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Diminished S1
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.
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.
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:
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:
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. 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
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
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.