Ventricular depolarisation

Cairns JA, Connolly SJ, Roberts R, et al. Randomised trial of outcome after myocardial infarction in patients with frequent or repetitive ventricular premature depolarisations CAMIAT. Canadian Amiodarone myocardial infarction arrhythmia trial investigators. Lancet. Mar 8 1997 349(9053) 675-682. 

Class I drugs have a local anaesthetic-like action, blocking the inward current in sodium channels. This depresses the fast depolarisation (phase 0) which initiates each action potential (Figure 8.5). This membrane-stabilising effect makes them valuable for the treatment of ectopic and tachycardic arrhythmias, such as atrial and ventricular fibrillation, extrasystoles, supraventricular and ventricular tachycardia. Class I drugs also decrease contractility. A sub-classification is made according to the effects on... 

Direct current (DC) electric shock applied externally is often the best way to convert cardiac arrhythmias to sinus rhythm. Many atrial or ventricular arrhythmias start as a result of transiently operating factors but, once they have begun, the abnormal mechanisms are self-sustaining. When a successful electric shock is given, the heart is depolarised, the... 

Figure 5.3 (A) Under normal conditions, the overall QRS vector (R) is made up of the sum of the different ventricular vectors (1 + 2 + 3 + 4). (B) When a necrotic (infarcted) area exists, the vector of infarction has the same magnitude as the previous vector, but has an opposite direction (3 ). This change of direction of the initial depolarisation electrical forces of a portion of the heart, the necrotic (infarcted) area, also implies the change of the overall vector direction (R ). (C) The development of...

According to the vector of infarction theory, the infarction Q wave is of the same magnitude but in opposite direction to the one normally generated by the infarcted area (Figure 5.3B, C). The vector of infarction, thus, moves away from the infarcted area (see Figs. 5.3-5.5). For this reason, the beginning of ventricular depolarisation changes its... 

In Figures 5.4 and 5.5 the changes that, as a consequence of the presence of the vector of infarction, are generated in the ventricular depolarisation loops in the presence of two prototype infarctions (anteroseptal and inferolateral areas, respectively) are represented. Said changes explain the presence of Q waves in the different leads by means of the loop-hemifield correlation. Some of the ECG morphologies and the QRS loops correlations in the seven types of infarctions, according to the classification... 

In the presence of complete LBBB, even when large ventricular areas are infarcted, the general direction of the depolarisation usually does not change. This... 

Figure 5.54 Inferior infarction associated with an SAH (A) When the necrosis is rather large and comprises the area where ventricular depolarisation is initiated in case of SAH (point A + C), the first vector of ventricular depolarisation (1), is neutralised by the infarction vector (Inf. V.) and the loop first goes directly upwards and then, due to the SAH (see lower FP image) instead of rotating in the clockwise direction downward, it rotates in the counter-clockwise direction upward (2). Consequently, a QS morphology...

Figure 5.55 Inferior infarction associated with an IPH (A) the vector of the first part of the activation (the sum of the normal activation initiating vector in the case of an IPH -see B(l) plus the infarction vector - Inf. V) moves away from the inferior wall more than that would be seen in an isolated IPH and is opposite to the final vector of ventricular depolarisation that is directed downwards...

Figure 5.57 Extensive anterior infarction including mid-anterior wall associated with IPH (A) the first ventricular depolarisation vector (1) generated in A + B areas in case of isolated IPH is directed upwards. However in case of extensive anterior infarction plus IPH, the infarction vector (Inf. V) is more important than the first depolarisation vector and all the loops move away from the infarcted area in the same direction of the second...

Figure 5.58 SAFI may mask small inferior infarction. (A) In this situation, when in the presence of an SAFI the area initiating the ventricular depolarisation (A + C) is spared by the necrosis, vector 1 that is directed downwards and rightwards can be only partially counterbalanced by the relatively small infarction vector (Inf. V). This allows the loop to initiate its movement downwards and rightwards.

As we have discussed previously ( cardiac memory in the intermittent LBBB and WPW syndrome), patients with intermittent right-ventricular stimulation, when the stimulus is conducted via the normal path (Figure 3.35), can show a cardiac memory phenomenon (lack of adequacy of the repolarisation to the depolarisation changes), which explains the anomalous repolarisation (negative T wave) that is sometimes observed, in sinus rhythm in the absence of IHD. It has been demonstrated that in this situation, the T wave is negative in precordial lead but is positive in I and VL (see Figure 3.35, p. 52). 

Figure 9.3 If the necrosis affects the areas of late ventricular depolarisation (in grey (C)), instead of pathologic Q wave, it will result in a change of the direction of the vectors of the second part of QRS, which is presented as slurrings in the terminal part of QRS in II, III,...

However, it could exhibit minimal changes in the mid-final portion of ventricular depolarisation (fractioned QRS) (Figures 9.3 and 9.4). 

Figure 9.5 (A) Three approximate starting points ( ) and the isochronal sequential lines of the ventricular depolarisation (Durrer et al., 1970). (B) Left lateral view of the correlation between the endocardial areas of initial...

Class IV anti-arrhythmic drugs usually interfere with calcium conductance such as verapamil hydrochloride. Verapamil inhibits the aetion potential of the upper and middle nodal regions of the heart where the slow inward ealeium-ion-mediated current contributes to depolarisation. This is responsible for the bloekade of slow-ehannel eonduetion in the atrioventricular node. It has been found to inhibit one limb of the re-entry circuit which is assumed to underlie most paroxysmal supraventricular tachycardias, thereby causing the reduction of ventricular rate in atrial flutter and fibrillation. 

Cifenline treated atrial fibrillation successfully in some patients [42] and is an effective therapy for chronic ventricular arrhythmias [43,44]. Its long half life in vivo allowed only twice a day dosage. This produced good patient compliance when it controlled ventricular arrhythmias throughout a two-year trial [45]. Another trial showed cifenline to be slightly superior to quinidine for patients with premature ventricular depolarisations [46]. 

Christophe B (2013) Simulation of early after-depolarisation in non-fading human ventricular myocytes can this help cardiac safety pharmacology Pharmacol Rep 65 1281-1293... 

Electrical activity generated by atrial depolarisation is recorded on the ECG as the P-wave. Atrial repolarisation occurs immediately, as the ventricles depolarise however, since the ventricular depolarisation occurs at the same time, the repolarisation wave for the P-wave of the atria is not observed on the ECG. Rather, a large QRS complex is observed to follow the P-wave. Ventricular depolarisation is a composite of the Q, R and S waves. The Q-wave represents depolarisation of the... 

The PR interval represents the time required for electrical impulse conduction from its origin at the onset of atrial depolarisation through the atrial conduction system to the ventricular myocardium. It generally represents conduction time across the AVN. Changes in this interval, in most species, reflect changes in Ca " channel function however, in the rat Na" channels are dominant (Botting et al. 1985). Unlike the PR interval, the QT interval represents the ventricular refractory period and includes depolarisation and repolarisation of ventricular muscle. In contrast to the atria, the AP in ventricular tissue is long ( 300 ms), which is a time interval that is similar to the duration of the QT interval. Thus, the QT interval is an approximate measure of ventricular repolarisation and thus channel function. 

The larger QRS complex represents the activation of the ventricles (ventricular depolarisation) (Fig. 2.13). After the electrical impulse arrives in the ventricles, the... 

The ST segment is measured from the end of the S wave to the start of the T wave (Fig. 2.17). The J point represents the junction where the S wave meets the isoelectric baseline. The ST segment represents the gap between ventricular depolarisation and repolarisation. During this period no additional electrical signals can pass through the myocardium. 

ECG waveforms are commonly made up of PQRS and T waves The P wave represents atrial depolarisation The QRS complex represents ventricular depolarisation The T wave represents ventricular repolarisation... 

Calculating the electrical axis is often considered one of the more complex elements of ECG interpretation. The electrical axis refers to the net or overall direction in which the electrical current travels in during ventricular depolarisation. This is achieved by adding together the sum of all of the individual vectors to determine the overall direction of the flow across the whole myocardium. Calculating the electrical axis is useful as it can provide additional evidence for the presence of various conditions. 

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