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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">To the Editor&#58;</span></p><p class="elsevierStylePara">Hyperkalaemia is one of the most severe electrolyte disorders&#44; especially in patients with chronic kidney disease &#40;CKD&#41; who are incapable of efficient renal potassium excretion&#46;<span class="elsevierStyleSup">1-4</span></p><p class="elsevierStylePara">High potassium levels lead to changes in transmembrane potential of the cells of skeletal and cardiac muscles&#44; the organs which are most clinically affected&#46;<span class="elsevierStyleSup">1-4</span></p><p class="elsevierStylePara">In patients with pacemakers&#44; hyperkalaemia can cause dysfunction of the device and therefore the patient&#8217;s life may be at risk&#46;<span class="elsevierStyleSup">4&#44;5</span></p><p class="elsevierStylePara">We report the case of a pacemaker malfunction due to hyperkalaemia in a patient with multiple risk factors for developing the aforementioned electrolyte disorder&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CASE REPORT</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">A 72-year-old female who came to the haemodialysis centre&#44; after the long weekend interdialytic period&#44; complaining of generalised muscle weakness&#44; to the point that it prevented her from walking&#46;</p><p class="elsevierStylePara">She had stage V CKD and had been on periodic haemodialysis for four years&#46; She had a single chamber pacemaker due to chronic atrial fibrillation with symptomatic bradycardia &#40;repeated syncope&#41;&#46; Other history findings included type 2 diabetes mellitus treated with oral anti-diabetic medication&#44; and high blood pressure&#46; Her regular medication included omeprazole&#44; amiodarone and aspirin &#40;none of which affected on potassium homeostasis&#41;&#46; Her adherence to medical treatment was poor and she often consumed unsuitable foods&#46; Physical examination was unremarkable except for the aforementioned muscle weakness&#46; The constants were correct and the patient was normoglycaemic&#46; The electrocardiogram &#40;ECG&#41; showed a pacemaker rate&#44; without any other abnormalities&#46; The urgent analysis revealed potassium levels of 8&#46;2mEq&#47;l&#46; While waiting for the haemodialysis session&#44; she began conventional treatment for hyperkalaemia&#44; with calcium gluconate&#44; intravenous salbutamol and an infusion of insulin and glucose being administered&#46;</p><p class="elsevierStylePara">Minutes after beginning this treatment&#44; the patient experienced a sudden decrease in her level of consciousness&#44; with undetectable blood pressure and signs of peripheral hypoperfusion&#46; At that moment&#44; the ECG showed failure of ventricular capture &#40;Figure 1&#41;&#46; Urgent haemodialysis was performed&#44; with both symptoms and electrocardiographic abnormalities being quickly and completely reversed&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Severe hyperkalaemia is a common problem in patients with advanced CKD&#46;<span class="elsevierStyleSup">1</span> It may affect 5&#37;-10&#37; of patients on chronic haemodialysis monthly&#46; It may also require urgent haemodialysis in up to 24&#37; of patients with end-stage CKD and it has a significant mortality rate&#46;<span class="elsevierStyleSup">1</span></p><p class="elsevierStylePara">Potential causes of hyperkalaemia in patients such as ours are multifactorial and may include&#44; in addition to CKD&#44; metabolic acidosis&#44; hyporeninemic hypoaldosteronism &#40;common in diabetics&#41;&#44; defects of cell Na<span class="elsevierStyleSup">&#43;</span>&#47;K<span class="elsevierStyleSup">&#43;</span>-ATPase and poor diet<span class="elsevierStyleSup">1-3 </span>&#40;recognised by our patient&#41;&#46;</p><p class="elsevierStylePara">In patients with cardiac pacemakers&#44; hyperkalaemia can cause various types of dysfunction of the device&#44; with very serious consequences&#46;<span class="elsevierStyleSup">4&#44;5</span> In our case&#44; there was a failure of ventricular capture&#46; In this situation&#44; excess of extracellular potassium increases the resting potential of the myocardial cell membrane&#46;<span class="elsevierStyleSup">4</span> If this potential exceeds the energy emitted by the pacemaker according to its programming&#44; cardiac muscle cell depolarisation is inhibited&#46; This situation is recognised in the ECG by the absence of depolarisation after the spicules&#46; The clinical manifestation&#44; which is clearly serious&#44; is asystole&#46;<span class="elsevierStyleSup">4&#44;5</span></p><p class="elsevierStylePara">In conclusion&#44; the presence of a cardiac pacemaker does not always protect the myocardium from the deleterious effects of hyperkalaemia&#46; Moreover&#44; the device requires a normal electrolyte balance for proper operation&#46; <span class="elsevierStyleBold">Therefore&#44; heart rate monitoring&#44; which is essential for all symptomatic hyperkalaemia&#44; should not be overlooked in patients with pacemakers&#46; Likewise&#44; the presence of a pacemaker must not be a decisive factor when urgent haemodialysis is indicated for severe hyperkalaemia&#46;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The authors declare that they have no conflicts of interest related to the contents of this article&#46;</p><p class="elsevierStylePara"><a href="grande&#47;11847&#95;16025&#95;49187&#95;en&#95;f111847&#46;jpg" class="elsevierStyleCrossRefs"><img src="11847_16025_49187_en_f111847.jpg" alt="12-lead electrocardiogram showing the failure of capture &#40;absence of QRS complexes after the first&#44; second and fourth spicules&#41;"></img></a></p><p class="elsevierStylePara">Figure 1&#46; 12-lead electrocardiogram showing the failure of capture &#40;absence of QRS complexes after the first&#44; second and fourth spicules&#41;</p>"
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