1. Basic Arrhythmias
© 2011 American Heart Association. Do not edit.

2. ECG Measurements PR interval 0.12  0.20 s QRS complex <0.12 s
QT interval Corrected for Heart Rate
Key Concept: In this slide, point out the major ECG intervals and their normal measurements and durations. Tell students that these will become important later for the measurement of atrioventricular blocks as related to the PR interval.

3. Heart Rate Estimation Pick a complex that falls on a heavy line
300
Key Concept: Describe to students a method to quickly estimate the heart rate. Have them memorize the rate intervals: 300, 150, 100, 75, 60, 50, 40, 30. This method estimates heart rate. There are other methods and tools available; however, this method does not require a 3- or 6-second strip and can be used easily at the bedside.
So about 75
Pick a complex that falls on a heavy line
Then estimate the rate by counting heavy boxes
Using 300, 150, 100, 75, 60, 50, 40, 30

4. Standard Monitoring Leads Lead 1
Key Concept: This is standard monitoring in lead 1. This slide and the next 2 slides are examples of the standard limb leads. Basic providers need to know only that the limb leads are “snapshots” of the 12-lead ECG. The leads differ in morphology and are not reliable as a diagnostic tool beyond monitoring. In this regard, emphasize that it is important to obtain a 12-lead ECG for diagnostic purposes in a stable patient when a significant change in rhythm occurs. Similarly, a postconversion 12-lead ECG should be done when a rhythm abnormality resolves or is converted to a normal rhythm. These ECGs may be invaluable in the diagnosis of an abnormal rhythm.

5. Standard Monitoring Leads Lead 2
Key Concept: This is standard monitoring in lead 2. Basic providers need to know only that the limb leads are “snapshots” of the 12-lead ECG. The leads differ in morphology and are not reliable as a diagnostic tool beyond monitoring. In this regard, emphasize that it is important to obtain a 12-lead ECG for diagnostic purposes in a stable patient when a significant change in rhythm occurs. Similarly, a postconversion 12-lead ECG should be done when a rhythm abnormality resolves or is converted to a normal rhythm. These ECGs may be invaluable in the diagnosis of an abnormal rhythm.

6. Standard Monitoring Leads Lead 3
Key Concept: This is standard monitoring in lead 3. Basic providers need to know only that the limb leads are “snapshots” of the 12-lead ECG. The leads differ in morphology and are not reliable as a diagnostic tool beyond monitoring. In this regard, emphasize that it is important to obtain a 12-lead ECG for diagnostic purposes in a stable patient when a significant change in rhythm occurs. Similarly, a postconversion 12-lead ECG should be done when a rhythm abnormality resolves or is converted to a normal rhythm. These ECGs may be invaluable in the diagnosis of an abnormal rhythm.

7. Rhythm Strip Interpretation
Basic Arrhythmias
Rhythm Strip Interpretation
Normal Sinus Rhythm
Sinus Bradycardia
Sinus Tachycardia

8. Initial Approach—Analysis 4 Questions
Rate?
Normal
Bradycardia, Tachycardia
Rhythm?
Regular or Irregular
Are there P waves?
Is each P wave related to a QRS with 1:1 impulse conduction?
QRS normal or wide?
Key Concept: Point out for the students that a standard, consistent, and
routine approach to rhythm analysis is key to success. One method is
developed in this slide and used in the self-directed learning module. Four
basic questions lead to correct analysis and diagnosis of the majority of rhythm
abnormalities:
Is the rate within the normal range for a sinus-initiated beat?
Is the rhythm regular or irregular?
Can P waves be identified; is there one P wave for each QRS complex; does an impulse conduct the P wave and QRS complex in a 1:1 ratio?
Is the QRS normal or wide?
For ACLS providers, knowing the answers to these questions will allow them
to navigate the appropriate algorithm and select the correct treatment or
strategy.

9. Arrhythmias—Etiology
Disturbance in Automaticity
Pacemaker speeds up
New pacemaker takes over
Disturbance in Conduction
Slowing or block in conduction of electrical impulse
Combination of Both
Reentry arrhythmias
Key Concept: Students at this level will not learn the mechanisms of arrhythmia generation and propagation in detail. However, a basic understanding is important to identify rhythm disorders and to serve as a foundation for more advanced discussion and rationale for therapy.

10. Normal Sinus Rhythm Rate Rhythm P waves P → QRS Therapy 60-100/min
Regular
Present
1:1 conduction
None
Key Concept: This slide is used to describe normal sinus rhythm.

11. Sinus Bradycardia Rate Rhythm P waves P → QRS Therapy <60/min
Regular
Present
1:1 conduction
Treat underlying cause
Key Concept: This slide is used to describe sinus bradycardia.

12. Sinus Tachycardia Rate Rhythm P waves P → QRS Therapy >100/min
Regular
Present
1:1 conduction
Treat underlying cause
Key Concept: This slide is used to describe sinus tachycardia.

13. What are the rate and rhythm?
Self-Assessment
What are the rate and rhythm? A B
Key Concept: This self-assessment slide demonstrates sinus rhythm. The top rhythm, A, is normal sinus rhythm, and B is sinus bradycardia. Rhythm C demonstrates a borderline sinus tachycardia, technically still NSR because the rate is 100/min and sinus tachycardia is defined as a rate exceeding 100 (NSR /min). C

14. If there is no pulse, what is this rhythm?
Self-Assessment
What is this rhythm? A
If there is no pulse, what is this rhythm?
Key Concept: The primary purpose of this slide is to introduce the concept of treating the patient, not the rhythm. After identifying normal sinus rhythm in A, ask the students to identify the rhythm in B. The rhythm is sinus bradycardia, but if no pulse could be detected, it is an arrest rhythm. The rhythm and clinical condition need to be evaluated together. Note that most ACLS therapy is based on the presence or absence of cardiac arrest or the presence of symptoms or serious signs associated with rhythm disturbances. B

15. Supraventricular Arrhythmias Premature Atrial Contraction (PAC)
Basic Arrhythmias
Supraventricular Arrhythmias
Premature Atrial Contraction (PAC)
Premature Atrial Beat (PAB) Atrial Premature Beat (APB) Premature Atrial Complex
Atrial Fibrillation
Atrial Flutter
Reentry Tachycardia
Key Concept: The next series of slides will present supraventricular rhythms. Different nomenclature is used for premature impulses. Here we will use the ACLS designation that defines them as premature contractions rather than beats, because not all contractions can be detected as a heart beat or pulse in the peripheral circulation. For example, weak contractions are often present in pulseless electrical activity, but these cannot be detected as beats by listening to the precordium or palpating the pulse. A small difference, but a beat is defined as a stroke or pulsation.

16. Premature Atrial Contraction (PAC)
QRS
Normal
Rate
Rhythm
P waves
P → QRS
Therapy
Sinus rate
Irregular—interrupted by PAC
Incomplete compensatory pause
Different morphology
Usually conducted with normal QRS
Treat underlying cause

17. Premature Atrial Contraction (PAC)
Sinus Node
Atrium
AV Node
Ventricle 
 PAC
Premature Beat Present
Pause (Incomplete) Sinus Node Reset 
QRS
Normal
Key Concept: Ladder diagrams can be complicated visual diagrams of rhythm disturbances, but they may be useful for some students. If you decide to include these, take care to “set up” the slide: use enough time to explain what is happening and focus in on the rhythm disturbance.
Since this is the first ladder diagram, remember to introduce the methodology and describe the landmarks.

18. Atrial Fibrillation Rate Rhythm P waves F → QRS Therapy
Rate
Rhythm
P waves
F → QRS
Therapy
Atrial rate cannot be measured
Ventricular rate—variable
Irregular (irregularly irregular)
Absent (fibrillation waves)
Conduction irregular
Slow ventricular rate
Treat underlying cause
Key Concept: This slide is used to describe atrial fibrillation. Note that normal P waves are absent and the rhythm is irregularly irregular.

19. Atrial Flutter Rate Rhythm P waves F → QRS Therapy
Normal
Rate
Rhythm
P waves
F → QRS
Therapy
Atrial rate /min (often 300)
Ventricular rate—variable
Regular (2:1 AV block common)
Absent (flutter waves)
Conduction regular (unless variable block)
Slow ventricular rate: terminate arrhythmia
Treat underlying cause
Key Concept: This slide is used to explain atrial flutter. Note that the most common flutter rate is an atrial rate of about 300 with 2:1, as in the bottom strip. Call students’ attention to the fact that the flutter wave may be missed (red arrows) if the rhythm strip is not carefully evaluated. Always look for flutter waves with a ventricular rate that is 150/min. Use the top rhythm to show the flutter waves as a sawtooth pattern when AV block is increased to 4:1. However, ask students first what the degree of AV block is, because most will forget to count the flutter wave now “buried” in the QRS complex.

20. Supraventricular Tachycardia (SVT)
AV Reentry Tachycardia
AV Nodal Reentry Tachycardia
Atrial Tachycardia 
Key Concept: In addition to AV block, supraventricular tachycardias are a challenge for the beginning provider. This slide shows 3 common types of SVT and distinguishes between AV reentry and AV nodal reentry tachycardia contrasted with atrial tachycardia due to an ectopic atrial focus. The initial treatment, however, remains the same: vagal maneuvers, followed by adenosine.
Connection between
atria and ventricle
Uses dual pathway
within AV node
Ectopic atrial focus

21. Supraventricular Tachycardia (SVT)
AV Reentry Tachycardia
What is different
between these
2 examples?
(Look carefully at
the arrow directions)
Connection between
atria and ventricle
Connection between
atria and ventricle
Key Concept: Here is the concept of reentry demonstrated in more detail by AV reentry with an accessory bypass tract between the atria and ventricles. These 2 illustrations differ in the pathway used for ventricular activation. On the right is antedromic conduction, and on the left is orthodromic conduction.
Question: Ask students if the QRS complex is narrow or wide and what difference exists between the 2 examples. Each shares use of the AV node in a reentry circuit.
After the students study the examples, it will be apparent that conduction is down the AV node on the right (antedromic) and up the AV node on the left (orthodromic). When conduction occurs down the AV node or antedromic activation of the ventricle occurs over normal pathways, the QRS complex is normal. When the impulse travels forward down the bypass tract, early activation of the ventricle occurs and a delta wave may appear on the ECG or the QRS complex may appear wide and bizarre.
Is the QRS complex
normal or wide for each?
Why?

22. Reentry (Paroxysmal) SVT
Usually onsets with PAC
QRS
Normal
Rate
Rhythm
P waves
P → QRS
Therapy
Atrial rate /min
Onset tachycardia abrupt
Regular
Present—inverted in leads 2, 3, and aVF
Conduction regular
Vagal maneuvers, adenosine,
synchronized cardioversion
Key Concept: This slide is used to explain classic reentry SVT. Note that reentry SVT usually is initiated with a premature beat.

23. What are the rate and rhythm?
Self-Assessment
What are the rate and rhythm? A
Key Concept: Make sure students now understand the difference between atrial fibrillation and atrial flutter. Also make sure students understand the difference between the ventricular rate and the atrial rate. As seen here, they may not always be the same. B

24. Clinical Correlation
This patient is unresponsive and BP is 70/50 mm Hg.
What is the rhythm?
What is your next action?
Key Concept: Here is another clinical correlation slide. This rhythm is reentry SVT with a ventricular response rate of about 170/min. However, for this patient to be this symptomatic, an acute process or underlying structural heart disease must be present. Without giving a detailed explanation of the ACLS Tachycardia Algorithm, note that this patient would require immediate intervention.

25. Basic Arrhythmias Ventricular Arrhythmias
Premature Ventricular Contraction (PVC)
Ventricular Premature Contraction (VPC) Premature Ventricular Beat (PVB) Premature Ventricular Complex
Ventricular Tachycardia
Ventricular Fibrillation
Asystole
Pulseless Electrical Activity (PEA)

26. Premature Ventricular Contraction (PVC)
Compensatory pause
Sinus node continues to discharge
2  HR
P wave obscured 
Key Concept: This is a basic slide describing the typical wide-complex morphology of a ventricular premature beat (VPB), also called a premature ventricular contraction (PVC). Stress the wide complex and note that the wide complex may appear narrow in some leads. A clue to a PVC is the compensatory pause. Discuss that in most instances the sinus node continues to discharge if retrograde conduction of the PVC through the AV node does not occur. In some instances, however, the PVC is conducted into the atria (retrograde conduction) and may “reset” the sinus node if it is early enough.

27. Mechanism PVCs Unidirectional Block Reentry  Purkinje Fiber
Key Concept: Some forms of ventricular tachycardia are initiated by a PVC and sustained by a mechanism called unidirectional block, a circus rhythm similar to other arrhythmias using 2 pathways with different refractory characteristics to propagate the arrhythmia. This is also how antiarrhythmic agents alter refractory periods or convert unidirectional block to bidirectional block. A rapidly firing automatic focus is another mechanism for VT.
Reentry
Muscle Fiber

28. PVC Morphology—Match the Name
Unifocal PVCs
Multifocal PVCs
Bigeminy
Ventricular Tachycardia
Torsades  
Key Concept: Although the names are not clinically important, students may need to know the common morphological names used to classify PVCs. 

29. Ventricular Tachycardia Monomorphic*
*Sustained—requires intervention for >30 seconds
Rate
Rhythm
P waves
P → QRS
Therapy
Atrial rate normal
Onset tachycardia abrupt
Regular
Present—obscured
Blocked—fusion complexes possible
Antiarrhythmic agent, cardioversion,
high-energy (defibrillation dose) shock
Key Concept: This illustrates monomorphic VT. VT can be sustained, usually degenerating into VF, or nonsustained. Whether treatment is initiated is determined by the clinical circumstances.

30. Polymorphic VT* Rate Rhythm P waves P → QRS Therapy
*Torsades de pointes—QT prolonged
Rate
Rhythm
P waves
P → QRS
Therapy
Atrial rate normal (obscured)
Onset tachycardia abrupt
Irregular
Present—obscured
Blocked—fusion complexes possible
Unsynchronized high-energy shock,
magnesium (beneficial with baseline QTC
prolongation)
Key Concept: This slide allows discussion of polymorphic VT. Note the “twisting around a point” or spindle shape that occurs and is typical of this morphology.

31. Ventricular Fibrillation
Coarse VF
Rate
Rhythm
P waves
P → QRS
Therapy
Chaotic, uncountable
Onset abrupt
Irregular
Absent; no normal QRS complexes
Not applicable
Immediate shock(s)
Key Concept: This illustrates ventricular fibrillation. It is an example of coarse VF with high-amplitude waveforms, which vary in size, shape, and rhythm.
Note: The exact mechanism of VF is not known. Two mechanisms are thought to occur in humans. The first is that an irritable focus initiates a series of multiple “wavelets” as demonstrated above. The second involves a “mother” rotor with spin-off daughter wavelets. Once initiated, VF can be sustained by the incessant recirculation of these wavefronts moving along constantly changing pathways at varying conduction velocities. To terminate VF, a defibrillation shock must extinguish these circuits at the same time, and the shock itself must not induce VF.

32. Ventricular Fibrillation
Fine VF
Rate
Rhythm
P waves
P → QRS
Therapy
Chaotic, uncountable
Onset abrupt
Irregular
Absent; no normal QRS complexes
Not applicable
Immediate shock(s)
Key Concept: This illustrates fine ventricular fibrillation. This VF has low-amplitude waveforms, which vary in size, shape, and rhythm.
Note: When VF persists it loses amplitude and frequency. This usually indicates that cardiac arrest has persisted for several minutes. The maintenance of coarse VF is energy dependent. As ATP stores are depleted and substrate is used up, VF deceases in amplitude and may be difficult to distinguish from asystole.

33. Asystole Rate Rhythm P waves P → QRS Therapy Absent None—“flatline”
Agonal Complexes
Pulseless Electrical
Activity
Rate
Rhythm
P waves
P → QRS
Therapy
Absent
None—“flatline”
Not applicable
CPR, vasopressor, atropine
Key Concept: This illustrates an “agonal rhythm” and asystole, or “flatline.”
Note: VF may “progress” to asystole as energy stores are used up and coarse VF degenerates to fine VF and finally asystole. It is also a common “postshock” rhythm when VF has persisted for several minutes. Some cardiac arrests, however, can occur as “bradyasystolic” arrests and terminate as above. That is, a bradycardia can deteriorate to a slow wide-complex agonal rhythm that finally ends in a straight line, or “asystole.” The agonal “beats” have no detectable pulse and so fit the definition of pulseless electrical activity if they are slow and organized. As cardiac arrest is prolonged, the right heart typically distends with blood in the absence of effective cardiac contractions.

34. Pulseless Electrical Activity (PEA)
ARTERIAL PRESSURE
Rate
Rhythm
Therapy
Variable—depends on baseline rhythm
PEA is not a single rhythm but any
organized rhythm without a pulse
Identify and treat underlying cause
CPR, vasopressor, atropine
Key Concept: This illustrates a supraventricular rhythm without a pulse.
Note: Pulseless electrical activity, although called an arrest rhythm, is not a single rhythm but any organized rhythm without a pulse. The causes of PEA are multiple and the prognosis dismal unless a cause can be rapidly identified and quickly corrected. The rhythm shown here is an SVT. This rhythm is associated with causes of PEA such as hypovolemia, tension pneumothorax, and hypoxia. In many cases this SVT will change to a slower rhythm with a progressively widening QRS complex as the patient deteriorates.

35. What are the rate and rhythm?
Self-Assessment
What are the rate and rhythm? A A B C
Key Concept: This self-assessment slide allows students to compare polymorphic with monomorphic VT. In slide B, polymorphic VT begins at point A, “twists” around the middle at B, and is above the baseline in C. B

36. Clinical Correlation
You see this rhythm on the monitor while standing next to the patient.
How many rhythms do you see?
What is your first action?
Key Concept: Have the students identify the 3 rhythms in this rhythm strip: normal sinus rhythm, frequent PVCs, and VF.

37. Atrioventricular Blocks Second-Degree AV Block
Basic Arrhythmias
Atrioventricular Blocks
First-Degree AV Block
Second-Degree AV Block
Third-Degree AV block
Key Concept: This next section will review atrioventricular blocks. These are often the most difficult arrhythmias for students to learn, so appropriate time, explanation, and review are necessary for beginners.

38. Atrioventricular Blocks Classification
Incomplete AV Block
First-Degree AV Block
Second-Degree AV Block
Type I—Wenckebach Mobitz I
Type II—Mobitz II
Key Concept: Use this slide to discuss the classification of atrioventricular block.
Complete AV Block
Third-Degree AV Block

39. Atrioventricular Block Normal AV Conduction
AV Nodal
Tissue
AV Node
His-Purkinje System P
QRS <0.12
seconds
Sinus Node
Underlying sinus rhythm
One P wave
PR interval 0.12 to second
One P wave for each QRS
Key Concept: For the healthcare providers, atrioventricular blocks are often the most difficult rhythms to understand and identify. This series of slides reviews the progression of atrioventricular block from first degree through third degree. Review in this slide again the normal conduction system, emphasizing the delay in the atrioventricular node and the normal limit of the PR interval. Note that there is one P wave that conducts through the AV node and stimulates ventricular excitation.

40. First-Degree AV Block Underlying sinus rhythm One P wave
AV Nodal
Tissue
His-Purkinje System P
QRS <0.12
>0.20 seconds
Sinus Node
Underlying sinus rhythm
One P wave
PR interval >0.20 second
One P wave for each QRS
Key Concept: This slide demonstrates delayed conduction through the AV node but still 1:1 atrioventricular conduction.
Clinical Correlation: No symptoms occur and no treatment is necessary.

41. First-Degree AV Block Underlying sinus rhythm One P wave
AV Nodal
Tissue
AV Node
His-Purkinje System P
QRS <0.12
>0.20 seconds
Sinus Node
Underlying sinus rhythm
One P wave
PR interval >0.20 second
One P wave for each QRS
Key Concept: This slide demonstrates delayed conduction through the AV node but still 1:1 atrioventricular conduction. The ECG is displayed, and the green arrows identify the limits of the prolonged PR interval.
Ask the students what the approximate duration of the PR interval is. Review the surface ECG measurements.
Clinical Correlation: No symptoms occur and no treatment is necessary.

42. Second-Degree AV Block—Mobitz I Wenckebach Phenomenon
Sinus Node P
Underlying sinus rhythm
P wave fails to periodically conduct
PR interval prolonged
One P wave for each QRS until block
AV Nodal
Tissue
Key Concept: This slide demonstrates delayed conduction through the AV node with progressive prolongation of the PR interval and, eventually, complete block of conduction—Mobitz I or Wenckebach phenomenon. The ECG shown and the green arrows identify the progressive prolongation and then block of conduction in the AV node.
Note that this conduction disturbance occurs in the part of the AV node innervated by the vagus nerve. Excess vagal stimulation may cause or contribute to this form of AV block, and treatment with atropine—rarely indicated—would be expected to improve conduction.
Clinical Correlation: No symptoms occur and no treatment is usually necessary.
>0.20 seconds
PR interval X
QRS
His-Purkinje System

43. Second-Degree AV Block—Mobitz II
PR intervals unchanged
AV Nodal
Tissue
AV Node
His-Purkinje System P
Often normal
QRS complex
Often Normal
Sinus Node 
Block
Underlying sinus rhythm
One P wave
PR interval usually normal, no prolongation
One P wave for each QRS until sudden block and dropped QRS
Key Concept: This slide demonstrates delayed conduction through the AV node without progressive prolongation of the PR interval and, eventually, sudden complete block of conduction—Mobitz II AV block. The ECG is displayed, and the green arrows identify the normal PR interval and then a “dropped QRS” due to block in conduction though the AV node. The PR interval is usually normal but may be prolonged at baseline.
Note that this conduction disturbance usually occurs in the part of the AV node not innervated by the vagus nerve. Mobitz II block with a wide QRS complex usually occurs in the infranodal conduction system (His-Purkinje). Treatment with atropine would not be expected to improve conduction of this form of block.
For a basic arrhythmia course, it is too complicated to discuss that high degrees of AV block, even complete heart block, may occur in the AV node. It would be confusing as well to note that 2:1 AV may be Mobitz I or Mobitz II and is a fourth type of category under AV block.
Clinical Correlation: No symptoms occur and no treatment is usually necessary. Mobitz II AV block should serve as a caution/warning that progression to high-degree AV block may progress. When this happens, the subsidiary pacemaker is low and slow in the conduction system and clinical deterioration may occur. So note that placement of transcutaneous pacing pads is appropriate and that any drug slowing conduction through the AV node should be stopped or withheld (eg, β-blockers, digoxin).
Now review with students the subsidiary pacemakers and their average escape rate.

44. Third-Degree AV Block—Junctional Escape
P waves unrelated to QRS
Underlying sinus rhythm (usual)
Escape junctional rate 40-60
PR interval variable
P waves unrelated to QRS
Narrow QRS = block above His junction
AV Node
His Purkinje System P
QRS <0.12
Sinus Node
QRS from
AV-His
escape  
Key Concept: This slide demonstrates complete block of the conduction through the AV node with P waves occurring regularly and unrelated to the QRS complex. The ECG is displayed, and the green arrows identify the P waves. Note for students that the atrial and ventricular rates are different and dissociated. Thus, complete AV block is one form of AV dissociation.
Also note that this conduction disturbance usually occurs in the part of the AV node not innervated by the vagus nerve. When this block occurs high in the His-bundle system, a QRS escape focus from the junctional pacemaker cells of the AV nodal tissue can occur, and a narrow QRS complex is generated as conduction occurs through the normal route. This will be contrasted in the next slide with the block lower in the His-Purkinje system.
Clinical Correlation: Symptoms from the arrhythmia will depend on the escape rate of the subsidiary pacemaker. If this is adequate to generate sufficient cardiac output, no symptoms or minimal symptoms may occur. But note that placement of transcutaneous pacing pads is appropriate and that any drug slowing conduction through the AV node should be stopped or withheld (eg, β-blockers, digoxin). This may become an unstable rhythm and immediate pacing may be required.
Now review with students the subsidiary pacemakers and their average escape rate if not done in the previous slide.

45. Third-Degree AV Block—Ventricular Escape
P waves unrelated to QRS
AV Node P
Sinus Node
His-Purkinje System
QRS >0.12
QRS from
His-Purkinje
escape 
Underlying sinus rhythm (usual)
Escape ventricular rate 30-40
PR interval variable
P waves unrelated to QRS
Wide QRS = block below His junction
Key Concept: This slide also demonstrates complete block of conduction through the AV node with P waves occurring regularly and unrelated to the QRS complex. The ECG is displayed, and the green arrows identify the P waves. Note again for the students that the atrial and ventricular rates are different and dissociated. Thus, complete AV block is one form of AV dissociation.
Also note that this conduction disturbance usually occurs in the part of the AV node not innervated by the vagus nerve. When this block occurs low in the His bundle system, a QRS escape focus from the ventricular pacemakers will occur, sometimes after a period of asystole, and a wide QRS complex is generated as conduction occurs aberrantly through the ventricle. This is in contrast to the normal QRS complex and higher escape rate in the previous slide.
Clinical Correlation: Symptoms from this arrhythmia usually occur, although patients may be minimally symptomatic at rest in the recumbent position in the absence of a serious coexisting problem (eg, myocardial infarction). If this is adequate to generate sufficient cardiac output, no symptoms or minimal symptoms may occur. Note that placement of transcutaneous pacing pads is appropriate and that any drug slowing conduction through the AV node must be stopped or withheld (eg, β-blockers, digoxin). If the patient is symptomatic and unstable, immediate pacing is indicated. Because this block usually occurs below the AV node, atropine would not be expected to increase heart rate.

46. AV Block—Which Type?    
Key Concept: AV block is historically the most difficult rhythm for healthcare providers to identify. This slide now allows assessment of the identification of AV block.
Questions: As the student identifies each AV block, ask what the clinical significance is. When the student identifies third-degree AV block in rhythm strip 1, ask where the escape focus is located. If needed, prompt students with “the QRS is wide.”
Answers:
Third-degree AV block
First-degree AV block
Second-degree AV block—Mobitz II (Wenckebach)
Second-degree AV block—Mobitz I 

47. What treatment is indicated?
Clinical Correlation
What treatment is indicated?
An athlete in the ED with a sprained ankle
A diabetic woman in the ED with chest tightness
Key Concept: This slide again emphasizes the need to correlate the clinical scenario and circumstances with symptoms and treatment. Remember to treat the patient and not the monitor.
Healthy athletes may have asymptomatic bradycardias that are physiologic. The diabetic woman likely has an acute coronary syndrome. If symptoms are determined to be due to the bradycardia, she would receive treatment.

48. What treatment is indicated?
Clinical Correlation
What treatment is indicated?
A 78-year-old woman with altered consciousness, BP 80/60 mm Hg
Key Concept: This rhythm is complete AV block with a wide-complex
ventricular escape rhythm at approximately 30 per minute. The patient is
symptomatic and unstable with altered consciousness and a low blood
pressure—likely due to the AV block.
Ask your students to identify the rhythm and what the treatment
might be.
Note that an external pacemaker is not immediately available.
Atropine may be ineffective (do not rely on atropine)—complete AV block with wide escape ventricular rhythm.
Dopamine or epinephrine infusions can be carefully titrated.
Expert consultation is indicated because a transvenous and permanent pacemaker will probably be necessary.
External pacer not immediately available

49. Transcutaneous—Transvenous Atrial, and Dual Chamber
Basic Arrhythmias
Pacing
Transcutaneous—Transvenous
Ventricular,
Atrial, and Dual Chamber
Key Concept: In the final section, healthcare providers will learn to recognize pacing artifacts and pacing morphology. Increasingly, healthcare providers will treat and monitor patients with artificial implanted pacemakers, and it will be necessary for them to recognize pacing artifact and appropriate capture and malfunction in order to properly recognize and treat arrhythmias. Use this section to give them a brief overview of pacing modalities and pacemaker rhythms.

50. Pacemakers Transcutaneous Transvenous Ventricular Atrial Dual Chamber –
Transcutaneous
Transvenous
Ventricular
Atrial
Dual Chamber
Key Concept: Having just reviewed third-degree AV block, it is now appropriate to review pacing and pacemakers briefly. Transvenous pacing is included in this basic course so that students are familiar with the different types of pacing. In their scope of practice, they may encounter paced rhythms and will need to distinguish these from artifact and normal rhythms.

51. Pacemakers – Transcutaneous 
Key Concept: In an emergent situation your students may be required to use a transcutaneous pacer. Pacing produces an electrical artifact on the rhythm strip, called a pacer spike. It also deforms the QRS complex. Inexperienced providers may confuse this with PVCs or VT.
FYI Guidelines 2010
Transcutaneous pacing is a second treatment for symptomatic bradycardia. Transcutaneous pacing can be painful and may fail to produce effective mechanical capture. If cardiovascular symptoms are not caused by the bradycardia, the patient may not improve despite effective pacing.
Transcutaneous pacing is noninvasive and can be performed by ECC providers at the bedside. Initiate transcutaneous pacing immediately if there is no response to atropine. Verify mechanical capture and reassess the patient’s condition. Use analgesia and sedation for pain control, and try to identify the cause of the bradyarrhythmia.
Transcutaneous pacing (TCP) may be useful for the treatment of symptomatic bradycardias. There are limited studies comparing TCP with drug therapy for the treatment of symptomatic bradycardia. A randomized controlled trial in which atropine and glycopyrrolate were compared with TCP showed few differences in outcome and survival, although the TCP group obtained a more consistent heart rate. In a study evaluating the feasibility of treatment with dopamine as compared with TCP, no differences were observed between treatment groups in survival to hospital discharge. TCP is, at best, a temporizing measure. TCP is painful in conscious patients, and, whether effective or not (achieving inconsistent capture), the patient should be prepared for transvenous pacing and expert consultation should be obtained. It is reasonable for healthcare providers to initiate TCP in unstable patients who do not respond to atropine (Class IIa, LOE B) or who are severely symptomatic (Class IIb, LOE C). Immediate pacing might be considered in unstable patients with high-degree AV block when IV access is not available (Class IIb, LOE C).

52. Pacemakers Transvenous Ventricular
Key Concept: This slide demonstrates a transvenous ventricular pacemaker. The arrow points to the pacer spike, which then is followed by a wide QRS complex due to abnormal ventricular depolarization.
As previously noted, this rhythm should not be confused with ventricular tachycardia.

53. Pacemaker Malfunction
Sinus Node
Pacemaker Malfunction
Key Concept: This slide shows pacer spikes that failed to capture the ventricle (arrows).
FYI Guidelines 2010: If the patient does not respond to drugs or transcutaneous pacing, transvenous pacing is probably indicated (Class IIa, LOE C).

54. Pacemakers Transvenous Atrial Dual Chamber A V “PR”
Key Concept: This rhythm strip demonstrates dual-chamber atrioventricular pacing. Used in permanent pacemakers, this mode is designed to simulate the normal physiology of atrial contraction followed by ventricular depolarization, allowing for the atrial contribution to cardiac output. This mode will not be seen in transcutaneous or temporary pacing but is included here for completeness. ACLS providers may encounter patients with AV sequential pacing, and they should not confuse this mode with pacemaker malfunction. A V
“PR”

55. Cardioversion – Synchronized Transcutaneous 
Key Concept: A single slide is presented to introduce the concept of cardioversion and distinguish this procedure from defibrillation and pacing. Ask the students what the difference is and when cardioversion is indicated.
Note what the vulnerable period is and why it is important to synchronize to avoid this period.
Ask what the complications of cardioversion are and how the students would avoid them (VF, cardioembolic event—for example, atrial fibrillation >48 hours in duration).
FYI Guidelines 2010: Synchronized Cardioversion
Synchronized cardioversion is shock delivery that is timed (synchronized) with the QRS complex. This synchronization avoids shock delivery during the relative refractory period of the cardiac cycle when a shock could produce VF. If cardioversion is needed and it is impossible to synchronize a shock, use high-energy unsynchronized shocks (defibrillation doses).
Synchronized cardioversion is recommended to treat (1) unstable SVT, (2) unstable atrial fibrillation, (3) unstable atrial flutter, and (4) unstable monomorphic (regular) VT. Shock can terminate these tachyarrhythmias by interrupting the underlying reentrant pathway that is responsible for them.

56. Cardioversion Energy Recommendations
Biphasic Waveform
Atrial Fibrillation J Initial
Atrial Flutter & SVT J Initial
Monomorphic VT J Initial
Increase the energy dose in a stepwise fashion for any subsequent cardioversion attempts
Use manufacturer-recommended doses  –
Key Concept: This slide is presented to show the current recommendations for energy used in cardioversion procedures using a biphasic defibrillator. For atrial fibrillation an initial dose of 120 to 200 J is recommended. For second and subsequent doses use escalating energy.
FYI Guidelines 2010: Synchronized Cardioversion
Healthcare providers should be familiar with doses recommended by the manufacturer.

57. Cardioversion Energy Recommendations
Monophasic Waveform
Atrial Fibrillation 200 J
Atrial Flutter & SVT 200 J
Monomorphic, Unstable With Pulse J
Polymorphic or Pulseless VT—Treat as VF with high-energy unsynchronized defibrillation doses
(Do not use low energy—high likelihood of causing VF in unsynchronized mode)  –
Key Concept: This slide is presented to show the current recommendations for energy used in cardioversion procedures using a monophasic defibrillator. Doses listed are initial recommended energies for specific rhythms. For second and subsequent doses use escalating energy.
Energy requirements may vary based on the rhythm.
Note that polymorphic VT (because it may rapidly deteriorate to VF and synchronization is not possible) and VT without pulses are treated with defibrillation energies—360 J monophasic or biphasic manufacturer-recommended dose (200 J if not specified).

58. Basic Arrhythmias
QUESTIONS?