Sound within the pulmonary artery was measured in 24 patients to determine if right ventricular failure modifies the amplitude of the pulmonary component of the second sound (P2). The amplitude of P2 in eight patients with right ventricular failure secondary to pulmonary hypertension (2610 ± 370 dynes/cm2) did not differ from P2 in eight patients with pulmonary hypertension not accompanied by right ventricular failure (3120 ± 710 dynes/cm2). In both groups, the amplitude of P2 exceeded control subjects (520 ± 70 dynes/cm2) (P \u3c .001 and P \u3c .01, respectively). The maximal rate of development of the pressure gradient across the closed pulmonary valve was higher in patients with right ventricular failure (580 ± 100 mm Hg/sec) than in control subjects (150 ± 30 mm Hg/sec) (P \u3c .001) and maximal negative dp/dt was also higher in patients with failure (750 ± 70 mm Hg/sec vs 190 ± 20 mm Hg/sec) (P \u3c .001). The maximal rate of change of the diastolic pressure gradient correlated linearly with maximal negative dp/dt (r=.89). These observations indicate that P2 is accentuated in patients with right ventricular failure secondary to pulmonary hypertension. The accentuation results from the augmented rate of development of the diastolic pressure gradient, which reflects an augmented right ventricular negative dp/dt. Therefore, an accentuated P2 remains valid as a clinical sign of pulmonary hypertension whether or not right ventricular failure occurs

Anbe, Daniel T.

Marzilli, Mario

Sabbah, Hani N.

Stein, Paul D.

English

Henry Ford Health System Scholarly Commons

Henry Ford Hospital Medical Journal Volume 28 Number 1 Article 17 3-1980 The Pulmonary Component of the Second Sound in Right Ventricular Failure Paul D. Stein Hani N. Sabbah Daniel T. Anbe Mario Marzilli Follow this and additional works at: https://scholarlycommons.henryford.com/hfhmedjournal  Part of the Life Sciences Commons, Medical Specialties Commons, and the Public Health Commons Recommended Citation Stein, Paul D.; Sabbah, Hani N.; Anbe, Daniel T.; and Marzilli, Mario (1980) "The Pulmonary Component of the Second Sound in Right Ventricular Failure," Henry Ford Hospital Medical Journal : Vol. 28 : No. 1 , 79-84. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol28/iss1/17 This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. Henry Ford Hosp Med Journal Vol 28, No 1, 1980 The Pulmonary Component of the Second Sound in Right Ventricular Failure Paul D. Stein, MD,* Hani N. Sabbah, BS,* Daniel T. Anbe, MD,* Mario Marzilli, MD** Sound within the pulmonary artery was measured in 24 patients to determ ine if right ventricular failure modifies the amplitude of the pulmonary component of the second sound (P2). The amplitude of P2 in eight patients with right ventricular failure secondary to pulmonary hypertension (2610 ± 370 dynes I cm^) did not differ from P2 in eight patients with pulmonary hypertension not accompanied by right ventricular failure (3120 ± 710 dynes/cm''). In both groups, the amplitude of P2 exceeded control subjects (520 ± 70 dynes/cmV (P < .001 and P < .01, respectively). The maximal rate of development of the pressure gradient across the closed pulmonary valve was higher in patients with right ventricular failure (580 ± 100 mm tig/sec) than in control subjects (150 ± 30 mm Hg/sec) (P < .001) and maximal negative dp/dt was also higher in patients with failure (750 ± 70 mm Hg/sec vs 190 ± 20 mm Hg/sec) (P < .001). The maximal rate of change of the diastolic pressure gradient correlated linearly with maximal negative dp/dt (r=.89). These observations indicate that P2 is accen-tuated in patients with right ventricular failure secondary to pulmonary hypertension. The accentuation results from the augmented rate of development of the diastolic pressure gradient, which reflects an augmented right ventricular negative dp/dt. Therefore, an accentuated P2 remains valid as a clinical sign of pulmonary hypertension whether or not right ventricular failure occurs. t ven though it is standard clinical practice to evaluate the intensity ofthe pulmonary component ofthe second sound (P2) during physical examination, only recently have the factors that affect its intensity been identified (1). The primary hemodynamic factor affecting intensity is the rate at which a pressure gradient develops across the valve after closure (1-4). The latter is strongly dependent upon the rate of fall of ventricular pressure (negative dp/dt) (4). In patients with myocardial infarction or left ventricular failure, the intensity of the aortic component of the second sound is reduced (5-7). We have shown that in patients wfth poor left ventricular performance this reduction re-sults from a diminished rate of change of the diastolic pressure gradient across the aortic valve which is second-Submitted for publication: July 2, 1979 Accepted for publication: July 25, 1979 • Department of Internal Medicine, Division of Cardiovascular Medicine, Henry Ford Hospital **Visit ing Investigator, Henry Ford Hospital; presently at Fisiologia Clinica C.N.R., Via Savi 8, 56100 Pisa, Italy Address reprint requests to Dr. Stein, Department of Internal Medicine, Henry Ford Hospital, 2799 W Grand Blvd, Detroit, Ml 48202 Supported in part by funds from the U.S. Public Health Service, National Heart, Lung and Blood Institute, Grant No. HL23669-01 ary to impaired isovolumic relaxation (4). It is therefore useful to inquire how the intensity of P2 is affected by right ventricular failure in pulmonary hypertensive heart disease. The purpose of this investigation is to determine if right ventricular failure in pulmonary hypertensive heart disease modifies the intensity of P2. We wil l explore the possibility of whether auscultation can give a clue to pulmonary hypertension once right ventricular failure develops, or whetherthe interpretation of the intensity of P2 should be modified in the presence of right ventricular failure. Methods Sound within the pulmonary artery was measured during diagnostic cardiac catheterization in 24 patients. Eight had normal pulmonary arterial pressure, eight had pulmonary hypertension without right ventricular failure, and eight had pulmonary hypertension with right ventricular failure. Patients were categorized as having a normal pulmonary artery pressure if ft did not exceed 30/12 mm Hg (8). Since right ventricular dysfunction has been observed in patients with right coronary disease (9, 10), they were excluded from the control group if narrowing of the right coronary artery was present. 79 stein, Sabbah, Anbe, and Marzilli Right ventricular failure was defined as the presence of hepatomegaly, ascites, or dependent edema in patients with an elevated (> 9 mm Hg) right atrial pressure (8). The diagnosis of right ventricular failure, therefore, was essen-tially a clinical diagnosis (11-13), although measured pres-sures were substituted for the physical sign of systemic venous hypertension. Patients were excluded if they had chronic obstructive pulmonary disease, since "emphysema heart" may differ from pulmonary hypertensive heart disease (14). The he-moglobin of control subjects, patients with pulmonary hypertension, and patients with pulmonary hypertension and right ventricular failure was 14.5 ± .8 gm/100 ml, 13.1 ± .7 gm/100 ml, and 13.1 ± .7 gm/100 ml, respectively. The cardiac diagnoses of the patients in this study are shown in Table I. Patients with pulmonary hypertension (51 ± 4 years), and those with pulmonary hypertension and right ventricular failure, (57 ± 3 years), were older than the TABLE I Cardiac Diagnoses Control Subjects No heart disease Coronary heart disease (left anterior descending only) Aortic insufficiency, mild Total Pulmonary Hypertension Coronary heart disease Mitral stenosis and/or regurgitation Cardiomyopathy Cause undetermined Total Pulmonary Hypertension with Right Ventricular Failure Coronary heart disease Aortic stenosis Cardiomyopathy Mitral stenosis and regurgitation Total control subjects (41 ± 4 years). None of the control sub-jects were treated with digitalis or propranolol. Six of the patients wfth pulmonary hypertension who were not in right ventricular failure were treated with digitalis, and all wfth right ventricular failure were treated with digitalis. None of the patients had electrocardiographic evidence of right ventricular hypertrophy. P pulmonale was present in one patient with pulmonary hypertension who was not in right ventricular failure. Complete right bundle branch block was present in one patient with right ventricular failure, and right axis deviation was present in one patient w i th right ventr icular fa i lure. Our cr i ter ia for making electrocardiographic interpretations have been previously described (15). Intracardiac sound and pressure were measured with a Millar Instruments catheter-tip micromanometer and re-corded on an Electronics for Medicine VR-6 photographic 1 O O O i -z LJ Q < • : a UJ c D 00 CO UJ Q: c < 8 0 0 6 0 0 o UJ CO O I O ± LU o 2 < X O < CE X < 5 4 0 0 2 0 0 P < . 0 0 1 P < . 0 0 1 ± P A - H T N C H F Fig. 1 Pulmonary component of the second sound in control subjects (C), patients wi th pulmonary hypertension (PA-HTN), and patients wi th pulmonary hypertension and right ventricular failure (CHF). Proba-bilities refer to comparisons of patients wi th PA-HTN to control subjects or comparisons of patients wi th CHF to control subjects. Second Sound TABLE II Central Hemodynamic Measurements PA Pressure (mm Hg) RV End-Diastolic Pressure (mm Hg) RA Mean Pressure (mm Hg) Heart Rate (beats/min) Cardiac Index (1/min/m2) Stroke Index (ml/stroke/m2) Pulmonary Vas-cular Resistance (dyne-sec-cm"5) RV Work (kg-m/min/m2) mean ± SEM mean ± SEM P mean ± SEM mean ± SEM P mean ± SEM P mean ± SEM P mean ± SEM P mean ± SEM P Control Subjects 18/7 ±1/1 2 ±0.3 4 ± 1 83 ± 6 2.9 ±.2 38 ± 3 53 ± 7 .40 ±.07 PA Hypertension (No CHF) 64/31 ± 4/2 7 ± 2 <.01 4 ± 1 90 ± 5 NS 2.1 ±.2 <.05 23±3 <.01 430 ± 80 <.01 1.11 ±.20 <.02 PA Hypertension (CHR 71/37 ±5/2 13±2 <.001 15±2 93 ± 3 NS 1.5±.1 <.001 18±1 <.001 490 ± 50 <.001 .91 ± .05 <.001 CHF: Congestive heart failure (right sided) PA: Pulmonary artery RV: Right ventricle Probabilities refer to comparisons wi th control subjects. recorder. Intracardiac sound pressure, referred to as intra-cardiac sound, was calibrated in dynes / cm^ The fre-quency response of the system and the method of calibration of intracardiac sound have been previously described (16). The rate at which a difference of pressure developed between the right ventricle and pulmonary artery during diastole was termed the rate of change of the diastolic pressure gradient. The rate of development ofthis pressure gradient across the closed pulmonary valve was calculated wfth the aid of a computer, as described previously (4). Results The amplitude of P2 in control subjects was 520 ± 70 dynes/cm^ It was higher both in patients with pulmonary hypertension (3120 ± 710 dynes/cm') (P < .01) (unpaired t-test) and in patients with pulmonary hypertension and right ventricular failure (2610 ± 370 dynes/cm^) (P < .001) (Fig. 1). The amplitude of P2 did not differ significantly between those with pulmonary hypertension who were in right ventricular failure and those who were not. Central hemo-dynamics are shown in Table II. Instantaneous values of the pressure gradient that de-veloped across the pulmonary valve after closure and throughout the duration of P2 are shown in a control patient, a patient wfth pulmonary hypertension, and a patient in right ventricular failure (Fig. 2). The rate of change of the diastolic pressure gradient can be judged from the slopes of these curves. The maximal rate of change of the diastolic pressure gradient across the closed pulmonary valve in control subjects was 150 ± 3 0 mm Hg/sec. ft was higher both in patients wfth pulmonary hypertension (590 ± 70 mm Hg/sec) (P < .001) and in patients with pulmonary hypertension and right ventricular HI Stein, Sabbah, Anbe, and Marzil l i T < CE cr UJ cr CL IS) < 45 4 0 -35 -30 -25 -20 1 5 10 -C O N T R O L Fig. 2 Instantaneous values of the diastolic pressure gradient across the closed pulmonary valve from the beginning (time 0) to the end of P2 in a control subject, a patient w i th pulmonary hypertension (PA-HTN), and a patient wi th right ventricular failure (CHF). The maximal rate of change of the diastolic pressure gradient is the steepest slope of the respective curves. J \ I L 10 15 20 25 30 35 40 TII^E ll^SEC) 45 8000 Q Z o CO Q Z O o LU CO O 1 -2 O UJ W MPOl UJ z > o u > CE < Z o -1 Q_ 6000 4000 2000 P <.01 P <.001 Fig. 3 The maximal rate of change of the diastolic pressure gradient across the pulmonary valve in control subjects (C), patients wi th pulmonary hyper-tension (PA-HTN), and patients wi th right ventricular failure (CHF). Probabilities refer to comparisons wi th control subjects. P A - H T N C H F 82 Second Sound failure (580 ± 100 mm Hg/sec) (P < .001) (Fig. 3). There was no significant difference between patients with pul-monary hypertension who were in right ventricular failure and those who were not in right vertricular failure. The maximal rate of fall of right ventricular pressure (max neg dp/dt) in control subjects was 190 ± 2 0 mm Hg/sec. It was higher both in patients with pulmonary hypertension (790 ± 80 mm Hg/sec) (P < .001) and in patients wfth right ventricular failure (750 ± 70 mm Hg/sec) (P < .001). Max neg dp/dt showed no significant difference between pa-tients with right ventricular failure and those not in right ventricular failure. The amplitude of P2 correlated linearly with the maximal rate of change of the diastolic pressure gradient that de-veloped across the closed pulmonary valve (r = .70). Elim-inating patients w i th right ventr icular fai lure d id not signfticantly improve the correlation (r = .71). The maximal rate of change of the diastolic pressure gradient correlated linearly with maximal negative dp/dt (r = .89) (Fig. 4). Discussion We recently described the hemodynamic and anatomic factors that interact to produce the accentuated P2 in patients wfth pulmonary hypertension (1) and in the present study showed that P2 remains accentuated in spite of the onset of right ventricular failure. This observation is consist-ent with the measured hemodynamic parameters that were encountered in patients with pulmonary hypertension and right ventricular failure, i.e., right ventricular maximal negative dp/dt was augmented relative to patients in whom pulmonary arterial pressure was normal. This augmentation resulted in a significant increase in the rate of change ofthe diastolic pressure gradient, which is a primary hemo-dynamic determinant o f the amplitude of P2 (1-3). The capability of the failing right ventricle to retain a faster than normal negative dp/dt parallels its capability to main-tain a high positive dp/dt (17). In patients with pulmonary hypertensive heart disease and right ventricular failure we observed that maximal dp/dt exceeded values in control subjects, and ^max and 1/p dp/dt remained normal (17). The accentuated P2 in patients wfth right ventricular failure secondary to pulmonary hypertension reflects the in-creased rate of change of the diastolic pressure gradient across the closed pulmonary valve primarily as a result of the capability of the failing right ventricle to retain a faster than normal negative dp/dt. In contradistinction, failure or poor performance of the left ventricle was accompanied by a lowerthan normal negative dp/dt (4). This phenomenon, through its effect upon the rate of change of the pressure gradient across the aortic valve, resulted in a diminished aortic component of the second sound (4). o o (0 m - CJ Q I i 0 0 6 0 0 2 0 0 0 300 600 900 1200 1500 M A X NEG D P / D T ( M M H G / S E C ) Fig. 4 Relation of maximal negative dp/dt to the maximal rate of change of the diastolic pressure gradient across the closed pulmonary valve. Open circles indicate patients wi th right ventricular failure. Closed circles indicate no failure. The amplftude of P2 in patients with right ventricular failure equaled or exceeded the amplitude of the aortic component of the second sound that we previously re-ported in patients with normal left ventricular function and normal aortic valves (4). The accentuation o f the pulmon-ary component of the second sound (whether or not ac-companied by right ventricular failure) reflects both an augmentation of the rate of development of the diastolic pressure gradient and the interaction of the anatomical structure of the aortic and pulmonary valves (1). The intensity of both components of the second heart sound may be affected by a variety of interacting hemo-dynami and anatomic factors (2, 3, 18). Aortic stenosis and aortic insufficiency affect the amplftude of the aortic com-ponent of the second sound (16, 19). Predictably, pulmon-ary stenosis and pulmonary insufficiency would have a similar effect upon the amplftude of P2. Mathematical analysis of semilunar valve vibrations that produce the second sound predicted additional factors that would also affect the intensity of the second sound. Such factors include the density and viscosity of blood, the volume and geometry of the ventricle, and the coefficient of sound absorption of the ventricular wall (3). In this study, we excluded patients wfth emphysema heart disease (14). The increased blood viscosity, due to the higher hematocrits of patients with emphysema, would diminish the intensity of their heart sounds (20). 83 stein, Sabbah, Anbe, and Marzilli Conclusion This study indicates that P2 is accentuated in patients wfth pulmonary hypertensive heart disease even after the de-velopment of right ventricular failure. Therefore, an accen-tuated P2 remains valid as a clinical sign of pulmonary hypertension, whether or not right ventricular failure occurs. References 1. Stein PD, Sabbah HN, Anbe DT Khaja F. Hemodynamic and ana-tomic determinants in amplitude of the aortic and pulmonary compo-nents of the second heart sound. Am J Cardiol 1978;42:539-44. 2. Sabbah HN, Stein PD. Investigation of the theory and mechanism of the origin of the second heart sound. Circ Res 1976;39:874-82. 3. Blick EF, Sabbah HN, Stein PD. One-dimensional model of diastolic semilunar valve vibrations productive of heart sounds. J Biomech 1979;12:223-27. 4. Stein PD, Sabbah HN, Khaja F, Anbe DT Exploration o f the cause of the low intensity aortic component of the second sound in non-hypotensive patients with poor ventricular performance. Circulation 1978;57:590-93. 5. Price W H , Brown AE. Alterations in intensity of heart sounds after myocardial infarction. Br Heart J 1968;30:835-39. 6. Stein PD, Sabbah HN, Bar I. Intensity of heart sounds in the evalua-t ion of patients f o l l o w i n g myocard ia l in farc t ion. Chest 1979; 75:679-84. 7. Fowler NO. Cardiac diagnosis. New York: Harper and Row, 1969:46. 8. Grossman W. Cardiac catheterization and angiography Philadelphia: Lea & Febiger, 1974:329. 9. Ferlinz J, Gorlin R, Cohn PF, Herman MV. Right ventricular perform-ance in patients w i t h coronary artery disease. C i rcu la t ion 1975:52:608-15. 10. Wells DE, Befeler B. Dysfunction of the right ventricle in coronary artery disease. Chest 1974;66:230-35. 11. FriedbergCK. Diseases of the heart. 3rd ed. Philadelphia: WB Saun-ders: 1966:807. 12. Wood P Diseases of the heart and circulation. 2nd ed. Philadelphia: IB Lippincott, 1962:285. 13. Burch GE, Giles TD. Considerations of selected aspects of physical signs of heart failure. In: Russek HI, ed. Cardiovascular disease, new concepts in diagnosis and therapy Baltimore: University Park Press, 1974:7. 14. Hecht H H . Heart fai lure and lung disease. C i rcu la t ion 1956; 14:265-90. 15. Stein PD, Dalen JE, Mclntyre KM, Sasahara AA, Wenger NK, Wil l is PW III. The electrocardiogram in acute pulmonary embolism. Prog Cardiovasc Dis 1975;17:247-57. 16. Sabbah HN, Khaja F, Anbe DT Stein PD. The aortic closure sound in pure aortic insufficiency. Circulation 1977;56:859-63. 17. Stein PD, Sabbah HN, Anbe DT Marzil l i M. Performance of the failing and non-failing right ventricle of patients with pulmonary hyperten-sion. Am J Cardiol 1979;44:1050-55. 18. Stein PD, Sabbah HN. Origin o f t h e second heart sound: Clinical relevance of new observations. Am J Cardiol 1978;41:108-10. 19. Sabbah HN, Khaja F, Anbe DT Folger GM Jr, Stein PD. Determinants ofthe amplitude of the aortic component of the second heart sound in aortic stenosis. Am J Cardiol 1978;41:830-35. 20. Stein PD, Sabbah HN. Accentuation of heart sounds in anemia: an effect of b lood viscosity. Am J Physiol (Heart Circ Physiol) 1978;4:H664-69. "4. 

The Pulmonary Component of the Second Sound in Right Ventricular Failure

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The Pulmonary Component of the Second Sound in Right Ventricular Failure

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