Laszlo Littmann, MD, PhD

A 57-year-old man hospitalized for treatment of multilobar pneumonia was noted to have a rapid, irregular heart rate on telemetry. He was hypoxemic and appeared to be in respiratory distress. A 12-lead electrocardiogram (ECG) demonstrated atrial fibrillation with rapid ventricular response, as well as what looked like distinct and regular P waves dissociated from the QRS complexes at a rate of about 44/min (Figure 1). What is the explanation and clinical significance of this curious finding?

What appear to be dissociated P waves actually represent respiratory artifact.^1–3 The sharp deflections mimicking P waves signify the tonic initiation of inspiratory effort; the subsequent brief periods of low-amplitude, high-frequency micro-oscillations represent surface electrical activity associated with the increased force of the accessory muscles of respiration.^1–3

Surface electromyography noninvasively measures muscle activity using electrodes placed on the skin overlying the muscle.⁴ Using simultaneously recorded mechanical respiratory waveform tracings, we have previously demonstrated that the repetitive pseudo-P waves followed by micro-oscillations have a close temporal relationship with the inspiratory phase of respiration.³ The presence of respiratory artifact indicates a high-risk state frequently necessitating ventilation support.

In addition, when present, respiratory artifact can be viewed as the “second vital sign” on the ECG, the first vital sign being the heart rate. The respiratory rate can be approximated by counting the number of respiratory artifacts in a 10-second recording and multiplying it by 6. A more accurate rate assessment is achieved by measuring 1 or more respiratory artifact cycles in millimeters and then dividing that number into 1,500 or its multiples.³ Based on these calculations, the respiratory rate in this patient was 44/min.

The presence of two atrial rhythms on the same ECG, one not disturbing the other, is consistent with the diagnosis of atrial dissociation.⁵ Atrial dissociation is a common finding in cardiac transplant recipients in whom the transplantation was performed using atrio-atrial anastomosis.⁶ Most other cases of apparent atrial dissociation described in the old cardiology and critical care literature probably represented unrecognized respiratory artifact.^7,8

An ECG from a different patient (Figure 2) demonstrates rapid respiratory artifact that raised awareness of severe respiratory failure. The respiratory rate calculated from spacing of the pseudo-P waves is 62/min, confirmed by simultaneous respirography.

A FREQUENT FINDING IN SICK HOSPITALIZED PATIENTS

Respiratory artifact is a frequent finding in sick hospitalized patients.³ Most commonly, it manifests as repetitive micro-oscillations.³ Pseudo-P waves, as in this 57-year-old patient, are less often observed; but if their origin is not recognized, the interpretation of the ECG can become puzzling.^1–3,7,8

Respiratory artifact is a marker of increased work of breathing and a strong indicator of significant cardiopulmonary compromise. Improvement in the patient’s cardiac or respiratory condition is typically associated with a decrease in the rate or complete elimination of respiratory artifact.³

Recognition of rapid respiratory artifact is less important in critical care units, where patients’ vital signs and cardiorespiratory status are carefully observed. However, in hospital settings where respiratory rate and oxygen saturation are not continuously monitored, recognizing rapid respiratory artifact can help raise awareness of the possibility of severe respiratory distress.

A 57-year-old man hospitalized for treatment of multilobar pneumonia was noted to have a rapid, irregular heart rate on telemetry. He was hypoxemic and appeared to be in respiratory distress. A 12-lead electrocardiogram (ECG) demonstrated atrial fibrillation with rapid ventricular response, as well as what looked like distinct and regular P waves dissociated from the QRS complexes at a rate of about 44/min (Figure 1). What is the explanation and clinical significance of this curious finding?

What appear to be dissociated P waves actually represent respiratory artifact.^1–3 The sharp deflections mimicking P waves signify the tonic initiation of inspiratory effort; the subsequent brief periods of low-amplitude, high-frequency micro-oscillations represent surface electrical activity associated with the increased force of the accessory muscles of respiration.^1–3

Surface electromyography noninvasively measures muscle activity using electrodes placed on the skin overlying the muscle.⁴ Using simultaneously recorded mechanical respiratory waveform tracings, we have previously demonstrated that the repetitive pseudo-P waves followed by micro-oscillations have a close temporal relationship with the inspiratory phase of respiration.³ The presence of respiratory artifact indicates a high-risk state frequently necessitating ventilation support.

In addition, when present, respiratory artifact can be viewed as the “second vital sign” on the ECG, the first vital sign being the heart rate. The respiratory rate can be approximated by counting the number of respiratory artifacts in a 10-second recording and multiplying it by 6. A more accurate rate assessment is achieved by measuring 1 or more respiratory artifact cycles in millimeters and then dividing that number into 1,500 or its multiples.³ Based on these calculations, the respiratory rate in this patient was 44/min.

The presence of two atrial rhythms on the same ECG, one not disturbing the other, is consistent with the diagnosis of atrial dissociation.⁵ Atrial dissociation is a common finding in cardiac transplant recipients in whom the transplantation was performed using atrio-atrial anastomosis.⁶ Most other cases of apparent atrial dissociation described in the old cardiology and critical care literature probably represented unrecognized respiratory artifact.^7,8

An ECG from a different patient (Figure 2) demonstrates rapid respiratory artifact that raised awareness of severe respiratory failure. The respiratory rate calculated from spacing of the pseudo-P waves is 62/min, confirmed by simultaneous respirography.

A FREQUENT FINDING IN SICK HOSPITALIZED PATIENTS

Respiratory artifact is a frequent finding in sick hospitalized patients.³ Most commonly, it manifests as repetitive micro-oscillations.³ Pseudo-P waves, as in this 57-year-old patient, are less often observed; but if their origin is not recognized, the interpretation of the ECG can become puzzling.^1–3,7,8

Respiratory artifact is a marker of increased work of breathing and a strong indicator of significant cardiopulmonary compromise. Improvement in the patient’s cardiac or respiratory condition is typically associated with a decrease in the rate or complete elimination of respiratory artifact.³

Recognition of rapid respiratory artifact is less important in critical care units, where patients’ vital signs and cardiorespiratory status are carefully observed. However, in hospital settings where respiratory rate and oxygen saturation are not continuously monitored, recognizing rapid respiratory artifact can help raise awareness of the possibility of severe respiratory distress.

A 57-year-old man hospitalized for treatment of multilobar pneumonia was noted to have a rapid, irregular heart rate on telemetry. He was hypoxemic and appeared to be in respiratory distress. A 12-lead electrocardiogram (ECG) demonstrated atrial fibrillation with rapid ventricular response, as well as what looked like distinct and regular P waves dissociated from the QRS complexes at a rate of about 44/min (Figure 1). What is the explanation and clinical significance of this curious finding?

What appear to be dissociated P waves actually represent respiratory artifact.^1–3 The sharp deflections mimicking P waves signify the tonic initiation of inspiratory effort; the subsequent brief periods of low-amplitude, high-frequency micro-oscillations represent surface electrical activity associated with the increased force of the accessory muscles of respiration.^1–3

Surface electromyography noninvasively measures muscle activity using electrodes placed on the skin overlying the muscle.⁴ Using simultaneously recorded mechanical respiratory waveform tracings, we have previously demonstrated that the repetitive pseudo-P waves followed by micro-oscillations have a close temporal relationship with the inspiratory phase of respiration.³ The presence of respiratory artifact indicates a high-risk state frequently necessitating ventilation support.

In addition, when present, respiratory artifact can be viewed as the “second vital sign” on the ECG, the first vital sign being the heart rate. The respiratory rate can be approximated by counting the number of respiratory artifacts in a 10-second recording and multiplying it by 6. A more accurate rate assessment is achieved by measuring 1 or more respiratory artifact cycles in millimeters and then dividing that number into 1,500 or its multiples.³ Based on these calculations, the respiratory rate in this patient was 44/min.

The presence of two atrial rhythms on the same ECG, one not disturbing the other, is consistent with the diagnosis of atrial dissociation.⁵ Atrial dissociation is a common finding in cardiac transplant recipients in whom the transplantation was performed using atrio-atrial anastomosis.⁶ Most other cases of apparent atrial dissociation described in the old cardiology and critical care literature probably represented unrecognized respiratory artifact.^7,8

An ECG from a different patient (Figure 2) demonstrates rapid respiratory artifact that raised awareness of severe respiratory failure. The respiratory rate calculated from spacing of the pseudo-P waves is 62/min, confirmed by simultaneous respirography.

A FREQUENT FINDING IN SICK HOSPITALIZED PATIENTS

Respiratory artifact is a frequent finding in sick hospitalized patients.³ Most commonly, it manifests as repetitive micro-oscillations.³ Pseudo-P waves, as in this 57-year-old patient, are less often observed; but if their origin is not recognized, the interpretation of the ECG can become puzzling.^1–3,7,8

Respiratory artifact is a marker of increased work of breathing and a strong indicator of significant cardiopulmonary compromise. Improvement in the patient’s cardiac or respiratory condition is typically associated with a decrease in the rate or complete elimination of respiratory artifact.³

Recognition of rapid respiratory artifact is less important in critical care units, where patients’ vital signs and cardiorespiratory status are carefully observed. However, in hospital settings where respiratory rate and oxygen saturation are not continuously monitored, recognizing rapid respiratory artifact can help raise awareness of the possibility of severe respiratory distress.

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.

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.