Applying a lateral pressure on the brachial artery above, say, 200 mm Hg, makes the artery close and no blood can flow past the occlusion. Thus, according to Beroulli, the energy that is produced by the heart and transferred through the artery will exercise a pressure towards the occlusion, i. e. a ‘wedge pressure’ (?), which equals the lateral pressure, since no energy is used to produce movement of the blood. If we lower the pressure in the spygmomanometer we will eventually reach a point where the pressure in the sphygmomanometer equals or is just below the wedge pressure in the artery, forcing the artery open. Blood will flow through the artery and produce the Korotkoff sound; and thus we can determine the systolic blood pressure. The systolic blood pressure could therefore be considered to equal the maximum energy per unit of blood volume produced by the heart at any given moment? ((N/m2) x m3 = Nm).

But the fact that the once closed artery now is open means that some of the energy produced by the heart will be used to move blood through the artery, lowering the lateral pressure again. So once the pressure is high enough to open the artery, that same pressure will be transformed into motion energy, making the lateral pressure fall and since the pressure of the spygmomanometer is just below the maximum wedge pressure, the artery will once again close..? And once it closes, the pressure will build up again and once more force the artery open; and if I am correct the walls of the artery would start to oscillate. At the same time the pulsatile energy produced by the heart will cause the total amount of energy in the closed artery to rise and fall, making the artery oscillate in systole and close in diastole.

If the continue to release the pressure in the sphygmomanometer, the ‘wedge pressure’ in the closed artery during diastole will eventually force the artery open, and the pressure in the sphygmomanometer at this moment would, according to me, represent the diastolic pressure. But at that point, why does the sound in the distal artery change? We would still have the oscillation, which I think now would be present during both systole and diastole.  Rather than the Korotkoff sound disappearing at this point, I would have guessed the sound would change to a  more constant murmur due to turbulence after the oscillating part of the artery. The oscillation would, if I am correct, continue until the point where the pressure in the sphygmomanometer no longer causes a deformation of the artery wall making the area of that section of the artery smaller than the surrounding vessel area. So the pressure we have reached where the turbulence completely disappears in the artery would rather represent the resistance to compressive stress of the vessel wall; maybe this pressure would correlate better to vessel wall changes and atheromatosis?

Where do I go wrong?

Basically you draw two lines, you mark out the P-waves on the upper line and the QRS-complexes on the lower one, and then you can start trying to decide which P-waves give rise to which complexes, and maybe even where there ought to have been P-waves but they are over-shadowed. This is what it might look like:

 (For further reading: Johnson NP, Denes P. Am J Cardiol. 2008 Jun 15;101(12):1801-4. Epub 2008 Apr 16.)

You get the basic idea? Pretty neat, huh? To me, it seems like a simple and appealing way of clearifying and interpreting complex ECGs and it is well worth a happy 124th birthday!

P. S. Speaking of arrythmias, I hope you have all seen the most wonderful and endearing cardiology tutor ever: http://www.youtube.com/watch?v=zvWzm7ICzhw Don’t you just want to marry this man and have his babies?

“What is the meaning of the atrial auricles?”

An interesting question! For my less educated readers, the atrial auricles are an anatomical part of the heart, or rather of the two atria, and they look rather like two floppy puppy-ears hanging down towards the ventricles. I have never thought about it before now, but the Kat is right; they do seem pretty pointless? Even worse, somtimes they can be the anatomical equivalent of a dark, dead-end ally, where shifty elements can gather planning mischief… So, readers, let’s put some light on the auricles!

“Hi! Read the news in Mats’ blog. I married into a family that sits around the table measuring their blood pressure once per day. I’m not joking! They pay attention to their heart beats and their blood and, well maybe if we all would some bad events would be avoided. Anyway, I do have a question:
I heard a doctor on tv say that people with a deep crease in their earlobes have an increased risk of suffering a heart attack. Living in an area where someone in the neighbourhood seems to be getting a heart attack once every two weeks (cigarettes, fat meat, baklava and no excercise) I started looking for deep creases and found one, not on my husband but on a relative. So, is it true about the crease and if so, where is the connection between the ears and the cardiovascular health of a person?”

Then this site is hopefully something for you. I hope this will be a site where you physiology nerds from all over the world can unite and discuss what’s on your hearts (pun intented, obviously).  Are you wondering about something but lacking the nerve to ask? Or have you ‘ruined’ to many perfectly nice family dinners trying to discuss the E/A ratio in patients with diastolic dysfunction? Now you can stop ruining your social life! Drop me a comment and I will publish your question on this blog. Maybe someone else have the answer, or at least a useful article or review where you can learn more.

Please be aware – asking good questions is the first step towards winning the Nobel Price. If you do have a really good question you might want to discuss the answer after you have published the article and not before…