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Electrocardiographic Passing Phenomenon (Flying Phenomenon or Yasser’s Phenomenon)

Background: Dynamic changes during an electrocardiographic recording are common alterations. These changes were commonly reported initially as an abnormal diagnosis by cardiologists despite they are unusual taking the opposite normal side. These changes may be passing as physiological or even transient changes. An electrocardiographic dynamic change with their urgent conversion from abnormal to normal way without any medical interference is the key to the new phenomenon.

is based on their rate. They are classified as follows: 1) Junctional bradycardia: Ventricular rate ˂40 bpm.

Category Causes
• Drug-induced  4) Junctional tachycardia: Ventricular rate >100 bpm [1]. If there is blockage for the sinoatrial node (SAN) electrical activity is blocked or is less than the automaticity of the atrioventricular node (AVN)/His Bundle a JR starts. Numerous conditions and medications can lead to a diseased SAN and lead to the AVN/His Bundle to take over due to the higher automaticity of the ectopic pacemaker [2][3][4]. Some of these conditions and medications are listed below [1] (Table 1).
Epidemiology: Junctional rhythm is typical among individuals who have a sinus node dysfunction (SND); and 1/600 cardiac patients more than the age of 65 in the US has SND. Patients with sick sinus syndrome (SSS); young children; and athletes who have increased vagal tone may also intermittently exhibit JR; especially during sleep. JRs are equally among males and females [5].

Histopathology:
The human heart has several pacemakers to locations in its conduction system which are independently able to conserve the heart beating. However, the rate of a heartbeat is linked the pacemaker site; and as we go down its conduction system; the rate of spontaneous depolarization at pacemaker sites decrease [6][7][8]. The SAN that can share in the AVN/His Bundle taking over as a pacemaker secondary to their intrinsic automaticity includes SAN fibrosis; atrophy; hypoplasia or amyloidosis. A normal SAN histopathology does not exclude reduced SAN automaticity contributing to a JR [9,10]. Pacemaker sites and their depolarization rates are as follow [1]: or SA block; or (e) a combination of causes (b) and (d) [11]. The increased automaticity of AV nodal cells is induced by sympathetic overactivity [11]. The accelerated junctional rhythm usually due to an acceleration of AVN pacemaker cells [11]. There was a report; however, of a case in which high nodal junctional rhythm (HNJR) suddenly changed to low nodal junctional rhythm (LNJR) during general anesthesia [11]. HNJR is what appears when the impulse reaches the atrium before the ventricle (P-wave preceding the QRS-complex) [12]. Therefore, the atrial kick is maintained; although it may not be ideally coordinated with ventricular contraction; and the patient's blood pressure (BP) usually remains stable [11].
Presentations: Patients presented with JR have a wide spectrum of symptoms. They may be asymptomatic. Symptoms often based on the causative agent of the JR, for example, a patient presenting with heart failure exacerbation may present with dyspnea, wheezing, and lower extremity edema1. Non-specific physical exam findings include pulsating veins and regular heart rate with the heart rate varying from 20 to over 100 beats per minute [13][14][15].
The key for a patient who presents with signs and symptoms of a JR is history and physical examination [13][14][15].
ECG with inverted P-waves in inferior leads (II, III, and aVF) indicates that the atrial activation is spreading from below upwards.
It is suggestive of a focus either in the low atrium or high junction.
A mid-JR will have no visible P-waves as the P-wave will be within the QRS due to the simultaneous activation of the atria and ventricles. In LNJR the P wave occurs after the QRS, in the ST-segment and is inverted in inferior leads (II, III, and aVF). In left atrial rhythm originating from the lower part, the P-waves are inverted in inferior leads as well as lateral leads [16]. Notching of the QRS-complex in the inferior leads which suggest the crochetage sign in the atrial septal defect (ASD) [16]. Low atrial rhythm can occur with sinus venosus ASD as the sinus node may be defective so that alternate focus arising in the low atrium gives the dominant rhythm [16]. The PR-interval is also shorter in LNJR and low atrial rhythm, more in the former than in the latter, due to obvious reasons [16]. An interesting case report in which left atrial rhythm mimicked myocardial infarction (MI) has been reported recently16. If there is a negative P-wave axis. So, there is now either low atrial rhythm or HNJR (both will have negative P-waves that are seen before the QRS-complex is LNJR with result in P-wave in, or after, the QRS [17].
Treatment: Junctional rhythm is a benign arrhythmia that often does not demand treatment [11,12,18,19]. Treatment for the JR is superfluous [11]. Treatment of a JR primarily based on the cause of the rhythm. If a patient is resistant to medical treatments without passing into junctional tachycardia, IV phenytoin can be given with monitoring for possible hypotension. In the pediatric population, persistent symptomatic junctional tachycardia is an indication for percutaneous radiofrequency ablation. In patients with sick sinus syndrome, or complete or high-grade AV block, a permanent pacemaker is indicated [20][21][22][23][24].
Prognosis: Prognosis is excellent if the JR is urgently recognized by a healthcare provider [1]. Periods of junctional rhythm are not necessarily accompanied by an increase in the mortality rate.
If there is a clear cause, such as CHB or SSS, then the morbidity or mortality is directly linked to that and not to the JR mechanism, which is serving as a "backup rhythm" during the periods of bradycardia [26]. Accelerated JR may be a sign of digitalis toxicity. A predominant junctional rhythm may be associated with structural heart disease (SHD), SSS, or both, during which the junctional escape rhythm supersedes the sinus rate and provides a safety mechanism [26].  [27]. PVCs are characterized by premature and bizarre-shaped QRS-complexes that are unusually long (typically >120 msec) and appear wide on the ECG. The QRS-complexes are not preceded by a P-wave, and the T-wave is usually large and oriented in a direction opposite the major deflection of the QRS [28].
Depending on whether there are one, two, or three normal beats between each PVC, the rhythm is called bigeminy, trigeminy, or quadrigeminy, etc. [29,30]. The two beats are figuratively similar to two twins (hence Bi-+ Gemini) indicates the number (2) [30,31].
Tri-is a multiplier suffix indicating the number (3) [31]. Quadri-is a multiplier suffix indicating the number (4) [30,31]. Penta-is a multiplier suffix indicates the number (5) [31]. So, PVCs Bigeminy means a cardiac arrhythmia in which every second beat is a ventricular premature complex (extrasystole) or one sinus beats between extrasystoles [31,32]. Trigeminy means a cardiac arrhythmia in which every third beat is a ventricular premature complex (extrasystole) or two sinus beats between extrasystoles. Quadrigeminy means a cardiac arrhythmia in which every fourth beat is a ventricular premature complex (extrasystole) or three sinus beats between extrasystoles [30,33]. Pentageminy means a cardiac arrhythmia in which every fifth beat is a ventricular premature complex (extrasystole) or four sinus beats between extrasystoles [30].
Epidemiology: It is more prevalent with increasing age [34].
The estimated prevalence of PVCs on standard 12-lead electrocardiography (ECG) was >1 PVCs /min occurs in 1% to 4% of adults in the general population and 40% to 75% in 75% of healthy persons using on 24-to 48-hour Holter monitoring [35][36][37][38][39][40]. The prevalence of PVCs depends on the co-morbidities of the patients being screened and the duration of monitoring [41].
Pathophysiology: Traditionally, they have been thought to be relatively benign in the absence of structural heart disease, but they represent an increased risk of sudden death in structural heart dis-ease36. In most cases, premature ventricular contractions have a focal origin [42]. Suggested pathophysiological mechanisms for PVCs are reentry, triggered activity, and enhanced automaticity [28].  [28,43].
Clinical significance, prognosis, and mortality: Patients are usually asymptomatic [28]. The clinical significance of PVCs depends on their frequency, complexity, and hemodynamic response [28]. Ischemic heart disease may be manifested and presented with ventricular arrhythmias like-premature ventricular contractions whatever the type [32]. The vast majority of patients with premature ventricular complexes are considered benign when they occur in patients without apparent SHD [44,45]. PVCs in patients without apparent SHD are safe once we rule out risk factors [44].
Workup: Required workup for premature ventricular contraction includes potassium levels, magnesium level, electrocardiography, and echocardiography [28]. The optimal indications for therapy for premature ventricular contractions have not yet been elucidated [28].

Management and Indications for Therapy:
The most common indication for treating PVCs in the absence of structural heart disease (SHD) is the presence of symptoms that are not improved by reassurance [45,46]. The presence of symptoms in patients with structural heart diseases is considering primary indication. Elimination of high burden PVCs (10%) in patients with impaired LV function can be associated with significant improvement of LV function [47,48], even when significant scarring is present [49,50].

Sinus arrhythmia
Introduction, definition, and description: Normal sinus rhythm (NSR) is the rhythm that arises from the SAN and identifies the known rhythm of the healthy heart [51]. The rate in NSR is generally regular but will vary depending on autonomic inputs into the sinus node. When there is an irregularity in the sinus rate, it is termed sinus arrhythmia (SA) [51]. Sinus arrhythmia is a common variation in the NSR [52,53]. Sinus rhythm with a beatto-beat variation in the P-P interval (the time between successive P waves), producing an irregular ventricular rate [54]. Sinus arrhythmia characteristically presents with an irregular rate in which the variation in the R-R interval greater than 0.12 seconds [52] or the P-P-interval of more than 120 ms (3 small boxes) [53][54][55]. There should be a 10% difference between the maximum and minimum cardiac cycle length [56]. The P-P interval gradually lengthens and shortens cyclically, usually corresponding to the phases of the respiratory cycle [55] with normal sinus P-waves with a constant morphology [53,54] (i.e. no evidence of premature atrial contractions) and constant P-R interval [53,54] (i.e. no evidence of Mobitz I AV block) [54]. So, P-waves are typically mono-form and in a pattern consistent with atrial activation originating from the SAN [52].
Epidemiology and risk factors: Sinus arrhythmia are a normal physiological phenomenon, most commonly seen in young, healthy people [54]. It is seen more often in children and young adults [52]. Sinus arrhythmia is a common incidental sign during routine ECG [52] Sinus arrhythmia is a common sign during telemetry [52,55].
It decreases in prevalence in the elderly, and those with multiple co-morbid conditions include diabetes and heart failure [52]. It is considered to be a normal variation found in healthy young adults [52,55]. Investigators found that the prevalence of respiratory SA in older individuals was less than 20 percent of that in those less than 31 years of age. Some suspect that this is due to age-related changes in the compliance of arterial walls and diminished vagal responses [57]. Sinus arrhythmia is especially easy to notice with slowing of the heart rate during sleep [56].

Presentation and ECG:
Often an asymptomatic and normal finding, the evaluation of sinus arrhythmia is limited. Generally, SA is at most mildly symptomatic (e.g., palpitations) [55]. On the ECG, sinus rhythm appears as a beat-to-beat variation in the P-P interval. Typically, this variation is greater than 120 msec: the P-P interval increases and decreases with inspiration and exhalation [52][53][54][55]. The P-wave morphology usually does not change56. If it does change, the changes are phasic and the P waves do not appear retrograde [56]. The heart rate varies due to reflex changes in vagal tone during the different stages of the respiratory cycle. Inspiration increases the heart rate by decreasing vagal tone. With the onset of expiration, vagal tone is restored, leading to a subsequent decrease in heart rate [54].

Pathogenesis and its variants: Respirations lead to
vagal stimuli resulting in R-R interval variations [52]. During respiration, the intermittent vagus nerve activation occurs, which results in beat to beat variations in the resting heart rate [52].
Atrioventricular conduction is normal [56]. Presumably, it may due to age-related decreases in carotid distensibility and baroreceptor reflex sensitivity [54]. Investigation on the pathogenesis of sinus arrhythmia continues but three main theorized mechanisms exist at this time. These include respiratory-phasic, non-respiratory-nonphasic, and non-respiratory-ventriculo-phasic sinus arrhythmia [52]. Respiratory SA is a common sign. It is a normal alteration in cardiac rhythm generated from the stimulation of the vagus nerve and changes in cardiac filling pressures during respiration [52]. Some studies have begun to associate sinus rhythm with obesity, diabetes mellitus, and hypertension (HTN) while others continue to support a reduction in sinus arrhythmia when these conditions are present [52]. One study suggested that the mediation of SA occurs through vagal stimulation [53,58]. The study suggested that baroreceptor signaling plays an important role in the generation of respiratory SA [59]. The investigators have evaluated the effects of diabetes mellitus on SA. They found that in patients with diabetes there is a reduction in SA, which investigators attributed to the autonomic effects of the disease [60]. In non-respiratory SA, electrocardiograms will appear similar to the respiratory type.
The two differ in that nonrespiratory SA is not associated with the respiratory cycle. While it can occur within healthy individuals, more often this type correlates with an underlying pathology [61]. This type was reported with digitalis overdose and traumatic intracerebral hemorrhage that associated with vasospasm, hypoxia, and increased intracranial pressure [62]. The ventriculo-phasic SA, when present, typically occurs in patients with third-degree AV block [52,53]. It occurs if there is coexistence for both sinus rhythm and high-grade or complete AV block. So, it is characterized by shorter P-P intervals when they enclose QRS-complexes and longer P-P-intervals when no QRS-complexes are enclosed [53].
However, they show good correlations with PVCs. Currently, the suggested mechanisms that ventriculophasic SA results due to a prolonged cardiac filling resulting in increased stroke volume (SV).
The increased SV triggers a carotid baroreceptor response. The ECG represents an interval shortening between the QRS and subsequent P-wave [52].
Differential diagnosis: A differential diagnosis for sinus arrhythmia would include frequent premature atrial contractions, AF, second-degree AV block, Mobitz I (Wenckebach phenomenon), type I sinoatrial exit block, and CHB [51,54]. Care should be taken to rule out other causes of arrhythmia including atrial fibrillation, flutter or multifocal atrial tachycardia with an ECG. P-waves will show uniform morphology [52].
Treatment: Upon confirming the diagnosis of SA on ECG, there are no further recommendations regarding treatment [52,55]. The patients rarely need cardiological evaluation for additional any treatment [52].
Prognosis: It is most common in young, healthy patients.
Typically, its presence is a prognostic indicator for good cardiovascular health [52,53]. Loss of SA may indicate underlying heart failure or structural heart disease [52].

Case Presentations
The  (Table 2).  Figure 1A). ECG recordings were taken one minute later and were completely normal without any medications ( Figure 1B)

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Local tenderness was elicited. The ECG recordings were showing accelerated junctional rhythm in the inferior leads (II, III, aVF) and all anterior leads (V1-6) ( Figure 3A). ECG recordings were taken two minutes later and were completely normal without any medications ( Figure 3B). Electrolytes profile, thyroid function tests, full blood picture, kidney function tests, and CPK were done. Otherwise of leukocytosis (14400) and increased CPK (473 IU/L), All other results of required investigations were normal. The echocardiography was normal. Troponin test was below the normal level. The patient was managed only with diclofenac potassium (tab., 25 mg/8 hours for 5 days). No recurrence for above ECG abnormalities on later serial ECG on follow up. Echocardiography was normal. Pleurisy was managed only with diclofenac (tab., 25 mg/8 hours for 5 days). No recurrence for above ECG abnormalities on later serial ECG tracings follows up. accelerated junctional rhythm (absent P-wave in all leads), sinus arrhythmia, and wide-spread T-wave inversions ( Figure 5A). ECG recordings were taken two minutes later and were completely normal without any medications ( Figure 5B). The patient admitted in ICU for ECG changes. Echocardiography and troponin test were normal.

Case 5: Accelerated junctional rhythm with suspected chronic myopericarditis
No recurrence of accelerated junctional rhythm on later serial ECG tracings. Otherwise of leukocytosis (16100) and increased ESR of 1st hour (53 IU/L), electrolytes profile, thyroid function tests, full blood picture, kidney function tests were normal. No recurrence for above ECG abnormalities on later serial ECG tracings follows up.
The patient was discharged after reassurance with further follows up.  Figure 6A). ECG recordings were taken one minute later and were completely normal ( Figure 6B). Patient pulse during the first ECG showed irregular regularity while pulse exam-     Figure 7A). ECG recordings were taken two minutes later and were the disappearance of pentageminy without any medications ( Figure 7B) bpm) ( Figure 8A). ECG recordings were taken one and half a minute later and were the disappearance of pentageminy without any medications ( Figure 8A)   lytes profile or thyroid function tests abnormalities were detected.

Case 9: Trigeminy with anxiety and old IMI
Echocardiography was normal. No recurrence for above ECG trigeminy on later serial ECG tracings follows up.

Case 10: Mixed ventricular and atrial quaderigeminy with left renal pain
A 43-year-old married driver Egyptian male patient presented to the emergency room with left loin pain. Upon examination BP of 140/80 mmHg, the pulse of 96 bpm, RR of 16 bpm, the temperature of 36.9 °C, and O 2 saturation with pulse oxymetry 99%. The ECG recordings were showing quaderigeminy ( Figure 10A). ECG re-cordings were taken one minute later and were completely normal without any medications ( Figure 10B). Electrolytes profile, thyroid function tests, full blood picture, kidney function tests, echocardiography, urine analysis, and abdominal ultrasound were done. Otherwise, present left ureteric stone on abdominal ultrasound showed and heavy oxalate salts (+++) on urine analysis, all other investigations were normal. The patient was managed only with diclofenac potassium 75 mg amp with reassurance for quadergeminy. No recurrence for above ECG abnormalities on later serial ECG tracings follow up. The patient was referred for a urologist for follows up.  Figure 11A). ECG recordings were taken one minute later and were near completely normal ( Figure 11B).
The patient was symptomatically improved with BP normalization within 6 hours. Initial laboratory workup was showing leukocytosis (17000), mild anemia (Hb; 9 g/dl. 3%, RBC; 3.8 M), elevated serum creatinine (1.7). The patient insisted on hospital discharge despite incomplete workup. ECG recordings were taken on the patient discharge with no trigeminy.   Figure 12A). ECG recordings were taken three minutes later and were completely normal without any medications ( Figure 12B). Electrolytes profile, thyroid function tests, full blood picture, and kidney function tests were done. All results of the required investigations were normal. Echocardiography was normal. The patient was managed only with reassurance for quaderigeminy. No recurrence for above ECG abnormalities on later serial ECG tracings follows up. and bigeminy through all ECG leads ( Figure 13A). ECG recordings were taken three minutes later and were completely disappearance only for bigeminy ( Figure 13B). The patient pulse during the first ECG showed irregular regularity with regular dropped beats while pulse examination was irregular regularity during the second ECG.
Bigeminy disappear without any medical interventions. The patient   The ECG recordings were showing sinus arrhythmia ( Figure 15A).
ECG recordings were taken one minute later and were completely normal without any medications ( Figure 15B). Electrolytes profile, thyroid function tests, full blood picture, and kidney function tests were done. All results of the required investigations were normal.
Echocardiography was normal. The patient was only managed with reassurance. No recurrence for above ECG abnormalities on later serial ECG tracings follows up.  Figure 16A). ECG recordings were taken one minute later and were completely normal without any medications ( Figure 16B). Electrolytes profile, thyroid function tests, full blood picture, and kidney function tests were done. All results of the required investigations were normal. Echocardiography was normal.
The patient was only managed with reassurance. No recurrence for above ECG abnormalities on later serial ECG tracings follows up.   Figure   17A). ECG recordings were taken four minute later and were com-pletely normal without any medications ( Figure 17B). Electrolytes profile, thyroid function tests, full blood picture, and kidney function tests were done. All results of the required investigations were normal. Echocardiography was normal. The patient was only managed with reassurance. No recurrence for above ECG abnormalities on later serial ECG tracings follows up.  showing sinus arrhythmia ( Figure 18A). ECG recordings were taken three minutes later and were completely normal without any medications ( Figure 18B). Electrolytes profile, thyroid function tests,

Discussion and Results
Age Figure 19 : Showing age averages.

Sex and percentages (%)
50% of the study cases are male (9 cases) and 50% are female

Reassurance but with organic cause
There is reassurance for all cases of the study (100%). But the reassurance with presence of organic cardiac cause was only in seven cases of this study (38.89%).
The Characteristic Criteria for the "Passing phenomenon" are a. The new "Passing phenomenon" is a transient electrocardiographic change that spontaneously reversed within a few seconds to a few minutes without any medical interventions and apparent hemodynamic impact.
b. The eighteen reported cases were variable in diagnosis.
c. The cases cannot be included in one specific category.
d. Not all cases have an organic cause.
e. The common denominator among the cases was the appearance of transient significant an electrocardiographic change with prompt and spontaneous disappearance of these changes within a few seconds to a few minutes without any medical interventions.
f. Otherwise, the medications for the basic pathology, all patients were lucky when no given medications or interference had happened.
g. All these ECG changes maybe not related to the diagnosis of relevant diseases.
h. These changes were transient.

Conclusion and Recommendations
a. The new "Passing phenomenon" is a transient electrocardiographic change that spontaneously reversed within a few seconds to a few minutes without any medical interventions and apparent hemodynamic impact.
b. Reassurance is the main immediate therapy unless there are otherwise sustaining electrocardiographic pathology.
c. Cellular electrolytes study may be advised future options for like these cases.
d. The electrophysiological study is the future advised investigation.