TRIPASS XR تري باس

 

10,62

Evaluation

CASE 26-3

QUESTION 1: S.J., a 75-year-old, 60-kg woman, was admitted to the hospital 4 days ago with peripheral

edema and pulmonary congestion consistent with a congestive heart failure exacerbation. Since admission, she

has been treated aggressively with furosemide 80 to 120 mg IV daily, which has generated approximately 3 L

of urine output each day. Today her lung sounds are clear and peripheral edema shows considerable

improvement with diuresis; however, she now complains of dizziness when she gets out of bed to go to the

bathroom. Physical examination reveals a tachycardic (heart rate [HR], 100 beats/minute), thin elderly woman

with poor skin turgor and slight muscle weakness. S.J.’s electrocardiogram shows flattened T waves and U

waves. Laboratory tests reveal the following:

Serum Na, 138 mEq/L

K, 2.5 mEq/L

Cl, 92 mEq/L

Creatinine, 0.9 mg/dL

BUN, 28 mg/dL

pH, 7.49

Paco2

, 46 mm Hg

HCO3

−

, 34 mEq/L

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

increased serum HCO3

− 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

pulmonary disease.

Causes

DIURETIC-INDUCED

CASE 26-3, QUESTION 2: What is the most likely cause of S.J.’s acid–base imbalance?

p. 563

p. 564

Common causes of metabolic alkalosis are listed in Table 26-6. The hypokalemic,

hypochloremic, metabolic alkalosis in S.J. most likely is the result of diureticinduced volume contraction. The incidence of this adverse effect is influenced by the

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).

62–64

Treatment

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

corrected.

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.

10 S.J.’s serum potassium is

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

indicated.

CASE 26-3, QUESTION 4: What other agents are available to treat S.J.’s alkalosis if fluid and electrolyte

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

renal dysfunction.

62,65,66

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

bicarbonate space.

10,62,63,65

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.

65 ABG

should be monitored at least every 4 hours during the infusion. HCl should not be

added to parenteral nutrition solutions.

66

RESPIRATORY ACIDOSIS

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

(a

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

ventilation.

67

Table 26-7

Common Causes of Respiratory Acidosis

Airway Obstruction Cardiopulmonary

Foreign body aspiration Cardiac arrest

Asthma Pulmonary edema or infiltration

COPD Pulmonary embolism

Adrenergic blockers Pulmonary fibrosis

CNS Disturbances Neuromuscular

Cerebral vascular accident Amyotrophic lateralsclerosis

Sleep apnea Guillain–Barré syndrome

Tumor Myasthenia gravis

CNS depressant drugs Hypokalemia

Barbiturates Hypophosphatemia

Benzodiazepines Drugs

Opioids Aminoglycosides

Antiarrhythmics

Lithium

Phenytoin

CNS, central nervous system; COPD, chronic obstructive pulmonary disease.

p. 564

p. 565

Evaluation

CASE 26-4

QUESTION 1: B.B., a 70-year-old man, is admitted to the hospital for treatment of an exacerbation of chronic

obstructive pulmonary disease (COPD). He complains of worsening shortness of breath and increased

production of sputum for the past 3 days. He has also noted a mild headache, a flushed feeling, and drowsiness

within the past 24 hours. He has a history of COPD, hypertension, coronary artery disease, and low back pain.

Current medications are tiotropium one inhalation daily, salmeterol dry powder inhaler one inhalation BID,

chlorthalidone 12.5 mg daily, long-acting diltiazem 240 mg daily, and diazepam 5 mg TID as needed for back

pain.

Vital signs include respiratory rate of 16 breaths/minute and HR of 90 beats/minute. Diffuse wheezes and

rhonchi are heard on chest auscultation. Laboratory tests reveal the following:

Na, 140 mEq/L

K, 4.0 mEq/L

Cl, 100 mEq/L

pH, 7.32

Paco2

, 58 mm Hg

Pao2

, 58 mm Hg

HCO3

−

, 29 mEq/L

B.B.’s baseline ABG at the physician’s office last month was pH, 7.35; Paco2

, 51 mm Hg; Pao2

, 62 mm Hg;

and HCO3

−

, 28 mEq/L. Which of B.B.’s signs and symptoms are consistent with the diagnosis of respiratory

acidosis?

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.

68

CASE 26-4, QUESTION 2: Is the respiratory acidosis present in B.B. consistent with an acute or a chronic

disorder?

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,

Paco2

, HCO3

−

), 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

increase in Paco2

; 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.

Causes

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-

6.

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.

DRUG-INDUCED

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

respiratory depressant drugs.

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

COPD.

Treatment

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

of COPD.

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

may be required.

54

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

present. When the excess CO2

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

tissues.

60,61,71

RESPIRATORY ALKALOSIS

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

, and a

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.

72,73

Evaluation

CASE 26-5

QUESTION 1: S.P., a 50-year-old, 80-kg woman, is admitted for treatment of presumed bacterial pneumonia.

She was in good health until 24 hours before presentation when she noted an abrupt onset of fever, a productive

cough with thick, yellowish sputum;

p. 565

p. 566

and chest pain on deep inspiration. She has taken aspirin 650 mg every 3 hours since the onset of fever, with

mild relief. Since arriving in the ED, she has become anxious and lightheaded and has developed tingling in her

hands, feet, and lips. Vital signs include the following: temperature, 38°C; respiratory rate, 24 breaths/minute;

HR, 110 beats/minute; and BP, 135/70 mm Hg. Physical examination reveals dullness to percussion, rales, and

decreased breath sounds over the left lower lung field.

Laboratory findings include the following:

Serum Na, 135 mEq/L

Cl, 105 mEq/L

pH, 7.49

Paco2

, 30 mm Hg

Pao2

, 90 mm Hg

HCO3

−

, 22 mEq/L

Gram stain of sputum reveals 25 white blood cells per high-power field and many gram-positive diplococci.

White blood cell count is 15,400 cells/μL with a left shift. A left lower lobe infiltrate is seen on chest radiograph.

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

). The history and physical

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

26-5, Question 3).

CASE 26-5, QUESTION 2: Which of S.P.’s signs and symptoms are consistent with the diagnosis of acute

respiratory alkalosis?

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

be evident.

5,6,10 Simple respiratory alkalosis rarely produces life-threatening

abnormalities.

Causes

CASE 26-5, QUESTION 3: What is the cause of the acid–base disorder in S.P.?

Table 26-8

Common Causes of Respiratory Alkalosis

CNS Disturbances

Bacteremia

Cerebrovascular accident

Fever

Hepatic cirrhosis

Hyperventilation

Anxiety-induced

Voluntary

Meningitis

Pregnancy

Trauma

Drugs

Progesterone derivatives

Respiratory stimulants

Salicylate overdose

Pulmonary

Pneumonia

Pulmonary edema

Pulmonary embolus

Tissue Hypoxia

High altitude

Hypotension

CHF

Other

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.

5,6,10,72–74 Based on

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

, as in

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.

Treatment

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

high.

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.

MIXED ACID–BASE DISORDERS

Evaluation

CASE 26-6

QUESTION 1: B.L., a 65-year-old man who was transferred from a long-term acute care facility 2 days

previously, is disorientated and lethargic. He was doing well until 1 week before admission, when the staff noted

that he was somnolent. He progressively became more lethargic and could no longer remember the names of

other persons. B.L. has a history of alcoholic cirrhosis, type 2 diabetes mellitus, and hypertension. Medications

before admission were nadolol 80 mg daily, isosorbide mononitrate 20 mg BID, glyburide 10 mg daily, and

spironolactone 50 mg BID. On admission, B.L. was disoriented to person, place, and time and was difficult to

arouse. Vital signs include the following: temperature, 37°C; respirations, 16 breaths/minute; HR, 70

beats/minute; and BP, 154/92 mm Hg. Physical examination revealed asterixis and mild ascites. Laboratory

studies included the following:

Na, 133 mEq/L Albumin, 3.2 g/dL

K, 4.3 mEq/L Ammonia, 120 μmol/L

Cl, 106 mEq/L pH, 7.43

BUN, 5 mg/dL Paco2

, 30 mm Hg

Creatinine, 0.7 mg/dL Pao2

, 90 mm Hg

Fasting glucose, 150 mg/dL HCO

3

−, 19 mEq/L

On admission, spironolactone was increased to 200 mg daily and lactulose 60 mL orally QID was started for

treatment of hepatic encephalopathy. Within the first 24 hours of lactulose therapy, B.L.

p. 566

p. 567

produced four loose, watery stools; however, his mental status worsened to the point of being unresponsive, his

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

K, 4.5 mEq/L Paco2

, 48 mm Hg

Cl, 105 mEq/L Pao2

, 58 mm Hg

BUN, 10 mg/dL HCO

3

−, 13 mEq/L

Creatinine, 1.2 mg/dL

Gram stain of peritoneal fluid revealed many WBC and gram-negative rods; the diagnosis of spontaneous

bacterial peritonitis with septic shock is made. Describe B.L.’s acid–base status on admission and at the current

time.

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

HCO3

− decreased by 0.5 mEq/L for each 1 mm Hg drop in Paco2

). B.L.’s history of

alcohol-induced liver disease is consistent with the diagnosis of chronic respiratory

alkalosis (Table 26-8).

8,10

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

and a low Paco2

. 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 13

yields a corrected HCO3

− of 22, which is normal. This suggests no additional

metabolic disturbances are present.

Causes

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

acidosis (Table 26-2).

75 The coexisting respiratory acidosis is most likely the result

of B.L.’s altered mental status and his diminished respiratory drive.

CASE 26-6, QUESTION 3: During the next 6 hours, B.L.’s hepatic encephalopathy, peritonitis, and acid–

base disorders are aggressively treated with lactulose, antibiotics, fluids, and mechanical ventilation. His most

recent ABG reveals the following:

pH, 7.45

Paco2

, 24 mm Hg

Pao2

, 90 mm Hg

HCO3

−

, 16 mEq/L

Ventilator settings are assist-control mode at 16 breaths/minute, tidal volume 700 mL, and inspired oxygen

concentration 40%. B.L. is noted to be more awake, anxious, and initiating 25 to 30 breaths/minute. What is the

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

− suggests

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.

76 B.L.’s

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.

KEY REFERENCES AND WEBSITES

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

after the reference.

Key References

Adrogue HJ, Madias NE. Management of life-threatening acid–base disorders: first of two parts. N Engl J Med.

1998;338:26. (54)

Adrogue HJ, Madias NE. Management of life threatening acid–base disorders: second of two parts. N Engl J

Med. 1998;338:107. (55)

Rose BD, Post TW. Metabolic alkalosis. In: Rose BD, Post TW, eds. Clinical Physiology of Acid–Base and

Electrolyte Disorders. 5th ed. New York: McGraw-Hill Medical; 2001:551. (62)

Rose BD, Post TW. Regulation of acid–base balance. In: Rose BD, Post TW, eds. Clinical Physiology of Acid–

Base and Electrolyte Disorders. 5th ed. New York: McGraw-Hill Medical; 2001:325. (4)

Rose BD, Post TW. Introduction to simple and mixed acid–base disorders. In: Rose BD, Post TW, eds. Clinical

Physiology of Acid–Base and Electrolyte Disorders. 5th ed. New York: McGraw-Hill Medical; 2001:535. (8)

Rose BD, Post TW. Metabolic acidosis. In: Rose BD, Post TW, eds. Clinical Physiology of Acid–Base and

Electrolyte Disorders. 5th ed. New York: McGraw-Hill Medical; 2001:578. (26)

Rose BD, Post TW. Respiratory acidosis. In: Rose BD, Post TW, eds. Clinical Physiology of Acid–Base and

Electrolyte Disorders. 5th ed. New York: McGraw-Hill Medical; 2001:647. (67)

Rose BD, Post TW. Respiratory alkalosis. In: Rose BD, Post TW, eds. Clinical Physiology of Acid–Base and

Electrolyte Disorders. 5th ed. New York: McGraw-Hill Medical; 2001:673. (74)

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p. 567

FLUID AND SODIUM DISORDERS

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.

Case 27-1 (Question 1),

Figure 27-1

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.

Case 27-2 (Questions 1, 2)

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.

Cases 27-4 through 27-7,

Figure 27-1

Hypovolemic hypotonic hyponatremia can occur with volume depletion

and decreased extracellular fluid. Calculation of sodium deficit will

determine how much sodium replacement is required.

Case 27-5 (Questions 1, 2)

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

as the use of diuretics.

Case 27-6 (Question 1)

Syndrome of inappropriate antidiuretic hormone is a common cause of

normovolemic hypotonic hyponatremia. Persistent ADH secretion

together with water ingestion results in hyponatremia.

Case 27-7 (Question 1)

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.

Case 27-7 (Questions 3, 4)

POTASSIUM DISORDERS

The sodium–potassium adenosine triphosphatase pump plays a pivotal

role in maintaining potassium homeostasis. Normalserum potassium

Case 27-8 (Questions 1, 2)

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.

Case 27-8 (Question 3)

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p. 569

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

-agonists, sodium

polystyrene sulfonate, sodium bicarbonate, and dialysis.

Case 27-9 (Question 1),

Case 27-10 (Questions 1, 2),

Table 27-3

CALCIUM DISORDERS

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.

Case 27-11 (Questions 1–3),

Table 27-4

PHOSPHATE DISORDERS

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.

Case 27-12 (Questions 1, 2)

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

replacement.

Case 27-12 (Questions 3, 4)

MAGNESIUM DISORDERS

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,

Case 27-13 (Questions 1, 2)

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

hypermagnesemia.

Case 27-13 (Questions 3, 4)

A common cause of hypermagnesemia is the use of magnesiumcontaining laxatives and antacids by patients with renal impairment.

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

excretion.

Case 27-14 (Questions 1–3)

BASIC PRINCIPLES

Body Water Compartments and Electrolyte

Composition

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

increases with age.

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.

1

The electrolyte composition differs between the intracellular and extracellular

compartments. Potassium, magnesium, and phosphate are the major ions in the

intracellular compartment,

p. 569

p. 570

whereas sodium, chloride, and bicarbonate are predominant in the extracellular

space.