Lupine Publishers | Non-Invasive Ventilation in the Treatment of Acute Respiratory Failure with COVID-19

 Lupine Publisher | Journal of Anesthesia & Pain Medicine

Abstract

Decades have passed since the first reports of the successful use of mask non-invasive ventilation (NIV) in the treatment of respiratory failure. The aim of the study is determining the benefits of NIV in acute respiratory failure in patients with COVID-19. The study included patients admitted to the intensive care unit of the surgical clinic of the AMU from April 1 to May 1, 2020. NIV has visible advantages over mechanical ventilation. But it must be remembered that even in experienced hands, NIV is successful only in 75-90% of all cases, which depends on many factors, such as the severity of ONE, the training and experience of medical personnel. As with many types of therapy, operations, and technologies, improvement in the results of this method can be expected as experience is gained. High minute lung ventilation (>10 L/min) during NIV may predict non-invasive lung ventilation.

Keywords: Non-invasive ventilation; Acute respiratory failure; COVID-19

Introduction

Decades have passed since the first reports of the successful use of mask non-invasive ventilation (NIV) in the treatment of respiratory failure [1,2]. Attempts to use NIV with positive pressure in acute respiratory failure have been made earlier - in the 1970s and 1980s, but in general this experience was not very successful, because at that time devices for intermittent breathing with positive pressure were usually used (intermittent positivepressure breathing), which were poorly tolerated by patients and were usually intended for aerosol therapy [3]. The appearance of convenient masks for conducting ventilation with continuous positive airway pressure (CPAP) and new modes of respiratory support (especially pressure support mode) gave an impetus to the widespread introduction of NIV in clinical practice [4-6]. In 1990- 2000, the accumulation of experience with NIV and the encouraging positive results of this method in several studies allowed NIV to be assigned the first-line treatment place in acute respiratory failure [7-9]. The most important advantage of NIV in acute respiratory failure is the reduction in mortality, which may be associated with a reduced risk of nosocomial pneumonia and other hospital infections [10]. In addition, compared with invasive respiratory support, NIV is associated with less risk of damage and subsequent remodeling of lung tissue. Before using NIV, you need to pay attention to some important aspects of the method. The effectiveness of NIV depends on the correct assessment of its capabilities and limitations, while in order to avoid delays in the use of tracheal intubation and mechanical ventilation, in turn, the selection of a suitable patient, the participation of trained medical personnel and the timely detection of NIV failure are required [5,11,12]. Proper patient selection is a key factor in achieving NIV success. When COVID-19 is complicated by acute respiratory failure, patients with hypercapnia and moderate respiratory acidosis are most suitable, although a combination of respiratory and metabolic acidosis also lends itself well to NIV therapy [13]. Severe respiratory acidosis significantly increases the chances of patient intubation, especially at pH <7.20 [14-17], but in routine practice, as experience shows, in some patients NIV can also be successfully performed at low pH values of 7.10 [18]. A coma condition is also a contraindication to NIV. As a rule, none of these factors is an absolute contraindication to NIV, but they should be taken into account when deciding on the beginning of NIV, as well as when ascertaining the inefficiency of the method and the need for tracheal intubation. Known predictors of NIV success or failure include the patient’s neurological status (Glasgow scale), overall disease severity (APACHE II scale), and high tachypnea [19]. The “ideal” patient during the NIV should be a sufficiently communicative patient to provide conditions for applying and fitting the mask and synchronization with a respirator. Agitated and restless patients usually do not tolerate the NIV procedure. Most often in clinical practice, nasal or facial masks are used. The severity of the patient’s condition may be a factor determining the appropriate type of mask: for example, patients with less severe respiratory failure (DN) are better adapted to nasal masks, which are more leaking when used, while in more severe situations, oronasal masks are better suited [20]. On the other hand, with the modern choice of various models of masks, individual characteristics and preferences of patients are considered. Tight fitting of the mask to the patient’s face allows to minimize leakage and improve the patient’s synchronization with the respirator. At the same time, with excessively tight contact of the mask with the patient’s skin, ulcerations and necrosis may develop. In patients with agitation, anxiety, and high tachypnea, sedation may be prescribed to improve synchronization, but the risk of excessive sedation and respiratory depression should be remembered [19].

The Aim of the Study

Determining the benefits of NIV in acute respiratory failure in patients with COVID-19.

Material and Research Methods

The study included patients admitted to the intensive care unit of the surgical clinic of the AMU from April 1 to May 1, 2020.

The Results of the Study

Our experience with NIV has shown that most patients treated with NIV tolerate this procedure relatively well already at the initial stage. However, in several patients, during the first minutes or hours of NIV, no improvement (clinical indicators and gas exchange) is observed or the procedure is poorly tolerated, the proportion of such patients is usually about 15-35%. Experience shows that longer attempts to use NIV without achieving a noticeable improvement only delay the time of tracheal intubation and mechanical ventilation, which significantly increases the risk of worsening respiratory failure, an unfavorable outcome, including death. Using NIV, we came to the conclusion that, in most cases, NIV therapy failures are detected quite early - on the first day from the initiation of respiratory support, however, in some patients, NVL therapy failure manifests itself later - 24-48-72 hours after the initial improvement. Lack of improvement in consciousness or respiratory acidosis 24 hours after onset is NIV another predictor of NIV failure. Indications for the implementation of NIV are as follows:

a. Symptoms and signs of acute respiratory failure: a) severe shortness of breath at rest; b) BH> 25 / min, participation in the breathing of the auxiliary respiratory muscles, paradoxical breathing.

b. Signs of gas exchange disturbance: a) PaCO2> 45 mm Hg. Art., pH <7.35; b) PaO₂ / FiO₂ <200 mmHg. Art.

c. The exclusion criteria for NIV in ODN are as follows:

d. Stop breathing.

e. Unstable hemodynamics (hypotension, uncontrolled arrhythmias, or myocardial ischemia).

f. Inability to protect the respiratory tract (cough and swallowing disorders)

g. Excessive bronchial secretion.

h. Signs of impaired consciousness (agitation or oppression), the patient’s inability to cooperate with medical personnel. i. Facial trauma, burns, anatomical disorders that prevent masking.

Indications for the termination of NIV and the transition to intubation of the trachea and mechanical ventilation include the following:

i. The patient’s inability to carry the mask due to discomfort or pain.

ii. The inability of the NIV to improve gas exchange within 2 hours: an increase or preservation of hypoxemia, despite the high values of PEEP and FiO2.

iii. Inability to mask ventilation to ease dyspnea. iv. The need for endotracheal intubation to remove secretions or protect the respiratory tract.

v. Instability of hemodynamics and ECG, instability with the phenomena of ischemia or clinically significant ventricular arrhythmias.

vi. The increase in encephalopathy.

vii. During the study, the following advantages of non-invasive ventilation were identified:

viii. Prevention of “mechanical” and infectious complications associated with intubation, reducing the risk of developing infectious complications and mechanical damage (trauma to the larynx and trachea, stenosis, and bleeding from the upper respiratory tract).

ix. Preservation of natural protective reflexes of the upper respiratory tract.

x. Preservation of physiological cough, the patient’s ability to talk, swallow, eat, cough up sputum.

xi. Increase patient comfort.

xii. Reduced need for muscle relaxants, opioids, and sedatives.

xiii. The possibility of discrete use and weaning from the apparatus.

In our clinic, NIV was performed using Salvia Elisa ventilator respirators in CPAP+PSV mode through a face mask. Used standard masks from Drager (Germany) or Respironics (USA). To determine the parameters of the gas and acid-base composition of the blood, an ABL500 gas analyzer with an OSM3 oximeter (Radiometer, Denmark) was used. Indicators of the function of external respiration were recorded from the display of the respirator. All data were recorded immediately before the start of ventilation. The level of PEEP and pressure support was set individually, based on the specific clinical situation. The ventilation parameters required by patients were as follows: PEEP - from 5 to 12 cm of water column, PSV - from 0 to 14 cm of water. column, FiO2 - from 0.3 to 0.6. At the initial stage, auxiliary ventilation was carried out in a continuous mode. Further, a gradual decrease in respiratory support was carried out in accordance with the degree of clinical improvement, after which they switched to NIV sessions for several hours a day until it was completely canceled. The criterion for successful NIV was the improvement of the arterial blood gas composition and the ability to avoid endotracheal intubation.

Clinical Case

Patient - a man aged 34 years, with complaints of alternating chronic cough, temperature 39.2º C, chills, headache, and shortness of breath. During auscultation of the lungs, crepitus was observed, moist rales in the lower lobes of the lungs, oxygen saturation 90%, and respiratory rate 30-34 per minute. Admission laboratory tests included: WBC - 14,64 x 109/L, LYM - 0,00 x 109/L, albumin - 3.01 g/dL, PI - 50.5%, PT - 14.8 sec., INR - 1.47, Fibrinogen - 128 mg/L, GRP 47.4 mg/L, D-Dimer> 1500 ng/mL, Ferritin - 1178 ng/mL, P / F> 180. Chest x-ray and CT are shown in the following (Figures 1-4).

Figure 1: X-ray upon admission.

Figure 2: Radiograph after improvement of the patient.

Figure 3: CT scan of the lungs upon admission.

Figure 4: CT scan of the same patient.

Non-invasive ventilation was carried out by an oral-nasal mask with a ventilator ELISA. Installation and adjustment of parameters was carried out according to the general condition and according to blood gas data: BH <35, pH> 7.30, neurological dysfunction according to the Kelly scale> 3-5, a modified scale for determining the participation of auxiliary respiratory muscles <3 points. For hypercapnia, the following parameters were set Ps - 12, PEEP - 6 cm water column, FiO2 -30-40%, and with hypoxemia - Ps - 12, PEEP - 5 cm water column, FiO2 -50-60. The median treatment period with NIV was 6 days. The average daily treatment time with NIV on the first day was 16.5 hours, on the second day - 17.2 hours and on the third day 15.7 hours. The patient was discharged on the 14^th day with improvement.

Conclusion

1. NIV has visible advantages over mechanical ventilation. But it must be remembered that even in experienced hands, NIV is successful only in 75-90% of all cases, which depends on many factors, such as the severity of ONE, the training and experience of medical personnel. As with many types of therapy, operations, and technologies, improvement in the results of this method can be expected as experience is gained.
2. High minute lung ventilation (>10 L/min) during NIV may predict non-invasive lung ventilation.

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Lupine Publishers | Unquestionable Wound Pain: Call for A Care-Plan Reform

 Lupine Publishers | Journal of Anesthesia & Pain Medicine

Opinion

Pain is a subjective experience and one that the medical healthcare profession will never fully be able to understand because the pain belongs to the patient. Ultimately, pain is whatever the patient experiences it to be, yet the traditional medical model approach is one that views the patient’s pain as something to be managed by the ‘professional’ [1,2]; who have been reported to often mismanage it [3]. Pain is in fact a personal encounter and one that is perceived differently both within and between individuals from one time to the next. This point must not only be acknowledged, but digested and acted upon, by healthcare providers working within the field of pain medicine. This paper concedes that pain is a biopsychological event that can only be fully managed by adopting a patient-centered and holistic approach to care. This proposition extends its focus to draw particular attention to those working in the field of wound care, due to the unique pain-related idiosyncrasies apparent among patients with acute and chronic wounds (from any origin: war/accident trauma; post-operative; foot/leg ulcers; burns/scars) that make them worthy of special attention in this matter.
In most recent years, wounds have been estimated to cost health services up to $96 billion globally [4] and this this figure is only set to rise due to self-compromising lifestyle and behavioral factors that lead to wound-promoting illnesses (for example obesity and diabetes) [5]. Pain has traditionally and consistently been dismissed as an overlooked aspect in wound care [6], yet pain has a detrimental and often devastating impact on wound healing [7] that negatively compromises an already weakened immune system [8]. Stress further perpetuates this deleterious cycle of events that tamper with effective wound healing, yet pain management does not take precedence in standard ‘wound care’ regimes. To illustrate, on reviewing the literature on various pain management guides, protocols and strategies specific to wound care published over the past twenty years (2000-2020), it became evident that, as with other types of pain, wound pain continues to be managed principally by pharmacological methods [9-12]. That is, guidance being offered from various commanding sources, from the World Health Organisation (WHO) to specialist wound and pain advocates [10-12] typically recommends a prescription care package of anti-inflammatory, non-steroidal medication (ibuprofen), which might be escalated to an oral pain killer (codeine) if the pain is greater and a stronger opiate analgesic (morphine) is offered when the pain becomes more severe. What this approach does is treat the symptom so is therefore less than optimum, because pain is more than just a symptom. Pain intensity, severity and duration are not only governed by physiological causes, but a psychological response. It has been reported that pain causes stress and stress negatively impacts healing [13]. Furthermore, pain perception (and therefore wound healing) is further compounded by anxiety; depression; and sleep deprivation as further by-products of stress [7].
Not only does this interacting biopsychosocial spiral of events impact on wound healing, but when it comes to pain from a wound, this topic becomes ever more complex due to the unique ways in which pain is manifested among patients with wounds. What makes wound pain distinct from pain caused by other illnesses (for instance cancer or arthritis), is that wound pain is consistently and blatantly visible to the sufferer. What this does is provides a constant reminder and red flag to notify the individual that there is something wrong. In fact, research has shown that wound pain is highest when dressings are removed [13], as opposed to being hidden by a dressing; and even when bandaged, the dressing remains a constant reminder of the fact that there is cause for concern. This form of biofeedback acts by conditioning a patient to a sense of heightened stress and unease that becomes amplified by an anticipatory response. This has been witnessed during such times when the wound becomes re-exposed, such as during dressing changes [13] and independently of pain sensation resulting from tissue disruption. A conditioned response therefore develops to prompt the physical system to experience pain. This anticipatory reaction explains pain perception as a bi-directional response. Not only can the physical body trigger warnings to the psychological self that there is a problem, but the mind can alert the body to feel pain. This mind-body dualism is magnified in the case of wound pain due to the high visibility of the source of the pain in question and this is precisely why pain regulation should be a focal point in any wound care plan due to its idiosyncratic qualities.
In order to bring pain medicine and treatment practice up to speed with contemporary integrated pain models [13], we need to consider holistic care packages that strategically intervene on both the physical and psychological levels of concern [6]. For example, empowering patients to self-manage their illness [1,14] both practically (e.g. wound dressing; patient-controlled analgesia) and mentally (e.g. cognitive reframing; stress management). Moreover, ‘treating’ the psychology should form an integrated part of any standard care package for wound patients [15], whereby continuous dialogue is used between patient and healthcare provider to monitor and reflect on aspects of the regimen. Patient pain diaries and monitoring of thoughts, feelings and behaviors can be achieved through use of self-support cognitive behavioral training for wound pain patients that facilitate restructuring negative coping strategies such as catastrophizing and fear self-statements [1].
Overall, it is aspired that this debate will provoke the attention of professionals working with patients with painful conditions to reconsider, firstly, that there is more to treating pain than a numbing of the symptom. As we appreciate, pain is an incredibly complex experience that cannot be managed reliably with medication alone. Secondly, wound pain is distinctive in that pain perception can be magnified by the unconcealed nature (or root cause) of the pain, which is unlike most other painful conditions. Finally, we wish readers to ponder over these germane issues right now, because despite witnessing scatterings within the literature of debates relating to the issues addressed here, it can be argued confidently, that all concerted efforts to get this message across to inform treatment plans thus far have failed, as we still do not see these viewpoints translated in to practice. We concede by reiterating that pain is subjectively owned by the patient and is therefore an un-questionable experience so can never be fully understood by a person outside of that experience; and call for a care-plan reform that guarantees a fully-integrated, biopsychosocial tailored package that responds to the voice of each patient.

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Lupine Publishers | Estimation of the Predictive Factors of Myocardial Ischemic Preconditioning in Elective Surgical Patients

 Lupine Publishers | Journal of Anesthesia & Pain Medicine

Abstract

Introduction: the physiological response to the aggression produced by the surgical trauma provides the effective treatment capacity in case of complications. Surgical intervention causes endocrine, metabolic, autonomic, immunological, and hematological changes.

Objective: to estimate the predictive factors of the second window of myocardial ischemic preconditioning in the patients proposed for elective surgical interventions.

Material and Methods: A quasi-experimental study was carried out in the period January to December 2019 at the Maria Curie Cancer Hospital in Camagüey with patients who met inclusion and exclusion criteria in preoperative consultation in the research period, to whom preconditioning was applied. Ischemic two hours before surgery. Chi squared and logistic regression was calculated as appropriate.

Results: Predictive factors such as essential arterial hypertension odds ratio 16,632, diabetes mellitus 12,157, age 60 years and over with odds ratios of 8,035, heart failure odds ratio 6,433, cerebrovascular disease odds ratio 6,135, and chronic kidney disease were estimated. Odds ratio 5,800 and chronic obstructive pulmonary disease with odds ratio 5,738.

Conclusion: the predictive factors of the second window of ischemic preconditioning were independent predictors of risk in elective surgical patients.

Keywords:Preconditioning; Elective surgical patient; Surgical stress; Predictive factors

Introduction

Knowledge of the physiological response to aggression produced by surgical trauma provides effective treatment capacity in the event of complications. Surgical intervention causes endocrine, metabolic, autonomic, immunological, and hematologic changes [1]. Somatic and autonomic afferent nerve impulses generated at the site of injury activate the endocrine response, while the inflammatory and immune response, mediated by hormones, begins to develop. and cytokines, secreted products of activated leukocytes, fibroblasts, and endothelial cells. The changes in the immune and endocrine systems in the face of surgical trauma, are objectified by the perioperative response of various markers. Surgical stress is a situation in which there is both an increase in the speed of generation of oxidizing species, free radicals (RL) and excited species, and a decrease in the activity of defense systems, resulting in higher concentrations, in the steady state of active oxygen species [2,3]. In these situations, the toxic effects of these RLs manifest and chemical reactions take place on lipids, proteins and carbohydrates inside the cells, which trigger irreversible damage and even death cellular. There are numerous diseases associated with the imbalance between oxidants and antioxidants, in the surgical patient from the preoperative period with personal pathological history, he becomes involved with the RL, through the physiological response of the diseases and the complexity of the surgical trauma as essential factors in the perioperative changes of hemostasis, the interaction of the endocrine and immune axis and of the drugs administered in the surgical anesthetic act [4]. The publication that describes the influence of anesthetics used during the perioperative period and the typical hormonal response generated by the surgical intervention and the patient is current. With modulation of adrenal response by the distribution of leukocytes and their immune functions. Anesthetics modify immune function by reducing the stress response and have a direct effect on immune cells [5]. The investigation was carried out with the objective of estimating the predictive factors of the second window of myocardial ischemic preconditioning in surgical patient’s elective for myocardial protection during major surgical intervention.

Material and Methods

General Aspects of the Study

This was a quasi-experimental investigation to estimate the predictive factors of the second window of myocardial ischemic preconditioning in elective surgical patients at the María Curie Cancer Hospital in Camagüey in the period from January to December 2019.

Definition of the Study Universe

The study population was delimited to 40 preconditioned patients 2 hours before the surgical intervention, an insufflated sphygmomanometer was placed at 200 mmHg for 5 minutes, after this time it is deflated, and 5 minutes are expected. This procedure is repeated 3 times. Blood draws are performed before and after the application of ischemic preconditioning. They are preconditioned and post conditioned patients who meet the inclusion and exclusion criteria.

Inclusion Criteria

Patients aged 20 years and over proposed for major elective surgical intervention.

Exclusion Criteria

Patients who do not offer their consent to participate in the research. Variables: age, sex, associated risk factors, antioxidant markers, discharge status, hospital stay, complications. The antioxidant markers before and after the preconditioning were determined: the concentration of reduced glutathione (GSH) by the method of Sedlak et al. [6] and malonic aldehyde (MAD).

Information Processing and Analysis Plan

Search and collection of information: A form was completed for each patient, complementing the information with data from the medical records.

Information processing: The database was compiled with the collected information, which was processed automatically using the SPSS statistical package. The information of the qualitative variables is summarized in descriptive statistics, related to the characterization of the patients operated on by the different surgical specialties, to determine the behavior of the activity of antioxidant and oxidant markers (preconditioning and postconditioning). The information resulting from applying the second window of ischemic preconditioning was processed according to the univariate and multivariate analysis for the study variables using the statistical program SPSS version 21. Implementing the chi-square test and logistic regression as appropriate. The understanding of the results obtained is facilitated through statistical tables and graphs, it was analyzed giving an answer to each proposed objective and comparing the results with those of other authors. Finally, after a synthesis work, conclusions and recommendations were issued [7].

Results and Discussion

N 40 Source: clinical history as can be seen in Table 1, most of the surgical oncology patients belong to the group of 60 years and more, for 77.5%. The evolution of the age pyramid, thanks to the increase in life expectancy and better healthcare, places cancer diseases in the forefront of surgery, influenced by the life expectancy at birth of 80.2 years for women and 76 years for the men. Cuba is among the three countries on the continent with the largest aging population, in 2000 it exceeded 1.6 million older adults and in 2014 it represented 17.9% of the total population, in 2015 the Cuban population was 18.5% and in 2018 21% of the population aged 60 and over 6.7 During the aging process, the adult heart undergoes numerous biochemical, ultrastructural, functional and anatomical changes that reshape cell structure, function and adaptive responses to stress. Histologically, a decrease in the number of myocytes and progressive hypertrophy of these are observed in both ventricles. Also, studies in humans demonstrated aging-related abnormalities in cardiac metabolism, coronary flow reserve, endothelial function. Age is an independent predictor of risk in patients with coronary heart disease, this is explained by the lack of adaptation to acute myocardial ischemia [8]. Ischemic preconditioning is a mechanism by which repetitive episodes of ischemia induce greater tolerance in the myocardium to subsequent episodes of aging as a biological process with interindividual variability leading to the progressive loss of physiological functional reserve, the alteration of these functions is not evident. in basal situation but it manifests itself in moments of stress such as illness and perioperative.

Table 1: Distribution of patients with ischemic preconditioning according to age group and sex.

Table 2: Frequency distribution of patients with ischemic preconditioning according to personal pathological history.

N 40 Source: clinical history

In Table 2, twenty-one patients out of forty preconditioned have a diagnosis of essential arterial hypertension with 52.5% followed by diabetes mellitus 42.5% and cardiovascular disease 32.5%. Comorbidity is more frequent and both cerebrovascular disease and lung processes, kidney failure, hypertension, and diabetes justify part of the increased risk of the surgical patient. However, it seems useful to recall other pathophysiological mechanisms that explain the elderly’s reduced response capacity such as endothelial dysfunction, microcirculatory disorders (rarefaction), increased precapillary resistance, and decreased ability to develop collateral circulation as clear. Limiting residual flow in the risk area and perfusion flow in the remote area [9,10]. In the myocardium, the possible loss of ischemic preconditioning, the accelerated drop in the reserve of high-energy phosphates (lower tolerance to ischemia), calcium overload and senile myomalacia are factors to consider. The primary changes of arterial aging produce important secondary changes in the heart and other terminal organs, including the brain and kidneys. The vascular aging process is accelerated by the presence of primary cardiovascular disease, including high blood pressure and atherosclerosis, as well as by other risk factors such as diabetes, smoking, and obesity. Morphological changes include a decrease in the number of myocytes, a thickening of the left ventricular wall, and a decrease in both the density of the conduction fibers and the number of cells in the sinus nodes [11]. These changes are readily apparent in terms of elevated mean arterial pressure and increased pulse pressure. Increased vascular stiffness leads to significant secondary cardiac responses, but in young people the heart pump and blood vessels are optimally coupled for maximum efficacy. The mere fact of treating the topic of aging and optimizing the preoperative period of the surgical patient with the application of preconditioning due to ischemia is the objective of the research Table 3.

Table 3: Frequency distribution of patients with ischemic preconditioning according to personal pathological history.

N 40 Source: clinical history

Interpreting the adjusted odds ratio (OR) for the variables of the equation as follows: In the estimated Logistic Regression function, the variable essential arterial hypertension had a significantly different regression coefficient of 0 (p = 0.01) and adjusted OR of 16,632 (95% CI 2,141; 20.54). In this analysis, the risk of not modulating (oxidative enzymatic response) is approximately 7 times greater in patients with positive oxidative stress markers than in negative ones, that is, the enzymatic response after preconditioning is at the expense of oxidants. The diabetes mellitus variable had a significantly different regression coefficient of 0 (p = 0.00) and adjusted OR of 12,157 (95% CI 2.487; 18.279), which implies that the risk of presenting enzymatic response to diabetes mellitus patients Oxidant expense is approximately 12 times greater than in those without a history of diabetes mellitus.
A patient 60 years and older after ischemic preconditioning is 8 times more likely to have an oxidative enzymatic response with OR (8,035) and 95% CI 2,703; 10,737. The variable Heart failure had a regression coefficient other than 0 (p = 0.00) and adjusted OR 6,433 (95% CI 2,705; 11,880), which implies the risk of presenting the oxidative enzymatic response in patients with a history of heart failure. After ischemic preconditioning, it is 6 times higher than in patients without a personal pathological history of heart failure, with a margin of 2 to 11 times. The variable cerebrovascular disease had a regression coefficient other than 0 (p = 0.00) and adjusted OR 6,135 (95% CI 2,843; 15,475), which implies the risk of presenting the oxidative enzymatic response in patients with a history of cerebrovascular disease. After ischemic preconditioning, it is 6 times greater than in patients without a personal pathological history of cerebrovascular disease, with a margin of 2 to 15 times. The variable chronic kidney disease had a regression coefficient other than 0 (p = 0.00) and adjusted OR 5,800 (95% CI 2,739; 10,270), which implies the risk of presenting the oxidative enzymatic response in patients with a history of disease. Chronic renal disease after ischemic preconditioning is 5 times higher than in patients without a personal pathological history of cerebrovascular disease with a margin of 2 to 10 times. The variable chronic obstructive pulmonary disease had a regression coefficient other than 0 (p = 0.00) and adjusted OR of 5,738 (95% CI 3,187; 11,271), which implies that the risk of presenting chronic obstructive pulmonary disease in surgical patients the oxidative enzymatic response after preconditioning being 5 times greater than in those without a personal history of chronic obstructive pulmonary disease with a margin of 3 to 11 times.

In 1986, Murry CE et al. 12. described the concept of ischemic preconditioning (PI) in dogs and since then it has been evaluated in multiple animal and human models.
PI (development of tolerance to acute ischemia) is a cellular mechanism capable of delaying, but not preventing cell death; This protection is transitory and lasts from 1 to 2 hours in anesthetized animals. During a brief episode of ischemia, adenosine, bradykinin, norepinephrine, and opioids that activate G receptors are released locally, culminating in the opening of ATP-dependent potassium channels. The signals leading to the opening of these channels are not fully defined, but include activation of phosphatidylinositol- 3-kinases, protein kinase C, and mitogen-activated protein kinase (MAPK). Multiple aging-related abnormalities at various levels of this cascade were demonstrated in animal models [13]. A clinical trial published in JAMA demonstrates a reduction in the incidence of postoperative renal failure in patients receiving IP compared to the control group (37.5 versus 52.5%) and a decrease in the need for renal replacement therapy. However, no differences were found in terms of mortality and adverse cerebral and cardiovascular events (although they were not the primary objective of the trial) [14]. Also, in 2015 two essays were published both in the New England Journal of Medicine. These are the ERICCA14 trial and the RIPHeart trial [15].
The ERICCA trial, multicentre on more than 1,000 patients, showed no difference in the primary endpoint (death, stroke, acute kidney failure or acute myocardial infarction). No differences were found either in the subgroup analyzes or in the secondary objectives (troponin values, length of stay in the Intensive Care Unit and mechanical ventilation, incidence of delirium and new atrial fibrillation). No adverse effects were observed in the intervention group [16] In the RIP Heart multicenter trial of more than 1,600 patients, no differences were found in the primary endpoint (death, acute myocardial infarction, need for revascularization or stroke), nor in the secondary endpoints (troponin elevation, acute kidney failure, need for inotropes, length of stay in the Intensive Care Unit and quality of life after the procedure). But, although PI seems to have beneficial effects, what role does it play in the case of elderly elective surgical patients in the local context? The enzymatic response obtained was oxidative in most of the elderly patients, which corresponds to 90%, showing no benefit. In a 2007 myocardial revascularization surgery study, 57 patients were randomized to receive or not receive remote ischemia-reperfusion cycles after anesthetic induction. The results showed a reduction in troponin levels at 72 hours in the treated group compared to the control group. Other trials confirm the cardioprotective effect reflected in reductions in postoperative troponin T, I or CKMB values. However, not all trials were positive in this regard and do not confirm these results. The routine uses of inhalational anesthetics or beta-blockers, which demonstrated their cardioprotective effect in several clinical trials, is very likely to mask the beneficial effects of PI. In any case, in a subsequent meta-analysis carried out by d’Ascenzo et al. A decrease in troponin values was observed in the postoperative period once possible confounding factors were controlled, such as the use of such volatile anesthetics during surgery [17]. Studies on IP, of different quality and with different objectives, conclude similarly in IP, offering benefits in terms of decreasing the values of markers for myocardial injury and incidence of kidney damage in the immediate postoperative period, but it does not seem to improve the short and medium term results when survival and cardiovascular and cerebral adverse effects are analyzed. On the other hand, cardioprotective drugs routinely used as inhalation anesthetics, beta-blockers, and anti-calcium are sufficient, without remote ischemia providing additional benefits. It is also not clear which group of patients benefits from the technique, what is the most appropriate method to perform it, and even whether or not it has no adverse effects.

Conclusion

Research suggests that the mechanism of ischemic preconditioning is diminished in elderly patients, confirming essential arterial hypertension, diabetes mellitus, age, heart failure, cerebrovascular disease, chronic kidney disease, chronic obstructive pulmonary disease as independent cardiovascular risk factors in cancer patients.

Acknowledgement

Zaily Fuentes Díaz: review, analysis and bibliographical selection; statistical processing; preparation of the final report; review and correction of the report; review and final approval. Gonzalo Fabián Orga García: field or assistance work; bibliographic review, analysis and selection; survey application, statistical processing; preparation of the final report; review and correction of the report; review and final approval. Orlando Rodríguez Salazar: review and correction of the report; review and final approval.
Jorge Lozano Casanova: sample processing and final approval. Tania Puerto Pérez: statistical processing; review and correction of the report and final approval.

Conflict of interest

The authors declare that does not exist an interest conflict.

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Lupine Publishers | Graded Phenomenon (Yasser’s Phenomenon); A Novel Electrocardiographic Phenomenon Change the Arrhythmia Directory; Retrospective-Observational Study

 Lupine Publishers | Journal of Anesthesia & Pain Medicine

Abstract

Background: Arrhythmias are one of the most serious disorders in cardiovascular and clinical medicine. Understanding the pathogenesis and mechanisms of arrhythmias is very advantageous to the appropriate management and treatment of all arrhythmia types. The “Graded phenomenon” is a novel directory phenomenon for understanding the arrhythmia. The principal of “Graded phenomenon” is based on catching the graded changes in serial ECG tracings or even single one regarding the arrhythmias.

Method of study and patients: My case study was an observational retrospective for a 30 case report series. The study was conducted in both Fraskour Central Hospital (Intensive Care Unit, and emergency room) and Physician Outpatient Clinic. The author reported the 30-cases thorough nearly 4 years, started from Jan 13, 2016, and, ended on February 9, 2020.

Results: The age mean is 58.3 years with male sex predominance (56.67%). The changes in graded phenomenon are classified into: Up-grading; 20%, down-graded; 10%, changed to NSR; 43.33%, changed to AF; 3.33%, changed to sinus tachycardia; 3.33%, therapeutic reversal; 3.33%, fixed –change; 10%, and variable change; 6.67%. The risk in the graded phenomenon is either high (40%), non-risk (43.33%), or still-risk (16.67%). The course in the graded phenomenon is either progressive (43.33%), regressive; 10%, intermittent; 6.67%, constant; 16.67%, transient; 20%, and non-fixed variation; 3.33%.

Conclusion: Graded phenomenon (Yasser’s phenomenon) is a novel electrocardiographic phenomenon change the arrhythmia directory. It is a crucial step for understanding arrhythmia. The phenomenon is a new strong guide for monitoring and follows up arrhythmic patients in cardiovascular patients.

Keywords: Graded phenomenon; Yasser’s phenomenon; A novel Electrocardiographic Phenomenon; Change the arrhythmia directory

Abbreviations: ABG: Arterial blood gases, AF: Atrial fibrillation, AMI: Acute myocardial infarction; ARVC: Arrhythmogenic right ventricular cardiomyopathy, BSOT: Bidirectional sectors of tachycardia, Congestive heart failure: CHF, CXR: Chest X-ray, ECG: Electrocardiograph, EADs: Early after-depolarizations, ED: Emergency Department, EPS: Electrophysiology studies, HR: Heart rate, HVS: Hyperventilation syndrome, ICU: Intensive care unit, IHD: ischemic heart disease, LVD: Left ventricular dysfunction, LVH: Left ventricular hypertrophy, MRI: magnetic resonance imaging, NSR Normal sinus rhythm, O2: Oxygen, PE: Pulmonary embolism, POC: Physician outpatient clinic, PVCs: Premature ventricular contractions, PVT: Polymorphic ventricular tachycardia, RA: Respiratory alkalosis, RBBB: Right bundle branch block, RBS: Random blood sugar, RR: Respiratory rate, SA Sinus arrhythmia, SAN: Sinus node, SCD: Sudden cardiac deaths, TdP: Torsades de pointes, VF Ventricular fibrillation, VT Ventricular tachycardia

Introduction

Arrhythmias

Scoping of arrhythmias: A heart arrhythmia is clearly described as a variation in the normal heart rate (HR) and/or rhythm regularity that is not physiologically justified [1]. Cardiac arrhythmias are happening if the electrical impulses that parallel your heartbeats don’t release precisely, causing tachycardia, bradycardia or irregularly [2]. Arrhythmia may be a serious problem especially if there are tachycardia or atrial fibrillation (AF) that can have serious consequences, including cardiac arrest and stroke [3]. Sudden cardiac death (SCD) is the cause of approximately 50 deaths due to cardiovascular disease (CVD) and nearly 15% of all mortality worldwide [4]. Almost 80% of SCD often due to ventricular arrhythmias [4]. Although most types of arrhythmia are benign, some will be predisposing to complications like stroke or heart failure [2]. Arrhythmias can kill 100,000 people in the UK annually [5].

Mechanisms of arrhythmias: Understanding the mechanisms of arrhythmias is key to the appropriate management of all arrhythmia types 6. The mechanisms responsible for cardiac arrhythmias may be divided into disorders of impulse formation, disorders of impulse conduction or a combination of both6 Table 1. Modified from Gaztan L et al [6], Automaticity is the property of cardiac cells to generate spontaneous action potentials. Spontaneous activity is the result of diastolic depolarization caused by a net inward current during phase 4 of the action potential, which progressively brings the membrane potential to threshold [1]. Abnormal automaticity includes both reduced automaticity, which causes bradycardia, and increased automaticity, which causes tachycardia. Arrhythmias caused by abnormal automaticity can result from diverse mechanisms [1]. Early Afterdepolarizations (EADs) are typically observed in cardiac tissues exposed to injury, altered electrolytes, hypoxia, acidosis, catecholamines, and pharmacologic agents, including antiarrhythmic drugs. Ventricular hypertrophy and heart failure also predispose to the development of EADs [7]. EAD-induced triggered activity is sensitive to the stimulation rate. Antiarrhythmic drugs with class III action generally induce EAD activity at slow stimulation rates [8]. The ring model is the prototypical example of reentry around an anatomic obstacle [9]. In 1914, Garrey suggested that reentry could be initiated without the involvement of anatomic obstacles and that “natural rings are not essential for the maintenance of circus contractions [10].

Table 1: Summary mechanisms of cardiac arrhythmias.

Premature Ventricular Contractions (PVCs)

Premature ventricular contractions scoping: Generally, PVCs are the most common cardiac arrhythmia in patients with or without structural heart diseases (SHD) [11,12].

Premature ventricular contractions Pathophysiology: Premature ventricular contractions are early depolarization of the myocardium originating in the ventricle [13] caused by an electrical impulse or ectopic rhythm from any part of the ventricles, including the ventricular septum before the sinoatrial impulse has reached the ventricles [14]. PVC is a common arrhythmia triggered by impulses arising outside the normal conduction pathway of the heart that occur even in people with no underlying heart disease [15]. PVCs often arise from a pre-excitation, mostly in the right ventricle [11]. A PVC is a sign of decreased oxygenation to the myocardium but is also found in healthy heart [16]. In most cases, PVCs have a focal origin [17]. This means that an abnormal automatism, triggered activity or reentrant mechanism have an electric impulse of focal origin. This site of the impulse propagates centrifugally to the rest of the ventricles resulting in after depolarizations [12,18].

Premature ventricular contractions and the prognostic value: Currently, PVCs are considered progenitors of SCD [17]. Moreover, the studies revealed that PVCs were independent predictors of sudden and non-sudden death [19]. The concept that ventricular fibrillation (VF) and ventricular tachycardia (VT) are preceded by PVCs [17].

PVCs as a precursor for ventricular tachycardia and ventricular fibrillation: PVCs have also been shown to trigger malignant ventricular arrhythmias in certain patients with idiopathic ventricular fibrillation and persistent VT [18-20]. Persistent VT is very dangerous, as it can trigger ventricular fibrillation (VF) and SCD [14]. Patients with PVC couplets are more inducer for VT than with single PVC [21]. A higher PVC burden (> 26 %/day) is associated with left ventricular dysfunction (LVD), especially, in patients without SHD [22].

Prognosis and frequency and multiform of PVCs: The high frequent PVCs can vary from 10,000 to 20,000 PVCs/day according to relevant studies [23]. Frequent PVCs are associated with AMI and SCD in patients without known CAD24. Some studies carry a significant risk of AMI and SCD if there are >30 PVCs per hour [24-26]. Reports have suggested that frequent PVCs increase the risk of SCD, cardiovascular events, and LVD [27]. Multiform PVCs are associated with an adverse prognosis in the general population [28]. There are red flags and risk markers for premature ventricular contractions with a higher risk for SCD Table 2. ARVC: Arrhythmogenic right ventricular cardiomyopathy, MRI: magnetic resonance imaging, Modified from Elsayed et al [2].

Long-QT syndrome and polymorphic ventricular tachycardia (PVT): Torsades de pointes (TdP) is a specific form of polymorphic ventricular tachycardia (PVT) in patients with a long QT-interval. It is characterized by rapid, irregular QRScomplexes, which appear to be twisting around the ECG baseline. This arrhythmia may cease spontaneously or degenerate into ventricular fibrillation. It causes significant hemodynamic compromise and often death. Diagnosis is by ECG. Treatment is with IV magnesium, measures to shorten the QT-interval, and directcurrent defibrillation when ventricular fibrillation is precipitated [29-31].

Table 2: Risk markers and red flags for PVC’s with a higher risk for SCD29.

Sinus Arrhythmia

Normal sinus rhythm: Normal sinus rhythm (NSR) is the rhythm that origins from the sinus node (SAN) and identify the known rhythm of the healthy heart [32]. The rate in NSR is commonly regular. But it varies depending on autonomic inputs into the SAN.

Sinus arrhythmia scoping: The term sinus arrhythmia refers to a normal phenomenon of alternating mild acceleration and slowing of the heart rate that occurs with breathing in and out respectively [33]. When there is an irregularity in the sinus rate, it is termed sinus arrhythmia (SA) [1]. Sinus arrhythmia is a common change in the NSR [34,35]. Sinus rhythm with a beat-to-beat variation in the P-P interval (the time between successive P waves), producing an irregular ventricular rate [36]. It is usually quite pronounced in children and steadily decreases with age. This can also be present during meditation breathing exercises that involve deep inhaling and breath holding patterns [37].

Sinus arrhythmia characteristics: Sinus arrhythmia characteristically presents with an irregular rate in which the variation in the R-R interval greater than 0.12 seconds34 or the P-P-interval of more than 120 ms (3 small boxes) [35-38]. There should be a 10% difference between the maximum and minimum cardiac cycle length [8]. The P-P interval gradually lengthens and shortens cyclically, usually corresponding to the phases of the respiratory cycle7 with normal sinus P-waves with both constant morphology [35, 36] and P-R interval [35, 36] Sinus arrhythmia is a physiological condition that most commonly occurs in the young healthy adults [34, 36] and children [34]. Sinus arrhythmia is a common incidental sign seen on routine Electrocardiogram (ECG) [34]. Often an asymptomatic and normal finding, the evaluation of sinus arrhythmia is limited. Generally, SA is at most mildly symptomatic (e.g., palpitations) [39].

Sinus arrhythmia prognostic value: Typically, its presence is a prognostic indicator for good cardiovascular health [34, 35]. Loss of SA may indicate underlying heart failure or structural heart disease [33].

Junctional Arrhythmias

Junctional arrhythmias nomenclature: The implicated nomenclature10 to recognize the type of junctional rhythms (JR) is based on their rate. They are classified as follows: 1. Junctional bradycardia: Ventricular rate ˂40 bpm [2]. Junction escape rhythm: Ventricular rate 40-60 bpm. 3. Accelerated junctional rhythm (AJR): Ventricular rate of 60-100 bpm. 4. Junctional tachycardia: Ventricular rate >100 bpm [40].

Junctional arrhythmias pathophysiology: If there is a 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 [41].

Junctional arrhythmias causative conditions: 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 [42-44]. Hyperkalemia, sick sinus syndrome, pericarditis, myocarditis, unstable angina, acute myocardial infarction, repair of congenital heart disease, atrial septal defect, tetralogy of Fallot, persistent left superior vena cava, adenosine, digoxin, calcium channel blockers, lithium, amitriptyline, clonidine, reserpine, inhalation anesthetics, cimetidine, isoproterenol infusion, narcotics, beta-blockers, and ivabradine implicated in causing junctional tachycardia [41].

Paroxysmal Supraventricular Tachycardia

Paroxysmal supraventricular tachycardia scoping: Paroxysmal supraventricular tachycardia (PSVT) accounts for intermittent episodes of supraventricular tachycardia with sudden onset and termination. PSVT is part of the narrow QRS-complex tachycardias with a regular ventricular response in contrast to multifocal atrial tachycardia (MAT), atrial fibrillation (AF), and atrial flutter [45].

Paroxysmal supraventricular tachycardia scoping: PSVT is often due to different reentry circuits in the heart, where less frequent causes include enhanced or abnormal automaticity and triggered activity. Reentry circuits include a pathway within and around the SAN, within the atrial myocardium, within the AVN or an accessory (AP) pathway involving the AVN. Different types of PSVT result depending on the existing circuits, and examples are: a. SANN: Sinoatrial node reentrant tachycardia.

b. Atrial myocardium: Atrial flutter, AF, and MAT.

c. AVN: Atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT) [46-48].

Methods of Study and Patients

My study was an observational-retrospective study for 30-case report series targeting the graded changes in arrhythmia using the serial electrocardiography (ECG) tracings. Premature ventricular contractions (PVCs), junctional arrhythmia, sinus arrhythmia, paroxysmal supraventricular tachycardia, and atrial fibrillation were the commonest goal in the study. The new phenomenon “Graded phenomenon” is a constellation of the graded changes in serial ECG tracings or even single one regarding the arrhythmic patients. The author reported the 30-cases of thorough nearly 4 years, started from January 13, 2016, and, ended on February 9, 2020. The study was conducted in both Fraskour Central Hospital (Intensive Care Unit, and emergency room) and Physician Outpatient Clinic (POC) Table 3.
a. The changes in the cases of “Graded phenomenon” are classified into:
1. Up-grading, 2. Down-grading, 3. Fixed change, 4. Spontaneously changed to normal sinus rhythm, 5. Spontaneously changed to another arrhythmia, 6. Therapeutic reversal.
b. The extension for arrhythmia in the cases of “Graded phenomenon” are classified into:
• The up-grading phenomenon with the right to the left extension

• The up-grading phenomenon with the left to the right extension.
• Up-grading bidirectional sectors of tachycardia (BSOT).
• Intermittent Wandering pacing rhythm with the left to the right extension.
c. The risk in arrhythmia in the cases of “Graded phenomenon” are: 1. High, 2. Non-risk, 3. Still-risk.

d. The principal of the “Graded phenomenon” (Yasser phenomenon) is based on catching the graded changes in serial ECG tracings or even single one regarding the arrhythmias. All cases were undergone to complete clinical examination and serial ECG tracings doing during follow up. Specific investigations were worked in the study. Serial ECG tracings, blood electrolytes (ionized calcium, sodium, potassium, and magnesium), complete blood counts, and random blood sugar nearly were done for all cases. Arterial blood gases, troponin test, d-dimmer, CPK-MB, echocardiography, helical thoracic computed tomography (TCT), and chest X-ray (CXR) were done in selected patients. Most of the cases were admitted to the ICU. Few cases were managed as clinic outpatients in POC with later follow up. Regards the remarks of the study method and data were summarized Table 3. For more details on general, clinical, and laboratory data for the cases see Tables 4-6. Table 3 showing remarks of the study method and data.

Table 3: Showing remarks of the study method and data.

1. Eligibility criteria, 2. Inclusion criteria, 3. All cases of arrhythmias with graded electrocardiographic (ECG) changes especially; premature ventricular contractions (PVCs), junctional arrhythmia, and sinus arrhythmia. Patient ages ranged from 11 and up to 88 years old, 4. Exclusion criteria: Purely non-arrhythmic disorders, 5. Limitations of the study: There are no limitations to the study

Cases Presentation

Case no. 1: (progressive Bigeminy Pvcs With Graded Phenomenon Right To Left Extension, Upgrading)

A 60-year-old married, housewife, Egyptian female, presented to the Emergency Room (ER) with orthopnea of progressive course. The patient admitted and managed in the intensive care unite (ICU) as chronic heart failure (CHF) with hypertensive crises (HC). She gave a history of diabetes and calcular cholecystitis. Clinically; the case manifested with heart failure. Serial ECG tracings were taken which showed an interesting progressive bigeminy PVCs was described as: “Graded phenomenon right to left extension, upgrading” (Figure 1). Bigeminy PVCs initially started in V1-6 leads (all chest leads) (Figure 1A), then extended to aVR, aVL, and aVF leads (Figure 1B), then I, II, and III leads to becoming total ECG bigeminy PVCs (Figure 1C). (Figure 1D), then into irregular PVCs (Figure 1E) lastly extended to runs of VT (Figure 1F). There is a mild renal impairment (serum creatinine: 2.86 and blood urea:95). The operator advised adding nitroglycerin IVI and diltiazem oral tablet. Despite there was a response but the recurrence was founded. The patient advised for further electrophysiological study (EPS). For more details see Tables 4-6.

Table 4: showing a summary of the history, clinical, and management data for the study cases.

Table 5: Showing laboratory data for the cases of study.

Table 6: Showing types of grading phenomenon, changes, course, and the risk.

Figure 1: ECG tracings showing bigeminy PVCs with “Graded phenomenon right to left extension, upgrading” only started in V1-6 leads (A-tracing; green color), then in Leads: II, III, and aVF with V1-6 (B-tracing; blue color), then to all ECG leads (C-tracing; brown color).

Case no. 2: (Progressive Polymorphic Ventricular Tachycardia (Pvt))

A 58-year-old married Egyptian housewife female patient presented to the POC with dizziness, dyspnea, and palpitations. The patient gave a history of psycho-familial troubles. Clinically, she had appeared myxedematos. There was sub-clinical hypothyroidism and congestive heart failure (CHF). Serial ECG tracings were taken which showed an interesting progressive polymorphic ventricular tachycardia (PVT) was described as: “Graded phenomenon left to the right extension, upgrading” (Figure 2). PVT initially started in part of I, II, and III leads (Figure 2A), then extended to the remaining part of I, II, and III leads (Figure 2B), then I, II, and III leads to then extended to part of aVR, aVL, and aVF leads (Figure 2C), lastly extend to V1,2, 3, and part of V4-6 (Figure 2D), then into irregular PVCs (Figure 2E) extended to runs of VT (Figure 2F). The patient advised for further electrophysiological study (EPS). For more details see Tables 4-6.

Figure 2: A-D ECG tracings; showing an interested progressive polymorphic ventricular tachycardia (PVT) “Graded phenomenon left to right extension, upgrading” started in part of I, II, and III leads (A-tracing; green color), then extended to the remaining part of I, II, and III leads (B- tracing; gold color), then extended to part of aVR, aVL, and aVF leads (C-tracing; light blue color), then extend to V1,2, 3, and part of V4-6 (D- tracing; dark blue color), E-tracing showing the disappearance of all PVT. There is evidence of QTc prolongation (470 ms, red rectangle and arrows) and prolonged R-interval (0.24 sec, lemon rectangle and arrows), superficial T-wave inversion in V1-3 leads.

Case No. 3: (Progressive Bidirectional Sectors Of Tachycardia (BSOT))

A 75-year-old married Egyptian housewife female patient presented to the POC with chest pain, dyspnea, and palpitations. The patient initially diagnosed as hypertensive crises with junctional tachycardia. Serial ECG tracings were taken which showed interesting progressive bidirectional sectors of tachycardia (PSOT) with a normal rhythm in between until becoming total tachycardia in all ECG tracing (Figure 3). PSOT initially started in first part of I, II, and III, aVR, aVL, and aVF leads (Figure 3A), then extended to last part of I, II, III, and aVR, aVL, and aVF and first part of, aVR, aVL, aVF, and V1-3 leads (Figure 3B), then first part of I, II, III, middle part of aVR, aVL, aVF and V1-3, and last part of I, II, III, and V4-6 leads (Figure 3C), then extend to last part of aVR, aVL, and aVF, and all V1-6 leads (Figure 3D), lastly it includes all ECG leads (Figure 3E). The patient advised for further electrophysiological study (EPS). For more details see Tables 4-6.

Figure 3: A-E ECG tracings showing “Graded phenomenon with an interested progressive bidirectional sectors of tachycardia (BSOT) with normal rhythm in between until become total tachycardia in the all ECG tracing” SOT initially started in first part of I, II, and III, aVR, aVL, and aVF leads (3 A tracing; blue color), then extended to last part of I, II, III, and aVR, aVL, and aVF and first part of, aVR, aVL, aVF, and V1-3 leads (3 B tracing; green color), then first part of I, II, III, middle part of aVR, aVL, aVF and V1-3, and last part of I, II, III, and V4-6 leads (3 C tracing; gold color), then extend to last part of aVR, aVL, and aVF, and all V1-6 leads (3 D tracing; green color), lastly it includes all ECG leads (3 E tracing; turquoise color).

Case No. 4: (Intermittent Wandering Pacing Rhythm (Wpr) With Progressive Extension From Left To Right)

An 11-year-old Egyptian boy student patient presented to the POC with pleuritic chest pain. There was no history of heart disease. Serial ECG tracings were taken which showed an interesting intermittent Wandering pacing rhythm (WPR) with progressive extension from left to right. It progresses until becoming total junctional rhythm in all ECG tracing except lead I and aVL, then spontaneously normalized (Figure 4). WPR initially started in I, II, and first part of III, aVR, aVL, and aVF leads, then sinus bradycardia in the remaining part of aVR, aVL, and aVF leads, then junctional rhythm (JR) in part of V1-3, lastly sinus bradycardia in the remaining part of V-3, and all V4-6 leads (Figure 4A), then JR including all ECG tracing except lead I and aVL (Figure 4B), then spontaneously normalized (Figure 4C). The patient advised for further electrophysiological study (EPS). For more details see Tables 4-6.

Figure 4: A-C Serial ECG tracings were taken which showed an interesting intermittent Wandering pacing rhythm (WPR) with progressive extension from left to right. It progresses until becoming total junctional rhythm in all ECG tracing except lead I and aVL, then spontaneously normalized. WPR initially started in I, II, and first part of III, aVR, aVL,and aVF leads (green arrows and color), then sinus bradycardia in the remaining part of aVR, aVL, and aVF leads (black and blue arrows, and color), then junctional rhythm (JR) in part of V1-3 (green arrows and color), lastly sinus bradycardia in the remaining part of V-3, and all V4-6 leads (black and blue arrows, and color) (4 A. ECG tracing), then JR including all ECG tracing except lead I and aVL (4 B. ECG tracing), then spontaneously normalized (4 C. ECG tracing).

Case No. 5: (Progressive Accelerated Junctional Rhythm (Ajr) With The Right To The Left Extension)

A 37-year-old married Egyptian housewife female patient presented to the POC with irritable bowel syndrome with chest tightness, and palpitations. She gave a history of anxiety due to delayed infertility. The patient initially diagnosed as anxiety with a junctional rhythm. Serial ECG tracings were taken which showed progressive accelerated junctional rhythm (AJR) with the right to the left extension. with a normal rhythm in between until becoming total junctional rhythm in the all ECG tracing, then spontaneously normalized (Figure 5). JR initially started in V1-6 leads (Figure 5A), then extended to all ECG leads except aVL (Figure 5B), then spontaneously normalized in all ECG leads (Figure 5C). The patient advised for further electrophysiological study (EPS). For more details see Table 4, 5, and 6.

Figure 5: A-C Serial ECG tracings showed junctional rhythm (JR) with progressive extension from right to left. with a normal rhythm in between until becoming total junctional rhythm in all ECG tracing, then spontaneously normalized. JR initially started in V1-6 leads (green arrows and color), with the remaining are sinus rhythm (blue arrows and color) (5 A. ECG tracing), then extended to all ECG leads except (brown arrows and color) (5 B. ECG tracing), then spontaneously normalized in all ECG leads (5 C. ECG tracing; yellow color).

Case no. 6: (Fixed Trigeminy In Anxiety And Old Imi)

Figure 6: A-D ECG tracings; A-C tracings showing fixed trigeminy PVCs (green arrows) with evidence of inferior myocardial infarction (black arrows). D-tracing (within 30 hours after the first ECG) showing complete showing normalization of all above trigeminy PVCs. There is an ECG artifact (lemon arrows).

A 50-year-old married Egyptian male teacher patient presented to the POC with dizziness and palpitations. The patient appeared anxious. Recent history of psychological stress. There was a history of old MI. The ECG recordings were showing fixed trigeminy PVCs through all ECG leads with VR; 66 bpm (Figure 6A-C). ECG recordings were taken within 30 hours after the first ECG later and were the disappearance of trigeminy PVCs after oral nitroglycerin retard capsule (2.5 mg twice daily). (Figure 6D). No recurrence for above ECG trigeminy on later serial ECG tracings follows up. For more details see Table 4-6.

Case No 7 (Pvcs Type Up-Grading In Suspected Pulmonary Embolism In Thrombophilia)

An 88-year-old married, worker, Egyptian male patient presented in the ER with tachypnea and palpitation. The patient gave a recent history of bilateral LL swelling. The patient has a history of hypertension, AF, multiple cerebrovascular strokes with bulbar palsy. At home, the patient missed his warfarin (3 mg). He was admitted to the ICU as suspected acute pulmonary embolism. Serial ECG tracings were done that showing PVCs type up-grading; A. tracing showing slow AF, sinus arrest, multiple PVCs, and inferior-anterior ST-segment depressions (Figure 7A). B. tracing showing polymorphic VT, AF waves, sinus arrest, and anterior ST-segment depressions (Figure 7B). C. tracing showing multifocal PVCs, inferior-anterior ST-segment depressions, and AF waves (Figure 7C). D. tracing showing inferior-anterior STsegment depressions and multifocal PVCs (Figure 7D). E. tracing showing runs of VT, inferior-anterior ST-segment depressions, and tremor artifact (Figure 7E). F. tracing showing runs of VT, inferior-anterior ST-segment depressions, multifocal PVCs, and tremor artifact (Figure 7F). Color duplex US showed extensive bilateral popliteal and leg veins. Plain Chest X-Ray view showed cardiomegaly, increased CTR, RV enlargement, RA enlargement bilateral enlargement of both pulmonary arteries, and oligemia of both lungs. Later echocardiography showed evidence of right-side dilatation with dysfunction. No more workup was done. The case was initially managed as APE. Unfortunately, the patient had died within 12 hours. For more details see Tables 4-6.

Figure 7: Serial ECG tracings showing PVCs type grading in suspected pulmonary embolism in thrombophilia; A. tracing showing slow AF, sinus arrest (brown arrows), multiple PVCs (green arrows), and inferior-anterior ST-segment depressions (blue arrows). B. tracing showing polymorphic VT (lemon arrows), AF waves (red arrows), sinus arrest (brown arrows), and anterior ST-segment depressions (blue arrows). C. tracing showing multifocal PVCs (green and purple arrows), inferioranterior ST-segment depressions (blue arrows), and AF waves (red arrows). D. tracing showing inferior-anterior ST-segment depressions (blue arrows) and multifocal PVCs (lemon and purple arrows). E. tracing showing runs of VT (red arrows), inferior-anterior ST-segment depressions (blue arrows), and tremor artifact (brown arrows). F. tracing showing runs of VT (red arrows), inferior-anterior ST-segment depressions (blue arrows), multifocal PVCs (purple arrows), and tremor artifact (brown arrows).

Case no. 8 (Fixed Pvcs Grading In Chf; Hexagimeny- Trigimeny- Trigimeny Hexagimeny: “6-3-3-6”)

An 87-year-old married Egyptian male farmer presented to the POC with palpitations. There was a history of compensated CHF and cirrhotic liver disease. ECG tracing was taken which showed an interested fixed PVCs grading in CHF; starting as hexagimeny, then trigimeny, then trigimeny hexagimeny as: (6-3-3-6) in a serial fixed manner. (Figure 8). For more details see Tables 4-6.

Figure 8: ECG tracing was taken which showed an interested “fixed grading in PVCs (red arrows); starting as hexagimeny, then trigimeny, then trigimeny (green arrows) hexagimeny (purple arrows) as: (6-3-3-6) in a serial fixed manner.

Case No. 9: (Fixed Pvcs Grading In Chf; Quadrigimeny- Bigimeny- Bigimeny Quadrigeminy “4-2-2-4”)

A 75-year-old married Egyptian female housewife presented to the POC with dizziness. There was a history of compensated chronic heart failure (CHF) and obstructive sleep apnea (OSA). ECG tracing was taken which showed an interesting fixed grading in PVCs; starting as Quadrigimeny-bigimeny-bigimeny quadrigimeny as: (4-2-2-4) in a serial fixed manner. (Figure 9). The patient advised for further electrophysiological study (EPS). For more details see Tables 4-6.

Figure 9: ECG tracing was taken which showed an interested “fixed grading PVCs (red arrows); starting as Quadrigimeny (purple arrows)-bigimeny-bigimeny (green arrows) quadrigimeny (purple arrows)” as: (4-2-2-4) in a serial fixed manner.

Case No. 10: (Non-fixed PVCs variation in grading in angina post-tramadol)

Figure 10: ECG tracing was taken which showed an interesting “Non-fixed variation grading PVCs”.

A 70-year-old married Egyptian male carpenter presented to ER with chest pain, dyspnea, and dizziness. He gave a recent history of ingested 3 tablets of oral tramadol (100 mg). There was a history of urinary bladder carcinoma. ECG tracing was taken which showed an interested “Non-fixed PVCs variation in grading” (Figure 10). The patient advised for further electrophysiological study (EPS). For more details see Tables 4-6.

Case No. 11: (Fixed bigeminal-quadrigeminal PVCs grading)

A 54-year-old married Egyptian male governmental officer presented to ER with palpitations. He gave a history of CHF. ECG tracing was taken which showed an interested “Fixed bigeminalquadrigeminal PVCs grading” (Figure 11). The patient advised for further electrophysiological study (EPS). For more details see Tables 4-6.

Figure 11: ECG tracing was taken which showed an interested “fixed bigeminal-quadrigeminal PVCs grading”.

Case No. 12: (Up-grading PVCs in CHF)

A 66-year-old married Egyptian male carpenter presented to the orthopnea. The patient had a recent history of CHF. He was admitted to the ICU as a CHF. Serial ECG tracing was taken which showed Up-grading from less frequent (trigeminy) to more frequent PVCs (bigeminy). The patient advised for further electrophysiological study (EPS) (Figure 12). For more details see Tables 4-6.

Figure 12: ECG tracing was taken which showed Up-grading PVCs from less frequent (trigeminy) to more frequent PVCs (bigeminy).

Case No. 13: (Insignificant isolated PVCs)

A 43-year-old married Egyptian female housewife presented to the POC with palpitations. There was a history of psycho-familial troubles. ECG tracing was taken which showed insignificant isolated PVCs. (Figure 13). The patient was managed with reassurance. For more details see Tables 4-6.

Figure 13: ECG tracing was taken which showed insignificant isolated PVCs (red arrows).

Case No. 14: (Insignificant isolated PVCs but important)

A 60-year-old married Egyptian female housewife presented to the ER with dizziness. There was a history of compensated chronic renal failure (CRF) on regular hemodialysis. She was admitted to ICU as symptomatic bradycardia. ECG tracing was taken which showed sinus bradycardia with few PVCs (Insignificant isolated PVCs but important) (Figure 14A). The above abnormalities reversed after atropine iv injection (1 mg). (Figure 14B). The patient advised for further electrophysiological study (EPS). For more details see Tables 4-6.

Figure 14: ECG tracings were taken which showed sinus bradycardia with few PVCs (an insignificant isolated PVCs but important) (tracing 14A). The above abnormalities reversed after atropine iv injection (1 mg). (tracing 14B).

Case No. 15: (Down-grading with less frequency of PVCs in CHF)

A 66-year-old married Egyptian male electrician presented to the orthopnea. The patient had a recent history of CHF. He was admitted to the ICU as a CHF. Serial ECG tracings were taken which showed Down-grading with less frequency of PVCs with ECG strip (Figure 15). The patient advised for further electrophysiological study (EPS). For more details see Tables 4-6.

Figure 15: ECG tracings were taken which showed ”down-grading PVCs” with ECG strip (red arrows). There is wavy triple an electrocardiographic sign (Yasser sign) for hypocalcemia in the anterior leads esp. V4-6 (green arrows).

Case No. 16: (Sinus arrhythmia spontaneously graded to normal)

A 66-year-old married housewife Egyptian female patient presented to the ER for follow up. The ECG recordings were showing sinus arrhythmia (Figure 16A). ECG recordings were taken one minute later and were completely normal without any medications (Passing phenomenon) (Figure 16B). The patient was only managed with reassurance. No recurrence for above ECG abnormalities on later serial ECG tracings follows up. For more details see Tables 4-6.

Figure 16: A. the initial ECG tracing showing sinus arrhythmia (green arrows) and with VR; 92 bpm. B. ECG tracing one minute later showing spontaneously normalization of all above changes.

Case No 17: (Sinus arrhythmia spontaneously graded to normal)

A 57-year-old married housewife Egyptian female patient presented to the ER for inguinal hernia preoperative preparation. The ECG recordings were showing sinus arrhythmia (Figure 17A). ECG recordings were taken one minute later and were completely normal without any medications (Passing phenomenon) (Figure 17B). The patient was only managed with reassurance. No recurrence for above ECG abnormalities on later serial ECG tracings follows up. For more details see Tables 4-6.

Figure 17: A. the initial ECG tracing showing sinus arrhythmia (green arrows) with VR; 76 bpm. B. ECG tracing one minute later showing spontaneously normalization of all above changes.

Case No 18: (PSVT spontaneously graded to AF)

A 43-year-old married Egyptian male worker presented to ER with palpitations and headache. He was a heavy cigarette smoker. He was admitted to the ICU as PSVT with HC. ECG tracing was taken which showed an interesting “PSVT spontaneously graded to AF” with ST-segment depressions in V3-6 leads (Figure 18). The patient advised for further electrophysiological study (EPS). For more details see Tables 4-6.

Figure 18: ECG tracings showing PSVT with ST-segment depressions in V3-6 leads (A. tracing; gold arrows) spontaneously graded to AF with few PVCs couplets (B. ECG tracing; green arrows), with complete normalization of all above changes with conversion to NSR after treatment (C. tracing).

Case No 19: (JT spontaneously graded to sinus tachycardia)

A 44-year-old married, driver, heavy cigarette smoker, Egyptian male patient presented in the ER with acute severe chest pain and palpitation. The chest pain was anginal The patient gave a recent history of using substance abuse. He was admitted to the ICU and managed in the ICU as unstable angina. ECG tracing was taken which showed an interested “JT spontaneously graded to sinus tachycardia” (Figure 19). For more details see Tables 4-6.

Figure 19: ECG tracings showing JT (A. tracing) spontaneously graded to sinus tachycardia (B. ECG tracing), with complete normalization of all the above changes with conversion to NSR after treatment (C. tracing).

Case No. 20: (Progressive AJR with the left to right extension in pleurisy and cold)

A 17-year-old single Egyptian male student presented to the POC with pleuritic chest pain. The patient had a recent history of a common cold. Serial ECG tracings were taken which showed progressive AJR with the left to the right extension. with a normal rhythm in between until becoming total JR in the all ECG tracing, then spontaneously normalized (Passing phenomenon). JR initially started in I, II, III, aVF, and part of V3-6 leads, except aVR, aVL, V1-2, and the remaining part of V3-6 lead, then extended to all ECG leads, then spontaneously normalized in all ECG leads. No recurrence for above ECG abnormalities on later serial ECG on follow up. The patient advised for further electrophysiological study (EPS. For more details see Tables 4-6.

Case No 21. (AJR and sinus arrhythmia with progressive extension from left to right in the prolapsed cervical disc)

A 56-year-old married Egyptian male teacher patient presented to POC with musculoskeletal chest pain. Chest pain associated with bilateral arm pain with weakness, paraesthesia, and numbness. The patient gives a history of lumbosacral herniated disc prolapse with the surgical repair 9 years ago. Local tenderness was elicited. The ECG recordings were showing AJR in the inferior leads; II, III, aVF (inverted P-wave), and aVR (upright P-wave) with sinus arrhythmia. ECG recordings were taken two minutes later and were completely normal without any medications (Passing phenomenon). MRI of the cervical spine showing herniated disc prolapse between C4 and C5 vertebrae with spinal stenosis. No recurrence of accelerated junctional rhythm on later serial ECG tracings. The patient was referred to the neurosurgeon after reassurance for further evaluation, management, and advised for further electrophysiological study (EPS). For more details see Tables 4-6.

Case No 22. (AJR with progressive extension from left to right in myositis)

A 43-year-old married housewife Egyptian female patient presented to POC with musculoskeletal chest pain. Local tenderness was elicited. The ECG recordings were showing AJR in the inferior leads ( II, III, aVF) and all anterior leads (V1-6). ECG recordings were taken two minutes later and were completely normal without any medications (Passing phenomenon). There are leukocytosis (14400) and increased CPK (473 IU/L). 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. For more details see Tables 4-6.

Case No 23: (AJR with progressive extension from left to right in pleurisy and cold)

A 47-year-old married male heavy smoker farmer Egyptian patient presented to the POC with pleuritic chest pain. The patient had a recent history of a common cold. Chest examining was showing pleuritic rub on listening. The ECG recordings were showing AJR with progressive extension from left to right (P-wave inversion through all ECG leads except aVR and V1-2 (upright P-wave) with VR;70 bpm. ECG recordings were taken one minute later and were completely normal without any medications (Passing phenomenon). 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. For more details see Tables 4-6.

Case No 24: (Down-Graded bigeminal RBBB)

A 70-year-old, heavy cigarette smoker, Egyptian farmer, the male patient presented in the ER with dizziness. The patient gave a history of IHD and HTN. The patient admitted to the intensive care unit (ICU). The initial emergency and serial ECG tracing showed down-graded bigeminal RBBB with ST-segment depression in III and V4-6 leads. He managed with nitroglycerin IVI. The next ECG tracing showed RBBB with trigeminy but with normalization of ST-segment depression. The third ECG tracing was taken after 30 minutes of nitroglycerin IVI within 6 hours of the ICU. It showed nearly complete disappearance of the above Abnormalities. The echocardiographic report showed evidence of IHD with apical and lateral wall hypokinesia with diastolic dysfunction and low ejection fraction (52%). The patient continued on nitroglycerin retard (2.5 capsules; BID) on discharge with no future problems. For more details see Tables 4-6.

Case No 25: (Up-grading PVCs in acute pulmonary embolism)

An 80-year-old, Egyptian worker, the male patient presented in the ER with tachypnea and acute confusion. His wife gave a recent history of diazepam amp (10 mg) injection for irritability. The patient admitted to the ICU with suspected acute pulmonary embolism. The initial emergency and serial ECG tracing showed RBBB with PVCs up-grading from less frequent to more frequent PVCs (bigeminy) with ST-segment depression in V4-6 leads. He managed as an acute pulmonary embolism. No recurrence for PVCs on later serial ECG tracings follows up. For more details see Tables 4-6.

Case No 26: (Down-grading PVCs in CHF and CVA)

An 82-year-old married housewife Egyptian female patient presented to the ER with orthopnea and hemiplegia. The patient gave a history of CHF and IHD. The patient admitted to the ICU as CVA with CHF. The initial emergency and serial ECG tracing showed Down-grading PVCs from more frequent (bigeminy) to less frequent PVCs (pentageminy) with wavy triple an electrocardiographic sign (Yasser sign) for hypocalcemia in the all leads. The echocardiographic report showed evidence of IHD with global hypokinesia, systolic dysfunction, and low ejection fraction (45%). For more details see Tables 4-6.

Case No 27: (Non-fixed variation on grading in CHF)

A 60-year-old married housewife Egyptian female patient presented to the POC with dizziness and palpitations. The patient gave a history of CHF, IHD, and HTN. The patient admitted to the ICU as frequent symptomatic PVCs. The initial emergency and serial ECG tracing showed Non-fixed variation on grading in CHF The echocardiographic report showed evidence of IHD with mild hypokinesia with ejection fraction (58%). For more details see Tables 4-6..

Case No 28: (Non-significant PVCs in old MI)

A 64-year-old, heavy smoker, Egyptian carpenter, the male patient presented in the ER with chest pain and palpitations. The patient admitted to the ICU as unstable angina. The initial emergency and serial ECG tracing showed Non-significant PVCs in evidence of old MI (pathological Q-wave in inferior leads; II, III, and aVF) leads. He managed as unstable angina. No recurrence for PVCs on later serial ECG tracings follows up. For more details see Tables 4-6..

Case No1 29 (Sinus arrhythmia spontaneously graded to normal)

A 34-year-old married worker Egyptian male patient presented to the ER for blood pressure follow up. The ECG recordings were showing sinus arrhythmia. ECG recordings were taken four minutes later and were completely normal without any medications (Pass phenomenon). The patient was only managed with reassurance. No recurrence for above ECG abnormalities on later serial ECG tracings follows up. For more details see Tables 4-6..

Case No 30 (Sinus arrhythmia spontaneously graded to normal with anxiety)

An 85-year-old married housewife Egyptian female patient presented to the emergency room with palpitation. The patient had a recent history of anxiety. ECG recordings were showing sinus arrhythmia. ECG recordings were taken three minutes later and were completely normal without any medications (Pass phenomenon). The patient was only managed with reassurance. No recurrence for above ECG abnormalities on later serial ECG tracings follows up. For more details see Tables 4-6.

Results, Findings, and Discussion

1. The Changes In “Graded Phenomenon” Is Classified Into:
1. Up-grading; 20% (6 cases), 2. Down Graded; 10% (3 cases), 3. Changed to NSR; 43.33% (13 cases), 4. Changed to AF; 3.33% (1 case), 5. Changed to sinus tachycardia; 3.33% (1 case), 6. Therapeutic reversal; 3.33% (1 case), 7. Fixed change; 10% (3 cases), 8. Variable change; 6.67% (2 cases) (Figure 20).

Figure 20: showing the graphical presentation for developmental changes in the “Graded phenomenon”.

2. The Course in “Graded Phenomenon” is Classified into: 1. Progressive; 43.33% (13 cases), 2. Regressive; 10% (3 cases), 3. Intermittent; 6.67% (2 cases), 4. Constant; 16.67% (5 cases), 5. Transient; 20% (6 cases), Non-fixed variation; 3.33% (1 cases) (Figure 21),

Figure 21: showing the graphical presentation for the course progression in the “Graded phenomenon”.

3. The risk in “Graded phenomenon” is classified into: 1. High risk; 40% (12 cases), 2. Non-risk; 43.33% (13 cases), 3. Still-risk; 16.67% (5 cases) (Figure 22).
4. Age averages mean (58.3), median (60), and, mode (60).
5. Sex averages: male Sex predominance: 17 cases (56.67%).
6. The Age mean:58.3 years with male Sex predominance;17 cases (56.67%).
7. The changes in “Graded phenomenon” are classified into: Up-grading; 20%, down-graded; 10%, changed to NSR; 43.33%, changed to AF; 3.33%, changed to sinus tachycardia; 3.33%, therapeutic reversal; 3.33%, fixed –change; 10%, and variable change; 6.67%.

Figure 22: showing the graphical presentation for risk outcomes in “Graded phenomenon”.

8. The risk in the “Graded phenomenon” is either high (40%), non-risk (43.33%), or still-risk (16.67%).
9. The course in the graded phenomenon is either progressive (43.33%), regressive; 10%, intermittent; 6.67%, constant; 16.67%, transient; 20%, and non-fixed variation; 3.33%.
10. The following are the principals for understanding the “Graded phenomenon”:
a. The “Graded phenomenon” (Yasser’s phenomenon) is a novel electrocardiographic phenomenon change the arrhythmia directory.
b. It is a crucial step for understanding the arrhythmia.
c. The phenomenon is a new strong guide for monitoring and follows up arrhythmic patients.
d. The principal of “Graded phenomenon” is based on catching the graded changes in serial ECG tracings or even single one regarding the arrhythmias.
e. The “Graded phenomenon” is a crucial step to repeat and reassessment arrhythmia management.
f. The graded changes in the serial ECG tracings or even single one regarding arrhythmias constitute the main topic for this research.

11. The changes in “Graded phenomenon” are:

a. Up-grading: It is meaning that the change either from low serious arrhythmia to higher serious arrhythmia, or more extension for the current serious arrhythmia, or ending to serious arrhythmia or just extension for a benign arrhythmia e.g. case No. 1. Up-grading may be included an up-grading type of arrhythmia as in case No. 7.
b. Down-grading: It is meaning that the change either from higher serious arrhythmia to low serious arrhythmia, or less extension for the current serious arrhythmia, or ending to the benign or non-serious arrhythmia e.g. case No. 15.
c. Fixed change: It is meaning that the current arrhythmia is constant in the serial ECG or even the single ECG tracing e.g. case No. 6.
d. Spontaneously changed to normal sinus rhythm: It is meaning that the current arrhythmia is spontaneously changed to normal sinus rhythm with no uses of medications or therapeutic maneuvers like DCC and Valsalva’s e.g. case No. 16 and17.
e. Spontaneously changed to another arrhythmia e.g. sinus tachycardia e.g. case No. 19 and atrial fibrillation e.g. case No. 18.
f. Therapeutic reversal: It is meaning that there is a new arrhythmic change after using the traditional antiarrhythmic e.g. case No. 14.
g. The extension for arrhythmia in “Graded phenomenon” are : The up-grading phenomenon with the right to left extension: It is meaning that the arrhythmic change starting from the right side of ECG tracing directed toward its left side e.g. case No. 1.
h. The up-grading phenomenon with the left to right extension: It is meaning that the arrhythmic change starting from the left side of ECG tracing directed toward its right side e.g. case No. 2.
i. Up-grading bidirectional sectors of tachycardia (BSOT): It is meaning that the arrhythmic change starting as sectors of tachycardia then gradually extend to both left and right side of ECG tracing until becoming complete tachycardia e.g. case No. 3.
j. Intermittent Wandering pacing rhythm with the left to right extension: It is meaning that the change occurring intermittent manner then extends from left to right e.g. case No. 4.

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12. The risk in arrhythmia with “Graded phenomenon” are:

a. High: This is meaning that there will be possible serious outcomes like; sudden cardiac deaths congestive heart failure, Torsades de pointes, and VT ventricular tachycardia e.g. case No. 1, 2, and 7.
b. Non-risk: This is meaning that there will not be possible serious outcomes e.g. case No. 1, 2, and 7.
c. Still-risk: This is meaning that there are no current possible serious outcomes but maybe with passing the time e.g. case No. 18, 24, and 26.

Conclusion and Recommendation

Graded phenomenon (Yasser’s phenomenon) is a novel electrocardiographic phenomenon change the arrhythmia directory. It is a crucial step for understanding arrhythmia. The phenomenon is a new strong guide for monitoring and follows up arrhythmic patients in cardiovascular patients. There are interlacing correlations between the “passing phenomenon” [49] and the current “Graded phenomenon” especially in cases of arrhythmia that is spontaneously changed to normal sinus rhythm with no uses of medications or therapeutic maneuvers like DCC and Valsalva’s e.g. case No. 16 and17. Electrophysiology studies (EPS) is recommended for more future study and understanding the “Graded phenomenon”. Physiological study for the cellular electrolytes may be advised future options for the “Graded phenomenon”.

Conflicts of Interest

There are no conflicts of interest.

Acknowledgment

I wish to thank Dr. Ameer Mekkawy; M.sc. for technical support, and both the emergency department and critical care unit nurses who make extra-ECG copies for helping me.

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