Presentation on theme: "Auscultation of the Heart. I. Auscultatory Valve Area 1. MV: apex, fifth left intercostal space, medial to the midclavicular line 2. PV: second left intercostal."— Presentation transcript:
Auscultation of the Heart
I. Auscultatory Valve Area 1. MV: apex, fifth left intercostal space, medial to the midclavicular line 2. PV: second left intercostal space 3. AV: second right intercostal space 4. AV 2 : left third intercostal space 5. TV: lower part of sternal 6. Other part
II. Auscultatory order Apex PV AV AV 2 TV III. Content of auscultation 1. Heart rate 2. Heart rhythm 3. Heart sound 4. Heart murmurs
1. HR Varies with age, sex. Physical activity and emotional status Normal adult: 60-80/min Sinus tachycardia: >100/min Sinus bradycardia: 60/min
2. Heart rhythm 1) Sinus arrhythmia 2) Premature beat: A sudden extrasystole of the heart in the basic of normal heart rhythm S 1 ; S 2 Pulse absent Ectopic point at atrial, AV node, ventricle
3) Atrial fibrillation: Mechanism: a very high frequency impulse coming from the atrial ectopic point, in multi-reentry Three inconsistence: ventricular rhythm S1 intensity Heart rate; pulse
3. Heart sound: S 1, S 2, S 3, S 4 S 1 : S 1 indicates the beginning of the ventricular constraction 1) Vibration of the closure of A-V valve 2) Opening of the semilunar valve 3) Acceleration of the blood in arteries
S 1 : Character of auscultation 1) Area: apex 2) Pitch 3) Lasting time: 4) Together with apex impulse
S 2 : Vibration of the closure of AV, PV, during the beginning of ventricular diastole, Indicates the beginning of ventricular diastole
S 2 : Character of auscultation 1) Area: loudest at the basic 2) Pitch 3) Lasting time
The differentiate between S 1 ~S 2 1) S 1 apex pitch , lasting time S 2 basic, pitch lasting time 2) Duration: S 1 __ S 2 S 2 __ S 1 3) Apical pulse
S 3 : Mechanism: In early diastole filling blood moves from atrium to ventricle, Produces the vibration of ventricle wall Character: at apex or superinternal of apex 0.12~0.18'' after S 2 frequency intensity S 4 : Occur late in diastole, with effective atrial contraction 0.11'' prior to S 1
4. Abnormal of heart sound Change in loudness Both S 1 and S 2 : Thinner chest wall Activity of the heart increased : Fat, edema, Pericardial effusion, heart failure
Change in S 1 : S 1 depends on: myocardial contraction filling degree of ventricle elastic and position of the valve S 1 : 1) MS 2) Tachycardia: in high fever, the diastolic period was shortened
S 1 : 1) Infarction 2) MI
Change of S 2 : S 2 depends on (1) the pressure within the great vessel (2) the situation of semiluner valves A 2 : hypertension P 2 : pulmonary hypertension in MS, MI A 2 : AS,AI P 2 : PS, PI
Change in quality of heart sound When the myocardial muscle is damaged severely, S 1 is similar to S 2. The heart sound like a pendular—pendular rhythm.Usuallyaccompany with tachycardia—embryocardia.
Splitting of heart sounds Splitting of S 1 : it is due to closure of MV and TV asynchronously loudest over the apex in RBBB
Splitting of S 2 : 1) In normal person, physiologic splitting –due to the closure of AV and PV asynchronously in inspiration 2) In pathological situation –delay of emptying time of one side of the heart such as ASD,MS.
3) The influence of respiration in inspiration: the pressure within the thorax , venous return to RV , so empty time to be delayed, PV closure more later.
4) Paradoxical splitting of S 2 –the abnormal is within the left heart,(AS), the emptying time of LV is delayed, the order of valve closure is reversed. In inspiration, the two components then more closer together or may be single.
5)Fixed splitting of S 2 : –in ASD, S 2 is widely split over the PV area with little or no change in the degree of splitting in either phase of respiration.
5. Extra sounds In diastolic period 1) Gallop: Three or four sounds are spaced to audibly resemble the center of a horse, the extra sounds occurs after S 2.
Protodiastolic gallop rhythm S 3 gallop, ventricular gallop rhythm. S 1 + S 2 + pathologic S 3
–In early diastole, the blood through into ventricle from atrium in failing myocardium, the ventricular wall tension is poor, produce vibration. Reflex that the ventricular function Auscultation character of S 3 gallop: –lower in pitch –After S 2 –Best hear at apex –Loudest at the end of expiration.
S 3 gallop: differ from normal S 3 –Occur in severe organic heart disease –HR>100 bpm –The interval time between S1 and S2 are almost equal, mimicking quality, normal S 3 is nearer from S 2 –Normal S 3 will disappear in standing or sitting position
Late diastolic gallop – S 4 gallop, atrium gallop At late diastole, related to atrial contraction. In LVEDP compliance Artial contraction occur precede S 1, far from S 2 low-pitch; best heard at apex Tensity: end of expiration (from LA) end of inspiration (from RA)
Occur in pressure overload, LVH, in myocardial damaged, LV compliance , such as BP , IHSS, CHD.
Summation gallop –Overlapping of S 3 G and S 4 G while HR
2) Opening snap –In MS –In early diastole of LV, the blood from LA LV, the opening MV suddenly stopped make itself vibration –After S 2. Brief in duration. –High in pitch. Indicate a flexible valve
3) Pericardial knock –In constrictive pericarditis after inflamation, pericardial constricted, limit the diastole of ventricle was limited, produce the vibration of ventrcular wall. – 0.1 after S 2, –Loudest at apex.
6. Extra sound in systolic period: 1) Early systolic ejection sound –Dilated great vessel, hypertention with in it. –After S 1, high in pitch. –PV area: PS, PH inspiration , expiration –AV area: BP ,AS
2) Middle and late systolic clicks – In MVP – Valve, tandae chordea redudent, floppy – Click: after S 1, close to S 2 best heard at apex lower in pitch
Heart murmur H M is abnormal sound Produce by vibration Within the heart or large arteries.
Mechanism –Blood velocity –Blood vascosity –Valve: narrowed or incompetent; organic or relative –Abnormal connection –Vibration of loose structure –Diameter of vessel or
Character of murmur Location: –Murmur of valvular origin are usually best heard over their respective valve area Timing: –Murmurs are timed according to the phase of cardiac cycle during which they occur. – SM, DM, CM. – Early, middle, late
Quality –Depend on: frequency and intensity of sound wave –Related to: pathology and hemodynamic changes of the heart –Soft, harsh, musical. –SM: blowing, harsh, musical (seagull) –DM: blowing, sigh-like, rumbling. –CM: machine-like, hum
Radiation: transmitted direction –With the bloodstream by which they are produced or propagated from their point of origin in many directions – AS – MR – MS
Intensity: –Related to : The severity of abnormal The velocity of blood flow The pressure gradient of valve The myocardial contraction
Six-point scale of for grading the intensity of heart murmur – Grade Ⅰ : basely audible – Grade Ⅱ : usually readily heard – Grade Ⅲ : loud – Grade Ⅳ : quite loud – Grade Ⅴ : even most pronounced – Grade Ⅵ : may be heard with the stethoscope removed from the chest wall.
PCG –Crescendo type –Decrescendo type –Crescendo-decrescendo type –Continuous –Regular
Physiological maneuver 1) Change the body position - Left recumbent: MS - Sitting, leaning forward: AI - Squatting from standing, supine position, raising two legs may increase venous return, SV CO - Murmur of MI, AI - Murmur of IHSS
2) Respiration - Deep inspiration: thorax pressure venous return , pulmonary circulation clockwise rotation of heart make murmur of TI, TS,PI - Expiration: - Valsalva maneuver: thorax pressure venous return M of IHSS
3) Exercise: - HR - Blood volume - Blood velocity make the murmur of MS
The clinical value of heart murmur 1. Important in diagnosis 2. Organic M : MS Relative M: valve, supporting tissues of the valve abnormal Functional M: increased flow across a normal valve
1. Systolic murmur 1) MV area : produced by MI –Organic: RHD, MVP Character: pan systolic Harsh, Loud >3/6 Radiate to the left axilla Maneuver insp exp
2) AV area—AS –Organic: RHD Character: Harsh, crescendo-decrescendo, radiate neck, Thrill, S2 –Relative: Arteriosclerosis, Dilation of aorta, HP
3) PV area –Most are functional: –Relative: ASD, PA dilation –Organic: congenital PS
4) TV area—TI –Most are relative, duo to dilate of RV character like MI, but increased in inspiration, organic SM are rare 5) Other position –VSD: harsh and loud Third-forth intercostal space Left to the sternal border Thrill
2. Diastolic murmur 1) MV area –Organic: RHD—MS, Apex Mid-late diastolic Rumbling, decrescendo-crescendo Thrill, S1 , OS
–Relative: LVH; AI; Austin-Flint murmur
2) AV area – AI rheumatic – decrescendo, sigh-like – best heard at aortic second area –radiate to the left side of the lower part of sternal
3) PV area –Most are produced by relative PI 4) TV area – It is rare in clinical
Continuous murmur –In patent ductus Arteriosus –Begins after S1, crescendo, peak intensity at S2, envelop S2, decreased at early- middle diastole producing a large diamond sharp. –Harsh, mimic the sound of machine rotating –Best heart at second intercostal space, left to sternal artery-vein fistula.
Pericardial friction sound It is produced by the rubbing on each other of the parietal and visceral surfaces of the roughened pericardium. During pericarditis In both systolic and diastolic Systolic component predominates Sometime only in systole
Harsh, Resemble massage the ear using the finger Best heard at 3th-4th in intercostal space Left to the sternal border Common cause is pericarditis (TB, non- specific, rheumatic) Also can been heard in AMI, uremia, SLE
Major symptom and sign of common diseases in circulatory system Mitral Stenosis (MS) –Rheumatic Commissural thickening, adherent fusion Orifice of MV stenosis,blood flow from LA LV was limited. LAP , LAH, Pulmonary V and capillary pressure dilatation, stasis, PAP RV over load RV failure LV filling CO
–Symptoms: Exertional dyspnea, cough, hemoptysis Paroxysmal noctunnal dyspnea –Signs: Mitral face, apical pulse left side Diastolic thrill at apex Cardiac waist prominence Diastolic murmur at apex OS S1 P2 splitting Graham-Steel murmur.
Mitral Insufficiency(MI) –Etiology: Rheumatic Non-rheumatic –Organic –Relative: duo to the LV enlargement. in systolic period, blood flow from LV LA LA filling degree P In diastolic period, LV accepts more blood→dilation CO
–Symptom: fatigue, palpitation, dyspnea –Sign : Apical pulse left, lower Apical beat heavy Cardiac dullness enlarged left Pausystolic, murmur at apex Radiate to left axilla, subscapular P2 spitting S1
Aortic Stenosis (AS) –Rheumatic, atherosclerosis, congenital Narrowed orifice of AV, the resistence of LV to output the blood LV contractility , LVH Aorta P blood flow in coronary A and peripheral A –Symptom: palpitation, fatigue, angina, syncope
–Sign: Apical impulse , to left Systolic thrill in AV area, pulse Cardiac dullness left Ejection SM in AV area, radiate to neck A2 splitting paradoxically
Aortic insufficiency(AI) –Rheumatic, arteriosclerosis, infective endocarditis, syphilis, –In AI, LV receives both blood from LA, AO volume overload LV dilation relative MI, relative MS Diastolic pressure , pulse pressure –Symptom: palpitation, angina
Peripheral vascular sign: pulse pressure water hammer pulse, carotic pulsation , Musset sign(moving head with each heart beat),capillary pulsation, pistol shot sound, Duroziez M.
Pericardial Effusion Inflammatory (TB, purulent) non inflammatory (rheumatism, uremia) Pericardial cavity P , limit the dilation of heart, blood flow from systemic venous to the RV , RV filling output
–Symptom: Depends on the volume and the velocity of effusion producing. Pericardial compression, dyspnea. Infection: fever, fatigue Cough, dysphagia – Sign: Cardiac impulse Apical pulsation Cardiac dullness enlarged, coincide with position
Pericardial friction rub Heart sound In massive effusion: neck vein engagement, inspiration Paradoxical pulse, venous pressure Ewart sign: the lung was pressed by the effusion, in the area of left scapula inferior angle with dullness, vocal fremitue, bronchovesicular breath sound