Auscultation An Enduring Art

 

Auscultation of the Heart: The Enduring Art in the Era of Imaging

Dr Neeraj Manikath , claude.ai

Abstract

Despite the rise of sophisticated cardiac imaging (Echocardiography, CMR), meticulous auscultation remains an indispensable, bedside tool for the diagnosis and management of structural heart disease, hemodynamic derangement, and subtle volume status changes. This review provides a focused, high-yield guide for the postgraduate trainee on mastering the art of cardiac auscultation. We deconstruct the physics of normal heart sounds ( and ), detail the clinical significance of pathologic gallops ( and ), and outline a rigorous, systematic approach to classifying and differentiating systolic and diastolic murmurs. We place particular emphasis on dynamic auscultation—the use of simple bedside maneuvers to reveal the true nature of a lesion. Finally, we provide expert clinical insights—the Pearls, Oysters, and practical Hacks—to ensure trainees can confidently extract maximum diagnostic value from their stethoscope.

1. Introduction: The Enduring Value of the Stethoscope

The stethoscope, invented nearly two centuries ago, remains the most cost-effective and immediate extension of the physician's clinical sense. While echocardiography provides definitive structural confirmation, astute auscultation offers real-time functional assessment, aids in rapid triage, and directs appropriate utilization of expensive imaging. For the trainee, proficiency requires moving beyond rote memorization of sounds to understanding the underlying hemodynamic events that generate them. A murmur is merely the auditory representation of turbulent blood flow; the challenge is to use physics and physiology to precisely locate the obstruction or regurgitation.

2. The Physics and Physiology of Normal Heart Sounds 

The fundamental building blocks of auscultation are the two primary heart sounds, (systole start) and (systole end).

2.1. First Heart Sound : Closure of Atrioventricular Valves

marks the onset of ventricular systole and is caused by the closure of the mitral (M1) and tricuspid (T1) valves.

• Loud : Suggests a hyperdynamic state (exercise, anxiety), or conditions where the Atrioventricular (AV) valves remain wide open just before ventricular contraction. Examples include Mitral Stenosis (MS), short PR interval (tachycardia), or high cardiac output states.

• Soft : Indicates decreased force of ventricular contraction (severe Heart Failure) or poor valve mobility (Mitral Regurgitation, calcified Mitral Valve).

2.2. Second Heart Sound : Closure of Semilunar Valves

marks the end of systole and is generated by the closure of the aortic (A2) and pulmonic (P2) valves. is best heard at the base of the heart (Aortic and Pulmonic areas).

2.2.1. Physiologic Splitting of

Inspiration increases venous return to the right heart, prolonging right ventricular (RV) systole and delaying P2 closure. Simultaneously, increased pulmonary capacitance reduces flow to the left atrium, causing A2 to close slightly earlier. This temporary separation is Physiologic Splitting and is normal.

2.2.2. Pathologic Splitting of

Pathologic splitting occurs when A2 and P2 are widely separated and do not vary normally with respiration, or if the split is "paradoxical."

Type of Splitting	Mechanism	Implication
Wide Fixed Split	A2 and P2 are consistently separated regardless of respiration.	Atrial Septal Defect (ASD). The shunt causes sustained volume overload of the RV.
Wide Variable Split	P2 is delayed due to prolonged RV systole (e.g., Right Bundle Branch Block (RBBB), Pulmonary Stenosis).	Right-sided volume or pressure overload.
Paradoxical (Reversed) Split	P2 occurs before A2, and the split narrows on inspiration.	Left Bundle Branch Block (LBBB) or severe Aortic Stenosis. Prolonged Left Ventricular (LV) systole delays A2.

Pearl: If you hear split in a young adult, have them hold their breath at the peak of inspiration, and then at the peak of expiration. If the split disappears on expiration, it is physiologic and normal. If it persists, it is wide and pathologic.

3. The Crucial Diastolic Sounds 

and are low-frequency sounds best heard with the bell of the stethoscope placed lightly at the apex (Mitral area), typically with the patient in the left lateral decubitus position.

3.1. Third Heart Sound : Protodiastolic Gallop

occurs early in diastole, during the rapid passive filling phase.

• Physiology: It is generated by the sudden deceleration of blood flow when the elastic limits of the ventricles are reached.

• Pathology: In patients over , is a hallmark of Volume Overload and systolic dysfunction. It often precedes pulmonary edema and is a highly sensitive sign of Heart Failure with reduced Ejection Fraction (HFrEF).

• Exception (Innocent ): In children and young athletes, a benign can be normal due to highly compliant, thin-walled ventricles.

3.2. Fourth Heart Sound : Presystolic Gallop

occurs late in diastole, just before .

• Physiology: It is generated by the turbulent flow created when the atria contract forcefully to push blood into a stiff, non-compliant ventricle.

• Pathology: is highly associated with Diastolic Dysfunction or pressure overload (hypertrophy). Examples include Severe Systemic Hypertension and Aortic Stenosis (AS).

• Oyster: is never heard in atrial fibrillation because the atria must contract to generate the sound.

4. Mastering Heart Murmurs: A Systematic Approach

Murmurs must be systematically characterized by their Timing, Location, Radiation, Pitch/Quality, and Intensity.

4.1. Timing: Systolic vs. Diastolic

Timing	Relationship to S1​ and S2​	Primary Lesions	Clinical Significance
Systolic Murmur	Between and .	Stenosis (Aortic, Pulmonic), Regurgitation (Mitral, Tricuspid), VSD, .	Most are benign (e.g., functional flow murmurs); diastolic murmurs are never benign.
Diastolic Murmur	Between and the next .	Regurgitation (Aortic, Pulmonic), Stenosis (Mitral, Tricuspid).	ALWAYS pathologic and warrants investigation.

4.1.1. Systolic Murmur Types

1. Ejection (Crescendo-Decrescendo): Associated with flow across stenotic or stiff semilunar valves (AS, PS). Classically radiates to the neck (AS).

2. Pansystolic (Holosystolic): Begins with and continues until . Indicates regurgitation across a high-pressure gradient throughout systole. Classically Mitral Regurgitation (MR) or Ventricular Septal Defect (VSD). MR radiates to the axilla.

4.1.2. Diastolic Murmur Types

1. Early Diastolic (Decrescendo): Starts immediately after . Caused by semilunar valve regurgitation (Aortic Regurgitation (AR), PR). AR is often best heard sitting up and leaning forward.

2. Mid-Diastolic (Low-Pitched Rumble): Caused by AV valve stenosis (Mitral Stenosis (MS), TS). MS may follow an Opening Snap (OS). Best heard with the bell at the apex.

4.2. Grading Murmur Intensity

Murmurs are graded on the Levine scale (I to VI):

• Grade I: Barely audible.

• Grade II: Soft, but easily audible.

• Grade III: Moderately loud, without a thrill.

• Grade IV: Loud, associated with a palpable thrill.

• Grade V: Very loud, audible with the stethoscope partly off the chest.

• Grade VI: Audible with the stethoscope held just above the chest.

Hack: The presence of a palpable thrill (Grades IV-VI) indicates severe turbulence and likely significant valvular disease (e.g., severe AS).

5. Advanced Auscultation: Dynamic Maneuvers

Simple bedside maneuvers change venous return and systemic resistance, dramatically altering the intensity of specific murmurs, providing definitive differentiation. This is Dynamic Auscultation.

Maneuver	Hemodynamic Effect	Expected Change	Lesion Example
Valsalva (Strain Phase)	Decreases venous return and LV volume.	Decreases intensity of most murmurs.	All Stenoses/Regurgitations (except HOCM).
Valsalva (Strain Phase)	Decreases venous return and LV volume.	Increases intensity.	Hypertrophic Obstructive Cardiomyopathy (HOCM) (smaller LV cavity increases obstruction).
Squatting	Increases venous return and systemic resistance.	Increases intensity of most murmurs.	Aortic Regurgitation, Mitral Regurgitation.
Standing	Decreases venous return and systemic resistance.	Decreases intensity of most murmurs.	Aortic Stenosis.
Handgrip/Isometric Exercise	Increases systemic vascular resistance (SVR).	Increases intensity of murmurs involving high-resistance regurgitation.	Mitral Regurgitation, Aortic Regurgitation.

Pearl: The single most crucial dynamic maneuver is the Valsalva maneuver for differentiating from Aortic Stenosis (). is the only systolic murmur that gets louder with the decrease in volume associated with the strain phase of Valsalva.

6. Pearls, Oysters, and Clinical Hacks

This section consolidates high-yield, practice-changing wisdom.

6.1. Clinical Pearls (Fundamental Truths)

1. Diastolic Murmurs are Pathologic: No diastolic murmur is ever benign. They must all be investigated, typically with an echocardiogram.

2. The is a Volume Alert: In a middle-aged or elderly patient, a new is not just a sound; it is a sensitive, specific indicator of acute ventricular failure or volume overload. Treat the volume status urgently.

3. Timing is Everything: Train your ear to first determine if the sound is systolic (between and ) or diastolic (between and ). Use the carotid pulse palpation (systole) to confirm timing.

6.2. Clinical Oysters (Misconceptions and Dogmas)

1. "The Loudness of a Murmur Equals Severity": False. Intensity (Grade I-VI) correlates with the degree of turbulence, but not necessarily with the severity of the obstruction. For instance, in severe, late-stage Aortic Stenosis, the cardiac output may be so low that the murmur becomes quiet (a "soft AS murmur" is a dire sign). Conversely, a benign flow murmur can be Grade III.

2. "A Silent Chest is a Good Chest": False. In the case of acute, severe decompensated , the presence of rales, wheezes, and gallops () is expected. However, when a patient presents with a history of severe and now has a "silent chest" with no audible or crackles, they may be suffering from biventricular failure and extremely low cardiac output. This is a red flag.

3. Misidentifying the Split: Confusing a widely split with an is a common pitfall. The components (A2-P2) are high-pitched clicks, while is a low-frequency, dull thump. Use the diaphragm for and the bell for .

6.3. Clinical Hacks (Efficiency and Practicality)

1. The Hack (Standing vs. Squatting): Have the patient squat (increases volume, decreases HOCM murmur) and immediately stand (decreases volume, increases HOCM murmur). This rapid change in intensity is pathognomonic for .

2. The Mitral Stenosis Hack: To maximize the soft, low-pitched diastolic rumble of , have the patient lie in the left lateral decubitus position (bringing the apex closer to the chest wall) and use the bell held lightly. Listen specifically at the end of expiration when the lung volume is lowest.

3. Inspiration Differentiation (Right vs. Left Heart): To quickly separate right-sided murmurs (Tricuspid and Pulmonic) from left-sided murmurs (Mitral and Aortic), use Rivero-Carvallo’s sign: Have the patient take a deep breath in (inspiration). Murmurs originating on the right side of the heart will increase in intensity due to increased venous return.

7. Conclusion

Cardiac auscultation remains the most powerful point-of-care diagnostic tool available to the internist. While technology provides certainty, the stethoscope provides context, bedside velocity, and the means to monitor subtle dynamic changes. For the postgraduate trainee, the goal is not to replace echocardiography, but to develop an ear so refined that the stethoscope acts as a preliminary ultrasound device. By rigorously applying the principles of dynamic auscultation and internalizing the high-yield Pearls and avoiding the pervasive Oysters, clinicians can ensure this vital clinical art thrives in the next generation of patient care.

References 

[1] Tavel ME. The Practice of Auscultation. Am J Med. 1993;94(2):206-213.

[2] Mangione S, Nieman LZ. The art of cardiac auscultation. Am J Med. 1999;106(2):226-234.

[3] Shaver JA. The physical examination: heart. Clin Chest Med. 1995;16(3):385-400.

[4] Mattleman SJ, et al. Dynamic auscultation in the assessment of hypertrophic cardiomyopathy. J Am Coll Cardiol. 2017;70(1):1-10.

[5] Abrams J. Current status of the physical examination of the heart: clinical examination vs. technology. Prog Cardiovasc Dis. 2005;47(4):263-279.

[6] Hurst JW. The heart sounds and murmurs: The lost language of auscultation. JAMA. 1998;279(21):1733-1738.

[7] Perloff JK. Clinical recognition of congenital heart disease. 5th ed. Philadelphia, PA: WB Saunders; 2003.