Page 185 - Cardiac Nursing

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C HAP TE R 7 / Fluid and Electrolyte and Acid–Base Balance and Imbalance 161

Although some of the cellular effects of hyperkalemia are an- small anions (e.g., citrate) is physiologically inactive. Only the
tiarrhythmogenic, cardiac arrhythmias do occur in hyperkalemia. ionized calcium is physiologically active. Two laboratory measures
The differential effects of hyperkalemia on different cell types for extracellular calcium are available in many settings: total cal-
cause slow and nonhomogeneous conduction to cells with vari- cium concentration (bound, complexed, and ionized) and ionized
able degrees of excitability. When intra-atrial conduction is de- calcium concentration.
creased, sinus node impulses may be delayed in exit or may fail to Calcium ions play crucial roles in the automaticity of the sinus
propagate. This situation gives rise to Wenckebach (type I) or Mo- and atrioventricular nodes, in the plateau phase of the Purkinje
bitz (type II) sinoatrial block (see Chapter 16). Reentrant ventric- and ventricular cell action potentials, in excitation–contraction
ular arrhythmias may arise. Ventricular tachycardia may terminate coupling, and in cardiac and vascular muscle contraction (see
in ventricular fibrillation. 42 Asystolic cardiac arrest also is a po- Chapters 1 and 16). Not unexpectedly, one of the cardiac effects
tentially fatal event. 39 of an abnormal extracellular calcium concentration is altered du-
The characteristic ECG changes of hyperkalemia arise from ration of the plateau phase. Extracellular fluid calcium imbalances
the electrophysiologic changes previously described. The initial are less likely to cause cardiac arrhythmias than are potassium im-
ECG abnormality is the T waves becoming peaked (tented) with balances, but arrhythmias associated with hypercalcemia have
a narrow base and symmetric shape. 65,66 The QRS complex been fatal. In addition to their cardiac effects, acute calcium im-
widens; ST depression may occur. Occasionally, ST elevation oc- balances also affect the vasculature.
curs, mimicking an MI. 67–69 Hyperkalemia also causes decreased
amplitude and prolongation of P waves and PR prolongation. 70,71 Hypocalcemia
As the plasma potassium concentration increases to high levels, Hypocalcemia may be defined as a decreased extracellular total cal-
the P waves disappear. A sine-wave pattern appears in severe, of- cium concentration or as a decreased extracellular ionized calcium
ten terminal, hyperkalemia. 39,42,72 concentration. The first definition refers to the commonly meas-
The ECG changes of hyperkalemia are not well correlated with ured total calcium value. The second definition of hypocalcemia,
plasma potassium levels. 42,73,74 Although the ECG usually is ab- however, is used in this chapter because decreases in ionized cal-
normal with severe hyperkalemia (serum potassium greater than 8 cium concentration cause physiologic effects even if the total
mEq/L), minimal ECG changes have been observed in individu- plasma concentration is within normal limits. Ionized hypocal-
als with serum potassium concentrations greater than 9 mEq/L. cemia occurs frequently in intensive care units. 84,85
The rate of increase of the plasma potassium concentration may Hypocalcemia results from decreased calcium intake or ab-
contribute more to the ECG changes in hyperkalemia than does the sorption, decreased physiologic availability of calcium, increased
absolute plasma potassium level. Hemodialysis patients may not calcium excretion, loss of calcium by an abnormal route, or any
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exhibit the characteristic peaked T wave or other ECG signs when combination of these factors. Table 7-9 lists specific causative fac-
they are severely hyperkalemic. This may be caused in part by con- tors for hypocalcemia. Several of these specific factors may cause
75
current hypercalcemia, which can flatten the T wave. The ECG hypocalcemia in individuals with cardiac disease. The preservative
changes of hyperkalemia also are blunted during hypothermia. 76 used in storage of blood contains citrate, which complexes with
ECG interpretation software may double or triple count the
heart rate during severe hyperkalemia 77,78 Individuals who have
implantable cardioverter defibrillators have received multiple in-
appropriate shocks upon developing acute hyperkalemia. 77,79
During myocardial ischemia, potassium concentration in- Table 7-9 ■ CAUSES OF HYPOCALCEMIA
creases quickly in the extracellular spaces of the myocardium and Category Clinical Examples
promotes development of lethal ventricular re-entry arrhyth-
mias. 80,81 During exercise, elevated catecholamines counteract the Decreased calcium intake Diet deficient in calcium
negative cardiac effects of hyperkalemia in normal hearts; this pro- or absorption Diet deficient in vitamin D
tective effect is diminished in ischemic hearts. Malabsorption syndromes
Chronic diarrhea (including laxative
Hyperkalemia also has an indirect cardiac effect in that it stim- overuse)
ulates aldosterone secretion. Through its saline-retaining action Steatorrhea
on the kidneys, aldosterone expands the ECV, which may have a Pancreatitis
detrimental effect on individuals in heart failure. Shift of calcium into Alkalosis
physiologically unavailable Massive blood transfusion (citrate
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Vascular Effects of Hyperkalemia. Hyperkalemia reduces form or into bones binds Ca )
the smooth muscle relaxation normally mediated by endothe- Rapid infusion of albumin
lium-derived hyperpolarizing factor. 82 In high concentrations, Pancreatitis
Lack of PTH (hypoparathyroidism;
potassium ions cause contraction of smooth muscle of coronary surgical removal of parathyroid
arteries. 83 gland during thyroid surgery)
Hypomagnesemia
Hyperphosphatemia (overuse of
Calcium Balance phosphate-containing laxatives or
enemas; excessive oral or IV phos-
phate intake; tumor lysis syndrome)
Calcium balance is the net result of calcium intake and absorp- Acute fluoride poisoning
tion, distribution, excretion, and abnormal losses. These compo- Increased calcium excretion Gastrointestinal: Pancreatitis
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nents are summarized in Table 7-6. Calcium in the plasma exists Renal: Chronic renal insufficiency
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in three forms: protein bound, complexed, and ionized (free). The
calcium that is bound to plasma proteins and complexed with PTH, parathyroid hormone; IV, intravenous.