I

acid-ba dentifying
se and
electro
ylyte
imbalan
ces

Abstract: Acid-base and electrolyte imbalances often complicate patient management

in acute care settings. Correctly identifying the imbalance and its cause is vital.
This article will review the physiology of acid-base and electrolyte balance, their
common disturbances, associated causes, clinical manifestations, and management
implications for nurse practitioners.

By Michael D. Gooch, MSN, RN, ACNP-BC, FNP-BC, ENP-BC,

CFRN, CTRN, CEN, NREMT-P

r. H, a 50-year-old male, presents to the ED via of carbon dioxide (PaCO2) 15.6 mm Hg, partial pressure

M emergency medical services. The paramedics and

family report the patient has a history of type 2
of oxygen (Pao2) 56 mm Hg, base excess (BE) -27, bicarbon-
ate (HCO3−) 3.9 mEq/L (mmol/L), and lactate (lactic acid)
diabetes, has been vomiting for the last 2 days, and has not 5.48 mmol/L.
taken his insulin. The paramedics also report his glucose The ED staff recognize that this patient is in acute distress
registered “high.” They initiated one I.V. line and started and requires aggressive resuscitation to manage his acidosis.
an infusion of 0.9% sodium chloride. On presentation, As the history and physical exam are completed, lab results
Mr. H appears very ill, looks emaciated, and older than his indicate the following: sodium (Na+) 130 mEq/L, potassium
stated age. As the assessment begins, his heart rate is 120 (K+) 5.4 mEq/L, chloride (Cl-) 89 mEq/L, carbon dioxide
beats/minute. He has classic Kussmaul respirations at 40 (CO2) less than 5 mmol/L, blood urea nitrogen (BUN)
mirjanajovic/istock ©

per minute, and his BP is 124/84. A second I.V. is inserted 51 mg/dL, creatinine 2.2 mg/dL, glucose 815 mg/dL, calcium
with a large bore needle, and a bolus infusion is initiated (Ca++) 8.6 mg/dL, anion gap 36 mEq/L, and positive serum
with 2 L of 0.9% sodium chloride. The patient’s peripheral acetone. This patient is in diabetic ketoacidosis (DKA);
venous blood gas is as follows: pH 7.008, partial pressure the labs show a metabolic acidosis with some respiratory

Keywords: acid-base imbalance, acidosis, alkalosis, anion gap acidosis, calcium, carbonic acid, electrolyte imbalance, hypercalcemia,
hyperkalemia, hypernatremia, hypocalcemia, hypokalemia, hyponatremia, potassium, sodium

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 Identifying acid-base and electroylyte imbalances

compensation, along with hyperglycemia, hyponatremia, ■ Acid-base imbalances

hypochloremia, and hyperkalemia. (See Lab reference ranges.) Metabolic acidosis: Hyperventilation is a primary response
to a respiratory acidosis and is seen as a secondary response
■ Homeostatic mechanisms to a metabolic acidosis. The patient in this scenario pre-
Electrolyte and acid-base imbalances may occur as the result sented in a metabolic acidosis, and to compensate, the pa-
of many diseases, medications, or toxins and are encoun- tient was displaying Kussmaul respirations to expel more
tered in patients across the lifespan. The impact on the CO2 in an attempt to lower the acid concentration and bring
patient varies as well, depending upon the exact imbalance the pH closer to a more compatible level. Kussmaul respira-
and the severity of that imbalance. Given the previous pa- tions are very deep, rapid respirations often seen in severe-
tient scenario, the patient was showing signs of organ dys- ly acidotic patients.2 However, alterations in carbon dioxide
function. Acid-base and electrolyte balance are critical levels (excess loss or accumulation) may be secondary to a
homeostatic mechanisms regulating the functions of all neuromuscular or ventilatory problem. On the opposite side,
body systems and processes. When the body’s pH falls out- if the patient was alkalotic, for example, from a significant
side the normal range of 7.4 ±0.05, homeostasis is inter- loss of H+ due to gastrointestinal (GI) losses, the minute
1,2
rupted, and cellular dysfunction will ensue. The pH value ventilation may be decreased to increase CO2 retention in
represents the amount of hydrogen ions (H+) in the blood. an effort to stabilize the pH.4,7 But this response is limited
Acidosis results from the accumulation of extra acids and/ in order to avoid hypoxia.
or the loss of base. Alkalosis is just the opposite; there is a The metabolic component is managed by the kidneys.
1,2
loss of acids and/or accumulation of base. The kidneys regulate how much of the body’s H+, meta-
bolic acids, and its primary base,
HCO3−, are lost or retained through the
Acid-base and electrolyte balance are critical renal tubules.2,6,7 This process is much
slower than respiratory changes and
homeostatic mechanisms regulating the
cannot quickly alter the pH. Base as well
functions of all body systems and processes. as acid may also be lost in significant
amounts from gastric suctioning, vom-
iting, or diarrhea. As in this case presen-
Circulating acids are classified as carbonic or respira- tation, the patient had been vomiting for the last 2 days, and
tory acids, or noncarbonic or metabolic acids. Carbonic acid on the blood gas analysis, his HCO3− was extremely low (3.9
(H2CO3) mainly results from carbohydrate metabolism. In mEq/L). This excess loss of base, in conjunction with the
the presence of carbonic anhydrase in the red blood cells, it presence of two other noncarbonic acids (ketones and lac-
+ −
is catalyzed to H and HCO3 , and CO2 and H2O are released tate) worsened this patient’s acidosis.
at the alveolar level. These reactions are summarized by CO2 Anion gap acidosis: As mentioned, an acidotic state may
+ H2O ↔ H2CO3 ↔ H+ + HCO3−.2,3 Noncarbonic acids, not just result from an imbalance of bicarbonate, carbon
including lactate and ketones, often result from the me- dioxide, or hydrogen ions. There are several other com-
tabolism of proteins and fats or the intake of foods contain- pounds that, when present, will lower the pH. This may result
ing sulfates or phosphates. The amount of acid produced or in an anion gap acidosis, as presented in this case. The anion
ingested each day must equal the amount removed, other- gap may be calculated using this formula: Na +−(Cl − +
2,4
wise, an imbalance occurs. HCO3−).6-8 Mr. H’s anion gap was 36, and a normal gap is
When discussing acid-base balance, there are two im- 12 ± 4 mEq/L; this, as with other values, may vary slightly
portant aspects to understand: chemical buffering and the from lab to lab. An elevated anion gap indicates the presence
secondary (compensatory) responses, which includes the of unmeasured anions in the blood, which may be related to
respiratory response and the metabolic response.4-6 Buffer- overproduction and/or decreased clearance.1,7,8 A mnemon-
ing occurs with the production of HCO3−, as shown in the ic used to help remember some of the causes of an anion gap
carbonic acid equation above, and is the fastest and most acidosis is MUDPILES.9,10 (See Causes of anion gap acidosis.)
2,6
common way the body regulates pH. The lungs regulate Methanol, or wood alcohol, commonly found in some
CO2 by way of the medulla and chemoreceptors located windshield wiper fluids, solvents, and solid fuels would be
throughout the body. The lungs are able to rapidly alter the metabolized to formaldehyde and then formic acid and
pH by changing the minute ventilation (minute ventilation will lead to death if ingested.3,8-10 Uremia, or kidney failure,
= respiratory rate x tidal volume) and amounts of exhaled as previously mentioned, can lead to a buildup of waste
CO2.1,2,4,6,7 (See Primary acid-base disorders and responses.) products and hydrogen ions.3,9 DKA, as with this patient’s

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 Identifying acid-base and electroylyte imbalances

presentation, is associated with the buildup of ketone bod-

ies from the breakdown of fat stores during catabolism.3,7-9 Lab reference ranges2,3,6,7
Propylene glycol, a double alcohol, is used as a preservative
in some food, tobacco, and pharmaceutical products (for Arterial blood gas
example, I.V. lorazepam [Ativan]). If a large amount is pH 7.35-7.45
ingested or absorbed by the body, it is metabolized to exces- Pao2 >80 mm Hg
sive amounts of lactic, pyruvic, and acetic acids.7,10 Inges- Paco2 35-45 mm Hg
tion of toxic amounts of iron or isoniazid, a common tu-
HCO3− 22-26 mEq/L
berculocidal antimicrobial, can lead to a metabolic +
BE 2–−2
acidosis.9,10 Lactic acidosis results from anaerobic metabo-
lism as a result of inadequate tissue perfusion.3,7-9 Chemistry values

Ethylene glycol, commonly known as an ingredient in Lactate <2 mmol/L

antifreeze, if ingested, is metabolized to glycolic and oxalic Na+ 135-145 mEq/L
acids and leads to kidney failure and death if not corrected.3,8-10 K+ 3.5-5.2 mEq/L
And lastly, salicylates (for example, acetylsalicylic acid [aspi- Cl− 96-106 mEq/L
rin]), normally used as an antipyretic, analgesic, or antiplate- Ca ++
8.5-10.5 mg/dL
let agent, are toxic if consumed in large quantities. In addition Ionized Ca++ 4.6-5.3 mg/dL
to being a weak acid, in toxic amounts, salicylates uncouple
BUN 7-20 mg/dL
oxidative phosphorylation and inhibit aerobic metabolism,
Creatinine 0.6-1.2 mg/dL
which leads to the overproduction of lactic and pyruvic ac-
ids.3,9,10 A nongap acidosis may develop as a result of severe Glucose 60-100 mg/dL

diarrhea, administration of large amounts of 0.9% sodium Anion gap 8-16 mEq/L
chloride, early kidney failure, or renal tubular acidosis.3,6,7
As with the patient in this case presentation, the initial
management of a metabolic acidosis is to restore perfusion drive due to a disease process (chronic obstructive pulmo-
with fluid resuscitation and identify the cause. In the setting nary disease), or from a central nervous system depressant,
of severe acidemia, a pH less than 7.0 and/or HCO3− less such as a benzodiazepine or opioid analgesic. Managing the
than 5 mEq/L, or a non-gap acidosis an infusion of sodium airway, providing adequate ventilations, and therefore, re-
bicarbonate may be indicated to buffer the pH.3,6,7,9 moving excess CO2, and/or reversing a central nervous system
Metabolic alkalosis: Metabolic alkalosis is most often (CNS) depressant, if needed, will help correct a respiratory
associated with an increase in serum bicarbonate as a result acidosis.
of depletion of chloride and sometimes potassium related Respiratory alkalosis: Respiratory alkalosis develops as
to excessive volume loss GI suctioning, vomiting, diarrhea, a result of hyperventilation. Treatment should be focused
or diuresis. In other patients, the alkalosis is due to miner- on correcting the cause, especially if the respiratory imbal-
alocorticoid excess.3,6,7,11 The correction of a metabolic al- ance is compensating for a metabolic imbalance. Another
kalosis is guided by the cause and the amount of Cl- in the cause of respiratory alkalosis, which is not a compensatory
urine. In patients with a urine Cl - less than 15 mEq/L mechanism, is improper mechanical ventilator settings.
(termed Cl-responsive), treatment begins with fluid and
electrolyte replacement.3,6,7,11 Acetazolamide (Diamox), a ■ Electrolyte imbalances
carbonic anhydrase inhibitor, promotes the loss of bicar- As seen with Mr. H, electrolyte imbalances are commonly
bonate by inhibiting reabsorption in the renal tubules and encountered with acid-base imbalances. Sodium is the most
may be utilized in patients with urine Cl- levels greater than abundant extracellular cation with a normal range of 135 to
25 mEq/L (termed Cl- unresponsive) and those with saline- 145 mEq/L. Sodium plays a crucial role in body water balance
resistant alkalosis.6,7,11 In severe refractory alkalemia, a pH as well as with nerve impulse conduction. (See Summary of
greater than 7.6 with organ dysfunction dilute I.V. hydro- electrolyte imbalances.)
chloric acid may be administered with caution.6,7,11 Hyponatremia: Hyponatremia is considered the most
Respiratory acidosis: The foundational management of common imbalance treated and can be of an acute or chron-
any imbalance is aimed at identifying and correcting the ic nature. Hyponatremia is often related to excess free water
cause. Imbalances related to the respiratory system are cor- intake but may also be related to kidney dysfunction or the
rected by managing the airway and ventilation. A patient syndrome of inappropriate antidiuretic hormone (SI-
with a respiratory acidosis may have a decreased respiratory ADH).7,12,13 Serum and urine sodium and osmolality values

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 Identifying acid-base and electroylyte imbalances

are needed for correct diagnosis and management. The analysis is critical to proper identification and management.
clinical presentations of both hyponatremia and hyperna- Treatment goals for patients with hypernatremia include
tremia are very similar and may include altered mental status, identifying the cause, correcting volume disturbances, and
muscle cramps, seizures, and weakness.13,14 Pseudohypona- correcting hypertonicity. Patients with hypernatremia may
tremia may be seen in patients with elevated serum glucose, be treated with infusions of 0.9% sodium chloride to restore
protein, or lipid levels, and evaluation of the serum osmolal- perfusion if needed; otherwise, half normal saline (0.45%
ity will help better identify these patients.3,6,7,13,15 This was the
sodium chloride) infusions are utilized. Loop diuretics may
case with Mr. H in this scenario. His hyperglycemia caused be used to promote natriuresis, and desmopressin (DDAVP)
a pseudohyponatremia. As his hyperglycemia resolved, his can be administered to increase renal reabsorption of water
sodium level normalized. Hyponatremia in a stable patient in patients with DI.6,7,9,15 In patients with hypernatremia,
may be corrected with free water restrictions, but the admin- cerebral edema may develop if the serum sodium is lowered
istration of hypertonic saline (3% sodium chloride) is often too quickly.6,7,12-14
required in the unstable or seizing patient.3,12,13,15 Hypokalemia: Unlike sodium, potassium is the most
Increasing the sodium by only 2 to 4 mEq/L is often abundant intracellular cation and often requires more ag-
enough to decrease cerebral edema and stop seizures.13,15 gressive correction. Potassium has a significant influence on
cellular resting membrane potential,
especially cardiac cells. Hypokalemia,
Patents with hypokalemia may complain less than 3.5 mEq/L, is often associated
with inadequate intake, GI and renal
of muscle cramps or weakness, which could
losses, hyperaldosteronism, or intracel-
progress to respiratory failure. lular shifts.
Patients with hypokalemia may
complain of muscle cramps or weak-
The use of a vasopressin antagonist may be beneficial in ness, which could progress to respiratory failure. Hypoka-
some patients, especially those with hyponatremia resulting lemia can be associated with flattened or inverted T waves,
3,6,7,12,13
from hepatic or cardiac failure or SIADH. Vasopressin the presence of a U wave, and ST depression; therefore, a
antagonists, often referred to as the “vaptans,” primarily 12-lead ECG should be obtained. Hypokalemia, depending
block the effect of vasopressin in the kidneys and prevent on the severity, should be corrected with oral replacement,
the reabsorption of free water.7,13 To prevent rapid fluid shifts which is considered the safest and/or I.V. replacement, which
and severe neurological complications, the serum sodium is the fastest.3,6,7,16 A dose of 10 mEq of K+ replacement will
should be corrected by no more than 1 to 2 mEq/L/hour increase the serum potassium by 0.10 mEq/L.6 Hypomag-
and no more than 10 to 12 mEq/L/day; however, these nesemia is sometimes associated with hypokalemia and must
numbers are often debated.6,7,9,13,14 Patients with chronic be corrected first in cases of refractory hypokalemia.2,3,16
sodium imbalances are at an increased risk for complications Hyperkalemia: Hyperkalemia, greater than 5.2 mEq/L,
and should be corrected at rate of no more than 8 mEq/L/ may be associated with acidosis, kidney disease, hypoaldo-
day.2,6,13 If Na+ is increased too rapidly, central pontine steronism, significant tissue trauma, and some medications,
myelinolysis or osmotic demyelination can occur.6,7,12-14 including: potassium-sparing diuretics, potassium supple-
Hypernatremia: Elevated serum sodium levels are fre- ments, succinylcholine, angiotensin-converting enzyme
quently associated with excessive water loss, including dia- inhibitors, angiotensin II receptor blockers, and renin in-
betes insipidus (DI).7,14 As previously mentioned, clinically, hibitors. Hemolysis is often a cause of a pseudohyperkale-
sodium imbalances present similarly; therefore, laboratory mia and should be considered, especially if the patient is

Primary acid-base disorders and responses2-7

Primary disorder Primary imbalance Pulmonary response Secondary response

Respiratory acidosis ↑ PaCO2 ↑ Respiratory rate ↑ HCO3
Respiratory alkalosis ↓ PaCO2 ↓ Respiratory rate ↓ HCO3
Metabolic acidosis ↓ HCO3 ↑ Respiratory rate ↓ PaCO2
Metabolic alkalosis ↑ HCO3 ↓ Respiratory rate ↑ PaCO2

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 Identifying acid-base and electroylyte imbalances

asymptomatic. As with hypokalemia, hyperkalemia can

cause muscle weakness, paralysis, and respiratory arrest. A Causes of anion gap acidosis9,10
12-lead ECG should be evaluated quickly for the presence
of peaked T waves, a prolonged PR interval, or widened M Methanol (ingredient in solid fuels, solvents,
windshield wiper fluid)
QRS if hyperkalemia is suspected or known. In severe
hyperkalemia, greater than 6.5 mEq/L, the QRS and T wave U Uremia (kidney failure)
will continue to widen and form a sine wave, which will D Diabetic ketoacidosis
lead to malignant dysrhythmias and death. The absence of P Propylene glycol (preservative
ECG changes does not rule out a hyperkalemic emergency, in some I.V. medications)
and lab evaluation is still warranted.17 If the patient is ex- I Ingestion, iron, isoniazid (INH)
periencing cardiac irritability, I.V. calcium administration L Lactic acidosis
will stabilize the cardiac cells by increasing the resting
E Ethylene glycol (common ingredient in antifreeze)
membrane potential, prevent life-threatening dysrhyth-
S Salicylates (aspirin)
mias for 30 to 60 minutes, and may be repeated if need-
ed.2,3,6,17 If the patient is taking digitalis, hypercalcemia may
potentiate toxicity and should be used with caution, and
acute toxicity will potentiate hyperkalemia. tetany (Trousseau sign and Chvostek sign), and hyperactive
There are two approaches to the management of hyper- deep tendon reflexes (DTRs) but can progress to laryngeal
kalemia: First, the K+ may be temporarily shifted back into stridor, seizures, and heart failure.6,7 The 12-lead ECG should
hepatic and muscle cells. This usually lasts 1 to 2 hours and be evaluated for a lengthened QT interval and bradycardia
allows time to prepare for more definitive measures. I.V. in- in hypocalcemia.
sulin is considered the fastest and most effective method.2,3,6,7,17 Depending on the severity, Ca++ may be replaced by oral
However, I.V. sodium bicarbonate administration may be or I.V. formulations.3,6,7,9,19 The patient’s phosphorus and
effective—especially in the setting of a metabolic acidosis.2,3,6,9 magnesium levels must be assessed and corrected, if needed,
High-dose beta2-agonist nebulization will also stimulate the before initiating Ca++ replacement.19
sodium-potassium pumps (Na-K-ATPase), though not as Hypercalcemia: Hypercalcemia, greater than 10.5 mg/
quickly or effectively and temporarily shift K+ back into the dL or ionized level greater than 5.3 mg/dL, is most often
cells.2,3,6,9,17 I.V. dextrose should be administered with insulin associated with hyperparathyroidism, and calcium levels
to prevent hypoglycemia, if needed. The combination of two greater than 14 mg/dL are often associated with malignan-
shifting methods is more effective at lowering the serum cies. Hypercalcemia is associated with muscle weakness,
potassium in an emergency than the use of a single agent.17 stupor, delayed DTRs, vomiting, and constipation. In pa-
Definitive correction is best accomplished with hemo- tients with hypercalcemia, the 12-lead ECG may show a
dialysis.2,3,7,17 The use of I.V. loop diuretics may help lower shortened QT interval and/or atrioventricular and bundle
serum potassium levels in patients with adequate renal branch blocks. In the setting of hypercalcemia, I.V. fluid
function, but their effects are slow and limited.3,9 Cation administration is often first utilized to correct hypovolemia
exchange resins (sodium polystyrene in sorbitol [Kayexalate] and improve kidney perfusion. Then the I.V. administration
may take 4 to 6 hours to be effective). There is limited evi- of a loop diuretic, a bisphosphonate, a glucocorticoid, and/
dence that it actually increases colonic potassium loss.18 The or an injection of calcitonin may be utilized depending on
use of an exchange resin with sorbitol has been associated the severity of the imbalance.3,6,7,9 I.V. bisphosphonates are
with numerous cases of bowel necrosis and should be used now viewed as the mainstay of treatment, are highly effective,
cautiously or avoided.3,7,17,18 but may take 1 to 2 days to show an effect.3,7,20,21 Calcitonin
Hypocalcemia: Calcium is also important for neuro- has the most rapid onset but has limited effect and may only
muscular function as well as bone health. Hypocalcemia, decrease the serum calcium by 2 mg/dL.3,6,7,20,21 Dialysis may
less than 8.5 mg/dL or ionized level less than 4.6 mg/dL, is be needed to correct a life-threatening imbalance.3,20,21
often associated with malabsorption from the GI tract, vi-
tamin D deficiency, and hypoparathyroidism, but is also ■ Case study revisited
seen with hyperventilation, alkalosis, massive blood transfu- As for Mr. H, he had multiple imbalances, including a life-
sions, and kidney failure. Occasionally, providers may en- threatening metabolic acidosis. This warranted admission
counter pseudohypocalcemia related to hypoalbuminemia. to an ICU. His anion gap acidosis and elevated lactate and
Patients with hypocalcemia often experience neuromus- hypovolemia were corrected with I.V. fluids and treatment
cular excitability, including paresthesias, muscle cramps/ focusing on the cause, which was DKA. I.V. insulin is a

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 Identifying acid-base and electroylyte imbalances

Summary of electrolyte imbalances2,3,6,7,9,12-17,19-21

Sodium (Na+) Potassium (K+) Calcium (Ca++)

Causes of hypo- Excess free water Renal and GI losses, Malabsorption,
intake, SIADH inadequate dietary intake hypoparathyroidism
Managementof hypo- Fluid restrictions, Oral or I.V. replacement; Oral or I.V. replacement;
(varies on severity) hypertonic saline infusion, check magnesium level check magnesium and
vasopressin antagonist phosphorus levels
Causes of hyper- Excess water loss, Hemolysis, tissue trauma, Malignancy,
diabetes insipidus medications, renal disease hyperparathyroidism
Management of hyper- I.V. fluid replacement, I.V. calcium to stabilize I.V. fluid replacement, I.V.
(varies on severity) natriuresis with a loop cardiac cells, I.V. insulin and bisphosphonate and/or
diuretic, vasopressin glucose to shift K+ back in the calcitonin, and/or dialysis
replacement cells, dialysis to remove the K+

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