Biology Reference
In-Depth Information
the sinoatrial node (or pacemaker), which causes contraction of the atria.
The contraction of the main pumping chambers, the ventricles, is
controlled by the atrioventricular node.
Recall that autonomic nervous system exerts control over HR through
the sympathetic and parasympathetic pathways. The sinoatrial node cell
membrane has beta-adrenergic (epinephrine- and norepinephrine-
binding) receptors which, on binding ligands released from sympathetic
nerve endings or the adrenal medulla, lead to the activation of cyclic
adenosine monophosphate (cAMP)-dependent protein kinase. The active
cAMP-dependent protein kinase phosphorylates cardiac ion channels
and results in cell depolarization, an action potential, and a heartbeat.
Consequently, HR rises after sympathetic stimulation. The sinoatrial
node cell membrane also contains muscarinic acetylcholine receptors.
When bound with acetylcholine from parasympathetic nerve endings,
they inhibit the process described above and HR falls. Thus, for as long
as the complex steps of intracellular signal transduction can be
successfully completed, the sinoatrial node can be viewed as an
amplifier of the input signals of the autonomic nervous system and HR
as the output signal. As the amounts of sympathetic and
parasympathetic activity vary, HR varies as well.
Now consider a severe illness like sepsis. In such an unfavorable
metabolic milieu, the optimal conditions for signal transduction are
unlikely; HRV becomes abnormal because sinus node cells, like all other
cells, are unable to respond normally to sympathetic and
parasympathetic inputs. In general, reduced HRV is a sign of system
isolation and disruption of the control mechanisms.
IV. QUANTIFYING HEART RATE AND HEART RATE
VARIABILITY
It is a cinematic clich´ to use the sound of a thumping heart in
suspenseful scenes—the beats becoming very slow and regular
when the character gets into trouble. Following the scientific literature
(and the movies), we could expect that before sepsis and SIRS the
HR would become more regular and would sometimes slow down.
Longer RRIs represent HR decelerations, while shorter RRIs represent
HR accelerations. Formulated scientifically, this means we should
see reduced baseline HRV and transient decelerations. To investigate
whether these expectations are correct, we need two components:
(1) Lots of HR data for healthy hearts and for hearts before
sepsis; and (2) methods quantifying HRV and distinguishing normal
from abnormal HR series, paying particular attention to HR
decelerations.
We begin by visually inspecting the HR time series of a baby who
developed sepsis. The baby was born 5 months prematurely, at
