Question Of The Day #28

question of the day


710 - hyperkalemia


855 - bradycardia

Which of the following is the most likely underlying cause for this patient’s condition?

This patient presents to the emergency department with vague and nonspecific symptoms of nausea, fatigue, and palpitations. The initial EKG (EKG #1) demonstrates a wide-complex tachycardia (QRS >120msec) with a regular rhythm. The differential diagnosis for wide-complex tachyarrhythmias include ventricular tachycardia (monomorphic ventricular tachycardia), torsades de pointes (polymorphic ventricular tachycardia), coarse ventricular fibrillation, supraventricular tachycardias with aberrancy (i.e. underlying Wolf Parkinson White Syndrome or Ventricular Bundle Branch Block), electrolyte abnormalities (i.e., Hyperkalemia), and from medications (i.e., Na channel blocking agents). If the history is unclear or the patient shows signs of instability, Ventricular tachycardia should always be the assumed tachyarrhythmia. This is managed with electrical cardioversion or with medications (i.e., amiodarone, procainamide, lidocaine), depending on the patient’s symptoms and hemodynamic stability.

The prior EKG for the patient (EKG #2) is helpful in showing that the patient does not have a wide QRS complex at baseline. There also are no EKG signs of Wolf Parkinson White Syndrome (Choice B) on EKG #2, making this choice incorrect. Signs of this cardiac pre-excitation syndrome on EKG include a shortened PR interval and a delta wave (slurred upstroke at the beginning of the QRS complex). Anxiety (Choice D) can cause sinus tachycardia and be a symptom associated with any arrhythmia, but it is not the underlying cause for this patient’s bizarre wide-complex tachydysrhythmia. On a closer look, the patient’s EKG (EKG #1) demonstrates tall, peaked T waves in the precordial leads. This supports a diagnosis of hyperkalemia. Other signs of hyperkalemia on EKG include flattened or absent P waves, widened QRS complexes, or a sine wave morphology. A common underlying cause of hyperkalemia is renal disease (Choice C). Ischemic heart disease (Choice A) is a common underlying cause for ventricular tachycardia. Ventricular tachycardia is less likely in this case given the presence of peaked T waves and the lack of fusion beats, capture beats, or signs of AV dissociation on the 12-lead EKG. Correct Answer: C 


  • Brady W.J., & Glass III G.F. (2020). Cardiac rhythm disturbances. Tintinalli J.E., Ma O, Yealy D.M., Meckler G.D., Stapczynski J, Cline D.M., & Thomas S.H.(Eds.), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill.
  • Burns, E. (2020). Ventricular Tachycardia – Monomorphic VT. Life in The Fast Lane. Retrieved from

Cite this article as: Joseph Ciano, USA, "Question Of The Day #28," in International Emergency Medicine Education Project, February 26, 2021,, date accessed: February 1, 2023

From Missed Hemodialysis to Multiple Arrhythmias

From Missed Hemodialysis to Multiple Arrhythmias

Case Presentation

A 78-year-old male, known case of Chronic Kidney Disease on maintenance hemodialysis, presented to the Emergency Department with dizziness and lethargy complaints about 2 days. He had missed his last hemodialysis session due to personal reasons. We could not elicit any further history details as was significantly dyspneic (no bystanders with him at the time of presentation). Hence, the patient was received in Bay 1 for immediate resuscitative measures. The patient was afebrile, conscious, and well oriented, but unable to communicate because of severe dyspnea.


HR – 142 beats/min
BP – not recordable
RR – 36 breaths/min
SpO2 – poor tracing, intermittently showed 98% on room air (15 LO2 via Non Rebreathing Mask was initiated nevertheless)


ECG on presentation
Monomorphic ventricular tachycardia

He was immediately connected to a defibrillator in anticipation of possible synchronized cardioversion. Simultaneously, the cause of the possible rhythm was being evaluated for and a thorough examination was carried out. On examination, his lung fields were clear. His left arm AV Fistula had a feeble thrill on palpation.

In suspicion of hyperkalemia as the cause of VT, patient was immediately started on potassium reduction measures while the point of care ABG report was awaited. He was treated with salbutamol nebulization 10mg, sodium bicarbonate 50 ml IV and 10% calcium gluconate 10ml IV. In view of hemodynamic instability, he was also started on intravenous noradrenaline infusion.

ABG Findings

pH – 7.010, pCO2 – 20.8 mmHg, pO2 – 125 mmHg, HCO3 – 7 mmol/L, Na – 126 mmol/L, K – 9.6 mmol/L

As hyperkalemia was confirmed, the patient was also given 200 ml of 25% dextrose with 12 units of Rapid-acting insulin IV. With the above measures, the patient’s cardiac rhythm came to a sine wave pattern. 

He was later taken up for emergency hemodialysis (HD) – Sustained Low Efficacy Dialysis (SLED) in the ICU, using a low potassium dialysate. Since his AV fistula was non-functioning, HD was done after placement of a femoral dialysis catheter. 2 hours into HD, the patient’s cardiac monitor showed a normal sinus rhythm. His hemodynamic status significantly improved. Noradrenaline infusion was gradually tapered and stopped by the end of the HD session, and repeat blood gas analysis and serum electrolytes showed improvement of all parameters. 

after hemodialysis

The patient was discharged 2 days later, after another session of hemodialysis (through AV fistula) and a detailed cardiology evaluation (ECHO – LVH, normal EF).

For the Inquisitive Minds

  1. The patient underwent a detailed POCUS evaluation, both in the ER and ICU. What findings do you expect to find on the RUSH examination for this patient?
  2. His previous ECHO report (done 1 month ago) mentioned left ventricular hypertrophy and normal ejection fraction. So what would be the reason behind the POCUS findings? Is it reversible?
  3. Why was the AV fistula non-functioning at the time of presentation? When would it have started to function again?
  4. Despite not having hypoxia, this patient was given supplemental oxygen. Did he really require it, and if so, what was the rationale?
  5. What was the necessity for carrying out SLED for this patient?
  6. Why was this patient not immediately cardioverted in the ER?
  7. If this patient had gone into cardiac arrest, what drugs would you have given for management of hyperkalemia?
  8. How differently would you have managed this patient?

Please give your answers and comments into "leave a reply" area below.

Cite this article as: Gayatri Lekshmi Madhavan, India, "From Missed Hemodialysis to Multiple Arrhythmias," in International Emergency Medicine Education Project, November 2, 2020,, date accessed: February 1, 2023

Hyperkalemia Treatment – Infographic

hyperkalemia treatment

Further Reading

Weisberg LS. Management of severe hyperkalemia. Crit Care Med. 2008 Dec;36(12):3246-51. doi: 10.1097/CCM.0b013e31818f22b. Review. PubMed PMID: 18936701.

Cite this article as: Kaushila Thilakasiri, Sri Lanka, "Hyperkalemia Treatment – Infographic," in International Emergency Medicine Education Project, January 8, 2020,, date accessed: February 1, 2023