Heart sounds are created by blood flow and vibrations of tissues during the cardiac cycle and can be classified as transient (of short duration) and heart murmurs (abnormal, longer, occurring during normally silent part of the cycle).
TRANSIENT HEART SOUNDS are:
- S1 – closure of AV valves at the beginning of the systole,
- S2 – closure of aortic and pulmonic valves after ejection,
- S3 – rapid ventricular filling in early diastole when the ventricles suddenly resist expansion,
- S4 – vibrations caused by blood flow into ventricles at atrial contraction.
Two heart sounds normally heard in dogs and cats are S1 and S2. S1 is loudest at the apex and S2 at the base. They can be used as a framework for the timing of cardiac cycle and abnormal sounds. Systole is a time period between S1 and S2 and diastole from S2 until the next S1. Diastolic sounds S3 and S4 are of lower frequency than S1 and S2 and normally not audible in dogs and cats. They are associated with diastolic ventricular filling. When one of them is heard, together with S1 and S2 they form a gallop rhythm.
- S3 gallop (ventricular gallop) usually indicates ventricular dilatation with myocardial failure and may be heard in dogs with dilated cardiomyopathy or advanced valvular heart disease and congestive failure.
- S4 gallop (atrial or presystolic gallop) is usually associated with increased ventricular stiffness as is seen with hypertrophic cardiomyopathy or hyperthyroidism in cats.
CARDIAC MURMURS are produced when blood flow becomes turbulent and creates vibrations within cardiovascular system. In case of audible murmur, the first diagnostic step is establishing its timing within cardiac cycle, determining PMI (point of maximal intensity) and grading intensity. Further evaluation with echocardiography is advisable, whenever heart disease is suspected.
By the timing, murmurs can be systolic, diastolic or continuous. Timing can be helpful in interpretation of murmur’s significance: low-intensity early systolic murmurs tend to be non-pathologic and the ones with duration of more than early systole or happening in diastole are usually indicative of a cardiac abnormality.
All valve areas should be auscultated. Localization of the PMI may guide us toward the origin of the murmur. PMI refers to the valve area at which the murmur is heard loudest and is defined by intercostal space or apex / base of the heart on right or left hemithorax.
Murmur intensity can be graded on a scale from I to VI. It may serve as a rough estimate of severity of a heart disease for some conditions (subaortic/pulmonic stenosis, mitral insufficiency), but is not reliable in conditions as myocardial disease or failure.
Murmurs are also described by phonographic shape:
- holosystolic (plateau-shaped): begins at S1 and has uniform intensity which fills whole systolic period; it is caused by turbulent blood flow throughout the systole
- crescendo-decrescendo (diamond-shaped or ejection): starts softly at S1, gets louder in the middle of systole as cardiac output or contractile strength increases and then diminishes; it occurs during blood ejection, because of ventricular outflow obstruction
- decrescendo: starts intensively at S1 or S2 and then tapers; duration depends on the pressure difference between the vessel and ventricle
- continuous (machinery): occurs throughout systole and diastole, is most intense at the time of S2 and becomes softer toward the end of diastole; it indicates persistent considerable pressure gradient between two connecting areas
- Puppy murmur: soft, low-grade, early systolic decrescendo (or ejection) murmur, heard over the outflow tracts (left base). It is non-pathologic and disappears by 4-5 months of age.
- Physiologic murmur: soft, low-grade early systolic decrescendo (or ejection) murmur, with PMI at the left base, that doesn’t indicate cardiac disorder but results from an altered physiologic state – anemia, fever, high sympathetic tone, etc., or athletic heart. Soft systolic ejection murmur is common in sight hounds and some other large breeds, related to large stroke volume in relation to the size of outflow vessels. Approximately one-third of healthy adult cats can have audible heart murmur, which varies with sympathetic tone and may disappear as heart rate slows or cat relaxes.
- Subaortic stenosis: narrowing after aortic valves causes systolic ejection murmur, heard best at the low left base. Because it radiates up the aortic arch, which curves toward right, can also be heard at the right base.
- Pulmonic stenosis: systolic ejection murmur, heard best at the left base.
- Mitral insufficiency: murmur is best heard at the left apex, usually holosystolic, but in early stages of the disease may be soft and decrescendo shaped. Its intensity is related to severity of the mitral valve disease.
- Tricuspid insufficiency: holosystolic murmur, loudest at the right apex. It is often accompanied by jugular pulsation.
- Ventricular septal defect: holosystolic murmur of low to moderate intensity, heard best at the right sternal border. A large ventricular septal defect may also cause the murmur of relative pulmonic stenosis.
Diastolic murmurs are uncommon in dogs and cats. The most common cause is aortic insufficiency from bacterial endocarditis (or less likely congenital malformation or degenerative aortic valve disease). Relevant pulmonic insufficiency is rare, but more likely with pulmonary hypertension. Diastolic murmurs are best heard at the left base and are decrescendo in configuration.
Continuous murmurs occur through whole cardiac cycle. Their most common cause is patent ductus arteriosus (PDA). Its murmur is loudest at high left base. Systolic component is usually louder (maximum intensity at the end of systole) and well heard over the whole chest, but in the diastole the intensity of the murmur decreases and can be more localized to the left base. Consequently, diastolic phase may be missed if only apex is auscultated.
Nelson R. W., Couto C. G.: Small Animal Internal Medicine, 4th Ed. Mosby Elsevier, 2009
Fuentes V. L., Johnson L. R., Dennis S.: BSAVA Manual of Canine and Feline Cardiorespiratory Medicine, 2nd Ed. BSAVA, 2010