Biology Reference
In-Depth Information
separately the mean values of contributions caused by accelerations
(measured by the logarithm of R
1
) and decelerations (measured by the
logarithm of R
2
).
It is evident that SA began increasing approximately 3 to 4 days before
sepsis, with the steepest increase in the last 24 hours. To statistically
compare the mean values of the baseline values of SA, ln(R
1
), and
ln(R
2
) 5 days before sepsis and those for the last 24 hours, a statistical
test called repeated measures analysis of variance (ANOVA) was
applied. This analysis is used when repeated measurements are made on
the same subject as we do for the SA values. Recall that the t-test is used
for testing the equality of the means for two groups. In effect, repeated
measures ANOVA extends the two-sample t-test for equality of two
independent population means to the more general setting of comparing
the means of groups formed by repeated measurements of the SA.
The data in Table 6-2(A) show that the difference between the
baseline group (5 days before sepsis) and the group containing the
SA values from the last 24 hours before sepsis was significant: F
¼
5.5,
p
¼
0.02.
Within the experimental group, analysis of the contribution of
accelerations (measured as the natural logarithm of R
1
) and of
decelerations (natural logarithm of R
2
) shows the surprising finding that
there was a significant fall in R
1
(F
0.02) before sepsis, but no
significant change in R
2
[the last two columns in Table 6-2(A)]. This is
readily interpreted to mean that a decrease in the extent and duration of
HR accelerations is more marked than an increase in decelerations,
which are more easily identified by eye.
¼
5.8, p
¼
As presented in Table 6-2(B), posttreatment SA returned to exactly
presepsis levels. A comparison of the two periods of health, 5 days
before sepsis versus posttreatment, showed no difference (F
0.01,
p > 0.99). A similar return toward baseline was observed for both
R
1
(accelerations) and R
2
(decelerations), although the second index,
R
2
, remained somewhat elevated. As expected, a comparison of
experimental-group infants' data when healthy to control-group infants
revealed no significant difference in SA (F
¼
0.13) and no
significance of the covariates BW and GA ( p-levels of 0.2 and 0.7,
respectively). Similarly, no significant differences in R
1
and R
2
were
observed between healthy and experimental infants in health
[Table 6-2(B)].
¼
2.4, p
¼
In closing, these analyses show that SA becomes elevated in the 24 hours
before sepsis and then, after a successful treatment, returns to its
baseline. Thus, SA may be a valid tool in the detection of sepsis in
prematurely born infants before the occurrence of any clinical
symptoms.
