THESIS

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thesis entitled

THE EFFECT OF VENTRICULECTOMY, PROSTHETIC LARYNGOPLASTY,

Date

0-7 639

AND EXERCISE, 0N UPPER AIRWAY FUNCTION IN
HORSES WITH LEFT LARYNGEAL HEMIPLEGIA

presented by

Kristie Karol Shappell

has been accepted towards fulfillment
of the requirements for

Master of Science degreein Large Animal Clinical

 

 

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THE EFFECT OF VENTRICULECTOMY, PROSTHETIC LARYNGOPLASTY AND EXERCISE
ON UPPER AIRWAY FUNCTION IN HORSES
WITH LEFT LARYNGEAL HEMIPLEGIA

By
Kristie Shappell

A THESIS

Submitted to
Michigan State University
in partial fulfillment of the requirements
for the degree of

MASTER OF SCIENCE

Department of Large Animal Clinical Sciences

1987

ABSTRACT

THE EFFECT OF VENTRICULECTOMY, PROSTHETIC LARYNGOPLASTY AND EXCERCISE
ON UPPER AIRWAY FUNCTION IN HORSES
WITH LEFT LARYNGEAL HEMIPLEGIA
BY

Kristie Karol Shappell

The effect of ventriculectomy and prosthetic laryngoplasty on upper airway
flow mechanics and blood gas tensions in exercising horses with left laryngeal
hemiplegia was assessed. Five adult horses were trained to stand, trot (4.5
m/s), and gallop (7.2 m/s) on a treadmill (6.38° incline). Inspiratory and
expiratory airflows (Ylmax: YEmax) were measured using a 14 cm diameter pneumo-
tachograph in a facemask. Inspiratory and expiratory transupper airway
pressures (PuI, Pug) were determined as pressure differences between barometric
and lateral tracheal pressures. Upper airway impedances (21, 25) were defined
as the ratio of peak Pu/V on inspiration or expiration. Blood collected from
exteriorized carotid arteries was analyzed for oxygen and carbon dioxide ten-
sions (Page, Pacoz), pH, hemoglobin content (Rb), and bicarbonate concentration
(HC03'). Heart rate (HR) was determined with a heart rate monitor.
Measurements were made with horses standing, trotting, and galloping before left
recurrent laryngeal neurectomy (LRLN) (baseline), 14 days after LRLN, 30 days
after ventriculectomy, and 14 days following prosthetic laryngoplasty. Results
were analyzed using a two-way analysis of variance with means compared using
Tukey'scu procedure (p < 0.05). Exercise before LRLN increased HR, respiratory
frequency, Yimax» YEmax. Pu}, Pug, Pacoz, and Hb, decreased Paoz, HC03' and pH,
and did not change ZI and Z5. After LRLN, Pu1 and 21 during exercise were
greater than baseline measurements. Ventriculectomy failed to improve upper
airway flow mechanics induced by LRLN, while prosthetic laryngoplasty was suc-

cessful in restoring upper airway flow mechanics to baseline values.

DEDICATION

To my Mom and Dad, June L. and Harry N.
Shappell, and to my main squeeze Randy
J. Krainock for their belief in my
abilities, support of my goals, and
their marvelous sense of humor and
perspective.

ACKNOWLEDGEMENTS

Dr. Frederik J. Derksen has shown me that quality research is neither
quick nor easy, but can be intellectually stimulating and physically exhilar-
ating. He has encouraged me to strive for a balance between my professional
and personal growth. He has been my mentor and friend and I will fondly
remember our conversations in which he was supportive and compassionate when I
experienced disappointment or frustration during my residency. I look forward
to continued exchanges.

Dr. John A. Stick has patiently provided surgical instruction, pertinent
both to my thesis research and clinic case management. He has been essential
in my development as a surgical resident, providing a forum for discussion of
case management, surgical technique and post operative care. Additionally,
his suggestions for surviving a long distance relationship were appreciated.

Dr. N. Edward Robinson has guided me towards critical evaluation and
interpretation of data emphasizing pertinenet physiology. His enthusiasm for
research was infectious and I enjoyed and appreciated our exchange of ideas
concerning the final manuscript of my thesis.

Additionally, Dr. Curtis Probst for his participation as a member of my
committee, and Doctors Christopher Brown, Frank Nickels and Edward Scott for
their instruction and guidance throughout my residency.

To these, my friends, thank you!

TABLE OF CONTENTS

Page
LIST OF TABLES iv
LIST OF FIGURES v
CHAPTER
I. INTRODUCTION 1
II. GENERAL LITERATURE REVIEW OF LARYNGEAL HEMIPLEGIA 2
A. Historical Perspective
8. Anatomy, Etiology and-Pathology
C. Diagnosis
D. Treatment
111. PRINCIPLES OF UPPER AIRWAY FLOW MECHANICS 15
IV. REVIEW OF ARTERIAL BLOOD GAS TENSIONS IN EXERCISING HORSES 20
V. EFFECT OF VENTRICULECTOMY PROSTHETIC LARYNGOPLASTY AND EXERCISE 23
ON UPPER AIRWAY FUNCTION IN EXERCISING HORSES WITH LEFT LARYNGEAL
HEMIPLEGIA
A. Materials and Methods
B. Results
C. Discussion
VI. SUMMARY AND CONCLUSIONS 47

LIST OF REFERENCES 49

LIST OF TABLES

Page
Effects of exercise on upper airway flow mechanics values, 27
blood gas tensions, and acid base parameters in five horses
before surgical intervention.
The effects of exercise on arterial oxygen and carbon dioxide 46

tensions following correction for arterial blood temperature (A)
or rectal temperature (R). *. -

iv

Figure

3a.

3b.

4a.

4b.

5a.

5b.

LIST OF FIGURES

Page

Schematic representation of Bernoulli's effect creating dynamic 18
collapse of a narrowed airway. Velocity of airflow, V1, increases

to V2 in the narrowed portion of the airway. Concurrently, the
intraluminal pressure, P1, decreases to P2 in the narrowed part of
the airway allowing collapse at that point.

Schematic representation of the face mask with the 14 cm diameter 24
pneumotachograph (A) and flow straightener element (B). Sites for
measurement of lateral tracheal pressure (PT) and mask pressure

(Pm)-

Inspiratory impedance at three levels of exercise before and after 29
surgical intervention. The asterisk (*) indicates the value is-
significantly different from baseline (before surgical intervention)

Expiratory impedance at three levels of exercise before and after 30
surgical intervention.

Peak transupper airway inspiratory pressure at three levels of exer- 31
cise before and after surgical intervention. The asterisk (*) indi-
cates the value is significantly different form baseline (before
surgical intervention).

Peak transupper airway expiratory pressure at three levels of exer- 32
cise before and after surgical intervention. The asterisk (*) indi-
cates the value is significantly different from baseline (before
surgical intervention).

Maximal inspiratory flow at three levels of exercise before and 33
after surgical intervention. The asterisk (*) indicates the value

is significantly different from baseline (before surgical
intervention).

Maximal expiratory flow at three levels of exercise before and after 34
surgical intervention. The asterisk (*) indicates the value is
significantly different from baseline (before surgical intervention)

Respiratory frequency at three levels of exercise before and after 35
surgical intervention. The asterisk (*) indicates the value is
significantly different from baseline (before surgical intervention).

LIST OF FIGURES (CONT'D)

Figure Page

7a. Arterial carbon dioxide tension at three levels of exercise before 36
and after surgical intervention. The asterisk (*) indicates the
value is significantly different from baseline (before surgical
intervention).

7b. Arterial oxygen tension at three levels of exercise before and after 37
surgical intervention.

8. Heart rate at three levels of exercise before and after surgical 38
intervention.

9. pH at three levels of exercise before and after surgical 39
intervention.

10. Hemoglobin concentration at three levels of exercise before and 40

after surgical intervention.

11. Bicarbonate concentration at three levels of exercise before and 41
after surgical intervention. (The asterisk (*) indicates the value
is significantly different from baseline (before surgical
intervention).

vi

I. Introduction

Abnormal inspiratory noise has been described in exercising horses since the
late 17th century.1 In the 19th century, it was shown that laryngeal hemiplegia
is one of the causes of abnormal inspiratory noise production in exercising hor-
ses and that this condition is caused by recurrent laryngeal nerve injury.2

Most modern surgical procedures used to correct left laryngeal hemiplegia in
horses (ventriculectomy, arytenoidectomy, and vocal cordectomy) are modifica-
tions of techniques used in the 18005.3 Williams reintroduced the technique in
1905 and the procedure was popularized by Hobday in 1936.4 Surgical therapy
remained unchanged until Marks (1970) described the use of a suture prosthesis
(prosthetic laryngoplasty) to treat laryngeal hemiplegia.5 Ventriculectomy has
been performed alone or in conjunction with the previously mentioned
procedures.5-5:7

Until recently, the efficacy of surgical procedures used to treat left
laryngeal hemiplegia was evaluated using subjective criteria such as reduction
of inspiratory noise during exercise and improved athletic performance.3»3:9 A
technique to objectively evaluate upper airway flow mechanics in exercising hor-
ses has been developed at the Pulmonary Laboratory at Michigan State
University.10 Using this technique, prosthetic laryngoplasty was shown to
reverse upper airway obstruction induced by left laryngeal hemiplegia. The
objectives of this study were twofold. First, to evaluate the effect of ventri-
culectomy on upper airway flow mechanics in exercising horses following left
recurrent laryngeal neurectomy. Second, to determine if prosthetic
laryngoplasty was an effective procedure for alleviating mechanical impairments
of upper airway flow measured following left recurrent laryngeal neurectomy in
horses exercising at greater speeds than previously measured with this tech-

nique.

II. General Review of Laryngeal Hemiplegia
A. Historical Perspective

In the late seventeenth century, Solleysel described inspiratory stridor in
exercising horses.1 The lay term "roaring“ was popularized in the nineteenth
century to describe this condition.2 The anatomic origin of this noise produc-
tion in horses was unknown until Bouley (1825) recognized left recurrent
laryngeal nerve damage at necropsy in a horse which “roared" while alive. This
prompted investigations by Dupuy (1825) and Gunther (1834).2 Independently,
these investigators sectioned the left recurrent laryngeal nerve and reported
abnormal noise production in exercising horses concomitant with "wasting” of
left laryngeal musculature in the same animals at necropsy. The importance of
differentiating between the causes of abnormal respiratory noise was emphasized
by Fleming, and he reserved the term “laryngismus paralytica“ for animals exhi-
biting inspiratory dyspnea during exercise.2 "Laryngismus paralytica“ described
both unilateral and, the less common, bilateral laryngeal paralysis. The term
"hemiplegia laryngis“ or laryngeal hemiplegia appeared in later literature to
describe the unilateral condition.3 Several diseases (e.g. strangles, bronchi-
tis, influenza, enlarged bronchial glands, etc.) have been purported to cause
left laryngeal hemiplegia, as these diseases preceded the development of
"roaring" in some individuals.

Diagnosis of laryngeal hemiplegia remained difficult until rigid- and
flexible-fiberOptic endosc0py became available in veterinary medicine.11 Using
endoscopy, differentiation of laryngeal hemiplegia from other causes of inspira-
tory stridor became possible.

In the late 19th century oral iodine, iron, mercury, and arsenic were recom-
mended medical therapy for laryngeal hemiplegia; alone, or in combination with

percutaneous strychine or electricity applied over the cricoarytenoideus dor-

3

salis muscle.12 Surgical therapy at that time included chemical cautery or
injection of counter irritants over the larynx, unilateral or bilateral vocal-
cordectomy, ventriculectomy, arytenoidectomy, and combinations of those
procedures.12 Surgical therapy remained unchanged until Marks (1970) described
use of a suture prosthesis (prosthetic laryngoplasty) to treat laryngeal
hemiplegia.5

The effects of medical and/or surgical therapy for left laryngeal hemiplegia
were only evaluated subjectively3:13:14 and reported ”success rates“ varied
depending on the criteria chosen for determining success (e.g. noise reduction,
improved racing times, etc.). Additionally, before the advent of the endoscope,
it was difficult to assess the effect of treatment because laryngeal hemiplegia
was likely misdiagnosed being confused with other diseases causing abnormal
upper respiratory noise during exercise.- In 1986, a method for measuring upper
airway resistance in exercising horses was reported.10 Following recurrent
laryngeal neurectomy, upper airway resistance was increased during inspiration
when compared with baseline values. Prosthetic laryngoplasty decreased inspira-
tory resistance towards baseline values. In the present study, I evaluated
ventriculectomy alone and then prosthetic laryngoplasty at greater treadmill
speeds than in the previous study by measuring upper airway flow mechanics in

exercising horses with left laryngeal hemiplegia.

B. Anatomy, Etiology, and Pathology

 

The intrinsic laryngeal musculature is symmetrically innervated at the level
of the larynx without evidence of nerve fiber decussation to the contralateral
side.15 Adductor muscles (cricoarytenoideus lateralis, arytenoideus transver-
sus, vestibularis, and vocalis muscles) and abductor muscles (cricoarytenoideus
dorsalis muscle) are innervated by the recurrent laryngeal nerve. The crico-
thyroideus muscle which tenses the vocal fold receives innervation from the cra-

nial laryngeal nerve.16 Innervation is symmetrical at the level of the larynx,

but the right and left recurrent laryngeal nerves have different anatomic path-
ways prior to innervating the larynx.15 The right and left vagi arise in the
medulla oblongata and exit the cranium through the jugular foramen. The nerves
descend, passing along the dorsal aspect of the guttural pouches, and sub-
sequently course along their respective jugular furrows into the thorax. There
the left recurrent laryngeal nerve (LRLN) branches from the vagus at the base of
the heart, dividing into two branches that eventually reanastomase, and pass
across the axial surface of the aorta and ligamentum arteriosum. The LRLN then
ascends passing along the dorsolateral aspect of the trachea to the level of the.
larynx. In contrast, the right recurrent laryngeal nerve (RRLN) branches from
the vagus 25-30 cm cranial to the LRLN at the level of the second rib and passes
medial to either the right subclavian or costocervical arteries before ascending
dorsolateral to the trachea until reaching the larynx.15 The average length of
the RRLN & LRLN are 76.0 cm and 97.6 cm, respectively.17

Neural pathology associated with laryngeal hemiplegia (LH) is characterized
by progressive loss of myelinated nerve fibers, most obvious in the distal part
of the recurrent laryngeal nerve.18 In addition, segmental demyelination and
remyelination have been observed. In chronic cases, increased endoneurial con-
nective tissue and nuclei with sporadic Wallerian or secondary degeneration have
been described.19 This neuropathology results in neurogenic atrophy of the
intrinsic laryngeal musculature. Endosc0pically20, failure to dilate the rima
glottis by abducting the arytenoid cartilages appears to be the major problem in
laryngeal hemiplegia, but histologically, both abductor and adductor muscles are
affected.21 Histologically, myofiber type grouping (resulting from interrup-
tion of innervation) myofiber atrOphy with fatty replacement of fibers, and
fiber hypertrophy in some areas (though atrophy is more pronounced) character-

izes changes in the laryngeal musculature.19:22-23 However, these changes must

be interpreted with caution because some clinically normal horses show histolo-
gic and gross changes compatible with the neuropathology and neurogenic atrophy
of LH. In one sample, 30% of clinically normal horses had histologic abnor-
malities of the laryngeal musculature.19 Changes in adductor muscles appeared
more severe than those in abductor muscles.21 In a sample of 75 horses, the
left intrinsic laryngeal musculature, excluding the cricothyroideus muscle,
weighed less than the musculature of the right side suggesting that a degree of
left-sided atrOphy may be present in many clinically normal horses. When com-
pared to normal horses, the difference between the weights of the right and left
intrinsic laryngeal musculature was significantly greater in one horse with
laryngeal hemiplegia.24 It has been suggested that atrophy of 50% of the left
cricoarytenoideus dorsalis muscle is necessary before clinical signs of inspira-
tory stridor are evident.17 1
Several causes have been proposed for laryngeal hemiplegia and these are
summarized as follows:
1. Congenital
2. Acquired
a. Toxic damage to the LRLN by chemical or bacterial toxins
b. Nutritional deficiencies
c. Nerve damage induced by viral infection
d. Mechanical damage to the LRLN by compression, stretching, or trauma.
Cook has suggested that LH is a congenital disease.25 In a single fetal
larynx, histochemical studies have shown muscle fiber grouping similar to that
present in animals with LH.21 The presence of this muscle fiber grouping
suggests that LH may have a congenital etiology. But, additional fetal larynxes
should be examined. Attempts to show that LH is an inherited condition has not

provided consistent results. A long-term study in South Africa was unable to

show that LH is inherited while another study suggested inheritance occurred as
a simple recessive.3»25

Laryngeal hemiplegia may occur concomitant with other diseases. Those
diseases that precede, or may be present concurrent with LH, have been proposed
as etiologies of the disease. Laryngeal paralysis has occurred in conjunction

with paralaryngeal abscess, infection with Staphlococcus aureu525, unilateral

 

rupture of the rectus capitis ventralis major and minor muscles leading to gut-
tural pouch mycosiSZ7, other bacterial infections which lead to lymph node
enlargement23, plant poisoning, lead poisoningZ9, organophosphate
intoxication30231, perivascular or perineural injections32, and lacerations
involving the jugular furrow.33 Additionally, plasma thiamin deficiency
recognized in some horses with laryngeal hemiplegia, is postulated to cause a
peripheral neuropathy similar to that observed in humans with beriberi (thiamin
deficiency).34 Neuropathy in other long peripheral nerves, as observed in
humans with beriberi, has been documented in horses with LH though this was not
correlated with thiamin deficiency in these horses. Additionally, thiamin defi-
ciencies in other species, like the cow, do not cause atr0phy of intrinsic
laryngeal musculature.35 A "dying back“ phenomena of distal degeneration of
peripheral nerves with few changes in central nuclei (anterior horn cells)35,
were similar to changes seen with thiamin deficiency. But, the changes were not
specific for thiamin deficiency as similar signs of degeneration occurred with
other neurotoxins. Bilateral laryngeal hemiplegia in an adult human male was
related to increased herpes simplex virus-complement fixation antibody titers
during the initial phase of the illness.37 Though herpes viruses play a role in
some equine disease, viral replication within peripheral nerves and resulting
damage does not explain the unilateral expression of the disease present in most

cases of equine laryngeal paralysis. In addition, most infectious disease

etiologies fail to explain the predominence of LH in large (16-17 hand) mature

male horses.38

In horses, the LRLN is longer than the right recurrent laryngeal nerve,16
and tension on the nerve resulting from the longer anatomic pathway of the
LRLN has been postulated to cause a neuropathy and atrOphy of laryngeal muscu-
lature. In addition, it has been suggested that anatomic variations of the
typical nerve routes might further lengthen the path the nerve travels and
cause additional tension along the LRLN.39 Experimentally, chronic slow
stretching of nerves in humans increases nerve length and fails to impair
nerve function.40 Therefore, the above explanation for the occurrence of LH
is unlikely. In addition, chronic tension on the LRLN does not explain muscle
and nerve histopathology observed bilaterally in clinically normal horses and
horses with LH.

Neural ischemia has been proposed as a mechanism for the neuropathy
observed in horses with LH36 because it causes similar neurohistologic
changes. However, vascular perfusion abnormalities with either bilateral or
unilateral vessel pathology have not been described as a feature of the
disease. Peripheral nerves have an extensive anastomotic blood supply which
is seldom occluded except by compression. Experiments to determine if ische-
mia of the LRLN would result in LH, are needed.

Since neural degeneration and laryngeal muscle atrophy have been observed
bilaterally, it has been suggested that another factor must be present to explain
the more commonly observed unilateral paralysis. Baker proposed that failure of
neural regeneration following degeneration of the LRLN could be the reason.8

In a New Zealand population of horses with LH, the cause of the disease was
undetermined (idiopathic) in 89% of the cases. Thus, although there is a
general consensus on the muscle and nerve pathology characterizing LH, the

etiology of the neural damage remains controversial in most cases.32

C. Diagnosis of Laryngeal Hemiplegia

Animals with laryngeal hemiplegia are usually presented for inSpiratory
dyspnea during exercise and in some cases exercise intolerance.32 Similar cli-
nical signs are observed in horses with other diseases that cause upper respira-
tory obstruction (e.g. laryngo-palatal dislocation or soft palate paresis41,
epiglottic entrapment or subepiglottic cysts42, rostral displacement of the
palatopharyngeal arch43, arytenoid chondritis44, nasal obstruction45, and severe
pharyngitis45). Clinical signs of lower respiratory tract inflammation and
obstruction47 may also mimic those of LH. These conditions can occur alone or
in conjunction with LH making a definitive diagnosis difficult. Diagnosis of LH
requires a thorough history to determine onset of clinical signs and a descrip-
tion of conditions under which inspiratory stridor or exercise intolerance are
present. Physical and lameness examinations and clinicopathologic evaluation
(complete blood count and blood chemistry profile) can be used to determine the
presence of systemic disease that may be causing exercise intolerance.

Three procedures for external palpation of the larynx have been suggested to
aid the diagnosis of LH.48 First, a prominent muscular process may be palpable
on the left side of the patient's larynx in chronic cases of LH in which the
left cricoarytenoideus dorsalis is atrOphied. Secondly, inspiratory stridor may
be elicited by depressing the muscular process on the affected side and reducing
the diameter of the laryngeal lumen (arytenoid depression test). Horses with LH
have abnormal muscular function and do not resist this manual depression.
Lastly, dorsal pressure on the cricotracheal ligament will cause obstruction and
inspiratory stridor when there is laxity of the cricotracheal ligament
(cricotracheal ligament intrusion test). Laxity of the cricotracheal liga-
ment has been observed in some animals with LH.

The laryngeal abductor (or slap) test should be included as a diagnostic‘

test for LH.49 Slapping of one side of the withers of a normal horse results in

contraction of laryngeal muscles and adduction of the contralateral arytenoid.
Failure of the contralateral arytenoid to adduct suggests it may be paralyzed
and supports a diagnosis of LH.

Following a physical examination at rest, the horse should be exercised when
feasible, to evaluate the severity of inspiratory stridor at different speeds.
Also, nasopharyngeal endoscopy should be done in unsedated animals before and
following exercise because endoscopy is important in differentiating between the
many causes of upper airway obstruction. Medial displacement of the affected
arytenoid cartilage relative to the normal resting position, shortening of the
vocal fold on the affected side43, and reduction of the cross sectional area of

the rima glottis50 have been described in horses with laryngeal hemiplegia.

0. Treatment

Modern surgical procedures (ventriculectomy, vocal cordectomy and
arytenoidectomy) used to treat laryngeal hemiplegia are modifications of nine-
teenth century surgical techniques.2:4 General anesthesia, allowing long
surgical procedures, enabled refinement of techniques and development of new
approaches. Ventriculectomy, or removal of the laryngeal ventricle, is thought
to lateralize the vocal fold, increasing the cross sectional area of the
laryngeal lumen.14 This technique was developed in the 1800's by Gunther, but it
was soon replaced by other procedures. Ventriculectomy was reintroduced by
Williams in 1905 and popularized by Hobday in 1936.4 The larynx is approached
through the cricothyroid ligament. The laryngeal ventricle on the side of the
affected arytenoid is everted, excised and the wound allowed to heal by second
intention. Skin, subcutaneous tissues, and the cricothyroid ligament also heal
by second intention. Recommendations for postoperative rest vary from 4-8 weeks

or until the skin incision is healed.4

10

In the past, only subjective criteria were used to evaluate the benefit of
ventriculectomy for treating LH. Noise reduction following ventriculectomy has
been reported in 20%4 to 30%8 of patients treated. Fifty to 95%4’3 of animals
are said to show improved athletic performance postoperatively. Suturing of the
ventricular orifice after ventrical removal is proposed to further improve
performance.7 Excision of the vocal ligament in conjunction with ventriculec-
tomy is practiced but the efficacy of vocal cordectomy has not been reported.6

Although ventriculectomy lateralizes the vocal folds, it may not prevent
laryngeal lumen obstruction by the affected arytenoid cartilage during inspira-
tion. Placement of a suture prosthesis to fix the arytenoid cartilage in an
abducted position has been described.5 Briefly, an approach is made between the
lingual facial and jugular veins and the omohyoideus muscle. The cricopharyn-
geal and thyropharyngeal muscles overlying the larynx are exposed. A nonabsor-
bable suture is inserted in the cricoid cartilage, lateral and parallel to its
dorsal midline. Suture material is drawn beneath the cricopharyngeus muscle,
advanced cranial, and inserted through the muscular process of the arytenoid
cartilage in a medial to lateral direction. Tension placed on the suture pulls
the corniculate process of the arytenoid cartilage caudal and lateral, enlarging
the laryngeal lumen. The surgical wound is closed in a routine manner. Many
surgeons perform a ventriculectomy in conjunction with the laryngo-
plasty.5»3’51952 Restoration of normal anatomic relationships, by lateraliza-
tion of the affected arytenoid, is one of the criteria used to evaluate the pro-
cedure, and Marks reported that in 88% of the cases prosthetic laryngoplasty
combined with ventriculectomy reestablished normal anatomic relationships within
the larynx.

Classification of the affected arytenoid as fully abducted with normal
movement, in an intermediate position with abnormal abduction, or in a para-

median position with no active abduction or adduction, is suggested for

11

selecting appropriate surgical therapy.48 Ventriculectomy alone has been
suggested to be appropriate for treating animals with an arytenoid in an inter-
mediate position while combined ventriculectomy and prosthetic laryngoplasty
have been suggested for treatment when the arytenoid is paralyzed in the para-
median position.48 The significance of the intermediate position is controver-
sial. Horses with arytenoids which move at different times (asychronous
movements) have been diagnosed as being affected with LH.53 Baker reported that
asynchrony or fluttering of the arytenoids, without paralysis, is not an early
indication of LH as progression to paralysis does not appear to occur. Thus,
asynchronous arytenoid movement may be normal in the horse.

.Modifications of the prosthetic laryngoplasty procedure have been reported.
They include different surgical approaches (e.g. dorsal to the lingual facial
and jugular veins)54, various materials for the prosthesis or multiple
prostheses55, and laryngoplasty alone or in conjunction with ventriculectomy.56
Until recently, the efficacy of prosthetic laryngoplasty had been evaluated by
subjective criteria, including respiratory noise reduction, endoscopically
determined arytenoid position, and athletic performance. Measuring the ampli-
tude of respiratory noise or determining the position of the arytenoid endosco-
pically are fraught with inter-observer error. Racing performances pre- and
postoperatively have been analyzed in an attempt to quantitate improvement in
athletic performance.52953 Spiers assessed the racing performances of horses
receiving one of four procedures involving modifications of prosthetic
laryngoplasty.57 An abductor muscle prosthesis without ventriculectomy, a
prosthesis with ventriculectomy, a prosthesis using a horizontal suture pattern
in the cricoid with ventriculectomy, and two prostheses with ventriculectomy
were compared. There was no statistically significant difference in the success
rate with these procedures, but horses receiving laryngoplasty without ventricu-

lectomy appeared to outperform all other animals except those in which two

12

abductor muscle prostheses had been placed. Animals which received a prosthetic
laryngoplasty with two prostheses had better racing performances than animals in
which only one prosthesis had been used. Combining ventriculectomy with
prosthetic laryngoplasty did not improve racing performance relative to prosthe-
tic laryngoplasty alone.

Postoperative complications after prosthetic laryngoplasty include coughing
(especially during feeding), formation of infected suture sinus tracts,
laryngeal luminal penetration by the prosthesis54, nasal discharge of food or
water, laryngeal swelling, and dysphagia or choking.56 Coughing is the most
common problem and may result from excessive abduction of the arytenoid,
distorting the palatopharyngeal arches, and blocking the lateral food channel.S8

Arytenoidectomy is usually performed as a salvage procedure following unsuc-
cessful laryngoplasty or used to treat laryngeal obstructions including aryte-
noid chondritis9 and ossification of laryngeal cartilages.59 The surgical
approach for this procedure is through the cricothyroid ligament and has been
described above. Insufficient exposure of the laryngeal lumen requires exten-
sion of the incision through either or both the thyroid and cricoid cartilages.8
Different portions of the affected arytenoid cartilage may be removed. In a
total arytenoidectomy, the entire cartilage is removed while, in a partial ary-
tenoidectomy, the muscular process is left lg gitg. When the subtotal aryte-
noidectomy is performed, the corniculate and muscular processes remain.
Submucosal dissection of the cartilage is extended laterally and dorsally until
the cartilage is removed. The laryngeal mucosa is sutured and the laryngotomy
incision is left to heal by second intention.8 Ventriculectomy and/or vocal
cordectomy are sometimes performed in conjunction with the arytenoidectomy.59
The success rates of partial and subtotal arytenoidectomy procedures have only

been subjectively assessed. Pasture soundness and return to athletic function

13

have been reported.9:59s50 Complications of total arytenoidectomies include
dysphagia and inhalation pneumonia. Those problems may have been partially
alleviated by the subtotal and partial arytenoidectomy procedures as they may
reduce foreign body aspiration. Although subtotal arytenoidectomy increases
laryngeal luminal diameter and exercise tolerance, 36% of the animals in one
study60 exhibited nasal discharge of food or water. Thus, arytenoidectomy
appears to improve performance but postoperative complications warrant using it
only in cases of upper airway obstruction where prosthetic laryngoplasty is
ineffective in enlarging the laryngeal lumen.

Several additional procedures have been advocated for treating laryngeal
hemiplegia in other species. Nerve-muscle pedicle transfers for reinnervation
of the cricoarytenoideus dorsalis muscle have been successful in humans61 and
dogs,62 but not in horses.63 Laryngeal pacemakers, or units providing electrical
impulses to abductor muscles of the larynx through nerve-muscle pedicles, have
also been investigated. An implantable instrument for muscle stimulation is not
available in the horse but it has been shown that lengthening of the trachea
during inspiration (as signaled by a strain gauge sutured across tracheal rings)
can trigger electrical stimulation of the cricoarytenoideous dorsalis muscle via
a nerve-muscle pedicle. This device would maintain upper respiratory function
until reinnervation of the nerve-muscle pedicle had occurred.64

Laryngeal pacemaker models have been developed to stimulate the cricoaryte-
noideus dorsalis without relying on nerve-muscle pedicle regeneration in dogs.
One type of electrical pacemaker stimulates the cricoarytenoideus dorsalis
through electrodes placed within the muscle. The pacemaker is attached to a
receiver coil implanted beneath the animals skin. Thoracic movements during
inspiration trigger a portable transmitter which signals the implanted receiver
coil causing an electrical impulse which stimulates the cricoarytenoideus dora

salis muscle.65

14

Laryngeal pacemakers are not available for clinical use but are attempts to pro-
vide a more physiologic means of maintaining respiration during LH.

Until recently, surgical correction of LH has only been evaluated using sub-
jective criteria. Our laboratory has developed a technique for objectively
measuring upper airway flow mechanics in normal animals and those with LH. This
allows comparison of the efficacy of surgical procedures in reducing airway
resistance resulting from laryngeal hemiplegia. Objective evaluation of
prosthetic laryngoplasty has been accomplished10 and it has been shown to be an
effective procedure for reducing upper airway resistance caused by laryngeal
hemiplegia. In this study, I describe the evaluation of ventriculectomy as a
technique for treatingleft laryngeal hemiplegia in horses and the success of
prosthetic laryngoplasty to reduce airway obstruction when animals with LH exer-
cise at high speeds. In the next section of this literature review, I will
discuss flow mechanics principles underlying the measurement technique used in

the study.

15

III. Principles of Upper Airway Flow Mechanics

The upper respiratory tract is a dynamic system in which changes in
respiratory tract geometry can be evaluated by measuring resistance to gas flow.
Poiseuille developed an equation describing laminar flow (V) in systems of
cylindrical tubes as a function of driving pressure (P). Driving pressure is

the pressure drop measured across a system. Poiseulle's equation,

8 “I/1H‘4 V

‘0
ll

incorporates the variables, rate of airflow (V), gas viscosity within a tube
(u), tube length (l), and tube radius (r).66 The most commonly described patterns
of airflow are laminar, transitional, and turbulent. Laminar flow occurs at low
flow rates when air streams are parallel to the sides of straight tubes.
Turbulent flow develops at higher flow rates, both within a straight cylinder
and at branch points which disrupt the parallel air streams. Transitional flow
is a combination of both flow types with laminar flow occuring in straight
portions of a system and turbulent flow at branch points. Since the pattern of
flow is not constant within the respiratory system, the Reynolds number (Re)
should be calculated to determine if flow is laminar, transitional, or
turbulent.57:68 Reynolds number is a dimensionless unit that incorporates gas
density (9), tube radius (r), gas viscocity (M). and flow rate (V) in the

following equation

-39.’
Re ‘ Mar V

If Reynolds number is greater than 3,000, turbulent flow will develop in the
system. If Reynolds number is less than 2,300, flow is primarily laminar. When
the Reynolds number is between 2300 and 3000, transitional flow is present. In

systems of laminar flow, Poiseulle's equation will describe the relationship

16

between pressure and flow. For a particular system, the variables in
Poiseulle's equation

8ul/1r4
can be considered equal to a constant K1. K1 represents the mechanical energy
loss within the system from laminar flow allowing a simplified equation

P = KlV
It has been suggested that in bronchioles, flow is probably laminar and that
turbulent flow occurs in the central airways especially during exercise when
airflows are high.69

When flow becomes turbulent, the pressure-flow relationship is dependent on

the density of the gas within the system examined and can be described by the

equation

p = K2up.25 90.75 91.75

The equation describes the driving pressure for turbulent flow. The effects of
incorporating both laminar and turbulent flow on driving pressure can be

described by Rohrer's equation

P = k3uV + kasz

where k3 is a constant representing the mechanical energy loss due to laminar
flow,,u.is the viscosity of the gas, k4 is the mechanical energy loss due to
turbulent flow, and p is the denisty of the gas. Changes in k3 and k4 reflect
changes in respiratory system geometry.67

Resistance (R) has been defined as the ratio of the change in pressure over
the change in flow (AP/AV). Resistance is the slope of the tangent to a
pressure-flow curve for a particular system measured at a specific V. Whenever

pressure and flow can be measured, resistance can be calculated.

17

The respiratory system is not composed simply of rigid tubes. Potential
energy is stored within the walls of compliant airways. Kinetic energy is pre-
sent in moving air masses, and frictional energy loss occurs as air streams con-
tact the walls of the airways. Therefore, R is inadequate to describe changes
in respiratory system geometry as it only includes resistive or frictional for-
ces and does not describe the combination of resistive, elastic, and/or inertial
elements that are present in the respiratory system.70 Impedance (Z) is a
complex parameter that incorporates all three elements (resistive, elastic, and
inertial).70 Impedance represents the magnitude of obstruction to oscillatory
flow within the portion of the respiratory system examined. The greater the
impedance, the greater the oscillatory pressure difference required to maintain
a given flow. Impedance is calculated from the ratio DP/AV at a specific fre-
quency of respiration.

During inhalation, a reduction in intraluminal pressure occurs so that
intraluminal pressures are negative relative to barometric and extraluminal soft
tissue pressures. The effect on the upper respiratory tract is primarily evi-
dent at the larynx and nasal ali as these areas are supported by cartilage
and muscular contraction is required to abduct cartilage structures and maintain
luminal diameter. In addition, the cross-sectional area of the larynx is small
relative to the pharynx and trachea.

If the cross sectional area of the larynx decreases, the velocity of flow
through that part of the upper reSpiratory tract increases. Consequently, the
intraluminal pressure decreases to allow conservation of energy within the
system (Bernoulli's principle) (Figure 1).

Failure of muscular contraction to abduct the arytenoid cartilages,
could result in dynamic collapse of the larynx, obstructing airflow. Slight
collapse of a portion of the airway will further reduce the cross-sectional

area of the respiratory tract causing increased airflow velocity at that point

18

 

 

l

 

 

 

 

Figure 1. Schematic representation of Bernoulli's effect creating dynamic
collapse of a narrowed airway. Velocity of airflow, V1 increases
to V2 in the narrowed portion of the airway. Concurrently, the
intraluminal pressure, P1, decreases to P2 in the narrowed part of

the airway.

19

and a further reduction in intraluminal pressure resulting in collapse of the
airway. On exhalation, airways do not collapse because the intraluminal pressure
is positive relative to barometric pressure and pressure in the extraluminal

soft tissues.

In normal animals, the arytenoid cartilages of the larynx can abduct and
the nostrils can dilate preventing dynamic collapse of the airways. Animals
with LH are unable to dilate the affected arytenoid and dynamic collapse
occurs. Increases in upper airway resistance, caused by laryngeal hemiplegia,
are alle viated by prosthetic laryngoplasty.10 The effect of other procedures
for treating laryngeal hemiplegia on airway resistance remains to be deter-
mined.

When evaluating the efficacy of ventriculectomy and prosthetic
laryngoplasty in horses with left laryngeal hemiplegia, I also measured
arterial blood gas tensions. The rationale for the use of these measurements

in this study is described in the next section of this literature review.

20

IV. Review of Arterial Blood Gas Tensions in Exercising Horses

Hypoxemia and concomitant normocapnia or hypocapnia have been observed in
horses competing in endurance rides.71 Hypercapnia and hypoxemia have also been
measured in horses exercising at high speeds on both a racetrack and treadmill
(8.5 m/s).72.73

The causes of hypoxemia are

1. reduced concentration of oxygen in inspired air,

2. unevenly matched ventilation and perfusion within the pulmonary system,

3. shunting of blood with low oxygen tension past unventilated regions of

the lung,
4. impairment of gas diffusion across the capillary endothelium and
alveolar walls, and

5. hypoventilation.59

In exercising horses, without pulmonary disease, breathing room air, it is
unlikely that the first reason contributes to hypoxemia. Exercise improves
matching of ventilation and perfusion in humans, reducing ventilation-perfusion
mismatch and shunting.74 In addition, membrane-diffusing capacity increases as
the blood volume of the pulmonary capillary bed increases.74 Diffusion impair-
ment or unmatched ventilation and perfusion are unlikely causes of the hypoxemia
associated with exercise. But, hypoventilation may be a factor. In humans
exercising strenuously, respiratory frequency increases and tidal volume
decreases.74 Possibly similar events are occurring in horses. If low oxygen
tension results from hypoventilation, then a rise in PACOZ should be observed.
The increase in PACOZ and concomitant reduction in PAOZ can be predicted from
the alveolar gas equation59

1-

_ , . R
PA02 ' PI02 ' PAC02 I E PAC02 Fl02 'E_' J

 

R
PAO2 is the partial pressure of oxygen in the alveolus, P102 is the oxygen ten-

21

sion of the inspired gas, PACO2 is the alveolar carbon dioxide tension, and R is
the respiratory quotient. The variables in parentheses provide a correction
factor (F) when air is breathed. F102 is the fractional concentration of the
inspired gas and R is the ratio of C02 production to oxygen consumption. A
simplification of the equation is:

PA

_ C0

The equation provides a useful estimate for PAOZ' Alveolar carbon dioxide ten-
sion is assumed to be equivalent to arterial carbon dioxide tension and the

latter is more easily measured.59.74 From the equation
P102 = (P3 - PHZO) F102

where barometric pressure (P3), water vapor pressure (PH20)’ and F102 are known,
P102 can be calculated.

If P102 was 147 mmHg and Paco2 was measured as 45.0 Torr, the alveolar gas
equation would predict a PA02 of 90.7 Torr. If Paco2 was measured as 50 Torr,
the predicted PA02 would be 85.4 Torr. 'Hypoxemia in horses exercising near
maximal velocity has been reported to be as low as 61.5 Torr.72 Therefore,
additional mechanisms have been suggested to explain the severe hypoxemia of
exercise. It is possible that increased cardiac output during exercise causes
decreased transit time of red blood cells through the pulmonary capillary vascu-

lature so the cells do not become fully saturated with oxygen.75 Reduced

alveolar oxygen tension may also result from a process called stratification
whereby the distance that oxygen must diffuse is increased because of the large
dead space in large species relative to smaller species.75

One study attempted to determine if pharyngeal lymphoid hyperplasia (PLH)

impaired athletic performance by causing airway obstruction.76 Blood gas ten-

sions were measured in exercising horses and no significant differences were

22

observed before and following chemical induction of pharyngitis. It was
suggested that upper airway obstruction was not a cause of exercise intolerance
in lymphoid hyperplasia because oxygen tensions were unchanged. But, a
controlled study correlating airway obstruction from pharyngeal lymphoid
hyperplasia and changes in blood gas tensions has not been reported. Arterial
blood gas tensions and acid-base balance were measured in one horse with
laryngeal hemiplegia.77 Hypercapnea and severe hypoxemia (Pao2 - 53.2 Torr,
Paco2 58.1 Torr) were measured during exercise, before any surgical interven-
tion. The oxygen and carbon dioxide tensions improved following prosthetic
laryngoplasty without ventriculectomy (PaoZ-83.6 Torr, Pac02-39 Torr). The
study suggested that hypoxemia occurring in normal exercising horses may worsen
when upper airway obstruction is present and that some surgical procedures may
be effective in improving blood gas tensions.

In this thesis, I propose to correlate changes in blood gas tensions and
acid-base balance with measurements of upper airway flow mechanics parameters
before any surgical intervention, in horses with laryngeal hemiplegia induced by
recurrent laryngeal neurectomy, and following corrective surgical procedures
(ventriculectomy and prosthetic laryngoplasty). If a correlation between upper
airway obstruction and blood gas tensions was found, measurement of blood gas
tensions could be helpful in diagnosing upper respiratory obstructive disease

and monitoring responses to procedures for treating the obstruction.

23

V. Effect of Ventriculectomy, Prosthetic Laryngoplasty and Exercise on Upper
Airway Function in Horses with Left Laryngeal Hemiplegia

A. Materials and Methods

Subjects -- Five adult horses (4.6 1 0.8 years of age, weighing 464 :_23 kg
[7 i SEMJ) were used in the experiments. Horses were immunized against the com-
mon respiratory virus infections (equine influenza and rhinopneumonitis) and
were pastured for one month prior to training. On endoscopic examination of the
upper airway, no abnormalities were found in any horse prior to the experiments.
Horses were trained to wear a face mask while walking, trotting, and galloping
over a 30 day period on a treadmill.a Animals were induced for all surgical
procedures with glycerol guiacolateb (500 ml of a 10% solution) and thiamylalc
(2 grams) given intravenously to effect, followed by endotracheal intubation and
maintenance on halothane and oxygen in a semiclosed circle anesthetic system.

Measurement Techniques--To measure inspiratory and expiratory airflow
rates, a fiberglass facemask was placed over the horse's nose and sealed to the
face with a rubber shroud. The mask allowed unimpeded dilation of the nostrils.
A 14 cm diameter pneumotachographd was mounted on the face mask (Figure 2). To
reduce mask pressure inhomogeneity, a flow straightener elemente was interposed
between the external nares and the pneumotachograph. The combined resistance of
the mask-pneumotachograph assembly was 0.04 cm H20/L/sec up to a flow rate of 70
L/sec. Pressure changes across the pneumotachograph were measured using a dif-

ferential pressure transducer.f After each experiment, the pneumotachograph-

 

TT’Jetline, DeSales Inc, Sand Lake, Mich.

b Glycerol guiacolate, Guaiacol Glyceryl Ether USP, Aceto Chemical Co.,
Flushing, NY.

C Biotal, Biocentic Division, Boehringer Ingelheim Animal Health Inc.,
St. Joseph, MO.

d Marian 6" Laminar Flow Straightener Element, Meriam Instruments, Grand
Rapids, Mich.

e Mesh SS screen, McMaster-Carr, Chicago, Ill.

Model DP 45-22, Validyne Sales, Northridge, Calif.

24

 

~
.I

O/

p. \\  

Figure 2. Schematic representation of the face mask with the 14 cm diameter
pneumotachograph (A) and flow straightener element (8). Sites for
measurement of lateral tracheal pressure (PT) and mask pressure

(Pm)-

25

transducer system was calibrated, using a rotameter flow meterg capable of
measuring flow rates up to 90 L/sec.

Transupper airway pressure (Pu) was defined as the pressure difference bet-
ween a side hole catheter in the trachea10 and barometric pressure (P3). The Pu
was measured using a differential pressure transducer.h To avoid phase dif-
ferences between flow and pressure signals caused by equipment, signals were
synchronized up to 10 Hz.78 All signals were recorded on a physiograph.1

Because inertia and airway deformation result in complex upper airway
pressure and flow relationships at high respiratory flow rates,70 pressure and
flow signals generated during exercise were not in phase. Therefore, peak Pu on
inspiration and expiration (Pu; and Pug, respectively) as well as peak airflow

rates on inspiration and expiration (VImax and ngax) were measured for a given

breath.10:70 Both inspiratory and expiratory impedance (21 and 25) were
calculated70 from the ratio of peak pressure and flow measurements which were
averaged for at least 10 breaths. Respiratory frequency (f) was determined from
the physiograph tracing. Heart rate (HR) was measured using a base apex lead
system and a heart rate computer.J

Arterial oxygen and carbon dioxide tensions (Pao2 and Pacoz) hemoglobin
content (Hb), bicarbonate concentration (HC03'), and pH, were measured in
samples taken from an exteriorized right carotid artery. Analyses were per-
formed using a blood gas analyzer.k Gas tensions were corrected for rectal

blood temperatures using standard equations.79

 

9 Model FP-2-37-P-10/77, Fisher and Porter Co, Warminster, Pa.
h Model DP 45-34, Validyne Sales, Northridge, Calif.

1 Model 8188, Gould Inc, Madison Hts, Mich.

J Equistat, Equine Biomechanics and Exercise, Unionville, Pa.

k Model A821, Radiometer, Copenhagen, Denmark.

26

Experimental Design--Measurements were made with horses on a treadmill
(incline 6.38°) while standing, trotting at 4.3 m/s, and galloping at 7.2 m/s.
While trotting and gallOping, horses were exercised for 2 minutes and data was
obtained during the last minute of each exercise period. Horses were allowed to
rest for two minutes between exercise periods or until their heart rate was
below 80/min.

Experiments were performed in healthy horses before surgical intervention
(baseline), 14 days following left recurrent laryngeal neurectomylo, 30 days
after left ventriculectomy as described by Hobday4 and 14 days following a modi-
fication of the prosthetic laryngoplasty procedure as described by Marks et al.5
A silicone treated polyester fiber1 suture material was substituted for the
elastic suture material used by Marks et al. In addition, surgical needles were
used to insert the prosthesis through the cricoid cartilage and muscular process
of the arytenoid cartilage (Martin's uterine, 1/2 circle, cutting edge 1860-30
and 1860-60”, respectively).

Statistical Analysis--A two-way analysis of variance was used to evaluate
the effects of exercise and the surgical procedures on upper airway flow mecha-
nics, blood gas tensions and heart rate. When F values were significant at P<

0.05, treatment means were compared using Tukey'sca procedure.14

8. Results
Prior to surgical intervention (baseline), increasing treadmill speed from
standing to the trot and gallop progressively increased HR, f, Vlmax, ngax,
PuI, Pug, Hb, and Pacoz, and decreased Paoz, pH, and HCO3', while 21 and Zg were
unchanged (Table 1).

 

I 5 Ticron, American Cyanamid Co, Pearl River, New York.

m Martins Uterine Needles, Anchor Products Co., Addison, IL.

27

Table I Effects of exercise on upper airway flow mechanics values, blood gas

tensions, and acid base parameters in five horses before surgical

 

 

intervention.

Exercise
Value Standing__ Trotting, Galloping
HR(m1n-1)(X§sE) 41.2:9.2 143.6:18.53 192.6:s.4a
f (min-1) 15.6:3.1 67.2_+_3.5a 88.8:7.53
1...... (Us) 4.31.5 38.014.73 56.3_+_3.2a.b
ngax (L/s) 4.9_+_1.o 40.715.“ 59.013.63.13
PuI (cm of H20) 2.71.4 20.913.83 29.714.0a.b
Pug (cm of H20) 1.81.4 9.53.0 11.911.5a
21 (cm of H20/L/s) £31.06 £31.06 .52:.06
25 (cm of HZO/L/s) 4131.11 321.02 211.03
P302 (Torr) 94.6_+_3.6 67.6:1.7al 55.6_+_2.9a-b
Paco2 (Torr) 37.8:.9 41.2:33 43.7:1.4a
pH 7.414;.007 7.3573016 7.2791.012a.b
HCO3' (mEq/L) 23.855 22.7_+_.9 20.011.0a
Hb (gm/dl) 12.6159 16.51.33 17.2_+_.3a.b

 

a Data significantly different from same measurement made while standing.

b Data significantly different from same measurement made while trotting.

28

Following recurrent laryngeal neurectomy, Z1 and PuI (Figure 3a and 4a)
were significantly increased at the trot and gallop compared to baseline. These
increases were unattenuated by ventriculectomy but were reversed after prosthe-
tic laryngoplasty. No significant differences in Zg and Pug (Figure 3b and 4b)
were observed between baseline measurements and those made following any surgi-
cal manipulation while animals were standing or moving at any treadmill speed.

When compared with baseline measurements at the gallop, VImax (Fig 5a) was
significantly decreased following recurrent laryngeal neurectomy. VImax
measured following ventriculectomy or prosthetic laryngoplasty was not signifi-
Cantly different from baseline measurements. Following recurrent laryngeal

neurectomy, ngax at the gallOp (Fig 5b) was unchanged compared to baseline

measurements. A significant reduction in ngax measured following ventriculec-
tomy was reversed by prosthetic laryngoplasty.

Following recurrent laryngeal neurectomy, f at the gallop (Fig 6) decreased
concomitant with an increase in Paco2 (Fig 7a) when compared with baseline
measurements. Paco2 and f were not statistically different from baseline
measurements following ventriculectomy or prosthetic laryngoplasty.

When compared with baseline measurements, left recurrent laryngeal neurec-
tomy, ventriculectomy, and prosthetic laryngoplasty had no effect on Pao2 (Fig
7b), HR (Fig 8), pH (Fig 9), or Hb (Fig 10). However, in standing horses following
ventriculectomy, there was a slight but statistically significant increase in

Paco2 (Fig 7a) and HC03' (F19 11)'

C. Discussion
Inspiratory and expiratory impedance remained unchanged with exercise while
significant increases in heart rate, respiratory frequency, inspiratory and

expiratory flow, inspiratory and expiratory pressure, arterial carbon dioxide

1.57

1 .04

2‘ (cm H20 ' L“1 - sec)
9
01
l

 

0.01

Figure 3a.

29

a;
- Control * I *
ZZI Neuroctorny
E Ventriculectomy * ,1.

[XXI Laryngoplasty 'f

 

 

 

 

 

Standing Trot

Inspiratory impedance at three levels of exercise before and after
surgical intervention. The asterisk (*) indicates the value is
significantly different from baseline (before surgical intervention)

3O

 

  

 

 

 

 

1.5-
IIIII Cmuurol
IZZ] Nourectorny
A [:1 Ventriculectomy
:9: [XXI Laryngoplasty
F: 1.0-4
I
.1
(3
N
I:
E 0.54
3
III
N
(I.
0.0-

 

Standing Goll10p

Figure 3b. Expiratory impedance at three levels of exercise before and after
surgical intervention.

31

   

    
   
       
       
       
       
      

75- *
- Control at
[22 Neuroctomy ,
E Ventriculectomy fl
[XXI Laryngoplasty
3 SO-J
N
I
I; 956%
V w
o
a? zs-l 50’:
9’4 ’34
a a:
c . 4
a
a:
‘0‘
()_J Inna-Ilvmoa 'mOA

 

 

 

 

 

Standing Trot GaIIOp

Figure 4a. Peak transupper airway inspiratory pressure at three levels of exer-
cise before and after surgical intervention. The asterisk (*) indi-
cates the value is significantly different from baseline (before
surgical intervention).

 

75-

8 504
N
I
E
8

E!" 25.1

04

Figure 4b.

32

- Control

1221 Neurectorny
[2:1 Ventriculectomy
[XXI Laryngoplasty

    

"‘ — '.'.‘

Standing . Trot GaIIOp

Peak transupper airway expiratory pressure at three levels of exer-
cise before and after surgical intervention. The asterisk (*) indi-
cates the value is significantly different from baseline (before
surgical intervention).

 

75-

f‘ 50-
c1
11
01
.4,

i 25.
':>

(3-

Figure 5a.

33

llIIliJontnol

ZZI Neurectorny
E2] Ventriculectomy
[XXI Laryngoplasty

 

W*

 

 

Standing Trot Gallop

Maximal inspiratory flow at three levels of exercise before and
after surgical intervention. The asterisk (*) indicates the value
is significantly different from baseline (before surgical
intervention).

34

 

 

 

 

75-1
lIIII chNrol
ZZI Neuractomy
E3 Ventriculectomy
[XE Laryngoplasty
1’.“ 501
o
o
n
.41
1g 25-l
' >
DJ

 

Standing Trot

Figure 5b. Maximal expiratory flow at three levels of exercise before and after
surgical intervention. The asterisk (*) indicates the value is
significantly different from baseline (before surgical intervention)

 

1 OO-
75-4

T: 50
u. .1

.5,

253
o_l

Figure 6.

35

- Control

iZZl Neurectomy
E: Ventriculectomy
[XE Laryngoplasty

 

   
 
  
  
   
  

   
 

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A

’9

  
  

O

   
   
  
  
 

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9
9%

A

  

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01

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O

     
  
   
  

O

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'9
of.

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V

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O

   

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‘5

   

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0

9'9
920

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a.

 

 

 

 

A

Standing Trot Gallop

 

Respiratory frequency at three levels of exercise before and after
surgical intervention. The asterisk (*) indicates the value is
significantly different from baseline (before surgical intervention).

75-

50-

Paco: (Torr)

 

251

Figure 7a.

36

IIIII (menthol

IZZ Nouroctomy
E Ventriculectomy
[XXI Laryngoplasty

  

 

 

 

 

  

A
Standing Trot

Arterial carbon dioxide tension at three levels of exercise before
and after surgical intervention. The asterisk (*) indicates the
value is significantly different from baseline (before surgical

intervention).

37

100-
- Control
221 Nouroctomy
E Ventriculectomy
IZXI Loryngoplooty
A 75..
S
b
6‘
6‘!
50-
251 /‘

 

 

 

 

 

 

Standing Trot

7b. Arterial oxygen tension at three levels of exercise before and after 37
surgical intervention.

38

- Control

[21 Nouroctomy

 
 

   
   

no»! . »

   
  

463C

«940. 49.0
o 0900 9

OK!»

ACV

  

   

          

 

  

 

 

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var

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033%

DA

AIVZO

19.0w

 

 

  

       

    

   

   

    

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7

 

 

:3 Ventriculectomy
[XX] Laryngoplasty

‘

v

049...
999.

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A

 

 

soJ

()—

Standing

Heart rate at three levels of exercise before and after surgical

intervention.

Figure 8.

39

 

7'5'1 - Control
EZSZIIWouroctOMHy
C21 Ventriculectomy
[XXI Laryngoplasty
7.4-
I
a.
7.3-
7.2-l

 

 

 

 

Standing » Trot Golloo

Figure 9. pH at three levels of exercise before and after surgical
intervention.

40

201
- Control

221 Neurectomy
[:23 Ventriculectomy
[XXI Laryngoplasty

:3

l——i
o 9"
’30 of

1.

 

V
A

v
A

'o
’9

(D
L
‘0

to.

o o
.920

V
A

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O>

Hb (gm ° dl—I)
.920.

’9

A,

o 9
0’9.

"

 

‘9

A

2020.

\
“0*
>20

 

 

 

 

 

 

 

 

 

Standing Trot Gallop

Figure 10. Hemoglobin eoncentration at three levels of exercise before and
after surgical intervention.

 

30-
L, 254
0'
DJ
.5,
l
5’ 204
C)
I

151
Figure 11.

41

- Control
221 Nouroctorny
EZZJ‘Vonhflcukuflxuny

XXI Laryngoplasty

 

 

 

 

Standing Trot Gallop

Bicarbonate concentration at three levels of exercise before and
after surgical intervention. The asterisk (*) indicates the value
is significantly different from baseline (before surgical
intervention).

42

tension and hemoglobin concentration were measured. Concurrently, significant
decreases in arterial oxygen tension, bicarbonate concentration, and pH were
measured (Table 1). Exercise results in tachypnea as well as progressive
hypoxemia, metabolic acidosis, and hemoglobinemia. Other investigators have
reported similar results.73:75981 During exercise, left recurrent laryngeal
neurectomy increases inspiratory impedance in the upper airway requiring larger
driving pressures (PuI) to generate Vimax equivalent to those measured prior to
surgical intervention. As the work of breathing increases, the ventilation
response to C02 is reduced69 and may in part explain the hypercapnia measured at
the gallop following left recurrent laryngeal neurectomy.

The larynx and nostrils are not ridgedly supported by bone or cartilage and
require muscular contraction to dilate and maintain a constant upper airway
intraluminal diameter during inspiration. Muscle contraction prevents dynamic
collapse of the airway and increased inspiratory impedance, especially during
exercise. Following left recurrent laryngeal neurectomy inspiratory impedance
increases, presumably as a result of altered airway geometry and intraluminal
obstruction by the paralyzed arytenoid and vocal ligament. Therefore, when com-
pared with baseline measurements at a given treadmill speed, inspiratory

pressure must increase to prevent a decrease in inspiratory flow.7o

Following ventriculectomy, healing of the everted laryngeal saccule by
fibrous scar tissue is thought to enlarge the diameter of the glottis by latera-
lization of the vocal cords.14 Some investigators report that retraction of the
paralyzed vocal ligament or arytenoid is not evident on endoscopic
examination.5914 The results of our study show that ventriculectomy failed to
alleviate the increased inspiratory impedance and the increased inspiratory

transupper airway pressure observed in exercising horses following left

43

recurrent laryngeal neurectomy. In contrast, prosthetic laryngoplasty effec-
tively improved upper airway flow mechanics returning inspiratory impedance and
pressure to baseline values. Therefore, if lateralization of the vocal cords
occurs following ventriculectomy, it is insufficient to prevent dynamic collapse
of the upper airway during exercise. Instead, it appears that stabilization of
the arytenoid cartilage by laryngoplasty is necessary to improve upper airway
flow mechanics in exercising horses with left laryngeal hemiplegia.lo

The effect of ventriculectomy was evaluated 30 days following the surgical
procedure when the fibroblastic phase of healing is complete in most tissues.82
It is therefore unlikely that additional time between ventriculectomy and the
measurement periods would have significantly altered the results of this study.

Flow rates obtained in this study (7: SEM, 59.0 1 3.6) were higher than
those previously reported by our laboratOry10 and were similar to those attained
by racing horses.33:84 Because the tendency for dynamic collapse of unsupported
structures increases as inspiratory flow rate increases85, our conclusions
regarding the effectiveness of ventriculectomy and prosthetic laryngoplasty may
be applicable to conditions encountered during racing.

Either procedure, the ventriculectomy or prosthetic laryngoplasty, increases
inspiratory flow (VImax) at the gallop when compared with measurements following
recurrent laryngeal neurectomy. This suggests ventriculectomy alone may improve
inspiratory flow. This result must be interpreted with caution as the pressure
difference across the airway causing the airflow (PuI) was still significantly
elevated at the gallop when compared with baseline measurements. However, the
decrease in expiratory flow (ngax) at the gallcp following ventriculectomy when
compared with baseline measurements and those made following ventriculectomy, or
prosthetic laryngoplasty, suggest ventriculectomy does reduce expiratory flow as

expiratory pressure (PuE) is not significantly reduced when compared with base;

44

line measurements. Possibly, the fibrosed ventricle following ventriculectomy
may cause partial obstruction of the airway or reduce airway compliance.

The reduction of respiratory frequency at the gallop following recurrent
laryngeal neurectomy probably resulted from the high inspiratory impedance.86
High inspiratory impedance limited inspiratory flow rates, and therefore
necessitated a reduction in respiratory frequency in order to maintain alveolar
ventilation. In spite of this change in respiratory pattern, hypoventilation at
the gallop still occurred. At the gallop, respiratory frequency is coupled with
stride frequency.87 Although we did not measure stride frequency or stride
length, if the coupling persisted in our horses with left laryngeal hemiplegia,
stride frequency must also have been reduced from control values.

Alternatively, increased stride length, uncoupling of stride, and respiratory
frequency or a change in the coupling ratio between stride and respiratory fre-
quencies could have occurred.

As has been previously reported, hypoxemia occurs in galloping horses even
without left recurrent laryngeal neurectomy. Blood gas tensions are routinely
corrected to rectal temperature. Increases in arterial blood temperature in
exercising horses has been previously reported33, though many studies use rectal
temperature to correct for temperature effects on blood gases.77a89 In a
separate experiment, right carotid artery blood temperature and rectal tem-
perature were concurrently measured in two horses using the same exercise proto-
col described above. Arterial temperatures were measured using a 6 French
thermistor-tipped cathetern and a thermodilution computer.o Rectal temperatures
remained unchanged while arterial blood temperatures increased markedly. For

each horse evaluated, arterial temperature increased at the trot and gallop,

 

n American Edwards Lab, Irvine, Calif.

0 Model 9520A Cardiac Output Computer, American Edwards Lab, Irvine, Calif.

45

1.6°C and 3.1°C, respectively, from a temperature of 36.6° measured while
standing. This suggests that during short periods of exercise as employed in
this study, rectal temperature is inappropriate for correcting blood gas ten-
sions as equilibration between core temperature and rectal temperature does not
occur. Therefore, for comparison, blood gas tensions were corrected again for
estimated changes in arterial blood temperature for each measurement period, and
the results are presented in Table 2. Unless otherwise mentioned, Pao2 and Paco2
discussed in the remainder of the paper refer to values obtained after correc-
tion for rectal temperature.

Before surgical intervention, mean Pao2 decreased significantly from 94.6
torr while horses were standing to 55.6 torr at the gallop. Hypoxemia of simi-
lar magnitude has been previously reported in exercising horses.72:73 The
mechanism for the decrease in Pao2 is unknown but hypoventilation is not the
sole cause.69 Because the Pao2 was unaffected by any of the surgical interven-
tions, exercise intolerance associated with left laryngeal hemiplegia is not due
to arterial hypoxemia.

Bisgard has suggested that face masks may change the ventilation pattern
during exercise and alter respiratory frequency and arterial blood gas tensions
in exercising ponies.75.35’90 It is possible that the face mask may have caused
hypoventilation by increasing dead space and thus altered arterial blood gas
tensions.7S However, the baseline Paco2 corrected for arterial temperature
(49.2 Torr) was similar to previously reported values for horses72:73 exercising
without a face mask. This suggests the face mask did not alter Pacoz.

In conclusion, ventriculectomy was ineffective in correcting upper airway
mechanical impairments to flow in exercising horses with left laryngeal hemiple-
gia. However, even when exercising at high speeds, upper airway obstruction in
horses with left laryngeal hemiplegia was successfully corrected using prosthe-

tic laryngoplasty.

46

Table 2 The effects of exercise on arterial oxygen and carbon dioxide tensions
following correction for mean arterial blood temperature (A) or mean

rectal temperature (R) in two horses.

 

 

Exercise
Value Standing Trotting Galloping
Pao2 Torr (A) 92.3 68.1 66.9
Pao2 Torr (R) 94.6 67.6 55.6
Paco2 Torr (A) 37.2 43.4 49.2

Paco2 Torr (R) 37.8 41.2 43.7

 

VI.

47

Summary and Conclusions

A technique was develOped to measure upper airway impedance in exercising

horses.

In normal horses, increasing the intensity of exercise progressively
increased HR, f, VImax, ngax, PuI, PuE, Hb, and Pacoz, decreased Paoz, pH,

and HCO3‘, while Z1 and Zg were unchanged.

Left recurrent laryngeal neurectomy increased Z1, PuI, Pacoz, concomitant

with a reduction in f and V1max.

Parameters measured following ventriculectomy were unchanged from those
measured following LRLN except for a decrease in ngax at the gallop and
increases in Paco2 and HCO3- while horses were standing. Therefore, ventri-
culectomy was ineffective in altering the increase in inspiratory impedence

measured after LRLN.

Parameters measured after prosthetic laryngoplasty were unchanged from base-
line measurements. Therefore, though prosthetic laryngoplasty was ineffec-
ive in improving blood gas tension and acid-base impairments, it was effec-

tive in reducing inspiratory impedence measured after LRLN.

Rectal temperatures may be inappropriate for correcting temperature effects
on blood gas tensions. Increased arterial blood temperature can be measured

after only two minutes of high intensity exercise.

Changes in blood gas tensions in exercising horses may be a poor indicator
of airway obstruction. Exercise in normal horses causes large changes in
blood-gas tensions that could mask the effects of an obstructive disease or

surgical procedure to treat the disease.

8.

48

The effect of the mask on airway flow mechanics parameters, blood gas ten-

sions, and acid-base parameters should be examined.

The effect of other upper airway diseases (entrapped epiglottis, rostral
displacement of the palatOpharyngeal arch, arytenoid chondritis, etc.) on
upper airway flow mechanics and blood gas tensions remains to be deter-
mined. Additionally, the efficacy of surgical procedures to treat
laryngeal hemiplegia and other diseases of the upper airway can be assessed

using the technique described in this thesis.

8.

49

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