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Introduction Disease of the cardiac valves and other cardiac structures frequently result in abnormal turbulent blood flow within the heart causing murmurs. Careful auscultation of heart murmurs is an extremely valuable tool in the diagnosis of many cadiac conditions. Heart murmurs will be discussed below. A review of heart sounds and valvular heart disease is available elsewhere. When normal laminar blood flow within the heart is disrupted, an audible sound is created by turbulent blood flow. Outside of the heart audible turbulence is referred to as a bruit, while inside the heart it is called a murmur. There are four major causes of cardiac murmurs. First, if blood is forced through a tight area, turbulent blood flow ensues. This is the case in valvular stenosis. As a general rule, the worse the stenosis, the louder the murmur, however if heart failure develops, adequate pressures to create turbulent blood flow may not be able to be achieved and the murmur may lessen or even disappear. Thus, the intensity of a murmur is not used to indicated severity of disease. A second cause of a murmur is valvular insufficiency in which blood abnormally travels backward through an incompetent valve causing turbulence when it meets normal, forward blood flow. If blood is forced through a congenital anomaly from one chamber to another, as in an atrial septal defect (ASD) or ventricular septal defect (VSD), a murmur is produced. Yet another cause of cardiac murmurs is increased flow of blood through a normal valve. In high output states such as anemia, thyrotoxicosis, or sepsis, a large amount of volume is passing through the cardiac valves and the normal laminar blood flow may be disturbed. Describing murmurs Murmurs are described by their timing in the cardiac cycle, intensity, shape, pitch, location, radiation, and response to dynamic maneuvers. Using the above, a clinician can accurately characterize the nature of a murmur and communicate their findings in a precise manner. Timing The timing of a murmur is crucial to accurate diagnosis. A murmur is either systolic, diastolic, or continuous throughout systole and diastole. Remember that systole occurs between the S1 and S2 heart sounds while diastole occurs between S2 and S1.  With the knowledge of the possible cardiovascular conditions that cause systolic or diastolic murmurs, the clinician can narrow their differential diagnosis. Thus, it is important to remember which lesions result in systolic murmurs and which result in diastolic murmurs. Stenosis of the aortic or pulmonic valves will result in a systolic murmur as blood is ejected through the narrowed orifice. Conversely, regurgitation of the same valves will result in a diastolic murmur as blood flows backward through the diseased valve when ventricular pressures drop during relaxation. Regarding the mitral and tricuspid valves, stenosis would result in a diastolic murmur and regurgitation a systolic murmur. Other murmurs will be discussed in their respective sections. A complete discussion of valvular heart disease is found elsewhere.
HOCM
= hypertrophic obstructive cardiomyopathy (a.k.a IHSS)
Once it is determined if the murmur is systolic or diastolic, the timing of the murmur within systole or diastole also becomes important when characterizing murmus. Systolic murmurs can be classified as either midsystolic (a.k.a. systolic ejection mumurs or SEM), holosystolic (pansystolic), or late systolic. A midsstolic murmur begins just after the S1 heart sound and terminates just before the P2 heart sound, so S1 and S2 will be distinctly audible. Conversely, a holosystolic murmur begins with or immediately after the S1 heart sound and extends up to the S2 making them difficult, if not impossible to hear. A mid-late systolic murmur begins significantly after S1 and may or may not extend up to the S2.
Grading Systolic murmurs are graded on a scale of 6 while diastolic murmurs are graded on a scale of 4 (see below). Often, grade 1 murmurs are not discernable to inexperienced clinicians, while grade 6 murmurs are heard even without the stethoscope on the chest and may actually be visible. The intensity of a murmur is primarily determined by the volume/velocity of blood flowing through a defect and the distance between the stethoscope and the lesion. For example, a very thin patient with severe aortic stenosis with a high pressure gradient across the valve (thus high velocity of blood flow) will have a loud murmur. Conversely, the exact same valvular lesion in a morbidly obese person or a person with severe COPD and a widened anterior-posterier chest diameter may be inaudible. Grading systolic murmurs
Grading diastolic murmurs
Shape The shape of a murmur describes the change of intensity throughout the cardiac cycle. Murmurs are either crescendo, decreshendo, creschendo-decreshendo, or uniform.  Pitch A murmur will be high pitched if there is a large pressure gradient across the pathologic lesion and low pitched if the pressure gradient is low. For example, the murmur of aortic stenosis is high pitched since there is usually a large pressure gradient between the LV and the aorta. Conversely, the murmur of mitral stenosis is low pitched since there is a lower pressure gradient between the LA and the LV during diastole. Remember high pitched sounds are heard with the diaphragm of the stethoscope while low pitched sounds are heard with the bell. Location The anatomic location the the murmur is best heard is an important factor in determining the etiology of the lesion. There are four main "listening posts" on the chest (see picture below).  P = pulmonic valve post (left upper sternal border or LUSB) T = tricuspid valve post (left lower sternal border or LLSB) M = mitral valve post (apex) E = "Erb's point" Note: Both the aortic and pulminc listening posts are considered to be near the "base" of the heart. In general, a murmur will be the most intense over whichever listening post corresponds to the diseased valve. Many murmurs will radiate to more than one listening post. For example, the murmur of aortic stenosis is best heard at the LUSB, however it may radiate to the apex. This radiation of the AS murmur is called the "Gallavaradin dissociation". Radiation While murmurs are usually most intense at one specific listening post, they often radiate to other listening posts or areas of the body. For example, the murmur of aortic stenosis frequently radiates to the carotid arteries and the murmur of mitral regurgitation radiates to the left axillary region. It is often difficult to distinguish if one murmur is radiating to multiple sites or if there are multiple murmurs present from many different causes. Dynamic auscultation and echocardiography is helpful in determining the exact lesion present. Systolic murmurs Midsystolic murmurs Midsystolic murmurs (a.k.a systolic ejection murmurs or SEM) include the murmurs of aortic stenosis (AS), pulmonic stenosis (PS), hypertrophic obstructive cardiomyopathy (HOCM) and atrial septal defects (ASD). A midsystolic murmur begins just after the S1 heart sound and terminates just before the P2 heart sound, so S1 and S2 will be distinctly audible. The term midsystolic is preferred to SEM since many lesions that produce midsystolic murmurs are unrelated to systolic ejection. Aortic stenosis (AS) The classic murmur of aortic stenosis is a high pitched, creshendo-decreshendo ("diamond shaped"), midsystolic murmur located at the aortic listening post and radiating toward the neck. The radiation of the AS murmur is often mistaken for a carotid bruit. The AS murmur is also well known to radiate to the cardiac apex on occassion, making it difficult to distinguish if MR is also present. This radiation of the AS murmur to the apex is known as "Gallavardin dissociation". It requries dynamic auscultation or echocardiography to determine if coexistant MR is the cause of the apical murmur in a patient with AS. The intensity of the murmur of AS is not a good indicater as to the severity of disease. As AS worsens, the LV begins to fail and the ejection fraction declines to the point where sufficient force to create turbulent flow is no longer produced, resluting in a decrease in the intensity of the murmur. While the intensity of the murmur may not be an accurate determinant of the severity of AS, the shape of the murmur can be very helpful. As AS worsens, it takes longer for blood to eject through the valve, so the peak of the creshendo-decreshendo murmur moves to later in systole. Thus mild AS would have an early peaking murmur while the murmur of severe AS peaks later in systole. Remember from the heart sounds section that the delay in aortic valve closure can cause a paradoxically split S2 heart sound and as the aortic valve becomes more heavily calcified, the intensity of the S2 heart sound declines. Also, in patients with bicuspid aortic valves, an ejection click may be heard just before the murmur begins.  Pulmonic stenosis (PS) The murmur of pulmonic stenosis is very similar to that of aortic stenosis. It is a midsystolic high-pitched creshendo-decreshendo murmur heard best at the pulmonic listening post and radiating slighlty toward the neck, however the murmur of PS does not radiate as widely as that of AS. The murmur of PS peaks early if the disease is mild and peaks later as the disease progresses. Also, the murmur of PS demonstrates increased intensity during inspiration due to the increased venous return to the right heart resulting in greater flow across the pulmonic valve. While the murmur of AS extends up to the A2 heart sound, the murmur of PS extends through the A2 sound up to the P2 heart sound. Severe PS results in decreased mobility of the pulmonic valve leaflets and thus a softer P2 sound. Also, as the PS worsens, the closure of the pulmonic valve is delayed, since more time is required to eject blood through the stenotic valve, resulting in a widely split S2 heart sound that still exhibits inspiratory delay. Note that the murmur of an ASD (see below) is also midsystolic, however it has a fixed split S2.  Atrial septal defect (ASD) The murmur produced by an ASD is due to increased flow through the pulmonic valve, thus it is remarkably similar to that of pulmonic stenosis. The difference lies in the intensity and splitting pattern of the S2 heart sound. The intensity of S2 should remain unchanged and may infact be accentuated if pulmonary hypertension develops. The S2 in fixed-split in a person with an ASD. This differs from the widened split S2 seen in severe PS. Also, the murmur of an ASD does not increase in intensity with inspiration.  Hypertrophic obstructive cardiomyopathy (HOCM) The murmur of HOCM is important to detect due to its clinical implications (see hypertrophic obstructive cardiomyopathy review). The murmur is high-pitched, creshendo-decreshendo, midystolic murmur heard best at the left lower sternal border. The murmur of HOCM does not radiate to the carotids like that of AS. The important auscultory features of HOCM that distinguish it from AS relate to dynamic auscultation (see below).  Pansystolic Murmurs Pansystolic murmurs are also known as holosystolic and include the murmurs of mitral regurgitation (MR), tricuspid regurgitation (TR), and ventricular septal defects (VSD). Since the intensity of these murmurs is high immediately after the onset of S1 and it extends to just before the S2, often the S1 and S2 sounds are overwhelmed by the murmur and may be difficult to hear. Mitral regurgitation (MR) The murmur of mitral regurgitation is described as a high-pitched, "blowing" holosystolic murmur best heard at the apex. The direction of radiation of the murmur depends on the nature of the mitral valve disease, however it usually radiates to the axilla. The intensity of the murmur of MR does not increase with inspiration helping to distinguish it from the murmur of tricuspid regurgitation.  Tricuspid regurgitation (TR) The murmur of tricuspid regurgitation is similar to that of MR. It is a high pitched, holosystolic murmur however it is best heard at the left lower sternal border and it radiates to the right lower sternal border. The intensity significantly increases with inspiration helping to distinguish it from MR. This inspiratory enhancement of the TR murmur is called "Carvallo's sign".  Ventricular septal defect (VSD) A ventricular septal defect produces yet another holosystolic murmur. Blood abnormally flows from the LV (high pressure) to the RV (low pressure) creating turbulent blood flow and a holosystolic murmur heard best at "Erb's point". The smaller the VSD, the louder the murmur.  Late Systolic Murmurs The murmur of mitral or tricuspid valve prolapse is the only significant late systolic murmur. Tricuspid valve prolapse is relatively rare and usually not clinically significant. Mitral valve prolapse (MVP) Mitral valve prolapse produces a mid-systolic click usually followed by a uniform, high-pitched murmur. The murmur is actually due to mitral regurgitation that accompanies the MVP, thus it is heard best at the cardiac apex. MVP responds to dynamic auscultation.  Diastolic Murmurs Diastolic murmurs include aortic and pulmonic regurgitation (early diastolic), and mitral or tricuspid stenosis (mid-late diastolic). Tricuspid stenosis is very rare and is discussed further in the valvular heart disease section. Aortic regurgitation (AR) The murmur of aortic regurgitation is a soft, high-pitched, early diastolic decreshendo murmur usually heard best at the 3rd intercostal space on the left (Erb's point) at end expiration with the patient sitting up and leaning forward. If the AR is due to aortic root disease, the murmur will be best heard at the right upper sternal border and not at Erb's point. As AR worsens in severity, the pressure between the LV and the aorta equalize much faster, thus the murmur becomes significantly shorter. In people with AR, an early diastolic rumble may also be heard at the apex due to the regurgitant jet striking the anterior leaflet of the mitral valve causing it to vibrate. This murmur is termed the Austin-Flint murmur. In addition to the above two murmurs, a systolic ejection murmur may be present in people with severe AR at the right upper sternal border simply due to the large stroke volume passing through the aortic valve with each systolic contraction of the LV.  Pulmonic regurgitation (PR) Pulmonic regurgitation produces a murmur that is often indistinguishable from that of AR. PR produces a soft, high-pitched, early diastolic decreshendo murmur heard best at the pulmonic listening post (LUSB). The murmur of PR increases in intensity during inspiration, unlike that of AR. The murmur of PR is clasically referred to as the "Graham-Steell murmur" after it's initial describers.  Mitral stenosis Mitral stenosis results in a uniquely shaped, low-pitched diastolic murmur best heard at the cardiac apex. The opening of the mitral valve produces an "opening snap" due to the high LA pressures, which is immediately followed by a decreshendo murmur as blood flows passively from the LA to the LV through the stenosed mitral valve creating turbulance. Immediately before the S1 sound, active LV filling occurs when the LA contracts and forces more blood through the stenosed mitral valve creating a late diastolic creschendo murmur. In the presence of atrial fibrillation, the active LV filling phase does not take place and the latter part of the MS murmur disappears. As MS worsens, LA pressure increases forcing the mitral valve open earlier in diastole. Thus, in severe MS, the opening snap occurs earier as does the initial decreshendo part of the murmur. The opening snap and murmur of MS also respond to dynamic auscultation.  Continuous Murmurs The murmur of a PDA is continuous throughout systole and diastole. Often the S2 heart sound is difficult to detect. The murmur begins just after S1 and creshendos peaking at S2, the decreshendos to S1.  Summary of
murmurs
  Dynamic Auscultation The use of dynamic auscultation to help determine the etiology of an abnormal heart sound or murmur is very easy to perform and can be very helpful. The most commonly used maneuvers include Valsalva, changes with respiration, squatting, rapid standing from a squatting position, post-ectopic beat changes, handgrip exercises/transient arterial occlusion, and inhalation of amyl nitrate. |
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