A continuous murmur is defined as one that begins in systole and extends through S2 into part or all of diastole. It need not occupy the entire cardiac cycle; therefore, a systolic murmur that extends into diastole without stopping at S2 is considered to be continuous even if it fades completely before the subsequent Sj. A physiologic classification of continuous murmurs as described by Myers320 is detailed in Table 10-13.
Table 10-13: Physiologic Classification of Continuous Murmurs
Continuous murmurs due to rapid blood flow Venous hum
Hyperemia of neoplasm (hepatoma rental cell carcinoma, Paget's disease)
Continuous murmurs due to high-to-low pressure shunts
Left-to-right atrial shunting (Lutembacher's syndrome, mitral atresia plus atrial septal defect)
Venovenous shunts (anomalous pulmonary veins, portosystemic shunts) Arteriovenous fistula (systemic or pulmonic) Continuous murmurs secondary to localized arterial ob- struction Coarctation of the aorta
SOURCE: From Myers JD. The mechanisms and significances of continuous murmurs. In: Leon DF, Shaver JA, eds. Physiologic Principles of Heart Sounds and Murmurs. Monograph 46. New York: American Heart Association; 1975:202. Reproduced with permission from the American Heart Association, Inc., and author.
High-velocity blood flow through veins and arteries may cause a continuous murmur. The cervical venous hum is a continuous murmur with diastolic accentuation and is easily heard in almost all children. This murmur also can be heard in healthy adults and is present in nearly all women in the later stages of pregnancy. High cardiac output states such as thyrotoxicosis and anemia are also associated with easily heard venous hums. This murmur is usually poorly heard in the supine position, and its presence in this position in an adult strongly suggests a hyperdynamic circulatory state. Peak intensity is in the supraclavicular fossa just lateral to the sternocleidomastoid muscle, and it is usually more prominent on the right side. When the murmur is loud, it may radiate below the clavicles and occasionally can be confused with the continuous murmur of patent ductus arteriosus. This error should never be made, however, because the cervical venous hum can be terminated easily by digital compression of the JVP.
The mammary souffle is another example of a continuous murmur occurring in 10 to 15 percent of pregnant women during the second and third trimesters and in the early postpartum period, particularly in lactating women, and is heard between the second and sixth anterior intercostal spaces. This murmur may be obliterated by firm pressure on the stethoscope or by digital pressure applied just lateral to the site of auscultation and therefore should not be confused with the continuous murmur of patent ductus arteriosus or with arteriovenous fistula. The mammary souffle disappears after termination of lactation. Other causes of continuous murmurs due to rapid blood flow through arterial or venous channels are outlined in Table 1013.
Continuous Murmurs due to High-to-Low-Pressure Shunts
A group of congenital cardiovascular anomalies has shunting from the high-pressure systemic (aortic) circulation to the low-pressure pulmonary arterial circulation, resulting in a large gradient between the two systems throughout the cardiac cycle. The murmur of patent ductus arteriosus is the classic example of this type of anomaly. It is heard best in the left infraclavicular area and the second left intercostal space. The peak intensity of the murmur is at the time of S2, after which it gradually wanes until it terminates before
S1.221 The length of the murmur is determined by the difference in the vascular resistance between the greater and lesser circulation. As the pulmonary vascular resistance increases, the diastolic pressure in the pulmonary artery approaches and finally reaches systemic levels, diminishing and finally abolishing diastolic flow and the diastolic portion of the murmur. With equilibration of aortic and pulmonary artery pressure, systolic flow across the shunt diminishes and finally disappears, leaving the ductus silent (Eisenmenger's patent ductus arteriosus). Surgically produced aortopulmonary connections (Blalock, Waterston, and Pott's shunts), as well as the murmur of aortic pulmonary window, have identical qualities, and the effect of pulmonary hypertension on their length is analogous. It is important to distinguish these types of continuous murmurs from to-and-fro murmurs. The latter is a combination of the systolic ejection murmur and a semilunar diastolic murmur. The classic example of a to-and-fro murmur is the murmur of aortic stenosis and regurgitation. The continuous murmur builds to a crescendo around S2, whereas the to-and-fro murmur has two components. The midsystolic ejection component decrescendos and may disappear as it approaches S2, leaving a silent period before the onset of the regurgitant murmur. Truncus arteriosus is a rare congenital anomaly and probably produces a continuous murmur only if there is coexisting pulmonary artery stenosis (see Chap. 63). In the presence of severe RV outflow obstruction, bronchial collateral arteries can enlarge their normal precapillary anastomoses with pulmonary arteries, and the resulting aortic pulmonary fistula can produce a continuous murmur. This murmur can be heard in the same location as the patent ductus but radiates widely, especially over the posterior thorax. Large bronchial collateral arteries producing such continuous murmurs are more common with pulmonary atresia but also occur with tetralogy of Fallot. Bronchial artery-pulmonary artery collaterals sufficient to produce continuous murmurs are also found in far-advanced bronchiectasis and sequestration of the lung (see Chap. 63).
An anomalous left coronary artery arising from the pulmonary artery may cause a continuous murmur when the left-to-right shunt flow is large; it is usually best heard at the left sternal border. In this condition, the origin of the right coronary artery is from the aorta, and the left-to-right shunt is from the high-pressure right coronary arterial bed through large arterial collaterals to the left coronary system, which empties into the low-pressure pulmonary artery.
Sinus of Valsalva aneurysms may cause continuous murmurs when they rupture into the right side of the heart. In almost all cases, rupture occurs from the right and noncoronary sinuses into the right atrium or the right ventricle.321 The murmur is heard maximally at the lower sternal border or xiphoid over the area corresponding to the fistulous tract. Diastolic accentuation of this murmur is an important sign to differentiate ruptured sinus from patent ductus arteriosus or arteriovenous fistula. Systolic suppression of the murmur is due to both mechanical narrowing of the fistulous tract during systole as well as the probable Venturi effect created by the rapid ejection of blood past the aortic origin of the fistula.
Coronary artery fistulas usually empty into the right atrium or ventricle and cause a continuous murmur that is best heard to either the left or the right of the lower sternal area. Since the majority of coronary flow occurs during diastole, the diastolic component of the murmur is louder. When the coronary artery fistula empties into a high-pressure right ventricle, only a diastolic murmur may be heard because the pressure gradient across the shunt is reduced during systole. Left-to-right shunting through an uncomplicated ASD produces no murmur audible on the chest wall because of the minimal pressure gradient and absence of turbulence. When mitral valve obstruction is present, as with Lutembacher's syndrome or mitral atresia, however, there can be a high-pressure gradient between the left and right atria across a small defect, and a continuous murmur may be present.322 This murmur increases in intensity with inspiration and decreases with the Valsalva maneuver. Occasionally, a small ASD is produced following transseptal catheterization or balloon valvuloplasty for mitral stenosis, and a continuous murmur is produced due to high-velocity flow resulting from the large pressure gradient from the left to the right atrium.
Total anomalous pulmonary venous drainage into a systemic vein may produce a continuous venous hum usually heard in the pulmonary area or the left infraclavicular area. Frequently, a constriction at the junction of the anomalous venous conduit and the innominate vein or superior vena cava may cause augmentation of the murmur (see Chap. 63).
Arteriovenous fistulas between peripheral vessels produce a classic continuous murmur with systolic accentuation caused by shunting of a large volume of blood at rapid flow rates from a high-pressure artery into a low-pressure vein. These murmurs are best heard at the site of the fistula. Local compression of the veins may decrease the intensity of the murmur by raising venous pressure and reducing the arteriovenous pressure gradient. Complete obliteration of the fistula will terminate the murmur, and if the shunt is of considerable magnitude, a baroreceptor-mediated reflex bradycardia may occur (Branham's sign). Likewise, a reflex tachycardia will occur on release of the obstruction. Pulmonary arteriovenous fistulas usually produce only a systolic murmur because the peripheral vascular resistance of the normal lung is very low, and the normally small diastolic pressure gradient from pulmonary artery to pulmonary vein is not significantly increased by the presence of the fistula.
Continuous Murmur Secondary to Localized Arterial Obstruction
Localized stenosis of systemic or pulmonary arteries may produce a continuous murmur or bruit if the obstruction is critical and adequate collateral flow is not available.323 Most partially obstructed arteries have only systolic murmurs that are delayed relative to cardiac systole, depending on the transit time of pulsatile flow from the heart to the site of obstruction. This lack of diastolic gradient is explained by the fact that the collateral arteries around the obstruction deliver adequate flow such that the diastolic pressure on either side of the localized obstruction is essentially equal. Thus a localized, partial arterial obstruction characteristically produces only a systolic murmur or bruit. If adequate collateral flow is not present, however, a diastolic and a systolic pressure gradient can be produced, together with a continuous murmur with systolic accentuation. Depending on the degree of inadequacy of collaterals, the murmur is truly continuous when collateral circulation is essentially nonexistent, or it extends only partially through diastole when collateral flow is somewhat compromised. Such is the case in severe coarctation of the aorta, where, in addition to the systolic and/or continuous murmurs heard over the thorax and produced by rapid blood flow through the tortuous intercostal collaterals, a continuous murmur may be produced at the site of the coarctation. This latter murmur is best heard over the back midline between the scapulae.
Continuous murmurs also may arise from branch pulmonary stenosis or partial obstruction of a major pulmonary artery occluded by a massive pulmonary embolus. Other common locations of continuous murmurs secondary to localized arterial obstructions are listed in Table 10-13. Common to all these murmurs is critical narrowing of the vessel with inadequate collateral flow such that a continuous pressure gradient is produced throughout the cardiac cycle. Murmurs produced by obstruction of major coronary arteries are rarely loud enough to be transmitted to the chest wall. When audible, they produce only diastolic murmurs, even with inadequate collateral circulation.
* This text is modified from Chap. 11 by N. Banks Anderson, Jr., in the ninth edition of The Heart.
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...