The Second Heart SoundDUBModerator- Dr. Arun Prasath M.D, D.M

Presenter- Varun V.

• S2 represents vibrations of cardiac structures and great vessels resulting from deceleration of blood mass at the end of systole when semilunar valves coapt to prevent diastolic reflux of blood into the ventricles.

• Crossover of AO-LV / PA-RV pressure precedes semilunar coaptation and cessation of forward flow.

• The sounds A2 and P2 represent abrupt tensing of the closed leaflets, as the valves, great vessels, ventricular outflow tract and blood mass oscillate with medium to high frequency vibrations.

• Most investigators have documented Aortic valve leaflet coaptation occurring synchronously with the major component of A2.

• Other studies suggest that valve closure immediately precedes A2.

• In the Pulmonary artery P2 follows RV-PA pressure crossover and pulmonic valve closure after an interval longer than in the left heart, particularly during inspiration.

• A2 and P2 coincide precisely with the respective incisura in the aorta and pulmonary artery pressure recordings.

The Hangout Interval

• The semilunar valves are expected to close at the point of cross-over of the pressures, however in reality these valves close slightly later (at the incisura of aorta and pulmonary artery pressure tracing).

• This time interval from the crossover of the pressures to the actual closure (occurrence of A2 and P2) is called “hangout interval”.

• The PA hangout interval typically is 2 to 5 times longer than aortic hangout interval.

• Due to higher pressure and less distensibility (complaint), the hang out interval on the aortic side is less than that of on the pulmonary side.

• The hang out interval is measured between the incisura of aorta and LV pressure at the same level on the left side and between the incisura of pulmonary artery and RV pressure at the same level on the right side.

Respiratory Effects of A2 & P2

• Intrathoracic pressure decreases with inspiration increased venous return prolonged RV ejection late P2.

• Inspiration may also reduce pulmonary venous return to the left heart, shortening the Q-A2 interval.

• PA hangout interval is inversely proportional to pulmonary vascular resistance.

• The highly compliant pulmonary vascular bed is affected by respiratory intrathoracic pressure changes more than the systemic vascular tree.

• The normal PVR is 10 – 20% that of systemic resistance.

• Forward flow into pulmonary artery thus continues over a longer period than flow into the aortaQ-P2 interval lengthens.

• Thus the inspiratory widening of A2 & P2.

How To Listen To S2

• Major vibrations of S2 are relatively high pitched.

• The diaphragm of the stethoscope should be used to auscultate S2.

• If A2 & P2 are separated by 20 msec or less, they will be heard as a single sound.

• When one sound is abnormally loud (like loud P2 in pulmonary htn.), a close splitting maybe detected. Although a very loud A2 or P2 may mask the softer component.

• A2 is louder than P2 in normal subjects.

• A2 is heard well at the 2nd right ICS (aortic area), 2nd left ICS (pulmonary area), and the cardiac apex.

• P2 normally does not radiate to the apex as a separate audible sound except in young or thin subjects, or with pulmonary hypertension.

• P2 is usually detected at 2nd to 4th left ICS.

• Slow regular respirations are best for auscultation.

• The upright position accentuates inspiratory separation of A2 and P2.

• The average A2 – P2 splitting interval is 30 to 40 msec.

• It may be as long as 70 - 80 msec.

• Any interval < 30 msec is considered ”narrow splitting”.

• In obese subjects S2 may be best heard in 1st left ICS.

• In COPD patients, the xiphoid area is often best site for S2 analysis.

• The cadence of S1 and S2 is most characteristic at the 2nd – 3rd ICS.

• S2 follows the palpable carotid and apical impulse.

Abnormalities of S2

• Increased or Loud A2 • Loud A2 occurs when there is increased flow or pressure in the central

aorta.• Aortic root dilatation can also increase the amplitude of A2.• Thickened aortic valve leaflets that retain good mobility is associated

with loud A2.• In certain congenital lesions involving the great vessels, A2 will be

loud because the aorta rises more anteriorly than usual or the pulmonary artery is displaced posteriorly.

• Tambour A2 – Systemic hypertension and Aortic aneurysm.

• Decreased A2• In valvular AS, aortic closure typically is diminished or absent because of

extensive leaflet distortion, fibrosis or calcification.• A2 is decreased in presence of aortic valve sclerosis with obstruction,

probably because the thickened valve tissue dampens oscillations of the leaflets.

• In AR, A2 is often diminished.

• Increased P2• Loud P2 almost always indicates pulmonary hypertension. • Since P2 is normally inaudible at the apex, the occurrence of two audible

components of S2 at the apex strongly suggests pulmonary hypertension.• Palpable P2 at the 2nd & 3rd ICS is a marker of elevated pulmonary

pressures.• In ASD with a large left to right shunt, the RV is enlarged and P2 can be

heard at the apex even in the absence of elevated PA pressures.

• Decreased P2• Valvular pulmonic stenosis is associated with a soft or even absent P2.• P2 is often delayed in pulmonic stenosis.• Augmentation of RV filling by squatting, mild exercise or leg elevation may

increase the intensity of a soft P2.• In severe TOF, P2 is inaudible. However in milder cases, a soft, delayed P2

may be recorded.• When P2 is soft or not audible, masking should be suspected.• Loud A2 may mask P2. A loud, narrowly split P2 may backwardly mask A2.• Loud, early opening snap may mask P2.

Splitting of S2

• Expiratory Splitting (Increased Q-P2)• Two audible components of S2 at end-expiration.• Held expiration may accentuate this finding.• Indicates an interval of at least 30 to 40 msec between the two

sounds.• RV systole shortens more than LV systole in sitting or standing

position, thus respiratory variation of S2 is enhanced when subject is upright.

• RBBB is the most common cause of expiratory splitting of S2. S1 may also be split in RBBB, in this setting P2 widens further with inspiration.

• PVCs of LV origin, LV epicardial pacing and some patients with WPW syndrome may have a delayed P2.

• Moderate to severe pulmonic stenosis produces delayed splitting of P2 on expiration.

• Audible expiratory splitting in patients with an ASD often persists after surgical repair, presumably because of persistently abnormal pulmonary artery compliance and a persistently prolonged hangout interval.

• Pulmonary hypertension is usually associated with a fixed Q-A2 and shortened Q-P2 (decreased hangout interval), resulting in narrow expiratory splitting.

• When RV failure or dysfunction accompanies pulmonary hypertension, S2 may be prominently split on expiration because of prolonged RV emptying.

• Pulmonic regurgitation may be associated with a prolonged RV systole and audible expiratory splitting.

• Expiratory Splitting (Decreased Q-A2)• Severe MR, VSD or pericardial tamponade may shorten LV systole.• In VSD, the Q-A2 interval may be short and the increased volume of RV

may prolong RV systole (increased Q-P2).• In pericardial tamponade, the reduction in LV stroke volume may be

greater than that of RV and expiratory splitting can be heard.• Some patients with severe pulmonary hypertension accompanying

pulmonary embolism may have shortened Q-A2, a normal or increased Q-P2 and prominent expiratory splitting.

• Other causes of expiratory splitting• Minor interventricular conduction delay• Pectus excavatum• Straight back syndrome

• Wide Inspiratory Splitting (Increased Q-P2)• RBBB, LV Pacing• RV failure will delay Q-P2. • In acute and chronic pulmonary embolization Q-P2 is increased.• In late pregnancy and in renal failure, the delayed Q-P2 reflects

hypervolemia.

• In valvular pulmonic stenosis, P2 is late and the degree of A2- P2 delay correlates with the severity of obstruction.

• Thus an A2-P2 interval of 100 msec. signifies severe stenosis with an RV-PA gradient greater than 100 mmHg.

• Because of markedly reduced PA diastolic pressure, the pulmonary closure sound is of low amplitude.

• When infundibular pulmonic stenosis is present, the correlation between the severity of obstruction and the length of A2- P2 interval is no longer valid.

• The RVOT contracts later than RV inflow region. In marked infundibular hypertrophy, a delay in RV outflow contraction may lengthen RV systole out of proportion to the actual measured gradient.

• Wide Inspiratory Splitting (Decreased Q-A2)• A large VSD with hyperkinetic pulmonary circulation and normal pulmonary

vascular resistance may demonstrate wide inspiratory splitting due to combination of decreased Q-A2 and increased Q-P2 intervals.

• The long systolic murmur of VSD may obscure A2. Thus for proper evaluation of S2 listen to A2 away from the peak murmur intensity (eg., at the apex and lower left sternal border).

• Patients with left atrial myxoma and pericardial tamponade have wide inspiratory splitting because of shortened LV systole.

• In constrictive pericarditis the RV stroke volume is relatively fixed and does not respond to respiratory alterations in venous return. LV filling may be diminished during inspiration resulting in a decreased Q-A2 and prominent wide inspiratory splitting.

• Shortened LV systole in severe MR is associated with an increased A2-P2 interval, particularly if there is associated RV failure. If LV failure occurs, LV systole is prolonged and the wide splitting disappears.

Fixed Splitting

• Failure to increase RV stroke volume with inspiration• In RV failure, acute and chronic pulmonary embolism and severe

pulmonary hypertension, inspiratory augmentation of RV filling may not be possible due to pressure overload of RV.

• In such cases LV filling may also be subnormal with decreased Q-A2 interval and prominent wide splitting.

• When RV systole is substantially prolonged (e.g., RBBB with CCF), A2-P2 will be wide and fixed.

• Simultaneous increase in RV & LV filling (ASD)• Wide and fixed splitting of S2 is the hallmark of ASD• There is prominent expiratory separation of A2- P2.• During inspiration the augmented venous return to volume overloaded RV

causes decrease in left to right shunt at atrial level and a resultant increase in LV filling.

• Both Q-P2 & Q-A2 increase simultaneously without a change in A2-P2 splitting interval.

• Simultaneous increase in RV & LV filling (VSD)• S2 is normal in VSD without pulmonary hypertension.• In VSD with markedly elevated pulmonary vascular resistance, the ventricles

act as a common chamber.• Ejection of blood from both ventricles into the great vessels with an

equivalent resistance results in inspiratory delay in each chamber with absence of respiratory motion of S2.

• This finding suggests that the defect is inoperable.

• Differential diagnosis of Wide Fixed split• Patients with LBBB & paradoxical splitting the presence of congestive

heart failure may result in fixed but reversed splitting of S2 (P2-A2).• A2-Opening snap complex in MS can be confused with a widely split S2.

Paradoxic Split

• Type I or classic reversed splitting of S2 • There is no split or single S2 during inspiration and split during

expiration with reverse sequence due to delay in A2 .• It occurs in delayed LV electromechanical systole i.e. increased Q-A2

interval. During expiration, prolonged LV systole causes A2 to follow P2 .

• During inspiration, Q-P2 normally increases, but Q-A2 shortens or remains unchanged (i.e. no split/single S2).

• Type II or partial reversed splitting of S2 • Normal inspiratory S2 splitting and expiratory splitting of S2 with reverse

sequence.• In lesser degrees of Q-A2 delay, or with a wide inspiratory lengthening of

the Q-P2 interval, inspiration still may result in normal A2-P2 and audible inspiratory splitting, although S2 reversal occurs in expiration.

• Type III reversed splitting of S2 • It is similar to Type II but A2 P2 separation is < 20 msec with reverse

sequence during expiration and S2 is heard as a single sound in both the phases of respiration.

• The most common cause of S2 reversal is LBBB.• Prolonged LV systole has 2 causes• Increased interval from the beginning of electrical activation &

beginning of LV isovolumetric contraction.• Prolongation of LV isovolumetric contraction time.

• S2 may be paradoxically split in lesser degrees of LBBB and type B WPW syndrome.

• RV pacing and PVCs of RV origin will produce audible paradoxic splitting of S2.

• Large stroke volume in LV volume overload conditions may result in prolonged Q-A2 and reversed splitting. (PDA and severe AR).

• In CAD or hypertension with acute or chronic LV dysfunction, reversed splitting of S2 is occasionally noted.

• Reversed splitting may be observed in valvular AS and hypertrophic cardiomyopathy.

• S2 splitting may vary from normal to paradoxic in the same patient from day to day in HCM.

• In these conditions reversed splitting is not related to total LV ejection time, which typically is normal in AS and short in HCM.

• Instead it is due to late aortic valve closure due to delayed LV-AO pressure crossover in patients with large gradients and slowed LV relaxation.

• Pseudoparadoxic splitting• In patients with COPD, deep inspiration may cause an artifactual muffling of

P2 due to interposition of expanded lung between the stethoscope and aorta.

• If S2 is audibly split in expiration, it may result in false diagnosis of reversed split as S2 appears ”single” during inspiration.

• Eisenmenger VSD, Single Ventricle• When a “common” ventricular chamber ejects blood into two vascular beds

with equivalent and high resistance, the RV and LV systoles are similar in length and S2 will be fused in all phases of respiration.

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