Atrial Bigeminy with Left Anterior Fascicular Block
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Patient: n/a
ECG description:
- Sinus tachycardia
- Supraventricular bigemeny
- One premature ventricular contraction
- Left Anterior Fascicular Block (LAD, initial R wave in II, III, aVF)
Discussion:
There is a baseline sinus tachycardia with a PR interval of 130ms, regularly interrupted by premature atrial contractions (PAC). Each PAC depolarizes the atria and resets the SA node, causing a change in automaticity and a noncompensatory extrasystolic pause. Judging by the PR interval as well as P axis and morphology of the premature beats, the ectopic pacemaker is atrial. The ectopic PR interval is 130ms, and it is plausible to think that the ectopic pacemaker is located near the SA node. The P wave axis is ca. 30 degrees, and the ectopic P wave axis is ca. 60 degrees, which means that the atria are depolarized anterogradely and in almost the same direction as from the SA node. QRS axis and morphology is slightly different in the QRS complex following the first premature beat and the second and third. Looking closely, we can see that P wave axis and morphology slightly differs from the first PAC to the next two. The PR interval however is the same. This could be due to multifocality, but since the PR interval is quite similar, the two foci must be very close to each other. After the third bigeminal beat, a broad QRS occurs. In spite of the aberrantly looking RBBB-like morphology, this is most likely a premature ventricular contraction (PVC). If this was aberrancy, it would be due a refractory right bundle branch that couldn’t cope with the rapid changes in automaticity caused by the PAC’s. However, the coupling interval before the broad complex is similar to the other coupling intervals, and this demonstrates that the RBB in fact handles the rapid changes in automaticity quite well. In the precordial leads, we can see a P wave following the PVC, suggesting that the atrias have been depolarized retrogradely from the PVC.
Add comment July 1, 2009
Sinus Arrest With Atrial Escape
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Patient: Woman, 55 y/o, using metoprolol. Diabetes Mellitus II, angina pectoris, adipositas. Admitted with general weakness and fatigue, dehydration and dyspnea. Blood pressure is 100/55. No signs of infection.
ECG description:
- Sinus rhythm with sinus arrest
- Axis within the normal quadrant, at ca. 0 degrees
- Poor R wave progression
- Low amplitude in limb leads
- Baseline artefact from patient movement
- T wave flat/inverted in I, aVL
Discussion: After two sinus beats, a two second atrioventricular asystole occurs, which is then terminated by atrial escape. By comparing the escape P wave with the P waves of the three sinus cycles (the two first and the very last on the ecg), we can see that both P wave morphology, axis and PR interval varies slightly. The PR interval in the sinus cycles is 170 ms, while the escape PR interval is 150 ms. This could indicate that the escape pacemaker is atrial ectopic, but is located in the near vicinity of the sinoatrial node. The sinus pause is longer than, but not a multiple of the normal interval, so this is most likely no SA block. There are also no signs of blocked atrial impulses or reciprocating impulses causing the pause. These observations are important to make, as sinus arrest is often confused with SA block and other mechanisms.
Add comment July 1, 2009
Dysrhythmia during hemodialysis
Arrhythmias frequently occur in patients undergoing hemodialysis. Shinichi, et al. (American Heart Journal, Vol. 131, Issue 6, 1996:1137-1144) reports that out of 221 patients receiving hemodialysis, a total of 65% (143 pts) had ECG abnormalities, excluding sinus tachycardia and sinus bradycardia. The study looks at ECG abnormalities, not only arrhythmias, and left ventricular hypertrophy has the highest prevalence in the sample group. This was followed by ventricular and supraventricular premature contractions, myocardial ischemia and nonspecific ST-T changes. Additionally, a wide range of other arrhythmias and electrocardiographic abnormalities were seen in the patients. The study discusses probable causes for the rather high prevalence of cardiac disorders and arrhythmias among these patients, but is not fully conclusive in it’s outcome. It points at although arrhythmias commonly appear during hemodialysis, the rather large (65%) prevalence is partly due to baseline cardiac conditions. The results indicate that a combination of changes in intra- and extracellular K levels, changes in other electrolyte levels such as Mg and Ca, rapid correction of metabolic acidosis and decreases of circulating blood volume, appear to trigger arrhythmias in patients with latent cardiac problems.
This case is from a 70 y/o man, initially operated for a perforated ulcus ventriculi. In the postoperative phase, severe sepsis and DIC (Disseminated Intravascular Coagulation) occured, and this participated in a following multiple organ failure including tubuar necrosis and total anuria. His medical history revealed no known cardiac disorders. These ECGs were obtained during a 6 hour session of hemodialysis which involved total fluid removal of 1000 ml.
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The baseline rhythm here is atrial fibrillation with rapid ventricular response. The QRS axis is at 30 degrees. The first beat is a premature ventricular contraction (PVC), which is then followed by two supraventricular beats being aberrantly conducted. The right bundle is still refractory after the PVC, and the following two supraventricular impulses are blocked in the RBB, and are being conducted aberrantly, thus causing a QRS with RBBB morphology.
Add comment June 21, 2009
Tachy-brady syndrome: A cascade of arrhythmias and various high degrees of AV block
The patient is an 80 y/o woman with known sick sinus syndrome, aortic sclerosis, aortic valve insufficiency, mitral valve insufficiency, tricuspidal valve insufficiency and left ventricular hypertrophy.
About the sick sinus syndrome and the tachy-brady syndrome
There are two types of Sick Sinus Syndrome (SSS): one with and one without associated tachyarrhythmias. SSS is due to many mechanisms related to SA-nodal failure, and in many patients with the syndrome more than one of the mechanisms are present. The most common mechanisms for SSS are severe, persistent sinus bradycardia, sinus arrest, both brief and sustained, with or without initiation of escape pacemakers, sometimes resulting in sustained asystole. Both Stokes-Adams attacks and sudden death is seen with SSS. When SSS is associated with tachyarrhytmhias, this is called the tachy-brady syndrome. Tachy-brady syndrome occurs in more than half of the patients with SSS.¹ The tachy-brady syndrome itself is not a specific condition, but more of a mixture of combinations of arrhythmias. I find it confusing that even the most profilic authors on this subject, as both Marriott² and Chou¹, tend to disagree on whether SSS should be considered part of the tachy-brady syndrome or vice versa. However, there seems to be consistency upon the fact that SSS can occur in two forms, with our without the associated tachycardias. Furthermore the tachy-brady syndrome is usually described as the condition where a tachycardia mechanism is directly associated with the mechanism of a bradycardia or the other way around. One author³ also differentiates between a tachy-brady syndrome and a brady-tachy syndrome, depending on what mechanism that initiates the next.
This series of telemetry strips from the patient described above, show the tachy-brady syndrome in action, manifested by a large and complex cascade of arrhythmic events. Note that there is a baseline first degree AV block at approximately 260 ms.
Note that each strip is not an exact continuation of the strip before it, meaning that i.e. strip number 2 can repeat some of the events in strip 1.
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Top strip: After 4 cycles of sinus bradycardia (43 bpm), atrial flutter occurs. The atrial rate is approximately 260 bpm, and 2:1 AV conduction occurs, resulting in a ventricular rate of 130 bpm. There are F waves (flutter waves) superimposed on each T wave.
Middle strip: Note that this strip is not an exact continuation of strip 1. The first 12 beats are the same. It shows however the atrial flutter persisting with the same AV ratio for several seconds.
Bottom strip: After a while, 4:1 conduction occurs for one cycle. The next cycle is interrupted by a PVC triplet, or a short run of ventricular tachycardia (VT). After the ventricular triplet, the AV node alternates with 2:1 and 3:1 conduction.
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Top strip: Atrial flutter still persists, while 2:1, 3:1 and 4:1 AV conduction occurs successively, before a four beat salvo of premature ventricular contractions occur. Such a salvo would also be considered non-sustained ventricular tachycardia. Following the salvo, AV ratio continues to vary and also with higher degrees of block. 2:1, 3:1 4:1 and 5:1 AV block occurs successively towards the end of the strip.
Middle strip: This strip is almost a repetition of the top strip, and can be ignored.
Bottom strip: Here we can see that even higher degree of AV block occurs, with AV ratio as high as 6:1 before progressively decreasing again.
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Top strip: This strip is recorded at 50mm/s, and shows the baseline atrial flutter being conducted with high degrees of AV block, and interrupted by a 5-beat run of ventricular tachycardia at 140 bpm.
Middle strip: Various degrees of AV block are seen throughout the strip. The deep, negative deflection towards the end is due to a loose electrode.
Bottom strip: AV block continues to vary, here mostly between a 2:1 and 3:1 ratio.
¹ Surawicz, Borys, Chou’s electrocardiography in clinical practice. Philadelphia: Saunders Elsevier, 2006:336-343, 6th edition.
² Wagner, Galen S., Marriott’s Practical Electrocardiography. Philadelphia: Lippincott Williams & Wilkins, 396-404, 10th edition
³ Sandøe, Erik and Bjarne Sigurd, Klinisk Elektrokardiografi. Bingen: Publishing Partners Verlag GmbH, 326-331, 1st edition.
Add comment June 18, 2009
Digitalis Intoxication: Slow Atrial Fibrillation with Ventricular Escape
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Patient: Woman, 82 y/o with permanent atrial fibrillation. Accidental digitalis intoxication. Serum digoxin level when arriving in the ER is 6.6 ng/ml. General fatigue, but no recent history of syncopal episodes.
ECG description:
- Irregular, narrow QRS bradycardia at approx. 35 bpm
- Atrial fibrillation with slow ventricular response
- Normal axis at ca. 60 degrees
- Prominent U waves, best seen in leads V2 -V3
- Cohn effect: ST segment depression and flattened T wave in leads V4-V6
- Poor R wave progression
- Low amplitude in limb leads
- Baseline noise artefact
Discussion: This 12 lead ECG displays atrial fibrillation with slow ventricular response. There is a high degree of AV block, resulting in a bradycardic rate at ca 35 bpm (50 mm/s). The axis is in the normal quadrant and at ca. 60 degrees. Limb leads show T wave flattening, and there is perhaps a slight ST segment depression visible in leads II and AVF. There is a quite prominent U wave. Normally, the U wave is best appreciated in the lateral precordial leads (V5-V6). Here however, it is seen in leads V2 and V3. The classic ST segment morphology induced by digitalis both at therapeutic and toxic serum levels, is the “coved” or “scooped”, or sometimes referred to as “bowl shaped” ST segment depression. It is sometimes described as if the ST segment has been dragged downwards from a point at the middle of the segment. Digitalis intoxications may however, manifest with or without the classic morphology even at high serum levels. The classic digitalis effect on the ST segment is sometimes called the Cohn Effect, named after Alfred E. Cohn, the American cardiologist, for his early 1900-century studies on the effect of digitalis on T wave morphology. It is generally recognized by ST segment depression together with T wave flattening in the same lead. Although this ECG lacks the coving ST segment, the Cohn effect is present in leads V4-V6.
Overall, digitalis has a positiv inotropic effect and a negative chronotropic effect. The negative chronotropy is due to both decreased automaticity of the SA node as well as prolongation of the refractory period of the AV nodal tissue, thus inducing higher degrees of AV block. It also increases AV nodal automaticity which often results in for instance accelerated junctional rhytm and junctional extrasystolia.
This ECG is in the low bradycardic range at around 35 bpm, which is due to the high serum levels of digoxin. Different AV ratios can occur, but 2:1 is rare. With second degree AV blocks, Wenckebach conduction is common. In this ECG it’s impossible to determine the AV ratio, due to atrial fibrillation, and one can only conclude that it is varying. Following is a continous rhythm strip (25 mm/s) of the patient that was obtained 10 minutes later, showing the development of higher degrees of AV block, resulting in long bradycardic cycles.
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Note the long, asystolic pauses. The first and third cycles are so long (>2 seconds) that ventricular escape occurs.
Add comment June 18, 2009
Hyperkalemia K⁺ 7.4 mM
Patient: Male, 84 y/o renal disease and diabetes mellitus type II. Presents in the ED with dyspnea and no chest while resting. He admits to having slight pressing chest pain during activity. His creatinine levels are 190 and his estimated glomerulus filtration rate is 22 ml/min. His potassium level is 7.4.
ECG description:
- Regular narrow complex bradycardia
- Ventricular rate 35 bpm
- No P waves
- Normal axis at ca. 60°
- Poor R wave progression
- QTc is 380 ms
ECG interpretation:
The ECG displays a junctional escape rhythm, a classic morphologic finding with hyperkalemia. With plasma potassium level above 7.0 mM, loss of P wave amplitude is expected, ultimately resulting in a depression of the PR segment. Complete flattening of the PR segment is usually seen when K+ levels exceed 8.0 mM. Here however, at 7.4 mM the P wave is completely absent.
Add comment June 7, 2009
Right Atrial Ectopic Tachycardia with 2:1 Atrioventricular Block
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Hearts point at ectopic P' waves, displaying a 2:1 AV ratio
Patient: Male, 65 y/o. Reoccuring episodes of atrial tachycardia.
ECG description:
- Regular, narrow complex supraventricular tachycardia
- 2 P’ waves per QRS (2:1 ratio) complex, best seen in V2
- Atrial rate is ca. 260 bpm
- Ventricular rate is ca. 130 bpm
- P’ wave morphology suggests right atrial focus
- QRS axis normal, ca. 10°
- Poor R wave progression
ECG interpretation:
With ectopic atrial rhythms, V1 as well as V2 are often good leads to use to look for and differentiate P’ waves and/or flutterwaves in. Here however, ectopic P’ waves are marked by ♥’s in V2, as they were easier to spot here. In V2 there are small, sharp, inverted P’ waves with a regular rate of ca. 260 bpm. Each QRS complex is preceded by 2 P’ waves. The ventricular rate is regular at ca. 130 bpm. 260:2 is 130 and this correlates with our presumption of a 2:1 atrioventricular block. The P’ waves in V1 are negative, which strongly suggests a right atrial focus (Kistler, et al., JACC, Vol. 48, No. 5, 2006).
2 comments June 4, 2009
Cardiac Arrest: Pulseless Electrical Activity (PEA) / Electromechanical Dissociation (EMD) ➔ Flatline
The prehospital ECG obtained in the patient's home, the moment before cardiac arrest. Click image for full scale version (will open in a new window)
Patient: Male 90 y/o. Previous medical history unknown. Sudden onset of chest pain and severe dyspnea in his home. EMS responds quickly and this ECG is obtained in home. The ECG shows an AV junctional rhythm in the bradycardic range. The patient is awake but in severe pain. During transport to the hospital, the patient goes into full cardiac arrest. ACLS is started and is continued during transport to the ER. On arrival in the ER, ACLS continues. The patient is pulseless, with agonal respiration. After a total of one hour of ACLS without result, the resuscitation attempt is called off.
These strips are obtained in the ER from the defibrillator pads and show the progression from Pulseless Electrical Activity (PEA) into a flatline on the monitor. Note: PEA is also sometimes referred to as Electromechanical Dissociation (EMD), which is perhaps a more precise description of the electrophysiologic phenomenon that occurs. EMD is simply the term for when electrical activity occurs in the myocardium, but fails in depolarizing the cells and causing contraction of the heart muscle. This means that PEA/EMD is an agonal rhythm, and that PEA per definition is equal to asystole. However, when people say asystole, they usually refer to a flat line on the monitor/ECG. The next strips show the progression from PEA/EMD into a flat line.
First strip show chest compressions at a rate of ca. 140 bpm, followed by a rhythm check that displays an agonal rhythm/PEA. Compressions then start again. The next strips are recorded from the defibrillator during the next minutes and show the gradual morphologic progression from PEA into what is commonly referred to as flatline.
2 comments June 1, 2009
Atrial Quadrigeminy
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Patient: Woman, 76 y/o. Admitted to the ER for palpitations. Medical history not available.
ECG description:
- Sinus rhythm
- Every fourth sinus beat is followed by a premature atrial contraction (PAC)
- PACs have fixed coupling interval, are preceded by an ectopic P wave and a short PR interval. P’ wave is upright in inferior leads.
- Normal, horizontal cardiac axis at ca. 10°
ECG interpretation:
Every fourth sinus beat is followed by a supraventricular extrasystole with a fixed coupling interval. This pattern is called quadrigeminy. The coupling interval is the interval between the sinus P wave and the ectopic P wave. While varying coupling intervals are often seen in parasystolia, a fixed coupling interval suggests the presence of an ectopic focus that due to increased automaticity decides to fire during normal sinus rhythm. The P wave preceding each premature beat is partially hidden in the preceding P wave, but the PR interval is clearly shorter than in the sinus cycles. This suggest that the PAC origins from a site nearby the sinus node, but closer to the AV junction. The PR interval exceeds 100ms, which suggests an atrial focus rather than a junctional, in which the PR interval would be expected to be shorter. In AV junctional extrasystolia, the atria is often depolarized in a retrograde fashion as the ectopic impulse starts around the AV junction and spreads upwards through the atrium. This normally produces inverted P waves in the inferior leads. Here however, the P wave is upright in the inferior leads, which also indicates an atrial focus.
Add comment May 25, 2009
Atrial Fibrillation With Multifocal PVC Triplet
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Patient: n/a
ECG description:
- Atrial fibrillation with varied ventricular response – ventricular rate 75-90 bpm
- Axis in the normal quadrant, at ca. 60°
- Early R-wave transition zone (V2)
- T wave inversion in leads inferior leads II, III, aVF and in precordial leads V4-V6
- Multiple and multiform/multifocal premature ventricular contractions (PVC)
- Multiform/multifocal PVC triplet
ECG description:
The three first beats of the ECG are PVCs in rapid succession. They are multiform and each have a different axis. Multiformity should not be considered as 100% specific to multifocality, as beats arising from the same ectopic focus can differ in morphology. However, it is common to both label and consider multiform extrasystoles as multifocal, as multifocality is a much more ominous sign of myocardial irritability. Three consecutive PVCs are per definition a short run of non-sustained ventricular tachycardia. However, the common term is a triplet or a salvo.
Add comment May 23, 2009
