Septic cardiomyopathy can be classified as a secondary form of cardiomyopathy,
the heart being involved in the systemic disease “sepsis”. The pathophysiology
of septic cardiomyopathy is much more complex than the pathophysiology of most of
the textbook heart diseases. This complexity is the consequence of the impact of
numerous toxins and sepsis mediators on the heart in the course of the disease.
Main trigger substances of septic pump failure are endotoxin, TNF-α, IL-1 and NO,
which interfere with receptors, inotropic signal transduction pathways, Ca2+ transients
and the contractile apparatus of the cardiomyocyte. These inflammatory mediators also
impair mitochondrial function of cardiac cells, with the consequence of cytopathic
hypoxia and energy depletion, but also increased production of reactive oxygen species
and induction of apoptosis in the organ.
Cardiac dysfunction is characterized by systolic as well as diastolic dysfunction of the
left and the right ventricle and – typically – by reversible dilation of the heart; diastolic
dysfunction of the left ventricle seems to be the prognostically most relevant alteration.
For compensation of the sepsis-induced vasoplegia resulting in a fall in blood pressure,
the diseased heart has to pump even more, to furnish the demands of circulation, which
further stresses the organ. Thus “afterload-related cardiac performance” (ACP) characterizes
the cardiac pump failure in sepsis much better than isolated measures of systolic
or diastolic dysfunction.
Septic cardiomyopathy is not a primary ischemic disease: Coronary macrocirculation
seems not impaired, while coronary microcirculation probably is. Drastic alterations are
seen in cardiac metabolism, with a strong reduction of free fatty acids fuelling, with
cytopathic hypoxia and some form of myocardial hibernation.
Also chronotropic and bathmotropic dysregulation characterizes septic cardiomyopathy:
resting heart rate is high and heart rate variability is reduced. This is the result of
cardiac autonomic dysfunction with a strongly depressed vagal as well as sympathetic
regulation in sepsis. Moreover, endotoxin interacts with the HCN channels of the
pacemaker current in sinus node, thereby contributing to the intrinsic impairment of
heart rate regulation.
The pathophysiology of septic cardiomyopathy is complex, the cardiac alterations can
be reversible and the impairments of heart function contribute to the unfavorable
prognosis of septic patients.
Keywords: ACP, Afterload-related cardiac performance, Apoptosis, Autonomic
dysfunction, Cardiac index, Cardiac output, Cardiomyopathy septic, Coronary
circulation, Cytopathic hypoxia, Diastolic dysfunction, Echocardiography, HCN
channels, Heart rate, Heart rate variability, If, Inotropy, Interleukin, Mitochondria,
Pacemaker current, Respiratory chain, Septic cardiomyopathy, Systemic vascular
resistance, Systolic dysfunction, TNF-α, Ventricular dilation.
