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THE HEART AND CIRCULATORY SYSTEM
Circulatory Dynamics
The cardiovascular system consists of two main structural units, the
heart and the blood vessels, which are jointly concerned in maintaining
the circulation of the blood and thereby ensuring normal exchange of
oxygen, carbon dioxide, electrolytes, fluid nutrients and waste
products between the blood and the body tissues. The autonomic
nervous system acts as an important regulator of the two components.
Either component may fail to function in an efficient manner
independently of the other. Of the two forms of circulatory failure, that
involving the heart is due to intrinsic factors, while in peripheral
circulatory failure there is defective venous return, the heart itself being
normal.
In heart failure two main effects are produced which are responsible for
the clinical signs shown by the affected animal. Although both effects
are produced simultaneously, one of them may be dominant, depending
upon the speed at which failure occurs. These effects result from failure
to maintain circulatory equilibrium and the nutrition of the tissues, most
particularly the oxygen requirements of the brain. Circulatory
equilibrium is deranged when the ventricular output is less than the
venous return, and this persists for a significant period. If this occurs
slowly, blood then accumulates in the veins and signs of congestive
heart failure develop. If cardiac output is markedly reduced then the
heart beat is suddenly arrested, producing acute heart failure.
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Peripheral circulatory failure is brought about by reduction in blood
volume, or by pooling of blood in the peripheral vessels as for example
in splanchnic vasodilatation. The end results are similar to those of
congestive heart failure although there is no primary defect of the heart
itself, the venous return being effectively ejected.
In the majority of animals, the heart has a considerable functional
reserve which maintains circulatory equilibrium under circumstances of
increased demand, such as those created by exercise and to a lesser
degree by pregnancy, lactation and digestion. The increased demands
are immediately met with by an increase in heart rate and an increase in
stroke volume. If the demands remain at an elevated level, a degree of
compensation may also be achieved through the development of cardiac
hypertrophy. Cardiac reserve can be eroded by many pathological processes, chemotherapeutic compounds and excessive physical exertion.
Diminution of cardiac reserve, which may be detected by assessing
exercise tolerance, is the first stage in heart disease. In the next stage,
when the cardiac reserve is completely lost, decompensation occurs
with inability to maintain circulatory equilibrium.
Regional Anatomy
In all species of domestic animals the chest is flattened laterally, usually
to a more marked degree in the lower two-thirds. The heart, suspended
at its base by the great vessels which traverse the mediastinum,
occupies a considerable part of the middle mediastinal region. The apex
of the heart is situated in the midline above the sternum.
In the horse the heart is asymmetrical in position, slightly more than half
of the organ being on the left of the median plane. The base, which is
directed dorsally, is situated on a level with the junction of the middle
and dorsal thirds of the dorsoventral diameter of the thorax, and
extends from opposite the second to the sixth intercostal space. The
apex is positioned centrally about 1 cm above the last sternal segment,
and about 2,5 cm anterior to the sternal diaphragm. The posterior
border is nearly vertical and approximates to a position opposite the
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sixth rib or interspace. The left surface of the heart, consisting almost
entirely of the wall of the left ventricle, covered by the pericardium, is in
contact with the lower third of the chest wall from the third to the sixth
rib. The relationship between the heart and chest wall on the right side
extends from the third to the fourth intercostal space only, because of
the relatively small cardiac notch in the right lung, and the degree of
cardiac asymmetry. Enlargement of the heart from any cause will
proportionately increase the area of contact between the organ and the
chest wall on the right side. Internally the heart contains four chambers
through which the flow of blood is directed, and regulated, by valves
situated at the entry or exit from the cavities. The right atrioventricular
orifice, guarded by the tricuspid valve, is situated opposite the fourth
intercostal space about 7 cm above the lower extremity of the fourth
rib. The pulmonary orifice, guarded by the pulmonary semilunar valve, is
opposite the third intercostal space immediately above the level of the
right atrioventricular orifice. The left atrioventricular orifice, guarded by
the mitral valve is situated opposite the fifth intercostal space about 10
cm above the sternal extremity of the fifth rib. The aortic orifice,
guarded by its semilunar valve, is opposite the fourth intercostal space
on a line level with the point of the shoulder.
In cattle, the degree of cardiac asymmetry is slightly greater than in the
horse. The base of the heart in this species extends from opposite the
third to about the sixth rib. The apex, which is median in position and
about 2 cm from the diaphragm, is opposite the articulation of the sixth
costal cartilage with the sternum. The posterior border, which is almost
vertical, is opposite the fifth intercostal space where it is separated from
the diaphragm by the pericardium. On the left side, the heart and
overlying pericardium are in contact with the chest wall from the third
rib to the fourth intercostal space. On the right side the extent of the
contact is limited to a small area opposite the ventral part of the fourth
rib, and the adjacent third and fourth interspaces. The right
atrioventricular orifice is opposite to the fourth rib almost 10 cm above
the costochondral junction; the pulmonary orifice, which is slightly
above this level, is opposite the third intercostal space; the left
atrioventricular orifice is mainly opposite the fourth intercostal space,
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and the aortic orifice is opposite the fourth rib, about 12 cm above the
sternal extremity.
In the dog the heart is placed so obliquely that the base, which is
opposite the ventral part of the third rib, faces mainly in an anterior
direction. The apex is blunt and positioned near the diaphragm on the
left of the median plane, opposite the seventh costal cartilage. The area
of contact between the heart and chest wall, through the overlying
pericardium, on the left side, extends from opposite the ventral parts of
the third to the sixth ribs. On the right side the area of contact is limited
to that extending between the fourth and fifth ribs.
Abnormal Types of Pulse
In order to extend and amplify the clinical information already obtained
by determining the pulse frequency and quality, attention should now
be directed towards detecting pulse abnormalities and interpreting their
possible significance. It must be appreciated that many of the variations
from the normal pulse reflect the functional status of the heart which is
influenced in a variety of ways. It should be remembered, however, that
pulse characters can also be significantly affected by extracardiac
factors, e.g. decreased amplitude because of reduced venous return as
well as from reduced contractile power of the myocardium. Reflex
acceleration of the heart occurs in painful conditions, e.g. spasmodic
colic, as well as in febrile diseases. In toxaemic and septicaemic
conditions all the circulatory components, including the myocardium,
blood vessels and medullary reflex centres, may be involved. The
myocardium and medullary reflex centres may also be influenced by
hypoxia in various forms of anaemia and in diseases, such as pneumonia,
which depress the pulmonary gaseous exchange. Diseases having the
latter effect will also cause cardiac disturbance because of the increased
resistance which develops in the pulmonary circulation. Other important
abnormalities of the pulse are due to primary heart diseases, which may
be functional or organic in character. Functional disease of the heart
occurs when no readily recognizable pathological lesion is observed,
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although it is probable that in many instances minute changes in
structure or biochemical lesions exist.
When cardiac disease is sufficiently severe to permit failure of
circulatory equilibrium along with inadequate oxygen provision to
meet the nutritional requirements of the tissues, obvious clinical signs
will be presented by the animal. The basic character of the cardiac
disease varies somewhat according to the species of animal involved.
In the horse, organic disease of the heart is infrequently encountered
(examples are endocarditis caused by Streptococcus equi,
Actinobacillus equuli and migrating Strongylus spp. larvae, and
pericarditis in occasional cases of strangles and of generalized infection
by Strep. faecalis); the commonest type in this species is functional in
character. In cattle organic heart disease, including subacute bacterial
endocarditis, post-vaccinal endocarditis in calves (Mycoplasma
mycoides), traumatic pericarditis, tuberculous pericarditis and the
pericarditis that occurs in pasteurellosis, is the most usual type,
although functional defects occur, sometimes only temporarily, as in
severe haemolytic anaemia, parturient paresis, etc. Endocarditis,
caused in lambs by Streptococcus spp. and Escherichia coli, and in older
sheep by Erysipelothrix insidiosa, and the pericarditis of pasteurellosis
are the most commonly encountered types of heart disease. In pigs,
endocarditis caused by Streptococcus spp. and Erysipelothrix insidiosa,
and pericarditis occurring in pasteurellosis, enzootic pneumonia,
salmonellosis and in Glasser's disease are the commonest forms of
heart disease encountered. In the dog, functional and organic disease
of the heart are of equal occurrence.
Disturbances of Pulse Rhythm
Irregular pulse. In this type of pulse the intervals between the individual
pulse waves vary in length. Irregularity of the pulse rhythm is invariably
associated with variations in pulse amplitude; it is particularly well
marked in atrial fibrillation, atrial flutter, disorders of the cardiac
intrinsic conduction mechanism and generalized myocarditis (true
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arrhythmia). During the course and convalescent phases of diseases such
as pneumonia and other severe febrile and toxaemic conditions that
impose increased work load on the heart, an intermittent pulse is often
a transitory feature; it also occurs with atrial and ventricular
extrasystoles (produced when impulses capable of stimulating
myocardial contraction originate at points apart from the sinoauricular
node) caused by focal myocarditis, also in digitalis and chloroform
intoxication and sometimes in space-occupying lesions of the brain. In
these circumstances the irregular ventricular contractions may not
always produce a pulse wave because of inadequate strength. The
detection of a pulse deficit enables extrasystolic arrhythmia to be
differentiated from heart block.
During respiration the pulse rate in some species (particularly dogs) is
appreciably more frequent during inspiration than during expiration
(respiratory sinus arrhythmia). It is usually most marked when
respiration is slow and deep. Sinus arrhythmia disappears on exercise or
following the injection of atropine, if the animal is healthy, but if the
pulse irregularity is the result of disease then it will, in many cases,
become more obvious during severe dyspnoea.
Intermittent pulse. In this type of pulse individual waves are absent from
an otherwise regular sequence. According to whether the waves are
dropped at regular intervals (e.g. every fourth wave) or not, the
condition is described as a regularly or irregularly intermittent pulse. If
there is a corresponding intermission in the heart beat, the condition is
described as deficient pulse. When, in spite of the pause in the pulse,
the heart beat occurs, although not strongly enough to produce a
perceptible pulse wave, the term intermittent pulse is applied; here,
obviously, the pulse rate is less than the heart rate.
An intermittent pulse is caused by many of the same diseases as
produce an irregular pulse, and is not infrequently encountered in
apparently healthy animals, particularly thoroughbred horses in which it
arises from partial atrioventricular node block (AV block). If any
irregularity in the pulse is abolished by exercise, excitement or following
the injection of atropine (inhibition of the vagus), the full effect of which
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is obtained only some hours later, it may be concluded that the pulse
deficit has no diagnostic significance unless it is accompanied by other
signs of cardiac disease, when as a rule the pulse arrhythmia will be
increased. Irregularity and intermission of the pulse may have various
origins: irregular development of stimuli at the sinoauricular node (SA
node block); irregular initiation of stimuli in the auricles (ectopic
pacemakers) (atrial flutter and atrial fibrillation) and in the whole cardiac
musculature (extrasystole) in focal myocarditis; and disturbances in the
conduction of the contractile impulse from the atria to the ventricles (AV
block).
Disturbance in Pulse Quality
Changes in pulse quality are attributable to variations in the stroke
volume of the heart, in the venous return and in the activity of the reflex
centres in the medulla. Pulse quality is classified according to certain
characteristics recognized by palpation:
Large strong pulse. In this pulse the artery is abnormally distended at
each pulsation, the amplitude is greater than normal and the wave is not
readily obliterated by digital pressure. It is indicative of persistent, or
temporary, elevation of blood pressure (hypertension) and reflects
increased cardiac stroke volume. This type of pulse may occur in athletic
animals because of ventricular hypertrophy; it is also detected in the
median artery of the horse in cases of acute laminitis, because of the
inflammatory hyperaemia of the foot; and in dogs during the earlier
stages of interstitial nephritis. It also appears transitorily after vigorous
exercise.
Small weak pulse. Here the artery is only poorly distended, and the
pressure wave is readily obliterated by finger pressure. It reflects
reduced stroke volume and occurs in myocardial asthenia, mitral
incompetence or stenosis, aortic stenosis and partial occlusion of the
artery at which the pulse is taken. In the last two, the pulse will show
other characters such as being slow and prolonged (see below).
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Soft pulse. The pulse wave is poorly developed and easily obliterated. It
occurs when the myocardium is debilitated by general septic or
toxaemic disease.
Unequal pulse. The individual pulse waves vary in amplitude and,
therefore, in strength, reflecting alterations in the stroke volume of the
heart. It occurs characteristically in sinus arrhythmia and in extrasystolic
arrhythmias.
Asymmetrical pulse. This is a pulse that has different qualities on the
right side of the body from those of the left, e.g. in unilateral
vasodilatation, and in iliac thrombosis. Slight differences of this type are
not uncommon in small animals.
Alternate pulse exists when a strong wave alternates with a weaker one.
Another form of alternating pulse occurs when there are groups of
continually weakening waves interspersed by a few stronger waves.
Both types of alternate pulse occur in severe cardiac weakness.
Water-hammer or Corrigan's pulse. The pulse wave rises rapidly until the
artery is overdistended, and then collapses equally quickly (Fig. 25c, p.
31). The wave is not readily obliterated. It is pathognomonic of either
insufficiency of the aortic valves or patency of the ductus arteriosus. A
form of this pulse occurs in severe anaemia as a result of the very low
arterial blood pressure.
Slow pulse. The pulse pressure wave rises slowly and collapses again in a
similar manner (Fig. 25d, p. 31). The artery is only moderate distended.
It occurs in stenosis of the aortic valve, complete A-V block and
sometimes in space-occupying lesions of the brain. It should not be
confused with infrequent pulse resulting from bradycardia.
Hard pulse. The wall of the artery is tense and hard, and the pulse wave
is not readily obliterated. It occurs in diseases associated with hypertension (nephritis), pain, increased muscular tone (tetanus) and local
hyperaemia (laminitis).
Wiry pulse. This pulse is hard and, at the same time, small. It occurs
when there is some degree of vasoconstriction. A wiry pulse is
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associated with painful diseases such as acute pleurisy, acute peritonitis,
acute and subacute endocarditis, the early stages of acute pericarditis
and intestinal volvulus.
Thready pulse. The pulse wave is small and readily obliterated. Its
significance is similar to that of wiry pulse although it may indicate that
the disease may have an unfavourable termination. This indication is
more clearly presented when repeated examinations reveal that the
pulse rate is progressively increasing, and that the amplitude is
decreasing, thus producing the so-called 'running down' pulse.
Dicrotic pulse. This type of pulse is appreciated only in very rare
instances. Following closely upon the main pulse wave, a second wave is
perceptible (caused by the slight, temporary rise in blood pressure
following closure of the aortic semilunar valves). It occurs in prolonged
and acute fevers, but sometimes occurs in the absence of demonstrable
disease. In the vast majority of animals the dicrotic pressure wave is
dissipated within a short distance of the heart.
Fremitus, i.e. a vibration or shaking of the arterial wall, instead of a pulse
wave, occurs when the lumen is reduced (arterial thrombosis, congenital
stenosis, stretching or kinking), in arteriovenous aneurysm of the
spermatic artery of the bull, in parasitic aneurysm of the anterior
mesenteric artery of the horse and in the middle uterine artery of the
cow in late pregnancy.
Distension of the Veins
Jugular Pulse
In many animals, engorgement of the jugular vein produces movement
which may be observed to involve that section of the vein which is
situated subcutaneously in the jugular furrow. This is described as a
jugular pulse. It may be negative or positive.
A negative jugular pulse occurs during the early part of cardiac systole
when the blood, being temporarily unable to enter the contracted right
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atrium, is dammed back in the jugular vein. This type of jugular pulse
takes the form of distension of the proximal part of the jugular vein,
arising presystolically, i.e. before the heart contracts, and gradually
extending from the lower part of the vein forwards. It is physiological,
readily observed in lean animals and particularly common in cattle.
Negative jugular pulse is exaggerated in tricuspid stenosis, heart block
and exudative pericarditis.
Positive jugular pulse consists of true pulse waves which run forward
from the shoulder towards the angle of the jaw. These regurgitation
waves are not only visible but are palpable as moderately strong
impulses. Positive jugular pulse occurs in tricuspid incompetence
because, during cardiac systole, the blood in the right ventricle is forced
backwards through the incompletely closed valvular orifice into the right
atrium and the jugular vein. In lacting cattle affected with tricuspid valve
insufficiency, a positive pulse may be detected also in the subcutaneous
abdominal (mammary) vein. This type of jugular pulse is systolic and
coincides with the arterial pulse; it is pathognomonic of tricuspid valve
incompetence. The existence of positive jugular pulse is indicated if,
following the application of digital pressure to the vein in the region of
the larynx, the engorgement disappears only after two or more cardiac
cycles.
In lean animals, the pulsation of the underlying carotid artery, noted
particularly at the entrance to the thorax, may be transmitted to the
overlying tissues and thereby simulate a positive jugular pulse. This
condition, which is termed false jugular pulse, is not obliterated by
compression of the jugular vein, whereas a true positive jugular pulse
will disappear.
Venous Stasis
The state of the venous system can be assessed by observing the jugular
vein, the smaller cutaneous veins, the auricular veins, the spermatic and
the subcutaneous abdominal veins. In long-coated animals, venous
distension is detected by palpation. In thin-skinned horses, such as
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thoroughbreds and hunters, when the coat is short, temporary
distension of the superficial veins is readily seen after active exertion.
Persistent dilatation of superficial veins occurs in all conditions in which
there is obstruction to the flow of blood on the venous side of the blood
vascular system. It is constantly present when the flow of blood into the
right side of the heart is delayed by incomplete emptying of the organ
during the preceding systolic contraction. It occurs in myocardial
dystrophy, heart block and cardiac and mediastinal neoplasia; in endocarditis; in congenital defects including patent interventricular septum,
patent foramen ovale, patent ductus arteriosus, and fibroelastosis; in
pericarditis and hydropericardium; and in pneumonia, chronic alveolar
emphysema, overdistension of the abdomen, etc. (Fig. 125). In the
broken-winded horse, the veins become distended after only a short
period of exercise, and remain dilated for much longer than in the
healthy animal, indicating the severity of the dyspnoea and its influence
on the pulmonary circulation and the heart. Occasionally, however,
engorgement of the veins may be the result of a purely local condition,
e.g. compression of a vein by a tumour or by a superficial inflammatory
process.
In myocardial asthenia, if distension of the jugular and other large
superficial veins is not already obvious, digital compression will rapidly
produce very marked dilatation. In vasogenic failure, occurring in
toxaemia and shock, the jugular vein is not engorged although the total
blood volume is normal, and digital compression slowly produces only a
slight distension of any of the superficial veins. In quiet dogs, the degree
of venous stasis may be estimated by placing the animal in lateral
recumbency, repeatedly raising the recurrent tarsal vein by digital compression and releasing the pressure with the leg held at various levels
relative to the heart. If venous pressure is normal, and the animal is in a
relaxed state, the vein should collapse rapidly when pressure is released
with the limb at any level above that of the heart.
Cyanosis is bluish discoloration of the skin and mucous membranes
caused by abnormally increased amounts of reduced haemoglobin in the
circulating blood. In animals it is most readily detected in the
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conjunctival and gingival mucosae. In all cases the haemoglobin
concentration shows little or no variation from normal, but the oxygen
tension of the arterial blood is low. Cyanosis is present in all types of
hypoxic hypoxia and in stagnant hypoxia, but not in anaemic hypoxia.
The existence of cyanosis can be determined by noting that the bluish
discoloration disappears temporarily when pressure is applied to the
mucosae or skin and the blood flow is stopped. Methaemoglobinaemia
is distinguished by noting that the discoloration of the mucosae and the
skin is brown rather than blue.
A varying degree of cyanosis occurs in all forms of heart disease; it is
most obvious in congenital heart defects and less so in acquired heart
disease. In pulmonary disease, cyanosis is rarely very obvious because
the circulation is impeded proportional to the degree of lung
dysfunction.
When venous engorgement persists it will cause oedema, usually
anasarca, ascites, hydrothorax and hydropericardium. The anasarca is
limited to the dependent parts, including the ventral surface of the
thorax and abdomen, the neck and the lower jaw. In severe congestion
the liver is enlarged to a varying degree, so that in the dog and cat the
thickened border of the organ can be palpated behind the right costal
arch.
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