Second heart sound, it's complications and significance

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second heart sound S2 aortic pulmonary component splitting diagram

This diagnostic graphic displays cardiac acoustic data from a patient with Atrial Septal Defect (ASD). The visualization consists of four vertically aligned panels spanning a 0.7-second time frame. The top two panels show successive Phonocardiogram (PCG) waveforms (PCG1 and PCG2), identifying the first heart sound (S1) at approximately 0.05s and a clearly split second heart sound (S2) between 0.3s and 0.4s. The S2 split is highlighted with pink circles, indicating the asynchronous closure of the aortic and pulmonary valves. The third panel, labeled 'Murmurgram,' represents the subtraction of the two PCG cycles, revealing high-amplitude signal activity in the systolic interval between S1 and S2, which corresponds to a mid-systolic murmur. The bottom panel is a Cyclic Spectral Profile (CSP) or spectrogram, illustrating frequency components of the heart sounds and murmur. The murmur exhibits frequency peaks reaching approximately 400-600 Hz. This dataset serves as an educational tool for identifying the fixed splitting of S2 and the associated systolic murmur characteristic of ASD.

This physiological waveform diagram displays a simultaneous recording of three cardiac parameters used for assessing cardiovascular hemodynamics. The top trace is an Electrocardiogram (ECG) showing standard QRS complexes representing ventricular depolarization. The middle trace is a Phonocardiogram (PCG) capturing acoustic vibrations of heart sounds, specifically the S1 and S2 sounds. The bottom trace is a Brachial Pulse Volume Waveform (bPVW) illustrating the peripheral arterial pressure pulse. Vertical markers indicate temporal relationships between these signals to calculate systolic time intervals. The 'QS2' interval is marked from the onset of the QRS complex on the ECG to the aortic component of the second heart sound on the PCG, representing the total electromechanical systolic interval. The 'bET' (Brachial Ejection Time) is delineated on the bPVW from the waveform foot to the dicrotic notch. An annotated formula shows the calculation of the Brachial Pre-ejection Period (bPEP) as the difference between QS2 and bET (bPEP = QS2 - bET). This diagram is an educational tool for understanding the non-invasive assessment of cardiac systolic function and arterial stiffness.

This diagnostic image displays a phonocardiogram tracing showing the amplitude waves of heart sounds recorded via an esophageal stethoscope. The waveform presents a rhythmic, repeating sequence of high-amplitude vertical spikes against a grid background. Key cardiac cycle components are labeled: 'S1' indicates the first heart sound (associated with mitral and tricuspid valve closure during ventricular systole) and 'S2' indicates the second heart sound (associated with aortic and pulmonic valve closure during ventricular diastole). Visually, S1 exhibits a slightly higher peak amplitude and sharper complex compared to S2. The interval between S1 and S2 represents the systolic phase, while the longer interval following S2 before the next S1 represents the diastolic phase. The baseline activity between these primary peaks is relatively stable with minimal noise, demonstrating the clinical utility of filtered esophageal recording for monitoring cardiac acoustic signals and assessing correlations between heart sound intensity and hemodynamic parameters like systolic blood pressure.

The image presents a dual-paneled physiological signal display from a patient with pulmonary hypertension, illustrating the synchronization of cardiac electrical and acoustic activity. Panel (a) shows a Lead II Electrocardiogram (ECG) trace over a 7.5-second interval. The y-axis measures amplitude in millivolts (mV), ranging from -0.2 to 0.6 mV. Green circular markers identify the detected R-waves, defining the beginning of each cardiac cycle. Panel (b) displays a corresponding heart sound signal (phonocardiogram) over the same time axis. The amplitude for the acoustic signal ranges from approximately -0.3 to 0.5 mV. Red vertical lines of varying heights indicate the detected components of the heart sound: shorter lines mark the first heart sound (S1) and longer lines mark the second heart sound (S2). This comparative visualization is used in clinical research to study the temporal relationships between electrical depolarization and mechanical valvular closure, specifically for detecting patterns or murmurs associated with pulmonary hypertension.

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The Second Heart Sound (S2)

1. Origin and Normal Physiology

The second heart sound (S2) corresponds to closure of the semilunar valves at the end of ventricular systole. It has two components:

A2 - aortic valve closure (occurs first, under higher systemic pressure)
P2 - pulmonic valve closure (occurs slightly after A2 due to lower pulmonary pressures and longer right ventricular ejection time)

S2 is a high-pitched sound, best heard with the diaphragm of the stethoscope. It is best auscultated at the second left and right intercostal spaces (pulmonic and aortic areas). Under normal circumstances, A2 and P2 have similar intensities when auscultated at the pulmonic position. P2 is normally audible only over the second left intercostal space; if it is heard elsewhere, pulmonary hypertension should be suspected.

Fuster and Hurst's The Heart, 15th Edition

2. Physiologic (Normal) Splitting of S2

During inspiration:

Enhanced venous return to right heart chambers
Increased pulmonary vascular capacitance
These together prolong right ventricular ejection time, delaying P2
Left ventricular ejection time does not change significantly

Result: On inspiration, A2 and P2 split apart (two distinct sounds). On expiration, P2 moves back toward A2 and they are heard as a single sound. This is physiologic splitting.

Heart sounds splitting diagram - normal, ASD, RBBB, LBBB, pulmonary hypertension

Harrison's Principles of Internal Medicine 22E

3. Abnormal Splitting of S2

Abnormal splitting can be classified into three types: paradoxical (reversed), persistent (wide), and fixed.

Audible expiratory splitting patterns: wide physiological, reversed, narrow

A. Paradoxical (Reversed) Splitting

P2 precedes A2 (reversed order)
Splitting is heard on expiration and disappears on inspiration (the opposite of normal)
Mechanism: delayed aortic valve closure due to prolonged LV ejection time (>300 ms)

Causes:

Cause	Mechanism
Left bundle branch block (LBBB)	Delayed LV lateral wall activation
Right ventricular pacing	Delayed LV activation
Severe aortic stenosis	Prolonged LV ejection against high resistance
Hypertrophic obstructive cardiomyopathy (HOCM)	Dynamic LV outflow obstruction (most common cause in practice)
Acute myocardial ischemia	Non-uniform LV contraction
Wolff-Parkinson-White type B	Accessory pathway delays LV activation

Note: In severe calcific aortic stenosis, A2 is often absent or inaudible, so paradoxical splitting is rarely appreciated despite the prolonged ejection time.

Patients with paradoxical splitting of S2 and reduced LV systolic function appear to respond favorably to cardiac resynchronization therapy (CRT).

Fuster and Hurst's The Heart, 15th Edition

B. Persistent (Wide) Splitting

S2 is widely split at baseline (both A2 and P2 audible)
With inspiration, the A2-P2 interval widens further (inspiratory increase, but not fixed)
Mechanism: underlying delay in P2, reflecting abnormal right ventricular ejection hemodynamics

Causes:

Right bundle branch block (RBBB) - most common cause in clinical practice
Severe pulmonary hypertension - increased RV afterload prolongs ejection
Severe MR - premature aortic valve closure (early A2 moves away from P2)
Idiopathic dilation of the pulmonary artery

C. Fixed Splitting

S2 is widely split at baseline AND the A2-P2 interval shows minimal or no change with respiration
Classic sign of ostium secundum atrial septal defect (ASD)

Mechanism in ASD: During expiration, normally decreased venous return would narrow the split. But in ASD, the drop in venous return is compensated by increased left-to-right shunting, keeping right ventricular preload relatively constant regardless of respiratory phase. This eliminates the respirophasic variation, producing a fixed split.

Other causes of fixed or widely fixed splitting:

RV volume overload (ASD, partial anomalous pulmonary venous return)
RV pressure overload (pulmonic stenosis)
RBBB
Occasionally normal in children
Fuster and Hurst's The Heart, 15th Edition; Harrison's Principles of Internal Medicine 22E

4. Abnormalities of S2 Component Intensity

Loud P2

Pulmonary arterial hypertension - the most important cause; P2 may be palpable in severe cases
Clinical significance by where P2 is audible:
- Left upper chest only: normal
- Left lower sternal border: moderate pulmonary hypertension
- Apex: severe pulmonary hypertension
Narrow or single S2 also occurs in pulmonary hypertension

Diminished / Absent P2

Increased anteroposterior thoracic distance (barrel chest, COPD) - most common cause of single S2 in practice
Pectus excavatum: paradoxically loud P2 (reduced AP dimension)
Severe valvular pulmonic stenosis - diminished or absent P2
Congenitally corrected transposition of the great arteries - posterior pulmonary valve position makes P2 inaudible; leads to a single, loud S2
Tetralogy of Fallot (TOF), pulmonary atresia, transposition of the great arteries (TGA)

Loud A2

Systemic arterial hypertension - increased aortic diastolic pressure causes A2 to be accentuated
Historically: "tambour-like" A2 in syphilitic aortitis (rarely seen today)

Diminished / Absent A2

Calcific aortic stenosis - classic finding; an absent A2 indicates severe disease
Important marker of disease severity: presence of a normal A2 in presumed "severe AS" should prompt investigation for subaortic or supravalvular obstruction

Single S2

Pulmonary hypertension (narrow split merges)
Single semilunar valve (pulmonary atresia, aortic atresia, truncus arteriosus)
Severe pulmonic stenosis (TOF, TGA) - P2 inaudible
Severe calcific AS
COPD (most common practical cause)
Occasionally normal
Fuster and Hurst's The Heart, 15th Edition; Harriet Lane Handbook, 23rd Ed

5. Clinical Summary Table

Pattern	Respiratory Behavior	Key Causes
Physiologic split	Split on inspiration, single on expiration	Normal
Wide physiologic split	Split on expiration, widens on inspiration	RBBB, severe MR, idiopathic PA dilation
Fixed split	No respiratory variation, always wide	ASD (secundum), PAPVR, severe PS
Paradoxical (reversed) split	Split on expiration, single on inspiration	LBBB, HOCM, severe AS, RV pacing, WPW type B
Narrow split / single S2	Barely audible or single throughout	Pulmonary hypertension, severe AS, COPD
Loud P2	-	Pulmonary hypertension (moderate to severe)
Absent A2	-	Severe calcific aortic stenosis

6. Diagnostic and Clinical Significance

S2 splitting and intensity provide crucial non-invasive information about valve function, ventricular conduction, and pulmonary/systemic pressures
Fixed splitting of S2 is a bedside hallmark of ASD before any murmur is identified
Paradoxical splitting suggests LV conduction delay or outflow obstruction; may predict CRT response
A loud, palpable P2 strongly suggests pulmonary arterial hypertension
Absent A2 is a bedside severity marker in aortic stenosis
Single S2 in COPD is the most common practical cause (obscured by lung hyperinflation)

Sources: Fuster and Hurst's The Heart, 15th Ed. | Harrison's Principles of Internal Medicine 22E | Harriet Lane Handbook, 23rd Ed.

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