Arrhythmias

Question 1

How are arrhythmias looked at on ECGs?

Answer 1

They can be observed using just one lead, provided that you can see both P waves and QRS complexes. The lead of choice to investigate arrhythmias is lead V1 because fo the proximity to the RA.
QRS complexes can be seen in any lead but the P wave is best observable from lead V1 and DII bc of the proximity.ì to the RA.

Question 2

What is regular sinus rhythm?

Answer 2

Normal p waves followed by a normal QRS complex. Bpm between 60 and 100 at rest.

Question 3

What is sinus tachycardia?

Answer 3

Normal rhythm with normal P wave morphology. BPM more than 100 but less than 150. Isn’t necessarily pathologic as it can be physiologic like during stress or exercise and even as a compensatory reaction to hypotension or anemia.

Question 4

What is inappropriate sinus tachycardia?

Answer 4

It is tachycardia but with an unidentifiable clinical cause to a physiological reaction. It is an exclusion diagnosis and many test should be run before defining it as inappropriate. The rate is usually below 150.

Question 5

What is Premature Atrial Complex?

Answer 5

A premature atrial complex (PAC) is a premature beat arising from a pacemaking tissue within the atria. There is an abnormal P wave, usually followed by a normal QRS complex.
The signal causing the beat doesn’t come form the sinus therefore the P wave is abnormal.
The QRS should be narrow as it shouldn’t have an effect on ventricular depolarization.
They fire very early so ventricular activation may not occur, or a reentrant atrial tachycardia may develop.

The pause after the premature beat should be less that 2 RR if it is more than 2 RR than it may be PVC.

Question 6

What is a first degree AV block? Criteria?

Answer 6

Regular rhythm, 1:1 ratio between P wave and QRS complex. The abnormalities lies in the PQ interval being linger than 200 ms. it isn’t really a block more like a delay from atrial activation to ventricular activation.
Could be caused by fibrosis of the conduction system which involves the purkinje fibers, old age, or disease involving the atria.

Question 7

What is a right bundle branch block?

Answer 7

PQ interval more than 200 ms, QRS complex more than 120 ms it is a complete block. V1 is M shaped this is because the first upward deflection is the septum slightly depolarizing the RV, then negative deflection due to the depolarization of the LV and finally another upward deflection due to the LV depolarizing completely the RV.
In V6 there is a positive deflection due to depolarization of LV, then a negative deflection due to LV depolarization of RV.

Question 8

What is a left bundle branch block?

Answer 8

QRS complex longer than 120 ms. V1 shows long negative R wave with positive skewed S wave. V6 shows absence of Q wave with positive tall notched R wave and negative skewed S wave.

Question 9

What is a third degree AV block? Criteria?

Answer 9

Regular rhythm, HR can differ between atria and ventricles, AV conduction is slow and the PQ interval is wider than 200 ms. There could be a true AV block where at least one P wave us not followed by a QRS complex. Often the atria try to compensate by increasing depolarization of the SA node. There are more P waves than QRS complexes.
There is a ventricular escape rhythm from the AVJ, usually not always.
Constant PP and RR, AV dissociation and an escape rhythm.

Question 10

What is a ventricular escape rhythm?

Answer 10

This rhythm occurs because a supraventricular node di not fire, basically the ventricles fire themselves. The rate is variable, the rhythm is regularly irregular, no P wave, no PQ interval and no PR interval. QRS will be wide, bizzarre looking greater than 110 ms.
The more downstream the block is the more significant is the bradycardia. This is because it takes longer to depolarize the ventricles if the block is in the purkinje fibers rather than the AVJ.

Question 11

Which arteries perfuse the hearts conduction system?

Answer 11

SA node : directly from the RCA.
AV node : has a direct artery coming from the RCA
His bundle, right and left bundles, and Purkinje fibers all are
supplied from the branches of the LAD which is a branch of
the LCA.
LAD provides branches for both the RBB and the left anterior
branch.
The left posterior branch perfusion depends on whether the heart is right or left dominant. Receives blood from the same branch supplying blood to the inferior part of the septum.

Question 12

Atrial pacing ECG?

Answer 12

Rate is usually between 60 and 100. Rhythm is regular. P wave is present and follows the classical spike which is the pacemaker firing into the atria. Narrow QRS. Very similar to sinus rhythm except the pacer spike.

Question 13

Ventricular pacing?

Answer 13

Rate is variable between 60 to 100, rhythm is regular. It just depolarizes the ventricles. P waves are absent bc there is no prior atrial depolarization, so no PQ or Pr interval. QRS is more than 120 ms and the classical pacer spike occurs before the QRS complex.

Question 14

What is a second degree AV block : Mobitz Type 1?

Answer 14

Regularly irregular rhythm, some P waves are not conducted. There is a progressive increase in the PR interval until it fails to conduct.
There are clusters of beats and then it stops and repeats therefore it is cyclical.
It is caused by increased vagal tone, MI, drugs, mitral valve surgery and hyperkalemia.
Can cause bradycardia and hypotension.

Question 15

What is a second degree AV block : Mobitz Type II?

Answer 15

It is a form of 2nd degree AV block in which there is intermittent non-conducted P waves without progressive prolongation of the PR interval. The rhythm is periodic and reproducible → regularly irregular. Sometimes fixed P to QRS ratio.

Caused by structural heart diseases, MI, fibrosis.
The block is located in 75% of the cases below the bundle of His (wide QRS) and 25% of the cases within the bundle of His (narrow QRS).

Can cause syncope, fatigue, chest pain, SCD and has a high risk of progression to complete heart block.

Question 16

What is second degree AV block : advanced block?

Answer 16

It is characterized by 2 consecutive non conducting P waves. It is just the few beats prior to a complete AV block and disassociation.

Question 17

What is a second degree AV block 2:1 AVB?

Answer 17

P wave to QRS complex ratio is 2:1. There aren’t enough conducted beats to clearly asses if there is a PQ progressive elongation. Clinically it is equivalent to a mobitz II. Requires particular pacemakers.

Question 18

What is premature ventricular complex?

Answer 18

It is an early beat fired autonomously from a ventricular focus. P waves normal but buried within the QRS. Opposite to PAC as it has a widened QRS complex. It is often benign but can be a sign of underlying conditions.
Some PVCs are called higher-risk PVCs as they come so
early even before the ventricles have completed the repolarization process. It is called the R on T phenomenon; which sometimes results in life-threatening arrhythmia like ventricular fibrillation.

Question 19

How are PVC categorized?

Answer 19

Monomorphic and polymorphic PVC.
It is clinically important to define the morphology because monomorphic PVCs point to a focal disease like a scar post-MI, inflammatory disease, or cardiomyopathy processes; if there is a disease area with a continuous firing, the origin of the PVC is just that focal point.
Instead, polymorphic PVCs are more complex because they indicate either a diffused disease or a disease external to the heart like iron or metabolic imbalances which create a sort of multifocal electrical activation of the heart.

Question 20

What is atrial fibrillation?

Answer 20

It is an irregularly irregular rhythm based on the QRS complexes, usually narrow QRS. Very fast atrial rate, single fibers or small groups of fibers are depolarizing and contracting independently, HR is around 120-150 bc of the refractory period of the AV node otherwise it would be much higher. The ECG looks like scribble with random QRS complexes.
Risk factors include hypertension, coronary artery disease, valvular diseases, obesity and diabetes.
One potential complication is stroke, bc the blood in the atria becomes more stagnant and is at a higher risk of forming a blood clot which could end up in the brain.

Question 21

How is atrial fibrillation classified?

Answer 21

Paroxysmal : AF comes and goes. Usually terminates within 7 days of onset without intervention. This can still over time cause stress to the heart.
Persistent : AF that isn’t able to spontaneously terminate after more than 7 days.
Long-standing : AF that is continuous for more than 1 year.
Permanent : Chronic AF.

Question 22

How do the ventricles response to atrial fibrillation?

Answer 22

If the ventricular rate is fast such as more than 150 bpm, the patient may become very symptomatic for palpitations and sometimes may experience syncope. If it is below 60 especially 40/30 bpm, the patient may experience syncope because of a too slow heart rate. More common in elderlies.

Question 23

How is atrial fibrillation treated and managed?

Answer 23

All patients, especially the elderly, should be on anticoagulants to avoid clotting. CHA2 DS2 VASc score is used to summarize stroke risk factors.

Restore rhythm control by direct current cardio version in hemodynamically compromised patients or pharmacological cardio version in hemodynamically stable patients.

Rate can be controlled using beta blockers, calcium channel blockers and amiodarone.

A pacemaker can also be a strategy.

Question 24

How does normal automaticity of the heart work?

Answer 24

Normal automaticity occurs within specialized pacemaker cells within the SA node, atria, AVJ and ventricles. It is dependent from the sympathetic effect causing the release of catecholamines stimulating B1 adrenergic receptors which increase HR. It is also dependent on the parasympathetic effect caused by the release of Ach from the vagus nerve which via the muscarinic receptor decrease depolarization and therefore decrease HR.
Automaticity is a balance between these two effects.

Question 25

What is the re entery circuit?

Answer 25

In normal conditions an electrical impulse should cease at the end of the cardiac cycle. An impulse that doesn’t cease at the end of the cardiac cycle but persists and reexcites the heart can cause clinically relevant tachyarrhythmias.

Reentry can be divided in two categories based on whether the circuit is large enough to be mapped. Microreentry and macroreentry.

Question 26

What is atrial flutter?

Answer 26

Atrial flutter is an SVT caused by a reentry circuit within the right atrium. It results in an atria rate of around 300 bpm and a ventricular rate depending on AV conduction ratio, usually 2:1 therefore 150 bpm in the ventricle. Higher degree blocks such as 3:1, 4:1 can occur.

Anticlockwise reentry—> most common form, 90% of cases. Inverted flutter waves in leads II,III, aVF. Positive flutter waves in V1.

Clockwise reentry—> uncommon, leads to opposite pattern.

ECG findings—> narrow complex tachycardia at around 150 bpm, saw tooth pattern seen in leads II, III and aVF.

Adenosine and/or vagal maneuvers can be used to differentiate between atrial flutter and AVNRT/AVRT, the first will cause the unmasking of flutter waves the latter will revert to sinus rhythm.

Question 27

What is AtrioVentricular Nodal Reentrant Tachycardia?

Answer 27

It is a subtype of SVT and a medical emergency. Typically paroxysmal in nature. A premature beat reaches the AV node it will find the fast pathway in the refractory period so it will travel through the slow pathway. By the time it reaches the end instead ceasing to exist, the fast pathway has recovered, therefore it loops back and will continue to excite the ventricles.

Typical AVNRT—> impulse runs down slow and back up through the fast pathway.
Atypical AVNRT—> 6% of cases. Impulse runs down the fast pathway and back up the slow pathway.

ECG findings—> 150-250 bpm, non discernible P waves, pseudo S wave which are retrograde P waves, QRS wave is normal unless they’re is an aberrant conduction.

Management—> patient may be instructed to undertake vagal maneuvers upon onset of symptoms such as carotid sinus massage or valsalva maneuver. Other strategies include adenosine, followed by beta blockers, calcium channel blocker, amiodarone. Cardio version is rarely used unless patient is hemodynamically unstable. Radio frequency catheter ablation can be offered to patients with frequent attacks.

Question 28

What is OAVRT and AAVRT?

Answer 28

Unlike AVNRT where the reentry circuit is located exclusively in the AV node in AVRT we have an accessory pathway that connect the atria to the ventricles.

In OAVRT, anterograde conduction is via in AV node producing a narrow complex rhythm.

In AAVRT, the anterograde conduction is via an accessory pathway producing a wide QRS complex. Often confused with Vtach.

Both have very high rates.

Question 29

How does the QT interval change in progressive degrees of hypokalemia?

Answer 29

Normal potassium range is between 3.5 to 5.2 mmol/L. 3.5 is the borderline level for having arrhythmias. Below 3 T waves starts becomes flat and biphasic because it takes more time to repolarize the atria. QT interval becomes longer.

Question 30

What is torsade de pointes?

Answer 30

It is a form of ventricular tachycardia arising from multiple ventricular foci.

Characterized by very fast rate, around 300 bpm, no p waves, wide QRS complex with various QRS amplitudes. Classical morphology resembles QRS complexes twisting around the isoelectric line.
It is associated to QT interval prolongation and hypokalemia. Can be initiated be a PVC on a T wave. Can manifest in short bursts which make the diagnosis harder as it lacks the classical twisting. It may also degenerate into VF.

Treatment include direct current cardio version, correction of electrolyte imbalances and anti arrhythmic drugs to reduce QT interval

Question 31

What is long QT syndrome? What is the physiology behind LQTS?

Answer 31

It is either congenital or acquired when triggered by certain medications (amiodarone, fluconazole, erythromycin, methadone, SSRI) and hypokalemia.
QT interval > 450 ms.
May present with syncope brought on by exercise, seizures, palpitations and cardiac arrest.
May lead to Torsades which could cause Vfib.

QT interval is defined as the time interval between the beginning of ventricular depolarization and the end of ventricular repolarization.

Question 32

Which are shockable vs unshockable rhythms?

Answer 32

Shockable : Pulsless Vtach, Vfib and SVT.
Unshockable : pulseless electrical activity and asystole.

Question 33

What is brugada syndrome?

Answer 33

It is a genetic disorder which is characterized by an inherited channelopathy that predisposes to cardiac arrhythmias and SDC.
The primary channel involved is the sodium, SCN5A most common mutation, but other channel may be involved as well. The exact mechanism is unknown.

Most patients are asymptomatic and SCD may be the first presentation although some patients present syncope, palpitations, chest pain and dyspnea.

Diagnosed by placing right precordial leads in the 2nd and 3rd intercostal space and to look for concave ST segments more than 2mm, J point elevation followed by a negative T wave. This is referred to as the Brugada sign and is the only ECG abnormality that is potentially diagnostic.

Question 34

What is the difference between tachyarrhythmias and bradyarrhythmias?

Answer 34

Tachyarrhythmias : are cause by an enhanced cardiac automaticity or re-entry phenomenon, heart rate increases. Causes might be ectopic heartbeats (atrial or ventricular), tachycardia, flutter, fibrillation.

Bradyarrhythmias : are a very important and relevant issue, especially in elderly, because they face problems in conduction system which usually is less and less active over time due to fibrosis. The firing of the SA and AV node will be reduced, and the HR will be progressively slower over time. When we define bradyarrhythmia, the HR is below 60.

Question 35

What are possible causes of atrio ventricular blocks?

Answer 35

Drugs, MI, IHD, degenerative diseases causing fibrosis and sclerosis in the conduction system, rheumatic diseases, infiltrative cardiomyopathies such as amyloidosis, hemochromatosis, sarcoidosis and tumors, neuromyopathies, infectious disease.

Question 36

Risk factors, clincal presentation, diagnosis, treatment of atrial fibrillation?

Answer 36

Consequences of atrial fibrillation include thromboembolism from thrombi developing in the atria and can embolization the brain most commonly, decreased EF, decreased QoL, increased need of hospitalization.

Comorbidities include IHD, DCM, RCM, HCM, excessive alcohol intake, myocarditis, hyperthyroidism and HF.

Clinical presentation : patient could be asymptomatic or report palpitations, fatigue, syncope and angina.

Diagnosed because of complete absence of P waves, irregularly irregular pattern, extremely high atrial HR.

Patients are prescribed beta blockers and calcium antagonists, and anticoagulation therapy to prevent thromboembolism. Patients are also scored on a scale that quantifies risk of stroke. Cardio version can be proposed.

Question 37

Treatment of atrial flutter?

Answer 37

Therapy strategy is very similar to AF bases on rate or rhythm control though drugs or ablation.

Question 38

What is ventricular fibrillation?

Answer 38

A PVC, R on T phenomenon, QT prolongation and SVT can all evolve into a VF. With this rhythm the patient is in cardiac arrest.

There are no identifiable P, QRS or T waves. The rate is between 150 to 500. Unless advanced life support is instituted this rhythm is inevitably fatal.

Question 39

What is ventricular tachycardia? Classification?

Answer 39

Ventricular tachycardia is a potentially life-threatening condition due to an abnormal rhythm generated in the working myocardial cells. The ventricles, therefore, do not follow the depolarization of the conduction system, as reflected by the broad QRS > 160 ms.

Can be classified as non-sustained VT which last less than 30 beats or 30 seconds or sustained VT lasting more than 30 beats or 30 seconds.
It can also be classified based on morphology, as it can be monomorphic or polymorphic (multiple ventricular foci).

ECG findings include notched S wave and and R-S interval > 100 ms.

Question 40

What is Wolf Parkinson White syndrome?

Answer 40

It is characterized by the presence of a congenital accessory pathway and episodes of tachyarrhythmias.

WPW syndrome is characterized by a double stimulation of the ventricles. A premature conduction wave via accessory pathways (pre-excitation) stimulates the portions of the ventricles nearest the atrium, then the ventricles depolarize as a result of the conduction wave which proceeds normally through the atrioventricular node.

Symptoms include palpitations, dyspnea, dizziness, syncope.

Classical findings include delta wave indicating pre excitation.

WPW treatment include vagal maneuvers, cardio version, catheter ablation and rate controlling drugs.