A Real Danger of Overdiuresis in Patients with HR

J Int Transl Med, 2014, 2(4):482-484; doi: 10.11910/2227-6394.2014.02.04.12

Open Access

Case Report

Furosemide Induced Electrolyte Imbalance: A

Real Danger of Overdiuresis in Patients with
Heart Failure
Yaseen Ali*, Amila M. Parekh*, Rahul K. Rao, Mirza R. Baig
Department of Medicine, Ohio University, 120 Chubb Hall Athens, Ohio, 45701, United States

ABSTRACT
Background: Chronic heart failure is one of the most common reasons for hospital admissions in
the United States. There have been several approaches for treating heart failure but loop diuretics
has been at the forefront to alleviate the symptoms. Loop diuretics have their own side effects as
with any medication use, and a lesser known and monitored one is metabolic alkalosis.
Case report: The patient was a 76-year-old female with past medical history of diabetes,
hypertension, chronic kidney disease, dyslipidemia and chronic heart failure who came to the
hospital with progressive shortness of breath for the past few days and was started on aggressive
diuresis with intravenous loop diuretics and well responded. On the morning of d 6 of her
admission, she was kept on the floor and started on BIPAP to correct hypercarbia and respiratory
acidosis due to metabolic alkalosis and back to baseline with normal mentation by the middle of
the day.
Conclusion: Hypokalemia due to the diuretic effect can cause alkalosis by resulting in the shift
of hydrogen ions intracellularly, stimulating the apical H+/K+ATPase in the collecting duct,
stimulating renal ammonia genesis, reabsorption, and secretion, leading to impaired chloride ion
reabsorption in the distal nephron and reducing the glomerular filtration rate (GFR). The patient
improved after being started on oxygen therapy and switched to acetazolamide as an alternative
diuretic, indicating that acetazolamide corrects the effect of metabolic alkalosis by causing
metabolic acidosis due to decrease reclamation of bicarbonate at the level of proximal convoluted
tubule.

Key words: Metabolic Alkalosis; Over-diuresis; Heart Failure

*Corresponding Author:

Yaseen Ali, Email: ya199312@ohio.edu;

Amila M. Parekh, Email: amilaparekhmd@gmail.com

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J Int Transl Med, 2014, 2(4):482-484

be altered, somnolent, and drowsy by the morning staff. She

Introduction
Chronic heart failure is one of the most common reasons for
hospital admissions in the United States[1-3]. In its simple definition,
a patient is diagnosed with heart failure when the heart is unable to
do its physiological work of pumping the blood to the peripheral
[4]

organs . As a result, the peripheral organs are at risk for chronic

ischemia leading to decreased function. More acutely since the heart
is unable to do its work, the excess volume of fluid can accumulate
leading to signs of fluid overload. Patients usually present with these
signs if chronic in an outpatient setting or if in the lungs can present
to the hospital with difficulty in breathing. Historically there have
been several approaches for treating heart failure but loop diuretics
has been at the forefront to alleviate the symptoms. Loop diuretics
have their own side effects as with any medication use, and a lesser
known and monitored one is metabolic alkalosis. We review a case

was alert to verbal and painful stimuli but was not following
commands. Rapid response team was activated and evaluated
the patient promptly by the bedside. Her initial vital signs were
normal except for tachycardia of 140, accucheck of 132, and
a respiratory rate of 8. Although the patient did not follow all
commands her physical exam was benign with resolving signs
of heart failure. Stat labs were ordered including CBC, CMP,
coagulation panel, PT/INR, cardiac enzymes, EKG, and a CXR.
Patient was placed on a non rebreather mask and a stat ABG
was obtained as well. An ABG disclosed 7.30 / 74/ 94 / 42 / 98,
a BMP that was made available revealed bicarbonate to be more
than 40 (internal lab cut off limit). Other studies were baseline.
As part of her work up she had a CT scan of the head which

where a patient developed metabolic alkalosis due to loop diuretics.

was unrevealing as well. Patient was kept on the floor and was

Case Report

By the middle of the day patient was back to baseline with

A 76-year-old female with past medical history of diabetes,

hypertension, chronic kidney disease, dyslipidemia and chronic
heart failure came to the hospital with progressive shortness of
breath for the past few days and was admitted via emergency
department with the primary diagnosis of acute decompensated
heart failure to the telemetry based on labs showing elevated
brain natriuretic peptide (BNP) of more than 1 500, previous
echocardiogram showing an ejection fraction of 25% with
systolic dysfunction, and physical signs such as jugular venous
distention, bilateral crackles in lungs with minimal wheezing,
and bilateral pitting leg edema. A chest X-ray obtained in
the emergency department revealed classic appearance of

started on BIPAP to correct hypercarbia and respiratory acidosis.

normal mentation. A brief review of her chart did not disclose
any inciting event or any causes of her metabolic alkalosis and
acute respiratory acidosis. Her medication profile has been the
same, no narcotics or benzodiazepines were administered except
for aggressive loop diuretics being administered. Her initial labs
revealed bicarbonate of 29 which progressively elevated to a
value of 42 at the time of the incident. It was presumed that the
patient had metabolic alkalosis due to loop diuretics and she was
switched to Acetazolamide.

Mechanism of Action of Loop

Diuretics

cardiomegaly with fluid overload.

Loop diuretics are a class of medications consisting of

After being admitted to the telemetry floor with presumed

act on thick ascending loop of henle via inhibiting the pump

Furosemide, Bumetanide, Ethacrynic acid, and Torsemide. They

diagnosis of heart failure; cardiology was placed on consult and

patient was started on aggressive diuresis with intravenous loop
diuretics and was diuresing well. Since she had prior admissions
for the same diagnosis, her weight was monitored daily apart
from intake and output as part of the standard heart failure
protocol. Her baseline weight was 225 lbs 2 months prior and at
this visit she had a weight of 243 lbs. Based on her increase in
weight it was presumed that she will need to be diuresed multiple
liters of fluid to attain resolution of her symptoms and revert her
back to her baseline status. Patients course was uncomplicated

responsible for reabsorption of Na/K/2 Cl. By inhibiting the

reabsorption of these ions they cause them to be lost in urine
and since water follows sodium; the kidneys ability to reabsorb
water is diminished. In effect, they cause significant diuresis and
are the most potent diuretics in class. Due to their mechanism of
action they can alter the electrolyte balance in the body leading
to various electrolyte losses and side effects per black box
warning.

Conclusion

and she was responding well to the standard regimen.

Metabolic alkalosis due to loop diuretics occurs due to multiple

On the morning of day 6 of her admission she was found to

Na/K/2 Cl pump and decrease their absorption. Due to the

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mechanisms. In essence, loop diuretics act by inhibiting the

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J Int Transl Med, 2014, 2(4):482-484

net decrease absorption of sodium chloride in thick ascending

this impairs renal excretion of the excess bicarbonate.

loop of henle, volume depletion occurs. The volume depletion

stimulates aldosterone secretion, which enhances sodium ion

The patient improved after being started on oxygen therapy,

reabsorption in the collecting duct and increases hydrogen ion

switched to acetazolamide as an alternative diuretic. Acetazolamide

[5]

and potassium secretion in this segment .

has been shown to correct the effect of metabolic alkalosis

by causing metabolic acidosis due to decrease reclamation of

Hypokalemia due to the diuretic effect can cause alkalosis

[5]

bicarbonate at the level of proximal convoluted tubule[6]. Our further

by five different mechanisms : First, hypokalemia results

research regarding this phenomenon did not reveal any published

in the shift of hydrogen ions intracellularly. The resulting

data but indeed represents an area of interest.

intracellular acidosis enhances bicarbonate reabsorption in the

collecting duct. Second, hypokalemia stimulates the apical H+/
K +ATPase in the collecting duct. Increased activity of this
ATPase leads to appropriate potassium ion reabsorption but

Declaration
All authors of this manuscript declare no conflict of interest.

a corresponding hydrogen ion secretion. This leads to a net

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