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MAGDI AWAD SASI 2013BY DR. MAGDI AWAD SASIDetailed analysis of cardiovascular examination 2012Cardiovascular HistoryRecord the date and time the history was taken.Name, Age, Occupation(s)Presenting Problem/ ComplaintRemember the questions you need to ask about each symptom?There are 4 main cardiovascular symptoms:1. Chest pain (character, radiation)2. Shortness of breath (exercise tolerance, orthopnoea, paroxysmal nocturnaldyspnoea)3. Presence and extent of oedema (ankle, leg or sacral)4. Palpitations (tap out rhythm, any dizziness or blackouts)Systemic ReviewDuring the history consider (and ask about) the main risk factors for IschaemicHeart Disease:1. Smoking2. Hypertension3. Diabetes mellitus4. Hyperlipidaemia5. Family historyPast Medical History (may ask under presenting complaint)e.g. angina, myocardial infarction, bypass operation, rheumatic fever, stroke,intermittentclaudicationSocial HistorySmoking (pack years), alcohol, stairsFamily HistoryAt what age did the relative have illness?Drug HistoryAllergies
MAGDI AWAD SASI 2013INTRODUCTIONW - Wash your hands.I - Introduce yourself (full name and role). Greet the patient with theirtitle and surname.P - Permission. Explain that you wish to examine their heart.E - Expose the necessary parts of the patient. Ideally the patient should beundressed from the waist up taking care to ensure the patient is not cold orunnecessarily embarrassed.R - Reposition the patient. In this examination the patient should besupine and reclined at 45 degrees.In the cardiovascular examination a lot of information can be obtained bylooking for peripheral signs of cardiovascular disease.The examination is therefore split into aA.peripheral examination and B. examination of the precordium.Adequate exposure and a quiet environment are critical.Peripheral ExaminationEnd of the Bed• Examine the patient for signs of breathlessness or distress.• It is also important to look at the surrounding environment for oxygen, fluidrestriction signs or GTN spray.Hands• To assess warmth, sweating and whether there is peripheral cyanosis.• Examine the nails for clubbing or signs of infective endocarditis (splinterhaemorrhages, Osler’s nodes and Janeway lesions).• Palpate the radial pulse and assess the rate and rhythm.Rate , rhythm , volume, special character, synchronicity, radiofemoral delaySmall volume = stenotic lesion mitral and aortic stenosis.Large volume = regurgitation lesion mitral and aortic regurgitation.
MAGDI AWAD SASI 2013Types of pulsesSlow rising pulse (delayed up strokes / parvus et tardus) Acarotid arterial pulse that is reduced (parvus) and delayed (tardus) argues foraortic valvular stenosis. Occasionally this also may be accompanied by apalpable thrill. If ventricular function is good, a slower upstroke correlates with ahigher transvalvular gradient. In left ventricular failure, however, parvus andtardus may occur even with mild aortic stenosis (AS).Pulsus bisferience = AR + ASPulsus paradocsus = acute sever asthma or cardiac tamponadePulsus paradoxus is an exaggerated fall in systolic blood pressure during quietinspirationPulsus alternans = LVFPulsus alternans is the alternation of strong and weak arterial pulsesdespite regular rate and rhythm.Collapsing pulse= hyperdynamic circulationA high volume pulse that hits the fingers suddenly and falls away justas quickly. It is exaggerated by raising the arm well above the level of theheart. This is a sign of aortic regurgitation. The pulse is examined with the armby the patient’s side; then briskly raise the arm• Measure the blood pressure. If theblood pressure is raised compare both arms.Face• Check eyes for corneal arcus and xanthelasma.• Inspect the conjunctivae for anaemia.• Check for mouth and tongue for central cyanosis.
MAGDI AWAD SASI 2013Check Jugular Venous Pressure (JVP)o With the head resting back on the pillow ask the patient to turn the head to theleft while the head of bed is elevated to 45.1 Think anatomically. The right IJ runs between the two heads (sternal andclavicular) of the sternocleidomastoid muscle (SCM) and up in front of the ear.2 Take your time. Look at the area in question for several minutes while thepatients head is turned to the left. The carotid artery is adjacent to the IJ, lying justmedial to it . The carotid impulse coincides with the palpated radial arterypulsation and is characterized by a single upstroke timed with systole. The venousimpulse (at least when the patient is in sinus rhythm and there is no tricuspidregurgitation) has three components a, c and v waves. When these are transmittedto the skin, they create a series of flickers that are visible diffusely within theoverlying skin. In contrast, the carotid causes a single up and down pulsation.Furthermore, the carotid is palpable. The IJ is not and can, in fact, be obliterated byapplying pressure in the area where it emerges above the clavicle.3. Shine a pen light tangentially across the neck. This sometimes helps toaccentuate the pulsations.4 . Hepatojugular reflux If you are still uncertain, apply gentle pressure tothe right upper quadrant of the abdomen for 5 to 10 seconds. This elicits Hepato-Jugular Reflux which, in pathologic states, will cause blood that has pooled in theliver to flow in a retrograde fashion and fill out the IJ, making the transmittedpulsations more apparent. Make sure that you are looking in the right area whenyou push as the best time to detect any change in the height of this column of bloodis immediately after you apply hepatic pressure.5 . The Angle of Louis
MAGDI AWAD SASI 2013The angle is the site of the joint which connects the manubrium with the restof the sternum.First identify the supra-sternal notch, a concavity at the top of themanubrium.Then walk your fingers downward until you detect a subtle change in theangle of the bone, which is approximately 4 to 5 cm below the notch. This isroughly at the level of the 2nd intercostal space.The vertical distance from the top of the column to this angle is added to 5cm,the rough vertical distance from the angle to the right atrium with the patientlying at a 45 degree angle.The sum is an estimate of the CVP.Normal is 7-9 cm.o Look for pulsation along the right internal jugular vein.o The height of the pulsation is measured vertically in cm from the sternal angle.Add 5cm to get the JVP.o You should know how the JVP can be differentiated from carotid pulsation
MAGDI AWAD SASI 2013Explain what youre doing (& why) before doing it .Expose the minimum amount of skin necessary - this requires "artful" use of gown& drapes (males & females)Examining heart & lungs of female patients:Ask pt to remove bra prior (you cant hear the heart well thru fabric)Enlist patients assistance, asking them to raise their breast to a position thatenhances your ability to listen to and palpate the heartDont rush, act in a callous fashion, or cause painPLEASE... dont examine body parts thru gown as:1. It reflects Poor technique2. Youll miss things3. Youll lose points on scored exams .
MAGDI AWAD SASI 2013INSPECTIONThe examination should be conducted in a warm, quiet room. Place the patient in a supine position withthe upper body elevated 30 to 45 degrees after all clothing has been removed from the chest. Explain tothe patient that you are going to examine the heart. Warm your hands and stethoscope, but warn thepatient that your hands may be cool at first. The most comfortable and satisfactory position for mostexaminers is on the patients right sideThe praecordium is the front of the chest overlying the heart.A. Look for abnormal chest shapeNormal chest =anterior posterior diameter 1/3- 2/3 of side to sideBarrel shaped = anterior posterior equal to side to sideCOPD, Bronchial asthma , BronchiectasisPigeon chest = pectus incavatum= sternum protruded outFunnel chest= pectus excavatum = sternum depressedB. Look for skin , scar , pulsation ,PacemakerMidline – sternotomy scar – CABG/valve replacement.Left – thoracotomy scar (diagonal from under left breast to left axilla) – mitrialvalvectomy for mitrial stenosis.Pacemaker – under skin inferior to left clavicle.Apical pulsation , parasternal pulsation , epigastric pulsationC. Look for respiratory movementThoraco abdominal in female , Abdominothoracic in maleAny change gives a clue to pathological process.D.Look for accessory musclesContracted sternomastoid , recession of intercostals muscles that gives aclue that the patient is dyspneic or he had a chronic respiratory diseasewith chronic dyspnea.NoteThis is the same even for chest inspection that for CVS concentrate onpulsation and for chest lok for respiratory movement.
MAGDI AWAD SASI 2013PALPATION1.Palpate trachea2.Apex beat = Point of Maximum Impulse (PMI)It is the lower most , outer most and most forceful pulsation.LOCATE the apex beat accurately with the flat of and fingers of your right hand.Try to pin down the precise location with the tip of your index finger. The normalsized and functioning ventricle will generate a penny sized impulse Count downthe ribs from the sternal angle= 2NDintercostals space. The normal apex beatshould be in the 5th intercostal space in the mid clavicular line. Decide if the apexbeat is normal or displaced.Locate the line “axillary, midclavicular “ , space “ 5th,6th,7th“ and character“ tapping,foreceful heaving or unsustained “..Apex beat not palpableNormal cause Obesity , thick chest , behind ribPathological cause barrel chest ,pericardial effusion,dextocardia.Rotating the patient to a left lateral decubitus position tips the hearttowards the chest wall and makes the apex beat easier to feel.
MAGDI AWAD SASI 20131.Mitral stenosisproduces a particularly characteristic cardiac apical impulse. The apicalimpulse often has a sharp tapping nature. This is because the first heartsound is loud because of forceful closure of the mitral valve and this forcefulclosure is transmitted to the chest wall as a ‘tap’. Same line and samespace “ tapping”2.Aortic stenosis- pressure load “heaving”A forceful or ‘thrusting’ apex, either in the normal position or slightlydisplaced to 6thintercostals space. This is usually due to concentric LVhypertrophy as a result of conditions such as aortic stenosis or hypertension.same line and change space. “forceful sustained”3. Mitral and aortic regurgitation- volume loadThe apical impulse may be displaced to the left and have a more diffuseheaving nature. This is usually when there is volume overload. A similartype of apex beat is often seen when there is sever LV dysfunction and theventricle is enlarged. If the patien has an audible gallop rhythm this cansometimes also be palpated with a hand placed over the cardiac apex. Lineand space changed.“forceful unsustained”D. Constrictive pericarditis , which is rare in many developed countries,but common in the developing world, can produce in-drawing of theintercostals spaces during systole because the LV is tethered to the chestwall by the diseased pericardium.Summary:For apex beat , check line , space and character.Palpation of the precordium of a female patient is bestdone by placing the palm of your right hand directlybeneath the patients left breast such that the edge ofyour index finger rests against the inferior surface of thebreast. Tell that patient what you are about to do (andwhy) before actually performing this maneuver.Remember that with age tissue turgor often declines,causing the breasts to hang below the level of the heart.
MAGDI AWAD SASI 2013Palpate the 2ndleft intercostals space “pulmonary area” for palpable 2ndheart sound which normally not felt.In pulmonary hypertension , the pulmonary artery dilates and producesan impulse in the second left intercostals space and the loud pulmonarycomponent of the S 2 may also be appreciated as a sharp snappingfeeling in this area.3.THRILLIt is a palpable vibratory sensation, often compared to the purring of a cat, andtypical of murmurs caused by very high pressure gradients. These, in turn,lead to great turbulence and loudness.Hence, thrills are only present in pathologic murmurs whose intensity is greaterthan 4/6. It should be checked in the four areas by palmer surface of the righthand at the junction of metacarpophalangeal surfaces.The commonest cause of a thrill is aortic stenosis.If present there should be an easily audible murmur present on auscultation.In mitral area= diastolic thrill , in aortic area= systolic thrill
MAGDI AWAD SASI 20131.Aortic area: “AA” 2ndparasternal right intercostals space2.Pulmonary area “ PA”:2ndparasternal left intercostals space3.Tricuspid area “TA” : 4thparaeternal left intercostals space4. Mitral area “MA” : 5thleft intercostals space-apex beat4.HEAVELeft parasternal (right ventricular) heaveA signifi cantly hypertrophied and/or dilated RV will producean abnormal impulse at the lower end of the sternum,usually to the left side. In a patient with lung disease andan abnormal RV this physical sign may be absent becausethe over-infl ated lung acts as a cushion between the heartand the chest wall and therefore prevents the impulse beingtransmitted to the surface. Heaves represent ventricular hypertrophyand feel as if your hand is being lifted of patient’s chest.Figure 1 AREAS TO BE PALPATED FOR THRILL
MAGDI AWAD SASI 2013Auscultation. Don’t auscultate over clothes or gown.. Warm your hands and stethoscope.. The most satisfactory position for examiner is on the patients right side.. Become comfortable with your stethoscope.. Learn how to use it correctly bell and diaphragm.. The most important "part" is what sits betwen the ear pieces!. Be isolated from surrounding and keep ear pieces tight to your ears..4 areas need to be auscultated 2 times change from diaphragm to bell.. 2 positions need to be done by the patient other than supine.. 2 radiation of the murmurs need to be checked.. Start from mitral area “apex beat”. OR aortic area!. start from MA - TA – PA – AA.These areas, although known as the mitral, tricuspid, pulmonary andaortic areas, in fact have no anatomical meaning. They are the keyareas where the heart sounds and murmurs radiating from thesevalves are traditionally considered to be best heard. Be prepared tohunt around slightly to find the optimum position for your stethoscopebut don’t move too quickly or you could miss a sound.
MAGDI AWAD SASI 2013Technique of auscultationA. Start from mitral area by putting the diaphragm of stethoscope andListen systematically to the cardiac cycle i.e. 1st and 2nd heartsounds (S1 and 2) and listen in the systolic and diastolic intervalsfor added sounds and murmurs. Time events with simultaneouspalpation of the carotid.B. Roll your patient slightly onto his left side and listen in the 5thICS with the bell for the low frequency mid diastolic murmur ofmitral stenosis. (Listen in full expiration).C. Auscultate in the axilla with the diaphragm for radiation andcomparative loudness of a systolic murmur. (e.g. the pan -systolic murmur of mitral regurgitation radiates to the axilla.)D. Go to TA then PA then AA ask patient to sit , lean forwardand exhale the air to check AA and listen at left lower sternaledge for high frequency diastolic murmur of aortic regurgetationE. auscultate with the diaphragm over bothcarotids for bruits and radiation ofmurmurs, (the ejection systolic murmur ofaortic stenosis radiates to the neck.)
MAGDI AWAD SASI 2013F. Use both the bell and diaphragm appropriately in the 4 areas –That the bell should only be placed lightly on the skin.The bell at the apex for low frequency sounds (i.e. murmurs)The diaphragm at the base for high frequency sounds.HEART SOUNDSHeart sounds are discrete bursts of auditory vibrations of varying intensity(loudness), frequency (pitch), quality, and duration.Start by listening to the heart sounds. To help you differentiate between the heartsounds they should be timed against the carotid pulse.SUMMARYS1 =1stheart sound best heard in MAMuffled with MR as it is masked by pansystolic murmurVery loud in MS with rumbling diastolc murmurTimed with carotid pulsationS2 =2ndheart sound heard in AALoud in PA in pulmonary HTN, loud in AA in systemic HTNTimed with carotid pulsation “delay”Soft A2 in AS , ARS3 = Left ventricular failure-gallop rhythmS4 = noncompliant ventricle LVHS3 AND S4 DIASTOLIC SOUNDS , LOW PITCHED.
MAGDI AWAD SASI 2013S1 & S2 ARE NORMAL SOUNDS . S3&S4 ARE PATHOLOGICAL.• The first heart sound is. The sound of the mitral and tricuspid valves closing.Systolic events tend to occur at the same time as the carotid pulse. Loudest at the apex.The S1 is muffled when there is an increased amount of tissue between theheart and the stethoscope, as occurs with pleural effusion, pericardialeffusion, emphysema, pneumothorax, and obesity.Conditions associated with a loud S1 include the following:Increased transvalvular gradient (MS, TS, atrial myxoma)Increased force of ventricular contraction (tachycardia, hyperdynamicstates [ie, anemia, fever, thyrotoxicosis, exercise, inotropic agents])Shortened PR interval - Tachycardia, preexcitation syndromes (ie,Wolff-Parkinson-White [WPW] syndrome)Conditions associated with diminished intensity of S1 include the following:Inappropriate apposition of the AV valves(ie, mitral regurgitation [MR], tricuspid regurgitation [TR], dilatedcardiomyopathy)Prolonged PR interval (ie, bradycardia, heart block, digitalis toxicity)Decreased force of ventricular contraction(ie, cardiomyopathy, myocarditis, myxedema, myocardial infarction [MI])Increased calcification of the AV valve(ie, calcific MS, postirradiation)Increased distance from the heart(ie, obesity, emphysema, pleural effusion, pericardial effusion)
MAGDI AWAD SASI 2013SO , S1 CAN BE HELPFUL FOR EVALUTING THE SEVERITY OF VALVULARLESION..• The second heart sound.Closure of the aortic and pulmonary valves at end of systole..Follows the apical impulse and carotid pulsation.. Best heard at the upper left sternal edge using thediaphragm of the stethoscope.A2 is best heard at the aortic area (second right intercostal space); P2 is bestheard at the pulmonary area. S2 is a high-pitched sound heard best with thediaphragm of the stethoscope. The intensity depends on valvular factors, thetransvalvular gradient, mechanical factors, and size of the great vessels.The intensity of A2 is increased in Systemic hypertension,Coarctation of the aorta,Aortic aneurysm,Thin individuals,and when the aorta is closer to the anterior chest wall as may occur withtetralogy of Fallot and transposition of the great arteries (TGA).The intensity of A2 is decreased with decreased aortic diastolic pressure ( AR),with improper valvular apposition ( AR or aortic dissection), calcific immobilevalves ( calcific aortic stenosis [AS]), and decreased systemic arterial pressure.The intensity of P2 is increased with pulmonary arterial hypertensionSplit S2Normally, the aortic valve closes slightly before the pulmonary valve. Thisdifference is more pronounced with inspiration due to increased RV strokevolume.The fixed-split S2- ASD, right heart failure
MAGDI AWAD SASI 2013Third Heart SoundThe third heart sound (S3) is a low-pitched, early diastolic sound audible duringthe rapid entry of blood from the atrium to the ventricle. When arising from theLV, it is best audible at the apex with the patient in left lateral decubitus positionwith breath held at end expiration. When it is of RV origin, S3 is best audible atthe left lower sternal border or the xiphoid with the patient in supine position.These are best heard with the bell of the stethoscope. Conditions associated withpathological S3 include the following:A. Systolic and/or diastolic ventricular dysfunction1. Ischemic heart disease2. MR or TR3. Sysetmic and pulmonary hypertension4. Acute aortic regurgitation5. Chronic AR with systolic dysfunctionB.Hyperkinetic states - Anemia, fever, pregnancy, thyrotoxicosis, AV fistulaC.Volume overload - Renal failureFourth Heart SoundThe fourth heart sound (S4) is a late diastolic sound that corresponds to lateventricular filling through active atrial contraction. It is a low-intensity soundheard best with the bell of the stethoscope. When of LV origin, S4 is best heard atthe apex with the patient in the left lateral decubitus position at end expiration.When of RV origin, it is heard best at the left lower sternal border. Maneuversthat increase the preload increase the intensity of S4 by increasing the separationof S4 from S1.Active atrial contraction is necessary for the generation of S4. Thus, S4 is notaudible with atrial fibrillation or flutter.Some of the conditions associated with S4 include the following:Ventricular hypertrophy - LV hypertrophy (systemic hypertension,hypertrophic cardiomyopathy, AS); RV hypertrophy (pulmonaryhypertension, pulmonary stenosis [PS])Ischemic heart disease - Acute MI,anginaVentricular aneurysmHyperkinetic states that cause forceful atrial contraction
MAGDI AWAD SASI 2013Both S3 and S4 need to be differentiated from splitting of the normal heartsounds. With splitting, the heart sounds are high pitched and best audiblewith the diaphragm, whereas the S3 or S4 are low-pitched sounds best audiblewith the bell of the stethoscopeIs there any audible sound other than heart sounds?MURMURS1.‘‘Inching’’ the stethoscope (i.e., slowly dragging it from site to site)can be the best way to avoid missing important findings.2. From MA TO TA THEN PA OT AA or THE REVERSE AA.3. Murmurs are common in MA AND AA THAT IS LEFT SIDE.Definition:The production of murmurs results from turbulent flow across valves. Three mainfactors have been attributed to cause a murmur:(1) high flow rate through normal or abnormal orifices(2) forward flow through a constricted or irregular orifice or into a dilated vessel orchamber, (3) backward or regurgitant flow through an incompetent valve.When evaluating a heart murmur, it is important to know the timing of themurmur in the cardiac cycle, the location, the duration, character, configuration,radiation, aggravating maneuvers, and diminishing maneuvers.Types of murmurs:1.Systolic (holosystolic, early/middle/late systolic)2.Diastolic (early/middle/late) or3.Continuous (ie, present in both systole and diastole).All diastolic murmurs and any systolic murmur above grade 2in severity requires further evaluation with echocardiography.
MAGDI AWAD SASI 2013TIMEThe timing of the murmur is determined by palpating the carotid pulse whilelistening to the murmur. The carotid upstroke corresponds to the onset ofsystole.LOCATIONThis is the area of the heart where the murmur is heard the loudest.While auscultating, one should concentrate on the apex, pulmonaryarea, tricuspid, and aortic areas, in addition to the axilla, base of theheart, and left fourth ICS for evidence of radiation of murmur.INTENSITY:The intensity of the murmur depends on the volume of blood flowacross the valve and the pressure gradient across which the bloodflow occurs.What is the Levine system for grading the intensity of murmurs?The intensity or loudness of a murmur is traditionally graded by theLevine system from 1/6 to 6/6. Increased intensity usually reflectsincreased flow turbulence. Thus, a louder murmur is more likely to bepathologic and severe.Grade I - Heard in a quiet room by an expert examinerGrade II - Heard by most examinersGrade III - Loud murmur without thrillGrade IV - Loud murmur with a thrillGrade V - Thrill with a very loud murmur audible with stethoscope placedlightly over the chestGrade VI - Thrill with a very loud murmur audible even with the stethoscopeslightly away from the chest
MAGDI AWAD SASI 2013Quality/character:Different murmurs have different qualities, such asharsh, blowing, rumbling, musical.Pitch:This can be high or low pitched depending on the frequency of themurmur. The high-pitched sounds are best audible with a diaphragmand the low-pitched sounds with the bell.
MAGDI AWAD SASI 2013Radiation:Murmurs tend to radiate to certain specific areas that are often characteristic of aparticular murmur. The murmur of MR radiates to the axilla or base of the heart,depending on which leaflet is involved. In the case of AS, the murmur radiates inthe direction of the jet of turbulent blood (ie, radiates to the carotids). Similarly,the aortic regurgitant murmur tends to radiate along the left sternal border.Configuration:This corresponds to the shape of murmur intensity over time. It can be a plateau,decrescendo, crescendo-decrescendo, or crescendo murmur.Maneuver affect on murmur:1.Affect of respirationThe murmurs generated from the right side of the heart increase in intensitywith inspiration by increasing the venous return to right side. ,Murmurs arising from the left side of the heart become more prominent withexpiration as blood is forced from lung to the heart.2.Standing up:This causes a peripheral pooling of blood and a net decrease in venous return.Most murmurs are thus decreased in intensity upon standing, except that ofhypertrophic obstructive cardiomyopathy (HOCM) and MVP, which becomemore prominent.3.Squatting:Squatting causes an increase in the afterload and venous return (ie, preload).The net effect is an increase in intensity of all the murmurs, except thoseassociated with MVP and HOCM, which become less prominent withsquatting.4.Hand grip:Hand grip is a form of isometric exercise and increases the afterload, arterialpressure, LV volume, and LV pressure. The net effect of these changes iscomplex and variable. Murmurs of MR, AR, and VSD worsen with hand grip,while those of HOCM and MVP are less prominent.
MAGDI AWAD SASI 2013Cardiac cycleAs a rule , the stenosis will be evident once blood flow through the valve and the valve isopened that with associated turbulent flow.The 2ndrule is the regurgitation will be evident once there is no blood flow through thevalve and valve closedIn systole, left and right ventricles contractAortic valve and pulmonary valves openedMitral and tricuspid valves closedAortic and pulmonary valves opened. If there is stenosis “AS/PS” , ejection systolicmurmur will be heard in aortic area/ pulmonary area which is harsh high pithched loud ofcrescendo- decrescendo in configuration as blood is pumped with high amount duringsystole which became more audible by sitting leaning and in full expiration in AS.Mitral valve and tricuspid valves closed. If there is regurgitation “MR/TR”, pansystolicmurmur will be heard in mitral area and tricuspid area which is blowing and high pitchedplateau in configuration which became more audible by telt to left side in apex beat inthe expiration and radiate to left axilla in MR.In diastole, left and rig ventricles relaxed.Mitral and tricuspid valves opened.Aortic and pulmonary valves closed .Mitral and tricuspid valves opened . If there is stenosis “MS/TS”, mid diastolic murmurwill be heard in mitral area and tricuspid area which is low-pitched rumbling , best heardwith the bell of the stethoscope placed over the cardiac apex with the patient in the leftlateral position in mitral stenosis in expiration with loud S1.Aortic and pulmonary valves closed. If there is regurgitation, “AR/PR” early diastolicmurmur will be heard in aortic area and pulmonary area which is high-pitched sound, isdecrescendo in configuration , and is most audible at the left sternal border or the rightsecond ICS just to the right of sternum, with the patient leaning forward at end expirationin AR.AS/PS = EJCETION SYSTOLIC MURMUMR/TR = PANSYSTOLIC MURMURAR/PR = EARLY DIASTOLIC MURMURMS/TS =MID DIASTOLIC MURMUR
MAGDI AWAD SASI 2013Systolic murmurs;1. Pansystolic murmur-Mitral regurgitationTricuspid regurgitationVentricular septal defectThese murmurs last throughout ventricular systole. They usually start at S1 andproceed through S2; the intensity of the murmur may overshadow both valveclosure sounds.These murmurs are typically produced by emptying of the high-pressureventricle during systole into chambers that have lower pressure at that time (theatria with MR or TR or the right ventricle in the case of VSD).The murmur of MR is blowing and high pitched and is best heard at the apexwith radiation to the axilla or the base of the heart. It is usually plateau inconfiguration. The MR murmur is increased during expiration, passive legraising, squatting, and handgrip and decreased in intensity with inspiration,Valsalva, and standing. The radiation of the murmur depends on which leafletis involved. A murmur generated by the deformity of anterior leaflet radiatesmore toward the axilla, thoracic spine, and scapula, while a murmur arisingfrom posterior leaflet involvement radiates to the base of the heartSevere MR . The presence of S3. Signs of pulmonary hypertension and right heart failureThe murmur of TR is best heard at the left lower sternal border. It is ablowing high-pitched murmur heard that increases in intensity withinspiration (Carvallo sign). It can result primarily from involvement of thetricuspid valve or secondarily from pulmonary hypertension. When due topulmonary hypertension, it is associated with a loud P2.In VSD with normal pulmonary arterial pressures, a holosystolic murmur canbe heard over the left lower sternal border at the level of the third and fourthICSs. This murmur depends on the orifice size of the septal defect. Thesmaller the defect, the greater the intensity of the murmur.
MAGDI AWAD SASI 20132.Ejection systolic murmur “mid to late systole”Aortico Obstructive Supravalvular - Supravalvular AS, aortic coarctation Valvular - AS, aortic sclerosis Subvalvular - HOCMo Increased flow, hyperkinetic states, aortic regurgitation, completeheart blocko Dilatation of the ascending aorta, aortitis, atheromaPulmonaryo Obstructive Supravalvular - Pulmonary artery stenosis Valvular - Pulmonary valve stenosis Subvalvular - Infundibular stenosiso Increased flow, hyperkinetic states, left-to-right shuntoThese murmurs are usually associated with ventricular outflow tractobstruction (which can be valvular, supravalvular, or subvalvular) or anabnormal amount of blood flow across normal valves as can happen inhyperdynamic states (hyperthyroidism, fever, pregnancy, anemia, renalfailure).AS/PSThe murmur associated with valvular stenosis (AS or PS) is usually a harsh murmurwhich is crescendo- decrescendo in configuration and high pitched.AS-associated murmurs are most audible at the right upper sternal border/rightthird ICS with the patient in the upright position and breath held at endexpiration. In some cases, it is audible at the apex, in which case it can be confusedwith the murmur of MR. Some of the findings that help delineate the murmur ofMR from that of AS include an audible S1, forceful apex, radiation to carotids,changes with atrial fibrillation, and post-PVC accentuation. The AS murmur usuallyradiates to the carotid arteries.
MAGDI AWAD SASI 2013Early diastolic murmursAre produced by either AR or pulmonary regurgitation.arThe AR murmur is a soft high-pitched sound, is decrescendo in configuration, and is mostaudible at the left sternal border or the right second ICS just to the right of sternum, withthe patient leaning forward at end expiration. The murmur radiates to the left lowersternal border if it is due to primary valve disease. In patients with aortic root disease, themurmur may radiate to the right sternal border. The murmur increases in intensity duringexpiration and decreases in intensity with hand grip. The S2 is usually muffled with AR.PRThe murmur of pulmonary regurgitation is best audible at the pulmonary area. Thecharacter, quality, and pitch of the murmur vary depending on the presence or absence ofpulmonary hypertension. In the presence of pulmonary hypertension, it is a high-pitched,decrescendo murmur also known as a Graham Steell murmur. S2 is usually loud inassociation with pulmonary regurgitation. In the absence of pulmonary hypertension, it is alow-pitched crescendo-decrescendo murmur.Mid- to late diastolic murmursThese murmurs are produced by the blood flow across stenotic AV valves.MS produces a low-pitched, mid-diastolic, rumbling murmur with presystolic accentuation,best heard with the bell of the stethoscope placed over the cardiac apex with the patient inthe left lateral position. S1 is loud. The murmur usually follows an OS, and the intervalbetween the A2 and OS is inversely proportional to the severity of obstruction.The murmur of MS is increased in intensity with expiration and maneuvers that increasecardiac output, such as exercise. The presystolic accentuation results from atrialcontraction in late diastole and is absent in patients with atrial fibrillation. The duration ofmurmur corresponds to the period in which the LA-LV diastolic pressure gradient ismaintained. This duration correlates with the severity of obstruction; the longer themurmur duration, the more severe the MS (provided the diastolic filling time is notshortened, as may happen in tachycardia) except in high cardiac output and pulmonaryhtpertension.D/D OF MID DIASTOLIC MURMUR:1. Tricuspid stenosis=tricuspid area2. Atrial myxoma- change by position3. Austin Flint murmur- due to AR4. Carey Coombs murmur-rhematic heart disease
MAGDI AWAD SASI 2013Continuous MurmursPDACoronary arteriovenous fistulaRuptured sinus of Valsalva aneurysmAortopulmonary windowAnomalous left coronary artery from the pulmonary arteryBronchial collateral circulationOpening SnapThe opening snap (OS) is a high-pitched diastolic sound produced by rapidopening of the mitral valve in MS or TS. When mitral in origin, it is best heardat the apex following the aortic sound A2, with the patient in left lateraldecubitus position.The time difference between the A2 and OS has a diagnostic implication. Thecloser the OS is to A2, the more severe the stenosis. The OS signifies when theleft atrial pressure exceeds the LV diastolic pressure and marks the beginning ofblood entry into the LV from the LA. The more severe the stenosis, the greaterthe LA pressure and the lesser the LA-LV early diastolic pressure gradient,leading to an early opening of the mitral valve. In general, the relation betweenA2 and the OS depends on LV pressure at A2 closure, LA pressure at A2 closure,and the rate of LV pressure decline.Pericardial rubIt indicates pericardial inflammation.• Inflammation of the pericardial membrane or pleural sac at the 3rdand 4thinterspace at the left sternal border. Louder during inspiration• Scratchy, like sandpaper being used, a match being struck, or leathersqueaking .• Sound present when the epicardial & pericardial surfaces, roughened byinflammation, slide over one another during atrial & ventricular systole &during the passive motion of rapid ventricular filling.
MAGDI AWAD SASI 2013• 3 components– Atrial Systolic (A)– Ventricular Systolic (V)– Ventricular Diastolic (D)Percardial Knock• Sharp, high-pitched sound present in 90% or more of patientswith constrictive pericarditis• Heard in diastole• Occurs .09 to .12 sec after S3• Occurs after Heart Surgery, radiation therapy, viral infection, TBpericarditis• Diaphragm of the stethoscope listen at the lower left sternalborderTumor Plops• Clues to a Myxoma– Cardiac silhouette on X-Ray consistent with atrialenlargement– An ECG showing signs of LA enlargement– Light-headedness– A very short presystolic murmur– Extra sound in diastole• Left Atrial Tumors– Loud, low-frequency thud heard in early diastole & causedby abrupt movements of the tumor inside the LA– It strikes the wall of the chamber or comes to a sudden haltas the pedicle reaches the limit its stretch
MAGDI AWAD SASI 2013SUMMARY SHEET OF CVS EXAMINATION1. INSPECTIONChest deformitySkin ,scars , pulsation, vesselsRespiratory movementsAccessory muscles of respiration2. PALPATIONTracheaApex beat- line , space , characterThrill- MA , TA ,PA & AA.Heave - left parasternal3. AUSCULTATIONStart in mitral area by diaphragm and listen for S1 ,S2 ,MFor murmur , site ,time ,radiation, character, grade ,pitch.Tilt pt to left lateral and use the bell to here diastole in MAChange the bell to diaphragm to auscultate axilla for PSMInch to TA and check S2 and ask pt to hold in inspirationInch to PA to hear P2 and murmurs if presentConcentrate on AA and ask pt to sit , lean ,and full expirationLastly check carotids by diaphragm for systolic radiation