Talk:Constrictive pericarditis/Archive 1

Good

Good article but and I have just learned of some of the people putting great information in here, for those working on this I complement you. I have some improvements or suggestions to this article.

1) differentiate between the 'chronic' constrictive pericarditis form(usually calcium seen in Xray and a pericardial knock upon ausculation) and the subacute (elastic) form where as 'chronic' is likened to being encased in a hard-candy shell, 'subacute' is likened to the heart being wrapped in rubberbands.

2)The explanation for the inspirational and expirational septal changes and filling patterns being attributed to:

"During inspiration, the negative pressure in the thoracic cavity will cause increased blood flow into the right ventricle. This increased volume in the right ventricle will cause the interventricular septum to bulge towards the left ventricle, leading to decreased filling of the left ventricle. Due to the Frank-Starling law, this will cause decreased pressure generated by the left ventricle during systole.

I believe this does not fully explain as to why this occurs. With inspiration, the diagphragm drops to create negative pressure to suck air into the lungs. NORMALLY, this intra-thoracic pressure drop is transmitted to the heart and lungs equally. While this describes the normal pull of blood by this action. It does not explain the decrease flow to the left ventricle. An incorporation of the notion should be added for ease of conceptualization and correctness of the heart via the pericardium disease shields the heart from the intrathoracic pressure drop THEREBY causing a 'pressure gradient' from the pulmonary vasculature (lungs) and the left atrium/ventricles causing less filling with inspiration. Less filling COMBINED with right heart filling causes the septal flattening. Which as noted in the septal region, it unloads the Starling mechanism reducing outflow. So there is just two sides to the pancake.

During expiration, the amount of blood entering the right ventricle will decrease, allowing the interventricular septum to bulge towards the right ventricle, and increased filling of the left ventricle and subsequent increased pressure generated by the left ventricle during systole.'''

The IVC should be plethoric in constrictive pericarditis and central venous pressure will be elevated already (resulting in the ascites and leg edema and jugular venous distention upon liver pressure during exam) so it is not the main cause to this mechanism although it plays a role. Its that with expiration the lung-heart pressure gradient is reversed or alleviated allowing full filling of the left ventricle and the septum is no longer moving posterior with inspiration.

What is it?

The lead doesn't tell me what CP is - only what causes it. My own attempt, based on the pathology section article and pericarditis would be this:

Constructive pericarditis is a medical condition characterized by a thickened, fibrotic pericardium, limiting the hearts ability to function normally.

I will be bold and insert this. Please feel free to improve it. NisJørgensen (talk) 12:03, 10 September 2014 (UTC)