Introduction
The practice of cardiac auscultation remains one of the
most widely used diagnostic techniques in veterinary
medicine. Technical considerations of cardiac auscultation
and interpretation of heart sounds and murmurs
are therefore of wide interest to the veterinary practitioner.
Although it may not be possible to establish the
diagnosis of a specific heart disease with the sole use
of a stethoscope, or in combination with a phonocardiogram
(PCG), optimal use can narrow down the list of
differential diagnoses substantially. A gentle approach
and a quiet environment are essential for the animal to
relax and for the auscultator to be undisturbed. It is also
essential to auscultate all cardiac areas to detect local
murmurs and, in the case of a heart murmur, the point
of maximum intensity (PMI).
Stethoscopes
There are a number of different types of stethoscope
commercially available. Most of the better quality
standard stethoscopes are adequate for use in veterinary
practice, but paediatric stethoscopes are not
recommended for most auscultation as a larger bell is
often needed for optimal amplification. It is essential
for the veterinary surgeon to become familiar with the
stethoscope, and how normal and abnormal heart
and lung sounds are perceived using this particular
instrument. It is also important to obtain a stethoscope
with earpieces that fit snugly. This helps to avoid discomfort
during prolonged auscultation and to reduce
the ‘leakage’ of sound around the earpieces. For most
veterinary surgeons, it is useful to angle the earpieces
to better fit the ear canal. Sound ‘leakage’ is one cause
of problems in the auscultation of abnormally lowintensity
heart sounds or failure to detect murmurs.
It is useful to have a stethoscope with bells and diaphragms
of different sizes. A small-sized bell can be
used to localize the PMI of murmurs, especially in small
dogs and cats. A larger diaphragm can be used to
determine whether or not the patient has normal heart
sounds. An open bell is sometimes useful to detect
low-frequency sounds (such as an S3 sound) that may
be inaudible using a diaphragm bell. Many standard
stethoscopes have unnecessarily long tubing for use
with small animals, and this may lead to dampening of
sounds. Fortunately, tubes can always be shortened to
an appropriate length of 36–46 cm (14–18 inches). A
sensor-based (non-microphone) stethoscope is also
available (Meditron™). This stethoscope can be connected
to a computer to store and filter the sounds as
PCGs with simultaneous electrocardiogram (ECG)
recordings. The ability to record, filter and analyse digital
PCGs offers substantial advantages.
Origin of murmurs
Blood flow in normal vessels and the heart is usually
laminar with minimal turbulence, and consequently
does not result in a heart murmur. Heart murmurs all
arise due to vibrations created within the cardiovascular
system, which may originate from turbulent
blood flow. However, not all animals with heart murmurs
have heart disease, as some individuals with
normal cardiovascular anatomy may have audible
murmurs in early systole. These murmurs may be
caused by high-velocity flow or low fluid viscosity
(e.g. in severe anaemia). Murmurs in small animals
that have a long duration in systole (more than 50%)
are often caused by pathological conditions such as
valvular regurgitation, shunting or obstruction of
blood flow.
Situations that can cause turbulent flow (and
therefore murmurs) include increased flow velocity in
a normal vessel (such as the aorta), or more commonly,
obstruction to blood flow or valvular incompetence.
Murmurs from shunts and valvular incompetence
are created by the combination of high-velocity
flow through a narrow orifice combined with flow
entering a cardiac structure of increased diameter.
Evaluation of the timing of murmurs is helpful in
the interpretation of the significance of a murmur. A
general rule is that holosystolic/diastolic murmurs
are often significant, meaning that they indicate heart
disease. Conversely, low-intensity early systolic murmurs
tend to be associated with insignificant flow
murmurs. Murmurs which have a duration of more
than early systole are usually indicative of a cardiac
abnormality.
Systole is defined as the time period between the
onset of S1 and the onset of S2. Diastole is defined as
the time period between the onset of S2 and the onset
of S1 (Figure 4.1). Systolic and diastolic murmurs can
also be characterized as early, mid or late, depending
on their location in systole or diastole. Holosystolic
murmurs fill the whole systolic period, and holodiastolic
murmurs fill all of the diastolic period.
Auscultation and the point of maximum intensity
General advice for cardiac auscultation
- It is important to minimize background noise. If a quiet environment is impossible to achieve, an electronic stethoscope with the option to amplify heart sounds is useful. Clients often take the opportunity to talk when the veterinary surgeon is quiet; therefore, it is a good idea to explain the need for a quiet environment before auscultation and that only fragments of the information that a client is trying to impart will be heard.
- Small animals should preferably be in a standing position on all four limbs during cardiac auscultation. If the animal is sitting, the forelimbs will cover the different PMIs and the diaphragm of the animal will be positioned in a more cranial direction, compressing the thorax, which may leave the heart sounds less audible. If the animal is in right or left lateral recumbency, the heart will move towards the dependent side, leaving the heart sounds less distinct on the non-dependent side.
- Dogs often pant, and auscultation should be carefully interpreted in these patients because panting generates disturbing sounds, and breathing sounds may be mistaken for murmurs. Warm examination rooms should be avoided and if the animal is panting, the client should be asked to manually close the mouth of the dog for brief periods of time. If this is not sufficient, manual occlusion of both the mouth and nostrils can allow a few seconds of undisturbed auscultation or PCG recording.
- Cats may purr, which often makes evaluation of heart sounds impossible. Blowing short bursts of expired air into the face of the cat or exposing the animal to visual stimuli, such as another animal, can be tried to stop the purring. Short occlusion of one or both nostrils can also be attempted or holding an alcohol-soaked cotton-wool ball near the cat’s nose. Holding the cat near a sink with running water often works
Grading of murmurs
Murmurs are graded on a scale of 1 to 6.
Low-intensity murmurs
• Grade 1 – a low-intensity murmur heard in a quiet
environment only after careful auscultation over a
localized cardiac area.
• Grade 2 – a low-intensity murmur heard
immediately when the stethoscope is placed over
the PMI.
Moderate-intensity murmurs
• Grade 3 – a murmur of moderate intensity.
• Grade 4 – a high-intensity murmur that can be
auscultated over several areas without any
palpable precordial thrill.
High-intensity murmurs
• Grade 5 – a high-intensity murmur with a
palpable precordial thrill.
• Grade 6 – a highintensity murmur with a
palpable precordial thrill that may even be heard
when the stethoscope is slightly lifted off the
chest wall.
Grading of murmurs may serve as a guide to
roughly estimate the severity of heart disease for
some conditions, such as aortic/pulmonic stenosis
and mitral regurgitation, but is less reliable in other
conditions, such as myocardial disease. Highintensity
murmurs often, but not always, indicate more severe
forms of heart disease. Exceptions include small
VSDs, which can generate very loud murmurs. Rarely,
degenerative mitral valve disease may generate very
strong vibrations of the valvular apparatus, causing
musical murmurs despite comparatively modest mitral
regurgitation. Other exceptions are lowintensity murmurs
that may be present in cases of myocardial failure
caused by dilated cardiomyopathy (DCM),
endstage degenerative mitral valve disease with multiple
small infarcts, and myocardial disease in cats.
Differential diagnoses for different cardiac murmurs
The general guidelines for the most common differential
diagnoses based on the intensity and PMI of murmurs
are presented in Figure 4.3.
Heart disease without murmurs
Fortunately, the majority of canine cardiac patients
have a murmur. However, some conditions are not
associated with heart murmurs. In a few of these
cases, altered heart sounds may be present (e.g.
gallop sounds), especially in advanced cases of
heart disease.
Examples of heart disease without murmurs
include: pericardial effusions; DCM; atrial septal
defects (ASDs, murmurs originating from a relative
pulmonic stenosis and which may be the result of
larger shunts, especially after exercise); and righttoleft
shunting with VSDs or PDA with pulmonary
hypertension. Cats with myocardial disease may have
no murmur at all.
Physiological flow murmurs in systole
Physiological flow murmurs are lowintensity, soft
murmurs caused by turbulent flow in the aorta or pulmonary
artery during early systole (Figure 4.4). The
PMI is over the outflow tracts (aortic/pulmonic area).
These murmurs do not indicate any underlying cardiac
disorder that may be identified by thoracic radiography,
echocardiography or postmortem findings. A
large stroke volume in relation to the size of the outflow
vessels of a normal heart may cause turbulent
flow and murmurs in young animals. These murmurs
can disappear within a few weeks, more commonly
within 4 to 5 months, or sometimes later during adolescence.
In some individuals (especially athletes)
these murmurs may remain in the adult animal.
These murmurs are usually of low intensity (grade
1–2) and comprise high-frequency sounds, sometimes
with medium-frequency sounds. They are early systolic
murmurs, meaning that they end before the middle
of systole and are usually of a decrescendo, but sometimes
of a crescendo–decrescendo, character.
Differential diagnosis
• Athletic heart.
• Severe anaemia.
• Low-grade aortic or pulmonic stenosis.
• Fever.
• Hyperthyroidism.
• Any condition leading to increased cardiac output
(e.g. pregnancy).
• Low-grade mitral regurgitation is sometimes
associated with early to mid-systolic murmurs.
PMI is over the mitral area in these dogs, in
contrast to physiological flow murmurs where the
PMI is over the aortic area.
Outflow tract stenosis in dogs
Pulmonic stenosis and aortic stenosis are two of the most common congenital malformations in dogs. Pulmonic stenosis is more common in small-breed dogs and aortic stenosis in large-breed dogs. These lesions are characterized by obstruction of the subvalvular, valvular or supravalvular area, causing turbulent blood flow. In contrast with aortic stenosis, the valvular form with fused cusps is more common in pulmonic stenosis. Supravalvular stenosis is less common. Acquired aortic stenosis may develop in association with bacterial endocarditis. Differentiation between aortic stenosis and pulmonic stenosis is best performed with echocardiography. The PMI is the pulmonic or aortic area at the left side of thorax (see Figure 4.3). Cases of low-grade stenosis often have a lowintensity murmur (grade 2–3). Cases of moderate stenosis often have a moderate-intensity murmur (grade 3–4). Cases with a severe degree of stenosis usually have a high-intensity murmur (grade 4–6). The murmurs are often of a crescendo–decrescendo character and occupy from 50–100% of the systole, with longer durations for severe obstructions.
Outflow tract obstruction murmurs in cats
Congenital pulmonic and aortic stenoses occur in cats but are much less common than in dogs. The most common cause of outflow tract obstruction murmurs in cats is hypertrophic cardiomyopathy (HCM). The PMI may be on either side of the thorax, or even sternal. Ejection murmurs can develop in cats with HCM if hypertrophy obstructs blood flow through the aortic or pulmonic outflow tracts (Figure 4.5). Dynamic left ventricular outflow tract obstruction is often caused by septal hypertrophy and systolic anterior motion of the mitral valve; dynamic right ventricular outflow tract obstruction may occur in cats with HCM or normal cats. Concurrent mitral regurgitation may complicate accurate identification of outflow tract murmurs
.Hyperthyroidism or renal disease with hypertension may cause secondary cardiac hypertrophy accompanied by obstruction to blood flow, creating low-intensity murmurs. Cats with more than two heart sounds (i.e. gallop rhythms) should always be examined with echocardiography as the majority of cases will have myocardial disease.
Tetralogy of Fallot
The audible murmur from tetralogy of Fallot is usually
caused by pulmonic stenosis, which is associated
with this complicated and uncommon congenital
heart disease. The polycythaemia that accompanies
tetralogy of Fallot causes hyperviscosity, which tends
to reduce the murmur intensity.
Patent ductus arteriosus
PDA occurs when the fetal ductus between the aorta
and the pulmonary artery fails to close post partum.
The ductus can close to different degrees, and consequently
the shunting of blood can range from insignificant
to very severe. The pressure in the aorta is
normally higher than the pressure in the pulmonary
artery, during both systole and diastole. Therefore,
blood is shunted through the ductus during the entire
cardiac cycle, causing a continuous murmur (Figure
4.6). In some cases, pulmonary hypertension may
develop, leading to reduced or even reversed shunting
during diastole and, if severe, in systole as well.
PDA is associated with a continuous heart murmur
(see Figure 4.3) with maximum intensity timed to the
peak pressure gradient between the aorta and the pulmonary
artery, which is at the end of systole. The
intensity of the murmur decreases during diastole, as
the pressure gradient decreases. The intensity and
radiation of the murmur also varies with the size of the
ductus. Small shunts have local low-intensity murmurs;
moderate shunts often have murmurs of moderate
intensity with some radiation; and severe shunts are
associated with intense murmurs that radiate widely. If
pulmonary hypertension develops, the murmur can
become systolic only and may even disappear as pulmonary
hypertension increases and polycythaemia
develops. Depending on the size and degree of shunting,
exercise intolerance and left-sided heart failure
may occur if surgical correction is not attempted.
Murmurs with the PMI at the apex of the heart
Differential diagnosis
• Mitral regurgitation.
– Myxomatous mitral valve disease (MMVD).
– Congenital mitral dysplasia.
– DCM.
– Endocarditis affecting the mitral valve
.
– Other causes of mitral regurgitation.
• (VSDs or tricuspid regurgitation may radiate to
the left side of the thorax but the PMI is usually at
the tricuspid area.)
MMVD is the most common cardiovascular lesion
causing murmurs in middle-aged or older small-breed
dogs. Progressive pathological changes of the atrioventricular
(AV) valves will, at some point, cause the
valves to become incompetent (Figure 4.7). Initially,
mitral regurgitation may cause intermittent, soft murmurs.
Over time, the murmur becomes holosystolic
and persistent (Figure 4.8), with increasing intensity
as the severity of the mitral regurgitation progresses.
The holosystolic ‘plateau’ shape of the murmur can be
explained by a similar degree of regurgitation throughout
systole.
The low-intensity of the murmur indicates that
only a small proportion of the stroke volume is regurgitated
during the early stages of the disease (see
Figure 4.3). As the disease progresses, forward stroke
volume is reduced as the regurgitant fraction
increases. However, this is counteracted by eccentric hypertrophy and increased ventricular filling, leading
to increased force of contraction according to the
Frank-Starling mechanism (see Chapter 15). Eccentric
hypertrophy in combination with hyperkinesis
maintains cardiac output despite an increasing degree
of mitral regurgitation, and the intensity of the murmur
and first heart sound increases. With further increase
in the severity of the disease, the second heart sound
decreases in intensity as forward stroke volume is
reduced (see Figure 4.3).
Congenital dysplasia of the AV valves can also
cause different degrees of mitral regurgitation. Many
dogs with DCM have no murmurs, but dilatation of the
mitral valve annulus and papillary muscle dysfunction
may cause mitral regurgitation with a systolic murmur
over the apex of the heart (mitral area). An audible
diastolic gallop (usually S3) may also be present. In
cases of DCM, heart sounds and murmurs are often
of a lower intensity than in animals with MMVD. This is
because reduced myocardial contractility prevents
the heart from generating forceful mitral regurgitation
jets and strong vibrations.
Murmurs with the PMI on the right side of thorax
Differential diagnosis
•VSDs.
• Tricuspid regurgitation caused by dysplasia,
degeneration or pulmonary hypertension.
• Aortic stenosis.
Ventricular septal defect
Although VSDs may occasionally be located in the
muscular portion of the septum, most commonly they
are found in the upper (perimembranous) portion of
the septum, just below the aortic valve. VSDs may
cause shunting of blood during systole from the LV to
the right ventricle (RV) because the systolic pressure
within the LV is normally considerably higher than in
the RV (Figure 4.9). The PMI is usually over the
cranioventral right hemithorax, but the murmur may
radiate to the left side of the thorax. Animals with a
VSD usually have a holosystolic murmur of low- or
moderate-intensity (see Figure 4.3). The intensity of
the murmur cannot be used to estimate the size or the
degree of shunting, as pulmonary hypertension may
reduce shunting in severe cases
Tricuspid regurgitation
Acquired or congenital lesions of the tricuspid valve
or right ventricular dilatation can cause valve
insufficiency during all or part of systole (Figure 4.10).
Dogs with tricuspid regurgitation commonly have
holosystolic murmurs, usually of low- to moderate
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