This video presents: 1. Cells taking part in the development of the conduction system of the hear. 2. Origin and development of the annulus fibrous (fibrous insulating ring). 3. Formation of the conduction pathway. 4. Difference of the His purkenje from the rest of the conduction system.

STUDY NOTES:

CONDUCTION SYSTEM OF THE HEART

SAN which is present near the opening of the superior vena cava. SA nodal cells have the highest intrinsic rhythm of spontaneous depolarization (roughly 60- 100/min) which makes them the automatic choice for the pacemaker of the heart.

The AVN is present behind the endocardial cushions and in front of the coronary sinus. It's important to remember that the coronary sinus is actually the attritioned left horn of the sinus venosus. AV nodal cells have the second highest intrinsic rhythm (40-60/min). This automatically makes AVN the as the pacemaker of heart in case there's a damage to the SA nodal cells.

Bundle of HIS originates from the AV node and subsequently branches into two within interventricular septum. These two branches are the right and left bundle branches which ends up forming the HIS Purkinje system that supplies the papillary muscles and the rest of the ventricular myocardium. Papillary muscles are part of the trabeculated region of the ventricles which are derived from the primordial ventricle. Although, Purkinje cells are specialized for conduction only, they still possess an intrinsic rhythm of 35/min which gives them the property of automaticity. Hence, Purkinje system is third in line to take over as the pacemaker of the heart if anything goes wrong with both the SA and AV nodal cells.

The SA and the AV node develop from the sinus venosus. Before the sinus venosus gets incorporated into the right atrium and forms the conducting system of the heart, the primitive atrium serves as the function of the pacemaker.Atrial myocytes around the sinus venosus develop a faster intrinsic rhythm thereby naturally taking over as the pacemaker cells. These myocytes are derived from mesoderm.This means that as the myocardial cells are developing to form atria, they develop this ability to depolarize spontaneously. This allows the primitive heart to start beating by the 22nd day and that too without a true pacemaker, hence the primitive atria starts depolarizing even before the pacemaker is formed. Since sinus venosus is at the caudal end of the heart tube and serves as the inflow region. The initial pulsations are in coherence with the direction of the blood flow i.e., from caudal to the cranial side of the developing heart tube.  Eventually as the sinus venosus is incorporated into the right atrium, the SA node develops from the sinus venosus near the entry of the superior vena cava. 

The AV node also develops from the sinus venosus near the opening of the coronary sinus. As the AV node develops, bundle of HIS also develops along with it from the sinus venosus. The bundle of HIS develops within the interventricular septum and divides into right and left bundle branches. The cells around the AV node which become consolidated into forming the Bundle of HIS exhibit the MSX-2 homeobox gene. Purkinje fibers are actually modified contractile myocytes which start to function as conducting fibers when they become connected with Bundle of HIS cells.

Another important structure is the fibrous septum which insulates the ventricles from the depolarization of the atria and vice versa. This fibrous skeleton of the heart develops from the epicardium which is the visceral pericardium of the heart. The cells of the epicardium are derived from the local mesodermal cells around the sinus venosus as well.

This video presents: Excitation contraction coupling in the heart tissue. Properties of the cardiac muscle compared to smooth and skeletal muscles Role of the extra cellular fluid calcium Beta agonists Action of actylcholine Cardiac glycocides (digitalis)

This video presents the 12 ECG leads and Einthoven's triangle. Leads presented are: 3 Bipolar Limb Leads 3 Unipolar Augmented Leads 6 Chest Leads Earth lead

CVS PHYSIOLOGY LECTURE # 17 STUDY NOTES:

ELECTROPHYSIOLOGY OF HEART

STRUCTURE OF THE CONDUCTING SYSTEM

The atria are separated from the ventricles by a ring of fibrous tissue. This fibrous demarcation acts as an insulator, thereby barricading the entrance of electrical activity from the atria into the ventricles. The functional structure of the heart requires it to fill the atria with blood before the ventricles. Therefore, it is important for the atrial musculature to contract first and force blood into the ventricles before the ventricles undergo contraction. After a time lapse of milliseconds, electrical activity in both the ventricles causes them to contract and pump blood to the pulmonary circuit and to the rest of the body.

Electrical activity in the cardiac muscle is initiated by the sinoatrial node (SAN), located near to the opening of superior vena cava. The SA node is comprised of a collection of modified cardiac cells that have the potential to generate electrical signals. Multiple pathways, originating from the SAN, carry electrical signals to the atrial muscles. Similarly, one of the pathways stimulates the atrioventricular node (AVN) present at the base of right atrium and limited by the coronary sinus, the atrial septum and the tricuspid valve (Coch’s triangle). Bundles of fibers arise from the AV node, pierce the atrioventricular fibrous ring and enter the ventricles. In the ventricles, the fibers recollect and divide into two bundles that run down the interventricular septum. These bundles are known as the bundle of His. Upon reaching the apex of the heart, the bundles of His give rise to Purkinje fibers that ascend along the ventricular walls in a fashion which allows for spread of electrical activity in an ascending fashion (from the apex to upwards). As the conduction fiberspass from atria to ventricles their diameter increases.

TYPES OF CELLS PRESENT IN THE CARDIAC SYSTEM

The cells of the cardiac system are primarily classified as follows:

• Functional Cells

• Electrical Cells

1) Functional cells of the heart are further divided into contractile cells and conducting cells. Contractile cells are basically muscular cells that are joined together at their ends forming intercalated discs. Gap junctions between cells within the intercalated discs allow movement of ions, thereby causing the heart to work as a syncytium (single unit). Hence, the contractile cells show properties of conduction as well. Conducting cells, on the other hand, are modified to allow passage of electrical current only and do not exhibit any contractile properties.In the embryonic stage they were contractile muscle cells which later became conducting cells.

2) Electrical cells are sub-classified into fast and slow fibers depending upon the conduction velocity and speed of depolarization which they exhibit. The rate at which an action potential travels through a conducting fiber depends on its diameter and the presence of various channels on its cell membrane. Purkinje fibers have the largest diameter relative to the rest of the fibers in the conducting system. Hence, Purkinje fibers have the highest conduction velocity. The diameter of His Purkinje fibers is 150 times larger than AV fibers and 6 times larger than Ventricular muscle fibers. In general, the conducting fibers in the heart also possess fast sodium channels on their cell membranes. The number of these fast sodium channels helps determine the rate of depolarization and hence, the conduction velocity.Velocity of conduction of His Purkinje fibers is 4m/sec while that of AV fibers is 2m/sec.

The two nodes (SAN & AVN), on the other hand, have slow calcium channels present on their cell membranes. They do not have sodium channels. Movement of ions through these channels results in a gradual increase in the membrane potential leading to slow depolarization of the nodes. They have slow depolarizing fibers.

Another determinant affecting conduction velocity is the presence of gap junctions between cardiac cells. Gap junctions facilitate movement of ions from one cell to another. Higher the number of these gap junctions, higher would be the conduction velocity as more cells get depolarized at a time. The AV node and its emergentfibers have the least number of gap junctions and hence, the conduction velocity is slowest. 

BEATS PER MINUTE:

The size of the cardiac cycle is determined by the formula

60 seconds

Number of beats per minute = 60/72=0.8 seconds.

DIRECTION OF IMPULSE TRAVEL

Before moving on, it should be noted that the two nodes (SAN & AVN) and all the conducting fibers in the heart muscle have an intrinsic ability to undergo depolarization. This explains why even if the heart is isolated from the rest of the body, it will resume its pacemaker activity and continue to beat on its own. An isolated SA node has the highest frequency of impulse generation, i.e. 100 beats/min. This intrinsic rhythm of the SAN is regulated down to 72 beats/min under the influence of the autonomic nervous system. Similarly, the AV node has the ability to depolarize at a rate of 60 beats/min. SA node, having a considerably higher frequency of depolarization, overrides the pace maker activity of the AV node. This causes the AV node to generate action potentials at a rate similar to SA node. Upon cessation of high frequency impulses from SA node, as happens during bundle blocks, due to ischemia or experimental destruction of SA Node the AV node is shown to beat at its own inherent frequency. There is a respective decrease in the frequency of depolarization as we move along the bundle of His and the Purkinje fibers. This relative difference in the intrinsic rhythm of different parts of the cardiac conduction system allows a uni-directional flow of impulses across the entire conducting system. 

It’s important to remember that, AV bundle is the only pathway which allows electrical transmission of impulses from atria to the ventricles. Moreover, the impulses are prevented from propagating in retrograde direction (back into the atria from the ventricles) by the fibrous atrioventricular ring or annulus (insulating layer). If the impulses were allowed to travel back into the atria through accessory pathways, the heart would lose its rhythmical beating and arrhythmias may ensue.

DURATION OF IMPULSES

Duration of impulses is important as it dictates periodic filling of the atria and ventricles and ejection of blood effectively. The duration of an impulse travelling along the conducting system can be briefly described as follows:

• It takes 0.03 seconds for an impulse to travel from SA node to the AV node. 

• The speed is substantially reduced as impulses reach AV node because of its smaller diameter (1*3*5mm) and fewer gap junctions. As a consequence, a time lapse of 0.09 seconds occurs within the AV node. Since, impulse transmission is the slowest within the AVN; it’s a site for various drugs that affect the heart rate.

• Travelling further, it takes 0.04 seconds for the impulse to move along the AV bundle and the bundle of His. 

• It takes another 0.06 seconds for the impulse to spread throughout the ventricular muscles as the fast Purkinje fibers allow rapid and instantaneous conduction of nerve impulses. This is made possible due to the large diameter of Purkinje fibers and presence of numerous gap junctions. The latter allows the ventricles to work as a syncytium, resulting in simultaneous contraction of the entire ventricular musculature. If simultaneous contraction of ventricles does not occur then arrhythmiasare induced and the person dies due to low cardiac output.

ACTION POTENTIAL:

The action potentials from SA node, Atria, AV node, Bundle of His, Ventricles are different from each other.  Nodal action potential from SA node does not have phase I, II but has phase 0, III, IV. If we superimpose all the Action potentials on the ECG the Ventricular muscle depolarization coincides with the QRS complex while that of Atrial muscle with P wave. Repolarization of atria is buried in the QRS complex while that of ventricle is T wave.

This video presents nodal action potentials. These action potentials occur in the cardiac tissues that exhibit automaticity. A comparison of the myocardial action potential with the nodal action potential is also made to make sure that you are not confused during the Steps.

STUDY NOTES:

NODAL ACTION POTENTIAL

NODAL ACTION POTENTIAL VS. VENTRICULAR ACTION POTENTIAL

The nodal tissues and the Purkinje fibers exhibit automaticity in their properties as they are able to undergo spontaneous depolarizations. In other words, these tissues do not require the need of an external stimulus or a trigger to undergo depolarization. This is in contrast to ventricular fibers that do not show automaticity. The reason behind this phenomenon can be explained as follow:

• The resting membrane potential (RMP) of nodal tissues is less negative than the RMP of ventricular fibers. This allows the nodal tissue channels to operate in a semi-activated state even during the resting phase of the action potential. The comparatively more negative ventricular fibers do not show this property and hence, are not easily activated by low voltage impulses.

• Secondly, the presence of fast sodium channels and slow calcium channels, in ventricular fibers and nodal tissue respectively, play an important role in the automaticity of a cell. The slow calcium channels in the nodal tissues are responsible for the peak voltage occurring during a nodal action potential. Whereas, in the ventricular muscle fibers, the fast sodium channels are responsible for the same voltage spike and the calcium channels are involved only during the plateau phase.

PHASES DURING AN ACTION POTENTIAL

SLOPE OF DEPOLARIZATION DURING NODAL ACTION POTENTIAL

There is a gradual increase in the RMP of nodal tissues from -55mV to -40mV. This is known as the slope of depolarization, after which occurs the Phase 0 of action potential. This slope is important as multiple factors, such as the ANS and certain drugs, act to alter this phase and bring about changes in the rate and rhythm of cardiac activity. An increase in the slope of depolarization will cause the SA Nodeto generate action potentials at a higher rate. Flattening of the slope will result in fewer numbers of action potentials in a given time which greatly decreases the rate at which the heart beats.

CONTROL OF HEART RATE & CONDUCTION VELOCITY

An isolated SA node has the highest intrinsic rhythm of impulse generation, i.e. 100 beats/min. This intrinsic rhythm of SA Node is regulated down to 72 beats/min under the influence of the autonomic nervous system. Similarly, the AV node has the ability to depolarize at a rate of 55 beats/min. SANode, having a considerably higher frequency of depolarization, overrides the pace maker activity of the AVNode. This causes the AV node to generate action potentials at a rate similar to SA node. Upon cessation of high frequency impulses from SA node, as happens during bundle blocks, the AV node is shown to beat at its own inherent frequency. Impulse generation of purkinje fibers is at a rate of 15-30 beats/min. There is a respective decrease in the frequency of depolarization as we move along the bundle of His and the Purkinje fibers. This relative difference in the intrinsic rhythm of different parts of the cardiac conduction system allows a uni-directional flow of impulses across the entire conducting system. 

As described above, the SA node has the highest rate of depolarization and therefore, it dictates the rate of cardiac activity. Altering with the mechanics of SA node will cause alterations in the rate of heart beat as a whole. Similarly, the velocity of conduction is controlled by the AV node(dimensions are 1*3*5 mm) and AV bundles as the speed of impulse travelling through them is the slowest. Time duration for conduction through these is 0.12 seconds. Velocity of impulse at AV node and AV bundle is 2 meters per second and 4 meters per second in purkinje fibers. Dromotropes act on these areas of the conducting system and cause changes in the velocity of impulse conduction.

DIFFERENT ION CHANNELS AND THEIR AFFECT ON THE ACTION POTENTIAL

1) VENTRICULAR ACTION POTENTIAL​​

• The Phase 0 of ventricular action potential is brought about by fast voltage gated sodium channels. This phase is referred to as the upstroke of action potential and corresponds to the QRS complex of the ECG.

• At the end of depolarization, there is a brief fall in the voltage of action potential as a result of opening of transient chloride and potassium channels. This isPhase 1 of the depolarization. Fast sodium channels transition to their inactivated state.

• L-type Calcium channels open in the Phase 2 of action potential. The inward calcium current balances the outward potassium current and there’s little change in membrane potential, which explains the plateau. During this plateau phase no change in the voltage is registered. Phase 2 or the plateau phase of the ventricular action potential corresponds to ST segment of the ECG.

• Phase 3 corresponds to repolarization during which Potassium channels open in response to voltage and ion concentration difference. By this time L-type Calcium channels, which were open during the plateau phase, have also closed. Repolarization corresponds to the T-wave on the ECG. Inward Potassium current enters via the:

▪ IK1 channels: Inward rectifying K channel 

▪ IKR channels: Slow and rapid delayed rectifying K channel 

• The action potential is brought back to the resting membrane potential (RMP) or Phase 4. The sodium-potassium ATP-ase is responsible for the maintenance of RMP until the arrival of the next action potential. Fast Na+, L-type Ca2+, and rectifying K+ channels (IKR) close, but IK1 channels remain open.

2) NODAL ACTION POTENTIAL

It’s important to understand that the nodal tissue (SA and AV) lacks fast Na+ channels. Thus, the upstroke of the action potential is mediated by inward calcium current rather than the sodium current. In addition, note that phases 1 and 2 are absent in the nodal tissue.

• The RMP (Phase 4) in nodal tissue is kept at -55mV by the Na-K ATPase pump. The less negative RMP of nodal tissue, compared to -70mV of ventricular tissues, allows it to exhibit automaticity. At -55mV, the fast sodium channels (also known as 'funny' channels) are in a semi-open state which causes leakage of positive ions into the nodal cells. Leakage of ions causes an increase in the membrane potential in a positive direction. The membrane potential gradually increases to -40mV. Upon reaching this threshold potential, the sodium channels close and remain closed for the rest of the action potential as they enter a state of refractoriness. 

• At this point the slow-gated T-type calcium channels open which creates the spike of depolarization (Phase 0). These differ from the L-type calcium channels (in the ventricular tissue) in that they open at a more negative membrane potential (-70 mV).The calcium ions that enter the cells during this phase are also involved in excitation-contraction coupling of the myosin light chains with actin filaments. 

• Repolarization (Phase 3) in nodal tissue is similar to that of ventricular muscle fibers. Inward Potassium current enters via the IK1 & IKR (rectifying K currents) channels. The fall in membrane potential will result in activation of the sodium-potassium ATPase and the cycle is repeated.

Why do we measure cardiac electrical activity (ECG)? Conduction medium of the heart ECG measurement from the body surfaces Properties of the ECG voltmeter ECG Paper Normal ECG

A healthy individual's standard wave form ECG waves ECG intervals ECG segments Interpretation of the ECG waveform

Dr. Syed presents the first chapter in the series of the EKG Interpretation lectures. This chapter contains:

1. EKG waves.

2. EKG segments.

3. EKG intervals.

4. Various shapes of the QRS complex and how to articulate them.

5. EKG paper properties.

Session 2 of the EKG interpretation.

Dr. Syed presents:

1. EKG leads setup.

2. Surfaces that the EKG leads look at.

3. Properties of QT interval.

4. QRS progression.

Dr. Syed presents:

The terminology used for the cardiac chamber enlargement.

Principles of the EKG changes when chamber enlargement is present.

Right atrial enlargement, EKG changes, diagnostic criteria, and the pathologies.

Left atrial enlargement, EKG changes, diagnostic criteria, and the pathologies.

Right ventricular enlargement, EKG changes, diagnostic criteria, and the pathologies.

Left ventricular enlargement, EKG changes, diagnostic criteria, and the pathologies.

Both ventricular enlargement, EKG changes, diagnostic criteria, and the pathologies.

This video presents the isoelectric lead method to determine the cardiac axis. (Digital media video)

This video presents the quadrant method to determine the cardiac axis. (Digital media video)

Lecture 2 Part 1.

Dr. Syed starts the set of talks on arrhythmias as part of the interpretation of the EKG series. Following topics are covered:

*How to detect arrhythmias?

*Types of arrhythmias.

*Sinus arrhythmias (first type) are presented as well.

Errata: Note the QRS complex duration is from 80ms to 120ms and not 1.2ms as I have incorrectly written.

Lecture 2 part 2

Dr. Syed continues the discussion of arrhythmias. In this talk he discusses:

Ectopic Rhythms

Identifying Atrial Ectopic Rhythms on the EKG

Identifying Junctional Ectopic Rhythms on the EKG

Identifying Ventricular Ectopic Rhythms on the EKG

Dr. Syed presents the first session in the series of supraventricular extrasystole. Topics covered are: Atrial Premature Beat/Premature Atrial Contraction (PAC) Junctional Premature Beat Difference between the Junctional Premature Beat and the Junctional Escape Beat Blocked Atrial Premature Beat

This video presents following topics:
Re-entry
Types of Supraventricular Tachycardia.
Mnemonic to remember supraventricular tachycardia.
Characteristics of Supraventricular Tachycardia.
AV Nodal Reentrant Tachycardia.
EKG changes
Pseudo R waves

Dr. Syed presents following topics about Atrial Flutter

1. Definition and difference from atrial tachycardia.

2. Types of Atrial Flutter (Typical and atypical.)

3. EKG changes.

4. Interpreting atrial flutter on an EKG.

5. Pathogenesis.

6. Clinical presentation.

7. Management:

    a) Pharmacological

    b) Cardioversion

    c) Pacing

    d) Radiofrequency ablation

Differences between multifocal atrial tachycardia, paroxysmal atrial tachycardia, and atrial fibrillation.

10% of the US population of 80 years of age and above suffer from atrial fibrillation. Sometimes, the patient does not notice atrial fibrillation for a long time, which results in sufficient cardiac remodeling. This makes establishing a sinus rhythm very difficult. 

In this video, Dr. Syed discusses the definition, presentation, pathology, EKG, and salient points of management of the atrial fibrillation. The following aspects are discussed in detail:

1. Loss of atrial function during the episodes of the atrial fibrillation.
2. The risk of thrombus formation and duration of fibrillation where this risk increases significantly so that cardioversion is contra-indicated.
3. Atrial fibrillation caused by failing heart and ischemic injury.
4. Cardiac remodeling at a macro and cellular level during the long-standing atrial fibrillation and why cardioversion becomes difficult.
5. Development of the reentry circuits and the need for catheter ablation.
6. EKG interpretation of the atrial fibrillation.
7. JVP changes (absence of the A wave) during the atrial fibrillation.
8. The absence of the S4 heart sound due to the atrial fibrillation where this abnormal sound is expected.
9. Pharmacological management and cardioversion approaches.
10. Catheter ablation indication and possible methods.
11. Clinical types/stages of atrial fibrillation.

EKG – difference between MAT and PAT

Posted on July 31, 2017

MAT stands for multifocal atrial tachycardia.

PAT stands for Paroxysmal atrial tachycardia.
A student going through drbeen’s EKG interpretation lectuers asked us the difference between MAT (multifocal atrial tachycardia) and PAT (paroxysmal atrial tachycardia).

Here is a quick summary of the differences:

1.  PAT is usually an extra focus/reentrant circuit in the atria. It is similar in pathology to PSVT but the location could be anywhere instead of near the coronary sinus (study our lecture on atrial flutter.) Due to the focus being away from the SA node, the P wave’s shape can be different but consistent. Usually, there also is a warm-up and cooling-down period.
2. MAT is due to many reentrant circuits (but not as many as in the atrial fibrillation). Because of multiple foci present in many locations in the atria, you will find P waves of many shapes. To diagnose a MAT you must identify three different shapes of the P waves in the EKG.

One more difference of the MAT and PAT from the PSVT is that carotid massage does not affect the heart rate in these conditions. Note: study this lecture to understand why it is difficult to cure arrhythmia due to reentrant circuits. (Hint: structural changes.)

MAT and PAT both have the common presentation of 100 to 200 bpm heart rate.

Visit drbeen.com for more lectures: https://www.drbeen.com/

Management notes

10% of the US population of 80 years of age and above suffer from atrial fibrillation. Sometimes atrial fibrillation is not noticed by the patient for a long time resulting in sufficient cardiac remodeling that establishing a sinus rhythm becomes very difficult. 

In this video talk, Dr. Syed discusses the definition, presentation, pathology, EKG, and salient points of management of the atrial fibrillation. Following aspects are discussed in detail:

1. Considerations for the treatment of the atrial fibrillation (AF.)
2. Cardioversion.
3. Anticoagulants and antiplatelets.
4. Antiarrhythmic.
5. Rate control.
6. Surgical approaches.

Considerations for Management

• Patient’s age and symptoms.
• Hemodynamic effects of the AF (LV function compromise, HF).
• Duration since the onset of the fibrillation.
  • <48 hours, unknown, >48 hours.
• Clinical stage of fibrillation.
  • Paroxysmal, persistent, permanent.
• Comorbidities.
• Risk of a cardiac incident.
• Risk of bleeding/stroke.
• Existing medication.

Electrical Cardioversion

• New onset AF associated with severe hypotension, pulmonary edema, and angina can be managed with electrical cardioversion. Usually, up to 48h of AF can be approached with cardioversion.
  • Assess the risk of stroke before cardioverting. (Use CHA2DS2-VASc score for assessment.)
    • Patients with prior embolic events, rheumatic mitral stenosis, hypertrophic cardiomyopathy with marked left atrial enlargement may not be cardioverted before careful consideration for the risk of stroke.
  • 200 Joule (sedation or anesthesia.)
    • Greater shock energy and different electrode placement may be tried if the shock fails to terminate AF.
    • If AF terminates and restarts then antiarrhythmic drugs (ibutilide) can be administered and then cardioversion attempted again.
• AF of unknown duration or greater than 48 hours must not be cardioverted. Following two choices are useful in such situations:
  • Give anticoagulants for 3 weeks before then cardiovert and then continue anticoagulants for at least 4 weeks after.
  • Perform transesophageal echocardiogram to detect a thrombus in the left atrial appendage. Cardiovert if there is no thrombus. Administer anticoagulants for at least 4 weeks after the cardioversion.
• Some patients may need continuous anticoagulation therapy instead of stopping after 4 weeks of cardioversion.

Medical Management

• Oral anticoagulants:
  • Vitamin K inhibitors.
  • Newer anticoagulants like:
    • Thrombin inhibitors (dabigatran.)
    • Factor Xa inhibitors (rivaroxaban, apixaban.)
  • Older anticoagulants like Warfarin are less used nowadays.
  • Immediate administration with Heparin is useful. This should give enough window of time to decide other therapies.
• Antiplatelet (Aspirin, Clopidogrel) have not shown efficacy for AF patients.
• Rate control:
  • Beta blockers.
  • Ca++ channel blockers. (Diltiazem, Verapamil.)
  • Na+/K+ ATPase inhibitor (Digoxin.) Especially when AV nodal blocking agent cannot be used.
• Rhythm Control (antiarrhythmic):
  • Class I
  • Class III

Anticoagulants/Stroke Prevention

• CHA2DS2-VASc score. (Indication of anticoagulants at a score of 2 or greater.)
  • Clinical Features:
    • CHF/LV Dysfunction: 1
    • HTN: 1
    • DM: 1
    • History of stroke, TIA or thromboembolism: 2
    • Vascular pathologies. History of MI, aortic atherosclerosis, PVD: 1
  • Age:
    • 65-74: 1
    • >= 75: 2
  • Sex:
    • Male: 0
    • Female: 1
• You can skip anticoagulants and antiplatelet, or administer Aspirin for a score of 0.
• Anticoagulants are administered at a score of 2 or higher, or to patients with prior history of stroke.
  • Anticoagulant may be considered even at a score of 1.
• Patients with rheumatic mitral stenosis or mechanical heart valves must receive vitamin K antagonists (Warfarin).
• Patients who have previously not received newer anticoagulants (Thrombin blocker and Factor Xa blockers) must get vitamin K antagonists as well.
• Keep in mind that 1% of the patients get intracranial hemorrhage or major bleeding that requires transfusion of fresh frozen plasma and vitamin K. (Monitoring is very important especially with the older anticoagulants.)
• Risk factors for bleeding are age >65-75 y, heart failure, anemia, excessive alcohol consumption, NSAID drugs usage, coronary stent patients on aspirin and a thienopyridine.
• Warfarin is superior to antiplatelet therapy.
  • It takes several days to achieve PT time/INR of greater than 2. Monitoring is needed. Hence newer anticoagulants are favored.
• Newer anticoagulants (dabigatran, rivaroxaban, and apixaban):
  • Shown marginal superiority over Warfarin (0.4%-0.7%.)
  • Promptly achieve the anticoagulant effect. Don’t need much dosage adjustment.
  • These are excreted by kidneys, hence severe renal failure patients cannot use these. Dose adjustment needed for modest renal failure.
  • •P-glycoprotein inducers and inhibitors also influence the excretion.
• Approach to the patient with paroxysmal AF and persistent AF is the same.
• Warfarin can be reversed by administering fresh frozen plasma and vitamin K.
• Reversing agents for the newer anticoagulants are lacking. However, they are excreted within 12 hours.
• Antiplatelet agents (aspirin, clopidogrel) are inferior to warfarin for stroke prevention in AF. Clopidogrel with aspirin is better than aspirin alone but have greater bleeding risk than aspirin alone.
• Chronic anticoagulants are contraindicated with patients with bleeding risks. In such patients, surgical removal of the left atrial appendage or catheter ablation is indicated.

Chronic Rate Control

• Usual goal is resting heart rate of <80 bpm and <100 bpm with light exertion (walking).
  • Note: if rate control is difficult then up to 110 bpm resting heart rate is acceptable provided symptoms are tolerable and ventricular function is normal.
• Rate control is important to alleviate symptoms and prevent ventricular damage due to chronic tachycardia.
• Rate control is important to also reduce the pace of or to prevent cardiac remodeling.
• Beta blockers, calcium channel blockers, and digoxin are used. Sometimes in combination.
• Rate control is incorrect if the patient experiences exertion related symptoms.
• If rate control fails with medications then catheter ablation is indicated. Sometimes AV Junction is ablated with a pace maker to manage ventricular rate. Sometimes there may be dyssynchronous ventricular rate for which biventricular pacing will be indicated.

Rhythm Control

• Rhythm control strategy includes the decision to administer antiarrhythmic or catheter ablation.
• Patient’s preference in light of risk and benefits is the guiding principle.
• Usually, the strategy is selected for following patients:
  • Symptomatic paroxysmal AF.
  • First episode of symptomatic persistent AF.
  • AF with difficult rate control i.e. patients that have structural changes.
  • AF compromising ventricular function.
  • AF aggravating heart failure.
• AV-nodal blocking agents are used.
• B-Adrenergic blockers and calcium channel blockers are used.
• These drugs help maintain sinus rhythm, improve symptoms, and have a low-risk profile. These drugs, however, have low efficacy to prevent AF episodes.
• Class I Na+ channel blockers (flecainide, propafenone, disopyramide) can be used if there is no significant structural heart change.
  • These have negative inotropic and proarrhythmic effect. Cannot be used in patients with coronary artery disease or patients with heart failure.
• Class III (sotalol and dofetilide) can be given to the patients with coronary artery disease.
  • 3% patients can develop prolonged QT and induce torsades des pointes.
  • Dofetilide should only be administered in a hospital with ECG monitors. Many physicians take the same approach with sotalol.
  • Amiodarone maintains sinus rhythm better in two-thirds of the patients.
    • It is also used after the open heart surgery to prevent a sudden onset of AF. 2g given over 2 days.
    • p-glycoprotein inhibitor.
    • Contraindicated in patients with heart block or SA node dysfunction. (Due to its class IV like behavior.)

Surgical Approach

• In patients with long standing AF (usually > 1 year) enough structural changes occur to the atrial tissue that reentrant circuits become permanent. In such patients, cardioversion will fail. If patient’s symptoms are disrupting their quality of life with permanent reentry circuits then catheter ablation is used.
• Catheter ablation can be done in two ways:
  • Usually, the tissue around the pulmonary veins is ablated trapping the reentrant signals in these areas.
  • If the restructuring is extensive, then a maze like path is formed in the atrial tissue that guides the impulse travel and prevents re-entry.
• In rare cases, catheter ablation can cause cardiac tamponade, stroke, esophageal injury, SA node injury requiring a pacemaker, and death.

Disclaimer

• All information contained in and produced by the drbeen corp., is provided for educational purposes only. This information should not be used for the diagnosis or treatment of any health problem or disease.
• THIS INFORMATION IS NOT INTENDED TO REPLACE CLINICAL JUDGMENT OR GUIDE INDIVIDUAL PATIENT CARE IN ANY MANNER.

Dr. Mobeen discusses following topics in the context of multifocal atrial tachycardia.

• Terms and definition of abnormal rate
• Definition of MAT
• Causes of MAT
• EKG representation
• Diagnostic criteria
• Pathological mechanisms behind the causative factors
• Treatment

Abnormal Impulse Terms

• Automaticity

  • Change in the heart rate driven by the pacemaker cells.

  • Sinus Tachycardia
  • Sinus Bradycardia
  • Sick sinus syndrome (alternating sinus tachycardia and sinus bradycardia.)

• Drivers

  • Non-nodal cardiac tissue that incorrectly starts to generate new impulses without the need to be triggered by another impulse. These ectopic foci are called drivers instead of pacemakers.

• Reentry

  • Entrapment of an impulse originated somewhere else in a reentrant circuit.
  • As the impulse cycles in this reentrant circuit, it sends new impulses to the neighboring cells.

• Triggered activity

  • An impulse giving rise to further impulses due to the abnormal state of myocardial cells.
  • Note: these cells in the abnormal state cannot produce a new impulse on their own, they need an impulse acting as a trigger.
  • Drugs that prolong action potential duration (APD), e.g. class III antiarrhythmic, can cause triggered activity.
  • This triggered activity is called afterdepolarization (AD). It is of two types.
    • Early Atrial Depolarization (AED). Caused by slow activation and prolonged action potential.
    • Delayed afterdepolarization (DAD). Caused by the Ca++ overload.

MAT

(A type of Supraventricular Tachycardia)

• Irregular rhythm occurring at the rate of 100 to 200 bpm.
  • The rate can be less than 100 bpm somtimes. In such cases, the arrhythmia is called wandering atrial pacemaker (WAP) or multifocal atrial rhythm.
  • Wandering atrial pacemaker can be detected in healthy individuals too.
  • If the rate is lesser than or equal to 60 then the term is multifocal atrial bradycardia.
• MAT occurrs due to the random firing of several different atrial foci.
• Common in patients with severe lung disease.
  • Older people with the chronic obstructive pulmonary disease (COPD,) and hypoxia.
  • Theophylline toxicity can also cause MAT. (Given in COPD.)
• MAT can occur with myocardial infarction.
• Low blood magnesium levels1 (<1.5 mg/dl) can lead to MAT.
  • Diuretics can cause hypomagnesemia.
  • Mg acts similar to Ca++ channel blockers.
  • Mg depletion reduces Na+/K+ pump action, leading to intracellular K+ depletion.
• Hypokalemia can lead to MAT. (<3.5 mg/dl or severe hypokalemia <2.5 mg/dl.)
• Rarely, digitalis toxicity in patients with heart disease can cause MAT.
• Treatment is usually not needed other than fixing the underlying disease.
  • Carotid massage has no effect as the rate is not originating from a pacemaker.

Clinical Presentation

• Patients are often asymptomatic.
• Exacerbated underlying disease symptoms may be present.
  • Shortness of breath, wheezing, productive cough, or the symptoms of acute metabolic derangement.
• Irregular heart rate/pulse.
• Heart rate > 100 bpm.
• Can worsen the systemic oxygenation in patients with advanced COPD.
• Can worsen the cardiovascular dynamics in patients with coronary artery disease or heart failure.
  • Signs and symptoms of exacerbated heart disease may be observed e.g. angina, dyspnea, and orthopnea.

MAT’s Diagnostic Criteria

• As the P waves appear from many different sites in the atria. The shapes of the P waves vary.
• For diagnosing MAT:
  • One must find three morphologies (shapes) of the P waves.
  • Note: one shape of a P wave can appear for a few beats before another shape of the P wave appears.
  • P waves must be separated by isoelectric lines.
  • Varying PR intervals, R-R intervals duration, and R-R intervals are observed.
• QRS complexes are of narrow type (no problem in the ventricle.)
  • Unless there are ventricular conduction pathologies present too.
• MAT is observed in about 3 patients out of every 1000 hospitalized adults.

EKG Presentation

(Credit: By Jer5150 - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=20243829)

Note the varying shapes of the p waves in the v6 rhythm lead at the bottom of this EKG image. You have to find at least three different shapes of p waves.

Difference of MAT and Atrial Fibrillation

• MAT usually has easily identifiable P waves before the QRS complex.
• There are clear isoelectric intervals between the P waves. Atrial fibrillation either does not have easily discernable P waves, or the P waves appear on the EKG with a higher frequency than the QRS complexes without isoelectric intervals between them.
• In atrial fibrillation, there is no discernible association between the P waves and the QRS complexes.
• In MAT PR intervals vary in size. Depends on the distance of the impulse origin from the AV node.

Chronic obstructive pulmonary disease (COPD) and MAT

• Hypoxia causes cell depolarization.
  • Na+/K+ pump function decreases due to the lack of ATP.
    • Reduced levels of hyperpolarizing currents.
    • Reduced pump activity leads to increased extracellular K+ levels. Which initially cause hyperpolarization but then cause depolarization because of increase extracellular K+ concentration.
  • Reduced ATP also slows down Na+ channels which causes action potential duration (APD) to become variable.
• Hypoxia affects the L-type Ca++ channel’s function.
  • These channels are important for the plateau phase of the cardiac action potential.
  • Disturbance in these L-type Ca++ channel function can result in life threatening arrhythmia. This happens as some cells end up with longer action potential duration and some with shorter durations. (An abnormal function of the L-type Ca++ channels.)
• In patients of severe COPD hypercapnia causes vasodilatation.
  • This, in turn, causes low blood pressure and the release of norepinephrine. Elevated levels of norepinephrine can cause arrhythmia.
    • APD shortening, resting membrane potential hyperpolarization, development of early afterdepolarizations cause arrhythmias.
    • https://books.google.com.pk/books?id=moq9BAAAQBAJ&pg=PA46&lpg=PA46&dq=mechanism+adrenaline+induced+arrhythmia&source=bl&ots=dQG2U-1x2L&sig=L4639d7lmGbSVsAVjq6MFDelo-w&hl=en&sa=X&ved=0ahUKEwiVyKad3rrVAhVKvI8KHfEcCb44ChDoAQgpMAI#v=onepage&q=mechanism%20adrenaline%20induced%20arrhythmia&f=false
  • Norepinephrine acts on beta receptors and triggers cAMP dependent PK-A. PK-A, in turn, acts on the L-type Ca++ channels in the cell membrane to increase Ca++ influx. PK-A also acts on the sarcoplasmic reticulum to release Ca++. Both of these effects increase the cardiac cell contractility. (In the heart the action is predominantly via beta 1 receptors.)
  • Norepinephrine also increases heart rate by its action on the Ca++ channels in the nodal tissue.

Treatment of the multifocal atrial tachycardia (MAT)

• Treat the underlying cause.
• Electrical cardioversion has no effect.
• Carotid massage has no effect.
• The following therapy can be applied (if the tachycardia due to MAT is causing hemodynamic issues.)
  • Ca++ channel blockers (verapamil.)
    • Verapamil is negatively inotropic and a vasodilator. It can cause severe hypotension in patients with heart failure. Use with caution.
  • Beta blockers (metoprolol.)
    • Patients with severe lung disease often cannot tolerate beta blockers.
  • Verapamil and beta blockers should not be given to patients with sinus node dysfunction or existing second or third-degree block without a pacemaker.
  • In patients with pulmonary disease start with calcium channel blockers. Use beta blockers with lots of care.
  • In patients who do not have pulmonary disease, you can start with beta blockers.
  • Amiodarone is effective but dangerous.
    • Long-term therapy with amiodarone is avoided due to its toxicity, especially pulmonary fibrosis.
  • Oxygen
  • Simultaneously correct magnesium and potassium levels.
  • Radiofrequency ablation of the AV node with a pacemaker installation is indicated in patients who are not responding to the drug therapy or who cannot tolerate drug therapy.

Disclaimer

• All information contained in and produced by the drbeen corp., is provided for educational purposes only. This information should not be used for the diagnosis or treatment of any health problem or disease.
• THIS INFORMATION IS NOT INTENDED TO REPLACE CLINICAL JUDGMENT OR GUIDE INDIVIDUAL PATIENT CARE IN ANY MANNER.

Notes on Paroxysmal Atrial Tachycardia (PAT)/Focal Atrial Tachycardia (Focal AT.)

Focal atrial tachycardia is caused by enhanced automaticity or re-entrant circuits giving rise to a flutter like atrial and consequently ventricular tachycardia.

Dr. Mobeen discusses:

• Properties of the focal atrial tachycardia (Focal AT.)
• Different terms used in this class of disorders e.g. focal atrial tachycardia, paroxysmal atrial tachycardia, atypical atrial flutter, etc.
• Causes of Focal AT.
• Pathophysiology of Focal AT.
• Clinical presentation.
• EKG representation.
• Medical and surgical treatment.

Abnormal Impulse Terms1

• Automaticity

  • Normal Enhanced Automaticity:
    • Change in the heart rate driven by the pacemaker cells.
    • Sinus Tachycardia
    • Sinus Bradycardia
    • Sick sinus syndrome (alternating sinus tachycardia and sinus bradycardia.)
  • Abnormal Enhanced Automaticity:
    • An increased pacemaker like activity of cardiac myocytes and Purkinje cells.

• Drivers

  • Non-nodal cardiac tissue that incorrectly starts to generate new impulses without the need to be triggered by another impulse (become automatic.) These ectopic foci are called drivers instead of pacemakers.

• Reentry

  • Entrapment of an impulse, that originated somewhere else, in a reentrant circuit.
  • As the impulse cycles in this reentrant circuit, it sends new impulses to the neighboring cells.

• Triggered activity

  • An impulse giving rise to further impulses due to the abnormal state of myocardial cells.
  • Note: these cells in the abnormal state cannot produce a new impulse on their own, they need an impulse acting as a trigger.
  • Drugs that prolong action potential duration (APD), e.g. class III antiarrhythmic, can cause triggered activity.
  • This triggered activity is called afterdepolarization (AD). It is of two types.
    • Early Atrial Depolarization (AED). Caused by slow activation and prolonged action potential.
    • Delayed afterdepolarization (DAD). Caused by the Ca++ overload.

1 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4823581/

https://www.uptodate.com/contents/enhanced-cardiac-automaticity

Paroxysmal Atrial Tachycardia (PAT) Characteristics

A type of Supraventricular Tachycardia

• Regular rhythm.
• Rate from 100 to 200 beats per minute (bpm).
• Usually, lasts for seconds or minutes. It can terminate and restart spontaneously. (It can become paroxysmal sustained tachycardia.)
• Incessant atrial tachycardia (incessant AT) is a term used when a patient has atrial tachycardia during the 90% of the monitoring time.
• The arrhythmia occurs due to the following abnormal impulses:
  • Enhanced automaticity of an ectopic atrial focus.
  • A reentrant circuit within atria.
  • Enhanced automaticity type may have a warm up and cool down period.
  • Reentrant form starts and stops abruptly as an atrial premature beat/contraction (PAC.) This is also called atypical atrial flutter.
• Normal healthy individuals of all ages can experience PAT.
• Digitalis toxicity can also cause PAT.

Causes of PAT/Focal AT

• Atrial stretch in patients with heart diseases. (Hypertension and cardiomyopathies.)
• Acute:
  • Myocardial infarction.
  • Pulmonary decompensation.
  • Infections.
  • Excessive alcohol ingestion.
  • Hypokalemia.
  • Hypoxia.
  • Stimulants.
  • Cocaine.
  • Theophylline.
• More commonly it occurs in healthy individuals and is benign.
• AT incidence is higher in patients that have undergone catheter ablation for atrial fibrillation.
• Digitalis toxicity causes AT as well due to increased central sympathetic outflow.

Site of Abnormal Focus

• The right atrium is involved in 63% of the cases and 37% involve the left atrium.
• Right atrium:
  • 35% tricuspid annulus.
  • 34% crista terminalis.
  • 17% coronary sinus ostium.
  • 9% perinodal tissue.
  • 4% RA appendage/auricle.
• Left atrium:
  • 67% pulmonary veins.
  • 17% mitral annulus.
  • 6% coronary sinus body.
  • 6% left intraatrial septum.
  • 4% LA appendage/auricle.

Clinical Presentation

• Palpitations during the episodes/runs.
• Rapid fluttering sensation in the chest or neck usually is associated with focal AT/PAT.
• Patients can, rarely, present with syncope. This usually occurs when the ventricular rate is 200 beats per minute or above.
• Symptoms of other cardiac comorbidities e.g. heart failure, angina may become exacerbated. (Dyspnea, chest pain, etc.)

PAT’s Diagnostic Criteria

• Heart rate greater 100 beats per minute.
• Driver/focus other than the SA node. (P wave morphology is different.)
• Sudden in onset and offset.
• An isoelectric interval between p waves.

EKG Presentation

• Heart rate greater 100 beats per minute.
• Driver/focus other than the SA node. (P wave morphology is different.)
• As the arrhythmia is focal (from a single point of origin) and sustained. EKG displays p waves that can have morphology from normal to abnormal. P wave morphology, however, will be consistent.
• The cycle length of tachycardia is variable.
• Warm up and cool down phases are short (a few beats.) Sinus tachycardia takes 30 seconds to minutes to warm up or cool down.
• Intermittent AV blocks may occur. These blocks, however, do not affect the PAT’s runs.
• The Same focal driver can erratically fire between runs, adding atrial ectopic p waves. These p waves will have the same morphology to the p waves during the PAT’s runs.

Mapping the origin of the focus

• An elaborate algorithm that predicted the arrhythmogenic focus in 93% of the patients has been devised.
• V1 is important:
  • Generally, a positive p wave or biphasic p wave with positive first is an indicator of the focus in the right atrium ( the majority of the cases.)
  • A negative p wave or biphasic p wave with the negative phase first is an indicator of the focus in the left atrium.
• Careful inspection of the p waves in the other leads can help locate the origin in possibly one of the following locations:
  • Coronary sinus, crista terminalis, right atrial appendage.
  • Interatrial septum.
  • Pulmonary veins, left atrial appendage.
• Locating the focus is important for the surgical ablation.

EKG Image

Photo credit: <a href="http://classconnection.s3.amazonaws.com/669/flashcards/3543669/jpg/proxymal_atrial_(supraventricular)_tachycardia-143E45A5E157FA1E468.jpg">Amazonaws.com</a>

PAT and PSVT

• Usually one cannot tell the difference between the focal atrial tachycardia (paroxysmal atrial tachycardia) and paroxysmal supraventricular tachycardia.
• Warm up and cool down rhythms are unique to PAT if present.
• Carotid massage does not affect PAT.
• PSVT can slow down or terminate with carotid massage.

Treatment of PAT

Consistent with 2015 American College of Cardiology/American Heart Association/Heart Rhythm Society (ACC/AHA/HRS)

• Acute

  • Rate, symptoms and hemodynamic status guides the acute treatment.
  • Treat the precipitating causes:
  • Administer potassium to hypokalemic patients.
  • If digitalis toxicity is suspected then discontinue digitalis and administer anti-digitalis antibodies if the hemodynamic status or other arrhythmias are life-threatening.
  • The vagal maneuver can be performed by the patient, or administer intravenous adenosine. (Both of these are usually less effective.)
  • IV beta blockers or nondihydropyridine Ca++ channel blockers (verapamil, diltiazem) can be given to hemodynamically stable patients.
  • IV Amiodarone can be better than the beta blockers, and verapamil and diltiazem.
  • Amiodarone can control acute tachycardia, terminate arrhythmia, and cause less hypotension.
  • Cardioversion may be tried but it is usually less effective for the following reasons:
  • Underlying pathology causing the arrhythmia may continue to trigger arrhythmias.
  • Enhanced automaticity of non-nodal tissue usually does not respond to cardioversion.
  • Hemodynamically unstable patients who fail to respond to above therapies may respond to chemical cardioversion with Amiodarone.

• Chronic suppressive or prophylactic

  • Patients with few or no symptoms and rare/brief spells of arrhythmia may not need chronic treatment.
  • Patients that do not respond to medical therapy or have been on drugs for a long time may need catheter ablation.
  • Patients that do not want catheter ablation may need amiodarone, or class Ic (flecainide, propafenone), or class III (sotalol) antiarrhythmic. Which drug to use should be consulted with a cardiologist experienced with arrhythmia management.
  • If catheter ablation also fails then cardiac pacemaker with AV nodal ablation may be considered.

• Treatment of incessant AT

  • Aggressive management to restore normal sinus rhythm should be made.
  • Beta blockers
  • Class Ic drugs (flecainide).
  • Usually, patients with incessant AT and LV systolic dysfunction that are not responding to medical therapy will need to undergo catheter ablation.

Drbeen Corp Disclaimer

• All information contained in and produced by the drbeen corp., is provided for educational purposes only. This information should not be used for the diagnosis or treatment of any health problem or disease.
• THIS INFORMATION IS NOT INTENDED TO REPLACE CLINICAL JUDGMENT OR GUIDE INDIVIDUAL PATIENT CARE IN ANY MANNER.

In this lecture we will discuss Ventricular Tachycardia, also known as V-Tach.
V-Tach is defined as rapid and repetitive firing of 3 or more PVCs in a row, with a rate of 100-250 beats per minute, originating in the ventricles of the heart. 

Ventricular Fibrillation is a terminal event for a dying heart. This talk discusses the:

• Primary pathophysiology
• Signs and symptoms
• EKG changes
• Management approach
• Potential outcomes

Dr. Syed discusses the EKG leads and normal waveform. {article:https://articles.drbeen.com/2016/05/22/electrocardiogram-clinical-review/}