Arrhythmic versus asphyxial cardiac arrest

We are comfortable thinking of cardiac arrest as one entity. That thinking is simplistic and flawed.  A recent review article highlights differences between two major categories of arrest. First some definitions. Arrhythmic cardiac arrest is primary cardiac arrest. It is caused by structural, electrical (channelopathy) or metabolic (eg electrolyte disturbance) disorders and the presenting rhythm is usually (though not always) VF or pulseless VT. Asphyxial arrest is the “respiratory code” which occurs as a result of respiratory failure and consequent hypoxemia or hypercapnia. VF may occur but it is almost never the presenting rhythm. These represent the main two causes of arrest. A third category, cardiac arrest as the end result of progressive circulatory shock, was not covered in the review.

The following sections from the body of the paper highlight key points:

Asphyxial CA is characterized by a prolonged time course and an important prearrest period where hypoxia (defined as critical reduction in arterial oxygen saturation or arterial oxygen tension), and hypercapnia (defined as increases in arterial carbon dioxide tension), progressively advance along with maintained but gradually deteriorating cardiopulmonary function...

Contrary to asphyxial, dysrhythmic CA leads to sudden and complete cessation of blood flow...

Although VF is a lethal tachyarrhythmia often associated with underlying cardiac disturbances and considered to be the immediate cause of CA, it can also occur during the asphyxial process. Ventricular fibrillation in this setting is uncommon, but not rare [15] . Asphyxia-induced or secondary VF has different underlying pathophysiologic mechanisms with regard to myocardial bioenergetics and electrophysiology...

The conversion of PEA and nonshockable rhythms to shockable during asphyxia is an interesting phenomenon and it seems that outcomes after asphyxial CA with asystole/PEA with subsequent VF are worse than after asystole/PEA without subsequent VF [20] . This is probably attributed to the fact that subsequent VF might be a marker of more severe myocardial dysfunction...

At cellular level, sudden CA of cardiac origin causes an immediate no-flow state with global ischemia, where high-energy phosphates are depleted rapidly. Especially in the brain, adenosine triphosphate (ATP) depletion is thought to occur within a few minutes [23] . On the contrary, asphyxial CA is characterized by progressive and global hypoxia with incomplete ischemia and results in gradually with the length of asphyxia ATP and phosphocreatine reduction. If ATP is depleted during hypoxia, necrosis occurs because of mitochondria transmembrane potential disruption, leading to cell swelling and ultimately to apoptosis and necrosis [24 25] . Depletion of cellular energy initiates biochemical cascades that lead to cell damage and death prior to the no-flow state...

Finally, maintained cardiovascular function during asphyxia prior to cardiac standstill results in CO 2 tissue production and accumulation in the alveoli, as there is no alveolar gas exchange. There are at least 5 laboratory studies that showed different patterns of end-tidal carbon dioxide ( et CO 2 ) levels during cardiopulmonary resuscitation (CPR) betpathophysiologic role. In particular, organ perfusion with hypoxemic blood during asphyxia prior to complete circulatory collapse may contribute to a different degree of reperfusion injury after ROSC compared with sudden dysrhythmic CA, affecting overall prognosis...

Although both asphyxial and dysrhythmic CAs lead to brain damage through global ischemia, it seems that significant histopathologic differences exist between the 2 conditions...

In summary, all available data support the assumption that the ischemic degree and final brain damage are greater and more severe after asphyxial CA than after dysrhythmic CA...

Myocardial dysfunction after resuscitated CA is a well-recognized and described component of the post-CA syndrome...

As for treatment implications based on the type of cardiac arrest, the authors suggest a traditional guideline based approach to asphyxial arrest versus cardiocerebral resuscitation as originally promulgated by the Arizona investigators for arrhythmic arrest. Post arrest hypothermia is recommended for both forms of arrest although it is more firmly established for arrhythmic arrest.