6 Respiration

Those physical actions by means of which air is brought into and is expelled from the lungs are not infrequently termed respiration. They should, more properly, be called ventilation because, in physiological terms, respiration includes both the chemical and physical processes which enable an organism to exchange gases with its environ­ment. In the case of higher organisms, including animals and man, survival is dependent upon the efficient functioning of a series of specialized structures which regulate the exchange between oxygen from the atmosphere and carbon dioxide in the tissues.

The physical features of respiration involve the diaphragm and intercostal muscles, which are in action during breathing. The volume and frequency of the respiratory movements are controlled by 'centres' in the brain stem which maintain inspiration and expiration. During inspiration, air enters the nose and mouth and, passing through the larynx, enters the trachea and makes its way to the pulmonary alveoli via the bronchi, bronchioles and alveolar ducts. The structure of the pulmonary alveoli is such, and the relationship with the numerous pulmonary capillaries so intimate, that exchange of oxygen and carbon dioxide occurs freely in normal conditions.

The exchange of these gases takes place by simple diffusion and is dependent on the pressure gradient (partial pressure) of the gas across the membrane separating the alveolar air and the blood in the alveolar capillaries. Although blood takes only about a second, at most, to pass through the capillaries, gaseous exchange is com­plete because of the enormous diffusing area.

Breathing is regulated by the respiratory centres consisting of an inspiratory centre and an expiratory centre in the medulla and a pneumotaxic centre in the upper pons. The in­spiratory and expiratory centres are reflexly influenced by afferent vagal stimuli from stretch receptors in the lungs, by afferent impulses from the carotid and aortic chemoreceptors, and from the higher levels of the brain. In addition the inspiratory centre is extremely sensitive to changes in the partial pressure of carbon dioxide and in hydrogen ion concentration, less so to changes in oxygen tension, in the blood.

It is not possible to diagnose any given disease, with certainty, by observations on the physical aspects of respiration alone, but it is sometimes possible tentatively to recognize specific entities by noting the character of the respiratory movements. Respiratory activity is assessed by noting the movements of the ribs and sternum, and flanks (in response to the expansion and contraction of the lungs and the movement of the diaphragm), preferably when the animal is in the standing position, as re­cumbency will have a modifying effect on respiration, more particularly in ailing animals.

This part of the clinical examination is best performed in conjunction with the general inspection, prior to the physical procedures, or the application of restraint. In selected cases exposing the animal to physical effort may be a necessary part of the examination, as a means for determining respiratory efficiency. The cli­nician should stand behind and to one side of the animal, so that both the thoracic and abdo­minal areas of the body are in view. It is advisable to observe the animal from both sides, in order to determine whether the respiratory movements are bilaterally similar. In quiet animals, deter­mining the frequency and rhythm of the respirations is facilitated by placing one hand on the lower part of the flank. The respiratory rate may also be determined by observing nostril move­ments, or more efficiently by auscultation over the thorax or trachea. The following points are noted: (a) rate or frequency (number/minute) (see Table 3); (4) type; (c) rhythm (regularity); and (d) quality (amplitude or depth of the res­piratory movements). Counting the frequency of the respirations is performed on the same basis as for the pulse. Physiological or abnormal variation may occur in any one or more of the four stated features.

The act of respiration is controlled volun­tarily and reflexly through the monitoring func­tion of the respiratory centres in the medulla oblongata. Particularly in the dog, excitement, fear or high environmental temperature and humidity may cause the animal to take sudden short breaths with great rapidity; this panting respiration (polypnoea) must not be confused with dyspnoea.

Clinical Assessment of Respiration

Respiratory Rate

The state of normal quiet breathing is called eupnoea. The rate of external respiration de­creases directly with the bodyweight in domestic animals, with the exception of cattle. Sheep and pigs have the fastest rate and horses the slowest.

Increased respiratory frequency occurs where-ever there is an increased demand for oxygen by the tissues. As a consequence it is seen when the animal is excited, after exercise or exposure to high environmental temperature or humidity and in obesity. It is a regular concomitant of fever and is observed in various pulmonary diseases, severe cardiac disease, obstruction of the upper respiratory passages, in conditions making respiration painful (pleurisy, peritonitis) and in

anaemia (deficiency of erythrocytes producing hypoxia). Increased respiratory rate, with or without an increase in the amplitude of the movements, is termed hyperpnoea. When there is increased respiratory frequency with reduction in depth of the associated movements the term polypnoea is applied.

Decreased or retarded respiratory frequency (oligopnoea) is rare; it occasionally occurs in animals with space-occupying lesions of the brain (chronic acquired and congenital hydrocephalus), in stenosis of the upper respiratory tract and in uraemia.

Type of Respiration

This is assessed by noting the way in which the observable respiratory movements are shared between the thoracic and abdominal walls (Fig. 26). The mechanics of respiration result from the opposing forces presented by the lungs which, because of their elastic tissue, tend to collapse, and the chest wall with its tendency to expand outwards. From the commencement of inspiration when the respiratory muscles con­tract, the intrapleural pressure becomes more subatmospheric. The contraction lowers the diaphragm and elevates the rib cage. In normal respiration, movement of the abdominal wall is a secondary effect; it varies in degree between species.

If the movements of both component parts are of equal extent, the respiration is said to be costo-abdominal in type. As a rule, normal respiration in horses is costo-abdominal, in dogs and cats it is mainly costal and in cattle, sheep and goats the movement of the abdominal com­ponent is greater. Predominantly costal or thora­cic type of respiration occurs as an abnormal manifestation when the action of the diaphragm —the principal muscle of respiration—is im­paired, e.g. by paralysis, rupture, abscessation, pressure by a neoplasm or accumulation of gas or fluid in an abdominal viscus or in the peri­toneal cavity; in diseases of the lungs, particu­larly those, such as pneumonia and acute pul­monary oedema, in which the entry of air into the lungs is impeded; and in peritonitis, in which movement of the abdominal wall and diaphragm is suppressed on account of pain.

A wholly abdominal type of respiration occurs in acute pleurisy because of the pain caused by movement of the thoracic wall; in tuberculous pleurisy, or thoracic nocardiosis with effusion in the dog and cat; in chronic alveolar emphy­sema (heaves) as a result of the decrease in the elastic collapse of the lungs which necessitates the voluntary use of the abdominal muscles to bring about the forcible expulsion of air during expiration; in paralysis of the intercostal muscles; and in those conditions in which the outward flow of air is impeded. In the initial stages of acute pleurisy, the fixation of the costal arch, resulting from the limitation of costal movement, produces the so-called pleuritic ridge, noted particularly in the horse.

Respiratory Rhythm

The three phases in each normal respiratory cycle are inspiration, expiration and pause. The

period of expiration is slightly longer than that of inspiration; the duration of the pause in healthy animals depends upon whether the ani­mal is relaxed and resting, or has recently been excited or exercised. During inspiration, con­traction of the intercostal muscles causes the costal arch to move outwards, and during in­spiration it moves inwards. Inspiration is the result of an active movement of the respiratory muscles (diaphragm, intercostal and abdominal muscles), initiated by the respiratory centres, whereas expiration is almost entirely passive, the elastic lungs contracting with the collapse of the thorax. In equine species, expiration has a biphasic character in that two peaks of expira­tory airflow occur. This is not associated with a double movement of the respiratory muscles, so that confusion with chronic alveolar emphysema does not arise.

Irregular respiration is not uncommon in normal animals, particularly the dog and pig (interrupted breathing or sniffing). Prolongation of inspiration is observed when there is partial obstruction of the upper respiratory tract and prolongation of expiration in pulmonary em­physema (chronic alveolar emphysema in horses, atypical pneumonia, parasitic pneumonia and anaphylaxis in cattle), when a double movement of the abdominal wall may be noted. In normal animals, any increase in the respiratory rate occurs at the expense of the pause period, which becomes correspondingly shorter. While in the majority of respiratory diseases involving the lungs, the cycle of respiration consists of two phases and the pause does not occur.

Dropped respirations (Fig. 27) cause the most marked change in respiratory rhythm. Charac­teristic forms of dropped respirations are recog­nizable. Cheyne-Stokes respiration is an ab­normal type of breathing in which a period of respiratory arrest (apnoea) occurs for 15-30 seconds, followed by a gradual increase and then a gradual decrease in the amplitude of the move­ments which are regularly succeeded by a further respiratory hiatus. It is characteristic of advanced renal and cardiac diseases, and severe toxaemia. Biot's respiration is characterized by recurring series of relatively shallow, rapid breaths (poly-pnoea), alternating with periods of apnoea; the intervals of respiratory arrest, and periods of activity, vary in length. It occurs in meningitis affecting particularly the region of the medulla oblongata. In syncoptic respiration, a pause is followed by deep breathing (hyperpnoea) that gradually becomes shallow until apnoea prevails. These three types of abnormal respiration should be regarded as indicating an unfavourable prognosis; they reflect decreased sensitivity of the respiratory centres in the medulla oblongata to carbon dioxide in the circulating blood.

Respiratory Depth

Normally there is great variation in the ampli­tude of the respiratory movements. Any form of exercise increases the depth of respiration be­cause of temporary hypoxia; at rest, amplitude is reduced. In deep breathing (hyperpnoea) the considerable movements of both the thoracic and abdominal walls are clearly visible. In shal­low breathing the movements of these compo­nents is very slight. Very deep respiration is said to be 'laboured', it occurs in dyspnoea. Irregula­rity in depth, and in the intervals between suc­cessive respirations, is commonly seen in dys­pnoea. Asymmetrical respiration occurs when there is unilateral deficiency or absence of move­ment; it is sometimes recognizable in severe disease in one lung, the amplitude of movement on the healthy side being normal or increased in extent, while that on the affected side is reduced to a variable degree, e.g. collapse or consolidation of one lung, unilateral pleural exudation, hydro-thorax or pneumothorax and rupture of the diaphragm with unilateral herniation of abdomi­nal viscera.

Dyspnoea

Any subjectively assessed difficulty in respira­tion, causing apparent distress to an animal, is known as dyspnoea. It may be a physiological occurrence following strenuous exercise but it more usually arises out of disease and is caused by hypoxia in association with hypercapnia. Dyspnoea may take the form of a change in the rate, type, rhythm or depth of respiration. Ac­cording to whether the difficulty arises at inspira­tion, at expiration or during both phases, dyspnoea is referred to as inspiratory, expiratory or indeterminate. In order to determine the degree of dyspnoea (slight, moderate or severe) it may be necessary to have the animal exercised. The more severe the dyspnoea, the correspon­dingly longer the recovery period after exertion (30-60 minutes or longer, instead of the usual 5-10 minutes in healthy animals). Obviously severe cases of dyspnoea can be recognized without recourse to exercise.

Inspiratory dyspnoea is a feature of all those diseases in which entry of air into the lungs or transfer of oxygen to the blood or tissues is inhibited, e.g. in stenosis of the air passages, bronchopneumonia, pulmonary oedema, pul­monary congestion, ruptured diaphragm, pleu­risy and hydrocyanic acid poisoning. When there is inflammation or congestion of the lungs or pleura, increased sensitivity of the Hering-Breuer reflex is a contributory cause of dyspnoea. In this form of dyspnoea the accessory respiratory movements become activated; dilatation of the nostrils; in cattle, dogs and cats, extension of the head and neck (Fig. 28) and opening of the mouth; costal type of respiration; depression of the intercostal spaces; forward movement of the body during each inspiration; outward rotation of the elbows; prolongation of inspiration. In the dog, the cheeks may be sucked inwards during inspiration (seen particularly in breeds with loose, mobile cheeks, when the mouth is closed or partially opened).

Expiratory dyspnoea occurs when the escape of air from the lungs is impeded, e.g. in pul­monary emphysema, as the result of the reduced elasticity of the lungs causing reduction in the volume of tidal air expelled and so leading to hypoxia, and in pleural adhesions. In these situa­tions the dyspnoea is caused by ambient hypoxia and by the forced expiration which is an attempt to restore the tidal volume to near normal. The clinical signs of this form of dyspnoea are: de­velopment of a groove in the anterior part of the flank, along the line of the costal arch—the so-called 'heaves line' (n.b. This is observed in transient form also, in lean, healthy horses following vigorous exercise); protracted expira­tion; double expiratory lift involving the ab­dominal muscles; 'pumping' of the anus (see below). In the dog, the lips and cheeks may be blown outwards.

Indeterminate dyspnoea is the commonest type. It is seen to occur in pneumonia, bronchitis, cardiac diseases such as failure of the left ven­tricle leading to congestion and oedema of the lungs, severe anaemia, acidosis, occasionally in meningitis, encephalitis or space-occupying lesions of the brain, stenosis of the nasal pas­sages, etc.—diseases in which there is a fairly severe disturbance of tissue respiration (hypoxia) or difficulty in both inspiration and expiration. Other factors which contribute to development of this form of dyspnoea include increased sen­sitivity of the Hering-Breuer reflex, and the influence of increased venous pressure on the respiratory centres.

'Pumping of the anus' is a sign which appears in severe dyspnoea, usually in association with dilatation of the nostrils, particularly in estab­lished chronic pulmonary emphysema in the horse. During inspiration, when the circum­ference of the abdomen is increased, the anus retracts into the plevic cavity, and at expiration, when the size of the abdominal cavity is reduced, more particularly during the second expiratory movement, the anus is protruded.

A double lifting movement involving the abdominal wall is observed during expiration when the elasticity of the lung is impaired. Pas­sive contraction of the lung, which is only partial, produces the first part of the double phased expiratory movement; the remainder of the tidal air has then to be actively expressed with the aid of the abdominal muscles, this being the second phase of the expiratory move­ment. A double expiratory lift of the abdominal muscles in the horse is usually indicative of chronic alveolar emphysema (broken wind). In calves, it is often seen in parasitic bronchopneumonia.

Abnormal Respiratory Noises

A hiccough (singultus) is a short, jerky in­spiration, caused by stimulation of the phrenic nerve producing sudden contraction of the diaphragm. It causes an abrupt sound which varies in volume according to the size of the animal, but in most cases it is much less obvious than in man. In the horse of intermediate or large size, a severe attack is associated with an inspiratory 'grunt', which is somewhat similar to the sound produced during attempted regurgita-tion in gastric tympany. The spasmodic contrac­tion of the diaphragm is readily identified by placing the hand on the thoracic wall, or near the costal arch in the region of the attachment of the diaphragm. In hiccough, the abdominal wall is jerked outwards (in spasm of abdominal muscles, the movement is inwards) because of the sudden increase in intra-abdominal pressure produced by the sharp contraction of the dia­phragm. When the horse is severely affected indoors, the sudden contractions may cause the stall and surrounding fittings to vibrate.

Other abnormal respiratory noises include sneezing due to nasal irritation; snoring caused by pharyngeal occlusion as in tuberculous lym­phadenitis of the retropharyngeal lymph nodes; roaring and whistling in paralysis of the intrinsic muscles of the larynx; grunting, which is a forced expiration against a closed glottis, and is associated with many painful conditions, par­ticularly those involving the respiratory tract; coughing (see p. 110) due to irritation of the pharynx, larynx, trachea and bronchi; and yawning, which is a prolonged inspiration, with the mouth opened widely and the soft palate raised, followed by an inspiration. In the dog it is accompanied by a fairly loud sound. The purpose of yawning is uncertain but when it occurs only occasionally it is not regarded as a sign indicating disease. Frequent yawning is observed in association with catarrhal gastritis, chronic 'hepatitis' and in some diseases of the brain, e.g. equine encephalomyelitis, dumb rabies. The yawning movements in rabies are suggested to be voiceless attempts to bellow or bark.

Respiratory Insufficiency

When it is functioning efficiently the respira­tory system oxygenates and removes carbon dioxide from the blood in the pulmonary circula­tion (ventilation or external respiration). Inter­ference with the gaseous exchange at this point, leading to reduced supply of oxygen for tissue (internal) respiration, can occur in a variety of respiratory diseases, e.g. pulmonary diseases (pneumonia, atelectasis, pleurisy, pneumothorax, pulmonary oedema and congestion, em­physema, neoplasia), partial occlusion of the respiratory passages as in bronchitis, rhinitis, tracheitis and neoplasia, etc. As a result the blood oxygen level decreases and the carbon dioxide concentration increases (hypercapnia), leading to greater respiratory activity through the overriding mediation of the respiration centres. In mild affections, in which internal respiration is only slightly disturbed, these functional changes alone may be effective in restoring tissue oxygenation to a normal state. When the interference is serious, because the extreme range of respiratory compensatory ac­tivity fails, respiratory insufficiency will develop and lead to hypoxia. Many of the important clinical signs of respiratory disease, therefore, arise from hypoxia due to respiratory insuffi­ciency, which may become severe enough to cause death from respiratory failure. The signs include changes in the character of the respira­tions which may be manifest as hyperpnoea or dyspnoea, cyanosis which is recognized as a bluish discoloration of the skin and visible mucous membranes and, depending upon the nature of the particular respiratory disease, coughing and nasal discharge.

Hypoxia

It is necessary in the consideration of the clinical aspects to remember that failure of tissue oxygenation can occur in other ways than by means of primary respiratory disease which produces ambient hypoxia. In this type of hypoxia the oxygen tension in the arterial blood is lower than normal so that haemoglobin is not saturated with oxygen to the normal extent. In anaemic hypoxia which occurs when there is a significant reduction in the blood haemoglobin concentration the total transporting capacity of the blood is inadequate to meet essential demands even although the percentage satura­tion and oxygen tension of the available haemo­globin are normal. This type of hypoxia occurs with anaemia due to any cause; a similar effect is produced when haemoglobin is converted to non-oxygen carrying pigments. In nitrite or chlorate poisoning haemoglobin is converted into methaemoglobin and in carbon monoxide poisoning conversion to carboxyhaemoglobin occurs; both these haemoglobin derivatives are stable products and are completely inactive in relation to oxygen transportation or release. In stagnant hypoxia the blood flow rate through the capillaries is reduced so that a tissue oxygen deficit occurs even although the oxygen satura­tion and tension of arterial blood and the total oxygen load are normal. This form of hypoxia occurs generally in congestive heart failure and in peripheral circulatory failure (arterial throm­bosis and embolism) and locally in venous obstruction. In histotoxic hypoxia which occurs in cyanide poisoning tissue oxidation is inhibited by paralysis of cytochrome oxidase even al­though the blood is fully oxygenated. Narcotics also depress tissue oxidation to a variable degree by inhibiting dehydrogenase systems.

The common causes of ambient hypoxia in animals are those diseases associated with lesions or dysfunctions of the respiratory tract and which reduce alveolar oxygen tension. These various diseases all cause a reduction in the vital capacity; they include pneumonia, in which the alveolar epithelium is altered, pulmonary atelec­tasis, pneumothorax, pulmonary oedema and congestion, and painful conditions such as pleurisy which decrease the amplitude of chest movements (tetanus, strychnine poisoning, botu­lism and tick paralysis also cause impairment of chest movements). A similar effect is produced in those diseases in which accumulation of exu-date causes partial obstruction of the air pas­sages. Depression of the respiratory centre by drugs, or in toxaemia, also causes this type of hypoxia. Other non-respiratory conditions which cause this state include low atmospheric oxygen tension (altitude disease) and congenital cardiac and vascular defects in which serious arterio-venous shunts occur.

The degree to which compensatory mecha­nisms come into operation in the various hypoxic states depends upon their rate of develop­ment. Almost immediately (except in anaemic hypoxia) the chemoreceptors situated in the carotid and aortic bodies mediate an increase in amplitude of the respiratory movements (hyper-pnoea). A compensatory increase in the heart rate and stroke volume leads to an increase in the minute volume of the heart; this degree of improvement is unlikely in cases of hypoxia caused by major congenital cardiac and vascula defects and in congestive heart failure. An in­crease in the erythrocyte population of the blood (polycythaemia) may follow almost at once as the result of contraction of the spleen (most likely to be marked in the horse) or at a later stage following increased erythropoiesis in the bone marrow. When in spite of these compensa­tory mechanisms tissue oxygen lack becomes severe the function of certain organs becomes impaired. Because of its high oxygen demands, dysfunction of the central nervous system appears as an early sign followed by cardiac decompensation, hepatic and renal dysfunction and reduction of motility and secretory activity of the digestive tract.

Respiratory Failure

This, which is the terminal stage of respiratory insufficiency, is recognized clinically by cessation of movement of the respiratory muscles follow­ing a period of diminishing activity of the res­piratory centres. The character of the respiratory failure, which can be asphyxial, paralytic or tachypnoeic, depending on the primary disease, may be suggested by the clinical signs. Asphyxial (dyspnoeic) failure gives rise to hypercapnia and hypoxia of varying severity, so that the respira­tory movements are dyspnoeic, with alternating periods of apnoea, and gasping, in the terminal phase. It occurs when tidal volume is seriously reduced in upper respiratory tract obstruction, in pneumonia and in pulmonary oedema. Depres­sion of the respiratory centres by anaesthetic agents, other toxic chemicals, nervous shock, acute heart failure and severe haemorrhage pre­cedes paralytic respiratory failure in which the respirations rapidly decrease in frequency and amplitude, and finally cease, without dyspnoea supervening. In all forms of hypothermia, hyperventilation of the lungs produces hypoxia and acapnia and because of the reduced carbon dioxide tension in the blood the respiratory movements become rapid and shallow—tachy­pnoeic respiratory failure. This is the least com­mon form of the condition.