PERCUSSION It is done to see the enlargement of the dullness of

the cardiac region

Left border APEX Right border RIGHT STERNAL MARGIN

USEFUL IN : Cardiac causes – Cardiomegaly, pericardial

effusion, pulmonary artery dilatation, dilated cardiomyopathy, etc.

See if the dullness extends beyond the apical impulse as in case of Pericardial effusion.

USEFUL IN : Respiratory causes : Pleural effusion,

hydropnemothorax, collapse, fibrosis.

To find the cause of displaced heart due to lung conditions

Presence of diaphragmatic hernia and eventration of diaphragm can be suspected.

AUSCULTATION Bread and butter of cardiovascular examination

Hearing abnormal heart sound is difficult because not

enough time is spent on auscultation. Auscultating only for few seconds may not be adequate.

It may be necessary to listen for a long time to each component of the cardiac cycle at each location of auscultation.

SITES OF AUSCULTATION

NORMAL HEART SOUNDS1 Closing of mitral and tricuspid valves at transition

from diastole to systole

S2 Closing of aortic and pulmonic valves at transition

from systole to diastole s1 termed as High pitched sounds(Best heard with LUB-DUB s2 diaphragm)

S1 Intensity of s1 is predominantly determined by its

mitral valve component.

Therefore, s1 is loudest at the apex

Intensity of s1 is related to the speed with which the mitral valve closes

Abnormalities of s1 Loud s1 Soft S1 Variable S1Short PR intervalMild mitral stenosisHyperdynamic states

Long PR intervalSevere mitral stenosis LBBB

COPDObesityPericardial effusion

AV dissociationAtrail fibrillation

Large PericardialEffusion Auscultatory alternansSevere LVdysfuction

S1 and the PR interval

S2 A relatively high pitched sound occuring at transition

from systole to diastole

Easiest to hear at the upper sternal boarder

Normally “split” during inspiration i.e. contribution from aortic and pulmonic valve are not simultaneous

S2

Expiration P2 S1 A2

Inspiration P2 S1 A2

Inspiration longer RV systole (delayed P2) shorter LV systole (early A2)

Abnormalities of the s2 splitExp S1 A2 P2

Insp

Normal

Exp

s1 P2Insp

Absent A2

Severe Aortic Valve Disease

Exp s1 A2 P2Insp

Wide SplitRBBB, Pre-excitation of LV, Pulm. HTN,Massive PE, Severe MR, Constrictive Pericarditis

Exp

S1 P2 A2 Insp

Reversed SplitLBBB, Pre-excitation of RV, Aortic Stenosis/Regurgitation, LV outflow tract ostruction

Exp

S1 A2 P2 Insp

Fused A2P2VSD with Eisenmenger’s Sydrome, Single Ventricle

Exp S1 A2 P2

Insp

Fixed split

ASD, Severe RV failure

LOUD P2 Suggestive of Pulmonary HTN

Exp.

S1 A2 P2 S1

Insp.

ABNORMAL HEART SOUNDS Sounds d/t abnormal ventricle : S3, S4

Sounds d/t abnormal valves: Aortic Ejection Click MVP Click Mechanical Valve Clicks Opening Snap

Sounds d/t abnormal pericardium: Pericardial Knock

Sounds d/t abnormal atrium: Tumor Plop

S3 A low pitched early diastolic sound

Easiest to hear at apex with patient in left lateral decuitus

Although occasionally heard in young healthy people and pregnant women, in those over the age of 40, it is usually pathologic and indicative of LV failure.

Actual mechanism of generation is not completely known but is probably d/t abrupt deceleration of blood as it attempts to fill a failing ventricle resulting in vibration of ventricular wall.

S3

Exp.

s1 s2 s3 s1

Insp.

s1 s2 s3 s1

S4 A low pitched, late diastolic sound(aka. Pre-systolic

sound)

It is always pathological and thought to be caused by atrial contraction into a stiff and non-compliant ventricle(might occur with systemic HTN, LVH or Ischemic Cardiomyopathy)

Has been described in patients in a-fib and a-flutter, thought mechanism for this has not been explained.

S4

Exp.

s1 s2 s4 s1

Insp.

s1 s2 s4 s1

‘GALLOPS’ “Gallop’’- refers to the presence of either S3 or S4 “Ventricular gallop” - S3 “Atrial gallop” - S4

On rare occasions, “Summation gallop” - S3+ S4 superimposed during tachycardia

s1 s2 s3 s4 s1 HR= 60

s1 s2 s3 s4 s1 HR= 80

s1 s2 s3 s4 s1 HR= 100

s1 s2 s3 s4 s1 HR=120

“CLICKS”

Timing Pitch Location Best Heard

Effect of Standing

Aortic ejectionClick

Mitral Valve Prolapse Click

Very early systole

Mid-Systole

High

High

Can be heard equally well everywhere

Apex

None

Click will occur earlier in systole

“CLICKS” An S1 or S2 caused by a mechanical valve will

acoustly sound similar to a click

These sounds are occasionally referred to as “mechanical valve click” or “prosthetic valve click”

An absent mechanical valve click in a patient who has received a mechanical valve may indicate valve dysfunction

SPLIT S1? The normal split of S1 is usually very narrow & not

appreciable

Causes of a prominently split S1:

1. S1 is actually split (RBBB, pre-excitation, idioventricular rhythm from the LV)

2. First component is actually as S1

3. Second component is actually an aortic ejection click

OTHER PATHOLOGIC SOUNDS “Opening Snap” – Low pitched, early diastolic sound heard

in mitral stenosis

“Pericardial Knok” – A sound acoustically similar to S3 that can be heard in constrictive pericarditis

“Tumor Plop”- A low frequency, early diastolic sound heard in

atrial myxoma . Can cause ‘functional mitral stenosis

HEART MURMURS

PHYSIOLOGY Produced by turbulent blood flow Called ‘bruits’ at other places, despite different

name- same phenomenon The chance that the flow will be turbulent in a

situation is dependent upon its Reynold’s number(NR)

NR = ρ.d.v/η ρ=density of fluid d=diameter of vessel or orifice v=velocity of flow η=viscocity of fluid

Thus, general mechanism of murmurs, - increased velocity of blood, through morphologically normal structures.eg. Hyperdynamic state

through narrowed structures(velocity increases with square of radius)

- decreased blood viscocity

ETIOLOGIES OF MURMURS BY MECHANISM

Mechanism

Examples

Decreased blood viscocity Anemia

Decreased diameter of vessel, valve or orifice

Valvular stenosis Coarctation of the aorta Ventricular Septal defect

Increased velocity of blood through normal structures

Hyperdynamic states (eg. Sepsis, hyperthyroidism)

Regurgitation in an incompetent valve

Valvular regurgitation

CHARACTERISTICS OF MURMURS Timing Location & Radiation Shape Pitch Intensity Quality Response to Maneuvers

TIMING Relative to cardiac cycle

Systolic or Diastolic or Both?

Single most characteristic that will aid in the association of abnormality

TIMING Timing Examples

Systolic(most common) 95%

Midsystolic Aortic/Pulmonic Stenosis Atrial Septal Defect HOCM

Holosystolic Mitral/Tricuspid Regurgitation Ventricular Septal Defect

Late Systolic Mitral Valve Prolapse

Diastolic Early Diastolic Aortic/Pulmonic Regurgitation

Mid/Late diastolic Mitral/Tricuspid Stenosis

Continous Patent Ductus Arteriosus

LOCATION

RADIATION Radiation describes other location(s) where the

murmur is audible, despite not being directly over the heart.

Murmurs generally radiate in the same direction as the turbulent blood is fowing.

Eg. AS to Carotid Artery TR to Ant. Right thorax MR to Axilla

SHAPE Describes how murmur intensity changes from onset to

completion Three basic shapes are heard: Crescndo Decrescendo Uniform( a.k.a. “holosystolic”)

Generally determined by the pattern of the pressure gradient driving the turbulent flow with the loudest segment occuring at the time of the greatest gradient since this will be the time of the highest velocity.

AORTIC STENOSIS

SYSTOLIC MURMURS

DIASTOLIC MURMURS

PITCH High pressure gradient High pitch (Eg. VSD )

Large volume of blood flow across low pressure gradient Low pitch (Eg. Mitral stenosis)

High pressure gradient Simultaneous high + and low pitch large volume of flow “Harsh” (Eg. Aortic stenosis)

INTENSITY How loud is volume? Largely graded on subjective scale. Grade I : Barely Audible Grade II: Soft, but easily heard Grade III: Loud Grade IV: Associated with a thrill Grade V: Can be heard with stethoscope only party in contact with chest wall Grade VI : Audible without the stethoscope

QUALITYMost subjective and non-characteristic

Pathology Frequently used adjective

Mitral Regurgitation

“Blowing”/ “Musical”

Mitral Stenosis “Rumbling” Aortic Stenosis “Harsh” Aortic Regurgitation

“Blowing”

Still’s Murmur “Musical”/ “Vibratory” PDA “Mahine-Like”

RESPONSE TO MANEUVERS

Squating from

supine position

Increased Venous return

Increased Stroke Volume

andIncreased LV End Diastolic Volume

Distinguishes:Aortc stenosis(increases intensity)

Hypertrophic Obstructive cardiomyopathy(decreases intensity)

Clenching Fists Afterload

Distinguishes:Mitral Stenosis( intensity)

Aortic Stenosis( or intensity)

TERMINOLOGY BEST AVOIDED Ejection Murmur A murmur produced by blood flowing forward through the aortic or pulmonic valves during systole.

Flow Murmur A murmur produced by lood flowing forward through a morphologically normal valve.

EPONYMOUS MURMURS A mid to late apical diastole rumble heard in AR which can mimic MS

The phenomenon in which the highest frequency components of an AS murmur radiates to the apex mimicking MR

A murmur of PR occuring in the setting of pulmonary HTN, usually described as high- pitched and “blowing”

A mid-diastolic murmur heard the apex during acute rheumatic fever

A diastolic murmur heard in steosis of left atrial decending artery

Austin Flint Murmur

Gallavardin Phenomenon

Graham Steel Murmur

Corey-Coombs Murmur

Dock’s Murmur