International Journal of Cardiology 190 (2015) 102
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Hyperkalemia induced sinoatrial block or atrial fibrillation? Tamer Kırat a,⁎, Nuri Köse b, İbrahim Altun b, Fatih Akın b a b
Yücelen Hospital, Deparment of Cardiology, Muğla, Turkey Sıtkı Koçman University, Faculty of Medicine, Department of Cardiology, Muğla, Turkey
a r t i c l e
i n f o
Article history: Received 13 April 2015 Accepted 15 April 2015 Available online 16 April 2015 Keywords: Hyperkalemia Atrial fibrillation Furosemide Bicarbonate
We read with great interest the case report by Pyung Chun Oh, et al. [1]. In this case report, the authors presented an acute severe hyperkalemic 74 year-old male patient who was treated successfully with intravenous fluid, intravenous (IV) calcium gluconate, IV insulin with 50% dextrose, Kayexalate enema and finally hemodialysis treatments. We would like to make a minor criticism about this case report and give a little additional information that may be important about treatment of acute severe hyperkalemia. In the first ECG, it is written as the rhythm is junctional and p waves aren't seen (i.e., sinoatrial block) which is typical for hyperkalemia. As is known, when the potassium level reaches to 8–9 mmol/L (8.2 mmol/L in the patient) the sinoatrial (SA) node activity may stimulate the ventricles without evidence of atrial activity, producing a sinoventricular rhythm. This occurs because the SA node is less susceptible to the effect of hyperkalemia and can continue to stimulate the ventricles without evidence of p waves [2]. It is cited that the patient had been in atrial fibrillation in the past medical records. Moreover, after treatment of hyperkalemia, the second and last ECGs revealed atrial fibrillation with slow and normal ventricular rate response, respectively. In close look at the first ECG, atrial fibrillation waves (f waves) can be seen and the ventricular rate is irregular which is against the diagnosis of junctional or sinoventricular rhythm. In view of this data, we think that it is possible to say that in the first ECG the patient is in atrial fibrillation with a very slow ventricular rate which accelerates after the therapy, rather than junctional or sinoventricular rhythm without atrial activity. In the management of acute severe hyperkalemia, apart from the mentioned IV calcium gluconate (which directly antagonizes the ⁎ Corresponding author at: Yücelen Hospital, Kötekli mevkii, 48000 Muğla, Turkey. E-mail address: [email protected] (T. Kırat).
http://dx.doi.org/10.1016/j.ijcard.2015.04.128 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
myocardial effects of hyperkalemia), IV insulin with 50% dextrose and nebulized albuterol (both which shift potassium into cells), Kayexalate enema (for elimination of potassium from the body by enteral route) and sodium bicarbonate in the article, IV loop diuretic therapy (for example furosemide 40–80 mg) might be of value [3,4,6] which removes the potassium from the body by renal route. IV furosemide therapy can be given in normal or edematous patients which has a short onset of action of 5–30 min and a duration of action of 2–6 h [4,6]. In addition, if the patient is volume-depleted, IV loop diuretic might be given with isotonic NaCl [7]. Finally, although bicarbonate therapy has been a traditional treatment for hyperkalemia, many studies showed that sodium bicarbonate fails to lower the serum potassium [4,5]. Moreover, in chronic renal failure, it may cause hypernatremia, hypocalcemia, metabolic alkalosis and hypervolemic state [5]. In light of these data, the use of bicarbonate therapy is no longer recommended in hyperkalemic patients without metabolic acidosis [7]. However, in patients with metabolic acidosis (bicarbonate b 22 mEq/L), bicarbonate can be given as a continuous infusion with close follow-up of the hydration, electrolyte and acid–base status [4,6]. Conflict of interest The authors report no relationships that could be construed as a conflict of interest. References [1] P.C. Oh, K.K. Koh, J.H. Kim, H. Park, S.J. Kim, Life threatening severe hyperkalemia presenting typical electrocardiographic changes — rapid recovery following medical, temporary pacing and hemodialysis treatments, Int. J. Cardiol. 177 (2014) 27–29. [2] H. Almukdad, Hyperkalemia revisited, Saudi J. Kidney Dis. Transpl. 18 (2007) 577–584. [3] 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 10.1: Life-threatening electrolyte abnormalities, Circulation 112 (24 Suppl.) (2005) IV-121–IV-125. [4] Y. Mushiyakh, H. Dangaria, S. Qavi, N. Ali, J. Pannone, D. Tompkins, Treatment and pathogenesis of acute hyperkalemia, J. Community Hosp. Intern. Med. Perspect. 4 (2012) 1. [5] K. Kamel, C. Wei, Controversial issues in the treatment of hyperkalemia, Nephrol. Dial. Transplant. 18 (2003) 2215–2218. [6] V. Carvalhana, L. Burry, Management of severe hyperkalemia without hemodialysis: case report and literature review, J. Crit. Care 21 (2006) 316–321. [7] J.C. Hollander-Rodriguez, J.F. Calvert Jr., Hyperkalemia, Am. Fam. Physician 73 (2006) 283–290.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Hyperkalemia induced sinoatrial block or atrial fibrillation? Tamer Kırat a,⁎, Nuri Köse b, İbrahim Altun b, Fatih Akın b a b
Yücelen Hospital, Deparment of Cardiology, Muğla, Turkey Sıtkı Koçman University, Faculty of Medicine, Department of Cardiology, Muğla, Turkey
a r t i c l e
i n f o
Article history: Received 13 April 2015 Accepted 15 April 2015 Available online 16 April 2015 Keywords: Hyperkalemia Atrial fibrillation Furosemide Bicarbonate
We read with great interest the case report by Pyung Chun Oh, et al. [1]. In this case report, the authors presented an acute severe hyperkalemic 74 year-old male patient who was treated successfully with intravenous fluid, intravenous (IV) calcium gluconate, IV insulin with 50% dextrose, Kayexalate enema and finally hemodialysis treatments. We would like to make a minor criticism about this case report and give a little additional information that may be important about treatment of acute severe hyperkalemia. In the first ECG, it is written as the rhythm is junctional and p waves aren't seen (i.e., sinoatrial block) which is typical for hyperkalemia. As is known, when the potassium level reaches to 8–9 mmol/L (8.2 mmol/L in the patient) the sinoatrial (SA) node activity may stimulate the ventricles without evidence of atrial activity, producing a sinoventricular rhythm. This occurs because the SA node is less susceptible to the effect of hyperkalemia and can continue to stimulate the ventricles without evidence of p waves [2]. It is cited that the patient had been in atrial fibrillation in the past medical records. Moreover, after treatment of hyperkalemia, the second and last ECGs revealed atrial fibrillation with slow and normal ventricular rate response, respectively. In close look at the first ECG, atrial fibrillation waves (f waves) can be seen and the ventricular rate is irregular which is against the diagnosis of junctional or sinoventricular rhythm. In view of this data, we think that it is possible to say that in the first ECG the patient is in atrial fibrillation with a very slow ventricular rate which accelerates after the therapy, rather than junctional or sinoventricular rhythm without atrial activity. In the management of acute severe hyperkalemia, apart from the mentioned IV calcium gluconate (which directly antagonizes the ⁎ Corresponding author at: Yücelen Hospital, Kötekli mevkii, 48000 Muğla, Turkey. E-mail address: [email protected] (T. Kırat).
http://dx.doi.org/10.1016/j.ijcard.2015.04.128 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
myocardial effects of hyperkalemia), IV insulin with 50% dextrose and nebulized albuterol (both which shift potassium into cells), Kayexalate enema (for elimination of potassium from the body by enteral route) and sodium bicarbonate in the article, IV loop diuretic therapy (for example furosemide 40–80 mg) might be of value [3,4,6] which removes the potassium from the body by renal route. IV furosemide therapy can be given in normal or edematous patients which has a short onset of action of 5–30 min and a duration of action of 2–6 h [4,6]. In addition, if the patient is volume-depleted, IV loop diuretic might be given with isotonic NaCl [7]. Finally, although bicarbonate therapy has been a traditional treatment for hyperkalemia, many studies showed that sodium bicarbonate fails to lower the serum potassium [4,5]. Moreover, in chronic renal failure, it may cause hypernatremia, hypocalcemia, metabolic alkalosis and hypervolemic state [5]. In light of these data, the use of bicarbonate therapy is no longer recommended in hyperkalemic patients without metabolic acidosis [7]. However, in patients with metabolic acidosis (bicarbonate b 22 mEq/L), bicarbonate can be given as a continuous infusion with close follow-up of the hydration, electrolyte and acid–base status [4,6]. Conflict of interest The authors report no relationships that could be construed as a conflict of interest. References [1] P.C. Oh, K.K. Koh, J.H. Kim, H. Park, S.J. Kim, Life threatening severe hyperkalemia presenting typical electrocardiographic changes — rapid recovery following medical, temporary pacing and hemodialysis treatments, Int. J. Cardiol. 177 (2014) 27–29. [2] H. Almukdad, Hyperkalemia revisited, Saudi J. Kidney Dis. Transpl. 18 (2007) 577–584. [3] 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 10.1: Life-threatening electrolyte abnormalities, Circulation 112 (24 Suppl.) (2005) IV-121–IV-125. [4] Y. Mushiyakh, H. Dangaria, S. Qavi, N. Ali, J. Pannone, D. Tompkins, Treatment and pathogenesis of acute hyperkalemia, J. Community Hosp. Intern. Med. Perspect. 4 (2012) 1. [5] K. Kamel, C. Wei, Controversial issues in the treatment of hyperkalemia, Nephrol. Dial. Transplant. 18 (2003) 2215–2218. [6] V. Carvalhana, L. Burry, Management of severe hyperkalemia without hemodialysis: case report and literature review, J. Crit. Care 21 (2006) 316–321. [7] J.C. Hollander-Rodriguez, J.F. Calvert Jr., Hyperkalemia, Am. Fam. Physician 73 (2006) 283–290.
