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Table of Contents
Year : 2021  |  Volume : 9  |  Issue : 3  |  Page : 195-196

The mystery of the “Fainting Patient”

Department of Internal Medicine, RAK Medical and Health Sciences University, Ras Al Khaimah, United Arab Emirates

Date of Submission26-Mar-2021
Date of Acceptance01-May-2021
Date of Web Publication16-Jul-2021

Correspondence Address:
Dr. Raghavendra Bhat
Department of Internal Medicine, RAK Medical and Health Sciences University, P.O. Box: 11172, Ras Al Khaimah
United Arab Emirates
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ajim.ajim_39_21

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How to cite this article:
Bhat R. The mystery of the “Fainting Patient”. APIK J Int Med 2021;9:195-6

How to cite this URL:
Bhat R. The mystery of the “Fainting Patient”. APIK J Int Med [serial online] 2021 [cited 2021 Sep 24];9:195-6. Available from: https://www.ajim.in/text.asp?2021/9/3/195/321659

  Brief Patient History Top

This lady walked into the Emergency with a complaint of attacks of fainting of recent onset. There was no such episodes in the past. There were no other co morbidities. ECG was taken is enclosed. Further enquiry revealed that her family physician had adviced her to take Azithromycin for respiratory infection.

  Observe Top
[Figure 1]
Figure 1: Long QT interval

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Heart rate is approximately 65/min. Rhythm is sinus as indicated by the normal P and normal PR interval. QRS is normal. QT interval is 0.44 s – prolonged. This patient was on azithromycin for respiratory infection and had a couple of fainting episodes.

Prolonged QT interval indicates delayed ventricular repolarization. This can result in ventricular tachycardia, syncopal attacks, seizures, and sudden death.

  1. What are the causes of prolonged QT interval?

  2. Congenital and acquired.

    1. Congenital

      1. Jervell–Lange–Nielsen syndrome: QT prolongation + deafness + syncopal episodes + sudden death (first described in 1957). Autosomal recessive
      2. Romano–Ward syndrome – QT prolongation + syncope + sudden death. Autosomal dominant
      3. Channelopathy.

    2. Acquired

      1. Electrolyte imbalance – hypocalcemia, hypokalemia, hypomagnesemia
      2. Drug-induced LQTS and torsades de pointes (TDP) due to the blockade of IKr (a major repolarization current of the heart)
      3. Myocardial Infarction (MI), Cerebrovascular accident (CVA)
      4. Brady arrhythmia.

  3. How do you measure the corrected QT Interval?

  4. By using the Bazett formula (QTc = QT X RR½)

  5. What is the danger if QT interval is prolonged?

  6. Greatly prolonged QT interval increases the risk of ventricular tachycardia

  7. Comment on the ST-T wave morphology in LQTS:

    • In LQTS 1 – T wave duration is long
    • In LQTS 2 – T waves can be small and notched
    • In LQTS 3 – T wave onset is unusually prolonged.

  8. What is TDP?

  9. It is a form of Polymorphic Ventricular Tachycardia, which starts with a premature ventricular complex following a sinus beat with a markedly prolonged QT interval and a bizarre T wave. A train of ventricular complexes of different sizes and shapes may follow. The first beat represents triggering from an early after depolarization

  10. What is the fate of TDP?

    • TDP reverts spontaneously to sinus rhythm in most instances.
    • In few other instances, it degenerates into ventricular fibrillation.

  11. What caused the LQTS in this patient?

  12. Antibiotic azithromycin.

  13. What are the causes of short QR interval syndrome?

    • Electrolyte imbalance
    • Hyperthermia
    • Digoxin.

  14. U waves were also noted in V4, V5, and V6.

  15. Digoxin, phenothiazines, some antiarrhythmics, and hypokalemia are known to cause it. None of these factors were present in this patient.

Final outcome – syncopal attacks stopped after discontinuing azithromycin.

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Conflicts of interest

There are no conflicts of interest.


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