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Examining the precordium The “precordium” refers to that part of the chest overlying the heart. Inspection Palpation Percussion Auscultation
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THE CARDIOVASCULAR HISTORY AND PHYSICAL EXAMINATION

Examining the precordiumThe precordium refers to that part of the chest overlying the heart.InspectionPalpationPercussionAuscultation

InspectionFor most of the cardiac examination, the patient should be supine with the upper body raised by elevating the head of the bed or table to about 30.Two other positions are also needed: (1) turning to the left side, and (2) leaning forward. The examiner should stand at the patients right side. Look for:

InspectionScarsCutaneous venous colllateralsChest shape and movements, precordial projection Apical impulseVisible pulsationsScars : A midline sternotomy scar usually indicates previous coronary bypass surgery or valve replacement.A left lateral thoracotomy may be evidence of previous closed mitral valvotomy, resection of coarctation, or ligation of a patent ductus arteriosus.Cutaneous venous colllaterals: over the anterior chest suggest obstruction of the superior vena cava or subclavian vein

Abnormal chest shape or movements:Unilateral asymmetry of the left side of the chest because of right ventricular hypertrophy before puberty.

Pectus excavatum (posterior displacement of the lower sternum) seen in Marfans syndrome and in mitral valve prolapse, and pectus carinatum ('pigeon chest') associated with Marfans syndrome , may displace the heart and affect palpation and auscultation.Barrel shaped chest can be related to COPD and cor pulmonale Pacemaker or implantable defibrillator, usually implanted over the left pectoral region.

Precordial projection congenital heart disease: tetralogy of Fallot Valvular heart disease-- MS,PS pericardial effusion (large , childhood)The second right intercostal space(2nd ICS-RS) aneurysm of aortic arch dilatation of ascending aortaAbnormal chest wall movements: in-drawing of the intercostal spaces during systole because the left ventricle is tethered to the chest wall by the diseased pericardium in chronic constrictive pericarditis.

Apical impulse: Careful inspection of the anterior chest may reveal the location of the apical impulse or point of maximal impulse.Abnormal apical impulse-Inward impulse:apex excavation in the systole is seen in : adhesive pericarditis prominent RV hypertrophy

Visible pulsationsIn the right second and third intercostal space, parasternal- a dilated or aneurysmal aorta.In the left second and third intercostal space-dilatation of the pulmonary artery or increased flow in the pulmonary artery. Left parasternal area in the 3rd, 4th, and 5th interspaces: right ventricular hipertrophy .Pulsation in the epigastric or subxiphoid area- right ventricular hipertrophy-Harzer signPulsation in the supraombilical area-abdominal aorta (in asthenic patients or in aneurysm of the abdominal aorta).

Cardiac palpationPalpation of the apical impulse (the apex beat)Palpation of visible pulsationsPalpable heart soundsPalpable murmurs: thrillsPericardial friction rubThe apex beat or apical impulse:The lowest and most lateral position on the chest wall where a cardiac impulse can be felt representing the brief early pulsation of the left ventricle as it moves anteriorly during contraction and touches the chest wall.

Palpation of the apex beat:Locate the apex beat by laying your fingers on the chest parallel to the rib spaces .Position of the patient for palpation of the apex beat: supine . If you cannot identify the apical impulse with the patient supine, ask the patient to roll partly onto the left sidethis is the left lateral decubitus position.Palpate again using the palmar surfaces of several fingers. If you find in this position the apex beat, count back 2 cm medially, as the apex beat moves laterally 2 cm-s . If you cannot find the apical impulse, ask the patient to exhale fully and stop breathing for a few seconds. Assess:LocationDiameterAmplitudeDurationLocation:The apex beat is normally found in the 5th left intercostal in the mid-clavicular line or 1-1,5 cm medial to the MCLDiameter In the supine patient, it usually measures less than 2.5 cm and occupies only one interspace. 3 cm or less in left sided position.AmplitudeIt is usually small and feels brisk and tapping. Some young persons have an increased amplitude, or hyperkinetic impulse, especially when excited or after exercise; its duration, however, is normal.

DurationDuration is the most useful characteristic of the apical impulse for identifying hypertrophy of the left ventricle. To assess duration, listen to the heart sounds as you feel the apical impulse, or watch the movement of your stethoscope as you listen at the apex. Estimate the proportion of systole occupied by the apical impulse. Normally it lasts through the first two thirds of systole, and often less, but does not continue to the second heart sound.Abnormalities of the apical impulse:AmplitudeReduced or impalpable apex beat: chest deformity, obesity, emphysema, a very muscular chest wall, pericardial effusion, a markedly dilated failing heart , ,death.Beware of dextrocardia. If no beat is felt, check the right side.Impalpable: apex beat is behind a rib.Increased amplitude:A hyperkinetic impulse results from increased stroke volume and does not necessarily signify heart disease, thus can be caused by hyperthyroidism, severe anemia, fever.An impulse may feel hyperkinetic when the chest wall is unusually thin, in young patients especially after exercise or excitement.

A forceful or thrusting apex either in the normal position or slightly displaced to the left is usually due to concentric left ventricular hypertrophy caused by pressure overload (e.g aortic stenosis, hypertension).Increased amplitude may also reflect volume overload of the left ventricle (e.g., mitral or aortic regurgitation). A heave is a palpable impulse that feels as though it 'lifts' your hand from the patient's chest.Displacement of the apex beat:Upward and to the left by pregnancy or a high left diaphragm.The apex may be displaced laterally in subjects with: chest deformity, or because of mediastinal shift (in these situations the trachea may also be deviated) secondary to a large pleural effusion, tension pneumothorax (away from the affected side)pneumonectomylung collapse (towards the affected side).

Diffusely displaced inferiorly and laterally (to the left) in: volume overload (e.g. mitral or aortic regurgitation) or severe left ventricular dysfunction with left ventricular enlargement.Diameter:Increased in pressure or volume overload.When a ventricle works under conditions of chronic pressure overload or increased afterload, its walls gradually thicken or hypertrophy. Volume overload (increased preload), in contrast, produces dilatation of the ventricle as well as thickening of its walls.

Duration:Sustained: impulse longer than expected (left ventricular hypertrophy, aortic stenosis, hypertrophic cardiomyopathy or hyperkinesia).Double impulse: (palpable atrial systole) characteristic of hyptertrophic cardiomyopathy.Palpation of visible pulsations:Left and right second and third interspaceLeft parasternal (right ventricular) heaveA significantly hipertrophied and/or dilated right ventricle will produce an abnormal impulse at the lower end of the sternum,usually to the left side

Apical beat modificationsNormalHyperkineticPressure OverloadVolume OverloadLocation5th ICS MCLNormalNormalDisplaced left and downwardDiameterLittle more than 2 cm in adultsNormalIncreasedIncreasedAmplitudeSmall, gentleIncreased

Increased

Increased

DurationUsually less than 2/3 of systoleNormalProlonged, may be sustained up to s2Often slightly prolongedExamples of causesAnxiety, severe anaemia, hyperthyroidosisAortic stenosis, systemic hypertensionAortic or mitral regurgitationPressure overload: means that the ventricle works under conditions of increased afterload, its walls gradually thickens (hypertrophy)Volume overload: means that the ventricle works under increased preload, this produces dilatation of the ventricle and also thickening of its walls.Palpable heart sounds:The 'tapping' apex beat: this is the description given to a palpable 1st heart sound in severe mitral stenosis.A palpable S2 a sharp snapping felt in the left 2nd interspacepulmonic area -suggests increased pressure in the pulmonary artery (pulmonary hypertension).A palpable S2 a sharp snapping felt in the right 2nd interspace-aortic area-suggests systemic hypertension.A brief mid-diastolic impulse indicates an S3-gallop, in cases of advanced heart failure.An impulse just before the systolic apical beat itself indicates an S4 gallop in cases of poor left ventricular distensibility during diastole.The opening snap of mitral stenosis felt at the apex. Palpable murmurs are called thrills and are felt as a shudder beneath your hand or rather like placing your hand on a purring cat.Thrills are the superficial vibratory sensations felt on the skin overlying an area of turbulence.One of characteristic signs of organic heart disease.The presence of a thrill indicates a loud murmur, 4/6 or louder.They are usually best felt using the heads of your metacarpal bones rather than the fingertips and applying very gentle pressure on the skin in the areas where the murmur is best heardCaused by severe valvular disease (If systolic: aortic stenosis, ventricular septal defect or mitral regurgitation; diastolic: mitral stenosis.)

Pericardial friction rub1) Precordium-4th ICS-LS2) both phases of the cardiac cycle3) systolic period, sitting erect and leaning forward, the end of expiration4) mechanism: rub of the visceral and parietal layers of pleura5) felt in acute pericarditisCardiac percussionPercussion may provide an estimate of a patients heart size the cardiac dullness.It is seldom used nowadays.With percussion we can determine the absolute cardiac dullness, where the heart is in direct contact with the chest, and the relative cardiac dullness, where we determine the dullness of the heart including those portions where the heart is partially covered by the lung.Superior margin: percussion in the mid-clavicular line downward, normally in the third intercostal space we find the cardiac dullness.Right margin: percussion in the right midclavicular line downward until we find the hepatic dullness, after that we change the position of the hand on the chest in vertical position and continue the percussion in a the latero-medial direction toward the sternum until we find dullness. Normally this will be at the right border of the sternum-sternal line.Inferior margin: is determined by the apical impulse and the superior margin of the liver.Left margin: it is a curve line between the apex and the superior margin of the third rib in the sternal line. The percussion is performed in a radial way in the supero-inferior and latero-median direction .

Abnormalities of cardiac dullnessRelative cardiac dullness is increased :In all directions:CardiomegalyPericardial effusionTransversally-to the left and right: right ventricular dilatation , hipertrophyDownward: left ventricular hipertrophy , dilatationRelative cardiac dullness is decreased or disappeared: emphysema, left sided pneumothorax, pneumopericardiumDextrocardiaModification of cardiac dullness due to extracardiac diseases:Abdominal: tumors, ascites, meteorism, gravidity, diaphragm paralysis CD is moved upwardsPulmonary: right pleural effusion, pneumothorax, lung tumor moves cardiac dullness to the leftLeft pulmonary atelectasis,pulmonary fibrosis toward the left

Cardiac auscultationIt is an important aspect of the clinical cardiovascular examination, but auscultatory skills are decreasing with the almost universal availability of echocardiography.Auscultation requires a stethoscope equipped with a bell and a diaphragm. The bell emphasizes low-pitched sounds such as the murmur of mitral stenosis. The diaphragm filters out these sounds and helps to identify high-pitched sounds such as normal heart sounds and most systolic murmurs.You must know :the surface anatomy of the heart to understand how and where the sounds and murmurs radiate and

basic cardiac physiology to appreciate their timings.Surface Projections of the Heart and Great VesselsThe right ventricle occupies most of the anterior cardiac surface.and to the left of the sternum.

The left ventricle, behind the right ventricle and to the left, forms the left lateral margin of the heart. Its tapered inferior tip is often termed the cardiac apex.

The cardiac cycle

Technique of cardiac auscultation1. Where to listen- areas of auscultation2. What and how to identify and describe by listening:the first and second heart soundsextra heart sounds (third and fourth heard in diastole)additional sounds, e.g. clicks and snapspericardial rubsmurmurs in systole and/or diastole.

Where to listen-areas of auscultation1. Mitral: at and around the cardiac apex. Sounds and murmurs arising from the mitral valve are usually heard best here.2. Tricuspid: 5th intercostal space at the left sternal edge. Sounds and murmurs originating in the tricuspid valve are heard best here.3. Pulmonary: 2nd intercostal space at the left sternal edge.4. Aortic: 2nd intercostal space at the right sternal edge.5. Erb-Botkin: 3rd intercostal space at the left sternal edge, for listening the murmur in aortic insufficiency.These areas do not relate exactly to the anatomical position of the valves but are the areas at which the sound of each valve can be best heard.

Practice is needed here and many hearts should be listened to in order to be familiar with the normal sounds.Make sure the room is quiet when auscultating.Position of the patient:The patient lying at approximately 45 .Left lateral decubitus (bringing the left ventricle close to the chest wall) for listening murmur of mitral stenosis, leftsided S3 and S4Sitting, leaning forward , exhaling completely and withholding breath for listening aortic regurgitation.Standing up for listening mitral valve prolapseAsk the patient to briefly stop breathing while you are listening. Normal heart valves make a sound when they close (lub-dub) but not when they open.Use a regular routine for auscultation. Sequence of auscultation is not important, one can start either at the apex or at the base, just do not leave out any of the areas of auscultation.You can then go back and concentrate on any abnormalities.First step should be identifying the two heart sounds. Simultaneously feel the carotid pulse with your thumb to time the sounds and murmurs. The carotid pulsation occurs with S1. Another way to recognize sounds is the duration of the pause: between sounds: the sound which appears after a longer pause (diastole) is S1Listen with the diaphragm at each area and then repeat using the bell. Listen over the carotid arteries and in the left axilla.

At each site :Identify the first and second heart sounds Assess their character and intensityNote any splitting (relation of splitting to respiratory phases, wideness of splitting)Concentrate in turn on systole (the interval between S1 and S2) and diastole (the interval between the S2 and S1). Listen for added sounds and then for murmurs (note location, timing, intensity, pitch, effect of resppiration)Use special positions as mentioned above.Use inspiratory or expiratory apneeaNote the character and intensity of any murmur heard.Sometimes listen after exercise.

Effects of respiration on auscultationIf a murmur or sound is made louder by inspiration it is nearly always right sided since right heart blood flow is increased during inspiration.If a murmur is made louder by expiration it may be left sided, but this is not definite since expelling air from the lungs decreases the amount of air between the heart and chest wall and may increase the intensity of any event whether its source is right or left sided.Normal heart soundsNormal findingsS1 and S2 are usually the only heart sounds heard on auscultation of a normal heart, although in young and athletic subjects a soft third sound S3 may be present.The first heart sound (S1) Is caused by the closure of the mitral and tricuspid valves at onset of ventricular systole andIt is best heard at the apex (mitral area)It has low intensity, it is low pitched and longer duration than S2.

The second heart sound (S2) Is caused by closure of the pulmonary and aortic valves at the end of ventricular systole , and Is best heard at the basis of the heart.The second sound is louder and higher pitched than the first sound, has a shorter duration and normally the aortic component is louder than the pulmonary one.Physiological splitting of the second heart sound occurs because contraction of the left ventricle slightly precedes that of the right ventricle so that the pulmonary valve closes after the aortic valve. This splitting increases at end-inspiration because the increased venous filling of the right ventricle further delays pulmonary valve closure. This separation disappears on expiration .Splitting of the second sound is best heard at the left sternal edge using the diaphragm. On auscultation, the clinician hears 'lub d/dub' (inspiration) 'lub-dub' (expiration).Heart sounds other than S1 and S2 are usually abnormal, but S3 and an ejection sound and very rarely S4 can occur in normal subjects.A third heart sound (S3) Is a low-pitched early diastolic sound best heard with the bell at the apex. It coincides with rapid ventricular filling immediately after opening of the atrioventricular valves. A third heart sound is therefore heard after the second as 'lub-dub-dum'. A third heart sound is a normal finding in children, young adults and during pregnancy.Ejection sound: an ejection sound occurs as the aortic or pulmonary valve opens and is close to S1 .Ejections sounds are sometimes heard in normal subjects but the most common cause in an asymptomatic patient is a bicuspid aortic valve.S4 also called atrial sound is exceptionnaly rare in normal subjects

Abnormalities of the heart soundsIntensity of heart sounds can be influenced by :Thickness and elasticity of the chest wallElasticity and density of the lungsPhases of respirationVentricle contractility and outputDistance from which valves are closingSpeed at which valves are closingThe consistency of the valves Duration of PR interval

Pathological third heart soundThis is a low frequency (can just be heard with the bell) sound occurring just after S2 at the end of rapid ventricular filling, early in diastole and is caused by tautening of the papillary muscles or ventricular distension. It can be heard as Da-da-dum or ken-tuck-y.Is usually pathological after the age of 40 yearsCombined with the normal heart sounds produces a triple rhythm or gallop rhythm as it resembles galloping horses-protodiastolic or ventricular gallopLeft sided S3 is best heart at the apex in the left lateral position during expirationRight sided S3 is best heard along the lower left sternal border or below the xifoid, in supine position, durin inspiration

Clinical implication of a pathological S3: LV impairment (decreased conpliance) or increased filling. The commonest causes are:left ventricular failure (IHD, hypertensive heart disease, MI, severe myocarditis)dilated cardiomyopathy, mitral regurgitationtricuspid regurgitationaortic regurgitation.In cardiac failure S3 is usually accompanied by a tachycardia and S1 and S2 are quiet.

4th heart sound (atrial sound or atrial gallop or pre-systolic gallop) occurs just before S1 in the late diastole.Clinical implication: left ventricular impairment or hypertrophy.It is soft and low pitched, best heard with the bell of the stethoscope at the apex.It is caused by decreased compliance or increased stiffness of the ventricular myocardium.Can be heard Da-lub dubor Ten-ne-ssee.Coincides with abnormally forceful atrial contraction and raised end diastolic pressure in the left ventricle.It is almost always pathological.Causes of left sided S4 (heard at the apex in left lateral position)hypertrophic cardiomyopathy aortic stenosis and systemic hypertensionischaemic heart disease

Causes of right sided S4 (best heard along the lower left sternal border or below the xifoid):Pulmonary hypertensionPulmonic stenosisOccasionally, a patient has both an S3 and an S4, producing a quadruple rhythm of four heart sounds.At rapid heart rates the S3 and S4 may merge into one loud extra heart sound, called a summation gallop.Additional or extra heart soundsExtra heart sounds in systole: Ejection clicksMid-systolic clicksExtra heart sounds in diastole:opening snappericardial knockMechanical prosthetic valves

Extra heart sounds in systole:Ejection click occur early in systole just after the first heart sound, caused by the opening of stiffened but not too calcified semilunar (aortic, plmonary)valves or by systemic or pulmonary hypertensionThis is a high-pitched sound , sharp, clicking quality, which can be heard with the diaphragm of the stethoscope at the aortic or pulmonary areas and down the left sternal edge.Clinical significance: indicate cardiovascular disease.Causes:Over the aortic area: aortic stenosis, bicuspid aortic valve, systemic hypertensionOver the pulmonary area: pulmonic stenosis, pulmonary hypertensionMidsystolic clicks Occur in mitral valve prolapse (abnormal systolic ballooning of part of the mitral valve into the left atrium) The prolapsing mitral valve tenses in mid/late systole and this produces single or multiple clicks. May be associated with a late systolic murmur .They are high pitched , clicking in quality and best heard at or medial to the apex with the diaphragm.Squatting delays the murmur, standing moves it closer to S1.

Extra heart sounds in diastole:Opening snapAn opening snap is commonly heard in mitral (rarely tricuspid) stenosis (if the valves are not calcified and almost immobile)The mitral valve normally opens immediately after S2. In mitral stenosis, sudden opening of the stiffened valve , due to high atrial pressure can cause an audible high-pitched snap, early in diastole, just after the second heart sound .May be followed by the murmur of mitral stenosis.The opening snap of mitral stenosis is best heard at the apex and over the left sternal edge in 4-5 th ICS, with the diaphragm.

Pericardial knock:May be heard in early diastole .Appears in constrictive pericarditisIs due to the high pressure atrium rapidly decompressing into a restricted LV producing an audible reverberation.Extra heart sounds in systole and diastole: pericardial friction rubIt is a superficial scratching , high pitched sound, comparable with creaking leather, best heard with the diaphragm of the stethoscope Often has systolic and diastolic components. It may be audible over any part of the precordium ,usually heard best in the 3rd interspace to the left of the sternum (Erb Botkin)and is often very localized, does not radiate.Intensity varies over time, increases when the patient leans forward and during expiration.It is most often heard in acute viral pericarditis and sometimes 24-72 hours after myocardial infarction.

MURMURSMurmurs are audible vibrations produced by turbulent flow through the heart, across an abnormal valve, septal defect or outflow obstruction, or by increased volume or velocity of blood flow through a normal valve.Murmurs are differentiated from heart sounds by their longer duration.Whatever constricts an orifice, whatever dilates a cavity, whatever establishes an orifice or cavity where none shall be, will disturb the even flow of blood and produce vibrations and a murmur.Samuel Jones Gee (18391911

Clinically murmurs can be:Innocent murmursFunctional or relative murmursOrganic murmursInnocent murmurs : no anatomic or physiologic abnormality exists Occur in a healthy heart in situations where the circulation is hyperdinamic,, e.g. normal children, during pregnancy, fever, anaemia and hyperthyroidism. They are always systolic, usually soft or moderate in intensity and with musical quality.It may require an echocardiogram to be sure that murmurs are innocent.

Functional or relative murmurs:Without anatomical lesions of the valvesThey reflect cardiac diseasesCan be caused by:Dilatation of great vesselsDilatation of valvular orificies (secondary to left or right ventricle dilatation)Papillary muscle dysfunctionCongenital heart disease (ASD, VSD)Organic murmurs: are produced by anatomical lesions of the valves, leading to stenosis or incompetence (insufficiency)

For each murmur heard, you should determine:1. Timing: relation to cardiac cycle (systolic, diastolic, systolo-diastolic)2. Pattern (shape)3. Intensity (loudness)4. Location of Maximal Intensity5. Radiation6. Character and pitch7. Variation of the murmur: with position, with respiration, with exercise

1. Timing: relation to cardiac cycle (systolic, diastolic, systolo-diastolic)Decide if you are hearing a systolic murmur, falling between S1 and S2, or a diastolic murmur.Murmurs that coincide with the carotid upstroke are systolic.Within systole or diastole they can be heard :At the beginning-early or proto-systolic , early or proto-diastolicIn the middle: mid-systolic, mid-diastolic, At the end : late systolic or telesystolic, late-diastolic or tele-diastolic or pre-systolic. Throughout the systole: pansystolic or holosystolic.

2. Pattern (shape)The shape of a murmur is determined by its intensity over time.A crescendo murmur grows louder : MS presystolic(only in sinus rhythm)A decrescendo murmur grows softer :AIA crescendodescrescendo murmur first rises in intensity, then falls :ASA plateau murmur has the same intensity throughout :MIContinuous :PDA

3. Intensity (loudness)Based on Levine 6 grade classification expressed as a fraction (1/6).Grade 1 Very faint murmur, heard by an expert in optimum conditions.Grade 2 Soft, heard by a non-expert in optimum conditions.Grade 3 Easily heard, moderately loud, without an associated thrill (palpable murmur)Grade 4 Loud murmur with barely palpable thrillGrade 5 Loud murmur with easily palpable thrill. May be heard when the stethoscope is partly off the chest.Grade 6 Loud murmur with thrill and audible with stethoscope removed from chest wall.Intensity can be influenced by the thickness of the chest wall, intervening tissues and transvalvular flow(pressure differerence, stroke volume). Obesitym well developed musculature, emphysema maz diminish the intsnity of the murmurs.624. Location of Maximal IntensityWhere the murmur is best heardThis is determined by the site where the murmur originates.For example, a murmur best heard in the 2nd right interspace usually originates at or near the aortic valve.5. Radiation-precordial and other (e.g. carotids) radiation of the murmur.Murmurs radiate in the direction of the blood flow causing the murmur to specific sites outwith the precordium.The radiation of cardiac murmurs is complex and any cardiac murmur from any structure can be heard anywhere in the chest. There are, however some typical radiations.The pansystolic murmur of mitral regurgitation radiates towards the left axilla.The systolic murmur of ventriculoseptal defect towards the right sternal edge.The ejection systolic murmur of aortic stenosis to the aortic area and the carotid arteries.

The murmur of aortic stenosis in elderly patients can be louder at the cardiac apex than it is over the aortic area, which is its classical site. This is because in elderly patients with hyperinflated lungs there is more lung between the upper part of the heart and the chest wall, than there is at the cardiac apex.

646. Character and pitchThe quality of murmurs is hard to define. Terms such as harsh, blowing, musical, rumbling, high or low pitched are used. Some examples: blowingMImusical MI of ischaemic cause (papillary muscle dysfunction -Mweschrei), calcified mitral or aortic valves (degenerative mitral regurgitation or aortic stenosis) rumblingMS sighing- AI Harsh AS machinery--PDAHigh-pitched murmurs often correspond with high-pressure gradients, so the diastolic murmur of aortic incompetence is higher pitched than that of mitral stenosis.7. Variation of the murmur:With positionWith respirationWith exerciseVariation with position:Some murmurs will become louder if you position the patient so as to let gravity aid the flow of blood creating the sound.Aortic regurgitation is heard louder if you ask the patient to sit up, leaning forwards, and listen at the left sternal edge.Mitral stenosis is louder if you ask the patient to lie on their left-hand side (listen with the bell at the apex).

Variation with respirationAsk the patient to breathe deeply whilst you listen. Right-sided murmurs (e.g. pulmonary stenosis) tend to be louder during inspiration and quieter during expiration (because of increasedvenous return.Left-sided murmurs are louder during expiration.Variation with exercise: murmurs are louder after exerciseDescription of a murmur: a medium pitched, grade 3/6, blowing holosystolic murmur, best heard at the apex, radiating to the left axilla (mitral regurgitation)

SYSTOLIC MURMURS1. Ejection systolic murmur

2. Pansystolic murmurs

3. Late systolic murmurs

1. Causes of ejection systolic or myd-systolic murmurs (S1 and S2 can be heard clearly)Increased flow through normal valves'Innocent systolic murmur':feverathletes (bradycardia , large stroke volume)pregnancy (cardiac output maximum at 15 weeks)Atrial septal defect (causing high pulmonary flow)Severe anaemia

Normal or reduced flow through stenotic valveAortic stenosisPulmonary stenosisOther causes of flow murmursHypertrophic obstructive cardiomyopathy (obstruction at subvalvular level)Aortic regurgitation (aortic flow murmur, relative stenosis)Aortic sclerosisPhysiopathology of ejection murmursThe flow of blood through a pathological structure generates the murmur and this flow is determined by the pressure difference on opposite sides of the responsible pathology (abnormal valve, septal defect, coarctation etc. )The sound generated (murmur) is louder when the pressure difference is greater.The murmur does not start until ejection begins and peaks when blood flow is greatest.The murmur stops before S2 since ejection is finished.Thus the murmur has a crescendo/decrescendo character.The murmur is flow dependent, meaning, that it gets softer and may disappear if transvalvular flow starts to fall when a lesion is very severe and causes heart failure.2. Causes of pansystolic or holosystolic murmursThis is a murmur that lasts for the whole of systole, S1 and S2 cannot be heard in all areas.All caused by a systolic leak from a high to a lower pressure chamber (regurgitant murmurs)Mitral regurgitationTricuspid regurgitationVentricular septal defectLeaking mitral or tricuspid prosthesisRegurgitant systolic murmurs through the AV valves, e.g. mitral regurgitation, may start immediately isovolumic contraction begins, before ejection, since the leak occurs as soon as the pressure rises in the ventricle and continues up until S2 or slightly beyond.

This is because there is a continuing pressure difference between the LV and the LA during this period of time. Often the S2 is swamped by the end of the murmur. 3. Late systolic murmursThere is an audible gap between S1 and the start of the murmur which then continues until S2. Typically due to tricuspid or mitral regurgitation through a prolapsing valve.In these cases the valve does not become incompetent until is has prolapsed and the murmur begins in mid-or even late systole and then continues up to and slightly beyond the second heart sound.Late systolic murmur may have a crescendo rather similar to an ejection systolic murmur but are much later in the cycle .DIASTOLIC MURMURS1. Early diastolic murmur2. Mid-diastolic murmurDiastolic murmurs can be extremely difficult to hear.They are often very low pitched and rumbling.Almost always they are produced by a heart disease.

1. Early diastolic murmurEarly diastolic murmurs occur from regurgitation through incompetent aortic or pulmonary valves.They are descrescendo and follow the S2. This is because the biggest pressure difference between the outflow vessel and the ventricle is at the beginning of the diastole.They are heard at the left sternal edge (occasionally louder at the right sternal edge) and are most obvious in expiration with the patient leaning forward. (brings the heart closer to the chest wall)Since the regurgitant blood volume must be ejected during the subsequent systole, significant aortic regurgitation leads to increased stroke volume and is almost always associated with a systolic flow murmur (relative stenosis)Pulmonary regurgitation is uncommon. It may be caused by pulmonary artery dilatation in pulmonary hypertension (Graham Steel murmur) or to a congenital defect of the pulmonary valve.

2. Mid-diastolic murmurA mid-diastolic murmur is usually caused by mitral stenosis. This is a low-pitched, rumbling sound which may follow an opening snap .It is best heard with the bell of the stethoscope at the apex with the patient rolled to the left side. The murmur can be accentuated by listening after exercise.The whole cadence sounds like 'lup-ta-ta-roo' where 'lup' is the loud first heart sound, 'ta-ta' the second sound and opening snap and 'roo' the mid-diastolic murmur.

If the patient is in sinus rhythm, left atrial contraction increases the blood flow across the stenosed valve leading to presystolic accentuation of the murmur. The murmur of tricuspid stenosis is similar but rare.An Austin Flint murmur is a mid-diastolic murmur caused by the vibration of the mitral valve during diastole as it is hit by flow of blood due to severe aortic regurgitation. Carey Coombs murmur: occurs in patients with mitral valvulitis and secondary valve incompetence due to acute rheumatic fever.It is a short, mid-diastolic rumble best heard at the apex, which disappears as the valvulitis improves. Can be distinguished from the diastolic murmur of mitral stenosis by the absence of an opening snap before the murmur.The murmur is caused by a increased blood flow across a thickened mitral valve. (relative stenosis)

CONTINUOUS MURMURSContinuous murmurs are rare in adults. These are murmurs heard throughout both systole and diastole murmur begins in the systole and continues through the second sound into all or part of diastole. The systolic component is usually louder than the diastolic component .Causes:1. Patent arterial duct2. Shunt-acute communication between the right and the left side3. Pericardial friction rub4. Venous hum1. Patent arterial duct, which connects the upper descending aorta and pulmonary artery in the fetus and normally closes just after birth. The murmur is best heard at the upper left sternal border and radiates over the left scapula. It is continuous and harsh described as 'machinery-like as it sounds like heavy machinery working in the background. 2. Most commonly in adults continuous murmurs are due to some acute communication developing between the right and the left side of the heart through which flow occurs both in systole and diastole. The commonest situation is a ruptured sinus of Valsalva, but infective endocarditis can lead to arteriovenosus and right/left heart communication.3. Pericardial friction rubIt is a superficial scratching , high pitched sound, comparable with creaking leather, best heard with the diaphragm of the stethoscope Often has systolic and diastolic components. It may be audible over any part of the precordium ,usually heard best in the 3rd interspace to the left of the sternum (Erb Botkin)and is often very localized, does not radiate.

RememberAuscultation remains an important clinical skill despite the ready availability of echocardiography. You must be able to detect abnormal signs to prompt appropriate investigation. Furthermore, certain auscultatory signs, such as the third or fourth heart sounds and pericardial friction, have no direct equivalent on echocardiography but are helpful prognostically.