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1st degree av block rhythm strip


1st degree av block rhythm strip

The typical ECG findings in Mobitz I (Wenckebach) AV block—the most with a benign conduction defect such as first-degree AV block. Individuals with first-degree atrioventricular block had a 2-fold or absence of atrial premature beats on a 10-second rhythm strip. termined from the surface ECG, has important clinical implications. The first A (atrid electrogram) wave is followed by a BH de-.
1st degree av block rhythm strip

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Understanding Atrioventricular Blocks

Cardiac Conduction System

The myocardium contains sets of specialized cells that form the conduction system of the heart, and are responsible for automaticity and rhythm maintenance. The specific areas are the sinoatrial (SA) node, internodal tracts, atrioventricular (AV) node, atrioventricular bundle, and Purkinje system.

SA Node

The SA node is a small collection of specialized cells and collagenous tissue located along the epicardial surface at the junction of the superior vena cava and the right atrium.2 The blood supply is via the sinus node artery and is from the initial branch of the right coronary artery in approximately 60% of individuals and takes its origin from the circumflex artery in the other 40%, with a few instances of lateral origin from either the right or left arteries or dual origins from both arteries.1 First citizens bank south hill va intrinsic rate of the SA node is 60-100 beats per minute (BPM) and the speed of conduction to adjacent cells within the SA node is 0.5 m/sec.

Internodal Tracts

The SA node and AV node have conduction pathways between the two that are the primary route of impulse transmission and are called internodal tracts. Three major internodal tracts exist: the anterior, middle, and posterior tracts.2 The anterior nodal tract (Bachmann bundle) extends into the left atrium and then travels downward through the atrial septum to the AV Node,2 the middle internodal tract (Wenckebach tract) curves behind the superior vena cava before descending to the AV node, and the posterior internodal tract (Thorel’s pathway) continues along the terminal crest to enter the atrial septum and then passes to the AV node.

internodal tracts

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Atrioventricular Node

The AV node is located beneath the endocardium on the right side of the atrial septum, anterior to the opening of the coronary sinus.2 Conduction through the AV node delays propagation of impulses from atria to ventricles and thus permits atrial systole to augment ventricular filling during late diastole, with an added 15-35% contribution to ventricular volume.5 In delaying transmission of the cardiac impulse from the atria to the ventricles, the AV node serves a critical function in augmenting ventricular filling during diastole and personal loan rates lightstream the ventricular response during atrial tachyarrhythmias.4 Impulse conduction is considerably slower as compared to any other region within the normal cardiac conduction system (0.05 m/sec) and this delayed speed allows for sufficient time for atrial depolarization and contraction prior to ventricular depolarization and contraction.2 When conduction slowing becomes exaggerated or heterogeneous within the AV node, abnormal rhythms ensue, such as pathological conduction block or reentrant tachycardias.4

His-Purkinje System

The Purkinje network functions to distribute a stimulus throughout the entire ventricles, leading to a much faster total activation of the ventricles than could be achieved by the spread of excitation solely through the ventricular muscle.3 The left bundle branch extends outward under the endocardium and forms several fascicles, which innervate various parts of the left ventricle.2 The anterior fascicle innervates the anterolateral wall of the left ventricle the anterior papillary muscle, and the posterior fascicle innervates the lateral and posterior ventricular wall and the posterior papillary muscle.2 The right bundle branch travels under the endocardium along the right side of the ventricular septum to the base of the anterior papillary muscle.2 The Purkinje cells have an intrinsic back up rate of 20-40 BPM when no signal is received from the SA node or AV node.

Understanding Atrioventricular Block

AV blocks are conduction delays or a complete block of impulses from the atria into the ventricles. AV block may be due to increased vagal tone that may be elicited during sleep, athletic training, pain, or stimulation of the carotid sinus. Damage of the conduction system secondary are banks open in massachusetts hereditary fibrosis or sclerosis of the cardiac skeleton are known as idiopathic progressive cardiac conduction disease. Ischemic heart disease causes 40% of AV blocks.6 AV blocks are also seen in cardiomyopathies, myocarditis, congenital heart diseases, and familial diseases. A plasma potassium concentration above 6.3 mEq/L may also cause AV block. They may be iatrogenic, from medications such as Verapamil, Diltiazem, Amiodarone, and Adenosine, or from cardiac surgeries and catheter ablations for arrhythmias.

AV blocks are further classified according to the degree of blockage and include first degree AV block, second degree AV block, and third-degree AV block.

First-Degree Atrioventricular Block

The measurement of conduction time between the atria and ventricles is represented by the PR interval on electrocardiograms (ECG). This component 1st degree av block rhythm strip the intra-atrial conduction, represented by the P wave, and the conduction from the AV node into the His-Purkinje system. Prolongation of the PR interval of more than 200 milliseconds is considered to be a first-degree AV block. These can be due to structural abnormalities within the AV node, an increase in vagal tone, and drugs that slow conduction such as digoxin, beta-blockers. and calcium channel inhibitors. It is important to note that in first degree AV block, no actual block occurs.

first degree av block

Second-Degree Atrioventricular Block

Second-degree atrioventricular blocks are occasional non-conducted P waves with prolonged RR intervals. There are two types under this classification. Mobitz type I (Wenckebach) occurs when there is an intermittent conduction block within the AV node that results in a failure to conduct an impulse from the atria into the ventricles. The impaired nodal conduction is progressive to the point that there is a total block. This causes an absent impulse into the ventricles, reflected by the disappearance of the QRS complex in the ECG. Mobitz type I is best website to buy jordans benign condition that rarely causes hemodynamic instability; asymptomatic patients need no further treatment. Symptomatic patients will require a pacemaker.

second degree AV block - mobitz type I

The Mobitz type II AV block is secondary to a disease involving the His-Purkinje system, in which there is a failure to conduct impulses from the atria into the ventricles. A block occurs after the AV node within the bundle of His, or within both bundle branches. The His-Purkinje system is an all-or-none conduction system; therefore, in Mobitz type II, there are no changes in the PR interval, even after the non-conducted P wave. Because of this, Mobitz type II has a higher risk of complete heart block compared to Mobitz type I.

Second degree AV block – Mobitz type II

Third-Degree Atrioventricular Block

A complete failure of the AV node to conduct any impulses from the atria to the ventricles is the main feature of third-degree atrioventricular block. There is AV dissociation and escape rhythms that may be junctional or ventricular, which represent perfusing rhythms. This is due to AV nodal disease or a disease involving the His-Purkinje system caused by coronary artery disease, enhanced vagal tone, a congenital disorder, underlying structural heart disease such as myocardial infarction, hypertrophy, inflammation or infiltration, Lyme disease, post-cardiac surgery, cardiomyopathies, rheumatologic diseases, autoimmune diseases, amyloidosis, sarcoidosis, or muscular dystrophy. At any time, the patient may suffer ventricular standstill that may result in sudden cardiac death. Pacemaker insertion is necessary to provide needed perfusion.

Third degree AV block (complete heart block)

References

  1. Busquet J, Fontan F, Anderson RH, Ho SY, Davies MJ. The surgical significance of the atrial branches of the coronary arteries. International Journal of Cardiology. 1984;6:223-234.
  2. Elisha S. Nurse Anesthesia. 6th St. Louis, Missouri: Elsevier; 2018.
  3. Liu BR, Cherry EM. Image-based structural modeling of the cardiac Purkinje network. Biomedical Research International. 2015. https://dx.doi.org/10.1155/2015/621034.
  4. Markowitz SM, Leman BB. A contemporary view of atrioventricular nodal physiology. Journal of Interventional Cardiac Electrophysiology. 2018;52:271-279.
  5. Meijler FL, Billette J, Jalife J, Kik MJ, Reiber JH, Stokhof AA, et al. Atrioventricular conduction in mammalian species: hemodynamic and electrical scaling. Heart Rhythm. 2005;2:188-96.
  6. Zoob M, Smith KS. The etiology of complete heart-block. British Medical Journal. 1963;2:1149.

Images

  1. 2019 Regents of the University of Minnesota. The conduction system of the heart. https://www.vhlab.umn.edu/atlas/physiology-tutorial/the-human-heart.shtml. Updated 2019. Accessed November 20, 2019.
  2. Burns E. ECG rhythm strip PR interval prolonged extreme 1st-degree AV block. https://lifeinthefastlane.com/ecg-library/basics/first-degree-heart-block/. Updated April 28, 2019. Accessed November 20, 2019.
  3. Patterson Harry. AV Block: 2nd-degree AV block, Mobitz I. https://lifeinthefastlane.com/ecg-library/basics/wenckebach/. Updated March 16, 2019. Accessed November 20, 2019.
  4. Burns E. ECG example of Mobitz II. https://lifeinthefastlane.com/ecg-library/basics/mobitz-2/. Updated May 20, 2019. Accessed November 20, 2019.
  5. Burns E. ECG strip 3rd-degree AV block complete heart block. https://lifeinthefastlane.com/ecg-library/basics/complete-heart-block/. Updated March 24, 2019. Accessed November 20, 2019.
Источник: https://resources.acls.com/free-resources/knowledge-base/bradycardia/understanding-atrioventricular-block

First Degree Heart Block - Heart Blocks.


Description

  • First Degree Heart Block will look like a typical sinus rhythm with one distinguishing feature.
  • The P-R interval will be constant throughout the tracing and measure greater than 0.20 seconds.
  • Rate, regularity, P wave morphology and QRS duration and morphology will be unaffected.
  • NOTE: The rate will be that of the underlying rhythm. If the friday may 1st is “normal”, it will be 60 – 100 bpm. If it is bradycardia, the rate will be less than 60 bpm.
  • First Degree Heart Block is the most common heart block.
  • People are born with it everyday. They will likely live a long and healthy life and die from some other malady.
  • Patients who develop a heart block during an MI bear close observation. This must be reported to the licensed healthcare practitioner immediately.

Example

Notice the following: the only abnormality when analyzing this tracing is the abnormal duration of the P-R interval.

heart block ecg image 102

Practice Strip

heart block ecg image 103

Analyze this tracing using the five steps of rhythm analysis.



Источник: https://ekg.academy

Electrocardiogram 3: cardiac rhythm and conduction abnormalities

The last of three articles on using an electrocardiogram to assess the heart’s electrical activity focuses on causes of cardiac rhythm and conduction abnormalities and how to spot them

Abstract

This is the last in a three-part series on using an electrocardiogram to assess the heart’s electrical activity. In this article, the focus is on cardiac rhythm and conduction abnormalities of the heart, which all have unique presenting characteristics. These characteristics include ectopic beats, tachycardias and atrioventricular block.

Citation: Jarvis S (2021) Electrocardiogram 3: cardiac rhythm and conduction abnormalities. Nursing Times [online]; 117: 8, 27-32.

Author: Selina Jarvis is honorary research nurse, Guy’s and St Thomas’ NHS Foundation Trust.

  • This article has been double-blind peer reviewed
  • Scroll down to read the article or download a print-friendly PDF here (if the PDF fails to fully download please try again using a different browser)
  • Click here to see other articles in this series

Introduction

This is the final article in a three-part series on use of an electrocardiogram (ECG), a non-invasive and quick investigation that assesses the electrical activity of the heart. Part 1 looked at the purpose of the test, cardiac electrophysiology and the practicalities of doing an ECG, while part 2 looked at interpretation, with a particular focus on cardiac ischaemia. In this article, the focus is on abnormalities in rhythm and electrical conduction that can be identified on an ECG.

Cardiac arrhythmias and conduction defects are common. They can be an acute problem presenting for the first time, or part of a chronic disease course complicated by acute decompensation at periods of illness. Some arrhythmias may cause little to no symptoms and are fairly benign, while others are of greater concern and may lead to serious symptoms; at worst, they may predate a cardiac arrest if not recognised and treated promptly.

Clinical assessment of arrhythmia

The following steps are key when assessing a patient presenting with an abnormal heart rhythm or conduction defect:

  • Take a history of open drive thru food near me complaint/symptom with which the patient presents;
  • Consider whether there are any features of cardiac compromise (specifically, shock, syncope or fainting, myocardial ischaemia, heart failure);
  • Consider any relevant past medical history;
  • Take note of medications that may be associated with the condition;
  • Ask about family history of arrhythmias, cardiac disease or sudden cardiac death;
  • Consider relevant investigations, such as electrolyte abnormalities. Excess, or deficiencies in, potassium, magnesium or calcium can affect the 1st degree av block rhythm strip of electrical charges inside and outside of cardiac cells, alter electrical signalling and cause arrhythmias;
  • Compare with previous ECG results if available.

Clinical symptoms

There are various potential symptoms associated with an arrhythmia. One common symptom is palpitations but this can mean different things to different people. Some report it as an increased awareness of a heartbeat or fluttering in the chest, while others may report feeling an extra or missing beat or complain of an irregular heart rate. You can ask patients to tap out the rhythm of the beat they felt onto a table with their hands or show you their device if they have recorded an event.

Symptoms may also include dizziness or syncope. Syncope may be due to a simple faint, often when standing for a long period of time or when standing up from a sitting/recumbent position (postural) or at rest, and can be related to aberrations in heart rhythm or conduction defects. Be aware that there may be causes of a cardiogenic or neurogenic nature (for example, seizures) to consider in the differential diagnosis.

Other symptoms are increased breathlessness, sweating or chest pain; these signs may be more common with tachycardias (see below). With the advent of fitness technology, such as smart watches, some patients may present with or without a history of symptoms after identifying abnormal activity on their ECG mobile app.

Recognising cardiac arrhythmias

When considering whether cardiac rhythms are normal, it is important to understand the electrical conducting system of the heart and how the ECG works, which were covered in parts 1 and 2 of this series. In summary, the sinoatrial node (SAN) is the natural pacemaker of the heart, generating a signal without an external stimulus. If this stops working, other slower potential pacemakers in the heart, such as the atrioventricular node (AVN) or bundle of His, can take over (Jarvis and Saman, 2018). In these circumstances, overall heart rate will be slower.

The key components of the cardiac conducting system are discussed below and listed with their usual intrinsic rates in Table 1.

Ectopic beats

Ectopic beats are common and characterised by single electrical impulses that originate away from the SAN as extra beats. They are generally benign and of 1st degree av block rhythm strip clinical significance. In the presence of an atrial ectopic (premature atrial contraction), an extra wave is seen within the P-wave (atrial depolarisation) so it looks different to normal on the ECG. Ventricular ectopic beats (premature ventricular contractions) look more dramatic, with a:

  • Large wave on the rhythm trace typically not preceded by chase business checking 300 offer P-wave;
  • Wide overall QRS complex (ventricular depolarisation) of more than 120 milliseconds (ms) and inverted T-wave (ventricular repolarisation) (Fig 1).

If there are isolated ectopic beats, there rabobank creditcard aanvragen likely to be little clinical significance or action needed (Omar et al, 2011). However sometimes there is a ventricular ectopic beat after every normal 1st degree av block rhythm strip complex; this is referred to as ventricular bigeminy and suggests some ventricular irritability.

If the patient is symptomatic with frequent ectopic beats, make sure you ask them about potential medications that can interfere with heart rate (for example, salbutamol, digoxin, over-the-counter cold and allergy drugs, or antiarrhythmic drugs), as well as high caffeine and alcohol consumption. Further investigations may be needed, such as checking electrolytes (potassium, magnesium and calcium) and thyroid function and, sometimes, a 24-hour or 48-hour Holter monitor or ECG may be required.

Sinus bradycardia

Sinus bradycardia is a slow heart rate of ≤60 beats per minute (bpm), due to the slowing down of the SAN. This may be physiological, often occurring in fit individuals like athletes, and may be related to an increase in the vagal tone of the heart caused by the vagus nerve (actually a group of nerves that control parasympathetic activity in the heart). 1st degree av block rhythm strip can also be caused by vomiting, straining (through vagal effects), beta-blocker drugs and raised intracranial pressure from head injury/pathology. It can also happen in the context of an inferior myocardial infarction in which the SAN is in the region supplied by an occluded coronary artery — usually, the right coronary artery affecting the sinoatrial artery.

Bradycardia can be caused by diseases such as sick sinus syndrome, when there is an irreversible dysfunction of the SAN that affects its ability to generate electrical impulses to the heart. This can cause a pause in electrical signals from the sinus (lasting seconds to minutes), or electrical impulses for which signals from the sinus are slow or blocked. The dysfunction can result in an alternating slow and fast heart 1st degree av block rhythm strip called bradycardia-tachycardia syndrome, or there may be atrioventricular block (described later in this piece). When there are symptoms due to sinus node problems, the patient may need to have a pacemaker inserted (National Institute for Health and Care Excellence, 2014a).

“It is important to keep an open mind to the potential causes and take a proper clinical history”

Sinus tachycardia

In sinus tachycardia, the SAN is firing at a rate of ≥100bpm, but the rest of the conducting system is normal. There are many benign causes, such as sinus tachycardia in response to pain or exercise, as an adaptation in pregnancy, a response to caffeine or a side-effect of medications such as salbutamol or digoxin.

Sinus tachycardia can also occur with fever, infection, dehydration, electrolyte (typically calcium, magnesium or potassium) abnormalities, and overactive thyroid. However, it can signify more-dangerous conditions, such as pulmonary embolism, and it is important to keep an open mind to the potential causes and take a proper clinical history.

Assessing tachycardias

A normal heart rate is 60-100bpm; tachycardia refers to a fast heart rate of >100bpm. It has different causes and the reason for the fast heart rate can originate from the atria or the ventricles. Tachycardia may be transient, lasting for seconds or minutes, but can also last for several days.

It is possible to differentiate between tachycardias that originate in the atria or ventricles by looking at the width of the QRS complex, which is normally 120ms. In tachycardia originating in the atria (supraventricular), the QRS is typically narrow (<120ms) compared with that originating in the ventricles (ventricular tachycardia), for which the QRS is broad (≥120ms).

Supraventricular tachycardia

Supraventricular tachycardia, with the characteristic narrow QRS complex, may originate in the atria or AVN. There are many different causes, including known cardiac or lung disease, particular medications, substance misuse, smoking, infection and pregnancy. The interpretation of an ECG should be done in a methodical way (Jarvis, 2021a). For tachycardia specifically, you should consider whether:

  • There are any P-waves;
  • The rhythm looks regular or irregular;
  • It is narrow or broad complex tachycardia based on the duration of the QRS complex (Ganz, 2019).

The most common sustained narrow complex tachycardia is atrial fibrillation (AF) (NICE, 2014b). There are several causes (Table 2) and a steep rise in prevalence with age. In AF, the atria have many mini circuits originating from small islets due to atrial remodelling. As a result, there is chaotic electrical activity with no concerted atrial depolarisation, which leads 1st degree av block rhythm strip an irregular, fast heart rhythm. As the electrical activity does not originate in the usual way from the SAN, there is a lack of P-waves and the rhythm strip of the ECG looks irregular (Fig 2a).

AF can spontaneously revert back to sinus rhythm or resolve once the underlying cause has been treated but the longer patients have the condition, the less likely it is to terminate spontaneously; they will need medications for rate control and anticoagulation due to the risk of clots forming in the fibrillating atria (Olshansky and Arora, 2019). As AF increases stroke risk by up to five times, it is crucial to consider anticoagulation based on a scoring system.

Atrial flutter – the causes and ECG features for which are outlined in Table 2 – is a supraventricular tachycardia that is regular, but the atrial rate is up to 300bpm and there are flutter waves that form a continuous sawtooth line. Although the atrial rate is 300bpm, the AVN has a delay due to its slower intrinsic rate so it is not able to transmit this fast rate and slows down atrial flutter typically to around 150bpm (Olshansky and Arora, 2019). This is a protective mechanism to prevent the impulses being transmitted into the ventricles. The result on the ECG is sawtooth-looking waves, instead of normal P-waves; not all of these are followed by a QRS complex so there are sometimes two P-sawtooth-waves preceding state bank of india near me branch QRS, which is referred to as a 2:1 block (Fig 2b).

Another narrow complex tachycardia that can occur at any age is atrioventricular-nodal re-entrant tachycardia (AVNRT), a common cause of paroxysmal supraventricular tachycardia caused by the formation of a re-entry circuit in the AVN or tissue around it (Knight, 2020). It develops suddenly, often with concomitant sudden onset of palpitations, and can relate to underlying structural heart disease but is precipitated by stress, alcohol, caffeine and other stimulants. On the ECG, there is a regular, narrow complex tachycardia with a heart rate of 120-220bpm. Fig 2c shows supraventicular tachycardia, which is a common type of AVNRT.

Management includes vagal manoeuvres to slow the AVN, such as carotid sinus massage of the neck or asking the patient to blow into a 50ml syringe (if not contraindicated). Otherwise, pharmacological control may be needed with adenosine (3mg intravenously over two seconds (s), followed by 6mg after 1-2 minutes, if required, then 12mg after 1–2 minutes). This can slow down the heart rate and help to identify a regular tachycardia.

Paroxysmal supraventricular tachycardia can be a result of AVNRT but, in younger patients, can be due to Wolff Parkinson White syndrome, in which an accessory pathway linking atria and ventricles bypasses the AVN, and for which there is a characteristic delta wave present on the ECG (Chhabra et al, 2020). With any supraventricular tachycardias, if there are any adverse features, electrical or chemical bank holiday fun fair near me may be required to bring the patient back into sinus rhythm.

Ventricular tachycardia

This is a broad complex tachycardia originating in the ventricles with a heart rate of >100bpm and a QRS complex of >120ms. For the most part, a broad complex tachycardia is likely to be due to a ventricular tachycardia and it is safest to consider this first, given the urgency for treatment.

In some cases, the problem may originate in the atria, such as with AF when a defect of electrical impulses down the bundle branches results in an ECG suggestive of a broad complex tachycardia. In this case of AF with a bundle branch block, there would be an absence of P-waves and the rhythm would be irregular, along with the broad QRS complex. Looking at the QRS complex may also be helpful in ventricular tachycardia because the heart rate keybank savings account apy regular and the QRS looks monomorphic (uniform) throughout the ECG trace.

It is crucial to recognise ventricular tachycardia on an ECG or cardiac monitor because it needs urgent medical attention; guidance on this can be found in the Resuscitation Council UK’s guidelines by Soar et al (2021).

Depending on whether there are adverse features and signs of haemodynamic compromise, such as shock, syncope, or chest pain, electrical cardioversion may need to be considered to bring the heart back into sinus rhythm. Pharmacological agents are another option for rate control and treatments include beta-blockers, calcium channel blockers or chemical cardioversion with amiodarone.

In polymorphic ventricular tachycardia (Fig 3a), the shape of the QRS complexes look very different to monomorphic complexes (Fig 3b). In a condition called torsades de pointes, the broad complex QRS complexes are polymorphic and look to be twisting around the electrical baseline with prolongation of the QT interval (Fig 3a). Torsades de pointes is a dangerous heart rhythm that can lead to dizziness and syncope; in addition, although in some cases it may spontaneously revert to sinus rhythm, it can also lead to a cardiac is rice milk good for you with ventricular fibrillation. After checking electrolyte levels and giving magnesium intravenously, if needed, electrical cardioversion may be required.

Causes of ventricular tachycardia and torsades de pointes are outlined in Table 2.

Conduction abnormalities

Conduction defects can be caused by problems at the level of the AVN or through the bundle of His and bundle branches.

Atrioventricular block

Atrioventricular (AV) block relates to a problem in conduction in, or in close proximity to, the AVN. When an electrical impulse leaves the atria and travels to the AVN, there is a delay which is represented by the PR interval (beginning of the P-wave to the start of 1st degree av block rhythm strip QRS complex) (Jarvis, 2021b). The maximum PR interval is 120-200ms (or three to five small squares of the ECG). If there is a delay in the PR interval, this is referred to as AV block or heart block of which there are key classes (Fig 4).

First-degree AV block (Fig 4a) is when there is a constant prolongation of the PR interval of ≥200ms. This is usually a benign state in which patients tend to be asymptomatic and it may not have been found had they not had an ECG.

There are two sub-types of the second-degree AV block: Mobitz type I and Mobitz type II. In both conditions, a P-wave is blocked from initiating a QRS complex. In Mobitz type I (also called Wenckebach), the disease is in the AVN; it is a more benign AV block than in Mobitz type Set up gmail account without mobile number and can be identified by a prolonged PR interval, which progressively increases on successive beats until there is a dropped beat (Fig 4b).

This differs from Mobitz type II in which the problem is below the AVN (most likely in the bundle of His or Purkinje fibres) and, intermittently, a non-conducted P-wave can be how much do you get for unemployment in louisiana (that is, there is no QRS complex). This can happen every other beat, referred to as 2:1 block (Fig 4c), or every third beat, referred to as 3:1 block. Mobitz type 1st degree av block rhythm strip is associated with a worse prognosis and can progress to third-degree heart block.

In third-degree AV block, there is an absence of conduction between the atria and ventricles, and a complete lack of relationship between the P-waves and QRS complexes (Fig 4d). In this case, the junctional cells found just before the bundle of His bifurcate into bundle branches and act as an escape pacemaker that takes over. This results in a heart rate of 40-60 bpm and is a serious condition with the risk of sudden loss of cardiac output. Avoiding those drugs that slow the AVN, correcting any electrolyte problems, giving atropine that blocks the vagal nerve (0.5mg intravenously every 3-5 minutes until a 3mg maximum dose is reached) can treat the AV block temporarily by bringing up the heart rate ready for urgent pacemaker insertion.

Table 3 summarises the differences in the ECG findings and causes of AV blocks.

Bundle branch blocks

In the normal heart at the level of the bundle of His, conducting fibres split into the right and left bundle branches, which conduct electrical impulses to the christopher and banks coupons september 2019 and left ventricles, respectively. This impulse usually occurs in synchrony and the ventricles contract simultaneously. If there is a block in one of the bundle branches due to damage, there may be a delay in the electrical impulse leading to that ventricle, causing a widened QRS complex exceeding 120ms. In the case of the right bundle branch block (Fig 5a), this can happen because of normal variation or due to diseases such as atrial septal defect, pulmonary embolus or cor pulmonale (heart failure due to lung disease).

Left bundle branch block can be seen in healthy people, but is also due to various cardiomyopathies, hypertension and fibrosis of the heart (Hampton and Adlam, 2019). Most patients with a bundle branch block (Fig 5b) are stable and intervention is only needed if they become symptomatic.

Conclusion

A good knowledge of the conducting system of the heart, including appreciating that depolarisation begins in the SAN and the route of the electrical impulse, is useful when understanding and identifying conduction defects and arrhythmias. This series has covered the principles and practicalities of ECG and how to take a methodical approach to its interpretation, while considering potential causes in context of the clinical situation and medical history.

Key points

  • Cardiac rhythm and conduction defects, such as atrial fibrillation, are common
  • They can be an acute problem presenting for the first time or part of the course of a chronic disease
  • When considering whether cardiac rhythms are normal, nurses need to understand the electrical conducting system of the heart
  • A clinical history should include medicines and current symptoms when assessing rhythm disorders
  • It is important to understand the unique patterns in rate and waveform on the electrocardiogram that are associated with different disorders

References

Chhabra L et al (2020) Wolff Parkinson White Syndrome. Treasure Island, FL: StatPearls Publishing.

Ganz LI (2019) Wide QRS complex tachycardias: approach to diagnosis. UptoDate.com, 4 November.

Hampton JR, Adlam D (2019) The ECG Made Practical. Elsevier.

Jarvis S (2021a) Electrocardiogram 2: interpretation and signs of heart disease. Nursing Times; 117: 7, 54-57.

Jarvis S (2021b) Electrocardiogram 1: purpose, physiology and practicalities. Nursing Times; 117:
6, 24-28.

Jarvis S, Saman S (2018) Cardiac system 1: anatomy and physiology. Nursing Times [online]; 114: 2, 34-37.

Knight BP (2020) Atrioventricular nodal reentrant tachycardia. UptoDate.com, 26 October.

National Institute for Health and Care Excellence (2014a) Dual-chamber Pacemakers for
Symptomatic Bradycardia due to Sick Sinus Syndrome without Atrioventricular Block. NICE.

National Institute for Health and Care Excellence (2014b) Atrial Fibrillation: Management. NICE.

Olshansky B, Arora R (2019) Mechanisms of atrial fibrillation. UptoDate.com, 22 October.

Omar AR et al (2011) Managing ventricular ectopics: are ventricular ectopic beats just an annoyance? Singapore Medical Journal; 52: 10, 707–713.

Soar J et al (2021) Adult Advanced Life Support: Guidelines. Resuscitation Council UK.

 

2021-07-26

NT Contributor

Источник: https://www.nursingtimes.net/clinical-archive/cardiovascular-clinical-archive/electrocardiogram-3-cardiac-rhythm-and-conduction-abnormalities-26-07-2021/

ECG Review: 2nd Degree AV Block, Mobitz Type II?

ECG Review

2nd Degree AV Block, Mobitz Type II?

By Ken Grauer, MD, Professor Emeritus in Family Medicine, College of Medicine, University of Florida. Dr. Grauer is the sole proprietor of KG-EKG Press, and publisher of an ECG pocket brain book.

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Scenario: Interpret the rhythm strip shown above. Does it represent 2nd degree AV Block, Mobitz Type II? Clinically — why is it important to distinguish between Mobitz I and Mobitz II 2nd degree AV block?

Interpretation: The rhythm in the Figure is slow but regular. The QRS complex is narrow, and a regular atrial rate is seen at 100/minute (arrows). Every other P wave conducts (as evidenced by the fact that a P wave does precede each QRS complex with a fixed PR interval!).

Traditionally — the AV blocks are divided into three degrees based on severity of the conduction disturbance:

• 1st degree AV block — in which all atrial impulses are conducted to the ventricles, albeit with delay (so that the PR interval exceeds 0.20 second).

• 2nd degree AV block — in which some (but not all) atrial impulses beach nourishment outer banks nc conducted to the ventricles.

• 3rd degree (or "complete") AV block — in which none of the atrial impulses are conducted to the ventricles, despite having more than adequate opportunity for conduction to occur.

Second degree AV blocks are further classified into three types:

• Mobitz I (AV Wenckebach) — in which the PR interval progressively lengthens until a beat is dropped. This is by far the most common form of 2nd degree AV block. Mobitz I usually occurs at the level of the AV node. As a result, the QRS complex is typically narrow. Mobitz I is generally associated with inferior infarction; it often spontaneously resolves, and typically responds to atropine (which works on the AV node).

• Mobitz II — in which there is a constant PR interval for consecutively conducted beats until one or more beats are dropped. Because Mobitz II typically occurs low down in the conduction system — the QRS complex is generally wide. This less common form of 2nd degree AV block is generally associated with anterior infarction; it usually does not respond to atropine — and is important to recognize because pacing will probably be needed.

• 2-to-1 AV Block — 1st degree av block rhythm strip which one never sees two consecutively conducted beats, so that you cannot tell if the PR interval is lengthening or not. As a result, it is impossible to know for sure whether this form of 2nd degree AV block represents Mobitz I or Mobitz II. This is precisely the situation seen in the Figure. We suspect this rhythm represents 2nd degree AV block, Mobitz Type I (Wenckebach) because: 1) Mobitz I is so much more common than Mobitz II; and 2) the QRS complex is narrow, as it almost always is with Mobitz I. Finding additional rhythm strips on this patient that clearly showed progressive lengthening of consecutively conducted QRS complexes before dropping a beat would strongly support our suspicion. Clinically the distinction is important because no treatment (other than perhaps atropine) is likely to be needed for Mobitz I (especially given that the ventricular rate 1st degree av block rhythm strip the above example is not overly slow at 50/minute). In contrast, pacing would probably be needed if the rhythm was Mobitz II.

Источник: https://www.reliasmedia.com/articles/131317-ecg-review-2nd-degree-av-block-mobitz-type-ii

Second Degree Atrioventricular Block


Related articles:AV blocks, first degree AV block, complete AV block.

With second-degree AV block an intermittent failure of the AV conduction occurs. Not all P waves are followed by a QRS complex, causing pauses in ventricular stimulation.

There are two types of second-degree AV block, type I, also called Mobitz type I or Wenckebach phenomenon, and type II, also called Mobitz type II.

This article will also discuss the second-degree AV block with conduction ratio 2:1 and advanced AV block.

Type I Second Degree AV Block. Mobitz type I or Wenckebach Phenomenon

In type I second-degree atrioventricular block (Wenckebach phenomenon) there is an AV conduction block with a progressive lengthening of PR interval of previous beats.

In other words: there is a progressive PR interval lengthening until a P wave is not conducted (Wenckebach phenomenon). Progressive shortening of the RR interval until a blocked P wave is also observed.

Type I Second Degree AV Block. Mobitz type I or Wenckebach Phenomenon

Type I second-degree AV block (Wenckebach phenomenon): Progressive lengthening of the PR interval until a P wave is blocked (red).

Electrocardiogram Findings

  • Progressive lengthening of the PR interval until a P wave is not followed by a QRS complex (blocked P wave).
  • Progressive shortening of the RR interval until a P wave is blocked.
  • RR interval containing the blocked P wave is shorter than the sum of two PP intervals 1.

Prolongation of the PR interval may not be progressive. If previous PR intervals are different from each other, it is also considered type I second-degree atrioventricular block 1 2.

At least two consecutive PR intervals are needed before the blocked P to determine the type of AV block.

Type I second-degree AV block is considered benign and is usually asymptomatic. In most patients there is no progression to more serious AV blocks. In elderly patients closer monitoring is recommended.

Type II Second-Degree AV Block. Mobitz type II

Type II second-degree AV block or Mobitz type II is less frequent, and almost always means severe disease of the conduction system 3.

It differs from the type I second-degree AV block by constant PR intervals, before and after the blocked P wave.

Electrocardiogram Findings

  • Constant PR intervals before and after the blocked P wave.
  • The PR 1st degree av block rhythm strip after the blocked P waves is similar to the previous PR interval.
  • RR interval containing the blocked P wave is similar to the sum of two PP intervals.
Type II Second-Degree AV Block. Mobitz type II

Type II second-degree AV block, Mobitz type II:
Constant PR before blocked P. Last beats with AV conduction ratio 2:1.

In second-degree AV block Mobitz type II, is usually located distal to bundle of His, especially if it is associated with bundle branch block 1.

Type II second-degree AV block may require pacemaker therapy for prognostic reasons and pacing may be indicated in asymptomatic patients 4.


2:1 Second-Degree AV Block

In 2:1 AV block the conduction ratio is 2:1, alternating a conducted P wave with a blocked P wave.

In the absence of two consecutive PR intervals is impossible to determine if the second degree AV block is type I or II, because is not possible to determine whether the PR varies 1.

2:1 Second-Degree Atrioventricular Block

2:1 second-degree AV block
Alternating conducted P waves with blocked P waves (red). PR intervals of conducted P waves is constant.

A long rhythm strip or 24 hours holter monitor may help to determine the type of block. Although occasionally is necessary an electrophysiological study.


High-grade or Advance Second-Degree AV Block

In advance second-degree AV block there are more than one consecutive blocked P wave, conduction ratio 3:1 or more.

Identifying the type of second-degree AV block in such instances is also difficult. A comparison of the PR intervals of the occasional captured complexes may help 1.

High-grade or Advance Second Degree AV Block

Advance second-degree AV block:
After a conducted P wave, there are two blocked P waves (red arrows)

This type of AV block has higher risk and poorer prognosis than previous ones, and can cause severe episodes of symptomatic bradycardia.

Advance AV block usually requires electronic pacemaker implantation.


Related articles:AV blocks, First degree AV block, complete AV block.

References

Источник: https://en.my-ekg.com/arrhythmias/second-degree-av-blocks.html

1st degree av block rhythm strip -

First Degree Heart Block - Heart Blocks.


Description

  • First Degree Heart Block will look like a typical sinus rhythm with one distinguishing feature.
  • The P-R interval will be constant throughout the tracing and measure greater than 0.20 seconds.
  • Rate, regularity, P wave morphology and QRS duration and morphology will be unaffected.
  • NOTE: The rate will be that of the underlying rhythm. If the rate is “normal”, it will be 60 – 100 bpm. If it is bradycardia, the rate will be less than 60 bpm.
  • First Degree Heart Block is the most common heart block.
  • People are born with it everyday. They will likely live a long and healthy life and die from some other malady.
  • Patients who develop a heart block during an MI bear close observation. This must be reported to the licensed healthcare practitioner immediately.

Example

Notice the following: the only abnormality when analyzing this tracing is the abnormal duration of the P-R interval.

heart block ecg image 102

Practice Strip

heart block ecg image 103

Analyze this tracing using the five steps of rhythm analysis.



Источник: https://ekg.academy

Understanding Atrioventricular Blocks

Cardiac Conduction System

The myocardium contains sets of specialized cells that form the conduction system of the heart, and are responsible for automaticity and rhythm maintenance. The specific areas are the sinoatrial (SA) node, internodal tracts, atrioventricular (AV) node, atrioventricular bundle, and Purkinje system.

SA Node

The SA node is a small collection of specialized cells and collagenous tissue located along the epicardial surface at the junction of the superior vena cava and the right atrium.2 The blood supply is via the sinus node artery and is from the initial branch of the right coronary artery in approximately 60% of individuals and takes its origin from the circumflex artery in the other 40%, with a few instances of lateral origin from either the right or left arteries or dual origins from both arteries.1 The intrinsic rate of the SA node is 60-100 beats per minute (BPM) and the speed of conduction to adjacent cells within the SA node is 0.5 m/sec.

Internodal Tracts

The SA node and AV node have conduction pathways between the two that are the primary route of impulse transmission and are called internodal tracts. Three major internodal tracts exist: the anterior, middle, and posterior tracts.2 The anterior nodal tract (Bachmann bundle) extends into the left atrium and then travels downward through the atrial septum to the AV Node,2 the middle internodal tract (Wenckebach tract) curves behind the superior vena cava before descending to the AV node, and the posterior internodal tract (Thorel’s pathway) continues along the terminal crest to enter the atrial septum and then passes to the AV node.

internodal tracts

Online accredited certifications

Atrioventricular Node

The AV node is located beneath the endocardium on the right side of the atrial septum, anterior to the opening of the coronary sinus.2 Conduction through the AV node delays propagation of impulses from atria to ventricles and thus permits atrial systole to augment ventricular filling during late diastole, with an added 15-35% contribution to ventricular volume.5 In delaying transmission of the cardiac impulse from the atria to the ventricles, the AV node serves a critical function in augmenting ventricular filling during diastole and limiting the ventricular response during atrial tachyarrhythmias.4 Impulse conduction is considerably slower as compared to any other region within the normal cardiac conduction system (0.05 m/sec) and this delayed speed allows for sufficient time for atrial depolarization and contraction prior to ventricular depolarization and contraction.2 When conduction slowing becomes exaggerated or heterogeneous within the AV node, abnormal rhythms ensue, such as pathological conduction block or reentrant tachycardias.4

His-Purkinje System

The Purkinje network functions to distribute a stimulus throughout the entire ventricles, leading to a much faster total activation of the ventricles than could be achieved by the spread of excitation solely through the ventricular muscle.3 The left bundle branch extends outward under the endocardium and forms several fascicles, which innervate various parts of the left ventricle.2 The anterior fascicle innervates the anterolateral wall of the left ventricle the anterior papillary muscle, and the posterior fascicle innervates the lateral and posterior ventricular wall and the posterior papillary muscle.2 The right bundle branch travels under the endocardium along the right side of the ventricular septum to the base of the anterior papillary muscle.2 The Purkinje cells have an intrinsic back up rate of 20-40 BPM when no signal is received from the SA node or AV node.

Understanding Atrioventricular Block

AV blocks are conduction delays or a complete block of impulses from the atria into the ventricles. AV block may be due to increased vagal tone that may be elicited during sleep, athletic training, pain, or stimulation of the carotid sinus. Damage of the conduction system secondary to hereditary fibrosis or sclerosis of the cardiac skeleton are known as idiopathic progressive cardiac conduction disease. Ischemic heart disease causes 40% of AV blocks.6 AV blocks are also seen in cardiomyopathies, myocarditis, congenital heart diseases, and familial diseases. A plasma potassium concentration above 6.3 mEq/L may also cause AV block. They may be iatrogenic, from medications such as Verapamil, Diltiazem, Amiodarone, and Adenosine, or from cardiac surgeries and catheter ablations for arrhythmias.

AV blocks are further classified according to the degree of blockage and include first degree AV block, second degree AV block, and third-degree AV block.

First-Degree Atrioventricular Block

The measurement of conduction time between the atria and ventricles is represented by the PR interval on electrocardiograms (ECG). This component includes the intra-atrial conduction, represented by the P wave, and the conduction from the AV node into the His-Purkinje system. Prolongation of the PR interval of more than 200 milliseconds is considered to be a first-degree AV block. These can be due to structural abnormalities within the AV node, an increase in vagal tone, and drugs that slow conduction such as digoxin, beta-blockers. and calcium channel inhibitors. It is important to note that in first degree AV block, no actual block occurs.

first degree av block

Second-Degree Atrioventricular Block

Second-degree atrioventricular blocks are occasional non-conducted P waves with prolonged RR intervals. There are two types under this classification. Mobitz type I (Wenckebach) occurs when there is an intermittent conduction block within the AV node that results in a failure to conduct an impulse from the atria into the ventricles. The impaired nodal conduction is progressive to the point that there is a total block. This causes an absent impulse into the ventricles, reflected by the disappearance of the QRS complex in the ECG. Mobitz type I is a benign condition that rarely causes hemodynamic instability; asymptomatic patients need no further treatment. Symptomatic patients will require a pacemaker.

second degree AV block - mobitz type I

The Mobitz type II AV block is secondary to a disease involving the His-Purkinje system, in which there is a failure to conduct impulses from the atria into the ventricles. A block occurs after the AV node within the bundle of His, or within both bundle branches. The His-Purkinje system is an all-or-none conduction system; therefore, in Mobitz type II, there are no changes in the PR interval, even after the non-conducted P wave. Because of this, Mobitz type II has a higher risk of complete heart block compared to Mobitz type I.

Second degree AV block – Mobitz type II

Third-Degree Atrioventricular Block

A complete failure of the AV node to conduct any impulses from the atria to the ventricles is the main feature of third-degree atrioventricular block. There is AV dissociation and escape rhythms that may be junctional or ventricular, which represent perfusing rhythms. This is due to AV nodal disease or a disease involving the His-Purkinje system caused by coronary artery disease, enhanced vagal tone, a congenital disorder, underlying structural heart disease such as myocardial infarction, hypertrophy, inflammation or infiltration, Lyme disease, post-cardiac surgery, cardiomyopathies, rheumatologic diseases, autoimmune diseases, amyloidosis, sarcoidosis, or muscular dystrophy. At any time, the patient may suffer ventricular standstill that may result in sudden cardiac death. Pacemaker insertion is necessary to provide needed perfusion.

Third degree AV block (complete heart block)

References

  1. Busquet J, Fontan F, Anderson RH, Ho SY, Davies MJ. The surgical significance of the atrial branches of the coronary arteries. International Journal of Cardiology. 1984;6:223-234.
  2. Elisha S. Nurse Anesthesia. 6th St. Louis, Missouri: Elsevier; 2018.
  3. Liu BR, Cherry EM. Image-based structural modeling of the cardiac Purkinje network. Biomedical Research International. 2015. https://dx.doi.org/10.1155/2015/621034.
  4. Markowitz SM, Leman BB. A contemporary view of atrioventricular nodal physiology. Journal of Interventional Cardiac Electrophysiology. 2018;52:271-279.
  5. Meijler FL, Billette J, Jalife J, Kik MJ, Reiber JH, Stokhof AA, et al. Atrioventricular conduction in mammalian species: hemodynamic and electrical scaling. Heart Rhythm. 2005;2:188-96.
  6. Zoob M, Smith KS. The etiology of complete heart-block. British Medical Journal. 1963;2:1149.

Images

  1. 2019 Regents of the University of Minnesota. The conduction system of the heart. https://www.vhlab.umn.edu/atlas/physiology-tutorial/the-human-heart.shtml. Updated 2019. Accessed November 20, 2019.
  2. Burns E. ECG rhythm strip PR interval prolonged extreme 1st-degree AV block. https://lifeinthefastlane.com/ecg-library/basics/first-degree-heart-block/. Updated April 28, 2019. Accessed November 20, 2019.
  3. Patterson Harry. AV Block: 2nd-degree AV block, Mobitz I. https://lifeinthefastlane.com/ecg-library/basics/wenckebach/. Updated March 16, 2019. Accessed November 20, 2019.
  4. Burns E. ECG example of Mobitz II. https://lifeinthefastlane.com/ecg-library/basics/mobitz-2/. Updated May 20, 2019. Accessed November 20, 2019.
  5. Burns E. ECG strip 3rd-degree AV block complete heart block. https://lifeinthefastlane.com/ecg-library/basics/complete-heart-block/. Updated March 24, 2019. Accessed November 20, 2019.
Источник: https://resources.acls.com/free-resources/knowledge-base/bradycardia/understanding-atrioventricular-block

Atrioventricular block electrocardiogram

Editor-In-Chief:C. Michael Gibson, M.S., M.D.[1]

Electrocardiogram

The main diagnostic modality used in determining whether a person has heart block, is the electrocardiogram.

  • First degree heart block consists of a prolonged PR interval of more than >200msec.
  • Second degree heart block consists of Mobitz type I and Mobitz type II heart block.
    • Mobitz I or Wenckebach block will show a progressive prolongation of the PR interval, until a ventricular beat is missed.
    • Mobitz II AV block consists of a constant PR interval with intermittent missed beats.
  • Complete heart block or third degree heart block will be depicted by a complete disassociation of atrial and ventricular beats.

EKG Examples

First Degree AV Block EKG Examples

Shown below is an EKG image showing sinus rhythm with a prolonged PR interval (>200ms.) which is first degree AV block. There is also a left axis deviation (axis between -30 and -90 degrees) with r waves in the inferior leads. This axis deviation is consistent with a left anterior fasicular block.

AVBlockEKG.jpg

Copyleft image obtained courtesy of ECGpedia, http://en.ecgpedia.org/wiki/Main_Page


Second Degree AV Block EKG Examples

Mobitz I Second Degree AV Block EKG Examples

Shown below is an EKG image of ventriculophasic reflex during second degree AV block Mobitz I. The PP interval where the blocked sinus beat occurs, is prolonged.

Ventriculophasic Reflex.jpg

Copyleft image obtained courtesy of ECGpedia, http://en.ecgpedia.org/wiki/File:De-Ventrfascreflex.jpg


Shown below are two rhythm strips showing Mobitz I A/V block with a gradual increase in the PR interval before the dropped p wave. Note the 2:1 block in the lower strip, and that one can not use this to determine if the block is Mobitz I or II as more than one conducted P wave is required to do this.

Mobitz type I block.jpg

Copyleft image obtained courtesy of ECGpedia,http://en.ecgpedia.org/wiki/File:E267.jpg


Mobitz II Second Degree AV Block EKG Examples

Shown below is an EKG image of two-to-one AV block, which can represent benign block within the AV node or disease of the His-Purkinje system. Certain electrocardiographic features and maneuvers can help in distinguishing where the location of block exists. A long PR interval with a narrow QRS suggests an intranodal block. A short PR interval with intraventricular conduction delay or bundle branch block suggests disease below the node. Responses to atropine, exercise and carotid sinus massage can be helpful in diagnosis. Atropine will improve AV nodal conduction but will worsen block within diseased His-Purkinje fibers. Exercise has a similar effect, improving conduction in cases where block exists only in the node, but worsening when block is subnodal. Alternatively, Carotid Sinus Massage will slow conduction when block occurs in the AV node, but will improve conduction in diseased His-Purkinje tissue by allowing for refractoriness to recover.

2to1AVBlock1.jpg

Copyleft image obtained courtesy of ECGpedia, http://en.ecgpedia.org/wiki/Main_Page

For more EKG examples of First Degree AV Block click here

References

Template:WHTemplate:WSCardiology

Источник: https://www.wikidoc.org/index.php/Atrioventricular_block_electrocardiogram

How to Recognize & Treat Heart Block

Learning Objectives

  • Understand the physiology and anatomy of the cardiac conduction system and normal conduction patterns.
  • Identifythe different degrees and types of AV block through accurate interpretation of rhythm disturbances.
  • Learnhow to treat AV block patients, including the administration of atropine and transcutaneous pacing.

Introduction

Cardiac rhythm interpretation is one of the most important skills EMS providers must master. It’s essential to be able to rapidly and accurately interpret rhythm disturbances, as patients with tachy- and brady-dysrhythmias may be unstable and require emergent assessment and treatment. While an in-depth review of all such arrhythmias is outside the scope of this article, we will focus on the diagnosis and treatment of a subset of bradydysrhythmias, specifically AV block and conduction delay.

Normal Conduction
Before discussing the abnormal electrical conduction in the heart, it’s important to first understand the anatomy of the cardiac conduction system and normal conduction patterns.

Cardiac anatomy

The heart is composed of three specialized cells: 1) pacemaker cells; 2) Purkinje cells; and 3) contractile cells.1 Pacemaker cells have a property called automaticity; they undergo spontaneous electrical depolarization that initiates an electrical impulse. The Purkinje cells conduct electrical impulses more quickly than other cells, so that electrical impulses are easily conducted through them. Contractile cells compose the large majority of the heart and will contract when the electric depolarization reaches them.

Typically, electrical impulses in the heart begin in the sinoatrial (SA) node, which is located in the right atrium and contains pacemaker cells. The sinus node artery supplies the SA node; it arises from the right coronary artery (RCA) about 55% of the time and the left circumflex artery (LCx) about 45% of the time.1 From the SA node, impulses then travel through the atrial myocardium to the atrioventricular (AV) node, which lies at the junction between the atria and the ventricles.2

A fibrous ring called the annulus fibrosis electrically insulates the atria and ventricles from one another; thus, the only way for electrical impulses to travel between the atria and ventricles is through the AV node.

The blood supply to the AV node is from the RCA in 90% of people and from the LCx in 10%.1 The distal continuation of the AV node is the bundle of His (sometimes referred to as the atrioventricular bundle), which is composed of Purkinje cells and travels down the intraventricular septum.1—3

The bundle of His separates into two distinct bundles a few millimeters below its junction with the AV node: the left and right bundle branches. The bundle of His is connected to the AV node, but is electrically insulated from the surrounding myocardium, thus allowing conduction only down the bundles rather than directly into the surrounding cardiac tissue. The bundle of His separates into the right and left bundle branches; the left bundle branch further subdivides into an anterior and posterior component.2

“Heart block” refers to a variety of conditions in which conduction from the atria to the ventricles is delayed. We will review the differing types of AV block along with associated causes and treatment.

Figure 2: First-degree AV block. Image courtesy Vanderbilt University School of Medicine

First-degree AV block

First Degree

First-degree AV block is due to delayed conduction in the atrium, AV node or in the His-Purkinje system.4,5 On an ECG, this manifests as a prolonged PR interval with a duration greater than 200 ms. Though the PR interval is prolonged, it should remain constant, and a P wave should precede every QRS complex. Most cases of first-degree AV block will also have a narrow QRS complex, indicating the block is in the proximal portion of the conducting system–likely the AV node itself;4,6 approximately 13% of first-degree AV block, though, may have a wide QRS, indicating a more distal block.4

Approximately 1—2% of the population may have a first-degree AV block as a normal variant; it has no relation to ischemic heart disease and no prognostic value. Clinically, these patients usually have a benign presentation.4 Most patients are asymptomatic and the AV block is found incidentally.4,7 Patients may rarely present with symptoms such as palpitations, dizziness, syncope or angina. Most of these symptoms are due to low cardiac output secondary to the AV block. First-degree AV block can also rarely be seen as a manifestation of acute rheumatic fever or more commonly from medication side effects.4

In an asymptomatic patient, no further investigation or treatment is recommended, though some recent literature has shown that patients with first-degree AV block have an increased risk of developing atrial fibrillation.4,7

Figure 3: Second-degree Type I AV block. Image courtesy Vanderbilt University School of Medicine

 Second-degree Type I AV block

Second Degree Type I
Second-degree type I AV block is also known as Mobitz type I or Wenkebach.4 Mobitz type I block is classically characterized by a progressive lengthening of the PR interval culminating in a dropped QRS complex. The site of the block is usually at or above the AV node, so the P wave and QRS complex will generally have a normal morphology and duration.4,6 As the PR interval lengthens, the R-R interval shortens on the rhythm strip.6 In the first beat of the series, the PR interval will be of normal duration; subsequent beats will have a progressively longer PR interval until the P wave is unable to reach the ventricles and cause a depolarization. This results in a dropped beat, after which the cycle begins again.4

The conduction disturbance in Mobitz type I block is in the AV node approximately 72% of the time, as opposed to within or below the bundle of His. Generally, these may be distinguished by the width of the QRS complex: A complex with normal duration indicates a block in the AV node whereas a widened QRS indicates a block either within or below the bundle of His.4 A simple way to remember this is that if conduction is delayed above the bundle of His, once it passes the block the impulse will still be conducted normally, so the QRS complex should appear normal.

Mobitz type I blocks can sometimes be seen in normal people while asleep and also in conditioned athletes, though both of these are rare findings. It can also be associated with acute myocardial infarction (MI) and as a result of antiarrhythmic or rate-controlling medications. Similar to a first-degree AV block, many patients will be asymptomatic at presentation.

Prognosis and treatment of Mobitz type I depends on symptoms and presence of underlying heart disease. Patients who are asymptomatic and have no heart disease generally don’t require treatment. Asymptomatic patients with underlying heart disease have a variable prognosis, but the prognosis is related to the progression of the underlying heart disease as opposed to the AV block itself. Progression to a higher grade of AV block is rare, unless the patient is experiencing an acute MI. In some patients, a Mobitz type I block will cause symptoms of hypoperfusion, such as dizziness, syncope or hypotension.

EMS providers who encounter symptomatic patients with Mobitz type I heart block should treat the patient with atropine to increase heart rate and therefore perfusion.4 Atropine should be given as a bolus dose of 0.5 mg, and the standard recommendation is to repeat a dose of 0.5 mg every three to five minutes as needed, with the total dose to not exceed 3 mg.4,7 If the first dose of 0.5 mg of atropine is ineffective, our recommendation is to increase the second dose to 1.0 mg one to two minutes after the initial dose is given. We feel waiting three to five minutes to give another 0.5 mg in a symptomatic patient isn’t aggressive enough in the prehospital setting. If atropine is ineffective and the patient remains symptomatic, temporary pacing may be indicated. As Mobitz type I block is generally benign, pacing is only indicated if the patient is hemodynamically unstable or has syncope, symptoms of acute congestive heart failure or ischemic chest pain.

Figure 4: 2:1 AV block. Image courtesy Vanderbilt University School of Medicine

2:1 AV block

Second Degree Type II
Second-degree type II AV block is also known as Mobitz type II.4 It’s also characterized by non-conducted P waves, or dropped QRS complexes. The PR interval in Mobitz type II may be normal or prolonged, but unlike Mobitz type I, it remains constant.4,6 The dropped beats will generally, but not always, occur at regular intervals.7 The QRS complex may be narrow but is more often widened, due to associated bundle branch blocks or the infranodal location of the block. The location of the block in Mobitz type II is distal to the bundle of His, either in the common bundle or the bundle branches. The block can be expressed as a ratio of P waves to QRS complexes; for example, three P waves to every two QRS complexes would be a 3:2 block.4,6

EMS providers must quickly recognize second-degree type II AV block as it’s a much more ominous rhythm than second-degree type I. Patients with Mobitz type II blocks may be unstable, and can suddenly progress to a third-degree heart block, so vigilance is warranted at all times.4,7 Patients with large anterior wall infarctions are at particular risk of progression to complete heart block. As with any bradycardia, the need for emergent treatment is dictated by patient stability.

Patients who are unstable at the time of assessment or progress to complete heart block will require immediate treatment. Although atropine can be tried early on, it’s generally unhelpful, as its predominant effect is to increase the sinus node’s rate and is less effective in increasing AV conduction.

Paramedics shouldn’t waste significant time with atropine if the initial dosing doesn’t improve the patient’s heart rate, as these patients usually require transcutaneous pacing. At the hospital, even asymptomatic patients are likely to undergo permanent pacemaker placement due to the risk of deterioration into complete heart block.4

Distinguishing between Mobitz type I and type II blocks is particularly difficult in patients who have a 2:1 AV block where every other beat is dropped.4,6 Unless a care provider is able to capture two consecutively conducted impulses, distinguishing between the two is impossible, and the rhythm can be referred to as a second-degree AV block with a 2:1 conduction pattern, or nontypeable AV block.4 A trick that can be used is to use the width of the QRS complex as a clue, as a wide QRS complex is more common in Mobitz type II and narrow QRS complex is more common in Mobitz type I.6 Symptomatic patients with a nontypeable second-degree AV block warrant a trial of atropine, particularly when the QRS is narrow, as this indicates a block above the bundle of His. Patients who have a stable, wide QRS 2:1 block or a block that evolves into a type II block aren’t likely to respond to atropine; rapidly switching to pacing is recommended for these patients.4

Second-degree AV block is considered high-grade or advanced when two or more consecutive P waves are blocked.4,6 In patients with an anterior MI, this is usually due to a second-degree type II AV block with co-existent bilateral bundle branch blocks.4 These patients are at particularly high risk for progression to complete heart block.6

Figure 5: Third-degree AV block. Image courtesy Vanderbilt University School of Medicine

Third-degree AV block

Third Degree
Third-degree, or complete AV block, is characterized by a complete dissociation between the atria and ventricles due to absence of conduction through the AV node.4,5 Since no atrial impulses reach the ventricles, the ventricular rate is determined by either a junctional or ventricular pacemaker, which is inherently slow.4 Both the P waves and QRS complexes will “march out” regularly on the ECG, yet be unrelated.6,7

Since the P wave is not generating a QRS complex they may be buried in the complex itself, or in the T wave. If there’s a junctional pacemaker, the QRS complex will be narrow with a rate of 40—60; a ventricular pacemaker will produce a wide QRS complex with a rate of 20—40. These rhythms are generally referred to as either junctional or ventricular “escape” rhythms.4 Ventricular escape rhythms are more likely to be acquired and generally associated with a poorer prognosis.6 The atrial pacemaker may be the SA node or an ectopic focus; thus, the atrial rate may be normal, bradycardic, tachycardic, flutter or fibrillation, while the ventricular rate will generally be bradycardic but regular.4,6 The atrial rate will generally be higher than the ventricular rate, although occasionally the two are very similar; in these cases the block is referred to as “isorhythmic.”4

There are many causes of complete heart block such as ischemia, electrolyte disturbances, tumors, cardiomyopathy, myocarditis, hypothyroidism and hypothermia. The incidence increases with advancing age.5 In adults, the most common causes are drug toxicity (generally from rate-controlling medications), coronary artery disease and degenerative processes.4 In children, the most common cause of complete AV block is congenital: abnormal development of the AV node.4

Third-degree heart block can occur in the setting of acute MI, and these patients are at high risk of hemodynamic instability.4,5 Symptoms are due to decreased cardiac output and may include dizziness, syncope, angina and sudden cardiac death. Elderly patients may only complain of weakness or fatigue. Patients with anterior MI are more likely to be unstable initially, or to suddenly develop instability, because anterior ischemia from occlusion of the left anterior descending artery will cause ischemia and delayed conduction of the bundle branches and conduction system distal to the bundle of His.4,5 In such patients, it’s prudent to place pacing pads at the initial encounter and prior to transport, in case of sudden need for transcutaneous pacing. If a transcutaneous pacemaker isn’t immediately available in the symptomatic patient, a trial of atropine is warranted, though unlikely to increase cardiac output.4

Use of Atropine
Atropine is a parasympatholytic agent; it has vagolytic action that predominantly increases the sinus node’s rate, thus it’s especially effective in sinus bradycardia. This decrease in vagal tone may sometimes also increase AV conduction. Along with this, it also acts on the more distal components of the conduction system. The goal when using atropine is to increase cardiac output and therefore systemic perfusion. It’s most effective in patients with acute myocardial ischemia or infarction, as opposed to patients with primary conduction system disease, as acute MI patients have heightened parasympathetic tone.8,9 As mentioned previously, studies have shown that atropine is more effective in patients with sinus bradycardia than AV block, and more effective with AV block occurring early in the course of acute MI.8

Prehospital administration of atropine has been shown to be safe and effective in bradycardia due both to acute MI and non-acute MI. Complications from atropine administration are rare and include ventricular fibrillation, ventricular tachycardia and symptomatic PVCs. Additionally, there’s thought that during an acute MI, atropine may worsen ischemia by increasing heart rate and therefore metabolic demand of the heart, though one must keep in mind that ischemia is also worsened by hypoperfusion due to the bradyarrhythmia itself. As with any drug, careful selection of patients and awareness of potential adverse effects of atropine are paramount for all providers.8 With any patient who’s symptomatic enough to require pharmacotherapy, always also plan for initiation of transcutaneous pacing in the event that the medication isn’t effective.7

Transcutaneous Pacing
In circumstances where atropine is not effective, providers must be prepared to initiate transcutaneous pacing. The purpose of cardiac pacing is to deliver an electrical current to the heart to stimulate contraction of the myocardium.10 Both pacing-only electrodes and multifunction electrodes are available; multifunction pads are capable of pacing, monitoring and defibrillation, and are more commonly found in the prehospital setting. It’s important to be familiar with the equipment available to you.

There are two options for pad application to the patient. The anterior-posterior configuration is preferred: The anterior pad is placed over the left anterior chest at the position of lead V3, and the posterior pad is placed on the back between the left scapula and the thoracic spine. Alternatively, the first pad is placed on the right upper chest and the second pad placed on the left side of the chest near the apex of the heart.7,10 This positioning may be preferable when the patient develops the need for pacing during transport or when access to the patient’s back may not be possible.

Once the pacemaker pads are applied to the patient, two variables must be adjusted on the machine: rate and output. Pacemakers operate on either a fixed-rate or demand mode. Fixed-rate pacing produces an electrical impulse at the set rate no matter the intrinsic cardiac activity of the heart, while demand pacing will only deliver an electrical impulse if the patient’s heart rate falls below the set rate. Fixed-rate pacing is used in the prehospital setting, and one should generally set a rate of between 60—90, depending on local protocols.10 The electrical output should begin on the lowest setting, and the provider should observe a pacing spike on the monitor. The current should then be increased by five to 10 mA at a time until a QRS complex and T wave appear after each pacer spike. This is termed “electrical capture.”

Once electrical capture has been achieved, one should next feel for a pulse to ensure mechanical capture. For transcutaneous pacing to be successful, you must have both electrical and mechanical capture. Once mechanical capture is achieved, the electrical output is turned down until mechanical capture is lost; this is the pacing threshold, and will generally be between 40 and 80 mA. The current should be increased five to 10 mA above the pacing threshold in order to ensure continued mechanical capture with the least amount of energy required.7,10

The pacing threshold often increases over time, so continually observe the patient and check pulses frequently; increase the current as needed to ensure mechanical capture.10 Keep in mind transcutaneous pacing can be quite painful, so consider providing pain management and sedation as appropriate. It’s not uncommon for transcutaneous pacing to be ineffective in increasing heart rate and thus cardiac output. In such cases, providers may need to move to more aggressive pharmacotherapy, such as a continuous epinephrine infusion, as guided by protocol.

References

1. Piktel JS: Chapter 22. Cardiac rhythm disturbances. In Tintinalli JE, Stapczynski JS, Cline DM, et al. (Eds.), Tintinalli’s emergency medicine: A comprehensive study guide, 7th ed. McGraw-Hill: New York, 2011. Retrieved Oct. 23, 2013, from www.accessmedicine.com/content.aspx?aID=6357092.

2. Kawashima T, Sasaki H. Gross anatomy of the human cardiac conduction system with comparative morphological and developmental implications for human application. Ann Anat. 2011;193(1):1—12.

3. Cabrera JA, Sanchez-Quintana D. Cardiac anatomy: What the electrophysiologist needs to know. Heart. 2013;99(6):417—431.

4. Hayden GE, Brady WJ, Pollack M, et al. Electrocardiographic manifestations: Diagnosis of atrioventricular block in the emergency department. J Emerg Med. 2004;26(1):95—106.

5. Barra SN, Providência R, Paiva L, et al. A review on advanced atrioventricular block in young or middle aged adults. Pacing Clin Electrophysiol. 2012;35(11):1395—1405.

6. Ufberg JW, Clark JS. Bradydysrhythmias and atrioventricular conduction blocks. Emerg Med Clin N Am. 2006;24(1):1—9.

7. Deal N. Evaluation and management of bradydysrhythmias in the emergency department. Emerg Med Pract. 2013;15(9):1—15.

8. Swart G, Brady WJ, DeBehnke DJ, et al. Acute myocardial infarction complicated by hemodynamically unstable bradyarrhythmia: Prehospital and ED treatment with atropine. Am J Emerg Med. 1999;17(7):647—652.

9. Brady WJ, Swart G, DeBehnke DJ, et al. The efficacy of atropine in the treatment of hemodynamically unstable bradycardia and atrioventricular block: Prehospital and emergency department considerations. Resuscitation. 1999;41(1):47—55.

10. Gibson T. A practical guide to external cardiac pacing. Nurs Stand. 2008;22(20):45—48.

Источник: https://www.jems.com/patient-care/how-recognize-treat-heart-block/

ECG Pointers: AV blocks – Part II

Author: Jamie Santistevan, MD (@jamie_rae_EMdoc – EM Physician, Presbyterian Hospital, Albuquerque, NM) // Edited by: Manpreet Singh, MD (@MPrizzleER – Assistant Professor of Emergency Medicine / Department of Emergency Medicine – Harbor-UCLA Medical Center) and Brit Long (@long_brit – EM Attending Physician, San Antonio, TX)

Welcome to this edition of ECG Pointers, an EMDocs series designed to give you high yield tips about ECGs to keep your interpretation skills sharp. For a deeper dive on ECGs, we will include links to other great ECG FOAMed! This is part II of our AV blocks series, so please check out part I here.


The Case:

A 73-year-old woman presents with two days of fatigue and dyspnea on exertion. She is asymptomatic at rest and her BP is 165/90. Here is her ECG:

There is bradycardia with a ventricular escape rate of 39. At first glance it appears that there is a progressively lengthening PR interval. Looking closer at the rhythm strip you see some additional P-waves buried in the T-waves of the first two beats*.

The pacer pads are placed on her chest and this strip is recorded:

P-waves are marching at their own rate of about 65, the ventricles are conducting at 36 bpm. The QRS duration is prolonged.

Because she is asymptomatic at rest and hemodynamically stable, you do not externally pace her in the ED, but she is transferred urgently to the cath lab for a placement of a permanent pacemaker.

Mobitz II and complete AV block:

Second-degree Mobitz type II and third-degree (complete) AV block almost always results from conduction systemfailure below the level of the AV node. The ventricular rhythm is determined by either junctional or ventricular escape beats. In complete heart block there is no conduction through the AV node; the atria and ventricles are completely dissociated and there is no relationship between the two. The dissociation can produce severe bradycardia or even ventricular standstill and sudden cardiac death.

Reversible causes most commonly are myocardial infarction with ischemia of the AV node and medications(e.g. beta blockers, calcium channel blockers). Nonreversible causes included fibrosis of the conduction system (e.g. Levs disease), cardiac surgery, autoimmune conditions (e.g. SLE) and infiltrative myocardial disease (e.g. amyloidosis, hemochromatosis) [1].

For patients who are symptomatic or hemodynamically unstable, immediate treatment should be initiated to maintain perfusion. These patients may require pharmacologic intervention as a temporizing measure (chronotropic agents such as epinephrine). A trial of atropine as a temporizing measure may be used, but pacing is the definitive treatment. External pacing with transcutaneous pacer pads can be used while inserting a transvenous pacemaker with eventual placement of a permanent pacemaker by cardiology.

Second-degree Mobitz type II: what to look for on the ECG:

  • There will be occasional non-conducted P-waves
  • The PR interval will be constant for all conducted beats
  • There is usually a fixed ratio of conduction between the atria to the ventricles (e.g. 3:2, 4:3).
  • The QRS complex may be wide (about 75% of cases)

https://lifeinthefastlane.com/ecg-library/basics/mobitz-2/

Third-degree (complete) AV block: what to look for on the ECG:

  • There is no association between the atria and ventricles (the PR interval is wildly inconsistent because of this)
  • The atrial rate is usually normal 70-100 bpm
  • The ventricular escape rate is usually 40-60 bpm
  • The QRS duration is usually wide

https://lifeinthefastlane.com/ecg-library/basics/complete-heart-block/

How to differentiate Mobitz I and II:

In Mobitz I block, the AV nodal cells progressively fatigue and then fail producing lengthening PR intervals. In Mobitz II the conduction system suddenly fails to conduct a beat, leaving the PR interval constant prior to sudden failure.

For patients with second degree AV block with a ratio of atrial to ventricular conduction of 2:1, the distinction between Mobitz type I and Mobitz type II cannot be made from the surface ECG alone.

https://en.wikipedia.org/wiki/Second-degree_atrioventricular_block

Other clues on the ECG may exist. In most cases of Mobitz I, the block occurs within the AV node and a junctional escape rhythm occurs with a rate between 40-60 bpm with a narrow QRS complex. When the block is below the AV node (Mobitz II and complete heart block), a ventricular escape rhythm produces a wide QRS complex with rates that are much slower (20-40 bpm) [2].

QRS complex duration and rate of ventricular conduction are not perfect clues because up to to one fourth of cases with Mobitz II may produce a junctional rhythm with a narrow QRS complex. Alternatively, Mobitz I may also occur in a patient with a pre-existing bundle branch block creating a wide QRS complex. The best way to know for certain is to observe patients for a period of time. A long rhythm strip should be recorded to watch for an occasional conduction pattern other than 2:1 (eg, 3:2, 4:3). A lengthening PR interval would suggest Mobitz type I (Wenckebach), and a consistent PR interval, Mobitz II.

Lastly, atropine could be administered to help distinguish the level of AV block. A lack of response to atropineis consistent with blockage occurring below the AV node and suggests Mobitz type II.

High-grade AV blocks:

Mobitz I and Mobitz II can occasionally produce high-grade blocks, with rates of atrial to ventricular conduction greater than 2:1:

Atrial to ventricular conduction is 3:1. There is a wide QRS complex with a rate of 33 (ventricular escape). The PR interval is the same for each conducted beat (there is still a relationship between the atria and ventricles). It is impossible to determine if this is Mobitz I or Mobitz II second-degree block.

In cases of high-grade blocks, bradycardia is severe. Regardless of type of block (Mobitz I or II), these patients often need pharmacologic intervention and pacemaker placement.

The top ECG pointers for Mobitz II and Complete AV block:

  • Mobitz II and complete AV block often occur due to blockade below the level of the AV node producing ventricular escape rhythms.
  • Distinguishing between Mobitz I and Mobitz II is difficulty when there is 2:1 conduction and may require a prolonged rhythm strip, evaluation of QRS duration and PR intervals and a trial of atropine.
  • High-grade second-degree blocks, Mobitz II and complete AV block require pacemaker placement.

But wait, there’s more ECG FOAMed:

References:

  1. Sauer WH. Etiology of atrioventricular block. Nov 2017. Uptodate.com
  2. Yealy, D. M., Kosowsky, J. M. (2014). Dysrhythmias. In Rosen’s Emergency Medicine: Concepts and Clinical Practice 8th edition(pp. 1034-1046). Philadelphia, PA: Elsevier Saunders.
Источник: http://www.emdocs.net/ecg-pointers-av-blocks-part-ii/
1st degree av block rhythm strip
1st degree av block rhythm strip

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