Editing Pulseless electrical activity (section)

==Causes==
These possible causes are remembered as the 6 Hs and the 6 Ts.<ref name=ACLS_2003_H_T>{{cite book |author=Mazur, Glen |title=Acls: Principles And Practice |publisher=Amer Heart Assn |location=[Dallas, TX] |year=2003 |pages=71–87 |isbn=0-87493-341-2 }}</ref><ref name=ACLS_2003_EP_HT>{{cite book |author1=Barnes, Thomas Garden |author2=Cummins, Richard O. |author3=Field, John |author4=Hazinski, Mary Fran |title=ACLS for experienced providers |publisher=American Heart Association |location=[Dallas, TX] |year=2003 |pages=[https://archive.org/details/aclsforexperienc00amer_0/page/3 3–5] |isbn=0-87493-424-9 |url-access=registration |url=https://archive.org/details/aclsforexperienc00amer_0/page/3 }}</ref><ref name="ECC_2005_7.2">{{cite journal |author=2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care |title=Part 7.2: Management of Cardiac Arrest |journal=Circulation  |date=December 2005 |volume=112 |issue=24 Suppl |pages=IV 58–66 |doi=10.1161/CIRCULATIONAHA.105.166557 |doi-access=free }}</ref> See [[Hs and Ts]]
* [[Hypovolemia|'''H'''ypovolemia]]
* [[hypoxia (medical)|'''H'''ypoxia]]
* [[Hydrogen|'''H'''ydrogen]] ions ([[Acidosis]])
* [[Hyperkalemia|'''H'''yperkalemia]] or [[Hypokalemia|'''H'''ypokalemia]]
* [[Hypoglycemia|'''H'''ypoglycemia]]
* [[Hypothermia|'''H'''ypothermia]]
* [[Tablet (pharmacy)|'''T'''ablets]] or [[Toxins|'''T'''oxins]]<!--Either-or; no need for {{which}}.-->
* [[Cardiac tamponade|Cardiac '''T'''amponade]]
* [[Tension pneumothorax|'''T'''ension pneumothorax]]
* [[Thrombosis|'''T'''hrombosis]] (e.g., [[myocardial infarction]], [[pulmonary embolism]])
* [[Tachycardia|'''T'''achycardia]]
* [[Physical trauma|'''T'''rauma]] (e.g., [[hypovolemia]] from blood loss)

The possible mechanisms by which the above conditions can cause pulseless in PEA are the same as those recognized as producing circulatory shock states. These are (1) impairment of cardiac filling, (2) impaired pumping effectiveness of the heart, (3) circulatory obstruction and (4) pathological vasodilation causing loss of vascular resistance and excess capacitance. More than one mechanism may be involved in any given case.{{citation needed|date=October 2014}}