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Ventricular pacemaker cells discharge at a slower rate than the SA or AV node. While the SA node typically initiates a rate of 70 beats per minute (BPM), the atrioventricular node (AV node) is usually only capable of generating a rhythm at 40-60 BPM or less. Ventricular contraction rate is thus reduced by 15-40 beats per minute. [3]
It is a protective mechanism for the heart, to compensate for the SA node no longer handling the pacemaking activity, and is one of a series of backup sites that can take over pacemaker function when the SA node fails to do so. It can also occur following a premature ventricular contraction or blocked premature atrial contraction. [3]
Electrical waves track a systole (a contraction) of the heart. The end-point of the P wave depolarization is the start-point of the atrial stage of systole. The ventricular stage of systole begins at the R peak of the QRS wave complex; the T wave indicates the end of ventricular contraction, after which ventricular relaxation (ventricular diastole) begins.
This can also be converted to an estimated maximal oxygen uptake score using the calculator below and the following formulas, where the value "T" is the total time completed (expressed in minutes and fractions of a minute e.g. 9 minutes 15 seconds = 9.25 minutes). As with many exercise test equations, there have been many regression equations ...
Figure 1: Idealized pressure–volume diagram featuring cardiac cycle components. Real-time left ventricular (LV) pressure–volume loops provide a framework for understanding cardiac mechanics in experimental animals and humans. Such loops can be generated by real-time measurement of pressure and volume within the left ventricle.
The loss of physiologic timing of atrial and ventricular contractions, or sometimes called AV dyssynchrony, leads to different mechanisms of symptoms production. This altered ventricular contraction will decrease cardiac output, and in turn will lead to systemic hypotensive reflex response with varying symptoms. [1] [2] [4] [5]
Since the next ventricular contraction occurs at its regular time, the filling time for the LV increases, causing an increased LV end-diastolic volume. Due to the Frank–Starling mechanism, the next ventricular contraction is more forceful, leading to the ejection of the larger than normal volume of blood, and bringing the LV end-systolic ...
As the left posterior fascicle is shorter and broader than the right, impulses reach the papillary muscles just prior to depolarization, and therefore contraction, of the left ventricle myocardium. This allows pre-tensioning of the chordae tendinae, increasing the resistance to flow through the mitral valve during left ventricular contraction. [5]