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162 PA R T II / Physiologic and Pathologic Responses

calcium ions. Large or rapid transfusions of citrated blood cause
hypocalcemia by decreasing the physiologic availability of calcium Table 7-10 ■ CAUSES OF HYPERCALCEMIA
in the blood. 86 The hypocalcemic effect of blood transfusions is Category Clinical Examples
84
greater in critically ill patients. Similarly, rapid administration of
proteinaceous plasma expanders such as albumin also decreases Increased calcium intake Milk-alkali syndrome
the physiologic availability of plasma calcium and may cause or absorption Excessive vitamin D
symptomatic hypocalcemia. Shift of calcium out of bone Hyperparathyroidism
Prolonged immobility
Hypocalcemia increases neuromuscular excitability. The clin-
Bone tumors
ical manifestations of hypocalcemia may include digital and pe- Multiple myeloma
rioral paresthesias, positive Chvostek’s sign, positive Trousseau’s Cancers that produce parathyroid
sign, muscle twitching and cramping, grimacing, hyperactive re- hormone-related peptide and other
flexes, tetany, carpopedal spasm, laryngospasm, seizures, cardiac bone-resorbing factors
Decreased calcium excretion Thiazide diuretics
arrhythmias, cardiac arrest, and hypotension (with acute
Familial hypocalciuric hypercalcemia
hypocalcemia).
Cardiac Effects of Hypocalcemia. Hypocalcemia prolongs
the plateau phase, thereby increasing the duration of the cardiac
reticulum rather than from the extracellular fluid. Any short-term
action potential. In addition, hypocalcemia slows atrioventricular
and intraventricular conduction to a moderate degree. 87 effects of hypocalcemia on the vasculature are more likely to arise
from alterations in cell membrane permeability than from alter-
These hypocalcemia-related changes in the myocardium usu-
ation in the contractile mechanisms. Acute (but not chronic)
ally are not great enough to give rise to significant cardiac ar-
hypocalcemia causes hypotension. The mechanisms involved are
rhythmias in clinical settings, although they may occasionally pre-
dispose to ventricular arrhythmias, including torsade de pointes. 88 not completely understood but likely include decreased peripheral
vascular resistance and impaired cardiac function.
Hypocalcemia does cause characteristic alterations in the ECG.
89
Hypocalcemia prolongs the ST segment. This finding is not un- Hypercalcemia
expected because hypocalcemia prolongs the plateau phase of the
Hypercalcemia results from increased intake or absorption of cal-
action potential. The prolongation of the ST segment causes a
prolonged QT interval. 39,90 The degree of prolongation of the cium, the shift of calcium from the bones into the extracellular
fluid, decreased calcium excretion, or any combination of these
QT interval is not a reliable indicator of the degree of hypocal- 1
factors. Specific causative factors are listed under these categories
cemia or of the decrease in ionized calcium concentration, but it
is influenced by the rate of decrease of the ionized calcium. 86 in Table 7-10. Note that thiazide diuretics, often administered to
people with cardiac disease, decrease the urinary excretion of
Concurrent hypomagnesemia magnifies the ECG effects of 25,97
calcium. Another type of diuretic should be substituted if
hypocalcemia. ECG changes in individuals with hypocalcemia
and hypomagnesemia may mimic MI. 91 hypercalcemia develops.
The clinical manifestations of hypercalcemia include anorexia,
Hypocalcemia impairs myocardial contractility and thus may
cause heart failure. 92–95 People who already have heart failure may nausea, vomiting, constipation, abdominal pain, polyuria, renal
calculi, skeletal muscle weakness, diminished reflexes, confusion,
decompensate if they become hypocalcemic. Hypocalcemia-
lethargy, possible personality change, frank psychosis, cardiac ar-
associated heart failure may be unresponsive to digitalis until the
rhythmias, and hypertension (with acute hypercalcemia).
hypocalcemia is corrected. The role of calcium ions in the regula-
tion of myocardial contraction is clear (see Chapter 16). Although Cardiac Effects of Hypercalcemia. Hypercalcemia short-
most of the calcium ions that initiate myocardial contraction ens the plateau phase of the cardiac action potential, thereby de-
come from the sarcoplasmic reticulum rather than directly from creasing the duration of the action potential. In addition, it in-
the extracellular fluid, entry of calcium from the extracellular fluid creases the rate of diastolic depolarization of sinus node cells and
is necessary to trigger calcium release from the sarcoplasmic retic- may increase the initial rate of increase and amplitude of the ac-
ulum. The depressive effect of hypocalcemia on myocardial con- tion potential. It may also delay atrioventricular conduction.
tractility may be most important in individuals who have pre-ex- Cardiac arrhythmias that have been reported to arise from hy-
isting downregulation of -adrenergic receptors. 91 In a normal percalcemia include various types of heart block, paroxysmal atrial
heart, hypocalcemia reduces stroke work at any particular left ven- fibrillation, and severe bradycardia. 98 Hypercalcemia potentiates
tricular end-diastolic pressure. This impairment is even greater in digitalis toxicity. 39 People using digitalis may acquire heart block
an ischemic heart. A classic study showed that patients who are if they become hypercalcemic. Sudden death has occurred in se-
administered albumin for resuscitation during hypovolemic shock vere hypercalcemia, possibly caused by ventricular fibrillation.
may also exhibit impaired myocardial contractility when the ion- The ECG in hypercalcemia reflects the short plateau phase in a
ized calcium binds to the albumin and becomes physiologically shortened ST segment. The QT interval is decreased as a result. 39
unavailable. 96 The length of the QT interval is a clinically unreliable index of the
extent of hypercalcemia. Hypercalcemia has been accompanied by
Vascular Effects of Hypocalcemia. Calcium ions play sev- lengthening of the QRS complex and diffuse flattening of
eral important roles in contraction of vascular smooth muscle. T waves. 99
They are involved in the action potential, the regulation of cell
membrane permeability, and in excitation–contraction coupling. Vascular Effects of Hypercalcemia. In people who have in-
In smooth muscle, as well as in cardiac muscle, contraction is ini- tact parathyroid glands, acute hypercalcemia causes vasoconstric-
tiated by an increase in cytoplasmic calcium. Most of the calcium tion and raises systolic blood pressure by impairing the vasodila-
ions that initiate the contraction come from the sarcoplasmic tory function of the endothelium. 100–102 Increased intracellular