Tachycardias are broadly categorized based upon the width of the QRS complex on the electrocardiogram (ECG). A narrow QRS complex (<120 milliseconds) reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the His bundle (ie, a supraventricular tachycardia). The site of origin may be in the sinus node, the atria, the atrioventricular (AV) node, the His bundle, or some combination of these sites. A widened QRS (≥120 milliseconds) occurs when ventricular activation is abnormally slow. The most common reason that a QRS is widened is because the arrhythmia originates below the His bundle in the bundle branches, Purkinje fibers, or ventricular myocardium (eg, ventricular tachycardia). Alternatively, a supraventricular arrhythmia can produce a widened QRS if there are either pre-existing or rate-related abnormalities within the His-Purkinje system (eg, supraventricular tachycardia with aberrancy), or if conduction occurs over an accessory pathway. Thus, wide QRS complex tachycardias may be either supraventricular or ventricular in origin.
Wolff–Parkinson–White syndrome (WPW) is one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals travelling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supraventricular tachycardia referred to as an atrioventricular reciprocating tachycardia.The incidence of WPW is between 0.1% and 0.3% in the general population.Sudden cardiac death in people with WPW is rare (incidence of less than 0.6%), and is usually caused by the propagation of an atrial tachydysrhythmia (rapid and abnormal heart rate) to the ventricles by the abnormal accessory pathway.
Tachycardias are broadly categorized based upon the width of the QRS complex on the electrocardiogram (ECG). A narrow QRS complex (<120 milliseconds) reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the His bundle (ie, a supraventricular tachycardia). The site of origin may be in the sinus node, the atria, the atrioventricular (AV) node, the His bundle, or some combination of these sites. A widened QRS (≥120 milliseconds) occurs when ventricular activation is abnormally slow. The most common reason that a QRS is widened is because the arrhythmia originates below the His bundle in the bundle branches, Purkinje fibers, or ventricular myocardium (eg, ventricular tachycardia). Alternatively, a supraventricular arrhythmia can produce a widened QRS if there are either pre-existing or rate-related abnormalities within the His-Purkinje system (eg, supraventricular tachycardia with aberrancy), or if conduction occurs over an accessory pathway. Thus, wide QRS complex tachycardias may be either supraventricular or ventricular in origin.
Wolff–Parkinson–White syndrome (WPW) is one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals travelling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supraventricular tachycardia referred to as an atrioventricular reciprocating tachycardia.The incidence of WPW is between 0.1% and 0.3% in the general population.Sudden cardiac death in people with WPW is rare (incidence of less than 0.6%), and is usually caused by the propagation of an atrial tachydysrhythmia (rapid and abnormal heart rate) to the ventricles by the abnormal accessory pathway.
Its a medical presentation describing how to approach to various cardiac arrhythmias in systematic way. Illustrated with more ECG photographs from standard sources.
AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of tachycardia (fast rhythm) of the heart. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medication, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node.
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
Its a medical presentation describing how to approach to various cardiac arrhythmias in systematic way. Illustrated with more ECG photographs from standard sources.
AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of tachycardia (fast rhythm) of the heart. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medication, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node.
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
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Some of the slides, i hide it from my real presentations for my own reference. Download to see all of them.
9. Inappropriate Sinus Bradycardia
Chronotropic Incompetence
• HR<60 that doesn’t increase appropriately with
exercise
• Usually defined as failure to attain 80% of
maximal age predicted HR (MAHR) on exercise
testing
• MAHR = 220 – Age
• e.g. failure to reach a HR of 120 in a 70 year old
patient
18. Tachycardia-Bradycardia Syndrome
• Bradycardia/sinus pauses interspersed with
atrial arrhythmias (AFL, A fib, A tach)
• Sinus arrest manifests after termination of
atrial arrhythmia (spontaneously or after DCCV)
• Sinus Node Recovery Time (SNRT) uses the
above observation to assess SA node function
in EP studies
20. Indications for pacing in SND
• Class I (recommended)
– SND with documented symptoms
– SND due to irreversible factors or due to essential
drug therapy
– Chronotropic incompetence
• Class III (NOT recommended)
– Asymptomatic
21. Bradycardias
• SA node dysfunction or • AV Blocks
Sick Sinus Syndrome – First Degree
– Inappropriate sinus – Second Degree
bradycardia • Mobitz I
– Sinoatrial exit Block • Mobitz II
– Sinus Pause/Arrest • 2:1 Block
– Tachycarda/Bradycardia – Third Degree
syndrome – High Grade AV Block
– Persistent Atrial Standstill
22. AV Blocks
• First Degree
• Second Degree
– Mobitz I
– 2:1 Block
– Mobitz II
• Third Degree
• High Grade AV Block
23. First Degree AV Block
• PR interval > 200msec
• If QRS is normal, block is usually at the level of
the AV node
• If QRS shows bundle branch block, block
maybe in His-Purkinje System
26. Second Degree Heart Block
Mobitz I or Wenchebach
• Progressive Prolongation of the PR interval
and shortening of the RR interval until a P
wave is blocked
• RR interval containing the non conducted P
wave is less than two PP intervals
• PR interval longer after the non conducted P
wave
• Grouped beating
28. Causes Features
• Normal • Usually asymptomatic
• Athletes • Usually narrow QRS complex
• Medications block at AV node
• Myocardial Infarction • The presence of bundle branch
block suggests the possibility
(inferior wall)
of block below the AV node in
• Acute rheumatic fever
His Purkinje system
• Myocarditis
30. Second Degree – Mobitz II
• Constant PR interval with intermittent
nonconducted P wave and no evidence for PACs
• RR interval between non conducted P waves is
equal to two PP intervals
• Each QRS is preceded by multiple P waves
• 3:1, 4:1 also called high grade AV block
• Other variations include 3:2
• 2:1 block maybe Mobitz I or Mobitz II
34. Management
• Usually require permanent pacing especially if
symptomatic due to high likelihood of
progression to high grade AV block and third
degree AV block
35. Differentiating mechanism of 2:1 block
Feature Mobitz I Mobitz II
QRS duration Narrow Wide
Response to increasing Improves Worsens
HR & AV conduction i.e.
exercise, atropine
Response to decreasing Worsens Improves
HR & AV conduction i.e.
carotid sinus massage
Acute MI Inferior Anterior
36. Third Degree AV block
• Atrial impulses consistently fail to reach the
ventricles, resulting in atrial and ventricular
rhythms that are independent of each other
• PR interval varies
• PP and RR intervals are constant
• Ventriculophasic sinus arrhythmia
– PP interval containing QRS is shorter than PP
interval without a QRS complex
46. P P P P P P P P P P P
3rd degree AV block, junctional escape
47. P P P P P P P P P P
3rd degree AV block, junctional escape
or high grade AV block
48. Problem
• 50 year old female with no PMH presents with
acute onset of shortness of breath on exertion
of 4 days duration
• HR 50/min, BP 140/80
• Initial ECG sinus bradycardia
• TropI 1.2
HR 46/min Put her on a treadmill reached HR of 137/min
3.4 and 4.8 second pauses Patient had acute coronary syndrome with lesion in proximal RCA involving the branch to the SA node, placed a dual chamber pacemaker
ACC/AHA guidelines
Prolongation of of the PR interval > 200ms, 1:1 conduction, P before every QRS complex, both P and QRS are normal
Progressive prolongation of the PR interval terminated in a non conducted P wave
