Differential diagnosis for elevated ammonia levels.
\r\n\t
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Dr. Wei Wu has received awards from many national societies for the originality and quality of his projects. He has authored 70 peer-reviewed papers in international journals.",coeditorOneBiosketch:"A pioneering researcher in obstetrics and holder of three registered patents. Dr. Qiuqin Tang's research interests include genetic and epigenetic risk factors of reproductive and developmental health. She has authored over 20 papers in international journals.",coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"178661",title:"Dr.",name:"Wei",middleName:null,surname:"Wu",slug:"wei-wu",fullName:"Wei Wu",profilePictureURL:"https://mts.intechopen.com/storage/users/178661/images/system/178661.jpeg",biography:"Dr. Wei Wu is an associate professor and associate department\nchair in the Department of Toxicology, Nanjing Medical University, China, where he received his Ph.D. in Toxicology in 2012.\nHe was a guest researcher at the National Institute of Environmental Health Sciences (NIEHS) between 2017 and 2018. Dr.\nWu is a member of different national and international societies\nin the fields of human reproduction and toxicology and has\nreceived awards from many national societies for the originality and quality of his\nprojects. Dr. Wu has authored seventy-three peer-reviewed papers in international\njournals. He has edited four books and collaborated on ten others as well as seventeen patents and in the organization of three international conferences. He is a\nreviewer for ninety-eight journals.",institutionString:"Nanjing Medical University",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"4",totalChapterViews:"0",totalEditedBooks:"4",institution:{name:"Nanjing Medical University",institutionURL:null,country:{name:"China"}}}],coeditorOne:{id:"184798",title:"Ms.",name:"Qiuqin",middleName:null,surname:"Tang",slug:"qiuqin-tang",fullName:"Qiuqin Tang",profilePictureURL:"https://mts.intechopen.com/storage/users/184798/images/13334_n.jpg",biography:"Qiuqin Tang is an attending doctor of The Women’s Hospital of Nanjing Medical University (Nanjing Maternity and Child Health Care Hospital). Her research interests include genetic and epigenetic risk factors of reproductive and developmental health. She has authored over 20 papers in international journals such as EBioMedicine, Clinical Epigenetics, Molecular Human Reproduction, Scientific Reports, and European Journal of Endocrinology. She has collaborated in four books and three patents. 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He is also the headmaster of the Family Planning Centre and Gynecological Cytology\nLaboratory at the same university. Dr. Tsikouras is a fellow of the\nInternational Academy of Clinical and Applied Thrombosis/Hemostasis. His scientific activities focus on paediatric and adolescence medicine, gynecological oncology, high-risk pregnancies. He is a reviewer for several international journals and has numerous scientific publications to his credit, including papers and book chapters. 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He\nis currently a professor in the Gynecology and Obstetrics Faculty\nof Medicine, University of Kiel, Germany, and honorary doctor\nat the Democritus University of Thrace, Alexandroupoli University Hospital He previously served as chief of the Department\nof Gynecology and Obstetrics at University Hospital RWTH Aachen,\nGermany. Dr. Rath is a reviewer for numerous journals and chief editor of Geburtshilfe und Frauenheilkunde (GebFra). 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Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"69494",title:"Ammonia",doi:"10.5772/intechopen.88044",slug:"ammonia",body:'\nAmmonia, a colorless gas with a unique odor is thought to be central to the pathogenesis of hepatic encephalopathy (HE). It is an important biomarker and may also serve as a prognostic indicator in acute liver disease where ammonia levels may be predictive of cerebral edema and herniation. In this chapter, we aim to review and discuss its role in HE understanding its rise and fall as part of the urea cycle, appropriate measurement and collection, and examine the paradigms differentiating acute liver failure with chronic liver disease. We want to recognize other diseases that may elevate ammonia levels and discuss how different treatments target its reduction.
\nThe homeostasis of ammonia is a multi-organ process involving the brain, gastrointestinal tract, muscles, adipose tissue, kidneys, and mainly the liver. A study involving patients with end-stage liver disease, revealed that branched-chain amino acids (BCAAs) (Figure 1) are not metabolized in the liver but rather by muscle, kidney, adipose, and brain tissue. This is in contrast to the aromatic amino acids (tyrosine, phenylalanine, methionine), which are metabolized and deaminated solely by the liver. BCAA supplementation leads to reductions in hyperammonemia as a result of the metabolism of BCAAs by skeletal muscle. The metabolism of BCAAs supplied carbon skeletons for the formation of α-ketoglutarate which combined with two ammonia molecules to form glutamine [1]. In a 1-year double-blind study of 174 patients with advanced cirrhosis who were randomized to receive BCAAs or equicaloric amounts of lactoalbumin, the group given BCAAs had a significantly decreased incidence of the combined endpoint of death and liver decompensation, as well as hospital admissions, compared with lactoalbumin [2]. In addition, a multi-center randomized study of 646 patients with cirrhosis who were given 12 g of BCAAs per day for 2 years, compared with diet therapy and a defined food intake, found a significant decrease in HE and refractory ascites in the treatment group [3]. Because of their poor palatability and high cost, BCAAs are not routinely recommended, but they were important tools in the proof of concept of liver’s importance in ammonia homeostasis.
\nBranched-chain amino acids.
The mechanism of how the liver processes the ammonia has been described and involves the following steps: ammonia is produced by the enterocytes from glutamine and by colonic bacterial catabolism of nitrogenous sources, such as ingested protein and secreted urea. It then enters the circulation through the portal vein where the liver metabolizes the majority of the ammonia converting it into urea or glutamine and preventing entry into the systemic circulation. These were demonstrated through careful studies of the urea cycle and its disorders [4].
\nThe increase in blood ammonia levels in advanced liver disease is a consequence of impaired liver function and of shunting of blood around/away from the liver. Muscle wasting, a common occurrence in these patients, also may contribute since muscle is also an important site for extrahepatic ammonia removal.
\nThe measurement serum ammonia concentration in patients suspected of having HE remains controversial. While it is well known that venous ammonia levels vary immensely and are not useful for screening or following HE [5], arterial ammonia concentrations more accurately correlate with HE as it is further discussed in this chapter. Furthermore, the grade of HE seems to be more closely related to the partial pressure of gaseous ammonia (pNH3) than the total arterial ammonia concentration, since gaseous ammonia readily enters the brain [6]. This can be easily calculated with ammonia levels when correlating with pH.
\nThe accuracy of ammonia determination is influenced by many factors, such as fist clenching, use of a tourniquet, and whether the sample was placed on ice [7]. It is largely recommended that it is tested within an hour of collection, though some agents (sodium borate/l-serine) could potentially stabilize for up to 12 h [8].
\nThus, ammonia should be collected in an extremity without trauma with arterial blood, collected in chilled tubes with ammonia-free sodium heparin (green top) or ethylenediaminetetraacetic acid (EDTA; purple top), placed on ice, and delivered rapidly to the laboratory (within an hour). Some chemicals could stabilize for posterior measurement, but more studies are needed to confirm that these agents will not influence in other reactions and measurements.
\nNormal values for ammonia concentration may differ depending on age groups. It can be often higher in newborns, with the upper limit of normal of ammonia concentration of healthy term infants at birth of 80 to 90 μmol/L, while normal values in children older than 1 month and adults are less than 50 and 30 μmol/L, respectively [9].
\nEarly studies had shown a correlation of levels of ammonia and worsening HE up to two times the upper limit of normality [6]. Further studies have not only cemented this correlation but have shown a more intricate relationship [10, 11]. It can predict the risk and frequency of HE episodes [12].
\nProof of the role of ammonia in pathogenesis of HE has come from the efficacy of therapies aimed to lower plasma ammonia in improving its symptoms. The mechanisms causing brain dysfunction in liver disease are still not known to the full extent. In coma of models of acute liver failure, the effects of ammonia are present in brain swelling, impaired cerebral perfusion, and reversible impairment of neurotransmitter systems [13].
\nStemming from this proof of concept, several studies have tried to elucidate the effects of hyperammonemia. First, ammonia is believed to be a direct neurotoxin potentialized by other toxins, such as mercaptans and short-chain fatty acids [14]. Second, it impairs the blood–brain barrier by changing the protein transport [15]. Third, it increases the intracellular osmolality of astrocytes leading to edema and extreme cases, herniation [13, 16]. Lastly, it increases oxidative stress. In one study, oxidative stress markers in the brain of patients with cirrhosis with severe hepatic encephalopathy included elevated levels of protein tyrosine-nitrated proteins, heat shock protein-27, and 8-hydroxyguanosine as a marker for RNA oxidation [17].
\nIn a recent study of patients with cirrhosis, there was significant evidence that ammonia levels correlate with not only the severity of hepatic encephalopathy but also the failure of other organs in cirrhosis and is an independent risk factor for 28-day mortality. This data provided evidence that the ammonia level has a clinically relevant utility in providing important prognostic information, signifying its potential role as a biomarker in identifying patients at high risk of mortality. A reduction in ammonia level was associated with improved survival, confirming it as a potential therapeutic target. Classically in urea cycle disorders ammonia levels above 200 μmol/L were considered a poor prognostic factor [18], but in this study in cirrhotics even ≥79.5 μmol/L was associated with increased mortality, indicating an additional role of ammonia in dictating clinical outcomes [11].
\nClassically, there was a clear distinction of the harmful effects of the ammonia in acute liver failure due to the osmotic component [13] and in lesser degree in chronic liver disease, stating that ammonia in cirrhosis increased morbidity and not mortality. But newer studies and prospective analysis shows that it can be harmful in similar way, increasing mortality [11]. Further studies are needed to corroborate both the utility and prognostic value of ammonia in the setting of chronic liver disease.
\nAmmonia levels may rise due to reasons other than acute or chronic liver disease. This may include increased urea absorption/production, decreased extra-hepatic removal, and reduced participation of liver (Table 1).
\nDifferential diagnosis for elevated ammonia levels.
Processes that increase urea absorption/production are the main conditions that make up the differential diagnosis. These conditions include gastrointestinal bleeding, renal disease, urinary tract infection with a urease-producing organism (e.g.,
Within the conditions that decrease extrahepatic removal of ammonia, diseases affecting the muscles such as severe muscle exertion/heavy exercise are worth noting.
\nReduced participation of liver in the removal of ammonia may occur in any cause of portosystemic shunting of blood, such as in hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease) and portal hypertension with collateral formation.
\nTwo other groups of conditions are considered controversial in their role in the development of hyperammonemia: congenital disorders (certain inborn errors of metabolism such as urea cycle defects and organic acidemia) and medication induced (valproic acid, barbiturates, narcotics, diuretics, alcohol, and salicylate-Reye syndrome). Some authors classify both as a cause for hyperammonemia while others would englobe in subgroups of liver diseases as they are believed to have similar pathophysiology [19, 20].
\nThe treatment HE resonates around decreasing ammonia. It can be achieved through three major mechanisms: decreasing ammoniagenic substrates, inhibiting ammonia production, and metabolic removal of ammonia (Table 2).
\nMechanisms used in treatment of hyperammonemia.
Enemas are the main treatment of this category. These are administered to patients at increased risk of aspiration. Different agents have been used, including tap water, milk/molasses, and lactulose. The efficacy of enema administration has not been evaluated [19].
\nThe use of laxatives, especially non-absorbable disaccharides, has been the cornerstone of the treatment HE. Oral lactulose or lactitol (the latter is not available in the United States) are thought to have an
Oral antibiotics have been used with the aim of modifying the intestinal flora and lowering stool pH to enhance the excretion of ammonia. Antibiotics are generally used as second-line agents after lactulose or in patients who are intolerant of non-absorbable disaccharides. Rifaximin given orally in a dose of 550 mg twice daily was approved in 2010 for the treatment of chronic hepatic encephalopathy and reduction in the risk of recurrence of overt encephalopathy in patients with advanced liver disease. The tolerability and side-effect profile of rifaximin are superior to those of lactulose, albeit at greater financial cost. Other antibiotics, including neomycin, paromomycin, metronidazole, and vancomycin, have been studied in small trials and case series, but some may have an increased side effect profile and the effectiveness of others are not well established.
\nAgents that may modify intestinal flora and modulate the generation or intestinal absorption of ammonia have been evaluated as potential treatments. Acarbose, an intestinal α-glucosidase inhibitor used to treat type 2 diabetes mellitus, inhibits the intestinal absorption of carbohydrates and glucose and results in their enhanced delivery to the colon. As a result, the ratio of saccharolytic to proteolytic bacterial flora is increased and blood ammonia levels are decreased. A randomized controlled double-blind crossover trial has demonstrated that acarbose improves mild hepatic encephalopathy in patients with cirrhosis and adult-onset diabetes mellitus. Similarly, probiotic regimens (such as
Sodium benzoate, sodium phenylbutyrate, and sodium phenylacetate, all of which increase ammonia excretion in urine, are approved by the FDA for the treatment of hyperammonemia resulting from urea cycle enzyme defects and may improve HE in patients with cirrhosis. Administration of sodium benzoate, however, results in a high sodium load, and the efficacy of this agent is not clearly established [21].
\nAdministration of zinc, which has been used because zinc deficiency is common in patients with cirrhosis. Furthermore, because it increases the activity of ornithine transcarbamylase, an enzyme in the urea cycle, it may also improve HE; however, clear efficacy has not been established. L-ornithine–l-aspartate (LOLA), a salt of the amino acids ornithine and aspartic acid that activates the urea cycle and enhances ammonia clearance, has been shown in several randomized controlled studies to improve HE compared with lactulose; however, this agent is not available in the United States.
\nExtracorporeal albumin dialysis using the molecular adsorbent recirculating system (MARS) has resulted in a reduction in blood ammonia levels and improvement in severe encephalopathy in patients with acute-on-chronic liver failure. Further studies are needed to clarify whether albumin dialysis has a role in treatment of HE [19].
\nFecal microbiota transplant is being studied prospectively in a few centers in North America. As an established treatment in
Studies are currently underway comparing different formulations of rifaximin, evaluating the difference between the immediate release against the sustained extended release.
\nOther antibiotics, cheaper and with safer profiles are being studied prospectively to compare with the current gold standard, rifaximin. One such antibiotic notably is nitazoxanide.
\nData regarding dialysis as a treatment modality has not been satisfactory in order to justify its regular use in the setting of HE. There are prospective studies evaluating other exchange therapies such as plasmapheresis as viable alternative treatment options especially in the setting of refractory HE.
\nAST-120, an oral spherical carbonaceous adsorbent approved and used in chronic kidney disease to decrease uremia by decreasing intestinal indole absorption and consequently indoxyl sulfate production [23] has been extrapolated to HE with promising results, but still in initial phases and further studies are needed to better characterize its role in the treatment of HE.
\nOur understanding of the interactive physiology between ammonia and HE has greatly increased since its first proposition by Hippocrates of Kos B.C. and its first description in 1860 by von Frerichs [22]. There are multiple effective treatments available and yet others in the horizon. However, there is still much more to be understood about the role of ammonia in HE and other factors may still be involved in the pathophysiology of portosystemic encephalopathy. The future of HE appears bright and future treatment options will hopefully improve the quality of life of patients with this potentially debilitating disease.
\nThe authors declare no conflict of interest.
\nbranched-chain amino acids
\nbefore Christ
\nethylenediaminetetraacetic acid
\nfecal microbiota transplant
\nhepatic encephalopathy
\nhereditary hemorrhagic telangiectasia
\nl-ornithine–l-aspartate
\nmolecular adsorbent recirculating system
\npartial pressure of gaseous ammonia
\nportosystemic encephalopathy
\nCardiac electrophysiology study (EPS) is helpful to assess the heart’s electrical system. This is an invasive percutaneous cardiac procedure used for the investigation and treatment of certain arrhythmias. During the examination, catheters are inserted to the appropriate position within the heart mainly via large veins to record the electrical signals of the heart and to pace from different localized areas. In this way, EPS can help evaluating the function of the conduction system, determining the mechanisms of brady- and tachyarrhythmias, and identifying areas which may be the targets of often curative catheter ablation. Many cardiac arrhythmias that previously required the use of potentially harmful antiarrhythmic drugs can now be routinely cured in the electrophysiology laboratory by means of transcatheter ablation techniques.
In this chapter, the basics of cardiac electrophysiological studies are presented.
Equipment necessary for EPS includes an operation table, fluoroscopy unit, recorders, programmable stimulator, a multichannel lead switching box, an oscilloscope, and emergency instruments. In addition, tools for vascular access and electrode catheters are also required [1]. A standard schematic set-up for typical EPS is shown in Figure 1.
Standard schematic set-up for typical electrophysiology study. Abbreviation: RF—radiofrequency.
Electrical signals from humans obtained by surface or intracardiac electrodes are <10 mV in amplitude. These electrocardiograms must be amplified and filtered before digitalization, displaying, and storage for interpretation and analysis [2]. Amplification means the increase of the signal’s amplitude. However, the signals are plagued with electrical noise, thus amplification results in increasing not only the original signals but the amplitude of noise also. For this reason, avoidance of extraneous signals is essential: all electrical tools used in EPS should be appropriately earthed and shielded. In addition, filtering is required to eliminate unnecessary components of the electrical signals. High-pass filters remove components below a given frequency, while low-pass filters eliminate high-frequency components of the electrical signal. Electrophysiological signals are often contaminated with power line noise (i.e., 60 Hz in North America and 50 Hz in Europe), thus notch filtering is often used to eliminate it [3].
Standard ECG devices run at 25 mm/s Increasing the paper output speed, subtle ECG findings hidden in the tracings become more evident. During an EPS, surface ECG leads and intracardiac electrocardiograms (IEGM) are generally displayed and interpreted at a sweep speed of 100 or 200 mm/s (Figure 2).
Same normal sinus beat at a paper speed of 25, 50, 100, and 200 mm/s.
For a standard EPS, a standard number of four catheters is necessary. Based on the operator’s decision, EPS is also feasible using only three diagnostic catheters. Diagnostic catheters have two or multiple electrodes, and for each pair of consecutive electrodes, a distinct intracardiac electrogram gets recorded. Traditionally, catheter placement is carried out under fluoroscopy guidance. In the EP lab, three main fluoroscopy projections are used: anteroposterior (AP), left anterior oblique (LAO), and right anterior oblique (RAO) views (Figure 3).
Standard catheter positions in left anterior oblique (LAO), anteroposterior (AP), and right anterior oblique (RAO) projections. Abbreviations: CS—coronary sinus decapolar catheter; HRA—high right atrium; RVa—right ventricle apex.
A diagnostic catheter is positioned from the femoral vein and contacted with the lateral wall of the right atrium at right atrium—superior vena cava junction.
The coronary sinus runs transversely in the left atrioventricular groove on the posterior side of the heart. A multielectrode catheter is inserted into the coronary sinus from femoral, jugular internal, or subclavian vein. For femoral approach, steerable catheters are used. CS catheter allows to record IEGMs coming from the left atrium and ventricle. Moreover, this position is easily reproducible and serves as a reference point during the EPS. Thus, CS catheters play an important role in EP labs.
For recording His bundle electrogram, a catheter is inserted via femoral vein to the high septal part of the right ventricle and pulled back slowly with clockwise torquing till characteristic His bundle electrogram appears.
A diagnostic catheter is advanced from femoral vein to apical right ventricle, which allows to record local ventricular IEGMs.
Generally, IEGMs mean the electrical activity between two electrodes at the tip of the catheter (bipolar recording) [4]. The main difference between surface ECG and IEGMs is that the surface ECG records a summation of the electrical activity of the heart, while in contrast, IEGMs show only the electrical activity of a localized area, i.e., IEGMs are local intracardiac electrograms. Importantly, these are displayed together on the monitor system facilitating accurate interpretations of the electrical signals (Figure 4).
Snapshot from an electrophysiology study. The upper four channels represent lead I, II, V1, and V6 of surface ECG. The paper speed is 200 mm/s. on the distal His (His d) channel, we can recognize three different wavefront characteristics of the His bundle: the first one is the A (atrial) wave (synchronous to P wave on surface ECG), the last is called V (ventricular) wave (synchronous to QRS complex on the surface ECG). In the middle, a sharp signal represents His bundle electrogram. AH interval could be measured from the beginning of A to the sharp His signal. HV interval is measured on the His bundle electrogram from the beginning of the His deflection to the earliest identified ventricular activity on the surface ECG. CS electrograms show atrial activation (synchronous to P wave on surface ECG again). Note that first activation occurs on CS 9,10 which is the proximal pair of electrodes. CS 9,10 is at the ostium of the coronary sinus, thus these electrodes are the closest to the sinus node. In the case of a correctly positioned CS catheter, CS 9,10 should be activated first during normal sinus rhythm. Finally, a local ventricular electrogram can be easily identified on the catheter at RVa position. Asterix represents PA interval.
After catheter placement, a routine EPS starts with the measurement of basic intervals [4]. Ideally basic intervals should be measured during sinus rhythm.
The PA interval represents the interval between the earliest atrial activation (recording in any channel) in the region of the sinus node and at the region of the atrioventricular node. Usually, the earliest atrial activation is represented by the P wave onset on the surface ECG. Normal value is 25–55 milliseconds (ms).
AH interval represents the conduction time from the low-right atrium at the interatrial septum through the atrioventricular (AV) node to the His bundle. It is measured between the atrial electrogram recorded by the His bundle catheter and the beginning of the His electrogram itself. The normal range is 55–150 ms [4]. The AH interval is sensitive to autonomic tone. A prolonged AH interval may indicate AV nodal disease or high vagal tone, whereas a shorter than normal AH can occur during sympathetic activation.
HV interval reflects conduction through the His-Purkinje system and is measured on the His bundle electrogram from the beginning of the His deflection to the earliest identified ventricular activity on the surface ECG. An HV interval of 35–55 ms is considered normal. In the presence of anterograde conducting accessory pathway, the HV interval may be shorter. Prolonged HV interval represents infrahisian conduction disturbances.
Time measurements are reported in milliseconds in the case of EP procedures. To characterize the heart rate, the cycle length (CL) is used instead of the frequency. CL represents the length of time between each atrial or ventricular beats. For example, a tachycardia with a heart rate of 150 beats per minute has a CL of 400 ms (Figure 5). The faster the heart rate the shorter the CL.
Atrial pacing at a cycle length of 400 ms, which means a rate of 150 beats per minute. Sharp pacing artifacts are present before P waves. P waves are negative in the inferior leads (pacing from coronary sinus ostium). Paper speed is 100 mm/s.
Besides IEGM recordings, electrode catheters previously inserted in the heart are also used for pacing. An external stimulator is connected to the catheters. When pacing starts, electrical current is passed by catheters resulting in cardiac cells’ depolarization near the catheter’s electrode. The depolarization of these cells generates an electrical wavefront, spreading over the heart as the impulse originating from the sinus node. As a result, stimulator pacing generates cardiac impulse artificially. Carefully positioned catheters can impulse the heart from almost any position. During the EPS, pacing is used to introduce electrical impulses in predetermined patterns and at precise time intervals. Such pacing is called programmed stimulation [1]. Programmed stimulation consists of the main type of pacing technique: burst and extrastimulus pacing.
Burst pacing consists of implementing a series of electrical impulses (so-called drive train) at a fixed cycle length. By definition, each impulse is called S1 and the difference between the impulses is the same (Figure 6).
Ventricular burst pacing from RVa position. Note the pacing artifact on RVa channel and before the QRS complexes. Pacing cycle length is fixed (500 ms). Paper speed is 50 mm/s.
Extrastimulus testing means introduction of a drive train (usually 8 beats, S1) followed by one or more extrastimuli with shorter coupling interval than the cycle length of the drive. S2 means the first programmed extrastimulus, S3 is used for the second, and so on (Figure 7).
Atrial extrastimulus testing from coronary sinus catheter (CS). The drive train consists of 8 beats at a cycle length of 400 ms is followed by an extrastimulus with a shorter coupling interval (300 ms). Ablation catheter (ABL) is in the His region showing His bundle electrogram. Paper speed is 50 mm/s.
During EPS, refractory periods of cardiac tissues can be characterized by measuring effective, functional, and relative refractory periods [5].
Most commonly used as it is part of a routine EPS. It represents the longest coupling interval that fails to capture the tissue or be conducted over the structure (Figure 8).
Programmed atrial stimulation from CS 9,10. Drive cycle length is 400 ms. Panel A shows ventricular contraction (i.e., QRS complex) after S2 extrastimulus at a coupling interval of 240 ms. However, Panel B represents atrioventricular block after S2 extrastimulus at a coupling interval of 230 ms. In this case, effective refractory period of the AV node (AVNERP) is 230 ms.
A routine EPS does not include the measurements of the functional and relative refractory period. Functional refractory period means the lower limit shortest “output” coupling interval that can be produced by any “input” interval. Relative refractory periods represent the point at which latency begins to occur. RRP means “input” interval to a tissue at which the “output” interval just begins to differ from the “input” interval.
This chapter summarized the basics of electrophysiological studies of the heart. The author sincerely hopes that the chapter may have contributed to a deeper understanding of the world of electrocardiograms.
The author declares no conflict of interest.
The Internet has irrevocably changed the dynamics of scholarly communication and publishing. Consequently, we find it necessary to indicate, unambiguously, our definition of what we consider to be a published scientific work.
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\\n\\nOther than the issue of originality, research misconduct is another major issue that all publishers have to address. IntechOpen’s Retraction & Correction Policy and various publication ethics guidelines identify both redundant publication and (self)plagiarism to fall within the definition of research misconduct, thus constituting grounds for rejection or the issue of a Retraction if the work has already been published.
\\n\\nIn order to facilitate the tracking of a manuscript’s publishing history and its development from its earliest draft to the manuscript submitted, we encourage Authors to disclose any instances of a manuscript’s prior publication, whether it be through a conference presentation, a newspaper article, a working paper publicly available in a repository or a blog post.
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\\n\\nSome basic information about the editorial treatment of different varieties of prior publication is laid out below:
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\\n\\nAll submitted manuscripts originating from a previously published conference paper must contain at least 50% of new original content to be accepted for review and considered for publication.
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\\n\\n2. NEWSPAPER & MAGAZINE ARTICLES
\\n\\nNewspaper and magazine articles usually do not pass through any extensive peer or editorial review and we do not consider them to be published in the scholarly sense. Articles appearing in newspapers and magazines rarely possess the depth and structure characteristic of scholarly articles.
\\n\\nSubmitted manuscripts stemming from a previous newspaper or magazine article will be accepted for review and considered for publication. However, Authors are strongly advised to report any such publication in an accompanying note to the External Editor.
\\n\\nAs with the conference papers and presentations, Authors should obtain any necessary permissions from the newspaper or magazine that published the work, and indicate that they have done so in a note to the External Editor.
\\n\\n3. GREY LITERATURE
\\n\\nWhite papers, working papers, technical reports and all other forms of papers which fall within the scope of the ‘Luxembourg definition’ of grey literature do not pass through any extensive peer or editorial review and we do not consider them to be published in the scholarly sense.
\\n\\nAlthough such papers are regularly made publicly available via personal websites and institutional repositories, their general purpose is to gather comments and feedback from Authors’ colleagues in order to further improve a manuscript intended for future publication.
\\n\\nWhen submitting their work, Authors are required to disclose the existence of any publicly available earlier drafts in a note to the Academic Editor. In cases where earlier drafts of the submitted version of the manuscript are publicly available, any overlap between the versions will generally not be considered an instance of self-plagiarism.
\\n\\n4. SOCIAL MEDIA, BLOG & MESSAGE BOARD POSTINGS
\\n\\nWe feel that social media, blogs and message boards are generally used with the same intention as grey literature, to formulate ideas for a manuscript and gather early feedback from like-minded researchers in order to improve a particular piece of work before submitting it for publication. Therefore, we do not consider such internet postings to be publication in the scholarly sense.
\\n\\nNevertheless, Authors are encouraged to disclose the existence of any internet postings in which they outline and describe their research or posted passages of their manuscripts in a note to the Academic Editor. Please note that we will not strictly enforce this request in the same way that we would instructions we consider to be part of our conditions of acceptance for publication. We understand that it may be difficult to keep track of all one’s internet postings in which the researcher´s current work might be mentioned.
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\\n\\nPolicy last updated: 2017-03-20
\\n"}]'},components:[{type:"htmlEditorComponent",content:'A significant number of working papers, early drafts, and similar work in progress are openly shared online between members of the scientific community. It has become common to announce one’s own research on a personal website or a blog to gather comments and suggestions from other researchers. Such works and online postings are, indeed, published in the sense that they are made publicly available. However, this does not mean that if submitted for publication by IntechOpen they are not original works. We differentiate between reviewed and non-reviewed works when determining whether a work is original and has been published in a scholarly sense or not.
\n\nThe significance of Peer Review cannot be overstated when it comes to defining, in our terms, what constitutes a published scientific work. Peer Review is widely considered to be the cornerstone of modern publishing processes and the key value-adding contribution to a scholarly manuscript that a publisher can make.
\n\nOther than the issue of originality, research misconduct is another major issue that all publishers have to address. IntechOpen’s Retraction & Correction Policy and various publication ethics guidelines identify both redundant publication and (self)plagiarism to fall within the definition of research misconduct, thus constituting grounds for rejection or the issue of a Retraction if the work has already been published.
\n\nIn order to facilitate the tracking of a manuscript’s publishing history and its development from its earliest draft to the manuscript submitted, we encourage Authors to disclose any instances of a manuscript’s prior publication, whether it be through a conference presentation, a newspaper article, a working paper publicly available in a repository or a blog post.
\n\nA note to the Academic Editor containing detailed information about a submitted manuscript’s previous public availability is the preferred means of reporting prior publication. This helps us determine if there are any earlier versions of a manuscript that should be disclosed to our readers or if any of those earlier versions should be cited and listed in a manuscript’s references.
\n\nSome basic information about the editorial treatment of different varieties of prior publication is laid out below:
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\n\nGiven that conference papers and presentations generally pass through some sort of peer or editorial review, we consider them to be published in the accepted scholarly sense, particularly if they are published as a part of conference proceedings.
\n\nAll submitted manuscripts originating from a previously published conference paper must contain at least 50% of new original content to be accepted for review and considered for publication.
\n\nAuthors are required to report any links their manuscript might have with their earlier conference papers and presentations in a note to the Academic Editor, as well as in the manuscript itself. Additionally, Authors should obtain any necessary permissions from the publisher of their conference paper if copyright transfer occurred during the publishing process. Failure to do so may prevent Us from publishing an otherwise worthy work.
\n\n2. NEWSPAPER & MAGAZINE ARTICLES
\n\nNewspaper and magazine articles usually do not pass through any extensive peer or editorial review and we do not consider them to be published in the scholarly sense. Articles appearing in newspapers and magazines rarely possess the depth and structure characteristic of scholarly articles.
\n\nSubmitted manuscripts stemming from a previous newspaper or magazine article will be accepted for review and considered for publication. However, Authors are strongly advised to report any such publication in an accompanying note to the External Editor.
\n\nAs with the conference papers and presentations, Authors should obtain any necessary permissions from the newspaper or magazine that published the work, and indicate that they have done so in a note to the External Editor.
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\n\nWhite papers, working papers, technical reports and all other forms of papers which fall within the scope of the ‘Luxembourg definition’ of grey literature do not pass through any extensive peer or editorial review and we do not consider them to be published in the scholarly sense.
\n\nAlthough such papers are regularly made publicly available via personal websites and institutional repositories, their general purpose is to gather comments and feedback from Authors’ colleagues in order to further improve a manuscript intended for future publication.
\n\nWhen submitting their work, Authors are required to disclose the existence of any publicly available earlier drafts in a note to the Academic Editor. In cases where earlier drafts of the submitted version of the manuscript are publicly available, any overlap between the versions will generally not be considered an instance of self-plagiarism.
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\n\nWe feel that social media, blogs and message boards are generally used with the same intention as grey literature, to formulate ideas for a manuscript and gather early feedback from like-minded researchers in order to improve a particular piece of work before submitting it for publication. Therefore, we do not consider such internet postings to be publication in the scholarly sense.
\n\nNevertheless, Authors are encouraged to disclose the existence of any internet postings in which they outline and describe their research or posted passages of their manuscripts in a note to the Academic Editor. Please note that we will not strictly enforce this request in the same way that we would instructions we consider to be part of our conditions of acceptance for publication. We understand that it may be difficult to keep track of all one’s internet postings in which the researcher´s current work might be mentioned.
\n\nIn cases where there is any overlap between the Author´s submitted manuscript and related internet postings, we will generally not consider it to be an instance of self-plagiarism. This also holds true for any co-Author as well.
\n\nFor more information on this policy please contact permissions@intechopen.com.
\n\nPolicy last updated: 2017-03-20
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