ABDULRAHMAN BASHIRE BENGHAZI CHILDREN HOSPITAL

Nov. 12
First introduce yourself to the patient and parent, (Let the child slowly accept you
as no threat as you talk with the parents; observe the patient as you talk with the
parent. Often the child is more comfortable when examined on a parents lap),
dont forget to wash your hands.
Next stand back and give a brief general description of the child.
Much information can be obtained by simple inspection of a patient, a quick look
when seeing the patient initially. General appearance should be assessed including
the patient looks well or sick.
Is the patient fussy or playful?
Look for any obvious findings consistent with chromosomal abnormality or
possibility of a syndrome (Down, Turner, Noonan, William, Marfan, Alagille
syndrome).
General growth parameter( in particular failure to thrive or short stature)
A. Height and weight should be performed and plotted on an appropriate growth
curve to compare to normal values for age and sex. Plot the measurements with
any known historical measurements such as birth weight to determine if a patient
has been growing well or has fallen on the growth curve.
Height:-
v Short ( Down, Noonan, Turner, heart disease causing failure to thrive)
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Nov. 12
v Tall ( Marfan, check arm span if you suspect this)
Weight:-
Failure to thrive ( congenital rubella, sever heart disease, cyanosis or
congestive heart failure)
Head circumference small ( congenital rubella).
B. Head and neck:-
Conjunctiva for pallor( anaemia), congestions ( chronic cyanosis)
Sclera for jaundice ( fragmentation hemolysis with artificial valve, hepatic
congestion with congestive heart failure)
Lips for cyanosis
Tongue for cyanosis
Gum hypertrophy for chronic cyanosis
Dental caries risk of SBE
C. Hands:-
Pallor , clubbing, splinter hemorrhage, oslers node, janeway lesions, peripheral edema
Roth spots are exudative, edematous hemorrhagic lesions of the retina.
Oslers nodes are painful, violaceous nodules on the pulp of the fingers and toes.
Janeway lesions are macular, blanching, nonpainful, erythematous lesions on the
palms are soles.
Splinter hemorrhages:- multiple linear reddish-brown marks found along the axis of
the finger- and toenails
D. ARTERIAL PULSES
The radial pulse is found at the wrist, lateral to the flexor carpi radialis tendon. Use
this to assess pulse rate and rhythm.
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Nov. 12
The brachial pulse is found in the antecubital fossa medial to the biceps tendon.
The carotid pulse is most easily palpable at the angle of the jaw, anterior to the
sternocleidomastoid muscle.
The heart rate and respiratory rate should be taken for a full minute rather than 15 s
and multiplying by 4, as there can be significant variation, particularly in younger
children.
Pulses should be assessed in both the upper and lower extremities. Take care to note
if pulses are easily palpable, and if regular in rate; also note the quality of the pulse.
A coarctation of the aorta should be suspected when the lower extremity pulses are not
equal in quality to that of the right upper extremity.
In an infant, palpate for pulse rate over the brachial artery.
In an older child or adult, the wrist is generally the optimal location.
Palpate the larger brachial and carotid arteries for a more reliable assessment of pulse
volume and character than is given by the radial puls
Table 416-4 -- PULSE RATES AT REST
AGE
LOWER LIMITS OF
NORMAL
AVERAGE
UPPER LIMITS OF
NORMAL
Newborn 70/min 125/min 190/min
111 mo 80 120 160
2 yr 80 110 130
4 yr 80 100 120
6 yr 75 100 115
8 yr 70 90 110
10 yr 70 90 110
sinus arrhythmia represents a normal physiologic variation in impulse discharges
from the sinus node related to respirations. The heart rate slows during expiration and
accelerates during inspiration.
Tachycardia may be a manifestation of anemia, dehydration, shock, heart failure, or
dysrhythmia.
Sinus bradycardia is due to slow discharge of impulses from the sinus node, the
heart's natural pacemaker. A sinus rate <90 beats/min in neonates and <60 beats/min
in older children is considered to be sinus bradycardia. It is commonly seen in well-
trained athletes; in healthy individuals (These rhythm changes, especially bradycardia,
appear more commonly during sleep and are not associated with symptoms. Usually,
ABDULRAHMAN BASHIRE BENGHAZI CHILDREN HOSPITAL
Nov. 12
no therapy is necessary). Sinus bradycardia may occur in systemic disease
(hypothyroidism or anorexia nervosa), and it resolves when the disorder is under
control. It may also be seen in association with conditions in which there is high vagal
tone, such as gastrointestinal obstruction or intracranial processes. complete heart
block : all forms of heart block are rare in children, it may occur in otherwise normal
children but is usually the result of structural heart disease, interacardiac surgery or
rheumatic carditis ( rare nowdays). Low birthweight infants display great variation in
sinus rate. Sinus bradycardia is common in these infants in conjunction with apnea,
and may be associated with junctional escape beats. Premature atrial contractions are
also frequent.
Sinus tachycardia Arrhythmia
Exercise Supraventricular tachycardia
Pain, anaemia, dehydration Atrial fibrillation
Fever Atrial flutter
Hyperthyroidism Ventricular tachycardia
Medication: sympathomimetics
Vasodilators
Slow heart rate (bradycardia, < 60/min)
Sinus bradycardia Arrhythmia
Sleep Carotid sinus hypersensitivity
Athletic training Sick sinus syndrome
Hypothyroidism Second-degree heart block
Medication: Complete heart block
beta-blockers, digoxin verapamil, diltiaze
Volume is the movement imparted to your fingers and reflects the pulse pressure - the
difference between systolic and diastolic blood pressure.
Character is the impression of the pulse waveform obtained. Pulse volume and
character are best appreciated from a major pulse, such as the carotid
The volume and character are assessed by palpation with index finger of the brachial
pulse or femoral in an infants.
A large volume pulse may be due to aortic regurgitation, or a high cardiac output
state. Exercise, emotion, heat and pregnancy are physiological factors causing
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Nov. 12
vasodilatation and increased cardiac output, which also occurs with fever,
thyrotoxicosis, anaemia, peripheral arteriovenous shunts and Paget's disease of bone.
A low volume pulse is associated with reduced stroke volume due to heart failure, or
peripheral vascular disease. The pulse may be thin and 'thready' in hypovolaemia due
to haemorrhage or dehydration.
Coarctation is a congenital narrowing of the aorta, usually situated immediately distal
to the left subclavian artery. In children with coarctation the upper limb pulses are
normal, while all lower limb pulses are reduced or impalpable. In adults, coarctation
usually presents with hypertension. Femoral pulses are usually palpable because of
the development of collaterals but are of low volume and delayed with respect to the
radial pulse.
Pulsus alternansis rare and describes a beat-to-beat variation in pulse volume in the
presence of a regular rhythm. It occurs in sever left ventricular failure and in sever
damage of the left ventricular muscle.
Pulsus paradoxusis a pulse that increases in volume on expiration and decreases in
volume in inspiration. This variation occurs in health but is not normally easy to detect.
This variation in pulse pressure is abnormal if it is exaggerated to the point that it is
clinically detectable. It occurs with severe airways obstruction e.g. acute asthma,
because of extreme changes in intrathoracic pressure, and in pericardial tamponade
due to a large pericardial effusion. Pulsus paradoxus is best assessed by measuring
the difference in systolic blood pressure during inspiration and expiration. A difference
> 15 mmHg is pathological.
During inspiration:-
intrathoracic pressure negativity the venous return End diastolic
ventricular volume with ventricular contraction, the stroke volume will increase
pulse volume decrease.
During expiration :-
Decrease stoke volume & increase pulse volume.
So change in intrathoracic pressure are superimposed on arterial blood pressure, SBP
& DBP rise & fall in parallel so there no consistent change in pulse pressure.
Normally the difference between inspiratory & expiratory systolic blood pressure is 5-
10 mmHg. But if the difference between inspiratory & expiratory systolic blood pressure
is more than 15 20 mmHg so pulsus paradoxus are detected clinically. That seen in
sever bronchial asthma and cardiac temponade due to a large pericardial effusion.
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Nov. 12
Bounding pulses (easily palpable) reflect runoff lesions such as aortic insufficiency or
a patent ductus arteriosus, but can also be seen in patients with sepsis. Diminished
pulses in all extremities is suggestive of ventricular dysfunction.
A. Regular rhythm :-
B. Irregular rhythm:-
Regularly irregular rhythm:- Extrasystoles extremely common in normal
children and disappear with exertion whereas pathological extrasystoles (
digoxin toxicity ) are exacerbated by exertion.
irregularly irregular rhythm:- atrial fibrillation ( very rare indeed) often
associated with structural defect and possible congestive heart failure,
causes of atrial fibrillation are:- ASD , open heart surgery or atrial surgery,
Ebesteins anomaly of tricuspid valve, rheumatic mitral stenosis.
Assess the respirations looking for tachypnea or increased work of breathing.
Tachypnea can occur secondary to increased pulmonary blood flow in left to right
shunt lesions such as a ventricular septal defect or a patent ductus arteriosus.
Increasing pulmonary congestion can cause the development of grunting, nasal flaring,
and intercostal and subcostal retractions, although most tachypnea associated with
pulmonary overcirculation is quiet tachypnea.
E. Blood pressure should be obtained in the right upper extremity and a lower
extremity, at a minimum, when evaluating patients for a suspected pathologic
cardiac murmur.
The most common method of measuring peripheral arterial pressure is
sphygmomanometry, or the Riva-Rocci method. The examiner places a cuff containing
an inflatable bladder around an arm or leg proximal to an accessible artery and
connected to a pressure gauge and a source of air pressure, usually a rubber bulb with
a pressure-relief valve. While palpating the pulse in the artery distal to the cuff, he or
she inflates the cuff, thus increasing pressure around the extremity.When the pulse is
no longer palpable, the examiner releases cuff pressure while listening over the artery
with the stethoscope bell. As cuff pressure decreases, a sequence of varying sounds
(the Korotkoff sounds) become audible.
The 1st Korotkoff sounds indicate systolic pressure. As cuff pressure is slowly
decreased, the sounds usually become muffled before they disappear. Diastolic
pressure may be recorded when the sounds become muffled (preferred) or when they
disappear altogether; the former is usually slightly higher and the latter slightly lower
than true diastolic pressure.
ABDULRAHMAN BASHIRE BENGHAZI CHILDREN HOSPITAL
Nov. 12
Initially, blood pressure in the right arm is measured. If elevated, measurements in the
left arm and legs are indicated to evaluate for possible coarctation of the aorta. (The
right arm is preferred, as the left arm may be involved in a coarctation of the aorta
and give a falsely low reading)
The blood pressure cuff should be of an appropriate size for the extremity with the
width of bladder 4050% of the circumference (or 125155% of the diameter) of the
limb and bladder length of 80100% of circumference. The correct size cuff is
important.
If the blood pressure cuff is too small, the blood pressure obtained will be artificially
high so it is better to err with a cuff that is too large than too small.
In infants, blood pressure can be determined by auscultation, palpation, or an
oscillometric (Dinamap) device that, when properly used, provides accurate
measurements in infants as well as older children.
Auscultation is the preferred method for blood pressure measurement, however, most
clinics utilize oscillometric devices to measure blood pressure as these devices are
convenient to use and decrease interobserver variability. The blood pressures obtained
by an oscillometric device tend to be higher than those obtained manually.
Blood pressure in the upper extremity is best obtained in a patient who has been sitting
for 35 min, the back supported, feet on the floor, and the arm supported at heart level
(level of the right atrium). The average of two to three blood pressure measurements
should be used. Following these guidelines will increase the likelihood of having a true
resting blood pressure.
For the lower extremity blood pressure, the patient should be supine and an
appropriate-sized cuff applied to either the calf or thigh (same rules for cuff size as for
the arm). In children, the lower extremity systolic blood pressure should be equal to or
slightly higher than the upper extremity blood pressure, often exceeding the upper
extremity blood pressure by 510 mmHg. If the systolic blood pressure in the lower
extremity is lower than the upper extremity by more than 10 mmHg, then a coarctation
of the aorta may be present.
The pulse pressure, or the difference between the systolic and diastolic blood
pressure, It is normally below 50 mm Hg or half the systolic pressure, whichever is
less. and results in bounding pulses.
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Nov. 12
A widened pulse pressure is seen in:-
aortic insufficiency,
truncus arteriosus
patent ductus arteriosus,
arteriovenous malformations.
increased cardiac output (low diastolic pressure) secondary to:-
* anemia,
* anxiety,
* conditions associated with increased catecholamine or
thyroid hormone secretion.
A narrow pulse pressure is seen with:-
pericardial tamponade,
aortic stenosis,
heart failure. conditions reducing cardiac output
myocarditis
Oxygen saturation should be obtained as part of the evaluation of a murmur in infants
in the first couple months of life and in all patients presenting with tachypnea or
complaints of cyanosis. Low oxygen saturations in infants with a heart murmur
suggests the possibility of cyanotic heart disease.
Blood pressure determination in both arms and a lower extremity will detect coarctation
of the aorta, lend support for the diagnosis of supravalvular aortic stenosis (blood
pressure higher in the right arm than in the left arm, due to the Coanda effect), and
help to assess the severity of aortic valve disease including aortic valve stenosis
(narrow pulse pressure) and aortic regurgitation (wide pulse pressure).
Though of little use in infants, in cooperative older children, inspection of the jugular
venous pulse wave provides information about central venous and right atrial
pressure. The neck veins should be inspected with the patient sitting at a 90-degree
angle. The external jugular vein should not be visible above the clavicles unless central
venous pressure is elevated. Increased venous pressure transmitted to the internal
jugular vein may appear as venous pulsations without visible distention; such pulsation
is not seen in normal children reclining at an angle of 45 degrees. Because the great
veins are in direct communication with the right atrium, changes in pressure and the
volume of this chamber are also transmitted to the veins. The one exception occurs in
superior vena cava obstruction, in which venous pulsatility is lost.
is bluish discolouration of normally pink area, it occur when a minimum of 5
gm deoxygenated Hb is present in the skin capillaries regardless of the total Hb,
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Nov. 12
corresponding to an arterial oxygen saturation of about 75% for HB concentration of
about 12-16 g/dl. The cyanosis develop less easily in anaemic child, more easily in
child with Polycythemia and not at all in child with an anemia with Hb less than 5gm/dl (
sever anaemia).
Cyanosis is most easily detected in the tongue, the mucous membranes of the mouth,
lips and the nail beds. Observation of the lips and mucous membranes for the
presence of cyanosis is best done in good daylight because fluorescent lighting
may produce a false cyanotic tinge. Cyanosis is associated with desaturation of 5 g
of hemoglobin and is difficult to detect unless the oxygen saturation is less than 85%.
If there is long-standing cyanosis, then digital clubbing may be present. Clubbing is
uncommon in early infancy. Clubbing, conjunctival injection and gum hypertrophy
indicate that the cyanosis is chronic.
Note for infants just press on the chin for check the mucous membrane where old
patient , observe for the tongue.
Peripheral cyanosis seen in the hands, lips and ears in cold weather as consequence
of cold induced vasoconstriction slowing the blood through the capillary bed
excessive removal of oxygen from the blood at the tissue level.
Peripheral cyanosis are associated with:-
Local venous obstruction
Vasomotor instability
Occasionally seen in shock, sepsis and CCF ( reduced cardiac output when
vasoconstriction divert the blood flow from the skin to other organ as brain)
Peripheral cyanosis is seldom seen in the tongue or buccal mucosa because they are
well perfused except in advanced circulatory failure.
Central cyanosis detected when the oxygen saturation of arterial blood fall below85%.
The central cyanosis may due to:-
Respiratory.
Cardiac. (Cyanotic congenital heart disease)
Central nervous system.
Hematological disorder. methemoglobinemia( patient is cyanosed but not
dyspniec)
Cyanosis in LL > UL in patient with infantile coarctation of aorta and in patient with
pulmonary hypertension with PDA.
Cyanosis in UL > LL in children with TGA with PDA.
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Nov. 12
The cardiac physical examination should be performed in a systematic manner to
assure complete evaluation of the patient. The physical examination typically begins
with inspection.
:-
Inspect the chest, assessing for any asymmetry. In Marfan syndrome, patients may
have pectus excavatum or carinatum. Chest wall abnormalities may alter findings on
electrocardiogram and chest x-ray.
Rule out chest deformity:-
kyphosis.
Scoliosis:- may alter the position of landmarks such as the cardiac apex.
Sternal deformity:-
pectus excavatum:- congenitally depressed sternum and costal
cartilages.
pectus carinatum:- ("pigeon chest") is characterized by protrusion
of the sternum and costal cartilages.
Harrisons sulcus:- indrawing of the lower rib flaring. may occur in
condition with increased pulmonary blood flow.
precordial bulge will cause the sternum and rib to bow forward,giving the
chest an over blown appearance. Patients with long-standing cardiomegaly
may develop a precordial bulge on the left side of the chest.
A visible cardiac impulse may also be seen during chest inspection and implies
hyperdynamic ventricular function.
Diffuse left parasternal pulse of right ventricular hypertrophy.
In second left intercostals space ( enlarged pulmonary artery).
In second right intercostals space or upper sternum ( aneurysm of the
aorta).
Epigastric pulsation ( enlargement of the right ventricle)
Scar on the anterior chest wall, posterior chest wall:-
Sternostomy scar = total correction.
Left side scar:-
Lt scar and no murmur = corrective operation in PDA.
corrective operation coarctation of the aorta.
Lt scar with ESM at the same side posteriorly = Palliative
operation, Banding of the pulmonary artery in huge VSD and
univentricle, Palliative operation done in infant > 2 month old.
ABDULRAHMAN BASHIRE BENGHAZI CHILDREN HOSPITAL
Nov. 12
Right side scar and machinery murmur:- BT shunt done in infant < 2
month old to decrease pulmonary blood flow .
:-
Palpation of the chest should be performed with the most sensitive part of the hand.
For some, this is the metacarpals and for others the fingertips. The apex beat is the
lowest & outermost point of definitive cardiac pulsation. The point of maximal
impulse should be noted, usually it is found in the midclavicular line in the fourth
intercostal space in children up to 4 years of age and the fifth intercostal space in
older children.
Palpation to detect the point of maximal pulsation of the heart may be same with apex
beat in left side dominance or another point rather than apex beat in right side
dominance.
The impulse may be displaced medially when there is right ventricular dominance or
laterally displaced in patients with left ventricular volume overload (left to right shunts,
aortic insufficiency, and mitral valve regurgitation).
Check the trachea position where in lung and pleura disease the trachea may be
deviated to one side but in cardiac disease the trachea is centrally located.
Pleural effusion.
Pneumothorax. Push the apex beat
So check the trachea position.
Pulmonary fibrosis.
Lung collapse. Pulling the apex beat
Apex beat may be difficult to feel in:-
Children < 2 year of age.
Pericardial effusion.
Heart failure.
Emphysema.
Dextrocardia (apex to the right) or mesocardia (apex to the middle).
Palpation also allows assessment for increased precordial activity such as a ventricular
tap or heave.
A tap is a more focal increased impulse typically related to hypertrophy of a ventricle.
Pulmonary hypertension pressure overload produce tap ( forceful & less
sustain impulse)
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Nov. 12
A heave is a diffuse impulse that occurs when there is volume overload of a ventricle.
ASD, VSD ( large) as well as AV Canal fluid overload forceful and sustained
impulse ( heave).
A thrill may be felt in association with a murmur and is a palpable vibratory sensation.
Thrills can be found anywhere in the precordium, suprasternal notch, supraclavicular
area, and over the carotid arteries..
The thrill at the apex is more easily felt with the child on the left side. Where basal
thrills are more easily felt with the child sitting up.
The location of the thrill usually correlates with the structural cardiac lesion causing a
cardiac murmur:-
1. Systolic thrill at the base of the heart are usually due to:-
Septal defect.
Aortic stenosis.
Occasionally pulmonary stenosis.
2. Continouos thrill at the base of the heart PDA
3. Systolic thrill in suprasternal notch( pulsatile) are usually due to:-
PDA.
Aortic insufficiency.
4. Systolic thrill at the lower left sternal border VSD.
5. Diastolic thrill at the apex mitral stenosis.
A palpable second heart sound may be noted in pulmonary hypertension or from
anterior positioning of the aorta, such as in transposition of the great arteries.
The first heart sound may be palpable in hyperdynamic states from any cause,
including exercise and fever.
Heart sounds may be felt during palpation in infants or patients with thin chest walls
and does not necessarily indicate cardiac pathology.
Abdominal palpation should assess the size of the liver. In young children the liver may
be at the costal margin or just below. If the liver is enlarged, this may be a finding
suggesting congestive heart failure.
ABDULRAHMAN BASHIRE BENGHAZI CHILDREN HOSPITAL
Nov. 12
:-
Auscultation of the heart should be performed sitting, supine, and standing if possible.
Sometimes, specific maneuvers may be required to bring out a cardiac murmur.
Proper equipment and the correct setting to perform auscultation are essential. A good
stethoscope has both a bell for low frequencies and a diaphragm for high frequencies.
To maximize the chances for successful auscultation the exam room should be quiet
and free from distractions.
Both the patient and the examiner should be comfortable. It is hard to concentrate on
the exam if performing bodily contortions. The patient should be unclothed, or at least
the stethoscope should be placed on the skin. Modesty may require the patient to be in
an exam gown. Younger children may be a challenge to examine as they may become
fussy or cry during the exam. With small children try simple maneuvers to calm or ease
the patient.
Auscultation should occur at least in the four main areas familiar to most providers,
pulmonary, aortic, mitral, and tricuspid areas, but should not be limited to just these
areas. Additional areas to examine are both infraclavicular areas, both carotids, the
axillae in the fourth or fifth intercostal space, and the posterior chest inferior and medial
to the scapula. Each area should be examined with the patient sitting, standing, and
lying down.
A complete auscultatory examination may take up to 510 min to complete properly.
:-
The first heart sound (S1) is caused by the closure of the mitral and tricuspid valves
(atrioventricular valves). The first heart sound is low-pitched and relatively long
compared to the second heart sound. S1 is best heard at the apex and precedes
systole and the carotid pulsation. To assist with determining which heart sound is S1,
the carotid pulsation can be palpated and S1 is always the heart sound that precedes
the carotid pulsation.
Normal splitting of S1 may be noted in some pediatric patients in the tricuspid area. A
normal split of S1 needs to be differentiated from an ejection click or an S4 gallop. In
normal splitting of S1, the splitting is less noticeable as one moves laterally and should
not persist at the anterior axillary line. If still present at the anterior axillary line, then
one should suspect presence of an ejection click.
Ejection clicks are often at a fixed interval to S1, while a split S1 should vary with the
respiratory cycle, increasing with inspiration. Usually, heart sounds are lower pitched
than ejection clicks.
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Nov. 12
Fixed splitting of S1 may occur in patients with interventricular conduction delays,
bundle branch block, and ventricular rhythms where one ventricle contracts earlier.
A loud S1 can be associated with high cardiac output states such as:-
anemia,
fever,
thyrotoxicosis,
exercise,
anxiety,
ASD
mitral stenosis,
arteriovenous fistula,
epinephrine administration.
S1 may be decreased in intensity in low cardiac output states such as:-
hypothyroidism,
cardiomyopathy,
mitral regurgitation,
myocarditis,
shock
when there is increased chest wall thickness or pericardial fluid present.
S1 is best heard at the apex and precedes systole and the carotid pulsation.if S1 isnt
well heard at the apex ask the patient to roll on the left side.
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Nov. 12
The second heart sound (S2) is produced by closure of the semilunar valves (aortic
and pulmonary) at the end of ventricular systole.it is immediately follow the carotid
pulse wave, it is usually heard at he upper left sterna. border. The aortic valve closure
(A2) occurs earlier and is louder than the closure of the pulmonary valve (P2).
Normally, there is variation in the splitting of S2 related to the respiratory cycle.
During inspiration, increase the venous return to the right side of the heart the
right ventricle fills more increased the right ventricular stroke volume delay
closure of the pulmonary valve . splitting S2
In exhalation, the right ventricle fills less resulting in P2 coming earlier with A2 and P2
occurring nearly simultaneously resulting in S2 usually becoming a single sound. This
normal or physiologic splitting of S2 (splitting during inspiration and single during
expiration) is best appreciated at the high left sternal border in the second to fourth
intercostal spaces.
There are some variations in S2 worth noting. A wide and fixed split S2 is noted in
patients with an atrial septal defect. This occurs from increased volume flowing through
the right heart and a decreased variation in right ventricular volume with respiration.
Additionally, the right ventricle is dilated resulting in further distance for electrical
activity to travel and excite the right ventricle, resulting in delay of right ventricular
emptying. As a result of these physiologic changes, the pulmonary component of S2
continues to occur later than the aortic component resulting in a fixed split S2.
The physiologic change that delays right ventricular emptying may result in a
widely split S2. This includes:-
1. right ventricular outflow tract obstruction (pulmonary valve stenosis or
subvalve stenosis),
2. severe mitral valve regurgitation (shortened left ventricular ejection time),
3. dilation of the main pulmonary artery (diminished recoil forces on the
pulmonary valve, delaying closure),
4. right bundle branch block,
5. premature ventricular contractions originating from the left ventricle.
A loud S2 occurs with increased diastolic blood pressure and decreased viscosity of
the blood (anemia). It may result from a loud A2 or P2.
A loud P2 may be heard in patients with:-
1. pulmonary hypertension.
2. increased pulmonary blood flow eg PDA, ASD, large VSD.
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Nov. 12
A loud A2 can be heard in:-
1. systemic hypertension,
2. coarctation of the aorta,
3. transposition of the great arteries,
4. aortic insufficiency.
Patients with a single semilunar valve (aortic atresia, pulmonary atresia, truncus
arteriosus) will have a single S2. Patients with transposition of the great arteries,
tetralogy of Fallot, or other cardiac defects that move the aorta anteriorly can result in a
loud single S2. Due to the fast heart rate in newborns, it is often difficult to appreciate if
there is a single S2.
Paradoxical splitting of S2 can also occur with A2 heard after P2.it is noted in:-
1. left bundle branch block,
2. hypertrophic obstructive cardiomyiopathy.
3. WolffParkinsonWhite syndrome,
4. aortic stenosis,
5. left ventricular outflow tract obstruction,
6. patent ductus arteriosus.
The reason for paradoxic splitting in these conditions is the delay in emptying of the left
ventricle by either electrical or anatomic changes.
Systolic ejection clicks are medium- to high-pitched sounds which closely follow S1.
They are associated with abnormalities of the semilunar valves or sometimes with
dilation of the aorta or pulmonary artery. Clicks are high pitched sounds, best
appreciated with the diaphragm of the stethoscope.
Aortic clicks are generally unchanged by the respiratory cycle and are called constant
early systolic ejection clicks. Aortic clicks can be heard at the second right intercostal
space but are often heard best at the apex.
The differential diagnosis for a patient with an aortic click includes:-
dilated aorta,
aortic stenosis,
bicuspid aortic valve.
Pulmonary ejection clicks may fade out or disappear with inspiration and are called
variable early systolic ejection clicks. Pulmonary clicks tend to be heard best at the
left upper sternal border (second intercostal space) during expiration. The differential
diagnosis for a patient with a pulmonary ejection click includes pulmonary valve
stenosis or a dilated pulmonary artery.
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A mid-systolic click is a high-pitched sound occurring in mid-systole usually associated
with mitral valve abnormalities such as mitral valve prolapse. If there is associated
mitral valve regurgitation with the mitral valve prolapse, then a regurgitant murmur can
be heard after the midsystolic click. The click should come later in systole with
squatting and heard better with the patient standing or with held expiration.
Gallops may also be heard during the cardiac cycle.
Early rapid filling of the ventricle,which follows the opening of the atrioventricular valve,
may produce the third heart sound (S3); An S3 gallop occurs early in diastole, low
pitched after second heart sound. increases with inspiration, and is heard with bell best
at the apex or just medial to the apex of the heart with the patient lying supine or on
their left side. An S3 gallop can be a normal finding in children, but a loud S3 suggests
pathology. Increased intensity of S3 occurs in excitement, anemia, or a large left to
right shunt.
ventricular filling related to the forceful expulsion of blood from the atrium into the
ventricle with atrial contraction may produce the fourth heart sound (S4). S4 gallops
occur before the first heart sound, low pitched, late in diastole and are associated with
atrial contraction. It is usually heard best with the patient recumbent, at the apex, and
during expiration utilizing the bell of the stethoscope.
Differential diagnosis for a patient with an S4 gallop includes:-
pulmonary hypertension,
pulmonary stenosis,
Ebsteins anomaly of the tricuspid valve,
tricuspid valve atresia,
total anomalous pulmonary venous return,
complete heart block.
A summation gallop (combination of S3 and S4) is often more intense than either
component. It is the most common gallop noted in pediatric patients and is commonly
associated with heart failure from large left to right shunts. A summation gallop is
pathognomonic for Ebsteins anomaly of the tricuspid valve.
:-
A complete description of a murmur includes a number of features: location, timing,
loudness, type, pitch, quality, and transmission. Given a complete description, most
cardiac murmurs can lead to a specific diagnosis, even without an echocardiogram.
Location:-
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Most practitioners are familiar with the usual areas of auscultation to include the
pulmonary, aortic, mitral, and tricuspid areas.
The pulmonary area is at the left upper sternal border or left second intercostal space
at the sternal edge.
The aortic area is at the right upper sternal border or second right intercostal space at
the sternal edge.
The mitral area is at the apex or fifth intercostal space in the midclavicular line.
The tricuspid area is at the left lower sternal border or fourth and fifth intercostals
spaces at the sternal edge.
Location of a murmur should be described by where it is the loudest (point of maximal
intensity) not by where it is heard by transmission.
Although these are the four primary areas for auscultation, the cardiac examination
should not be limited to these four areas.
Additional areas to auscultate include:-
the infraclavicular areas,
over the carotid arteries,
each axilla (at about the fourth and fifth intercostal space),
the posterior aspect of the chest just medial and inferior to each scapula.
Examining all these areas allows for full evaluation of a cardiac murmur.
Timing:-
Murmurs can occur in systole, diastole, or be continuous. At times this is difficult to
assess, particularly in younger patients or patients with high heart rates. Palpating a
pulse while performing auscultation may allow one to determine the timing of a
murmur. Also, a continuous murmur does not mean it is always present; instead the
murmur just needs to spill past S2 into diastole to qualify as continuous. Murmurs can
occur early, mid, or late in either diastole or systole:
Early systolic murmurs start abruptly but taper and disappear before S2 and are
associated with a small muscular ventricular septal defect that becomes occluded
during systole.
Mid-systolic murmurs are the most common type of murmur heard and include the
benign flow murmurs and murmurs associated with aortic or pulmonary stenosis.
Mid- to late systolic murmurs begin midway through systole and are often heard in
association with midsystolic clicks and insufficiency of mitral valve prolapse.
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Early diastolic murmurs are from aortic insufficiency or pulmonary insufficiency and
have a decrescendo pattern.
Mid-diastolic murmurs are typically flow rumbles from increased flow across the
atrioventricular valves associated in large shunt lesions such as ventricular septal
defects.
Late diastolic murmurs are typical of mitral or tricuspid valve stenosis and occur
with atrial contraction.
Diastolic murmurs are always felt to be pathologic in origin.
Murmur intensity
Grade
1 Only noted when concentrating
2 Easily heard
3 Very easily heard
4 Easily heard and associated thrill
5 Heard with stethoscope on edge on chest
6 Heard with stethoscope off the chest
Listening Areas for Common Pediatric Heart Murmurs
Area Murmur
Upper right sternal border Aortic stenosis, venous hum
Upper left sternal border Pulmonary stenosis, pulmonary flow murmurs,
atrial septal defect, patent ductus arteriosus
Lower left sternal border Still's murmur, ventricular septal defect,
tricuspid valve regurgitation, hypertrophic
cardiomyopathy, subaortic stenosis
Apex Mitral valve regurgitation
Maneuvers
There are a variety of maneuvers that can be performed at the bedside that allow the
murmur to be heard better and help to further define the etiology of the murmur.
Maneuvers tend to change the volume of blood flow through the heart. The simplest of
the maneuvers is patient position, hence the recommendation to examine a patient
sitting, supine, and standing. Other maneuvers include Valsalva, exercise, respiration,
transient arterial occlusion, response after a premature ventricular contraction, and use
of amyl nitrite.
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Postural changes are the easiest maneuvers to perform as this only requires the
patient to sit, stand, or lie down, making it very likely the patient will comply.
Standing is similar to the strain phase of a Valsalva causing a decrease in venous
return, decrease in stroke volume, decreased systemic vascular resistance, and an
increase in heart rate.
These physiologic changes make the murmur of hypertrophic cardiomyopathy and the
mid-systolic click of mitral valve prolapse increase in intensity. Murmurs that are flow
related such as pulmonary flow murmur, aortic stenosis, aortic regurgitation, and mitral
regurgitation murmurs are decreased in intensity with standing.
Squatting increases systemic vascular resistance, increases venous return, and
increases stroke volume while decreasing heart rate. These physiologic changes
decrease the murmur associated with hypertrophic cardiomyopathy and increases the
flow-related murmurs of aortic stenosis, mitral regurgitation, aortic regurgitation,
and pulmonary flow murmur.
A supine position favors immediate increased systemic venous return to the right
heart and shortly after to the left heart. There is an increase in stroke volume which
increases the intensity of many murmurs, including:-
v Stills murmur.
v the benign pulmonary flow murmur of adolescence.
v tricuspid valve diastolic murmur (flow rumble) associated with an atrial septal
defect.
v patent ductus arteriosus.
v pulmonary valve stenosis.
left lateral supine position with the patient rolled up onto their left side while lying on
the exam table brings the heart closer to the lateral chest wall and raises the intensity
of mitral valve murmurs, both regurgitation and stenosis. This position also increases
an S3 gallop.
Other maneuvers to assist in cardiac auscultation require cooperation by the patient or
equipment but may assist in determining the etiology of a murmur.
A Valsalva maneuver has four physiologic phases but is clinically a two-part process
with a strain phase and a release phase. Phase I occurs as strain commences lasting
only 13 s and is usually undetectable at the bedside. In phase II of the Valsalva, there
is a decrease in systemic venous return, blood pressure, and pulse pressure. Right
heart filling is decreased and cardiac output decreases.
After 3 or 4 s, there is arterial and venous constriction and increased heart rate. This
part of a Valsalva is clinically appreciable. Phase III begins with release of the strain
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which is very brief and difficult to perceive at the bedside.
Phase IV is composed of an overshoot of systemic blood pressure which causes a
decrease in heart rate, which can be easily detected at the bedside. Venous return is
increased above the baseline prior to the Valsalva and there is a time delay between
the filling of the right ventricle and the left ventricle. Right-sided cardiac murmurs
usually return to baseline in one to four cardiac cycles, leftsided murmurs in five to ten
cycles.
Valsalva maneuver (phase II) decreases both systemic and pulmonary venous return
to the heart and is particularly effective in reducing an innocent Stills murmur and
decreases the intensity of all left-sided murmurs except mitral valve prolapse and
hypertrophic cardiomyopathy.
In the release phase of Valsalva (phase IV), the murmurs of mitral valve prolapse and
hypertrophic cardiomyopathy are decreased.
Innocent heart murmurs are a common finding on examination of children and there
are four benign systolic murmurs and two benign continuous murmurs. In general,
benign cardiac murmurs are :-
grade 3 or less in intensity,
never have an associated thrill,
never occur solely in diastole.
Most of the innocent murmurs are accentuated by increased cardiac output related to
fever, anemia, or activity.
Characteristics of innocent cardiac murmurs:-
Grade 12/6
Left sternal border
Systolic ejection murmur
Normal intensity and physiologic splitting of S2
No other cardiac sounds or murmurs
No evidence of ventricular hypertrophy or dilation
Murmur does not increase with Valsalva or squat to stand
Asymptomatic
Family history negative for HCM or sudden death
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The benign murmur common to early infancy is referred to as peripheral pulmonary
artery stenosis or pulmonary flow murmur of newborns. Prior to birth, there is
minimal flow into the branch pulmonary arteries so the branches are relatively small.
Also, the branches arise from the main pulmonary artery at a sharper angle than seen
later in life. After birth, there is a marked increase in pulmonary blood flow often
creating a murmur as the blood makes the turn from the main pulmonary artery into the
branch pulmonary arteries. The murmur of peripheral pulmonary stenosis is often
initially heard at a couple of weeks of age when the physiologic nadir of the blood
count occurs.
A peripheral pulmonary stenosis murmur is usually louder in the axillae and back, but
may be heard anteriorly at the left upper sternal border. The murmur is ejection in
character and grade 1 or 2 in loudness. The pitch of the murmur is similar to breath
sounds and may be difficult to separate from the rapid respiratory noises in infancy, so
can easily be missed. This murmur can be differentiated from valvar pulmonary
stenosis as there is no associated ejection click. It is more common in premature
infants and often resolves by 69 months of age.
If the murmur persists past this age, then consider diagnosis of:-
true branch pulmonary artery stenosis,
Williams syndrome,
congenital rubella.
A Stills murmur is a common vibratory murmur (The murmur is often described as
musical in nature) heard in children, most often between the age of 2 and 6 years. It
can however be heard in infancy and may persist into adolescence. usually resolves by
adolescence.
Stills murmurs are low to medium in pitch, maximal at the left lower sternal border and
out to the apex, and typically grade 13 in loudness. The murmur is usually louder and
the vibratory component easier to appreciate when the patient is supine. In some
children the murmur may only be noted in the supine position. The intensity of the
murmur often changes with respiration and position and may be attenuated in the
sitting or prone position.
A Stills murmur will be louder in conditions with increased cardiac output, so when a
patient is seen for evaluation of a fever, the murmur may be heard for the first time.
A pulmonary flow murmur is a common murmur heard in late childhood and
adolescence, ages 814 years. It is a crescendo-decrescendo murmur heard best at
the left upper sternal border without further radiation and usually grade 23 in
loudness. The murmur is more pronounced in patients with pectus excavatum or
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kyphoscoliosis, The murmur likely due to the right ventricular outflow tract being closer
to the chest wall. It also seems to be more common in athletic individuals who may
have an increased stroke volume.
In addition to a pulmonary flow murmur, the differential diagnosis of a murmur at the
left upper sternal border would include one related to an atrial septal defect or to
pulmonary valve stenosis. In an atrial septal defect, there is a fixed split S2 and there
may be an increased right ventricular impulse on palpation. With pulmonary valve
stenosis, there often is an ejection click present and the murmur tends to be of a
longer and higher grade than in the benign flow murmur.
A murmur related to the carotids, or a carotid bruit, can be heard in children and
young adults. It is a crescendo-decrescendo murmur heard best above the clavicles
and radiates to the neck. Carotid bruits are low to medium in pitch, of abrupt onset,
brief, and maximal in the first part of systole. The murmur is felt to be due to flow from
the common carotid into the internal and external carotid arteries. Unlike carotid bruits
heard in adults, this is a benign finding in children.
A venous hum is a common continuous murmur heard in children 26 years of age.
It is usually loudest in the infraclavicular area and more common on the right side.
The murmur is low in pitch and louder in diastole. A venous hum murmur is often only
heard with the patient sitting upright and will dissipate with gentle occlusion of the
internal jugular vein on the same side of the neck as the murmur is heard or turning the
head toward the side of the murmur. The murmur may be accentuated by having the
patient look away from the side of the murmur. A venous hum is thought to occur from
flow from the internal jugular vein into the superior vena cava.
The following is a brief overview of cardiac murmurs associated with some of the more
common structural cardiac defects.
The murmur associated with an atrial septal defect:-
It Is not related to the flow across the atrial septum, but due to an increase in flow
across the pulmonary valve.
The murmur is grade 13, best at the left upper sternal border, medium pitched,
and ejection (crescendo-decrescendo) in nature.
The murmur may radiate to the lung fields (axillae and back).
The finding setting the murmur of an atrial septal defect apart from a benign
pulmonary flow murmur is fixed splitting of S2. This is due to decreased
variability of right ventricular volume with respiration and an enlarged right
ventricle resulting in prolonged ventricular contraction.
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Additional findings seen in some large atrial septal defects are a diastolic flow
rumble associated with flow across the tricuspid valve and an increased right
ventricular impulse.
Patients with atrial septal defects are often asymptomatic and the murmur is
often picked up during routine examination in childhood.
A ventricular septal defect (VSD) murmur:-
Is a holosystolic murmur usually heard best at the left lower sternal border,
grade 16, high pitched, and harsh in nature.
The murmur can radiate to the right lower sternal border and to the apex.
systolic thrill may be present at the left sternal edge.
With large ventricular septal defects, a gallop may be present on auscultation
and increased precordial activity noted on palpation.
There may be a diastolic flow rumble associated with increased flow across the
mitral valve.
Normal 1
st
and 2
nd
heart sound.
VSD murmurs are rarely heard in the first couple of days of life with the exception
of small muscular VSDs where the flow is directed anteriorly.
Most VSD murmurs are noted by 24 weeks of age.
A patent ductus arteriosus (PDA) murmur:-
Is described as a continuous machinery-like murmur
heard best at the left upper sternal border or left infraclavicular area,
grade 16, that can radiate to the back.
The murmur may also sound like other murmurs heard at the left upper sternal
border such as pulmonary valve stenosis. The key to differentiate the murmur
from pulmonary stenosis is that it is continuous, that is, it spills into diastole.
There may be widened pulse pressures (bounding pulses) and increased left
ventricular activity volume overload displaced the apex beat.
Patients may have a flow rumble across the mitral valve and a systolic ejection
murmur across the aortic valve because of increased flow in the left heart.
A PDA murmur may initially be only heard in systole due to the minimal pressure
gradient seen in diastole. As the pulmonary vascular resistance decreases to
normal levels in the first few weeks of life, the more classic continuous nature of
the murmur will be noted.
A pulmonary stenosis murmur:-
is a systolic ejection murmur at the left upper sternal border but the murmur
doesnt radiate to the carotids.
ranging from grade 1 to 6, A thrill may be present in the suprasternal notch or
upper left sternal border.
Usually there is an ejection click associated with valvar pulmonary stenosis.
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An increased right ventricular impulse parasternal heave of right
ventricular hypertrophy.
The murmur of aortic stenosis:-
is a systolic ejection murmur heard best at the right upper sternal border.
It is high pitched ranging from grade 1 to 6, harsh in nature, and radiates to the
carotids.
There is usually an aortic ejection click at the apex.
A thrill may be present at the right upper sternal border or in the suprasternal
notch.
An increased left ventricular impulse may be noted by palpation.
A murmur from mitral valve regurgitation:-
Is holosystolic and heard best at the apex.
a grade ranging from 1 to 3.
The murmur is high pitched and blowing in nature, radiating to the left lower
sternal border, left axilla, and left posterior chest.
When associated with mitral valve prolapse, there is a mid-systolic click prior to
the murmur being noted.
Coarctation of the aorta gives a variable murmur that is rarely greater than grade 3. It
is a systolic ejection type murmur, maximal at the left scapula or just below, but may be
heard anteriorly at the left upper sternal border. There is an increase in left ventricular
activity on palpation, and decreased lower extremity pulses. If the coarctation is
severe, there may be a continuous murmur present. A murmur associated with a
coarctation may not be noted until the ductus closes (2448 h for functional closure)
and may not be readily heard until complete remodeling of the aorta has occurred in
several weeks.
Mitral valve prolapse is not truly a murmur, but a mid-systolic click associated with
prolapse of the valve leaflets. Additionally, mitral valve prolapse may be associated
with a murmur of mitral regurgitation occurring after the click.
The murmur associated with hypertrophic cardiomyopathy is a grade 13 systolic
ejection murmur that is medium in pitch and heard best at the mid or lower left sternal
border. The murmur increases when going from a squat to a stand or during the strain
phase of a Valsalva
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Patients with Noonan syndrome have features characteristic of Turner syndrome but
possess a defect on chromosome 12 and may be male or female.
Clinically, these children have the findings of:-
epicanthal folds, low-set ears.
webbing of the neck,
pectus excavatum,
shield chest with widely spaced nipples,
short stature, ,
increased carrying angle of the arms.
Common cardiovascular defects include:-
pulmonary stenosis in association with a dysplastic pulmonary valve,
atrial septal defect,
hypertrophic cardiomyopathy.
On occasion, there may be dysplasia of all cardiac valves.
The syndrome appears as an autosomal dominant disorder; multiple members of a
family are often affected.
Patients with Williams syndrome characteristically have:-
elfin facies:
full face.
broad maxilla, rounded cheeks
small mandible with full mouth and large upper lip (philtrum),
flattened bridge of the nose & upturned nose,
broad forehead.
mental retardation (IQ range 41-80)
idiopathic hypercalcemia of infancy.
Additional features include loquacious personality, hypersensitivity to sound, spasticity,
hypoplastic nails, dental anomalies (partial anodontia, microdontia enamel hypoplasia),
joint hypermobility, nephrocalcinosis, hypothyroidism, and poor weight gain.
a strikingly affable personality despite variable degrees of developmental delay, and
has an identifiable genetic abnormality. Supravalvular aortic stenosis and pulmonary
artery branch stenosis are the common cardiovascular abnormalities associated with
this syndrome.
.
Marfan syndrome also has autosomal dominant inheritance; it manifests as a
connective tissue disorder in which the elastic fibers are disrupted, causing cystic
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Nov. 12
medial necrosis of the aorta, as well as joint laxity and subluxation of the ocular
lens.
Affected patients are tall, with increased limb length compared with the trunk.Their
arm span exceeds their height.
The cardiovascular abnormalities nearly always found in this syndrome include
aneurysmal dilation of the aorta and aortic sinuses and mitral valve
prolapse.
Associated aortic and mitral valve regurgitation are common