CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 3, May/June 2014
AFRICA
107
diseases or rhythm disorders, those taking drugs known to
influence QT interval, patients with ECG abnormalities such
as atrial fibrillation, conduction delay, bundle branch blocks,
immeasurable T waves, and those with stroke, obstructive lung
diseases, malignancies and those who received hyperbaric
oxygen therapy.
On admission to the emergency department, blood samples
were obtained for blood gas analysis, total blood cell counts and
biochemical parameters. COHb measurements were performed
with Synthesis 45 (Italy).
Baseline 12-lead ECGs were recorded with a paper speed of
25 mm/s and standardisation of 1.0 mV/cm in all patients. The
QT intervals were measured from the onset of the QRS complex
to the end of the T wave, defined as the return T-P baseline. When
U waves were present, the QT intervals were measured to the
nadir of the notch between the T and U waves. QT
c
interval was
calculated using the Bazett’s formula. The QT
c
dispersion (QT
cd
)
is the difference between minimum and maximum QT
c
intervals.
T
p
T
e
interval was measured from the peak of the T wave
to the end of the T wave. The end of the T wave was defined
as the junction of the T wave with the isoelectric line. The
difference between minimum and maximum T
p
T
e
intervals on
ECG (T
p
T
e.max
–T
p
T
e.min
) was considered T
p
T
e
dispersion. T
p
T
e
/QT
ratio and T
p
T
e
/QT
c
ratio were also calculated. Two experienced
cardiologists (ZI and MY), who were unaware of the patient’s
clinical condition, took two measurements of the QT and T
p
T
e
interval from each measurable lead.
Statistical analysis
The data are presented as mean
±
SD. The independent-
samples
t
-test was used to compare continuous variables and
the chi-square test was used for categorical variables. Pearson’s
correlation coefficients were determined for the relationship
of COHb levels with ECG parameters (QT
c
, QT
cd
, T
p
T
e
, T
p
T
e
dispersion and T
p
T
e
/QT
c
). A
p
-value
<
0.05 was accepted as
statistically significant. Statistical analyses were performed
using SPSS 11.0 (SPSS Inc., Chicago, IL).
Results
A total of 67 patients (28.5
±
9.0 years, 44 female) were
included in the study. Eight (27%) among the CO-intoxicated
patients were smokers. Clinical characteristics of the patients
are presented in Table 1. Mean COHb level was 27.6
±
7.4%.
Mean duration of CO exposure was 164
±
111 minutes and
mean emergency department arrival time was 68
±
123 minutes.
We found a negative correlation between the time to emergency
department arrival and COHb level (
r
=
–0.568,
p
=
0.001). We
also found a negative correlation between age and COHb level
(
r
=
–0.469,
p
=
0.01).
Seven patients among the CO-intoxicated patients had
sinus tachycardia on the ECG records taken at the emergency
department. The mean heart rate of the CO-intoxicated patients
was found to be mildly higher than that of the normal subjects.
However, the difference was not statistically significant (
p
>
0.05) (Table 1).
The QT
cd
durations of CO-intoxicated patients were
significantly longer than that of normal subjects (63.1
±
10.9 vs
42.1
±
4.3 ms;
p
=
0.0001) (Table 2). The QT
cd
value was detected
to be above 60 ms in 19 subjects of the CO-intoxicated patients
(63%) and in none of the normal subjects (
p
<
0.001).
The T
p
T
e
dispersion value of the CO-intoxicated patients was
significantly higher than that of normal subjects (41.4
±
13.0
vs 33.2
±
4.9 ms;
p
=
0.001). T
p
T
e
/QT
cd
ratio was lower in the
CO-intoxicated patients compared to the normal subjects (1.52
±
0.29 vs 2.0
±
0.34;
p
=
0.001).
Pearson’s correlation analysis revealed that a moderately
significant positive correlation was present only between T
p
T
e
dispersion and COHb levels (
r
=
0.39,
p
=
0.03) (Fig. 1).
Correlations between electrocardiographic measurements and
COHb levels of the patients are presented in Table 3.
Discussion
Our results showed that T
peak
–T
end
dispersion and QT
c
dispersion
were higher in CO-intoxicated patients compared to normal
subjects. T
p
T
e
/QT
cd
ratio was lower in CO-intoxicated patients
compared to normal subjects. We found a positive correlation
only between T
peak
–T
end
dispersion and COHb level. Our results
indicated that T
p
T
e
dispersion may be one of the reasons for
arrhythmia caused by CO poisoning.
CO may lead to persistent or reversible myocardial damage,
mainly due to myocardial hypoxaemia and direct action of CO on
the heart.
13
Binding to myoglobin may reduce oxygen availability
in the heart and cause arrhythmias and cardiac dysfunction.
14
Cardiovascular effects of CO poisoning include tachycardia,
Table 1. Clinical characteristics of the study population.
CO-intoxicated
patients (
n
=
30)
Normal subjects
(
n
=
37)
p
*
Age (years)
30.8
±
11.3
26.0
±
5.2
>
0.05
Gender (F/M)
19/11
25/12
>
0.05
BMI (kg/m
2
)
23.1
±
5.5
24.6
±
6.9
>
0.05
Mean heart rate (beats/min)
92.5
±
16.2
82.0
±
13.0
>
0.05
SBP (mmHg)
118.7
±
9.6
122.1
±
8.7
>
0.05
DBP(mmHg)
78.2
±
8.4
72.1
±
7.5
>
0.05
CO exposure time (min)
163.5
±
110.9
COHb (g/dl)
27.6
±
7.4
Time to ED arrival (min)
68.3
±
123.1
Smoker,
n
(%)
8 (27)
11 (30)
>
0.05
BMI, body mass index; SBP, systolic blood pressure; DBP, diastolic blood
pressure; ED, emergency department.
Table 2. Electrocardiographic measurements of the groups.
CO-intoxicated
patients (
n
=
30)
Normal subjects
(
n
=
37)
p
*
QT interval (ms)
355.7
±
90.7
359.6
±
26.4 0.51
QT
c
interval (ms)
382.1
±
11.4
403.7
±
19.7 0.31
T
p
T
e
/QT
c
time (ms)
0.26
±
0.02
0.20
±
0.02 0.16
T
p
T
e
/QT
d
time (ms)
1.78
±
0.32
1.85
±
0.27 0.2
T
p
T
e
/QT
cd
time (ms)
1.52
±
0.29
2.0
±
0.34 0.001
T
p
T
e
dispersion (ms)
41.4
±
13.0
33.2
±
4.9 0.001
T
p
T
e
/QT time (ms)
0.26
±
0.04
0.23
±
0.02 0.11
QT
d
interval (ms)
57.2
±
10.8
55.1
±
3.7 0.1
QT
cd
interval (ms)
63.1
±
10.9
42.1
±
4.3 0.0001
T
p
T
e
time (ms)
87.5
±
19.0
83.1
±
8.3 0.21
