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Hyperkalaemia, pseudohyperkalaemia and electrocardiographic correlates
242
Letters to the Editor
Hyperkalaemia, pseudohyperkalaemia and electrocardiographic correlates Eftychios Siniorakis, Spyridon Arvanitakis ⁎, Georgios Psatheris, Nikos Flessas, Eftychios Prokovas, Nikos Exadactylos Department of Cardiology, Sotiria Chest Diseases Hospital, Athens, Greece
a r t i c l e
i n f o
Article history: Received 27 November 2009 Accepted 4 December 2009 Available online 13 January 2010 Keywords: Hyperkalaemia Pseudohyperkalaemia Electrocardiogram Right bundle branch block
We enjoyed the article by Gogas BD et al. reporting the electrocardiographic consequences of a hyperkalaemia case [1]. In the same article, the authors mention briefly the condition known as pseudohyperkalaemia. Every time the value of serum potassium (Ks) exceeds the respective value in plasma (Kp) by 0.4 mEq/l, the phenomenon of pseudohyperkalaemia is present [2]. The arrhythmogenic effects of hyperkalaemia, and the consequent changes of the electrocardiogram, depend upon the concentration of potassium in the plasma, not in the serum. Ks represents exclusively an in vitro condition, by definition. Several factors can affect the Ks values, creating false alarms of hyperkalaemia. In particular, several myeloproliferative haematologic diseases, with hypererythraemia, leukocytosis and thrombocytosis, are prone to provoke spectacular discrepancies between Ks and Kp values [3]. Increased Ks, under those circumstances, is due to excessive in vitro release of intracellular potassium from platelets, leucocytes and erythrocytes, with Kp remaining within the normal range. Hyperkalaemia is not rare. If the phenomenon exists unrecognized, diagnostic and therapeutic pitfalls are awaited. With these points in mind, every time clinical circumstances make the existence of pseudohyperkalaemia likely, the electrocardiogram should be interpreted in comparison with the Kp values [4]. To illustrate this we discuss two cases. A woman with idiopathic thrombocytosis (platelets= 1200 ×103/µL) presented with a Ks value of 8.4 mEq/l, validated in repeated measurements. She did not mention any cardiac problems in her past medical history, and her electrocardiogram was normal (Fig. 1). When a simultaneous Kp was requested, the in vivo value was 5.1 mEq/l,
explaining the lack of clinical and electrocardiographic abnormalities. Pseudohyperkalaemia in this case was found to be related to the increased release of potassium from platelet granules during coagulation. Another patient suffering from diabetic nephropathy, was admitted because of decompensated heart failure, with a Ks value of 3.0 mEq/l. The admission electrocardiogram appears in Fig. 2A. Frusemide and small doses of potassium sparing diuretics were administered. On day 3, renal function had deteriorated and Ks was 7.8 mEq/l. At the same time, the electrocardiogram changed into right bundle branch block (Fig. 2), not an uncommon finding in hyperkalaemia [5]. Kp was concordant with the Ks value, excluding pseudohyperkalaemia. After therapeutic manipulations, the electrocardiogram returned to its baseline pattern after a few hours, when the Ks value dropped to 6.2 mEq/l. There are several controversies regarding the ability of the electrocardiogram to predict hyperkalaemia [6]. There are cases of severe hyperkalaemia with quite normal electrocardiograms, and others of only mild hyperkalaemia with typical electrocardiographic signs. When discrepancies between the elevated Ks values and clinical and electrocardiographic patterns ensue, the trough value of potassium in circulating blood should be requested, by measuring Kp. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [7]. References [1] Gogas BD, Iliodromitis E, Leftheriotis D, Flevari P, Rallidis L, Kremastinos D. Instantaneous electrocardiographic changes and transient sinus rhythm restoration in severe hyperkalaemia. Int J Cardiol 2011:e40–2. [2] Sevastos N, Theodossiades G, Archimandritis A. Pseudohyperkalaemia in serum: a new insight into an old phenomenon. Clin Med Res 2008;60:30–2. [3] Nomura M, Nakasuji M, Nakamura M, Imanaka N, Tanaka M, Kawashima H. A pitfall in intraoperative electrolyte management for patients with pseudohyperkalaemia caused by thrombocytosis. Masui 2009;58:1300–2. [4] Kapoor AK, Ravi A, Twomey PJ. Investigation of outpatients referred to a chemical pathologist with potential pseudohyperkalaemia. J Clin Pathol 2009;62:920–3. [5] Barbosa PR. Unveiling electrocardiographic mysteries. Int J Cardiol 2007;121:326. [6] Martinez-Vea A, Bardaji A, Garcia C, Oliver JA. Severe hyperkalaemia with minimal electrocardiographic manifestations: a report of seven cases. J Electrocardiol 1999;32:45–9. [7] Coats AJ. Ethical authorship and publishing. Int J Cardiol 2009;131:149–50.
Fig. 1. A normal electrocardiogram accompanies this case of pseudohyperkalaemia (serum potassium 8.4 mEq/l).
⁎ Corresponding author. 10 Evrou Str. Athens, 11528, Greece. Tel.: +30 210 7484760. E-mail address: [email protected] (S. Arvanitakis).
Letters to the Editor
243
Fig. 2. Baseline electrocardiogram in a patient with renal failure, and serum potassium of 3.0 mEq/l (A). Right bundle branch block appears when the level of serum potassium raises to 7.8 mEq/l (B).
0167-5273/$ – see front matter © 2009 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2009.12.022
Swings and roundabouts: Intravascular Optical Coherence Tomography (OCT) in the evaluation of the left main stem coronary artery M.A. Moharram a,b, T. Yeoh a, H.C. Lowe a,b,⁎ a b
Cardiology Department, Concord Hospital, Concord, NSW, Australia Anzac Research Institute, University of Sydney, Sydney, NSW, Australia
a r t i c l e
i n f o
Article history: Received 24 December 2009 Accepted 14 February 2010 Available online 11 March 2010 Keywords: Stent Left main coronary Optical coherence tomography Intravascular ultrasound
The imaging detail provided by Intravascular Ultrasound (IVUS) has contributed to 2 recent advances in the treatment of atherosclerotic left ⁎ Corresponding author. Cardiology Department, Concord Hospital, Hospital Rd, Concord, NSW, 2139, Australia. Tel.: +61 2 9767 5000; fax: +61 2 9767 6994. E-mail address: [email protected] (H.C. Lowe).
main stem coronary artery disease. First, the imaging of stent strut expansion has contributed to an increasing acceptance of left main stem stenting as an alternative to surgery [1], and second, precise measurements of the plaque area and residual lumenal area have allowed for improved quantification of left main lesion severity [2]. The novel intracoronary imaging technique of Optical Coherence Tomography (OCT) is currently being evaluated for a variety of coronary indications, with a resolution of up to 4–16 μm, although generally only relatively superficial structures are observed [3]. Its utility in the left main coronary artery is unknown. In a patient with a prior drug-eluting stent to the mid and distal left main coronary artery, angiographic, IVUS and OCT evaluations were undertaken (Fig. 1A–E). Angiography suggested mild ostial disease and satisfactory stent deployment (Fig. 1A). OCT revealed stent strut position with markedly improved precision compared to IVUS, in the mid portion of the left main coronary artery, as expected (Fig. 1B, C). However, although OCT gave unequivocal images of the left main ostium — with
Letters to the Editor
Hyperkalaemia, pseudohyperkalaemia and electrocardiographic correlates Eftychios Siniorakis, Spyridon Arvanitakis ⁎, Georgios Psatheris, Nikos Flessas, Eftychios Prokovas, Nikos Exadactylos Department of Cardiology, Sotiria Chest Diseases Hospital, Athens, Greece
a r t i c l e
i n f o
Article history: Received 27 November 2009 Accepted 4 December 2009 Available online 13 January 2010 Keywords: Hyperkalaemia Pseudohyperkalaemia Electrocardiogram Right bundle branch block
We enjoyed the article by Gogas BD et al. reporting the electrocardiographic consequences of a hyperkalaemia case [1]. In the same article, the authors mention briefly the condition known as pseudohyperkalaemia. Every time the value of serum potassium (Ks) exceeds the respective value in plasma (Kp) by 0.4 mEq/l, the phenomenon of pseudohyperkalaemia is present [2]. The arrhythmogenic effects of hyperkalaemia, and the consequent changes of the electrocardiogram, depend upon the concentration of potassium in the plasma, not in the serum. Ks represents exclusively an in vitro condition, by definition. Several factors can affect the Ks values, creating false alarms of hyperkalaemia. In particular, several myeloproliferative haematologic diseases, with hypererythraemia, leukocytosis and thrombocytosis, are prone to provoke spectacular discrepancies between Ks and Kp values [3]. Increased Ks, under those circumstances, is due to excessive in vitro release of intracellular potassium from platelets, leucocytes and erythrocytes, with Kp remaining within the normal range. Hyperkalaemia is not rare. If the phenomenon exists unrecognized, diagnostic and therapeutic pitfalls are awaited. With these points in mind, every time clinical circumstances make the existence of pseudohyperkalaemia likely, the electrocardiogram should be interpreted in comparison with the Kp values [4]. To illustrate this we discuss two cases. A woman with idiopathic thrombocytosis (platelets= 1200 ×103/µL) presented with a Ks value of 8.4 mEq/l, validated in repeated measurements. She did not mention any cardiac problems in her past medical history, and her electrocardiogram was normal (Fig. 1). When a simultaneous Kp was requested, the in vivo value was 5.1 mEq/l,
explaining the lack of clinical and electrocardiographic abnormalities. Pseudohyperkalaemia in this case was found to be related to the increased release of potassium from platelet granules during coagulation. Another patient suffering from diabetic nephropathy, was admitted because of decompensated heart failure, with a Ks value of 3.0 mEq/l. The admission electrocardiogram appears in Fig. 2A. Frusemide and small doses of potassium sparing diuretics were administered. On day 3, renal function had deteriorated and Ks was 7.8 mEq/l. At the same time, the electrocardiogram changed into right bundle branch block (Fig. 2), not an uncommon finding in hyperkalaemia [5]. Kp was concordant with the Ks value, excluding pseudohyperkalaemia. After therapeutic manipulations, the electrocardiogram returned to its baseline pattern after a few hours, when the Ks value dropped to 6.2 mEq/l. There are several controversies regarding the ability of the electrocardiogram to predict hyperkalaemia [6]. There are cases of severe hyperkalaemia with quite normal electrocardiograms, and others of only mild hyperkalaemia with typical electrocardiographic signs. When discrepancies between the elevated Ks values and clinical and electrocardiographic patterns ensue, the trough value of potassium in circulating blood should be requested, by measuring Kp. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [7]. References [1] Gogas BD, Iliodromitis E, Leftheriotis D, Flevari P, Rallidis L, Kremastinos D. Instantaneous electrocardiographic changes and transient sinus rhythm restoration in severe hyperkalaemia. Int J Cardiol 2011:e40–2. [2] Sevastos N, Theodossiades G, Archimandritis A. Pseudohyperkalaemia in serum: a new insight into an old phenomenon. Clin Med Res 2008;60:30–2. [3] Nomura M, Nakasuji M, Nakamura M, Imanaka N, Tanaka M, Kawashima H. A pitfall in intraoperative electrolyte management for patients with pseudohyperkalaemia caused by thrombocytosis. Masui 2009;58:1300–2. [4] Kapoor AK, Ravi A, Twomey PJ. Investigation of outpatients referred to a chemical pathologist with potential pseudohyperkalaemia. J Clin Pathol 2009;62:920–3. [5] Barbosa PR. Unveiling electrocardiographic mysteries. Int J Cardiol 2007;121:326. [6] Martinez-Vea A, Bardaji A, Garcia C, Oliver JA. Severe hyperkalaemia with minimal electrocardiographic manifestations: a report of seven cases. J Electrocardiol 1999;32:45–9. [7] Coats AJ. Ethical authorship and publishing. Int J Cardiol 2009;131:149–50.
Fig. 1. A normal electrocardiogram accompanies this case of pseudohyperkalaemia (serum potassium 8.4 mEq/l).
⁎ Corresponding author. 10 Evrou Str. Athens, 11528, Greece. Tel.: +30 210 7484760. E-mail address: [email protected] (S. Arvanitakis).
Letters to the Editor
243
Fig. 2. Baseline electrocardiogram in a patient with renal failure, and serum potassium of 3.0 mEq/l (A). Right bundle branch block appears when the level of serum potassium raises to 7.8 mEq/l (B).
0167-5273/$ – see front matter © 2009 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2009.12.022
Swings and roundabouts: Intravascular Optical Coherence Tomography (OCT) in the evaluation of the left main stem coronary artery M.A. Moharram a,b, T. Yeoh a, H.C. Lowe a,b,⁎ a b
Cardiology Department, Concord Hospital, Concord, NSW, Australia Anzac Research Institute, University of Sydney, Sydney, NSW, Australia
a r t i c l e
i n f o
Article history: Received 24 December 2009 Accepted 14 February 2010 Available online 11 March 2010 Keywords: Stent Left main coronary Optical coherence tomography Intravascular ultrasound
The imaging detail provided by Intravascular Ultrasound (IVUS) has contributed to 2 recent advances in the treatment of atherosclerotic left ⁎ Corresponding author. Cardiology Department, Concord Hospital, Hospital Rd, Concord, NSW, 2139, Australia. Tel.: +61 2 9767 5000; fax: +61 2 9767 6994. E-mail address: [email protected] (H.C. Lowe).
main stem coronary artery disease. First, the imaging of stent strut expansion has contributed to an increasing acceptance of left main stem stenting as an alternative to surgery [1], and second, precise measurements of the plaque area and residual lumenal area have allowed for improved quantification of left main lesion severity [2]. The novel intracoronary imaging technique of Optical Coherence Tomography (OCT) is currently being evaluated for a variety of coronary indications, with a resolution of up to 4–16 μm, although generally only relatively superficial structures are observed [3]. Its utility in the left main coronary artery is unknown. In a patient with a prior drug-eluting stent to the mid and distal left main coronary artery, angiographic, IVUS and OCT evaluations were undertaken (Fig. 1A–E). Angiography suggested mild ostial disease and satisfactory stent deployment (Fig. 1A). OCT revealed stent strut position with markedly improved precision compared to IVUS, in the mid portion of the left main coronary artery, as expected (Fig. 1B, C). However, although OCT gave unequivocal images of the left main ostium — with