Animal Coat Colours (Mainly of Horses and Cattle) Mentioned ...
Apneic oxygenation in anesthetized ponies and horses
-
Upload
independent -
Category
Documents
-
view
2 -
download
0
Transcript of Apneic oxygenation in anesthetized ponies and horses
Veterinary Research Communications, ]1 (1987) 281-291 281 Geo Abstracts Ltd, Norwich - pr in ted in Eng]and
APNEIC OXYGENATION IN ANESTHETIZED PONIES AND HORSES
C. A. BLAZE 1 and N. E. ROBINSON 2
1Department of Large Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, Michigan 48824, U.S.A.
2Departments of Physiology and Large Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, Michigan 48824
ABSTRACT
Blaze, C .A. and Rob inson , N . E . , 1987. Apneic o x y g e n a t i o n in a n e s t h e t i z e d ponies and ho r se s . Ve t e r i na ry Research Communications, 11(3) , 281-291
Apneic oxygenation was studied in six ponies for 30 minutes, and six horses for 10 minutes. Arterial blood was sampled at regular intervals for measure- ment of oxygen and carbon dioxide tensions (PaO 2 and PaCO 2) and calculation of alveolar-arterial oxygen tension difference (PAO2--PaO2). In both groups of animals, PaO 2 decreased rapidly during the first 3 minutes of apnea, then more slowly. Although the mean value was above 100 mmHg at 10 minutes, there was considerable inter-animal variability. Before apnea, PAO2--PaO 2 was slightly, but not significantly, larger in horses than in ponies and increased in both groups during the first 3 minutes of apnea, after which the increase was slower. There was no significant difference between ponies and horses up to 10 minutes, suggesting that PAO2--PaO 2 is independent of body size. In ponies, the PAO 2- PaO 2 did not change significantly between 10 and 30 minutes. Final PaO 2 could not be correlated with initial PaO 2 or initial PAO2--PaO 2. The rate of rise of PAO2--PaO 2 could not be predicted from baseline values. The rate of rise of PaCO 2 was similar and fairly constant in ponies and horses, and did not con- tribute to the rapid initial decrease in PaO 2. It appears that apneic oxygena- tion should not be used in the equine species, since it is impossible to predict in which animals the technique is safe for more than a few minutes.
INTRODUCTION
Apneic oxygenation means the oxygenation of arterial blood by flow of
oxygen down the trachea. Prerequisites for oxygenation of greater than a few
minutes duration are replacement of alveolar nitrogen with oxygen before apnea,
an unobstructed airway, oxygen as the ambient gas rather than room air, and
an adequate circulation.
Apneic oxygenation is not a new concept, having been studied extensively
by Draper and Whitehead (1944, 1949) and Draper et ai. (1949) in dogs, and by
Holmdahl (1956) in dogs and rabbits. Other workers studied the technique in
cats (Tenney, 1956), and in man (Enghoff et al., 1951; Frumin et al., 1959).
In humans, the technique has been used for procedures such as bronchoscopy,
but no reports could be found of its use in the equine species.
0165-7380/87/S03.50 (~) 1987 Geo Abstracts Ltd
282
A common su rg i ca l p r o c e d u r e in the horse is l a ryngotomy, usual ly with v e n -
t r i cu l ec tomy . D u r i n g th i s p r o c e d u r e , which is done in dorsal r e c u m b e n c y , the
e n d o t r a c h e a l t u b e is u s u a l l y removed to allow maximum su rg ica l access to the
l a r y n x . The most i m p o r t a n t problem caused by th i s is a dramatic decrease in a r -
t e r i a l oxygen t e n s i o n , to va lues as low as 35 mmHg (Blaze, pe r sona l obse r va t i on ) .
This s t u d y was d e s i g n e d to assess whether apne ic o x y g e n a t i o n can be used
in the equ ine species to p rov ide adequa te oxyge na t i on of a r t e r i a l blood.
MATERIALS AND METHODS
Six adu l t ponies and six adul t ho r se s , of both sexes and in good h e a l t h ,
were u s e d in th is s t u d y . Ponies weighed from 145 to 186 kg (mean 169 k g ) ,
and ho r se s weighed from 409 to 586 kg (mean 497 k g ) .
Af te r o v e r n i g h t f a s t i n g , ponies were p remedica ted with xy laz ine (0.5 mg / kg
i n t r a v e n o u s l y ) (Rompun , Bayve t Labora to r i e s , Shawnee, K a n s a s ) , the j u g u l a r
ve in was c a t h e t e r i z e d , and anes the s i a was i n d u c e d with a g iyce ry l gua iaco la te -
(Gecola te , Summit Hill Labora to r ies , Avalon, New Je r sey ) th iamyl (Biotal , Bio-
Ceut ic Labora to r i e s , St . Joseph , Missouri) m i x t u r e g iven i n t r a v e n o u s l y to effect .
Af te r i n t u b a t i o n with a cuf fed endo t r achea l t u b e , ponies b r e a t h e d 100% O 2
t h r o u g h a demand va lve (Hudson demand t u b e va lve , Model 5040, Hudson Oxygen
T h e r a p y Sales, Wadsworth, Ohio) , and a n e s t h e s i a was main ta ined with i n c r e m e n -
tal bo lus i n j ec t ions of the g l y c e r y l gu ia iaco la te - th iamyla l mix tu re . A p e r i p h e r a l
a r t e r y was c a t h e t e r i z e d and the c a t h e t e r c o n n e c t e d to an ane ro id manometer via
an e x t e n s i o n se t , and ponies were placed in dorsa l r e c u m b e n c y in a padded
V - t r o u g h .
A small a rea o f the v e n t r a l neck , j u s t a n t e r i o r to the thorac ic in le t , was
c l ipped and s c r u b b e d . A 10 gauge , 4 - inch needle was i n s e r t e d t h r o u g h the
sk in , be tween t r achea l r i n g s and into the t r achea l lumen. The e n d o t r a e h e a l
t u b e was s l i gh t l y moved a n t e r i o r l y so tha t the needle lumen was not o b s t r u c t e d .
The e x t e r n a l end of the needle was sealed with a 3-way s topcock and c onne c t e d
to r u b b e r t u b i n g which would d e l i v e r o x y g e n to the t r achea once apnea was i n -
duced . This s t age of p r e p a r a t i o n was u sua l l y completed within 45 minu tes of
i n d u c t i o n . Heart and r e s p i r a t o r y ra tes were r e c o r d e d , as well as mean a r t e r i a l
blood p r e s s u r e i n d i c a t e d by the ane ro id manometer . Body t e m p e r a t u r e was
measu red rec ta l ly with a cl inical m e r c u r y the rmomete r . When a n e s t h e t i c dep th
was j u d g e d to be adequa t e acco rd ing to accep ted methods of c h e c k i n g pa l pe b r a l
r e f l exes a n d v i ta l s i g n s , manual ven t i l a t ion was b e g u n by p r e s s i n g the b u t t o n
on the demand va lve to in f la te the l u n g s . The ponies were g iven at leas t I0
l a rge b r e a t h s , at approx imate ly 4 - second i n t e r v a l s , and a base l ine a r t e r i a l blood
sample was anaerob ica l ly d rawn from the a r t e r i a l c a t he t e r , sealed, and placed on
an ice s l u s h .
283
Succinylcholine chloride (Succostrin HP, E.R. Squibb and Sons, Inc.,
Princeton, New Jersey) (0.1 mg/kg intravenously) was injected and an infusion
of succinyleholine chloride begun immediately at 2.2 mg/kg/hr while manual
ventilation was continued. When muscle fasciculation ceased, manual ventilation
was stopped, an arterial blood sample was drawn, and simultaneously the 3-way
stopcock on the tracheal needle was turned to allow oxygen to flow into the
trachea at 2 I/min. The demand valve was removed from the endotracheal tube
to p r o v i d e an o p e n a i r w a y for t h e e s c a p e of e x c e s s g a s .
A r t e r i a l b lood s amp le s for b lood gas a n a l y s i s were d r a w n at 1," 2, 3, 4, a n d
5 m i n u t e s a f t e r t h e o n s e t of a p n e a , a n d t h e n e v e r y 5 m i n u t e s up to a n d i n -
c l u d i n g 30 m i n u t e s . The a n a e r o b i c a l l y d r a w n s amp le s were s e a l e d a n d p l a c e d on
ice u n t i l a n a l y z e d . D u r i n g a p n e a , i n c r e m e n t a l d o s e s of t h e a n e s t h e t i c m i x t u r e
were g i v e n , c o r r e s p o n d i n g to t h e r e q u i r e m e n t s of t h e p o n y b e f o r e a p n e a , a n d
v i t a l s i g n s were m o n i t o r e d . The s u c c i n y l c h o l i n e i n f u s i o n was t e r m i n a t e d at
a b o u t t h e 28 th m i n u t e . At 30 m i n u t e s , t h e d e m a n d v a l v e was r e p l a c e d on t h e
e n d of t h e e n d o t r a c h e a l t u b e , a n d t h e l u n g s were i n f l a t e d s e v e r a l t imes wi th
o x y g e n . S i m u l t a n e o u s l y , t h e 3 -way s t o p c o c k was t u r n e d to seal t h e e x t e r n a l
e n d of t h e t r a c h e a l n e e d l e . Mechan ica l v e n t i l a t i o n c o n t i n u e d u n t i l s p o n t a n e o u s
v e n t i l a t i o n r e s u m e d , u s u a l l y w i th in 4 to 5 m i n u t e s of t e r m i n a t i o n of t h e s u c c i n y l -
cho l ine i n f u s i o n .
H o r s e s were f a s t e d o v e r n i g h t , p r e m e d i c a t e d wi th x y l a z i n e (0.44 m g / k g i n t r a -
v e n o u s l y ) , a n d a n e s t h e s i a was i n d u c e d i n t r a v e n o u s l y wi th a g l y c e r y l g u a i a c o l a t e -
t h i amy la l m i x t u r e to e f f e c t . A c u f f e d e n d o t r a c h e a l t u b e was p l a c e d in t h e
t r a c h e a , a n d m e c h a n i c a l v e n t i l a t i o n was b e g u n wi th a h a l o t h a n e - ( H a l o t h a n e USP,
H a l o c a r b o n L a b o r a t o r i e s , H a c k e n s a c k , New J e r s e y ) o x y g e n m i x t u r e . A p e r i p h -
e r a l a r t e r y was c a t h e t e r i z e d a n d v i t a l s i g n s were m o n i t o r e d . H o r s e s we re p l a c e d
in d o r s a l r e c u m b e n c y a n d were v e n t i l a t e d for a minimum of 48 m i n u t e s b e f o r e
a p n e a was i n d u c e d .
A 1.5 cm d i a m e t e r p l a s t i c t u b e was p l a c e d a g a i n s t t h e n e c k , wi th one e n d at
t h e l eve l of t h e t h o r a c i c i n l e t , a n d a m a r k was made on t h e t u b e to c o r r e s p o n d
wi th t h e l eve l of t h e i n c i s o r t e e t h . Th i s t u b e would be u s e d l a t e r to d e l i v e r
o x y g e n to t h e h o r s e d u r i n g a p n e a . When a n e s t h e t i c d e p t h was s t a b i l i z e d , a
b a s e l i n e a r t e r i a l b lood sample was d r a w n .
S u c c i n y l c h o l i n e c h l o r i d e (0 .1 m g / k g i n t r a v e n o u s l y ) was i n j e c t e d a n d an i n -
f u s i o n of t h i s d r u g b e g a n at 2.2 m g / k g / h r . Mechan ica l v e n t i l a t i o n c o n t i n u e d ,
a n d at t h e time when musc le f a s c i c u l a t i o n s c e a s e d , an a r t e r i a l b lood sample was
d r a w n , v e n t i l a t i o n was s t o p p e d , a n d t h e p r e m a r k e d p l a s t i c t u b e wi th o x y g e n
f lowing t h r o u g h i t a t 15 I / ra in , was q u i c k l y i n s e r t e d i n t o t h e e n d o t r a c h e a l t u b e .
A r t e r i a l b lood samples were d r a w n at t h e same t ime i n t e r v a l s as in t h e p o n i e s .
The s u c c i n y l c h o l i n e i n f u s i o n was s t o p p e d a t l0 m i n u t e s , t h e p l a s t i c t u b e
284
c a r r y i n g 0 2 was removed from the e n d o t r a e h e a l t u b e , and manual ven t i l a t i on
was r e s u m e d . All samples were ana lyzed wi th in an hour . Blood gas va lues
were c o r r e c t e d to body t e m p e r a t u r e . Alveolar o x y g e n t ens ion (PAO 2) was ca l -
c u l a t e d from the formula . PAO 2 = [(PB--PH2 O) x FIO2--PaCO2], where PB is ba r o -
metr ic p r e s s u r e , PH20 is s a tu r a t ed vapor p r e s s u r e of water, FIO 2 is f rac t iona l con-
e e n t r a t i o n of i n s p i r e d o x y g e n and PaCO 2 is a r t e r i a l ca rbon dioxide t e n s i o n .
A l v e o l a r - a r t e r i a l o x y g e n t ens ion d i f fe rence (PAO2--PaO 2) was t hen de t e r mi ne d .
Data were ana lyzed by factor ia l ana ly s i s of va r i a nc e . When s i gn i f i c a n t F
va lues were o b t a i n e d , factor means were compared u s i n g T u k e y ' s ~ s t a t i s t i c .
RESULTS
F i g u r e s 1 and 2 i l l u s t r a t e the changes in a r t e r i a l oxygen and c a r b o n dioxide
t e n s i o n s in ponies and h o r s e s , r e s p e c t i v e l y . Ar t e r i a l oxygen t ens ion dec reased
PONIES
• P o 0 2 30O
,oor l . . . * * "10 so~'w~PaCOz I I i i 0 5 I0
Minutes
40
HORSES 400 '1
( 300
"6
~ 2 0 0 "
~o~
0 5 K) Minutes
~50
40
O
ZO
Io
Fig. I . Changes in a r t e r i a l o x y g e n a n d c a r b o n dioxide t e n s i o n s d u r i n g 10 minu tes of apne ic o x y g e n a t i o n in pon ies .
Fig. 2. Changes in a r t e r i a l o x y g e n and c a r b o n dioxide t e n s i o n s d u r i n g I0 minu tes of apne ic oxyge na t i on in ho r se s .
r a p i d l y in bo th pon ies and hor ses d u r i n g the f i r s t 3 minu tes , t h e n dec reased
more slowly up to l0 minu t e s . Al though the mean value was above 100 mmHg in
both g r o u p s of animals at l0 minu tes of apnea , t he r e was c o n s i d e r a b l e i n t e r -
animal v a r i a b i l i t y . The lowest va lues of PaO 2 were 76.1 mmHg and 53.7 mmHg
i n pon ies and in h o r s e s , r e s p e c t i v e l y . In pon ies , c a rbon dioxide t e n s i o n i n -
c r e a s e d at a r a t e of 5.31_+0.31 mmHg/min d u r i n g the f i r s t l0 minu tes of apnea .
I n h o r s e s , the r a t e of i n c r e a s e was 5.46+_0.64 mmHg/min. The h i g h e s t value of
PaCO 2 a f t e r l0 minu tes was 98.5 mmHg in a p o n y a nd 106.4 mmHg in a ho r se .
Ca rbon dioxide t e n s i o n i n c r e a s e d more slowly d u r i n g the r e m a i n i n g 20 minutes
(3.67_+0.25 mmHg/min) . The mean va lue of PaCO 2 at 30 minutes was 146.6-+7.4 mmHg,
285
The decrease in pH was similar in both groups of animals; pH averaging 7.15_ +
0.01 and 7.19+0.03 at 10 minutes in ponies and horses, respectively. Mean pH
of ponies at 30 minutes of apnea was 6.99_+0.02. Table 1 shows blood gas values
and alveolar-arterial oxygen tension difference in ponies during 30 minutes of
apnea. Table 2 shows acid base status, and oxyhemoglobin saturation in horses
during 10 minutes of apneic oxygenation.
F igu re s 3 and 4 i l l u s t r a t e the a l v e o l a r - a r t e r i a l o x y g e n t e n s i on d i f f e r ences
d u r i n g 10 minu te s of apnea in ponies and h o r s e s . A l though the PAO2--PaO 2
before apnea was s l i gh t l y l a r g e r in ho r ses t han in pon ies , the d i f f e r ence was not
s i g n i f i c a n t . The re was a r ap id i n c r e a s e in PAO2-PaO 2 d u r i n g the f i r s t 3 minu tes
in both g r o u p s , and the PAO2-PaO 2 t hen i n c r e a s e d more slowly a f t e r 3 minu t e s .
At no time up to 10 minu tes was t he r e a s i gn i f i c a n t d i f f e rence in PAO2-PaO 2 be -
tween ponies and h o r s e s . PAO2-PaO 2 in ponies r emained c o n s t a n t be tween 10
and 30 minu t e s .
DISCUSSION
This study suggests that it is not possible to maintain acceptable blood
gases for more than a few minutes in anesthetized ponies and horses using the
technique of apneic oxygenation. The mean arterial oxygen tension remained
above 100 mmHg for 10 minutes in both ponies and horses. There was, however,
a great deal of inter-animal variability in the PaO 2 after 10 minutes of apnea. In
3 of 6 horses, PaO 2 was less than 70 mmHg at I0 minutes. This variability was
also apparent in ponies, one having a PaO 2 of 107.8 mmHg at 10 minutes, from a
baseline value of 443.2 mmHg, and another having a PaO 2 of 188.7 mmHg at 10
minutes, from a baseline value of 332.7 mmHg, PaO 2 values lower than 70 mmHg
were seen in one horse at 3 minutes of apnea, and in one pony at 15 minutes of
apnea, The lowest value of PaO 2 in a pony was 66.6 mmHg at 20 minutes of
apnea, suggesting that apneic oxygenation may be useful for periods up to 15
minutes in some ponies. However, pH at this time was 7.039 and PaCO 2 was
122.6 mmHg. This great variability in PaO 2 between animals makes lhe technique
of apneic oxygenation unsuitable for routine use.
Because the increase in PaCO 2 was similar and fairly constant in both ponies
and horses, the magnitude of hypoxemia was not determined primarily by the rate
of carbon dioxide accumulation in the alveoli. The primary determinant of the
degree of hypoxemia was the initial PAO2-PaO 2, and its rate of increase. In
both ponies and horses, the rate of increase was rapid during the first 3 minutes,
then became slower after that time. The PAO2-PaO 2 actually decreased slowly
from 15 to 30 minutes, although this decrease was not significant. The initial
PA02-PaO2 was slightly, but insignificantly, larger in, horses than in ponies,
but the rate of increase was similar in both groups, suggesting that this
286
The dec rease in pH was similar in both g r o u p s of animals ; pH a v e r a g i n g 7 .15- +
0.01 and 7.19-+0.03 at 10 minutes in ponies and ho r se s , r e s p e c t i v e l y . Mean pH
of pon ies at 30 minu tes of apnea was 6.99-+0.02. Table 1 shows blood gas va lues
a n d a l v e o l a r - a r t e r i a l o x y g e n t e n s i o n d i f fe rence in ponies d u r i n g 30 minu tes of
apnea . Table 2 shows acid base s t a t u s , and oxyhemoglobin s a tu r a t i on in horses
d u r i n g 10 minu tes of apne ic o x y g e n a t i o n .
F i g u r e s 3 and 4 i l l u s t r a t e the a l v e o l a r - a r t e r i a l o x y g e n t ens ion d i f f e rences
d u r i n g 10 minu tes of apnea in ponies and h o r s e s . Al though the PAO2-PaO 2
before apnea was s l i gh t l y l a r g e r in horses t h a n in pon ies , the d i f f e rence was
not s i g n i f i c a n t . The re was a r ap id i nc r ea se in PAO2-PaO 2 d u r i n g the f i r s t 3
minu tes in both g r o u p s , and the PAO2-PaO 2 t h e n i n c r e a s e d more slowly a f te r 3
m i n u t e s . At no time up to 10 minutes was the re a s ign i f i can t d i f fe rence in
PAO2-PaO 2 be tween pon ies and ho r se s . PAO2-PaO 2 in ponies remained c o n s t a n t
between i0 and 30 minutes.
DISCUSSION
This s t u d y s u g g e s t s tha t it is not poss ib le to mainta in acceptab le blood
gases for more t han a few minutes in a n e s t h e t i z e d ponies and horses u s i n g the
t e c h n i q u e of apne ic o x y g e n a t i o n . The mean a r t e r i a l oxygen t ens ion remained
above 100 mmHg for 10 minu tes in both ponies a nd ho r se s . The r e was, how-
e v e r , a g rea t deal of i n t e r - a n i m a l va r i ab i l i t y in the PaO 2 a f te r 10 minu tes of
apnea . In 3 of 6 h o r s e s , PaO 2 was less t h a n 70 mmHg at 10 minu te s . This
v a r i a b i l i t y was also a p p a r e n t in ponies , one h a v i n g a PaO 2 of 107.8 mmHg at 10
m i n u t e s , from a base l ine va lue of 443.2 mmHg, and a n o t h e r h a v i n g a PaO 2 of
188.7 mmHg at 10 m i n u t e s , from a base l ine va lue of 332.7 mmHg. PaO 2 va lues
lower t h a n 70 mmHg were seen in one horse at 3 minu tes of apnea , a nd in one
pony a t 15 min tues of apnea . The lowest va lue of PaO 2 in a pony was 66.6
mmHg at 20 minu tes of apnea , s u g g e s t i n g tha t apneic oxyge na t i on may be use fu l
for pe r iods up to 15 minu tes i n some p ° n i e s . However, pH at th is time was
7.039 and PaCO 2 was 122.6 mmHg. This g rea t va r i ab i l i t y in PaO 2 be tween
animals makes the t e c h n i q u e of apneic o x y g e n a t i o n u n s u i t a b l e for r o u t i n e use .
Because the i n c r e a s e in PaCO 2 was similar and fa i r ly c o n s t a n t in both
pon ies a n d h o r s e s , the magn i tude of hypoxemia was de te rmined by the
ra t e of i n c r e a s e of PAO2-PaO 2, and not p r i m a r i l y by the ra te of ca rbon
d i o x i d e accumula t ion i n the a lveol i . In both ponies and ho r se s , t h e
r a t e of i n c r e a s e was r ap id d u r i n g the f i r s t 3 m i n u t e s , t h e n b e c a m e
s lower a f t e r tha t t ime. The PAO2-PaO 2 a c t u a l l y d e c r e a s e d s l o w l y f r o m
15 to 30 m i n u t e s , a l t h o u g h th i s decrease was not s ign i f i can t . The i n i t i a l
PAO2-PaO2 was s l i gh t ly , bu t i n s i g n i f i c a n t l y , l a r g e r in ho r ses t h a n in pon ies ,
bu t the r a t e of i n c r e a s e was s imilar in both g r o u p s , s u g g e s t i n g t h a t t h i s
TA
BL
E
1
Blo
od
gas
va
lue
s,
an
d a
lve
ola
r-a
rte
ria
l o
xy
ge
n t
en
sio
n g
rad
ien
ts d
uri
ng
30
min
ute
s o
f ap
neic
ox
yg
en
ati
on
in
si
x
po
nie
s.
(Mea
n
_+ S
.E.)
Tim
e in
M
inu
tes
Aft
er
Ind
uc
tio
n o
f A
pn
ea
0
5
10
15
20
25
30
PaO
2 m
mH
g
381.3
+_18.0
1
83
.4+
_2
6.9
"
120.4
+_19.8
*
93.6
-+11.5
*
84
.0+
9.8
*
82.5
-+7.1
*
84.7
-+5.3
*
% S
AT
. 9
9.8
+-0
.02
9
7.7
+-1
.26
9
3.8
+1
.72
" 8
9.6
+-2
.36
*
85
.5+
-3.1
9"
85
.2_
+2
.35
*
85
.6+
1.8
9.
PA
O2
-PaO
2 m
mH
g
29
5.6
-+1
6.9
4
53
.3+
-26
.8*
489.3
-+19.7
*
51
6.0
+-1
2.8
" 5
10
.2+
-12
.7"
501.0
+10.2
*
482.0
_+
II.0
*
pH
7
.49
+-0
.03
7
.26
+_
0.0
1"
7
.15
+_
0.0
1"
7
.10
+_
0.0
1"
7
.05
_+
0.0
2
*
7.0
2+
_0
.01
" 6
.99
+0
.02
*
PaC
O 2
mm
Hg
36
.4+
_2
.6
69.8
+3.5
*
89.5
+3.1
*
103.7
+3.8
*
119.2
+4.1
*
130.0
+4.3
*
14
6.6
+7
.4"
HC
O 3
- m
Eq/L
2
7.7
+-0
.6
29
.2_
+1
.0"
29.1
+-0
.8"
29
.7+
_0
.7
*
30.5
+-0
.8*
30
.8+
_1
.0"
32
.3_
+1
.2
*
B.E
. m
Eq/L
4
.0+
1.0
1
.5_
+0
.7
0.0
2+
0.7
*
-1.7
+1
.2"
-1.9
-+0
.6"
-2.1
+-1
.3"
-2.1
_+
1.5
*
PaO
2
PaC
O 2
PA
O 2
- P
aO 2
% S
AT
.
HC
O 3
-
B.E
.
= a
rte
ria
l o
xy
gen
te
nsi
on
.
-- a
rte
ria
l c
arb
on
dio
xid
e t
en
sio
n.
= a
lve
ola
r-a
rte
ria
l o
xy
ge
n d
iffe
ren
ce
.
= p
er
ce
nt
sa
tura
tio
n o
f h
em
og
lob
in.
= s
eru
m b
ica
rbo
na
te.
= b
ase
e
xc
ess
.
= i
nd
ica
tes
sig
nif
ica
nt
dif
fere
nc
e f
rom
b
ase
lin
e v
alu
es.
CO
288
g r a d i e n t is i n d e p e n d e n t of body size. The f inal PaO 2 was not co r re l a t ed with
the in i t i a l PAO2-PaO 2, or with the in i t ia l PaO 2, making it impossible to p red i c t
in which ho r se s apne ic o x y g e n a t i o n can be u sed safe ly .
TABLE 2
Acid-base status, and oxyhemoglobin saturation, during minutes of apneic oxygenation in six horses (mean ± S.E.)
Time in minu tes a f te r i n d u c t i o n of apnea
0 5 i0
pH 7.51±0.03 7.25±0.03* 7.19±0.03"
HCO 3 25.0±0.63 29.9±0.79* 30.9±0.83*
BE 2.45±0.60 1.56±0.88 0.5±0.01"
% S a t u r a t i o n 99.8±0.06 93.1±2.41" 89.4±3.02*
* Ind ica te s s i g n i f i c a n t l y d i f f e r en t from base l ine va lue .
It was e x p e c t e d tha t the ra te of i n c r e a s e of PAO2-PaO 2 would be c ons i s -
t e n t l y g r e a t e d in ho r se s t han in pon ies , l e ad ing to a more r a p i d deve lopment of
hypoxemia . It is known tha t a l a rge PAO2-PaO 2 g r a d i e n t develops soon a f te r
i n d u c t i o n in ho r ses and remains fa i r ly c o n s t a n t d u r i n g a n e s t h e s i a , whether
ven t i l a t i on is s p o n t a n e o u s or con t ro l led (Hall et a l . , 1968; Gillespie et a l . , 1969;
Hall, 1971). Recumbency alone can cause a PAO2-PaO 2 g r a d i e n t to develop in
pon ie s , e v e n when u n a n e s t h e t i z e d (Hall, 1984). It was expec t ed tha t func t iona l
r e s i d u a l capac i ty would dec rease more r ap id ly and tha t ven t i l a t ion pe r f u s i on
600
5OO I
E E 400
50(~
PONIES
I I 0 5 I0
M inutes
80 600-
"tO
0
50
40
500- :I: "5
4 0 0 -
I 0 5
Minutes
HORSES
IO
30
"tO
6O "O o
50
40
Fig. 3. A l v e o l a r - a r t e r i a l o x y g e n t en s ion d i f f e r e n c e dur ing 10 minu tes of apne ic o x y g e n a t i o n in pon ies .
Fig. 4. A lveo l a r - a r t e r i a l o x y g e n tens ion d i f ference d u r i n g I0 minutes of apne ic oxyge na t i on in ho r se s .
289
inequalities would be greater in larger and heavier horses. There was consid-
erable variability in the rate of increase of the PAO2-PaO 2 gradient and in the
baseline PAO2-PaO 2 within each group of animals. The rate of rise of PAO 2-
PaO 2 could not be predicted from the baseline value.
An important determinant of the duration of apnea before gross hypoxemia
occurs is the composition of the alveolar gas. If alveoli are filled with air,
alveolar PO 2 decreases rapidly towards the mixed venous PO 2, which itself is
declining continuously as the PaO 2 decreases. Gross hyp0xia and hypoxemia
occur in about 90 seconds. However, when the lungs are ventilated with oxygen
for periods greater than 30 minutes before apnea is induced, most of the nitro-
gen is eliminated from the body, and PAO 2 does not reach inadequate levels for
a longer period. When oxygen diffusing across the alveolar capillary membrane
is being replaced constantly by a stream of oxygen flowing down the trachea,
no nitrogen is added to the alveoli from the ambient gas, and PAO 2 decreases
only as fast as the PACO 2 increases. This greatly prolongs the duration of
apnea before gross hypoxia develops. The deficiency of nitrogen in the alveoli
tends to increase the likelihood of alveolar collapse, which may contribute to the
rapid increase in PAO2-PaO 2 gradient which occurred in this study.
The mean increase in PaCO2.during I0 minutes was 5.31+_0.31 mmHg/min in
ponies and 5.34_+0.64 mmHg/min in horses, which compares well with values re-
ported by Hubbell and Muir (1985) during several minutes of apnea after con-
trolled ventilation. This slow and steady rise results from the rate of pro-
duction of CO 2 and the capacity of the body stores (Nahas and Verosky, 1966;
Nunn, 1969). Although the decrease in pH associated with hypercarbia would
displace the oxyhemoglobin dissociation curve to the right (Bohr effect), this
should not compromise oxygen delivery to the tissues. Even at a pH of 7.19,
hemoglobin in arterial blood was still 89.4% saturated in horses, and the lowest
degree of arterial hemoglobin saturation in ponies was 85.2% at a pH of 7.02.
The Bohr effect of acidosis facilitates the delivery of oxygen to the tissues.
The increase in cardiac output that is normally associated with hypercarbia
should also improve perfusion of the tissues and increase oxygen delivery.
Therefore, apneic oxygenation should not compromise tissue oxygen delivery.
Flow rates of 0 2 into the trachea during apnea were set at 2 1/min for
ponies and 15 I/min for horses, which were adequate for the metabolic 0 2 re-
quirement, which Thomas (1981) reported as 2.2-+0.3 ml/kg/min in horses and
Parks (1983) reported as 9.2+-1 ml/kg/min in ponies. The flow rate for ponies
was set to exceed metabolic 0 2 requirement. The flow rate in horses was that
which is generally recommended for oxygen insufflation during recovery from
general anesthesia.
290
A major p rob lem with apne ic o x y g e n is the r e t e n t i o n of CO 2 a n d p r o -
g r e s s i v e r e s p i r a t o r y a c i d o s i s . The mean PaCO 2 of 86.6 mmHg o b s e r v e d in
h o r s e s at 10 minu te s of a p n e a would no t be u n u s u a l in t hose a n e s t h e t i z e d and
b r e a t h i n g s p o n t a n e o u s l y . However , h y p e r c a r b i a may c o n t r i b u t e to a r r h y t h m i a ,
especially during halothane anesthesia (Eberly et al., 1968). Even though mean
oxygenation in ponies was adequate at 30 minutes (84.6 mmHg), the concomitant
hypercarbia and possibility of severe arrhythmia may be the limiting factor to
the safe duration of apnea. The narcotic effect of high CO 2 in horses is not
known, but it is possible that in ponies, where the mean PaCO 2 was above
90 mmHg at 15 minutes of apnea, the requirement for anesthetic agent may have
been considerably reduced.
Apnea was maintained in both groups of animals by infusion of succinyl-
choline. A previous report (Hildebrand and Hewitt, 1983) has demonstrated a
rise in body temperature and metabolic acidosis associated with succinylcholine
infusion in ponies. These changes were not observed in this study.
ACKNOWLEDGMENTS
The a u t h o r s wish to t h a n k Dr . A. O r t e n b u r g e r , Dr . D. Daun t , and
Mr. S. Ba i ley for t h e i r a s s i s t a n c e . Th is s t u d y was f u n d e d b y the A g r i c u l t u r a l
E x p e r i m e n t S t a t i on of Michigan S ta te U n i v e r s i t y .
REFERENCES
DeMoor, A., Desmet, P. and Verschooten, F., 1974. Influence of change of body position on arterial oxygenation and acid base status in the horse in l a t e r a l r e c u m b e n c y a n a e s t h e t i z e d with ha lo thane and e f f i c i ency of p o s t - a n a e s t h e t i c o x y g e n . Zen tb l . V e t . . M e d . , 21A: 525-531.
D r a p e r , W.B. a n d Whi tehead , R . W . , 1944. Dif fus ion r e s p i r a t i o n in t he d o g a n e s t h e t i z e d b y p e n t o t h a l sod ium. A n e s t h e s i o l o g y , 5: 262-273.
D r a p e r , W.B. and Whi tehead , R . W . , 1949. The phenomenon of d i f fu s ion r e s p i r a t i o n . A n e s t h . A n a l g . , 28: 307-318.
D r a p e r , W . B . , Whi tehead , R . W . , S p e n c e r , J . N . , B e s h o r e , D . L . G . a n d P a r r y , T . M . , 1947. S tud i e s on d i f fu s ion r e s p i r a t i o n : I l l . A lveo la r g a s e s and v e n o u s b lood pH o f dogs d u r i n g d i f fu s ion r e s p i r a t i o n . A n e s t h e s i o l o g y , 8: 524-533.
E b e r l y , V . E . , G i l l e sp ie , J . R . , T y l e r , W.S. and Fowler , M.E . , 1968. Ca rd io - v a s c u l a r v a l u e s in t he h o r s e d u r i n g ha l0 thane a n e s t h e s i a . Am. J . Vet . R e s . , 29: 305-314.
E n g h o f f , H . , Holmdahl , M.H. and Risholm, L . , 1951. Dif fus ion r e s p i r a t i o n in man. N a t u r e , 168: 830.
F ra io l i , R . L . , S h e f f e r , L . A . and S t e f f e n s o n , J . L . , 1973. Pu lmonary and c a r d i o v a s c u l a r e f f e c t s of apne ic o x y g e n a t i o n in man. A n e s t h e s i o l o g y 39: 588-596.
F r u m i n , M . J . , E p s t e i n , R.M. and Cohen , G . , 1959. Apne ic o x y g e n a t i o n in m a n . A n e s t h e s i o l o g y , 20: 789-798.
G i l l e sp ie , J . R . , T y l e r , W.S. an'd Hall, L . W . , 1969. Card iopu lmonary d y s f u n c t i o n in a n e s t h e t i z e d , l a t e r a l l y r e c u m b e n t h o r s e s . Am, J . Vet. R e s . , 30: 61-72.
Hall, L . W . , 1971. D i s t u r b a n c e s of c a r d i o p u l m o n a r y func t ion in a n a e s t h e t i z e d h o r s e s . Equ ine Vet . J . , 3: 95-98.
291
Hall, L . W . , 1984. C a r d i o v a s c u l a r and p u l m o n a r y e f f e c t s of r e c u m b e n c y in two consc ious p o n i e s . Equ ine Vet . J . , 16: 89-92.
Hall, L .W. , Gi l l e sp ie , J . R . a n d T y l e r , W . S . , 1968. A l v e o l a r - a r t e r i a l o x y g e n t e n s i o n d i f f e r e n c e s in a n a e s t h e t i z e d h o r s e s . Br . J . A n a e s t h . , 40: 560-567.
H i l d e b r a n d , S .V . and Howit t , G . A . , 1983. S u c c i n y l c h o l i n e i n f u s i o n a s s o c i a t e d with h y p e r t h e r m i a in pon i e s a n e s t h e t i z e d with h a l o t h a n e . Am. J. Vet. R e s . , 44: 2280-2284.
Holmdahl , M . H . , 1956. P u l m o n a r y u p t a k e of o x y g e n , a c i d - b a s e metabo l i sm, and c i r c u l a t i o n d u r i n g p r o l o n g e d a p n e a . Ac ta Ch i r . Seand. , (Suppl . 212): 1-128.
Hubbe l l , J . A . E . and Muir , W.W., 1985. Rate of r i s e of a r t e r i a l c a r b o n d iox ide t e n s i o n in the h a l o t h a n e a n e s t h e t i z e d h o r s e . J . Am. Vet . Med. A s s o c . , 186: 374-376.
Lees , P. and T a v e r n o r , W . D . , 1970. I n f l uence of h a l o t h a n e a n d ca t echo l amines on h e a r t r a t e and r h y t h m in t he h o r s e . Br . J . P h a r m a c o l . , 39: 149-159.
Mitchel l , B. a n d L i t t l e j ohn , A . , 1974. The e f fec t of a n a e s t h e s i a and p o s t u r e on the e x c h a n g e of r e s p i r a t o r y g a s e s and on the h e a r t r a t e . Equine Vet . J . , 4: 177-178.
Nahas , G .G. and V e r o s k y , M., 1966. The s t o r a g e of CO 2 d u r i n g apne i c o x y g e n a t i o n . A n n . N.Y. Acad° S c i . , 133: 134-141.
Nunn, J . F . , 1969. A p p l i e d R e s p i r a t o r y P h y s i o l o g y , 2nd Ed i t ion . London , B u t t e r w o r t h s , p p . 358-359.
P a r k s , C.M. and Manohar , M., 1983. D i s t r i b u t i o n of b lood flow d u r i n g mode ra t e and s t r e n u o u s e x e r c i s e in pon ies ( E q u u s c a b a l l u s ) . Am. J . Vet . R e s . , 44: 1861-1866.
Riebold , T . W . , Goble , D .O . and G e i s e r , D . R . , 1982. La rge Animal A n e s t h e s i a , P r i n c i p l e s and T e c h n i q u e s , I s t Ed i t i on . Iowa S ta te U n i v e r s i t y P r e s s , Ames, p p . 17-19.
R u g h , K . S . , G a r n e r , H . E . , Ha t f i e ld , D . G . and H e r r o l d , D . , 1964. A r t e r i a l o x y g e n and c a r b o n d iox ide t e n s i o n s in consc ious l a t e r a l l y r e c u m b e n t p o n i e s . Equine Vet . J . , 16: 185-188.
T e n n e y , S . M . , 1956. Mechanism of h y p e r t e n s i o n d u r i n g d i f f u s i o n r e s p i r a t i o n . A n e s t h e s i o l o g y , 17: 768-776.
Thomas , D . P . and F r e g i n , G . , 1981. C a r d i o r e s p i r a t o r y and metabol ic r e s p o n s e s to t r eadmi l l e x e r c i s e in t he h o r s e . J . App l . P h y s i o l . , 50: 864-868.
Weaver , B . M . Q . and Walley, R . V . , 1975. Vent i l a t ion and c a r d i o v a s c u l a r s t u d i e s d u r i n g mechan ica l c o n t r o l of v e n t i l a t i o n in h o r s e s . Equine Vet . J . , 7: 9-15.