Approach to Murmurs

Overview

Encountering an added sound while auscultating the chest can be exciting and confusing. You need to determine:

• Whether it is a murmur (occurring due to altered blood flow) or an additional heart sound or extra cardiac in origin.
• Is the sound pathological? Diastolic murmurs are never benign and systolic murmurs that radiate and have a thrill are always pathological

Once you have ascertained the above then try to describe the murmur as done below:

• How to assess a murmur. To further describe the murmur you need to determine its:
  • When does it occur?
  • How loud is it? (Grading)
  • Location
  • Does it radiate
  • Pitch and quality
• Grading of murmurs
  • Grade 1 – Very soft; only heard when you listen for awhile
  • Grade 2 – Soft but detectable immediately
  • Grade 3 – Clearly audible; no palpable thrill
  • Grade 4 – Loud with associated thrill
  • Grade 5 – Very loud and audible with stethoscope only partially touching chest
  • Grade 6 – Heard without stethoscope
  Diastolic murmurs are graded to 4; Systolic to grade 6
• Features of a benign murmur
  • Soft
  • Mid-systolic
  • Heard at left sternal edge
  • No radiation
  • No other cardiac abnormalities

Extra cardiac sounds don’t follow the predictable pattern of the cardiac cycle and can be altered by changes in posture and respiration.

Aortic Regurgitation

This is the retrograde flow of the blood from the aorta into the left ventricle during diastole due to dysfunction of the aortic valve

• Etiology
  • Acute
    • Infective endocarditis
    • Traumatic/ atraumatic aortic rupture
    • Iatrogenic – percutaneous aortic balloon valvuloplasty, prosthetic valve dysfunction, and perivalvular leak or dehiscence of a prosthetic valve
    • Medications that increase cardiac contraction hence increased stress on aortic valve such as dopamine agonists (bromocriptine)
  • Chronic causes
    • Congenital – unicuspid, bicuspid (most common) and quadricuspid valves
    • Rheumatic heart disease (Most common cause)
    • Myxomatous valve degeneration
    • Senile valvular calcifications
    • Aortic dilation causes
      • Marfan syndrome
      • Ehler-Danlos syndrome
      • Aneurysm
      • Aortic dissection
      • Syphilis
      • Trauma
      • Systemic hypertension
      • Ankylosing spondylitis
      • Age related changes
  • Other
    • Antiphospholipid syndrome
    • Systemic lupus erythematosus
    • Rheumatoid arthritis
    • Reiter syndrome
    • Psoriatic arthritis
    • Takayasu vasculitis
    • Behcet disease
    Correlations have also been made between AR and Turner Syndrome
• Pathophysiology
  • Acute AR
    • Backward flow of blood from the aorta into the left ventricle increases the end diastolic volume faster than the left ventricle can stretch to accommodate the increased volume causing increased left ventricular diastolic pressures
    • This leads to increase in pressure in the left atrium and pulmonary vasculature causing pulmonary edema (they develop dyspnea), altering coronary blood flow ( causing myocardial ischemia) and reducing stroke volume
  • Chronic AR
    • The left ventricle compensates by enlarging (sacromeres are laid in series)
    • Compensatory mechanisms fail causing a drop in ventricular wall compliance
• History
  • Often asymptomatic
  • Cough
  • Palpitations
  • Dyspnea on exertion
  • Chest pain
  Acute cases may present in cardiogenic shock Chronic cases may present with the following additional features:
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
  • Syncope
• Physical examination There are manoeuvres to help better appreciate the murmur:
  • Ask patient to sit forward and auscultate over the left lower sternal border (3rd – 4th ICS) with the diaphragm of your stethoscope during expiration – Early diastolic murmur
  A murmur at the right sternal border is associated more often with aortic dissection than it is with any other cause of AR.Acute AR
  • Hypotension
  • Cyanosis
  • Tachycardia (to compensate for reduced stroke volume)
  • Arterial pulsus alterans
  • Normal or elevated pulse pressure
  • Normal apical impulse
  • Diminished S1
  • S3 sound – indicates patient has developed heart failure
  Chronic AR
  • Widened pulse pressure
  • Displaced apical beat – lateral or inferior
  • Diminished S1
  • Soft S2
  If the pulse pressure is noticed to become more narrow and the patient has an S3, this may be a sign the patient has developed heart failure.Eponymous signs of AR
  • de Musset’ sign – Head nodding with pulse
  • Muller’s sign – Systolic pulsations of uvula
  • Corrigan’s sign – Visible carotid pulsations
  • Quincke’s sign – Capillary nail bed pulsation in finger with light compression of finger nail
  • Traube sign – Pistol shot sound over femoral arteries
  • Duroziez sign – Systolic murmur over the femoral artery with proximal compression of the artery, and diastolic murmur over the femoral artery with distal compression of the artery
  • Becker sign – Visible systolic pulsations of the retinal arterioles
  • Hill sign – Popliteal cuff systolic blood pressure 40 mm Hg higher than brachial cuff systolic blood pressure
  • Pulsus bisferiens -A biphasic pulse with two systolic peaks seen on pressure tracings
  • Waterhammer Pulse – Peripheral arterial pulses are rapidly dissipated or “bounding”. This finding can be accentuated by raising the extremities.
• Austin Flint Murmur
  • Regurgitant jet of the aortic regurgitation causes premature closing of the mitral valve
  • Mid-diastolic
  • Low-pitched

Aortic Stenosis

Common valvular disorder that causes left ventricular outflow obstruction. Common in the elderly.

• Etiology
  • Congenital
    • Congenital aortic stenosis – presents in infancy
    • Bicuspid aortic valve – superimposed calcification; presents in early to mid adulthood
  • Acquired
    • Rheumatic valve disease
    • Senile degenerative aortic stenosis
    • Alkaptonuria
    • Systemic lupus erythematosus
    • Ochronosis
    • Irradiation
    • Homozygous type II lipoproteinemia
    • Fabry disease
    • End-stage renal disease
• Pathophysiology
  • Left ventricular (LV) obstruction caused by the stenosis of the valve increases LV systolic pressure.
  • It also results in increased LV ejection time (LVET), decreased aortic pressure, and increased LV end-diastolic pressure.
  • The increased afterload, in addition, to an increase in LV volume overload, leads to an increase in LV mass, ultimately leading to LV dysfunction and failure.
  • Myocardial oxygen consumption increases with increased LV systolic pressure, LV mass, and LVET, while myocardial perfusion time decreases with increased LVET. Hence, LV function further deteriorates with increased myocardial oxygen consumption and decreased myocardial oxygen supply
• History Asymptomatic stage (10-20 years) Classic triad of:
  • Chest pain – anginal in nature
  • Exertional dyspnea
  • Syncope
  As well as heart failure symptoms (ie, paroxysmal nocturnal dyspnea, orthopnea, dyspnea on exertion, and shortness of breath). Extra-cardiac symptoms:
  • GI bleeding – seen in severe aortic stenosis and is often associated with angiodysplasia or other vascular malformations
  • Emboli from calcific deposits on aortic valve to brain, kidney.
  • Features of infective endocarditis
• Physical examination
  • Pulsus parvus et tardus – A slow-rising, late-peaking, and a low-amplitude carotid impulse
  • Mid-systolic ejection murmur, heard best over the right second intercostal space, with radiation into the right neck
  • Second heart sound may lack a split and can be heard as a single sound during inspiration
  In elderly persons with calcific aortic stenosis, however, the murmur may be more prominent at the apex, because of radiation of its high-frequency components (Gallavardin phenomenon). This may lead to its misinterpretation as a murmur of mitral regurgitation.

Mitral Regurgitation

This is the reversal of blood flow from the left ventricle to the left atrium in the systolic phase of the cardiac cycle

• Etiology
  • Rupture of the chord/papillary muscle from:
    • Trauma; direct, drug induced, radiation induced
    • ST-segment elevation myocardial infarction (STEMI)
  • Infection/inflammation
    • Rheumatic heart disease – most common cause in developing countries
    • Infective endocarditis
  • Causes of left ventricular structural change
    • Ischemic heart disease
    • Cardiomyopathies
    • Atrial fibrillation
    • Congestive heart failure
  • Degenerative mitral valves such as myxomatous degeneration – most common cause in developed countries
  • Hereditary connective tissue disorders – Marfan syndrome, Ehler’s Danlos Syndrome, Osteogenesis Imperfects
• Pathophysiology Can be divided into acute vs chronic or primary vs secondary Acute MR
  • Acute mitral regurgitation causes a rapid rise in left atrial pressure (because left atrial compliance is normal) and marked symptomatic deterioration.
  • Severe cases can cause heart failure without left ventricular dilation
  Chronic MR
  • There is gradual dilatation of the LA with little increase in pressure and therefore relatively few symptoms.
  • The LV dilates slowly and the left ventricular diastolic and left atrial pressures gradually increase as a result of chronic volume overload of the LV.
  • Elevation in left atrial pressures can result in left atrial enlargement, atrial fibrillation, pulmonary congestion, and pulmonary hypertension.
  • Ventricular dilation causes dysfunction and heart failure
  Primary MR
  • Pathological disruption in the integrity of the mitral valve apparatus itself in many ways:
    • Myxomatous degeneration causing lengthened and redundant mitral flaps
    • Progressive thickening of mitral leaflets from RHD, IE, drugs, radiation causing restricted movement
    • Progressive calcific degeneration seen in old age
    • Rupture of a cord or perforation of a leaflet
  Secondary MR
  • Pathology due to structural changes in the left ventricle (LV), causing failure of coaptation of mitral leaflets due to annular dilatation
  • Causes enumerated under etiology
• Carpentier’s Classification
  • Type I – normal leaflet motion with normal coaptation (leaflet perforation, cleft)
  • Type II – abnormal coaptation with excessive leaflet motion (either due to excess of tissue/excess of motion- mitral valve prolapse)
  • Type IIIa – abnormal apposition of leaflets due to restricted leaflet motion both in systole and diastole (mostly from organic leaflet issues such as rheumatic heart disease)
  • Type IIIb – abnormal apposition of leaflets due to restricted leaflet motion in systole (from LV remodeling)
• History
  • Prior history of:
    • Prior bacterial or viral infections
    • Rheumatic fever
    • Trauma
    • Ischemic events
    • Invasive cardiac/noncardiac procedures
    • Family history
  • Fatigue
  • Dyspnea
  • Exercise intolerance
  • Orthopnea
  • Paroxysmal nocturnal dyspnea (PND)
  • Progressive signs of congestive heart failure (CHF)
  • Palpitations (from associated arrhythmias)
  Chronic mitral regurgitation produces a symptom complex that is similar to that of mitral stenosis but sudden-onset mitral regurgitation usually presents with acute pulmonary oedema. Hereditary mitral valve prolapse is usually associated with autonomic symptoms:
  • Anxiety
  • Panic attacks
  • Arrhythmias
  • Exercise intolerance
  • Palpitations
  • Atypical chest pain
  • Fatigue
  • Orthostasis
  • Syncope or presyncope
  • Neuropsychiatric symptoms
• Physical examination General examination:
  • Low normal blood pressure
  • Asthenic body habitus
  • Low body weight or body mass index (BMI)
  • Lower waist-to-hip ratio
  • Straight-back syndrome
  • Scoliosis or kyphosis
  • Pectus excavatum
  • Hypermobility of the joints
  • Arm span greater than height (which may be indicative of Marfan syndrome)
  Systemic examination:
  • Hyperactive eprecordium due to LV volume overload
  • Displaced apex beat due to left ventricular dilation
  • Characteristic holosystolic murmur present at the apex and radiating to the left axilla; may be associated with a thrill
  • Loud S3 sound due to increased blood flow through mitral valve
  • In mitral valve prolapse you have – Mid to late systolic click which may or may not be followed by a high-pitched, mid-to-late systolic murmur at the cardiac apex.

Mitral Stenosis

Form of valvular heart disease characterized by the narrowing of the mitral valve orifice.

• Etiology
  • Rheumatic fever.
  • Calcification of the mitral valve leaflets
  • Congenital heart disease
    • The association of atrial septal defect with rheumatic mitral stenosis is called Lutembacher Syndrome
  • Infective endocarditis
  • Mitral annular calcification
  • Endomyocardial fibroelastosis
  • Malignant carcinoid syndrome
  • Systemic lupus erythematosus
  • Whipple disease
  • Fabry disease
  • Rheumatoid arthritis.
• Pathophysiology
  • Normal mitral valve area is 4-6cm2. Symptoms start when it reduced below 2-2.5 cm2. Severe mitral stenosis occurs with a valve area of less than 1 cm2.
  • As the mitral valve narrows, a pressure gradient is formed between the left atrium and left ventricle requiring more atrial contractions (atrial kick) to push blood into the left ventricle.
  • This increased LA pressure causes pulmonary hypertension – pulmonary venous congestion – dyspnea
  • Pulmonary hypertension leads to right ventricular hypertrophy and dilatation, tricuspid regurgitation and right heart failure.
  • Sustained elevated pressures in the LA causes enlargement of the LA and subsequent atrial fibrillation which reduces blood flow from the LA to LV causing a decrease in cardiac output and eventually heart failure.
• History
  • Asymptomatic (presents 20-40 years after rheumatic fever bout) but can be triggered by:
    • Fever
    • Severe anemia
    • Thyrotoxicosis
    • Exercise
    • Excitement
    • Pregnancy
    • Atrial fibrillation
  • Palpitations
  • Chest pain
  • Fatigue
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
  • Hemoptysis
  • Thromboembolism from the Afib
  • Features of right sided heart failure: ascites, edema, and hepatomegaly
• Physical examination
  • Mitral facies
    • Pinkish-purple patches on the cheeks
  • Signs of right-sided heart failure – jugular venous distension, parasternal heave, hepatomegaly, ascites
  • Apical impulse may be laterally displaced
  • Left parasternal heave (right ventricular hypertrophy due to pulmonary hypertension)
  • Loud S1 due to forceful closing of the valve
  • The P2 (pulmonic) component of the second heart sound (S2) will be loud if severe pulmonary hypertension is due to mitral stenosis.
  • An opening snap (OS) will be heard due to the forceful opening of the mitral valve when the pressure in the left atrium is greater than the pressure in the left ventricle.
  • This is followed by a mid-diastolic murmur which is low and rumbling in character; best heard over the apex in the left lateral position with the bell of your stethoscope
  Graham Steell murmur: soft, blowing, decrescendo early diastolic murmur of pulmonary incompetence caused by pulmonary hypertension not caused by intrinsic pulmonary valvular defect but by mitral stenosis.