Could it be because of O2 and nutrient changing into CO2 and body waste?
Do not change the molecules causes the volume change?
Seems to be the end-diastolic filling due to atrial contraction.
Seems to be the end-diastolic filling due to atrial contraction.
The peak of systole is more related to the volume of blood in the ventricle and the electrolytes that cause the contraction of the myocardium. Other factors that may play a part in systole is Ischemia (poor blood supply) of the cardiac muscles. Cardiac muscle contraction is caused in response to electrical signal. Electrical signals, in heart, are not transmitted through O2 and nutrient changing into CO2 and body waste. The corresponding Electrocardiogram is not showing signs of O2 and nutrient changing into CO2 and body waste. A 12 lead ECG for comparison would help diagnose it along with prolonged reading of pressure and volumes as shown in the figure.
This is a not-so-good picture from a textbook. The designated part of the curve is intended to show the effect of atrial contraction on ventricular volume (as Thierry suggested). It should have stopped rising a little bit earlier than it does (I enlarged the picture on my screen), but it is purely schematic and not a real-life recording.
The curve rises as the ventricular volume increases; the "extra bump" at the top is the increase due to the atrial contraction. The ventricular volume curve follows the change over time and has nothing to do with plotting Oxygen consumption.
The proportion of filling following atrial contraction is limited to 10-15% of the total filling volume at rest, but increases during exercise. To give an extreme example, the whale has a resting HR of 2 pm and does not need atrial contraction, being in total AV dissociation. When diving, AV synchrony is restored.
In diseased hearts, such as in overload states (valvular regurgitation), in the presence of diastolic dysfunction or in the particular case of mitral stenosis, the contribution of atrial contraction can rise to 50% or more of the total filling volume. These ventricles are highly dependent on atrial compensatory mechanisms for maintaining output and keeping filling pressures under control. These ventricles therefore are vulnerable to the consequences of afib, leading to prompt haemodynamic failure.
Hello Seyed,
I wish I have explanation for you. But I do not. Done a lot of work on this topic. Maybe it will help you if I attach pdf file to this posting with ECG synchronized LV volume trace from larger mammal. Also I have measured Aortic pressure right close to Aortic valve (using TEE as a guide for the Pressure catheter). It is also included. What is very strange is the non-linearity (steepness) of this LV volume trace, not only its rather interesting bump... but also its non linear nature. Is this example theoretical or this describes a patho-physiology of some sort?
Filip, thank you for the nice recording. How was volume measured here? By a conductance catheter?
Your picture shows nicely that real-life recordings are quite different from the text-book schematics that students are subjected to. However, starting at the schematics, with proper explanation and practical experience these students can become experts in the end.
The peak indicate EDV in normal human the EDV value is 120 ml/min
After atrial contraction is complete, the atrial pressure begins to fall causing a pressure gradient reversal across the AV valves. This causes the valves to float upward (pre-position) before closure. At this time, the ventricular volumes are maximal, which is termed the end-diastolic volume (EDV). The left ventricular EDV (LVEDV), which is typically about 120 ml, represents the ventricular preload and is associated with end-diastolic pressures of 8-12 mmHg and 3-6 mmHg in the left and right ventricles, respectively.
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