Medical

1. Clinical approach for cardiac
patients
DR TEWODROS G.(MD,CARDIOLOGIST)

2. P/E of cardiac patients
• ‘The trouble with doctors is not that they don’t know enough, but
that they don’t see enough’
Sir Dominic J. Corrigan (1802-80)

3. GENERAL APPREANCE
• Acutely VS chronically sick looking
• Color
• Pale , cyanotic, jaundiced
• Mental status
• Dysmorphic features
• Down syndrome
• Trisomy 18 syndrome
• Turner syndrome

4. Growth Pattern
• Weight , length/height, head circumference
• Different patterns of growth impairment are seen in different types of
CHD.
• Cyanotic patients have disturbances in both height and weight.
• Acyanotic patients, particularly those with large left-to-right shunts, tend to
have more problems with weight gain than with linear growth.
• The degree of growth impairment is proportional to the size of the shunt.
• Acyanotic patients with pressure overload lesions without intracardiac shunt
grow normally.
• If length or head circumference is also affected, additional congenital malformations or
metabolic disorders should be suspected.

5. Vital signs
• It includes BP, HR, RR, temperature and SO2
• They should be taken according to the above order.
• Blood pressure
• On initial visit, BP should be measured both upper extremities and at least
one lower extremity.
• The standard technique for measuring BP should be used.
• The width of the bladder of the blood pressure cuff should be approximately 40% of the
circumference of the upper arm midway between the olecranon and the acromion
• The length of the bladder of the cuff should encircle 80 % of the circumference of the
upper arm at the same position.
• A cuff that is too small results in falsely high readings, whereas a cuff that is
too large records slightly decreased BP.

7. • The BP should be taken with the patient's right arm supported at the
level of the heart.
• The right arm is preferred in repeated measures of BP for consistency and
comparison with standard tables.
• In addition, the possibility of coarctation of the aorta would lead to falsely
low BP readings in the left arm.
• Allowing the arm to hang below the heart will elevate BP levels by the added
hydrostatic pressure induced by gravity.
• The BP should be taken at least twice on each visit, with the
measurements separated by 1 – 2mins to allow the release of trapped
blood.
• A new diagnosis of HTN should not be made until the SBP and/or DBP
measurement is ≥95th percentile or ≥130/80 mmHg on at least three
separate visits.

8. The blood pressure should be measured with the arm supported and the cubital
fossa at the level of the heart. The stethoscope bell is placed over the brachial
artery pulse below the bottom edge of the cuff, which should be about 2 cm above
the cubital fossa

9. • Mean arterial pressure
• It is a mean perfusion pressure.
• It provide another indication of overall circulatory pressure load.
• It is estimated by formula ( diastolic blood pressure + 1/3 x [systolic pressure –
diastolic pressure]).
• Orthostatic hypotension
• Definition:
• Blood pressure decrease of >20 mm Hg systolic or >10 mmHg diastolic when the patient
is assessed first in the supine position and then again after 2 minutes with the patient
standing or sitting with legs dangling.
• The presence of a tachycardia with orthostatic hypotension consistent with
volume depletion.
• Hypotension without a concomitant increase in the pulse rate raises the
possibility of autonomic dysfunction.

10. Vital Signs cont…
• Heart rate
• Peripheral pulses: rate, volume and rhythm should be assessed
• For infant apical heart rate can be taken by auscultation at apex.
• If there is a discrepancy of > 20 beat/min between apical and peripheral heart
rate count, called pulse deficit( atrial fibrillation…)
• The normal pulse rate varies with the patient’s age and status.
• Increased pulse rate may indicate excitement, fever, CHF, or arrhythmia.
• Hyperthermia associated with infection should be accompanied by an
increase in the pulse rate of approximately 10 beats/min for each 1° C
increase in temperature (Liebermeister's rule).

11. • In pediatric patients the pulse should be counted for one full minuts
• The pulse rhythm can be regular or irregular.
• Irregular rhythms are classified as either
• Regularly irregular, where the irregular beat can be anticipated at a fixed
interval.
• Commonly occurs with second-degree atrioventricular block (either
Mobitz I or II) or with atrial flattur.
• Irregularly irregular, where the irregular beat occurs without predictability.
• An irregularly irregular pulse implies that the examiner cannot anticipate
when the next beat will occur
• Commonly occurs with multifocal atrial tachycardia, or atrial fibrillation.

12. • Respiratory Rate
• Should be counted for one full minute.
• Periodic breathing: common in young infants related with developmental
related immaturity of the respiratory center.
• The RR is faster in children who are crying, upset, eating, or feverish.
• The most reliable respiratory rate is that taken during sleep.
• After finishing a bottle of formula, an infant may breathe faster than normal
for 5 to 10 minutes.
• The normal RR varies with age, and it is decreases as age increases.
• Temperature
• Core Vs peripheral
• Should be measured at regular interval( like every 2hr) for children suspected
to have infection like infective endocarditis.

13. CVS examination
• The cardiovascular physical examination includes:
Inspection, palpation, and auscultation of the heart as well as
Examination of the arterial and venous pulses.

14. Examination of the arterial pulse
• Carotid, radial, brachial, femoral, posterior tibial, and dorsalis pedis
pulses should be routinely examined bilaterally to ascertain any
differences in the pulse amplitude, contour, or upstroke.
• The brachial arterial pulse is examined to assess the volume and
consistency of the peripheral vessels.
• Simultaneous palpation of the radial and femoral pulses is important
to determine if there is a delay in pulse transmission.
• Normally the femoral pulse appreciated first in most normal children.
• A delay in the onset of the femoral pulse, generally associated with a
diminished amplitude, suggests coarctation of the aorta.

15. Pulse pressure
• It is the difference between the systolic and diastolic pressure.
• The change in pulse pressure is proportional to the volume
change(stroke volume), but inversely proportional to arterial
compliance.
• The normal value is approximately 30 to 40mmgh.
• If it is more than 40mmgh, it is called elevated or wide pulse pressure
• If it is lower than 25% of the systolic BP, it is called low or narrow pulse
pressure.
• Clinical conditions associated with wide or narrow pulse pressure
include???

16. • PULSUS PARADOXUS
• Some respiratory variation of pulse amplitude should be observed during
examination of the arterial pulse.
• Systolic arterial pressure normally falls during inspiration, although the
magnitude of decrease usually does not exceed 8 to 12 mmHg.
• A more marked inspiratory decrease in arterial pressure exceeding 20 mmHg
is termed pulsus paradoxus.
• The term pulsus paradoxus does not indicate a phase reversal; rather, it is an
exaggeration of normal reduction of systolic pressure during inspiration.
• Pulsus paradoxus is an important physical finding in cardiac tamponade.
• It can also occur in COPD, in constrictive pericarditis and restrictive
cardiomyopathy.

17. Mechanisms of pulses paradoxes
• Pulsus paradoxus can be thought of as a direct result of competition
(ie, enhanced chamber interaction) between the right and left sides
of the heart for limited space;
• For the right heart to fill more, the left heart must fill less.
• Although enhanced chamber interaction is the most important
mechanism, several other complex mechanisms contribute.
• Under normal conditions, inspiration increases systemic venous
return and right heart volumes increase; the free wall of the right
ventricle expands into the unoccupied pericardial space with little
impact on left heart volume.

21. MEASUREMENT OF
PULSUS PARADOXUS
a) The cuff pressure is raised about 20 mm
Hg above the systolic pressure
b) The pressure is lowered slowly until
Korotkoff sound 1 is heard for some but
not all cardiac cycles, and the reading is
noted(line A)
c) The pressure is lowered further until
systolic sounds are heard for all cardiac
cycles, and the reading is noted (line B)
d) If the difference between readings A and
B is greater than 10 mm Hg, pulsus
paradoxus is present

22. Cardiac tamponade without pulsus paradoxus
• Coexisting disease that significantly elevates left ventricular diastolic
pressure (eg, systemic hypertension, aortic stenosis) or right
ventricular diastolic pressure (eg, pulmonary hypertension with cor
pulmonale)
• An intracardiac shunt or significant valvular regurgitation (eg, aortic
regurgitation)
• "Low pressure" tamponade, as in the presence of dehydration and
hypovolemia, where a pericardial effusion that would not otherwise
cause cardiac compression can affect cardiac function.

23. • Bounding arterial pulse
• Usually occurs with wide pulse pressure ( systolic minus diastolic BP).
• It occur in many conditions associated with increased stroke volume such as AR, PDA,
large arteriovenous fistulas, hyperkinetic states, thyrotoxicosis anemia, and extreme
bradycardia.
• Weak, thready pulses are found in clinical conditions like CHF or
circulatory collapse.
• If it is only on the legs, suggestive of CoA.
• Peripheral signs of aortic stenosis and aortic regurgitation
• Reading assignment

24. Neck veins
• Neck veins distention suggests impaired right ventricular filling.
• It may not be apparent in infants and toddlers because of their relatively
short neck and relatively increased subcutaneous tissues.
• The most common indication is to use jugular venous pressure (JVP) to
estimate whether right atrial pressure (RAP) is high or low and to assess how
RAP changes over time, including its response to medical therapy.
• RAP estimation is an important component of the evaluation of heart failure.
• Since left HF is a major cause of elevated right heart pressures, estimation
of RAP using the JVP can aid in initial diagnosis of HF as well as in
detection of HF exacerbation.

25. • The right internal jugular vein (IJV) pulse is generally preferred for assessing right
heart hemodynamics since the right IJV and right brachiocephalic vein are in a
direct line with the superior vena cava.
• Neck vein distention is best observed with the patient positioned 30 to 45 degree
upright.
• Measurement of the height of the neck vein distention above the sternal angle is
used to estimate the central venous pressure.
• If the measured height is > 3cm, right atrial pressure is elevated.
• The normal venous pressure is 1 to 8 cm of water (or blood) or 1 to 6 mmHg
(1.36 cm of water is equal to 1.0 mmHg).
• The RAP is estimated by adding the height of the jugular venous column above the sternal
angle (JVP height) to the vertical distance from the mid-right atrium to the sternal angle.
• We estimate RAP by adding 5 cm to the vertical height in cm of the JVP column above the
sternal angle.

26. Jugular venous pulse relations

27. Distinguishing venous from arterial pulsations
Characteristics of pulse Venous pulsations Arterial pulsations
Number of pulsations Multiple Single
Body position Higher in horizontal position and lower in
vertical position
No change
Abdominal compression May increase No change
Compression at root of neck Pulsations cease Maintained

28. IN pediatric cardiac
examination it is preferred to
position the child at 30 degree

30. Abnormal head movement
• Bobbing of the head may be seen in patients with significant aortic
regurgitation.
• This is caused by increased carotid arterial pulsations striking the angles of
the mandibles.
• The patient appears to be nodding “yes.”
• Patients with significant tricuspid regurgitation will exhibit lateral
head movement.
• This occurs when regurgitant blood in the superior vena cava strikes the right
mandibular angle.
• The patient appears to be nodding “no.”

31. Precordial examination
• INSPECTION
• Precordial activity
• Precordial bulge
• Point of maximal impulse
• It is usually located in the 4th ICS in the midclavicular line.
• In dextrocardia, it is on the right side.
• It is displaced downward and laterally with left ventricular volume
overload.
• Left ventricular hypertrophy does not usually alter the location of the PMI.

32. PALPATION
• Palpation includes PMI, thrill, heaves and heart sounds.
• The location of PMI suggests the ventricular dominance.
• Heart sounds normally not palpable.
• In patient with PAH and elevated pulmonary arterial diastolic pressure, the
pulmonary valve closure(P2) often palpable at LUSB.
• Precordial heave
• Parasternal heave – right ventricular enlargement
• Apical heave – left ventricular enlargement
• Thrills are palpable equivalent of murmurs
• Timing and location is very important(systolic or diastolic)

34. Auscultation
• STETHOSCOPES
• Many stethoscopes have a separate bell and diaphragm.
• The bell is most effective at transmitting lower frequency sounds, while the
diaphragm is most effective at transmitting higher frequency sounds.
• The diaphragm should be pressed firmly against the chest to detect high
frequency sounds.
• The bell should be pressed lightly against the chest to detect low frequency
sounds.
• Auscultation of heart sounds:
• The heart sound should be identified and analyzed before the analysis of
heart murmurs.

35. Heart sounds
• The classic hypothesis for the genesis of
the first heart sound (S1) relates to
mitral and tricuspid valve closure.
• Best heard at apex (MV) and LLSB(TV).
• S1 occur coincident with the upstroke of
the carotid pulse.
• S2 occur by closure of the semilunar
valves( PV and AV).
• S2 has two components and the A2 best
heard at RUSB and P2 at LUSB.
• A2 is widely transmitted to the right
second interspace, along the left and
right sternal border, and to the cardiac
apex.
• P2 poorly transmitted.

37. • MV closure begins a few milliseconds before onset of
the rise of the LV pressure pulse.
• The intensity of S1 is primarily determined by the
intensity of mitral valve closure and is normally maximal
over the cardiac apex.
• Several factors contribute to the S1 intensity:
 Mitral valve position at the onset of systole
 The rate of mitral valve closure
 Mobility of the mitral valve
 The PR interval
 Strength of ventricular systole
• S1 normally is louder than S2 over the apex and along
the LLSB; intensity is reduced if S1 is softer than S2
over these areas.
• S1 intensity is likely to be accentuated if S1 is much
louder than S2 over the left or right second interspace.

38. • Increased intensity of S1
• The intensity of valve closure is increased when the MV remains widely open
at end-diastole and then closes rapidly as occurs with an elevated peak rate
of rise of LV systolic pressure.
• The greater distance of travel of the leaflets from the open to the closed
position and the increased velocity of closure contribute to the increased
intensity of S1.
• Clinical situations in which this occurs include:
Increased transvalvular gradient (mitral valve obstruction as in MS or atrial
myxoma)
Increased transvalvular flow (left-to-right shunt in PDA, VSD, and high output
state)
Shortened diastole (tachycardia)
Short PR intervals (preexcitation syndrome)

39. • Decreased intensity of S1
• Restricted valve mobility and lack of apposition of the leaflets decrease the
intensity of S1.
Thus, S1 is soft when the mitral valve is immobile due to calcification and fibrosis,
despite a significant transvalvular gradient.
• S1 may also be reduced when the leaflets are semi-closed prior to the onset
of systole or when the velocity of closure is reduced, as can occur with LV
dysfunction. Examples:
Decreased apposition of MV leaflets: RVHD (MR, sever MS)
In contrast, mitral regurgitation due to perforation of the valve leaflets from bacterial
endocarditis may not be associated with a reduced intensity of S1.
• S1 is usually soft when the PR interval is prolonged since semi-closure of the mitral valve
occurs following atrial systole and before ventricular systole begins.
• S1 is soft in some patients with left bundle branch block.

40. • Decreased intensity of S1
• Premature closure of the MV can occur in severe acute AR due to a rapid rise
in LV diastolic pressure; the mitral valve may be virtually closed at the onset
of systole, resulting in a markedly decreased intensity of or even absent S1.
• Hemodynamically significant AS may be associated with a soft S1.
Semi-closure of the mitral valve due to a powerful atrial contraction and an abnormally
elevated LV diastolic pressure before the onset of ventricular systole is the most likely
explanation.
• S1 is frequently soft in patients with dilated cardiomyopathy.
The decreased S1 is almost invariably associated with a significantly reduced LV ejection
fraction and elevated pulmonary capillary wedge pressure.
The mechanism for a soft S1 include semi-closure of the mitral valve due to an elevated
LV diastolic pressure and decreased velocity of valve closure due to myocardial
dysfunction may contribute.

41. • Variation in the intensity of S1
• Varying intensity of S1 may be evident in the following situations:
• AF and premature beats; mechanism is variation in the velocity of valve
closure related to changes in the RR cycle length.
• Changing intensity of S1 occurs in atrioventricular dissociation, whether the
heart rate is slow or fast (eg, in complete heart block or ventricular
tachycardia).
The changing intensity is due to random variation of the PR interval; the short PR interval
is associated with an increased intensity and the long PR interval with a decreased
intensity.
The pulse is regular in atrioventricular dissociation; thus, the varying intensity of S1 in a
patient with a regular pulse almost always suggests atrioventricular dissociation.

42. Summery of Causes of first heart sound (S1) abnormalities
Abnormality Causes
Increased intensity of S1
Atrioventricular valve obstruction
Mitral Mitral stenosis and left atrial myxoma
Tricuspid Tricuspid stenosis and right atrial myxoma
Increased transvalvular flow
Mitral
Patent ductus arteriosus; ventricular septal
defect; atrial septal defect
Forceful ventricular systole Tachycardia ; mitral valve prolapse
Short PR interval Pre-excitation syndrome
Decreased intensity
Immobility of mitral valve Calcific mitral stenosis
Lack of apposition of the mitral leaflets Rheumatic mitral regurgitation
Presystolic semiclosure of the atrioventricular valves
Long PR interval; acute AR; significant AS;
dilated cardiomyopathy
Conduction anomaly Left bundle branch block

43. SECOND HEART SOUND (S2)
• The genesis of the second heart sound (S2) consists of two components: aortic
and pulmonary valve closure sounds, traditionally designated as A2 and P2.
• The two components of S2 are best heard with the over the left second
interspace close to the sternal border.
• The relative intensity of A2 is almost always greater than P2 over the left second
interspace.
• S2 is usually single during expiration.
• Separation of A2 and P2 occurs during inspiration, allowing comparison of the
relative intensities of these two components.

44. • Intensity of A2 and P2
• The major determinants of A2 intensity include:
Aortic pressure,
Relative proximity of the aorta to the chest wall
Size of the aortic root,
Degree of apposition of the valve leaflets and their mobility.
• The intensity of P2 is determined by:
Pulmonary arterial pressure, particularly the diastolic pressure
Size of the pulmonary artery,
Degree of apposition of the pulmonary valve leaflets
• The intensity of P2 is determined by comparing its intensity with A2.
• An increased P2 intensity is suggested when it is louder over the left second interspace or
when there is transmission to the cardiac apex.

45. • Increased intensity of A2
• Increased intensity of A2 often occurs in systemic hypertension, coarctation of the aorta.
• The intensity of A2 is significantly increased when the aortic root is relatively anterior and
closer to the anterior chest wall, as in TOF and TGA.
• Increased intensity of P2
• The most common cause of an increased P2 intensity is pulmonary PAH of any etiology.
• In almost all cases ASD, P2 is accentuated despite low pulmonary artery diastolic pressure
and pulmonary vascular resistance.
• A dilated pulmonary artery and considerable right ventricular (RV) dilatation may
contribute.
• Decreased intensity of A2
• Sever AR: due to lack of apposition of leaflets and decreased arterial diastolic pressure
• Sever AS: restricted valve mobility and relatively low arterial pressure

46. • Decreased intensity of P2
• A decreased intensity of P2 occurs when there is lower pulmonary artery
diastolic pressure, except with atrial septal defect.
• P2 is soft and delayed with significant RV outflow obstruction, as in patients
with pulmonary valve stenosis.
• P2 is absent in patients with severe pulmonary insufficiency due to a
congenitally absent pulmonary valve.
• SINGLE S2
• Apparent: obesity, emphysema, pericardial effusion
• Absent A2: severe aortic stenosis, severe aortic regurgitation
• Absent P2: sever pulmonary valve stenosis, absent pulmonary valve,
pulmonary atresia, tetralogy of Fallot, truncus arteriosus and TGA.
• The second heart sound often becomes single and loud during pulmonary
hypertension, as the timing of pulmonary closure becomes earlier.

47. • Splitting of S2
• Splitting of S2 is best heard with the diaphragm of the stethoscope over the
left second interspace.
• This is a normal physiologic splitting which occur almost always during inspiration.
• Mechanisms:
1. Increased right ventricle blood ejection time
2. Increased pulmonary hangout interval
• A2 occurs on average 0.02 seconds after LV systolic pressure falls below the aortic pressure.
• P2 occurs on average 0.03 to 0.009 seconds after right ventricular systolic pressure falls below the
pulmonary arterial pressure.
• So the time interval b/n the lowest ventricular systolic pressure and closure of the AV and PV is
called hangout interval
• The hangout time is inversely proportional to the impedance to blood flow in the
systemic arterial and pulmonary arterial systems.
• During inspiration, pulmonary vascular impedance declines with a further increase in the
pulmonary hangout time.

48. Mechanisms of S2 splitting

50. Normal inspiratory splitting of S2

51. Wide splitting of S2
• Wide variable S2 splitting:
• Inspiratory splitting is greater than expiratory. It occurs:
• Pressure overload: Pulmonary stenosis
• Electrical delay: RBBB
• Early aortic valve closure: MR, VSD with low pulmonary vascular resistance
• Wide and fixed S2 splitting:
• The splitting occurs equally in both phases of respiration.
• RV volume overload: ASD, PAPVC
 The mechanism of wide expiratory splitting of S2 appears to result from
isolated shortening of LV ejection time while the RV ejection time
remains normal, and an increase in pulmonary hangout time due to
decreased pulmonary vascular impedance.

52. Paradoxical split of S2
• It occurs when A2 follows P2 during the expiratory phase of respiration.
• The splitting of S2 is then maximal during expiration and the splitting is less or S2
becomes single during inspiration with the normal inspiratory delay of P2.
• It may result from either conduction disturbances or hemodynamic causes:
Conduction disturbance: LBB, preexcitation of the RV (WPW syndrome).
Hemodynamic factors – A markedly prolonged LV ejection time may delay
A2 sufficiently to cause reversed splitting of S2.
Increased resistance to LV outflow: AS, systemic hypertension
Isolated increment in LV stroke volume: PDA, aortic regurgitation
Increased aortic hangout time: PDA, AR and AS

53. Wide and variable splitting of S2

54. Wide fixed splitting

55. Paradoxical split of S2

57. Summary of abnormal S2
Wide splitting of S2 with maintained inspiratory delay of P2
Delayed activation and completion of RV ejection: RBB, WPW syndrome of left ventricle
Prolonged RV ejection time: PAH with RV failure, RV outflow obstruction (eg. PS)
Increased pulmonary hangout time: Idiopathic dilatation of the pulmonary artery, Mild PS
Decreased left ventricular ejection time (early A2): MR, VSD with low pulmonary vascular resistance
Wide and fixed splitting of S2
Interatrial communication; atrial septal defect; common atrium. RV failure of any cause
Reversed splitting of S2
Delayed LV activation and completion of ejection: LBB, Pre-excitation of the right ventricle (WPW syndrome)
Prolonged LV ejection time:
• Increased resistance to left ventricular ejection: AS, obstructive hypertrophic cardiomyopathy, hypertension
• Isolated increase in left ventricular forward stroke volume: AR, PDA
• Myocardial dysfunction: mild to moderate LV dysfunction, myocardial ischemia or infarction
Increased aortic hangout time (not the sole cause): AR, PDA, AS

58. THIRD (S3) AND FOURTH (S4) HEART SOUNDS
• S3 and S4 are low-frequency diastolic sounds that appear to originate
in the ventricles.
• Auscultated best by the bell of the statoscope
• S3 occurs as passive ventricular filling begins at early diastole
• S3 can be heard and recorded in healthy children.
• If it heard in the context of tachycardia, it is most likely to be pathological
gallop than a normal sound.
• If the ventricle resistant to further distention, the poorly compliant
myocardium will vibrate, producing S4.
• Audible S4 always pathologic and are found often in pt with CHF.

59. S3 and S4 sounds

60. • S4 is a low frequency sound heard at the end of diastole just before
S1.
• It is associated with rapid ventricular filling during atrial
contraction and is heard in CHF and condition of decreased
ventricular compliance.
• Its presence, often in the context of tachycardia, may sound like
gallop.
• When gallop rhythm is heard, it is often difficult to distinguish
whether third or fourth heart sound heard.
• This is often called `summation gallop` as it may represent one or both
of those sounds, S3 and S4.

61. • Gallops — An abnormal S3 and S4 tend to be louder and of higher pitch (sharper)
and are frequently referred to as gallops.
• S3 is the ventricular gallop and S4 is the atrial gallop sound.
• S3 and S4 can be fused during tachycardia to produce a loud diastolic filling
sound, termed a "summation gallop" .
• An S3 gallop is an important and common early finding of CHF associated with
dCMP and may also be heard in patients sever chronic MR and AR.
• An S3 often occurs in high-output states such as thyrotoxicosis, pregnancy, or
anemia.
• S4 gallop is most frequently observed in patients with decreased LV
dispensability.
• Thus, S4 is common in hypertensive heart disease, aortic stenosis, and hypertrophic
cardiomyopathy.
• Left ventricular hypertrophy, which is present in all these conditions, contributes to decreased left
ventricular distensibility.

64. • Ejection clicks
• Are high frequency early systolic sound and occur soon after S1.
• Aortic valve clicks heard at apex or right upper sternal border, and don’t vary
with respiration.
• They occur in conditions where the aortic valve is stenotic or the aorta is dilated (e.g.,
TOF, truncus arteriosus).
• Not heard in sub or supra valvular AS.
• Pulmonary valve clicks are heard at left sternal border and louder with
expiration.
• They are associated with mild to moderate pulmonary stenosis, are vary with
respirations, often disappearing with inspiration.
• Mid diastolic click
• A midsystolic, apical click is heard in the diagnostic finding of mitral valve prolapse.
• A midsystolic click may be accompanied by a late systolic murmur.
• Standing after squatting may accentuate a mitral valve click or regurgitant murmur.

65. • PERICARDIAL KNOCK
• It is an early diastolic murmur just after S2, but before S3.
• Ventricular filling is confined to early diastole in constrictive pericarditis and terminates with
a sharp S3; this is termed a "pericardial knock.“ Best heard at apex or LLSB.
• Opening snap
• The opening snap is a high-frequency, early diastolic sound associated with mitral or tricuspid
valve opening.
• This opening of the atrioventricular valves, which is normally silent, becomes audible in the
presence of pathologic conditions.
• Mitral stenosis is the most frequent and important cause of an opening snap.
• The opening snap results from rapid opening of the mitral valve to its maximal open position;
thus, mobility of the valve contributes to its genesis.
• PERICARDIAL FRICTION RUB
• It is generated by the friction of two inflamed layers of the pericardium.
• Pericardial rubs are of scratching or grating quality and appear superficial. They are best
heard with the diaphragm of the stethoscope. Best heard at apex.

66. Heart murmurs
• Cardiac murmurs are the direct result of blood flow turbulence.
• The amount of turbulence and consequently the intensity of a cardiac
murmur depend on:
• The size of the orifice or vessel through which the blood flows
• The pressure difference or gradient across the narrowing
• The blood flow or volume across the site
• Murmurs are generally the loudest near the point of origin since
sound radiates away from its source.
• Murmur description:
• Murmurs should be described according to their intensity, pitch, timing
(systolic or diastolic), area of maximal intensity, and radiation to other areas.

67. • Auscultation for murmurs should be carried out across the upper
precordium, down the left or right sternal border, and out to the apex
and left axilla.
• Auscultation should also always be performed in the right axilla and
over both sides of the back.
• During auscultation of a cardiac murmur, always remember the
cardiac cycle which will help you easily to recognize the origin of the
murmur.
• The intensity of a murmur is primarily determined by the quantity
and velocity of blood flow at the site of its origin.
• Six grades are used to classify the intensity of a murmur:

68. • Grade I: faintest murmur that can be heard (with difficulty; murmur
usually softer than first [S1] and second [S2] heart sounds)
• Grade II: faint murmur but has the same intensity as S1 and S2
• Grade III: louder than S1 and S2 without a palpable thrill
• Grade IV: loud and is associated with a palpable thrill
• Grade V: very loud with a thrill and can be heard with slightest touch
of the stethoscope
• Grade VI: loudest and can be heard without a stethoscope.
• Based on the timing of the murmur in relation to S1 and S2, it is
classified in to systolic, diastolic and continuous murmur.

69. Timing of murmur VS phases of cardiac cycle

70. Phase 1
• This phase is called ventricular diastole
• 80% of atrial blood flows to ventricles
passively. This is called early diastolic
period.
• Then the pressure in the atrium and
ventricles equalized.
• Then the rest 20% atrial blood flows to
ventricles by atrial contraction. Called late
diastolic phase.
• Then the ventricular pressure is much
higher than the atrial pressure, leads to
AV valve closure(S1 will be heard).
• After S1 heard, the semilunar valves(AV
and PV) remain closed.
• The ventricles undergo isovolumic
contraction.

71. Phase 2
• It is called isovolumic contraction.
• It is early systolic phase, and the
murmurs are early systolic murmur
• In this phase if there are murmurs which
are heard immediately after S1, the
origins are either AV valve
insufficiency(MR or TR) or VSD.
• So such types of murmurs are only
maximally heard at LLSB or apex
• These phases murmur(early systolic
murmurs) their locations as follows
1. If it is heard at LLSB(tricuspid area), the
origins are TR or VSD.
2. If it is heard at apex, it is only MR.
• If the duration of these murmurs extend
in to S2, called holosystolic or pansystolic
murmurs

72. Phase 3
• Now the ventricles developed enough pressure
to open the semilunar valves.
• Then ejection of blood from ventricles to great
arteries via semilunar valve occur.
• If murmur heard at this “ejection phase” is
called ejection systolic murmur(ESM)
• It is heard some time after S1 is heard.
• The origins of the murmurs are only due to
ventricular outflow tract obstruction.
• They heard maximally on their respective site
1. The origin of the ESM at RUSB, it is due to left
ventricular out flow tract obstruction(AS)
2. The origin of the ESM at LUSB, it is due to right
ventricular out flow tract obstruction(PS).
• Then systolic phase is over and semilunar
valves closed(S2 heard).

73. Phase 4
• This phase is called early diastolic phase.
• If you hear murmurs just after S2 heard, is
called early diastolic murmur.
• The origin of the murmurs are only due to
semilunar valve regurgitation.
• They mostly maximally heard at either RUSB or
LUSB
1. EDM due to aortic regurgitation maximally
heard at LUSB or RUSB
2. EDM due to pulmonary regurgitation
maximally heard at LUSB.

74. Phase 5
• This phase is called mid diastolic phase.
• If you hear murmurs sometime after S2 heard,
is called mid diastolic murmur.
• The origin of the murmurs are only due to AV
valve stenosis or increased flow through it
• They mostly maximally heard at either LLSB or
apex.
1. MDM due to mitral stenosis or increased
blood flow through it maximally heard at apex
2. MDM due to tricuspid stenosis or increased
flow through it maximally heard at LLSB.

75. Systolic murmurs
• Systolic murmurs are classified as ejection, pansystolic, or late systolic
according to the timing of the murmur in relation to S1 and S2.
• Systolic ejection murmurs start a short time after a well-heard S1 ,
increase in intensity, peak, and then decrease in intensity.
• It is related to either increased flow of blood across a normal semilunar
valves or stenosis of semilunar valves.
• Semilunar valve, subvalvular or supravalvular stenosis: AS or PS.
• Increased volume and/or velocity of blood flow via aortic or pulmonary valve
• Hyperdynamic states such as anemia(decreased viscosity), thyrotoxicosis, pregnancy
• Can be caused by excessive volume through the pulmonary valve are heard in ASD,
pulmonary valve regurgitation, and anomalous pulmonary venous drainage.
• Excessive blood flow via AV in AR, PDA and systemic arteriovenous malformations.

77. • Early systolic murmur
• Obscures S1 and extends for a variable length in systole but does not extend up to S2
• Early systolic murmurs may result from mitral regurgitation (acute sever MR or mild chronic
MR), tricuspid regurgitation, or large ventricular septal defect (with PAH).
• Pansystolic or holosystolic (PSM)
• The murmurs begin almost simultaneously with S1 and continue throughout systole.
• It obscures both S1 and S2.
• It must be related to blood exiting the contracting ventricle via either an abnormal opening
(VSD) or AV (mitral or tricuspid) valve insufficiency.
• Late systolic murmurs
• The murmur starts at late systole and extends into S2
• It is caused by mitral valve prolapse.
• It is best heard with the diaphragm of the stethoscope, over the cardiac apex.
• It is usually preceded by single or multiple clicks
• Location and DDX of systolic murmurs:

79. DIASTOLIC MURMURS

80. • Early diastolic murmurs
• Early diastolic murmurs, most often due to aortic or pulmonary regurgitation.
• They typically start at the time of semilunar valve closure and their onset
coincides with S2.
• An aortic regurgitation murmur begins with A2; pulmonary regurgitation
begins with P2.
• Mid-diastolic murmurs
• Mid-diastolic murmurs result from turbulent flow across the atrioventricular
valves during the rapid filling phase because of mitral or tricuspid valve
stenosis and an abnormal pattern of flow across these valves.
• Mid-diastolic murmurs may occur in the presence of normal atrioventricular
valves when the flow across the valve is markedly increased in mid-diastole.
• Mitral regurgitation and left to right shunt lesions are the usual causes
• Austin Flint murmur — An apical diastolic rumbling murmur in patients with pure AR.

81. • CONTINUOUS MURMURS
• Continuous murmurs are defined as murmurs that begin in systole and extend
up to diastole without interruption.
• These murmurs almost always are vascular in origin.
• They result from blood flow from a higher pressure vessel to a lower system
associated with a persistent pressure gradient between these areas during
systole and diastole.
• Continuous murmurs are caused by the following:
I. Aortopulmonary or arteriovenous connection (e.g., PDA, arteriovenous fistula,
persistent truncus arteriosus)
II. Disturbances of flow patterns in veins (e.g., venous hum)
III. Disturbance of flow pattern in arteries (e.g., COA, PA stenosis).
• The murmur of PDA has a machinery-like quality.
• This murmur is maximally heard in the left infraclavicular area.
• With pulmonary hypertension, only the systolic portion can be heard.

82. • Venous hum is a common innocent murmur that is audible in the
upright position, in the infraclavicular region, unilaterally or bilaterally
• It is usually heard better on the right side.
• The murmur’s intensity also changes with the position of the neck.
• When the child lies supine, the murmur usually disappears.
• Less common continuous murmurs of severe COA may be heard over the
intercostal collaterals.
• The continuous murmurs of peripheral pulmonary artery stenosis may be heard
over the right and left anterior chest, the sides of the chest, and in the back.
• The combination of a mid-systolic murmur (e.g., VSD, AS, or PS) and a diastolic
murmur (e.g., AR or PR) is referred to as a to-and-fro murmur .

83. Innocent murmurs
• Innocent heart murmurs, also called functional murmurs, arise from
cardiovascular structures in the absence of anatomic abnormalities.
• More than 80% of children have innocent murmurs of one type or another
sometime during childhood.
• All innocent heart murmurs (as well as pathological murmurs) are accentuated or
brought out in a high-output state, usually during a febrile illness.
• In general, innocent murmurs are low in intensity, and low in frequency.
• Most innocent murmurs, with the exception of the venous hum, are systolic
ejection in timing.
• Innocent murmurs are not associated with abnormalities in the palpation exam
and are associated with normal heart sounds.

85. Diagram of common innocent murmurs in children

86. • All innocent heart murmurs are associated with normal ECG and
radiography findings.
• When one or more of the following are present, the murmur is more
likely pathologic and requires cardiac consultation:
1. Symptoms
2. Abnormal cardiac size or silhouette or abnormal pulmonary vascularity on
chest roentgenograms
3. Abnormal ECG findings
4. Diastolic murmurs
5. A systolic murmur that is loud (i.e., grade 3 of 6 or with a thrill), long in
duration, and transmits well to other parts of the body
6. Cyanosis
7. Abnormally strong or weak pulses
8. Abnormal heart sounds