Effect of Cigarette Smoking and Breathing Carbon
Monoxide on Cardiovascular Hemodynamics in
Anginal Patients
By WILBERT S. ARONOW, M.D., JOHN CASSIDY, M.D., JACK S. VANGROW, M.D.,
HAROLD MARCH, M.D., JOHN C. KERN, M.D., JOHN R. GOLDSMITH, M.D.,
MAHAVEER KHEMKA, M.D., JAMES PAGANO, M.D., AND MICHAEL VAWTER, M.D.
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SUMMARY
Smoking high-nicotine cigarettes caused a significant increase in systolic and diastolic arterial pressure,
heart rate, left ventricular end-diastolic pressure, and coronary sinus, arterial, and venous CO levels, no
significant change in left ventricular dp/dt, aortic systolic ejection period, and cardiac index, and a significant decrease in stroke index and coronary sinus, arterial, and venous P02 levels in eight anginal patients
with documented coronary disease. One week later, these patients inhaled 150 ppm of carbon monoxide until their increase in coronary sinus CO was similar to that produced after smoking their third cigarette. Inhaling carbon monoxide caused a significant increase in left ventricular end-diastolic pressure and coronary
sinus, arterial, and venous CO levels, no significant change in systolic and diastolic arterial pressure, heart
rate, and systolic ejection period, and a significant decrease in left ventricular dp/dt, stroke index, cardiac
index, and coronary sinus, arterial, and venous PO2 levels. Nicotine caused the increased systolic and
diastolic arterial pressure and heart rate after smoking. Carbon monoxide caused the negative inotropic
effect which increased the left ventricular end-diastolic pressure and decreased the stroke index after smoking.
Additional Indexing Words:
Nicotine
Heart rate
Arterial pressure
Stroke index
Coronary heart disease
Cardiac index
Left ventricular contractility
Coronary sinus
MOKING CIGARETTES causes anginal patients to have a significant decrease in exercise performance before the onset of angina
pectoris.1-3 Smoking high-nicotine cigarettes",4'5 or
low-nicotine cigarettes2'4 causes a significant increase
in heart rate and in blood pressure but no significant
change in systolic ejection period in anginal patients
with documented coronary heart disease. This increase in blood pressure and in heart rate does not occur after smoking non-nicotine cigarettes.3 4,6
However, smoking high-nicotine, low-nicotine, or
non-nicotine cigarettes increases the carboxyhemoglobin level3 4' 7 which decreases the amount of oxygen available to the myocardium. Therefore, anginal
patients develop angina sooner after exercise follow-
ing cigarette smoking for at least two reasons: (1) increased myocardial oxygen demand caused by
nicotine and (2) reduced oxygen delivery to the
myocardium, whether or not nicotine is present.
We5 demonstrated in a hemodynamic study that
smoking high-nicotine cigarettes significantly increased the systolic and diastolic arterial pressure,
heart rate, and left ventricular end-diastolic pressure,
did not significantly affect the left ventricular dp/dt,
systolic ejection period, and cardiac index, and
significantly decreased the stroke index and coronary
sinus, arterial, and venous PO2 levels in 10 patients
with angina pectoris due to documented coronary
heart disease. These data caused us to wonder
whether a negative inotropic effect on the myocardium caused by an increase in carboxyhemoglobin
level or by nicotine was responsible for the significant
decrease in stroke index in our anginal patients after
smoking. Therefore, in eight anginal patients with
coronary artery disease, we evaluated the effect of cardiovascular hemodynamics of smoking high-nicotine
cigarettes and of breathing sufficient carbon monoxide
to raise the coronary sinus carboxyhemoglobin level
similar to that occurring after smoking.
From the Cardiology Section, Medical Service, Long Beach
Veterans Administration Hospital, the University of California
College of Medicine, Irvine, and the California State Department
of Public Health, Berkeley, California.
Address for reprints: Wilbert S. Aronow, M.D., Chief, Cardiology
Section, Veterans Administration Hospital, Long Beach, California
90801.
Received February 11, 1974; revision accepted for publication
March 21, 1974.
340
3 4ir0(culation. V olue .50. Alglst 1.974
SMOKING AND CARBON MONOXIDE IN ANGINA
Materials and Methods
Eight men, mean age 51 6 years, with severe angina
pectoris who needed cardiac catheterization and coronary
angiography were subjects. All eight patients smoked
between 20 and 30 cigarettes daily. Informed consent was
obtained from the eight men who participated in this study
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after the nature of the procedures was fully explained.
All eight subjects abstained from smoking for 12 hr prior
to their right and left heart cardiac catheterizations, each of
which was performed twice, one week apart. The cardiac
catheterizations were performed at 8 a.m., with the patients
in the fasting state. The patients did not take any
medications within 24 hr of their cardiac catheterization.
None of the patients received any beta-adrenergic blocking
drugs within two weeks of this study.
The right and left heart cardiac catheterizations were performed with pressures measured with Statham model P23
Db catheter tip pressure transducers and recorded with an
Electronics for Medicine recorder. The maximal rate of left
ventricular pressure rise (left ventricular dp/dt) was
calculated by electronic means with an Electronics for
Medicine RC Differentiator model RC-1. After the pressure
measurements were obtained, blood was drawn
simultaneously from catheters in the coronary sinus, aorta,
and main pulmonary artery and analyzed for P02 with a
Beckman 160 physiological gas analyzer and for carboxyhemoglobin with an Instrumentation Laboratory 182
CO-oximeter. Then the cardiac output was determined by
the indocyanine green dye dilution method. Duplicate
determinations were made.
After the above control measurements were made during
the first cardiac catheterization, the subject then smoked 4/5
of his first standard brand, nonfilter cigarette (containing 1.8
mg of nicotine) at his normal pace, inhaling the smoke. The
cigarettes were marked at the % point. Immediately after
this cigarette was smoked, mesurements (except for cardiac
output) were obtained in the same order stated above. Five
minutes after the subject finished smoking his first cigarette,
he smoked 4/5 of his second cigarette. Measurements were
then made as after cigarette 1. These measurements were
repeated 30 min after smoking cigarette 2 (immediately
prior to smoking cigarette 3). Immediately after smoking
%
of cigarette 3, these measurements and duplicate determinations of the cardiac output were made.
341
After the above control measurements were made during
the second cardiac catheterization, the patient then
breathed 150 ppm of carbon monoxide from a tank through
a mask. We used a Bird Mark 7 Respirator with pressure settings and flow rates reduced and a built-in expiratory leak so
that significant positive pressure was not applied. The
patients breathed carbon monoxide until their increase in
coronary sinus CO was similar to that experienced after
smoking their third cigarette.
Left ventriculography and coronary angiography were
not performed until after completion of the above
measurements. Coronary angiography revealed greater than
75% narrowing of one or more major coronary vessels in all
eight anginal patients.
The t-test for correlated means was used to analyze the
data after breathing carbon monoxide and the cardiac index
and stroke index data after smoking. An analysis of variance
test was done to analyze the data (excluding cardiac index
and stroke index) obtained after smoking. In order to test
the difference between the means, a least significant
difference (LSD) was computed by multiplying the t-table
value for the 0.05, 0.01, and 0.001 levels by the square root
of 2 times the mean square error divided by the degrees of
freedom for the study periods. A LSD for the 0.05, 0.01, and
0.001 levels was compared with each difference between the
study periods means. If the difference between the study
periods means exceeded the LSD at the 0.05, 0.01, or 0.001
levels, then the difference was significant at that level.
Results
None of the patients developed angina pectoris during the study periods. The aortic systolic ejection
period did not significantly change after smoking or
after breathing 150 ppm of carbon monoxide.
Table 1 indicates the aortic systolic and diastolic
pressure for each anginal patient before and after
smoking and before and after breathing 150 ppm of
carbon monoxide. The mean aortic systolic pressure
was significantly increased after smoking compared to
the control period (LSD = 2.9; P < 0.001). The mean
aortic diastolic pressure was significantly increased
after smoking compared to the control period
ible 1
Aortic Systolic and Diastolic Measurements After Smoking atnd After
in Eight Anginal Patients (mm Hg)
Pt.
Control
no.
140/88
122/74
118/68
114/70
110/66
126/78
132/82
120/76
122.8
1
2
3
4
6
7
8
Mean
-9.7
75.3
1 SD
4o7.4
(Circulaztimi, Yo<tlmme}
.;(.
.X1tigitst 1974
After
After
cig. 1
cig. 2
1.50/92
134/82
126/72
126/78
152/94
136/82
128/74
126/78
120/72
134/82
142/88
132/84
122/74
133.0
-9.6
81.3
7.1
134.5
136/84
142/88
134/84
-9.5
82.3
-o6.9
30 min.
after
eig.
2
146/90
126/76
122/70
120/72
116/68
130/80
138/85
124/78
127.8
-9.9
77.4
Breathing Carbon Monoxide
After
cig.
3
152/94
136/82
130/74
128/80
122/74
136/84
144/90
132/84
Control
134/84
126/78
122/70
116/68
114/70
124/76
126/80
124/80
135.0
123.3
9.4
6.2
82.8
7,5.8
-I7.5-7.0
I5.8
-96.6
After
carbon
monoxide
132/82
132/82
118/68
114/67
110/68
128/78
126/78
122/80
122.8
X.2
75.4
ARONOW ET AL.
342
Table 2
Heart Rate Measurements After Smoking and After Breathing Carbon Monoxide in Eight Anginal
Patients (beats/min)
Pt.
no.
1
2
3
4
5
6
7
8
Mean
1 SD
Control
After
cig. 1
After
cig. 2
62
78
74
68
76
80
66
72
72.0
- 6.2
70
90
86
84
90
92
75
84
83.9
-7.7
73
92
88
86
90
92
78
86
30 min
after
85.6
6.8
= 2.5; P < 0.001). Thirty minutes after smoking cigarette 2, the aortic systolic and diastolic
(LSD
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significantly decreased compared to
after cigarette 2 (P < 0.001) but were still significantly
increased compared to the control period (P < 0.01
for aortic diastolic pressure; P < 0.001 for aortic
systolic pressure). The mean aortic systolic and
diastolic pressure did not significantly change after
breathing 150 ppm of carbon monoxide.
Table 2 shows the heart rate for each anginal
patient before and after smoking and before and after
breathing 150 ppm of carbon monoxide. The mean
heart rate was significantly increased after smoking
compared to the control period (LSD = 3.6;
P < 0.001). Thirty minutes after smoking cigarette 2,
the mean heart rate was significantly decreased compared to after cigarette 2 (P < 0.001) but was still
significantly increased compared to the control period
(P < 0.001). The mean heart rate did not significantly
change after breathing 150 ppm of carbon monoxide.
Table 3 reveals the left ventricular dp/dt for each
anginal patient before and after smoking and before
pressure were
After
cig. 2
cig. 3
Control
68
84
82
76
82
86
70
80
78.5
-6.6
74
94
90
88
92
93
78
86
86.9
-7.3
66
80
72
70
74
78
69
70
72.4
-4.7
After
carbon
monoxide
64
82
74
72
70
76
72
67
72.1
0.a
and after breathing 150 ppm of carbon monoxide. The
mean left ventricular dp/dt was not significantly
changed after smoking compared to the control period
but was significantly decreased after breathing 150
ppm of carbon monoxide (t = 18.16; P < 0.001).
Table 4 indicates the left ventricular end-diastolic
pressure for each anginal patient before and after
smoking and before and after breathing 150 ppm of
carbon monoxide. The mean left ventricular enddiastolic pressure was significantly increased after
smoking cigarette 1 compared to the control period
(LSD = 0.8; P < 0.01) and after smoking cigarettes 2
and 3 (LSD = 1.2; P < 0.001) but was not
significantly changed 30 minutes after smoking the
second cigarette. The mean left ventricular enddiastolic pressure was significantly increased after
breathing 150 ppm of carbon monoxide (t = 3.74;
P < 0.01).
Table 5 shows the cardiac index for each anginal
patient before and after smoking and before and after
breathing 150 ppm of carbon monoxide. The mean
cardiac index
was
not
significantly changed after
Table 3
Left Ventricular dp/dt Measurements After Smoking and After Breathing Carbon Monoxide in
Eight Anginal Patients (mm Hg/sec)
Pt.
no.
Control
1
2
3
4
5
6
7
8
1500
1400
1525
9215
Mean
1 SD
975
1050
After
cig. 1
1475
1375
1600
975
1025
112.5
102,5
975
1100
1188
1200
1219
-246
=219
After
cig. 2
1430
1350
1575
975
1000
1150
1050
1150
1213
221
30 min
after
cig. 2
1475
1325
1.550
1000
1000
1075
1025
1125
1197
-222
After
cig. 3
Control
1550
1375
1625
950
950
1100
1000
1150
1214
1525
1350
-270
=219
1500
1000
1025
1100
1050
1075
1203
After
carbon
monoxide
1325
1175
1275
860
825
950
850
900
1020
=205
Circulation, Voltme .50, Autgust
1974
343
SMOKING AND CARBON MONOXIDE IN ANGINA
Table 4
Left Ventricular End-Diastolic Pressure Measurements After Smoking and After Breathing Carbon
Monoxide in Eight Anginal Patients (mm Hg)
Pt.
no.
1
2
3
4
6
7
8
Mean
i 1 SD
Control
After
cig. 1
After
cig. 2
30 min
after
cig. 2
6
10
8
11
10
12
9
10
9.5
11.9
7
12
9
12
11
12
10
11
10.5
=1.8
8
12
10
12
12
12
10
11
10.9
i1.5
6
11
8
11
10
12
9
10
9.6
' 1.9
After
cig. 3
8
12
10
12
12
12
11
12
11.1
i1.5
Control
8
10
9
10
11
12
8
10
9.8
-1.4
After
carbon
monoxide
10
11
9
11
12
12
9
12
10.8
1.3
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smoking compared to the control period but was
significantly decreased after breathing 150 ppm of
carbon monoxide (t = 14.44; P < 0.001).
Table 6 illustrates the stroke index for each anginal
patient before and after smoking and before and after
breathing 150 ppm of carbon monoxide. The mean
stroke index was significantly decreased after smoking
(t = 18.16; P < 0.001) and was significantly decreased
after breathing 150 ppm of carbon monoxide
(t = 16.80; P < 0.001).
Table 7 reveals the coronary sinus CO level for each
anginal patient before and after smoking and before
and after breathing 150 ppm of carbon monoxide. The
coronary sinus CO level was significantly increased
after smoking compared to the control period
(LSD = 0.23; P < 0.001). Thirty minutes after smoking cigarette 2, the coronary sinus CO level was
significantly decreased compared to after smoking
cigarette 2 (P < 0.001) but was still significantly increased compared to the control period (P < 0.001). A
significant increase in mean coronary sinus CO level
occurred after breathing 150 ppm of carbon monoxide
(t = 37.17; P < 0.001).
Table 8 reveals the arterial CO level for each
anginal patient before and after smoking and before
and after breathing 150 ppm of carbon monoxide. The
arterial CO level was significantly increased after
smoking compared to the control period (LSD = 0.17;
P < 0.001). Thirty minutes after smoking cigarette 2,
the arterial CO level was significantly decreased compared to after smoking cigarette 2 (P < 0.001) but was
still significantly increased compared to the control
period (P < 0.001). A significant increase in mean
arterial CO level occurred after breathing 150 ppm of
carbon monoxide (t = 57.67; P < 0.001).
Table 9 reveals the venous CO level for each
anginal patient before and after smoking and before
and after breathing 150 ppm of carbon monoxide. The
venous CO level was significantly increased after
smoking compared to the control period (LSD = 0.17;
P < 0.001). Thirty minutes after smoking cigarette 2,
the venous CO level was significantly decreased com-
Table 5
Cardiac Index Measurements After Smoking and After
Breathing Carbon Monoxide in Eight Anginal Patients
(L/min/m2)
Table 6
Stroke Index Measurements After Smoking and After
Breathing Carbon Monoxide in Eight Anginal Patients
(ml/ beat/rm2)
Pt.
no.
Control
1
2
3
4
5
6
7
8
Mean
2.97
3.20
3.34
3.03
2.89
3.27
3.04
SD
Circolation.
3.09
3.10
-.15
After
After
cig. 3
Control
carbon
monoxide
2.95
3.29
3.21
3.20
2.61
2.62
3.28
3.06
2.85
3.07
3.12
2.92
3.07
.16
3.31
3.06
2.66
2.69
2.17
V'oltme .50. Auigtust 1974
2.85
3.12
3.10
3.06
3.11
.14
2.60
2.68
2.50
2.57
-.17
Pt.
Control
1
2
3
4
5
6
7
8
48
41
45
44
38
41
46
43
43.3
=1=3.2
Mean
-
After
no.
1 SD
cig. 3
40
35
37
35
31
33
40
34
35.6
3.3
Control
49
40
46
46
39
40
45
44
43.6
3.6
After
carbon
monoxide
39
32
36
37
31
34
37
37
35.4
2.8
ARONOW ET AL.
344
Table 7
Coronary Sinus CO After Smoking and After Breathing Carbon Monoxide in Eight Anginal
Patients (%)
Pt.
no.
1
2
3
4
15
6
7
8
Mean
1
SD
Control
After
cig. 1
After
cig. 2
2.5
2.7
2.6
3.2
3.5
3.4
2.0
1.7
2.6
2.4
1.8
2.1
2.4
2.8
2.2
2.81
i.,50
3.8
4.2
4.2
3.1
3.1
3.0
3.5
2.9
3.48
-.53
1.5
2.24
-.39
Downloaded from http://circ.ahajournals.org/ by guest on July 31, 2017
pared to after smoking cigarette 2 (P < 0.001) but was
still significantly increased compared to the control
period (P < 0.001). A significant increase in mean
venous CO level occurred after breathing 150 ppm of
carbon monoxide (t = 47.62; P < 0.001).
Table 10 reveals the coronary sinus PG2 level for
30 min
after
cig. 2
3.5
4.0
3.8
2.8
2.9
2.8
3.2
2.7
3.21
4. 0
After
cig. 3
4.3
4.7
4.4
3.5
3.6
3.
3.8
3.4
3.90
Control
After
carbon
monoxide
2.0
2.1
2.4
1.8
2.5
2.3
1.7
1.5
2.04
-.35
3.8
4.1
4.2
3.4
4.4
4.1
3.4
3.5
3.86
-3.39
1
each anginal patient before and after smoking and
before and after breathing 150 ppm of carbon monoxide. The mean coronary sinus P02 level was
significantly decreased after smoking compared to the
control period (LSD = 0.81; P < 0.001). Thirty
minutes after smoking cigarette 2, the mean coronary
Table 8
Arterial CO Measurements After Smnoking and After Breathing Carbon Monoxide in Eight Anginal
Patients (%)
Pt.
no.
Control
2.4
2.8
2.7
2.1
1
2
3
4
5
6
7
8
Mean
i 1 SD
1.7
1.8
2.2
1.6
2.16
-A.45
After
cig. 1
After
cig. 2
3.5
3.8
3.8
3.0
2.7
2.7
3.2
2.5
3.15
.51
4.1
4.4
4.4
3.6
3.3
3.3
3.8
3.2
3.76
-.49
30 min.
after
eig. 2
3.5
4.0
3.9
3.0
2.9
2.8
3.2
2.7
3.25
=.50
After
cig. 3
4.5
4.9
4.7
3.9
3.9
3.7
4.1
3.6
4.16
.48
Control
2.0
2.2
2.4
i.8
2.4
2.3
1.7
1.6
2.05
.32
After
carbon
monoxide
4.1
4.4
4.6
3.8
4.7
4.4
3.8
3.9
4.21
.36
Table 9
Venous CO Measurements After Smoking and After Breathing Carbon Monoxide in Eight Anginal
Patients (%)
no.
Control
cig. 1
After
After
cig. 2
1
2
3
4
5
6
7
8
2.6
2.9
2.8
2.2
1.8
1.9
2.3
1.7
2.28
-.46
3.3
3.6
3.6
2.8
2.5
2.5
3.0
2.3
2.95
.51
3.9
4.3
4.2
3.3
3.1
3.1
3.6
3.0
3.56
.52
Pt.
Mean
1 SD
30 min.
after
eig. 2
3.6
4.1
4.0
3.1
3.0
2.9
3.6
2.8
3.35)
.50
After
cig. 3
Control
After
carbon
monoxide
4.3
4.7
4.6
3.7
3.7
3.5
3.9
3.4
3.98
-.53
2.2
2.3
2.5
2.0
2.7
2.4
1.8
1.7
2.20
-.35
3.9
4.2
4.4
3.6
4.5
4.2
3.6
3.6
4.00
=.37
Circulation, Volume 50, August 1974
345
SMOKING AND CARBON MONOXIDE IN ANGINA
Table 10
Coronary Sinus P02 Measurements After Smoking and After Breathing Carbon Monoxide in Eight
Anginal Paflients (mm Hg)
Pt.
no.
Control
1
2
3
20
22
22
21
23
22
20
24
21.8
-1.4
4
5
6
7
8
Mean
A
1 SD
After
cig. 1
After
cig. 2
30 min.
after
cig. 2
19
18
20
19
19
21
20
19
21
20
18
22
19.6
1.5
20
22
20
19
23
20.5
-1.4
21
21
20
22
21
19
23
20.8
1.4
was significantly increased compared
after smoking cigarette 2 (P < 0.001) but was still
significantly decreased compared to the control period
(P < 0.001). A significant decrease in mean coronary
sinus P02 level occurred after breathing 150 ppm of
carbon monoxide (t = 25.00; P < 0.001).
Table 11 shows the arterial P02 level for each
anginal patient before and after smoking and before
and after breathing 150 ppm of carbon monoxide. The
mean arterial P02 level was significantly decreased
after smoking cigarettes 2 and 3 compared to the control period (LSD = 1.40; P < 0.001). Thirty minutes
after smoking cigarette 2, the mean arterial P02 level
was significantly increased compared to after smoking
cigarette 2 (P < 0.05) but was still significantly
decreased compared to the control period (P < 0.001).
A significant decrease in mean arterial P02 level occurred after breathing 150 ppm of carbon monoxide
(t = 19.86; P < 0.001).
Table 12 indicates the venous PO2 level for each
anginal patient before and after smoking and before
and after breathing 150 ppm of carbon monoxide. The
sinus PO2 level
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to
After
cig. 3
Control
17
19
19
19
20
19
18
21
19.0
-1.2
22
23
20
21
21
22
20
21
21.3
1.0
After
carbon
monoxide
19
19
17
18
18
19
17
18
18.1
-0.8
P02 level was significantly decreased
after smoking compared to the control period
(LSD = 0.86; P < 0.001). Thirty minutes after smoking cigarette 2, the mean venous P02 level was
significantly increased compared to after smoking
cigarette 2 (P < 0.001) but was still significantly
decreased compared to the control period (P < 0.001).
A significant decrease in mean venous P02 level occurred after breathing 150 ppm of carbon monoxide
(t = 25.97; P < 0.001).
mean venous
Discussion
The increase in carboxyhemoglobin levels after
smoking34' 7 reduces myocardial oxygen delivery. We
found in this study that smoking caused a significant
increase in coronary sinus, arterial and venous CO
levels and a significant decrease in coronary sinus,
arterial, and venous P02 levels with partial recovery
within 30 minutes after smoking.
Ayres and co-workers8 showed that an acute rise of
the venous carboxyhemoglobin level from 0.66% to
8.69% in four patients with coronary heart disease
Table 1 1
Arterial P02 Measurements After Smoking and After Breathing Carbon Monoxide in Eight Anginal
Patients (mm
Pt.
no.
1
2
3
4
5
6
7
8
Mean
i
1 SD
Hg)
After
After
30 min.
after
Control
eig. 1
cig. 2
cig. 2
84
82
86
83
85
83
84
82
83
83.5
=1=1.4
81
84
81
83
82
85
81
84
87
83
86
82
85
81
85
84.1
-2.0
Circuilation, Volutme 50, Atugutst 1974
80
80
82
83
80
80
82
81.6
1.4
83
82.3
1.8
After
eig. 3
80
83
80
83
79
81
78
81
80.6
1.8
Control
86
88
84
87
81
84
83
87
85.0
2.4
After
carbon
monoxide
83
85
80
84
78
81
79
84
81.8
2.6
ARONOW ET AL.
346
Table 12
Venous P02 Measurements After Smoking aid After Breathing Carbon Monoxide in Eight Anginal
Pr.tientt (mm Hg)
30 min.
Pt.
no.
1
2
3
4
.o
6
7
8
Mean
1 SD
=
Control
After
rig. 1
After
cig. 2
37
39
38
39
40
38
37
43
38.9
=i=1.9
36
37
37
37
39
37
35
42
37.5
-2.1
34
36
35
36
37
35
34
40
35.9
-2.0
Downloaded from http://circ.ahajournals.org/ by guest on July 31, 2017
caused a 20% average decrease in mixed venous oxygen tension. This greater reduction in mixed venous
oxygen tension relative to the rise in venous carboxyhemoglobin level was due to a leftward shift of
the oxyhemoglobin dissociation curve, with tighter
binding of oxygen to hemoglobin in the presence of
carboxyhemoglobin. Myocardial oxygen extraction
and extraction ratios also significantly decreased and
the myocardial lactate extraction ratio significantly
changed to production in their coronary heart disease
patients.
Regan and associates" demonstrated a significant increase in mean arterial pressure and in heart rate but
no significant change in cardiac index after eight
patients with a healed myocardial infarction smoked
two standard nonfilter brand cigarettes in about 25
minutes. Pentecost and Shillingford'0 observed a
significant increase in heart rate and in arterial
pressure, no significant change in cardiac output, and
an average reduction of 8% in stroke volume after 14
patients with a previous myocardial infarction smoked
one standard brand cigarette. Frankl and co-workers'1
showed a significant rise in heart rate but no significant change in stroke volume or cardiac output after
eight patients with a healed myocardial infarction
smoked two standard filter tip cigarettes within 10
minutes. Summers and associates12 demonstrated a
significant increase in heart rate and in aortic systolic
and diastolic pressure but no significant change in
systolic ejection period after 15 anginal patients with
angiographically documented coronary artery disease
smoked two regular commercial cigarettes for a total
of eight to 10 minutes.
Nicotine absorbed during smoking increases
catecholamine discharge from the adrenal medulla
and from chromaffin tissue in the heart, causing an increase in blood pressure and in heart rate.`1 Nicotine
also acts on chemoreceptors in the carotid and aortic
bodies reflexly causing an increased blood pressure
after
rig. 2
After
eig. 3
35
33
35
34
36
36
Control
35
33
37
38
39
38
40
37
38
41
36.9
1.9
39
41
31.1
-2.0
38.5
-1.4
37
36
37
38
36
35
After
carbon
monoxide
33
34
35
34
35
33
34
36
34.3
1.0
and heart rate.'4 In addition, low concentrations of
nicotine can stimulate sympathetic ganglion cells.
In this study, we observed a significant increase in
arterial systolic and diastolic pressure and in heart rate
after smoking but not after breathing 150 ppm of car-
bon monoxide. These hemodynamic changes partially
recovered within 30 minutes after smoking.
Therefore, the rise in blood pressure and in heart rate
after smoking cigarettes can be attributed to absorbed
nicotine.
We also demonstrated no significant change in left
ventricular dp/dt after smoking but a significant
decrease in left ventricular dp/dt after inhaling 150
ppm of carbon monoxide. The increase in heart rate,
blood pressure, and positive inotropic effect induced
by nicotine should have increased the left ventricular
dp/dt after smoking. However, these factors were
offset by a negative inotropic effect caused by carbon
monoxide, resulting in no significant change in left
ventricular dp/dt after smoking.
The stroke index significantly decreased in our
anginal patients both after smoking cigarettes and
after breathing 150 ppm of carbon monoxide. The
negative inotropic effect on the myocardium caused
by an increase in carboxyhemoglobin level after smoking and after breathing 150 ppm of carbon monoxide
was responsible for the significant decrease in stroke
index in our anginal patients. The nicotine absorbed
while smoking did not significantly affect the stroke
index because its positive inotropic effect was offset by
an increase in heart rate and afterload. The negative
inotropic effect caused by inhaling carbon monoxide
also significantly raised the left ventricular enddiastolic pressure after smoking.
Finally, the cardiac index in our anginal patients
did not significantly change after smoking cigarettes
but significantly decreased after breathing 150 ppm of
carbon monoxide. The rise in heart rate due to
nicotine compensated for the decrease in stroke
Circulation, Volume .50 Auigust 1974
347
SMOKING AND CARBON MONOXIDE IN ANGINA
volume produced by the carbon monoxide inhaled
during smoking, resulting in no significant change in
cardiac index after smoking. However, the cardiac index was significantly decreased after breathing 150
ppm of carbon monoxide because the inhaled carbon
monoxide significantly decreased the stroke index and
did not significantly affect the heart rate.
6.
7.
8.
Acknowledgment
The authors wish to express their appreciation to Michael W.
Isbell, C.P.T., for his technical assistance and to Reed Boswell,
Ph.D., for biostatistical analysis of the data.
References
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Effect of Cigarette Smoking and Breathing Carbon Monoxide on Cardiovascular
Hemodynamics in Anginal Patients
WILBERT S. ARONOW, JOHN CASSIDY, JACK S. VANGROW, HAROLD MARCH,
JOHN C. KERN, JOHN R. GOLDSMITH, MAHAVEER KHEMKA, JAMES PAGANO and
MICHAEL VAWTER
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Circulation. 1974;50:340-347
doi: 10.1161/01.CIR.50.2.340
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1974 American Heart Association, Inc. All rights reserved.
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