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Digoxin Effect and Digoxin Intoxication
Digoxin effect
The following are the ECG changes that are observed at therapeutic levels of digoxin (observation of these findings does not necessarily imply the presence of digoxin inoxication):
- Sagging type ST segment depression.
- Flattened, negative or biphasic T waves.
- QT interval shortening.
- U wave amplitude may increase.
Clinical significance of the digoxin effect
In patients with therapeutic levels of digoxin levels, the sagging type ST segment depression starts from the isoelectric line and there is no J point depression.
In patients with therapeutic levels of digoxin levels, the J point depression may be due to
- tachycardia
- coronary artery disease
- left ventricular hypertrophy
In patients with therapeutic levels of serum digoxin and normal coronary arteries, ST segment depression may develope during treadmill exercise test.
Digoxin intoxication
Almost any type of arrhythmia may be observed.
The most common arrhythmia observed in digoxin intoxication is ventricular premature contraction (VPC). However, VPC is not specific for digoxin intoxication. On the other hand, observation of
bidirectional VPC in a patient under digoxin therarapy should raise the possibility of digoxin intoxication.
Digoxin depresses conduction in atrioventricular (AV) node and may result in:
- AV blocks
- Sinus bradycardia
- Sinoatrial exit block
Atrial tachycardias or ventricular tachycardias may be seen. Ventricular tachycardias may be monomorphic or bidirectional.
Although there is no diagnostic ECG finding of digoxin intoxication, observation of any of the following ECG findings strongly suggests digoxin intoxication:
1. Atrial tachycardia with block: atrial rate is > 100/minute, ventricular rate is < 100/minute.
2. Bidirectional VPC or bidirectional ventricular tachycardia.
3. Equalization of R-R intervals in a patient with atrial fibrillation.
Clinical significance of digoxin intoxication
May cause ventricular tachycardia or ventricular fibrillation resulting in death.
AV block or significant decrease in heart rate may cause syncope.
What to do in digoxin intoxication
Digoxin should be withdrawn immediately.
Drugs that may increase serum levels of digoxin (spironolactone, verapamil, diltiazem, amiodarone or carvedilol) should be withdrawn immeadiately.
Hypokalemia, if present, should be corrected. Hypokalemia exacerbates arrhythmias in digoxin intoxication. Since heart failure patients often use diuretics, hypokalemia is frequently observed in this group of patients.
If there is no hemodynamic instability, withdrawal of digoxin and monitorization of cardiac rhythm is usually sufficient.
Temporary cardiac pacemaker may be implanted if there is AV block and syncope.
Digoxin-specific Fab-fragments act immediately and should be preferred in patients with life threatening arrhythmias.
Antiarrhythmic drugs may be used if ventricular arrhythmias are observed. However, remember that antiarrhythmic drugs may cause or worsen AV block while suppressing ventricular arrhythmias.
Electrical cardioversion may result in ventricular fibrillation or asystole in patients with digoxin intoxication. Therefore, the use of electrical cardioversion is relatively contraindicated in this group of patients.
References
J Electrocardiol 2018;51:450-451.
J Electrocardiol 2017;50:909-911.
Indian Heart J 2016;68 Suppl 2:S223-S225.
Intern Med 2011;50:2243.
Circulation 2006;113:e156-157.
Am J Med 2003;115:70-71.
Am J Geriatr Cardiol 2001;10:59.
Pacing Clin Electrophysiol 1987;10:1371-1377.
J Am Coll Cardiol 1985;5(5 Suppl A):91A-98A.
ECG 1. 2:1 AV block is seen in a patient with digoxin intoxication. Of every 2 P waves, one P wave is conducted and the other
P wave is not conducted. The patient's serum digoxin level was above 5 ng/mL.
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ECG 2a. Slow ventricular rate in a patient with atrial fibrillation and digoxin intoxication. Serum digoxin level is 3.0ng/mL.
The second beat on the left side is a ventricular premature systole (VPS).
At first glance, atrial fibrillation with a slow ventricular response may give the impression of complete AV block.
In complete AV block, the QRS intervals are regular.
In atrial fibrillation with a slow ventricular response, the QRS intervals are still irregular.
The QRS intervals in the above ECG are irregular (atrial fibrillation with slow ventricular response).
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ECG 2b. The same patient's ECG 8 days later. The ventricular rate is increased.
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ECG 3. First degree AV block and sagging type ST segment depression is observed in a patient with digoxin intoxication.
The serum digoxin level is above 4ng/mL.
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ECG 4a. This patient had syncope with a serum digoxin level of 25 ng/mL. The basic rhythm is nodal rhythm with no preceding
P waves. There are also attacks of ventricular tachycardia. If antiarhhythmic therapy is initiated without temporary pacemaker
implantation, the heart rate will probably decrease more.
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ECG 4b. The ECG of the same patient a few minutes later. Basic rhythm is junctional rhythm with narrow QRS complexes and
no preceding P waves. Ventricular couplet is also seen. If antiarhhythmic therapy is initiated without temporary pacemaker
implantation, the heart rate will probably decrease more.
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ECG 5. This heart failure patient under digoxin therapy also has accompanying hypothyroidism. There are intermittent nodal
beats with no preceding P waves. Some sinus beats have P waves preceding the QRS complex. The U waves are best seen
in middle chest leads (in C2 of the above figure) and especially during bradycardia. The amplitude of the U wave increases
in patients under digoxin treatment.
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ECG 6. This patient is under digoxin therapy and has a serum Digoxine level of 0.7 ng/mL (within normal limits).
The observation of sagging type ST segment depression only suggests Digoxine effect.
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ECG 7. Atrial fibrillation with slow ventricular response in a patient with Digoxin intoxication.
Dr. Huseyin Narcı has donated the above ECG to our website.
Click here for a more detailed ECG
ECG 8. This patient with atrial fibrillation has normal coronary arteries. He is under Digoxin therapy.
The sole sagging type ST segment depression in leads C4 to C6 show Digoxin effect, but not necessarily Digoxin intoxication.
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ECG 9. The ECG above is from a patient with heart failure under Digoxin therapy and shows ECG signs of Digoxin intoxication:
Sagging type ST segment depression may be seen as a Digoxin effect or may be a sign of Digoxin intoxication.
However, this patient also has bidirectional VPCs ( positive and negative VPCs) which suggest Digoxin intoxication.
Digoxin overdose has resulted in a significantly slow heart rate.
The basic rhythm is atrial fibrillation: RR intervals are irregular and no P waves preceed the QRS complexes.
Click here for a more detailed ECG
ECG 10. The ECG above is from a dilated cardiomyopathy patient taking Digoxin. He has normal coronary arteries.
There is atrial fibrillation and ST depression.
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ECG 11. Sagging-type ST segment depression is seen in leads V3-V5 of the ECG above. It belongs to a 72 years-old woman
with normal coronary arteries and atrial fibrillation.
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ECG 12. Right bundle branch block and atrial fibrillation in a 74 years-old woman. She is taking Digoxin to control heart rate.
Sagging-type ST segment depression is seen in leads V2 to V4.
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ECG 13. The ECG above is from a 67 years-old woman with a diagnosis of alcoholic dilated cardiomyopathy and
paroxysmal atrial flutter. She was admitted to Cardiology department because of repeated pre-syncope.
She was on carvidilol, quinapril, spironolactone, bumetanide, atorvastatin and digoxin therapy.
Her ECG on admission is seen above. This is a junctional escape rhythm in the setting of digitalis intoxication.
Sinus bradycardia, sinus arrest and sinus Wenckebach conduction are not uncommon in digitalis toxicity.
The reason why the sinus node is inhibited in this patient is due to digitalis intoxication with extreme sinus bradycardia/SA
block combined with overdrive suppression by the retrograde P waves. The slow junctional escape rhythm conducts
retrogradely - suggested by the superior P wave axis - with a long ventriculoatrial (VA) interval. Besides slowing the antegrade
atrioventricular (AV) conduction, it has also been shown that digitalis slows/blocks the retrograde fast pathway conduction.
The reason why the retrograde impulse conducts via the retrograde slow pathway - suggested by the long VA interval - is
probably due to retrograde fast pathway block in the setting of digitalis intoxication or due to the absence of retrograde fast
pathway conduction. The impulse then re-enters the ventricle via the fast pathway and initiates the so-called
ventricular echo beat (Figure 8). The RP interval is longer than the PR interval, signifying that the impulse is travelling
in a retrograde fashion via the slow pathway and then antegradely down to the ventricle via the fast pathway.
Click here for a more detailed ECG
The ECG above has been used with the permission of Netherlands Heart Journal.
Click here to read the relevant article by Alzand B.S.N.
Figure 13. Above is the ladder diagram explanining the mechanism of the group beating in ECG 8.
An AV nodal escape rhythm is travelling in a retrograde fashion to the atrium via the slow pathway
and then antegradely to the ventricle (echo beat) via the fast pathway.
The ECG above has been used with the permission of Netherlands Heart Journal.
Click here to read the relevant article by Alzand B.S.N.
ECG 14. Atrial fibrillation and sagging type ST segment depression in a 55 years-old woman.
She has severe mitral stenosis and is taking Digoxin to control heart her rate.
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ECG 15. The above ECG is from an old woman with hypertension, severe left ventricular systolic dysfunction and atrial fibrillation.
She is under Digoxin therapy. Sagging type ST segment depression and prominent U waves are seen.
The ventricular rate is decreased due to Digoxin use. Left bundle branch block is also seen.
Click here for a more detailed ECG
ECG 16. The ECG above is from a 70 years-old woman with atrial fibrillation and normal coronary arteries.
She is under Digoxin therapy. Sagging type ST segment depression is seen.
Prominent U waves are not seen due to high ventricular rate.
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ECG 17. The above ECG is from an old man under Digoxin therapy.
He had previously undergone stent implantation of LAD and Cx coronary arteries.
Sagging type ST segment depression and prominent U waves are seen. The rhythm is atrial fibrillation.
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ECG 18a. The ECG above is from a 72 years-old man who has been hospitalized for acute cerebrovascular accident.
Cardiology consultation was requested for attacks of tachycardia.
The rhythm is atrial fibrillation in the presence of left bundle branch block (LBBB).
ECHOcardiogram showed left ventricular dilation and systolic dysfunction with significant mitral valve stenosis.
The patient had been on Digoxin therapy for a long time. His serum potassium level was measured below 3 mmol/L.
Hypokalemia increases the risk of Digoxin toxicity.
Click here for a more detailed ECG
ECG 18b. Then, his 24-hour cardiac rhythm was recorded by a 3-channel Holter recorder.
The Holter tracing above is from the same man and shows that aberrant conduction developes when heart increases.
(Acceleration-dependent left bundle branch block type aberration in this patient)
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ECG 18c. The above Holter tracing is from the same man.
Conduction without aberration, aberrant conduction and ventricular couplet VPCs are seen.
VPCs are the most frequently observed ECG abnormality in patients with Digitalis intoxication.
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ECG 18d. The above Holter tracing is from the same man.
Conduction without aberration, aberrant conduction and non-sustained ventricular tachycardia are seen.
The last beat of the VT attack is a fusion beat.
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ECG 18e. The above Holter tracing is from the same man.
Conduction without aberration, aberrant conduction and bidirectional VPCs are seen.
In patients on Digoxin therapy, bidirectional VPCs should raise the suspicion of toxicity.
Click here for a more detailed ECG
ECG 18f. The above Holter tracing is from the same man.
Conduction without aberration and non-sustained bidirectional ventricular tachycardia attack are seen.
Bidirectional ventricular tachycardia is typical for Digoxin intoxication.
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ECG 18g. The above Holter tracing is from the same man.
Conduction without aberration, aberrant conduction, short-lasting bidirectional VT attack and VPCs are seen.
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ECG 18h. The above Holter tracing is from the same man and shows conduction without aberration,
aberrant conduction and non-sustained ventricular tachycardia with a different morphology.
Digoxin decreases the excitability of cardiac conduction system while increasing the excitability of myocardial cells.
This is the reason why VPCs and Ventricular Tachycardia attacks with different morphologies may be seen.
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ECG 18i. The above Holter tracing is from the same man and shows conduction without aberration,
aberrant conduction and non-sustained ventricular tachycardia with another morphology.
Digoxin decreases the excitability of cardiac conduction system while increasing the excitability of myocardial cells.
This is the reason why VPCs and Ventricular Tachycardia attacks with different morphologies may be seen.
Click here for a more detailed ECG
ECG 18j. The above Holter tracing is from the same man.
Conduction without aberration, aberrant conduction and artifact are seen.
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ECG 19. The ECG above is from an 82 years-old man. The rhythm is atrial fibrillation.
He has a dilated left ventricle and significant mitral valve insufficiency. He is under Digoxin therapy.
Digoxine related prominent U waves are seen.
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ECG 20. The above compact ECG is from a 70 years-old man with coronary artery disease,
atrial fibrillation and incomplete left bundle branch block. He is under Digoxin therapy.
Leads V5 and V6 show sagging type ST segment depression which is typical for Digoxin effect.
ECG 21. The ECG above is from a 69 years-old man with coronary artery disease and heart failure.
He had previously undergone coronary artery bypass graft surgery.
His left ventricular Ejection Fraction was reported as 30% (low). He also has an ICD pacemaker.
The rhythm is atrial fibrillation. The ventricular rate is very low due to concomitant Amiodarone and Digoxin use.
Both Amiodarone and Digoxin decrease ventricular response during atrial fibrillation.
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ECG 22. The ECG above is from a 75 years-old woman with chronic renal insufficeny and heart failure (left ventricular
systolic dysfunction). At the time the above ECG was recorded, her serum potassium level was measured as 8.6 mmol/L.
She was also under Digoxin therapy. Renal failure eases the occurrence of Digoxin intoxication.
Nodal rhythm is seen. P waves are not visible.
QRS complexes are widened and the T waves in right precordial leads are relatively prominent.
The above ECG was recorded at a paper speed of 25mm/second.
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ECG 23. The ECG above is from a 68 years-old woman with systemic hypertension and atrial fibrillation.
She is taking Digoxin tablets.
Sagging-type ST depression is seen in most of the leads.
The ventricular response is slow due to Digoxin effect. RR intervals are irregular.
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ECG 24. Above is an ECG from a 72 years-old man.
He had undergone surgery for hemodynamically significant pulmonary stenosis, 42 years ago.
ECHOcardiography on the same day with the ECG showed 25 mmHg peak systolic pulmonary gradient.
The right ventricle was dilated and hypertrophic, while both atria were also dilated.
The rhythm is atrial fibrillation: irregular RR intervals without P waves.
The patient is taking Digoxin. Sagging type ST segment depression is due to Digoxin effect.
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ECG 25a. Above is a 3-channel rhythm tracing from a 87 years-old woman with mild renal impairment.
She has been on Digoxin and Metoprolol (beta blocker) therapy for atrial fibrillation.
She was consulted to Cardiology because of "bradycardia".
At first glance, it may look as if there are P waves with a prolonged PR interval.
But the basic rhythm is atrial fibrillation and there are no P waves. Seemingly P waves are QRS complexes.
While monitoring this rhythm, a monitor may sense only the VPCs and may give "bradycardia" alarm.
QRS complexes with different morphologies are bidirectional VPCs.
If you observe bidirectional VPCs on the ECG of a patient under Digoxin therapy, remember the possibility of Digoxin intoxication.
This ECG was recorded at a standard paper speed (25mm/s) and calibration (10 mm/mV).
Dr. Sirli Bulut has donated the above ECG to our website.
Click here for a more detailed ECG
ECG 25b. The 3-channel rhythm tracing above also belongs to the same patient.
It is the continuation strip of the ECG 25a.
The basic rhythm is atrial fibrillation. P waves are absent.
Bidirectional VPCs are seen.
If you observe bidirectional VPCs on the ECG of a patient under Digoxin therapy, remember the possibility of Digoxin intoxication.
Dr. Sirli Bulut has donated the above ECG to our website.
Click here for a more detailed ECG
ECG 25c. The 3-channel rhythm tracing above also belongs to the same patient.
It is the continuation strip of the ECG 25b.
Dr. Sirli Bulut has donated the above ECG to our website.
Click here for a more detailed ECG
ECG 25d. The ECG above belongs to the same patient. It was recorded 2.5 hours after the ECG 25c.
This ECG was recorded at a standard paper speed (25mm/s) but at a calibration of 20 mm/mV.
Now it is clear that the seemingly P waves in ECG 25a are QRS complexes.
At a calibration of 20 mm/mV, the U waves also can be seen.
The basic rhythm is atrial fibrillation. P waves are absent.
Digoxin and Metoprolol therapy causes low ventricular rate.
Dr. Sirli Bulut has donated the above ECG to our website.
Click here for a more detailed ECG
ECG 25e. The above 3-channel 12-lead ECG belongs to the same patient.
It was recorded immediately after the ECG 25d.
This ECG also has a calibration of 20 mm/mV at a paper speed of 25mm/s.
At a calibration of 20 mm/mV, the U waves can be seen easily.
Dr. Sirli Bulut has donated the above ECG to our website.
Click here for a more detailed ECG
ECG 25f. The above 3-channel ECG tracing belongs to the same patient.
It was recorded immediately after the ECG 25e.
This ECG also has a calibration of 20 mm/mV at a paper speed of 25mm/s.
VPCs with different morphologies are seen. Digoxin increases excitability of myocardial cells (positive bathmotrop).
When a patient under Digoxin treatment shows multifocal VPCs and atrial fibrillation with a slow ventricular rate, the possibility of Digoxin intoxication must be remembered.
When AV block increases, ventricular escape beats (not ventricular premature beats) start to appear.
Dr. Sirli Bulut has donated the above ECG to our website.
Click here for a more detailed ECG
ECG 25g. The above 3-channel ECG tracing belongs to the same patient.
It was recorded immediately after the ECG 25f.
This ECG also has a calibration of 20 mm/mV at a paper speed of 25mm/s.
VPCs with different morphologies are seen. Digoxin increases excitability of myocardial cells (positive bathmotrop).
When a patient under Digoxin treatment shows multifocal VPCs and atrial fibrillation with a slow ventricular rate, the possibility of intoxication must be remembered.
Dr. Sirli Bulut has donated the above ECG to our website.
Click here for a more detailed ECG
ECG 25h. The above 3-channel ECG tracing belongs to the same patient.
It was recorded immediately after the ECG 25g.
Short-lasting idioventricular rhythm emerges due to complete AV block.
Dr. Sirli Bulut has donated the above ECG to our website.
Click here for a more detailed ECG
The following are the ECG changes that are observed at therapeutic levels of digoxin (observation of these findings does not necessarily imply the presence of digoxin inoxication):
- Sagging type ST segment depression.
- Flattened, negative or biphasic T waves.
- QT interval shortening.
- U wave amplitude may increase.
Clinical significance of the digoxin effect
In patients with therapeutic levels of digoxin levels, the sagging type ST segment depression starts from the isoelectric line and there is no J point depression.
In patients with therapeutic levels of digoxin levels, the J point depression may be due to
- tachycardia
- coronary artery disease
- left ventricular hypertrophy
In patients with therapeutic levels of serum digoxin and normal coronary arteries, ST segment depression may develope during treadmill exercise test.
Digoxin intoxication
Almost any type of arrhythmia may be observed.
The most common arrhythmia observed in digoxin intoxication is ventricular premature contraction (VPC). However, VPC is not specific for digoxin intoxication. On the other hand, observation of
bidirectional VPC in a patient under digoxin therarapy should raise the possibility of digoxin intoxication.
Digoxin depresses conduction in atrioventricular (AV) node and may result in:
- AV blocks
- Sinus bradycardia
- Sinoatrial exit block
Atrial tachycardias or ventricular tachycardias may be seen. Ventricular tachycardias may be monomorphic or bidirectional.
Although there is no diagnostic ECG finding of digoxin intoxication, observation of any of the following ECG findings strongly suggests digoxin intoxication:
1. Atrial tachycardia with block: atrial rate is > 100/minute, ventricular rate is < 100/minute.
2. Bidirectional VPC or bidirectional ventricular tachycardia.
3. Equalization of R-R intervals in a patient with atrial fibrillation.
Clinical significance of digoxin intoxication
May cause ventricular tachycardia or ventricular fibrillation resulting in death.
AV block or significant decrease in heart rate may cause syncope.
What to do in digoxin intoxication
Digoxin should be withdrawn immediately.
Drugs that may increase serum levels of digoxin (spironolactone, verapamil, diltiazem, amiodarone or carvedilol) should be withdrawn immeadiately.
Hypokalemia, if present, should be corrected. Hypokalemia exacerbates arrhythmias in digoxin intoxication. Since heart failure patients often use diuretics, hypokalemia is frequently observed in this group of patients.
If there is no hemodynamic instability, withdrawal of digoxin and monitorization of cardiac rhythm is usually sufficient.
Temporary cardiac pacemaker may be implanted if there is AV block and syncope.
Digoxin-specific Fab-fragments act immediately and should be preferred in patients with life threatening arrhythmias.
Antiarrhythmic drugs may be used if ventricular arrhythmias are observed. However, remember that antiarrhythmic drugs may cause or worsen AV block while suppressing ventricular arrhythmias.
Electrical cardioversion may result in ventricular fibrillation or asystole in patients with digoxin intoxication. Therefore, the use of electrical cardioversion is relatively contraindicated in this group of patients.
References
J Electrocardiol 2018;51:450-451.
J Electrocardiol 2017;50:909-911.
Indian Heart J 2016;68 Suppl 2:S223-S225.
Intern Med 2011;50:2243.
Circulation 2006;113:e156-157.
Am J Med 2003;115:70-71.
Am J Geriatr Cardiol 2001;10:59.
Pacing Clin Electrophysiol 1987;10:1371-1377.
J Am Coll Cardiol 1985;5(5 Suppl A):91A-98A.
ECG 1. 2:1 AV block is seen in a patient with digoxin intoxication. Of every 2 P waves, one P wave is conducted and the other
P wave is not conducted. The patient's serum digoxin level was above 5 ng/mL.
Click here for a more detailed ECG
ECG 2a. Slow ventricular rate in a patient with atrial fibrillation and digoxin intoxication. Serum digoxin level is 3.0ng/mL.
The second beat on the left side is a ventricular premature systole (VPS).
At first glance, atrial fibrillation with a slow ventricular response may give the impression of complete AV block.
In complete AV block, the QRS intervals are regular.
In atrial fibrillation with a slow ventricular response, the QRS intervals are still irregular.
The QRS intervals in the above ECG are irregular (atrial fibrillation with slow ventricular response).
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ECG 2b. The same patient's ECG 8 days later. The ventricular rate is increased.
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ECG 3. First degree AV block and sagging type ST segment depression is observed in a patient with digoxin intoxication.
The serum digoxin level is above 4ng/mL.
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ECG 4a. This patient had syncope with a serum digoxin level of 25 ng/mL. The basic rhythm is nodal rhythm with no preceding
P waves. There are also attacks of ventricular tachycardia. If antiarhhythmic therapy is initiated without temporary pacemaker
implantation, the heart rate will probably decrease more.
Click here for a more detailed ECG
ECG 4b. The ECG of the same patient a few minutes later. Basic rhythm is junctional rhythm with narrow QRS complexes and
no preceding P waves. Ventricular couplet is also seen. If antiarhhythmic therapy is initiated without temporary pacemaker
implantation, the heart rate will probably decrease more.
Click here for a more detailed ECG
ECG 5. This heart failure patient under digoxin therapy also has accompanying hypothyroidism. There are intermittent nodal
beats with no preceding P waves. Some sinus beats have P waves preceding the QRS complex. The U waves are best seen
in middle chest leads (in C2 of the above figure) and especially during bradycardia. The amplitude of the U wave increases
in patients under digoxin treatment.
Click here for a more detailed ECG
ECG 6. This patient is under digoxin therapy and has a serum Digoxine level of 0.7 ng/mL (within normal limits).
The observation of sagging type ST segment depression only suggests Digoxine effect.
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ECG 7. Atrial fibrillation with slow ventricular response in a patient with Digoxin intoxication.
Dr. Huseyin Narcı has donated the above ECG to our website.
Click here for a more detailed ECG
ECG 8. This patient with atrial fibrillation has normal coronary arteries. He is under Digoxin therapy.
The sole sagging type ST segment depression in leads C4 to C6 show Digoxin effect, but not necessarily Digoxin intoxication.
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ECG 9. The ECG above is from a patient with heart failure under Digoxin therapy and shows ECG signs of Digoxin intoxication:
Sagging type ST segment depression may be seen as a Digoxin effect or may be a sign of Digoxin intoxication.
However, this patient also has bidirectional VPCs ( positive and negative VPCs) which suggest Digoxin intoxication.
Digoxin overdose has resulted in a significantly slow heart rate.
The basic rhythm is atrial fibrillation: RR intervals are irregular and no P waves preceed the QRS complexes.
Click here for a more detailed ECG
ECG 10. The ECG above is from a dilated cardiomyopathy patient taking Digoxin. He has normal coronary arteries.
There is atrial fibrillation and ST depression.
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ECG 11. Sagging-type ST segment depression is seen in leads V3-V5 of the ECG above. It belongs to a 72 years-old woman
with normal coronary arteries and atrial fibrillation.
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ECG 12. Right bundle branch block and atrial fibrillation in a 74 years-old woman. She is taking Digoxin to control heart rate.
Sagging-type ST segment depression is seen in leads V2 to V4.
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ECG 13. The ECG above is from a 67 years-old woman with a diagnosis of alcoholic dilated cardiomyopathy and
paroxysmal atrial flutter. She was admitted to Cardiology department because of repeated pre-syncope.
She was on carvidilol, quinapril, spironolactone, bumetanide, atorvastatin and digoxin therapy.
Her ECG on admission is seen above. This is a junctional escape rhythm in the setting of digitalis intoxication.
Sinus bradycardia, sinus arrest and sinus Wenckebach conduction are not uncommon in digitalis toxicity.
The reason why the sinus node is inhibited in this patient is due to digitalis intoxication with extreme sinus bradycardia/SA
block combined with overdrive suppression by the retrograde P waves. The slow junctional escape rhythm conducts
retrogradely - suggested by the superior P wave axis - with a long ventriculoatrial (VA) interval. Besides slowing the antegrade
atrioventricular (AV) conduction, it has also been shown that digitalis slows/blocks the retrograde fast pathway conduction.
The reason why the retrograde impulse conducts via the retrograde slow pathway - suggested by the long VA interval - is
probably due to retrograde fast pathway block in the setting of digitalis intoxication or due to the absence of retrograde fast
pathway conduction. The impulse then re-enters the ventricle via the fast pathway and initiates the so-called
ventricular echo beat (Figure 8). The RP interval is longer than the PR interval, signifying that the impulse is travelling
in a retrograde fashion via the slow pathway and then antegradely down to the ventricle via the fast pathway.
Click here for a more detailed ECG
The ECG above has been used with the permission of Netherlands Heart Journal.
Click here to read the relevant article by Alzand B.S.N.
Figure 13. Above is the ladder diagram explanining the mechanism of the group beating in ECG 8.
An AV nodal escape rhythm is travelling in a retrograde fashion to the atrium via the slow pathway
and then antegradely to the ventricle (echo beat) via the fast pathway.
The ECG above has been used with the permission of Netherlands Heart Journal.
Click here to read the relevant article by Alzand B.S.N.
ECG 14. Atrial fibrillation and sagging type ST segment depression in a 55 years-old woman.
She has severe mitral stenosis and is taking Digoxin to control heart her rate.
Click here for a more detailed ECG
ECG 15. The above ECG is from an old woman with hypertension, severe left ventricular systolic dysfunction and atrial fibrillation.
She is under Digoxin therapy. Sagging type ST segment depression and prominent U waves are seen.
The ventricular rate is decreased due to Digoxin use. Left bundle branch block is also seen.
Click here for a more detailed ECG
ECG 16. The ECG above is from a 70 years-old woman with atrial fibrillation and normal coronary arteries.
She is under Digoxin therapy. Sagging type ST segment depression is seen.
Prominent U waves are not seen due to high ventricular rate.
Click here for a more detailed ECG
ECG 17. The above ECG is from an old man under Digoxin therapy.
He had previously undergone stent implantation of LAD and Cx coronary arteries.
Sagging type ST segment depression and prominent U waves are seen. The rhythm is atrial fibrillation.
Click here for a more detailed ECG
ECG 18a. The ECG above is from a 72 years-old man who has been hospitalized for acute cerebrovascular accident.
Cardiology consultation was requested for attacks of tachycardia.
The rhythm is atrial fibrillation in the presence of left bundle branch block (LBBB).
ECHOcardiogram showed left ventricular dilation and systolic dysfunction with significant mitral valve stenosis.
The patient had been on Digoxin therapy for a long time. His serum potassium level was measured below 3 mmol/L.
Hypokalemia increases the risk of Digoxin toxicity.
Click here for a more detailed ECG
ECG 18b. Then, his 24-hour cardiac rhythm was recorded by a 3-channel Holter recorder.
The Holter tracing above is from the same man and shows that aberrant conduction developes when heart increases.
(Acceleration-dependent left bundle branch block type aberration in this patient)
Click here for a more detailed ECG
ECG 18c. The above Holter tracing is from the same man.
Conduction without aberration, aberrant conduction and ventricular couplet VPCs are seen.
VPCs are the most frequently observed ECG abnormality in patients with Digitalis intoxication.
Click here for a more detailed ECG
ECG 18d. The above Holter tracing is from the same man.
Conduction without aberration, aberrant conduction and non-sustained ventricular tachycardia are seen.
The last beat of the VT attack is a fusion beat.
Click here for a more detailed ECG
ECG 18e. The above Holter tracing is from the same man.
Conduction without aberration, aberrant conduction and bidirectional VPCs are seen.
In patients on Digoxin therapy, bidirectional VPCs should raise the suspicion of toxicity.
Click here for a more detailed ECG
ECG 18f. The above Holter tracing is from the same man.
Conduction without aberration and non-sustained bidirectional ventricular tachycardia attack are seen.
Bidirectional ventricular tachycardia is typical for Digoxin intoxication.
Click here for a more detailed ECG
ECG 18g. The above Holter tracing is from the same man.
Conduction without aberration, aberrant conduction, short-lasting bidirectional VT attack and VPCs are seen.
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ECG 18h. The above Holter tracing is from the same man and shows conduction without aberration,
aberrant conduction and non-sustained ventricular tachycardia with a different morphology.
Digoxin decreases the excitability of cardiac conduction system while increasing the excitability of myocardial cells.
This is the reason why VPCs and Ventricular Tachycardia attacks with different morphologies may be seen.
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ECG 18i. The above Holter tracing is from the same man and shows conduction without aberration,
aberrant conduction and non-sustained ventricular tachycardia with another morphology.
Digoxin decreases the excitability of cardiac conduction system while increasing the excitability of myocardial cells.
This is the reason why VPCs and Ventricular Tachycardia attacks with different morphologies may be seen.
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ECG 18j. The above Holter tracing is from the same man.
Conduction without aberration, aberrant conduction and artifact are seen.
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ECG 19. The ECG above is from an 82 years-old man. The rhythm is atrial fibrillation.
He has a dilated left ventricle and significant mitral valve insufficiency. He is under Digoxin therapy.
Digoxine related prominent U waves are seen.
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ECG 20. The above compact ECG is from a 70 years-old man with coronary artery disease,
atrial fibrillation and incomplete left bundle branch block. He is under Digoxin therapy.
Leads V5 and V6 show sagging type ST segment depression which is typical for Digoxin effect.
ECG 21. The ECG above is from a 69 years-old man with coronary artery disease and heart failure.
He had previously undergone coronary artery bypass graft surgery.
His left ventricular Ejection Fraction was reported as 30% (low). He also has an ICD pacemaker.
The rhythm is atrial fibrillation. The ventricular rate is very low due to concomitant Amiodarone and Digoxin use.
Both Amiodarone and Digoxin decrease ventricular response during atrial fibrillation.
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ECG 22. The ECG above is from a 75 years-old woman with chronic renal insufficeny and heart failure (left ventricular
systolic dysfunction). At the time the above ECG was recorded, her serum potassium level was measured as 8.6 mmol/L.
She was also under Digoxin therapy. Renal failure eases the occurrence of Digoxin intoxication.
Nodal rhythm is seen. P waves are not visible.
QRS complexes are widened and the T waves in right precordial leads are relatively prominent.
The above ECG was recorded at a paper speed of 25mm/second.
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ECG 23. The ECG above is from a 68 years-old woman with systemic hypertension and atrial fibrillation.
She is taking Digoxin tablets.
Sagging-type ST depression is seen in most of the leads.
The ventricular response is slow due to Digoxin effect. RR intervals are irregular.
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ECG 24. Above is an ECG from a 72 years-old man.
He had undergone surgery for hemodynamically significant pulmonary stenosis, 42 years ago.
ECHOcardiography on the same day with the ECG showed 25 mmHg peak systolic pulmonary gradient.
The right ventricle was dilated and hypertrophic, while both atria were also dilated.
The rhythm is atrial fibrillation: irregular RR intervals without P waves.
The patient is taking Digoxin. Sagging type ST segment depression is due to Digoxin effect.
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ECG 25a. Above is a 3-channel rhythm tracing from a 87 years-old woman with mild renal impairment.
She has been on Digoxin and Metoprolol (beta blocker) therapy for atrial fibrillation.
She was consulted to Cardiology because of "bradycardia".
At first glance, it may look as if there are P waves with a prolonged PR interval.
But the basic rhythm is atrial fibrillation and there are no P waves. Seemingly P waves are QRS complexes.
While monitoring this rhythm, a monitor may sense only the VPCs and may give "bradycardia" alarm.
QRS complexes with different morphologies are bidirectional VPCs.
If you observe bidirectional VPCs on the ECG of a patient under Digoxin therapy, remember the possibility of Digoxin intoxication.
This ECG was recorded at a standard paper speed (25mm/s) and calibration (10 mm/mV).
Dr. Sirli Bulut has donated the above ECG to our website.
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ECG 25b. The 3-channel rhythm tracing above also belongs to the same patient.
It is the continuation strip of the ECG 25a.
The basic rhythm is atrial fibrillation. P waves are absent.
Bidirectional VPCs are seen.
If you observe bidirectional VPCs on the ECG of a patient under Digoxin therapy, remember the possibility of Digoxin intoxication.
Dr. Sirli Bulut has donated the above ECG to our website.
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ECG 25c. The 3-channel rhythm tracing above also belongs to the same patient.
It is the continuation strip of the ECG 25b.
Dr. Sirli Bulut has donated the above ECG to our website.
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ECG 25d. The ECG above belongs to the same patient. It was recorded 2.5 hours after the ECG 25c.
This ECG was recorded at a standard paper speed (25mm/s) but at a calibration of 20 mm/mV.
Now it is clear that the seemingly P waves in ECG 25a are QRS complexes.
At a calibration of 20 mm/mV, the U waves also can be seen.
The basic rhythm is atrial fibrillation. P waves are absent.
Digoxin and Metoprolol therapy causes low ventricular rate.
Dr. Sirli Bulut has donated the above ECG to our website.
Click here for a more detailed ECG
ECG 25e. The above 3-channel 12-lead ECG belongs to the same patient.
It was recorded immediately after the ECG 25d.
This ECG also has a calibration of 20 mm/mV at a paper speed of 25mm/s.
At a calibration of 20 mm/mV, the U waves can be seen easily.
Dr. Sirli Bulut has donated the above ECG to our website.
Click here for a more detailed ECG
ECG 25f. The above 3-channel ECG tracing belongs to the same patient.
It was recorded immediately after the ECG 25e.
This ECG also has a calibration of 20 mm/mV at a paper speed of 25mm/s.
VPCs with different morphologies are seen. Digoxin increases excitability of myocardial cells (positive bathmotrop).
When a patient under Digoxin treatment shows multifocal VPCs and atrial fibrillation with a slow ventricular rate, the possibility of Digoxin intoxication must be remembered.
When AV block increases, ventricular escape beats (not ventricular premature beats) start to appear.
Dr. Sirli Bulut has donated the above ECG to our website.
Click here for a more detailed ECG
ECG 25g. The above 3-channel ECG tracing belongs to the same patient.
It was recorded immediately after the ECG 25f.
This ECG also has a calibration of 20 mm/mV at a paper speed of 25mm/s.
VPCs with different morphologies are seen. Digoxin increases excitability of myocardial cells (positive bathmotrop).
When a patient under Digoxin treatment shows multifocal VPCs and atrial fibrillation with a slow ventricular rate, the possibility of intoxication must be remembered.
Dr. Sirli Bulut has donated the above ECG to our website.
Click here for a more detailed ECG
ECG 25h. The above 3-channel ECG tracing belongs to the same patient.
It was recorded immediately after the ECG 25g.
Short-lasting idioventricular rhythm emerges due to complete AV block.
Dr. Sirli Bulut has donated the above ECG to our website.
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