Biology Reference
In-Depth Information
introduction to understanding the terminology used in describing
HR data and patterns.
III. HEART RATE AND HEART RATE VARIABILITY
In searching for a surveillance strategy for early warning of sepsis or
NEC, it is important to keep in mind the clinical understanding of these
conditions. As mentioned previously, the current hypothesis is that the
clinical syndrome of sepsis, SIRS, is brought about by the infant host's
response to such insults as bacterial infection. The major host response at
the molecular level is the release of cytokines—small circulating
peptides that serve as mediators of the inflammatory response. They
play the role of invisible messengers or ligands that bind to specific
targets (receptors) on the cell surface. Various studies suggest that SIRS
may be caused by an imbalance between cytokines' proinflammatory
and anti-inflammatory effects. In sepsis, circulating cytokines are
important in triggering and maintaining the inflammatory response, and
their quantities are correlated with the severity of illness. For example,
elevated levels of circulating cytokines have been found up to 2 days
before the diagnosis of clinical sepsis—see Kuster et al. (1998). Of
particular interest to our investigation are the widespread effects of
cytokines on signal transduction processes and, specifically, their
potential to interfere with the normal control of HR by the sympathetic
and parasympathetic nervous systems.
Signal transduction at the cellular level refers to the mechanism by
which signals are transmitted from the outside of the cell to the inside.
One of the mechanisms of signal transduction may involve small ion
movement, either into or out of the cell. These ion movements result in
changes in the electrical potential of the cells that propagate the signal
along the cell. Other mechanisms of signal transduction may involve the
coupling of ligand-receptor interactions to cascades of intracellular
events that alter enzyme activities and protein conformations. Signal
transduction leads to alterations in cellular activity and to changes in the
program of genes expressed within the responding cells. For example, it
has been shown by Oddis and Finkel (1997) that specific cytokines
(acting as ligands and binding receptors on the cell surface) may
increase HR. Interestingly, the same cytokines have also been shown to
reduce HR responses to certain drugs.
Figure 6-2 presents an electrocardiogram (EKG), which is a record of the
electrical activity in the heart muscle during the heartbeat cycle. The
markers at the peaks pinpoint the time of occurrence of sequential
heartbeats. The characteristic that quantifies HR is the interbeat interval
(RRI). The RRI is the elapsed time (usually measured in milliseconds)
from one heartbeat to the next (e.g., the distance between two
sequential markers [so a larger RRI corresponds to a slower HR]).
