How I Approach… A young puppy with a heart murmur
Puppy murmurs are a common clinical finding for many practitioners. They are typically detected during routine primary vaccination appointments and are therefore found as “incidental” murmurs, although occasionally some will be found after clinical signs of heart disease are identified.
Puppy murmurs are often found, but can vary greatly in their significance.
Understanding cardiac anatomy and physiology will assist with localization and timing of murmurs.
Assessment and accurate description of the murmur will enable creation of a differential diagnosis list.
Early identification and management of many congenital cardiac abnormalities result in a better long-term outcome for the patient.
Referral to a cardiologist is warranted with any cardiac murmur to allow for accurate diagnosis using echocardiography.
IntroductionPuppy murmurs are a common clinical finding for many practitioners. They are typically detected during routine primary vaccination appointments and are therefore found as “incidental” murmurs, although occasionally some will be found after clinical signs of heart disease are identified. Owners can be very distressed by the diagnosis of a puppy murmur, and the guidance and reassurance of their veterinarian is essential. Knowledge of the differential diagnosis, and the significance and approach for each type of murmur, is needed to help better guide appropriate management in each case. Referral to a cardiologist should always be considered and offered to the owner if a clinically significant murmur is identified.
What is a murmur?
Murmurs are sound waves created by vibrations caused by turbulent or regurgitant blood flow in the heart or nearby vasculature (the chamber walls, valves and walls of blood vessels). Blood must move at high velocity to produce turbulence or a regurgitation which creates a murmur loud enough to detect. The key is the difference in pressure across two chambers; for example, a mitral regurgitation forces blood into the low pressure left atrium (approximately 10 mmHg) from the high pressure left ventricle (approximately 120 mmHg) in systole, therefore moving blood with an overall pressure difference of 110 mmHg and causing local tissue vibrations which translate into a detectable sound.
It is important to note that shunting of blood through defects may not always cause a murmur. Movement of blood between two low pressure systems will not create a murmur loud enough to hear, for example with an atrial septal defect. Furthermore, some shunts will originate left to right, with the high-pressure differential between the systemic and pulmonary circulations. However, over time chronic overload of the right side can increase right-sided pressures until they equate and then surpass left-sided pressures, resulting in a right to left shunt; this may translate into a dramatic worsening of clinical signs but with loss or significant reduction in the murmur.
What is important in the history and signalment?
Even in routine health check/vaccination appointments, a thorough history must be taken. Should you suspect a murmur, pay particular attention to the cardiovascular history, including exercise tolerance, resting respiratory rate/effort and any coughing. Check if the puppy has been wormed appropriately for lungworm and heartworm prophylaxis (in countries where this is prevalent). Note if there have been any other concerns with the littermates or whether either of the parents were reported as having heart disease or a murmur. Importantly, note the breed; signalment can be useful in guiding you towards a differential diagnosis, although the rules are not absolute.
How do I diagnose a murmur in a puppy?
Auscultation is a skill learnt during veterinary training, but is honed with practice. Auscultation of puppies can be challenging; they can be wriggly, noisy and very non compliant, and it may be necessary to try and calm the puppy to enable better examination. Options include lifting the animal from the table and cradling in your arms with the stethoscope placed on the chest (Figure 1), or giving the puppy a brief feed and then allowing it to relax with the owners before attempting again (as they often then fall asleep).
How do I describe a murmur?If a murmur is identified it is essential to grade, localize and time the murmur wherever possible. This will lay the foundation for your differential diagnosis list. Murmurs are classically described using a grading system of 1-6 (Table 1), which defines the “loudness” of the murmur in relation to the normal heart sounds. Importantly, grade 5 and 6 murmurs have a concurrent palpable “thrill”. Palpation of the thoracic wall must be performed in all cases (Figure 2). This can be done by placing the flat palms onto the puppy’s chest, cranio-ventrally (as though you were about to lift it up) and paying particular attention to the dorsal axillary region.
|Intermittent, hard to hear, quieter than heart sounds, very focal
|Constant, hard to hear, quieter than heart sounds, focal
|As loud as heart sounds, easy to hear, can be focal
|Louder than heart sounds, easy to hear, radiates
|As 4 with palpable thrill
|As 5 but murmur can be heard with stethoscope away from chest
What other aspects of the physical examination are important?
Murmur assessment is just one aspect of a full and thorough cardiovascular clinical examination. Mucous membrane color should be noted. In a normal healthy puppy these will be pink, with a brief capillary refill time (less than 2 seconds). Look for cyanosis and include assessment of mucous membranes at both cranial (gingiva) and caudal (vulva or prepuce) sites. Right to left shunting cardiac abnormalities will cause cyanosis, and dependent on the location of the shunt differential cyanosis may be seen (see below).
Respiratory rate/effort and pulmonary auscultation should be noted. Again, with a lively, wriggly puppy it can be more difficult to ascertain, but taking time to allow the puppy to relax (and preferably fall asleep) can allow for better assessment.
Assessment of the pulses should be made routinely, ideally whilst also auscultating the heart to ensure pulses are matching with heart rate. The character of the pulses should be noted, paying particular attention to weak pulses and hyperdynamic, “bounding” pulses (see below).
Assessment of the abdomen should be made to look for organomegaly or evidence of ascites (ballottement should be performed) which can be indicative of right sided heart failure (Figure 3). Assess the neck to look for jugular distension, and performing a hepatojugular reflux test (gentle compression of the abdomen whilst assessing for jugular distension) can help this.
Heart rate and rhythm should also be noted, and the details documented. Rhythm is important to assess, and any doubts over this can be followed up with an electrocardiograph (ECG) to confirm presence of a sinus rhythm or to diagnose arrhythmias (see below).
What other diagnostics can I perform?History and physical examination will be the mainstay of your initial diagnostics, but further investigations include blood pressure measurement, thoracic radiography and an ECG. Referral to a cardiologist for accurate echocardiography, particularly in more complex congenital abnormalities, is recommended.
How do I make a differential diagnosis?
The following is a summary of the most likely differential diagnoses based on murmur description and localization, but the list is not exhaustive, and occasionally murmurs will not follow the “rules”. Brief notes regarding treatment are included where appropriate. Finally, very rare complex congenital abnormalities can occur, which can mimic more typical murmurs, and you should always be mindful of that.
The left apex defines the region of the mitral valve. At this location blood moves from the left atrium across the valve into the left ventricle during diastole. During systole the mitral valve closes and blood is ejected from the left ventricle out through the aorta.
Systolic murmurs occur due to regurgitation across the mitral valve. In a puppy, the defect is likely to be congenital and therefore mitral valve dysplasia is considered to be the main differential.
Prevalence is similar between purebred and crossbreed dogs 1, although English Bull Terriers and German Shepherd dogs are predisposed 2 3. Cases of mitral dysplasia may be more likely to show clinical signs 4 when compared to other congenital abnormalities, but this will relate to age at diagnosis, with younger dogs less prone to show signs.
Diastolic murmurs at the left apex are rare and difficult to appreciate. These are filling murmurs, related to the movement of blood from the left atrium to the left ventricle, and are consistent with mitral valve stenosis. This can be an extension of severe mitral valve dysplasia, but can be a defect in its own right, with a narrowed mitral valve orifice causing dramatic increases in left atrial pressures 5. Again English Bull Terriers are thought to be predisposed, and also Newfoundlands. Outcome in these cases is very poor, with a reduced life span (typically around 2-3 years) 6.
In general, when faced with mitral dysplasia and stenosis, the overall treatment will be management of heart failure when or if this develops in the longer term. Arrhythmias such as atrial fibrillation may also develop and therefore rate management control with anti-arrhythmic therapy may be indicated.
This location covers the valve annulus of both the pulmonary and aortic arteries. Again murmur timing should enable assessment of outflow versus regurgitant murmurs. Systolic murmurs over this region are consistent with turbulence in blood exiting across the valve annulus, leading to a suspicion of aortic or pulmonic stenosis.
Pulmonic stenosis (PS) is the most common congenital heart disease found in dogs (accounting for 32% of all congenital cardiac problems in a recent study 7) and classically identified as a harsh, ejection-type (crescendo-decrescendo) murmur. PS is caused by either fused (type A) or dysplastic (type B) valves, with or without a hypoplastic annulus 8. It is impossible to differentiate the two types based on auscultation alone, and therefore referral for echocardiography is essential. Pulmonic stenosis can be graded as mild, moderate or severe, with a worse long-term outcome for those in the latter category 9. Murmur grade can assist in differentiating the degree of severity, but it is defined objectively by pressure gradient across the stenosis via echocardiography. Breed predispositions include Boxers, Bulldogs (English and French) and Staffordshire Bull Terriers 7. Balloon valvuloplasty can be highly successful in type A PS, improving the long-term outcome, but the outlook for severe cases without valvuloplasty is poor 10. Other treatments may include beta-blockers (e.g., atenolol) but these should be discontinued once heart failure occurs. Pulmonic stenosis can also be associated with coronary artery aberrancy (typically in brachycephalic breeds) and angiography must be performed in these cases prior to balloon valvuloplasty to ascertain the coronary anatomy.
Tetralogy of Fallot (pulmonic stenosis, right ventricular hypertrophy, ventricular septal defect and overriding aorta) can present with a murmur of pulmonic stenosis. This is a rare condition (approximately 1% of congenital abnormalities 7) and should not be diagnosed without echocardiography; cases typically have a guarded long-term prognosis.
Aortic stenosis is identified when there is an increased velocity in blood flow exiting the aorta, caused by obstruction just below the valve (subaortic stenosis, or SAS), at the valve (aortic stenosis), or above the valve (supravalvular stenosis). In dogs, SAS is by far the most common form and accounts for approximately 20% of all congenital cardiac defects 7. SAS is found more commonly in purebred dogs, with Newfoundlands, Boxers, Bull Terriers, Rottweilers, Golden Retrievers, Dogue de Bordeaux, Irish Terriers and Bouvier des Flandres predisposed 1 7. SAS is defined as mild, moderate or severe based on echocardiographic assessment of pressure differentials across the aortic obstruction. Outcomes in mild cases are good, with a normal predicted lifespan. However, severe aortic stenosis is associated with a poor long-term prognosis (estimated median survival 19 months) and increased risk of sudden death 11. Treatment includes beta-blockers, but again these must be withdrawn should signs of heart failure occur, and whilst this class of drug make physiological sense, there is no evidence to suggest it improves long-term outcome in severe cases 12. Interventional therapy with a cutting balloon valvuloplasty has been described 13, but long-term outcomes following this procedure have not been documented. SAS severity can alter with age, therefore final grading of the condition is typically performed once the patient is skeletally mature 14. However, this should not delay early referral to a cardiologist to confirm diagnosis as timely introduction of beta blockade may be necessary.
Diastolic murmurs over the left base are consistent with aortic and pulmonic insufficiency. These are rare and difficult to determine. Increased pulmonary pressures, consistent with pulmonary hypertension can cause an audible pulmonary regurgitation murmur if the severity degree is high enough. In this situation the puppy should be investigated for causes of pulmonary hypertension, including parasitic disease. Aortic insufficiency is rare, and may be associated with aortic valvular dysplasia, endocarditis (very rare) or systemic diastolic hypertension.
A continuous murmur at the left heart base is pathognomonic for a patent ductus arteriosus (PDA). This accounts for approximately 20% of congenital cardiac abnormalities 7 with females predisposed 15 and an over-representation of German Shepherd Dogs 7 16. It is important to recognize this murmur, as a significant proportion of these patients can be effectively “cured” by surgery to close the defect. Definitive diagnosis requires echocardiography, although murmur character, bounding pulses and thoracic radiography can be highly suggestive, the latter typically demonstrating a “three knuckle sign” on dorsoventral views consistent with dilation of the ascending aorta, proximal pulmonary artery and the left auricle (Figure 4). Puppies can initially be asymptomatic, but significant left-sided volume overload occurs over the longer term, leading to dilation and remodeling of the left side of the heart and increased filling pressures. Ultimately, cases will typically go into left-sided congestive heart failure, and long-term prognosis for a PDA is poor without closure. Right to left shunting can also occur, and can usually be characterized by the loss of the previously detected loud murmur and decompensation in clinical signs, with differential cyanosis, pulmonary hypertension and polycythemia. Closure of the PDA is advised and can be done interventionally using specially designed implants by a cardiologist. An alternative is surgical ligation of the ductus via thoracotomy, which can be performed in animals too small to gain access via the vascular system.
This identifies the location of the tricuspid valve, and murmurs associated with this region are related to passage of blood from the right atrium to the right ventricle. Typically, these are systolic, regurgitant murmurs and are associated with tricuspid valve dysplasia. This condition accounts for approximately 3% of all canine congenital heart disease cases, with Labrador Retrievers being over-represented 7. In the long term, cases of tricuspid dysplasia can progress to right-sided heart failure, and therefore early recognition of this defect allows for better case management. Diastolic murmurs are not typically detectable due to the low-pressure differentials across this valve in diastole and are therefore a rare finding.
This identifies the right ventricular wall, and a murmur in this region is typically a left to right shunting ventricular septal defect (VSD). VSD murmurs demonstrate an interesting paradox; the louder they are, the smaller and less clinically significant the defect. Very small defects (restrictive VSDs) allow a small volume of blood to pass through at high velocity, thus causing a loud murmur. Alternatively, a wide VSD allows a large volume of blood to pass and can equate left and right ventricular pressures, thus moving the blood at a slower velocity and causing a much quieter murmur. Clinical signs of a VSD can vary dependent upon the degree of defect; small restrictive VSDs can remain asymptomatic, whereas large VSDs have severe volume overload and progression to heart failure. VSDs are seen in approximately 7.5% of congenital cardiac cases and commonly occur in conjunction with another defect such as pulmonic stenosis 7.
Again, for tricuspid dysplasia and VSD, the overall treatment will be management of heart failure when or if this develops in the longer term. Arrhythmias such as atrial fibrillation may also develop and therefore rate management control with anti-arrhythmic therapy may be indicated.
It is worth pointing out that a large proportion of puppies can present with an ”innocent” murmur. These are typically low grade (< 3/6), early systolic and with a “musical” quality, localized on the left apical or basilar regions. They are not related to structural heart disease, and are thought to occur due to changes in blood viscosity. Essentially, these murmurs should disappear over time, usually by approximately 20 weeks of age 17.
In summary, puppy murmurs are a common clinical finding, typically presenting incidentally initially, rather than with overt clinical signs. Identifying and describing the murmur will enable better assessment of possible differential diagnoses, and therefore diagnostics and management. In the majority of congenital heart diseases, early identification allows for better long-term outcomes, with some conditions being potentially curable. In other cases there is no real evidence to suggest that any pre-emptive medical therapy will delay onset of heart failure, but it is generally recommended that owners are made aware of the severity of the heart condition, and this may be guided by referral to a cardiologist and having echocardiography. However, close monitoring for progression to failure by monitoring exercise tolerance and resting respiratory rate and effort is the main short-term objective if a heart condition is not treated at first diagnosis.
- Bellumori TP, Famula TR, Bannasch DL, et al. Prevalence of inherited disorders among mixed-breed and purebred dogs: 27,254 cases (1995-2010). J Am Vet Med Assoc 2013;242:1549-1555.
- Dukes-McEwan J. Mitral dysplasia in Bull Terriers. Vet Annual 1995;35:130-146.
- Litu SK, Tilley LP. Malformation of the canine mitral valve complex. J Am Vet Med Assoc 1975;167:465-471.
- Tidholm A. Retrospective study of congenital heart defects in 151 dogs. J Small Anim Pract 1997;38:94-98.
- Trehiou-Sechi E, Behr L, Chetboul V, et al. Echoguided closed commissurotomy for mitral valve stenosis in a dog. J Vet Card 2011;13:219-225.
- Lehrnkuhl LB, Ware WA, Bonagura JD. Mitral stenosis in 15 dogs. J Vet Intern Med 1994;8:2-17.
- Oliveira P, Domenech O, Silva J, et al. Retrospective review of congenital heart disease in 976 dogs. J Vet Intern Med 2011;25:477-483.
- Bussadori C, Amberger C, Le Bobinnec G, et al. Guidelines for the echocardiographic studies of suspected subaortic and pulmonic stenosis. J Vet Card 2000;2:15-22.
- Locatelli C, Spalla I, Domenech O, et al. Pulmonic stenosis in dogs: survival and risk factors in a retrospective cohort of patients. J Small Anim Pract 2013;15:445-452.
- Francis AJ, Johnson MJS, Culshaw GC, et al. Outcome in 55 dogs with pulmonic stenosis that did not undergo balloon valvuloplasty or surgery. J Small Anim Pract 2011;52:282-288.
- Kienle RD, Thomas WP, Pion PD. The natural clinical history of canine congenital subaortic stenosis. J Vet Intern Med 1994;8:423-431.
- Eason BD, Fine DM, Leeder D. Influence of beta blockers on survival in dogs with severe subaortic stenosis. J Vet Intern Med 2014;28:857-862.
- Javard R, Bélanger MC, Côté E. Comparison of peak flow velocity through the left ventricular outflow tract and effective orifice area indexed to body surface area in Golden Retriever puppies to predict development of subaortic stenosis in adult dogs. J Am Vet Med Assoc 2014;245:1367-1374.
- Kleman ME, Estrada AH, Maisenbacher HW. How to perform combined cutting balloon and high pressure balloon valvuloplasty for dogs with subaortic stenosis. J Vet Card 2012;14:351-361.
- Van Israel N, French AT, Dukes-McEwan J, et al. Review of left-to-right shunting patent ductus arteriosus and short-term outcome in 98 dogs. J Small Anim Pract 2002;43:395-400.
- Van Israel N, Dukes-McEwan J, French AT. Long-term follow-up of dogs with patent ductus arteriosus. J Small Anim Pract 2003;44:480-490.
- Szatmári V. Differentiation between innocent cardiac murmurs and murmurs caused by congenital cardiac anomalies with auscultation in asymptomatic puppies. In Proceedings, ECVIM Congress 2015, Lisbon, Portugal.