CHOICE OF STETHOSCOPE
Cardiac auscultation begins with proper choice of a stethoscope. The cardiac stethoscope should contain separate tubes for each ear. It should have both a bell and a diaphragm.
There are cardiac stethoscopes that do not have a bell. The bell effect is created by light pressure on the stethoscope. Firm pressure makes the stethoscope behave like it should with a diaphragm. The difference between the diaphragm and the bell is that the bell allows low frequency sounds, which permits hearing gallops and rumbles. The diaphragm filters those out.
The high-pitched murmurs of aortic insufficiency and some cases of mitral insufficiency are better heard with the use of the diaphragm that filters out the low frequency components of other distracting heart sounds.
Distant, faint heart sounds may be heard better by asking the patient to exhale. It should be kept in mind however, that held expiration affects some auscultatory findings. Deep inspiration followed by slow deliberate exhalation may slow the heart rate briefly prolonging the cardiac cycle and thus providing more time to listen to a particular murmur.
Patients with barrel chests due to lung disease can be positioned semi-sitting and the stethoscope can be applied in the subxiphoid region. Heart sounds in these patients may become more audible when the stethoscope is tilted toward the heart. The patient should be instructed as follows: "take a deep breath in, breathe out slowly, hold your breath as long as you can comfortably, then just breathe normally".
FIRST HEART SOUND
The intensity of the first heart sound can be affected by different conditions. One common cause of a muffled first heart sound can be confirmed by looking a the EKG. PR interval prolongation indicates a delay between late diastolic maximal mitral leaflet separation and mitral leaflet closure (due to the long interval between the P wave and the QRS). Hence, a patient with first degree heart block will typically have a soft first heart sound.
For the same reasons a patient with variable PR interval (Mobitz I second degree AV block or third degree heart block) can have changing intensity of the first heart sound. Lyme carditis, anatomically corrected transposition and maternal lupus can all cause complete heart block.
A loud first heart sound is also correlated with certain conditions. Wolff-Parkinson-White syndrome (short PR interval) and mitral stenosis are two examples.
In a patient with a short PR interval, the first heart sound is loud due to the short time interval between maximal mitral leaflet opening (after the P wave) and mitral leaflet closure (after the QRS).
A loud first heart sound should also raise the possibility of mitral stenosis. One would then listen for the other characteristic auscultatory components of mitral stenosis; specifically, the opening snap followed by a diastolic rumble with presystolic accentuation.
Splitting of the first heart sound can be heard at the lower left sternal border. This is the tricuspid area and the softer tricuspid component of the first heart sound may not transmit much beyond this area; making this the best place to hear the widely transmitted mitral component of the first heart sound together with the softer tricuspid component.
The tricuspid component may become "snappier" and more distinct on inspiration. (Potain PC. Note sur les dedoublements normaux des bruits du coeur. Bull et Mem Soc Med Hop, Paris 1866;3:138).
The splitting is best heard with the diaphragm (not the bell) of the stethoscope.
There has been controversy about the origin of the components of the first heart sound. Proof that the first component is due to mitral closure stems from the fact that it is loudest in the mitral area, precedes the carotid upstroke and coincides with echocardiographic mitral valve closure.
Early systolic ejection sounds should be distinguished from split first heart sounds as follows:
The intensity of the first heart sound varies in
patients with atrial fibrillation. Nevertheless,
it may be difficult to ascertain that this indeed
is the case with rapid "irregularly irregular" heart sounds.
In this case, an easy approach for detecting variable intensity
of the first heart sound consists of sliding the stethoscope
away from the area of maximal intensity to the point where the first heart
sound is completely inaudible.
Once the ear is trained, it may be easier to detect a first heart sound that actually disappears completely and returns intermittently.
The point of maximal intensity of the first heart sound should be identified. The stethoscope is then moved in various directions to a point where the first heart sound muffles and intermittently disappears with the variable cycle lengths. If the first sound disappears in all cycles, the stethoscope is slowly inched back in the direction of the point of maximal intensity until it is heard intermittently.
SECOND HEART SOUND
The second heart sound splits on inspiration. This is best heard in the pulmonic area during normal breathing. During inspiration right ventricular filling increases, and right ventricular ejection is prolonged - resulting in delayed pulmonic valve closure.
The aortic component of the second heart sound is the major contributor even in the areas where the pulmonic component is most audible.
The normal pulmonic component (P2) is relatively softer and is usually best heard in the upper left sternal area. Inspiratory delay in the pulmonic component separates it from the aortic component, resulting in audible splitting of the second heart sound. The pulmonic component (manifested as audible inspiratory splitting of the second heart sound) may also be normally audible in the upper right sternal area, but not at the apex. Thus, audible inspiratory splitting of the second heart sound at the apex should be considered abnormal and may be a manifestation of a loud P2, since only the aortic component should be heard.
Normal patients should have a single heart sound at some point in expiration. In examining the normal patient, one should always develop the habit of timing the splitting of the second heart sound with respiration.
Fixed splitting of the second heart sound should prompt suspicion of a secundum atrial septal defect. Patients with secundum atrial septal defects also have right bundle branch block on the EKG, which even in the absence of an atrial septal defect, is associated with exaggerated inspiratory splitting of the second heart sound.
It is possible to encounter persistent splitting of the second heart sound in the absence of cardiac disease in patients who are only examined in the supine position. Sitting or standing will yield a single second heart sound in these patients by decreasing venous return.
Patients with left bundle branch block have paradoxical splitting of the second heart sound. It is split on expiration and becomes single on inspiration. This is due to the fact that the normal sequence of aortic valve closure followed by pulmonic valve closure is reversed. The first audible sound is the pulmonic second heart sound followed by the aortic second heart sound. Patients with electronic pacemakers in the right ventricular apex manifest the same paradoxical splitting during cardiac pacing. Careful auscultation during intermittent demand pacing can detect the paced beats by timing the splitting with the respiratory cycle.
Severe aortic stenosis typically prolongs left ventricular ejection time. Because the left ventricular ejection time is prolonged, the aortic valve closure sound becomes delayed resulting in paradoxical splitting of the second heart sound. The mechanism is as follows: the delayed aortic valve closure sound does not move with respiration but it now follows rather than precedes the pulmonic component. The pulmonic component continues to move as usual durin the respiratory cycle. In expiration it audibly precedes the aortic component resulting in audible splitting of the second sound. In inspiration the pulmonic component is delayed, coinciding with the aortic component, manifesting as a single second heart sound. This can be used for following patients with aortic stenosis together with the time to peak of the crescendo decrescendo murmur. The timing of the peaking of aortic stenosis murmurs is a useful index of severity. It goes along with left ventricular ejection time and with delayed closure of the aortic valve.
Patients with left bundle branch block can have an underlying cardiomyopathy or other cardiac disease. The presence of left bundle branch block provides reason to pursue a cardiac evaluation. Paradoxical splitting of the second heart sound on auscultation may be the first clue to the presence of left bundle branch block.
There are several causes for a loud aortic component: systemic hypertension, coarctation of the aorta, transposition of the great vessels.
The pulmonic component is loud with pulmonary hypertension and soft with pulmonic stenosis. Yet, both these conditions are associated with increased amplitude of the jugular venous 'a' wave.
Atrial septal defect and pulmonic stenosis can be present in association. Normal auscultation of the second heart sound can exclude this combination by using the normal inspiratory splitting of the second heart sound as confirmation of the presence of audible pulmonic valve closure. A normal single second heart sound in expiration excludes the atrial septal defect.
FOURTH HEART SOUND
The fourth heart sound, also called S4 gallop, atrial gallop, or presystolic gallop is a low frequency sound that is best heard with the bell of the stethoscope held lightly against the skin. Forceful pressure may obliterate it. Increasing and decreasing the pressure during auscultation can help differentiate an S4 followed by S1 from S1 followed by an ejection sound. Both S1 and ejection sounds have high frequency components that remain audible even when the bell is pressed down.
Some very low frequency components of S4 may be palpable at the apex without being audible. The search for an S4 should therefore combine palpation with auscultation. By looking at one's fingers as they palpate the precordium it may also be possible to see the S4. So an S4 can be heard, felt and seen in some patients.
Due to the loss of atrial contraction the S4 disappears with onset of atrial fibrillation.
Having the patient cough several times may elicit a previously inaudible gallop.
When both S3 and S4 are present, the quadruple rhythm is reminiscent of a locomotive and can be phonated as: "ta ra ta ta". An increase in the heart rate will shorten diastole and can bring S3 and S4 together resulting in a single loud diastolic sound called summation gallop. This may also happen in patients with a long P-R interval. Carotid sinus pressure during auscultation may separate the converging diastolic sounds by slowing the heart rate.
Loud diastolic sound produced during the rapid ventricular filling phase. It usually occurs later than the opening snap of mitral stenosis. The two are easily confused because both are high pitched. The opening snap is more widely transmitted across the precordium.
The pericardial knock occurs earlier than the S3 gallop, is louder and higher pitched than the S3. The knock is heard with the diaphragm over a larger area than the S3. The S3 is best heard with a lightly applied bell.
The pericardial knock becomes louder with inspiration, squatting, and any other maneuvers that increase venous return. It can have an associated palpable diastolic thrust. The palpable diastolic thrust is not pathognomonic. It has also been described in mitral insufficiency in association with an audible loud "ventricular knock". The mechanism of both entails structural restriction of diastolic filling - a so called "cocktail shaker" motion of the heart. The restricting structure is either a pericardial shell in constriction, or the actual chest wall in mitral insufficiency.
In some patients the pericardial knock may actually be louder than both S1 and S2. Following pericardiectomy the knock may disappear, or become softer and/or occur later in diastole.
Patients with constrictive pericarditis have systolic retraction of the apex in addition to the pericardial knock as well as a prominent "y" descent of the jugular pulse.
Some patients with constrictive pericarditis may have an unusual splitting of the second heart sound. There may be abrupt and short-lived splitting of S2 at the onset of respiration.
JUGULAR VENOUS INSPECTION
Inspection of the jugular veins requires practice. In many patients it is difficult to see jugular venous pulsations. A common misconception is to look at the external jugular veins and forget about the internal jugular pulsations. The internal jugular pulsations convey information about right atrial and right ventricular activity. It is most important to recognize the A wave and the V wave. The A wave and V wave are more easily distinguished in patients with slow heart rates, and with the help of palpating the carotid upstroke. The A wave typically precedes the carotid upstroke, whereas the V wave will coincide with, or follow the carotid upstroke. Therefore, the typical cardiac physical examination involves palpation of the carotid upstroke with one hand, while the eyes focus on the internal jugular pulsations and the other hand moves the stethoscope.
Internal jugular pulsations sometimes need to be enhanced by a tangential light on the neck to create shadows that will bring out the pulsations. A classic finding that is not easily diagnosed until one has seen a few cases is a prominent Y descent that follows the V wave. Prominent Y descent is associated with constrictive pericarditis.
Venous neck pulsations can be differentiated from
Venous pulses are:
Some of the difficulty in the jugular venous exam resides in the variability of the A and V waves. Both occur in diastole. The duration of diastole is more variable than the duration of systole.
In addition to examining the neck veins for jugular venous distension it is possible to estimate the venous pressure by inspecting the dorsal veins of the extended hand. The hand is lowered until the veins fill. It is then raised slowly to the height at which they just begin to collapse. The difference in height between the arm and the heart is roughly the venous pressure in millimeters of blood.
The recumbent patient can place one hand on the anterior aspect of their thigh and the other hand on the bed. The dorsal hand veins on the thigh are compared to those on the bed. There is venous hypertension if the veins in both hands are distended.
AUSTIN FLINT MURMUR
This is an apical mid to late diastolic murmur. It was described in 1862 by Austin Flint. It has a rumbling quality similar to the sound of distant thunder. It resembles the diastolic rumble of mitral stenosis. Amyl nitrite inhalation decreases the Austin Flint murmur and increases the loudness of the diastolic rumble of mitral stenosis.
Two pulse wave peaks may be palpated during one cardiac cycle. The pulse is called dicrotic when the second pulse peak is palpated in diastole. The second (diastolic) peak of a dicrotic pulse is obliterated by finger pressure. In contrast, a systolic second peak (bisferiens pulse) is accentuated by finger pressure.
Palpation of the radial pulse should use three fingers (the third finger blocks a possible distal retrograde pulse from the hand). The first finger gradually increases the pressure proximally. The middle finger palpates the pulse during the compression. With experience, the amount of compression can be used to estimate the systolic blood pressure.
Alternating strong and weak pulse amplitude during regular heart rhythm is called pulsus alternans. Very light palpation of the radial or femoral pulse should be used. The amount of pressure should be as light as the pressure created by blowing on the examiner's fingertips! The weak pulse may sometimes be too faint to feel.
The tactile diagnosis can also be dramatically confirmed with a blood pressure cuff. On slowly deflating the cuff, the Korotkoff sounds are first heard at half the heart rate. With further lowering of the cuff pressure, the rate of Korotkoff sounds suddenly doubles.
Continuous murmurs are rare in adult internal medicine practice, but when found they need to be distinguished. The cause could be either a benign or a significant abnormality that may actually require cardiac surgery.
Specifically, an aneurysm of the sinus of Valsalva can increase in size and at one point rupture into the right ventricle or into the right atrium. At that time the patient develops a continuous murmur and may also develop heart failure. The onset of heart failure associated with a new continuous murmur should prompt the diagnosis, which can be confirmed with echocardiography.
Another commonly known cause of a continuous murmur is the presence of a persistent ductus arteriosus. In an adult this is rare, and ductal ligation is a definitive cure. It is also possible to close the ductus with catheter devices such as coils.
Another cause of continuous murmurs can be an aortopulmonary Window. This is a connection between the aorta and the pulmonary artery (different from a truncus arteriosus). Coronary artery fistulas can also cause continuous murmurs.
There are several benign causes of continuous murmurs. A venous hum can be heard in children, and when present it can be shown to be benign by applying pressure on the neck over the jugular vein. This will cause the hum to decrease in loudness or actually disappear.
During pregnancy, a mammary souffle can be heard over one or both breasts. Compression of the area where the murmur is heard may make that murmur disappear as well.
STANDING FLEXION POSITION FOR AUSCULTATION
Pericardial rubs can be very faint. A potentially useful technique consists of listening with the patient lying face down, chest propped up by leaning on their elbows. A less awkward approach is to have the patient stand, lean forward, and support the elbows on a table or a counter - the standing flexion position. (JAMA 1965;195:146-147)
This technique also makes it possible to increase the patient's heart rate by some form of upright exercise with immediate post exercise stethoscope access while the rate is still fast.
VENTRICULAR SEPTAL DEFECT
Ventricular septal defects are also associated with characteristic physical findings. The systolic murmur of a ventricular septal defect is heard at the left sternal border. It can be heard very high up in the second intercostal space in supracristal defects. The timing of the murmur is important because it may provide evidence of associated pulmonary hypertension. A late systolic murmur is more ominous. Murmurs from ventricular septal defects can vary with the respiratory cycle. Typically, the murmur will increase on expiration. At that time it is also possible to come to a mistaken conclusion about the second heart sound. Specifically, the second heart sound may be widely split in patients with ventricular septal defects due to the fact that the pulmonic closure sound is delayed. When the murmur of the defect becomes louder on expiration, it can actually extend all the way through to the aortic component of the second heart sound, masking it. Therefore, on auscultation the mistaken impression is that the second heart sound has become single, when in fact it remains split with the aortic component simply being masked by the more prominent murmur. Fixed splitting of the second heart sound is commonly known to be associated with secundum atrial septal defects, but this can also be present in patients with ventricular septal defect.
There are four phases during the Valsalva maneuver.
Phase one is the onset of straining with increased intrathoracic pressure. The heart rate does not change but blood pressure rises.
Phase two is marked by the decreased venous return and consequent reduction of stroke volume and pulse pressure as straining continues. The heart rate increases and blood pressure drops.
Phase three is the release of straining with decreased intrathoracic pressure and normalization of pulmonary blood flow.
Phase four marks the blood pressure overshoot (in the normal heart) with return of the heart rate to baseline.
Phase two can be used to distinguish fixed left ventricular outflow obstruction (valvular aortic stenosis) from dynamic obstruction. During phase two the murmurs of hypertophic obstructive cardiomyopathy and mitral valve prolapse may increase as a result of the decreased stroke volume. Most other murmurs (including valvular aortic stenosis) decrease in intensity.
It is important to continue listening after Valsalva release. Phase four auscultation is useful in distinguishing left-sided from right-sided murmurs. Right-sided murmurs that decrease in intensity during phase two will return to baseline intensity almost immediately after Valsalva release. Left-sided murmurs require five to ten cardiac cycles to return to baseline.
TECHNICAL HINTS FOR CARDIAC PERCUSSION
Percussion of the heart should be performed from the right side of the patient.
The left hand is placed on the chest when the examiner is right handed.
The middle finger of the left hand is placed by separating it fron the rest of the fingers and hand. It should be placed in the intercostal spaces rather than on top of the ribs. It should be bent in an arc so that only the distal two thirds of the finger are in contact with the chest wall.
All soft tissue under the finger should be compressed firmly.
The fingers of both hands should be as parallel to each other as possible.
One should strike at a 90 degree angle to prevent sideways displacement of the percussed finger (with resultant muffling of sounds).
One should strike briskly with motion at the wrist only. The striking finger should be promptly removed to prevent muffling of the elicited percussion sound.
The point of impact should be just proximal to the nail.
Br Heart J 1989 Feb;61(2):144-8
Relation of third and fourth heart sounds to blood velocity during left ventricular filling.
Vancheri F, Gibson D.
Cardiac Department, Brompton Hospital, London.
To investigate the relation between changes in left ventricular inflow velocity and the timing of third and fourth heart sounds, simultaneous phonocardiograms and continuous wave Doppler traces were recorded in 48 patients (aged 17-78) with heart disease and in 21 normal children. The onset of the first vibration of the third heart sound coincided with peak left ventricular inflow blood velocity to within 5 ms in all but two of the patients. The mean (SD) difference between the two events was 5 (5) ms, which did not differ significantly from zero. The relation was similar in patients with primary myocardial disease (11), and in those with valve disease (26), hypertension (five), and coronary artery disease (four). In the normal children, the mean interval was 2.5 (5) ms--not significantly different from zero. By contrast, the first deflection of the fourth heart sound consistently preceded the timing of peak atrial inflow velocity by 55 (10) ms. Agreement was much closer between the onset of atrial flow and the onset of the atrial sound (mean difference 1 (5) ms, not significantly different from zero). Gallop sounds seem to be closely related to changes in ventricular inflow velocity, and thus to the effects of forces acting on blood flow. The forces underlying the third sound seem to arise within the ventricle and are responsible for sudden deceleration of flow during rapid ventricular filling. The fourth sound, occurring at the onset of the "a" wave, is more likely to arise from dissipation of forces causing acceleration of blood flow--that is, atrial systole itself.
Circulation 1981 Sep;64(3):464-71
Clinical significance and hemodynamic correlates of the third heart sound gallop in aortic regurgitation. A guide to optimal timing of cardiac catheterization.
Abdulla AM, Frank MJ, Erdin RA Jr, Canedo MI.
The hemodynamic and clinical data of 42 patients with chronic significant aortic regurgitation and 31 normal subjects were examined. Of the patients with aortic regurgitation, 28 had a third heart sound (S3) gallop and 14 did not. There was no significant difference in the severity of regurgitation between the patients with or without an S3 gallop. However, all patients with an S3 gallop had an abnormality increased left ventricular residual volume and depressed contractile state. These findings were supported by the hemodynamic data of two patients who underwent cardiac catheterization before and after the development of an S3 gallop. We conclude that the S3 gallop in patients with chronic AR reflects left ventricular dysfunction, rather than more severe degrees of regurgitation per se, and may therefore be useful for selecting patients for cardiac catheterization and consideration for prosthetic aortic valve replacement.
Am Heart J 1977 Nov;94(5):633-6
Echocardiographic correlate of presystolic pulmonary ejection sound in congenital valvular pulmonic stenosis.
Flanagan WH, Shah PM.
A presystolic ejection click was present in a patient with congenital valvular pulmonic stenosis. The coincidence of this sound with presystolic pulmonary valve opening was demonstrated by simultaneous phonoechocardiography. Hemodynamic confirmation of this observation was made by demonstrating presystolic crossover of RV-PA pressures. This sound was distinguished on phonocardiogram as a high frequency sound separate from a lower frequency presystolic (S4) gallop.
Angiology 1976 May;27(5):300-10
When does a fourth sound become an atrial gallop?
Perez GL, Luisada AA.
A study of the fourth sound was conducted on 100 normal subjects (ages 1-88 years) and 42 clinical cases with either aortic stenosis, systemic hypertension or coronary heart disease. This study was based on the graphic recognition of a presystolic sound when the tracing was taken with the use of one or more of 5 different high pass filters. Attention was paid to the existence of the fourth sound, its magnitude, and its vibrational frequency. In general it was accepted that a magnitude of 1/2 of the first heart sound or a frequency of 30 Hz denoted a pathologic fourth sound. However, exceptions were found among normal subjects, so that only the combination of the two criteria could be considered highly significant for a pathologic phenomenon (gallop). Patients with aortic stenosis presented an increase in magnitude of the fourth sound but incidence and vibrational frequency were similar to those of controls. Patients with hypertension had a greater incidence of fourth sounds, especially in middle age (100%); middle age patients usually had a greater magnitude while older patients had more often an increase in vibrational frequency. Patients with coronary heart disease (evidence of old infarcts) had an increase in the incidence, magnitude, and vibrational frequency in comparison with controls. These data and the cause of the fourth sound are discussed. The fourth sound has been repeatedly studied in the past, both as an auscultatory finding and a graphic phenomenon. Attempts were made for separating the normal fourth sound from that denoting a pathological phenomenon but, so far, no clear cut criteria for the differentiation have been obtained. We thought, therefore, that a new study was indicated.
Br Heart J 1975 Dec;37(12):1277-80
Transmission of audible praecordial gallop sounds to right supraclavicular fossa.
DiDonna GJ, O'Rourke RA, Peterson KL, Karliner JS.
To evaluate the significance of audible gallop sounds in the right supraclavicular fossa we performed simultaneous external heart sound recordings at 50 and 100 Hz at the left ventricular apex, left sternal border, and right supraclavicular fossa in 50 patients with audible gallop sounds at the left ventricular apex. In each patient heart sounds were recorded with a simultaneous jugular phlebogram, apex cardiogram, and carotid pulse tracing. In 44 patients an apical fourth heart sound coincident with the 'a' wave of the apex cardiogram was recorded, and in 32 (73%) the fourth heart sound was audible and recordable in the right supraclavicular fossa. A left ventricular third heart sound, coincident with the rapid filling wave of the apex tracing, was present in 25 patients but was recorded in the right supraclavicular fossa in only 7 (28%). Intracardiac phonocardiography (high-fidelity catheter) was performed in six patients with left ventricular gallop sounds and in each instance arterial transmission of the third or fourth heart sound, or both, was present. Five additional patients had a prominent jugular venous 'a' wave, but only two had a soft parasternal fourth heart sound. Intracardiac phonocardiography in these five patients failed to reveal transmission of right ventricular gallop sounds to the superior vena cava. We conclude that since left ventricular gallop sounds commonly are transmitted to the right supraclavicular fossa auscultation in this area is often helpful in their detection. In addition, a prominent jugular venous 'a' wave sometimes produces recordable presystolic vibrations that are occasionally audible as well.
Am J Med 1996 Feb;100(2):149-56 Comment in: Am J Med. 1996 Dec;101(6):664.
Intensity of murmurs correlates with severity of valvular regurgitation.
Desjardins VA, Enriquez-Sarano M, Tajik AJ, Bailey KR, Seward JB.
Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA.
PURPOSE: To evaluate the relationship between the intensity of murmurs and severity of mitral and aortic regurgitation. PATIENTS AND METHODS: Consecutive patients with chronic isolated aortic (n = 40) or mitral (n = 170) regurgitation undergoing echocardiographic quantitation of regurgitation between 1990 and 1991 were studied. Regurgitant volume and fraction were measured using two simultaneous methods (quantitative Doppler echocardiography and quantitative two-dimensional echocardiography); the intensity of the regurgitant murmur (grade 0 to 6) was noted by physicians unaware of the study. RESULTS: Correlations between murmur intensity and regurgitant volume and fraction were good in aortic regurgitation (r = .60 and r = .67, respectively; P < 0.001) and mitral regurgitation (r = .64 and r = .67, respectively; P < 0.001) but weaker (r = .47 and r = .45, respectively) in the subset of mitral regurgitation of ischemic or functional cause. Murmur intensity grades > or = 3 for aortic regurgitation and > or = 4 for mitral regurgitation predicted severe regurgitation (regurgitant fraction > or = 40%) in 71% and 91% of patients, respectively. Murmur grades < or = 1 for aortic regurgitation and < or = 2 for mitral regurgitation predicted "not severe" regurgitation in 100% and 88% of patients, respectively. Murmur grades 2 for aortic regurgitation and 3 for mitral regurgitation were not correlated to degree of regurgitation. The severity of regurgitation was the most powerful determinant of intensity of murmur. CONCLUSIONS: Murmur intensity correlates well with the degree of chronic organic aortic and mitral regurgitation, and can be used as a predictor of regurgitation severity and as a simple guideline for diagnostic testing in these patients.
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