of urine output each day. Today her lung sounds are clear and peripheral edema shows considerable
waves. Laboratory tests reveal the following:
Urine Cl concentration is 60 mEq/L. What acid–base disorder is present in S.J.?
Using the stepwise approach to the evaluation of acid–base disorders as
previously described, S.J.’s elevated pH is consistent with alkalosis.
Furosemide-induced diuresis may be a clue to her acid–base disorder. The
− and increased Paco2 suggest primary metabolic alkalosis
with respiratory compensation. S.J.’s anion gap is 12, suggesting no additional
metabolic acid–base abnormalities are present. A Paco2 of 46 mm Hg suggests
normal respiratory compensation for metabolic alkalosis. Appropriate treatment of
the metabolic alkalosis should return her Paco2
to normal if there is no underlying
CASE 26-3, QUESTION 2: What is the most likely cause of S.J.’s acid–base imbalance?
Common causes of metabolic alkalosis are listed in Table 26-6. The hypokalemic,
type, dose, and dosing frequency of the diuretic.
Diuretics cause metabolic alkalosis (sometimes referred to as a “contraction
alkalosis”) by the following mechanisms. First, they enhance excretion of sodium
chloride and water, resulting in extracellular volume contraction. Volume contraction
alone will cause only a modest increase in plasma bicarbonate; however, volume
contraction also stimulates aldosterone release. Aldosterone increases distal tubular
sodium reabsorption and induces hydrogen ion and potassium secretion, resulting in
alkalosis and hypokalemia. In addition, hypokalemia induced by diuretics will
stimulate intracellular movement of hydrogen ions to replace cellular potassium,
producing extracellular alkalosis. Hypochloremia also is important in sustaining
metabolic alkalosis. In a hypochloremic state, sodium will be reabsorbed,
accompanied by bicarbonate generated by secreted hydrogen (Fig. 26-1).
CASE 26-3, QUESTION 3: How should S.J.’s acid–base imbalance be corrected and monitored?
Treatment of metabolic alkalosis depends on removal of the cause. S.J.’s diuretic
therapy should be temporarily discontinued until her volume status and electrolytes
can be restored. The initial goal is to correct fluid deficits and replace chloride and
potassium by infusing sodium and potassium chloride. As long as hypochloremia
exists, renal bicarbonate excretion will not occur and the alkalosis will not be
63 The severity of alkalosis dictates how rapidly fluid and electrolytes
should be administered. In patients with hepatic or renal failure or congestive heart
failure, infusion of large volumes of sodium and potassium salts can produce fluid
overload or hyperkalemia. Thus, fluid and electrolyte replacement should proceed
cautiously, and these patients should be monitored closely for these complications.
Potassium chloride should be administered to correct S.J.’s hypokalemia. The
amount of potassium required to replace total body stores is difficult to determine
accurately because 98% of the potassium in the body is intracellular. Although wide
variation exists, for each 1 mEq/L decrease in K+
from an ECF concentration of 4
mEq/L, the total body K+ deficit is about 4 to 5 mEq/kg.
2.5 mEq/L, which correlates with a decrease of about 350 mEq in total body
potassium stores. S.J. should be treated with the chloride salt to ensure potassium
retention and correction of alkalosis. Potassium replacement can be achieved over
the course of several days with supplements of 100 to 150 mEq/day given either
orally in divided doses or as a constant IV infusion. S.J.’s laboratory tests for BUN,
creatinine, chloride, sodium, and potassium should be monitored during sodium and
potassium chloride therapy. As noted earlier, hypercapnia should disappear after
correction of the alkalemia, and can be confirmed with an ABG, if clinically
replacement does not correct the arterial pH?
Patients unresponsive to sodium and potassium chloride therapy or those at risk for
complications with these agents can be treated with acetazolamide, hydrochloric acid
(HCl), or a hydrochloric acid precursor. The most commonly used agent is
acetazolamide, a carbonic anhydrase inhibitor that blocks hydrogen ion secretion in
the renal tubule, resulting in increased excretion of sodium and bicarbonate. Although
the serum bicarbonate concentration often improves with acetazolamide, metabolic
alkalosis may not completely resolve. Other concerns with the use of acetazolamide
include its ability to promote kaliuresis and its relative lack of effect in patients with
A solution of 0.1 N HCl may be administered to patients who require rapid
correction of alkalemia. The dose of HCl is based on the bicarbonate excess using
Eq. 26-8, where the factor 0.5 × body weight (kg) represents the estimated
Parenteral hydrochloric acid is prepared extemporaneously by adding the
appropriate amount of 1 N HCl through a 0.22-μm filter into a glass bottle containing
5% dextrose or normal saline. The dilute solution should be administered through a
central venous catheter in the superior vena cava to reduce the risk of extravasation
and tissue damage. The infusion rate should not exceed 0.2 mEq/kg/hour.
should be monitored at least every 4 hours during the infusion. HCl should not be
added to parenteral nutrition solutions.
Respiratory acidosis occurs as a result of inadequate ventilation by the lungs. When
the lungs do not excrete CO2 effectively, the Paco2
rises. This elevation in Paco2
functional acid) causes a fall in pH (Eq. 26-3). Common causes of respiratory
acidosis are listed in Table 26-7. They generally can be categorized into conditions
of airway obstruction, reduced stimulus for respiration from the CNS, failure of the
heart or lungs, and disorders of the peripheral nerves or skeletal muscles required for
Common Causes of Respiratory Acidosis
Airway Obstruction Cardiopulmonary
Foreign body aspiration Cardiac arrest
Asthma Pulmonary edema or infiltration
Adrenergic blockers Pulmonary fibrosis
CNS Disturbances Neuromuscular
Cerebral vascular accident Amyotrophic lateralsclerosis
Sleep apnea Guillain–Barré syndrome
CNS depressant drugs Hypokalemia
CNS, central nervous system; COPD, chronic obstructive pulmonary disease.
obstructive pulmonary disease (COPD). He complains of worsening shortness of breath and increased
rhonchi are heard on chest auscultation. Laboratory tests reveal the following:
B.B.’s baseline ABG at the physician’s office last month was pH, 7.35; Paco2
, 28 mEq/L. Which of B.B.’s signs and symptoms are consistent with the diagnosis of respiratory
A stepwise evaluation reveals a respiratory acidosis. A history of COPD and
physical findings of dyspnea, headache, drowsiness, and flushing support the ABG
evaluation. Respiratory acidosis also can cause more severe symptoms, including
CNS effects, such as disorientation, confusion, delirium, hallucinations, and coma.
These CNS abnormalities probably are partly caused by the direct effects of carbon
dioxide. Hypoxemia (decreased Pao2
), which commonly accompanies respiratory
acidosis, also contributes to these symptoms. Elevated Paco2 causes cerebral
vascular dilation, resulting in headache caused by increased blood flow and
increased intracranial pressure. Cardiovascular effects typically include tachycardia,
arrhythmias, and peripheral vasodilation.
Following the stepwise approach, it is determined that B.B. has a respiratory
acidosis. He has a normal AG. Comparing his current to previous values (e.g., pH,
), it appears B.B. has an acute-on-chronic respiratory acidosis because
his baseline Paco2 was 51 mm Hg with an acute worsening to 58 mm Hg. In
respiratory acidosis, increased renal reabsorption of bicarbonate compensates for the
; however, at least 48 to 72 hours are needed for this compensatory
mechanism to become fully established.
10 Patients with COPD commonly present
with an acute-on-chronic respiratory acidosis similar to B.B.
CASE 26-4, QUESTION 3: What potential causes of respiratory acidosis are present in B.B.?
Respiratory acidosis often is caused by airway obstruction, as shown in Table 26-
67,68 Chronic obstructive airway disease is a common cause of both acute and
chronic respiratory acidosis. Upper respiratory tract infections, such as acute
bronchitis, can worsen airway obstruction and produce acute respiratory acidosis.
B.B.’s drug therapy also may be contributing to respiratory insufficiency. Many drugs
(Table 26-7) decrease ventilation, but usually these drugs only significantly affect
patients who are predisposed to respiratory problems because of underlying
diseases. Because B.B. has COPD, he may be more sensitive to drugs affecting
respiration. The benzodiazepines, barbiturates, and opioids minimally decrease
respiration in normal subjects and in most patients with COPD when given in usual
therapeutic doses. These drugs, however, can cause significant respiratory
insufficiency when administered either in large doses or in combination with other
68 B.B.’s diazepam may be contributing to
hypoventilation and respiratory acidosis and should be withdrawn from his regimen.
Nonselective adrenergic blocking drugs should be used cautiously in patients with
CASE 26-4, QUESTION 4: How should B.B.’s respiratory acidosis be treated?
As with most cases of respiratory acidosis, treatment primarily involves
correction of the underlying cause of respiratory insufficiency. In this case, treatment
of acute bronchospasm with a β-adrenergic agent, such as inhaled albuterol, is
warranted. Corticosteroids, such as methylprednisolone (60–125 mg every 6–12
hours initially), are commonly used in hospitalized patients with acute exacerbations
69 Antibiotic therapy with a β-lactam with or without a β-lactamase
inhibitor should be considered in hospitalized patients producing purulent, largevolume secretions.
70 B.B’s respiratory status should be monitored closely during his
hospitalization. If the acidosis, hypercarbia, or associated hypoxemia worsen,
noninvasive positive-pressure ventilation or intubation with mechanical ventilation
Treatment with IV sodium bicarbonate is not recommended in most cases of acute
respiratory acidosis because of the risks associated with bicarbonate therapy (see
Case 26-2, Question 4) and because an absolute deficiency of bicarbonate is not
is excreted, arterial pH should return to normal.
Hypercapnia should not be overcorrected, because hypocapnia results in decreased
lung compliance, increases dysfunctional surfactant production, and shifts the
oxyhemoglobin dissociation curve to the left, restricting the release of oxygen to
Respiratory alkalosis usually is not a severe disorder. Excessive rate or depth of
respiration results in increased excretion of carbon dioxide, a fall in Paco2
rise in arterial pH. Common causes of respiratory alkalosis are presented in Table
26-8. Many conditions can cause respiratory alkalosis by stimulating respiratory
drive in the CNS. In addition, pulmonary diseases can stimulate receptors in the lung
to increase ventilation, and conditions that decrease oxygen delivery to tissues also
can stimulate ventilation, causing respiratory alkalosis.
cough with thick, yellowish sputum;
decreased breath sounds over the left lower lung field.
Laboratory findings include the following:
What acid–base disorder is present in S.P.?
Steps 1 to 3 in the evaluation of the ABG values, as described previously, indicate
a respiratory alkalosis (increased pH, decreased Paco2
findings of deep, rapid breathing and tingling sensations are clues to the etiology.
This disorder is most likely acute because her HCO3
− concentration is normal. She
does not have an AG. If a large AG were present, it would suggest she has a
coexisting metabolic acidosis, possibly caused by salicylate intoxication (see Case
CASE 26-5, QUESTION 2: Which of S.P.’s signs and symptoms are consistent with the diagnosis of acute
S.P.’s paresthesias of the extremities and perioral region, lightheadedness,
tachycardia, and increased rate and depth of respiration are common signs and
symptoms of respiratory alkalosis. Confusion and decreased mental acuity also may
5,6,10 Simple respiratory alkalosis rarely produces life-threatening
CASE 26-5, QUESTION 3: What is the cause of the acid–base disorder in S.P.?
Common Causes of Respiratory Alkalosis
Excessive mechanical ventilation
Rapid correction of metabolic acidosis
CHF, congestive heart failure; CNS, central nervous system.
Common causes of respiratory alkalosis are listed in Table 26-8.
physical examination, laboratory findings, and chest radiograph, S.P. appears to have
an acute bacterial pneumonia. Pneumonia and other pulmonary diseases can result in
stimulation of ventilation and respiratory alkalosis, even with a normal Pao2
this case. The anxiety S.P. is experiencing also may be contributing to respiratory
alkalosis by producing the familiar anxiety–hyperventilation syndrome. Although
salicylate intoxication is a potential cause of respiratory alkalosis because of the
direct respiratory stimulant effect of salicylate,
74 S.P. displays few other symptoms of
salicylate intoxication (e.g., nausea, vomiting, tinnitus, altered mental status, elevated
AG metabolic acidosis). The total aspirin dose reportedly ingested (65 mg/kg in 24
hours) is not large enough to be associated with significant risk for toxicity.
CASE 26-5, QUESTION 4: What is the appropriate treatment for S.P.’s respiratory alkalosis?
Similar to respiratory acidosis, treatment of respiratory alkalosis usually involves
correcting the underlying disorder. Initiation of appropriate antibiotic therapy for a
community-acquired pneumonia is indicated in this case (see Chapter 67, Respiratory
Tract Infections). Simple respiratory alkalosis is unlikely to cause life-threatening
symptoms, although mortality rates for critically ill patients with this disorder can be
68 The well-known remedy of rebreathing expired air from a paper bag for
treatment of hyperventilation associated with anxiety appears to be effective for this
cause of respiratory alkalosis and may be helpful for S.P.
QUESTION 1: B.L., a 65-year-old man who was transferred from a long-term acute care facility 2 days
studies included the following:
Na, 133 mEq/L Albumin, 3.2 g/dL
K, 4.3 mEq/L Ammonia, 120 μmol/L
Fasting glucose, 150 mg/dL HCO
treatment of hepatic encephalopathy. Within the first 24 hours of lactulose therapy, B.L.
BP dropped to 100/60 mm Hg, and his breathing became labored and eventually required mechanical
ventilation. At the time of intubation, his laboratory values were as follows:
Na, 137 mEq/L Arterial pH, 7.06
An evaluation of B.L.’s first ABG results using Steps 1 and 2 (in the section
Evaluation of Acid–Base Disorders) reveals abnormal Paco2 and serum bicarbonate
values, suggesting the existence of an underlying acid–base abnormality. The
direction of change in his Paco2 and serum HCO3
, along with a pH of 7.43, suggests
a respiratory alkalosis is the primary disorder. His calculated AG of 8 is not
increased. Examination of the ranges of expected compensation in Table 26-3 reveals
that these values are indeed consistent with chronic respiratory alkalosis (serum
− decreased by 0.5 mEq/L for each 1 mm Hg drop in Paco2
alcohol-induced liver disease is consistent with the diagnosis of chronic respiratory
The second set of ABG reveals severe acidosis. B.L.’s serum bicarbonate has
fallen from 19 to 13 mEq/L, and his Paco2 has increased acutely from 30 to 48 mm
Hg. Because these values have changed in opposite directions, a mixed acid–base
abnormality should be suspected.
The diagnosis of a mixed metabolic and respiratory acidosis can be confirmed by
applying the stepwise approach outlined previously. If the acidosis were purely
metabolic in nature, a serum HCO3
− of 13 mEq/L should result in hyperventilation
. B.L.’s Paco2 of 48 mm Hg is high, which would be consistent with
coexistent respiratory acidosis. The anion gap is 19, indicating an AG metabolic
acidosis is present. The excess AG (AG – 10 = 9) added to B.L’s HCO 3
− of 22, which is normal. This suggests no additional
metabolic disturbances are present.
CASE 26-6, QUESTION 2: What are possible causes for the mixed acidosis in B.L.?
The AG should be calculated in all patients with a metabolic acidosis. B.L.’s
calculated AG has increased from 8 to 19 mEq/L (11 and 22 mEq/L, respectively,
after adjusting for hypoalbuminemia), suggesting that an elevated AG acidosis is now
present. Septic shock from bacterial peritonitis can produce profound hypotension,
which leads to tissue hypoperfusion, generation of lactic acid, and a subsequent
elevation in the AG. Other causes of elevated AG metabolic acidosis can be
excluded with additional laboratory data (e.g., serum ketones, glucose, osmolal gap).
Although diarrhea and spironolactone should be considered in the differential
diagnosis, these are usually associated with hyperchloremic, normal AG metabolic
75 The coexisting respiratory acidosis is most likely the result
of B.L.’s altered mental status and his diminished respiratory drive.
recent ABG reveals the following:
current acid–base status and probable cause?
Evaluation of the ABG reveals a pH at the upper limit of normal with significant
decreases in both Paco2 and serum HCO3
− concentration. This clinical scenario is
most consistent with a mixed acute respiratory alkalosis and ongoing metabolic
acidosis. The time frame in which B.L.’s Paco2 decreased from 48 to 24 mm Hg is
consistent with acute respiratory alkalosis. B.L.’s low serum HCO3
ongoing metabolic acidosis as a result of his septicemia. The metabolic acidosis
should improve with time, given adequate antibiotic therapy and supportive measures
that maintain BP and increase oxygen delivery to the tissues.
The acute respiratory alkalosis in this case is most likely caused by the mechanical
ventilator, B.L.’s anxiety, or sepsis. In the assist-control mode, any inspiratory effort
by B.L. results in the delivery of a fully assisted breath by the ventilator.
anxiety and resultant tachypnea are resulting in over ventilation, producing excessive
CO2 elimination and respiratory alkalosis. Appropriate changes in the therapy may
include use of an anxiolytic, an analgesic if needed to treat pain, changing the
ventilator settings, or probably a combination of these strategies.
A full list of references for this chapter can be found at
http://thepoint.lww.com/AT11e. Below are the key references and websites for this
chapter, with the corresponding reference number in this chapter found in parentheses
Electrolyte Disorders. 5th ed. New York: McGraw-Hill Medical; 2001:551. (62)
Base and Electrolyte Disorders. 5th ed. New York: McGraw-Hill Medical; 2001:325. (4)
Electrolyte Disorders. 5th ed. New York: McGraw-Hill Medical; 2001:578. (26)
Electrolyte Disorders. 5th ed. New York: McGraw-Hill Medical; 2001:647. (67)
Electrolyte Disorders. 5th ed. New York: McGraw-Hill Medical; 2001:673. (74)
COMPLETE REFERENCES CHAPTER 26 ACID–BASE
Kellum JA. Disorders of acid–base balance. Crit Care Med. 2007;35(11):2630.
Electrolyte Disorders. 5th ed. New York: McGraw-Hill Medical; 2001:299.
Greenlee MM et al. The renal H,K-ATPases. Curr Opin Nephrol Hypertens. 2010;19(5):478.
Base and Electrolyte Disorders. 5th ed. New York: McGraw-Hill Medical; 2001:325.
Koeppen BM. The kidney and acid–base regulation. Adv Physiol Educ. 2009;33(4):275.
Gluck SL. acid–base. Lancet. 1998;352(9126):474.
Adrogue HJ et al. Assessing acid–base disorders. Kidney Int. 2009;76(12):1239.
department. Emerg Med J. 2001;18(5):340.
Anaesthesia. 2002;57(11):1109.
Hood VL et al. Protection of acid–base balance by pH regulation of acid production. N Engl J Med.
Gabow PA. Disorders associated with an altered anion gap. Kidney Int. 1985;27(2):472.
Winter SD et al. The fall of the serum anion gap. Arch Intern Med. 1990;150(2):311.
experiences. Ren Fail. 2002;24(5):671.
in human patients. J Lab Clin Med. 2000;136(5):379.
conditions. Postgrad Med. 2000;107(3):249.
Kraut JA et al. Approach to patients with acid–base disorders. Respir Care. 2001;46(4):392.
Electrolyte Disorders. 5th ed. New York: McGraw-Hill Medical; 2001:578.
Endocrinol Metab. 1984;13(2):333.
Swenson ER. Metabolic acidosis. Respir Care. 2001;46(4):342.
DuBose TD, Jr. Hyperkalemic metabolic acidosis. Am J Kidney Dis. 1999;33(5):XLV.
Waters JH et al. Cause of metabolic acidosis in prolonged surgery. Crit Care Med. 1999;27(10):2142.
Izzedine H et al. Drug-induced Fanconi’s syndrome. Am J Kidney Dis. 2003;41(2):292.
Kellum JA. acid–base disorders and strong ion gap. Contrib Nephrol. 2007;156:158.
exchangers in renal regulation of acid–base balance. Semin Nephrol. 2006;26(5):334.
Clin North America. 2000;18(4):809.
therapy. Am J Kidney Dis. 1987;10(5):329.
Electrolyte Disorders. 5th ed. New York: McGraw-Hill Medical; 2001:619.
possible risk factors. Aids. 2002;16(10):1341.
infusion. Crit Care Med. 2000;28(5):1631.
patients. Am J Kidney Dis. 1999;33(5):892.
Brent J et al. Fomepizole for the treatment of methanol poisoning. N EnglJ Med. 2001;344(6):424.
Adrogue HJ. Mixed acid–base disturbances. J Nephrol. 2006;19(Suppl 9):S97.
Group. N EnglJ Med. 1999;340(11):832.
Am J Kidney Dis. 2001;38(2):339.
Rao RB et al. Acid–base disorders. N EnglJ Med. 1998;338(22):1627; author reply 1628.
Laffey JG. Acid–base disorders in the critically ill. Anaesthesia. 2002;57(2):198.
Crit Care Clin. 1998;14(3):457.
Electrolyte Disorders. 5th ed. New York: McGraw-Hill Medical; 2001:551.
Galla JH. Metabolic alkalosis. J Am Soc Nephrol. 2000;11(2):369.
Khanna A et al. Metabolic alkalosis. Respir Care. 2001;46(4):354.
Bistrian BR et al. Acid–base disorders. N EnglJ Med. 1998;338(22):1628.
Electrolyte Disorders. 5th ed. New York: McGraw-Hill Medical; 2001:647.
Epstein SK et al. Respiratory acidosis. Respir Care. 2001;46(4):366.
disease. Department of Veterans Affairs Cooperative Study Group. N EnglJ Med. 1999;340(25):1941.
Laffey JG et al. Hypocapnia. N EnglJ Med. 2002;347(1):43.
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Foster GT et al. Respiratory alkalosis. Respir Care. 2001;46(4):384.
Electrolyte Disorders. 5th ed. New York: McGraw-Hill Medical; 2001:673.
Tobin MJ. Mechanical ventilation. N EnglJ Med. 1994;330(15):1056.
Plasma osmolality is maintained within normal limits through a delicate
balance between water intake and excretion. Antidiuretic hormone
(ADH) plays an important role in maintaining fluid balance in the body.
Signs of volume depletion include orthostatic hypotension, dry mucous
membranes, and poor skin turgor. Because water and sodium are
inherently linked, the assessment of volume status and selection of
replacement fluid require examination of sodium concentration.
Aldosterone is the main regulatory hormone for sodium homeostasis. A
patient may have hypotonic, isotonic, or hypertonic hyponatremia
depending on the plasma osmolality. Normalserum sodium
concentration is 135–145 mEq/L.
Hypovolemic hypotonic hyponatremia can occur with volume depletion
and decreased extracellular fluid. Calculation of sodium deficit will
determine how much sodium replacement is required.
Hypervolemic, hypotonic hyponatremia is caused by a disproportionate
accumulation of ingested water relative to sodium. It is also observed in
patients with heart failure, liver and renal failure, and nephrotic
syndrome. Management includes sodium and water restriction, as well
Syndrome of inappropriate antidiuretic hormone is a common cause of
normovolemic hypotonic hyponatremia. Persistent ADH secretion
together with water ingestion results in hyponatremia.
Neurologic symptoms may be manifested in acute or severe
hyponatremia. Low plasma osmolality causes water to move into the
brain resulting in cerebral edema, increased intracranial pressure, and
central nervous system symptoms. Rapid or overly aggressive
correction of hyponatremia can result in osmotic demyelination.
The sodium–potassium adenosine triphosphatase pump plays a pivotal
role in maintaining potassium homeostasis. Normalserum potassium
concentration is 3.5–5.0 mEq/L. Clinical manifestations of hypokalemia
include muscle weakness and electrocardiography (ECG) changes.
Potassium repletion should be guided by close monitoring of serum
potassium. Oralsupplementation is usually preferred. Patients who
cannot tolerate oral potassium or who have severe/symptomatic
hypokalemia can receive intravenous potassium. In general, the rate of
potassium infusion should not exceed 10 mEq/hour to prevent phlebitis.
Hyperkalemia can be caused by chronic kidney disease and medications
that inhibit the renin–angiotensin–aldosterone system. Intravenous
calcium is administered to antagonize the cardiac effects (ECG changes
and ventricular arrhythmias) of hyperkalemia. Other treatment
strategies include the use of insulin and glucose, β2
polystyrene sulfonate, sodium bicarbonate, and dialysis.
Normalserum calcium is 8.5–10.5 mg/dL (corrected for serum albumin
as calcium is protein-bound). Hypercalcemia can be caused by
dehydration, malignancy, hyperparathyroidism, vitamin D intoxication,
sarcoidosis, and other granulomatous disease. Clinical presentation of
hypercalcemia includes signs and symptoms involving the neurologic,
cardiovascular, pulmonary, renal, gastrointestinal, and musculoskeletal
systems. First-line treatment for hypercalcemia is hydration and
diuresis. Calcitonin and bisphosphonates are alternative agents used in
the management of hypercalcemia.
Hypophosphatemia can develop as a result of impaired intestinal
phosphorus absorption, increased renal elimination, or shift of
phosphorus from extracellular to intracellular compartments. Normal
serum phosphorus concentration is 2.7–4.7 mg/dL.
Clinical effects of hypophosphatemia can involve multiple organ systems
and are attributed to impaired cellular energy stores and tissue hypoxia
secondary to ATP depletion. Phosphorus supplementation can be
administered orally or intravenously, depending on the signs and
symptoms, and severity of hypophosphatemia. Renal function, serum
phosphorus, calcium, and magnesium need to be monitored closely.
Diarrhea is a common dose-related side effect of oral phosphorus
Magnesium depletion (normalserum magnesium, 1.8–2.4 mEq/L) can
result in abnormal function of the neurologic, neuromuscular, and
cardiovascular systems. Typical findings include Chvostek and
Trousseau signs, muscle fasciculation, tremors, muscle spasticity,
convulsions, and possibly tetany. As serum magnesium does not reflect
total body stores, symptoms are more important determinants of the
urgency and aggressiveness of magnesium replacement.
Oral magnesium replacement is indicated in asymptomatic patients with
mild depletion. Urinary excretion of magnesium increases during
intravenous replacement. Thus, replenishment of magnesium stores
usually takes several days. After intravenous magnesium administration,
the patient should be monitored for hypotension, marked suppression of
deep tendon reflexes, ECG and respiration changes, as well as
Potentially life-threatening complications of severe hypermagnesemia
include respiratory paralysis, hypotension, and complete heart block.
Intravenous calcium should be administered to antagonize the
respiratory and cardiac manifestations of magnesium. Diuretics may be
given to patients with good renal function to enhance urinary magnesium
Body Water Compartments and Electrolyte
In newborns, approximately 75% to 85% of body weight is water. After puberty, the
percentage of water per kilogram of weight decreases as the amount of adipose tissue
1,2 Body water constitutes 50% to 60% of the lean body weight
(LBW) in adult men but only 45% to 55% in women because of their greater
proportion of adipose tissue. The water content per kilogram of body weight further
decreases with advanced age. Total body water (TBW) is usually calculated as 0.6 ×
LBW in men and 0.5 × LBW in women.
Two-thirds of the total body water resides in the cells (intracellular water). The
extracellular water can be divided into different compartments—the interstitial fluid
(12% LBW) and the plasma (5% LBW) are the two major compartments. Other
compartments of the extracellular fluid (ECF) include the connective tissues and
bone water, the transcellular fluids (e.g., glandular secretions), and other fluids in
sequestered spaces, such as the cerebrospinal fluid.
The electrolyte composition differs between the intracellular and extracellular
compartments. Potassium, magnesium, and phosphate are the major ions in the
whereas sodium, chloride, and bicarbonate are predominant in the extracellular
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