This is from a young person with palpitations, on no medications, and with no known heart disease. There was no syncope or history of cardiac disease.
Sinus arrhythmia is unlikely because, in sinus arrhythmia, the rate usually gradually slows and then gradually speeds up. Here, the long R-R intervals are nearly exactly the same as each other, and nearly exactly double the short R-R intervals, which are, in turn, nearly exactly identical to each other. It can't be sinus pause or arrest because the pause is less than 2 seconds. Also, sinus pause would not start up again at a multiple of the other P-P intervals.
Thus, it is almost certainly sinoatrial exit block. This means that the underlying sinus node depolarizes at a constant rate, but occasionally does not "exit" the sinus node and depolarize the atrium; hence, no P-wave.
The fact that the long intervals are not EXACTLY double the short ones argues only weakly against this because the sinus rate is not always exactly the same.
Why is the P-wave after the first long interval different from the others? Dr. Karim explained:
"The sinus node is a very long structure, extending from SVC/RA junction coming down on the RA wall.
Of course, without the actual SA recordings, no one can say for sure, but we essentially rely on the P-wave morphology and axis to make a determination about the origin of those p-waves.
"The exit site of the Sinus node activity is usually high up and therefore P-waves are usually positive. Sometimes, the exit site from sinus node can vary in the same person and can potentially result in slightly different morphology.
"The P-wave in question is different, but still appears like sinus to me, with a slightly lower exit and therefore the positivity is not as pronounced. The pause that occurs afterwards shows the p-wave that’s similar to other sinus p-waves."
Furthermore, the fact that the sinus node impulse is exiting at different parts of the long sinus node suggests that it is being blocked from its normal exit, and supports sinoatrial exit block.
Final explanation of this case, which I believe is SA exit block second degree type II (with an interesting twist):
SA block in this case: Suppose the impulse cannot exit using the normal transitional (T) cells (SA block), but does succeed in travelling down the SA node and exiting elsewhere. Then you get a different P-wave morphology, as we have in this case. In this case: the first PQRS is normal. The second sinus impulse is completely blocked and there is no p-wave or QRS. The third is partly blocked, but exits the SA node in a different area and you get a PQRS but with a different P-wave morphology. Then there are 7 normal beats, but the 11th sinus impulse is completely blocked but the 12th exits normally and the P-wave morphology is normal.
Management: The patient was admitted, had an uneventful overnight stay except was diagnosed with hyperthyroidism, and discharged. He will get follow up for the sinus abnormality. Patients with asymptomatic SA block do not need treatment (palpitations would not be a significant symptom). Patients with syncope or near syncope must be evaluated further.
Sinus Node Dysfunction (SND):
Partly adapted from the AHA/ACC guidelines for pacemaker insertion (JACC 2008; 51(21):e1-e62) and from online textbook UpToDate:
"SND refers to a broad array of abnormalities in sinus node and atrial impulse formation and propagation. These include persistent sinus bradycardia and chronotropic incompetence without identifiable causes, paroxysmal or persistent sinus arrest with replacement by subsidiary escape rhythms in the atrium, AV junction, or ventricular myocardium." (ACC/AHA)
Anatomy and Pathology of SND
The sinoatrial (SA) node has pacemaker, or "P" cells and transitional, or "T" cells which transmit the impulse from the P cells to the atrium. It may be diseased due to ischemic, infiltrative, inflammatory, or fibrotic changes, or to excessive vagal tone, beta blockers, calcium channel blockers, or hyperkalemia.
1. Sinus pause: At least 2 seconds of pause
2. Sinus arrest: I could not find a definition, except that there is a complete absence of P-waves. If an escape beat comes within 3 seconds, is that sinus arrest or sinus pause? Lower pacemakers (AV node, bundle of HIS, right or left bundle, ventricle) which produce "escape" rhythms do not always function, so asystole is a possible outcome of sinus arrest.
Etiology of sinus pauses and arrest: alteration in the impulse rate of the P cells. Therefore, the pause length is variable and not necessarily a multiple of the basic sinus rate. Pauses up to 3 seconds during carotic sinus massage (vagal stimulation) are within normal limits. But symptomatic carotid sinus hypersensitivity may be an indication for a pacer.
3. Sinoatrial nodal exit block (SA exit block): SA pacemaker, or P cells, are working but the impulse is not transmitted by the T cells to the surrounding atrial tissue. So there is no P-wave. The sinus impulse is invisible on the surface ECG if there is no P-wave (the P-wave comes from atrial activity).
3a. First Degree SA Block: slowing of impulse exit only. This cannot be seen on the surface ECG
3b. Second Degree SA Block:
Type I: (Wenckenbach): progressivley decreasing P-P intervals prior to a pause; the pause has a dduration less than 2 P-P cycles.
Type II: P-P interval is a multiple of the normal P-P intervals
3c. Third Degree SA Block: the impulse does not reach the atrium at all and thus cannot be differentiated from sinus arrest on the surface ECG.
Sick Sinus Syndrome findings include:
1. chronic, inappropriate, sinus bradycardia, which may be symptomatic if there is failure of "escape" rhythms
2. Sinus pauses, sinus arrest, and sinoatrial exit block
3. Alternating bradycardia and atrial tachyarrhythmias, including atrial fib (tachy-brady syndrome)
Not all patients with sick sinus syndrome need a pacemaker immediately, but if you encounter a patient who has symptomatic sinus pauses in the ED (syncope or near syncope) and you are not sure that it is sinus arrhythmia, as I see it, you cannot safely send the patient home without further evaluation, usually by a cardiologist. Although the serious outcomes may take some time to manifest (see paper below), I don't know of any way to predict that they won't happen immediately in your symptomatic ED patient, unless you can find and reverse an identifiable cause such as hyperkalemia or drug effect. Anyone with any better information on this, please comment and I will edit this.
Natural History of Sick Sinus Syndrome
In this study of 35 patients with sick sinus syndrome, as diagnosed by (1) age at least 45 years; (2) mean sinus rate at rest less than 45 beats/min, and/or intermittent sinoatrial block in at least 1 standard electrocardiogram recorded during diurnal hours on different days; (3) symptoms attributable to sinus node dysfunction, such as syncope or dizziness, and/or easy fatigue or effort dyspnea, the patients were followed up for up to 4 years (mean 17 ± 15 months). During follow-up, 20 patients (57%) had cardiovascular events that required treatment: 8 had syncope (23%); 6 had overt heart failure (17%); 4 patients had chronic atrial fibrillation (11%); and 2 patients had poorly tolerated episodes of paroxysmal tachyarrhythmias (6%). Actuarial rates of occurrence of all events were 35%, 49%, and 63%, respectively, after 1, 2, and 4 years. At univariate analysis, age at least 65 years, end-systolic left ventricular diameter at least 30 mm, end-diastolic left ventricular diameter at least 52 mm, and ejection fraction less than 55.