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A 64-year-old man with chronic kidney disease and recent upper gastrointestinal hemorrhage suffered pulseless electrical activity and cardiac arrest. Cardiopulmonary resuscitation was started, with three attempted but failed electrical cardioversions. Return of spontaneous circulation required prolonged resuscitation efforts, including multiple rounds of epinephrine, calcium, and sodium bicarbonate. The standard 12-lead electrocardiogram (Figure 1) showed an irregular wide-QRS-complex rhythm, with right bundle branch block and right-superior-axis deviation.
What was the cause of the pulseless electrical activity and the features on the electrocardiogram?
The presentation of cardiac arrest with pulseless electrical activity usually has a grave prognosis, and in the acute setting, the cause may be difficult to establish. However, several conditions that cause this presentation have treatments that, applied immediately, can lead to quick and sustained recovery.1
Electrocardiography can be a powerful tool in the urgent evaluation of pulseless electrical activity.2,3 Narrow-QRS-complex pulseless electrical activity is often caused by mechanical factors such as cardiac tamponade, tension pneumothorax, pulmonary embolism, and major hemorrhage.3 Pulseless electrical activity associated with a wide QRS complex and marked axis deviation, as in this patient, is usually the result of a metabolic abnormality, most often hyperkalemia3; additional indicators of severe hyperkalemia include ST-segment elevation in the anterior chest leads (including the Brugada pattern4) and, as in this patient, “double counting” of the heart rate by the interpretation software (Figure 1).5,6
Based on the suspicion of a metabolic cause, the serum potassium was tested and was 8.9 mmol/L (reference range 3.5–5.0). The patient was given intravenous calcium, sodium bicarbonate, glucose, and insulin, and 2 hours later the serum potassium had decreased to 7.1 mmol/L. At that time, the electrocardiogram (Figure 2) showed a regular rhythm with ectopic P waves, probably an ectopic atrial tachycardia. There were now narrow QRS complexes with J-point depression, upsloping ST segments, and tall, hyperacute T waves in the chest leads—a pattern recently described in proximal left anterior descending coronary artery occlusion.7 The electrocardiographic similarities in hyperkalemia and acute myocardial infarction are probably the result of potassium accumulation in the ischemic myocardium associated with acute coronary occlusion.7
The patient had a full recovery, both clinically and on electrocardiography.
- Saarinen S, Nurmi J, Toivio T, Fredman D, Virkkunen I, Castrén M. Does appropriate treatment of the primary underlying cause of PEA during resuscitation improve patients’ survival? Resuscitation 2012; 83:819–822.
- Mehta C, Brady W. Pulseless electrical activity in cardiac arrest: electrocardiographic presentations and management considerations based on the electrocardiogram. Am J Emerg Med 2012; 30:236–239.
- Littmann L, Bustin DJ, Haley MW. A simplified and structured teaching tool for the evaluation and management of pulseless electrical activity. Med Princ Pract 2014; 23:1–6.
- Littmann L, Monroe MH, Taylor L, Brearley WD. The hyperkalemic Brugada sign. J Electrocardiol 2007; 40:53–59.
- Littmann L, Brearley WD, Taylor L, Monroe MH. Double counting of heart rate by interpretation software: a new electrocardiographic sign of severe hyperkalemia. Am J Emerg Med 2007; 25:584–586.
- Tomcsányi J, Wágner V, Bózsik B. Littmann sign in hyperkalemia: double counting of heart rate. Am J Emerg Med 2007; 25:1077–1078.
- de Winter RJ, Verouden NJ, Wellens HJ, Wilde AA; Interventional Cardiology Group of the Academic Medical Center. A new ECG sign of proximal LAD occlusion. N Engl J Med 2008; 359:2071–2073.
A 64-year-old man with chronic kidney disease and recent upper gastrointestinal hemorrhage suffered pulseless electrical activity and cardiac arrest. Cardiopulmonary resuscitation was started, with three attempted but failed electrical cardioversions. Return of spontaneous circulation required prolonged resuscitation efforts, including multiple rounds of epinephrine, calcium, and sodium bicarbonate. The standard 12-lead electrocardiogram (Figure 1) showed an irregular wide-QRS-complex rhythm, with right bundle branch block and right-superior-axis deviation.
What was the cause of the pulseless electrical activity and the features on the electrocardiogram?
The presentation of cardiac arrest with pulseless electrical activity usually has a grave prognosis, and in the acute setting, the cause may be difficult to establish. However, several conditions that cause this presentation have treatments that, applied immediately, can lead to quick and sustained recovery.1
Electrocardiography can be a powerful tool in the urgent evaluation of pulseless electrical activity.2,3 Narrow-QRS-complex pulseless electrical activity is often caused by mechanical factors such as cardiac tamponade, tension pneumothorax, pulmonary embolism, and major hemorrhage.3 Pulseless electrical activity associated with a wide QRS complex and marked axis deviation, as in this patient, is usually the result of a metabolic abnormality, most often hyperkalemia3; additional indicators of severe hyperkalemia include ST-segment elevation in the anterior chest leads (including the Brugada pattern4) and, as in this patient, “double counting” of the heart rate by the interpretation software (Figure 1).5,6
Based on the suspicion of a metabolic cause, the serum potassium was tested and was 8.9 mmol/L (reference range 3.5–5.0). The patient was given intravenous calcium, sodium bicarbonate, glucose, and insulin, and 2 hours later the serum potassium had decreased to 7.1 mmol/L. At that time, the electrocardiogram (Figure 2) showed a regular rhythm with ectopic P waves, probably an ectopic atrial tachycardia. There were now narrow QRS complexes with J-point depression, upsloping ST segments, and tall, hyperacute T waves in the chest leads—a pattern recently described in proximal left anterior descending coronary artery occlusion.7 The electrocardiographic similarities in hyperkalemia and acute myocardial infarction are probably the result of potassium accumulation in the ischemic myocardium associated with acute coronary occlusion.7
The patient had a full recovery, both clinically and on electrocardiography.
A 64-year-old man with chronic kidney disease and recent upper gastrointestinal hemorrhage suffered pulseless electrical activity and cardiac arrest. Cardiopulmonary resuscitation was started, with three attempted but failed electrical cardioversions. Return of spontaneous circulation required prolonged resuscitation efforts, including multiple rounds of epinephrine, calcium, and sodium bicarbonate. The standard 12-lead electrocardiogram (Figure 1) showed an irregular wide-QRS-complex rhythm, with right bundle branch block and right-superior-axis deviation.
What was the cause of the pulseless electrical activity and the features on the electrocardiogram?
The presentation of cardiac arrest with pulseless electrical activity usually has a grave prognosis, and in the acute setting, the cause may be difficult to establish. However, several conditions that cause this presentation have treatments that, applied immediately, can lead to quick and sustained recovery.1
Electrocardiography can be a powerful tool in the urgent evaluation of pulseless electrical activity.2,3 Narrow-QRS-complex pulseless electrical activity is often caused by mechanical factors such as cardiac tamponade, tension pneumothorax, pulmonary embolism, and major hemorrhage.3 Pulseless electrical activity associated with a wide QRS complex and marked axis deviation, as in this patient, is usually the result of a metabolic abnormality, most often hyperkalemia3; additional indicators of severe hyperkalemia include ST-segment elevation in the anterior chest leads (including the Brugada pattern4) and, as in this patient, “double counting” of the heart rate by the interpretation software (Figure 1).5,6
Based on the suspicion of a metabolic cause, the serum potassium was tested and was 8.9 mmol/L (reference range 3.5–5.0). The patient was given intravenous calcium, sodium bicarbonate, glucose, and insulin, and 2 hours later the serum potassium had decreased to 7.1 mmol/L. At that time, the electrocardiogram (Figure 2) showed a regular rhythm with ectopic P waves, probably an ectopic atrial tachycardia. There were now narrow QRS complexes with J-point depression, upsloping ST segments, and tall, hyperacute T waves in the chest leads—a pattern recently described in proximal left anterior descending coronary artery occlusion.7 The electrocardiographic similarities in hyperkalemia and acute myocardial infarction are probably the result of potassium accumulation in the ischemic myocardium associated with acute coronary occlusion.7
The patient had a full recovery, both clinically and on electrocardiography.
- Saarinen S, Nurmi J, Toivio T, Fredman D, Virkkunen I, Castrén M. Does appropriate treatment of the primary underlying cause of PEA during resuscitation improve patients’ survival? Resuscitation 2012; 83:819–822.
- Mehta C, Brady W. Pulseless electrical activity in cardiac arrest: electrocardiographic presentations and management considerations based on the electrocardiogram. Am J Emerg Med 2012; 30:236–239.
- Littmann L, Bustin DJ, Haley MW. A simplified and structured teaching tool for the evaluation and management of pulseless electrical activity. Med Princ Pract 2014; 23:1–6.
- Littmann L, Monroe MH, Taylor L, Brearley WD. The hyperkalemic Brugada sign. J Electrocardiol 2007; 40:53–59.
- Littmann L, Brearley WD, Taylor L, Monroe MH. Double counting of heart rate by interpretation software: a new electrocardiographic sign of severe hyperkalemia. Am J Emerg Med 2007; 25:584–586.
- Tomcsányi J, Wágner V, Bózsik B. Littmann sign in hyperkalemia: double counting of heart rate. Am J Emerg Med 2007; 25:1077–1078.
- de Winter RJ, Verouden NJ, Wellens HJ, Wilde AA; Interventional Cardiology Group of the Academic Medical Center. A new ECG sign of proximal LAD occlusion. N Engl J Med 2008; 359:2071–2073.
- Saarinen S, Nurmi J, Toivio T, Fredman D, Virkkunen I, Castrén M. Does appropriate treatment of the primary underlying cause of PEA during resuscitation improve patients’ survival? Resuscitation 2012; 83:819–822.
- Mehta C, Brady W. Pulseless electrical activity in cardiac arrest: electrocardiographic presentations and management considerations based on the electrocardiogram. Am J Emerg Med 2012; 30:236–239.
- Littmann L, Bustin DJ, Haley MW. A simplified and structured teaching tool for the evaluation and management of pulseless electrical activity. Med Princ Pract 2014; 23:1–6.
- Littmann L, Monroe MH, Taylor L, Brearley WD. The hyperkalemic Brugada sign. J Electrocardiol 2007; 40:53–59.
- Littmann L, Brearley WD, Taylor L, Monroe MH. Double counting of heart rate by interpretation software: a new electrocardiographic sign of severe hyperkalemia. Am J Emerg Med 2007; 25:584–586.
- Tomcsányi J, Wágner V, Bózsik B. Littmann sign in hyperkalemia: double counting of heart rate. Am J Emerg Med 2007; 25:1077–1078.
- de Winter RJ, Verouden NJ, Wellens HJ, Wilde AA; Interventional Cardiology Group of the Academic Medical Center. A new ECG sign of proximal LAD occlusion. N Engl J Med 2008; 359:2071–2073.
