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HEART SOUNDS

1. FIRST HEART SOUND


S1 is produced by the closure of the mitral and tricuspid valves in early systole and is
loudest near the apex of the heart. Its high frequency sound. Best heard with the
diaphragm of the sthetoscope.
Mitral closure usually precedes tricuspid closure, they are separated by only about
0,01 seconds . an execption occurs in patients with right bundle branch block) in
whom these componets may be audibly split because of delayed right ventricular
contraction and late closure of the tricuspid valve.
3 factors determine of the intensity of S1 :
a. The distance separating the leaflets of the open valves at the onset of
ventricular contraction (relates to the electrocardiograph PR interval, the period
between the onset of atrial and ventricular activation. Atrial contraction at the
end of diastole forces the tricuspid and mitral valve leafets apart
b. The obility of the mitral and tricuspid leaflets (normal, r rigid because of
stenosis)
c. The rate of rise of ventricular pressure
Cause of altered intensity of the first heart sound (S1)
Accentuated S1
a. Shortened PR interval ( because the valve leafets have less time to drift back
together and are therefore forced shut from a relatively wide distance
b. Mild mitral stenosis, impeded low through the mitral valve cause a
prolonged diastolic pressure gradient between the left atrium and ventricle,
which keeps the mobile portions of the mitral leafets farther apart than
normal during late diastole. Because the leafets are relatively wide apart at
the onset of systole, they are forced shut loudly when the left ventricle
contratcs
c. High cardiac output states or tachycardia (e.g exercise) because diastole is
shortened and the leafets have less time ti drift back together before the
ventricle contract

Diminished S1

a. Lengthened PR interval: first degree AV nodal block


Abnomarlity prolongrd PR interval, which delays the onset of ventricular
contractions. Consequently, following atrial contraction, the mitral and
tricuspid valves have additional time to foat back together so that the
leafets are forced closed from only a small distance apart and the sound is
softened
b. Mitral regurgitation
Mitral leafets may not come into full contact with one another as they close,
c. in severe mitral stenosis, the leafets are nearly fixed in position throughout
the cardiac cycle, and that reduced movement lessens the intensity of s1
d. stiff left ventricle ( left ventricular hypertrophy due to systemic
hypertension) hypertrophied chamber, atrial contraction generates a
higher than normal ventricular pressure at the end of diastole. This greater
pressure causes the mitral leafets to drift together more rapidly, so that
they are forced closed from a smaller tan normal distance when ventricular
contraction begins, thus reducing the intensity of S1

2. SECOND HEART SOUND


Results from the closure of the aortic and pulmonic valves and therefore has aortic
(A2) and pulmonic (P2) components unlikeS1, which is usually heard only as a single sound,
the componets of S2 vary with the respiratory cycle: they are normally fused as one sound
during expiration but become audibly separated during inspiration, a situation termed
normal or physiologic splitting.
One explanation for normal splitting of S2 is as follows. Expansion of the chest
during inspiration causes the intrathoracic pressure to become more negative. The negative
pressure transiently increases the capacitance (and reduces the impedence). As the result,
there is a temporary delay in the diastolic back pressure in the pumonalry artery
responsible for the closure of the pulmonic valve. Thus, P2 is delayed that its occurs later
during inspiration than during expiration.
Inspiration has the opposite effect on aortic valve closure. Because the capacitance
of the intrathoracic pulmonary veins is increased by the negative pressure generated by
inspiration, the venous return to the left atrium and ventricle temporarily decreases reduced
filling of the LV diminishes the stroke volume during the nect systolic contraction and
therefore shortens the time required for LV emptying. Therefore, aortic valve closure (A2)
occurs slightly earlier in inspiration than during expiration. The combination of an earlier A2
and delayed P2 during inspirations causes audible separation of the two component. Best
heard with the diaphragm of the stethoscope and splitting of s2 is usuall most easily
appreciated near the second left intercostal space nest to the sternum.
Abnormalities of s2 include alterations in its intensity and changes in the pattern of
splitting. The intensity of s2 depends on the velocity of blood coursing back toward the
valves from the aorta and pulmonary artert after the completion of ventricular contraction.
And the suddenness with shich that motion is arrested by the closing valves. In systemic
hypertension or pulmonary arterial hypertension, the diastolic pressure in the respective
great artery is higher than normal, such that the velocity of the blood surging toward the
valve is augmented and s2 is accentuated. Conversely, in severe aortic or pulmonic valve
stenosis, the valve comissures are nearly fixed in position, such that the contribution of the
stenotic valve to s2 is dimished.
There are three types of abnormal splitting patterns of s2 widened, fixed and
paradoxical.
Widened splitting of s2 reders to an increase in the time interval between
A2 and P2, such that the two componets are audibly separated even
during expiration and become more widely separated in inspiration. This
pattern is usuallt the result of delayed closure of the pulmonic valve, which
occurs in right bundle branch block and sometimes in pulmonic valve
stenosis
Fixed splitting of s2 is an abnormality widened interval betwee A2 and P2
that persists unchanged through the repiratory cycle. The most common
abnormality that causes fixed splitting of s2 is an atrial septal defect. In that
condition, chronic volume overload of the right sided-circulation results in
hgh capacitance, low resistance ulmonary vascular system. This alteration
in pulmonary artery heodynamic delays the back pressure responsible for
the closure of the pulmonic valve. Thus P2 occurs later than normal, even
during expiration, such that there is wider than normal separation of A2
and P2. The pattern of splitting doesnt change during repiratory cycle
because (1) inspiration doesnt substantially increase further the already
elevated pulmonary vascular capacitance and (2) augmented filling of the
right atrium from the systemic veins during inspiration is counterbalanced
by a reciprocal decrease in the left to right transatrial shunt, eliminating
respiratory variations in right ventriculat filling.
Paradoxical splitting 9also tered reversed splitting) refers to audible
seperations of A2 dan P2 during expirations that fuses into a single sound
on inspiration. The opposite of the normal situation. It reflects an abnormal
delay in the closure of the aortic such that P2 precedes A2. In adults, the
most common cause Is left bundle branch block (LBBB). In LBBB, the spread
of electrical activity through the left ventricle is impaired, resulting in
delayed ventricular contraction and late closure of the aortic valve, causing
A2 to abnormality follow P2 with wide separation between them.this results
in narrowing and often superimposition, of the two sounds, thus, there is
no apparent split at the height of inspiration. In addition to LBBB
paradoxical splitting may be observed under circumstances in which left
ventricular ejection is greatly prolonged, such as aortic stenosis.

EXTRA SYSTOLIC HEART SOUNDS


Extra systolic heart sounds may occur in early- , mid-, or late systole.

a. Early extra systolic heart sounds


Abnormal early systolic sounds or ejection clicks, occurs shortly after s1 and coincide
with the opening of the aortic or pulmonic valves. These sounds have a sharp, high-
pitched quality, so thet are heard best with the diaphragm of the stetoscope placed over
the aortic and pulmonic areas. Ejection clicks indicate the presence of aortic or
pulmonic valve stenosis or dilation of the pulmonary artery or aorta. In stenosis of the
aortic or pulmonic valve, the sound occurs as the deformed valve leaflets reach their
maximal level of ascent into the great artery, just prior to blood ejection. At that
moment, the rapidly ascending valve reaches its elastic limit and decelerates abruptly.
An action thought to result in the sound generation. In dilation of the root of the aorta
or pulmonary artery, the sound is associated with sudden tensing of the aortic or
pulmonic root with the onset of blood flow into the vessel. The aortic ejection click is
heard at both the base (represented by the aortic ad pulmonary regions0 and the apex
of the heart and doesnt vary wth respiration. In contrast, the pulmonic ejection click is
heard only at the base, and its intensity dimishes during inspiration

b. Mid- or late extra systolic heart sounds


Clicks occurring in mid- or late systole are usually the result of systolic prolapse of the
mitral or tricuspid , in which the leafets bulge abnormally from the ventricular side of
the AV junction into the atrium during ventricular contraction, often accompanied by
valvular regurgitation. They are loudest over the mitral or tricuspid auscultatory
regions, respectively

EXTRA DIASTOLIC HEART SOUNDS

Extra heart sound in diastole include the opening snap (OS), the third heart sound (S3), the
fourth heart sound (S4) and the pericardial knock.

a. Opening snap
Opening of the mitral and tricuspid valves is normally silent, but mitral or tricuspid
valvular stenosis (usually the result of rheumatic heart disease) produces a sound,
termed as snap, when the affected valve opens. Its a sharp, high-pitched sound and
its timing doesnt vary significantly with respiration. In mitral stenosis (which is much
more common than is tricuspid valve stenosis), the OS is heard best between the apex
and the left sternal border, just after the aortic closure sound (A2), when the left
ventricular pressure falls below that of the left atrium.
Because of its proximity to A2, the A2-OS sequence can be confused with a widely split
second heart sound. However, careful auscultation at the pulmonic area during
inspiratin reveals theee sound occurring in rapid sucession, which coreespond to aortic
closure (A2), pulmonic closure (P2) and then the OS.

b. THIRD HEART SOUND (S3)

When present an S3 occurs in early diastole, following the opening the AV valves, during
the ventricular rapid filling phase. Its a dull, low-pitched sound best heard with the
bell of the stethoscope. A left=sided S3 is typically loudest over the cardiac apex while
the patient lies in the left lateral decubitus position. A right-sided S3 is better
appreciated at the lower left sternal border. Production of the S3 appears to result
from tensing of the chordae tendinae during rapid filling and expansion of the
ventricle.

An S3 is a normal finding in children and young adults. In these grops, an S3 implies the
presence of a supple ventricle capable of nrmal rapid expansion in early diastole.
Conversely, when heard in middle-aged or older adults, an s3 is a sign of disease
resulting from a dilated ventricle (e.g patient with heart failure due to impaired systolic
contraction) or from the increased transvalvular flow that accompanies advanced
mitral or tricuspid regurgitation. A pathologic s3 is sometimes reffered to as a
ventricular gallop
c. Fourth heart sound (S4)
When an s4 is present, it occurs in late diastole and coincide with contraction of the
atria. This sound is generated by the left or right atrium ejecting blood into a stiffened
ventricle. Thus an s4 usually indicated the presence of cardiac diseasespesificially a
decrease in ventricular compliance typically resulting from ventricular hypertrophy or
myocardial ischemia. Like an s1, the s4 is dull, low-pitched sound and is best heard with
the bell of the stethoscope. In the case of the more common left sided s4, the sound is
loudest at the apex, with the patient lying in the lateral decubitus position. S4 is
sometimes reffered to as an atrial gallop.

d. Quadruple rhythm or summation gallop

In a patient with both an s3 and s4. Those sound is conjuction with s1 and s2, produce a
quadruple beat. If a patient with a quadruple rhytm develops tachycardia, diastole
becomes shorter in dartion. The s3 and s4 coalesce, and a summation gallop results.
The summation of s3 and s4 is heard as a long middiastolic, low-pitched sound, often
louder tha s1 and s2

e. Pericardial knock
A pericardial knock is an uncommon, high pitched sound that occurs in patients with
severe constrictive pericarditis. It appeard early in diastole soon after s2 and can be
confused with an OS or an S3, however the knock appears slightly later in diastole than
the timing of an OS and is louder and occurs earlier than dose a ventricular gallop. It
results from the abrupt cessation of ventricular filling that occurs when the expanding
ventricle meet a rigid pericardium in early diastole, which is the hallmarl of constrictive
pericardiditis

MURMURS

A murmur is the sound generated by turbulent blood flow. Under normal conditions, the movement
of blood through the vascular bed is laminar,smooth and silent. However as a result of
hemodynamic and or structural changes, laminar flow can become distrurbed and produce an
audible noise. Murmurs result from any of the following mevhanism:

1. Flow across a partial obstruction (e.g aortic stenosis)


2. Increase flow thorugh normal structures (e.g aortic systolic murmur associated with the high
output state, such anemua)
3. Ejection into a dilated chamber (e.g aortic systolic murmur associated with aneurysmal
dilation of the aorta)
4. Regurgitant flow across an incompetemt valve (mitral regurgitation)
5. Abnormal shunting of blood from one vascular chamber to a loer pressure chamber (e.g
ventricular septal defect (VSD))
Murmurs are described by therir timing, intensity,pitch, shape, location, radiation and response to
maneuvers. Timing refers to wether the murmur occurs during systole or diastole or is continuous
(i.e begins in systole and continues into diastole). The intensity of the murmur is typically quantified
by a grading system grade 1/6 6/6 and in the case of diastolic murmurs 4/4

Pitch refers to the frequency of the murmur, ranging from high to low. High frequency murmur are
caused by large oressure gradients between chamber (e.g aortic stenosis) and are best
appreciated using the diaphragm chest piece of the sthetoscope. Low frequency murmurs impy
less of a pressure gradient between chambers (e.g mitral stenosis) and are best heard using the
stethoscopes bell piece.

Shape describes how the murmur changes in the intensity from its onset to its complection for
example a crescendo-drecendo (or diamond shape) murmur first rises and then falls off in
intensity. Other shapes include dresescendo (i.e the murmur begins at its maximum intensity then
becomes softer) and uniform (the intensity of the murmur doesnt change)

Location refers to the murmurs region of maximum intensity and is usually described in terms of
specific ausculatatory areas

a) Aortic area = second to third right intercostal spaces, next to the sternum
b) Pulmonic area = second to third left intercostal spaces, next to the sternum
c) Tricuspid area = lower left sternal border
d) Mitral area = cardiac apex

From their primary locatons, murmur are often heard to radiate to other areas of the chest, and
such patterns of transmission relate to the direction of the turbulent flow. Finally similar types of
murmurs can be distinguished from another by simple bedside maneuvers, such as standing upright,
valsava (forceful expiration against a closed airway), or clenching of the fists, eaxh of which alters
the hearts loading conditions and can affect the intensity of many murmurs.

EXAMPE = A grade III/VI high pitched, crescendo-drescendo systolic murmur, loudest at the upper
right sternal border, with radiatiom toward the neck.

A. Systolic murmurs
Systolic murmurs are subdivided into systolic ejection murmurs, pansystolic murmurs and
late systolic murmur.
A sysytolic murmur is typical of aortic or pulmonic valve stenosis. It begins after the
first heart sound and terminates before or during s2 depending on its severity and
wheater the obstruction is of the aortic or pulmonic valve. The shape of the murmur
is of the crescendo-decrescendo type (i.e intensity rises and then falss)
the ejection murmur of aortic stenosis begins in systole after s1, from which its
separated by a short audible gap. This gap corresponds to the period of isovlumetric
contraction of the left ventricle (the period after the mitral valve has closed but
before the aortic valve has opened. The murmur becomes more intense as flow
increase across the aortic valve during the rise in left ventricular pressure
(crescendo). Then as he ventricle relase, forward flow drcerease and the murmur
lessens In intensity (decrescendo) and finally ends prior to the aortic component of
s2. The murmur may be immediately precede by an ejection click, especially in mild
forms of aortic stenosis.

Diastolic murmurs
BASIC ELECTROPHYSIOLOGY

Rhythmic contraction of the heart relies on the organized propagation of electrical impulses along its
conduction pathway.the marker of electrical stimulation, the action potential is created by a
sequence of ion fuxes through specific channels in the sarcolemma. To provide a basis for
understanding how electricl impulses lead to cardiac contraction, the process of cellular
depolarization and repolarizato is reviewed here. Cardiac cells capable of electrical excitation are of
three electrophysiology types, thr properties of which have been studied by intracellular
microelectrode and patch clamp recording:

1. Pacemaker cells (e.g SA node, AV node)


2. Specialised rapidly conductings tissues (e.g Purkinje fibers)
3. Ventricular and atrial muscle cells

The sarcolemma of each of these cardiac cells types is a phospholipid bilayer that, by itseld, is
largely impermeable to ions. There are specialized proteins interspersed throughout the
membrane that serve as ion channels, passive contrasporters, and active transporters. These
help to maintain ionic contrecation gradients and charge differentials betwee the inside and the
outside of the cardiac cells. Note that normally the Na and ca concentractions are much higher
outside the cell, and the k concentration is much hiher inside.

The movement of specific ion across the cell membrane severs as the basis of the action potential.
Passive ion movement depend on two major factors:

(1) the energetic favorability

(2) the permeability of the membrane for the ion

1. ENERGETICS
The two major forces that drive the direction of passive ion flux are the concentration
gradient and the transmembrane potential (voltage) . molecules diffuse from areas of high
contrecation to areas of lower concentration, and the gradient between these values is a
determinant of the rate of ion flow. For example, the extracellular Na concentration is
normaly 145 mM, while the concentration inside the myocyte is 15 mM. as a result, a strong
diffusive force tends to drive na into cell, down its concetrtion gradient.
The transmembrane potential of cell exerts an electrical force on ion (i.e like charges repel
one another, and opposite charges attract). The transmembrane potential of a myocyte at
rest is about -90 mV (the inside of the cell is negative relative to the outside). Extracellular
Na, a positively charged ion, is therefore attracted to the relativey negatively charged
interior of the cell. Thus, there is a strong tendency for Na to enter he cell and remain there,
because of the steep concentration gradient and the electrical attraction.

2. Permeability
If there is such a strong force driving Na into the cell. Instead permeability of the membrane
is dependent on the opening of specific ion channels, specialized protein that span the
cellmembrane and contain hydrophilic pores through which certain charged atoms can pass
under specific circumstance. The permeability of the cardiac myocyte cellular membrane for
sodium is minimal in the resting state because the channels that conduct that ion are
essentially cosed. However there is a slight leak of sodium ions into the cell at rest. This
small inward current of positively charged ions explains why the actual resting potential is
slightly less negative than would be predicted if the cell membrane wew truly only
permeable to potassium. The sodium ions that slowly leakinto the myocyte at rest (and the
much larger amount that enters during the action potential) are continuously removed from
the cell and returned to the extracellular environment by NaK-ATPase, as previously
described

CARDIAC MUSCLE CELL

Until stimulated, the resting potential of a cardiac muscle cell remains stavle, at approximately -90
mV.this resting state before depolarization is knows as phase 4 of tge action potential. Following
phase 4, four additional phases charactereize depolarization and repolarization pf te cell

POTENSIAL AKSI SEL OTORITMIK JANTUNG

a. Fase 0 (Depolarisasi cepat)


Dibawah keadaan normal, serat otot jantung dapat berkontraksi sekitar 60-100 kali/menit
oleh karena impuls listriik yang dihasilkan oleh nodus SA. Aksi ini merubah potensial
isthirahat membrane dan membiarkan masuknya aliran Na (sodium) secara cepat kedalam
sel melalui natrium channel. Dengan masuknya ion natrium (bersifat positif) kedalam sel.
Maka potensial dalam membrane sel akan menjadi lebih positf sehingga ambang
potensialnya kan naik (depolarisasi) sekitar 30 mV

b. Fase 1 (repolarisasi awal)


Segera seteah fase 0, channel untuk ion K (potassium) terbuka dan melewatkan ion kalium
keluar dari dalam sel. Hal ini membuat potensial membrane sel menjadi lebih turun sedikit

c. Fase 2 (plateu)
Segera setelah repolarisasi awal, untuk mempertahankan ambang potensial di membrane
sel maka ion kalsium (Ca) akan segera masuk sementara ion kalium tetap keluar. Dengan
begini ambang potensial membrane sel akan tetap datar untuk mempertahankan kontraksi
sel otot jantung.

d. Fase 3 (repolarisasi cepat)


Aliran lambat ion kalsium berhenti, akan tetapi aliran ion kalium yang keluar membrane sel
tetap terjadi sehingga potensial membrane menjadi turun (lebih negative) dan disebut
dengan repolarisasi

e. Fase 4 9isthirahat/resting state)


Potensial membrane menjadi ke fase isthirahat dimana potensialnya sekitar -90 mV.
Dikarenakan ion natrium yang berlebihaan didalam sel dan ion kalium yang berlebihaan
diuar sel dikembalikan ketempat semula dengan pompa natrium-kalium, sehingga ion
natrium kembali keluar sel dan ion kalium kembali kedala sel
GAGAL JANTUNG

o GJ dianggap remodelling progresif akibat beban/penyakit pada miokard


sehingga pencegahaan progresivitas dengan peghambat neurohormonal
(neurohumoral blocker) seperti ACE-inhibitor, angiotensin receptor blocker
atau penyekat beta diutamakan di samping obat konvensional )diuretic dan
digitalis)