Inspection of the precordium should begin at the foot of the bed. The subject should be supine with the legs horizontal and the head and trunk elevated to approximately 15-30 degrees. Asymmetry of the thoracic cage due to a convex bulging of the precordim suggests the presence of heart disease since childhood, such as congenital heart disease and rheumatic heart disease, with skeletal molding to accommodate cardiac enlargement. In the adult, precordial bulge may be produced from the massive pericardial effusion.
2. Apical impulse
The apical impulse is occurring early in systole. In adults the apical impulse normally is located in the left fifth intercostal space, either at or medial to the mvl and about 2-2.5 cm diameter, it serves the examiner as a marker for the onset of cardiac contraction.
Displacement of the apical impulse:
Some heart diseases cause the left ventricular hypertropy dilatation or both, the apical impulse is displaced laterally and inferiorly and sustained, and it may be shifted to the left and upward in right ventricular hypertrophy, dilatation or both. It can be found at the right fifth intercostal space in dixtrocardiac and can not be found in massive pericardial effusion.
Thoracic disease: pneumothorax and pleural effusion will displace the apical impulse to the normal side. Pleuraladhesion and ateleotasis will result in a displacement of impulse toward the diseased side.
Abdominal disease: The apical impulse also can be displaced by large mass, massive ascites.
The apical impulse may have increased amplitued and duration in those persons with a thin chest, anemia, fever, hyperthyroidism and anxiety. The examiner should always observe the shape and contour of patint’s chest. Depressions of the sternum, Kyphosis of dorsal spine, scoliosis often alter the shape and position of the apical impulse.
Abnormal pulsations in the other areas.
Right vertricular hypertophy (RBH). The impulse is clearly seen in left third fourth intercostal space.
Pulmonary emphysema with RVH, usually the pulsation can be found inferior the xiphoid process.
In asending or arch aortic aneurysm, one may detect abnormal pulsations in aortic area, with bulging or pulsation in systole.
Pulmonary hypertension with dilatation the pulsation in systole may be detected in left second intercostal space to the edge of sternum.
Usually inspection and palpation are discussed together because there is an intimate relationship between these two processes in the heart examination. Palpation not only confirms the results in inspection, but also discovers diagnostic signs. Through careful palpation, the examiner should aim to determine the location and size of the cardiac apex impulse, characterize its contour, and identify any abnormal precordial pulsations. The palm of the hand, ventral surface of the proximal metacarpals, and fingers should all be used for palpation because each is useful for optimal appreciation of certain movements.
Usage of the palpation confirms the precordial pulsation’s location. Amplitude, duration and intensity. In left ventricular hypertrophy (LVH) the impulses are very forceful, sustained throughout systole and has a great amplitude. The apical impulse may have decreased amplitude and duration in those patients with myocarditis. In massive pericardial effusion the impulse cannot be palpable.
Thrills are actually palpable fine vibrations, most commonly produced by blood from one chamber of the heart to another through a restricted or narrowed orifice, it may occur in systole, diastole, presystole and at times may be continuous. Any thrill should be described as to its location, its time in cardiac cycle, and its mode of extension or transmission. The intensity of the thrill varies according to the velocity of the blood, the degree of narrowing of the orifice and which it is produced and difference in pressure between the two chambers of the heart. Quality of a thrill depends on the frequency of vibration producing it, rapid vibrations result in fine thrills whereas slower vibrations produce coarser thrill.
Pericardial friction rub is a to-and-fro grating sensation, which is usually present during both phases of cardiac cycle, often rubs are more readily palpated with the patient sitting erect and leaning forward during the end period of deep inspiration. The rub is caused by a fibrinous pericarditis. In the presence of pericardial effusion the rub will usually disappear because of the separation of visceral and parietal layers by the accumulated fluid.
The chest is percussed to confirm the cardiac borders, size contour and position in the thorax, patient should lie supine on an examining table or sit on the chair, with the physician at his right side. Usually we employ indirect percussion for percussing heart borders. It is outlined by percussing in the 5th, 4th, 3rd and 2nd interspace on the left sequentially, starting near the axilla and moving medially until cardiac dullness is encountered. The beginner should mark with a skin pencil where the note changes. The distance from left midsternal line to the left border should be measured and recorded, measurement should be made along a straight line paralleled to the transverse diameter in the thorax.
The heart borders
The base of the heart, formed by both atria, corresponds to a line crossing the sternum obliquely, from the lower border of the second left costal cartilage, at a point just to the left of its juction with the sternum, to upper border of the third right costal cartilage, at a point 2 cm lateral to its sternal junction.
The right border of the heart: It confirms with a curved line with its convexity toward the right, extending from the upper border of the third right costal cartilage 2 cm lateral to its junction with the sternum, to the sixth right chondrosternal articulation.
The left border of heart. It is formed by the left ventricle and the atrium and is represented by a curved line with its convexity directed upward and toward the left, extending from the 5th left interspace 1.5 cm medial to the Mvl, to the lowerborder of the second left costal cartilage 1-2 cm, to the left of its articulation with the sternum.
The inferior border: It is formed by the RV and a lesser extent by the L V, is represented by a line drawn from the 5th chondrosternal articulation to the site of the cardiac impulse in the left 5th intercostal space 1-2 cm to the M. V. I.
Normal relative dullness of the heart
Right Intercostal space Left (cm)
2-3 II 2-3
2-3 III 3.5-4.5
3-4 IV 5-6 (cm)
In normal person the distance from the 5th to the midsternal line is about 7-9 cm.
Changing cardiac dullness
Left ventricular enlargement, the cardiac dullness will be extended to the left and downward, the heat silhouette is like a shoe. It is frequently seen in aortic regurgitation and called aortic heart.
Right ventrucular enlargement, the cardiac dullness will extended to left and upward. The right ventricular is severely enlarged the right border of the hert will extended to the right.
Left atrium and pulmonary dilatation
Both the left artrium and pulmonary artery enlarged, the pulmonary artery will be exaggerated to leftward. The cardiac silhoutte is like a pear and called mitral heart, it is frequentlyseen in mitral valve stenosis. Aortic dilation, aneurysm of aorta, pericardial effusion, all those diseases may cause the base border of heart enlargement, so that the base border of the heart will be widened.
Congestive heart failure, myocarditis, myocardiopathy and pericardial effusion may cause the heart silhouette extending both to right and left. Especially in presence of pericardial effusion, percussion at times may be helpful in outlinging the changing cardiac silhouette resulting from a change in the patient’s position.
AUSCULTATION OF THE HEART
The purpose of auscultation of the heart is to find the normal and abnormal sounds of the heart. It plays a very important role in the diagnosis of heart disease. It is a very interesting thing to master the auscultation, but it is difficult.
For a thorough examination, auscultation must be done with the patient in a sitting, lying, and left lateral recumbent position, and change the position of patient in order to detect some abnormal sounds and murmurs. while the patient roll onto his left side, the murmur at the apex will be hear more clearly. Exercise is valuable for increasing the intensity of faint murmurs. In auscultation, sometimes let the patient holding the breath at the end of expiration, the murmur will be hear easier.
I. Auscultatory Valve Areas
Sounds produced by each valves of the heart may propagate to different area at the pericardial area following the blood stream. At this area, one can hear the sound clearest in auscultation. It is called “auscultatory valve area”. The auscultatory valve area does not correspond with the anatomic location of the valve themselves.
l. Mitral valve area: it is at the apex, in the fifth left intercostal space, medial to the midclavicular line.
2. Aortic valve area: there are two auscultatory area of AV, one is located in the second right intercostal space, just lateral to the sternum. The other is at the third or fouth intercostal space, left to the sternum border. We call it the second auscultatory area of AV.
3. Pulmonary valve area: in the second intercostal space just lateral to the sternum.
4. Tricuspid valve area: at the lower part of the sternal near the xiphoid.
The physician should adopt a systematic way of listening: start at the apex, then move to the PV area , AV area, second AV area, TV area. Beside, according the clinical feature, the other part of pericardium, neck, axilla, and back may be examined.
Ⅱ. The Content of Auscultation
It includes rate, rhythm, heart sound, murmur and pericardial friction sound.
1. Heart rate: It means how many beats per minute. It normally varies with age, sex, physical activity and emotional status.
In normal adults: 60-80/min
Sinus tachycardia : >1OObeats/min in adults;
Sinus bradycardia : <=60 beats/min in adults.
2.Heart rhythm: It is regular in Normal adults, but young adult and children may sinus arrhythmia. The most common arrhythmias in clinical practice are: premature beat (extrasystole) and atrial fibrillation.
Premature beat is a sudden extrasystole of the heart in the basis of normal heart rhythm ,and followed by a longer compensatory pause.
The characteristic auscultation of extrasystole is:
(l) The intensity of S1 is increased;
(2) The intensity of S2 is decreased or even disappeared;
(3) The peripheral arterial pulse is absent.
Atrial fibrillation: It is the common arrhythmia in clinical. It is caused by a very high frequency impulse coming from the atrial ectopic point or caused by the circus movement of the ectopic impulse. The clinical auscultatory characters are “three inconsistence”;
(1) The ventricular rhythm has absolutely no regularity;
(2) The intensity of S1 is inconsistence;
(3) The rate of heart and pulse are unconcerned.
3. Heart sound
A. Normal heart sounds
In most of normal individuals there are four heart sounds. The first and second sounds can be heard with ease in normal subjects. However, the third sound only can be heard in young person and children. The fourth sound is frequently inaudiable.
The producing mechanism of heart sound
1) S1: Although several cardiac events play a part in the production of the S1 , the vibration of the closure of the atrioventricular valves is the most important and accounts for most of the sounds that are heard. The S1 indicates the beginning of the ventricular contraction. Phonocardiographic analysis shows four components in the S1, which have been related to the various events occuring at the onset of systole:
(a) Development of tension in the ventricular musculature;
(b) Closure of the Atrioventricular valves;
(c) Opening of the semilunar valves and the onset of ventricular ejection;
(d) Acceleration of the blood in the arteries during maximum ejection.
Often some residual vibrations of auricular origin occur at the very beginning of the S1.Normally, only the components due to the closure of the AV valves and the opening of the similar valves are heard, but the either components may be heard under abnormal circumstance.
S1 can be heard at any part of pericardium, loudest at apex, lower in pitch than those of the S2,with 55-58 Hz in frequency, last about 0.1 second, longer than those of the S2.
2) S2: The second heart sound is mainly produced by the vibration of the closure of the semilunar valves during the beginning of the ventricular diastole. It is a composite sound result from closure of both the aortic and pulmonary valves. The vibration of the relax of ventricular muscle in diastole, the moving of blood flow within the great vessels, the opening of MV and TV, are taken part in the formation of S2. The exist of S2 is an indicator of the beginning of ventricular diastole. It can be heard at any part of pericardium and loudest at the basic. The S2 is high in frequency and shorter in lasting duration than the S1 It has a snapping-like tone.
3) S3: The third heart sound is heard in most children and some adults. It occurs in early diastole approximately 0.12-0.18 second after the S1. Being lower in both frequency and intensity. It occurs during the phase of early diastolic filling, the blood moves into ventricle rapidly from atrium, produces the vibrating of ventricle wall. Usually it is heard clearly at the apex or superinternal of the apex.
4) S4: The fourth heart sound occurs late in diastole or just prior to the S1 about 0.l second , produced in the ventricle during the ventricular filling associated with an effective atrial contraction. It is also low in frequency and intensity and rarely heard under normal conditions.
b. The differentiate between S1 and S2:
1) The S1 has a lower pitch, a longer lasting time. It is maximal in intensity at the apex. The S2 has a higher pitch, a shorter lasting time. It is maximal in intensity at the basic;
2) The duration between the S1 to S2 is shorter (has a shorter pause) than the duration between the S2 to the S1 of next cardiac cycle (has a longer pause);
3) The S1 is synchronized with the apical pulse. and is mimic coincident to the aortic artery pulse. The S2 is produced after the apical impulse.
B. Abnormal Heart Sounds
Change in loudness
1) Both the S1 and S2 are affected simultaneously: Both increased; both decreased;
2) Change of S1:It depends on the myocardial contraction, the filling degree of ventricle, the elastic and position of the valve.
(1) In the situation of high fever, hyperthyroidism and ventricular hypertrophy,
(2) In MS
(3) In complete AV block
(1) It occurs in myocardial infarction;
(2) In mitral insufficiency;
(3) In aortic insufficiency.
In arrhythmia, the S1 at apex may be louder or weaker.
3) Change of the S2:It mainly depends on the pressure within the aorta and pulmonary artery and the situation of semilunar valves.
(1) S2 Increased at aortic valve area :It is due to the pressure increased within the aorta.
(2) S2 increased at pulmonary valve area: It is due to pulmonary hypertension.
(3) S2 decreased at aortic valve area: It is due to aortic pressure diminished.
(4) S2 decreased at pulmonary valve area: It is due to the pressure diminished within the pulmonary artery.
b. Change of the quality of the heart sound
If the myocardial muscle is damaged severely, the heart sound like a pendular, it is called pendular rhythm. If accompany with tachycardia, like the heart sound of embryo, it is called embryocardia.
c. Splitting of heart sounds.
Splitting of S1 :It is due to the closure of MV and TV asynchronously, loudest over the apex. It may occur in normal children and young person, and usually occur in right bundle branch block.
Splitting of S2:It can be heard in following conditions.
(1) In normal person;
(2) In pathological situation: conditions that cause an over volume to empty or delay of emptying time of one side of the heart will produce splitting of the S2.
(3) The influence of respiration: in inspiration, the pressure within the thorax is decreased and the venous return to right heart is increased. The RV require a slightly longer period to empty it itself, the PV closure does not occur until the ventricle has emptied itself, so make the S2 splitting slightly in normal condition. In pathological situation, if the splitting of S2 is due to the abnormal of right side of the heart, inspiration will produce the S2 splitting more.
If the abnormal is within the left side of the heart, such as AS, the emptying time of left ventricle is delayed. The order of valve closure may be reversed, the two components then more closer together or may be single, this is referred to as paradoxical splitting of S2.
(4) Fixed splitting of S2: in the usual case of ASD, the S2 over the PV area is widely split, with little or no change in .the degree of splitting during either phase of respiration. This is referred to as fixed splitting.
d. extra sounds:
The extra sounds in systolic period
1) Early systolic ejection sound:
In the presence of dilatation of the aorta or pulmonary artery, or in the hypertension of aorta or pulmonary artery, it can be heard.
(1) Pulmonary early systolic ejection sound : It can be heard after S1 with a high pitch sharp. They are best heard at the left side of the sternal border, in the 2-3 intercostal space. These sound are not transmit to the apex. It can be heard in obvious pulmonary dilation and pure PS.
(2) Aortic early systolic ejection sounds: It appear after the S1, have the equal quality of pulmonary artery early systolic click. They are heard over the base of heart as well as at the apex.
2) Mid and late systolic click:It occurs in MVP. The redudent and floppy of the tandae chordea can not control the mitral valve at annul level and prolapse into the LA at late systolic period. In systolic period the pathological tandea chordea suddenly be tight, produce vibration, so the click occurs. Sometime it may produce MI, so there is SM after the click.The click usually occurs after the S1 close to the S2, best heard at apex. The pitch is lower that in early systolic click.
The extra sounds in diastolic period:
(l) Protodiastolic gallop rhythm:
It is termed S3 gallop orS3 gallop. It is the pathologic counterpart of the S3 and occurs at the time of rapid diastolic ventricular filling.It is a brief low-pitched sound It occurs at middle diastole at the end of rapid filling phase of diastole. In the early diastole, the blood through into the ventricle from the atrium in failing myocardium, the tension is poor, produce the vibration of the ventricular wall.. It reflexes that the LV function is decreased.
(2) Presystolic gallop:
The extra sound in prespstolic gallop is pathological S4.It is termed as S4 gallop or atrium gallop.It occurs in late diastole and is temporally related to atrial contraction . It is due to the increasing contraction of atrium.It occurs precede the the S1. It is low-pitched, best heard at the apex or 3-4 intercostal space, left to the sternal border.
(3) Summation gallop:
It is termed the middle diastolic gallop, produced by the overlapping of early diastolic gallop and presystolic gallop while the heart rate is quite faster.
2) Opening snap of MV:
It occurs after the S2 in MS. This sound is brief in duration and high in pitch than other gallop sounds. It is due to the vibration of the opening AV valve suddenly stopped during the blood from LA into LV in early diastole of the ventricle. The opening snap of the MV usually indicates a flexible valve, and its presence is, an evidence that the valve is probably suitable for mitral commisurotomy operation.
3) Pericardial knock:
In the presence of constrictive pericarditis, at time an extra sound is heard in diastole, occuring shortly after the second heart sound. This is reffered to as the pericardial knock. It may be heard all over the precordium and loudest at the apex and left side at lower part of the sternal. It is due to the constriction of the pericardial after inflammation, the diastole of ventricle are eliminated at the ventricular rapid filling phrase in early diastole, the ventricular diastole has to stop suddenly produces the vibrate of ventricular wall.
In some pathological situation, when the presystolic gallop and protodiastolic gallop both sounds are present, a quadruple rhythm results. The heart rate usually increased , the presystolic gallop and protodiastolic gallop usually summate together, this is the summation gallop.
In the therapy of pacemaker, there are some abnormal heart sounds, murmur and extra sounds. The pacemaker sound is produced by the contraction of the local intercostal muscle due to the leakage of the electric current stimulate the intercostal nerves.
In the patients suffering from valvular disease, after the operation of valvular replacement, the prosthetic valve as in mechanical valve, the abnormal heart sound are produced by the crush of metal stent or metal annuls of the valve, such as the click sounds.
2) It should be differentiate from the heart sounds;
3) It has a very important clinical value.
2. Mechanism of production:
Mechanism of production:
Heart murmurs are abnormal sounds produced by vibrations within the heart itself or in the walls of the large arteries. It usually caused by one of the following mechanisms:
l). Increased velocity of blood flow though normal valves;
2). Forward flow though narrowed or deformed valves;
3). Backward or regurgitant flow through incompetent valve;
4). Abnormal connection;
5). Vibration of loose structure within the heart;
6). Increase with diameter of a major vessels.
3.Characterized of murmurs:
1. Location: murmurs of valvular origin are usually best heard over their respective auscultatory valve area.
2. Timing: murmurs are timed according to the phase of the cardiac cycle during which they occur. There are three basic types of murmurs: systolic, diastolic and continuous.
3. Quality: the quality of murmur depends on the frequency and intensity of the sound wave, and related close to the pathology and hemodynamic changes of the heart. We usually describe the SM as blowing, harsh or musical. About the DM, it may be describe as blowing, sigh-like and rumbling. The CM are described as machine-like and hum.
4.Radiation: some murmurs are transmitted with the direction of the bloodstream by which they are produced, other murmurs are propagated from their point of origin in many directions.
5.Intensity: the intensity of murmurs are related to several factors:
(1) the severity of abnormal;
(2) the velocity of blood flow;
(3) the pressure gradient of crossing valve.
The most widely used system (Levine and Harvey)for grading the intensity of heart murmur is six-point scale: grade 1 murmur is barely audible and is often missed on the first cardiac examination, grade 2 is usually readily heard and slightly louder than grade 1, grade 3 and 4 are quite loud and grade 5 is even more pronounced, grade 6 may be heard with the stethoscope just removed from the chest wall.
A murmur that increases in intensity after its onset termed “crescends”. If it decreases in intensity, it is referred to as “decrescends”. If the first portion of a murmur is increases in character and the latter portion is decreased it is then referred to as a “diamond-sharped” murmur.
6.Physiological maneuver : The examiner may intervene in several ways to modify sounds and murmurs for the purpose of better recognition and differentiation. Some of the most helpful maneuver are discussed below:
1.Change the body position: it may produces some heart sound or murmur increase or decrease. The murmur of mitral stenosis is more evident in left recumbent position. In sitting position, leaning forward, held respiration in the end of deep expiration, is useful to the ausculation of aortic insufficiency murmur. Prompt squatting from standing position or raising two legs at supine position may increase venous return, therefor increase the strock volume and cardiac out put, increase the murmur of MI and AI .The murmur of hypertrophic obstructive cardiomyopathy is decreased in squatting and increased in standing position.
2.Respiration: respiration may change the output volume of left and right ventricle, then inflence the tensity of the murmur. During deep inspiration, the pressure with in the thorax decreased, the venous return increases, the blood volume of pulmonary circulation increases, therefore the output volume of right side heart is large than those of left side heart and the heart has a clock wise rotation along long axis ,the tricuspid valve closes to the chest wall more, produce the murmur of TI,TS,PI increase in intensity. It is in the opposite way during expiration.
3.Exercise: exercise increases heart rate, blood volume of circulation and blood velosity, so the murmur due valvular stenosis will increase.
Ⅳ.The clinical value of murmur in each valve area of auscultation.
Heart murmur usually is a feature of the disease of cardiac or vessels. It may appear in rare normal individuals. The abnormal which produce the murmur may be organic, relative, and functional.we call it organic, relative, and function murmur. The term “relative M” indicates the valves itself is not involved but the supporting tissues of the valves are abnormal. It consist the dilation of the valve annulus, the damage of chordae tendineae, the enlargement of cardiac chamber or great vessels, and produce a relative stenosis or insufficiency of the orifice of the valve. The functional M usually reveals in systolic period in part of healthy child or young person or in the situation due to increasd flow across a normal valve.
1) MV area: the murmur at apex is produced by mitral insufficiency. Its origin and cause may be organic, relative or functional.
Organic MI most are due to rheumatic heart disease, MVP and dysfunction of papilly muscule. It is a pansystolic M,overlap the S1,high-pitched, blowing in charter, more harsh, louder than 3/6 degree in decresento type and frequently radiate toward the left axilla. It is diminished in inspiration, increased in expiration. It is best heard in left supine position.
Relative MI: It is due to the dilated LV. It is heard in hypertensive heart disease,acute rheumatic fever, dilated cardiomyopathy and severe enemia.The M is in soft charter and less in radiation.
Functional MI: the valve is normal but the blood flow is quite faster. It is heard in high fever, enemia in middle degree, hyperthyroidism, usually is less than 2/6 degree, in soft charter, more local in area, does not radiateto other part. The M will disappear when the cause producing faster velosity of the blood flow disappeared. It is heard in part of the normal adult.
When valvular insufficiency exists, the ventricular pressure remains above atrial pressure throughout systole. When the aortic and pulmonary valves close, the ventricular pressure is still well above the atrial pressure, thus the murmur of Mi is heard throughout systole and for a brief period following the S2.
2) AV area: it is heard in organic AS. The murmur is harsh in charicter, cresendo-decresendo type, radiate toward the neck following the great vessels, usually are accompanying with systolic thrill and S2 is diminished at AV area.It is also heard in relative lesion of AV, such as dilation of aorta due aortic arteriosclerosis, hypertensive heart disease.
3) PV area: it is an ejection murmur, most of them are functional.It can be heard in part of normal children and young person. It is soft and weakness in charter. This murmur may exist in relative stenosis of the orifice of pulmonary artery, due to pulmonary artery dilation in pulmonary hypertension,such as ,MS, ASD.The organic murmur in this area are produced in congenital PS. It is louder in intensity, harsh in quality, diamond-shaped, usually accompanying with systolic thrill. The S2 decreased in this area.
4) TV area: The systolic murmur in this area indicates Ti, most are relative TI due to dilate of right ventricle. It is a blowing SM, increased in inspiration. The organic SM are very rare here. .
5) Other position: In VSD, a loud and harsh SM can be heard at third and fourth intercostal space, left to the sternal border, usually are accompanying with systolic thrill.
(2) Diastolic murmur:
Most of them are produced by organic lesion of the valve. In rheumatic MS,an mid-late rumbling diastolic murmur can be heard at the apex, cresendo-sharped, in low-pitch. It is generally confirmed to a rather small area, best hears in left recumbent position at the end of expiration, usually are accumpanying with louded S1, OS of MV and diastolic thrill.
The DM of relative MS may occurs in AI.It is termed Austin Flint murmur. Do not accompanying with louding S1 or OS.The mechanism are the blood regurgitating from the aorta into LV stricking the MV area up,produce relative stenosis of MS.
2) AV area: The murmur begins immediately after the AV closure sound.It is usually heard in rheumatic AI. The murmur are sigh-like, decresedo, may radiate to the left side of the lower part of sternal. It is best heard at the aortic second area,
3) PV area: The diastolic murmur at this area, most are produced by relative Pi. The Grahan Steell murmuris also a relative murmur.
4) TV area: It is rare in clinical.
Continuous murmur: Murmurs which extend from systole into diastole are called continuous murmur, such as in Patent Ductus Arteriosus. It is a continunous murmuur, harsh in quality, mimic the sound of machine rotating.It is best heard at second intercostalspace, left to the sternal border. The murmuer begins after S1, middle pitch,cresendo type, recher peak intensity at late systole, envelop the S2 and decreased at early-middle diastole, produceing a large diamond sharp, persistent from systole to diastole, the peak of diamond is at the top of S2. Continuous murmur can also be heard in arterio-vein fistula.
Pericardial friction rub
The pericardial friction rub is produced by the rubbing on each other of the parietal and visceral surfaces of the roughened pericardium during pericadiatis.
The sound is usually in both systolic and diastolic, with a to-and-fro character, but the systolic component predominates, and sometime the sound is heard only during systole. In general, the sound is harsh, resemble massage the ear using the finger. At times, it is soft, it seems closer to the ear than the heart sounds. The rub is most commonly heard at the third to fourth intercostal space left to the sternal border. It is best heard in the sitting position leaning forward and held breath.The common cause of pericardial friction rub is pericarditis(TB,non-spicific, rheumatic). It also can be seen in acute myocardial infarction, uremia and SLE.
F. THE BLOOD VESSELS
The palpation of artery is an important step in the cardiovascular examination. From here We can get data of the patient above the general condition, the function of circulation, and some cardiovascular abnormalities. So it has an important value in the clinical diagnosis.
The arterial pulse can be papated at any point where the arteeainst a firmer surface usually bone.
l. First pay attention to the intensity and the beginning time of the radial A. and compare the radial A. in both sides if it is equal or not.
2. The pulse intensity may not be equal between the upper and lower extremitries.
3. Compare the pulse of artery of both lower extremtries at the relevant position.
In examining the pulse, It Is important bear In mind the following points: rate, rhythm, consistency, intensity, wave form and condition of the arterial wall.
c. tention: The tention of pulse depends on the level of the arterial systolic pressure.
d. Intensity: The intensity depends on the arterial filling degree and the resistance of peripheral vessels, it also depends on the cardiac output and pulse pressure.
e. Wave form
The arterial pulse starts at the instant the valve opens and left ventricular ejection begins. This results in an abrupt sharp rise in aortic pressure, since blood enters the aorta much faster than it flows to the more distal arteries. During the systolic phase of left ventricular ejection a large portion of the blood is temporarily stored in the proximal aorta. Once the aortic pressure reaches a peak it begins to fall as ventricular ejection slows, and blood continues its flow in the peripheral arteries. As the ventricle relaxes there is a transient reversal of flow from the central arteries to the ventricle and the aortic valve closes. The aortic pressure continues to decrease during diastole as blood flow continues to the peripheral vessels.
The pulse wave is composed of an ascending limb, peak, and descending limb. There is a small notch near the peak of the ascending limb and a similar notch on the descending limb.
l. Water hammer pulse.
A strong bounding pulse with a tall rapid ascending limb and an equally rapid decending limb .It is called a water-hammer or collapsing pulse.
2. Pulsus alternans.
Pulsus alternans is charterized by a regulary alternating pulse, in which every other beat is weaker than the preceding beat. Actually, there is an alternating series of high and low pulse waves caused by an alternating contractile force of the left ventricle. Since the weak beats are but slightly weaker than the strong beats, this arrhythmia may be overlooked unless the examiner is skilled or alerted to its possibility. It is more likely to be detected when the patient is sitting or standing. It must be distinguished from bigeminy.Consequently it is a valuable indication of left ventricular failure .
3. Dicrotic pulse.
In dicrotic pulse there are two impulses that are palpable during diastole. It usually occurs in the presence of high fever and may be palpated in both the carotid and peripheral arteries.
4. Paradoxical pulse.
Paradoxical pulse is charterized by a decrease in the amplitude or an actual imperceptibility of the pulse that occure during the inspiratory phase of respiration. This phenmenon is caused mainly by pooling of blood in the pulmonary circuit during inspiration resulting from the expansion of the lungs and an increase in the negative intrathoracic pressure. In turn this results in a decrease in the return of blood to the left side of the heart, a decrease in left ventricular output, and thus a decrease in arterial blood pressure. When the systolic blood pressure falls more than 10 mm.Hg during inspiration the pulse is refferred to as paradoxical. The most accurate means of identifying a sphygmomanometer, since it can be easily overlooked while palpating the radial artery. The presence of a paradoxical pulse should suggest the possibility of massive pericardial effusion, constrictive pericarditis. f.Consistency of the arterial wall.
This is best accomplished by expressing the blood from a distal segment of the radial artery that has been ocluded by digital pressure. The trun consistency of this vessel can then be determined by means of palpation. Normally the wall of an artery under these circumstances is soft and pliable. In arteriosclerosis the wall offers more resistance to compression by the palpating finger, and the vessel may be rolled easily between the examining digits. This is often referred to as a “pipe stem” artery may be beaded in consistency and tortuous in its couse. In elderly persons the examiner may actually visualize these snakelike pulsating arteries under the skin of the arms and forearms.
2. Pistol-shot sound
3. Duroziez's sign.
4. Pathological sound: including systolic murmur and continuous murmur.
Measurement of Arterial Blood Pressure
For routine measurement, the patient may be either sitting or lying in the supine position. The patient should have been resting for some time. Bare the arm and affix on it the collapsed cuff smoothly, so the distal margin of the cuff is at least 3 cm proximal to the antecubital fossa. The cuff is evenly and firmly wrapped about the arm with the center of the inflatable portion over the brachial artery, place the chestpiece of the stethoscope over the brachial A. at the antecubital fosse. The radial pulse is palpeted and inflate the cuff to a pressure about 30 cm of mercury about the point where the palpable pulse disappears. Open the valve slightly ,so the pressure drops gradually(2 mm/second). From this point, observation may be made by either auscultation or palpation. Press the bell of the sterhoscope hightly over the brachial A. and note the pressure reading at which sounds first become audible, this reading is taken as the systolic pressure. As the blood pressure cuff is further deflated, the sounds undergo changes in intensity and quality. As the cuff pressure approaches diastolic, the sounds often quite suddenly become dull and muffled and then cease. The point of complete cessation of sounds is the best index of the diastolic pressure.
The systolic pressure is depended on the myocardial contractility and the cardiac output. The diastolic pressure is depended on the resistance of peripheral vessels. The cardiac output decreasing or the peripheral vesseular resistance decreasing may produces the blood pressure drop.
Under normal circumstances there is little or no significant difference in the blood pressure in the two upper extremities. In certain instances-for example, aortic aneurysm or obstruction of the innominate artery-there may be a significant discrepancy in the blood pressure in the upper extremities.
Blood pressure is somewhat variable and depends on sex, race,and climatic conditions. Some serious causes of low blood pressure(hypotension) include Addison’s disease, acute myocardial infarction, hemorrhage, and shock. Among the causes of high blood pressure(hypertension) are essential hypertension, chronic glomerulonephritis, pheochromocytoma, renal artery stenosis, and coarctation of the aorta.
G. MAJOR SYMPTOM AND SIGN
OF COMMON DISEASE IN CIRULARORY SYSTEM
Mitral stenosis(MS) results from recurrent rheumatic activity. During the course of M.S., the flow of blood is damped from left atrium to left ventricle in diastole, left ventricle filling is then decreased, and the left atrial pressure is increased, left atrium is overfilled, causing dilatation and hypertrophy of it. The high atrial pressure induces a dilatation and stasis of pulmonary vein and capillary. Then pulmonary artery pressure increased gradually due to the increased pulmonary circulatory resistance and pulmonary arterial sclerosis developed later on. The right ventricle is overloaded and then the compensatory hypertrophy and dilatation occur. Right ventricular failure may be present finally.
There is no symptom, or only a slight in a case of mild or moderate M.S. Major symptoms (due to left atrial dysfunction)are as follows. Exertional dyspnea, cough, hemoptysis and occasional paroxysmal nocturnal dyspnea.
Inspection: The so-called “Mitral Facies” May be present. The apical pulse may extend to left side.
Palpation: diastolic thrill may be felt at apex.
Percussion: The cardiac dull area extend to left in early stage and later on to right. A prominence of “cardiac waist” may be present, making the heart to form a pea –shaped dullness.
Ausculation : A loud snappy first sound and a localized cresendo rumbling diastolic murmur in the mid-late stage may be hear at apex, which can be clearer when the patient in lying in left lateral position. The opening snap may be present. The pulmonary second sound may be accentuated or splitting. Moist rales at the base of lung may be appeared.
X - ray. The lung markings are increased. The heart shadow showed a “ Mitralized contour”. Barium meal of esophagus may show an enlargement of the left atrium which compresses the esophagus backwardly. Enlargement of right ventricle may be present in late stage.
EKG: A broad p wave with a notch “Mitral P” and enlargement of right ventricle may be present.
Echo: Double -spike of mitral anterior leaflet disappeared and flat curve may be seen. Anterior and posterior leaflets move in same direction. Right ventricular enlargement may be seen in late stage.
Mitral Insufficiency (MI)
The main cause of MI is rheumatism, and MI may be produced by left ventricular dilatation due to any cause. During left ventricular contraction the blood regurgitates into the left atrium, so that the filling degree and pressure were augmented for the left atrium and them the compensatory dilatation of left atrium occurs. During the left ventricular diastole the left ventricle accepts more blood flow from left atrium and from left ventricle regurgitate. Consequently, the left ventricle bears blood volume so heavily during the left ventricular contraction that the compensatory dilatation and hypertrophy of the left ventricle occur gradually.
The patient has fatigue, palpitation in the early stage. If without heart failure, the patient feels no symptom for a long time.
Inspection: The apical beat is displaced to left and lower.
Palpation: The apical beat is heavy.
percussion, cardiac dullneus enlarged toleft, or right in late stage. Auscultation: a grade Ⅲ or more pansystolic blowing murmur may be heard and transmitted to the left axilla and supscapular region. The first heart sound was decreased and masked by the murmurs. The pulmonary second heart sound was accentuated.
X-ray shows dilated left ventricle and left atrium and pulmonary congetion.
EKG shows left ventricular hypertrophy.
The valvular deformity in aortic stenosis may be the result of rheumatic fever but also occur on the basis of a congenital defect or atherosclerosis. Calcific stenosis may occur when the underlying pathologic condition is either rheumatic or sclerotic.
In aortic stenosis blood is forced under great pressure by the left ventricle through a narrowed aortic valve into the aorta. The resistance of output the blood in left ventricle is increased. The wall thickening of LV gatting high and high due to the constraction of LV increased. The mean pressure of aorta is decreased, the blood flow in coronary artery and periphelow artery is decreased.
The main symptom are palpation, fatigue,,angina, even syncope.
Signs: The apical impulse is increased,and displaced laterally.A systolic thrill may palpable at the second intersapace lateralal to the sternal with a pulsus parvus..In auscultatioin, there is a murmur , systolic in time, loud, harsh, and usually has a crescendo-decrescendo charter. The murmur is ejection in nature, beginning shortly after the first heart sound and ending just before the aortic component of the second sound. The murmur is heard over the right second interspace lateral to the sternum and radiated widely, frequently to the right side of the neck and especially to the apex. The aortic component of the second sound is delayed in most cases and is absent in a few. Consequently, there is either a single second heart sound, or a reversed splitting of the second sound, the aortic component occurring after the pulmonary.
Etiology: The cause of aortic insufficiency are rheumatic fever, the commonest, and arteriosclerosis and infective endocarditis. Syphilis is a less common cause of A.I. in our country now.
In aortic insufficiency, the left ventricle receives both blood from left atrium and aortic regurgitation, the augmentation of stroke volume leads to compensatory, left ventricular dilatation and hypertrophy and relative M.I. The regurgitant jet from aorta hits the anterior mitral leaflet and causes it moving toward left atrium during diastole, result in relative mitral stenosis, Because the blood leaks to the left ventricle in diastole, the diastolic pressure is decreased causing an increase in pulse pressure and other signs of peripheral vessels due to A.I.
Symptom: The patient may be free symptom or only feels palpitation in the early signs:
Inspection: Patient looks pale, the apical impulse is diffuse and displaced laterally or inferiorly.
Palpation: The apical impulse is displaced laterally and inferiorly, lifting impulse may be felt.
Percussion: cardiac dullness is enlarged laterally and inferiorly. The “cardiac waist” is decreased. The cardiac dullness shows a boot-shaped shadow.
Auscultation: First heart sound is decreased at apical area and the aortic second heart sound decreased or disappeared. A blowing diastolic murmur is audible in the aortic area or third intercostal space left to sternum and transmitted to apex. A soft blowing systolic murmur at apex may be heard due to the relative mitral insufficiency.
If there is relative mitral stenosis, a rumbling murmur in early-mid diastole at apex may be heard, it is called “Austin-Flint” murmur.
Peripheral varcular signs due to increased pulse pressure are as follow: (l) Moving of head with each heart beat, i.e. Musset sign; (2)Carotid pulsation; (3)Capillary pulsation; water hammer pulse; pistolshot sound; Duroziez dicrotic murmur etc.
The commonest causes of pericardial effusion are inflammatory( tubercurosis or purulent disorders)and noninflammetory ( Rheumatism, nephrosis). For a slight effusion, there is no effect on heart and hemodynamics. If pericardial effusion increased rapidly or gradually but massive, the elevated pressure of pericardial cavity limit the dialate of the heart,influnce the blood flow retun from systemic venus to the right ventricle, the ventricular filling and out put were reduced, produceing a serious hymodynsmic changes.
The severity of symptom depends on the pericardial effusion volume and the velosity of effusion producing.patients may complainpericardial compression, dyspnea. If the effusion compresses the neighboring organs, cough, hiccup, dysphagia may be present. In addition, there are inflammatory symptoms of fever, sweating, fatigue and pericardial pain.
Inspection: It is dyspnea in a sitting, leaning forwarl posture. The cardiac impulse decreased or disappeared.
Palpation: Apical pulsation reduced or absent, with fast and small pulse, paradoxlcal pulse may be present.
Percussion: Cardiac dullness is enlarged and almost coincide with posture.
Auscultation: A faint heart sound and sometimes pericardial friction rub may be heard. Ewa's sign with dullness below the angel of left scapula as associated with the increased vocal fremitus , broncbial breath. Elevated venous pressure, small pulse pressure and positive hepatojugular reflex may be present.