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Approach to the Patient with a Heart Murmur

Chapter 44 | Part 2: Cardinal Manifestations and Presentation of Diseases · Part 2 – Cardinal Manifestations & Presentation · Chapter 44

Key Clinical Points

  1. Timing is the primary step in identification: Systolic (S1 to S2), Diastolic (S2 to S1), or Continuous (systole to diastole).
  2. Murmur intensity is graded 1–6; Grade ≥ 3 typically signifies important structural heart disease and high blood flow velocity.
  3. Gallavardin effect: Aortic stenosis (AS) murmur becomes higher-pitched at the apex due to radiation.
  4. Carvallo's sign: Tricuspid regurgitation (TR) murmur intensity increases with inspiration.
  5. Acute severe mitral regurgitation (MR) is a medical emergency; the murmur may be absent in 50% of cases.
  6. VSD murmurs change from holosystolic to early systolic as pulmonary hypertension develops and right ventricular pressure rises.
  7. MVP click moves closer to S1 with standing (decreased preload) and away with squatting (increased preload).
  8. Austin Flint murmur: A lower-pitched mid to late diastolic murmur at the apex in severe aortic regurgitation (AR).
  9. Graham Steell murmur: A decrescendo early to mid-diastolic murmur of pulmonic regurgitation (PR) best heard at the second left interspace.
  10. Continuous murmurs indicate a persistent pressure gradient between two chambers or vessels during both systole and diastole (e.g., PDA).

1. DEFINITION & OVERVIEW

• Definition: Heart murmurs are caused by audible vibrations due to increased turbulence from accelerated blood flow through normal or abnormal orifices, flow through a narrowed or irregular orifice into a dilated vessel or chamber, or backward flow through an incompetent valve, ventricular septal defect (VSD), or patent ductus arteriosus (PDA). • Timing: The primary step in identification. ◦ Systolic: Begin with or after S1 and terminate at or before S2. ◦ Diastolic: Begin with or after S2 and end at or before the subsequent S1. ◦ Continuous: Not confined to one phase; begin in early systole and proceed through S2 into all or part of diastole. • Duration: Determined by the length of time over which a pressure difference exists between two cardiac chambers (LV/Aorta, RV/PA) or great vessels. • Configuration: ◦ Crescendo: Increasing intensity. ◦ Decrescendo: Decreasing intensity (e.g., chronic AR). ◦ Crescendo-decrescendo: Diamond shape (e.g., AS). ◦ Plateau: Constant intensity (e.g., chronic MR). • Intensity: Graded on a scale of 1–6. ◦ Grade 1: Very soft, heard only with great effort. ◦ Grade 2: Easily heard but not particularly loud. ◦ Grade 3: Loud but not accompanied by palpable thrill. ◦ Grade 4: Very loud and accompanied by a thrill. ◦ Grade 5: Loud enough to be heard with only the edge of the stethoscope touching the chest. ◦ Grade 6: Loud enough to be heard with the stethoscope slightly off the chest. ◦ Clinical Note: Murmurs of grade 3 or greater usually signify important structural heart disease and high blood flow velocity. Small, restrictive VSDs are often Grade ≥ 4 due to high velocity; low-velocity events (e.g., ASD) are usually silent. • Location & Radiation: Identification of location/radiation facilitates accurate identification of the specific valve involved.

2. ETIOLOGY & PATHOPHYSIOLOGY

• Mechanism: Defined by the pressure gradient between chambers and the geometry of the orifice. • Systler Murmurs (Table 44-1): ◦ Early Systolic: Acute MR, VSD, Muscular, Nonrestrictive with pulmonary hypertension, TR with normal pulmonary artery pressure. ◦ Midsystolic: Aortic stenosis (AS) [Obstructive: supravalvular, valvular, subvalvular; Increased flow: hyperkinetic states, AR, complete heart block], Pulmonic stenosis (PS) [Obstructive: supravalvular, valvular, subvalvular; Increased flow, left-to-right shunt (e.g., ASD)]. ◦ Late Systolic: Mitral valve prolapse (MVP), acute myocardial ischemia, Tricuspid valve prolapse (TVP). ◦ Holosystolic: Atrioventricular valve regurgitation (MR, TR), Left-to-right shunt at ventricular level (VSD). • Diastolic Murmurs: ◦ Early Diastolic: Aortic regurgitation (AR) [Valvular: congenital, rheumatic, endocarditis, prolapse, trauma, post-valvotomy; Dilation of valve ring: dissection, hypertension, etc.], Pulmonic regurgitation (PR) [Valvular: post-valvotomy, endocarditis, rheumatic fever, carcinoid; Dilation of valve ring: pulmonary hypertension, Marfan syndrome; Congenital]. ◦ Mid-Diastolic: Mitral stenosis (MS), Carey-Coombs murmur (acute rheumatic fever), Increased flow across nonstenotic mitral valve (MR, VSD, PDA, high-output states, complete heart block), Tricuspid stenosis, increased flow across tricuspid valve (TR, ASD, anomalous pulmonary venous return), Atrial tumors (myxoma), Severe AR (Austin Flint murmur). • Continuous Murmurs: ◦ Patent ductus arteriosus (PDA), Proximal coronary artery stenosis, Coronary AV fistula, Mammary souffle of pregnancy, Ruptured sinus of Valsalva aneurysm, Pulmonary artery branch stenosis, Aortic septal defect, Bronchial collateral circulation, Cervical venous hum, Small (restrictive) ASD with MS, Anomalous left coronary artery, Intercostal AV fistula.

3. CLINICAL FEATURES

• Systolic Murmurs: ◦ Early Systolic: Begin with S1; end before S2. (e.g., Acute MR, VSD). ◦ Midsystolic: Crescendo-decrescendo; AS is most common. → Gallavardin effect: AS murmur becomes higher-pitched at the apex due to radiation. ◦ Late Systolic: Best heard at apex; often MVP (nonejection click followed by mid-late systolic murmur). ◦ Holosystolic: MR (best at apex → axilla), TR (best at lower left sternal border, increases with inspiration/Carvallo's sign), VSD (mid to lower left sternal border with palpable thrill). • Diastolic Murmurs: ◦ Early Diastolic: AR (high-pitched, blowing, decrescendo); PR (Graham Steell murmur; decrescendo early to mid-diastolic). ◦ Mid-Diastolic: MS (low-pitched, best heard with bell in left lateral decubitus). → Austin Flint murmur: Lower-pitched mid to late diastolic murmur at apex in severe AR. • Continuous Murmurs: ◦ PDA: Best heard lateral to upper left sternal border. ◦ Ruptured sinus of Valsalva: Continuous murmur of abrupt onset at upper right sternal border. ◦ Cervical venous hum: Systolic and diastolic components (to-fro murmur) → high-grade carotid artery stenosis. • Physical Exam Maneuvers: ◦ Standing: Decreases preload; MVP click moves closer to S1; AS/HOCM intensity increases. ◦ Squatting: Increases preload/afterload; MVP click moves away from S1; duration of murmur shortens. ◦ Valsalva: Decreases preload/afterl; AS intensity increases; MR remains constant. ◦ Carotid Pulse: Parvus et tardus (small, delayed upstroke) → severe AS; Bisferiens pulse → mid-systolic closure of aortic valve. ◦ Jugular Venous Pulse: c-v waves in TR; prominent c-v wave with sharp Y descent in MR.

4. DIFFERENTIAL DIAGNOSIS

• Systolic Murmur Differential: ◦ AS vs. MR: AS increases with maneuvers increasing afterload (squatting); MR intensity varies with afterload (decreases with vasodilators). ◦ HOCM: Increases with maneuvers that increase obstruction (standing, Valsalva). ◦ MVP: Click moves closer to S1 with standing; away with squat/Valsalva. • Diastolic Murmur Differential: ◦ AR vs. PR: AR radiates along left sternal border (primary) or right sternal border (root); PR intensity increases with inspiration. ◦ MS vs. Austin Flint: Austin Flint lacks opening snap and responds to vasodilator challenge. • Continuous Murmur Differential: ◦ PDA: Best heard lateral to upper left sternal border. ◦ Ruptured sinus of Valsalva: Upper right sternal border. ◦ Cervical bruit: Indicates high-grade carotid artery stenosis.

5. DIAGNOSTIC APPROACH

  1. Initial Assessment: Identify murmur timing, intensity (1–6), and response to maneuvers (Standing, Squatting, Valsalva).
  2. Holosystolic Murmur Differentiation (Flowchart 44-5): ◦ Identify Holosystolic Murmur → ◦ If [Non-ejection click, response to Valsalva, or stand-guard] → Primary Mitral Regurgitation. ◦ If [S_3, S_4, displaced/enlarged LV, or apical impulse] → Secondary Mitral Regurgitation. ◦ If [Normal P_2] → Primary or Secondary Tricuspid Regurgitation. ◦ If [Narrow splitting of S_2, loud/palpable P_2, prominent right anterior-left inferior] → Secondary Tricuspid Regurgitation due to severe pulmonary hypertension. ◦ If [Favors ventricular septal defect] → Ventricular Septal Defect.
  3. Specific Diagnostic Clues: ◦ Gallavardin effect: AS murmur radiates to apex and becomes higher-pitched. ◦ Carvallo's sign: TR intensity increases with inspiration. ◦ Austin Flint murmur: Diastolic rumble at apex in severe AR. ◦ Graham Steell murmur: Diastolic murmur of PR. ◦ Parvus et tardus: Small and delayed carotid upstroke → severe AS. ◦ Bisferiens pulse: Mid-systolic closure of aortic valve. ◦ Opening snap: Present in MS, absent in MR. ◦ Nonection click: Present in MVP, absent in HOCM.
  4. S2 Splitting Dynamics (Figure 44-8): ◦ Wide splitting: Delay in P_2 (e.g., RVB) or early closure of A_2 (e.g., severe MR). ◦ Reversed splitting: Delay in A_2 (paradoxical movement; with inspiration P_2 moves toward A_2, interval narrows). ◦ Narrow splitting: Pulmonary hypertension (both A_2 and P_2 heard during expiration at narrow interval).

6. MANAGEMENT & TREATMENT

  1. Acute/Post-MI Complications: ◦ Acute MR (Papillary muscle rupture): Medical emergency; requires medical stabilization and prompt referral for surgical repair.
  2. Infective Endocarditis / Rheumatic Fever: ◦ Initiate antibiotic use or prophylaxis as indicated.
  3. General Management: ◦ Restriction of physical activity as indicated. ◦ Family screening as indicated.
  4. Surgical/Procedural Planning: ◦ Use TTE to assess suitability for valve repair; evaluate lesion severity, ventricular size, and systolic function.

7. PROGNOSIS & COMPLICATIONS

• Acute MR (Papillary Muscle Rupture): ◦ Clinical Presentation: Chest pain, hypotension, pulmonary edema; murmur may be absent in 50% of cases. • VSD Progression: ◦ Murmur becomes limited to first portion of systole as pulmonary hypertension develops → rise in right ventricular pressure. • Chronic AR: ◦ Signs: Wide pulse pressure, Corrigan's pulse (water-hammer), Quincke's pulsations. ◦ Acute vs. Chronic: Acute AR is shorter duration and lower pitched than chronic AR. • Chronic MR: ◦ "MR begets MR": Enlargement of left atrium leads to further stretching of the annulus and more MR. ◦ Findings: Enlargement and leftward displacement of LV apex beat.

8. SPECIAL CONSIDERATIONS

• Pediatric Considerations: ◦ Still's murmur: Benign grade 2, vibratory or musical midsystolic murmur at mid/lower left sternal border. ◦ Congenital Valvular AS: Early ejection sound (click) usually audible; signifies flexible, noncalcified bicuspid valve. • Pregnancy Considerations: ◦ Mammary souffle of pregnancy: Continuous murmur. ◦ High-flow states (Pregnancy, hyperthyroidism, anemia): Often present with grade 1 or 2 midsystolic murmurs at the left sternal border.

9. KEY PEARLS & CLINICAL TRAPS

• Acute MR is a medical emergency; murmur may be absent in 50% of cases. • VSD murmur changes from holosystolic to early systolic as pulmonary hypertension develops. • Austin Flint murmur distinguished from MS by absence of opening snap and response to vasodilator challenge. • Gallavardin effect: AS murmur radiates to apex and becomes higher-pitched. • Carvallo's sign: TR intensity increases with inspiration. • Continuous murmurs imply a pressure gradient between two chambers/vessels during both systole and diastole. • S2 Splitting: Narrow splitting of S_2 → pulmonary hypertension; Reversed S_2 → aortic stenosis + pulmonary hypertension.

Reference Tables

TABLE 44-1 Principal Causes of Heart Murmurs Systolic Murmurs Early systolic

Harrison's 22e, p.284

Early systolic
Mitral
Acute MR
VSD
Muscular
Nonrestrictive with pulmonary hypertension
Tricuspid
TR with normal pulmonary artery pressure
Midsystolic
Aortic
Obstructive
Supravalvular–supravalvular AS, coarctation of the aorta
Valvular–AS and aortic sclerosis
Subvalvular–discrete, tunnel or HOCM
Increased flow, hyperkinetic states, AR, complete heart block
Dilation of ascending aorta, atheroma, aortitis
Pulmonary
Obstructive
Supravalvular–pulmonary artery stenosis
Valvular–pulmonic valve stenosis
Subvalvular–infundibular stenosis (dynamic)
Increased flow, hyperkinetic states, left-to-right shunt (e.g., ASD)
Dilation of pulmonary artery
Late systolic
Mitral
MVP, acute myocardial ischemia
Tricuspid
TVP
Holosystolic
Atrioventricular valve regurgitation (MR, TR)
Left-to-right shunt at ventricular level (VSD)
Early Diastolic Murmurs
AR
Valvular: congenital (bicuspid valve), rheumatic deformity, endocarditis,
prolapse, trauma, post-valvotomy
Dilation of valve ring: aortic dissection, annuloaortic ectasia, medial
degeneration, hypertension, ankylosing spondylitis
Widening of commissures: syphilis
Pulmonic regurgitation
Valvular: post-valvotomy, endocarditis, rheumatic fever, carcinoid
Dilation of valve ring: pulmonary hypertension; Marfan syndrome
Congenital: isolated or associated with tetralogy of Fallot, VSD, pulmonic stenosis
Mid-Diastolic Murmurs
Mitral
MS
Carey-Coombs murmur (mid-diastolic apical murmur in acute rheumatic fever)
Increased flow across nonstenotic mitral valve (e.g., MR, VSD, PDA,
high-output states, and complete heart block)
Tricuspid
Tricuspid stenosis
Increased flow across nonstenotic tricuspid valve (e.g., TR, ASD, and
anomalous pulmonary venous return)
Left and right atrial tumors (myxoma)
Severe AR (Austin Flint murmur)
Continuous Murmurs
Patent ductus arteriosus Proximal coronary artery stenosis
Coronary AV fistula Mammary souffle of pregnancy
Ruptured sinus of Valsalva aneurysm Pulmonary artery branch stenosis
Aortic septal defect Bronchial collateral circulation
Cervical venous hum Small (restrictive) ASD with MS
Anomalous left coronary artery Intercostal AV fistula

TABLE 44-2 Dynamic Auscultation: Bedside Maneuvers That Can Be Used to Change the Intensity of Cardiac Murmurs (See…

Harrison's 22e, p.289

    1. Respiration
      2. Isometric exercise (handgrip)
      3. Transient arterial occlusion
      4. Pharmacologic manipulation of preload and/or afterload
      5. Valsalva maneuver
      6. Rapid standing/squatting
      7. Passive leg raising
      8. Post-premature beat