Atrial fibrillation ecg strip: Understanding the EKG Signal – Atrial Fibrillation: Resources for Patients

22.09.197026.07.2021 by alexxlab

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Understanding the EKG Signal – Atrial Fibrillation: Resources for Patients

By Steve S. Ryan, PhD

An electrocardiogram, ECG (EKG), is a test used to measure the rate and regularity of heartbeats, as well as the size and position of the chambers, the presence of any damage to the heart, and the effects of drugs or devices used to regulate the heart.

The ECG signal strip is a graphic tracing of the electrical activity of the heart. It measures the length of time it takes for the initial impulse to fire at the Sinus Node and then ends in the contracting of the Ventricles.

Schematic diagram of normal sinus rhythm for a human heart as seen on ECG

The first upward pulse of the EKG signal, the P wave, is formed when the atria (the two upper chambers of the heart) contract to pump blood into the ventricles. In A-Fib you will see many “fibrillation” beats instead of one P wave. A characteristic sign of A-Fib is the absence of a P wave in the EKG signal.

The next large upward spike segment, the QRS Complex, is formed when the ventricles (the two lower chambers of the heart) are contracting to pump out blood. The normal duration (interval) of the QRS complex is between 0.08 and 0.10 seconds.

The next section, the ST segment, measures the end of the contraction of the ventricles to the beginning of the rest period before the ventricles begin to contract for the next beat.

The next slight rising section, the T wave, measures the resting period of the ventricles.

These pulses are caused by the movement of positively and negatively charged ions (sodium, calcium, potassium, magnesium) through proteins called ion channel receptors. (For an excellent discussion and explanation of the science behind the movement of these chemical ions, see Restart Your Heart by Dr. Aseem Desai, p. 21.)

ECG (EKG) Strip: Atrial Fibrillation

In the case of Atrial Fibrillation, the consistent P waves are replaced by fibrillatory waves, which vary in amplitude, shape, and timing (compare the two illustrations below).

ECG recorder: special graph Paper

The output of an ECG recorder is a graph (or sometimes several graphs, representing each of the leads) with time represented on the x-axis and voltage represented on the y-axis. A dedicated ECG machine would usually print onto graph paper which has a background pattern of 1mm squares (often in red or green), with bold divisions every 5 mm in both vertical and horizontal directions.

Diagram of electrocardiogram paper. Click for Video: Cardiac Conduction System

Interpreting a ECG strip involves counting the squares of the tracing. For example, by counting the squares of a heart in Normal Sinus Rhythm, you can calculate the heart rate.

Video: Cardiac Conduction System and its Relationship with ECG‬

Animation with narration about the heart’s conduction system. Schematic diagram and explanation of normal sinus rhythm for a human heart as seen on ECG (3:34 min.) Click on image to go to the video page.

Resources & Photo Credits for this article

• Schematic diagram of normal sinus rhythm for a human heart as seen on ECG (with English labels). Wikimedia Common, Public Domain. Last accessed April 13, 2014, URL: http://commons.wikimedia. org/wiki/File%3ASinusRhythmLabels.svg

• Diagram of electrocardiogram paper. Public Doman. Wikipedia.org. Last accessed April 13, 2014, URL: http://en.wikipedia.org/wiki/File:ECG_Paper_v2.svg

Updated August 2020

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Validation of an algorithm to reveal the U wave in atrial fibrillation

ECG databases

Two ECG databases were used in this work according the requirements of the sub-studies as described below. The study was approved by the University of Hull and Northumberland Local Research Ethics committees and all methods were performed in accordance with the relevant guidelines and regulations.

Validation study

The database comprised recordings from 25 patients for which both AF and SR recordings in the same patient were available. Fourteen suitable recordings were available from the PAF Prediction Challenge database from PhysioNet²³. A further 11 historical recordings from routinely collected ECG during electrophysiological studies at Castle Hill Hospital were used. The requirement for individual patient consent was waived as the study did not impact clinical care and all data were anonymised. Recording duration for AF or SR was a minimum of 4 minutes and recordings had sampling rate of either 128 Hz (PhysioNet) or 1953Hz. The PhysioNet recordings comprised two unspecified leads²³ whereas the others had standard 12-lead ECG. As the lead with the most prominent U wave⁸ lead V4, or if V4 was not available (i. e. PhysioNet recordings) the lead with the most prominent U wave, was analysed.

Number of beats study

The requirement for this database was the availability of long duration AF recordings to ensure a large number of ventricular beats to be used in the beat averaging algorithm. For this purpose, an existing database of 15 minute, 12-lead ECG recordings from 10 AF patients was used. Patients gave informed consent for these recordings. It is the same database used in our preliminary study⁸. The sampling rate was 500 Hz and lead V4 was analysed in this study.

U wave extraction algorithm

AF recordings

U waves were extracted using a beat averaging algorithm. The average beat was formed using only beats with similar preceding RR interval. Careful selection of qualifying beats with respect to preceding RR interval and their alignment ensured optimum U wave extraction and minimised the effects of heart rate dependency of U wave timing and amplitude. The ECG processing workflow is illustrated in Fig. 6 and comprises (i) R wave detection, (ii) RR histogram, (iii) selection of qualifying beats and (iv) calculation of the average beat and identification of the U wave.

Figure 6

Signal processing workflow to extract U waves from AF recordings. R wave peaks () were detected in the ECG lead (a) from which the RR histogram (bin size RR_bin = 100 ms) was created (b). Beats meeting the selection criteria (RR_i−1 = RR_mode ± 50 ms and RR_i > RR_min) were extracted from the ECG lead and aligned to the R peak (R_i) (c). The average beat (d) was calculated from the collection of beats over the interval corresponding to the grey area in (c) revealing the U wave.

R wave peaks (R_i) were detected automatically and confirmed by visual inspection (Fig. 6a). If present, ectopic beats and their adjacent intervals were removed. RR intervals were calculated (RR_i−1 = R_i − R_i−1). The RR histogram with bin size (RR_bin) of 100 ms was constructed so that the number of beats (N_beats) at specific RR intervals could be identified (Fig. 6b). To ensure the average beat was generated using the maximum number of beats with similar RR intervals, only beats falling within the bin with the most number of beats were selected (Fig. 6c). In other words, qualifying beats had RR_i−1 = RR_mode ± 50 ms, where RR_mode was the histogram bin with most number of beats. A further requirement was to exclude beats with short following RR intervals (RR_i) that would otherwise contaminate the averaged U wave, therefore beats with RR_i less than a threshold (RR_min) of 650 ms were excluded. All qualifying beats were aligned to their R wave peak (R_i) (Fig. 6c), and the average beat in each lead was calculated as the mean amplitude across the beats (Fig. 6d). The presence of a U wave was identified from the average beat (Fig. 6d). It is important to note that it is the preceding RR interval (RR_i-1) which is important to consider rather than the RR interval containing the U wave (RR_i) since our preparatory work indicated that the preceding RR interval is the major determinant of U wave amplitude.

SR recordings

With good quality SR recordings, the U wave can be readily seen without significant processing. However most clinical recordings present some noise and by applying the same beat averaging algorithm as for the AF recordings the resulting noise reduction allows for optimal presentation of U waves. Hence SR recordings were processed by the same algorithm used for the AF recordings. However, in SR at fast heart rates the P wave can impinge on the U wave so it was necessary to extend the RR_min interval to ensure that any following P waves would not contaminate the beat averaged U wave.

Data analysis

Validation study

For each patient the presence or absence of U waves in the average beat was assessed visually and independently by two observers (MSA, PL). A positive validation outcome was defined as the presence of U waves of same polarity and morphology in both SR and AF recordings from the same patient, otherwise a negative validation outcome was recorded. Validation outcomes were recorded in a contingency table and statistical significance of agreement between U wave presence in AF and SR assessed by McNemar’s test. U wave amplitude from baseline to U peak was measured automatically but confirmed visually. Stable baseline amplitude was estimated from a 10-sample window in the electrically quiescent period before the onset of the QRS complex in AF recordings and before the onset of the P wave in SR recordings. Significance of differences in amplitude between SR and AF recordings was assessed by paired t-test.

Number of beats study

To determine the effect of the number of beats (N_beats) on the quality of extracted U waves in AF recordings, the algorithm was systematically iterated with diminishing number of beats used for beat averaging at each iteration. Trials were conducted where the number of beats was systematically reduced from 100 beats (reference) in steps of 10 down to 10 beats (i.e. N_beats = {100, 90, 80, 70, 60, 50, 40, 30, 20, 10}).

Rather than discard some beats for trials where N_beats was less than 100, multiple sub-trials were conducted so that all 100 beats were analyzed across all the sub-trials. This was achieved by dividing the 100 beats into contiguous groups of 10 beats. For each N_beats trial, 10 sub-trials were conducted, systematically including the appropriate number of groups of 10 beats so that over the 10 trials all the beats were used. See the example in Figure A1 (supplementary document).

Noise reduction and hence U wave quality was quantified by U wave amplitude since U waves contaminated by noise have larger amplitude than clean U waves. Amplitude measurement was as described for the validation study. Differences between U wave amplitude for each N_beats trial and reference U wave (N_beats = 100 beats) were calculated as ΔU amp = U amp (N_beats) − U amp (N_beats = 100)) and statistical differences with respect to zero amplitude difference assessed by within subjects ANOVA and post-hoc t-test. All tests were two-sided and p-values less than 0.05 considered statistically significant.

Heart Rhythm Monitor with Instant Atrial Fibrillation Detection

“It is the right kind of solution for patients, because it’s a lifetime solution and Afib is a lifetime condition. I’m very impressed by the device.”

Dr. Hugh Calkins, MD, Director, Cardiac Arrhythmia Service, Professor of Medicine

Physician

“I wish I had had it years ago, so I wouldn’t have visited the ER so often…”

Frank (patient)

Patient

“The algorithm for detecting atrial fibrillation is extremely accurate. Another benefit to me has been the quality
of the strips recorded compared to other single lead heart rhythm monitors. These high quality recordings are
useful in identifying and monitoring other conditions as well as afib recurrence. ”

Robert Baker, MD, FACC, Nevada Cardiology Associates

Physician

“I have had the monitor for several years and have to tell you that this unit has saved my wife and I many days of anxiety and stress in knowing that I was not in Afib…”

Sherman (patient)

Patient

“The AfibAlert is beneficial in the clinical research arena to monitor for recurrence of atrial fibrillation after ablation.
The quality of the ECGs it captures is excellent. In addition, patients find it extremely easy to use which yields high
compliance”

John N. Catanzaro, MD, Assistant Professor of Medicine, University of Florida Health – Jacksonville

Physician

“I’ve had my AfibAlert for about nine months (Afib, for four years). It is easy to use and has taught me a lot about my particular Afib patterns. My meds were keeping my heart rate down most of the time and so I thought I wasn’t fibrillating unless I had one of the big, obvious episodes; the monitor taught me that I was fibrillating quite often at low heart rates, too. I’m not sure I would ever have figured this out by myself. I only wish I had discovered AfibAlert a year or two earlier.”

Mary (patient)

Patient

Atrial fibrillation | ACLS-Algorithms.com

The most common cardiac arrhythmia, atrial fibrillation, occurs when the normal electrical impulses that are generated by the SA node are overwhelmed by disorganized electrical impulses in the atria.

These disorganized impulses cause the muscles of the upper chambers of the heart to quiver (fibrillate) and this leads to the conduction of irregular impulses to the ventricles.

For ACLS, atrial fibrillation becomes a problem when the fibrillation produces a rapid heart rate which reduces cardiac output and causes symptoms or an unstable condition.

When atrial fibrillation occurs with a (RVR) rapid ventricular rate (rate > 100 beats/min), this is called a tachyarrhythmia. This tachyarrhythmia may or may not produce symptoms. Significant symptoms that occur are due to a reduction in cardiac output.

The following is a list of the most common symptoms.

palpitations or chest discomfort
shortness of air and possibly respiratory distress
hypotension, light-headedness and possibly loss of consciousness
peripheral edema, jugular vein distention, and possibly pulmonary edema

For the purpose of ACLS, it is important to be able to recognize atrial fibrillation when the patient is symptomatic. On an ECG monitor, there are two major characteristics that will help you identify atrial fibrillation.

No p-waves before the QRS on the ECG. This is because there are no coordinated atrial contractions.
The heart rate will be irregular. Irregular impulses that the ventricles are receiving cause the irregular heart rate.

When the heart rate is extremely rapid, it may be difficult to determine if the rate is irregular, and the absence of p-waves will be the best indicator of atrial fibrillation.

ACLS Treatments:

For the purposes of ACLS atrial fibrillation is treated when the arrhythmia/tachyarrhythmia produces hemodynamic instability and serious signs and symptoms.

For the patient with unstable tachycardia due to a tachyarrhythmia, immediate cardioversion is recommended. Drugs are not used to manage unstable tachycardia. The appropriate voltage for cardioverting unstable atrial fibrillation is 120-200 J.

Cardioversion of stable atrial fibrillation should be performed with caution if the arrhythmia is more than 48 hours old and no anticoagulant therapy has been initiated due to the risk of emboli that can cause MI and stroke.

Below is a short video which will help you quickly identify atrial fibrillation on a monitor.
Please allow several seconds for the video to load. (5.11 mb)

Click for next Rhythm Review: Other Tachycardias

Optimizing Heart Rate and Controlling Symptoms in Atrial Fibrillation

Abstract

Atrial fibrillation (AF) is the most common arrhythmia noted in clinical practice and its incidence and prevalence are on the rise. The single most important intervention is the evaluation and treatment of stroke risk. Once the risk for stroke has been minimized, controlling the ventricular rate and treating symptoms become relevant. In this review article, we emphasize the importance of confirming and treating the appropriate arrhythmia and correlating symptoms with rhythm changes. Furthermore, we evaluate some of the risk factors for AF that independently result in symptoms, underlining the need to treat these risk factors as part of symptom control. We then discuss existing and novel approaches to rate control in AF and briefly cover rhythm control methods.

Disclosure: The authors have no conflicts of interest to declare.

Received: 06 January 2016

Accepted: 03 February 2016

Citation:US Cardiology Review 2016;10(1):26–9

Correspondence: KL Venkatachalam, Department of Cardiology, Mayo Clinic Florida, 4500 San Pablo Road, Davis 7, Jacksonville, FL 32224, USA. E: [email protected]

Open access:

The copyright in this work belongs to Radcliffe Medical Media. Only articles clearly marked with the CC BY-NC logo are published with the Creative Commons by Attribution Licence. The CC BY-NC option was not available for Radcliffe journals before 1 January 2019. Articles marked ‘Open Access’ but not marked ‘CC BY-NC’ are made freely accessible at the time of publication but are subject to standard copyright law regarding reproduction and distribution. Permission is required for reuse of this content.

Atrial fibrillation (AF) is the most common pathologic clinical arrhythmia lasting more than 30 seconds, and its incidence and prevalence continue to increase. It has been estimated that 5.9 % of patients aged >65 years suffer from AF.¹ In the Rotterdam study, 17. 8 % of patients over 85 had AF.² The lifetime risk for developing AF in both men and women above age 40 is one in four.³ This arrhythmia, with its attendant comorbidities, poses a substantial physical, psychologic, and financial burden on the populace and is a significant public health concern. Evaluating and managing AF appropriately at the primary care level (by minimizing risk factors) and recognizing and treating the arrhythmia immediately will play important roles in containing this epidemic. This review article addresses the recognition of AF and the importance of distinguishing it from other arrhythmias with an irregular pulse. It discusses the available options for stroke reduction and examines the correlation between symptoms and rhythms. It then reviews existing and potentially novel approaches to rate and rhythm control and their role in controlling symptoms in patients with AF.

Types of Atrial Fibrillation

The type of AF determines treatment, and we will use the definitions from the most recent American Heart Association/American College of Cardiology/Heart Rhythm Society (AHA/ACC/HRS) guidelines on AF from 2014. ⁴ Paroxysmal AF (PAF) terminates spontaneously or with intervention within 7 days of onset. Persistent AF lasts >7 days and often requires pharmacologic or electrical cardioversion. Long-standing persistent AF lasts >12 months. This is an important change to the definition since cardioversion and ablation success rates diminish substantially in patients with long-standing persistent AF. Permanent AF describes the situation where the patient and physician have decided to stop pursuing a rhythm control strategy.

Confirming the Arrhythmia

The most common clue for suspecting that a patient may be in AF is the irregularity of the pulse. As medical students, we are all taught to associate an “irregularly irregular” pulse with AF. However, there are several arrhythmias that can produce irregularly irregular pulses and a few that produce regularly irregular pulses, which can also feel irregularly irregular if they have not been assessed for an adequate period of time. Irregularly irregular pulses are present in AF, atrial flutter with variable atrioventricular (AV) conduction, wandering atrial pacemaker, multifocal atrial tachycardia, and frequent premature atrial and ventricular complexes. Regularly irregular pulses may be noted in patients with sinoatrial exit block as well as second degree AV block. If the pulse is not monitored for an adequate interval the pattern of irregularity may not be perceived, and a wrong conclusion may be drawn.

An electrical rhythm strip is still the only reliable way to identify these arrhythmias. Patients now have access to home blood pressure (BP) monitors, pulse oximeters, and single lead rhythm monitors, which indicate the presence of irregularity.^5,6 This does not constitute proof of AF. Even computer-based ECG diagnostics frequently get the above arrhythmias confused, and simply reading the verbal report of an ECG without looking at the rhythm strips for oneself will result in an erroneous diagnosis (see Figure 1). Implanted pacemaker and defibrillator diagnostics can also confuse supraventricular tachycardia with AF or atrial flutter and simply using the presence of atrial high rate (AHR) episodes from a pacemaker check as proof of AF is not appropriate. The stored electrograms need to be evaluated to confirm the arrhythmia before treatment can be suggested.

Based on present knowledge, only AF and atrial flutter pose a significant stroke risk and require risk-factor-based anticoagulation. Also, the treatment for typical atrial flutter (counterclockwise isthmus dependent flutter) is significantly different from the treatment of AF since typical atrial flutter can be ablated relatively easily with excellent success rates (90 %). The clinician is obliged to offer patients the appropriate treatment choices based on risk and efficacy, and identifying the correct arrhythmia is the first step.

Evaluating and Treating Stroke Risk

Once AF has been confirmed, estimating a patient’s stroke risk in AF is paramount, as an embolic stroke due to inadequately treated AF is the surest way to negatively impact quality of life (QoL) in these patients. Several algorithms have been developed over the past 25 years and the CHA2DS2-VaSc scoring system has been most recently validated.^7–9 With nonvalvular AF and a CHA2DS2-VASc score of 0 (i.e., aged <65 years with lone AF), both the US and European guidelines agree that it is reasonable to omit antithrombotic therapy. However, the two guidelines differ in their recommendations for patients with a CHA2DS2-VaSc score of 1. The US guidelines allow for antiplatelet therapy, anticoagulation, or neither, based upon an assessment of the risk for bleeding complications and patient preferences; whereas the European guidelines recommend anticoagulation as the only option. Both guidelines agree that at a CHA2DS2-VaSc score of ≥2 anticoagulation should be instituted.^4,10 Warfarin, dabigatran, rivaroxaban, apixaban, and edoxaban have been approved for this use. Patients who are intolerant, or have a contraindication, to the use of anticoagulants would be candidates for a left atrial appendage occlusion, whose efficacy has been validated recently. ¹¹

Symptoms Related to Atrial Fibrillation

Patients may present with a variety of symptoms related to AF. The most common symptoms include palpitations, dyspnea, and fatigue. Additionally, chest pain, lightheadedness, presyncope, and syncope may be also reported. More than half of patients with AF experience a decrease in exercise tolerance defined by lowered New York Heart Association functional class. In addition to simple awareness of having an irregular rhythm, there are multiple potential mechanisms for these symptoms, including loss of atrial contraction, loss of AV synchrony, bradycardia, tachycardia, or even tachycardia-mediated cardiomyopathy. Understanding the type of symptom and the mechanism behind it are important steps in determining the optimal treatment strategy for patients with AF.

Figure 1: Electrocardiogram Rhythm Strips Showing a) Atrial Fibrillation; b) Atrial Flutter with Variable Atrioventricular Block; c) Multifocal Atrial Tachycardia; and d) Sinus Rhythm with Frequent Premature Atrial Complexes

Figure 2: An Example of the Lack of Symptom–Arrhythmia Correlation on Event Monitoring

Correlating Symptoms with Rhythm

While patients may present with a variety of symptoms in AF, these may also be noted in a host of other conditions including pulmonary disease, poorly controlled hypertension (or due to the BP medications themselves), obstructive sleep apnea, obesity, or deconditioning. ^12–14 Therefore, it is important to confirm that the patient’s symptoms are, in fact, related to AF before beginning treatment. This is typically achieved with prolonged rhythm monitoring, ranging from 1 to 30 days depending on the frequency of symptoms. This approach can identify symptomatic bradycardia, prolonged pauses, tachycardia, or simply awareness of conversion into or out of AF. However, it is important to correlate the patient’s symptoms temporally with an episode of AF, as noted in Figure 2. Having episodes of paroxysmal AF on a particular day should not result in symptoms on another day, and concluding that AF produced these symptoms will result in needless testing and therapy. Additionally, an exercise electrogram can be utilized to identify poor rate control or chronotropic incompetence as potential causes for dyspnea on exertion or exercise intolerance. Once the AF and symptoms have been correlated, appropriate therapy can be instituted.¹⁵ Anxiety in the presence of palpitations is common; allaying a patient’s fears regarding the arrhythmia and using a systematic approach to treating the risk factors and controlling AF will go a long way toward improving QoL in these patients. ¹⁶

Figure 3: Rate Control Recommendations from the 2014 American Heart Association/American College of Cardiology/ Heart Rhythm Society Guideline for Atrial Fibrillation Management

Figure 4: Drug Selection for Rhythm Control in Atrial Fibrillation from the 2014 American Heart Association/American College of Cardiology/Heart Rhythm Society guideline for Atrial Fibrillation Management.

Lifestyle Modification

In addition to considering pharmacologic or procedural treatment options for AF management, it is important to address modifiable risk factors. Obesity, obstructive sleep apnea, hypertension, type 2 diabetes, and alcohol consumption have all been identified as independent risk factors for the development of AF. Properly evaluating and treating these risk factors may help minimize episodes of AF and also tackle the symptoms.^17–21 Caffeine intake has also often been discouraged for patients with AF. However multiple studies have demonstrated no association between caffeine exposure and risk for AF, and there is even evidence to suggest that caffeine consumption in moderate amounts may actually decrease the occurrence of AF.²² Finally, exercise can improve symptoms throughout the spectrum of AF. In fact, multiple studies have demonstrated that exercise training in adults with permanent AF significantly improves rate control (at rest and with exertion), functional capacity, muscle strength, activities of daily living, and QoL.²³

Approaches to Rate Control in Atrial Fibrillation

Controlling heart rate (ventricular response) is a well-established approach to treating patients with minimally symptomatic AF. Beta blockers, calcium channel blockers, and digitalis (see Figure 3) are commonly used to accomplish this goal. ^24,25 The Atrial Fibrillation Follow- up Investigation of Rhythm Management (AFFIRM) trial used 80 beats/ min as a reasonable resting heart rate in AF. More recently, the Rate Control Efficacy in Permanent Atrial Fibrillation II (RACE-II) trial compared strict versus lenient rate control and demonstrated that a lenient rate control strategy does not increase morbidity. The criticism levelled against this study is that most patients in the control and treatment groups had heart rates below 90 beats/min and the results were really based on an intention-to-treat analysis.^26,27

In active individuals, digitalis is not as helpful for rate control since sympathetic drive during activity can overwhelm the vagotonic action of digitalis. However, it can be useful in conjunction with a beta blocker or calcium channel blocker since it can control ventricular rate without reducing BP. Anti-arrhythmic drugs (AADs), even if they fail to maintain sinus rhythm, can provide rate control without lowering BP. Amiodarone has strong AV nodal blocking activity and may be effective in this application. There is mounting evidence that the hyperpolarization- activated cyclic nucleotide-gated (HCN) channels, responsible for funny current (If) modulation, are also present in the AV node and could be targeted to achieve rate control. The prototypical drug to modulate If in the sinus node is ivabradine.²⁸ Recent case reports highlight the rate- controlling effect of ivabradine in AF through its additional action on the AV node, and this may turn out to be a very useful drug for this purpose, though presently this would be an off-label use of this medication.^29–31

The extreme approach in the continuum of rate control is AV node ablation, with pacemaker implantation. This technique has fallen out of favor over the past 20 years due to the rapid incorporation of AF ablation into clinical practice. Nevertheless, AV node ablation with pacemaker implantation remains a very effective technique to control symptoms and improve QoL, particularly in the elderly population, often intolerant of rate-controlling medications. ^32–33

Managing Rhythm Control in Atrial Fibrillation

In patients who are symptomatic from AF, despite good control of heart rate, a rhythm-control strategy should be implemented. Success at maintaining sinus rhythm long-term is highest with good control of underlying risk factors (hypertension, sleep apnea, and obesity). Cardioversion as a means of establishing that AF is responsible for symptoms is a very reasonable first step, even if the long-term success of this approach is only 30–35 %. Once the symptom-rhythm correlation has been established and risk factors have been controlled, AADs may be attempted. The 2014 ACC/AHA/HRS AF guidelines provide a systematic approach to trying AADs (see Figure 4), based on the patient’s co-morbidities.⁴ Ranolazine in conjunction with dronedarone or ivabradine may also play an important role in effective rate control of AF.^30,34 Intolerance of AADs or breakthrough AF while on AADs should prompt consideration of an invasive approach. The specific technique (radiofrequency ablation, cryoablation, focal impulse and rotor modulation, laser ablation, or a surgical maze procedure in patients undergoing cardiac surgery) is not as important as the decision to attempt the intervention, and the risks and benefits of this approach need to be discussed with patients in detail. The success rate for all ablative methods for paroxysmal AF has been reported between 66–89 % at 1 year. In long-standing persistent AF, multiple ablation procedures may often be required.^35,36

Conclusion

AF should be considered a chronic condition, and like other chronic conditions, such as hypertension and diabetes, should be treated with risk factor control and symptom management. Since the morbidity associated with this condition and with the available treatment options is considerable, exhaustive attempts to confirm the diagnosis of AF must be made early. Symptom-rhythm correlation is an important part of this evaluation. Advances in heart rate control, rhythm management, and stroke prevention over the next decade will aid in reducing the burden of AF.

EKG Interpretive skills

Print version of Knowledge bytes used in this lesson.

Close the window to return to the lesson after printing.

The rate of paper (i.e. of recording of the EKG) is 25 mV/s
which results in:

1 mm = 0.04 sec (or each individual block)

5 mm = 0.2 sec (or between 2 dark vertical lines)

Distance between Tick marks = 3 seconds (in the rhythm strip)

The voltage recorded from the leads is also standardized on the
paper where 1 mm = 1 mV (or between each individual block vertically) This results in:

1 mm = 0. 1 mV

5 mm = 0.5 mV (or between 2 dark horizontal lines)

10 mm = 1.0 mV

Heart rate calculation:

Normal range at rest is between 60-100 beats per minute (bpm).

The basic way to calculate the rate is quite simple. You take
the duration between two identical points of consecutive EKG waveforms such as the R-R
duration. Take this duration and divide it into 60. The resulting equation would be:

Rate = 60/(R-R interval)

A quicker way to obtain an approximate rate is

to go by RR or PP interval. If it is 1 big box (0.2 secs) then the rate is
60/0.2 = 300 bpm. The rest of the sequence would be as follows.

1 big box = 300 beats/min (duration = 0.2 sec)

2 big boxes = 150 beats/min (duration = 0.4 sec)

3 big boxes = 100 beats/min (duration = 0.6 sec)

4 big boxes = 75 beats/min (duration = 0.8 sec)

5 big boxes = 60 beats/min (duration = 1.0 sec)

Count the number of RR intervals between two Tick marks (6 seconds) in the rhythm
strip and multiply by 10 to get the bpm. This method is more effective when the rhythm is
irregular.

Rhythm can be quite variable. It could be

Regular : RR interval constant

Basically regular
- Premature ectopic beat
- Escape ectopic beat

Regularly irregular : RR interval variable but with a pattern. Normal and ectopic
beats grouped together and repeating over and over.

Irregularly irregular. RR interval variable with no pattern, totally irregular

Normal:

Normal sinus rhythm (NSR): indicates that the rate is between 60 and 100,
inclusive, and that the P waves are identifiable and are of the same morphology
throughout. The RR interval or PP intervals between beats are same.

Sinus arrhythmia: There is a cyclical acceleration of
heart rate with inspiration and slowing with expiration. The beat to beat interval
is slightly different.The rhythm is regularly irregular, in the sense that there is a
pattern to irregularity. This is termed sinus arrhythmia.

P wave

Represents discharge of SA node and depolarization of both atria

Normal:

The best lead to look at the P wave is V1.

Normal P wave is upright and rounded

The P wave in general should not be more than 1 box wide

The P wave in general should not be more than 1 box tall.

The p wave is biphasic in

The P wave contour is constant

Abnormal:

If P wave exceeds the normal range for duration or voltage,
it generally means that either or both atria is enlarged (hypertrophied)

If P wave contour
Peaking of P wave (Voltage increase) suggests Right atrial hypertrophy

Broad slurred (increased duration) suggests Left atrial hypertrophy

When biphasic the initial positive wave is prominent with RA hypertrophy and the
negative deflection is prominent wit LA hypertrophy

If the P wave contour changes between beats it could mean that there is an
ectopic atrial focus

QRS

QRS complex is a series of wave forms following P wave.

Naming convention:

Q wave: first downstroke of the QRS complex. Usually very small
or absent.

R wave: first upward deflection of the QRS complex. Upward
deflections occurring after an S wave are noted by a “prime mark” such as R’

S wave: the first downward deflection occurring after the R
wave.

A monophasic negative QRS complex is called QS.

Normal

Duration: 0.08-0.12 seconds (2-3 horizontal boxes)

Contour is same between beats

Abnormal

Duration:

Delay in conduction through the ventricles leads to prolongation of QRS complex

Prolonged: Bundle branch blocks, drug toxicity, electrolyte
imbalance

Shortened: WPW

Contour

Change of contour between beats suggests ectopic foci

Abnormal but constant contour suggests

Bundle branch blocks

Drug toxicity

Electrolyte imbalance

Q wave

Normal:

Usually very small or absent

Normal in III and AVR .

Abnormal:

A Q wave is significant if it is greater than 1 box wide (0.04
secs) in leads other than III and AVR

Greater than 1/3 the amplitude of the QRS complex.

Greater than 1/4th of R wave

Abnormal Q waves: indicate presence of infarct

T wave

First upward deflection after QRS complex. Represents: ventricular
repolarization

Normal:

In general, T waves are in the same direction as the largest
deflection of the QRS (normally the R wave).

Negative in AVR

Inverted T waves in precordial leads V1, V2, V3 can be seen in
normal, young athletes

Low T voltage changes may occur in the absence of any heart disease
at all.

Abnormal:

T wave changes can be primary or secondary.

Primary T wave change refer to abnormal repolarization

Secondary T wave changes are caused by QRS changes. T
wave changes caused by bundle branch block or ventricular hypertrophy are secondary.

Tall peaked T waves

Electrolyte imbalance = Hyperkalemia causes tall
peaked T waves. overall maximum of 15 mV but this is not sensitive. T
wave looks like an isosceles triangle.

Low voltage T waves

Hypokalemia causes low voltage T waves and
prominent U waves. T waves less than 1mV in the limb leads and less than 2mV in the
precordial leads.

low T voltage and sagging or flattened ST
segments. these changes may occur in the absence of any heart disease at all.

Inverted T waves

Inverted T waves that are symmetrical,
“round-shouldered” can be caused by coronary ischemia. especially when it occurs
in a pattern as previously described for ST segment changes. .

Inverted T waves in precordial leads V1, V2, V3 can be seen in
normal, young athletes, as well as CNS diseases.

U wave

What it represents is not certain.

This upright wave, when present, follows the T wave.

Abnormal:

The presence of U waves may indicate Hypokalemia.

Hypokalemia is associated with flat T waves, U waves. U waves taller than T
waves.

PR interval

Represents: atria to ventricular conduction time (through His bundle) It
includes P wave and PR segment.

Normal duration: 0.12-2.0 seconds (3-5 horizontal boxes). This
is measured from the onset of the P wave to the onset of the QRS complex regardless if the
initial wave is a Q or R wave.

Abnormal duration:

Prolonged:

If the PR interval is greater than 0.2 sec, then an AV block is present. There are several
types of AV blocks:

1st degree AV Block: PR>0.20 sec.

2nd degree AV Block: 2 types:
Type I (Mobitz I or Wenckeback): increasing PR interval until a QRS complex is
dropped. It is usually benign.

Type 2 (Mobitz II): QRS dropped without any progressive increase in PR interval
(i. e., PR interval is constant but still >0.20 sec).

3rd degree AV Block: atria and ventricles are electrically
dissociated. Therefore, P waves and QRS complexes will occur independent of each other. As
always, use the QRS complexes to determine heart rate.

Shortened:

A PR interval that is <0.12 sec when associated with prolonged QRS should
prompt evaluation for Wolff-Parkinson syndrome (WPW).

ST segment

Represents early phase of repolarization of ventricles.

Begins at the end of S wave and ends at the beginning of T wave.

In normal situations, it serves as the isoelectric line from which to measure
the amplitudes of the other waveforms.

ST segments are usually isoelectric and normal.

When examining the ST segment, evaluate elevations or depressions
0.06 seconds after the J point (since the ST segment can at times be sloping).

Abnormal:

This segment is important in identifying pathology such as
myocardial infarctions (elevations) and Ischemia (depressions).

ST segment elevation

In general, an ST segment elevation indicates infarction.

ST segment elevation is a current of injury – can be seen in pericarditis
as well as Prinzmetal’s angina.

Early repolarization causes ST segment elevation in the lead of normal EKG’s.

The location of the ST elevations on the EKG can help to
identify a location of the infarct:
Anterior Wall Infarct (corresponding to Left Anterior Descending Artery): V1, V2

Lateral Wall Infarct (Circumflex Artery): V3, V4

Inferior Wall Infarct (can be combination of Circumflex or Right Coronary
Artery): V5, V6, I, avl

when in all leads suggests Pericarditis

ST segment depression

In general, an ST segment depression indicates Ischemia

ST segment depression can be Ischemia as in exercise EKG’s or
subendocardial injury current.

Digitalis causes ST segment sagging and shortens the Q-T interval.

QT and QTc (corrected QT) interval

QT represents the duration of activation and recovery of the ventricular muscle.

This duration varies inversely with the heart rate

Since the duration of QT varies inversely with the heart rate, the QT is not
used, but rather the corrected QT is.

QTc interval

QTc = QT + 1.75 (ventricular rate – 60)

Normal:

The normal QTc is approximately 0.41 seconds. It tends to be slightly longer for
females and increases slightly with age.

Abnormal:

Prolonged QT

Quinidine Toxicity

Hypocalcemia

Shortened QT
May be shortened in hypocalcemia.

Machine learning detection of Atrial Fibrillation using wearable technology

Abstract

Background

Atrial Fibrillation is the most common arrhythmia worldwide with a global age adjusted prevalence of 0.5% in 2010. Anticoagulation treatment using warfarin or direct oral anticoagulants is effective in reducing the risk of AF-related stroke by approximately two-thirds and can provide a 10% reduction in overall mortality. There has been increased interest in detecting AF due to its increased incidence and the possibility to prevent AF-related strokes. Inexpensive consumer devices which measure the ECG may have the potential to accurately detect AF but do not generally incorporate diagnostic algorithms. Machine learning algorithms have the potential to improve patient outcomes particularly where diagnoses are made from large volumes or complex patterns of data such as in AF.

Methods

We designed a novel AF detection algorithm using a de-correlated Lorenz plot of 60 consecutive RR intervals. In order to reduce the volume of data, the resulting images were compressed using a wavelet transformation (JPEG200 algorithm) and the compressed images were used as input data to a Support Vector Machine (SVM) classifier. We used the Massachusetts Institute of Technology (MIT)—Beth Israel Hospital (BIH) Atrial Fibrillation database and the MIT-BIH Arrhythmia database as training data and verified the algorithm performance using RR intervals collected using an inexpensive consumer heart rate monitor device (Polar-H7) in a case-control study.

Results

The SVM algorithm yielded excellent discrimination in the training data with a sensitivity of 99.2% and a specificity of 99.5% for AF. In the validation data, the SVM algorithm correctly identified AF in 79/79 cases; sensitivity 100% (95% CI 95.4%-100%) and non-AF in 328/336 cases; specificity 97.6% (95% CI 95.4%-99.0%).

Conclusions

An inexpensive wearable heart rate monitor and machine learning algorithm can be used to detect AF with very high accuracy and has the capability to transmit ECG data which could be used to confirm AF. It could potentially be used for intermittent screening or continuously for prolonged periods to detect paroxysmal AF. Further work could lead to cost-effective and accurate estimation of AF burden and improved risk stratification in AF.

Citation: Lown M, Brown M, Brown C, Yue AM, Shah BN, Corbett SJ, et al. (2020) Machine learning detection of Atrial Fibrillation using wearable technology. PLoS ONE 15(1):
e0227401.

https://doi.org/10.1371/journal.pone.0227401

Editor: Elena G. Tolkacheva, University of Minnesota, UNITED STATES

Received: March 25, 2019; Accepted: December 4, 2019; Published: January 24, 2020

Copyright: © 2020 Lown et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Data Availability: All relevant data has been included in the paper and the Supporting Information files.

Funding: Funded by NIHR (NIHR SPCR) FR 11: Project No:318 https://www.spcr.nihr.ac.uk/projects/screening-for-atrial-fibrillation-using-economical-and-accurate-technology-safety-2013-a-pilot-study The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The funder provided support in the form of salaries for authors ML, but did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. The specific roles of these authors are articulated in the ‘author contributions’ section.” MB is affiliated with Leonardo MW Ltd. but did not receive any funding from any organisation for this work.

Competing interests: MB is affiliated with Leonardo MW Ltd but did not receive any funding from any organisation for this work. This does not alter our adherence to PLOS ONE policies on sharing data and materials.

Introduction

Atrial Fibrillation is the most common arrhythmia worldwide with a global age adjusted prevalence of 0.5% in 2010.[1] Numerous studies have reported a growing epidemic of AF with an expected doubling of its prevalence by 2030.[1]AF is linked with up to 1/3 of all strokes and as a significant proportion is asymptomatic it can often go undiagnosed. [2] There has been increased interest in detecting AF due to its increased incidence and the possibility to prevent AF-related strokes.[3] Anticoagulation treatment using warfarin or direct oral anticoagulants is effective in reducing the risk of AF-related stroke by approximately two-thirds and can provide a 10% reduction in overall mortality.[4] Screening for AF has been the subject of much recent debate by expert committees.[3]

There has been recent interest in the use of consumer devices for the detection of arrhythmias including AF.[5,6] Wrist-worn heart-rate sensors that measure heart rate using Light Emitting Diodes (LEDs) have become increasingly popular but their accuracy has been questioned and some manufacturers advise the heart rate measurement should be considered an estimate and suggest using a chest heart rate sensor for increased accuracy.[7] LED based wrist sensors have been shown to underestimate heart-rate during AF and thus may be less accurate for detecting AF. [8] Because ECG confirmation is mandated by guidelines for the diagnosis of AF, devices which sense an ECG signal may have the advantage of providing a verifiable ECG trace and would therefore be a preferred screening tool.[9] Although consumer chest heart rate sensors may be less comfortable than wrist based sensors, they are inherently designed to be compact, lightweight, unobtrusive, have long battery lives and should be accurate when used in sub-optimal settings such as during exercise. Consumer devices are now available which transmit ECG data in addition to heart rate enabling accurate AF detection by a cardiologist and automated algorithms.[10]

Consumer devices do not generally have algorithms incorporated for the detection of AF. In terms of diagnostic algorithms, machine learning has the potential to improve patient outcomes particularly where diagnoses are made from large volumes or complex patterns of data. Recently, machine learning algorithms have been developed to detect diabetic retinopathy with high accuracy[11] and to detect breast cancer metastases with a higher accuracy than pathologists. [12] In this research we aimed to investigate if an inexpensive consumer chest heart rate monitor device could be used along with a highly discriminative machine learning algorithm to accurately detect AF.

Methods

The study complies with the declaration of Helsinki, and the protocol was approved by the London—City & East Research Ethics Committee in June 2016 (ref 16/LO/1173). Informed consent was obtained from all participants (trial registration ISRCTN: 17495003). We developed the algorithm using an online database of RR intervals obtained from Holter recordings containing segments of sinus rhythm, AF and other arrhythmias.[13] We used 60 consecutive intervals to construct a Lorenz plot (a correlated scatter-plot of consecutive RR interval changes vs the previous change (ΔRR[k], ΔRR[k-1]) depicting heart rate variability). The patterns of data in the Lorenz plots for regularly irregular intervals such as bigeminy can distinguished from the more random pattern of AF. [14] We de-correlated the Lorenz plot using the following direct transformation derived from first principles (see S1 Appendix):
(1)

Where X is the difference between the two consecutive, discrete RR intervals and Y is the previous value of X ie. X = RR(k)–RR(k-1) and Y = X(k-1). We then compressed the de-correlated Lorenz plot using a wavelet-transformation (as used in the JPEG 2000 image compression algorithm[15]) to reduce the volume of data (to an 8×8 pixel image) presented to the machine learning algorithm (a Gaussian Support Vector Machine (SVM)) and hence the volume of training data required. Overtraining was avoided using crossfold-validation through the dataset.[16] (K-fold cross validation partitions data into k randomly chosen subsets (or folds) of roughly equal size. One subset is used to validate the model trained using the remaining (k-1) subsets. This process is repeated k times such that each subset is used exactly once for validation. We used 5-fold cross validation and the data was split randomly across records in the entire training dataset). This process is depicted in Fig 1 which depicts the original Lorenz plots, de-correlated Lorenz plots and subsequent compressed images used to train the SVM for 60 interval segments of normal sinus rhythm, bigeminy and AF. 60 consecutive RR intervals were used for training and in the validation data.

We trained the SVM using the Massachusetts Institute of Technology (MIT)—Beth Israel Hospital (BIH) Atrial Fibrillation database (comprising approximately 250 hours from 25 subjects; approximately 95 hours of AF (319 episodes), 2 hours of atrial flutter (40 episodes) and 163 hours of other rhythms) and the MIT-BIH Arrhythmia database (comprising approximately 24 hours of data from 47 subjects including complex ventricular, junctional, and supraventricular arrhythmias). We used the RR intervals and rhythms annotated in the database and did not employ a separate QRS detection algorithm. The MITBIH-AF database yielded 7,744 consecutive 60 beat sequences of AF, and 10,467 non-AF; the MIT-BIH Arrhythmia yielded 134 AF and 1404 non-AF consecutive 60-beat sequences.

We validated the algorithm using data from a case-control study of 415 participants aged > 65yrs (79 with AF at the study visit and 336 without) attending 3 general practice surgeries in Hampshire, UK for a single screening visit.[17] Following informed consent, 60 consecutive R-R intervals were obtained from participants at rest using the Polar H7 (PH7) heart rate monitor (via Bluetooth) and an iPad by study nurses. The participants each had a 12-Lead ECG, which were interpreted independently by 2 cardiologists, with a 3^rd cardiologist adjudicating disagreements. The PH7 is an inexpensive device (cost price £26) and has been shown to measure RR intervals accurately.[18]

Results

Training data

In the training data, the SVM algorithm yielded excellent discrimination with a sensitivity of 99.2% and a specificity of 99.5% for AF.

Validation / Trial data.

The SVM algorithm correctly identified AF in 79/79 cases; sensitivity 100% (95% CI 95. 4%-100%) and non-AF in 328/336 cases; specificity 97.6% (95% CI 95.4%-99.0%). Several control cases had non-AF arrhythmias including heart block, bigeminy and sinus arrhythmia[19]. Fig 2 shows Lorenz plots (standard / correlated) for the incorrectly classified (false positive) cases.

Discussion of results

The SVM algorithm demonstrated excellent discrimination with sensitivity and specificity both exceeding 99% for the training data set. This compares favourably with other algorithms results using the same databases in the literature.[20–22] Furthermore, we have validated the algorithm performance with clinical data obtained using an in expensive consumer device and achieved excellent discrimination with sensitivity and specificity both within 2% of the training data set results. High performing algorithms such as the SVM could greatly reduce clinical workload in terms of clinician confirmation of AF in positive cases. Visual inspection of the Lorenz plots of the false positive cases indicates several cases with clustering of RR intervals (case 021 and 118) which is not suggestive of atrial fibrillation and thus algorithm modifications or further training could possibly lead to improvements in performance.

The accuracy of the Polar-H7 and SVM algorithm also compares favourably with the accuracy of commercial devices designed and approved to detect AF.[23,24] The accuracy of the consumer device and algorithm was comparable to a cardiologist’s interpretation of single-lead ECGs.[25] Although it is not currently implemented commercially, a variant of the Polar-H7 device can transmit single lead ECG data which could be used to confirm the AF diagnosis. A newly available similar device that also provides a rhythm strip has been used clinically to detect AF and the ECG strip was sufficient for reliable confirmation of AF compared with a Holter monitor.[10] Smartphones are becoming more widely used among the elderly and in developing countries and in conjunction with inexpensive wearable technology, present an opportunity for cost-effective screening for AF. If these products are to be used in future for the diagnosis of AF, they would need to be registered as medical devices with either FDA approval (US) or a CE mark (EU).

Current guidelines make identical recommendations for anticoagulation regardless of AF pattern or burden (defined as the amount of time spent in AF). Reviews of recent evidence however suggests that higher AF burden is associated with higher risk of stroke[26]. Developments in monitoring technologies and algorithms will likely change the landscape of long-term AF monitoring and could allow better definition of the significance of changes in AF burden over time and to improved risk stratification and potentially improved patient outcomes. Inexpensive devices such as the Polar-H7 and Suunto Movesense[10] together with further algorithm development and implementation could lead to cost-effective methods for prolonged and continuous monitoring for AF detection. In addition, they could also potentially be used where clinically appropriate for the investigation of palpitations and syncope and the detection of other arrhythmias. The SVMs utility could potentially be used to classify patterns generated by other arrhythmias from the Lorenz plots which would potentially be an advantage over methods employing statistical analysis. This should be considered for future research.

Conclusions

Acknowledgments

We thank the CRN Wessex team and in particular Kerry Gunner, Clare Grocott, Julie Kennedy, Vivian Sparshott and the trial manager Kate Martinson.

The views expressed are those of the authors(s) and not necessarily those of the NIHR, the NHS or the department of Health or Leonardo MW Ltd.

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Atrial fibrillation or atrial fibrillation

Atrial fibrillation (AF, synonym – atrial fibrillation) irregular and often frequent contractions of the heart, increasing the risk of stroke, heart failure and other cardiac complications.

At atrial fibrillation “upper” cardiac chambers – the atria contract chaotically and irregularly, while their normal coordination with the contractions of the two “lower” chambers of the heart – the ventricles – is disturbed.

The most common symptoms of AF are palpitations, shortness of breath and general weakness.

Episodes (seizures, paroxysms) AF can be short, sometimes asymptomatic (“silence”), but can last for several days, months or more and be regarded as a permanent form. AF itself is usually not a life-threatening condition, but it can lead to the development of a severe clinical situation requiring emergency medical care.

This type of arrhythmia can lead to the development of serious complications, such as the formation of blood clots in the heart cavity, which are transferred in the direction of blood flow to the vessels of other organs, primarily the brain, causing blockage of the lumen and cessation of blood flow through the vessel, respectively, the development of ischemia , up to organ infarction.

Treatment of AF can be medication and / or interventional, affecting the cardiac conduction system.

Symptoms : Some people do not feel AF symptoms and arrhythmias are only detected on physical examination.But for some, the symptoms may be as follows:

Palpitations that feel irregular, unpleasant, or “coups”
Weakness, fatigue,
Light-headedness, dizziness
Decreased exercise tolerance (tolerance).
Shortness of breath, feeling short of breath
Chest pain

Any first documented episode of AF (ECG , Holter ECG monitoring ) is considered newly diagnosed AF, regardless of the duration and severity of symptoms.

Atrial fibrillation can be:

Paroxysmal – sinus rhythm recovers on its own, usually within 48 hours. Although paroxysmal AF can last up to 7 days, this period is of key importance.

Persistent – the duration of the episode exceeds 7 days, while medical or electrical cardioversion is required to restore the rhythm.

Long-term persistent – persistent AF lasts ≥1 year and rhythm control strategy is selected.

Permanent – the patient and the doctor consider it possible to maintain AF. Constant drug therapy is carried out to control the rhythm. Accordingly, cardioversion is by definition not performed in these patients. If rhythm restoration is expected, the arrhythmia is called “long-term persistent AF”.

When should I see a doctor? If you feel symptoms of AF, especially if shortness of breath increases, chest pains appear, you should immediately consult a doctor.

Possible causes of AF:

High blood pressure – arterial hypertension
Heart valve disease – acquired and congenital heart defects
Thyroid diseases and other metabolic disorders
Use of harmful substances – smoking, alcohol, drugs
Sick sinus syndrome (natural pacemaker)
Lung pathology
Postponed heart surgery
Infection
Stress due to severe surgical operations
Sleep apnea syndrome
Ischemic heart disease – angina pectoris, previous myocardial infarction

Atrial flutter

Atrial flutter (AT), a condition similar to AF, but with less chaotic and more ordered heart rhythm.Sometimes it can be combined or transformed into FP and vice versa. Complications and prognosis are similar to those of AF.

AF and TP if properly treated do not affect a person’s lifespan

Risk factors

Age , the older the person, the greater the risk of developing AF.
Heart disease
Arterial hypertension
Chronic diseases – diabetes mellitus, thyroid diseases, chronic kidney disease, lung diseases, etc. Drinking alcohol . For some people, drinking alcohol can trigger an episode of atrial fibrillation. Binge drinking may put you at an even higher risk.
Obesity
Heredity .

Complications:

Stroke , the risk depends on age (the older, the greater the risk), concomitant pathology (see above), high blood pressure, history of previous strokes, the presence of heart failure, etc.
Heart failure – a situation where your heart cannot circulate as much blood as needed by the body’s tissues.

Treatment FP

Drug treatment should be carried out as directed and under the supervision of a physician, taking into account all factors, symptoms, risks and characteristics of the course of the pathology. In general, the objectives of the treatment are:

Heart rate control
Prevention of blood clots
Reducing the risk of stroke

Sometimes the treatment of choice is catheter or surgical procedures

There are several surgical treatments for AF, with ablation being the most commonly used and effective.Ablation is a minimally invasive operation, the essence of which is to cauterize a small area of the heart using a special catheter. In order to accurately establish the area where the arrhythmia occurs, an electrophysiological study is performed before the operation. Cauterization is carried out using the radio frequency method. After cauterization, scarring of the myocardium occurs, which prevents the conduction of an electrical signal that causes abnormal atrial contractions. With ablation, all functions of the muscle tissue surrounding the scar are preserved, and the sinus rhythm of the heart is restored.

The decision on the choice of surgical or medical treatment should be made in conjunction with your treating cardiologist.

90,000 Atrial fibrillation (atrial fibrillation) – what the patient should know

Atrial fibrillation (AF), or atrial fibrillation (many doctors still call it that), is one of the most common rhythm disturbances. It is more common in older people than in young people.Let’s see together why it occurs – the causes of atrial fibrillation – and how it can be dangerous to humans.

In the human heart there are not only muscle cells (myocardium), which contract and provide the heart as a pump for pumping blood, but also special cells that produce electric current and conduct it to the myocardium. The so-called conducting system of the heart, through which an electrical impulse propagates, consists of these special cells.In a healthy heart, an electrical impulse that stimulates heart contraction occurs in the right atrium, in the sinus node. Therefore, a normal heart rhythm is called sinus rhythm. From the sinus node, the impulse propagates along the fibers of the conducting system in the atria, causing them to contract. Blood is pumped through the open mitral and tricuspid valves into the ventricles of the heart. Then the impulse enters the atrioventricular node (atrioventricular), which is a kind of checkpoint into the ventricles.Fibers called “bundle branch legs” emerge from it. Moving along the bundle of His, the impulse leads to a contraction of the ventricles and the release of blood into the aorta and pulmonary artery.

In a healthy heart, the formation of an impulse occurs at regular intervals, from 60 to 90 times per minute. In different situations, the pulse rate of the same person is 60 (for example, in a state of rest and rest), and 90 (with physical exertion, excitement) beats per minute. By changing the heart rate, a healthy heart adapts to the body’s changing oxygen needs.The same happens with blood pressure, which can change during the day from 100/70 to 140/90 mm Hg. Art. (normal).

What is atrial fibrillation?

At atrial fibrillation (atrial fibrillation) the electrical impulse moves through the atria chaotically, instead of a “friendly” contraction, the atria tremble, “flicker”. Due to the fact that the muscle fibers of the atria contract at different times, there is no single contraction and ejection of blood into the ventricles.Since the atria begin to contract not only chaotically, but also very often, the atrioventricular node passes by far not all contractions to the ventricles, an equal period of time is not observed. Therefore, when you try to count your heart rate, the intervals between beats will be different and your heart rate will be “uneven.” Please also note that the pulse has become different in filling – one contraction is stronger, while the other can barely be detected under the fingers. The reason for this is the disorganized work of the heart.Part of the contractions of the ventricles occurs when they have had time to fill with blood, and part – with empty ventricles, “at idle”.

Forms

Atrial fibrillation (atrial fibrillation) can be paroxysmal or chronic. If the attacks of arrhythmias (paroxysms) do not last long (from several minutes to 7 days) and the normal rhythm is restored spontaneously, this form of atrial fibrillation is called paroxysmal.

Can atrial fibrillation be hazardous to health?

Atrial fibrillation (atrial fibrillation) in most cases does not threaten your life directly, as it happens with ventricular tachycardia, ventricular fibrillation. To a greater extent, atrial fibrillation affects the accelerated development of heart failure, reducing the quality of human life. However, in certain situations, patients with atrial fibrillation are in danger. The chaotic contraction of the muscle fibers of the atria leads to the fact that instead of a complete one-step emptying of blood from the atria into the ventricles, the blood begins to stagnate in the atria.Conditions arise for the formation of blood clots (thrombi), which sometimes move with the blood flow into the ventricles and further into the systemic circulation. Such travel thrombi (emboli) can clog the vessels of the brain (causing a stroke), extremities, and internal organs. The complication can be fatal.

The most favorable conditions for the formation of blood clots are created when chronic (permanent) form of atrial fibrillation , or if paroxysm atrial fibrillation lasts more than 2 days.In addition, AF (atrial fibrillation) contributes to the onset and progression of heart failure and coronary insufficiency. In patients with heart rhythm disturbances, the quality of life is significantly reduced: a constant feeling of the danger of arrhythmia at any time, complete dependence on the availability of medical care.

Symptoms of atrial fibrillation (atrial fibrillation)

Atrial fibrillation, or atrial fibrillation , manifests itself in different ways: AF paroxysmal (chronic and persistent), persistent.With paroxysmal fibrillation , attacks of varying duration occur, from several minutes to 7 days. Such attacks stop spontaneously. With a stable form of atrial fibrillation , paroxysms do not go away on their own, last more than 7 days, to restore the sinus rhythm, the help of doctors is needed (drug treatment or electric pulse therapy). With a constant form of atrial fibrillation , the sinus rhythm cannot be restored.

Most often atrial fibrillation begins with a paroxysmal form, further attacks become more frequent, longer, the sinus rhythm is more and more difficult to restore, and then it is not possible at all – atrial fibrillation turns into a permanent form .For any form of atrial fibrillation, drug treatment is required, which should be carried out under the supervision of a physician. Atrial fibrillation can be detected during a screening mass ECG study, for example, when recording a stationary ECG during a medical examination or accidentally, when recording an ECG over the phone at a sports center, pharmacy or laboratory. Sometimes paroxysm of atrial fibrillation can develop during exercise tests, such as bicycle ergometry (VEM).But most often paroxysms of atrial fibrillation (atrial fibrillation) can be registered during long hours of ECG recording on a special small wearable monitor – Holter monitoring .

Causes of atrial fibrillation (atrial fibrillation)

Causes that lead to atrial fibrillation (atrial fibrillation) can be different. Atrial fibrillation can be an independent disease (idiopathic form), but more often atrial fibrillation occurs in people suffering from cardiovascular diseases: heart valve defects, coronary heart disease, hypertension, cardiomyopathies, pericarditis and myocarditis, heart surgery.Also at risk of getting atrial fibrillation are people suffering from thyroid pathology (hyperfunction of the thyroid gland – thyrotoxicosis, or “toxic goiter”). Sometimes rhythm disturbance is the first manifestation of thyroid disease, therefore at the first paroxysm of atrial fibrillation doctors always examine it.

The following video (in English) tells in great detail and clearly about atrial fibrillation:

Alcohol abuse is also a common cause of atrial fibrillation .Frequent alcohol intake disrupts the level and balance of electrolytes in the blood (potassium, sodium and magnesium ions are very important for the work of any muscles, but primarily the heart) and has a direct toxic effect on the heart, leading to expansion of the atria and ventricles, and a decrease in contractile function. The appearance of atrial fibrillation in patients with chronic lung diseases, against the background of general serious diseases, pathology of the gastrointestinal tract (reflux esophagitis, hiatal hernia) is also one of the causes of atrial fibrillation, or atrial fibrillation.

Atrial fibrillation: what to do, how to treat it?

Diagnosis of atrial fibrillation (atrial fibrillation) is based on an electrocardiogram (ECG) recording. Sometimes atrial fibrillation is asymptomatic and is detected by chance, for example, when an ECG is recorded with prof. examination or during inpatient treatment for another disease. However, most often the patient goes to the doctor with complaints of interruptions in the work of the heart, attacks of rapid, uneven heartbeat, which may be accompanied by weakness, shortness of breath, sweating, dizziness, feeling of “internal trembling”, pain in the heart and a decrease in blood pressure.When an attack occurs suddenly, you should definitely consult a doctor or call an ambulance. It is very important that the ECG recording was made exactly at the time of the attack – the doctor will be able to accurately determine the nature of the arrhythmia, diagnose and prescribe the correct treatment.

If seizures occur often enough, but they cannot be “caught” on a conventional ECG, the patient is referred for daily ECG monitoring (Holter, Holter monitoring). Within 24 hours (and more, depending on the device), the patient’s ECG is recorded and electronically recorded with a special palm-sized device that the patient carries with him.The record is processed on a computer, and if during the examination the patient had arrhythmia attacks, they will be recorded and documented. The doctor will receive all the information he needs.

It may happen that a seizure does not occur during Holter monitoring. Re-examination will be required, and so on until the arrhythmia is “caught”. If attacks are rare, it is very difficult to do this. In such cases, the doctor may recommend a study that allows you to provoke the onset of an attack – transesophageal atrial pacing (TEE).When conducting a NSPP through the patient’s nose, a thin electrode is inserted into the esophagus, which is installed at the level of the atria and, using a special device, allows electrical impulses to be applied to the heart. When AF paroxysm occurs, an ECG is recorded, then the sinus rhythm is restored. CHSP is carried out only in a hospital, in special departments specializing in the treatment of cardiac arrhythmias.

Paroxysm of atrial fibrillation – what to do?

If this is the first time you have a bumpy heartbeat, you should see a doctor right away or call an ambulance.Even if you feel good. Remember – it is very important to record the seizure on an ECG. The attack may end on its own after a while, but it is necessary to restore the correct rhythm within the first two days. The more time elapses from the onset of paroxysm, the more difficult it is for the heart to restore normal functioning and the higher the risk of blood clots in the chambers of the heart. If more than two days have passed since the onset of an attack, or you do not know exactly the time of its onset, it is necessary to restore the heart rhythm only under the supervision of a doctor after examining the heart chambers by echocardiography, EchoCG (to exclude already formed blood clots) and special preparation with blood thinners (to prevent thrombus formation).

If paroxysms of atrial fibrillation (atrial fibrillation) occur frequently, it is necessary, together with your doctor, to develop a plan for your actions during an attack. With good tolerance of arrhythmia and with short (no more than 24 hours) attacks of arrhythmia, which often end on their own, no special action can be taken. It is necessary to continue taking the drugs recommended by the doctor without changing the dose. If an attack occurs, your doctor may recommend a single dose of an antiarrhythmic drug in addition to basic therapy, or a temporary increase in the dose of medication you are already taking.If, during paroxysm of atrial fibrillation, the state of health significantly worsens, or the arrhythmia continues for more than a day, an appointment with a doctor is mandatory.

Which is “better” – seizures or persistent atrial fibrillation (atrial fibrillation)?

For a long time, doctors believed that the only optimal result of treatment was the restoration of the correct, sinus rhythm. And now, in most cases, the doctor will advise you by all means to restore and maintain sinus rhythm.However, not in all cases. Studies have shown that in the case of the impossibility of effectively maintaining the restored sinus rhythm (when the heart constantly “breaks” into atrial fibrillation), constant atrial fibrillation (atrial fibrillation) with drug-controlled heart rate of about 60 beats per minute is safer than frequent paroxysms of atrial fibrillation (especially protracted, requiring the administration of high doses of antiarrhythmic drugs or electro-pulse therapy).

The doctor decides on the advisability of restoring sinus rhythm or maintaining a permanent form of atrial fibrillation. In each case, such a decision is individual and depends on the cause of the development of arrhythmia, the disease against which it arose, on its tolerance and effectiveness of the treatment of atrial fibrillation carried out to maintain the correct rhythm.

An attack that lasted more than two days should be treated only under the supervision of a doctor, after special training.In case of successful restoration of sinus rhythm, the doctor will correct constant antiarrhythmic therapy and advise taking blood thinners for at least a month after cardioversion.

Treatment of atrial fibrillation (atrial fibrillation)

There are several ways to treat atrial fibrillation (atrial fibrillation) – to restore sinus rhythm. This is the intake of antiarrhythmic drugs by mouth, the introduction of antiarrhythmic drugs intravenously and cardioversion (electric pulse therapy, EIT).If the doctor conducts the restoration of the rhythm in the clinic or at the patient’s home, most often they start with intravenous drugs, then take pills. The procedure is carried out under ECG control, the doctor monitors the patient for 1-2 hours. If the sinus rhythm is not restored, the patient is admitted to the hospital. In the hospital, drugs can also be administered intravenously, but if the time is limited (the duration of the attack is approaching the end of the second day) or the patient does not tolerate paroxysm well (there is a decrease in blood pressure, i.e.EIT is used more often.

Cardioversion is performed under intravenous anesthesia, so the electrical discharge is painless for the patient. The success of rhythm restoration depends on many factors: the duration of the attack, the size of the cardiac cavities (in particular, the left atrium), sufficient saturation of the body with an antiarrhythmic drug), etc. EIT efficiency approaches 90-95%.

If the paroxysm of atrial fibrillation lasts more than two days, it is possible to restore the rhythm only after special preparation.The main stages are taking blood thinners under the control of a special analysis (INR) and performing transesophageal echocardiography (TEE) before EIT to exclude blood clots in the cardiac cavities.

Attacks of atrial fibrillation – how to prevent?

In order for the paroxysms of atrial fibrillation not to recur, the patient must constantly take an antiarrhythmic drug. For the purpose of prevention. Today there are many antiarrhythmics, the choice of the drug must be made by the doctor.A patient with atrial fibrillation needs a cardiologist’s observation, during which a regular examination is carried out (for example, EchoCG once a year, or daily Holter monitoring, if necessary, to assess the effectiveness of treatment), correction of treatment. The selection of drug therapy is always, for any disease, a very painstaking task that requires literacy and perseverance on the part of the doctor and understanding and diligence on the part of the patient. Not only the effectiveness, but also the tolerability of the treatment can be individual.

Failure of drug therapy for atrial fibrillation may be an indication for surgical treatment. In the left atrium (near the confluence of the pulmonary veins) there are zones in which electrical impulses are formed that can trigger atrial fibrillation. Increased electrical activity in these areas can be detected using a special electrophysiological examination (EPI). A special catheter is inserted into the cavity of the heart, the information obtained allows you to draw up an electrical “map” and determine the trigger (“starting”) sites.The study is carried out under local anesthesia and is safe enough for the patient. After determining the “trigger” areas, an operation is performed – radio frequency ablation of trigger zones (RFA). The catheter, using high-frequency current, destroys these areas and disrupts the start of arrhythmia. In four out of five cases, atrial fibrillation no longer recurs. In an animated form, the RFA process of trigger zones in atrial fibrillation is presented in the video.

Atrial fibrillation has become permanent

In a certain proportion of patients suffering from atrial fibrillation attacks, sooner or later there comes a time when it is no longer possible to restore sinus rhythm.Atrial fibrillation becomes permanent. As a rule, this happens in patients with a significantly increased size of the left atrium (4.5 cm or more). Such a dilated atrium is simply unable to maintain sinus rhythm. With a permanent form, the patient also needs medical supervision.

The goals of treatment are keeping the heart rate within 60-70 beats per minute at rest, preventing the formation of blood clots in the cavities of the heart and reducing the risk of thromboembolic complications.

Control of heart rate is carried out with beta-blockers, digoxin or calcium antagonists (verapamil group), selecting an individual dose of the drug according to the principle “the higher the dose, the less frequent the heart rate.” At the optimal dose, titration is terminated and the patient receives it daily. The effectiveness of heart rate control can be assessed using daily Holter ECG monitoring. If the decrease in the frequency of the rhythm cannot be achieved with pills, doctors resort to surgical methods. The arrhythmologist isolates the atria from the ventricles and implants a pacemaker that is programmed for a certain number of heartbeats at rest and adapts to stress.

To prevent thrombus formation, drugs that “thin” the blood are used, that is, they slow down the processes of blood coagulation. For this purpose, aspirin and anticoagulants (most often warfarin) are used. To date, the approach to the tactics of anticoagulant therapy has been determined on the basis of an assessment of the risk of thromboembolic complications and the risk of bleeding while taking these drugs, and is approved in the National Russian Recommendations of the VNOK.

Many patients are afraid to start taking medications, as the instructions indicate complications such as bleeding.You should be aware that before prescribing anticoagulants, the doctor always weighs the benefits and risks of drug treatment, and prescribes only when he is completely sure that the benefits significantly outweigh the risks. Strict adherence to the recommendations and regular monitoring of blood tests (international normalized ratio (INR) for patients receiving warfarin) plus your awareness of the main mechanisms of action of the drug and the tactics of your actions at the first sign of bleeding make such treatment completely predictable and as safe as possible.

Relatively recently, in Russia, to prevent the development of stroke in patients with chronic atrial fibrillation, they began to perform endovascular occlusion of the left atrial appendage. The operation is an alternative to the use of anticoagulants in patients for whom these drugs are contraindicated, or for those who are shown to use warfarin, but for one reason or another they do not receive it. Over 90% of blood clots that cause cardioembolic strokes in non-valvular atrial fibrillation form in the appendage (appendage) of the left atrium, due to a decrease in blood flow velocity.This operation is performed in the X-ray operating room under double control – transesophageal echocardiography and fluoroscopy.

Computed tomography data are preliminarily analyzed. For access, puncture and catheterization of the femoral vein are performed. The instruments are passed along the guide to the right atrium, after positioning is performed, the atrial septum is punctured and through this puncture the guide enters the left atrium. Then the choice of the site of implantation and selection of the size of the occluder is made.The occluder is installed in the mouth of the left atrial appendage, stopping the blood flow in it and, thus, excluding the appearance of blood clots in this anatomical formation. In Krasnoyarsk, such operations are performed at the Regional Clinical Hospital.

Cardiologists of the Center for Contemporary Cardiology have not only all modern functional and laboratory methods for diagnosing diseases that cause atrial fibrillation , but also vast experience in diagnosing and treating various forms of atrial fibrillation .

About atrial fibrillation – read also AFIB Matters (in Russian)

90,000 Clinical Study Paroxysmal Atrial Fibrillation: Electrophysiological Study – Clinical Study Register

Acceptability	Criteria: Inclusion criteria: – Patient from 18 to 75 years old. – The patient has at least one episode of persistent (> 30 s) paroxysmal atrial fibrillation. documented 12-lead ECG, Holter monitor, transtelephone event monitor, telemetry strip or pacemaker, respectively, implantable cardioverter defibrillator (ICD) within 12 months prior to enrollment – Patient has symptomatic paroxysmal atrial fibrillation (PAF), refractory or intolerable.to at least one class I-IV antiarrhythmic drug – The patient is willing and able to comply with the requirements of the study protocol, including the specified follow-up schedule – The patient provides written informed consent prior to enrollment in the study. Exclusion criterion: – Failure to meet inclusion criteria – Active systemic infection – Recent (within 3 months) cardiac events, including myocardial infarction, acute coronary syndrome, percutaneous coronary intervention (PCI), or valve or coronary bypass surgery – Reversible causes of arrhythmias, including disease thyroid gland, spicy alcohol.intoxication, recent (less than 3 months) major surgery – Patient has left atrial diameter> 5.0 cm – Patient has persistent or long-term persistent atrial fibrillation (AF) – Left ventricular ejection fraction <35% - New York Heart Association ( NYHA) Class III or IV - Previous Left Atrial Ablation Procedure, Surgical or Catheter Ablation - Patient has an intracardiac angina thrombus, has had a ventriculotomy or atriotomy. - Patient has moderate to severe structural heart disease, as evidenced by transthoracic or transesophageal echocardiogram of all four chambers of the heart (ventricular dysfunction or valve disease) - Tricuspid or mitral valve replacement or repair - If a woman of childbearing age is pregnant or breastfeeding - The patient is bleeding diathesis or suspicion of a procoagulant state.- The patient has contraindications to long-term antithromboembolic therapy (e.g. acetylsalicylic acid, heparin, warfarin) - Presence of a condition that prevents proper vascular access - Heart disease in which corrective surgery is expected within 6 months - Renal failure requiring dialysis - The patient has a known sensitivity to contrast agents (if necessary during the procedure) that cannot be adequately controlled by premedication (or completely excluded) - The patient has other anatomical or comorbid conditions that, in the opinion of the investigator, the opinion may limit the patient's ability to participate in the study or comply with follow-up requirements or affect the scientific validity of the study results - The patient is currently participating in another clinical study.- The patient is unlikely to live more than one year Floor: All Minimum age: 18 years old Maximum age: 75 years Healthy volunteers: No

Acceptability

Criteria:

Inclusion criteria: – Patient from 18 to 75 years old. – The patient has at least one episode of persistent (> 30 s) paroxysmal atrial fibrillation. documented 12-lead ECG, Holter monitor, transtelephone event monitor, telemetry strip or pacemaker, respectively, implantable cardioverter defibrillator (ICD) within 12 months prior to enrollment – Patient has symptomatic paroxysmal atrial fibrillation (PAF), refractory or intolerable.to at least one class I-IV antiarrhythmic drug – The patient is willing and able to comply with the requirements of the study protocol, including the specified follow-up schedule – The patient provides written informed consent prior to enrollment in the study. Exclusion criterion: – Failure to meet inclusion criteria – Active systemic infection – Recent (within 3 months) cardiac events, including myocardial infarction, acute coronary syndrome, percutaneous coronary intervention (PCI), or valve or coronary bypass surgery – Reversible causes of arrhythmias, including disease thyroid gland, spicy alcohol.intoxication, recent (less than 3 months) major surgery – Patient has left atrial diameter> 5.0 cm – Patient has persistent or long-term persistent atrial fibrillation (AF) – Left ventricular ejection fraction <35% - New York Heart Association ( NYHA) Class III or IV - Previous Left Atrial Ablation Procedure, Surgical or Catheter Ablation - Patient has an intracardiac angina thrombus, has had a ventriculotomy or atriotomy. - Patient has moderate to severe structural heart disease, as evidenced by transthoracic or transesophageal echocardiogram of all four chambers of the heart (ventricular dysfunction or valve disease) - Tricuspid or mitral valve replacement or repair - If a woman of childbearing age is pregnant or breastfeeding - The patient is bleeding diathesis or suspicion of a procoagulant state.- The patient has contraindications to long-term antithromboembolic therapy (e.g. acetylsalicylic acid, heparin, warfarin) - Presence of a condition that prevents proper vascular access - Heart disease in which corrective surgery is expected within 6 months - Renal failure requiring dialysis - The patient has a known sensitivity to contrast agents (if necessary during the procedure) that cannot be adequately controlled by premedication (or completely excluded) - The patient has other anatomical or comorbid conditions that, in the opinion of the investigator, the opinion may limit the patient's ability to participate in the study or comply with follow-up requirements or affect the scientific validity of the study results - The patient is currently participating in another clinical study.- The patient is unlikely to live more than one year

Floor:

All

Minimum age:

18 years old

Maximum age:

75 years

Healthy volunteers:

Atrial fibrillation ecg clip art – Medical Diagnostic Center Starlab

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Extrasystoles

Extrasystoles (premature contractions) are divided into ventricular and supraventricular.

Ventricular extrasystoles differ from supraventricular:

a wide QRS complex, unlike the usual “correct” complexes
by the absence of an atrial P wave (this symptom is not absolute, since a normal excitation wave can be generated by the atrium, and soon after that, ectopic excitation of the ventricles will independently occur, which will be recorded on the ECG as a P wave followed by a wide deformed complex). Holter programs like to mistakenly label such complexes as WPW.
The absence of the so-called compensatory pause (that is, the RR interval between the preceding ES complex and the subsequent one is strictly equal to either twice the “correct” interval, or a single such interval in the case of an interstitial extrasystole.

↓ In this picture, a single ventricular extrasystole presumably from LEFT ventricle (the shape of the complex is similar to the blockade of the RIGHT bundle branch – see the page about conduction disorders).

↓ Ventricular bigeminy – the correct alternation of one normal complex and one ventricular extrasystole (a type of allorhythmy – the correct alternation).Extrasystoles presumably from RIGHT ventricle (have the morphology of LEFT bundle branch block).

↓ Ventricular polymorphic bigeminy – the shape of the extrasystole in the center differs from those at the edges, which means that the sources of origin of extrasystoles are different.

↓ Ventricular trigeminia – the correct alternation of two normal complexes and one ventricular extrasystole.

↓ Intercalary ventricular premature beats is located between normal rhythmic contractions.Some lengthening of the RR interval between the complexes adjacent to the extrasystole is explained as follows. The atrial P wave arose on time, but it is practically absorbed by the extrasystole T wave. The echo of the P wave is a small notch at the end of the T of the extrasystole in lead V5. As you can see, the PR interval after extrasystole is increased, since there is a partial refractoriness of the AV conduction after extrasystole (probably due to the reverse conduction of the impulse from the ventricles along the AV node).

↓ Paired monomorphic ventricular premature beats .

↓ Paired polymorphic ventricular extrasystole (extrasystoles from different sources, therefore a different form of complexes). The paired VES is a “small embryo of ventricular tachycardia.”

Group (from 3 pcs) extrasystoles according to modern views refer to jogging tachycardia, supraventricular or ventricular.

↓ The refractory ventricular extrasystole blocked the conduction of the normal atrial impulse to the ventricles (a normal rhythmic atrial P wave is visible after the extrasystole T wave).

Supraventricular (supraventricular) extrasystoles are narrow (similar to normal) premature QRS complexes. They may have in front of them an atrial P wave (atrial ES) or not (AV-nodal extrasystoles). After atrial ES, a compensatory pause is formed (the RR interval between complexes adjacent to ES is greater than the “normal” RR interval.

↓ Supraventricular (supraventricular) bigeminy – correct alternation of one rhythmic contraction and one extrasystole.

↓ Supraventricular (supraventricular) bigeminy and aberrant extrasystole (aberrant conduction like blockade of the right bundle branch (“ears” in V1-V2) in the second extrasystole).

↓ Supraventricular (supraventricular) trigeminia – correct repetition of two rhythmic complexes and one extrasystole (note that the P waveform in extrasystoles differs from that in “normal” complexes.This suggests that the source of ectopic excitation is in the atrium, but different from the sinus node).

↓ Intercalated supraventricular extrasystole . In the first “normal” complex after extrasystole, there is a slight increase in the PQ interval, caused by the relative refractoriness of the AV conduction after ES. The extrasystole itself, possibly from the AV node, since the atrial P wave in front of the ES is not visible (although it can be “absorbed” by the T wave of the previous complex) and the shape of the complex is somewhat different from the “normal” neighboring QRS complexes.

↓ Paired supraventricular extrasystole

↓ Blocked supraventricular premature beats . At the end of the T wave of the second complex, a premature P wave of atrial extrasystole is visible, however, refractoriness does not allow excitation to the ventricles.

↓ A series of blocked supraventricular extrasystoles of the bigeminy type.
. After the T wave of the previous complex, an altered atrial P wave is visible, immediately after which the ventricular complex does not arise.

Paroxysmal tachycardia

Paroxysmal tachycardia is called with an abrupt beginning and ending (as opposed to gradually “accelerating” and “slowing down” sinus). Like extrasystoles, there are ventricular (with wide complexes) and supraventricular (with narrow). Strictly speaking, a run of 3 complexes, which seemed to be called a group extrasystole, is already an episode of tachycardia.

↓ Run of monomorphic (with the same complexes) ventricular tachycardia of 3 complexes, “triggered” by supraventricular extrasystole.

↓ Jogging perfectly monomorphic (with very similar complexes) ventricular tachycardia.

↓ Start of episode of supraventricular (supraventricular) tachycardia (with narrow complexes similar to normal).

↓ This picture shows an episode of supraventricular (supraventricular) tachycardia against the background of a permanent left bundle branch block. The “wide” QRS complexes, similar to ventricular ones, immediately draw attention to themselves, however, the analysis of the previous complexes leads to the conclusion about the presence of constant LBBB and the supraventricular nature of the tachycardia.

Atrial flutter

↓ The main ECG sign of atrial flutter is a “saw” with a frequency of “teeth” usually 250 per minute or more (although in this particular example, an elderly person has a frequency of atrial impulses of 230 per minute). Atrial impulses can be delivered to the ventricles in different ratios. In this case, the ratio changes from 3: 1 to 6: 1 (The invisible sixth and third teeth of the “saw” are hidden behind the ventricular QRS complex). The ratio can be either constant or variable, as in this episode.

↓ Here we see atrial flutter with conduction options 2: 1, 3: 1, 4: 1 and 10: 1 with a pause of more than 2.7 seconds. Let me remind you that one of the teeth of the “saw” is hidden under the ventricular QRS complex, therefore the figure in the ratio is one more than the visible number of atrial contractions.

↓ This is a fragment of a recording of the same patient with a constant 2: 1 conduction, and here no one can say for sure that the patient has flutter. The only thing that can be assumed by the rigid (practically unchanged RR interval) rhythm is that this tachycardia is either from the AV node, or atrial flutter.And then if you convince yourself that the complexes are narrow :).

↓ This is the diurnal HR trend for the same patient with atrial flutter. Notice how exactly the upper limit of heart rate is “cut” to 115 beats per minute (this is because the atria produce impulses with a frequency of 230 per minute, and they are conducted to the ventricles in a two-to-one ratio). Where the trend is below 115, there is a variable conduction rate greater than 2: 1, hence a lower heart rate per minute.Where higher – a single episode of AF.

Atrial fibrillation

The main ECG sign of atrial fibrillation is significantly different adjacent RR intervals in the absence of an atrial P wave.In resting ECG, minor fluctuations in the isoline are very likely to be fixed (atrial fibrillation itself), however, with Holter recording, interference can neutralize this sign.

↓ Start an atrial fibrillation episode after normal sinus rhythm (from the fifth beat).Tachysystolic form.

↓ Atrial fibrillation itself is visible (serration of the isoline) – according to the old classifications, “large-wave” – in the chest leads. Bradystole. Complete blockade of the right bundle branch block (“ears” in V1-V2)

↓ “Small-wave”, according to the old classifications, atrial fibrillation, is visible in almost all leads.

↓ Rhythmogram with constant atrial fibrillation: there are no two equal adjacent RR intervals.

↓ Rhythmogram when changing from fibrillation to sinus rhythm and vice versa. An “island of stability” with a lower heart rate in the middle of the picture is an episode of sinus rhythm. At the beginning of the episode of sinus rhythm, the sinus node “pondered” whether it should turn on or not, hence the long pause.

↓ The heart rate trend in atrial fibrillation is very broad, often with a high average heart rate. In this case, the patient has an artificial pacemaker programmed for 60 beats per minute, so all frequencies below 60 beats / min are cut off by the pacemaker.

↓ Heart rate trend in paroxysmal atrial fibrillation. The signs of AF are “high” and “wide” trend, sinus rhythm is a narrow band that is significantly “lower”.

Ventricular rhythm

↓ Ventricular rate run . It cannot be called “tachycardia” in the usual sense of the word, but usually the ventricles emit impulses with a frequency of 30-40 per minute, so for the ventricular rhythm it is quite “tachycardia”.

Pacemaker migration

↓ Note the change in the P waveform on the left and right sides of the picture.This proves that the momentum on the right side of the picture comes from a different source than on the left side. Lead II shows early repolarization syndrome .

↓ Migration of the pacemaker by the type of bigeminy (Call “extrasystole” contraction with a clutch interval of more than a second does not turn the tongue). Correct alternation of positive and negative atrial P waves in adjacent complexes.

Diagnosis of atrial fibrillation on ECG

Atrial fibrillation, or, as it is also called, atrial fibrillation, is a pathological change in heart rhythm, in which an electrical impulse in the atria moves randomly with a frequency of 350-700 beats per minute, which makes normal contraction of the atrial muscles impossible.

Atrial fibrillation in a patient may be suspected by a physician during an assessment of the pulse and auscultation of the heart, but the final confirmation of the diagnosis can only be an ECG study.

Cardiogram procedure

The process of taking an electrocardiogram is painless and non-invasive, and the availability of this research method is wide: an electrocardiograph can be found in any hospital.

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Only a DOCTOR can deliver an EXACT DIAGNOSIS to you !
We earnestly ask you NOT to self-medicate, but to make an appointment with a specialist !
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Taking an electrocardiogram is not such a simple matter as it seems at first glance.Much in the process of diagnostic research depends not only on the patient, but also on the professionalism of the doctor, therefore, without special preliminary preparation, they are not allowed to the procedure.

Taking an ECG consists in the correct placement of the electrodes. At the same time, it is important for the patient himself to follow a number of recommendations before the study, so as not to accidentally influence its results.

The recommendations are as follows:

it is forbidden to overeat before the procedure;
It is recommended not to smoke 12 hours before the procedure;
alcohol consumption is prohibited before the procedure;
before the procedure, it is necessary to exclude for a while the intake of certain medications that may affect the results, but this can be done only after consulting a doctor, self-withdrawal of drugs is unacceptable;
you can not get carried away on the eve of hard physical work or be exposed to severe stress;
coffee is also prohibited on the eve of the procedure.

Failure to comply with these simple recommendations will nullify the entire value of the study, since most of the listed factors provoke the appearance on the ECG, at best, of signs of tachycardia, and sometimes other pathologies.

Before the procedure, the patient is advised to sit and calm down for a few minutes in order to calm down and mentally prepare for the study (this way, the effect of the so-called “white coat syndrome” – a sharp jump in blood pressure accompanied by an attack of tachycardia can be avoided).

When the patient is ready, he is asked to undress to the waist, and also to free the legs from the tissue at least to the middle of the shin. That is why it is recommended to wear light and loose clothing that can be easily removed for the study.

After undressing, the patient lies down on the couch. Now his main task is to lie still and wait until the research is over.

In the meantime, the nurse or doctor will lubricate the electrodes with a special gel, which will improve adhesion to the skin, and place the electrodes.During the study, the patient must lie still, therefore it is recommended to immediately take a comfortable position.

The study does not last long, and at the end of the study, the patient is given the results, which are deciphered by the attending physician.

What to look for

The reasons why atrial fibrillation develops can be easily explained scientifically. To do this, the doctor must first of all find out from the patient information about whether there are any lesions of the cardiovascular system, and especially the heart muscle itself.

Methods for the treatment of permanent atrial fibrillation are described here.

It is also required to clarify whether the person has recently undergone any surgical interventions directly on the heart or in the immediate vicinity of it.

If the interventions were very recent, then the development of arrhythmias is a normal phenomenon that should decline over time, but still needs therapy and monitoring.

It is also imperative to clarify whether the patient’s history has the influence of the following factors:

pathological changes in the mitral valve;
lesions of the heart muscle by rheumatic diseases, damage in the general organism by pathologies of the rheumatoid type;
ischemic heart disease in various forms;
heart failure of various forms;
cardiomyopathy;
diseases of the chronic bronchopulmonary system.

Full physical health reduces the risk of developing atrial fibrillation to zero, and the absence of diseases of the cardiovascular system significantly reduces it.

Odds ratio

When calculating the ratio of the coefficients, the doctor usually estimates how many atrial waves visible on the ECG preceded the appearance of the ventricular complex. Even ratios, such as 1: 2, 1: 4, etc., which are characteristic of atrial flutter, and not fibrillation, are considered more favorable prognostically.

The analysis of the ratio of the ratios is important. Its rates according to the 1: 2-1: 4 principle are more favorable and, more often than not, are tolerated by patients more easily than the odd ratio characteristic of fibrillation.

Also, the coefficient helps in the differential diagnosis of atrial flutter and atrial fibrillation. Fibrillation is characterized by the irregularity of the coefficient and its oddness, although in a number of cases an odd coefficient occurs also during flutter (this happens rarely, but even in the case of oddness during flutter, the coefficient remains regular).

This is due, first of all, to the fact that with an even rate of contraction, the atria remain coordinated, while with an odd one, complete desynchronization occurs. That is why patients generally tolerate flutter more easily than atrial fibrillation.

Atrial fibrillation is an insidious pathology with its own characteristics. Its development is difficult to predict due to the fact that the jump in the heart rate occurs too abruptly as soon as the conduction coefficient changes.

An important diagnostic element is the symptoms that must be looked for when diagnosing atrial fibrillation. The main criterion is the heart rate. In addition to the heart rate, the characteristics of cardiac pathology in each individual patient are also assessed.

In the clinical diagnosis of this cardiac pathology, an assessment of the arterial pulse plays an important role. In atrial fibrillation, the arterial pulse is usually characterized as arrhythmic, while in atrial fibrillation it will be rhythmic and rapid.

Despite the importance of assessing the arterial pulse, its assessment is still not the main method of clinical differential diagnosis. It is not used for these purposes due to the fact that a ratio of 4: 1 can be a sign that the heart rate is kept within 85 beats per minute.

Conclusion An ECG in atrial fibrillation can only be performed by a doctor, since only he is able to assess all the factors and fully carry out differential diagnostics between atrial fibrillation and flutter.

The therapy that is prescribed to the patient in a particular case depends on the correctness of the diagnosis, therefore it is extremely important to distinguish between diseases.

Display of atrial fibrillation on ECG

Signs of atrial fibrillation on the ECG are characterized by the following features, which are important to pay attention to when evaluating the results of an electrocardiogram and making a diagnosis:

P wave completely disappears in all leads;
P wave is replaced by a set of waves of different amplitude and width, which are called f waves;
the frequency of these waves can reach 200-400 beats per minute;
characteristic waves that do not have a clear consistency are best seen in leads aVF, II, III, V1 and V2;
the rhythm of the ventricles changes, becoming irregular, which is characterized by a change in the intervals between the R waves;
the ventricular complexes themselves do not undergo any diagnostically significant changes, maintaining the correct shape without dilatation.

In some cases, atrial flutter can be, like fibrillation, irregular.

In this case, the differential diagnosis of pathologies is carried out according to the following criteria:

with atrial fibrillation, the ventricular complexes will be located arrhythmically;
P wave will be completely absent;
, characteristic small waves f will be determined;
heart rate will be around 300 beats per minute, and sometimes more.

Naturally, most experienced doctors pay attention to the rhythm of the ventricular complexes, since this criterion in differential diagnosis plays the greatest role and is the most obvious.

If the first diagnostic criterion is in doubt, then special attention is paid to the third and fourth criteria.

So, the flutter is characterized by the correctness of the waves, they are called large waves F. These waves resemble in their appearance the teeth of a saw and the interval between them is always the same.Also, flutter is characterized by a heart rate that does not exceed 300 beats per minute.

An experienced physician usually only needs the first criterion to make a correct diagnosis.

The basics of anticoagulant therapy for atrial fibrillation are described in this article.

How to provide first aid for atrial fibrillation – read here.

It is important to determine the correct diagnosis and differentiate atrial fibrillation from atrial flutter, since the therapy of diseases and their prognosis are different.

So, with fibrillation, full-fledged drug treatment is required, which the patient will have to adhere to all his life, while the issue of flutter is most often solved using the catheter ablation procedure, which allows you to completely get rid of the disease.

Atrial fibrillation on the ECG: description and signs

Diagnosis of a disease such as atrial fibrillation is impossible without an ECG. The pathology is characterized by an abnormal heart rhythm, chaotic contraction and excitation of the atria, the so-called atrial fibrillation.The diagnostic procedure provides an opportunity to get acquainted with the full picture of the course of the pathological process, thanks to which the doctor manages to establish the correct diagnosis. Based on the data obtained, the cardiologist prescribes a course of therapy.

How atrial fibrillation looks on the ECG

Atrial fibrillation is a rhythm disturbance in which, during one cardiac cycle, irregular excitation and contraction of individual muscle fibers of the atria occurs

Heart disease requires a comprehensive study.These include cardiac arrhythmias. The first diagnostic measure to which a cardiologist refers a patient is an ECG.

On the electrocardiogram, the bioelectric activity of the heart is reflected in the form of teeth, intervals and sections. Their length, width, distance between the teeth normally have certain values. Changing these parameters allows the doctor to determine abnormalities in the work of the heart muscle.

Changes in the ECG make it possible to establish whether the patient suffers from atrial fibrillation (flickering) or atrial flutter.Deciphering the result will make it clear exactly what worries the patient. Atrial flutter is characterized by an accelerated, but correct rhythm of heart contractions, while during fibrillation the rhythm is disturbed, different groups of muscle fibers in the atria contract inconsistently with each other. Since the heart rate reaches high numbers with these violations (up to 200 beats per minute), it is impossible to determine by ear, using a phonendoscope, the form of arrhythmia. Only the ECG gives the doctor the information he needs.

First signs

The electrocardiogram displays symptoms characteristic of the disease.Atrial fibrillation on the ECG will look like this:

There is no P wave on any electrocardiographic lead (this wave is a mandatory component of a normal ECG).
The presence of irregular f waves throughout the entire cardiac cycle. They differ from each other in amplitude and shape. In certain leads, these waves are recorded best. These include V1, V2, II, III. aVF. These waves are caused by atrial fibrillation.
Irregularity of R-R ventricular complexes (irregularity, different length of R-R intervals).It indicates an abnormal ventricular rhythm;
QRS complexes differ in their unchanged appearance and in the absence of signs of deformity.

On the ECG, a fine- or large-wave form of atrial fibrillation is distinguished (depending on the scale of the waves f).

Symptoms as the disease progresses

Chest pain is one of the possible symptoms of atrial fibrillation

Clinical symptoms of atrial fibrillation become more pronounced as the disease progresses.They can vary significantly from patient to patient.

Signs of atrial fibrillation, which appear on the electrocardiogram, are supplemented by symptoms that are palpable to the patient himself. We are talking about such painful conditions:

profuse sweating;
weakness;
heart palpitations;

90,023 chest pains.

A patient with chronic atrial fibrillation may not even be aware of his illness if it is characterized by an asymptomatic course.In this case, only the result of an electrocardiographic study can determine the presence of pathology.

The types of electrocardiographic manifestations, that is, the symptoms that are seen on the ECG, correspond to the clinical signs of the patient’s disease. Thanks to this competent specialist, it is possible to unmistakably understand what exactly bothers the patient and what kind of help he needs to provide.

Recommendations of doctors

The procedure for taking an electrocardiogram is not difficult.It is only required to adhere to the step-by-step implementation of the action plan, with which each specialist is familiar. He will explain in detail what the patient should do at the time of diagnosis. The total duration of the procedure does not exceed 10 minutes on average.

Electrodes are fixed on the patient’s body, the position of which is changed by the doctor or laboratory assistant to obtain various ECG leads.

ECG decoding

It is not recommended to undergo the procedure after eating, drinking alcohol, drinks containing caffeine or cigarettes

Arrhythmia of heart contractions can only be recognized by a competent specialist who conducts a description of the ECG in atrial fibrillation.Decoding of the results obtained is available only to a doctor. If the case is urgent, then the task can be assigned to a paramedic, who repeatedly had to remove and decipher the ECG.

The patient can also try to decipher his ECG. To do this, he needs to study the medical literature in order to assess the location and height of the teeth, the size of the intervals between them. Without basic knowledge of the ECG, a person runs the risk of making a serious mistake.

Other diagnostic methods

In standard situations, a person is diagnosed with atrial fibrillation based on his complaints and the symptoms of the disease identified during the initial diagnosis.Interviewing the patient and the result of electrocardiographic diagnostics is quite enough if there are no serious complications of the disease.

If the ECG does not provide sufficient information about the patient’s condition, then the cardiologist sends him for additional studies:

Echocardioscopy.
Radiography.
Biochemical analyzes of blood and urine.
Transesophageal study of the cardiac conduction system.

An important stage in the study of a patient with atrial fibrillation is differential diagnosis: it is necessary to distinguish the disease from other pathological conditions that may have similar symptoms with it.Differential diagnosis is carried out with the following pathologies:

sinus tachycardia;
atrial flutter;
supraventricular paroxysmal tachycardia;
ventricular paroxysmal tachycardia.

The ECG results allow the cardiologist to distinguish atrial fibrillation from the aforementioned heart conditions.

ECG frequency

Regular examination by a cardiologist will promptly reveal the presence of violations in the work of the heart

Patients may ask questions about the frequency of electrocardiography in order to check the status of the cardiovascular system.This diagnostic option is absolutely safe for human health. During the procedure, the indicators of the bioelectric activity of the heart are simply taken. In this case, no negative effects on the body occur.

The frequency of the ECG is dependent on several factors. Doctors recommend that all people be checked for the prevention of atrial fibrillation about 1 time per year. If a person’s profession is associated with serious stress, then he should visit a cardiologist once every six months.Seniors should be checked every 3 months. They fall into a risk group, so regular checking of the cardiovascular system is mandatory for them.

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References

Atrial fibrillation or atrial fibrillation

Atrial fibrillation ecg clip art – Medical Diagnostic Center Starlab

Extrasystoles

Paroxysmal tachycardia

Atrial flutter

Atrial fibrillation

Ventricular rhythm

Pacemaker migration

Diagnosis of atrial fibrillation on ECG

Cardiogram procedure

What to look for

Odds ratio

Display of atrial fibrillation on ECG

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First signs

Symptoms as the disease progresses

Recommendations of doctors

ECG decoding

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ECG frequency

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