limits chest expansion)
metabolic acids, moving the pH back toward normal, even nerves) Respiratory muscle fatigue
though the blood chemistry remains abnormal. 140 Excretion of Severe hypokalemia
more metabolic acids raises the bicarbonate ion concentration be- Poliomyelitis
Guillain–Barré syndrome
cause fewer bicarbonate ions are used in buffering. Thus, renal Myasthenia gravis
compensation for respiratory acidosis restores the 20:1 ratio of bi- Kyphoscoliosis
carbonate to carbonic acid, even though the absolute values of Pickwickian syndrome (obesity limits chest
expansion)
both are elevated. Restoring the 20:1 ratio normalizes the pH. Re- Suppression of respiratory Opioids
nal compensation for respiratory acidosis takes 3 to 5 days to be neurons in brainstem Barbiturates
3
fully effective. Compensated respiratory acidosis is characterized (medulla) (problem in the Anesthetics
by elevated Pa CO2 (the sign of the primary problem), elevated bi- brainstem) Sleep apnea (central type)
carbonate ion concentration (the sign of the renal compensation),