Electrical Heart Function

CLINICAL EXAMPLES: SUPRAVENTRICULAR TACHYARRHYTHMIAS

Supraventricular tachyarrhythmias the origins are above the ventricles from all structures above the fibrous skeleton including the atrium but also including the av node. The category of supraventricular arrhythmias is containing a number of different arrythmias: atrial fibrillation, an atrial flutter, and then there is a category that is in general called supraventricular tachycardia.

One form of supraventricular tachycardia is caused within the AV node: it's actually a reentrant circuit in the av node. The impulses circling around in site of the av node, at least atrial site side and ventricular site, the AV node exciting at the high-speed the atria and exciting at the high-speed but in the normal way the conduction system, the His Bundle, the left and right bundle branches and as a result will be a normal excitation of the ventricles but fast (P-waves that are in somewhere to be found in the QRS complex or

after the QRS complex). It has been discovered that the atrioventricular node, symbolically depicted here with an entry from the atria in an exit to the ventricles, has two major conduction pathways: one is fast and the other is slow so normally the electrical impulse that comes from the atria travels along the fast pathway in the His Bundle and excites the ventricles. It also travels in the retrograde way in the slow pathway and meets there slow conducted impulse and dies. If, for some reason, there is a prolonged effective refractory period in the fast pathway, so that this actually it is a functional block that depends on the rhythm and, when an impulse arrives relatively early from the atria, it will be blocked here because the tissue is still refractory and the impulse will be conducted through the slow pathway. Then, it will be conducted out and retrogradely enter the fast pathway, finds there no longer refractory tissue because time has passed and the tissue is conducting and then the

re-entry circuit is complete and both aria and ventricles will be excited at a higher rate.

Normal sinus rhythm: the AV node has a slow conducting and a fast conducting pathway, parallel excitation results in a collision of the excitation wavefronts in the slow pathway.

1. a premature supraventricular beat is blocked in the fast pathway (Effective Refractory Period);
2. the slow pathway conducts the impulse (normal activation order of the ventricles, and is retrogradely conducted by the fast pathway;
3. this starts the reentry.

Another form of supraventricular tachycardia is called atrial ventricular reciprocating tachycardia (AVRT) and the re-entry circuit that is included in this tachycardia contains not only supraventricular but also ventricular structures.

The anatomical substate of these tachycardia is an extra electrical connection called accessory pathway between the atria and ventricles. This connection is a remnant of the development of the heart in the fetal stage. It is possible.

thatthis accessory pathway conduct only from atria towards ventricular muscle orreverse: it's also possible that bi-directional conduction is possible (I have tomake a remark here: in the picture looking at an accessory pathway betweenthe right atrium and right ventricle but accessory pathways can happeneverywhere in the heart so this is only an example).

If the accessory pathwayconducts the electrical impulse in the direction from the atrium to the ventricle, the right ventricular muscleis excited before the normal regular excitation fire the right bundle branch is reaching this anatomical structure.This means that if you look at the ECG, the QRS complex is starting in the strange way and the strange waythe waves that we see in front of the right of a curious complex is called Delta wave, caused by thephenomenon of pre-excitation. This phenomenon is called pre-excitation syndrome or Wolff-Parkinson-WhiteSyndrome.

35 Electrical Heart FunctionOrthodromic AVRT – The most

Common (95%) type of AVRT. The existence of an accessory pathway, conducting in either direction, makes it possible that a reentrant circuit is formed due to a functional block at a given moment. The most likely reentrant circuit is the orthodromic one, where the impulse is normally conducted, fired by AV node and then conducted back to the atria through the accessory pathway. This will result in narrow QRS complexes because the activation of the ventricle occurs in a normal and efficient way using the ventricular conduction system and the rhythm is very fast because it immediately circles around and returns for next time in the AV node. This tachycardia is about 150 beats per minute or faster.

Antidromic AVRT Least common (5%) type of AVRT: electrical activation of the ventricles occurs via the accessory pathway, and the electrical impulse travels back to the atria by retrograde AV conduction. Because of the abnormal activation order of the ventricles, QRS complexes are wide.

Combination of

prevention and management of pre-excitation and atrial fibrillation VT/VF. These include: 1. Medications: Antiarrhythmic drugs can be prescribed to control the heart rate and rhythm in patients with atrial fibrillation. These medications help to prevent the occurrence of ventricular tachycardia or fibrillation. 2. Cardioversion: In cases of atrial fibrillation, electrical cardioversion may be performed to restore the normal rhythm of the heart. This procedure involves delivering a controlled electric shock to the heart to reset its electrical signals. 3. Ablation: Ablation therapy is a minimally invasive procedure that is used to destroy the accessory pathway responsible for pre-excitation. During this procedure, a catheter is inserted into the heart and radiofrequency energy is used to destroy the abnormal pathway. 4. Implantable Cardioverter Defibrillator (ICD): In patients at high risk for ventricular tachycardia or fibrillation, an ICD may be implanted. This device continuously monitors the heart's rhythm and delivers a shock if a life-threatening arrhythmia is detected. 5. Lifestyle modifications: Making certain lifestyle changes, such as avoiding triggers like caffeine or alcohol, managing stress, and maintaining a healthy weight, can help reduce the risk of pre-excitation and atrial fibrillation VT/VF. It is important for patients with pre-excitation and atrial fibrillation to work closely with their healthcare team to develop an individualized treatment plan. Regular follow-up appointments and monitoring are necessary to ensure the effectiveness of the chosen therapies and to prevent complications.

Supraventricular tachycardia, one of the most used treatments is catheter ablation. This procedure involves locating and destroying the anatomical structure responsible for these arrhythmias, such as part of the AV node or accessory pathways. In the clinic, performing this ablation procedure requires advanced equipment, which we will discuss later in this course.

Clinical examples of ventricular tachyarrhythmias involve the ventricles and do not involve any supraventricular structures. Ventricular arrhythmias can occur in various settings, including:

• Ventricular tachycardia (VT): old myocardial infarction, idiopathic dilated cardiomyopathy, hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia, myocarditis
• Torsade de Pointes (TdP): long QT syndrome, medication (antiarrhythmics, antibiotics, antipsychotics)
• Ventricular fibrillation (VF), the most serious one

that lead to death: acute and old myocardial infarction; WPWas in VTHere we see some examples of ventricular tachyarrhythmia:Ventricular fibrillation/flutter and pulseless ventricular tachycardia need to be terminated by an electricalshock (defibrillation). When this happens at an unexpected moment is will be external defibrillation withexternal electrodes but when patients are known for an increased risk, because I have already had such aserious read me or they are belonging to this group and ICD (implantable cardioverter defibrillator) isindicated. 37 Electrical activity07 - ECG lead systems, vectorcardiogram, axes1. Lead vector – To understand the electrocardiogram (ECG) better we need to discuss two concepts: theheart vector (discussed in the 5 lecture) and the lead vector. These two concepts are essential tounderstand ECG. William Einthoven made his contribution to the “creation” of the ECG, is often called“the father of electrocardiography” and hereceived a Nobel prize for his work in 1924. Einthoven defined the circuit "Einthoven triangle", in which the electrical activity of the heart is lumped in heart vector H (which is not based on dipole theory, but is simply the electrical activity). This vector H is projected on an equilateral triangle, on the three leads I, II, III. Notes that all leads are equally sensitive, and the directions are very schematic. The amplitude in lead I, II and III is associated with heart vector H, and if H changes direction or size, it will change ECG amplitude in each lead. The extremity leads I, II and III have been called "Einthoven leads". Few decades later, when the dipole concepts emerged, the Frank torso model was developed, in which the equivalent dipoles are located at fixed positions in the thorax (1 and 2), representing the lumped total electrical activity of the heart at a given moment. The torso is simply filled with a conducting medium, for example salt, and with every

combination of surface electrodes, that gives a sort of ECG leads (3 and 4) in order to see what happens on the surface of torso.

Torso model by Burger developed a better model in which were introduced the effect of the internal inhomogeneities (due to the lungs). Burger developed the lead vector concept, so how interpret the ECG in terms of relation in what happens in the electrocardiogram and what happens in the heart. The idea is that each ECG lead is associated with a lead vector that represents the directionality (i.e. spatial orientation of the lead vector) and the sensitivity (i.e. lead vector magnitude) of the ECG lead.

The ECG amplitude at given moment t V(t) in a lead is equal to the dot product of the heart vector (dipole vector p(t)) and the fixed lead vector c: V(t)=c*p(t). Graphically seen, the ECG amplitude equals the magnitude of the projection of the heart vector on the lead vector, multiplied by the magnitude of the lead vector. It is important to remember is that the spatial

orientamento del vettore di guida può differire considerevolmente dalla posizione fisica degli elettrodi dell'ECG. Il vettore di guida esprime l'omogeneità del conduttore di volume (torace) attraverso il quale la corrente extracellulare nel cuore causa i potenziali della superficie corporea/l'ECG. Il triangolo di Burger ha sostituito il triangolo di Einthoven. È una rappresentazione grafica dei concetti del vettore di guida. Ci sono due triangoli e ancora qui c'è un vettore cardiaco H, che viene proiettato su questi vettori di guida e ci dà l'ampiezza dell'ECG. Il triangolo interno è formato dai vettori di guida I', II' e III', e la direzione del vettore di guida I non è orizzontale ma leggermente verso l'alto, mentre i vettori di guida II' e III' misurano più verticalmente rispetto alla rappresentazione di Einthoven. Dobbiamo amplificare l'ampiezza nei vettori di guida II' e III' (questa amplificazione è rappresentata dal triangolo esterno). Il vettore di guida III è il vettore di guida più sensibile perché ha il vettore di guida più lungo ed è per questo motivo che il

The relative distance between the inner and outer triangle is larger in lead III than lead II. So, finally the ECG amplitude is measured in leads I, II and III of the outer triangle.