Cardiac Auscultation

melissa r. cundangan, m.d.

department of internal medicine

Cardiac Auscultation
principles: (1) performed in a quiet room (2) focus on the phase of the cardiac cycle (3) timing in relation to other observable events in the cardiac cycle: a. carotid arterial pulse b. the apical impulse, c. JVP

Heart Sounds
vibrations associated with the abrupt acceleration or deceleration of blood first heart sound: closure of the atrioventricular (AV) valves second heart sound:closure of the semilunar valves

FIRST HEART SOUND (S1)

mitral (M1) and tricuspid (T1) valve closure best heard at the lower left sternal border intensity influenced by:
(1) the position of the mitral leaflets at the onset of ventricular systole; (2) the rate of rise of the left ventricular pressure pulse; (3) the presence or absence of structural disease of the mitral valve; and (4) the amount of tissue, air, or fluid between the heart and the stethoscope.

FIRST HEART SOUND (S1)

loud if : diastole is shortened ( tachycardia) AV flow is increased short PR interval (<160 msec) early stages of rheumatic mitral stenosis (valve is pliable and remains open at
the onset of isovolumetric contraction because of the elevated left atrial pressure)

FIRST HEART SOUND (S1)

soft S1 may be due to: slow rise of the left ventricular pressure pulse (contractile dysfunction) long PR intervals (>200 msec) imperfect closure due to reduced valve substance (MR)

FIRST HEART SOUND (S1)

late stages of mitral stenosis (anterior mitral leaflet is immobile because of rigidity and calcification) beta-adrenergic receptor blockers poor conduction of sound through the chest wall
mechanical ventilation obstructive lung disease Obesity pendulous breasts pneumothorax pericardial effusion

FIRST HEART SOUND (S1)

Splitting 1030 ms is a normal phenomenon Widening is due most often to complete right bundle branch block
(delay in onset of the right ventricular pressure pulse)

SECOND HEART SOUND (S2)

Comprises: aortic (A2) and pulmonic (P2) valve closure best heard: 2nd left ICS (supine position) A2 is normally louder than P2 and can be heard at most sites across the precordium
pulmonary hypertension: both components heard at the lower left sternal border or apex, or when P2 can be palpated at the 2nd left ICS intensity of A2 decreases with aortic stenosis intensity of P2 decreases pulmonic stenosis

SECOND HEART SOUND (S2)

normal, or physiologic splitting
A2-P2 interval increases during inspiration narrows with exhalation

A2-P2 interval widens with:

CRBBB (delayed pulmonic valve closure) severe mitral regurgitation (premature aortic valve closure) Unusually narrow but physiological splitting of S2, with an increase in the intensity of P2 relative to A2, indicates PA hypertension.

SECOND HEART SOUND (S2)

Fixed splitting:
A2-P2 interval is wide and remains unchanged during the respiratory cycle Ex: ostium secundum atrial septal defect

Reversed, or paradoxical, splitting

pathological delay in aortic valve closure CRBBB RV apical pacing severe aortic stenosis HOCM myocardial ischemia

SYSTOLIC HEART SOUNDS

1. EJECTION SOUND sharp, high-pitched early systolic sound closely follow the first heart sound coincides in timing to the upstroke of the carotid pulse

EJECTION SOUND
occur in: semilunar valve stenosis congenital bicuspid aortic or pulmonic valve patients with aortic or pulmonic root / artery dilation normal semilunar valves

The ejection sound that accompanies pulmonic valve disease decreases in intensity with inspiration, the only right-sided cardiac event to behave in this manner Ejection sounds disappear as the culprit valve loses its pliability over time

SYSTOLIC HEART SOUNDS

2. NONEJECTION CLICKS / MIDSYSTOLIC CLICKS occur after the upstroke of the carotid pulse occur with or without a late systolic murmur often denote prolapse of one or both leaflets of the mitral valve probably result from chordae tendineae that are functionally unequal in length

SYSTOLIC HEART SOUNDS

2. NONEJECTION CLICKS / MIDSYSTOLIC CLICKS best heard along the lower left sternal border and at the left ventricular apex usually occur later than the systolic ejection sound Standing: ventricular preload decreases and the click and murmur move closer to S1 Squatting: ventricular preload increases, the prolapsing mitral valve tenses later in systole, and the click and murmur move away from S1

DIASTOLIC HEART SOUNDS

1. OPENING SNAP (OS) a brief, high-pitched, early diastolic sound occurs a short distance after S2 heard best at the lower left sternal border and radiates well to the base of the heart usually due to stenosis of an AV valve (mitral valve) intensity decreases with progressive calcification and rigidity of the anterior mitral leaflet

DIASTOLIC HEART SOUNDS

1. OPENING SNAP (OS) The A2-OS interval is inversely related to the height of the mean left atrial pressure (height of the left atriumLV diastolic pressure gradient ) and ranges from 0.04 to 0.12 s The OS of tricuspid stenosis occurs later in diastole than the mitral OS

DIASTOLIC HEART SOUNDS

2. PERICARDIAL KNOCK high-pitched early diastolic sound corresponds in timing to the abrupt cessation of ventricular expansion after atrioventricular valve opening and with the prominent y descent seen in the jugular venous waveform in patients with constrictive pericarditis

DIASTOLIC HEART SOUNDS

3. TUMOR PLOP a low-pitched sound; appreciated only in certain positions arises from the diastolic prolapse of the tumor across the mitral valve (left atrial myxoma) may have the timing of an opening snap, but it is usually lower-pitched.

DIASTOLIC HEART SOUNDS

4. THIRD HEART SOUND (S3)

rapid filling phase of ventricular diastole a low-pitched sound produced in the ventricle 0.140.16 s after A2 normally present in children, adolescents, and young adults, and in patients with high cardiac output

DIASTOLIC HEART SOUNDS

4. THIRD HEART SOUND (S3) In older adults (> 40 y/o) it indicates: systolic heart failure/impairment of ventricular function AV valve regurgitation other conditions that increase the rate or volume of ventricular filling disappear with treatment of heart failure.

DIASTOLIC HEART SOUNDS

left-sided S3 is a low-pitched sound best heard with the bell piece of the stethoscope at the left ventricular apex during expiration and with the patient in the left lateral decubitus position right-sided S3 heard at the lower left sternal border or in the subxiphoid position with the patient supine may become louder with inspiration

DIASTOLIC HEART SOUNDS

5. FOURTH HEART SOUND (S4) low-pitched, presystolic sound produced in the ventricle during ventricular filling atrial filling phase of ventricular diastole indicate presystolic ventricular expansion best heard with the bell piece of the stethoscope loudest at the left ventricular apex when the patient is in the left lateral position accentuated by mild isotonic or isometric exercise in the supine position

DIASTOLIC HEART SOUNDS

5. FOURTH HEART SOUND (S4) associated with an effective atrial contraction (absent in atrial fibrillation) occurs when diminished ventricular compliance increases the resistance to ventricular filling The incidence of an audible S4 increases with increasing age common among patients with:
left ventricular hypertrophy (hypertrophic cardiomyopathy) ischemic heart disease or myocardial ischemia. systemic hypertension aortic stenosis, and acute mitral regurgitation

DIASTOLIC HEART SOUNDS

5. FOURTH HEART SOUND (S4) right-sided S4
present in patients with right ventricular hypertrophy secondary to either pulmonic stenosis or pulmonary hypertension accompanies a prominent presystolic a wave in the JVP

frequently accompanies delayed AV conduction, even in the absence of clinically detectable heart disease

HEART MURMURS
result from audible vibrations caused by increased turbulence Intensity Timing location Radiation response to various physiologic maneuvers configuration

SYSTOLIC MURMURS
1. Holosystolic (Pansystolic) Murmurs

generated when there is flow between two chambers that have widely different pressures throughout systole The pressure gradient occurs early in contraction and lasts until relaxation is almost complete.

Holosystolic (Pansystolic) Murmurs

begin before aortic ejection, with S1 and end after S2. Ex. MR, TR, VSD

SYSTOLIC MURMURS
2. Midsystolic Murmurs
also called systolic ejection murmurs often crescendo-decrescendo in shape occur when blood is ejected across the aortic or pulmonic outflow tracts

Midsystolic Murmurs
starts shortly after S1 ends before the ventricular pressure falls enough to permit closure of the aortic or pulmonic leaflets gets louder as the velocity of ejection increases diminishes as ejection declines Most are benign, functional murmurs and originate from the pulmonary outflow tract

SYSTOLIC MURMURS
murmur of aortic stenosis is the prototype of the left-sided midsystolic murmur valvular aortic stenosis
murmur is usually maximal in the second right intercostal space, with radiation into the neck may disappear over the sternum and reappear at the apex (Gallavardin Phenomenon)

SYSTOLIC MURMURS
hypertrophic cardiomyopathy
murmur originates in the left ventricular cavity usually maximal at the lower left sternal edge and apex, with relatively little radiation to the carotids.

SYSTOLIC MURMURS
The age and the area of maximal intensity aid in determining the significance of midsystolic murmurs. Midsystolic aortic and pulmonic murmurs are intensified during the cardiac cycle following a premature ventricular beat, while those due to mitral regurgitation are unchanged or softer

SYSTOLIC MURMURS
3. Early Systolic Murmurs
begin with the first heart sound and end in midsystole
Ex. large ventricular septal defects with pulmonary hypertension

SYSTOLIC MURMURS
4. Late Systolic Murmurs

faint or moderately loud, highpitched apical murmurs probably related to papillary muscle dysfunction caused by infarction or ischemia or to their distortion by left ventricular dilation

 common in patients with myocardial infarction or diffuse myocardial disease

Late systolic murmurs following midsystolic clicks are due to late systolic mitral regurgitation caused by prolapse of the mitral valve into the left atrium

DIASTOLIC MURMURS
1. EARLY DIASTOLIC MURMUR
begin with or shortly after S2 high-pitched murmurs of aortic regurgitation or of pulmonic regurgitation due to pulmonary hypertension generally decrescendo, since there is a progressive decline in the volume or rate of regurgitation during diastole. The diastolic murmur of aortic regurgitation is enhanced by an acute elevation of the arterial pressure, such as occurs with handgrip.

MIDDIASTOLIC MURMUR
usually arise from the mitral or tricuspid valves occur during early ventricular filling

Due to disproportion between valve orifice sizes and flow rate the duration of the murmur is more reliable than its intensity as an index of the severity of valve obstruction

 may be generated across the mitral valve in cases of mitral regurgitation, patent ductus arteriosus, or ventricular septal defect, and across the tricuspid valve in cases of tricuspid regurgitation or atrial septal defect. related to the very rapid flow across an AV valve usually follow an S3 tend to occur with large left-to-right shunts or severe AV valve regurgitation

 In acute, severe aortic regurgitation, the left ventricular diastolic pressure may exceed the left atrial pressure, resulting in a middiastolic murmur due to "diastolic mitral regurgitation." In severe, chronic aortic regurgitation, a murmur is frequently present that may be either middiastolic or presystolic (AustinFlint murmur)

PRESYSTOLIC MURMUR
begin during the period of ventricular filling that follows atrial contraction usually due to AV valve stenosis same quality as the middiastolic-filling rumble, but are usually crescendo, reaching peak intensity at the time of a loud S1

 corresponds to the AV valve gradient, which may be minimal until the moment of right or left atrial contraction. most characteristic of tricuspid stenosis
A right or left atrial myxoma may occasionally cause either middiastolic or presystolic murmurs that resemble the murmurs of mitral or tricuspid stenosis.

CONTINUOUS MURMUR
begin in systole, peak near S2, and continue into all or part of diastole. result from continuous flow due to a communication between high- and lowpressure areas that persists through the end of systole and the beginning of diastole EX. patent ductus arteriosus
When pulmonary hypertension is present, the diastolic portion may disappear, leaving the murmur confined to systole

 may also result from:

congenital or acquired systemic arteriovenous fistula coronary arteriovenous fistula anomalous origin of the left coronary artery from the pulmonary artery, and communications between the sinus of Valsalva and the right side of the heart

may also be due to disturbances of flow pattern in constricted systemic (e.g., renal) or pulmonary arteries when marked pressure differences between the two sides of the narrow segment persist

 a continuous murmur in the back may be present in coarctation of the aorta pulmonary embolism may cause continuous murmurs in partially occluded vessels mammary souffle an innocent murmur heard over the breasts during late pregnancy and in the early postpartum period may be systolic or continuous

 innocent cervical venous hum

continuous murmur usually audible over the medial aspect of the right supraclavicular fossa with the patient upright usually louder during diastole and can be abolished instantaneously by digital compression of the ipsilateral internal jugular vein

Keith, Wagener, and Barker classification of hypertensive retinopathy Grade Islight or modest narrowing of the retinal arterioles, with an arteriovenous ratio 1:2 Grade IImodest to severe narrowing of retinal arterioles (focal or generalised), with an arteriovenous ratio < 1:2 or arteriovenous nicking Grade IIIbilateral soft exudates or flameshaped haemorrhages Grade IVbilateral optic nerve oedema

Arteriovenous nicking

Flame shaped hemorrhages

papilledema

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