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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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Patient: Woman, ca. 60 y/o, sudden onset of palpitations and dyspnea. Prehospital EKG showed rapid atrial fibrillation, but she converted spontaneously during transport. When presented in the ER, she still feels palpitations, although not as rapid and intense as they were.
ECG description:
- Sinus rhythm with varying rate, ca. 55-70 npm
- Multiple premature atrial complexes
- Left Axis Deviation (LAD). Axis at approx. – 40°.
- Left Anterior Fasicle Block (LAD, QRS<120ms, no sign of LVH)
- Deep Q waves in V1-V2
- Poor R wave Progression (PRWP)
ECG interpretation: Sinus rhythm with Left Anterior Fasicle Block and Multiple Premature Contractions
ECG comments: The postextrasystolic pause can be compensatory or non-compensatory, depending on whether the premature depolarization of the atria has reset the SA Node or not. When the premature atrial depolarization resets the SA Node, the node will use a variable time period to restart, causing a pause. This pause is longer than the normal PP interval, but not twice as long. If the SA Node is not reset, the pause will be an exact multiple or twice as long as the normal PP interval.
This is measured by adding the PP interval of the coupling interval with the PP interval of the pause. If the sum of these is equal to the normal PP interval, the pause is compensatory. If it is shorter than the normal PP interval, the pause is non-compensatory. See this previous post, where distinguishing between compensatory and non-compensatory pauses is explained.
Why are these PACs and not PJCs?
It is not very usual for PACs to present with compensatory pauses as in this ECG. PACs usually present with non-compensatory pauses, as an atrial depolarization usually resets the SA node. Still, I’d like to think that the ectopic beats here are atrial. If they were junctional, the P waves would fall close to or right after the QRS. With a PJC the PR interval is usually 10 ms or less when the P wave precedes the QRS complex. With PJC, P waves are also inverted in the inferior leads. Another suggestion that this ECG shows PACs, is that the configuration of the premature P wave differs from that of the sinus P waves, which is because the premature impulse originates in a different part of the atria and depolarizes them in a different way.
From measuring the normal intervals, coupling intervals and postextrasystolic pauses, you can see that all the pauses in this ECG are compensatory, except one: The second PAC in the first strip is followed by a pause that is less the sum of the normal PP interval and the coupling PP interval.
Lastly, this ECG shows a Left Anterior Fasicle Block, based on Left Axis Deviation, narrow QRS (>120ms) and no sign of Left Ventricle Hypertrophy measuring by the Sokolow-Lyon index).
December 30, 2008
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ECG description:
- Sinus rhythm, regularly irregular, at approximately 90 bpm
- PR interval normal and constant at 140ms
- Multiple premature atrial complexes
- Atrial trigeminy pattern with compensatory postextrasystolic pauses
- Axis normal at approx. 60°
ECG conclusion: Atrial Trigeminy with Compensatory Postextrasystolic Pauses.
Recognition of Premature Atrial Complexes (PAC)
Every second beat is followed by a premature atrial complex (PAC). A PAC is recognized by a premature QRS complex preceded by a premature P wave. As the pacing comes from the atria, the QRS complex is narrow and has the same morphology as the normal beats. PACs often gets mistaken for junctional premature beats, as the premature P wave easily gets hidden in the preceding T wave. Whenever presented with premature beats, always scan the T waves for hidden P waves. With completely hidden P waves, the giveaway is often a too tall T, which is taller than the other T waves in the same lead. Premature atrial impulses arise from irritable automaticity foci in the heart, and can be induced by several factors, as adrenaline (epinephrine) released by adrenal glands, increased sympathetic stimulation, precense of caffeine, amphetamines, cocaine or other β1 receptor stimulants. Also, digitalis toxicity can lead to PACs. When an automaticity focus in the atria becomes irritable due to one or several of the factors mentioned, it may spontaneously fire an impulse. Such a premature impulse will depolarize the surrounding myocardial tissue, and will show on the ECG as a premature beat. As irritable foci in the atria will lead to atrial contraction, a p wave will preceed the premature QRS complex. Since the impulse starts in the atria, it usually gets conducted normally through to the ventricles via the AV node, which shows on the ECG as a normal PR interval (unless underlying AV block of any kind) and a QRS complex that is similar to the other sinus beats on the ECG.
Different intervals during sinus arrhythmia
A premature beat is premature because it occurs earlier than expected. To be able to tell if a beat is premature, one needs to look at the preceding beats, comparing the normal beat intervals to the interval preceding the premature complex. If the RR or PP interval preceding an early beat is shorter than the normal RR or PP intervals, the beat is considered premature. There are three types of intervals during arrhythmias, that are important to understand the underlying mechanism when dealing with premature beats. These may be named differently in the books and literature, but the concept is the same:
Normal interval (N_int): The interval (PP or RR), ususally in milliseconds or millimetres between the beats in the underlying rhythm.
Coupling interval(C_int): The interval (PP or RR) between a normal sinus beat and the following premature beat.
Postextrasystolic pause (P_ex): The following pause after a premature beat. A postextrasystolic pause can be compensatory (where the SA node is not reset) and non-compensatory (where the SA node is reset).
The Postextrasystolic Pause: Difference between compensatory and non-compensatory
The cycle pause after a PVC is called a post-extrasystolic pauses. Such pauses are divided into two kinds: Compensatory Post-Extrasystolic Pauses and Non-Compensatory Post-Extrasystolic Pauses. These names are often too long to use, so the terms compensatory pause and non-compensatory pause are used instead.
Compensatory Post-Extrasystolic Pause
A PVC starts in the ventricles from an irritable, often hypoxic focus. Therefore, it only depolarizes the ventricles, not the SA Node. Therefore, the SA Node is not reset. So the SA Node fires as planned and on schedule. Often, if you use your caliper and measure PP intervals, you can spot that timely P within a PVC. The problem is though, that when the sinus node fires, the ventricles are still refractory, and the sinus impulse doesn´t get conducted. When this impulse reaches the ventricles, they´re not ready, and can´t depolarize. So there is a pause after the PVC as the ventricles finish repolarizing, making them receptive to the next sinus generated cycle. Remember that since the depolarization begins in the ventricular tissue, the SA Node will never know anything about this premature impulse. And if it doesn´t get depolarized by the impulse, it will not reset and will keep on pacing. And if the SA Node is not reset, the compensatory pause will be an exact multiple of the regular PP interval. So by measuring PP intervals, you can check if the pause is compensatory or not.
Non-Compensatory Post-Extrasystolic Pause
With non-compensatory pauses, the SA Node is reset and starts a new sinus cycle. The non-compensatory pause is not an exact multiple of the regular PP interval. The SA Node is usually reset by Premature Atrial Contractions (PACs) or Premature Junctional Contractions (PJCs). PVCs are sometimes followed by a non-compensatory pause, but only very rarely. Remember, for the SA Node to be depolarized by a PVC, there will have to be retrograde conduction through the AV Node. This is not very usual, but can happen. The take-home advice here, is that with non-compensatory pauses, you are usually dealing with a PAC or a PJC.
The Postextrasystolic Pause: Distinguishing compensatory pauses from non-compensatory pauses
By measuring and comparing intervals, and by setting up two simple formulas, we can check if a postextrasystolic pause is compensatory or not.
Compensatory: The pause is so long , that the distance between the two normal beats that surround the premature beat, is twice as long the normal interval in the underlying rhythm.
Non-compensatory: The pause is longer than the normal interval in the underlying rhythm, but not long enough for the coupling interval and the compensatory pause to double the length of the normal interval.
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As we can see here, the normal interval is 31mm. The sum of the coupling interval and the postextrasystolic pause is 62mm. The pause is compensatory, which means the SA node has not been reset. It continues to pace, undisturbed and unknowingly of the premature beat that just occured. By positioning a caliper on the normal interval and moving this distance two times to the right, you will land exactly on the P wave that follows the postextrasystolic pause. Remember that if the SA node had been reset, it would start a new cycle, and therefore the postextrasystolic pause would be shorter.
December 10, 2008
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Short anamnesis: Male patient, around 70 years of age. Admitted to the ER with ARF (acute renal failure). Serum potassium (kalium) levels at the time of the ecg recording were 7.8 mmol/l.
ECG description:
- Sinus rhythm, approx. 75 bpm
- Normal axis (although deviated towards the left at approx. 0°)
- Tall, tented/peaked T waves.
- One PVC (premature ventricular complex) at the end of the recording
Comments: With severe hyperkalemia like this, one would perhaps also suspect to find a widening of the QRS complex and small P waves, which would be a classic presentation. The QRS in this ecg seems to be normal at about 80ms. The P-waves also seem normal.
November 7, 2008
