Sepsis-associated cardiac arrest is a relatively common
occurrence with especially poor outcomes. A review paper, published in Journal
of Critical Care, discusses the epidemiology of sepsis-associated in-hospital
cardiac arrest in adults and children, the relevant physiology responsible for
its pathogenesis and poor outcomes, and potential therapeutic interventions
based on this pathophysiology.
Over 200,000 patients suffer an in-hospital cardiac arrest
(IHCA) each year in the United States, with only one-fourth surviving to
hospital discharge. The precise mechanisms by which septic shock leads to
cardiac arrest have not been explicitly characterised. However, the cardinal
manifestations of septic shock, including vasodilation, hypovolemia, and
myocardial dysfunction, along with concurrent hypoxemia, acidosis, and
metabolic derangements likely form the basis of the complex pathophysiologic
pathways that both contribute to cardiac arrest and impede successful return of
spontaneous circulation (ROSC) in these patients, according to researchers.
Prompt recognition and treatment of septic shock are the
first steps in preventing IHCA in these patients. Early goal-directed therapy
aimed at optimising intravascular volume status and correcting metabolic
derangements, in addition to timely administration of antimicrobials and other
source control measures can reduce mortality in septic shock.
"Recognition of sepsis-associated cardiac dysfunction,
likely a major precipitator of cardiac arrest, is important. This can be
accomplished through clinical examination, measurement of serum levels of
natriuretic peptides, and echocardiography, and should trigger the use of
inotropic support in addition to vasopressors," the authors note.
High-quality cardiopulmonary resuscitation (CPR) with
emphasis on appropriate chest compression rate, depth, and recoil; vasopressor
administration; and timely defibrillation has been shown to increase the
likelihood of ROSC, survival to hospital discharge, and satisfactory neurologic
recovery following IHCA. Given the higher rate of adverse outcomes from IHCA in
the setting of septic shock, the authors say further work is necessary to
identify targeted therapeutic interventions to enhance CPR and improve outcomes
specifically in sepsis-associated IHCA.
The higher rates of post-ROSC mortality with
sepsis-associated IHCA reflect the overall severity of disease and degree of
multiple organ dysfunction in these patients, which is not simply corrected
with ROSC.
Derangements in vascular tone and intravascular volume
status persist and likely worsen after cardiac arrest, the authors explain.
While aggressive fluid resuscitation may have preceded or accompanied
resuscitation from cardiac arrest, relative intravascular hypovolemia can
persist and further volume administration may be indicated.
"Experimental conditions that model sepsis-associated
IHCA need to be developed to test novel CPR algorithms and post-resuscitative
therapies. Most importantly, sepsis-associated cardiac arrest provides a prime
example for the need to tailor therapies to the physiologic response of the
patient. Understanding and targeting sepsis-related pathophysiology before,
during, and after cardiac arrest has great potential to improve patient
outcomes," the study concludes.
Source: Journal of Critical Care
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