Chloride deficit (hypochloremia) Serum chloride <96 mEq/L

Contributing Factor: Addison’s disease, reduced chloride intake or absorption untreated

diabetic ketoacidosis, chronic respiratory acidosis, excessive sweating, vomiting, gastric
suction, diarrhea, sodium and potassium deficiency, metabolic alkalosis, loop, osmotic, or
thiazide diuretic use, overuse of bicarbonate, rapid removal of ascetic fluid with a high sodium
content, intravenous fluids that lack chloride (dextrose and water), draining fistulas and
ileostomies, heart failure, cystic fibrosis.
Signs and Symptoms: Agitation, irritability, tremors, muscle cramps, hyperactive deep
tendon reflexes, hypertonicity, tetany, slow, shallow respirations, seizures, dysrhythmias, coma
Labs indicate: ↓ serum chloride, ↓ serum sodium, ↑ pH,
↑ Serum bicarbonate, ↑ total carbon dioxide content, ↓ urine chloride level

CHLORIDE DEFICIT (HYPOCHLOREMIA)

Chloride control depends on the intake of chloride and the excretion and
reabsorption of its ions in the kidneys. Chloride is produced in the stomach as
hydrochloric acid; a small amount of chloride is lost in the feces. Chloride-deficient
formulas, salt restricted diets, GI tube drainage, and severe vomiting and diarrhea
are risk factors for hypochloremia. As chloride decreases
(Usually because of volume depletion), sodium and bicarbonate ions are retained by
the kidney to balance the loss. Bicarbonate accumulates in the ECF, which raises
the pH and leads to hypochloremic metabolic alkalosis.

Clinical Manifestations
The signs and symptoms of hypochloremia are those of acid–base and electrolyte
imbalances. The signs and symptoms of hyponatremia, hypokalemia, and metabolic
alkalosis may also be noted.
Metabolic alkalosis is a disorder that results in a high pH and a high serum
bicarbonate level as a result of excess alkali intake or loss of hydrogen ions. With
compensation, the PaCO2 increases to 50 mm Hg. Hyperexcitability of muscles,
tetany, and hyperactive deep tendon reflexes, weakness, twitching, and muscle
cramps may result. Hypokalemia can cause hypochloremia, resulting in cardiac
dysrhythmias. In addition, because low chloride levels parallel low sodium levels, a
water excess may occur. Hyponatremia can cause seizures and coma.

Assessment and Diagnostic Findings

The normal serum chloride level is 96 to 106 mEq/L(96–106 mmol/L). Inside the cell,
the chloride level is 4 mEq/L. In addition to the chloride level, sodium and potassium
levels are also evaluated because these electrolytes are lost along with chloride.
Arterial blood gas analysis identifies the acid–base imbalance, which is usually
metabolic alkalosis. The urine chloride level, which is also measured, decreases in
hypochloremia.

Medical Management
Treatment involves correcting the cause of hypochloremia and contributing
electrolyte and acid–base imbalances. Normal saline (0.9% sodium chloride) or half-
strength saline (0.45% sodium chloride) solution is administered IV to replace the
chloride. The physician may reevaluate whether patients receiving diuretics (loop,
osmotic, or thiazide) should discontinue these medications or change to another
diuretic. Foods high in chloride are provided; these include tomato juice, salty broth,
canned vegetables, processed meats, and fruits. A patient who drinks free water
(water without electrolytes) or bottled water will excrete large amounts of chloride;
therefore, this kind of water should be avoided. Ammonium chloride, an acidifying
agent, may be prescribed to treat metabolic alkalosis; the dosage depends on the
patient’s weight and serum chloride level. This agent is metabolized by the liver,
and its effects last for about 3 days.

Nursing Management
The nurse monitors intake and output, arterial blood gas values, and serum
electrolyte levels, as well as the patient’s level of consciousness and muscle
strength and movement. Changes are reported to the physician promptly. Vital
signs are monitored and respiratory assessment is carried out frequently. The nurse
teaches the patient about foods with high chloride content.
ACUTE AND CHRONIC RESPIRATORY
ALKALOSIS (CARBONIC ACID DEFICIT)
Respiratory alkalosis is a clinical condition in which the arterial pH is greater than
7.45 and the PaCO2 is less than 38 mm Hg. As with respiratory acidosis, acute and
chronic conditions can occur. Respiratory alkalosis is always due to
hyperventilation, which causes excessive “blowing off” of CO2 and, hence, a
decrease in the plasma carbonic acid concentration. Causes can include extreme
anxiety, hypoxemia, the early phase of salicylate intoxication, gram-negative
bacteremia, and inappropriate ventilator settings that do not match the patient’s
requirements. Chronic respiratory alkalosis results from chronic hypocapnia, and
decreased serum bicarbonate levels are the consequence. Chronic hepatic
insufficiency and cerebral tumors are predisposing factors.

Clinical Manifestations
Clinical signs consist of lightheadedness due to vasoconstriction and decreased
cerebral blood flow, inability to concentrate, numbness and tingling from decreased
calcium ionization, tinnitus, and at times loss of consciousness. Cardiac effects of
respiratory alkalosis include tachycardia and ventricular and atrial dysrhythmias

Assessment and Diagnostic Findings

Analysis of arterial blood gases assists in the diagnosis of respiratory alkalosis. In
the acute state, the pH is elevated above normal as a result of a low PaCO2 and a
normal bicarbonate level. (The kidneys cannot alter the bicarbonate level quickly.)
In the compensated state, the kidneys have had sufficient time to lower the
bicarbonate level to a near-normal level. Evaluation of serum electrolytes is
indicated to identify any decrease in potassium as hydrogen is pulled out of the
cells in exchange for potassium; decreased calcium, as severe alkalosis inhibits
calcium ionization, resulting in carpopedal spasms and tetany; or decreased
phosphate due to alkalosis, causing an increased uptake of phosphate by the cells.
A toxicology screen should be performed to rule out salicylate intoxication. Patients
with chronic respiratory alkalosis are usually asymptomatic, and the diagnostic
evaluation and plan of care are the same as for acute respiratory alkalosis.

Medical Management
Treatment depends on the underlying cause of respiratory alkalosis If the cause is
anxiety, the patient is instructed to breathe more slowly to allow CO2 to accumulate
or to breathe into a closed system (such as a paper bag). A sedative may be
required to relieve hyperventilation in very anxious patients.
Treatment for other causes of respiratory alkalosis is directed at correcting the
underlying problem.
MIXED ACID–BASE DISORDERS
At times patients can simultaneously experience two or more independent acid–
base disorders. A normal pH in the presence of changes in the PaCO2 and plasma
HCO3
− concentration immediately suggests a mixed disorder. The only mixed disorder
that cannot occur is a mixed respiratory acidosis and alkalosis, because it is
impossible to have alveolar hypoventilation and hyperventilation at the same time.
An example of a mixed disorder is the simultaneous occurrence of metabolic
acidosis and respiratory acidosis during respiratory and cardiac arrest.

COMPENSATION
Generally, the pulmonary and renal systems compensate for each other to return
the pH to normal. In a single acid–base disorder, the system not causing the
problem will try to compensate by returning the ratio of bicarbonate to carbonic
acid to the normal 20_1. The lungs compensate for metabolic disturbances by
changing CO2 excretion. The kidneys compensate for respiratory disturbances by
altering bicarbonate retention and H+ secretion.
In respiratory acidosis, excess hydrogen is excreted in the urine in exchange for
bicarbonate ions. In respiratory alkalosis, the renal excretion of bicarbonate
increases, and hydrogen ions are retained. In metabolic acidosis, the compensatory
mechanisms increase the ventilation rate and the renal retention of bicarbonate. In
metabolic alkalosis, the respiratory system compensates by decreasing ventilation
to conserve CO2 and raise the PaCO2. Because the lungs respond to acid–base
disorders within minutes, compensation for metabolic imbalances occurs faster than
compensation for respiratory imbalances.