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HEART AND LUNGSOUNDSReading for IVMS Heart and LungAuscultation Page

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Contents

Articles

Heart sounds 1

Heart murmur 7

Aortic valve stenosis 12

Mitral regurgitation 22

Pulmonary valve stenosis 30

Tricuspid insufficiency 32

Atrial septal defect 35

Functional murmur 44

Aortic insufficiency 46

Mitral stenosis 53

Tricuspid valve stenosis 59

Pulmonary valve insufficiency 61

Patent ductus arteriosus 63

Wheeze 68

Stridor 70

Rhonchi 72

Crackles 73

Pertussis 75

References

Article Sources and Contributors 82

Image Sources, Licenses and Contributors 84

Article Licenses

License 85

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Heart sounds 1

Heart sounds

Normal heart sounds

Normal heart sounds as heard with a stethoscope

Problems playing this file? See media help.

Front of thorax, showing surface relations of bones, lungs (purple), pleura (blue),

and heart (red outline). The location of best auscultation for each heart valve are

labeled with "M", "T", "A", and "P".

First heart sound: caused by atrioventricular valves - Mitral (M) and Tricuspid (T).

Second heart sound caused by semilunar valves -- Aortic (A) and

Pulmonary/Pulmonic (P).

Heart sounds are the noises generated by

the beating heart and the resultant flow of

blood through it. Specifically, the sounds

reflect the turbulence created when the heart

valves snap shut. In cardiac auscultation, an

examiner may use a stethoscope to listen forthese unique and distinct sounds that

provide important auditory data regarding

the condition of the heart.

In healthy adults, there are two normal heart

sounds often described as a lub and a dub

(or dup), that occur in sequence with each

heartbeat. These are the first heart sound

(S1) and second heart sound (S

2), produced

by the closing of the AV valves and

semilunar valves, respectively. In addition

to these normal sounds, a variety of other

sounds may be present including heart

murmurs, adventitious sounds, and gallop

rhythms S3

and S4.

Heart murmurs are generated by turbulent

flow of blood, which may occur inside or

outside the heart. Murmurs may be

physiological (benign) or pathological (abnormal). Abnormal murmurs can be caused by stenosis restricting the

opening of a heart valve, resulting in turbulence as blood flows through it. Abnormal murmurs may also occur withvalvular insufficiency (regurgitation), which allows backflow of blood when the incompetent valve closes with only

partial effectiveness. Different murmurs are audible in different parts of the cardiac cycle, depending on the cause of

the murmur.

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Heart sounds 2

Diagram showing relations of opened heart to front of thoracic wall.

Ant. Anterior segment of tricuspid valve. A O. Aorta. A.P. Anterior

papillary muscle. In. Innominate artery. L.C.C. Left common carotid

artery. L.S. Left subclavian artery. L.V. Left ventricle. P.A.

Pulmonary artery. R.A. Right atrium. R.V. Right ventricle. V.S.

Ventricular septum.

Primary heart sounds

Normal heart sounds are associated with heart valves

closing, causing changes in blood flow.

S1

The first heart tone, or S1, forms the "lub" of "lub-dub"

and is composed of components M1

and T1. Normally

M1

precedes T1

slightly. It is caused by the sudden

block of reverse blood flow due to closure of the

atrioventricular valves, i.e. tricuspid and mitral

(bicuspid), at the beginning of ventricular contraction,

or systole. When the ventricles begin to contract, so do

the papillary muscles in each ventricle. The papillary

muscles are attached to the tricuspid and mitral valvesvia chordae tendineae, which bring the cusps or leaflets

of the valve closed; the chordae tendineae also prevent

the valves from blowing into the atria as ventricular

pressure rises due to contraction. The closing of the

inlet valves prevents regurgitation of blood from the

ventricles back into the atria. The S1 sound results from

reverberation within the blood associated with the

sudden block of flow reversal by the valves.[1] If M1

occurs slightly after T1, then the patient likely has a

dysfunction of conduction of the left side of the heartsuch as a left bundle branch block.

S2

The second heart tone, or S2, forms the "dub" of "lub-dub" and is composed of components A

2and P

2. Normally A

2precedes P

2especially during inspiration when a split of S

2can be heard. It is caused by the sudden block of

reversing blood flow due to closure of the semilunar valves (the aortic valve and pulmonary valve) at the end of

ventricular systole and the beginning of ventricular diastole. As the left ventricle empties, its pressure falls below the

pressure in the aorta. Aortic blood flow quickly reverses back toward the left ventricle, catching the pocket-like

cusps of the aortic valve, and is stopped by aortic valve closure. Similarly, as the pressure in the right ventricle fallsbelow the pressure in the pulmonary artery, the pulmonary valve closes. The S

2sound results from reverberation

within the blood associated with the sudden block of flow reversal.

Splitting of S2, also known as physiological split, normally occurs during inspiration because the decrease in

intrathoracic pressure increases the time needed for pulmonary pressure to exceed that of the right ventricular

pressure. A widely split S2 can be associated with several different cardiovascular conditions, including right bundle

branch block, pulmonary stenosis, and atrial septal defect.

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Heart sounds 3

Extra heart sounds

The rarer extra heart sounds form gallop rhythms and are heard in both normal and abnormal situations.

S3

Rarely, there may be a third heart sound also called a protodiastolic gallop, ventricular gallop, or informally the

"Kentucky" gallop as an onomatopoeic reference to the rhythm and stress of S1 followed by S2 and S3 together

(S1=Ken; S2=tuck; S3=y).

"lub-dub-ta" or "slosh-ing-in" If new, indicates heart failure or volume overload.

It occurs at the beginning of diastole after S2 and is lower in pitch than S1 or S2 as it is not of valvular origin. The

third heart sound is benign in youth, some trained athletes, and sometimes in pregnancy but if it re-emerges later in

life it may signal cardiac problems, such as a failing left ventricle as in dilated congestive heart failure (CHF). S3 is

thought to be caused by the oscillation of blood back and forth between the walls of the ventricles initiated by blood

rushing in from the atria. The reason the third heart sound does not occur until the middle third of diastole is

probably that during the early part of diastole, the ventricles are not filled sufficiently to create enough tension for

reverberation.It may also be a result of tensing of the chordae tendineae during rapid filling and expansion of the ventricle. In other

words, an S3 heart sound indicates increased volume of blood within the ventricle. An S3 heart sound is best heard

with the bell-side of the stethoscope (used for lower frequency sounds). A left-sided S3 is best heard in the left

lateral decubitus position and at the apex of the heart, which is normally located in the 5th left intercostal space at the

midclavicular line. A right-sided S3 is best heard at the lower-left sternal border. The way to distinguish between a

left and right-sided S3 is to observe whether it increases in intensity with inspiration or expiration. A right-sided S3

will increase on inspiration, while a left-sided S3 will increase on expiration.

S4

S4 when audible in an adult is called a presystolic gallop or atrial gallop. This gallop is produced by the sound of

blood being forced into a stiff or hypertrophic ventricle.

"ta-lub-dub" or "a-stiff-wall"

It is a sign of a pathologic state, usually a failing or hypertrophic left ventricle, as in systemic hypertension, severe

valvular aortic stenosis, and hypertrophic cardiomyopathy. The sound occurs just after atrial contraction at the end of

diastole and immediately before S1, producing a rhythm sometimes referred to as the "Tennessee" gallop where S4

represents the "Ten-" syllable. It is best heard at the cardiac apex with the patient in the left lateral decubitus position

and holding his breath. The combined presence of S3 and S4 is a quadruple gallop, also known as the

"Hello-Goodbye" gallop. At rapid heart rates, S3 and S4 may merge to produce a summation gallop, sometimes

referred to as S7.Atrial contraction must be present for production of an S4. It is absent in atrial fibrillation and in other rhythms in

which atrial contraction does not precede ventricular contraction.

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Heart sounds 4

Murmurs

Heart murmurs are produced as a result of turbulent flow of blood strong enough to produce audible noise. They are

usually heard as a whooshing sound. The term murmur only refers to a sound believed to originate within blood flow

through or near the heart; rapid blood velocity is necessary to produce a murmur. It should be noted that most heart

problems do not produce any murmur and most valve problems also do not produce an audible murmur.

Murmurs can be heard in many situations in adults without major congenital heart abnormalities:

Regurgitation through the mitral valve is by far the most commonly heard murmur, producing a

pansystolic/holosystolic murmur which is sometimes fairly loud to a practiced ear, even though the volume of

regurgitant blood flow may be quite small. Yet, though obvious using echocardiography visualization, probably

about 20% of cases of mitral regurgitation do not produce an audible murmur.

Stenosis of the aortic valve is typically the next most common heart murmur, a systolic ejection murmur. This is

more common in older adults or in those individuals having a two, not a three leaflet aortic valve.

Regurgitation through the aortic valve, if marked, is sometimes audible to a practiced ear with a high quality,

especially electronically amplified, stethoscope. Generally, this is a very rarely heard murmur, even though aortic

valve regurgitation is not so rare. Aortic regurgitation, though obvious using echocardiography visualization,

usually does not produce an audible murmur.

Stenosis of the mitral valve, if severe, also rarely produces an audible, low frequency soft rumbling murmur, best

recognized by a practiced ear using a high quality, especially electronically amplified, stethoscope.

Other audible murmurs are associated with abnormal openings between the left ventricle and right heart or from

the aortic or pulmonary arteries back into a lower pressure heart chamber.

Gradations of

Murmurs[1]

(Defined based on use of an acoustic, not a high-fidelity amplified electronic stethoscope)

Grade Description

Grade 1 Very faint, heard only after listener has "tuned in"; may not be heard in all positions. Only heard if the patient "bears

down" or performs the Valsalva maneuver.

Grade 2 Quiet, but heard immediately after placing the stethoscope on the chest.

Grade 3 Moderately loud.

Grade 4 Loud, with palpable thrill (a tremor or vibration felt on palpation)[2]

Grade 5 Very loud, with thrill. May be heard when stethoscope is partly off the chest.

Grade 6 Very loud, with thrill. May be heard with stethoscope entirely off the chest.

Though several different cardiac conditions can cause heart murmurs, the murmurs can change markedly with the

severity of the cardiac disease. An astute physician can sometimes diagnose cardiac conditions with some accuracy

based largely on the murmur, related physical examination, and experience with the relative frequency of different

heart conditions. However, with the advent of better quality and wider availability of echocardiography and other

techniques, heart status can be recognized and quantified much more accurately than formerly possible with only a

stethoscope, examination, and experience.

Effects of inhalation/expiration

Inhalation pressure causes an increase in the venous blood return to the right side of the heart by increasing

intrathoracic negative pressure making it more negative (pulling blood into the right side of the heart via a

vacuum-like effect). Therefore, right-sided murmurs generally increase in intensity with inspiration. The increased

(more negative) intrathoracic pressure has an opposite effect on the left side of the heart, making it harder for theblood to exit into circulation. Therefore, left-sided murmurs generally decrease in intensity during inspiration.

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Heart sounds 5

With expiration, the opposite haemodynamic changes occur: left-sided murmurs generally increase in intensity with

expiration. If a patient lies supine with his legs up at a 45-degree angle, venous return to the right side of the heart

produces effects similar to inhalation-increased blood flow.

Interventions that change murmurs

There are a number of interventions that can be performed that alter the intensity and characteristics of abnormalheart sounds. These interventions can differentiate the different heart sounds to more effectively obtain a diagnosis

of the cardiac anomaly that causes the heart sound.

Other abnormal sounds

Clicks Heart clicks are short, high-pitched sounds that can be appreciated with modern non-invasive imaging

techniques.

Rubs The pericardial friction rub can be heard in pericarditis, an inflammation of the pericardium, the sac

surrounding the heart. This is a characteristic scratching, creaking, high-pitched sound emanating from the rubbing

of both layers of inflamed pericardium. It is the loudest in systole, but can often be heard at the beginning and at theend of diastole. It is very dependent on body position and breathing, and changes from hour to hour.

Surface anatomy

The aortic area, pulmonic area, tricuspid area and mitral area are areas on the surface of the chest where the heart is

auscultated. Heart sounds result from reverberation within the blood associated with the sudden block of flow

reversal by the valves closing. Because of this, auscultation to determine function of a valve is usually not performed

at the position of the valve, but at the position to where the sound waves reverberate.

Pulmonary valve (to pulmonary trunk) left second intercostal space left upper sternal border

Aortic valve (to aorta) right second intercostal space right upper sternal border

Erb's point Left third intercostal space medial left sternal border

Mitral valve (to left ventricle) left fifth intercostal space medial to left midclavicular line

Tricuspid valve (to right ventricle) left fifth intercostal space lower left sternal border

Recording heart sounds

Using electronic stethoscopes, it is possible to record heart sounds via direct output to an external recording device,

such as a laptop or MP3 recorder. The same connection can be used to listen to the previously recorded auscultation

through the stethoscope headphones, allowing for more detailed study of murmurs and other heart sounds, forgeneral research as well as evaluation of a particular patient's condition.

Notes and references

[1] http:/ /en.wikipedia. org/wiki/Heart_sounds#endnote_Abnormal_sounds

[2] "thrill". (http://www2.merriam-webster. com/cgi-bin/mwmednlm?book=Medical& va=thrill) Medline Plus Medical Dictionary.

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Heart sounds 6

External links

University of Michigan Heart Sound and Murmur Library. (http://www.med.umich.edu/lrc/psb/heartsounds/

index.htm)

Heart Sounds & Murmurs. (http://www.dundee.ac.uk/medther/Cardiology/hsmur.html) University of

Dundee.

Auscultation Assistant. (http://www.med.ucla.edu/wilkes/intro.html) UCLA Heart Sounds - Heart Murmurs. (http://www.practicalclinicalskills.com/heart-sounds-murmurs.aspx)

practicalclinicalskills.com

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Heart murmur 7

Heart murmur

Cardiac murmurs and other cardiac sounds

Auscultogram from normal and abnormal heart sounds

ICD-10 R01[1]

ICD-9 785.2[2]

-785.3[3]

DiseasesDB 29151[4]

MedlinePlus 003266[5]

MeSH D006337[6]

Murmurs are pathologic heart sounds that are produced as a result of turbulent blood flow that is sufficient to

produce audible noise. Most murmurs can only be heard with the assistance of a stethoscope ("or auscultation").A functional murmur or "physiologic murmur" is a heart murmur that is primarily due to physiologic conditions

outside the heart, as opposed to structural defects in the heart itself. Functional murmurs are benign (an "innocent

murmur").

Murmurs may also be the result of various problems, such as narrowing or leaking of valves, or the presence of

abnormal passages through which blood flows in or near the heart. Such murmurs, known as pathologic murmurs,

should be evaluated by an expert.

Heart murmurs are most frequently categorized by timing, into systolic heart murmurs and diastolic heart murmurs.

However, continuous murmurs cannot be directly placed into either category.

Classification

Murmurs can be classified by seven different characteristics: timing, shape, location, radiation, intensity, pitch and

quality.

Timing refers to whether the murmur is a systolic or diastolic murmur.

Shape refers to the intensity over time; murmurs can be crescendo [7], decrescendo [8] or crescendo-decrescendo.

Location refers to where the heart murmur is usually auscultated best. There are four places on the anterior chest

wall to listen for heart murmurs; each of the locations roughly corresponds to a specific part of the heart and

should be auscultated with the patient lying supine. The four locations are:

Aortic region - the 2nd right intercostal space.

Pulmonic region - the 2nd left intercostal spaces.

Tricuspid region - the 5th left intercostal space.

Mitral region - the 5th left mid-clavicular intercostal space.

Additional maneuvers can be performed for additional auscultation:

Left lateral decubitis.

With the patient sitting upright.

With the patient leaning forward and exhaling.

Radiation refers to where the sound of the murmur radiates. The general rule of thumb is that the sound radiates

in the direction of the blood flow.

Intensity refers to the loudness of the murmur, and is graded according to the Levine scale, from 1 to 6:

1.1. The murmur is only audible on listening carefully for some time.

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Heart murmur 8

2.2. The murmur is faint but immediately audible on placing the stethoscope on the chest.

3.3. A loud murmur readily audible but with no palpable thrill.

4.4. A loud murmur with a palpable thrill.

5.5. A loud murmur with a palpable thrill. The murmur is so loud that it is audible with only the rim of the

stethoscope touching the chest.

6.6. A loud murmur with a palpable thrill. The murmur is audible with the stethoscope not touching the chest but

lifted just off it.

Pitch may be low, medium or high and is determined by whether it can be auscultated best with the bell or

diaphragm of a stethoscope.

Quality refers to unusual characteristics of a murmur, such as blowing, harsh, rumbling or musical.

A mnemonic to remember what characteristics to look for when listening to murmurs is SCRIPT: Site, Configuration

(shape), Radiation, Intensity, Pitch and quality, and Timing in the cardiac cycle.

The use of two simple mnemonics may help differentiate systolic and diastolic murmurs; PASS and PAID.

Pulmonary and aortic stenoses are systolic while pulmonary and aortic insufficiencies (regurgitation) are diastolic.

Mitral and tricuspid defects are opposite.

Interventions that change murmur sounds

Inhalation leads to an increase in intrathoracic negative pressure, which increases the capacity of pulmonary

circulation, thereby prolonging ejection time. This will affect the closure of the pulmonary valve. This finding,

also called Carvallo's maneuver, has been found by studies to have a sensitivity of 100% and a specificity of 80%

to 88% in detecting murmurs originating in the right heart. specifically positive Carvallo's sign describes the

increase in intensity of a tricuspid regurgitation murmur with inspiration.[9]

abrupt standing

Squatting, by increasing afterload and increasing preload.

Handgrip maneuver, by increasing afterload Valsalva maneuver. One study found the Valsalva maneuver to have a sensitivity of 65%, specificity of 96% in

detecting hypertrophic obstructive cardiomyopathy (HOCM). Both standing and Valsalva maneuver will decrease

venous return and subsequently decrease left ventricular filling, resulting in an increase in the loudness of the

murmur of hypertrophic cardiomyopathy, since outflow obstruction is increased by decreasing preload.

Alternatively, squatting increases systemic vascular resistance, increasing afterload and helping to hold the

obstruction in a more open configuration, decreasing the murmur. Maximum handgrip exercise also results in a

decrease in the loudness of the murmur.[10]

post ectopic potentiation

Inhaled amyl nitrite is a vasodilator that diminishes systolic murmurs in left-to-right shunts in ventricular septal

defects, and reveals right-to left shunts in the setting of a pulmonic stenosis and a ventricular septal defect. methoxamine

positioning of the patient. That is, putting patients in the left lateral position will allow a murmur in the mitral

valve area to be more pronounced.

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Heart murmur 9

Anatomic sources of murmur

Systolic

Aortic valve stenosis typically is a crescendo/decrescendo systolic murmur best heard at the right upper sternal

border sometimes with radiation to the carotid arteries. In mild aortic stenosis, the crescendo-decrescendo is early

peaking whereas in severe aortic stenosis, the crescendo is late-peaking, and the S2 heart sound may be obliterated.

Stenosis of Bicuspid aortic valve is similar to the aortic valve stenosis heart murmur, but a systolic ejection click

may be heard after S1 in calcified bicuspid aortic valves. Symptoms tend to present between 40 and 70 years of age.

Mitral regurgitation typically is a holosystolic murmur heard best at the apex, and may radiate to the axilla or

precordium. A systolic click may be heard if there is associated mitral valve prolapse. Valsalva maneuver in mitral

regurgitation associated with mitral valve prolapse will increase left ventricular preload and move the murmur onset

closer to S1, and isometric handgrip, which increases left ventricular afterload, will increase murmur intensity. In

acute severe mitral regurgitation, a holosystolic murmur may not be heard.

Pulmonary valve stenosis typically is a crescendo-decrescendo murmur heard best at the left upper sternal border,

associated with a systolic ejection click that diminishes with inspiration and sometimes radiates to the left clavicle.

Tricuspid valve regurgitation presents as a holosystolic murmur at the left lower sternal border with radiation to theleft upper sternal border. Prominent v and c waves may be seen in the jugular venous pulse. The murmur will

increase with inspiration.

Hypertrophic obstructive cardiomyopathy (or hypertrophic subaortic stenosis) will be a systolic

crescendo-decrescendo murmur best heard at the left lower sternal border. Valsalva maneuver will increase the

intensity of the murmur, as will changing positions from squatting to standing.

Atrial septal defect will present with a systolic crescendo-decrescendo murmur best heard at the right upper sternal

border due to increased volume going through the pulmonary valve, and is associated with a fixed, split S2 and a

right ventricular heave.

Ventricular septal defect (VSD) will present as a holosystolic murmur at the left lower sternal border, associatedwith a palpable thrill, and increases with isometric handgrip. A right to left shunt (Eisenmenger syndrome) may

develop with uncorrected VSDs due to worsening pulmonary hypertension, which will increase the murmur intensity

and be associated with cyanosis.

Flow murmur may be heard at the right upper sternal border in certain conditions, such as anemia, hyperthyroidism,

fever, and pregnancy.

Diastolic

Aortic valve regurgitation will present as a diastolic decrescendo murmur heard at the left lower sternal border or

right lower sternal border (when associated with a dilated aorta). This may be associated with bounding carotid and

peripheral pulses (Corrigan's pulse, Waterhammer pulse), and a widened pulse pressure.

Mitral stenosis typically presents as a diastolic low-pitched decrescendo murmur best heard at the cardiac apex in the

left lateral decubitus position. It may be associated with an opening snap. Increasing severity will shorten the time

between S2 and the opening snap.

Tricuspid valve stenosis presents as a diastolic decrescendo murmur at the left lower sternal border, and signs of

right heart failure may be seen on exam.

Pulmonary valve regurgitation presents as a diastolic decrescendo murmur at the left lower sternal border. A

palpable S2 in the second left intercostal space correlates with pulmonary hypertension due to mitral stenosis.

Continuous and Combined Systolic/Diastolic

Patent ductus arteriosus may present as a continuous murmur radiating to the back.

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Heart murmur 10

Severe coarctation of the aorta can present with a continuous murmur: a systolic component at the left infraclavicular

region and the back due to the stenosis, and a diastolic component over the chest wall due to blood flow through

collateral vessels.

Acute severe aortic regurgitation is associated with a three phase murmur, specifically a midsystolic murmur

followed by S2, followed by a parasternal early diastolic and mid-diastolic murmur (Austin Flint murmur). Although

the exact cause of an Austin Flint murmur is unknown, it is hypothesized that the mechanism of murmur is from thesevere aortic regurgitation jet vibrating the anterior mitral valve leaflet, colliding with the mitral inflow during

diastole, with increased mitral inflow velocity from the narrowed mitral valve orifice leading to the jet impinging on

the myocardial wall.

Another not that common cause of a continuous murmur is a ruptured sinus of valsalva. Usually the murmur is well

heard in the aortic area and along the left sternal border.

Murmur Types and Disease Associations

Continuous Machinery Murmur, at the left upper sternal border

Classic for a patent ductus arteriosus, and in serious cases associated with poor feeding, failure to thrive andrespiratory distress. Other examination findings may include widened pulse pressures and bounding pulses.

Systolic Murmur loudest below the left scapula

Classic for a coarctation of the aorta which is often seen in Turner's Syndrome, (gonadal dysgenesis), an

X-linked disorder with a part missing of the X-chromosome. Other findings of this murmur is radio-femoral

delay, and different blood pressures in the upper and lower extremities.

Harsh holosystolic murmur at the left lower sternal border

Classic for a ventricular septal defect. It is in these children that the delayed-onset cyanotic heart disease

occurs known as Eisenmenger syndrome, which is a reversal of the left-to-right heart shunt as the right

ventricle hypertrophies, causing a right-to-left shunt and resulting cyanosis.Widely split fixed S

2and systolic ejection murmur at the left upper sternal border

Classically due to a patent foramen ovale or atrial septal defect, which is lack of closure of the foramen ovale.

This produces a left-to-right shunt initially, thus does not produce cyanosis, but causes pulmonary

hypertension. Longstanding uncorrected atrial septal defects can also result in Eisenmenger's syndrome with

resultant cyanosis.

Cooing dove murmur

The cooing dove murmur is a cardiac murmur with a musical quality (high pitched - hence the name) and is

associated with aortic valve regurgitation (or mitral regurgiation before rupture of chordae). It is a diastolic murmurwhich can be heard over the mid-precordium.[11]

References

[1] http:/ /apps.who. int/classifications/icd10/browse/2010/en#/R01

[2] http:/ /www.icd9data. com/getICD9Code.ashx?icd9=785. 2

[3] http:/ /www.icd9data. com/getICD9Code.ashx?icd9=785. 3

[4] http:/ /www.diseasesdatabase.com/ddb29151. htm

[5] http:/ /www.nlm.nih. gov/medlineplus/ency/article/003266. htm

[6] http:/ /www.nlm.nih. gov/cgi/mesh/2009/MB_cgi?field=uid& term=D006337

[7] http:/ /en.wiktionary.org/wiki/crescendo

[8] http:/

/

en.wiktionary.org/

wiki/

decrescendo[9] Harrison's Internal Medicine 17th, chapter 5, "Disorders of the cardiovascular system," question 32, self assessment and board review

[10] Harrison's Internal Medicine 17th, chapter 5, "Disorders of the cardiovascular system," question 86-87, self assessment and board review

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Heart murmur 11

[11] https://www.jstage.jst.go. jp/article/ihj1960/22/5/22_5_861/_pdf

External links

Information on heart murmurs in children (http://heartcenter.seattlechildrens.org/conditions_treated/

heart_murmurs.asp) from Seattle Children's Heart Center

Heart Murmurs in Pediatric Patients (http:/

/

www.

aafp.

org/

afp/

990800ap/

558.

html) Lehrer, Steven. Understanding Pediatric Heart Sounds. Elsevier 2002.

Hanifin, Christopher.Heart Sounds: A Cardiac Auscultation Primer. CreateSpace, 2010

Texas Heart Institute (http://www.texasheartinstitute.org/education/cme/explore/events/eventdetail_5469.

cfm) Scroll down to listen to heart murmurs.

The Auscultation Assistant (http://www.med.ucla.edu/wilkes/intro.html) Provides recordings of heart

murmurs.

Heart murmurs in children (http://www.gosh.nhs.uk/medical-conditions/search-for-medical-conditions/

heart-murmurs-innocent/heart-murmurs-innocent-information/) information for parents.

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Aortic valve stenosis 12

Aortic valve stenosis

Aortic valve stenosis

Classification and external resources

In the center is an aortic valve with severe stenosis due to rheumatic heart disease. The valve is surrounded by the aorta. The pulmonary trunk is atthe lower right. The right coronary artery, cut lengthwise, is at the lower left. The left main coronary artery, also cut lengthwise, is on the right.

ICD-10 I35.0[1]

, I06.0[2]

, Q23.0[3]

ICD-9 395.0[4]

, 396.0[5]

, 746.3[6]

DiseasesDB 844[7]

MedlinePlus 000178[8]

eMedicine med/157[9]

Aortic valve stenosis (AS) is a disease of the heart valves in which the opening of the aortic valve is narrowed.

[10]

The aortic valve is the valve located between the left ventricle of the heart and the aorta, the largest artery in the

body which carries the entire output of blood to the systemic circulation. Aortic stenosis is now the most common

valvular heart disease in the Western World.

Signs and symptoms

Symptoms related to aortic stenosis depend on the degree of valve stenosis. Most people with mild to moderate

aortic stenosis are asymptomatic. Symptoms usually present in individuals with severe aortic stenosis, though they

may occur in those with mild to moderate aortic stenosis as well. The three cardinal symptoms of aortic stenosis are

syncope, anginal chest pain and dyspnea or other symptoms of heart failure such as orthopnea, exertional dyspnea,

paroxysmal nocturnal dyspnea, or pedal edema.

Angina

Angina in the setting of heart failure also increases the risk of death. In patients with angina, the 5 year mortality rate

is 50%, if the aortic valve is not replaced.

Angina in the setting of AS is secondary to the left ventricular hypertrophy (LVH) that is caused by the constant

production of increased pressure required to overcome the pressure gradient caused by the AS. While the

myocardium (i.e., heart muscle) of the LV gets thicker, the arteries that supply the muscle do not get significantly

longer or bigger, so the muscle may become ischemic (i.e., does not receive an adequate blood supply). The ischemia

may first be evident during exercise, when the heart muscle requires increased blood supply to compensate for theincreased workload. The individual may complain of exertional angina. At this stage, a stress test with imaging may

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Aortic valve stenosis 13

be suggestive of ischemia.

Eventually, however, the cardiac muscle will require more blood supply at rest than can be supplied by the coronary

artery branches. At this point there may be signs of ventricular strain pattern (ST segment depression and T wave

inversion) on the EKG, suggesting subendocardial ischemia. The subendocardium is the region that becomes

ischemic because it is the most distant from the epicardial coronary arteries.

Syncope

Syncope (fainting spells) from aortic valve stenosis is usually exertional.[11] In the setting of heart failure it increases

the risk of death. In patients with syncope, the 3 year mortality rate is 50%, if the aortic valve is not replaced. [citation

needed]

It is unclear why aortic stenosis causes syncope. One popular theory is that severe AS produces a nearly fixed

cardiac output.[citation needed] When the patient exercises, their peripheral vascular resistance will decrease as the

blood vessels of the skeletal muscles dilate to allow the muscles to receive more blood to allow them to do more

work. This decrease in peripheral vascular resistance is normally compensated for by an increase in the cardiac

output. Since patients with severe AS cannot increase their cardiac output, the blood pressure falls and the patient

will syncopize due to decreased blood perfusion to the brain.

A second theory as to why syncope may occur in AS is that during exercise, the high pressures generated in the

hypertrophied LV cause a vasodepressor response, which causes a secondary peripheral vasodilation that, in turn,

causes decreased blood flow to the brain resulting in loss of consciousness. Indeed, in aortic stenosis, because of the

fixed obstruction to bloodflow out from the heart, it may be impossible for the heart to increase its output to offset

peripheral vasodilation.

A third mechanism may sometimes be operative. Due to the hypertrophy of the left ventricle in aortic stenosis,

including the consequent inability of the coronary arteries to adequately supply blood to the myocardium (see

"Angina" below), arrhythmias may develop. These can lead to syncope.

Finally, in calcific aortic stenosis[12] at least, the calcification in and around the aortic valve can progress and extendto involve the electrical conduction system of the heart. If that occurs, the result may be heart block - a potentially

lethal condition of which syncope may be a symptom.

Density-Dependent Colour Scanning Electron

Micrograph SEM (DDC-SEM) of cardiovascular

calcification, showing in orange calcium

phosphate spherical particles (denser material)

and, in green, the extracellular matrix (less dense

material).[]

Congestive heart failure

Congestive heart failure (CHF) carries a grave prognosis in patients

with AS. Patients with CHF attributable to AS have a 2 year mortality

rate of 50% if the aortic valve is not replaced.[citation needed] CHF in the

setting of AS is due to a combination of left ventricular hypertrophy

with fibrosis, systolic dysfunction (a decrease in the ejection fraction)

and diastolic dysfunction (elevated filling pressure of the LV).

Associated symptoms

In Heyde's syndrome, aortic stenosis is associated with gastrointestinal

bleeding due to angiodysplasia of the colon. Recent research has

shown that the stenosis causes a form of von Willebrand disease by

breaking down its associated coagulation factor (factor VIII-associated

antigen, also called von Willebrand factor), due to increased turbulence around the stenosed valve.

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Aortic valve stenosis 14

Complications

Notwithstanding the foregoing, the American Heart Association has recently changed its recommendations regarding

antibiotic prophylaxis for endocarditis. Specifically, as of 2007, it is recommended that such prophylaxis be limited

only to those with prosthetic heart valves, those with previous episode(s) of endocarditis, and those with certain

types of congenital heart disease.[citation needed]

Since the stenosed aortic valve may limit the heart's output, people with aortic stenosis are at risk of syncope anddangerously low blood pressure should they use any of a number of medications for cardiovascular diseases that

often coexist with aortic stenosis. Examples include nitroglycerin, nitrates, ACE inhibitors, terazosin (Hytrin), and

hydralazine. Note that all of these substances lead to peripheral vasodilation. Under normal circumstances, in the

absence of aortic stenosis, the heart is able to increase its output and thereby offset the effect of the dilated blood

vessels. In some cases of aortic stenosis, however, due to the obstruction of blood flow out of the heart caused by the

stenosed aortic valve, cardiac output cannot be increased. Low blood pressure or syncope may ensue.

Etiology

Illustration depicting aortic stenosis

Aortic stenosis is most commonly caused by age-related progressivecalcification of a normal (three-leafed) aortic valve (>50% of cases)

with a mean age of 65 to 70 years old. Other causes of aortic stenosis

include calcification of a congenital bicuspid aortic valve [13] (30-40%

of cases) and acute rheumatic fever post-inflammatory (less than 10%

of cases).[14] Rare causes of aortic stenosis include Fabry disease,

systemic lupus erythematosus, Paget disease, hyperuricemia, and

infection.

Normal aortic valves have three leaves (tricuspid), but some

individuals are born with an aortic valve that has two leaves (bicuspid).

Typically, aortic stenosis due to calcification of a bicuspid valve

appears earlier, in the 40s or 50s, whereas aortic stenosis due to

calcification of a normal tricuspid aortic valve appears later, usually in

the 70s and 80s.

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Aortic valve stenosis 15

Pathophysiology

Simultaneous left ventricular and aortic pressure

tracings demonstrate a pressure gradient between

the left ventricle and aorta, suggesting aortic

stenosis. The left ventricle generates higher

pressures than what is transmitted to the aorta.

The pressure gradient, caused by aortic stenosis,

is represented by the green shaded area. (AO =

ascending aorta; LV = left ventricle; ECG =

electrocardiogram.)

The human aortic valve normally consists of three leaflets (trileaflets)

and has an orifice of 3.0-4.0 square centimeters. When the left

ventricle (LV) contracts, it forces blood through the valve into the

aorta and subsequently to the rest of the body. When the LV expands

again, the aortic valve closes and prevents the blood in the aorta from

flowing backward into the left ventricle. In aortic stenosis, the opening

of the aortic valve becomes narrowed or constricted (stenotic) (i.e., due

to calcification). Degenerative aortic stenosis, the most common

variety, and bicuspid aortic stenosis both begin with damage to

endothelial cells from increased mechanical stress. Inflammation is

thought to be involved in the earlier stages of the pathogenesis of AS

and its associated risk factors are known to promote the deposition of

LDL cholesterol and a highly damaging substance known as

Lipoprotein(a) into the aortic valve resulting in significant damage and

stenosis over time.

As a consequence of this stenosis, the left ventricle must generate a

higher pressure with each contraction to effectively move blood

forward into the aorta. Initially, the LV generates this increased

pressure by thickening its muscular walls (myocardial hypertrophy).

The type of hypertrophy most commonly seen in AS is known as

concentric hypertrophy, in which the walls of the LV are

(approximately) equally thickened.

In the later stages, the left ventricle dilates, the wall thins, and the systolic function deteriorates (resulting in impaired

ability to pump blood forward). Morris and Innasimuthu et al. showed that different coronary anatomy is associatedwith different valve diseases. Research is ongoing to see if different coronary anatomy might lead to turbulent flow

at the level of valves leading to inflammation and degeneration.[15][16][17]

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Aortic valve stenosis 16

Risk factors

Risk factors known to influence disease progression of AS include lifestyle habits similar to those of coronary artery

disease such as hypertension, advanced age, being male, hyperlipidemia, diabetes mellitus, cigarette smoking,

metabolic syndrome, and end-stage renal disease.

Diagnosis

Phonocardiograms from normal and abnormal

heart sounds

Aortic stenosis is most often diagnosed when it is asymptomatic and

can sometimes be detected during routine examination of the heart and

circulatory system. Good evidence exists to demonstrate that certain

characteristics of the peripheral pulse can rule in the diagnosis. In

particular, there may be a slow and/or sustained upstroke of the arterial

pulse, and the pulse may be of low volume. This is sometimes referred

to as pulsus parvus et tardus. There may also be a noticeable delay

between the first heart sound (on auscultation) and the corresponding

pulse in the carotid artery (so-called 'apical-carotid delay'). In similarmanner, there may be a delay between the appearance of each pulse in

the brachial artery (in the arm) and the radial artery (in the wrist).

The first heart sound may be followed by a sharp ejection sound

("ejection click") best heard at the lower left sternal border and the

apex, and, thus, appear to be "split". The ejection sound, caused by the

impact of left ventricular outflow against the partially fused aortic

valve leaflets, is more commonly associated with a mobile bicuspid

aortic valve than an immobile calcified aortic valve. The intensity of

this sound does not vary with respiration, which helps distinguish it

from the ejection click produced by a stenotic pulmonary valve, which will diminish slightly in intensity during

inspiration.

An easily heard systolic, crescendo-decrescendo (i.e., 'ejection') murmur is heard loudest at the upper right sternal

border, at the 2nd right intercostal space, and radiates to the carotid arteries bilaterally. The murmur increases with

squatting, decreases with standing and isometric muscular contraction, which helps distinguish it from hypertrophic

obstructive cardiomyopathy (HOCM). The murmur is louder during expiration, but is also easily heard during

inspiration. The more severe the degree of the stenosis, the later the peak occurs in the crescendo-decrescendo of the

murmur.

The second heart sound (A2) tends to become decreasedand softer as the aortic stenosis becomes more severe. This

is a result of the increasing calcification of the valve preventing it from "snapping" shut and producing a sharp, loudsound. Due to increases in left ventricular pressure from the stenotic aortic valve, over time the ventricle may

hypertrophy, resulting in a diastolic dysfunction. As a result, one may hear a fourth heart sound due to the stiff

ventricle. With continued increases in ventricular pressure, dilatation of the ventricle will occur, and a third heart

sound may be manifest.

Finally, aortic stenosis often co-exists with some degree of aortic insufficiency (aortic regurgitation). Hence, the

physical exam in aortic stenosis may also reveal signs of the latter, for example an early diastolic decrescendo

murmur. Indeed, when both valve abnormalities are present, the expected findings of either may be modified or may

not even be present. Rather, new signs that reflect the presence of simultaneous aortic stenosis and insufficiency,

e.g., pulsus bisferiens, emerge.

According to a meta analysis, the most useful findings for ruling in aortic stenosis in the clinical setting were slow

rate of rise of the carotid pulse (positive likelihood ratio ranged 2.8130 across studies), mid to late peak intensity of

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Aortic valve stenosis 17

the murmur (positive likelihood ratio, 8.0101), and decreased intensity of the second heart sound (positive

likelihood ratio, 3.150).

Other peripheral signs include:

sustained, heaving apex beat, which is not displaced unless systolic dysfunction of the left ventricle has developed

A precordial thrill

narrowed pulse pressure

Electrocardiogram

Although aortic stenosis does not lead to any specific findings on the electrocardiogram (ECG), it still often leads to

a number of electrocardiographic abnormalities. ECG manifestations of left ventricular hypertrophy (LVH) are

common in aortic stenosis and arise as a result of the stenosis having placed a chronically high pressure load on the

left ventricle (with LVH being the expected response to chronic pressure loads on the left ventricle no matter what

the cause).

As noted above, the calcification process that occurs in aortic stenosis can progress to extend beyond the aortic valve

and into the electrical conduction system of the heart. Evidence of this phenomenon may rarely include ECG

patterns characteristic of certain types of heart block such as Left bundle branch block.

Heart catheterization

Cardiac chamber catheterization provides a definitive diagnosis, indicating severe stenosis in valve area of 40 < 1.0

Critical aortic stenosis >70 < 0.6

Echocardiogram (heart ultrasound) is the best non-invasive tool / test to evaluate the aortic valve anatomy and

function.

The aortic valve area can be calculated non-invasively using echocardiographic flow velocities. Using the velocity of

the blood through the valve, the pressure gradient across the valve can be calculated by the continuity equation or

using the modified Bernoulli's equation:

Gradient = 4(velocity) mmHg

A normal aortic valve has a gradient of only a few mmHg. A decreased valvular area causes increased pressure

gradient, and these parameters are used to classify and grade the aortic stenosis as mild, moderate or severe. The

pressure gradient can be abnormally low in the presence of mitral stenosis, heart failure, co-existent aorticregurgitation and also ischaemic heart disease (disease related to decreased blood supply and oxygen causing

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Aortic valve stenosis 18

ischaemia).

Echocardiogram may also show left ventricular hyperthrophy, thickened and immobile aortic valve and dilated aortic

root. However, it may appear deceptively normal in acute cases.

Chest X-ray

Chest X-ray can also assist in the diagnosis, showing calcific aortic valve, and, in longstanding disease, enlarged leftventricle and atrium.

Management

Treatment is generally not necessary in people without symptoms. In moderate cases, echocardiography is performed

every 12 years to monitor the progression, possibly complemented with a cardiac stress test. In severe cases,

echocardiography is performed every 36 months. In both moderate and mild cases, the patient should immediately

make a revisit or be admitted for inpatient care if any new related symptoms appear.

Medical ManagementThe effect of statins on the progression of AS is still unclear. The latest trials do not show any benefit in slowing AS

progression, but did demonstrate a decrease in ischemic cardiovascular events. Angiotensin-converting enzyme

(ACE) and angiotensin II receptors have been found in stenotic aortic valves. This leads to the hypothesis that the

renin-angiotensin system may play a role in the progression of the disease. To date, there is no randomized trial

examining the impact of ACE inhibitors in AS. Innasimuthu et al. showed that patients on bisphosphonates have less

progression of aortic stenosis and some regressed.[19][20][21] This finding led to multiple trials which is ongoing.

Subsequent research has failed to confirm the initial positive result.

In general, medical therapy has relatively poor efficacy in treating aortic stenosis. However, it may be useful to

manage commonly coexisting conditions that correlate with aortic stenosis:

Any angina is generally treated with beta-blockers and/or calcium blockers. Nitrates are contraindicated due to

their potential to cause profound hypotension in aortic stenosis.[22]

Any hypertension is treated aggressively, but caution must be taken in administering beta-blockers

Any heart failure is generally treated with digoxin and diuretics, and, if not contraindicated, cautious inpatient

administration of ACE inhibitors. As for angina, nitrates are contraindicated.

Since calcific aortic stenosis shares many pathological features and risk factors with atherosclerosis, and since

atherosclerosis may be prevented and/or reversed by cholesterol lowering, there has been interest in attempting to

modify the course of calcific aortic stenosis by lowering cholesterol levels with statin drugs. Although a number of

small, observational studies demonstrated an association between lowered cholesterol and decreased progression,

and even regression, of calcific aortic stenosis, a recent, large randomized clinical trial, published in 2005, failed tofind any predictable effect of cholesterol lowering on calcific aortic stenosis. A 2007 study did demonstrate a

slowing of aortic stenosis with the statin rosuvastatin. However, a large randomized controlled trial published in the

New England Journal of Medicine in 2008 failed to find any beneficial effect of intensive cholesterol lowering on

the course of aortic stenosis.

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Aortic valve stenosis 19

Aortic valve replacement

In adults, symptomatic severe aortic stenosis usually requires aortic valve replacement (AVR). While AVR has been

the standard of care for aortic stenosis for several decades, currently aortic valve replacement approaches include

open heart surgery, minimally invasive cardiac surgery (MICS) and minimally invasive catheter-based

(percutaneous) aortic valve replacement.

Apicoaortic conduit

Apicoaortic Conduit (AAC), or Aortic Valve Bypass (AVB), has been shown to be an effective treatment for aortic

stenosis.[23] There is long-term stability of the left ventricular hemodynamics after AVB, with no further biologic

progression of native aortic valve stenosis. Once the pressure gradient across the native valve is substantially

reduced, the narrowing and calcification of the native valve halts.

Surgical Valve Replacement

A diseased aortic valve is most commonly replaced using a surgical procedure with either a mechanical or a tissue

valve. The procedure is done either in an open-heart surgical procedure or, in a smaller but growing number of cases,

a minimally invasive cardiac surgery (MICS) procedure.

Percutaneous (Transcatheter)Aortic Valve Replacement

Globally more than 40,000 patients have received transcatheter aortic valve replacement. For patients who are not

candidates for surgical valve replacement, transcatheter valve replacement may be a suitable alternative. When

selecting the optimal therapy for individual patients, the percutaneous (transcatheter) approach must be carefully

weighed against the excellent results achieved with conventional surgery.

Balloon valvuloplasty

For infants and children, balloon valvuloplasty, where a balloon is inflated to stretch the valve and allow greaterflow, may also be effective. In adults, however, it is generally ineffective, as the valve tends to return to a stenosed

state. The surgeon will make a small incision at the top of the patient's leg and proceed to insert the balloon into the

artery and then inflate it to get a better flow of blood around the patient's body. [24]

Prognosis

If untreated, severe symptomatic aortic stenosis carries a poor prognosis with a 2-year mortality rate of 50-60% and a

3-year survival rate of less than 30%.

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Aortic valve stenosis 20

Epidemiology

Approximately 2% of people over the age of 65, 3% of people over age 75, and 4% percent of people over age 85

have aortic valve stenosis.[25] The prevalence is increasing with the aging population in North America and

Europe.[26]

History

Aortic stenosis was first described by French physician Lazare Riviere in 1663.

References

[1] http:/ /apps.who. int/classifications/icd10/browse/2010/en#/I35. 0

[2] http:/ /apps.who. int/classifications/icd10/browse/2010/en#/I06. 0

[3] http:/ /apps.who. int/classifications/icd10/browse/2010/en#/Q23. 0

[4] http:/ /www.icd9data. com/getICD9Code.ashx?icd9=395. 0

[5] http:/ /www.icd9data. com/getICD9Code.ashx?icd9=396. 0

[6] http:/ /www.icd9data. com/getICD9Code.ashx?icd9=746. 3

[7] http:/

/

www.

diseasesdatabase.

com/

ddb844.

htm[8] http:/ /www.nlm.nih. gov/medlineplus/ency/article/000178. htm

[9] http:/ /www.emedicine. com/med/topic157. htm

[10] Aortic stenosis (http://www.mountsinai. org/Other/Diseases/Aortic stenosis) at Mount Sinai Hospital

[11] Chapter 1: Diseases of the Cardiovascular system > Section: Valvular Heart Disease in:

[12] Miller, J. D. Cardiovascular calcification: Orbicular origins.Nature Materials12, 476-478 (2013).

[13] Ricardo Zalaquett, Cristbal Campl, et al. (2005). "Ciruga reparadora de la vlvula artica bicspide insuficiente".Rev Md Chile, 133(3):

pp. 279-86. (http://www.scielo. cl/scielo.php?script=sci_arttext&pid=S0034-98872005000300002& lng=es&nrm=iso) ISSN 0034-9887.

[14][14] VOC=VITIUM ORGANICUM CORDIS, a compendium of the Department of Cardiology at Uppsala Academic Hospital. By Per Kvidal

September 1999, with revision by Erik Bjrklund May 2008

[15] G. Morris, Innasimuthu A L, J.P. Fox, R.A. Perry; The association of heart valve diseases with a dominant left coronary circulation

European Heart Journal, 2009; 30:682

[16] GM Morris, A L Innasimuthu, JP. Fox, RA. Perry, The Association of Heart Valve Diseases with Coronary Artery Dominance The

Journal of Heart Valve Disease 2010;19:389-393

[17] Innasimuthu A L, Morris G, Rao G K, Perry R A; Left Dominant Coronary arterial system and Aortic stenosis: an association, cause or

effect Heart 2007; 93 (Suppl 1): A39.

[18] Yale atlas of echocardiography (http://www.yale.edu/imaging/echo_atlas/entities/aortic_stenosis_senile.html)

[19] Innasimuthu A L, Katz W E; Effect of Bisphosphonates in Progression of Aortic Stenosis Echocardiography 2010; Jan;28(1):1-7.

[20] Nathaniel S, Saligram S, Innasimuthu AL, Aortic stenosis: an update World Journal of Cardiology 2010; 2(6): 135-139

[21] Innasimuthu A L, Katz W E; Effect of Bisphosphonates in Progression of Aortic Stenosis Journal of the American College of Cardiology

2009; 53:A413

[22][22] 1 Rutherford SD, Braunwald E. Chronic ischaemic heart disease. In: Braunwald E, ed. Heart disease: A textbook of cardiovascular

medicine. 4th ed. Philadelphia: WB Saunders, 1992:1292-1364.

[23] Vliek CJ, Balaras E, Li S, Lin JY, Young CA, DeFillippi CR, Griffith BP, Gammie JS,Early and Midterm Hemodynamics After Aortic

Valve Bypass (Apicoaortic Conduit) Surgery, Ann Thorac Surg 2010;90:13643.

[24] Mayo Clinic > Aortic valve stenosis > Treatments and drugs (http://www.mayoclinic. com/health/aortic-valve-stenosis/DS00418/DSECTION=8) Retrieved September 2010

[25][25] Stewart BF, Siscovick D, Lind BK, Gardin JM, Gottdiener JS, Smith VE. Clinical factors associated with calcific aortic valve disease.

Cardiovascular Health Study. J Am Coll Cardiol. 1997; 29: 630-634.

[26][26] clinical Anesthesiology by Edward Morgan

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Aortic valve stenosis 21

External links

Aortic valve stenosis (http://www.dmoz.org/Health/Conditions_and_Diseases/Cardiovascular_Disorders/

Heart_Disease/Valvular/Aortic_Valve//) at the Open Directory Project

Aortic Stenosis (http://www.gosh.nhs. uk/medical-conditions/search-for-medical-conditions/

aortic-valve-stenosis/aortic-valve-stenosis-information/) information for parents.

Aortic Stenosis Infographic (http://www.heart-valve-surgery.com/heart-surgery-blog/2013/04/01/aortic-stenosis-infographic/) for patients, their family members and friends.

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Mitral regurgitation 22

Mitral regurgitation

Mitral regurgitation

Classification and external resources

Mitral regurgitation (schematic drawing)

During systole, contraction of the left ventricle causes abnormal backflow (arrow) into the left

atrium.

1 Mitral valve

2 Left Ventricle

3 Left Atrium

4 Aorta

ICD-10 I05.1[1]

, I34.0[2]

, Q23.3[3]

ICD-9 394.1[4]

, 424.0[5]

, 746.6[6]

DiseasesDB 8275[7]

MedlinePlus 000176[8]

eMedicine emerg/314[9]

MeSH D008944[10]

Mitral regurgitation (MR), mitral insufficiency or mitral incompetence is a disorder of the heart in which the

mitral valve does not close properly when the heart pumps out blood. It is the abnormal leaking of blood from theleft ventricle, through the mitral valve, and into the left atrium, when the left ventricle contracts, i.e. there is

regurgitation of blood back into the left atrium.[11] MR is the most common form of valvular heart disease.