Hospital Practice
ISSN: 2154-8331 (Print) 2377-1003 (Online) Journal homepage: http://www.tandfonline.com/loi/ihop20
Supraventricular Tachycardia in Sepsis: What Mechanism? E. William Hancock To cite this article: E. William Hancock (1991) Supraventricular Tachycardia in Sepsis: What Mechanism?, Hospital Practice, 26:3, 36-41, DOI: 10.1080/21548331.1991.11707710 To link to this article: http://dx.doi.org/10.1080/21548331.1991.11707710
Published online: 06 Jul 2016.
Submit your article to this journal
View related articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ihop20 Download by: [University of Otago]
Date: 10 November 2016, At: 01:46
ECG Casebook E. WILLIAM HANCOCK, Editor
Supraventricular Tachycardia in Sepsis: What Mechanism? A 28-year-old man was seen in the emergency room for weakness, dyspnea, and chest pain. One week earlier he had been seen elsewhere for acute chest pain. He was found at that time to have a large right pneumothorax and was treated with a chest tube for two days. He improved and left the hospital against medical advice. At home he rapidly became sicker. with increasing weakness and chest discomfort. He was taking large doses of acetaminophen and felt increasingly "dopey." He was a thin, acutely ill man. His temperature was 35.2°, pulse 156 and regular, blood pressure 94/85. and respirato:ry rate 24. His skin was pale, warm. and moist. Breath sounds were diminished to absent over the entire right chest. with marked dullness in the lower half and normal to increased resonance in the upper half. Jugular venous pressure was not elevated. and the cardiac examination was unremarkable except for tachycardia The hematocrit was 41 and white cell count 30,900, with 40% polymorphonuclear and 37% band forms. Serum electrolytes and chemical screening panel were normal. An arterial blood sample showed a Po 2 of 52, Pco 2 of 35. and pH of 7.40. The chest roentgenogram showed extensive consolidation in the right lower lung field, with a moderately large pneumothorax in the upper third of the right chest. The electrocardiogram is shown. What is the rhythm diagnosis? What.further cardiac diagnostic studies should be performed? What should be the immediate cardiac therapy? 1-11-111
36
Hospital Practice March 15. 1991
aVR-aVL-aVF
(continues)
Analysis of the ECG (continued)
The ECG shows a regular rhythm at 156, with narrow QRS complexes. The QRS complexes are normal except for borderline left-axis deviation and borderline evidence of incomplete right bundle branch block. There are apparent P waves in the usual position before the QRS complex; these are upright in lead V1 but inverted in leads II, III, and aVF. The P-R interval is noticeably shorter in V1 than in II. III, and aVF. Further study shows good evidence of a second P wave immediately after the QRS complex in lead V1 • It may then be seen that leads II, III, and aVF also show good evidence of a second nadir of atrial activity immediately following the QRS complex. Thus, there is an atrial tachyarrhythmia at a rate of 312, with a 2:1 AV conduction ratio. The atrial waveform in lead V1 has· the appearance of discrete P waves separated by an isoelectric baseline, while in leads II, III, and aVF, it is more like a continuous sawtooth. This is the classic appearance of atrial flutter with a 2:1 AV conduction ratio. In the initial emergency setting, there was uncertainty
about the type of supraventricular tachycardia in this patient. An intravenous infusion of adenosine was given, and the results are shown in a second ECG. Ventricular asystole for 5.5 seconds was recorded, revealing classic atrial flutter as the underlying atrial rhythm mechanism. The QRS complexes returned with a varying AV conduction ratio, and the 2: 1 conduction ratio returned in less than 10 seconds after the adenosine infusion was administered. Since the patient was hypotensive and acutely ill, the question of reverting the atrial flutter to sinus rhythm was a consideration. This is not reliably accomplished by drug therapy and would probably require an intervention such as rapid overdrive atrial pacing or cardioversion. It appeared that sepsis and hypovolemia might be more important contributors than the arrhythmia to the hypotension and should be treated first. In fact, the blood pressure did respond to intravenous volume replacement and antibiotics. The patient was given digoxin, which slowed the ventricular rate by increasing the AV conduction ratio. The atrial flutter reverted spontaneously to sinus rhythm several days later.
Further examination showed no evidence of underlying heart disease. The occurrence of atrial flutter in this patient was attributed to the stress associated with severe infection. The pneumothorax and empyema were treated by chest tube drainage, followed by thoracotomy to close the bronchopleural fistula The patient made a satisfactory recovery. Adenosine was introduced relatively recently as an agent for reverting reentrant supraventricular tachycardias to sinus rhythm. It is tending to replace verapamil for this purpose because of its very brief duration of action and its lesser risk of causing hypotension. Adenosine is also useful as a diagnostic test in atrial tachyarrhythmias of uncertain type, by virtue of its blocking effect on AV conduction. Prolonged pauses due to transient complete AV block (as seen in this case) have occurred with adenosine more frequently than with verapamil. It is prudent to give adenosine in very small doses initially, repeating the infusion in progressively higher doses, to avoid such excessive pauses. o Dr. Hancock Is Professor of Medicine, Cardiology Division, Stanford University School of Medicine.
Continuous Monitor Lead
Hospital Practice March 15, 1991
41
ISSN: 2154-8331 (Print) 2377-1003 (Online) Journal homepage: http://www.tandfonline.com/loi/ihop20
Supraventricular Tachycardia in Sepsis: What Mechanism? E. William Hancock To cite this article: E. William Hancock (1991) Supraventricular Tachycardia in Sepsis: What Mechanism?, Hospital Practice, 26:3, 36-41, DOI: 10.1080/21548331.1991.11707710 To link to this article: http://dx.doi.org/10.1080/21548331.1991.11707710
Published online: 06 Jul 2016.
Submit your article to this journal
View related articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ihop20 Download by: [University of Otago]
Date: 10 November 2016, At: 01:46
ECG Casebook E. WILLIAM HANCOCK, Editor
Supraventricular Tachycardia in Sepsis: What Mechanism? A 28-year-old man was seen in the emergency room for weakness, dyspnea, and chest pain. One week earlier he had been seen elsewhere for acute chest pain. He was found at that time to have a large right pneumothorax and was treated with a chest tube for two days. He improved and left the hospital against medical advice. At home he rapidly became sicker. with increasing weakness and chest discomfort. He was taking large doses of acetaminophen and felt increasingly "dopey." He was a thin, acutely ill man. His temperature was 35.2°, pulse 156 and regular, blood pressure 94/85. and respirato:ry rate 24. His skin was pale, warm. and moist. Breath sounds were diminished to absent over the entire right chest. with marked dullness in the lower half and normal to increased resonance in the upper half. Jugular venous pressure was not elevated. and the cardiac examination was unremarkable except for tachycardia The hematocrit was 41 and white cell count 30,900, with 40% polymorphonuclear and 37% band forms. Serum electrolytes and chemical screening panel were normal. An arterial blood sample showed a Po 2 of 52, Pco 2 of 35. and pH of 7.40. The chest roentgenogram showed extensive consolidation in the right lower lung field, with a moderately large pneumothorax in the upper third of the right chest. The electrocardiogram is shown. What is the rhythm diagnosis? What.further cardiac diagnostic studies should be performed? What should be the immediate cardiac therapy? 1-11-111
36
Hospital Practice March 15. 1991
aVR-aVL-aVF
(continues)
Analysis of the ECG (continued)
The ECG shows a regular rhythm at 156, with narrow QRS complexes. The QRS complexes are normal except for borderline left-axis deviation and borderline evidence of incomplete right bundle branch block. There are apparent P waves in the usual position before the QRS complex; these are upright in lead V1 but inverted in leads II, III, and aVF. The P-R interval is noticeably shorter in V1 than in II. III, and aVF. Further study shows good evidence of a second P wave immediately after the QRS complex in lead V1 • It may then be seen that leads II, III, and aVF also show good evidence of a second nadir of atrial activity immediately following the QRS complex. Thus, there is an atrial tachyarrhythmia at a rate of 312, with a 2:1 AV conduction ratio. The atrial waveform in lead V1 has· the appearance of discrete P waves separated by an isoelectric baseline, while in leads II, III, and aVF, it is more like a continuous sawtooth. This is the classic appearance of atrial flutter with a 2:1 AV conduction ratio. In the initial emergency setting, there was uncertainty
about the type of supraventricular tachycardia in this patient. An intravenous infusion of adenosine was given, and the results are shown in a second ECG. Ventricular asystole for 5.5 seconds was recorded, revealing classic atrial flutter as the underlying atrial rhythm mechanism. The QRS complexes returned with a varying AV conduction ratio, and the 2: 1 conduction ratio returned in less than 10 seconds after the adenosine infusion was administered. Since the patient was hypotensive and acutely ill, the question of reverting the atrial flutter to sinus rhythm was a consideration. This is not reliably accomplished by drug therapy and would probably require an intervention such as rapid overdrive atrial pacing or cardioversion. It appeared that sepsis and hypovolemia might be more important contributors than the arrhythmia to the hypotension and should be treated first. In fact, the blood pressure did respond to intravenous volume replacement and antibiotics. The patient was given digoxin, which slowed the ventricular rate by increasing the AV conduction ratio. The atrial flutter reverted spontaneously to sinus rhythm several days later.
Further examination showed no evidence of underlying heart disease. The occurrence of atrial flutter in this patient was attributed to the stress associated with severe infection. The pneumothorax and empyema were treated by chest tube drainage, followed by thoracotomy to close the bronchopleural fistula The patient made a satisfactory recovery. Adenosine was introduced relatively recently as an agent for reverting reentrant supraventricular tachycardias to sinus rhythm. It is tending to replace verapamil for this purpose because of its very brief duration of action and its lesser risk of causing hypotension. Adenosine is also useful as a diagnostic test in atrial tachyarrhythmias of uncertain type, by virtue of its blocking effect on AV conduction. Prolonged pauses due to transient complete AV block (as seen in this case) have occurred with adenosine more frequently than with verapamil. It is prudent to give adenosine in very small doses initially, repeating the infusion in progressively higher doses, to avoid such excessive pauses. o Dr. Hancock Is Professor of Medicine, Cardiology Division, Stanford University School of Medicine.
Continuous Monitor Lead
Hospital Practice March 15, 1991
41
