heart murmurs 2 by nuhman10

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                             HEART SOUNDS AND MURMURS
                                     James A. Shaver, MD
The student should be able to:
       a.     draw the relationship between intracardiac and arterial pressures versus the
              normal and abnormal heart sounds;
       b.     classify the types of systolic and diastolic murmurs on a pathophysiologic basis;
       c.     list the factors that influence the intensity of normal and abnormal heart sounds

The student should be able to:
       a.     understand the mechanisms of production of normal and abnormal heart sounds;
       b.     appreciate the relationship between driving pressure, flow velocity, and the
              resultant turbulence in the production of murmurs;
       c.     appreciate the concept of pulmonary and systemic vascular impedance and how it
              affects the timing and intensity of the second heart sound

The student should be able to:
       a.     predict the effect of altered hemodynamics on the timing and intensity of heart
              sounds and murmurs

The student should be able to:
       a.     differentiate systolic ejection murmurs versus pansystolic regurgitant murmurs by
              both their “murmur envelopes” as well as by their response to physiologic and
              pharmacologic maneuvers
       b.     differentiate diastolic rumble and pandiastolic regurgitant murmurs by both their
              “murmur envelopes” as well as by their response to physiologic and
              pharmacologic maneuvers
       c.     diagram the ausculatory findings of common valvular heart abnormalities

The student should be able to:
       a.     diagnose the valvular lesion, given the diagram of the abnormal heart sounds and
       b.     predict alterations of intracardiac systolic and diastolic pressures on the basis of
              abnormal heart sounds and murmurs

The student should be able to:
       a. appreciate the value of cardiac auscultation in the overall evaluation of the cardiac
                                    CARDIAC AUSCULTATION

                                        Heart Murmurs

A cardiac murmur is defined as a relatively prolonged series of auditory vibrations of varying
intensity (loudness), frequency (pitch), quality, configuration, and duration. Most authorities
now agree that turbulence is the prime factor responsible for most murmurs; it occurs when
blood velocity becomes critically high.

The clinician’s description of a murmur should include its timing (systolic, diastolic, or
continuous), location, radiation, and intensity. The location and radiation of a murmur are
multifactorially determined by the site of origin, intensity, and direction of blood flow. The
intensity of the murmur as heard at the chest wall is determined by the transmission
characteristics of the tissue intervening between the source of the murmur and the stethoscope.
Obesity, emphysema, and significant pleural or pericardial effusions will decrease the intensity
of the murmur, whereas a thin, ascetic body type will often accentuate it.

Systolic Murmurs. Systolic murmurs may be classified as systolic ejection or pansystolic
regurgitant. Systolic ejection murmurs (SEM) are caused by forward flow across the left or right
ventricular outflow tract, whereas pansystolic regurgitant murmurs are caused by retrograde flow
from a high-pressure chamber into a lower-pressure chamber (Figure 1). A more detailed
breakdown of this classification based on the physiologic mechanisms of production of these
murmurs is shown in Figure 2.
        Classification of Murmurs Based on Physiologic Mechanism of Production

Systolic murmurs are graded from 1 to 6. A grade 1 murmur is audible only after the listener has
tuned in. Grade 2 is the faintest systolic murmur audible immediately after placing the
stethoscope on the chest. Grade 5 is a loud murmur that cannot be heard with the stethoscope
removed from the chest wall but can be heard with just the edge of the stethoscope touching the
skin. A grade 6 murmur is audible with the stethoscope removed from the chest wall. Grade 3
and 4 are intermediate. Systolic murmurs of grade 3 or more in intensity are usually
hemodynamically significant. Systolic thrills are usually associated with grade 4 or louder
murmurs. A murmur’s intensity varies directly with the velocity of blood flow, which in turn is
directly related to the pressure head that propels the blood across the murmur-producing area.
Systolic ejection murmur. The midsystolic ejection murmur begins shortly after the left or
right ventricular pressure exceeds aortic or pulmonary diastolic pressure sufficiently to open the
aortic or pulmonic valve (Figure 3).

                                   Left Ventricular Ejection Dynamics

    Figure 3
    Left ventricular ejection dynamics are illustrated by simultaneous recording of left ventricular and aortic pressure,
    aortic flow velocity and tine intensity envelope of murmur. During normal left ventricular ejection (left panel), peak
    flow velocity is early, with two-thirds of ventricular volume ejected during first half of systole. Murmur threshold
    may be exceeded during early peak flow and the corresponding murmur envelope is inscribed. Center panel shows
    exaggeration of the normal left ventricular ejection pattern, with large stroke volume as seen high –output states.
    With critical left ventricular outflow obstruction (right panel), rapid early ejection is no longer possible; flow velocity
    is increased and a contour becomes rounded and prolonged, producing a typical diamond-shaped murmur of aortic
The contour of the time-intensity pattern, or murmur envelope, parallels the contour of flow
velocity, and the murmur is heard when the sound produced by the peak turbulence exceeds the
audible threshold. The intensity of SEMs is related directly to peak flow velocity during
ventricular ejection. Any condition that increases forward flow, such as exercise, anxiety, or the
increased stroke volume associated with a long diastolic pause following a premature beat
(Figure 4), will increase the intensity of the murmur. Likewise, conditions that decrease stroke
volume or its rate of ejection (congestive heart failure or negative inotropic drugs) will decrease
the intensity of the murmur.
Figure 4                                                          Figure 4
Left ventricular ejection dynamics are demonstrated with a        The effect of a premature ventricular contraction (PVC) on
simultaneous flow probe in the central aorta, together with       peak aortic flow velocity and the intensity of a systolic
the aortic phonocardiogram. Note that at rest, a very short       ejection murmur. Following a long diastolic filling period
ejection murmur is recorded simultaneously with peak flow         with a greater filling of the left ventricle, there is a more
in the central aorta. Following exercise, there is a marked       forceful contraction resulting in larger stroke volume and
increase in the peak aortic flow, and associated with this is a   peak flow, and in turn, resulting in a louder systolic
significant increase in the systolic ejection murmur due to the   ejection murmur. Beat-to-beat variations in the intensity
turbulence produced by the high flow during early ejection.       of a systolic murmur caused by premature atrial or
Any maneuver which increased flow during systole will             ventricular contractions, and in patients with atrial
increase the intensity of a systolic ejection murmur.             fibrillation, allow differentiation between ejection and
                                                                  pansystolic regurgitant murmurs.

                                              Innocent Murmurs

Innocent murmurs are systolic ejection in nature and are found in patients without evidence of
physiologic or structural abnormalities of the cardiovascular system (Figure 5). This definition
excludes murmurs produced by minor structural abnormalities such as a prolapsing mitral valve,
even if such murmurs are hemodynamically insignificant. Although systolic murmurs produced
by high cardiac output are functional, physiologic, and flow related, they are excluded from this
definition because of the associated altered physiologic state. Innocent murmurs are less than
grade 3 in intensity and vary considerably with body position and level of activity, and from one
examination to another. They are found in approximately 30% to 50% of all children and are
common in adolescents and young adults. In elderly persons, innocent murmurs caused by flow
across the left ventricular outflow tract may have a musical quality and are frequently heard best
at the apex.

                                                                               Figure 5
                                                                               This is an example of an innocent systolic
                                                                               ejection murmur (SEM) as recorded in a 16
                                                                               year old boy. The murmur is soft, crescendo-
                                                                               decrescendo, and ends well before S2.
                                                                               Normal physiologic splitting is present, and
                                                                               no diastolic filling sounds are recorded. The
                                                                               carotid pulse is normal. The murmur was
                                                                               recorded in the pulmonary artery during
                                                                               diagnostic catheterization by intracardiac
                                                                               phonocardiography, confirming its right-
                                                                               sided origin.
                                                                      Because both innocent murmurs and systolic
                                                                      ejection murmurs associated with physiologic
                                                                      or structural abnormalities of the
                                                                      cardiovascular system have the same
                                                                      mechanism of production, it is not the nature
                                                                      of the murmur itself that allows the differential
                                                                      diagnosis, but rather the associated cardiac
                                                                      findings. Therefore, the “company the
                                                                      murmur keeps” establishes the proper
                                                                      diagnosis; the innocent murmur must be found
                                                                      in the setting of an otherwise normal
                                                                      cardiovascular examination (Figure 6).

                                             Right and LV Outflow Obstruction

        A prominent systolic ejection murmur is almost always present with obstruction to right or left
        ventricular outflow, which may be located at the valvular, supravalvular, or subvalvular level.
        These murmurs are crescendo-decrescendo in nature, and their murmur envelope closely
        parallels the instantaneous ventricular-great vessel pressure gradient (Figure 7). As long as the
        cardiac output is maintained, the intensity and duration of the murmur increase as the stenotic
        lesion progressively narrows. When cardiac output decreases, the intensity of the murmur
        decreases, although careful auscultation will usually reveal that the murmur still has a
        prolonged duration.

Figure 7
Simultaneous phonocardiogram, left ventricular and central aortic pressure are recorded in a 23 year old patient with
congenital Valvular aortic Stenosis. After a premature ventricular contraction (PVC) note the marked increase in the
                                              Pansystolic Regurgitation This increased gradient results in an
peak left ventricular pressure and the gradient across the stenotic aortic valve. Murmur
increase in the stroke volume across the stenotic valve and results in a marked increase in the intensity and duration of
the systolic ejection murmur. The murmur envelope of the systolic ejection murmur corresponds to the instantaneous
pressure difference between the left ventricle and central aorta. Also note the marked decrease in the intensity of the
murmur during the premature systole which correlates with the markedly decreased pressure gradient on this beat.
         Pansystolic regurgitant murmurs are produced from retrograde flow from a chamber of high
         pressure to one of low pressure (Figure 1). Because there is usually a large pressure differential
         between the two chambers throughout systole, the murmurs are pansystolic in duration, high
         pitched in blowing and quality and plateau-like in configuration. The pansystolic murmur of
         mitral regurgitation is heard best at the apex, often radiating into the axilla. There is a good
         correlation between the intensity of the murmur and the degree of mitral regurgitation which is
         closely related to the pressure gradient causing the regurgitant flow from the left ventricle into
         the left atrium (Figure 8). Interventions at increased left ventricular pressure such as hand grip,
         the squatting position of vasoconstrictor drugs increase the intensity of the regurgitant murmur
         where as measures which decrease the left ventricular pressure (inhalation of amyl nitrite)
         decrease the intensity of the murmur. In contrast to systolic ejection murmurs, these murmurs
         very little with changes and forward cardiac output or beat-to-beat changes in stroke volume
         (Figure 9).

Figure 8
The simultaneous apex phonocardiogram, left ventricular and left atrial pressures are recorded in a patient with moderately
severe mitral regurgitation. During the control observation, there is a significant pressure gradient between the left ventricle and
the left atrium and this is associated with a Grade IV pansystolic murmur which is recorded well at the apex. Following the
inhalation of amyl nitrite, the peak left ventricular pressure, the height of the left atrial V wave and the left ventricular left atrial
pressure gradient are markedly decreased. Associated with this is a marked decrease in the intensity of the pansystolic murmur.
In contrast, following the infusion of phenylephrine, a potent peripheral vascular constrictor, there is a marked increase in the
peak left ventricular pressure, the height of the left atrial V wave, and the pressure differential between the left ventricle and the
left atrium. Associated with this is a marked increase in the intensity of the apical pansystolic murmur due to the increased
retrograde flow as a result of the increased pressure gradient between the left ventricle and left atrium.
Figure 9
There is little variation in the intensity of the pansystolic murmur with variation in cycle. This lack of marked variation
is very helpful in differentiating apical pansystolic murmurs vs ejection murmurs that are also heard at the apex,
particularly in the elderly patient.

 left sternal border; however when a large right ventricle occupies the apex, it may be heard well
 lateral to the midclavicular line. It is usually easily identified by its typical augmentation and
 intensity with inspiration (Figure 10). Simultaneous observation of the JVP while listening to
 this murmur will help define its right-sided origin, revealing prominent V waves with rapid Y
 descents that augment with inspiration. The murmur of a ventricular septal defect is heard at the
 parasternal border of the fourth, fifth and sixth intercostals spaces, frequently associated with a
 systolic thrill. In contrast to mitral regurgitation, the murmur does not radiate well to the axilla
 and its intensity does not correlate with the degree of left to right shunting, nor does it have any
 respiration variation characteristic of tricuspid regurgitation.

    Figure 10
    The murmur of severe tricuspid regurgitation (TR) increases in intensity with inspiration and is associated
    with a very prominent V wave, having a rapid Y descent. The onset of the V wave in severe tricuspid
    regurgitation is early, as shown by a prominent systolic (S) wave.
Not all regurgitant murmurs are pansystolic. Common variants of regurgitant murmurs are
illustrated in Figure 11, and the typical response of the late systolic murmur of mitral prolapse to
postural changes is shown in Figure 12.

  Figure 11
  In addition to the classic pansystolic regurgitant murmur seen in mitral regurgitation, tricuspid regurgitation and
  ventricular septal defect variants exist. In patients with small ventricular septal defects, the murmur which starts with
  S1 may suddenly stop during early or mid-systole. The proposed explanation is that as ventricular volume becomes
  smaller after maximal ejection, the defect seals shut and the murmur ceases. In acute mitral regurgitation, the
  regurgitant murmur may end well before A2 as the results of an extremely high left atrial V wave that abolishes the
  left ventricular –left atrial pressure gradient during late systole. S1 may be soft if a flair mitral leaflet is present and is
  preceded by a prominent S2. Audible expiratory splitting with an accentuated P 2 is present. Mid-to late systolic
  regurgitation murmurs may be due to papillary muscle dysfunction as well as to prolapsed of them mitral or tricuspid
  valve. In the latter conditions, the valve is competent in early systole, but as ventricular volume decreases, the
  leaflets become incompetent and the murmur begins and builds in late systole to become maximal at the same S 2.

          Figure 12

Diastolic Murmurs. Diastolic murmurs are caused by either structural abnormalities of the
atrioventricular and semilunar valves or increased flow across anatomically normal
atrioventricular valves. In contrast to some systolic ejection murmurs that are innocent, diastolic
murmurs should never be considered innocent. They have two basic mechanisms of production.
Diastolic filling murmurs or rumbles are due to forward flow across the atrioventricular valves,
whereas diastolic regurgitant murmurs are due to retrograde flow across an incompetent
semilunar valve (Figure 13). A further breakdown of this classification based on the mechanism
of production of each murmur is shown in Figure 14.

Diastolic filling murmurs (rumbles). Diastolic rumbles are caused by forward flow across the
atrioventricular valves, and their onset is delayed from their respective semilunar closure sound
by the isovolumic relaxation period (Figure 13). When the atrial pressure exceeds the declining
ventricular pressure, the atrioventricular valves open and filling begins. There are two phases of
rapid ventricular filling, early diastole and presystole, the time at which these murmurs tend to be
most prominent.

                                               Heart Murmurs

Figure 13
Right panel: Flow diagram. Diastolic filling murmurs or rumbles are caused by forward flow across the atrioventricular
valves, where as diastolic regurgitant murmurs are caused by retrograde flow across an incompetent semilunar valve.
Left panel: Diagrammatic representation of the diastolic filling murmur and the diastolic regurgitant murmur as related to
high-fidelity left ventricular (LV), aortic, and left atrial (LA) pressure. The diastolic filling murmur occurs during the
diastolic filling period and is separated from the second heart sound (S2) by the isovolumic relaxation period (IRP). The
rumbling murmur is most prominent during rapid early ventricular filling and presystole, terminated with the first heart
sound (S1). The diastolic regurgitant murmur begins immediately after S2 and continues in a decrescendo fashion up to
S1, closely paralleling the aortic-left ventricular diastolic pressure gradient.
         Classification of Murmurs Based on Physiologic Mechanism of Production

The diastolic rumble of the stenotic mitral
valve is heard best at the apex. As long as
the stenotic valve has mobility, the murmur
is introduced by an opening snap and is
most prominent during the two phases of
rapid ventricular filling (Figure 15). The
duration of the mitral rumble correlates
well with the duration of the diastolic
gradient across the mitral valve, whereas
its intensity is related to both the severity
of the obstruction and the forward flow
across the stenotic valve. In normal sinus
rhythm, the presystolic murmur crescendos
up to S1. The diastolic rumble of the
stenotic tricuspid valve is usually heard in        Figure 15
xiphoid area just off the left sternal border. In   In mild mitral Stenosis, the diastolic gradient across valve is
                                                    limited to the phases of rapid ventricular filling in early
contrast to the presystolic murmur of mitral
                                                    diastole and presystole. The rumble occurs during either or
stenosis, which crescendos up to the                both periods. As the stenotic process becomes severe, a large
                                                    gradient develops across the valve during the entire diastolic
                                                    filling period and the rumble persists through out the
                                                    diastolic filling period. As the left atrial pressure becomes
                                                    higher, the time from aortic valve closure sound (2) to the
                                                    opening snap (OS) shortens. In severe mitral Stenosis,
                                                    secondary pulmonary hypertension results in a louder
                                                    pulmonic valve closure sound (P2) and splitting interval
                                                    usually narrows. S1, first heart sound; S2, second heart
loud S1, the earlier onset of right atrial systole relative to left atrial systole results in a presystolic
tricuspid murmur with a crescendo-decrescendo configuration, which ends before S1 and
increases with inspiration (Figure 16).

                 The Effect of Respiration on the Murmur of Tricuspid Stenosis

  Figure 16
  In tricuspid stenosis (TR), note the crescendo-decrescendo presystolic murmur of TS is coincident with the rapid rise
  and decline of the A wave.
Short mid-diastolic flow rumbles, often introduced by S3, are also produced by high flow across
the normal or regurgitant atrioventricular valve (Figure 17).

                                          Diastolic Flow Rumbles

    Figure 17
    Diastolic flow rumbles are caused by high flow across the atrioventricular valves in patients having atrial septal
    defect (ASD), ventricular septal defect (VSD), and patient ductus arteriosus. Shunting through the atrial septal
    defect results in high flow across the tricuspid valve, producing the tricuspid flow rumble (TFR). In both VSD
    and PDA, left-to-right shunting through the VSD or PDA, causes high flow across the mitral valve, resulting in a
    mitral flow rumble (MFR). With both MR and TR, the large regurgitation volume causes increased flow during
    early diastole across the atrio ventricular valve, resulting in MFR and TRF, respectively, both being introduced
    by a prominent third heart sound (S3). With inspiration, there is a significant increase in the intensity of the
    pansystolic regurgitant tricuspid murmur (PRM), the S3, and the TFR. No significant changes in the intensity of
    the diastolic flow rumbles occur with inspiration in patients have ADS, VDS, PDA or MR. A 2, aortic valve
    closure sound; M1, mitral valve closure sound; P2, pulmonary valve closure sound; SEM, systolic ejection
    murmur, T1, tricuspid valve closure sound.
      Pandiastolic aortic regurgitant murmurs. When the aortic valve becomes incompetent, a
      blowing high-pitched decrescendo diastolic murmur develops (Figure 13). The murmur of aortic
      regurgitation resulting from deformity of the aortic valve is usually best heard in the third and
      fourth left parasternal areas. When the murmur is heard best to the right of the sternum
      (Harvey’s sign), however, the clinician should be alerted to a possible aortic root etiology for the
      regurgitation. The murmur of mild aortic regurgitation is frequently quite faint and may be
      overlooked if the examiner does not listen with the patient sitting up and leaning forward, with
      the diaphragm of the stethoscope pressed firmly against the chest wall during held forced
      expiration. Pharmacological agents or maneuvers that increase or decrease the diastolic aortic
      left ventricular pressure gradient will increase or decrease the intensity of the regurgitant
      murmur. For example, prompt squatting or hand grip often elicits a faint aortic regurgitant
      murmur at the bedside, whereas inhalation of amyl nitrite will markedly decrease an easily heard
      aortic regurgitant murmur.

      In many patients, combined aortic stenosis and regurgitation are present when the deformed
      aortic valve is both obstructive and incompetent. In this situation, the classic to-fro murmur of
      aortic stenosis and regurgitation is present (Figure 18). Unlike a continuous murmur that reaches
      its peak intensity at about the time of S2, the to-fro murmur has two separate components that can
      be clearly distinguished by the presence of a silent period before the onset of the regurgitant

      Pulmonary regurgitation is most commonly found when severe pulmonary hypertension is
      present with dilation of the pulmonary artery. This type of pulmonary regurgitant murmur
      (Graham Steell’s murmur) is identical in contour and pitch to that of aortic regurgitation, both
      murmurs being produced by similar hemodynamics. Although these murmurs cannot be
      differentiated by their acoustic qualities, the Graham Steell’s murmur is almost always
      accompanied by physical findings of severe pulmonary hypertension.

Figure 18
During abnormal communication between high-pressure and low-pressure systems, large pressure gradient exists
throughout the cardiac cycle, producing continuous murmurs. A classic example is patent ductus arteriosus. At times, this
type of murmur is confused with a to-fro murmur, which is a combination of a systolic ejection murmur and the murmur of
semilunar valve incompetence. The classic example of to-fro murmur is aortic stenosis and regurgitation. The continuous
murmur builds to a crescendo around second heart sound (S 2) where as the to-fro murmur has two components, a mid-
systolic and early diastolic component with a silent period between the two murmurs.
Continuous murmurs. A continuous murmur                                           Table I
is defined as one that begins in systole and          Physiologic classifications of continuous
extends through S2 into part or all of diastole. It   murmurs
does not necessarily have to occupy the entire
cardiac cycle; thus a systolic murmur that
extends into diastole without stopping at S2 is       A     Continuous murmurs caused by rapid blood flow
                                                            1. Venous hum
considered to be continuous, even if it fades               2. Mammary souffle
away before the subsequent S1. Continuous                   3. Hemiangioma
                                                            4. Hyperthyroidism
murmurs can be congenital or acquired.                      5. Acute alcoholic hepatitis
Although it is beyond the scope of this lecture to          6. Hyperemia of neoplasm (hepatoma renal cell carcinoma,
                                                                 Paget’s disease)
detail the many conditions that may cause a           B.    Continuous murmurs caused by high-to-low pressure shunts
continuous murmur, a few of the more common                 1. Systemic artery to pulmonary artery (patent ductus
                                                                 arteriosus, aortopulmonary window, truncus arteriosus,
clinical conditions are reviewed. A more                         pulmonary atresia, anomalous left coronary,
complete physiologic classification of                           bronchiectasis, sequestration of the lung)
                                                            2. Systemic artery to right heart (ruptured sinus of valsalva,
continuous murmurs is provided in Table I.                       coronary artery fistula)
                                                            3. Left-to-right atrial shunting (Lutembacher’s syndrome,
                                                                 mitral atresia plus atrial septal defect)
The differential diagnosis of a continuous                  4. Venovenous shunts (anomalous pulmonary veins,
murmur should include the benign cervical                        portosystemic shunts)
                                                            5. Arteriovenous fistula (systemic or pulmonic)
venous hum heard commonly in children, in             C.    Continuous murmurs secondary to localized arterial
nearly all pregnant women, and in persons with              obstruction
                                                            1. Coarctation of the aorta
high cardiac output. This murmur is usually                 2. Branch pulmonary stenosis
poorly heard in the supine position, and its                3. Carotid occlusion
                                                            4. Ciliac mesenteric occlusion
                                                            5. Renal occlusion
                                                            6. Femoral occlusion
                                                            7. Coronary occlusion

                                             presence in an adult in this position strongly suggests
                                             a hyperdynamic circulatory rate. Its peak intensity is
                                             in the supraclavicular fossa just lateral to the
                                             sternocleidomastoid muscle and is usually more
                                             prominent on the right side, peaking in early diastole.
                                             A cervical venous hum can be terminated easily by
                                             digital compression of the JVP (Figure 19). Another
                                             benign continuous murmur is a mammary souffle,
                                             which occurs in 10% to 15% of pregnant women
                                             during the second and third trimesters and in early
                                             postpartum lactation. This murmur may be
                                             obliterated by firm pressure on the stethoscope or by
                                             digital pressure lateral to the site of auscultation.

                                             A patent ductus arteriosus is a classic example of a
                                             cardiovascular congenital anomaly in which there is
                                             shunting from a high-pressure systemic to the low-
                                             pressure pulmonary circulation, resulting in a large
                                             pressure gradient between the two circulations
                                             throughout the cardiac cycle. This murmur is heard
                                             best in the left infraclavicular area and the second left
intercostal space, and peaks in intensity at the time of S2.

Atriovenous fistulas between peripheral vessels produce a classic continuous murmur with
systolic accentuation caused by the shunting of blood at high flow rates from a high-pressure
artery into a low-pressure vein. This condition should always be considered as a potential cause
for heart failure. These murmurs are best heard at the site of the fistula and local compression on
the venous side decreases its intensity. Complete obliteration of the fistula abruptly terminates
the murmur.

Continuous murmurs in adults are also caused by severe localized arterial obstructions.
Although partially occluded arteries usually have only a delayed systolic murmur, this murmur
may be continuous if the obstruction is critical, and adequate collateral flow is not available.
Such murmurs are commonly heard directly over the carotid, subclavian, and femoral arteries.
Continuous murmurs caused by obstruction of the renal or mesenteric arteries can also be heard
by careful auscultation over the back or abdomen, respectively.

   1.        All of the following statements regarding cardiac murmurs are true but one:

             a. The regurgitant murmur of aortic regurgitation will increase in intensity with an
                abrupt squatting.
             b. The pansystolic murmur of tricuspid regurgitation will increase in intensity with
             c. The late systolic murmur of mitral valve prolapse will begin later in systole with
                the assumption of an upright posture.
             d. The systolic ejection murmur of severe calcific aortic stenosis may become nearly
                inaudible with congestive heart failure and low cardiac output.
             e. The continuous murmur of a patent ductus arteriosus peaks in intensity around the
                second heart sound while the to-fro murmur of aortic stenosis and aortic
                regurgitation is silent around the second heart sound.

   2.        All of the following statements regarding innocent murmurs are true but one:

             a. Innocent murmurs are always systolic ejection in nature.
             b. Innocent murmurs are frequently seen in “the company” of a physiologic S3 in
             c. Innocent murmurs are frequently introduced by a loud ejection sound.
             d. Innocent murmurs are usually grade 1 to grade 3 in intensity and vary from exam
                to exam as well as with changes in position.
             e. The functional systolic ejection murmurs of anemia or thyrotoxicosis are not
                considered innocent because of the altered physiologic state, even though there is
                no structural cardiac abnormality.

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