Page 189 - Cardiac Nursing

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C HAP TE R 7 / Fluid and Electrolyte and Acid–Base Balance and Imbalance 165

Phosphate Balance The signs and symptoms of severe hypophosphatemia include
anorexia, nausea, malaise, diminished reflexes, paresthesias, mus-
Phosphate balance is the net result of phosphate intake and ab- cle aching, muscle weakness, rhabdomyolysis, severe debility,
sorption, distribution, excretion, and abnormal losses. These com- acute respiratory failure, hemolysis (possible hemolytic anemia),
ponents are summarized in Table 7-6. Phosphate is necessary for confusion, stupor, seizures, coma, and impaired cardiac function.
many cell metabolic processes and is a component of ATP, the cel- These effects of hypophosphatemia are caused primarily by
lular energy source. decreased intracellular ATP and by decreased 2,3-biphosphoglyc-
The normal range of serum phosphate concentration is 2.5 to erate (BPG) in the red blood cells. Decreased erythrocyte BPG
4.5 mg/dL. Mild or moderate hypophosphatemia (1.0 to 2.4 mg/dL) causes tissue hypoxia by increasing hemoglobin–oxygen affinity,
may be asymptomatic. Severe hypophosphatemia, with a serum which reduces oxygen release. Administration of phosphate to
phosphate less than 1 mg/dL, usually has dramatic clinical mani- hypophosphatemic individuals increases erythrocyte BPG, which
festations. decreases hemoglobin–oxygen affinity and allows greater tissue
oxygenation. 130
Severe Hypophosphatemia
Hypophosphatemia is caused by decreased intake or absorption of Cardiac Effects of Severe Hypophosphatemia. Severe hy-
phosphate, shift of phosphate into cells, or increased phosphate pophosphatemia impairs myocardial function by decreasing car-
1
excretion. Specific causative factors included in these categories diac contractility. This cardiac impairment may progress to acute
130,132
are presented in Table 7-13. congestive failure or congestive cardiomyopathy. The de-
Of importance to people with cardiac disease is the decrease in creased cardiac performance of hypophosphatemia is reversed by
129,132
plasma phosphate concentration that occurs with intravenous glu- the intravenous administration of phosphate.
cose administration. Glucose infusion by itself does not usually Cardiac arrest can occur from sudden severe hypophos-
cause severe hypophosphatemia; however, if glucose infusion is phatemia caused by the refeeding syndrome, a situation that arises
combined with other factors, such as diuretics that increase phos- when a malnourished person with low phosphate stores begins to
phate excretion, severe hypophosphatemia may occur. Insulin, as receive oral or parenteral nutrition. The plasma phosphate con-
well as glucose, promotes the movement of phosphate into cells. centration falls rapidly within a few days of beginning nutritional
Catecholamines and -adrenergic agonist drugs also shift phos- repletion because a sudden increase in cellular metabolism de-
133,134
phate into cells and predispose to hypophosphatemia. 129 pletes the individual’s phosphate stores. The sudden phos-
Hypophosphatemia is common in chronic alcoholism. 130,131 phate depletion leads to lack of ATP and cellular dysfunction.
Individuals with newly diagnosed alcoholic cardiomyopathy The role of severe hypophosphatemia in cardiac arrhythmias is
need to have their phosphate levels checked. If they undergo al- not well understood. Arrhythmias do occur in these individuals.
cohol withdrawal, then they will likely be hyperventilating and However, many people who have severe hypophosphatemia also
respiratory alkalosis will develop, which also causes hypophos- have hypokalemia or hypocalcemia or multiple electrolyte imbal-
phatemia; therefore, their phosphate levels will need continued ances, so it may be difficult to isolate the effect of the decreased
monitoring. phosphate.
Vascular Effects of Severe Hypophosphatemia. Clini-
cally, any vascular effects of severe hypophosphatemia are difficult
to separate from the cardiac effects. Mean arterial pressure in hy-
Table 7-13 ■ CAUSES OF HYPOPHOSPHATEMIA pophosphatemic individuals increases after phosphate reple-
tion. 132 It is possible that this effect is caused by a vascular as well
Category Clinical Examples
as a myocardial action; however, clearly the cardiac effect pre-
Decreased phosphate intake Prolonged or excessive antacid use dominates in most situations.
or absorption Starvation
Malabsorption syndromes
Chronic diarrhea SUMMARY OF FLUID
Chronic alcoholism
Shift of phosphate into cells Total parenteral nutrition AND ELECTROLYTES
Rapid cell proliferation (refeeding after
starvation or malnutrition; leukemic Fluid balance is determined by the interplay of fluid intake, dis-
blast crisis)
Respiratory alkalosis (hyperventilation) tribution, excretion, and fluid loss through abnormal routes. The
Insulin two types of fluid imbalances are ECV imbalances and osmolal-
Epinephrine, -adrenergic agonists ity imbalances. ECV imbalances are increases or decreases in the
Infusion of IV glucose, fructose, or amount of fluid in the vascular and interstitial compartments.
lactate Osmolality imbalances are alterations in the concentration of
Increased phosphate excretion Diabetic ketoacidosis
Alcohol withdrawal body fluids and result in movement of water into or out of cells
Diuretic phase after severe burns caused by osmosis. Extracellular volume and osmolality imbal-
Infusion of IV bicarbonate ances may occur concurrently or separately in people with cardiac
Renal tubular acidosis disease.
Diuretic therapy
Glucocorticoid therapy A normal plasma electrolyte concentration is necessary for op-
Phosphate loss by abnormal route Emesis timal cardiovascular function. Because electrolytes play important
Hemodialysis roles in the generation of action potentials and the contraction of
cardiac and smooth muscle, electrolyte imbalances exert cardiac
IV, intravenous. and vascular effects. The effects of a specific electrolyte imbalance