Post on 10-Jan-2017
transcript
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