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|Year : 2014 | Volume
| Issue : 3 | Page : 338-340
Hyperkalemia induced pseudo-myocardial infarction in septic shock
Department of Emergency Medicine, Singapore General Hospital, Singapore
|Date of Submission||10-Mar-2013|
|Date of Decision||07-Apr-2014|
|Date of Acceptance||25-May-2013|
|Date of Web Publication||14-Aug-2014|
Dr. S E Pothiawala
Department of Emergency Medicine, Singapore General Hospital
Source of Support: None, Conflict of Interest: None
Hyperkalemia is an acute life-threatening disorder presenting to the emergency department. Patients with hyperkalemia may manifest characteristic electrocardiographic changes including tented T waves, widening of the QRS complex and loss of P waves, sine wave pattern and eventually asystole. There have been only few reports of hyperkalemia causing ST segment elevation on electrocardiogram simulating an acute myocardial infarction. This case describes pseudo-myocardial infarction due to hyperkalemia and septic shock. Rapid determination of serum potassium levels by bedside blood gas analyzers serves to be a useful guide. ST segment elevation related to hyperkalemia will resolve with successful reduction of the serum potassium levels by appropriate therapy. It is important for physicians to be aware of this condition as this will aid in initiating correct therapy and prevent the patient from unnecessary interventions and the associated risk of complications.
Keywords: Electrocardiography, hyperkalemia, pseudo-myocardial infarction
|How to cite this article:|
Pothiawala S E. Hyperkalemia induced pseudo-myocardial infarction in septic shock. J Postgrad Med 2014;60:338-40
| :: Introduction|| |
Hyperkalemia is an acute life-threatening disorder commonly seen in the emergency department. It can produce several characteristic electrocardiographic (ECG) changes. It rarely produces ST-segment elevation simulating an acute myocardial infarction (AMI). "Pseudo-infarction" is a rare manifestation of hyperkalemia; with very few cases documented in the literature until date. This case describes pseudo-myocardial infarction secondary to hyperkalemia in septic shock.
| :: Case Report|| |
A 75-year-old man was presented to the emergency department by an ambulance with complaints of generalized weakness. He lived alone and was noted by the social worker to be progressively weak for the whole of previous week. He had not being eating well. No further history could be elicited from the patient owing to his clinical condition. He was not known to have any past medical history from the medical records.
On initial assessment, he was drowsy and dehydrated. He was tachycardic with a heart rate of 124 beats/min and blood pressure of 76/38 mm Hg. He attempted to communicate with occasional slurred words. His pupils were bilaterally equal and reactive to light. The airway was patent and lungs were clear. His abdomen was soft and non-tender. There were no external signs of injury. There was a foul-smelling cauliflower shaped mass over the glans penis, suspicious for penile cancer.
The patient's blood glucose was 5.3 mmol/L. Intravenous access was established and after 1.5 L of normal saline, his blood pressure increased to 129/92 mm Hg. The ECG showed ST elevation in V2-V5 with tall T waves [Figure 1]. Immediate venous blood testing on the blood gas analyzer showed a potassium level of 7.8 mmol/L.
|Figure 1: Electrocardiograph showing anterior pseudo-myocardial infarction, ST elevation in V3-5 marked by arrows|
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The initial ECG was suspicious for an acute anterior myocardial infarction; however, the identification of severe hyperkalemia led to suspicion of ST elevation secondary to hyperkalemia. The patient was also more alert by then and denied any complaints of chest pain. He was immediately treated with 10 ml of 10% calcium gluconate, 10 units of intravenous insulin with 40 ml of 50% dextrose and oral resonium (sodium polystyrene sulfonate). A repeat ECG 45 min later showed complete resolution of the ST segment elevation [Figure 2] and hence the patient was not considered for coronary angiogram.
|Figure 2: Electrocardiograph showing resolution of ST elevation in V3-5, marked by arrows|
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The laboratory tests showed a raised white blood cell count of 44.69 × 10 9 /L with neutrophils 94.1% and hemoglobin of 16.6 g/dL. Biochemical results showed the following serum concentrations: Sodium 154 mmol/L, potassium >8 mmol/L, urea 23.9 mmol/L, creatinine 265 μmol/L and glucose 5.5 mmol/L. His troponin T was 0.09 μg/L (normal < 0.03 μg/L) likely secondary to sepsis and acute renal failure and normal creatine kinase (CK) and CK-MB levels. The chest radiograph showed lucency over the left mid zone. His repeat potassium was 5.1 mmol/L. He was given intravenous antibiotics in view of septic shock with acute kidney injury and was admitted to the hospital. The patient died on day 3 of the hospital stay due to severe sepsis.
| :: Discussion|| |
Hyperkalemia induced ECG changes range from T wave changes to fatal dysrhythmias. Peaked and tented T waves may be seen with potassium concentrations of 5.5-6 mmol/L. A wide QRS complex and prolonged PR interval occurs with potassium of 6.5 mmol/L. P wave amplitude decreases with potassium level of 7 mEq/L and as the levels reach >8 mmol/L, it produces a classic sine-wave pattern, eventually leading to ventricular fibrillation and asystole. These ECG changes are due to the physiological effect of potassium on the myocardial cells. The ECG changes may not correlate with serum potassium concentration and they depend upon rate of the rise of potassium, acid-base status, other electrolyte disturbances and effects of other medications. ,
ST segment elevation or "pseudoinfarction" is a rare manifestation of hyperkalemia. Levine et al. reported four cases of ST segment elevation resembling AMI or pericarditis due to hyperkalemia and they coined the term "dialyzable currents of injury."  It is unsure whether the ST elevation is a primary repolarization abnormality or an artifact caused by the merging of the terminal R' portion of the QRS complex with the T wave.  ST segment elevation could be attributed to a hyperkalemic diastolic current of injury and to a combination of diastolic and systolic current of injury. In some cases of hyperkalemia related pseudoinfarction, along with the ST segment elevation, ECG abnormalities consistent with hyperkalemia, like intraventricular conduction delay or tall peaked T waves, are reported. , Hyperkalemia triggering coronary spasm also needs to be considered.  Acute transient ST segment elevation has also been reported in septic shock in the absence of hyperkalemia and coronary vasospasm was proposed as the underlying mechanism. ,
Early diagnosis and treatment of hyperkalemia is dependent on the physician's ability to recognize the ECG changes of hyperkalemia; although, ECG alone is not reliable for diagnosis.  Rapid determination of serum potassium levels by bedside blood gas analyzers serves to be a useful guide, directing immediate treatment of hyperkalemia. ST segment elevation due to hyperkalemia will resolve with appropriate treatment. Urgent dialysis may occasionally be needed. This response to therapy can be noted on serial ECG monitoring.
There have been few reports of pseudoinfarction in patients with hyperkalemia and diabetic ketoacidosis. ,,,,,, There have been no reports published in the literature of hyperkalemia secondary to septic shock and acute renal failure causing pseudo-infarction changes on ECG.
The patient we described had initial ECG findings suggestive of an AMI. There are ECG clues that can aid in differentiating ST elevation of hyperkalemia from myocardial injury. A short normal QTc interval and narrow and tented T waves are suggestive of hyperkalemia. A long QTc interval and broad-based T waves are more suggestive of myocardial injury.  The ECG changes in this case showed markedly elevated ST segments with concavity upward and pointed T waves. It is this change that is slightly different from the early hyperacute changes of AMI and should prompt suspicion of hyperkalemia. The effects of hyperkalemia may be uneven throughout the ventricles, being more marked in some myocardial regions, thus leading to ST-elevation pattern confined to some ECG leads. It has been postulated that differences occur in accumulation or depletion of ions in the extracellular space in different zones of the heart.  Patient responded to the management of hyperkalemia and ST elevation returned back to the baseline. The ischemic basis of the ECG changes could not be absolutely excluded as angiography was not performed, but the rapid normalization of ST elevation on treatment of hyperkalemia makes ischemia a rather unlikely cause.
This case depicts acute anterior pseudo-myocardial infarction on ECG, which is a rare manifestation of hyperkalemia with septic shock. ST segment elevation related to hyperkalemia will resolve with successful reduction of the serum potassium levels. With the current emphasis on reducing door-to-balloon times in patients presenting with ST elevation myocardial infarction, it is important for physicians to be aware of this condition. This will aid in initiating correct therapy and prevent the patient from unnecessary interventions and the associated risk of complications.
| :: References|| |
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