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60-1
HYPOKALEMIA AND
HYPOMAGNESEMIA
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CASE SUMMARY
A 45-year-old Caucasian woman with a history of nonischemic
cardiomyopathy with ICD placement, pulmonary hypertension,
hypertension, hypothyroidism, asthma, diabetes, and other medical problems presents to the emergency department with increased
shortness of breath. History, physical examination, and diagnostic
tests are indicative of an acute exacerbation of chronic heart failure
with volume overload. Laboratory evaluation reveals hypokalemia,
hypomagnesemia, hyponatremia, hypocalcemia, and hypoalbuminemia. The patient has multiple possible causes for the electrolyte
abnormalities, including diuretic use. Correction of the serum
calcium concentration for hypoalbuminemia suggests that no treatment is required for hypocalcemia. The reader is asked to develop a
cohesive plan to diurese the patient and treat both the hypokalemia
and hypomagnesemia on an inpatient basis.
QUESTIONS
Problem Identification
1.a. Create a list of the patient’s drug therapy problems.
• Hypokalemia, hypomagnesemia, hyponatremia that are not
treated; pseudohypocalcemia
• Hypervolemia secondary to HF
• Hyperglycemia
• Medications without an indication: omeprazole, loratadine,
meclizine, and folic acid
• Untreated pulmonary hypertension
1.b.What information (signs, symptoms, and laboratory values) indicates the presence and severity of the electrolyte
abnormalities?
Hypokalemia:
• The normal range for serum potassium concentration is 3.5–
5.0 mEq/L. Mild hypokalemia is defined as a serum potassium
between 3.0 and 3.5 mEq/L; moderate hypokalemia is defined
as a serum potassium of 2.5–3.0 mEq/L; and severe hypokalemia is defined as a level <2.5 mEq/L. This patient has moderate
hypokalemia (2.8 mEq/L).
• The signs and symptoms of hypokalemia are quite variable,
depend on the acuteness of the electrolyte loss, and are usually
not observed until the serum potassium concentration falls
below 3.0 mEq/L. Most symptoms are caused by changes in the
cellular resting potential and membrane excitability, which are
related to the ratio of intracellular-to-extracellular potassium.
Hypokalemia causes a hyperpolarization of the resting membrane potential, resulting in impaired muscle contraction.
Many patients with mild hypokalemia have no symptoms,
but as hypokalemia progresses, nonspecific symptoms such
Hypomagnesemia:
• The normal range for serum magnesium is 1.5–2.0 mEq/L.
This patient’s level of 1.3 mEq/L signifies a mild magnesium
deficit; however, serum magnesium is not an accurate indicator of body magnesium stores because magnesium is a major
intracellular cation.
• The patient does not exhibit any signs or symptoms of hypomagnesemia such as tremor, twitching, or palpitations. Refer
to the textbook chapter on potassium and magnesium homeostasis for a complete discussion of hypomagnesemia.
• The patient also appears to have hypocalcemia (see below),
which often accompanies hypomagnesemia.
Hyponatremia:
• The normal range for serum sodium is 135–145 mEq/L.
This patient’s level of 130 mEq/L signifies mild hyponatremia. Symptoms of hyponatremia are often not seen until
the sodium drops to <125 mEq/L (nausea and malaise). A
serum sodium between 115–120 mEq/L often correlates with
symptoms of headache, lethargy, confusion, or unsteadiness.
Once the serum sodium drops to <115 mEq/L, a patient may
develop delirium, seizures, coma, respiratory arrest, or death.
This patient does not exhibit any of these symptoms.
Hypocalcemia:
• The normal range for total calcium is 8.5–10.5 mg/dL. The occurrence of signs and symptoms of hypocalcemia may be directly
related to the time course over which the abnormality occurs.
Currently, she is not showing any signs of hypocalcemia. See
the textbook chapter on calcium and phosphorus homeostasis
for a complete discussion of hypocalcemia. With a total serum
calcium concentration of 8.3 mg/dL, the patient appears to be
hypocalcemic, but a serum albumin is necessary to correctly
assess total serum calcium concentrations because of calcium’s
affinity for albumin. A normalized or corrected calcium concentration (Cacorr) can be calculated with the following equation:
Cacorr = O
bserved calcium + 0.8 (normal albumin
– observed albumin)
Cacorr = 8.3 mg/dL + 0.8 (4.0 – 3.0) = 9.1 mg/dL
Because the corrected calcium is within the normal range,
this suggests that the patient’s ionized calcium is within normal limits and no calcium replacement is necessary.
1.c. What are the potential causes of the electrolyte disorders in
this patient?
Hypokalemia:
• Diuretic use is the most common pharmacologic cause of
hypokalemia. Both thiazide and loop diuretics can cause an
increase in the renal excretion of potassium, and the incidence of hypokalemia is related to both dose and treatment
Copyright © 2017 by McGraw-Hill Education. All rights reserved.
Hypokalemia and Hypomagnesemia
Denise R. Sokos, PharmD, BCPS
• Hypokalemia can result in a variety of cardiac arrhythmias, ranging from bradycardia to ventricular fibrillation; however, they
are very rare. In patients with cardiovascular ischemia or heart
failure, even small decreases in serum potassium can result in
arrhythmias. An ECG was performed in this patient, and hypokalemia-associated ECG changes (broad T waves and the occurrence of a U wave) were not found. Polyuria and polydipsia may
also occur in chronic hypokalemia. The patient is also hypomagnesemic, which often occurs in conjunction with hypokalemia.
CHAPTER 60
60
as generalized weakness and fatigue can occur. Patients with
a chronic loss of potassium may have few symptoms because
intracellular potassium moves extracellularly, thus restoring
the intracellular-to-extracellular potassium ratio.
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SECTION 5
duration.1 In addition to increased renal losses of potassium,
hypovolemia induced by the diuresis causes the release of
aldosterone, which can further increase potassium loss. A
potassium-sparing diuretic can be used in combination with a
potassium-wasting diuretic to prevent hypokalemia. This particular patient is receiving furosemide, metolazone, spironolactone, and a potassium supplement. The spironolactone and
potassium are not sufficient to offset the potassium-wasting
effects of the furosemide and metolazone in this case.
Renal Disorders
• Diarrhea is one of the most common nonpharmacologic causes
of hypokalemia. The normal concentrations of potassium and
bicarbonate in the stool are very high (approximately 10
and 40 mEq/L, respectively) and increase proportionally
with the volume of stool. Diarrhea may cause both decreased
absorption and increased secretion of potassium. The loss of
bicarbonate and potassium commonly causes a hypokalemic
metabolic acidosis. This patient does not complain of diarrhea
but may have GI losses due to her magnesium supplementation, which often causes diarrhea. Diuretic-induced hypokalemia usually results in metabolic alkalosis, and the patient does
appear to have a metabolic alkalosis based on serum bicarbonate levels; however, arterial blood gases are not available.
• Insufficient intake of potassium is rarely a cause of hypokalemia due to the kidney’s ability to efficiently conserve potassium. However, in periods of increased losses, intake may not
be sufficient to make up for the amount of potassium loss. The
patient is prescribed a potassium supplement, but the dose is
inadequate to overcome her losses.
• Hypomagnesemia is often a concomitant disorder in patients
with hypokalemia, especially those taking diuretics. Diabetic
ketoacidosis is another clinical situation in which hypokalemia
and hypomagnesemia commonly occur together. Hypomagnesemia may lead to increases in both renal and fecal losses of
potassium via decreased intracellular transport of potassium.
Hypomagnesemia exacerbates hypokalemia via increasing
distal potassium secretion in the nephron.2 Therefore, hypokalemia cannot be corrected until hypomagnesemia is corrected.
A serum magnesium concentration should always be checked
in patients with persistent hypokalemia, especially those resistant to replacement therapy.
Hypomagnesemia:
• Both thiazide and loop diuretics inhibit the reabsorption of
magnesium, and hypomagnesemia commonly occurs with
diuretic use.3 In fact, more than one-third of patients receiving thiazide or loop diuretics have this electrolyte disorder
(refer to the textbook chapter on potassium and magnesium
homeostasis). Proton-pump inhibitors are also known to cause
hypomagnesemia, although the mechanism is unclear.
• Diarrhea (especially if chronic) can result in significant magnesium losses, as intestinal fluids contain approximately
14 mEq/L of magnesium. Although this patient is not complaining of diarrhea, she is taking a magnesium supplement,
which can cause diarrhea.
• Malnutrition commonly results in hypomagnesemia because
of decreased magnesium intake and increased renal elimination of magnesium. The patient is hypoalbuminemic, which
may be suggestive of malnutrition; however, this patient is
obese. Therefore, the hypoalbuminemia is more likely related
to heart failure than to malnutrition.
Hyponatremia:
• There are three classifications of hyponatremia: hypervolemic
hyponatremia, euvolemic hyponatremia, and hypovolemic
Copyright © 2017 by McGraw-Hill Education. All rights reserved.
hyponatremia. In a heart failure patient exhibiting signs and
symptoms of fluid overload, the most likely classification is
hypervolemic hyponatremia (a.k.a. dilutional hyponatremia).
In this case, there is an excess of sodium and fluid, but the
excess fluid predominates. Heart failure exacerbations lead to
tissue hypoperfusion, which triggers ADH secretion, causing
reabsorption of water in the collecting tubules of the kidneys.
This culminates in hyponatremia.
• Medications (eg, diuretics) can also cause hyponatremia. In
this case, the thiazide diuretic is the most likely cause. There
are three contributing factors to thiazide-induced hyponatremia: excess free-water intake, reduced free-water clearance,
and renal sodium and/or potassium losses. Thiazide diuretics
inhibit sodium reabsorption in the distal convoluted tubule
leading to an inhibition of urinary dilution capacity. Additionally, due to diuretic action and an increase in ADH, sodium
losses may be higher than water losses.
• Hypokalemia can also cause hyponatremia because sodium
will enter cells to account for the reduction of intracellular
potassium to maintain cellular electroneutrality.
Hypocalcemia:
• Hypoalbuminemia is the most common cause of laboratoryreported hypocalcemia. In this case, a corrected calcium
concentration should be calculated or an ionized calcium
concentration measured. Hypoalbuminemia is common
in chronic heart failure and may be related to an underlying inflammatory process. In this patient, the decrease in
albumin concentration may also be a dilutional effect related
to volume overload. Heart failure can induce a catabolic
state leading to cachexia, but this is not the case in this obese
patient.
1.d.What additional information is needed to satisfactorily
assess this patient’s electrolyte disorders?
• For evaluation of the hypokalemia, urinary sodium, potassium, and osmolality, with concurrent serum values, are
usually necessary to investigate the source of losses and the
patient’s volume status. If the urinary potassium is <20 mEq/L,
then extrarenal losses are more likely. Urinary potassium
concentrations of >20 mEq/L generally indicate renal potassium losses. In this patient, urinary potassium concentrations
should be elevated because the patient is receiving furosemide
and metolazone. Spironolactone decreases urinary potassium
levels, thus further complicating the diagnostic utility of the
test and making it unnecessary.
• Low urinary sodium concentrations indicate a volumedepleted state; however, because of the patient’s current
diuretic use, urinary sodium concentrations are expected
to be high. The patient’s clinical presentation suggests volume overload (ie, edema in the pulmonary vasculature and
lower extremities, shortness of breath). Because of this and
the normal pathology associated with heart failure, urinary
sodium concentration would not provide valuable assessment information.
• Urinary osmolality is normally 900–1400 mOsm/kg. In a
hypokalemic state, the osmolality slowly decreases over weeks
but generally does not fall below 300 mOsm/kg. Because of
this, urine output normally stays below 3 L per day. Maximal
osmolality begins to fall when the total body potassium deficit
exceeds 200 mEq and reaches a minimum with a deficit of
400 mEq (the reflective serum concentration should be below
3.0 mEq/L). This is in contrast to diabetes insipidus, where
the osmolality may be below 150 mOsm/kg. Because of this
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Desired Outcome
2.What are the goals of pharmacotherapy in this patient?
Primary outcomes:
• Replace potassium and magnesium deficiencies without
overcorrecting.
• Treat hyperglycemia and prevent hypoglycemia.
• Prevent further losses of electrolytes.
Secondary outcomes:
• Prevent future heart failure exacerbations.
• Prevent venous thromboembolism.
• Continue to treat hypertension, asthma, hypothyroidism, and
anxiety disorder.
• Treat pulmonary hypertension.
• Discontinue unnecessary medications.
• Ensure preventive health measures are up to date or scheduled.
Therapeutic Alternatives
3.What feasible pharmacotherapeutic alternatives are available
for treatment of hypervolemia, hypokalemia, and hypomagnesemia in this patient?
Hypervolemia:
• The patient has clinical signs and symptoms of significant
volume overload probably due to her recent diet choices.
Although she is taking furosemide, metolazone, and spironolactone orally, she is retaining excess fluid. Heart failure
patients have a delay in the time of absorption as well as a
delay in the overall extent of absorption of oral furosemide
causing an unpredictable response. Some patients respond
more favorably to torsemide or bumetanide, as they are more
bioavailable. Current practice guidelines recommend intravenous loop diuretics as the first choice for the treatment of acute
fluid overload.4
• Loop diuretics have a relatively short half-life, and sodium
reabsorption in the tubule resumes after the tubule concentration of the diuretic declines. To obtain an adequate diuresis,
some patients may require dosing of the diuretic several times
per day. Some providers may choose to use a continuous
IV infusion. However, there is not a statistically significant difference in symptoms, diuresis, or outcomes between continuous infusion and intermittent doses. Provider preference will
dictate whether multiple daily doses or continuous infusions
are used.
• The addition of intravenous vasodilator therapy should be
considered if the response to diuretic therapy is not adequate.
The patient’s blood pressure is adequate at the time of presentation and vasodilator therapy could be used if needed.
• Note that the treatment of hypervolemia will also treat the
hyponatremia in this patient.
Hypokalemia:
• Because the kidneys are the primary regulators of potassium
excretion, a patient’s renal function should be assessed before
instituting potassium replacement. In patients with renal
insufficiency, potassium replacement should be approached
cautiously, because hyperkalemia may develop. The patient’s
IBW kg (female) = 45.5 kg + 2.3 (height in inches above 60)
IBW = 45.5 kg + 2.3 (5) = 57 kg
For drug dosing, use the Cockcroft–Gault equation to
calculate the patient’s CLcr:
CLcr (female) =
CLcr =
(140 – age) × IBW(kg) × 0.85
72 × SCr
(140 – 45) × 57 kg × 0.85
72 × 1.0 mg/dL
CLcr = 64 mL/min
Based on this calculation, this patient does not have renal
insufficiency. Note that to correctly calculate CLcr, use IBW
rather than total body weight (TBW). If the patient’s TBW
(87 kg) were used in the above equation, the result of 96 mL/min
would be an overestimation of her true renal function.
• Potassium chloride, phosphate, and bicarbonate salts are the
available formulations of potassium and are equally efficacious.
The oral route is preferred unless there are life-threatening
symptoms or the patient is unable to tolerate oral intake.
Chloride salts are generally used in patients with alkalosis to
replenish chloride stores depleted by diuretic use, vomiting, or
nasogastric suctioning. Normally, sodium is reabsorbed in the
renal tubules with chloride; however, when chloride stores are
depleted, hydrogen and/or potassium ions are exchanged for
sodium ions. When hypokalemia occurs, hydrogen ions are
exchanged for sodium, resulting in a metabolic alkalosis. Chloride and fluid replenishment decrease the exchange of hydrogen ions for sodium ions in the renal tubules, therefore helping
to correct the alkalosis. Phosphate salts should be reserved for
concomitant hypophosphatemia. Bicarbonate salts are used
in metabolic or renal tubular acidosis to replace bicarbonate.
• Oral potassium is available in four dosage forms: elixirs, powders, capsules, and tablets. The extended-release tablets are
available as wax-matrix or microencapsulated formulations.
The microencapsulated formulations are preferred because
they disintegrate better in the stomach and cause less GI erosion. The elixir is the least expensive formulation but has very
poor patient adherence during chronic therapy because of its
unpleasant taste and resulting nausea. Regardless of the preparation used, all products are well absorbed.
• Parenteral potassium replacement is the preferred route when
the patient is unable to take oral medications, when signs and
symptoms of hypokalemia are present, or when hypokalemia is life threatening. In general, 10–20 mEq/hour can be
safely administered and repeated based on serum potassium
concentrations. In rare instances of severe hypokalemia with
life-threatening symptoms, a rate of 40–100 mEq/hour may be
used. ECG monitoring is required if potassium is to be administered at a rate of 20 mEq/hour or greater and may be warranted if administration exceeds 10 mEq/hour. The maximum
concentration for peripheral administration is 40 mEq/L;
higher concentrations may be painful and cause venous irritation. When potassium is administered through a central line,
10–20 mEq/100 mL may be given over 1 hour, with concurrent ECG monitoring. Whenever parenteral therapy is used,
frequent laboratory monitoring is necessary.5 High variability
exists in dosing recommendations; therapy should be guided
by the patient’s condition and laboratory results.
Copyright © 2017 by McGraw-Hill Education. All rights reserved.
Hypokalemia and Hypomagnesemia
• Treat hypervolemia and hyponatremia.
current weight is 87 kg, but she is obese, and her ideal body
weight (IBW) should be calculated to accurately estimate her
creatinine clearance (CLcr):
CHAPTER 60
patient’s diuretic use and history of heart failure, the urine
osmolality will be difficult to interpret.
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Hypomagnesemia:
SECTION 5
• As with potassium, the kidneys are the primary regulators
of magnesium homeostasis, and renal function should be
assessed before initiating magnesium replacement. In the setting of renal insufficiency, the risk of hypermagnesemia with
replacement is much greater. This patient’s CLcr is 64 mL/min,
indicating that she does not have impaired renal function.
Patients are not considered to have clinically important renal
dysfunction until their CLcr is <60 mL/min.
Renal Disorders
• Oral magnesium gluconate or oxide may be given in most
situations and is the treatment of choice for asymptomatic
patients. Magnesium gluconate is the preferred agent because
magnesium oxide can cause an osmotic diarrhea.
• IV magnesium sulfate is warranted when the serum concentration is <1.0 mEq/L or when acute symptoms are present.
For life-threatening symptoms, give a 2 g IV bolus over
1 minute followed by an infusion of 0.5 mEq/kg lean body
weight (LBW) over 5–6 hours. An additional 0.5 mEq/kg LBW
should be administered as a continuous infusion over the next
18 hours. For serum concentrations of <1.0 mEq/L without lifethreatening symptoms, a total of 1.0 mEq/kg LBW should be
given over 24 hours. Initially, one-half of the dose (0.5 mEq/kg
LBW) should be given as an infusion over 2–6 hours (not to
exceed 150 mg/min), with the remainder of the dose given
as a continuous infusion. Extended replacement is warranted
because even when severe deficiencies are present, approximately 50% of an administered dose is excreted in the urine.
Optimal Plan
4.a. Given the therapeutic alternatives outlined above, what is
the most appropriate therapy for treatment of hypervolemia, hypokalemia, and hypomagnesemia in this patient?
Hypervolemia:
• This patient developed edema on an oral dose of furosemide
80 mg BID; practice guidelines recommend initiating an intravenous dose that is equal to or exceeds her oral dose.4 The oral
bioavailability of furosemide has large intra- and interpatient
variability. In general, the bioavailability is considered to be
50%. That is, 40 mg orally is equivalent to 20 mg intravenously.
A reasonable choice is to start with furosemide 80 mg IV
BID. Monitoring should include the laboratory parameters of
BUN, serum creatinine, and the BUN/SCr ratio and the physical examination findings of pulmonary and lower-extremity
edema, supine and standing vital signs, volume intake, urine
output, and daily weights.
• Spironolactone is not available intravenously and the oral
formulation should be continued at its current dose. Consider
discontinuing the metolazone, as it may be a contributor to the
hyponatremia. While hospitalized, her fluid status can be balanced with intravenous loop diuretic dose titration.
Hypokalemia:
• The first step in the assessment of this patient’s hypokalemia
is to calculate the potassium deficit. In the early phases of
hypokalemia, a 1 mEq/L decrease in the serum potassium concentration reflects a 100–200 mEq total body loss. However,
once the serum potassium is <2.5 mEq/L, a further 1 mEq/L
drop in serum potassium represents total body deficits of
200–400 mEq. This patient’s deficit is approximately 200 mEq.
This implies that a single dose will not be sufficient to correct
her serum potassium. For mild deficits, 40–80 mEq per day is
appropriate. More severe deficits may require 300–400 mEq
Copyright © 2017 by McGraw-Hill Education. All rights reserved.
per day with frequent monitoring. These are only estimates
as potassium replacement is guided by the serum potassium
concentration.
• Because the patient is receiving a higher dose of IV furosemide,
intravenous potassium chloride should be administered to correct her current potassium deficit and to replace the potassium
she will lose. A starting dose of 60 mEq IV in divided doses is
appropriate. Her oral supplements may be continued. Additional IV doses of KCl will likely be necessary to replenish her
stores. During replacement therapy, intracellular potassium
must be restored before changes will be reflected in the serum
potassium. Laboratory results will determine the dose and
frequency of additional KCl doses.
• Because this patient is also hypomagnesemic, magnesium
replacement is necessary for potassium replacement to be
successful.
Hypomagnesemia:
• The patient is currently taking magnesium oxide 400 mg PO
TID for hypomagnesemia. Increase the dose to 800 mg PO BID
with close monitoring of serum levels, because she will likely
have additional losses with the higher dose of furosemide.
The dose may be increased as necessary to maintain normal
serum magnesium levels. Intravenous magnesium sulfate may
be indicated if the serum level falls below 1.0 mEq/L. In that
scenario, give 1 mEq/kg LBW (55 mEq); one-half of the dose
as a bolus infusion over 2–6 hours, and the remainder as a
continuous infusion on day 1. On days 2–5, give 0.5 mEq/kg
LBW per day (30 mEq) as a continuous infusion. To be practical, doses should be rounded to the nearest 5 mEq or 0.5 g of
magnesium sulfate.
Treatment Summary:
• Continue the spironolactone. Increase the magnesium oxide
dose to 800 mg PO BID. Intravenous KCl 20 mEq given over
2 hours × 3 with telemetry ECG monitoring (because of KCl at
a rate of 10 mEq/hour and the heart failure) is an appropriate
initial strategy. Continue the oral KCl 80 mEq BID. Discontinue the oral furosemide and initiate furosemide 80 mg IV
BID with the monitoring outlined above. If the diuresis is
inadequate, there are two options: (1) if the 80-mg dose does
not provide an increase urine output, then a higher dose will
be necessary; (2) if the 80 mg dose increases urine output,
but there is rebound sodium resorption during time when
the diuretic blood levels are low, then additional daily doses
would be necessary. Multiple daily doses provide more diuresis
and less physiologic disturbance than larger single doses. The
diuretic dose should be titrated to alleviate symptoms and
reduce extracellular fluid volume excess.
4.b.What therapy changes should be made for the patient’s
heart failure and hyperglycemia?
• For the treatment of heart failure, she is receiving all of the
recommended medications at appropriate doses except for
digoxin. The recommended dose is 0.125 mg per day. Clinical practice guidelines recommend decreasing the dose to
avoid toxicity; especially in the setting of hypokalemia as the
arrhythmogenic potential of digoxin is enhanced in the setting
of hypokalemia. Increasing the spironolactone dose to 50 mg
daily is not recommended because of the risk of hyperkalemia; adjusting the potassium dose is preferred. This patient’s
requirement for supplemental potassium is unusual; in most
clinical scenarios when spironolactone is initiated potassium
supplementation is discontinued or titrated downward as most
60-5
Outcome Evaluation
5.What clinical and laboratory parameters are necessary to
evaluate the therapy for the desired therapeutic outcome and
prevention of adverse effects?
• While the patient is hospitalized, monitor serum potassium
concentrations initially every 4 hours (after every 30–40 mEq
has been given). After initial replacement, potassium should be
monitored daily until stable.
• Monitor magnesium concentration twice daily initially, and
then every few days after the electrolytes are stable.
• A 12-lead ECG does not need to be monitored for her electrolyte
abnormalities alone unless signs and symptoms of hypokalemia
or hyperkalemia are present. However, the majority of patients
admitted with acute exacerbations of heart failure are continuously monitored via telemetry during their hospitalization.
• Monitor HR (inpatient and outpatient) because the digoxin
dose is being reduced. In heart failure, the beta-blocker dose is
titrated to a HR of 50–60 bpm or the target dose recommended
in practice guidelines. Adjustments could be made as necessary in the future.
• Monitor renal function daily while hospitalized to assess for
the development of azotemia secondary to the diuresis.
• Measure fluid intake, urine output, and vital signs (especially
for hypotension) every shift. The patient’s weight and lowerextremity edema should be assessed daily.
• Monitor other electrolytes daily to assess for the development
of hypo- or hyper-electrolyte disorders (or any time signs or
symptoms of a disorder are noted). These monitoring guidelines are valid only during hospitalization; outpatient monitoring is less intensive and much more difficult. After this patient
is discharged, she should return in approximately 3 days to
have her serum magnesium and potassium concentrations
measured. She should then return weekly for serum magnesium and potassium concentration measurements until stable.
• Monitor the patient for signs of toxicity from the electrolyte
replacement therapy:
✓Discontinue potassium therapy if the serum levels are
>5.0 mEq/L, if peaked T waves are noticed on ECG, or if
there is a sudden onset of muscle weakness. Additionally,
the patient should be monitored for pain and phlebitis with
IV therapy and GI irritation when switched to oral therapy.
✓Discontinue magnesium therapy if the serum concentrations are >2.0 mEq/L. Additionally, monitor the patient for
muscle weakness and cardiac and respiratory abnormalities.
✓Monitor the serum phosphate and chloride concentrations
during potassium and magnesium replenishment. If the
serum phosphate concentration drops below 2.5 mg/dL,
potassium phosphate can be used instead of potassium chloride. Magnesium sulfate is also compatible with potassium
phosphate in solution.
Patient Education
6.What information should be provided to the patient to
enhance adherence, ensure successful therapy, and minimize
adverse effects?
Potassium chloride (eg, K-Dur tablets):
• This medication is a potassium supplement called K-Dur. The
dose is 80 mEq (four tablets) three times a day. This dose may
go up or down if your blood levels show too much or too little
potassium in your body. Continue to take this medicine as
prescribed until your doctor tells you to stop.
• Potassium is essential for the proper function of the heart, kidneys, muscles, nerves, and digestive system. Normally, people
get enough potassium from their diet, but because you take
diuretics (water pills), your body loses too much potassium.
• Take this medicine right after each meal. Take it with a full
glass of water or juice and swallow the tablets whole. If you
cannot swallow the tablets whole, break them in half and take
each half separately with a glass of water.
• If you forget to take a dose, take it as soon as you remember. If
it is <4 hours until your next dose, skip the missed dose completely; never take a double dose.
• Side effects of potassium tablets are generally very mild; you
may notice some abdominal discomfort, nausea, vomiting,
or diarrhea. If you develop confusion or a tingling, burning
sensation in your arms or legs, notify your doctor because your
dose may be too high. Do not adjust the dose on your own.
• Store this medicine at room temperature and out of reach of
children.
Magnesium (eg, Mag-Ox):
• This medication is a 400 mg tablet called magnesium oxide or
Mag-Ox. Magnesium is essential for the proper functioning of
your muscles, heart, and digestive tract. Because you are taking
water pills (diuretics), your body loses too much magnesium
and it needs to be replaced.
• Your doctor prescribed two tablets two times a day, and you
should continue this dose until he/she tells you to stop taking
the medicine. The dose may increase or decrease if your blood
levels show too much or too little magnesium in your body.
• Swallow each tablet with a full glass of water.
• If you forget to take a dose, take it as soon as you remember
and then take any remaining doses at evenly spaced intervals
throughout the day. Do not take doses any closer than 4 hours
apart; do not take a double dose. If you miss a dose, simply skip
the missed dose and go on with your usual regimen.
• Magnesium tablets may cause diarrhea in some patients. If you
develop diarrhea, notify your physician.
• Store this medicine at room temperature and out of the reach
of children.
Copyright © 2017 by McGraw-Hill Education. All rights reserved.
Hypokalemia and Hypomagnesemia
• In an attempt to control the patient’s hyperglycemia while
hospitalized, her current basal and prandial insulin should be
continued. Correction insulin (ie, supplemental insulin that is
used in addition to basal and prandial insulin) should be added
to her regimen to treat premeal hyperglycemic episodes. Her
glycemic goals are premeal blood glucose <140 mg/dL and
random blood glucose <180 mg/dL. To prevent hypoglycemia,
consider adjusting the insulin regimen if blood glucose levels
fall to <100 mg/dL.
If IV therapy is administered, the patient should be supine
(especially for the bolus) and blood pressure should be
monitored. The patient may complain of flushing or sweating during IV magnesium administration.
CHAPTER 60
patients will develop hyperkalemia. Also, consider changing
her diuretic regimen from furosemide to torsemide because
of the increased bioavailability. This might offset the need
for metolazone and better balance her fluid status and serum
sodium. Refer to the textbook chapter on heart failure for a
complete description of the treatment options.
60-6
■■ FOLLOW-UP QUESTIONS
SECTION 5
1.What changes should be made to the patient’s medication
regimen at hospital discharge to prevent future electrolyte
imbalances?
• Increase the potassium chloride dose to 80 mEq PO TID with
careful monitoring.
• Increase the magnesium oxide to 800 mg PO BID with careful
monitoring.
Renal Disorders
2.Develop a plan to monitor this patient’s electrolytes after hospital discharge.
• The patient should return for follow-up within 3 days to assess
her laboratory parameters. If stable, the electrolytes can be monitored weekly for 2–3 weeks and then less frequently once stable.
Given this patient’s severity of disease and comorbidities, it is
likely that she will require more frequent monitoring and dosage adjustments of her potassium and magnesium supplements.
3.What vaccinations should this patient receive?
• The pneumococcal polysaccharide vaccine (PPSV23) is recommended because she is considered high risk for invasive
pneumococcal disease (due to diabetes, chronic heart disease,
and asthma).
• The CDC’s 2015–2016 influenza vaccination recommendations
state that all individuals aged 6 months and older receive the
vaccine each influenza season regardless of underlying medical
conditions. Trivalent and quadrivalent vaccines are available;
the CDC does not recommend one vaccine over another.
Copyright © 2017 by McGraw-Hill Education. All rights reserved.
• Varicella vaccination is appropriate if a reliable history of
infection is not obtainable.
• Tetanus booster (Td) every 10 years. (Note: Tetanus, diphtheria, pertussis [Tdap] vaccine should replace a single dose of Td
in adults <65 years who have not previously received a dose of
Tdap. Adults >65 years without an indicator condition may
also be immunized.)
• Because of her diabetes, the hepatitis B vaccination is indicated.
• Any other vaccine as necessary if the patient is unable to provide documentation of childhood immunizations.
REFERENCES
1. Cohn JN, Kowey PR, Whelton PK, Prisant M. New guidelines for
potassium replacement in clinical practice. A contemporary review by
the National Council on Potassium in Clinical Practice. Arch Intern
Med 2000;160:2429–2436.
2. Huang CL, Kuo E. Mechanism of hypokalemia in magnesium deficiency. J Am Soc Nephrol 2007;18:2649–2652.
3. Ayuk J, Gittoes NJL. How should hypomagnesaemia be investigated
and treated? Clin Endocrinol 2011;75:743–746.
4. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for
the management of heart failure: a report of the American College of
Cardiology Foundation/American Heart Association Task Force on
Practice Guidelines. Circulation 2013;128:e240–e327.
5. Kraft MD, Btaiche IF, Sacks GS, Kudsk KA. Treatment of electrolyte
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