TRIPASS XR تري باس

 

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. 9-1).81–83

Treatment

CASE 9-3, QUESTION 3: How should K.E.’s acid–base imbalance be corrected and monitored?

Treatment of metabolic alkalosis depends on removal of the

cause. K.E.’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.82 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 K.E.’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 K.E.’s serum potassium is 2.5 mEq/L, which correlates with a decrease of about 350 mEq in total body potassium

stores. K.E. 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. K.E.’s laboratory tests for BUN,

creatinine, chloride, sodium, and potassium should be monitored

184 Section 1 General Care

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 9-3, QUESTION 4: What other agents are available

to treat K.E.’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.81,84,85

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. 9-9, where the factor 0.5 × body

weight (kg) represents the estimated bicarbonate space.10,81,82,84

Dose of HCl (mEq) = 0.5 × Body weight (kg)

× (plasma bicarbonate − 24) (Eq. 9-9)

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.84 ABG should be monitored at least

every 4 hours during the infusion. HCl should not be added to

total nutrient solutions.85

Precursors of hydrochloric acid, such as ammonium and

arginine hydrochloride, are not recommended.81 The adverse

effect profile of these agents has significantly limited their role.84

Ammonium hydrochloride is metabolized to HCl and NH3 in

the liver. Severe ammonia intoxication with CNS depression

can occur during rapid infusion of ammonium hydrochloride or

in patients with liver disease.81 Arginine can cause rapid shifts

in potassium from the intracellular to the extracellular space,

resulting in dangerous hyperkalemia.81

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 (Eqs. 9-3 and 9-5). Common causes of respiratory

acidosis are listed in Table 9-7. 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.86

Evaluation

CASE 9-4

QUESTION 1: B.B., a 56-year-old man, is admitted to the

hospital for treatment of an exacerbation of chronic obstructive pulmonary disease (COPD). He complains of worsening

TABLE 9-7

Common Causes of Respiratory Alkalosis

CNS Disturbances

Bacterial septicemia

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.

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 ipratropium inhaler two puffs four times a day (QID), salmeterol dry powder inhaler one inhalation twice a day (BID),

hydrochlorothiazide 25 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

HCO−

3 , 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

HCO−

3 , 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.87

CASE 9-4, QUESTION 2: Is the respiratory acidosis present

in B.B. consistent with an acute or a chronic disorder?

185Acid–Base Disorders Chapter 9

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, HCO−

3 ), 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 9-4, 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 9-7.86,87 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 9-7) 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.87 B.B.’s diazepam may

be contributing to hypoventilation and respiratory acidosis and

should be withdrawn from his regimen. Nonselective adrenergic

blocking drugs should not be used in patients with COPD.

Treatment

CASE 9-4, 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 ipratropium or 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.88 Antibiotic therapy with a β-lactam or β-lactamase

inhibitor should be considered in hospitalized patients producing purulent, large-volume secretions.89 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.67

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 9-2, 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

TABLE 9-8

Laboratory Values in Simple Acid–Base Disorders

Primary Compensatory

Disorder Arterial pH Change Change

Metabolic acidosis ↓ ↓HCO−

3 ↓Paco2

Respiratory acidosis ↓ ↑Paco−

2 ↑HCO−

3

Metabolic alkalosis ↑ ↑HCO−

3 ↑Paco2

Respiratory alkalosis ↑ ↓Paco−

2 ↓HCO−

3

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.74,75,90

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 9-8. 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.91,92

Evaluation

CASE 9-5

QUESTION 1: S.P., a 35-year-old, 60-kg woman, is admitted

for treatment of presumed bacterial pneumonia. She was in

good health until 24 hours before presentation when she

noted a fever; onset of a productive cough with thick, yellowish sputum; and chest pain on deep inspiration. She has

taken aspirin 650 mg every 4 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

HCO−

3 , 22 mEq/L

Gram stain of sputum reveals 25 white blood cells (WBC)

per high-power field and many gram-positive diplococci.

WBC 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