Why Is There a Delay between Atrial and Ventricular Contractions

by bamsco April. 19, 22 3 Comments

Echocardiographic techniques to optimize AV and VV delays have been comprehensively described in recent reports [27, 93, 94]. In general, echocardiography is a widely used and non-invasive technique without significant stress for the patient. However, these optimization techniques are subject to higher intra- and inter-observer variability than invasive measurements. Nevertheless, echocardiography remains a cornerstone of CRT as it is able to assess the response to CRT versus reverse remodeling and identify other factors that could affect non-response to CRT (e.B. insufficiency of RV, pulmonary hypertension, valvular heart disease). During a single cardiac cycle, the atria and ventricles do not beat at the same time; Ear contraction occurs before ventricular contraction. This delay allows a correct filling of the four chambers of the heart. Remember that the left and right heart pumps work in parallel. The diastolic phase of the cardiac cycle begins with the opening of the tricuspid and mitral valves (atrioventricular valves). The atrioventricular valves open when the pressures in the ventricles fall below those in the atria. This can be seen here for the left heart, where the mitral valve opens when the left ventricular pressure falls below the left ear pressure. At this time, passive filling of the ventricle begins.

In other words, blood that has accumulated in the atria behind the closed atrioventricular valves quickly enters the ventricles, leading to an initial drop in ear pressure. Later, the pressure in the four chambers increases as the atria and ventricles continue to fill passively in unison, with blood returning to the heart through the veins (pulmonary veins in the left atrium and the superior and inferior vena cava in the right atrium). In the systolene phase, blood is forced to flow from both atria into their respective ventricles, as the atrial muscles contract due to depolarization of the atria. There is a period called isovolumetric contraction, during which the ventricles contract, but the pulmonary and aortic valves are closed because the ventricles do not have enough strength to open them. The atrioventricular valves remain closed even during the period of isovolumetric contraction. The crescent-shaped valves open when the ventricular muscle contracts, producing higher blood pressure in the ventricle than in the artery shaft. When the heart muscle relaxes, the diastolen phase begins again. Expression of connexin at the mRNA level in different regions of the human atrioventricular compound (VA). A: Anatomy of the AV node. Left: Heart seen from behind with a window cut into the right atrium to expose the AV node (in red). Modified by Li et al.10Right: Exploded view of the nested area on the left.

B: Relative frequency of mRNA for 4 connexin isoforms in different regions of the AV compound of the human heart. The mean values ±SEM are displayed (n = 6). De Greener et al.3 Ao = Aorta; CN = compact node; CS = coronary sinus; FO = oval pit; INE = Lower nodal extension; IVC = inferior vena cava; LBBB = left beam branch block; BP = pulmonary artery; PB = penetrating beam; RA = right atrium; RBBB = right beam branch block; RV = right ventricle; SVC = Superior Vena Cava. Twelve-channel electrocardiogram recording during VR stimulation (left panel), LV stimulation (center panel) and biventricular stimulation (BV) with a VV delay of 80 ms (right panel). The total activation time, defined as the time between the beginning of the step and the end of the QRS complex, specified between the two vertical dotted lines of each panel. During VR stimulation, the total activation time is 218 ms; However, it is increased to 274ms during BT stimulation. During BV stimulation, this delayed activation can be compensated by pre-activation of LV 80 ms before rv Throughout the cardiac cycle, the atria collect oxygen-depleted blood that returns to the heart from the peripheral circulation and coronary circulation (right atrium) or pulmonary circulation (left atria). During diastole, the accumulation of blood in the atria creates a pressure gradient that forces the opening of the AV valves, so that about 75% of this blood can enter the ventricle, which leads to a gradual increase in ventricular diastolic pressure (point A).

In late diastole, the contraction of the atria leads to the remaining 25% of the blood in the ventricles, which leads to a further increase in ear and ventricular pressure (point B). This is followed by a contraction of the ventricle, which signals the appearance of mechanical systole. When the ventricles contract, the pressures they contain quickly exceed the ear pressure. This pressure gradient pushes back the brochures of the AV valves and forces them to close (point C). The appearance of ventricular contraction also creates tension on the papillary muscles, which exert additional force on the edges of the leaves to ensure proper alignment of the valves, which helps in their closure. Another ventricular contraction causes the ventricular pressure to exceed the diastolic pressures in the pulmonary artery and aorta, forcing the crescent valves to open (point D). This allows the ventricles to empty their contents into the lung and circulation of the system. Because the crescent-shaped valves are open, the continuous contraction of the ventricles increases the pressure in the pulmonary artery and aorta. Completion of ventricular sputum causes the pressure in the ventricles to fall below that of the pulmonary artery and aorta. This allows blood in the pulmonary artery and aorta to push back the crescent-shaped valves and close them (point E).

The cardiac cycle then begins again with the ventricles filling with blood that has accumulated in the atria. The structure and functioning of the atrioventricular (AV) node has remained mysterious due to its great complexity. In this review article, we incorporate advances in knowledge regarding connexin expression in the AV node. The complex structuring of 4 different connexin isoforms with ultra-low to high single-channel conductance values explains the dual-track electrophysiology of the AV node, the presence of 2 node extensions, longitudinal dissociation in the penetrating beam and, most importantly, how the AV node maintains slow conduction between the atria and ventricles. It has been shown that the complex structuring of connexins is the result of the embryonic development of the cardiac conduction system. Finally, it is argued that the deregulation of connexin could be responsible for the malfunction of the AV node. Ritter`s formula. This method was initially proposed for patients with complete heart block [102]. Although it was only presented in abstract form and no further validation was published, its use was extrapolated to the CRT population without further validation.

The formula defines the optimal AV delay as the AV interval that connects the end of the A wave with the closure of the mitral valve or the beginning of ventricular contraction. For this purpose, the time elapsed between the beginning of the QRS complex and the moment of the end of wave A (QS interval) is measured at both a long AV (AVlong) and a short (AVshort) delay. The optimal AV delay is calculated from the following formula: AVopt = AVlong − (QAshort − QAlong). Ritter`s formula was also compared to the QuickOpt and AV-VTI algorithm for AV optimization using LV dP/dt max as the gold standard. This study showed that Ritter`s formula was the least accurate [80]. Optimization of VV during exercise has only been studied sporadically, using different optimization methods and involving a limited number of patients. Lafitte et al. reported a change in interventricular dysysynchrony (defined as mechanical interventricular delay) during bicycle training tests in 60% of the 65 patients with heart failure [48]. In contrast, Valzania et al. showed no significant change in interventricular mechanical delay during the dobutamine stress test [53]. Two other small studies have shown that the optimal VV delay changes during bike load tests in about 55% of patients [52, 54].

In one study in patients with atrial fibrillation and no intrinsic AV conduction, a decrease in optimal VV delay was noted with an increase in pacemaker rate [55]. Meluzin`s method. A simplified method to fuse the end of atrial contraction with mitral valve closure has been proposed by Meluzin [104]. A long AV delay is programmed and the pulsed Doppler transmission input pattern is recorded. The time between the end of the A wave and the beginning of systolic mitral regurgitation is calculated. This time is subtracted from the AV delay programmed to determine the optimal AV interval. The method was only validated in one study involving 18 patients that showed significantly higher cardiac output, measured by thermodilution by comparing optimal AV delay with longer and shorter AV delays [104]. Obviously, the use of this method depends on a clear mitral regurgitation signal.

In a CRT population, the PATH-CHF (PAcing THerapies in Congestive Heart Failure) study showed a significant acute hemodynamic effect of variation in AV delay in vrv, VL and biventricular stimulation [28, 29]. Interestingly, the optimal AV delay for left ventricular dP/dt max (LV dP/dt max) for VR and biventricular stimulation was significantly shorter than that of the responder group. This variable acute hemodynamic response to various AV delays was also observed in the PATH-CHF-II study [30]. This could be explained by the fact that during left ventricular stimulation, a left atrioventricular delay is set, which should be longer to allow fusion with the intrinsic conduction of the normally conductive branch of the right beam (Fig. 1). In all but one of these studies [39], VV delay optimization was performed in addition to the previous AV optimization. In the overall CRT population, the benefit of VV optimization is relatively small compared to simultaneous biventricular stimulation: van Gelder et al. . .

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