Conduction Disorders (PEARLS)

The NCCPA™ PANCE Cardiology System Content Blueprint covers 10 different conduction disorders

Conduction Disorders Quick Cram

Normal sinus rhythm	Regular rhythm of the heart cycle stimulated by the SA node with an average heart rate of 60-100 bpm
Sinus tachycardia	Sinus rhythm but with a heart rate over 100 bpm
Sinus bradycardia	Sinus rhythm with a resting heart rate of < 60 bpm in adults or below the normal range for age in children
Atrial fibrillation/flutter	Irregularly irregular rhythm with disorganized and irregular atrial activations and an absence of P waves Regular, sawtooth pattern and narrow QRS complex
Atrioventricular block	First Degree AV Block: PR interval is longer than 0.2 seconds or one block on EKG Type I Second Degree (Wenckebach): progressive lengthening of the PR interval, then missed QRS complex Type II Second Degree (Mobitz): fixed PR interval with occasional dropped QRS complexes Third Degree AV Block: no association between the P wave and QRS complex
Bundle branch block	Left: R and R’ (upward bunny ears) in V4-V6 Right: R and R’ (upward bunny ears) in V1-V3
Paroxysmal supraventricular tachycardia	Narrow complex tachycardia
Premature Beats	PVC: Early wide, bizarre QRS, no p wave seen PAC: abnormally shaped P wave PJC: Narrow QRS complex, no p wave or inverted p wave
Sick sinus syndrome	Brady-tachy: Arrhythmia in which bradycardia alternates with tachycardia Sinus arrest: prolonged absence of sinus node activity (absent P waves) > 3 seconds
Sinus arrhythmia	Normal, minimal variations in the SA Node's pacing rate in association with the phases of respiration. Heart rate frequently increases with inspiration and decreases with expiration
Torsades de pointes	Polymorphic ventricular tachycardia that appears to be twisting around a baseline
Ventricular fibrillation	Erratic ventricular rhythm without identifiable P waves, QRS complexes, or T waves
Ventricular tachycardia	Wide complex tachycardia with three or more consecutive ventricular premature beats

Normal Sinus Rhythm

Patient will present as → a 37-year-old woman with a history of hypertension presents to the emergency department with complaints of shortness of breath. She was placed on a telemetry monitor. An EKG is performed and demonstrates a regular rhythm at a rate of 75 bpm. A normal P wave precedes each QRS complex, P waves are upright in leads I and II and inverted in aVR, the PR interval remains constant, and each QRS complex is < 100 ms wide.

Normal sinus rhythm refers to both a normal heart rate and rhythm.

Normal heart rates are from 60 to 100 beats per minute.
Electrical impulse originates in the sinoatrial node (SA).
P waves are upright and appear before each QRS and have the same shape.
Intervals between the P waves are regular although some variations can occur with respiration.

Sinus Tachycardia

Patient will present as → a previously healthy 34-y/o long-distance runner who sustained a prolonged viral illness followed by persistent fatigue. She was evaluated 6 months later for excessive heart rate increases with minimal exertion (walking across the room) associated with palpitations. She developed near syncope with running and was unable to keep up with her mother for more than a 500-m jog. Her resting heart rate was 95 b.p.m. without orthostatic changes in pulse or blood pressure. Heart rate with minimal exercise was 190 b.p.m., which slowed gradually upon rest; this was reproducible.

Sinus tachycardia is a normal sinus rhythm but with a heart rate over 100 bpm.

It is a normal response to exercise, excitement, and some illnesses

Sinus Bradycardia

Patient will present as → a 65-year-old woman with a past medical history notable for squamous cell carcinoma of the vallecula. Her vital signs are HR 48 bpm, BP 90/70 mmHg, RR 11 rpm, and T 98.2F. The ECG demonstrates normal sinus rhythm with a rate of 48 beats/min.

Sinus bradycardia is a sinus rhythm with a rate of 40-60 bpm

Go to top

Atrial fibrillation

Patient will present as → a 65-year-old woman with palpitations. Her past medical history is notable for chronic obstructive pulmonary disease (COPD) for which she has been hospitalized once in the last year. On exam her T 98.4F, HR 86, BP 105/70, RR 18, SpO2 94% on room air consistent with her baseline. The ECG demonstrates low-amplitude fibrillatory waves without discrete P waves and an irregularly irregular pattern of narrow QRS complexes.

Irritable sites in the atria fire very rapidly, between 400-600 bpm

This very rapid pacemaking caused the atria to quiver
The ventricles beat at a slower rate due to the AV node is blocking of some of the atrial impulses

Presentation:

Elderly, excessive alcohol use
Symptoms range from syncope, dyspnea, palpitations to no symptoms
Irregularly irregular pulse

EKG: Low-amplitude fibrillatory waves without discrete P waves and an irregularly irregular pattern of QRS complexes

Treatment:

Rate: Calcium channel blocker (diltiazem, verapamil) or beta-blocker (metoprolol)
Rhythm:
- Duration <48 hours - cardioversion, amiodarone (obtain echo to determine if a clot is present prior
  to cardioversion)
- Duration >48 hours - anticoagulation for 21 days prior to cardioversion

Anticoagulation is determined by CHA2DS2-VASc or CHADS2 scoring to assess the risk of stroke

0 points – no therapy or 81–325 mg/day of aspirin
1 point – either 81–325 mg/day of aspirin or anticoagulation
2 or more points – anticoagulation

Atrial Flutter

Patient will present as → a 74-y/o presents for her annual physical examination and notes increasing fatigue over the prior 3 months. Her history is notable for longstanding, but now well-controlled, systolic hypertension. A physical examination demonstrates a blood pressure of 130/70 mm Hg and an irregular pulse of approximately 120 bpm at rest. The ECG shows continuous and regular atrial activation with a sawtooth pattern, most obvious in leads II, III, and aVF.

There are two types of atrial flutter

Type I (also called classical or typical) has a rate of 250-350 bpm
Type II (also called non-typical) are faster, ranging from 350-450 bpm

EKG: Regular, sawtooth pattern (F-waves), narrow QRS complex

Occasionally occurs in COPD, congestive heart failure, atrial septal defect, coronary artery disease

Similar treatment as atrial fibrillation

Go to top

Atrioventricular block

1st degree AV block: PR interval > .2 seconds
2nd degree AV block (Mobitz) two types:
- Mobitz type 1 (Wenckebach) – longer, longer, drop now you’ve got a Wenckebach
- Mobitz type 2 – some get dropped some get through now you’ve got Mobitz 2
3rd degree (complete block): P’s and Q’s don’t agree now you’ve got 3rd degree

First degree AV block

Patient with first-degree AV block will present as → a 68-year-old female with a history of hypertension and hyperlipidemia presents for a routine check-up. She reports feeling generally well but mentions occasional episodes of mild fatigue, which she attributes to aging. She denies any chest pain, shortness of breath, or palpitations. Her medications include lisinopril and atorvastatin. Vital signs are within normal limits. Physical examination is unremarkable. An EKG is performed as part of her evaluation, which reveals a consistent prolongation of the PR interval greater than > 0.2 seconds (200 ms), consistent with a first-degree AV block. There are no other abnormalities noted on the EKG. The patient is reassured, as first-degree AV block is often a benign finding, especially in asymptomatic patients.

PR interval > .2 seconds

First-degree heart block is actually a delay rather than a block. It is caused by a conduction delay at the AV node or bundle of His. This means that the PR Interval will be longer than normal (over 0.20 seconds) without disruption of atrial to ventricular conduction.

(PR interval longer than 1 big box 0.20 seconds)

Second degree AV block Type 1 (Wenckebach) and Type 2 (Mobitz)

Type I: Wenckebach block

Patient with Mobitz Type I (Wenckebach) second-degree AV block will present as → a 55-year-old male, with no significant medical history, presents to the clinic complaining of occasional lightheadedness and palpitations, particularly during his morning jogs. He denies any chest pain, shortness of breath, or syncope. On examination, his vitals are stable, but his pulse is irregularly irregular. An ECG is performed, revealing a pattern of progressively lengthening PR intervals followed by a non-conducted P wave, a characteristic finding of Mobitz Type I (Wenckebach) second-degree AV block. The patient is referred to cardiology, who discusses the potential treatment options, which may include lifestyle modifications, medication adjustments, and possibly pacemaker implantation if his symptoms are deemed related to the observed AV block.

Wenckebach (longer, longer, longer drop now you've got a Wenckebach)

With second-degree heart block, Type I (Wenckebach) some impulses are blocked but not all. More P waves can be observed vs QRS Complexes on a tracing
Each successive impulse undergoes a longer delay. After 3 or 4 beats the next impulse is blocked
On an EKG tracing, PR Intervals will lengthen progressively with each beat until a QRS Complex is missing. After this blocked beat, the cycle of lengthening PR Intervals resumes
The Wenckebach pattern tends to repeat in P:QRS groups with ratios of 3:2, 4:3 or 5:4

Type II: Mobitz

Patient with Mobitz Type II second-degree AV block will present as → a 68-year-old female with a history of hypertension presents to the emergency department complaining of dizziness and episodes of near-syncope over the past few days. She reports no chest pain, shortness of breath, or palpitations. Her blood pressure is slightly elevated, and her pulse is slow and irregular. An ECG reveals intermittent, non-conducted P waves without progressive prolongation of the PR interval, consistent with Mobitz Type II second-degree AV block. The patient is informed about the nature of her condition, the need for a pacemaker, and the associated risks and benefits.

MOBITZ 2 (some get dropped some get through now you've got mobitz 2)

With Mobitz Type II blocks, the impulse is blocked in the bundle of His. Every few beats there will be a missing beat but the PR Interval will not lengthen.

Third-degree AV block (complete heart block)

Patient with third-degree (complete) AV block will present as → a 75-year-old male with a history of coronary artery disease presents to the clinic with fatigue and episodes of lightheadedness. He denies chest pain but notes increasing shortness of breath on exertion. On examination, his pulse is slow, and blood pressure is on the lower side. An ECG is performed, revealing a complete heart block (third-degree AV block) characterized by atrial and ventricular rhythms that are independent of each other. The ECG shows no acute ischemic changes. Due to the high risk of progression to asystole and the potential for sudden cardiac arrest, he is immediately admitted for cardiac monitoring. Cardiology is consulted, and they recommend urgent pacemaker placement.

P’s and Q’s don’t agree now you've got 3rd degree

With this block, no atrial impulses are transmitted to the ventricles.

As a result, the ventricles generate an escape impulse, which is independent of the atrial beat. In most cases, the atria will beat at 60-100 bpm while the ventricles asynchronously beat at 30-45 bpm.

There is no electrical communication between the atria and the ventricles, causing complete AV dissociation. P waves do not match the QRS one-for-one

Go to top

Bundle branch block

Patient with left bundle branch block (LBBB) will present as → 68-year-old female with a history of hypertension and type 2 diabetes presents to the emergency department with palpitations and mild shortness of breath. She mentions a recent increase in fatigue but denies chest pain. Her blood pressure is elevated, and a regular but fast heart rate is noted. An ECG is performed, showing a left bundle branch block (LBBB) characterized by wide QRS complexes and an RSR’ pattern in V4-V6 that looks like a W in V1 and M in V6. The ECG also reveals a fast ventricular rate. The patient is stable, without signs of heart failure or acute coronary syndrome. Cardiology is consulted, and they recommend further evaluation to rule out underlying ischemic heart disease, given her risk factors and new-onset LBBB.

With this conduction block, either the left or right bundle branch is blocked intermittently or fixed

The QRS complex is wider than normal (> 0.12 sec.)

Using a 12 lead EKG, blocks in either the left or right bundle branch may be diagnosed.

QRS complex > .12 seconds
May be due to MI
Left: R and R’ (upward bunny ears) in V4-V6
Right: R and R’ (upward bunny ears) in V1-V3

Go to top

Paroxysmal supraventricular tachycardia

Summary of supraventricular tachycardia:

Heart rate: 150-250 BPM

Types:

Paroxysmal supraventricular tachycardia (PSVT) – no structural abnormalities
AV nodal reentrant tachycardia (AVNRT) – a small extra pathway exists in or near the AV node
Wolff Parkinson White (WPW) – presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles – Bundle of Kent fibers and delta wave on EKG
Atrial tachycardia (AT) is responsible for about 5 percent of PSVTs. It occurs when an electrical impulse fires rapidly from a site outside the sinus node and circles the atria, often due to a short circuit. In AT, the ECG shows identical P waves with a consistent rhythm.
- Multifocal atrial tachycardia (MAT): Characterized by multiple ectopic foci within the atria firing electrical impulses erratically, resulting in a rapid and irregular atrial rhythm. The ECG shows different P wave shapes originating from different atrial locations.

Treatment:

Valsalva for stable patients
Adenosine for symptomatic patients
Definitive treatment: Radiofrequency ablation
WPW- do not administer adenosine or calcium channel blockers

Paroxysmal supraventricular tachycardia (PSVT)

A faster-than-normal heart rate beginning above the heart's two lower chambers in the atria, AV junction, or SA node associated with no structural abnormalities

Atrioventricular nodal reentrant tachycardia (AVNRT)

A small extra pathway exists in or near the AV node
If an electrical impulse enters this pathway, it may start traveling in a circular pattern that causes the heart to abruptly start beating fast and regular

Wolff-Parkinson-White Syndrome

Patient will present as → a 25-year-old female patient with complaints of sudden onset of a pounding heartbeat, which is regular and “too rapid to count.” She reports that the episodes begin and terminate abruptly and are associated with shortness of breath and chest discomfort. On exam, the patient appears anxious, her heart rate is 170 bpm. EKG demonstrates a shortened PR interval, widened QRS, and delta waves.

This occurs when the impulse travels between the atria and ventricles via an abnormal path, called the bundle of Kent

The impulse, not being delayed by the AV node, can cause the ventricles to contract prematurely
EKG characteristics include a shorter PR Interval, longer QRS complex, and a delta wave (click here)

Multifocal Atrial Tachycardia

Patient will present as → a 72-year-old man is admitted for exacerbation of COPD. On the third day, he reports dizziness associated with occasional chest pain. His telemetry reveals an irregular rhythm with a pulse of 124/min. The EKG demonstrates an irregularly irregular rhythm, rate of 120 bpm, discrete P waves before every QRS complex with 4 different P wave morphologies.

When multifocal atrial tachycardia occurs, multiple (non-SA) sites are firing impulses.

EKG: Rapid, irregular rhythm > 100 bpm. At least 3 distinct P-wave morphologies
The PR Interval varies
Ventricular rhythm is irregular

Go to top

Premature Beats

Patient will present as → a 24-year-old college student complaining of a feeling as though his heart is momentarily stopping followed by a feeling of his heart in his throat. He appears anxious and reports a weight loss of about 7 lbs. over the past 3 months. On auscultation of his heart, you notice an occasional skipped beat, followed by a brief pause and then a regular rhythm. His laboratories reveal a TSH of 0.001 and on his EKG, you notice a wide, bizarre QRS complex, greater than 0.12 sec and no identifiable p wave.

Premature atrial contractions (PAC), Premature junctional complexes (PJC) and premature ventricular contractions(PVC)

Typically benign. May cause palpitations.
Increased frequency with stimulants (Ie. Caffeine)

EKG: Irregular beats (three types)

PVC – widened QRS
PAC – abnormally shaped P wave
PJC – narrow QRS usually measured at 0.10 sec or less

Every 3rd beat – trigeminy. Every other beat- bigeminy

Treatment: None or beta-blockers if symptomatic

Premature atrial beats

Patient will present as → a 44-year-old man presents with several months of nearly constant palpitations and “skipped beats.” His past medical history is notable for hypertension and obesity, treated with gastric bypass surgery 9 years prior. He denies alcohol and illicit drug use. An EKG performed to assess his current symptoms of palpitations is notable for sinus rhythm with an abnormal (non-sinus) P wave followed by a normal QRS complex. Holter monitoring documented a 19% burden of unifocal PACs.

This occurs when an ectopic site within the atria fires an impulse before the next impulse from the SA node

EKG: An abnormal (non-sinus) P wave is followed by a QRS complex
- If the ectopic site is near the SA node, the P wave will likely have a shape similar to a sinus rhythm. But this P wave will occur earlier than expected.

Premature junctional beats

Patient will present as → a 30-year-old woman presented to our outpatient clinic describing a 3-year history of palpitations. An EKG performed in the clinic demonstrates several premature narrow QRS complexes without a preceding p wave.

Premature junctional complex (PJC) occurs when an irritable site within the AV node fires an impulse before the SA node. This impulse interrupts the sinus rhythm

EKG: Narrow QRS complex, either (1) without a preceding P wave or (2) preceded by an abnormal P wave with a PR interval of < 120 ms
The QRS complex will be narrow, usually measured at 0.10 sec or less

Premature ventricular contractions

Patient will present as → a 24-year-old woman presents to your clinic with complaints of anxiety along with occasional palpitations. She reports that when they occur she feels a pause in her heart followed by an extra hard beat often times felt in her throat. Laboratory evaluation reveals a TSH of 0.02. EKG demonstrates normal sinus rhythm with occasional broad QRS complexes (≥ 120 ms) with abnormal morphology.

Premature ventricular complexes (PVCs) occur when a ventricular site generates an impulse. This happens before the next regular sinus beat.

EKG: Broad QRS complex (≥ 120 ms) with abnormal morphology.
Look for a wide QRS complex, equal or greater than 0.12 sec
The QRS complex shape can be bizarre
The P wave will be absent

Go to top

Sick sinus syndrome

Patient will present as → a 45- year-old male admitted to the hospital because of several months of sudden onset of recurrent weakness accompanied by flushing of the face and dizzy spells. The patient also had recurrent spells of chest pain localized to the sternal area. The symptoms last for 10-15 seconds and sometimes 30 seconds to a minute and go away without treatment. During his stay in the ICU, the patient had similar symptoms several times, and the monitor showed long periods of asystole with no ventricular activity. This was associated with blood pressure drops, and the patient felt dizzy. The echocardiogram is within normal limits.

Population: Elderly

Historically referred to as sick sinus syndrome (SSS), now commonly known as sinus node dysfunction (SND), is a collective term used to describe dysfunction in the sinus node's automaticity and impulse generation

Sinus bradycardia: Sinus rhythm with a resting heart rate of < 60 bpm in adults, or below the normal range for age in children
Sinus pause: pause < 3 seconds
Sinus arrest: pause > 3 seconds
Tachy-Brady Syndrome: Episodes of alternating sinus tachycardia and bradycardia

Treatment: Pacemaker

Go to top

Sinus arrhythmia

Patient will present as → an 18-year-old student radiographer presents with a five-month history of blackouts which had latterly been occurring three or four times a day. They invariably occurred when she was standing, and from her description, there was no reason to think that the blackouts were other than vasovagal attacks, but their frequent occurrence was inconvenient. There were no other symptoms and no previous medical complaints. The pulse rate was 60 beats per minute and irregular; blood pressure was 100/60 mmHg with no postural drop. A three-minute electrocardiogram recorded during spontaneous respiration showed marked variation in the P-P intervals induced by respiration with an amplitude of 20-1%, well outside the normal range.

Sinus arrhythmia represents normal, minimal variations in the SA Node pacing rate in association with the phases of respiration.

Heart rate frequently increases with inspiration and decreases with expiration

Go to top

Torsades de pointes

Patient will present as → a 68-year-old woman with a history of chronic heart failure and recent hospitalization for pneumonia presents to the emergency department complaining of sudden onset dizziness and palpitations. She reports adherence to her medication regimen, which includes a diuretic and an antibiotic she started a week ago. On examination, she appears anxious, her blood pressure is 100/60 mmHg, and her heart rate is irregular and fast. An ECG reveals a polymorphic ventricular tachycardia with a characteristic twisting of the QRS complexes around the baseline, consistent with Torsades de Pointes. Her serum potassium and magnesium levels are found to be low. The patient is immediately given intravenous magnesium, and her antibiotic is reviewed, revealing that it is known to prolong the QT interval. The offending antibiotic is discontinued, and she is admitted for cardiac monitoring, electrolyte repletion, and evaluation of her heart failure management to prevent recurrence of this arrhythmia.

Torsade de Pointes is a special form of ventricular tachycardia

EKG: Polymorphic ventricular tachycardia that appears to be twisting around a baseline
Etiology: Hypokalemia or hypomagnesemia
Treatment: IV Magnesium sulfate

Go to top

Ventricular fibrillation

Patient will present as → a 72-year-old male who develops coarse ventricular fibrillation while being monitored following an uneventful colonoscopy. He is immediately defibrillated using a biphasic defibrillator at 120 joules. The countershock is successful, and he is converted to a sinus tachycardia. He has resumed spontaneous breathing.

Chaotic irregular deflections of varying amplitude and no useful contractions

No identifiable P waves, QRS complexes, or T waves
Rate 150 to 500 per minute
Amplitude decreases with duration (coarse VF -> fine VF)

Treat with unsynchronized cardioversion

Unsynchronized cardioversion - start CPR
Give 3 sequential shocks (120, 150, 180); assess rhythm
If VF persists --> do CPR and intubate
Administer two doses amiodarone 2-4 min. Administer 1 mg IV bolus epi every 3-5 minutes (will ↑ myocardial blood flow and ↓ cerebral blood flow and ↓ defib threshold)

An implantable cardioverter-defibrillator may be necessary

Ventricular tachycardia

Patient will present as → a 68-year-old female who arrives at the emergency department after a syncopal episode at work. Physical exam reveals an obese, unresponsive female with bilateral nonpalpable radial, carotid, and distal pedal pulses. Vital signs are as follows: T 99.4 F and BP 88/47. An emergent EKG is obtained (seen here).

A sequence of three PVCs in a row is ventricular tachycardia.

The rate will be 120-200 bpm.
There are several different varieties of VT — the most being Monomorphic VT

Ventricular Tachycardia (Monomorphic)

Monomorphic ventricular tachycardia occurs when the electrical impulse originates in one of the ventricles. The QRS complex is wide. Rate is above 100 bpm.

EKG: Wide complex tachycardia

Treatment:

Stable- amiodarone, lidocaine
Unstable- CPR and defibrillation

Ventricular Tachycardia (Polymorphic)

Polymorphic ventricular tachycardia has QRS complexes that vary in shape and size. If a polymorphic ventricular tachycardia has a long QT Interval, it could be Torsade de Pointes.

Pacemaker Rhythm

Patient will present as → a 78-year-old man who was admitted with 3 days history of fluttering in the chest, shortness of breath, and epigastric pain radiating to the back. His medical history includes exertional angina, unobstructed coronaries in 2015, hypercholesterolemia, and a single-chamber permanent pacemaker for complete heart block in 1995. The patient is conscious and tachycardiac with a blood pressure of 105/70 mm Hg. His chest is clear with signs of congestive heart failure. Blood chemistry results showed normal serum sodium, potassium, calcium, and magnesium. His cardiac troponin is >1000. ECG demonstrates ventricular tachycardia with a pacing spike followed by a P wave or QRS complex.

Atrial and ventricular pacing can be seen on the ECG as a pacing stimulus (spike) followed by a P wave or QRS complex, respectively.

EKG: The appearance of the ECG in a paced patient is dependent on the pacing mode used, placement of pacing leads, device pacing thresholds, and the presence of native electrical activity

EKG Pacing Spikes: Vertical spikes of short duration, usually 2 ms.
It May be difficult to see in all leads

Go to top

Back to PANCE Blueprint Cardiology (13%)

PANCE Blueprint...

PANCE Blueprint...

PANCE Blueprint...

PANCE Blueprint...

PANCE Blueprint...

PANCE Blueprint...

PANCE Blueprint...

PANCE Blueprint...

PANCE Blueprint...

PANCE Blueprint...

PANCE Blueprint...

PANCE Blueprint...

PANCE Blueprint...

PANCE Blueprint...

PANCE Blueprint Cardiology (13%)

Conduction Disorders (PEARLS)

Conduction Disorders Quick Cram

NCCPA™ CONTENT BLUEPRINT

Teacher

Stephen Pasquini PA-C

Role : PA-C