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.
June 18, 2009
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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.
June 18, 2009
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.
June 7, 2009
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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).
June 4, 2009
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.
June 1, 2009
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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.
May 25, 2009
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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.
May 23, 2009
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Patient: Young female person with cardiac arrest. Initial ventricular fibrillation that was defibrillated x 3. Then asystole and long resuscitation ( 45 min) before ROSC was achieved.
ECG description:
- Regular junctional rhythm
- Ventricular rate 76 bpm
- No visible P waves preceding QRS
- Extreme right axis deviation – axis indeterminate
- Poor R wave progression
- Prolonged QT interval. QTc = 485 ms
ECG interpretation:
The ECG shows a regular, narrow-complex rhythm with no visible P waves. Sinoatrial pacing has failed, and an ectopic site in the AV junction has taken over pacing. Junctional automaticity normally provides heartrates in the range of 40 to 60 bpm, but here the rate is right below 80 bpm. When the rate of junctional impulse discharge is moderately increased like here, it is called an accelerated AV junctional rhythm (AJR). Chou (2008:389-391) states that AJR is seen predominantly in patients with heart disease. The QT interval is prolonged, with a QTc of 485 ms. Prolonged QT often occurs after CPR.
Calculating corrected QT-time (QTc) with Bazett’s Formula
QTc = QT / √ RR
QT is measured in milliseconds, while RR is measured in seconds. To calculate the RR interval in seconds, we use 60/heart rate. 60/80 is 0.75.
We enter this into Bazett’s formula and get:
QT = 420 / √ 0.75
QT = 420 / √ 0.866
QT = 484.988 ≈ 485 ms
May 23, 2009
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Patient: Male, 91 y/o. Admitted to the hospital after he fell in his home and was found after 24 hours on the floor. No complaints over chest pain. He is put under observation for commotio cerebri. Cerebral CT scan is negative. Known angina pectoris and has had one AMI in 1983 (vessel unknown). He has a prerenal kidney failure. Troponine level on admittance is 0.04. 8 hours later it is 0.03.
ECG description:
- Regulary irregular supraventricular rhythm
- Sinus rhythm
- Premature atrial contractions (PAC) in trigeminal pattern
- Normal cardiac axis
- Poor R wave progression
- Q wave in lead III
- 2mm horizontal ST-depression in leads V2-V4
ECG interpretation:
Sinus rhythm is interrupted by premature atrial contractions (PAC). Every second sinus beat is followed by a PAC, resulting in a trigeminal pattern. Each PAC resets the sinus node, and is therefore followed by a non-compensatory postextrasystolic pause, contributing to slowing the rhythm down. The ectopic P waves are best seen lead V1, where they are upright/positive. In the inferior leads (II, III, aVF), the same P waves are inverted. This indicates that the ectopic focus lies in or around the AV junction, depolarizing the atria in a retrograde fashion – away from the inferior leads, making the P wave negative. You will probably note that the first P wave in the ECG is negative in lead III. This could lead to confusion, as it would suggest that also this beat is ectopic. However, a diphasic or inverted sinus P wave in lead III is normal in small amounts of the population (Chou 2008:8). Also, note that the last P wave in the ECG has the same P wave axis and morphology as the rest of the ectopic P waves. Although it doesn’t seem to be much premature, it comes from the same ectopic pacemaker. It also breaks the trigeminal pattern.
Premature atrial contractions (PAC) and postextrasystolic pauses
Since we’re on the subject, let’s do a quick recap of the essentials regarding PACs and their pauses.
- A PAC originates from an ectopic site in the atria, and therefore produces a P wave morphology that differs from that of the sinus P wave. It will also produce a normal QRS, as the premature atrial impulse will conduct through His-Purkinje normally. Unless of course, some kind of intraventricular conduction delay is present or if aberrant conduction of the impulse occurs. A PAC produces a pause in the heart rhythm, which can be seen on the ECG. A PAC will usually depolarize the whole atrium (logically, since there is nothing there to stop the impulse from spreading all over the place). When the impulse therefore reaches the sinus node, the node will be “reset” and start a “new” sinus rhythm. This will be manifested on the ECG as a pause, which will be longer than the sinus cycle.
- Such a pause is either labeled a compensatory or a non-compensatory postextrasystolic pause. To differentiate these pauses, we need to look at the three intervals: the normal interval, the coupling interval and the postextrasystolic pause. The normal interval is the basic cycle in the ECG, in this ECG it is the sinus cycle, the cycle starting with the third P wave and ending with the fourth P wave in this ECG. The coupling interval is the interval between the sinus P wave and the premature P wave. The postextrasystolic pause is the pause after the premature beat, consisting of the interval between the premature P wave and the sinus P wave following the pause.
- Now, if the coupling interval + postextrasystolic pause is less than twice of the normal interval, the pause is non-compensatory. If the two added intervals equals twice or more than twice the length of the normal interval, the pause is compensatory. With PACs, non-compensatory pauses are the common finding. Only very rarely, a premature beat originating near or in the AV junction can spread only in the anterograde direction and avoid resetting the sinus node and thereby produce a compensatory pause.
- Now, let’s take a look at lead III from this ECG. By using a ruler or a caliper we will find that the coupling interval + the postextrasystolic pause is less than twice the length of the normal interval. Which is what we expected to find. This is a premature atrial contraction producing a non-compensatory pause.
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May 20, 2009
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This ECG is from a healthy, 29 year old caucasian male with no medical history.
- Sinus bradycardia with varied ventricular rate
- Normal cardiac axis at approx 60 °
- Flattened T wave in aVL
- Voltage criteria (Sokolow-Lyon index) suggests Left Ventricular Hypertrophy
Sinus Bradycardia
Sinus bradycardia is normally considered clinically significant when then rate drops under 50 beats/min. However during sleep and in healthy, young individuals (especially athletes), heart rate may be as slow as 40 bpm without compromising cardiac output. Chou (2008: 329-330) states that a rate as slow as 35 bpm may be seen, but in healthy individuals the rate is usually > 40 bpm during waking hours. Increased vagal tone is often the cause of sinus slowing. In sinus bradycardia, the sinoatrial node fires slower than in normal sinus rhythm. The cell automaticity in the SA node is prolonged. When considering the action potential, this is equivalent with a longer phase 4 repolarization. This again manifests electrocardiographically as a prolonged TP segment.
Respiratory Sinus Arrhythmia
Variations in heart rate commonly occur in relation to the respiratory cycle. In respiratory sinus arrhythmia the heart rate increases with inspiration and decreases with expiration, due to changes in vagal tone during the respiratory cycle. Sinus arrhythmia occurs more frequently when the sinus rate is slow. This arrhythmia is considered benign and normal. Prevanlence is higher in infants and young individuals and tends to decrease with age.
May 17, 2009
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