3History “S2 is the key to auscultation” : Aubrey Leathem Respiratory variation first described by Potain (1866)Term “Hangout interval” coined by shaver laboratory.
4Genesis of S2During systole blood flow from LV to Aorta & RV to PA. Once pressure in the great vessels becomes more than corresponding ventricle and hang out interval is over, blood flow reverses , this retrograde flow is stopped suddenly by semilunar valves when the elastic limits of the tensed leaflets are met during closure of valves
5This causes vibrations in the cardiohemic system This causes vibrations in the cardiohemic system. High frequency generated from this vibration is the Second heart sound.
7Hang out intervalIt is the time interval from the crossover of the pressure between RV and PA or LV and Aorta during the ejection phase of systole to the actual closure of the Pulmonary or Aortic valve respectively.
8Cardiac cycle recorded by high fidelity catheter tipped manometer
10Factors influencing the duration of Hangout interval Pressure in the arteriesVascular resistanceCompliance of Vessels
11Aorta is a higher pressure and less compliant vessel so hangout interval of aortic is less than the pulmonary sidePulmonary circulation is Low pressure ,low resistance, high capacitance circulation .So hang out interval more
12Features of S2 Frequency Higher than S1(S1 25-45Hz , S2 50HZ) Duration 0.11 sec( Shorter than S Sec)Components of S2Aortic component (A2) & Pulmonary component (P2)Timing of A2 coincidesIncisura of Aortic pressure traceTiming of P2 coincidesIncisura of pulmonary artery pressure traceNormally A2 – P2 interval : During inspirationDuring expiration40-50 msec<30msecNormally A2 is earlier and Louder than P2Normally A2 heard in Aortic area, Pulmonary area , and ApexNormally P2 heard at pulmonary area only (P2 heard at apex only if PHN Present or If the apex is formed by RV (eg ASD))
13Reasons for Higher frequency S2 compared to S1 The tautness of the semilunar valves more compared to A-V valves.The Greater elastic coefficient of the taut arterial walls that provide the principal vibrating chambers for the second sound,in comparison with the much looser, less elastic ventricular chambers that provide the vibrating system for the first heart sound.
14Why S2 duration shorter than S1? Normally duration of S1 is secondand S2 is 0.11 second .The reason is that, semilunar valves are more taut than the A-V valves, so they vibrate for a shorter time than do the A-V valves.
22Normal splitting of S2Normal A2 P2 interval During expiration : < 30 msec During inspiration : ms Splitting occurs because of delayed P2 (73%) and early A2 (27%).
23Factors affecting normal splitting of S2 Age :As age increases split duration decreases. SingleS2 during both phases of respiration is a normalfinding in subjects with age >40yrsDepth of respirationPosition of body :In recumbent position prominent splittingin both phases of respiration is a normal finding
25Recent views regarding inspiratory widening of split Complex interplay of dynamic changes in pulmonary vascular impedence and changes in pulmonary and systemic venous return. Net effect is prolonged RV ejection and a concomittent decrease in LV ejection causing widening of split in inspiration.
26Inspiration causes more negative intrathoracic pressure 1) Increased venous return2) Increase capacitance of the pulmonary vesselsPulmonary hang outinterval increases & RV ejection time increasesDecreased pulmonary venous flowto the left atrium. So LV ejectiontime decreases so A2 occurs earlySo A2 P2 interval > 30 msec
28Abnormal splitting can be either absent/inaudible split (single S2) or presence of audible expiratory splitting both in supine and upright position
29Abnormal Splitting of S2 includes Persistent physiological splitWide fixed split of S2Reverse split of S2Narrow Physiological split with Loud P2No Split : ie Single S2Expiratory splitinterval> 30msec
43Reverse or paradoxical splitting splitting S2 Split>30msec during expiration with reversal of sequence ie P2-A2Presence of reverse splitting always indicate significant underlying Heart diseaseAlmost all cases of reversed split are due to dalayed A2
44Types of Reversed split Type 1 or classic : Only this type is audibleclinicallyType 2Detected PhonographicallyType 3
45Type 1 Reversed splitNo split during inspiration. But splitting during expiration with reverse sequence due to delay in A2It occurs due to delayed LV Electro mechanical systole
46Type 2 or Partially Reversed splitting of S2 Normal Inspiratory splitting But Expiratory splittingof S2 with Reverse sequenceIt resemble wide fixed split.But during expirationsequence of sound is P2-A2
47Type 3 Reversed splitting of S2 ie similar to type 2 but difference is that A2 P2 and P2-A2 seperation is ≤30 ms and so S2 is heard as a single sound in both phase of respiration
48Clinical recognition of Reversed split of S2 Trace the two components of S2 to the apex.If the second component of S2 is tracable up to apex , reverse split present.(normally only first component of S2(ie A2) is tracable up to apex, And second component is heard only at pulonary area.In reverse split A2 is the second component.)
49Clinical recognition of Reversed split of S2 Valsalva testingNormally S2 becomesReversed split S2 becomesStrain phaseSplit narrowswidensRelease phaseSplitt narrows
50Differentiation of P2-A2 in reversed Split Auscultate from pulmonary area to apex concentrating on the two components of S2.The component which disappears at apex is the pulmonary component.
51Causes of Reversed spliting Due toDelayed A2Early P2
52Causes of Delayed A2 Delayed Electrical activation of LV Complete LBBB RV pacingRV ectopic beatProlonged LV mechanical systoleComplete LBBBSevere ASSevere HTN (Rarely)Chronic ischemic heart d/sDuring episode of anginapectoris(rarely)
53Causes of Delayed A2 . . .contiued. Decreased Impedance of systemic circulation egPost stenotic dilatation aortaChronic severe AR,PDA.
55Reversed splitting in LBBB In proximal type: Delayed activation of LVIn peripheral type: There is prolonged mechanical systole (primarily isovolumic contraction time increased).In most cases of LBBB varying degrees of both mechanism coexist with one predominating
56Reversed split in angina pectoris It occurs rarelyProposed mechanisms are1) Prolonged isovolumetric contractiontime of ischemic LV2) Systemic hypertension prolongingLVETime3) Transient LBBB
57Reverse splitting in HTN In HTN Loud A2 with normal split is the common findingReverse split occurs rarely especially in acute hypertension . Due to increased LV ejection & isovolumetric contraction time
59Single S2In this there is absent splitting both in inspiration and expiration
60Single S2: Mechanism If only one semilunar valve present: eg: Aortic or Pulmonary atresia,Persistent truncus arteriosisWhen P2 inaudible: TGA, TOF, Severe PS, PAWhen Delayed A2 coincides with P2: Severe AS
61When early P2 coincides with A2 : Severe PHTN, VSD+PHTNAny condition producing Paradoxical split with A2-P2 interval ≤ 30msecA2 sound drowned by murmur of AS/MR/VSD
63Factors influencing the intensity of S2 Size of the vesselPressure in the vessel beyond the valveRate of change of Diastolic pressure gradient across the valve.Flow across the valvePosition Of Vessels(Anterior/Posterior)Valve anatomy
64S2 intensity relation to the rate of change of the diastolic pressure gradient that develops across the valvesIt is the driving forces accelerating the blood mass retrograde into the base of the great vessels. This pressure gradient is the result of the level of diastolic pressure in the great vessel and the rate of pressure decline in the ventricle.,
65Accentuted A2 Causes Increased flow across the valve Hyperkinetic StatesAnteriorly placed AortaTGAPulmonary atresiaPTAIncreased size of the vesselAscending aorta aneurysmRoot dialatation:Syphilitic ARAnkylosing SpondylitisBicuspid Aortic valvewith post stenoticdilatationIncresed pressure in thevessel beyond the valveSystemic HypertensionCoactation of aorta
66Diminished A2 Occurs due to distortion of aortic leaflet eg Aortic sclerosis, Calcific AS, Valvular ARAortic atresia(HLHS).
67Loud P2 Increased size of the vessel: Increased flow across the valve Idiopathic dilatation of pulmonary artery,ASDIncresed pressure in the vessel beyond the valve:PHTNIncreased flow across the valveHyperkinetic StatesASDDistance From the site of origin of sound to the chest wall:Thin Chest wallStraight Back syndrome
68Grading Of Loud P2 Grade 1: P2= A2 Grade 2: P2>A2 Localised to Pulmonary areaGrade 3: P2>A2 But heard Beyond thepulmonary artery
69Relation Between P2 intensity and Pulmonary pressure Pulmonary Systolic pressureMean pulmonary pressureGrade 1Mild PHTN30-49 mm of Hg21-34 mm of HgGrade 2Moderate PHTN50-75 mm of Hg35-50mm of HgGrade 3Severe PHTN> 75mm of Hg> 50 mm of Hg
70Diminished P2 Thick chest wall: Obesity Poor conduction of sound : COPDThickened leaflet and diminished valve mobilityPS & Dysplastic PVTOF>60 yr oldDecreased Diastolic Gradient pressure in PA:PS,Tricuspid atresia
72Mitral stenosis Mild to Moderate MS without PHTN: Normal A2 & P2 Severe MS With PHTN : S2 narrow split P2 Loud
73Mitral Regurgitation Wide and Fixed in MR : MR+ ASD Wide variable split : Severe MRWide and Fixed in MR :MR+ ASDReverse splitting in MR:MR due to HCM
74P2 in Mitral regurgitation In MR with giant Left atrial enlargement .P2 is more prominent even with slight increase in pulmonary hypertension.It is due to the enlarged LA displaces the pulmonary artery anteriorly closer to the chest wall
75Aortic stenosis Reverse split : Due to Delayed A2 in Severe AS Single S2 : If A2 is Absent/soft or A2 drowned in themurmur
76Aortic regurgitation S2 Split normally split/Reverse split A2 loud If ARDue to root dilatationA2 soft if AR due to Valvular disease.
77Pulmonary hypertension Spectrum of the width of splitting can happen in PHTN depending on the selective prolongation of RV systole.In PHTN hangout interval will always be narrow
78Spliting of S2 in PHTN Narrow physiological split with Loud P2 Wide variable splitting of S2 with Loud P2Fixed splitting in PHTN due1) If RV failure: Due to inability ofcompromised RV to accept theaugmented venous return associatedwith inspiration2) Altered vascular impedence in pulmonarycirculation
80ASD Wide fixed split with loud p2 in absence of PHTN is the hallmark of ASDP2 Loud because Dilated P2 is close to the chest wall.
81Fixed split in ASD Mechanism: Fixed : Inspiratory augmentation of systemic venous return produces less Left to Right shunt and it causes delayed A2. And expiratory decrease in systemic venous return causes increased Left to right shunt producing early A2.
82VSD Small VSD : Normal S2 split with normal intensity P2 Moderate VSD: Normal split with moderateaccentuation of P2Large VSD : Wide variable Split withLoud P2VSD with PS physiology :Single Loud S2
83PDA Small PDA : Normal S2 split and normal intensity P2 but S2 masked bycontinous murmurLarge PDA: Normal S2 split with accentuatedP2. Occationally paradoxicalsplitting can be seen.
84Pulmonary stenosis Mild PS: Normal S2 Split with decreased intensity P2Moderate – Severe PS: Wide Variable SplitWith Diminished P2Severe PS : P2 absentDysplastic pulmonary valve : P2 can be normal or inaudible depending severity of stenosis
85BISCUSPID AORTIC VALVE In the absence of significant AS or AR S2 normally split with accentuated A2If significant AS: S2 Reversed split
86COA Normally splitting S2 with accentuated A2 due to hypertension sometimes reverse split can also happen
87S2 in Ebsteins anomalyS2 is often single because pulmonary closure is inaudible due to low pressure in pulmonary trunkWide splitting of S2 can happen if complete RBBBParadoxical split occurs if Type B WPW association
88S2 in Anomalous pulmonary venous connection If Associated ASD : Wide fixed splitIf Atrial septum intact: S2 normal split with normal respiratory variation
89S2 in Eissenmenger syndrome ASD Eissenmenger syndrome: S2 narrow fixedsplitVSD Eisenmenger syndrome: Single Loud P2PDA Eisenmenger syndrome:Closely split S2 with Loud P2