syndrome
CHARGE syndrome TOF, truncus arteriosus,
aortic arch anomalies (e.g.
vascular ring, interrupted
aortic arch)
Coloboma, choanal atresia, growth or mental retardation, genitourinary
anomalies, ear anomalies, genital hypoplasia
(AS: aortic stenosis; ASD: atrial septal defect; ECD: endocardial cushion defect; HOCM: hypertrophic
obstructive cardiomyopathy; LVH: left ventricular hypertrophy; PA: pulmonary artery; PS: pulmonary
stenosis; TOF: tetralogy of Fallot; VSD: ventricular septal defect); CHDs: congenital heart diseases;
PDA: patent ductus arteriosus)
SYSTEMIC EXAMINATION
All cardiovascular examination has to be simultaneously timed with carotid pulse. Findings synchronous
with carotid upstroke is systolic and if it is asynchronous, it is diastolic.
Inspection and Palpation of Heart
Palpation of CVS (Fig. 4E.2)
Tips of fingers For localizing the pulsations
Metacarpal heads For appreciating the thrills
Heel of hand For appreciating the heave
Fig. 4E.2: showing sites of hand for palpation of pulses, thrills and heave.
Chest deformity and associated clinical diseases:
Chest deformity Associated diseases
Barrel shaped Chronic obstructive pulmonary disease and cor pulmonale
Broad shield like chest Turner syndrome
Noonan syndrome
Pectus carinatum Marfan’s syndrome
Noonan syndrome
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Pectus excavatum Marfan’s syndrome
Homocystinuria
Straight back syndrome Loss of normal kyphosis
Expiratory splitting of S2
Midsystolic murmur
Prominent pulmonary artery
Male gynecomastia Digitalis or spironolactone
Female hypomastia Mitral valve prolapse (MVP)
Topographical Areas of the heart (Fig. 4E.3):
Fig. 4E.3: Illustration showing areas of heart.
Precordial Bulge
Patient in supine position, stand at the foot end of the bed and look for precordial bulge
If present, indicates right ventricular dilatation in childhood
Classically seen only with congenital heart diseases like atrial septal defect (ASD)
Costal cartilage fuses by 16 years of age, so cardiac diseases which are acquired beyond 16 years
may not have a precordial bulge
Acquired heart disease that can produce precordial bulge is juvenile mitral stenosis.
Causes of precordial bulge:
Cardiovascular causes
Ribs involved, e.g. cardiac enlargement of long duration Ribs not involved, e.g. pericardial effusion
Noncardiovascular causes
Skeletal deformity
Bronchogenic carcinoma
Mediastinal growth
Apical Impulse
Definition
It is the outermost and lowermost point of maximum cardiac impulse (PMI) in early systole which imparts
a perpendicular gentle thrust to a palpating finger followed by a slight medial retraction in the late
systole.
Method of Examination of Apical Impulse
First observe the position of apical impulse, then comment on the charact
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Patient should be in supine position
First palpate the apex with the palm (Fig. 4E.4), then localize it with fingertip (Fig. 4E.5)
Observe the amplitude and duration of the lift of the palpating finger
If apical impulse is not palpable in supine position, the patient can be put in left lateral position and
examination done.
Fig. 4E.4: Palpating the apex with palm flat on the chest.
Fig. 4E.5: Localizing the apex with the fingertip.
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Fig. 4E.6: Location of cardiac impulse.
Features of normal cardiac impulse:
Location Left 5th ICS, 1–2 cm medial to MCL (or) ≤10 cm from the midsternal line (Fig. 4E.6)
Extent <3 cm diameter or one ICS
Duration <50% of systole
(ICS: intercostal space; MCL: midclavicular line)
Mechanism of normal apical impulse:
Anterior and counter clockwise rotation of left ventricle (LV) due to isovolumic contraction during early
systole and medial retraction due to clockwise rotation of the LV during late systole.
Abnormalities of apex (Fig. 4E.7)
Absent (Not seen nor felt) Cardiovascular causes
Pericardial effusion
Dextrocardia
Noncardiac causes
Behind rib
Obesity or thick chest wall
COPD/emphysema
Left sided pleural effusion
Left sided pneumothorax
Tapping Mitral stenosis (palpable S1—closing snap)
Hyperdynamic Increased in amplitude
Duration is >1/3–<2/3 of systole
Occupies more than one intercostal space (hence called diffuse apex)
Occurs in LV volume overload conditions
Physiological
Thin chest
Pectus excavatum
High output states
Pathological
AR
MR
VSD
PDA
AV fistula
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Heaving Increase in amplitude
Duration is >2/3 of systole
Confined to one intercostal space
Occurs in LV pressure overload
AS
Systemic hypertension
HCM
Coarctation of aorta
Double apical impulse HOCM
LV aneurysm
LV dyssynergy
Triple or quadruple or wavy impulse HOCM
Retractile Severe TR
See-saw apex LV aneurysm
(AR: aortic regurgitation; AS: aortic stenosis; AV fistula: arteriovenous fistula; COPD: chronic obstructive
pulmonary disease; HOCM: hypertrophic obstructive cardiomyopathy; LVH: left ventricular hypertrophy;
MR: mitral regurgitation; PDA: patent ductus arteriosus; VSD: ventricular septal defect); LV: left
ventiricular; TR: tricuspid regrurgitation)
Fig. 4E.7: Apicogram showing different types of cardiac apex.
Which Ventricle is Causing the Apical Impulse?
The heart during systole, becoming smaller, generally withdraws from the chest wall except for the
apex. The effect of this withdrawal on the chest wall can be observed as an inward movement of the
chest wall during systole called “Retraction”.
The presence of lateral retraction identifies the apical impulse to be formed by the right ventricle,
which is an abnormal state.
A wide area apex beat with medial retraction implies left ventricular enlargement.
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Right ventricular (RV) apex vs. left ventricular (LV) apex:
RV apex LV apex
Apex rotated and shifted laterally Apex may be shifted down and out
Lateral retraction Medial retraction
Note: In adhesive pericarditis/constrictive pericarditis—systolic retraction of the apex followed by
diastolic expansion is—Skoda’s sign.
Displacement of apex
Upward
displacement
Children
Ascites
Abdominal tumor
Pericardial effusion
Downward
displacement
Mediastinal growth
Aortic aneurysm
Lateral
displacement
If trachea is also shifted along with the displacement of apex beat, then it is due to mediastinal shift as a result of
conditions such as lung fibrosis, collapse, pneumothorax or skeletal abnormalities
If the trachea is central but the apex is displaced, the causes may be:
Left ventricular enlargement: The apex will be displaced downwards and laterally.
Right ventricular enlargement: The apex will displaced laterally
Left Parasternal (LPS) Pulsation/heave
Produced either by right ventricle (RV) or left atrium (LA).
Normally RV activity is neither visible nor palpable.
Examination of LPS Area
Heel of hand with wrist cocked up (Fig. 4E.8) or ulnar border of hand is applied over 3/4/5 ICS in left
sternal margin (Fig. 4E.9) and felt for the pulsations.
In children or thin patients, parasternal heave can be demonstrated by placing a pen over the
parasternal area parallel to the sternal margin and watched for the movement of the tip of the pen.
In case of difficulty in appreciating the parasternal heave from breathing, ask the patient to
momentarily hold the breath.
Fig. 4E.8: Examination of parasternal heave (with heel of the hand in cocked up position).
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Fig. 4E.9: Examination of parasternal heave (by placing ulnar border).
All India Institute of Medical Science (AIIMS) Grading of Parasternal Heave
Grade I Grade II Grade III
Visible
Not palpable
Visible
Palpable
Obliterable
Visible
Palpable
Not obliterable
Ill-sustained >50% of systole Full systole
How to Differentiate RV and LA Parasternal Heave?
RV parasternal heave LA parasternal heave
Synchronous with apex
Systolic
Not synchronous with apex
Diastolic
Conditions where LPS pulsations are seen
Physiological Children
Reduced AP diameter
Right ventricular hypertrophy
associated
Pressure overload
Pulmonary HTN
Pulmonary stenosis
Volume overload
TR
ASD
VSD
Normal RV Moderate to severe MR (jet or squid effect)–regurgitant jet of blood into LA pushes the RV
anteriorly
Regional wall motion abnormality (RWMA) of LV–dyskinetic motion of LV septum pushes
RV forwards during the systole
Note:
There is no parasternal heave in TOF
In MS with MR there is both LAE and RVH, hence very prominent parasternal heave seen
(AP: anteroposterior; ASD: atrial septal defect; HTN: hypertension; LAE: left atrial enlargement; LV: left
ventricular; MR: mitral regurgitation; RVH: right ventricular hypertrophy; TR: tricuspid regurgitation; VSD:
ventricular septal defect); LA: left atrium; RV: right ventiricular)
Aortic and Pulmonary Pulsations (Base of the Heart)
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Examined in sitting and leaning forward position with breath held in expiration (Erb’s maneuver—
described in auscultation section).
Aortic area Pulmonary area
Right 2nd ICS area Left 2nd ICS area
Visible pulsations
Aneurysm of aorta
Chronic AR
Pulmonary HTN
Pulmonary artery dilatation
Pulmonary artery aneurysm
Hyperdynamic pulmonary artery circulation
Palpable heart sounds
A2 (sHTN)
Ejection click (bicuspid aortic valve)
P2 (pHTN)—diastolic shock
Ejection click (pulmonary stenosis)
Palpable murmurs
AS
AR (dilated root—AR)
PS
PDA (Gibsons area—left 1st ICS)
Graham steel murmur
(AR: aortic regurgitation; AS: aortic stenosis; HTN: hypertension; pHTN: pulmonary hypertension; sHTN:
systemic hypertension; ICS: intercostal space; PDA: patent ductus arteriosus; PS: pulmonary stenosis)
Sternoclavicular Pulsations
Suprasternal pulsations Aneurysm of arch of aorta
Thyroidea ima artery
Right sternoclavicular joint Aortic dissection
Aneurysm of aorta
Aortic regurgitation
Right aortic arch
Blalock-Taussig shunt
Epigastric Pulsations
The subxiphoid region should be palpated by placing the thumb/index finger/palm of the hand over the
epigastrium with the fingertip pointing towards the patient’s head (Fig. 4E.10).
Gentle pressure is applied downward (posteriorly) and upward towards the head.
The patient should be asked to take a deep inspiration in order to move the diaphragm down. This
facilitates the palpation of the right ventricle.
If the impulse were palpable pushing the tip of the thumb/fingertips downward (toward the feet), it
would indicate a palpable right ventricular impulse.
Transmitted abdominal aortic pulsations will cause the impulse to strike the pulp/palmar aspect of the
thumb/hand.
Transmitted hepatic pulsations are felt from the right side onto lateral surface of the examining finger.
Causes of epigastric pulsations
Cardiac causes RVH (due to any cause)
Aortic causes Thin build
Aneurysm of descending aorta
Aortic regurgitation
Hepatic causes Presystolic/diastolic: TS
Systolic: TR
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(RVH: right ventricular hypertrophy; TR: tricuspid regurgitation; TS: tricuspid stenosis)
Fig. 4E.10: Demonstration of epigastric pulsations.
Other Pulsations
At back Suzman’s sign in coarctation of aorta
Pulmonary arteriovenous fistula
At neck Aortic regurgitation
Carotid aneurysm
Subclavian artery aneurysm
Thrills
Thrills are palpable murmurs (grade IV or more intensity).
It is described as purring of the cat.
Best felt with head of the metacarpal bones.
Can be systolic, diastolic or continuous.
Area Timing Cause
Mitral (apex) Systolic Severe MR
Diastolic MS
Left sternal border Systolic VSD
Pulmonary area Systolic PS
Aortic area Systolic AS
Diastolic Acute severe AR
Left 1st ICS Continuous PDA or rupture of sinus of Valsalva
Note: As a rule, thrills in the apex of heart are diastolic and thrills in the base of the heart are systolic (exceptions are systolic thrill
of acute severe MR and diastolic thrill of acute severe AR).
(AR: aortic regurgitation; AS: aortic stenosis; ICS: intercostal space; MR: mitral regurgitation; MS: mitral
stenosis; PDA: patent ductus arteriosus; PS: pulmonary stenosis; VSD: ventricular septal defect)
Other Sounds Palpable at Apex
Low frequency sounds
LV S3 LVF, MR
LV S4 (LVEDP >15–18 mm Hg) AS
HCM
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MR/AR
CAD
Pericardial knock Constrictive pericarditis
High frequency sounds
S1 Tapping apex of MS
OS Early diastolic sound in MS
Ejection systolic click AS (congenital—bicuspid aortic valve)
Tumor PLOP LA/RA myxoma
Murmurs (thrills)
Systolic MR
AS
VSD
Diastolic MS
(AR: aortic regurgitation; AS: aortic stenosis; CAD: coronary artery disease; HCM: hypertrophic
cardiomyopathy; LA: left atrial; LV: left ventricular; LVF: left ventricular failure; MR: mitral regurgitation;
MS: mitral stenosis; PDA: patent ductus arteriosus; RA: right atrial; VSD: ventricular septal defect).
Other Palpable Sounds in Parasternal Area
Low frequency sounds
RV S3 (increased flow to ventricles) RV failure
Chronic TR
ASD
RV S4 (against increased pressures of ventricle) PS
Decreased RV compliance
High frequency sounds
OS TS
Murmurs (thrills)
Systolic TR
Diastolic TS
(ASD: atrial septal defect; OS: opening snap; PS: pulmonary stenosis; RV: right ventricular; TR: tricuspid
regurgitation; TS: tricuspid stenosis)
Note:
Palpable S1 Tapping apex
Palpable S2 Diastolic shock (palpable P2)
Constrictive pericarditis Diastolic knock or pericardial knock
Dilated vessels:
Dilated veins: caudal flow [superior vena cava (SVC) obstruction]; cranial flow [inferior vena cava
(IVC) obstruction]
Collaterals are seen with coarctation of the aorta (COA)
For example, Suzman’s sign—seen in COA where collaterals are seen in interscapular and
infrascapular region.
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Scars (Fig. 4E.11)
Median sternotomy
(Generally done when there is need for connecting a heart lung machine)
Coronary artery bypass grafting (CABG)
Lateral thoracotomy All valve replacement surgeries
Patent ductus arteriosus (PDA) surgery scar
Fig. 4E.11: Image showing different surgical scars for cardiac disease.
Tracheal Tug (Oliver’s Sign)
Raise the chin of patient and apply the upward pressure on two sides of cricoid cartilage (Fig. 4E.12).
Positive Downward pull with each heartbeat Aortic aneurysm
False positive Due to mediastinal mass
False negative Do not move with heartbeat Thrombosed aortic aneurysm
Percussion
Determination of Heart Border
Right heart border:
Percuss from above downward in midclavicular line up to the liver dullness (Fig. 4E.13).
Start percussing one space above the liver dullness (Fig. 4E.14), from the right midclavicular line to
the sternum keeping the pleximeter finger parallel to the sternal edge (Figs. 4E.15A and B).
Repeat this in two more consecutive spaces above.
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Fig. 4E.12: Demonstration of Oliver’s sign.
Dullness corresponding to right sternal margin Normal
Dullness outside the right sternal edge Pericardial effusion
Dextrocardia
Cardiac enlargement
Right atrial enlargement
Mediastinal mass
Lung pathology
Left heart border:
Palpate the apex.
In same ICS go to the midaxillary line and start percussing medially.
Direction of percussion should be parallel to the apparent left heart border (Figs. 4E.16A and B).
Normally Corresponds to the apex
Dullness outside apex seen in Large pericardial effusion
Left ventricular aneurysm
Fig. 4E.13: Percuss from above downward in midclavicular line up to the liver dullness.
Fig. 4E.14: Now, go one space above the liver dullness.
Fig. 4E.15A: Illustration showing direction of percussion of right heart border.
Fig. 4E.15B: Change the direction of percussing finger parallel to heart border and move medially till
you get dullness (due to right heart border).
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Fig. 4E.16A: Illustration showing direction of percussion of left heart border.
Fig. 4E.16B: Percussion for left heart border from mid axillary line and start percussing medially with
percussing finger parallel to the apparent heart border.
Note: Position of pleximeter while percussing the heart border showing should be always parallel to the
presumed borders of heart as showed in Figure 4E.17.
Fig. 4E.17: Illustration showing placement of pleximeter finger during percussion of heart borders.
Percussion of Aortic and Pulmonary Areas
For aortic area: Start percussing parallel to the right sternal edge and percuss laterally.
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For pulmonary area: Start percussing parallel to the left sternal edge and percuss laterally.
Normally it is resonant.
Aortic area Pulmonary area (Fig. 4E.18)
Resonant (normal) Resonant (normal)
Dullness
Dilated aorta
Aortic aneurysm
Superior mediastinal mass
Dullness
Dilated PA
PAH
PDA
(PA: pulmonary artery; PAH: pulmonary arterial hypertension; PDA: patent ductus arteriosus)
Note:
*Rotch sign—seen with moderate to large pericardial effusion causing obliteration of cardiohepatic
angle.
Fig. 4E.18: Percussion of left 2nd intercostal space.
Auscultation
Hearing of human beings:
Capability is 20–20,000 Hz
Sensitivity is 1,000–5,000 Hz
Minimum time gap to differentiate two sounds by human ear is 20 ms.
Characters of cardiac sounds:
Loudness: Implies amplitude or intensity.
Pitch: Implies frequency.
Difference between low and high frequency heart sounds
Low frequency High frequency
<125 Hz >300 Hz
Low pitch High pitch
Rough
Rumbling
Soft
Blowing
For example:
S3, S4, pericardial knock
MDM (TS/MS)
For example:
S1, S2, ESC, OS
Systolic murmur of (MR, AR)
Better appreciated with Bell of stethoscope by applying low Better appreciated with Diaphragm of stethoscope by applying
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pressure over the chest piece. firm pressure over the chest piece
(AR: aortic regurgitation; ESC: early systolic click; OS: opening snap; MDM: mid-diastolic murmur; MR:
mitral regurgitation; MS: mitral stenosis; TS: tricuspid stenosis)
Topographical areas of heart (Fig. 4E.19)
Mitral area Corresponds to apex (normally in left 5th ICS 1–2 cm medial to mid clavicular line
Tricuspid area Lower left sternal edge corresponding to 5th ICS
Aortic area Right 2nd ICS
Neoarotic area
(Erb’s neo aortic area)
Left 3rd ICS
Pulmonary area Left 2nd ICS
Other areas
Axilla PSM of MR
Epigastrium PSM of TR
Carotid artery Conduction of AS murmur
Carotid bruit
Gibson’s area Left 1st ICS (PDA)
Roger’s area Left 4th ICS (VSD)
Interscapular area Coarctation of aorta
Aneurysm of descending aorta
Subclavian artery (supraclavicular area) Bruit over this area heard in aortoarteritis
Femoral artery Durozier’s murmur of AR
(AR: aortic regurgitation; AS: aortic stenosis; ICS: intercostal space; MR: mitral regurgitation; PDA:
patent ductus arteriosus; PSM: Pansystolic murmur; TR: tricuspid regurgitation; VSD: ventricular septal
defect)
Fig. 4E.19: Illustration of areas of auscultation.
Sequence of Auscultation
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Position of patient during auscultation
Left lateral decubitus Mitral area
Supine Tricuspid area
Sitting and leaning forward (Erb’s maneuver) Aortic or pulmonary area
CARDIAC CYCLE AND HEART SOUNDS
Fig. 4E.20: Cardiac cycle.
Cardiac Cycle Duration (Fig. 4E.20)
Assuming heart rate of 72, each heartbeat is approximately 0.8 seconds in which 0.5 seconds is diastole
and 0.3 seconds is systole.
Heart sounds (Figs. 4E.21A and B)
S1 Closing of mitral and tricuspid valves
Marks the onset of ventricular systole
S2 Closing of aortic and pulmonary valves
S3 Rapid filling phase of ventricle
S4 Filling of ventricle due to atrial contraction
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Others
Clicks Systolic sounds are called clicks which can be either ejection click or nonejection clicks
Snaps Diastolic sounds indicating opening of mitral and tricuspid valves.
Pericardial knock Diastolic sounds (early)
Seen in constrictive pericarditis
Fig. 4E.21A: Image showing different heart sounds. (EC: ejection click; MSC: mid systolic click; OS:
opening snap)
Fig. 4E.21B: Different cardiac events and heart sounds.
Heart Sounds
First Heart Sound (S1)
Two audible components (M1 and T1)
Two inaudible components (muscular in origin coinciding with beginning of LV contraction and
opening with semilunar valves respectively)
Order of appearance (1st inaudible component → M1 → T1 → 2nd inaudible component)
M1–T1 interval = 20 ms
It is loudest at apex
Coincides with carotid upstroke
Determinants of S1
Structural integrity of valve
Position of the valve at the onset of ventricular systole
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PR interval (inversely proportional)
Increased ionotropic activity of heart (directly proportional)
Loss of isovolumetric contraction leads to soft S1 (MR, AR, VSD)
Thoracic cavity and chest wall (high frequency murmurs are more attenuated with soft tissues).
Variations of S1
Loud Soft Variable
MS (mild to moderate), TS
ASD (loud T1)
Tachycardia
Short PR interval
Hyperdynamic
circulation
Thin people
Muffled in pan-systolic murmurs—MR, TR (here valves are wide
and do not coaptate)
MS (severe calcific)
AR (increased LV filling and premature closure of mitral valve)
Bradycardia
Long PR, heart blocks,
Obesity, emphysema, effusion
Atrial fibrillation
Ventricular tachycardia (AV
dissociation)
Complete heart blocks (cannon
sound)
When do you say loud S1?
When S1 is heard with the same intensity as of mitral area in the base of heart (aortic and pulmonary areas)
Splitting of S1
Wide splitting Reverse splitting (T1→ M1)
Ebstein’s anomaly
ASD
Complete RBBB
LV pacing
Ectopics
Severe MS
Complete LBBB
RV pacing
Note: In ebstein’s anomaly one can hear S1 split, S2 split, OS, S4 and pulmonary ejection click.
(AR: aortic regurgitation; ASD: atrial septal defect; AV: atrioventricular; LV: left ventricular; MR: mitral
regurgitation; TR: tricuspid regurgitation; MR: mitral regurgitation; MS: mitral regurgitation; MS: mitral
stenosis; TS: tricuspid stenosis; RBBB: right bundle branch block; LBBB: left bundle branch block)
Second Heart Sound (S2)
Two components (A2 and P2)
A2 → P2
A2-P2 time interval is <30 ms (expiration) and 40–50 ms (inspiration).
Heard best in base of the heart (pulmonary and aortic areas).
The loudest component of S2 in pulmonary area is A2.
The loudest component of S2 in aortic area is A2.
Hang out interval: The time interval from the crossover of pressures between ventricles and the
arteries to the actual closure of valves is called hang out interval.
Mechanism of normal split of S2:
During inspiration there is an increase in the capacitance of pulmonary vascular bed à this results
in the delay of rise of pulmonary arterial pressure resulting in prolonged pulmonary hang out
interval.
Early A2 (contributes around 27%).
Delayed P2 (contributes for 73%).
Physiological split is inspiratory and disappears on standing, due to decreased venous return (while
pathological split persists on standing).
Variations of S2 (Fig. 4E.22)
A2
Loud Soft
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Hyperdynamic state, sHTN
Aneurysm of aorta
Aortic root dilatation (e.g. syphilis, ankylosing spondylosis)
TGA
Pulmonary atresia
AS
AR
Aortic sclerosis (elderly)
Thick chest wall, obesity, emphysema
When do you say loud A2?
Normally A2 is loudest at the base (aortic and pulmonary area). A2 is considered to be loud if the intensity in the mitral area is
same as the base of the heart
P2
Loud Soft
Hyperkinetic states
pHTN
Dilation of pulmonary trunk
Aneurysm of pulmonary artery
Thin chest wall
Condition with L → R shunt
PS
Dysplastic pulmonary valve
Thick chest wall, obesity, emphysema
When do you say loud P2?
Normally A2 is louder than P2 even in pulmonary area but if P2 is as loud as A2 in pulmonary area, it is considered as loud P2
Single S2
Severe AS, aortic atresia
Severe PS, pulmonary atresia
Fallot’s tetralogy (A2 becomes loud and P2 disappears)
(AR: aortic regurgitation; AS: aortic stenosis; pHTN: pulmonary hypertension; PS: pulmonary stenosis;
sHTN: systemic hypertension; TGA: transposition of the great arteries)
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Fig. 4E.22: Variations of 2nd heart sound.
Splitting of 2nd heart sound
Narrow split Wide and variable split Wide and fixed split
Severe pHTN Chest deformity: Funnel chest and straight back syndrome
Due to early A2: MR, VSD
Due to late P2: RBBB, LV pacing, ectopics from LV
ASD
Severe RV failure
Acute pulmonary embolism
Note: Why do you get wide fixed split in ASD?
Wide split is due to Fixed split is due to
Increased RV ejection time
Prolonged pulmonary hangout
interval
RBBB
Free communication between two atria equalizes the pressure during inspiration and
expiration
Already prolonged pulmonary hangout interval cannot be further prolonged
Paradoxical split (reverse split)
P2 comes before A2
Split is prominent and wider during expiration, while it narrows during inspiration
Causes due to either early P2 or late A2
Early P2 Late A2
Complete LBBB
RV pacing
PVCs of RV
Severe AS
Severe sHTN
HCM
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