ANESTHESIA

AND ANALGESIA.
. . Current Researches VOL.54, NO.6,Nov.-DEc.,1975

783

Treatment of Bronchospasm During Anesthesia

MARTIN I . GOLD, M.D.*

During anesthesia, wheezing and difficult breathing are dangerous, requiring prompt therapy.
The pressurized i s o p r o t e r e n o l cartridge described in this report may be interposed conveniently in the anesthesia breathing system,
is inexpensive, and provides accurate dosage.
This device proved effective in treating bronchospasm and decreasing wheezing and secretions in 11 out of 12 cases. The mean (-+.SEM)

peak airway pressure was 43 (C 2) torr before

and 31 (& 2) torr after treatment; mean Pacon
was lowered from 60 (rt 6) to 47 (24) torr;
mean pH increased from 7.24 (i. 0.03) to 7.33
(r+0.03), and mean percent increase i n Paoz
was 32 (& 13.4). No cardiac arrhythmias,
tachycardia, o r rise in blood pressure were
observed.

during anesthesia is of
serious concern to the clinician.l-;
While fluorocarbon administration may create complications, pressurized (Freon@)
isoproterenol in 250 mcg doses inhaled in
the awake asthmatic patient creates effective bronchodilation.T.8

proterenol nebulization. The syndrome of

wheezing, troublesome secretions, and/or
retractions together with high peak PA occurred usually 10 to 40 minutes after tracheal intubation. One unintubated patient
developed this condition during spinal anesthesia (mask, N,0-02, FIO, = 0.5). All patients had radial arteries punctured for gas
Isoproterenol administration during anes- analysis, immediately before the Mistomthesia has improved over the years.4.s713
eter-casette was interposed (figure).
A casette into which the Freon-pressurized
cartridge? fits interposed with 15 mm adapThe patient was removed from the venters between the Y-piece of the circle sys- tilator and placed on a rebreathing bag.
tem and the endotracheal tube has been This was followed by 2 depressions of the
This device is inexpensive, con- Mistometer valve, 125 mcg/depression,
venient, creates accurate dosage and avoids timed with manually induced inspiration.
rainout into anesthesia tubing (figure).
The fractional inhalation concentration of
The purpose of the present investigation oxygen (FIo,), tidal volume (VT),$and
was to study the response to nebulized iso- respiratory rate before treatment were measproterenol in 11 anesthetized patients with ured and maintained constant during and
after isoproterenol administration. All pabronchospasm (table 1).
tients (except the patient receiving spinal
anesthesia) were mechanically ventilated.
PROCEDURE
After 10 minutes a second sample of arterial
Eleven patients who developed broncho- blood was drawn. I n each patient the ECG
spasm during anesthesia-one twice during (lead 11) recorded cardiac rhythm.
the same surgical procedure-were studied.
Clinical observations and physiologic measRESULTS
urements, including peak airway pressures
(peak PA) a t the mouth (Air Shields venAfter 11 of 12 treatments, clinical imtilator manometer), Pao,, Paco,, and p H provement occurred: wheezes disappeared
were made before and 10 minutes after isoRONCHOSPASM

iIsuprel Mistometefi, Winthrop Laboratories.

$Measured by a Beckman D-2 O? analyzer and

Wright respirometer, respectively.

Professor, Department of Anesthesiology, University of Miami School of Medicine; Chief, Anesthesia

Service, Veterans Administration Hospital, Miami, Florida 33152.
Paper received: 1/13/75
Accepted for publication: 4/29/75

784

ANESTHESIA
AND ANALGESIA..
. Current Researches VOL.54, NO.6, Nov.-DEc., 1975

FIGURE.
Position of nebulizer in anesthesia circuit.

or were ameliorated, difficult breathing improved (retractions) and the amount of

secretions, after aspiration, decreased or disappeared (table 2 ) . One patient (#12)
worsened clinically although Pao, mse. The
mean ( + SEM) peak PA was 43 (t 2)
torr before and 31 ( 2 2) torr after treat-

ment; mean Paco, was lowered from 60

( k 6) to 47 (f4 ) torr and mean pH increased from 7.24 ( k 0.03) to 7.33 ( k 0.03)
(p<0.05, paired t-test). Since the no,
ranged from 0.4 to 1, the difference between
the mean Pao2's (before and after) was
clinically meaningless; however, the mean

TABLE 1
Patient Characteristics
Patient
number

Age

Surgery

Primary anesthetic

Prior pulmonary
disease

Other disease

66 Thyroidectomy

Halothane

None

Hyperparathyroidism

52 Gastrectomy

Halothane

Pulmonary
aspiration

Obesity, liver disease

Extreme obesity

56 Cholecystectomy

Halothane

None

55 Neck dissection

Morphine-NzO-02

Cardiac asthma Previous myocardial

infarction

59 Laryngectomy,
radical neck
dissection

Fentanyl-NZO-02

COPD"

Cachexia. anemia

Sarcoidosis
and asthma

Arrested TB, alcoholism

1:

Bilateral
31 temperomandibular Halothane
joint dissection
8

59 Hip nailing

Halothane

COPD

Previous pulmonary
embolus

73 Transurethral
resection

Spinal anesthesia

COPD

Recurrent bladder tumor

10

70 Closure
suprapubic fistula

Halothane

COPD

11

37 Lumbar discectomy Halothane

12

53 Cystoscopy and
cystogram

Halothane

*Chronic obstructive pulmonary disease.

None
COPD

Obesity, diabetes,
massive, hydronephrosis,
uremia, hypertension

Bronchospasm . . . Gold

785
TABLE 2
Effect of lsoproterenol
~

Effect of

Clinical
.
.
improvement
Patient
number

after
isoproterenol

Fioz

VT, ml

Status

isoproterenol

Peak PA,
torr

Pooz,
torr

Blood gases
Pacop,
torr

PH

+++

0.4

900

35
30
-14

100
140
40

55
45
-18

7.38
7.39
0

Before
After
70 A

0.5

950

+++

40
29
-27

80
95
19

62
45
-27

7.28
7.35
1

0.5

1100

Before
After
% A
Before
After

50
138
176

29
29
0

7.40
7.40
0

+++

40
30
-25

0.4

900

40
20
-50

70
98
40

100
66
-34

7.12
7.30
3

50
40
-20

88
110
25

62
42
-32

7.20
7.38
3

40
30
-25

81
93
15

75
64
-15

7.03
7.11
1

30
20
-33

140
155
11

83
55
-34

7.15
7.28
2

50
40
-20

160
200
25

45
34
-24

7.33
7.43
1

50
25
-50

240
350
46

65
52
-20

7.20
7.32
2

62
55
-11

7.25
7.28
0

Yo

Before
After

% A

++

0.5

1000

0.9

850

+++

0.9

850

+++

0.4

900

++

1.o

750

Before
After

10

+++

0.6

950

Before
After

Before
After
% A
Before
After

% A
Before
After
% A
Before
After

%a
% A
70 A

11

+++

0.6

900

Before
After

12

1.0

900

Before
After

Mean

SE

50
35
-30

126
165
31

50
40
-20

7.31
7.43
2

45
45
0

320
390
22

35
31
-11

7.21
7.23
1

Before
After

43
31
-25

132
174
39

60
47
-21

7.24
7.33

Before
After

2
2

6
4

0.03
0.03

70 A
YO

% A

13.4:k

*SE of percent
= change

DISCUSSION

monary disease; 8 patients did. Eight received halothane; two, N,O-0,-narcotic; and
one, spinal anesthesia. After the 12 treatments, only one patient was clinically unimproved.

Most patients were elderly men undergoing major operations. One patient with
breathing difficulties was treated successfully twice. Three patients had no prior pul-

Objectively, isoproterenol consistently

lowered peak PA, raised Pao, and pH, and
lowered Pacoz. These changes were statistically significant at p<0.05. IsoproterenoI

percent increase, 39 ( k 13.4) was derived

from the percent increase in Pao, for each
patient.

786

ANESTHESIAAND ANALGESIA
. . . Current Researches VOL.54, NO.6, Nov.-DEc., 1975

use was not associated with cardiac arrhythmias, tachycardia, or significant changes in
blood pressure. In the recovery room, all
patients were observed carefully for 4 hours,
and no bronchospasm developed except in
one patient who had aspirated.
Few investigations have related blood-gas
changes to bronchospasm and bronchodilator therapy during anesthesia.3.l-l In status
asthmaticus, halothane anesthesia is clinically beneficial, without changes in blood
gases and pulmonary mechanics.3 In conscious asthmatic patients, isoproterenol and
other bronchodilators make patients feel
better and improve their overall breathing
function, but their Pao, worsens because of
a change in venti1ation:perfusion ratios.
However, this may not occur in asthmatics
given high FIO,.~
Isoproterenol helps the bronchospastic
both subjectively and objectively.s This
study is a continuation of this concept, the
primary difference being that anesthetized
patients breathing FIO,Sabove 0.21 were
utilized: most of these patients were not
true asthmatics. The exact mechanism for
relief of bronchospasm by isoproterenol has
not been established on a clinical basis. It
is believed that nebulized isoproterenol is
carried into the airways with spontaneous
or positive pressure breathing, absorbed,
and carried to bronchial smooth muscle.
Subsequently, clinical conditions and blood
gas values improve.1 Opposing evidence
exists indicating that the lungs play a minor
role in the absorption and catabolism of
inhaled isoproterenol.18 The technic described in this investigation represents objective and clinical evidence that bronchospasm under anesthesia may be successfully
treated.

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