Introduction
The prognosis of cardiac arrest (CA) remains poor, despite the advances
in treatment in recent years (1). The primary goal of cardiopulmonary
resuscitation (CPR) is to achieve the return of spontaneous circulation
(ROSC). Deciding when to stop CPR and not knowing how long the CPR will
take and how it will end are the main problems for rescuers. Biomarkers,
such as Interleukin-6, High sensitive C reactive protein, and S-100 B
protein, have been studied as an early marker of post-CPR prognosis and
predictors for ROSC (2,3). However, these biomarkers are not routinely
performed in the emergency department, add cost, and incur a time delay.
These delays diminish their value for CA patients. Studies of routinely
available laboratory markers have shown that high blood sugar, low
potassium, high platelet count, and elevated lactate levels are
associated with poor prognosis in patients with CA. Nevertheless, a
consensus has not been achieved on a standardized biomarker in this
regard (4–7). For healthcare professionals, blood gas analysis with
rapid results is an important tool in terms of diagnosis and treatment
of reversible causes of CA (hypoxia, hyperpotassemia, hypopotassemia,
hypovolemia, and acidosis). Carboxyhemoglobin (COHb) and methemoglobin
(MetHb) levels can be easily measured by blood gas analysis and do not
require additional costs.
COHb and MetHb are variants of normal hemoglobin. Both molecules are
formed from hemoglobin as a result of different biochemical processes
(8). COHb is formed by the binding of carbon monoxide (CO), which is
formed endogenously by hemoglobin metabolism or exogenously inhaled (8).
It has been reported that CO is involved in various functions, such as
vasodilation, angiogenesis, vascular remodeling, and inflammatory
response (8,9). The reported blood COHb level is approximately 1.0% in
non-smokers and 5.5% in patients with a smoking history (10). In some
studies, it has been reported that high and low COHb levels are
associated with poor clinical prognosis in various pathological
conditions, including pulmonary embolism (PTE), acute ischemic heart
disease, and critically ill patients in intensive care units (ICU)
(11–13).
MetHb formation results from oxidative processes in which one or more of
the four iron atoms in the hemoglobin molecule are converted to a ferric
state and, thus, unable to bind oxygen. When naturally produced nitric
oxide (NO) interacts with hemoglobin endogenous MetHb is formed. Large
amounts of NO can be produced in various critical diseases, such as
sepsis or septic shock (14). Increased free NO levels in the circulation
can cause the formation of MetHb (15,16). In conclusion, it has been
reported that MetHb levels increase in patients with sepsis and PTE
(11,14). To our knowledge, no study has yet investigated the predictive
value of COHb and MetHb levels in CA cases.
This study aimed to investigate the role of the COHb and MetHb levels in
predicting the ROSC in patients with non-traumatic cardiac arrest who
underwent CPR and to determine the predictive value of the COHb and
MetHb levels in patients who achieve ROSC.