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Journal of the association of physicians of india • december 2013 • VOL. 61
case reports
Low Dose Methylprednisolone Induced
Bradycardia
HS Darling+, V Marwah*, AK Rajput$, PP Varma# , KK Singh@
Abstract
Methylprednisolone induced arrhythmias, especially bradycardia, are well known. Most of the available
reports suggest the occurrence of these arrhythmias with high dose intravenous therapy. We, hereby
report a case of low dose methylprednisolone induced bradycardia.
Introduction
H
igh dose intravenous methylprednisolone is an important therapeutic modality
for many autoimmune conditions. Adverse effects of this therapy include
hypertension, hyperglycaemia, fluid and electrolyte disturbances and cardiac
arrhythmias (both tachyarrhythmias as well as bradyarrhythmias). 1 Here we report a
33 year old male patient who developed sinus bradycardia during therapy with low
dose intravenous methylprednisolone for clinically and radiologically suspected acute
eosinophilic pneumonia. Bradycardia recovered after cessation of steroid therapy.
Case Report
Resident Medicine, *Graded
specialist, Respiratory
Medicine, $Senior Advisor, Med
and Respiratory Medicine,
#
Senior Consultant, Med and
Nephrology, @ Chief Consultant,
Medicine and Neurology, Army
Hospital, Research and Referral,
New Delhi
Received: 21.12.2011;
Revised: 25.05.2012;
Accepted: 04.06.2012
+
920 
A 33 year old male, was admitted as a case of sepsis with acute lung injury. On fifth day
of admission, he developed rapidly worsening dyspnoea and hypoxaemia. Chest X-ray
showed bilateral peripheral fluffy opacities with central sparing (photographic negative
of pulmonary oedema). He had to be intubated and put on mechanical ventilatory
support. On the basis of clinical suspicion and radiological picture, he was suspected
to be suffering from acute eosinophilic pneumonia and was initiated on intravenous
methylprednisolone 40 mg three times a day as an infusion over 30 minutes each. By
next day, his oxygenation status improved, however he developed sinus bradycardia
(minimum HR 38/min). Clinically his BP and cardiovascular system examination was
normal. His serum potassium was 4.3 meq/dL, serum calcium (corrected) was 9.8 mg/
dL and serum magnesium was 1.9 mg/dL. ECG showed sinus bradycardia (Figure 1)
and 2D-Echo showed structurally normal heart. Methylprednisolone was suspected
to be the culprit and hence was stopped. He recovered from bradycardia 42 hours
after the last dose (Figure 2). Thereafter, he was put on low dose oral steroids and
was extubated the same day.
Discussion
Intravenous methylprednisolone is an important therapeutic modality for treating
many life threatening diseases. Rhythm disorders have been reported in 1% to 82% of
patients receiving such therapy 2 and these include sinus bradycardia, atrial fibrillation/
flutter, and ventricular tachycardia. The available literature suggests that bradycardia
occurs with high dose steroids (intravenous methylprednisolone at a dose of 30 mg/
Kg body weight). It has been reported after single and consecutive daily doses, and
its onset may occur as early as during administration of the methylprednisolone to as
© JAPI • december 2013 • VOL. 61
51
Journal of the association of physicians of india • december 2013 • VOL. 61 140
120
100
80
Pul(bpm)
60
T(oF)
40
MAP
20
D
D
Fig. 1 : Electrocardiogram showing bradycardia, HR 46/min
while on methylprednisolone
ay
-1
ay (8 a
-1 m
(8 )
D
p
ay
-1 m)
D (8
ay
a
-1 m)
(
D
ay 8 p
-2 m)
(
D
ay 8 a
-2 m)
(
D
ay 8 pm
-3
(8 )
D
ay
a
-3 m)
(
D
ay 8 p
-4 m
D (8 )
ay a
-4 m)
(
D
ay 8 p
-5 m)
(8
D
ay
a
-5 m)
(8
D
pm
ay
-6
)
D
(
ay 8 a
-6 m)
(8
pm
)
0
Fig. 3 : Comparison of HR, axillary temperature and mean
arterial pressure on twice daily basis (blue stars indicate
days of methylprednisolone therapy)
triggering a reflex bradycardia (iv) reaction to
excipients in the steroid preparations. Our patient was
normotensive, had normal haemoglobin, haematocrit
and serum electrolytes, hence it is difficult to postulate
a definite cause for bradycardia. Possibly underlying
aetiology was multifactorial.
Fig. 2 : Electrocardiogram showing normal sinus rhythm after
stoppage of methylprednisolone
Conflicts of interest
None identified.
late as several days afterward. 3 The late development
of arrhythmias may make it difficult to identify
methylprednisolone as the cause, if the association
is not appreciated. The patient in our case developed
bradycardia after about 36 hours of the first dose of
intravenous methylprednisolone (Figure 3).
Conclusion
Pa t i e n t s m a y r e m a i n a s y m p t o m a t i c o r m a y
experience palpitations, altered sensorium and even
cardiac arrest. Meticulous cardiac monitoring is
necessary and depending upon the clinical status,
they might require administration of chronotropic,
antiarrhythmic agents or temporary cardiac pacing.
The reported duration of arrhythmias has varied
from hours to days. Our patient recovered after 42
hours of last methylprednisolone dose (Figure 3).
The exact mechanisms underlying the development
of arrhythmias due to steroids is unknown, however
the proposed mechanisms include (i) direct action
on the myocardial cell membrane and via alterations
in cardiovascular sensitivity to catecholamines 4 (ii)
alteration of the stimulation threshold of myocardial
cells due to rapid electrolyte shifts across myocardial
cell membranes 5 (iii) methylprednisolone induced
expansion of plasma volume 6 and hypertension,
References
© JAPI • december 2013 • VOL. 61
Sinus bradycardia, can occur following low dose
regimen of methylprednisolone. A high index of
suspicion is required to make this diagnosis and
stoppage of drug can rapidly revert the bradycardia.
1.
Jonathan D. Akikusa, MBBS, Brian M. Feldman, MD etal: Pediatrics
2007;119:e778-782
2.
Garrett R, Paulus H. Complications of intravenous methylprednisolone
pulse therapy. Arthritis Rheum 1980;23:677
3.
Kucukosmanoglu O, Karabay A, Ozbarlas N, Noyan A, Anarat A.
Marked bradycardia due to pulsed and oral methylprednisolone
therapy in a patient with rapidly progressive glomerulonephritis.
Nephron 1998;80:484
4.
Hall ED, Plaster M, Braughler JM. Acute cardiovascular response to a
single large intravenous dose of methylprednisolone and its effects
on the responses to norepinephrine and isoproterenol. Proc Soc Exp
Biol Med 1983;173:338–343.
5.
Fujimoto S, Kondoh H, Yamamoto Y, Hisanaga S, Tanaka K Holter
electrocardiogram monitoring in nephrotic patients during
methylprednisolone pulse therapy. Am J Nephrol 1990;10:231–236.
6.
Anzai Y, Nishikawa T. Heart rate responses to body tilt during spinal
anesthesia. Anesth Analg 1991;73:385–390.
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