IVMS Heart and Lung Auscultation Sounds

The notes that follow represent brief descriptions of the physiologic / pathophysiologic auscultation sound mp3s provided as a component module in the IVMS Mini-Med School Course for USMLE Step 1 Review, available at http://www.imhotepvirtualmedsch.com/heart-and-lung-auscultation-sounds-mp3s.php

For a more detailed discussion of the topics herein, please access/ download the learning modules companion note set. Heart and Lung Sounds: Reading for IVMS Heart and Lung Auscultation Page , an illustrated discussion of various heart sounds, murmurs and lung sounds as they relate to the anatomy, physiology, pathology, pathophysiology and diagnosis of common cardiovascular and pulmonary diseases. I. Systolic Murmurs(8)
1) Aortic Stenosis AS most commonly arises from one of three conditions. A patient may be born with a congenital stenosis, or acquire the stenosis from secondary conditions such as rheumatic heart disease or idiopathic calcification of the valves. Persons born with an abnormal bicuspid valve are particularly susceptible to calcification later in life. The murmur of aortic stenosis is typically a mid-systolic ejection murmur, heard best over the aortic area or right second intercostal space, with radiation into the right neck. This radiation is such a sensitive finding that its absence should cause the physician to question the diagnosis of aortic stenosis. It has a harsh quality and may be associated with a palpably slow rise of the carotid upstroke. Additional heart sounds, such as an S4, may be heard secondary to hypertrophy of the left ventricle which is caused by the greatly increased work required to pump blood through the stenotic valve. Because the second heart sound is largely generated by the sudden closing of the aortic valve, a poorly mobile and stenotic aortic valve may cause S2 to become quieter or even absent. N.B. - Although S2 is normally created by the
closure of the aortic valve followed by the pulmonary valve, if the closure of the aortic valve is delayed enough, it may close after the pulmonary, creating an abnormal paradoxical splitting of S2.

Aortic stenosis is a progressive disease, with typical symptoms and clinical findings to match its course. A good mnemonic to remember the march of symptoms related to undiagnosed aortic stenosis is ASC, or Aortic Stenosis Complications. One of the early symptoms is Angina, which is usually stable and exertion-related. A more serious and later condition is Syncope, again associated with exercise. Finally, the hypertrophied left ventricle can no longer meet demands, and Congestive heart failure may ensue. On examination, the phase during systole at which the murmur peaks can help to determine the severity of the disease. An early-peaking murmur is usually associated with a less stenotic valve, while a late-peaking murmur has a more severe degree of stenosis. This is because a more stenotic valve takes longer for the ventricle to generate the terrific pressures needed to force the blood past the lesion.

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2) Early Aortic Stenosis This is an early-peaking murmur of AS. Note that the murmur is in early systole, with a harsh quality and a crescendo-decrescendo shape. Because this is early-peaking, it would suggest an earlier stage of aortic stenosis than a late-peaking murmur. 3) Late Aortic Stenosis This is a late-peaking murmur of AS. Note that the murmur is in later systole, with a harsh quality and a crescendo-decrescendo shape. Because this is late-peaking, it would suggest a more severe stage of aortic stenosis than an early peaking murmur. Additionally, there is a nearly-absent S2, again indicating that the valve is poorly mobile and severely diseased 4) Mitral Valve Prolapse The pathophysiology of MVP is varied, but can be thought of as an inability of the papillary muscles or chordae tendineae to completely tether the mitral valve during the late stages of systole. As the left ventricle chamber decreases in size, the papillary muscles and/or the chordae fail to maintain tension on the mitral valve, and it prolapses with a brief regurgitant period into the left atrium. This is a common syndrome which frequently is associated with young adult women, and can present as attacks of palpitations, anxiety, or light-headedness. Although it is usually a mild symptom, patients with mitral valve prolapse with evidence of regurgitation by echo should be given antibiotic prophylaxis during invasive procedures to help prevent bacterial endocarditis. Following a normal S1 and briefly quiet systole, the valve suddenly prolapses, resulting in a midsystolic click. The click is so characteristic of MVP that even without a subsequent murmur, its presence alone is enough for the diagnosis. Immediately after the click, a brief crescendodecrescendo murmur is heard, usually best at the apex. In stark contrast to most other murmurs, MVP is enhanced by Valsalva maneuvers and decreased by squatting. This is because those maneuvers which decrease the volume of the left ventricle (Valsalva, standing) will cause the prolapse to occur sooner and more severely, while those that increase venous return and diastolic filling (squatting) and thereby enhance the ventricular volume, help to maintain tension along the chordae and to keep the valve shut. The only other murmur which, for similar reasons, responds in this paradoxical way to these common maneuvers is hypertrophic cardiomyopathy, also known as idiopathic hypertrophic subaortic stenosis. 5) Mitral Regurgitation MR is usually either a congenital condition or a consequence of rheumatic heart disease, marked left ventricular dilatation, acute infective endocarditis, or papillary muscle dysfunction secondary to acute or prior myocardial infarction. This murmur is usually best heard at the apex, with radiation into the axilla. Because the mitral valve is unable to contain the blood within the ventricle for the entire systolic period, it is a holosystolic murmur. The quality of the murmur is usually described as blowing, and, as subtly demonstrated in the sample you are hearing, it is often associated with an S3 because of

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the left atrial volume overload. Although S1 is due to a combination of mitral and tricuspid valve closure, the mitral valve is the louder aspect. Because the valve closure in mitral regurgitation is incomplete, S1 may be noticeably quieter. Finally, in severe regurgitation, the pressure in the left ventricle quickly equalizes with venous pressure in the left atrium during the start of diastole. The result is that the aortic valve may close prematurely and may, although not present in this sample, occasionally result in a widely split S2. A maneuver which may increase the intensity of mitral regurgitation is transient arterial occlusion. When blood pressure cuffs are used to completely occlude the brachial artery for a short period, the resultant increase in arterial resistance causes the left ventricle to increasingly favor the regurgitant mitral valve as an outlet for flow. This flow increase will enhance the intensity of the murmur. 6) Pulmonary Stenosis Pulmonary stenosis is an infrequent cause of significant murmurs, and is often a part of congenital disorders, such as tetralogy of Fallot, Williams syndrome, and Noonan syndrome. The murmur of pulmonary stenosis is heard best in the pulmonic area, the second intercostal space along the left sternal border. The murmur can be heard radiating into the neck or the back, has a crescendo-decrescendo shape, and a harsh quality. Because it takes longer for the right ventricle to eject its load of blood through the stenotic valve, the closure of the pulmonary valve is delayed. This widens the slight gap between the closure of the aortic and pulmonary valves in S2 to a noticeable degree, and a significant splitting of S2 can be heard, as is well demonstrated in this audio example. Finally, maneuvers which increase venous filling and blood flow into the right ventricle, such as deep inspiration, will tend to increase the intensity of the murmur. 7) Ventricular Septal Defect VSD is usually best heard over the tricuspid area, or the lower left sternal border, with radiation to the right lower sternal border because this is the area which overlies the defect. It is characteristically a holosystolic murmur because the pressure difference between the ventricles is generated almost instantly at the onset of systole, with a left to right shunt continuing throughout ventricular contraction. If the defect persists without treatment, irreversible pulmonary hypertension may develop with reversal of the shunt into a right to left flow pattern (Eisenmenger syndrome). There is usually no diastolic component to the murmur, as the pressure between the ventricles during diastole is not sufficiently different to generate an audible flow. Because the flow pattern is usually left to right, the right ventricle suffers from volume overload and takes longer to eject the stroke volume. This causes a slight delay in the closing of the pulmonary valve, and a widely split S2 may result.

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8) Atrial Septal Defect In ASD because the pressure in the left atria initially exceeds that in the right, the blood flows in a left to right shunt. This high volume of blood next passes into the right ventricle, and the ejection of the excess blood through a normal pulmonary valve produces the prominent midsystolic flow murmur as heard in this sample. This murmur is best heard over the pulmonic area of the chest, and may radiate into the back as with the murmur of pulmonary stenosis. The most characteristic feature of an atrial septal defect is the fixed split S2. As mentioned in the murmur overview, a split S2 is caused physiologically during inspiration because the increase in venous return overloads the right ventricle and delays the closure of the pulmonary valve. With an atrial septal defect, the right ventricle can be thought of as continuously overloaded because of the left to right shunt, producing a widely split S2. Because the atria are linked via the defect, inspiration produces no net pressure change between them, and has no effect on the splitting of S2. Thus, S2 is split to the same degree during inspiration as expiration, and is said to be fixed.

II. Diastolic Murmurs

1) Aortic Regurgitation You are listening to a typical murmur caused by aortic valve regurgitation. Aortic regurgitation is mostly seen in males, with a 3:1 ratio as compared to females. In 2/3 of cases, the regurgitation is secondary to rheumatic heart disease, and may have a component of aortic stenosis. Aortic regurgitation may also be primarily congenital or associated with syphilis infection, Marfan syndrome, or valvular deterioration due to infective endocarditis. The murmur of aortic regurgitation is complex. The left ventricle is typically dilated secondary to extreme volume overload, as it must handle both the forward flow delivered from the left atria as well as the regurgitant flow from the aorta. This large volume of blood is ejected rapidly during systole, and an early mid-systolic flow murmur is frequently audible over the right upper sternal border with radiation into the neck. The most notable aspect of the murmur is the diastolic sound produced as the blood flows retrograde back into the left ventricle. This murmur is usually characterized as blowing, decrescendo, and heard best in the third left intercostal space. In severe regurgitation, it may be holodiastolic. It radiates widely along the left sternal border. Finally, a third murmur, known as an Austin Flint murmur, may be detected. This is a soft, rumbling, low-pitched, late diastolic murmur which is heard best at the apex. It is thought to be due to a functional mitral valve stenosis, as the backflow of blood from the aorta presses on the anterior leaflet of the mitral valve, slightly occluding the flow from the atria. The atrial kick just before systole accentuates this flow, producing the Austin Flint murmur. Any maneuver which increases systemic vascular resistance will increase the murmur of aortic regurgitation, as it will tend to favor backflow into the ventricle. This includes handgrip and isometric excercise.

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2) Mitral Stenosis You are listening to a typical example of the murmur produced by mitral valve stenosis. As opposed to aortic regurgitation, mitral stenosis has a female preponderance, with the female:male ratio being about 2:1. Almost all cases of mitral stenosis are rheumatic in origin, although congenital causes can occur. The murmur of mitral stenosis is best heard at the apex with little radiation. It is nearly holodiastolic with pre-systolic accentuation due to the atrial kick. It is usually described as lowpitched, decrescendo, and rumbling, and can be heard best with the patient in the left lateral decubitus position. The murmur appears about 0.08 seconds after S2, and is heralded by an opening snap. This is a brief, loud sound which is caused as the stenotic valve suddenly halts its normal opening at the start of diastole.

III. Rubs, Gallops, and Continuous Murmurs

1) Friction rub It is caused by the beating of the heart against an inflamed pericardium or lung pleura, which itself have a wide variety of etiologies. This sound is usually continuous, and heard diffusely over the chest. It typically has three components, one systolic and two diastolic. The systolic occurs with ventricular contraction, and the diastolic occurs during both rapid ventricular filling and atrial contraction. It is accentuated when the patient sits up and leans forward, and may be accentuated during inspiration. If the rub completely disappears when the patient holds his breath it is more likely due to pleural, not pericardial, origin. 2) Third heart sound or S3 Shortly after S2, the closing of the semilunar valves, the AV valves open and diastole begins. Diastole is itself further divided into several stages, the first being that of rapid filling, where 80% of the blood stored in the atria during systole is transferred to the ventricles. At the end of this stage, about 140-160 msec after S2, an S3 may be heard if the volume which has been transferred is abnormally large, as in mitral regurgitation. It can be thought of as a sound which is generated when the ventricle is forced to dilate beyond its normal range because the atrium has overloaded volume. An S3 is usually heard best with the bell of the stethoscope placed at the apex while the patient is in the left lateral decubitus position. The presence of an S3 is usually normal in children and young adults, but pathologic in those over the age of 40. 3) Fourth heart sound or S4 The late stage of diastole is marked by atrial contraction, or kick, where the final 20% of the atrial output is delivered to the ventricles. If the ventricle is stiff and non-compliant, as in ventricular hypertrophy due to long-standing hypertension, the pressure wave generated as the atria contract produces an S4. It is heard best with the bell of the stethoscope at the apex.

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4) Patent ductus arteriosis This vascular channel between the aorta and pulmonary artery remains open in a small percentage of newborns, with a resultant left to right shunt. This murmur is best heard over the upper left sternal edge, associated with a thrill, and is characteristically continuous and machinery-like. If untreated, the high flow through the pulmonary artery will eventually lead to irreversible pulmonary hypertension with reversal of the shunt flow to right to left (Eisenmenger syndrome). It should be differentiated from a venous hum, a common innocent murmur often heard in children. You may hear short breaks in the otherwise continuous murmur, which is an artifact of looping the sound by your computer.

Lung Sounds
Breath Sounds - Normal Vesicular breath sounds are normal. Other types of breath sounds include tracheal (very loud, high pitch, harsh), bronchial (loud, high pitch, tubular), and bronchvesicular (moderately loud, medium pitch, rustling). Vesicular breath sounds are heard over most of the peripheral lung fields, and are described as soft, low pitched, and with a gentle rustling quality. The sample you are listening to has had the volume enhanced to the point where you can detect the heart sounds in the background. You will also notice that this patient seems to be hyperventilating, with a respiratory rate of approximately 25. Breath Sounds - Crackles Also known as rales, these abnormal breath sounds are usually caused by excessive fluid within the airways. This fluid could be due to an exudate, as in pneumonia or other infections of the lung, or a transudate, as in congestive heart failure. You will notice that crackles sound just as they are named, and are typically inspiratory. The crackles in this example are particularly wet sounding, with dry crackles sounding more like rubbing hair together next to your ear or like the sound of opening Velcro. Breath Sounds - Wheezes Wheezes are characteristically an expiratory sound associated with forced airflow through abnormally collapsed airways with residual trapping of air. Although commonly associated with asthma, wheezes may also be due to other causes such as airway swelling, tumor, or obstructing foreign bodies.

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References and further study: 1) The Auscultation Assistant Available at: http://www.med.ucla.edu/wilkes/inex.htm Accessed November 25, 2013 2) 3) 4) 5) Heart Sounds Podcast Series-James M. Wilson, MD (A IVMS mp3 Folder) IVMS Folder-Cardiovascular Notes, Curves and Calculations IVMS Folder-Audio-Heart and Lung Auscultation Sounds Cray, MI. Heart and Lung Sounds: Reading for IVMS Heart and Lung Auscultation Page, e-Notes Guide. http://www.scribd.com/doc/186914662/HEART-AND-LUNG-SOUNDSReading-for-IVMS-Heart-and-Lung-Auscultation-Page

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