Editing Cardiac tamponade (section)

==Pathophysiology==
[[File:Blausen 0164 CardiacTamponade 02.png|thumb|250px|[[Hemopericardium]], wherein the [[pericardium]] becomes filled with [[blood]], is one cause of cardiac tamponade.]]
The pericardium, the double-walled sac surrounding the heart, consists of a fibrous pericardium layer on the outside and a double-layered serous pericardium on the inside.<ref>{{cite journal |last1=Sharma |first1=Nitish K. |last2=Waymack |first2=James R. |title=Acute Cardiac Tamponade |journal=StatPearls |date=4 August 2021 |pmid=30521227 |url=https://www.ncbi.nlm.nih.gov/books/NBK534806/ |access-date=22 November 2021}}</ref> Between the two layers of the serous pericardium is the pericardial space, which is filled with lubricating serous fluid that prevents friction as the heart contracts.<ref>{{cite journal |last1=Vogiatzidis |first1=Konstantinos |last2=Zarogiannis |first2=Sotirios G. |last3=Aidonidis |first3=Isaac |last4=Solenov |first4=Evgeniy I. |last5=Molyvdas |first5=Paschalis-Adam |last6=Gourgoulianis |first6=Konstantinos |last7=Hatzoglou |first7=Chrissi |title=Physiology of pericardial fluid production and drainage |journal=Frontiers in Physiology |date=18 March 2015 |volume=6 |page=62 |doi=10.3389/fphys.2015.00062 |pmid=25852564 |pmc=4364155 |doi-access=free }}</ref> The outer layer of the heart is made of fibrous tissue<ref name=Thibodeau>{{cite book |vauthors=Patton KT, Thibodeau GA |title=Anatomy & physiology |publisher=Mosby |location=St. Louis |year=2003 |isbn=978-0-323-01628-5 |edition=5th }}</ref> which does not easily stretch, so once excess fluid begins to enter the pericardial space, pressure starts to increase.<ref name=Mattson/> Consequently, the heart becomes compressed due to its inability to fully relax.<ref name=":1">{{Citation|last1=Stashko|first1=Eric|title=Cardiac Tamponade|date=2021|url=http://www.ncbi.nlm.nih.gov/books/NBK431090/|work=StatPearls|place=Treasure Island (FL)|publisher=StatPearls Publishing|pmid=28613742|access-date=2021-11-24|last2=Meer|first2=Jehangir M.}}</ref>

If fluid continues to accumulate, each successive diastolic period leads to less blood entering the ventricles. Eventually, increasing pressure on the heart forces the [[interventricular septum|septum]] to bend in towards the [[left ventricle]], leading to a decrease in [[stroke volume]].<ref name=Mattson/> This causes the development of [[obstructive shock]], which if left untreated may lead to [[cardiac arrest]] (often presenting as [[pulseless electrical activity]]).<ref>{{cite journal | last1=Standl | first1=Thomas | last2=Annecke | first2=Thorsten | last3=Cascorbi | first3=Ingolf | last4=Heller | first4=Axel R. | last5=Sabashnikov | first5=Anton | last6=Teske | first6=Wolfram | title=The Nomenclature, Definition and Distinction of Types of Shock | journal=Deutsches Ärzteblatt International | volume=115 | issue=45 | date=2019-02-03 | pages=757–768 | pmid=30573009 | doi=10.3238/arztebl.2018.0757 | pmc=6323133 }}</ref> The decrease in stroke volume can also ultimately lead to a decrease in cardiac output, which could be signaled by tachycardia and hypotension.<ref name=":1" />