inhaler use
TRANSCRIPT
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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.
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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-
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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
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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
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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
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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.
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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
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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.
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.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
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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 phonocardiographicrecording. This list is not all inclusive and variations in timing within the cardiac cycle can befound among both systolic and diastolic murmurs (i.e., murmurs may be early, middle, or late inoccurrence). 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 mitralinsufficiency); diastolic murmurs may assume a rumbling quality. More than one murmur mayalso 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
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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 MurmursFlow 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 forextra 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
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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 murmuris 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 ofa patient's hemoglobin.
A sensor is placed on a thin part of the patient'sanatomy, usually a fingertip orearlobe,or in the case of a neonate, across a foot, and a light containing bothred and infraredwavelengths is passed from one side to the other. Changing absorbance of each of the twowavelengths is measured, allowing determination of the absorbances due to the pulsingarteriablood alone, excluding venousblood, skin, bone, muscle, fat, and (in most cases)fingernail polish.[1] Based upon the ratio of changing absorbance of the red and infraredlight caused by the difference in color between oxygen-bound (bright red) and oxygenunbound (dark red or blue, in severe cases) blood hemoglobin, a measure ofoxygenation
(the per cent ofhemoglobinmolecules bound with oxygen molecules) can be made.
Contents
[hide]
1 Indication
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2 History 3 Limitations 4 See also
5 References
[edit] Indication
Pulse oximetry data is necessary whenever a patient'soxygenation is unstable, includingintensive care,critical care, and emergency department areas of a hospital. Data can alsobe obtained frompilots in unpressurized aircraft,[2] and for assessment of any patient'soxygenation inprimary care. A patient's need for oxygen is the most essential element tolife; no human life thrives in the absence of oxygen (cellular or gross). Although pulseoximetry 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 alsomeasure 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 hypoventilationis impaired with the use of supplemental oxygen, as it is only when patients breathe roomair that abnormalities in respiratory function can be detected reliably with its use.Therefore, the routine administration of supplemental oxygen may be unwarranted if thepatient is able to maintain adequate oxygenation in room air, since it can result inhypoventilation 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 tomeasure O2 saturation.[citation needed]
In 1949 Wood added a pressure capsule to squeeze blood out of ear to obtain zero settingin an effort to obtain absolute O2 saturation value when blood was readmitted. Theconcept is similar to today's conventional pulse oximetry but suffered due to unstablephotocellsand light sources. This method is not used clinically. In 1964 Shaw assembledthe first absolute reading ear oximeter by using eight wavelengths of light.Commercialized by Hewlett Packard, its use was limited to pulmonary functions andsleep laboratoriesdue to cost and size.[citation needed]
Pulse oximetry was developed in 1972, byTakuo Aoyagi, a bioengineer, atNihonKohden using the ratio of red to infrared light absorption of pulsating components at themeasuring site. Susumu Nakajima, a surgeon, and his associates first tested the device inpatients, reporting it in 1975.[3] It was commercialized by Biox in 1981 and Nellcor in1983. Biox was founded in 1979, and introduced the first pulse oximeter to commercialdistribution in 1981. Biox initially focused on respiratory care, but when the companydiscovered that their pulse oximeters were being used in operating rooms to monitoroxygen levels, Biox expanded its marketing resources to focus on operating rooms in late
http://en.wikipedia.org/wiki/Pulse_oximetry#History%23Historyhttp://en.wikipedia.org/wiki/Pulse_oximetry#Limitations%23Limitationshttp://en.wikipedia.org/wiki/Pulse_oximetry#See_also%23See_alsohttp://en.wikipedia.org/wiki/Pulse_oximetry#References%23Referenceshttp://en.wikipedia.org/w/index.php?title=Pulse_oximetry&action=edit§ion=1http://en.wikipedia.org/wiki/Oxygenationhttp://en.wikipedia.org/wiki/Oxygenationhttp://en.wikipedia.org/wiki/Intensive_carehttp://en.wikipedia.org/wiki/Intensive_carehttp://en.wikipedia.org/wiki/Critical_carehttp://en.wikipedia.org/wiki/Emergency_departmenthttp://en.wikipedia.org/wiki/Aircraft_pilothttp://en.wikipedia.org/wiki/Pulse_oximetry#cite_note-1%23cite_note-1http://en.wikipedia.org/wiki/Primary_carehttp://en.wikipedia.org/wiki/Carbon_dioxidehttp://en.wikipedia.org/wiki/Hypoventilationhttp://en.wikipedia.org/wiki/Wikipedia:Citation_neededhttp://en.wikipedia.org/wiki/Wikipedia:Citation_neededhttp://en.wikipedia.org/w/index.php?title=Pulse_oximetry&action=edit§ion=2http://en.wikipedia.org/wiki/Wikipedia:Citation_neededhttp://en.wikipedia.org/wiki/Wikipedia:Citation_neededhttp://en.wikipedia.org/wiki/Photocellhttp://en.wikipedia.org/wiki/Photocellhttp://en.wikipedia.org/wiki/Sleep_laboratoryhttp://en.wikipedia.org/wiki/Sleep_laboratoryhttp://en.wikipedia.org/wiki/Wikipedia:Citation_neededhttp://en.wikipedia.org/wiki/Wikipedia:Citation_neededhttp://en.wikipedia.org/wiki/Wikipedia:Citation_neededhttp://en.wikipedia.org/w/index.php?title=Takuo_Aoyagi&action=edit&redlink=1http://en.wikipedia.org/w/index.php?title=Takuo_Aoyagi&action=edit&redlink=1http://en.wikipedia.org/w/index.php?title=Nihon_Kohden&action=edit&redlink=1http://en.wikipedia.org/w/index.php?title=Nihon_Kohden&action=edit&redlink=1http://en.wikipedia.org/wiki/Pulse_oximetry#cite_note-2%23cite_note-2http://en.wikipedia.org/wiki/Bioxhttp://en.wikipedia.org/wiki/Pulse_oximetry#History%23Historyhttp://en.wikipedia.org/wiki/Pulse_oximetry#Limitations%23Limitationshttp://en.wikipedia.org/wiki/Pulse_oximetry#See_also%23See_alsohttp://en.wikipedia.org/wiki/Pulse_oximetry#References%23Referenceshttp://en.wikipedia.org/w/index.php?title=Pulse_oximetry&action=edit§ion=1http://en.wikipedia.org/wiki/Oxygenationhttp://en.wikipedia.org/wiki/Intensive_carehttp://en.wikipedia.org/wiki/Critical_carehttp://en.wikipedia.org/wiki/Emergency_departmenthttp://en.wikipedia.org/wiki/Aircraft_pilothttp://en.wikipedia.org/wiki/Pulse_oximetry#cite_note-1%23cite_note-1http://en.wikipedia.org/wiki/Primary_carehttp://en.wikipedia.org/wiki/Carbon_dioxidehttp://en.wikipedia.org/wiki/Hypoventilationhttp://en.wikipedia.org/wiki/Wikipedia:Citation_neededhttp://en.wikipedia.org/w/index.php?title=Pulse_oximetry&action=edit§ion=2http://en.wikipedia.org/wiki/Wikipedia:Citation_neededhttp://en.wikipedia.org/wiki/Photocellhttp://en.wikipedia.org/wiki/Sleep_laboratoryhttp://en.wikipedia.org/wiki/Wikipedia:Citation_neededhttp://en.wikipedia.org/w/index.php?title=Takuo_Aoyagi&action=edit&redlink=1http://en.wikipedia.org/w/index.php?title=Nihon_Kohden&action=edit&redlink=1http://en.wikipedia.org/w/index.php?title=Nihon_Kohden&action=edit&redlink=1http://en.wikipedia.org/wiki/Pulse_oximetry#cite_note-2%23cite_note-2http://en.wikipedia.org/wiki/Biox -
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1982. A competitor,Nellcor(now part ofCovidien, Ltd.), Incorporated in 1982, andbegan to compete with Biox for the US operating room market in 1983. Prior to itsintroduction, a patient's oxygenation could only be determined by a painfularterial bloodgas, a single point measure which takes a few minutes processing by a laboratory. (In theabsence of oxygenation, damage to the brainstarts in 5 minutes withbrain death in
another 1015 minutes). In the US alone, approximately $2 billion was spent annually onthis measurement. With the introduction of pulse oximetry, a non-invasive, continuousmeasure of patient's oxygenation was possible, revolutionizing the practice of anesthesiaand greatly improving patient safety. Prior to its introduction, studies in anesthesiajournals estimated US patient mortality as a consequence of undetected hypoxemia at2,000 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 USincluded pulse oximetry. From the operating room, the use of pulse oximetry rapidlyspread throughout the hospital, first in the recovery room, and then into the variousintensive 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 toomuch oxygen. Furthermore, obtaining an arterial blood gas from a neonatal patient isextremely difficult.[citation needed]
In 1996, Masimo, a California-based company, introduced the first pulse oximeter able toprovide accurate measurements during periods of patient motion or low peripheralperfusion, long thought to be limitations of pulse oximetry technology that could not beovercome. [4] The ability to provide accurate measurements under these difficult clinicalconditions meant pulse oximetry could be used outside the operating room, wherepatients were generally well perfused and not moving, allowing for adoption in neonatalintensive care units, ambulances, and other challenging settings. [5]
By 2008, the accuracy and capability of Pulse Oximetry had continued to increase, andhad 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 Oximetryin 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 byNonin Medical, enabling clinicians to remotely monitor patients pulses and oxygensaturation levels. It also allows patients to monitor their own health through online patienthealth records and home telemedicine system.[10]
[edit] LimitationsThis is a measure solely of oxygenation, not ofventilation, and is not a substitute forblood gaseschecked in a laboratory as it gives no indication of base deficit,carbondioxide levels, bloodpH, or bicarbonate HCO3-concentration. The metabolism ofoxygen can be readily measured by monitoring expired CO2. Saturation figures also giveno information about blood oxygen content. Most of the oxygen in the blood is carried by
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hemoglobin. In severe anemia, the blood will carry less total oxygen, despite thehemoglobin being 100% saturated.
Falsely low readings may be caused by hypoperfusionof the extremity being used formonitoring (often due to the part being cold or fromvasoconstrictionsecondary to the use
of vasopressor agents); incorrect sensor application; highly calloused skin; and movement(such as shivering), especially during hypoperfusion. To ensure accuracy, the sensorshould return a steady pulse and/or pulse waveform. Falsely high or falsely low readingswill occur when hemoglobin is bound to something other than oxygen. In cases ofcarbonmonoxide poisoning, the falsely high reading may delay the recognition ofhypoxemia(low blood oxygen level). Methemoglobinemia characteristically causes pulse oximetryreadings in the mid-80s. Cyanide poisoningcan also give a high reading because itreduces oxygen extraction from arterial blood (the reading is not false, as arterial bloodoxygen 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 noninvasivemeasurement of the dyshemoglobins is a pulse co-oximeter. Pulse CO-Oximetry wasinvented in 2005 by Masimo and currently allows clinicians to measure totalhemoglobinlevels in addition to carboxyhemoglobin, methemoglobinand PVI, which initial clinicalstudies have shown may provide clinicians with a new method for noninvasive andautomatic assessment of patient fluid volume status.[11][12][13] Appropriate fluid levels arevital to reducing postoperative risks and improving patient outcomes as fluid volumesthat are too low (under hydration) or too high (over hydration) have been shown todecrease wound healing, increase risk of infection and cardiac complications.[14]
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