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 highpitched 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 lowpitched 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












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 forward while holding his or her breath in exhalation. up and leaning

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 highpressure 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 Grade 2 Grade 3 Grade 4 Grade 5 a very faint murmur that seems to fade in and out a soft but easily detectable murmur a moderately loud murmur a loud murmur that is associated with a thrill(palpable vibration) a very loud palpable murmur that is audible with the stethoscope

partly off Grade 6

the chest wall. 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 (crescendodecrescendo), 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 crescendodecrescendo 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, middiastolic 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.


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]