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Chapter 10: THE HISTORY, PHYSICAL EXAMINATION, AND CARDIAC AUSCULTATION

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Figure 10-1: Ellis-van Creveldsyndrome. A. Typical "lip tie" due to multiple frenulum. B. Polydactyly. This patient has a large septal defect.

Figure j0-2: Holt-Oram syndrome: fingerized thumb (arrow) associated with an atrial septal defect.

Figure j0-3: Cornelia de Lange's syndrome: low hairline, hirsutism, bushy brows, phocomelia, and a single thumblike digit. May be associated with ventricular septal defect. Figure j0-4: Pierre Robin syndrome: hypoplastic mandible associated with a ventricular septal defect.

Figure j0-5: Ehlers-Danlos syndrome. A. Hyperextensible skin. B. Lax joints. Redundant chordae tendineae and arterial rupture may occur.

Figure ^-6: Pseudoxanthoma elasticum: grooved skin in a typical location. Arterial calcification may occur.

Figure j0-7: Marfan's syndrome. A. Long, narrow face. B. Arachnodactyly and positive wrist sign. C. High-arched palate. D. Ectopia lentis associated with aortic aneurysm and severe aortic regurgitation in a teenage girl.

Figure j0-8: Fabry's disease: dark-red angiokeratomas on the penis may be linked with coronary artery disease.

Figure j0-9: Trisomy 18 syndrome: tightly clenched fist with overlapping index and fifth fingers. A ventricular septal defect was present.

Figure 10-10: Turner's syndrome: epicanthal folds, pigmented moles, hypertelorism, and scars on the neck where webs have been removed. May be associated with coarctation of the aorta.

Figure 10-11: Fetal alcohol syndrome: midface hypoplasia, absent philtrum, and microcephaly associated with a ventricular septal defect.

Figure 10-12: (Plate 29) Symmetric cyanosis. Equal cyanosis and clubbing of hands and feet due to transposition of great vessels and a ventricular septal defect without patent ductus arteriosus.

Figure 10-13: (Plate 30) Differential cyanosis. Cyanosis of fingers (left) greater than that of toes due to transposition of great vessels with patent ductus arteriosus. Figure jP-H: (Plate 3j Differential cyanosis. Clubbing of left hand (compare thumbs) and cyanosis of left hand and all toes due to patent ductus arteriosus with pulmonary hypertension and normally related great vessels. (Courtesy of Dr. Joseph K. Perloff, University of California, Los Angeles.)

Figure 10-15: (Plate 32) Tuft erythema. Erythema of fingertips due to small right-to-left shunt from AV canal defect.

Figure 10-16: (Plate 33) Clubbing due to bacterial endocarditis.

Figure 10-17: (PLATE 34) Bacterial endocarditis: A. Valvular infection associated with a tender, purplish nodule (Osler's node) in the finger pad (arrow). B. Osler's node. Figure Noonan's syndrome: ptosis, hypertelorism, and low-set ears associated with valvular pulmonic stenosis.

Figure 10-19: Rubinstein-Taybi syndrome may be associated with a variety of congenital heart defects. (From Silverman ME, Hurst JW. The hand and heart. Am J Cardiol ^68; 22:7j8. Reproduced with permission from the publisher and authors.)

Figure 10-20: Multiple lentigines syndrome: dark-brown macular lesions of the abdomen associated with hypertrophic subaortic stenosis. (From Silverman ME. Visual clues to diagnosis. Primary Cardiology, October 1986. Reproduced with permission from the publisher and author.)

Figure 10-21: Scleroderma: clawlike hand deformity and shiny, tight skin. May be linked with myocardial fibrosis.

Figure 10-22: CREST syndrome. Telangiectasia of the face in a patient with Raynaud's phenomenon and sclerodactyly.

Figure 10-23: Systemic lupus erythematosus: butterfly rash associated with pericardial, myocardial, and endocardial disease.

Figure 10-24: (Plate 35) Rheumatoid arthritis: with ulnar deviation of the fingers, flexion of the distal interphalangeal joints with hyperextension of the proximal interphalangeal joints.

Figure 10-25: Polychondritis. A,B. Destruction of cartilage of the nose, producing a "saddle nose" in association with aortic regurgitation. (Courtesy of Dr. Warren Sarrell, Anniston, AL.)

Figure 10-26: Ankylosing spondylitis: immobile, curved spine with forward jutting of head. May be seen with AV block or aortic regurgitation. (From Silverman ME. Visual clues to diagnosis. Primary Cardiology, June 1987. Reproduced with permission from the publisher, author, and patient.) Figure 10-27: (Plate 36) Marked pectus excavatum.

Figure 10-28: Friedreich's ataxia (photographs from different patients). A. Kyphoscoliosis. B. Pes cavus. Myocardial fibrosis and hypertrophy are often present. (From Silverman ME. Visual clues to diagnosis. Primary Cardiology, June 1987. Reproduced with permission from the publisher and authors.)

Figure 10-29: Acromegaly. Coarse facial features, folds of skin, and prognathism are associated with myocardial hypertrophy and fibrosis. (From Silverman ME. Visual clues to diagnosis. Primary Cardiology, February1987. Reproduced with permission from the publisher, author, and patient.)

Figure 10-30: (Plate 37) Hyperkeratotic lesions encrusted on the soles of the feet in Reiter's syndrome.

Figure 10-31: Lyme arthritis: annular expanding rash with a clear central area. May be associated with pericarditis and AV block. (From Silverman ME. Visual clues to diagnosis. Primary Cardiology, December 1986. Reproduced with permission from the publisher and author.)

Figure 10-32: (Plate 38) Dermatomyositis. A violaceous hue and edema of upper eyelid may be associated with myocardial disease.

Figure 10-33: Amyloidosis. Enlarged tongue may be a sign of an infiltrative cardiomyopathy. (From Silverman ME. Visual clues to diagnosis. Primary Cardiology,

November1987. Reproduced with permission from the publisher, author, and patient.)

Figure 10-34: Hyperlipidemia: xanthomata associated with coronary artery disease. A. On the extensor tendons of the hand. B. On the Achilles tendon (arrow).

Figure 10-35: Klippel-Trenaunay syndrome: hypertrophy of left side of face and tongue in a patient with port-wine stains, gigantism of digits, and varicose veins.

Figure 10-36: Supravalvular aortic stenosis: turned-up nose, broad cheeks, large mouth with peg-shaped teeth, and large ears.

Figure 10-37: (Plate 39) Hereditary hemorrhagic telangiectasia. Telangiectasia under nails. (From Silverman ME, Hurst JW. The hand and the heart. Am J Cardiol 1968; 22:609. Used with permission from the publisher.)

Figure 10-38: (Plate 40) Hereditary hemorrhagic telangiectasia. Telangiectasia of tongue and lips may be associated with a pulmonary arteriovenous fistula. Figure 10-39: (Plate 41) Tuberous sclerosis. Adenoma sebaceum may be associated with rhabdomyomas of the myocardium.

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Figure 10-40: (Plate 42) Horizontal ear creases often are associated with the presence of extensive CAD.

Figure 10-41: Micromanometer and catheter tip flow velocity as change in contour of pressure waves (above) and flow waves (below) between the ascending aorta and the saphenous artery. (From Vlachopoulos C, O'Rourke MF. The arterial pulse. Curr Probl Cardiol 2000; 25:296-346.)

Figure 10-42: Schematic representation of the normal carotid arterial pulse, five types of abnormal pulses, and pulsus alternans. ECG, electrocardiogram; phono, phonocardiogram; S1, S2, first and second heart sounds; S, systole; D, diastole.

Figure 10-43: Pressure waves recorded directly in the ascending aorta (top) and brachial artery (bottom) under control conditions (left) and after 0.3 mg sublingual nitroglycerin (right) in a human adult. X, height the pressure would have without reflection (R). (From Kelly et al.,162a with permission.)

Figure 10-44: Elevation in RA pressure observed during abdominal pressure in patient with mild congestive heart failure. (From Ewy GA. The abdominojugular test: Technique and hemodynamic correlates. Ann Intern Med 1989; 109:456. Used with permission from the publisher and author.)

Figure 10-45: Schematic representation of the normal JVP, four types of abnormal JVPs, and the JVPs in three arrhythmias. See text under "Normal Venous Pulse" for definition of H, A, Z, C, X, V, and Y.

Figure 10-46: Right ventricular (RV) and right atrial (RA) pressure curves and simultaneous ECG from a patient with severe tricuspid regurgitation. Note ventricularization of the RA pressure curve.

Figure 10-47: (Plate 43) Retinal cotton-wool spot. Cotton-wool spots are most frequently found close to the optic disk. Although they occur in acute uncontrolled systemic hypertension, the more common cause now, in younger patients, is infection with the human immunodeficiency virus (HIV). This normotensive 37-year-old man had no visual symptoms and no other retinopathy. There is a myopic crescent at the temporal disk edge, which is not abnormal. He died of complications related to the acquired immunodeficiency syndrome (AIDS) 2 years later.

Figure 10-48: (Plate 44) Disk swelling and hard exudate in a macular "star" pattern. In this hypertensive patient with periarteritis nodosa, vascular leakage has led to the deposit of hard exudates around the fovea. Radial perifoveal connective tissue results in the star pattern of the exudate. Note also that the optic disk is edematous, with blurred margins, secondary to hypertension.

Figure 10-49: (Plate 45) Background diabetic retinopathy. Retinal microaneurysms, dot-and-blot hemorrhages, and a few fine upper temporal hard exudates are diagnostic of early diabetic retinopathy. The patient had no visual symptoms, but retinopathy of this magnitude can often be seen in patients with insulin-requiring diabetes of 15 or more years' duration.

Figure 10-50: (Plate 46) Proliferative diabetic retinopathy with preretinal hemorrhage. When neovascularization develops, preretinal and vitreous hemorrhages are much more likely to occur. Easily visible neovascularization either in the periphery of the retina, as in this diabetic patient, or at the disk is an indication for immediate panretinal laser photocoagulation.

Figure 10-51: Proliferative diabetic retinopathy, left eye. There is extensive neovascularization of the disk with an associated small intravitreal hemorrhage that obscures the upper temporal vessels. Along the inferior temporal arcade is another area of neovascularization. These new vessels are incorporated in fibrous membranes that may tent up the vessels and cause traction detachments of the retina, as at the lower right edge of the photograph.

Figure 10-52: (Plate 47) Branch retinal vein obstruction. Thickening of the retinal arterial wall in diabetes and hypertension may compromise the lumen of the vein, where they share a common adventitial sheath at an arteriovenous crossing. The resulting obstruction produces hemorrhage retinopathy in the drainage area of the affected vein. Note here how the flame-shaped pattern of blood outlines the arcuate pattern of the nerve fibers as they run toward the optic disk.

Figure 10-53: (Plate 48) Embolic retinal arterial obstruction (A and B). Cholesterol crystals may dislodge from the walls of the heart, aortic arch, or carotids. Carried into the retinal circulation as Hollenhorst plaques, they seldom obstruct the arterioles completely. Although amaurosis fugax is more common, the embolic burden may occasionally be so large as to produce retinal infarction. Note in the photograph of the macular area (A) that this patient's fovea remains red, while there is a pale, cloudy swelling nasal to it. This has produced a half "cherry-red" spot. With complete central retinal artery occlusion, the red foveal area is completely surrounded by pale swollen retina. Hollenhorst cholesterol plaques can be seen in both the upper and lower temporal retinal arteries. In A, the inferior temporal arteriole demonstrates "boxcar" segmentation of the blood column, indicative of very slow flow.

Figure 10-54: (Plate 49) Neovascularization after branch retinal vein obstruction. New vessels may develop late after obstruction of a branch of the central retinal vein. These most often serve to shunt flow around the obstructed vessel site and are thus not as exuberantly proliferative as those seen in diabetic retinopathy. Figure 10-55: Retinal emboli often lodge at bifurcations, as in this patient with carotid atherosclerosis. Note that the embolic material often seems larger than the containing vessel, as in the embolus at the lower left edge of the photograph. Emboli may damage the vessel wall and cause leakage, as can be seen by the exudate deposited about the inferior embolus. Hollenhorst cholesterol plaques rarely obstruct arterial flow completely, and this patient maintained vision.

Figure 10-56: (Plate 50) Calcific retinal embolus associated with aortic valvular disease. Calcific aortic valvular disease and valve replacement surgery may result in retinal emboli. Like cholesterol emboli, these calcific flecks lodge at arterial bifurcations but seldom obstruct flow completely. They are white and glitter in the ophthalmoscope beam. Somewhat similar emboli may be seen after the intravenous injection of illicit drugs expanded with talc.

Figure 10-57: (Plate 51) Retinal hemorrhages after cardiac catheterization. Following cardiac catheterization, symptomatic and asymptomatic retinal hemorrhages may occur. The latter are more common. Presumably, these are the result of embolic events. Note, in this recently catheterized patient, the two oval hemorrhages and a small area of cloudy swelling just inferior and temporal to the fovea.

Figure 10-58: Exudative diabetic retinopathy, right eye, illustrating microaneurysms, dot-and-blot hemorrhages, and venous engorgement with extensive deposits of hard, yellow exudate.

Figure 10-59: (Plate 52) A. Retinal arteriosclerosis. This 75-year-old hypertensive woman has marked arteriosclerosis of the upper temporal retinal arteriole and its branches. When the narrowed blood column can no longer be seen, the thickened wall produces the "silver-wire" appearance seen here. Where the arteriole crosses its associated vein, the course of the vein is altered, and its blood column cannot be seen. This venous "nicking" and "banking" is associated with impairment of outflow, and the affected veins become darker, larger, and more tortuous. B. Low-power view showing the silver-wire arteriole. Figure 10-60: Seven areas to be examined for abnormal cardiovascular pulsations by inspection and palpation. (From Schlant RC, Hurst JW. Examination ofthe Precordium: Inspection and Palpation. New York: American Heart Association; 1990:1-28. Used with permission from the publisher and authors.)

' Figure 10-61: Graphic representation of apical movements in health and disease. Heavy line indicates palpable features. P2, pulmonary component of second heart sound; A, atrial wave, corresponding to a fourth heart sound (S4) or atrial gallop; F, filling wave, corresponding to third heart sound (S3) or ventricular gallop. (From Willis P IV. Inspection and palpation of the precordium. In: Hurst JW, ed. The Heart, 7th ed. New York: McGraw-Hill; 1990:164. Reproduced with permission from the publisher and author.)

s Figure 10-62: The apex phonocardiogram is displayed simultaneously with the cardiac cycle, as recorded by high-fidelity catheter-tipped micromanometers in the central aorta, left ventricle (LV), and left atrium (LA). The first high-frequency component of M1 is coincident with the downstroke of the left atrial c wave and is separated from left ventricular-left atrial pressure crossover by an interval of 30 ms. (From Shaver JA, Saderni R, Reddy PS, et al. Normal and abnormal heart sounds in cardiac diagnosis: I. Systolic sounds. Curr Probl Cardiol 1985; 10:10-53. Reproduced with permission from the publisher and authors.)

' Figure 10-63: Base and apex phonocardiograms are recorded simultaneously with the mitral valve echocardiogram in a 62-year-old man who developed acute mitral regurgitation secondary to rupture of the chordae tendinae of a myxomatous valve. During diastole, multiple echoes arise from the flail posterior mitral leaflet (PML), and during early ventricular systole, effective mitral valve closure does not occur, resulting in an inaudible low-frequency vibration on the apex phonocardiogram. During systole, there is separation of the anterior (AML) and posterior mitral leaflets, resulting in severe mitral regurgitation. The murmur has a crescendo-decrescendo contour simulating the murmur of aortic stenosis ending prior to A1. Wide physiologic splitting of S1 is present. The prominent S4 present on the apex phonocardiogram was associated with an apical presystolic impulse. (From Shaver JA. The physical examination in cardiac diagnosis. Cardiol Consult 1985; 6:3. Reproduced with permission from the publisher and author.)

' Figure 10-64: Simultaneous phonocardiograms are recorded with the mitral valve echocardiograms in three patients: mitral stenosis (left), left atrial myxoma (center), and prolapse of the mitral valve (right). In each condition, a loud M1 is present and coincident with the closing point of the mitral valve echocardiogram. Common to each condition is wide separation of the mitral leaflets at the onset of LV systole, with high-velocity closure occurring over a large excursion. In the left panel, a mobile stenotic valve is demonstrated, and a loud opening snap is coincident with the E point. In the center panel, an early diastolic tumor plop (TP) is coincident with the maximal excursion of the tumor during its rapid descent into the ventricle. Note the presystolic crescendo murmur (PSM) occurring during the rapid closure of the mitral valve in both mitral stenosis and left atrial myxoma. In the right panel, a pansystolic murmur (PSM) with late systolic accentuation is secondary to the prolapse of the mitral valve with late systolic hammocking. (From Shaver JA. Current uses of phonocardiography in clinical practice. In: Rapaport E, ed. Cardiology Update: Reviews for Physicians. New York: Elsevier; 1981:370. Reproduced in part (center panel) with permission from the publisher and author. Copyright 1981 by Elsevier Science Publishing Co, Inc.)

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Figure 10-65: External sound, equisensitive LV and left atrial pressures (catheter-tipped micromanometer), LV dP/dt, and left atrial sound are recorded simultaneously with the mitral valve echocardiogram in a patient with hemodynamically significant mitral stenosis. A significant presystolic gradient is present due to atrial contraction, and the onset of the rapid closure of the mitral valve (B) is delayed until the LV pressure exceeds left atrial pressure. This occurs 40 ms after the beginning of the LV pressure rise at a time when LV dP/dt is much higher than normal. Following left atrial-left ventricular pressure crossover, there is rapid ventriculogenic closure of the mitral valve (BC), resulting in a very loud M1 coincident with the C point of the mitral valve echocardiogram. Its separation from A2 is determined by both the level of the left atrial pressure and the rate of LV pressure decline. (From Shaver JA, et al. Normal and abnormal heart sounds in cardiac diagnosis: I. Systolic sounds. Curr Probi Cardiol 1985; 10:10-53. Reproduced with permission from the publisher and the authors.)

Figure 10-66: Base and apex phonocardiograms are recorded simultaneously with the aortic valve echocardiogram in a young man with valvular aortic stenosis. A prominent aortic valvular ejection sound (AVES) is recorded at the apex and is coincident with the maximal excursion of the aortic valve in early systole. It is followed by a crescendo-decrescendo systolic ejection murmur (SEM) that ends well before a loud A2. Figure 10-67: Simultaneously recorded base and apex phonocardiograms and mitral valve echocardiogram (MVE) demonstrating the frequent association of a late systolic murmur with a prominent late systolic click. Although the murmur is well transmitted to the base, the click transmits poorly. In the first two complexes, an additional softer click precedes the click murmur complex. The last complex shows only a single click, demonstrating the variability of the auscultatory findings even at rest. The large click occurs at maximal prolapse, and the smaller click occurs near the onset of echocardiographic prolapse. Figure 10-68: A midsystolic nonejection sound (C) occurs in mitral valve prolapse and is followed by a late systolic murmur that crescendos to S1. With assumption of the upright posture, venous return decreases, the heart becomes smaller, the C moves closer to S1, and the mitral regurgitant murmur has an earlier onset. With prompt squatting, both venous return and afterload increase, the heart becomes larger, the C moves toward S2, and the duration of the murmur shortens. (From Shaver JA. Examination ofthe Heart, Part IV: Auscultation. Dallas: American Heart Association; 1990:13. Reproduced with permission from the publisher and the authors.)

Figure 10-69: The cardiac cycle recorded by high-fidelity catheter-tipped micromanometers. The aortic (A2) and pulmonic (P2) closure sounds are coincident with the incisurae of their respective arterial traces. Although the LV and RV mechanical systoles are nearly equal in duration, the RV systolic ejection period terminates after LV ejection because of an increased right-sided "hangout" interval. (From Shaver JA. The second heart sound: Newer concepts: I. Normal and wide physiological splitting. Mod Concepts Cardiovasc Dis 1997; 46:7. Reproduced with permission from the American Heart Association and the authors.)

Figure 10-70: (Left) The base and apex phonocardiograms are recorded simultaneously with the aortic valve echocardiogram. The first high-frequency component of A2 is coincident with the completion of closure of the aortic valve. (Right)) Base and apex phonocardiograms are recorded with the pulmonary valve echocardiogram. The first high-frequency component of P1 is coincident with the completion of closure of the pulmonic valve. (From Shaver JA, et al. Normal and abnormal heart sounds in cardiac diagnosis: I. Systolic sounds. Curr Probi Cardiol 1985: 10:43. Reproduced with permission from the publisher and the authors.)

' Figure 10-71: (Top) Normal physiologic splitting. During expiration, A2 and P2 are separated by less than 30 ms and are appreciated as a single sound. During inspiration, the splitting interval widens, and A2 and P2 are clearly separated into two distinctly audible sounds. (Bottom) Audible expiratory splitting. In contrast to normal physiologic splitting, two distinct sounds are easily heard during expiration. Wide physiologic splitting is due to delay in P2. Reversed splitting is due to delay in A2, resulting in paradoxical movement; i.e., with inspiration, P2 moves toward A2, and the splitting interval narrows. Narrow physiologic splitting is seen in pulmonary hypertension, and both A2 and P2 are heard during expiration at a narrow splitting interval due to an increased intensity and high-frequency composition of P2. (From Shaver JA. Examination ofthe Heart, Part IV: Auscultation. Dallas: American Heart Association; 1990:17. Reproduced with permission from the publisher and the authors.)

' Figure 10-72: (Left) Wide physiologic splitting of S2 is seen in a patient with complete right bundle branch block. Audible expiratory splitting that widens normally with inspiration is present. Note also the wide splitting of the first heart sound into its mitral (Mj) and tricuspid (Tj) components, as recorded at the apex. (Right)) The base phonocardiogram is recorded simultaneously with high-fidelity catheters in the right ventricle and pulmonary artery during cardiac catheterization. There is marked prolongation of the Q to the onset of the RV pressure rise of 96 ms, resulting in wide physiologic splitting of S2. The delayed P2 is secondary to delayed activation of the right ventricle. (From Shaver JA. Current uses of phonocardiography in clinical practice. In: Rapaport E, ed. Cardiology Update: Reviews for Physicians. New York: Elsevier; 1981:337. Reproduced originally in part (left panel) with permission from the publisher and author, and from Shaver JA, et al. Normal and abnormal heart sounds in cardiac diagnosis: I. Systolic sounds. Curr Probl Cardiol 1985; 10:48. Reproduced in total with permission from the publisher and authors.)

s Figure 10-73: (Upper left) Sound and pressure correlates of S2 in a 45-year-old woman with a normotensive atrial septal defect (shunt 2:1). Wide, fixed splitting of S2 is demonstrated; P2 and A2 are coincident with their respective incisurae, and the duration of the "hangout" interval is nearly equal to the A2-P2 interval. (Upperright) Simultaneous RV and LV pressures clearly show that the duration of RV and LV systole is equal. (Lower left) Sound and pressure correlates of a patient with idiopathic dilatation of the pulmonary artery. P2 is coincident with the incisura of the pulmonary artery and separated from the RV pressure tracing by a "hangout" interval of 90 ms (almost identical to the splitting interval). (Lowerright) Similar sound and pressure correlates in a patient with mild valvular pulmonic stenosis and aneurysmal dilatation of the pulmonary artery. Most of the delay in P2 is due to a wide "hangout" interval of 56 ms. In each patient all pressures are recorded by catheter-tipped micromanometers. (From Shaver JA, et al. Second heart sound: The role of altered greater and lesser circulation. In: Leon DF, Shaver JA, eds. Physiologic Principles of Heart Sounds and Murmurs. Monograph 46. New York: American Heart Association;1975:63. Reproduced originally in part (top panel) with permission from the publisher and the authors, and from Shaver JA. The second heart sound: Hemodynamic determinants. Acta Cardiol 1985; 40:12. Reproduced in total with permission from the publisher and authors.)

' Figure 10-74: A. The S4 occurs in presystole and is frequently called an atrial, or presystolic, gallop. B. The S3 occurs during the rapid phase of ventricular filling. It is a normal finding and is commonly heard in children and young adults, disappearing with increasing age. When it is heard in a patient with cardiac disease, it is called a pathologic S3, or ventricular gallop, and usually indicates ventricular dysfunction or AV valvular incompetence. C. In constrictive pericarditis, a sound in early diastole, the pericardial knock (K), is heard earlier and is louder and higher-pitched than the usual pathologic S3. D. A quadruple rhythm results if both S4 and S3 are present. E. At faster heart rates, the S3 and S4 occur in rapid succession and may give the illusion of a middiastolic rumble. F. When the heart rate is sufficiently fast, the two rapid phases of ventricular filling reinforce each other, and a loud summation gallop (SG) may appear; this sound may be louder than either the S3 or S4 alone. (From Shaver JA. Examination of the Heart, Part IV: Auscultation. Dallas: American Heart Association; 1990:27. Reproduced with permission from the publisher and the authors.)

' Figure 10-75: (Top) A physiologic S3 (normal variant) recorded in a 24-year-old woman without evidence of cardiovascular disease. The onset of the S3 occurs during the rapid filling wave (RFW) of the ACG between the O and F points. The remainder of the cardiovascular examination was entirely within normal limits. (Bottom) A very prominent S3 gallop is recorded in a patient with severe congestive cardiomyopathy (COCM). On physical examination, there was a small-volume carotid pulse and marked engorgement of the neck veins with elevated venous pressure. The ACG shows a very prominent presystolic pulsation (a), and an extremely rapid filling wave is present. The onset of the S3 occurs during the RFW of the ACG. The first heart sound is soft. (From Shaver JA. Early diastolic events associated with the physiologic and pathologic S3. J Cardiogr. 1984; 14(suppl 5):30. Reproduced with permission from the publisher and the authors.)

' Figure 10-76: Atrial diastolic (ADG) and ventricular diastolic gallops (VDG) are recorded in an adult with severe calcific aortic stenosis. The ADG is associated with a prominent presystolic apical impulse (a), and the VDG occurs during the rapid filling wave of the ACG. The carotid pulse has a very slow rate of rise and a markedly prolonged LV ejection time. The classic diamond-shaped systolic ejection murmur (SM) is present at the base and apex. Note the higher-frequency composition of the SM at the apex but preservation of the crescendo-decrescendo pattern. (From Shaver JA. Current uses of phonocardiography in clinical practice. In: Rapaport E, ed. Cardiology Update: Reviews for Physicians. New York: Elsevier; 1981:356. Reproduced with permission from the publisher and author. Copyright 1981 by Elsevier Publishing Co., Inc.)

' Figure 10-77: Midsystolic ejection murmurs are caused by forward flow across the LV or RV outflow tract, whereas pansystolic regurgitant murmurs are caused by retrograde flow from a high-pressure cardiac chamber to a low-pressure one. (Left) Diagrammatic representation of the midsystolic ejection murmur and the pansystolic regurgitant murmur, as related to LV, aortic, and left atrial (LA) pressures. The systolic ejection murmur occurs during the period of LV ejection; the onset of the murmur is separated from S1 by the period of isovolumic contraction and the crescendo-decrescendo murmur terminates before A2. The pansystolic regurgitant murmur begins with, or may replace, S1, and the murmur continues up to and through A2 as LV pressure exceeds left atrial pressure during the period of isovolumic relaxation. The murmur has a plateau configuration and varies little with respiration. (Right) Flow diagram. (Left panel reproduced from Reddy PS, Shaver JA, Leonard JJ. Cardiac systolic murmurs: Pathophysiology and differential diagnosis. Prog Cardiovasc Dis 1971; 14:19. Entire figure reproduced with permission from Shaver JA. Systolic murmurs. Heart Dis Stroke 1993; 2:10.)

B+'Si Figure 10-78: The simultaneous time-intensity course of the murmur "envelope," aortic flow velocity, and LV and central aortic pressure. During normal LV ejection (left), peak flow velocity is early, with two-thirds of the ventricular volume ejected during the first half of systole. The murmur threshold may be exceeded during the early peak flow and the corresponding murmur envelope inscribed. (Center) Exaggeration of the normal pattern of LV ejection with a high stroke volume, as in high-output states. With critical aortic stenosis (right), rapid early ejection is no longer possible; the flow velocity is increased, and the contour becomes rounded and prolonged, producing the typical diamond-shaped murmur of aortic stenosis. (Modified from Reddy PS, et al. Cardiac systolic murmurs: Pathophysiology and differential diagnosis. Prog Cardiovasc Dis 1971; 14:4. Reproduced with permission from the publisher and the authors.)

' Figure 10-79: The differential diagnosis of the innocent murmur versus the pathologic systolic murmur is made by the "company the murmur keeps." The innocent murmur must be found in the setting of an otherwise normal cardiovascular examination. C, midsystolic nonejection sound; AVES, aortic valvular ejection sound; PVES, pulmonic valvular ejection sound; AR, aortic regurgitation. (From Shaver JA, et al. Examination of the Heart, Part IV. Auscultation. Dallas: American Heart Association; 1990:40. Reproduced with permission from the publisher and the authors.)

' Figure 10-80: Effect of the long diastolic filling period following a premature ventricular contraction (PVC) on the intensity of a systolic ejection murmur (SEM). There is a marked increase in the intensity of the aortic stenosis murmur recorded at the base and at the apex. Despite the higher-frequency content of the apical murmur, this response clearly identifies this murmur as ejection in nature. (From Paley H. Left ventricular outflow tract obstruction: Heart sounds and murmurs. In: Leon DF, Shaver JA, eds. Physiologic Principles of Heart Sounds and Murmurs. Monograph 46. Dallas: American Heart Association; 1975:112. Reproduced with permission from the publisher and the author.)

' Figure 10-81: In valvular pulmonic stenosis with intact ventricular septum, RV systolic ejection becomes progressively longer with increasing obstruction to flow. As a result, the murmur becomes louder and longer, enveloping the aortic closure sound. At the same time, pulmonic closure occurs later; splitting becomes wider but is more difficult to appreciate because the aortic closure sound is lost in the murmur; and the pulmonic closure sound becomes progressively softer due to the low pulmonary artery pressure. With increasing severity of pulmonic stenosis, the pulmonary ejection sound may fuse with S1. In severe obstruction with concentric hypertrophy and decreased RV compliance, an S4 appears. In tetralogy of Fallot, with increasing obstruction at the infundibular area, more and more RV blood is shunted across a silent VSD with less flow across the obstructed RV outflow tract. With increasing obstruction, the murmur becomes shorter, earlier, and fainter. The pulmonic closure sound is absent in severe tetralogy of Fallot. The dilated aorta receives almost all the cardiac output from both ventricular chambers, and there is an aortic ejection sound (Aej). (From Leonard J, et al: Examination ofthe Heart, Part 4: Auscultation. Dallas: American Heart Association; 1974:45. Reproduced with permission from the publisher and authors.)

' Figure 10-82: (Left) The phonocardiogram of a patient with severe valvular pulmonic stenosis as recorded at the second left intercostal space (2LICS) and the apex. The long ejection murmur (ESM) has late systolic peaking and spills through A2. There is a marked delay in P2, which is very small in amplitude. (Right) At cardiac catheterization, the markedly delayed P2 is shown to be secondary to a very large systolic pressure gradient, and its decreased intensity is due to the low pulmonary artery pressure at the time of valve closure. The late peaking of the ejection murmur correlates with the maximal pressure gradient between the right ventricle and the pulmonary artery. (From Curtiss EI, et al. First and second heart sound. In: Horwitz LD, ed. Signs and Symptoms in Cardiology. Philadelphia: Lippincott; 1985:200. Reproduced with permission from the publisher and authors.)

' Figure 10-83: Simultaneous base and apex phonocardiograms are recorded with the carotid pulse and ACG in the left and center panels, respectively, in a 54-year-old man with hypertrophic cardiomyopathy. The carotid pulse rises rapidly and has a late systolic plateau and a prolonged ejection period. Prominent S4 and S1 are demonstrated and are associated with the a wave and the rapid filling wave (RFW), respectively, of the ACG. Note the late systolic bulge (LSB) on the ACG. S2 is single. A loud, grade 5 systolic ejection murmur is present and is of greatest intensity at the apex. In the right panel, the apical systolic murmur is recorded together with the M-mode echocardiogram. Simultaneous high-fidelity LV and central aortic pressures are recorded by catheter-tipped micromanometers. Marked thickening of the interventricular septum and SAM of the mitral valve are present on the echocardiogram. A large systolic pressure gradient is demonstrated beginning shortly after the onset of the SAM. (From Shaver JA, et al. Phonoechocardiography and intracardiac phonocardiography in hypertrophic cardiomyopathy. Postgrad Med J. 1986; 62:538. Reproduced with permission from the publisher and the authors.)

' Figure 10-84: Diastolic filling murmurs or rumbles are caused by forward flow across the AV valves, whereas diastolic regurgitant murmurs are caused by retrograde flow across incompetent semilunar valves. (Left) Diagrammatic representation of the diastolic filling murmur and the diastolic regurgitant murmur as related to LV, aortic, and left atrial (LA) pressures. The diastolic filling murmur occurs during the diastolic filling period and is separated from S2 by the isovolumic relaxation period. The rumbling murmur is most prominent during rapid, early ventricular filling and presystole, terminating with S1. The diastolic regurgitant murmur begins immediately after S2 and continues in a decrescendo fashion up to S^, closely paralleling the aortic LV diastolic pressure gradient. (Right) Flow diagram. (From Shaver JA. Diastolic murmurs. Heart Dis Stroke 1993; 1:98-103. Reproduced with permission from the American Heart Association.)

' Figure 10-85: Diagram contrasting the auscultatory findings in chronic and acute aortic regurgitation. In chronic aortic regurgitation, a prominent systolic ejection murmur (SEM), resulting from the large forward stroke volume, is heard at the base and apex and ends well before S2. The aortic diastolic regurgitant murmur begins with S2 and continues in a decrescendo fashion, terminating before S1. At the apex, the early diastolic component of the Austin Flint (AF) murmur is introduced by a prominent S3. A presystolic component of the AF is also heard. In acute aortic regurgitation, there is a significant decrease in the intensity of the SEM compared with chronic aortic regurgitation because of the decreased forward stroke volume. S1 is markedly decreased in intensity because of preclosure of the mitral valve, and at the apex the presystolic component of the AF murmur is absent. The early diastolic murmur at the base ends well before S1 because of the equilibration of the LV and aortic end-diastolic pressure. Significant tachycardia is usually present. (From Shaver JA. Diastolic murmurs. Heart Dis Stroke 1993; 1:98-103. Reproduced with permission from the American Heart Association.)

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Hurst's the Heart: Chapter 10, Figure Index

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