Sorry about length: relevant quotes from wikipedia articles. Stuff after ------ is mine.
Right heart my emphasis [my addition]
Oxygen-depleted blood from the body leaves the systemic circulation [includes head] when it enters the right heart, more specifically the right atrium through the Superior (upper) vena cava and Inferior (lower) vena cava. The blood is then pumped through the tricuspid valve (or right atrioventricular valve), into the right ventricle. Blood is then pumped through the semilunar valve and into the pulmonary artery [for the lungs].
Tricuspid insufficiency (TI), a valvular heart disease also called [tricuspid regurgitation (TR)], refers to the failure of the heart's tricuspid valve to close properly during systole[, when the heart is pumping used blood to the lungs]. As a result, with each heart beat some blood passes from the right ventricle to the right atrium, the opposite of the normal direction.
Although congenital causes of tricuspid insufficiency exist, most cases are due to dilation of the right ventricle. Such dilation leads to derangement of the normal anatomy and mechanics of the tricuspid valve and the muscles governing its proper function. The result is incompetence of the tricuspid valve. Common causes of right ventricular dilation include left heart failure, pulmonary hypertension, and right ventricular infarction. One notable exception to right ventricular dilation as a cause of tricuspid insufficiency occurs in right-sided endocarditis (i.e. infection affecting the right side of the heart). In that case, there is direct damage to the tricuspid valve as a result of infection.
Other diseases can directly affect the tricuspid valve. The most common of these is rheumatic fever, which is a complication of untreated strep throat infections.
Tricuspid regurgitation occurs in roughly less than 1% of people and is usually asymptomatic. It may be found in those with a type of congenital heart disease called Ebstein's anomaly.
Other infrequent causes of tricuspid regurgitation include:
* Carcinoid tumors, which release a hormone which damages the valve
* Connective tissue diseases such as Marfan syndrome
* Rheumatoid arthritis
* Radiation therapy
Another important risk factor for tricuspid regurgitation is use of the diet medications called "Fen-Phen" (phentermine and fenfluramine) or dexfenfluramine
Tricuspid insufficiency may be asymptomatic, especially if right ventricular function is well preserved. Conversely, edema, vague upper abdominal discomfort (from a congested liver), and fatigue (due to diminished cardiac output) can all be present to some degree.
On examination, the jugular venous pressure is usually elevated, and 'CV' waves can be seen. The liver may be enlarged and is often pulsatile (the latter finding being virtually diagnostic of tricuspid insufficiency). Peripheral edema is often found. In severe cases, there may be ascites and even cirrhosis (so-called 'cardiac cirrhosis).
Diagnosis is usually made by echocardiography although the find of a pulsatile liver and/or the presence of prominent CV waves in the jugular pulse is also essentially diagnostic.
No valve separates the superior vena cava from the right atrium. As a result, the (right) atrial and (right) ventricular contractions are conducted up into the internal jugular vein and, through the sternocleidomastoid muscle, can be seen as the jugular venous pressure. In tricuspid valve regurgitation, these pulsations are very strong.
Main article: Jugular venous pressure
The jugular venous pressure (JVP) is an indirectly observed pressure over the venous system. It can be useful in the differentiation of different forms of heart and lung disease.
Classically 3 upward deflections and 2 downward deflections have been described. The upward deflections correspond with (1) atrial contraction, (2) ventricular contraction (and resulting bulging of tricuspid into the right atrium during isovolumic systole), and (3) atrial venous filling. The downward deflections correspond with (1) the atrium relaxing (and the tricuspid valve moving downward) and (2) the filling of ventricle after tricuspid opens.
The azygous vein (which receives blood from the rib cage) joins it [the Vena Cava] just before it enters the right atrium, at the upper right front portion of the heart. It is also known as the cranial vena cava in animals.
====>>found all this stuff on wikipeda
It seems the azygous is lower down. drains the ribcage, and ends up at the vena cava. Only way returning blood (this is also true of all the veins below the heart) can get upward against gravity is by suction from the right atrium. There must be some negative pressure available from the heart muscle during systole, which pulls the blood up, against gravity. It is only during the other interval, diastole, when the heart contracts, that there could be reflux strong enough to reach the brain.
At the end of the suction part of the cycle (usually called "relaxation") the tricuspid is suppose to close, and in this case it is stuck open. The heart goes on to pump blood into the lungs. Instead of just the lungs, the used blood will in the case of tricuspid insufficiency be forced towards the brain.
"In tricuspid valve regurgitation, these pulsations are very strong." Does this mean normal (no tricuspid problems) people have pulse of jugular pressure? If true, that would mean tricuspid problems result only in existing pulsations become stronger than usual?
It sounds like a lot of people have (asymptomatic) tricuspid regurgitation, and those who *are* symptomatic (note how some of the symptoms soond familiar) could include PwMS.
It also seems that if the motor centers are on the left, for limbs on the right, and vice versa we could see if bad drainage from the left corresponds with brain injuries on the left, in people with only one internal jugular. Of coure alternative explanations always exist, but if the iinjured side always corresponds to the missing jugular side, at least the CCSVI theory is not contradicted, and may be easier believed. Does that make sense?