PHONOCARDIOGRAPHY

Phonocardiography is a procedure that graphically depicts heart sounds and

murmurs on a strip chart recorder. It has been used since the early 1900s to visually

display the vibrations emanating from the heart and great vessels during different

phases of the cardiac cycle. Since the availability of Doppler echocardiography,

phonocardiography is used less often)

Phonocardiograms are used to confirm the clinical diagnosis of specific valvular

disease; precisely time cardiac events; and make possible the distinguishing of extra

sounds, splitting of sounds, and identification and classification of murmurs. It should

be noted, however, that the phonocardiogram will not make cardiac events audible,

but rather will display them visually, permitting precise timing and correct diagnosis

(Figures 4.19 and 4.20).

The human ear can detect sound vibrations in the range of 20 to 20,000 Hz and since

most heart sounds are in the 20 to 500 Hz range, they are audible. However, since

the human ear can hear more easily in the high frequency range, some of the sounds

go undetected or are difficult to Interpret, Very low - pitched sounds produced within

the chest are not detected as sound but rather as palpable vibration. During the

course of the phonocardiogram, certain frequency ranges can be filtered out or

amplified inorder to zero-in on specific sounds.

FIGURE 4.19

Phonocardiogram and carotid pulse tracing (CPT). The ECG is monitored on lead II (Lit) with the

phono tracing obtained from the left sternal border. S, ~ first heart sound; S2 = second heart

sound.
Technique of Phonocardiography

After the patient is connected to the phonocardiography machine, the microphones

are placed on the chest over the base and apex of the heart, and the sound recording

is done. An M-mode echocardiogram can be done at the same time so that a

comparison between auscultatory events and valve movements can be made.

Pharmaacologic agents and physiologic measures are often used to bring about

and/or accentuate heart sounds and murmurs. When the patient is asked to speed or

slow his breathing pattern in order to make certain murmurs more evident, the

inspiratory and expiratory cycles are marked off manually by the technician to

provide a point of reference.

Patient Preparation

No physical preparation is necessary for a pphonocardiogram. The procedure should

be explained to the patient.It should be stressed that extreme quiet is nessecary

during the procedure. Also patients should be told that they may be given medication

or asked to alter their breathing pattern during the procedure to enhance heart

sounds or murmurs.

FIGURE 4.20

Phonocardiogram from a 60-year-old male with aortic stenosis. Demonstrates the crescendo-
decrescendo murmur during systole (SM). The ECG is monitored in lead II (LI1).

NORMAL HEART SOUNDS

Physical assessment remains a clinically important diagnostic tool in the

evaluation of heart sounds and murmurs. Cardiac auscultation is perhaps one of the

most challenging aspects of physical assessment. Heart sounds are transient

vibrations thought to be secondary to sudden tension on the valve leaflets. Heart

sounds originating from each particular, valve are usually recorded best from their

respective auscultatory areas on the chest.

A quiet environment is of fundamental importance in the detection of most cardiac

sounds, especially those of high frequency that might otherwise go unnoticed.

Proper use of a good quality stethoscope is also important. Although the stethoscope

does not accentuate heart sounds, it does have a limited ability to filter out unwanted

sounds and allow the examiner to focus in on a specific range of heart sounds.

Desirable characteristics of a stethoscope include proper-fitting earpieces, tubing

length of approximately 10 to 12 inches, double tubing (separate or encased), and a

chest piece with a diaphragm and a bell. The diaphragm is used for listening to high-

pitched sounds and should be held firmly on the chest wall. The bell is used for

listening to low-pitched sounds and should be held with the lightest pressure
necessary to maintain skin contact. Firm pressure on the bell filters out the low-

pitched sounds it is designed to detect.

First Heart Sound

The first heart sound, S1 occurs at the onset of systole. The sound itself is relatively

high pitched and originates from vibrations produced after the closure of the mitral

and tricuspid valves. The mitral valve component is louder than the tricuspid valve

component due to the higher pressure on the left side of the heart. The mitral valve

also closes a fraction of a second sooner than the tricuspid valve.

The is heard best over the apex of the heart. Occasionally both components

of S1

(M1) = mitral valve component; T1 = tricuspid valve component) can be heard by

placing the diaphragm of the stethoscope over the tricuspid area. This is called

normal splitting of S1.

Many factors can have an effect on the intensity of S1. The S1 is loudest when the

mitral valve closes rapidly and when the mitral valve leaflets are widely separated at

end-diastole. Some conditions that cause an increase in the intensity of S1 are

tachycardia, rapid atrioventricular conduction (short PR interval), and hyperdynamic

states such as exercise and fever that increase the force of contraction of the left

ventricle. Mitral stenosis without calcification of valve leaflets is also associated with

a loud S1. The intensity of S1 decreases when the atrioventricular conduction is slow

(long PR interval) because the mitral valve is already partially closed at end-diastole.

Decreased left ventricular contractility and mitral stenosis with calcification of valve

leaflets are also associated with a soft S1.

First heart sounds can vary in intensity and duration when the atria and ventricles

are asynchronous, as in complete heart block, atria] fibrillation, and ventricular

tachycardla. This is because leaflet separation and rate of closure In the mitral valve

vary with eac h beat.

It is sometimes difficult to differentiate S1 from S2 during rapid heart rates – ie. as

systole and diastole approach equal duration. It is helpful to bear in mind that S1 is

consistent with the apical impulse and just precedes the carotid impulse.

Second Heart Sound

The second heart sound, S2, occurs at the onset of diastole. The origin of the second

sound is due to vibrations produced after closure of the aortic and pulmonic valves.

The S2 is a high-pitched sound that is loudest at the base of the heart. The aortic

valve component is louder than the pulmonic valve component and the aortic valve

normally closes just before the pulmonic valve. This separation is augmented during

active inspiration as pulmonic valve closure is delayed due to increased venous

return to the right side of the heart. This normal splitting of the components of S2 (A2

= aortic component; P2 = pulmonic component) is usually easily identifiable with the

phonocardiogram and is frequently audible with the stethoscope.5 The components

of the second heart sound are heard best over the pulmonic area with the diaphragm

of the stethoscope. Erb's point is an area on the chest where many murmurs of aortic

and pulmonic origin are transmitted (Figure 4.21).

The S2 can also be abnormally split and is then termed paradoxical (reversed)

splitting. It is heard characteristically during inspiration, with S2 occurring before A2.

The most common cause of paradoxical splitting is left bundle branch block.

Wide splitting of S2 occurs in situations where right ventricular systole is delayed, as

in right bundle branch block, pulmonic stenosis, and left ventricular pacing. It is

actually an accentuation of normal splitting. Wide splitting is most pronounced in

inspiration and often present in expiration.

Fixed splitting is manifested by wide splitting throughout the respiratory cycle with

no change between inspiration and expiration. It occurs most commonly with atrial

septal defect.

The intensity of S2,can vary as well. Increased intensity of A2 is indicative of arterial

hypertension. Aortic stenosis causes a decreased intensity of A2. Similarly,

pulmonary hypertension causes the P2 to increase in intensity whereas pulmonic

stenosis causes the P2 to decrease in intensity.

EXTRA HEART SOUNDS

Third Heart Sound

The third heart sound, S3, is an early diastolic sound. The sound is generated from

vibrations produced during rapid filling of the ventricles in patients with ventricular

dysfunctions and overfilled ventricles as in CCF. It can also be a normal variant in

individuals up to 30 years of age. It is a low-frequency pitch that often can be

detected on phonocardiogram when it cannot be heard at the bedside. For purposes

of specific timing, it occurs approximately 0.15 second after A2. The S3 can be

augmented in the left lateral decubitus position and in conditions where the venous

return is increased. It is heard best at the apex with the bell. An S3 may also be

heard over the lower left sternal border in patients with right ventricular failure.

Fourth Heart Sound

The fourth heart sound, S4, is a low-pitched, presystolic sound. It is secondary to a

forceful atrial contraction into a ventricle that has decreased compliance. Chronic

ischemia, ventricular hypertrophy, car-diomyopathy, and idiopathic hypertrophic

subaortic stenosis are some of the conditions in which an S4 may be heard. The S4 is

also easily detectable on the phonocardlogram. It occurs prior to the S1, and for

timing purposes, about 0.14 second after the onset of the P-wave. Like the S3, it can

be heard best at the apex in the left lateral decubitus position with the bell.
Summation Gallop

The summation gallop is the triple sound complex that is heard during a tachycardia

in individuals that have both an S3 and an S4. These two sounds fuse together at

high heart rates to form a diastolic sound. This happens because atrial contraction

and rapid ventricular filling occur simultaneously with rapid heart rates.

Ejection Clicks

Ejection clicks are high-frequency sounds that can immediately follow S1 They are

frequently heard in pulmonary and systemic hypertension. Aortic ejection clicks are

heard in aortic stenosis, aortic insufficiency, and aortic dilatation. These sounds are

heard best at the apex. Pulmonary ejection clicks are heard in pulmonary stenosis

and pulmonary hypertension and are heard best in the pulmonic area. Because of

the timing of ejection clicks relative to the cardiac cycle, they can be mistaken for a

split S1. The distinction can be made based on the location in which the "double

sound" is heard. The split S1 is best heard over the tricuspid area.

Clicks that occur in mid - to late-systole are related to the billowing of a mitral valve

leaflet in mitral valve prolapse. Sometimes more than one click will be present. It is

believed that these sounds are due to the chordae being pulled taut suddenly during

systole when the mitral valve billows back into the left atrium. The intensity and
timing of a mid- or late-systolic click may vary with changes in position and with

respiration. It is most easily detected with the diaphragm at the apex of the heart.

Opening Snap

Opening snaps are high-pitched sounds that occur upon opening of a stenosed mitral

or tricuspid valve. The sound is thought to occur as a result of sudden tension on the

partially open valve leaflets very early in diastole. Opening snaps closely follow A2

and are heard best at their respective auscultatory areas with the diaphragm (Figure

4.22).

Pericardial Friction Rub

A pericardial friction rub is a high-pitched, grating sound resembling the

characteristic sound heard when using sandpaper. Some people compare it to the

sound produced when a lock of hair is held in front of the ear and rubbed between

the fingers. It occurs in pericarditis and may have as many three components. The

pericardial friction rub Is usually heard best with the diaphragm at the right and left

sternal border. It may be accentuated with the patient sitting up and leaning

forward while holding his or her breath in exhalation.

FIGURE 4.22

Heart sounds and the cardiac cycle. Extra heart sounds are graphically depicted as they would

appear in the cardiac cycle. Always be aware of the effect of splitting and timing on heart sounds:

St = first heart sound; S2 = second heart sound; S3 = third heart sound;

S4 = fourth heart sound; E = ejection click (early systolic); M = ejection click (mid systolic); L =

ejection click (late systolic); OS = opening snap.

.0.20 sec

-------Low frequency sounds ---------High frequency sounds

MURMURS

Murmurs are auscultatory events that have a longer duration than heart sounds. On

the phonocardiogram they are recorded as a series of vibrations. (Figure 4.23).

Murmurs occur because of turbulent blood flow that results from flow through

stenotic or regurgitant valves, increased velocity of blood flow, decreased blood

viscosity (e.g. anemia), flow into a dilated chamber, shunting of blood from a high-

pressure chamber into a low-pressure chamber, or increased cardiac output (e.g.

fever or exercise). Murmurs may occur in any part of the cardiac cycle and may be

normal in some individuals. Often, however, they represent a specific dysfunction

within the heart.

Murmurs are evaluated according to their timing in the cardiac cycle, location, and

Intensity. The Intensity of a murmur is objectively rated on a six-point grading scale;

Grade 1 a very faint murmur that seems to fade in and out

Grade 2 a soft but easily detectable murmur

Grade 3 a moderately loud murmur

Grade 4 a loud murmur that is associated with a thrill(palpable vibration)

Grade 5 a very loud palpable murmur that is audible with the stethoscope
partly off the chest wall.

Grade 6 a very loud palpable murmur that is audible with the stethoscope held

off the chest wall

FIGURE 4.23

Murmurs.

Graphic representations of how the indicated murmurs would appear on a phonocardiographic

recording. This list is not all inclusive and variations in timing within the cardiac cycle can be
found among both systolic and diastolic murmurs (i.e., murmurs may be early, middle, or late in
occurrence). Often, certain murmurs will begin with a click or opening snap. In addition, the
prefixes pan- or holo- are applied to those murmurs that persist throughout systole or diastole
(e.g the holosystolic murmur of mitral insufficiency). Systolic murmurs are often described as
producing a harsh or blowing sound (especially the pansystoiic regurgitant murmur of mitral
insufficiency); diastolic murmurs may assume a rumbling quality. More than one murmur may
also occur, producing a combination of sounds.

Heart murmurs are also classified as harsh, rough, blowing, rumbling, musical,
or
Machinery like. They may be high, medium, or low pitched, and they may be
localized or radiate along the precordium. Finally, murmurs may be classified
according to their intensity and may be diagrammed with a specific shape that
represents that intensity. For instance, they may be diamond shaped (crescendo-
decrescendo), progressively increase in intensity (crescendo), progressively decrease
in intensity (decrescendo), or remain the same intensity throughout the duration of
the murmur.
Systolic Murmurs
Systolic murmurs may be classified as flow murmurs, ejection murmurs, or
regurgitant murmurs. Ejection murmurs occur as blood flows forward through the
semilunar valves during systole. Regurgitant murmurs occur as blood flows backward
through an incompetent atrioventricular valve during systole.
Flow Murmurs
Flow murmurs occur as a result of physiologic changes associated with increased
cardiac output, such as those consistent with tachycardia and anemia, and fluid
overload. They are the most common type of murmur and are not indicative of any
type of heart disease.26 Flow murmurs are usually heard best at the base of the
heart with the diaphragm.
Pathologic Ejection Murmurs
These murmurs are due to stenosis of the aortic or pulmonic valves. Aortic stenosis is
the most common cause. The murmur of aortic stenosis is harsh and crescendo-
decrescendo in nature. It is audible with the diaphragm in the aortic area and may
radiate down the left sternal border or up into the carotid arteries.

Regurgitant (Pansystolic) Murmurs

Systolic regurgitant murmurs characteristically have a more even intensity and often
last throughout systole (i.e., they are "pansystolic"). Pansystolic murmurs often
obscure the first and second heart sounds. Mitral regurgitation represents the most
common type of pansystolic murmur, which usually has a blowing quality. It is heard
best with the diaphragm at the apex and may radiate to the axilla. In individuals
with mitral valve prolapse, a late systolic mitral regurgitant murmur may be present.
Blood flow from the left ventricle Intothe right ventricle in ventricular septal defect
will also produce a pansystolic murmur . This is usually a loud murmur with an
associated thrill that may be audible over most of the anterior precordium. Tricuspid
regurgitation, although uncommon, is another cause of pansystolic murmurs.
Diastolic Murmurs
Diastolic murmurs always indicate some type of pathology. They are frequently of
shorter duration than systolic murmurs and, therefore, are sometimes mistaken for
extra sounds. The most common diastolic murmurs are those of mitral stenosis and
aortic insufficiency (regurgitation). Other causes are tricuspid stenosis and
pulmonary insufficiency. Diastolic murmurs are classified as either mid or early.
The murmur of mitral stenosis is often difficult to hear. It is a low-pitched, mid-
diastolic rumbling murmur heard best at the apex with the bell of the stethoscope. It
is usually very localized and often it will only be audible with the patient lying in the
left lateral decubitus position.
The murmur of aortic insufficiency is a high-pitched, blowing, early-diastolic murmur
that is heard best with the diaphragm in the aortic area and sometimes down the left
sternal border. This murmur maybe accentuated with the patient sitting up and
leaning forward while holding his or her breath in exhalation. The Austin-Flint murmur
is a mid-diastolic murmur found in patients with severe aortic insufficiency without
mitral valve disease. The sound is produced by blood flow across a rapidly closing
mitral valve. The murmur is usually pandiastolic and rarely accentuated just prior to
systolic ejection.
At times, the sounds of a murmur can be heard throughout both systole and diastole.
Such murmurs are called continuous murmurs and may reflect a single event (as
occurs in patent ductus arteriosus) or may be the fusion of two or more events that
must be differentiated. Accurate assessment in this circumstance is made by
considering the location, intensity, and character of the murmur (Figure 4.23). For
example, the patent ductus normally closes shortly after birth, so its appearance in
an adult individual is uncommon. The machinery like sound it produces is the result
of turbulent blood flow between the aorta and the pulmonary artery and thus is best
heard in the aortic or pulmonic region. However, the murmur combination of aortic
stenosis and aortic insufficiency may be a real possibility in the older individual and is
best appreciated in the aortic area or at the apex; these may be frequent radiation of
the sound into the carotid arteries.

Pulse oximetry is a non-invasive method allowing the monitoring of the oxygenation of

a patient's hemoglobin.

A sensor is placed on a thin part of the patient's anatomy, usually a fingertip or earlobe,
or in the case of a neonate, across a foot, and a light containing both red and infrared
wavelengths is passed from one side to the other. Changing absorbance of each of the two
wavelengths is measured, allowing determination of the absorbances due to the pulsing
arteria blood alone, excluding venous blood, skin, bone, muscle, fat, and (in most cases)
fingernail polish.[1] Based upon the ratio of changing absorbance of the red and infrared
light caused by the difference in color between oxygen-bound (bright red) and oxygen
unbound (dark red or blue, in severe cases) blood hemoglobin, a measure of oxygenation
(the per cent of hemoglobin molecules bound with oxygen molecules) can be made.

Contents
[hide]

• 1 Indication
 • 2 History
• 3 Limitations
• 4 See also

• 5 References

[edit] Indication
Pulse oximetry data is necessary whenever a patient's oxygenation is unstable, including
intensive care, critical care, and emergency department areas of a hospital. Data can also
be obtained from pilots in unpressurized aircraft,[2] and for assessment of any patient's
oxygenation in primary care. A patient's need for oxygen is the most essential element to
life; no human life thrives in the absence of oxygen (cellular or gross). Although pulse
oximetry is used to monitor oxygenation, it cannot determine the metabolism of oxygen,
or the amount of oxygen being used by a patient. For this purpose, it is necessary to also
measure carbon dioxide (CO2) levels. It is possible that it can also be used to detect
abnormalities in ventilation. However, the use of pulse oximetry to detect hypoventilation
is impaired with the use of supplemental oxygen, as it is only when patients breathe room
air that abnormalities in respiratory function can be detected reliably with its use.
Therefore, the routine administration of supplemental oxygen may be unwarranted if the
patient is able to maintain adequate oxygenation in room air, since it can result in
hypoventilation going undetected.[citation needed]

[edit] History
In 1935 Matthes developed the first 2-wavelength ear O2 saturation meter with red and
green filters, later switched to red and infrared filters. This was the first device to
measure O2 saturation.[citation needed]

In 1949 Wood added a pressure capsule to squeeze blood out of ear to obtain zero setting
in an effort to obtain absolute O2 saturation value when blood was readmitted. The
concept is similar to today's conventional pulse oximetry but suffered due to unstable
photocells and light sources. This method is not used clinically. In 1964 Shaw assembled
the first absolute reading ear oximeter by using eight wavelengths of light.
Commercialized by Hewlett Packard, its use was limited to pulmonary functions and
sleep laboratories due to cost and size.[citation needed]

Pulse oximetry was developed in 1972, by Takuo Aoyagi, a bioengineer, at Nihon

Kohden using the ratio of red to infrared light absorption of pulsating components at the
measuring site. Susumu Nakajima, a surgeon, and his associates first tested the device in
patients, reporting it in 1975.[3] It was commercialized by Biox in 1981 and Nellcor in
1983. Biox was founded in 1979, and introduced the first pulse oximeter to commercial
distribution in 1981. Biox initially focused on respiratory care, but when the company
discovered that their pulse oximeters were being used in operating rooms to monitor
oxygen levels, Biox expanded its marketing resources to focus on operating rooms in late
1982. A competitor, Nellcor (now part of Covidien, Ltd.), Incorporated in 1982, and
began to compete with Biox for the US operating room market in 1983. Prior to its
introduction, a patient's oxygenation could only be determined by a painful arterial blood
gas, a single point measure which takes a few minutes processing by a laboratory. (In the
absence of oxygenation, damage to the brain starts in 5 minutes with brain death in
another 10–15 minutes). In the US alone, approximately $2 billion was spent annually on
this measurement. With the introduction of pulse oximetry, a non-invasive, continuous
measure of patient's oxygenation was possible, revolutionizing the practice of anesthesia
and greatly improving patient safety. Prior to its introduction, studies in anesthesia
journals estimated US patient mortality as a consequence of undetected hypoxemia at
2,000 to 10,000 deaths per year, with no known estimate of patient morbidity.[citation needed]

By 1987, the standard of care for the administration of a general anesthetic in the US
included pulse oximetry. From the operating room, the use of pulse oximetry rapidly
spread throughout the hospital, first in the recovery room, and then into the various
intensive care units. Pulse oximetry was of particular value in the neonatal unit where the
patients do not thrive with inadequate oxygenation, but also can be blinded with too
much oxygen. Furthermore, obtaining an arterial blood gas from a neonatal patient is
extremely difficult.[citation needed]

In 1996, Masimo, a California-based company, introduced the first pulse oximeter able to
provide accurate measurements during periods of patient motion or low peripheral
perfusion, long thought to be limitations of pulse oximetry technology that could not be
overcome. [4] The ability to provide accurate measurements under these difficult clinical
conditions meant pulse oximetry could be used outside the operating room, where
patients were generally well perfused and not moving, allowing for adoption in neonatal
intensive care units, ambulances, and other challenging settings.[5]

By 2008, the accuracy and capability of Pulse Oximetry had continued to increase, and
had allowed for the adoption of the term High Resolution Pulse Oximetry (HRPO).[6][7][8]
One area of particular interest in the area of Pulse Oximetry, is the use of Pulse Oximetry
in conducting portable and in-home sleep apnea screening and testing.[6][9]

In 2009, the World's first Bluetooth-enabled fingertip pulse oximeter was introduced by
Nonin Medical, enabling clinicians to remotely monitor patients’ pulses and oxygen
saturation levels. It also allows patients to monitor their own health through online patient
health records and home telemedicine system.[10]

[edit] Limitations
This is a measure solely of oxygenation, not of ventilation, and is not a substitute for
blood gases checked in a laboratory as it gives no indication of base deficit, carbon
dioxide levels, blood pH, or bicarbonate HCO3- concentration. The metabolism of
oxygen can be readily measured by monitoring expired CO2. Saturation figures also give
no information about blood oxygen content. Most of the oxygen in the blood is carried by
hemoglobin. In severe anemia, the blood will carry less total oxygen, despite the
hemoglobin being 100% saturated.

Falsely low readings may be caused by hypoperfusion of the extremity being used for
monitoring (often due to the part being cold or from vasoconstriction secondary to the use
of vasopressor agents); incorrect sensor application; highly calloused skin; and movement
(such as shivering), especially during hypoperfusion. To ensure accuracy, the sensor
should return a steady pulse and/or pulse waveform. Falsely high or falsely low readings
will occur when hemoglobin is bound to something other than oxygen. In cases of carbon
monoxide poisoning, the falsely high reading may delay the recognition of hypoxemia
(low blood oxygen level). Methemoglobinemia characteristically causes pulse oximetry
readings in the mid-80s. Cyanide poisoning can also give a high reading because it
reduces oxygen extraction from arterial blood (the reading is not false, as arterial blood
oxygen is indeed high in early cyanide poisoning).

Pulse oximetry only reads the percentage of bound hemoglobin. It can be bound to other
gasses such as carbon monoxide and still read high even though the patient is hypoxemic.
The only noninvasive methodology that allows for the continuous and noninvasive
measurement of the dyshemoglobins is a pulse co-oximeter. Pulse CO-Oximetry was
invented in 2005 by Masimo and currently allows clinicians to measure total hemoglobin
levels in addition to carboxyhemoglobin, methemoglobin and PVI, which initial clinical
studies have shown may provide clinicians with a new method for noninvasive and
automatic assessment of patient fluid volume status.[11][12][13] Appropriate fluid levels are
vital to reducing postoperative risks and improving patient outcomes as fluid volumes
that are too low (under hydration) or too high (over hydration) have been shown to
decrease wound healing, increase risk of infection and cardiac complications.[14]