CD Contents VIDEO: The Technique of Performing an Echo Echo Made Easy® Fourth Edition Atul Luthra MBBS MD DNB Diplomate National Board of Medicine a sanjea pue smaiq [eEUUON *S GE 04g UI suondang aining val 9¢ yp jeaBeydosasuey 8¢ SMOpUIM O4>g PIepUeIS A Le oypy W>BOYISUEL AUK smopulm O43 “y #2 _19\ddoq 10}05 jo suonedtiddy 61 J2|ddog 10/05 jo sajdioung oypg sajddog 40105 * 81 OY>3 Jo suone: dy 1221 By} ZL tajddog anem pasing 91 1a\ddog anem snonunuoy Ve rL 0493 apour-uonow EL 04>3 jeuo!suaUIp-omp oyay jeuoHUaAUOD “Z 5 1aiddog jo sajdioung 1 punosesyn jo sajdioung coupg ue SEEM s}ua}uU0D LHET «eho nase tasy 6. Ventricular Dysfunction + Left Ventricular Systolic Dysfunction 58 * Left Ventricular Diastolic Dysfunction 69 ght Ventricular Systolic Dysfunction 75 1. Cardiomyopathies \ + Dilated Cardiomyopathy 80 i i * Restrictive Cardiomyopathy 85% + Hypertrophic Cardiomyopathy 88 8. Coronary Artery Disease + Indications for Echo in Coronary Artery Disease 96 = Myocardial Ischemia 97 + Myocardial Infarction 97 + Left Ventricular Dysfunction 103 + Right Ventricular Dysfunction 106 + Acute Mitral Regurgitation 107 + Ventricular Septal Defect 109 + Left Ventricular Aneurysm 109 * Ventricular Mural Thrombus = 177 * Acute Pericardial Effusion 112 * Coronary Artery Anomalies 112 + Simulating Conditions 113 + Stress Echocardiography 114 9. Systemic Hypertension + indications for Echo in Hypertension 117 + Left Ventricular Hypertrophy 117 70. Pulmonary Hypertension #* + Detection of Pulmonary Hypertension 123 + Estimation of Pulmonary Hypertension 126 58 80 96 117 123 mM. Diseases of Aorta * Dilatation of Aorta 135 + Aneurysm of Aorta 136 © @ Coarctation of Aorta 1370) a 4 * Dissection of Aorta 139 Congenital Diseases > 142 Ventricular Septal Defect 143" Ayer ge Atrial Septal Defect 145) 1 “+ Patent Ductus Arteriosusq149 6?) + Tetralogy of Fallot 150 * Eisenmenger Reaction 152 * Quantification of Shunt 753 Valvular Diseases 155 Mitral Stenosis 156 + Mitral Valve Prolapse 165 @) + Flail Mitral Leaflet 168 & + Mitral Annular Calcification 170 se* Mitral Regurgitation 172 + Tricuspid Stenosis 179 + Tricuspid Regurgitation 182 + Ebstein Anomaly 188 + Aortic Stenosis 190 * Aortic Regurgitation 207 4 + Pulmonary Stenosis 217 % + Pulmonary Regurgitation 214 Pericardial Diseases 218 14, g° *” Pericardial Effusion 218 @) © Cardiac Tamponade 222 A\ constrictive Pericardi 224UL 61g) yBua|anem ayp st says “(KouaNbOy ayy 4932946) puoDas e ul $2)2A> a4) 3101 PUODas aUO Ul a>UEYSIp Paxy e sjenen punos ‘souls ‘payejas-saiui aie yyBuajanem pue Aouanbal4 syead annnoasuoa ‘om Lasmiag aruersip ayn s| anem aya yo YBUE} ay! Iey pue asi 40 2}942 auo UI unos fq pajjanen auersip ays si BUBIaNeM w [punos jo Yaad se sauaisi) 942 Aq paersaidde s| A>uanbald) w 7H 0000001 = 2H 901 = (ZHI) ZuayeBau \2H 0001 =2H

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Relationship between frequency and wavelength: (A) High frequency, short wavelength; (8) Low frequency, long wavelength (Therefore, Velocity = Frequency x Wavelength) Velocity of sound is expressed in meters per second (m/sec) and is determined by the nature of the medium through which sound propagates. In soft tissue, the velocity is 1540 m/sec. Intensity of sound is nothing but its loudness or amplitude expressed in decibels. Higher the intensity of sound, greater is the distance upto which it is audible. The normal audible range of sound frequency is 20 Hz to 20 KHz. Sound whose frequency is above what is audible to the human ear (more than 20 KHz) is known as ultrasound. The technique of using ultrasound to examine the heart is known, as echocardiography or simply echo. Electricity and ultrasound are two different forms of energy that can be transformed from one to the other by special crystals made of ceramic such as barium titanate. Ultrasound relies on the property of such crystals to transform electrical current of changing voltage into mechanical vibrations or ultrasound waves. This is known as the piezoelectric (pressure electric) effect (Fig. 1.2) ‘When electrical current is passed through a piezoelectric crystal the crystal vibrates. This generates ultrasound waves which are transmitted through the body by the transducer which houses several such crystals, | What lean Eeh Returning signat r~ Transmitted ultrasound Reflected ultrasound a~ aw~ Fig. 1.2. The piezoelectric effect in ultrasound Most of these ultrasound waves ate scattered or absorbed by the tissues, without any obvious effect. Only a few waves are reflected back to the transducer and echoed. Reflected ultrasound waves again distort the piezoelectric crystals and produce an electrical current. These reflected echoes are processed by filtration and amplification, to be eventually played on the cathode-ray-tube. The reflected signal gives information about the depth and nature of the tissue studied, Most of the reflection occurs at interfaces between tissues of different density and hence a different echo-reflectivity. The magnitude of electrical current produced by the reflected ultrasound determines the intensity and brightness on the play screen On the gray-scale, high reflectivity (from bone) is white, low reflectivity (from muscle) is gray, and no reflection (from ait) is black (Table 1.1). The location of the image produced by the reflected ultrasound depends upon the time lag between transmission and reflection of ultrasound. Deeper structures are shown on the lower portion of the display screen while superficial structures are shown on the upper peers |(fouanbay, Jamo}) Nok wou Keme S306 11 uaym ueyy (Auanbay 124614) NOK saypeoucide 11 Uayan JaYBIY S! 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Ue gaqunosua Jaanpsues ayy kq payeiauab sanem punosesyn uayM = paquosqe pue pasanieas (janissaiGoid s196 3nq uon>auip [eulBy0 sy sulerulew 2) (wnipaw Wuoylun e yBnouyy paytwsued si punosenjn Uy aw “(€'1 ig) uaaids ay2 uo abews seINBueL ayy Jo xade aun ze s| s2onpsuen ayy asneraq 51 si4s “uonuod “uaai0s Jamo] aya Ul ap>UNUaAYaT “A ‘uaaias sadn ayp ul apinuan 346IY “Y ‘e\dsip jensia yo xade ayy ve | aonpsued, €*4 “Bld ua9u08 49M07, vaeis eddy Jeonpsued, ‘psnGRR @ ceo madetasy This means that the nature of sound depends upon the relative motion of the listener and the source of sound. The change of fequency (Doppler shift) depends upon the speed of the automobile and the original frequency of the horn sound, Ultrasound reflected back from a tissue interface gives information about the depth and echo-reflectivity of the tissue. On the other hand, Doppler utilizes ultrasound reflected back from moving red blood cells (RBCs). The Doppler principle is used to derive the velocity of blood flow. Flow velocity is derived from the change of frequency that occurs between transmitted (original) and reflected (observed) ultrasound signa The shift of frequency (Doppler shift) is proportional to ratio of velocity of boo: to speed of sound and to the original frequency. It is calculated “rom the following formula: Fy: Doppler shift V = Velocity of blood F, : Original frequency C : Speed of sound Therefore, velocity of blood flow is: vybe F Further refinement of this formula is: f, veo foxC 2F, xCos 0 The original frequency (F,) is multiplied by 2 since Dopp er shift occurs twice, during forward transmission as well as during backward reflection. Cosine theta (Cos 0) is applied as a correction for the angle between the ultrasound beam and blood flow. The angle between the beam and flow should be less than 20° to ensure accurate meastrement. Cos 0 is 1 if the beam is par. velocity is observed. Cos 8 is 0 if the beam is perpendicular to blood flow and no velocity is detected. It is noteworthy that for Doppler echo, maximum velocity information is obtained with the ultrasound beam aligned parallel to the direction of blood flow being studied. This is in sharp contrast to conventional echo, where best image quality is obtained with the ultrasound beam aligned perpendi- cular to the structure being studied. Since, the original frequency value (2 x F,) is in the denominator of the velocity equation, it is important to remember that maximum velocity information is obtained using a low frequency (2.5 MHz) transducer. There isa direct relationship between the peak velocity of blood flow through a stenotic valve and the pressure gradient across the valve. Understandably when the valve orifices small, blood flow has to accelerate in order to eject the same stroke volume, This increase in velocity is measured by Doppler. The pressure gradient across the valve can be calculated using the simplified Bernaulli equation: Ap=4v P: Pressure gradient (in mm Hg) V: Peak flow velocity (in m/sec) This equation is frequently used during Doppler evaluation of stenotic valves, regurgitant lesions and assessment of intracardiac shunts. The velocity information provided by Doppler complements the anatomical information provided by standard M-mode and 2D Echo. 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This time is requica/!@ order to switch-over into the receiver mode. = Tolocate the@l2city,a’sample volume’ indicated by a small box or circle, jlaced over the 2D image at the region of interest. The ‘sapdilé volume’ can be moved in depth along the path of pw j4lundicated as a broken line, until a maximum velocit ed (Fig. 1.7) 1 cen precisely localize the site of origin of a velocity .¢ CW/ Doppler. ® Because of the t me delay in receiving the reflected ultrasound signal, PW Doppler cannot accurately detect high velo exceeding 2 m/sec. "However, PW Doppler provides a spectral tracing of better quality than does CW Doppler (Fig. 1.8) = The single crystal of PW Doppler can emit a fresh pulse only after the previous pulse has returned. The time interval between pulse repitition is therefore the sum of the time taken by the | c Fig. 1.7 Doppler signal from various levels of LV: A.LV apex. B. 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UoneBouayul Jo uidap ayy se sasea.pap Jug au ‘painseaw Bulag 43129) 221mg ueyl 4918846 aq Pinoys (4¥d) AouantRN cho mace cassie w Mv La am Fig. 2.1 Two-dimensional echo (2D Echo) views: (A) Parasternal long-axis (PLAX) view; (8) Apical four-chamber (A4CH) view impos tion of simultaneously reflected dots, builds up a real-time image on the display screen. Production of images in quick succession creates an anatomical cross-section of structures. Any image frame can be frozen, studied on the screen or printed out on thermal paper or on X-ray film, = 2D echo is useful to evaluate the anatomy of the heart and the relationship between different structures (Fig. 2.1). = Intracardiac masses and extracardiac pericardial abnormalities can be noted. The motion of the walls of ventricles and cusps of valves is visualized. = Thickness of ventricular walls and dimensions of chambers can be measured and stroke volume, ejection fraction and cardiac output can be calculated. ® 2D image is also used to place the ‘cursor line’ for M-mode echo and to position the ‘sample volume’ for Doppler echo, Kes * In the M-mode tracing, ultrasound is transmitted and received along only one scan conventionatecho (i ERE Ivs Fig. 2.2 Motion-mode echo (M-mode echo) levels: (A) Mitral valve (MY) level; (8) Aortic valve (AV) level This line is obtained by applying the cursor to the 2-D image and aligning it perpendicular to the structure being studied. The transducer is finely angulated until the cursor line is exactly perpendicular to the image. M-mode is displayed as a continuous tracing with two axes. The vertical axis represents distance between the moving structure and the transducer. The horizontal axis represents time. Since only one scan line is imaged, M-mode echo provides greater sensitivity than 2D echo for studying the motion of moving cardiac structures. Motion and thickness of ventricular walls, changing size of cardiac chambers and opening and closure of valves is better displayed on M-mode (Fig. 2.2). imultaneous ECG recording facilitates accurate timing of cardiac events. 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Architecture of valve leaflets and size of orifice. ® Positioning for M-mode image and Doppler echo. M-Mode Echo Cavity size, wall thickness and muscle mass. Excursion of ventricular walls and valve cusps. ming of cardiac events with synchronous ECG. Timing of flow pattern with color flow mapping, CW Doppler Grading the severity of valvular stenosis. & Assessing degree of valvular regurgitation. = Quantifying the pulmonary artery pressure. = Scanning the heart for high velocity signal. PW Doppler = Assessment of left ventricular diastolic function. © Calculation of stroke volume and cardiac output. = Estimation of orifice area of stenotic aortic valve. ® Localization of flow pattern seen on CF mapping. = Localization of signal picked up on CW Doppler. ® Application of spectral tracing for calculations. Wall thickness, chamber volume, ejection fraction. = The color flow map Cea awa at Color Doppler Echo PRINCIPLES OF COLOR DOPPLER * Color Doppler echocardiography is an automated version of the pulsed-wave Doppler. It is 2lso known as real-time Doppler imaging. * Color Doppler provides a visual display of blood flow within the heart, in the form of a color flow map. rightly called a “non-invasive angiogram” al as well as ce it simultaneously displays both anato functional information. = After a burst of ultrasound is reflected back along a single scan-line, as in pulsed-wave Doppler, it is analyzed by the autocorrelator of the echo-machine, = The autocorrelator compares the frequency of the returning signal with the original frequency. It automatically assigns a color-code to the frequency difference. = Analysis of several sample volumes down each scan-line and of several such scan-lines using multigate Doppler, creates a color- encoded map of the area being interrogated. ™ The color flow map encodes information about direction as wel as velocity of blood flow. When this map is superimposed on the image sector of interest, appropriate interpretation is made. ™ The colors assigned to blood flow towards the transducer are shades of red white colors assigned to flow away from the transducer are hues of blue (Fig. 3.1).sdew moy 4009 3iNdsqo PU SasNIINAAS JeUUOU WOY SI>e}aUe 40/03 Ww YBIY Uleb pue Mo] Jay ay BUNIES ‘sa;!>0IaA mo] 04) 10109 ssitu ABW mo} WIeB pue YyBry sary ay BuMas Jewnido aq isnW SBUIAS WIeS-10J0D PUR JaYY-AWDOIBA SUL = (pe “‘Biy) Aejdsip 20]09 34} S1i0}sip pue ,2s/0U punosByDeq, 10 eau 9[e2s-KeIB sa2npul YSiy 00} ule6-anssn ay Buns “aBew je>1woyeue Up SuN|g mo] 003 UIeB-anssia ayy BuMras ‘eouadaja1 jeunyons Sous ysnfaq isnt BuNRas UleB-anssiaa[ers-Kes6 ay, w ‘dew moy 10102 pos e pue abew! jeriwioreue jewindo ue uaamyag yo-apen e uayo s! eu) Jeuy au, Aejdsip jensia ayy azjwndo 03 auop 51 sys ‘payeinBue Aj46ys 51 92npsueR ayn ‘pazijensia uaaq sey dew iojo> ayy Uay\ 7 eso Busey sanding) apeus anjen Apoian 1010) on aig uonewioju} 2s Aeidsig. | oy 10 2900 jon2ads | ranted s1es0u e Buoys maya saquiey>-sno4 e Wou} anjen jesus 9OUAIS e jo dew Moy 1010) Z"E “Bid (E°€ 614) aBewW! oyda puepueys ay) Uo pasodwiiadns pue pakejdsip Ajjeriewoine aie sdew moy 10/09 ‘uo PaUAN 5] 40/03 a4) ‘pauyergo s| aBew je>WoreUe Ue eUO wo Suibew! ‘0y>e PAepuers 10} auop se MopUIM je2!de 40 jeWIaIseLed jensn 943 Ul pape|d s| saonpsuen ay sajddog anem-pasind pue oya JeuonuaAuos so rey 03 se|!WUIs | 49}4doq 40]09 Jo anbiuYDaI ay. = anbyuyray “Ve 3]qeLul pazuewuins aie ajddog anem-pasind woy paulerqo a2e jearads e pue dew Moy 40]03 e Uaamiag sarUaJayIp ay. ‘rajddog anem-pasind uo paniasqo Bulserje Jo yuedserunod 10]03 ayy st ‘Ay)20)9A YBIY ‘a4 sauljino pue,,punoue sdeum, 3! Se “@POI-10]0> Jo [esiOAed SIL “(ve ‘B1g) ‘Mo}|a4 pue uaad6 ‘auewenbe Jo sapeys YIM Waned rIesoW & se Uaas SI SIL ‘dew Moy s0j09 ayy OIU! a2DUELIeA 1002 sasoduu} -aadns 41 Wuaingin; sauioraq AD0]aA YBIY ye Moy poojg UaYM, 2461] Pue YyBug seadde san20,@0 YB1y a]1YM yep pue |jnp zeadde sanDoj9A mo} ‘S10ja!ay) saIYBUG Ajan\ssasBo1d 5196 MOY aya 02 pauBisse any 10 apeys aya ‘saseas2U! Moy POO|qJo Ay!D0J9A 943 SY spaemol pay Aemy anig, :UOUBAUOD LHW BY} YIM BdUepIOD2e UI si 19f paojo>-pau e Buoys main Jaquiey>-unoj & Woy anjen jentus jeUUOU e Jo dew Moy 10}03) y= =[EIA OF iscccsy Fig. 3.3. Color flow map of ventricular outflow tract from a five-chamber view showing a blue jet oA a | 9 A lor flow map of a regurgitant aortic valve from a five-chamber view showing a mosaic jet Fig. 3.4 Advantages ® The major advantage of color Doppler echo is the rapidity with h normal and abnormal flow patterns can be visualized interpreted. The spatial orientation of color flow mapping is easier to comprehend for those not experienced in Doppler. Conventional wave Dopplertracings have to be understood, before interpretation, Doppler improves the accuracy of sampling with pulsed- wave and continuous-wave Doppler by helping to align the Doppler beam with the color jet. This facilitates localization of e regurgitation and intracardiac shunts. ColorDoppierecho EMM ye phenomenon of aliasing, a disadvantage in pulsed- ve Doppler, is advantageous during color flow mapping. tion of color variance in the flow map is easily recognized asa mosaic pattern. tro. imitations Like all other echo modalities, color Doppler may be limited by non-availability of a satisfactory echo window or by ment of the ultrasound beam with blood flow direction. pulsed-wave Doppler, color Doppleris sensitive to pulsed epetition frequency (PRF) of the transducer and the depth of the cardiac structure being interrogated. Color Doppler may inadvertently miss low velocities if the flow signal is weak. This occurs especially if the velocity filter setting is high and the color gain setting is low. Color Doppler may spuriously pick up artefacts from heart muscle and valve tissue which falsely get assigned a color. This occurs especially if the velocity filter setting is low and the color gain setting is high (Fig. 3.5). Complex cardiac lesions may produce a multitude of blood flows in a small area, in both systole and diastole. The result, is a confusional riot of color, hindering rather than helping an accurate diagnosis. Fig. 3.5 Color flow map of the left ventricle from a five-chamber view 1owing artefacts from the IV septum‘uonenGinBas jeeojn> 2UaA Jo aai6ap ay ssasse 01 pasn ose s! zis JeUIe 02 eae af jo ones ayn Bune|n|e> pue eaxe raf ainjosqe ayy Buunseaw a jaquuey> Buynie2e1 ay Jo UoNOd je35Ip au ordn paddew yanas alum aueld anjen ayy 01 pauyuo> W ‘dn paypid aq ues moy 20}09 Yy>1Yym ordn jp Bulssasse dq paynuenb aq ue> uonerbinBaszeinalen (o}s] 1ue1161nBe4 31:3Ua299 JO UONDaIEp ayy anordLu aq saquiey> ayy Jo yypim pue yBUa} aya Uy yaonpsuen ayy areinBue 07 Aressa2au S131 jareuno9e aq ued 191 je>IGojoyred eyo Anjawioa6 pue 15 au) ‘UONEBONAIU! 10) sMOPUIM pue smaiA ajdaynuy BuIsn Aq “2012 Ja||eWUs @ sjeanai ssouDe raf awes ayy BuIULEDs ay n6u9] sy Buoje parebouarul fy ® (°¢ 614) 132 MOYINO JeINDIRUaA ya] a4 ul dew moy e sasne> uoneUBinBai 311408 ayym dew Moy Ne Ya] & U!s)]NSa1 UO}eY6inBa4 jen ‘aduUeIsUL 104 VaqUIEY Bulniarai ayy Ul dew Moy 10}0> e saanposd anjen quenGinBai yw janed Moy |eUuOU ayy Woy I9UNSIp dew-moy e se na: ayy sdejdsip 31 "saayen ayy Jo suojsal yueNGinGas ue asouBelp ue> 1a|\ddoq 40/0) « »61e| & saonpoid jo Aysanas ayy arewnse suo}sa7 jue3/6nBey wunnye yal aun urate Buymoys main XV"Id WON AAJeA [EIU 1UeI!6iNBas e jo dew Moy 10j0 L°€ “Bld (0493 Jayddog s0}09 | ussned 21esou @ 0} 10}09 ul aBueYy> Buymoys mata saquiey>-2ny @ Woy anjea 21U0B 3NOUaIS Jo dew Moy 10j09 9°E “Bld uoReqUeL0 Weag jelje1ed e sauinbai jeubIs sajddog ‘aut ajtym LoReIUalio Weag se/n>!puadiad saunbas uswe:nseaLl Jeoiworeue aouis.ynoyp Aijeanzeid s1 siyp YanamoH ‘ma1n Ja|ddoq 4002 ayy Woy S2yHO JNOUAIS ayR ainseaW O3 [API aq PINOM 3] w jeub)s sa\ddog au se jjam se aBewl 3uoreUe ayy YI0q JO Suswoo|g sasne> eae payi>je> ayy aew 03 ule6 ayy dn Buyin, ‘gale payl>je> ayp ul aBewl! ay2 Jo 3no. sdoup Ae|dsip moy 40102 ay) ‘snjnuue Jo siayea| anjen aya Jo UONe>Y!>Ie> SI B19y UY aBeut je21woreue ayy syoysip pue smays AnuaanpeUl jeub)s sajddog ayy ancidu! 02 Jaanpsuen aya Jo uoneinbuy | ‘parewinsaiapun sia6 sisouais Jo aasBap ayy asje 10 Moy Poo|q \| | J UoN>auIp ay) 0} jajjeied aq 03 sey [eUBIs ajddog 40/09 24, “(9'€ 614) moy auajnquni pue AD0}9A pasea.oul GuLAy!U6|s Mo}joX pue uaau6 ‘sueWenbe | Jo wianied 21esow e sawinsse 40}09 raf ayy “BUIMoMeU Jo aus ayy 3e 1a/ padeys ,ewey-a[pues, e saanpoid anjen eo sisoUaIS ‘MOY [PWUOU Woy IDUNSIP se ya{ JUeYNsad ay pu eaie 2nouars ay SAejdsip Aljensin | "sanjeA 2eIpse> aya Jo SUoIsa| >ijouays ayeruenb pue azije20} ‘AjnUap! Ue> Jajddog 10}0) | suo|sa7 20Ua35, | ERE C ole Ren lee ERC FA PEC Cha(gE ise ay Fig. 3.8 Color flow map of an atrial septal defect from PSAX view showing a jet from the left atrium to right atrium of less than 25% indicates mild, 25 to 50% suggests moderate and more than 50% represents severe valvular regurgitation, Intracardiac Shunts * Anatrial septal defect produces a mosaic color flow map crossing from the left atrium to the right atrium. Because of low velocity, the color map is sometimes missed (Fig. 3.8) tricular septal defect produces a mosaic color flow map extending from the left ventricle to the right ventricle across the septum. The width of the map approximates the size of the septal defect. ® Appatent ductus arteriosus produces a retrograde mosaic color flow map extending from the descending aorta to the pulmonary Echo Windows Conventional echocardiography is performed from the anterior chest wall (precordium) and is known as transthoracic echo. Echocardiography can also be performed from the esophagus which is known as transesophageal echo. For transthoracic echo, the subject is asked to lie in the ion on his or her left side with the head semirecumbent pos lightly elevated. The left arm is tucked under the head and the right arm, the right side of the body. This position opens the intercostal spaces through which echocardiography can be performed, while most of the heart is masked from the ultrasound beam by the ribs. Better images are obtained during expiration when there is least jr-tissue’ interface. Ultrasound is transmitted from a transducer having a frequency of 2.5 to 3.5 MHz for echo in adults, This frequency is used to study deep seated structures because of better penetration. A transducer frequency of 5.0 MHzis suitable for pediatric echo, since the heart is more superficial in children, Ultrasound jelly is applied on the transducer an} the chest at the site of an “echo window’, s along placed on“wmnipsesuiag ~ apuauanay6iy ~ Jem souBIsog uimdas a) ~ ajunuan yer - aAlea [eI winne yay - anjenaquoy - euoe jewixorg — USSSSSIMTIUIS TOPMOTSTYOUSPIEMOY SUIS uon2au1p 0p LEW 258ds Uip= PUL SHPS EUISTS YS uontsod soonpsuelL (zy “B1s) (AIA XV1d) MaIA Sixy-Bud7 jeuTaIseIET euiashydwa Kseuowing — Ayuuoyap jen say — Ausaqo piqiow aianas - Suonendis Bujmoljo} yp Ul Wwiojad 01 yndysip Ajje>1uyra aq Kew OYDa>!DeIOYISUeLL yansasqo auies ayy Aq suo|se320 1Ua1ayJIp UO 40 sianiasqo yualayip hq pauuoyiad salpnas yim pasedwuod aq ue) sabe oyra pazipiepuers 7 @ ‘SMOpUIM O43 ‘Aydeiboipse0y29 Buinp pasn ,smopuim, piepuers ay, Lb “Bd leoidy reisooqng, jewosered jewaysered wer Bry jeweysesdng -sBun| pue squ hq punosexyin jo uondiosqe 10 a6euu Jo Bupysewi yonuanoyaim ‘poob $1 smopuim wow sanem punosesiin Jo uoneNauag * Suosea oma 10} 1ueuiodu a1e smopulm piepuers {Jeuiaiseidns — ourasered wu -creso3GNs = TedW - v (PUIG yay — ‘ore asa4 I (L'p'614) ,SMOpUlM 04>, palje> axe YDIYm “aonpsueN yz a2e/d 01 pasn aie jjemysay> ovayue ayy UO SUORe>0| PepUeIS w SMOGNIM OHD3 GUVGNVLS ‘aBew ays auny-auy, 03 (as wpoppAUE 10 asyMy}D0)9) pareyou pue saIaIUL Jo aIMIoNNS 24} sNd0J OU} BUG 03 “(KjJoHaJUI 40 KjJoUadns) pay aq UeDI) “saBeUuy 049 yUaLayIp 104 'UoRDaIIP pue uone20} Jo sua} Ul ‘pauon|sod Aiqeuen s! Jeonpsuen ai ‘smajA O4>a SNOLeA Bu!U}eVqGo 404 'YONDa1Ip 1>a1100 au) UL NAME ©2 49p10 ur ‘apis 3u0 Uo 0p 10 aul} 22u0s9)01 8 sey JaaM a1e smopuym jeride pue jewiarsesedehowindowd” i ED RVOT PV PA Fig. 4.4. PSAX view: pulmonary artery (PA) level = Bytilting the transducer on an axis between the left hip and right shoulder, short-axis cuts are obtained at different levels, from the aorta to the LV apex (Fig. 4.3). ® This angulation of the transducer from the base to apex of the heart for short-axis views is known as "bread-loafing’, Short Axis Levels (Fig. 4.3) Pulmonary artery Aortic valve level Mitral valve level Papillary muscle Left ventricle. Fig. 4.3 The parasternal short-axis (PSAX) views yaune = Most echo studies begin with this view. It sets the stage for subsequent echo views. Pulmonary Artery (PA) Level (Fig. 4.4) Parasternal Short-Axis Views (PSAX Views) (Fig. 4.3) Structures seen: = Transducer position: Left sternal edge; 2nd-~4th space = Pulmonary artery = Marker dot direction: Points towards left shoulder (90° clockwise = Pulmonary valve from PLAX). = RVoutflow tract.ded sara xvsd £*¥ "6 omen Jana} (We) apsnus Aa (e-.21) lem souaiuy (o£) Wa [e1patuosarsog (Ge) Wd esarejouanuy tuees seanonas (£61) 1227 (Wd) a/2SNY) AuoyItdog winidas seinsuqUa,A « syoyea| anjen ex = @2YHO BAIEA [EUW w suaas saampnas winuge ya] puey6iy ajpujuan ya] puewy6y = (9°p 614) J2A27 (AW) aAjDA [OA suvas saunjonays ‘ap|Noys Ya] spxeMOy SIUIOd :UOR2aNIP OP JEW pen MOyINO AY = jeay 8uj Jo xade :uonisod yeonpsuelL anjea pidsnaul a» wimdasjeueaiu) a» (g'p *614) (MaIN ASW) MaIA JaquIEYD-p [e>I1dy cannes sdsn> anjenanioy ‘auidns a1ow salj pue Lonisod jesare} fier seinionne yal aup Woy sprenmyBu y>eq suum rafqns ayn ‘smaia jeridesoj = (71-26) wmdas Ala (6-29) lem s0uajut a (5'y 615) [2427 (Ay) aAJOA 2nIOy [ano] (AWN) anfeA JONNU:MOIAXYSE OP “Bid [P89] (AY) anjen aRu0R=MaIA XYSd $b Giaide Easy po en | = Transducer position: as in A4CH view. = Marker dot direction: as in A4CH view. Structures seen: As in A4CH view. Additionall = LVoutflowtract = Aortic valve = Proximal aorta. socal ies = For subcostal view, the position of the subject is different from that used to obtain parasternal and apical views. = The subject lies supine with the head held slightly low, feet planted on the couch and the knees slightly flexed. = Better images are obtained with the abdomen relaxed and during the phase of inspit mn. Transducer position: under the xiphisternum = Marker dot position: points towards left shoulder. Fig. 4.8 Apical 4-chamber (A4CH) view tricuspid valves Apical 5-Chamber View (ASCH view) (Fig. 4.9) ® The ASCH view is obtained after the A4CH view by slight downward tilting of the transducer. The Sth chamber added is the left ventricular outflow tract (LVOT) Structures seen: As in A4CH view. = The subcostal view is particularly useful when transthoracic echo is technically difficult because of the following reasons: ~ Severe morbid obesity ~ Chest wall deformity ~ Pulmonary emphysema. © The following structures are better seen from the subcostal view than from the apical 4-chamber view: ~ Inferior vena cava Descending aorta Interatrial septum Pericardial effusion. 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UORISod sua ‘spiom 194.0 Uw ‘Apog aus jo apis 443} aur Bugle sary we ya} ay) pue peay aug vepun payam s1 we 34611 ay, “apis 46H 34a Uo UORISod quaquundasjuias aya Ul s9y):>a/qns ay) mala jeUsesered 1611104 mala jeusayseseg 1y61y “Argue Aeuowing = euoe Bulpusssy suaas semanas ‘mel 149] SP1eMO} SJULOd :YONNZauIp IOP JEW w ‘ytou |ewayseadns :uo}ysod seanpsuedl “MOpUIM OY>a S14 UO BuLLe|q OU ney uonedidsay Jo aseyd ayy pue $63] 40 sue Jo UoN|sod ay yal ayR spremos AnYBIIs pareros s) peay AUL “stapinoys ayy Japun mojtd e BulDe\d kq PapuarxaiadAy 429" YL YRIM ouIdns say] a>a{qns ays ‘malA jeUIarserdns 104 MaIA eurarserdng,Useful supplement to transthoracic echo, which cannot examine the posterior aspect of the heart. Structures such as left atrial appendage, descending aorta and pulmonary veins can only t visualized by TEE. Disadvantages It is a semi-invasive procedure which is uncomfortable to the patient, more time consuming and carries a small risk of serious complications such as oropharyngeal or esophageal trauma, cardiac arrhythmias and laryngo-bronchospasm (Table 4.1), ® Itrequires short-term sedation, oxygen administration and ECG monitoring since, there are chances of hypoxia, arrhythmia and occur, = TEE is contraindicated in the presence of active bleeding or coagulopathy, esophageal abnormalities, unstable cervical arthritis and poor cardiopulmonary status (Table 4,2). = The transesophageal echo (TEE) views are significantly different from standard transthoracic echo views. Novel TEE images require a comprehensive understanding of the spatial relationship between cardiac structures. ieee ‘Major + Esophageal rupture or perforation + Laryngospasm or bronchopasm + Sustained ventricular tachycardia Minor nate Absolute + Uncooperative patient + Poor cardiorespiratory status + Esophageal obstruction + Tracheoesophageal fistula + Active bleed or coagulopathy Relative ~ Lage esophageal varices {Por esophages surgery * Unstobleceniatarthits (Lanta dstcation It would be beyond the scope and against the philosophy of this book to understand and learn these views in detail. Nevertheless, the indications for TEE are duly mentioned at appropriate places, in several chapters of the book. Ta Three-Dimensional Echo * Two-dimensional echocardiography (2-D echo) provides a 2-D view of the 3-D heart. Therefore, a series of integrated 2-D views are required to mentally construct a three-dimensional (3-D) image of the structure of the heart. ™ To accurately perform this task, knowledge of the precise relationship of each 2-D image with the other is vital but not always feasible. ® For instance, while quantifying cardiac chamber volume and function with 2-D echo, one makes certain assumptions about cardiac geometry to apply specific formulae for calculations. © Aschambers get distorted in shape by infarction and remodeling, these geometric assumptions lose their accuracy as do the calculated values from formulae.“uoIsnyiad jeipies0hw 1 01 Bulujeviad uoReWojU! aanerauend se jjam se aanewenb anueyua 03 Arijiqe ay2 sey GulGews ysesu0d jerpser0KW ‘uone|nsdesua pidi| Aq 10 uoNeaiuos jentueyraton>a|a Kq 194R19 paonpoid ase y>iym sajqgnqousiw se sisixa iuabe yseNUOD ay) w “uoysnj220 reuoi0> 03 parejar si2aJap UoIsnyJad 40 Moy poojq jeIp1eD04wW paanpad J0 Sea.e ayeauljap Ajayeino>e 03 "\uabe yse1yUOD >1UoseRIIN Ue Jo Uonediidde ayp sanjonuy AydesBoipses0yra isenUo> je1pses0KWy aw yaa ase2qU05 JeIpser0KW Bunsa an euare Je>1Ul]> ayp UI Ajanisuarxa pasn Bulag 03 J003 yoseasas e Ajos9Ui Bulag wo anow 0} jenUaIod ayp sey aiyaiay O42 G-2a14, w a6ew) eun-|ea1 hq parejdas aq UoOs |j1m Uo!INI3SUO>Da1 @GeW BUIYJO anisuaiUl-ioge| pue aUUN ‘sanjona ABC|OUY>Ia Jeonpsuen pur saimew aiemyos pue aiempiey saindwo> sy “uonysinb>e ‘@6ew! 2e1p1e> arajduwoD 40} pauinbau awn ayy aonpe1 03 jenuaiod aya sey (0429 G-€) AydesBorpies0y>a |euolsuaWp-2914, = ‘sdiysuonejas Jeamanas jo uoneeidde ayp aoueyua o4 ‘sa6ew! a4 30 uoNe101 Aq suonsafoid snouen wo pamaja aq ue> oye G-€ 34, = “saseasip ueay Jeyua6uod ur paniasqo sdiysuonejas jemonas xajdwo> pue sa\ddog 40109 Aq dn paypid syaf yuenGinGar 2uUa>Da 'so2y0 anjea 2ROUars je>1IaWUUASe ANAS 03 |NYasn KjJe|N>;Ued s| OYDa rE uaUUSsasse a1NAWNjOA JeIN>|;NUAA UI LONeDI|ddesy sopIsag w ‘woe>ynuenb 403 sasnaanuis >e1pie> yo adeys 2y2 Inoge UoNduinsse ayn3WOa6 GuIyewW Jo UOsindwo> ayy pue sauejd abeu G-2 Jo op annsu0ra1 CE anjJuB0> 10) pau up sareingo (0422 G+€) AydesGorpies0y>e jeuo!susWIp-aa1y,GUE roast cosy * Patients of acute coronary syndrome with both abnormal wall motion and abnormal perfusion have worse event-free survival when compared to patients with normal myocardial perfusion. = Inthe acute setting, contrast imaging can identify patients with the “no-reflow” phenomenon which is characterized by lack of recovery in microvascular perfusion despite successful opening of the occluded coronary artery by intervention or thrombolysis. The long-term prognosis of these“no-reflow’ patients is adverse and they are observed to have significant deterioration in regional and global systolic function at follow-up. = Inthe chronic setting, contrast imaging can also identify viability of the perfusion bed subtended by the occluded coronary artery, when contrast injection into an adjacent coronary artery produces enhancement. This is clinical relevant because revascularization after myocardial infarction results in improved function only when viable myocardium is demonstrable. Finally, during exercise or dobutamine stress echocardiography, real-time assessment of myocardial perfusion improves the sensitivity of the test in detecting angiographically significant stenosis, compared to wall motion analysis alone. Tissue Doppler Imaging ® During day-to-day echocardiography, left ventricular function is routinely evaluated by two-dimensional (2-D) and motion-mode (M-mode) techniques, However, visual evaluation of LV function using these modalities suffers from the limitations of being significantly subjective and provides only semi-quantitative data. Moreover, visual assessment has limited ability to detect subtle changes in LV function and in timing of wall motion, throughout entire systole and diastole. Tissue Doppler imaging is a more objective and highly quantitative method to accurately assess regional and global left ventricular systolic and diastolic function. This technique can measure a variety of myocardial func- tional parameters which include tissue velocity, acceleration, displacement and strain rate. Tissue Doppler imaging has been used as a diagnostic tool in specific situations including assessment of myocardial ischemia, evaluation of diastolic dysfunction and differentiation between restrictive cardiomyopathy and constrictive pericarditis. Myocardial ischemia is diagnosed by velocity imaging as reduced systolic ejection velocity and higher postsystolic shortening velocity. Findings on strain imaging are reduced systolic shortening along with systolic lengthening. Heart failure with preserved ejection fraction (HFPEF) accounts fora significant chunk of heart failure patients particularly in the elderly population. These patients have isolated or predominant diastolic heart failure allowing for the fact that ejection fraction (EF) may fail to identify mild systolic dysfunction. ‘Additionally, there are patients who do not have heart failure but have impaired diastolic function such as patients with systemic hypertension and diabetes mellitus. The characteristic findings in diastolic dysfunction observed by tissue Doppler imaging is reduced early diastolic mitral annulus velocity, which correlates with peak LV lengthening velocity. This abnormality is observed across the entire range of diastolic dysfunction from impaired relaxation (reduced E/A ratio) through pseudo-normal filling (normal €/A ratio) to restrictive filling (increased E/A ratio). Patients with constrictive pericarditis have normal systolic function and ventricular relaxation while those with restrictive cardiomyopathy have impairment of both parameters.apoUIUaAA yal JO [ABT “€ AIBA Jesatu JO [ABT °Z AJWA 214408 JO [AI “L 'sjana| ¢ aay Ie BUIPIODa1 aPOW-W axeW = “Mala sixe-Bug] jeusaysesed ay2 YM Wes we :5Mmo}jOy Se st Apnas AydesGoIp1es0439 pajleiap pue 2ewarsks e 40) 2newayrs paise66ns y w SSUO|SUAWIP [WOU YrIM seIILUeY 3g 0 pue saBew oysa jewuou ayerraidde 0} 1uewoduuy 5131 ‘240j9194L JewuoU ayp Jo 1461] ayy UI pamaA aq Ajuo Ue> |EWUoUge SUL w ps pue a2uaniadxe s1y 02 jeuonsodoud pue yuapuadap soreiado AjYBIY 51 0422 Ue JO ‘Aayjenb ay pnys aug pauuojiad sey oym uodn Ajleay spuadap 0YDda WOH) PaALaP UOREWHOJUI Jo an|eA ayp ‘SS9]IYVEAIN w “sajdiound Je21Bojo1sdyd pue si9ey je>IsAyd ajduyjs uodn paseq axe sainzeay oypa Auewiaouls ‘puersiapun 03 fsea ayinb s| Aydei6orpie20423. = “uopoury je>160)015hyd ynoge sn [jay saBew! 2wWeUXp ‘jJeIap je1WoIeUe apiaosd sowie YM ueay a4) INOge UOReWOJUI jeuonDUNy PUe yeunronays jo juNoWe jenueIsqns e sapinoid WesGoIpieDr0y>9 34. = oe NOILVLSUdYaINI OH): sanjea pue smal, [eWJON Eee ae 1 | } ‘s1Da{qns jewuou ana pue spipsesuad aansiysuos yam asoun ‘siuaned assy uaamiag saniojan Bury jeawisuen UL deyaro jenuersqns s} ait seasaym Aypedofwolpse> aanouasei Jo aane>|pul a10W St AyD0/@A snjnuue jeiw >10IseIp Kjsea panpel ‘aspba ionaasessr™ © Rotate the transducer by 90° clockwise. Angulate it from the base to apex to obtain short-axis views at these 4 levels: nonary artery level 2. Aortic valve level 3. Mitral 4. Papillary muscle level. Go on to the apical 4-chamber view. Measure ventricular volumes in systole and diastole (to assess LV systolic function) Turn on the color flow mapping for abnormal flow patterns due to valvular diseases or septal defects. Place the pulsed wave (PW) Doppler ‘sample volume’ in the LV cavity at the tips of MV leaflets in the diastolic position (to assess LV diastolic function). Angulate the transducer anteriorly to obtain the apical 5-chamber view. Place the’sample volume’ in the aortic valve to obtain the flow velocity integral (FVI). Calculate the stroke volume and from it the cardiac output. Use continuous wave (CW) Doppler to scan the apical chamber view for high velocity signal, if abnormal flow is bserved on color flow mapping. pulsed wave (PW) Doppler to localize an abnormal flow seen on color flow mapping or a high velocity signal picked on W Doppler. Use other echo windows (subcostal, suprasternal and right parasternal) as and when indicated Rotate the transducer by 45° anticlockwise and obtain the apical 2-chamber view. EES ae a must be borne in mind that normal value ranges of derived dimensions, depend upon several factors. These factors include height, sex, age and the level of physical activity, wean A EA Normal values are higher in these subject — Male gender ~ Tall persons ~ Trained athletes ~ Elderly patients. Therefore, correction for these factors is made by indexing cardiac dimensions to body surface area (BSA) using the formula: height (cm) x weight (kg) BSA(m!)= ry = Normal dimensions are estimated from small populations of ‘average’ persons and may not apply to unusually small or tal subjects, to the elderly or to athletes. ee = Some findings on echo may be normal and must be carefully understood to avoid overdiagnosis of heart disease (Fig. 5.1). HaQ 1.5.1 Normal structural variants seen on echo: ‘A. Moderator band in right ventricle. B. False tendon in the left ventricle. C. Mitral annular ring calcification D. 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Dimensions of proximal aorta from PLAX view Mitral Valve Level (Fig. 5.6) AML D-E excursion 20-35 mm AML E-F slope 18-120 mm/sec Parasternal Long-Axis View (PLAX View) Epointto septum an Note The PLAX view is used to measure the dimensions of the aortic sinus of Valsalva, aortic root and the anterior aortic swing - The diameter of the aortic rootis measured between the leading (Fig. 5.4), edges of the anterior and posterior aortic walls. Aortic annulus 17-25 mm ~ Thediameter of the left atrium is measured between the leading Sinus of valuaive 23-36mm edges of the anterior and posterior atrial walls. Sinotubular junction 18-26 mm t Aortic root (tubular) 20-37 mm vs terior aortic swing 7-15 mm Aortic valve orifice area —-2.5-3.5 cm? M-Mode Scan PLAX Aortic valve level (Fig. 5.5) Aortic root diameter 20-37 mm Aortic cusp separation 15-26 mm LvPw Left atrial diameter 19-40 mm Fig, 5.6 M-mode scan PLAX view; mitral valve levelWd) 19YeI| [eI OWDISOg 7 Clwy) 29ye9] Jew souaruy “1 ss]ayeal Z JO SIS|SUOD AAA [eI AY, a AIPA [RU S3ATVA TWWHON AU Zee WARE By-ZE (2as/u € | Ueawl) ras/u 81-60 yndino 2e1p1e> BUIN}OA a{ONS Apojan mono 240y (mata HOSW) MeIA Jaquieyd-s [eridy (pas/ui (0 ueaw) pas/w £0-€'0 (pass 610 ueaw) w/|W SL FSB (Maia HPW) Mal, Jequiey-p [erIdy wud o-y ww op-6L ww Ze-02z (pas sz ueaw) 2as/WO'L-S'0 ww $181 Aypojen moyul pidsnouL AOIaA Moy! [AU Dy}0XSAS-pua a~UN|OA AT 21J02SeIP-PUB SLUNIOA AI AdYHO aAIeA eI w [2n27 anjOA [DAI Jayswelp [euye ya] UosuaWIp 1001 HOY w 12037 2A]OA 2104 Aypojan moyino Aseuowind sayawielp Aiaue K1euowlInd a Janay Aiauly Asouow)ng (MIA XWSd) MIA SIXW-}40Ys JeUsarsesed Sanjen pue smain |eWON sajpnis je11as azedwo> 04 sap10 24} Mojaq asn{ painseaw ase a|>LIUaA ya] aY2J0 SUOISUAUUI >Yy| — “suoise2d0 1uasayip UO pauuoyiad jena] prepuers siy, — 39Yed| [esIW JO}NaIUe BYR Jo aBpa aay, 310N 9652-08 uon>ey uonzafe A7 %6Sb-0€ Buluarsoys jeuonrey 07 wu s > SSOUH>IYD [TEM-381) AY wu €2-2 uoisuawip jeusaiul Ay ww 2-2 (as3A7) 2H03shs-pua sarowierp A wi 75-98 1SeIp-Pua La}WLeI Ay ww p16 (2110354s) uojsin9xe jem 401129504 wu 6-9 (2110284s) uoysindxa jerdas-pj wu LL-9 Jem 4OUaISOg wnw Z1-9 joxseip) ssauyoiua jerdas-p) (£5 61g) Janay sojnaygua, ana] sejnouauen ‘main Xd UeDs apOU-W £°S°BIdFig. 5.8 M-mode tracing of the mitral valve © Motion of both the leaflets is visualized by M-mode scanning from the PLAX view. ® The excursion of the AML can be divided into the following waves and slopes (Fig. 5.8) E Anterior and posterior motion during entire diastole. D-E slope : Anterior motion during rapid diastolic filling. E-F slope : Posterior motion during end-diastolic relaxation. Aawave Anterior motion during atrial systolic contraction )e amplitude of motion of the PML is less than that of the AML and in an opposite direction. Tricuspid Valve Lricuspid valve consists of 3 leaflets: 1. Large anterior leaflet (ATL), 2. Snail septal leaflet (STL) 3. Tiny posterior leaflet (PTL). ® The ATL motion is visualized by M-mode scanning from the PLAX view in the right ventricle, anterior to the IV septum. © The excursion of the ATL is very similar to that of the AML of mitral valve described above (Fig. 5.9), | Fig, 5.9 M-mode tracing of the tricuspid valve = The STL is only recorded when there is dilatation of the right ventricle or clockwise rotation due to emphysema. = The amplitude of motion of the STL is less than that of the ATL and in a direction opposite to ATL excursion. = The PTL is not visualized on M-mode tracing. Aartic Valve «The aortic valve consists of 3 cusps: 1. Anterior right coronary cusp (RCC) 2. Posterior non-coronary cusp (NCC) 3. Middle left coronary cusp (LCC). The RCC and NCC are visualized by M-mode scanning from the PLAX view (Fig. 5.10). = During systole, the anterior and posterior cusps move away from each other and towards the anterior and posterior aortic walls respectively. = This creates a box- of a parallelogram. * During diastole, the cusps oppose to forma central closure line in the aortic lumen. The closure line is equidistant from the anterior and posterior aortic walls. ke systolic opening of the valve, in the shape‘anjen A1euowind ay jo Suen apow-W Li's “Bl “wreaq punosenin ay3 01 anjer au Jo AyinbI}qo 0} anp pazijensia Ajuanbayul aie sdsn>yyBu pue souaiue ayL “(LU'S 614) dsm (yay) souarsod ay si mata xvid ay woy Bujuuess apowl-w Aq papiopar Aljensn dsn> A|UO By, ‘dsn>ay6iy - sno 1ovaquy - dsno (4Ja)) 1ouaysog — sd5n9 € JO 5}S}SUOD anjen AJeuoW|Nd ay, anten Ateuowing anja 2NUOR ay Jo BuDeN aPOW-W OL's “BIS dno Areuosoouon, uy esnsoig voRow JoHasod yo\seip : adojs 4-3 - uonow BuIsop syorsés : adojs3-a - ajoysks Buyinp aajeauado : adojsg-> - fae Sungedo onow Bujuado 203s: adojs 3-g — ub s (1.5 B14) sadojs Buymoyjoy aya ou Papinip 36 Je 3ayea| AeuoW|nd so1193S0d ay Jo UOISINDXa ay, = Ge S8N BA Pur SMAI, JEULION |Ventricular Dysfunction ‘Assessment of ventricular function, particularly of the left ventricle, is the most common and the most important application of echocardiography. Presence of left ventricular (LV) dysfunction is a reliable prognostic indicator in all forms of cardiac disease. It has important therapeutic implications and many a time, clinical management is altered when an abnormality of ventricular function is detected. Ventricular dysfunction can be classified as: = Left ventricular systolic dysfunction~ = Left ventricular diastolic dysfunction- = Right ventricular dysfunction. Sm SUED ene hea eee In order to understand LV systolic dysfunction, it is important to know the normal indices of left ventricular function. Normal Indices LV wall thickness in diastole = 6-12 mm interventricular septum (IVS) = 6-11 mm LV posterior wall (LVPW) LV wall excursion in systole = 3-8 mm interventricular septum (IVS) = 9-14 mm LV posterior wall (LVPW) icutar Dysfunction i BEES nal = 354.5 mlat end-systole (LVESV) © 85.415 ml at end-diastole (LVED\ Fractional shortening 30-45% (9% change in LV dimension) LV ejection fraction (9 change in LV volume) Echo Features of LV Systolic Dysfunction M-Mode LV Level * During ventricular systole, the interventricular septum (IVS) and the left ventricular posterior wall (LVPW) move towards each other. = The amplitude of this motion is reduced in the presence of LV systolic dysfunction (Fig. 6.1). Lvew Fig. 6.1 M-mode scan of the left ventricle showing: A. Reduced excursion of IVS and LVPW; B. 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B18 SUOISUOWIP AT = ‘(Md 1) |]eM 1onaysod ay Jo IY) 01 (SAI) LMdas ayy Jo Guru jeipies0pua ay) Woy Uaye} aie SluaWaINseAW = sdn yayeE] (AW) aAIeA JENN Jo JaAa| ayL I “(XVId) MAIA SIXe-BUO} Jewarseied ay: ul Buen apow-w aup UO painseaw are (GQ3A1) ajo seIp-pua pue (GS3A7) a]01SAs-pud UL UOISUBWUIP |EUsaIU! AT» (a) ajorshs (>) aorseyp ma. HOY Ha) IOSKs (y) BOASEIp=MaIA XT 4aqaweIp A] WO Buruayoys jeuoNrey Jo UONeUIWAIIG Z°9°614 fseaapew ours ff| Fig. 6.3 Simulation of left ventricle cavity as an ellipsoid, Major axis (L) is twice the minor axis (D) Lv volume = D* by the cubed equation The normal range of ejection fraction is 50 to 75%. Reduced ejection fraction is an indicator of LV systolic dysfunction. However, the ejection fraction also depends upon ventricular loading (preload and afterload). The normal diastolic thickness of the left ventricular walls, that interventricular septum (IVS) and left ventricular posterior wal (LVPW), is 6 to 12 mm. Walls thinner than 6 mm indicate to stretching due to cardiomyo- pathy or scarring due to myocardial infarction. Walls thicker than 12 mm indicate the presence of left ventricular hypertrophy. Normally, the walls should thicken in systole. Reduced systolic thickening of walls indicates presence of LV systolic dysfunction, either global (cardiomyopathy) or regional (myocardial infarction). 2D Echo A4CH View 2-Decho canalso be used to estimate LV volume in end-diastole (LVEDV) and end-systole (LVESV). Verticuaroystunction ERR ® This is done by tracing the LV endocardial borders of a systolic and a diastolic LY frame while the software of the echo machine calculates the LV volumes. * From these volumes, the ejection fraction (EF) is calculated: _ LVEDV ~LVESV EF LVEDV 100% = The above method of calculating LV volume relies on manual tracing of the ventricular endocardial outline. Alternatively, LV volume can be calculated totally by the computer using the Simpson's method. = By this method, the left ventricle is divided into 20 sections of equal thickness. The computer takes multiple short-axis slices at different levels (Fig. 6.4). The volume of each slice is the area multiplied by its thickness. The sum of volumes of all sI volume of the left ventricle, Area of each slice = n(D/2P Dis diameter ‘esis the Fig. 6.4 Estimation of the left ventricular volume by Simpsons method; DisLV diameterquaurwioid ey] 1n9s0 Kew JuaWaINseawL Ul $10119 MdAT PUP SALI saDe4uns |eIpaedopua uaeMIaq U9xe} a1e SUOISUALLIP [PUIAIU! 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This should always be borne in mind. = Measurement of LV dimensions can be unreliable in the, Presence of abnormal wall motion due to infarction and abnormal septal motion due to left bundle branch block or RV volume overload. = Reduced LV systolic function is usually but not always associated with increased LV dimensions. = For instance, a large akinetic segment of the LV wall following myocardial infarction may impair LV systolic function but LV dimensions may be within the normal range. ® Anexperienced echocardiographer can often give a reasonably good visual assessment of LV systolic function from the PLAX view, without actual measurements. = However, this rough assessment may be unreliable for serial evaluation of LV function and when LV volumes critically influence the timing of a surgical intervention Venwiculordystunction (i ERAS There may be interobserver and even more surprisingly, intraobserver variations in the measurement of LV dimensions, LV volumes and therefore in the computing of fractional shortening and ejection fraction Often these are due to variations in the frame frozen for calculations and in the delineation of the endocardial surface. While calculating LV volumes, certain geometrical assumptions are made about LV shape which are not always valid, particularly ina diseased heart. This often occurs in regional LV dysfunction. Post-infarction LV remodelling increases LV sphericity and causes alteration of the normal ellipsoid shape of the left ventricle. When assessing LV systolic function, one must allow for effects of volume loading and drug therapy. Fluid overload and antiarthythmic drugs with negative ionotropy may further impair LV function. In presence of mitral regurgitation (MR), ejection fraction (EF) may be normal despite reduced contractility of the LV. This is because the left atrium offers less resistance to ejection than does the aorta. Conversely, in presence of aortic stenosis (AS), ejection fraction (EF) may be low despite normal contractility of the LV. This is because the left ventricle has to overcome a high transaortic resistance during ejection. Therefore, after surgery (valve repair or replacement) for MR, the EF falls and after surgery for AS, the EF rises. The calculation of cardiac output from peak aortic flow velocity by Doppler is invalid if the aortic valve is regurgitant or stenotic, because of increased aortic flow velocity. The measurement of aortic valve diameter (D) at the aortic annulus is not only difficult but any inaccuracy is magnified, since the D value is squared.sarepaid uayo pue saseasip Ueay Jo AaN1eA e Ul S1ND30 xej—1 ST Argo Aujiqeu! ayy 10 uonsunyskp >yoseIq ‘uonUaNe Jo [ep yea e pareme sey uonounyskp >10ISeIp AT ‘s1eOK UB) Uw Tore CPOs Mk Aue Ene een “Aypedokworpie> pareyip uetp Joyres siIpreD0KU ouBeip ayy Joney uoNenbinBas jentws Jo Uo|ssas5a1 pue ides Buymoys soyra [eH25 « “UoISHaAU! BALM | qu erpieskypey Bunsas Buymoys 933 UR PUL SSOUIH! aIUGE} JO Aioxsiy WOYs @ a1e spIp1eD0Kw Jo saimeay BuReHUDIEYIP OY, w “winipies0ku atp Jo uonewueyu! 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SIIPIED0AW siupserohw ainry yo vonouUny 7 Jo jaULaAciduut suawanoidut > pasned aney Ae Yin ‘ainjtej Ywedy Jo waunean Grup sae pantasqo aq Kew Uonsunyskp 3H}015As JOUNLY KUO AEULLIS ‘Bunsay ssans 40 UoNJexe Aq 3no 1yBNoAG Ng S94 ye snoingo aq 10U Aew UoDUNY >HoIsks Jo SANeUUOUe BANS = ‘Adexayy 01 asuodsas ay osje ing aseasip axa jo Asoysiy jeameu aun ssasse A]UO YOU UPD sweIBOIPIEIO4>@ |eHES = “Ayyedoxuiorpie> pareyip Jo sisoubelp ay 10) eUaIUD JUE}OCLUI Ue s} UONDUNYSAP >H}OISKS Aj] JO a2UaSAId = ‘AsaBins @nmn3@1109 Jo Burtuy ayy ul ajo4 yerana> e skeid uondunyskp 21}0154s Jo 1asUo “LeU DNSOUBOId & Bulag sapisag = “‘uon2unyskp JOASAs 7 asNeD AjaeW|N |NM UNYs 1Y6H-01-Yya} e 40 UONeUH -1nB21 Je|NA|eA 03 ANP aj>1LNUAA 49] B41 Jo BUIPEOLaAG aLUN|OA “aseasip ueay antsuariadAy Jo a6ers paresuadwio2ap yp Jo asUO at sere>1pUt 4! ‘UoRDUNYsAp >1}0ISks A sdojanap Aydoniaddy seinounuan ya] yum uoisuariedAyjojuanede usyM ‘AiaBins ssedhq K1euoso ay ainpacoid uonezueinasenas e Jaye auio>1no 110d pue ares jealains 1aMo} @ aney santjewouge UoRoW Jem or UORIppe U! LON>UNyskp DHOISks A] BACY OYM aseasip AydUse A1eUOI0> Jo sjuaneg w# “uonert|duit 3nsouBoud asianpe ue saliie> aseasip deipie> Jo wo} Xue UI UON2UTYSKP DOISkS 7 Jo @uasaid ay. w uonounyskq >1]03SKs 7 JO a2UedyIUBI: SIIPIEDOAW JeuIA arndy ~ aseasip jeipierocw rewg a” snsousue smanp iuaied ~ aDayep jerdas sejnsuuan, ~ qunys 16-01-4397. uoneu6inbar nioy ~ uonew6in6as jen — PeOHaAO awUN}OA AT = SISOUaIS anjen IL0y uorsuariaday aiwiarshs PeOLaN ainssad AT we aseasip jassan ajduy ~~ sioiejur jes ajdnjnyw — ueyul abe} ajbus — aseasip kiayie A1eu010>,_a ue sasne> UDUILLOL “UORDUN|sAP 21}0354S AT ur ayeUIUIND AjaIeLUNIN aseasip de1pseD Jo SLUIO} |e ‘KIJoINIeId UONDSUNJSAQ d1}03sks A130 Sdsne> cae won2unysha se;n21n49, | concen RY(IRENA ccro macesay the decline in LV systolic performance. A recently introduced terminology is heart failure with preserved ejection fraction or HFPEF. Normal Diastole Diastole is divided into 4 discrete periods: 1. Relaxation phase: AV closure to MV opening (1) 2._Early rapid filling: MV opening to end of filling (2) 3. Diastasis phase: equilibration phase (3) 4. Atrial systole: active atrial contraction (4) and 2 comprise the phase of myocardial relaxation which is an active energy dependent process. 3and 4 comprise the phase of myocardial distensibility which is a passive stiffness dependent process. Therefore, there are 2 patterns of diastolic dysfunction: 1. Slow-relaxation pattern 2. Restrictive pattern Echo Features of LV Diasto! Dysfunction M-Mode MV Level = Motion of the anterior mitral leaflet (AML) during normal diastole has a characteristic M-shape (E-A pattern). In the presence of LV diastolic dysfunction, AML excursion is diminished, A wave i taller than the E wave and the E : A ratio is reduced. These abnormalities occur due to stiffness of left ventricle and greater atrial contribution to ventricular filling. These signs are neither highly sensitive nor specific for the Presence of diastolic dysfunction. et ‘ VenvicularDysfuncion i EAI! 2-D Echo PLAX View =) 2-D echo cannot directly assess LV However, it can detect certain associated abnormal ventricular hypertrophy, wall motion abnormality, myocardial infiltration or pericardial thickening, ®) Coexistent abnormalities of systolic function may be detected along with LV diastolic dysfunction. (@) The diastolic flow pattern from the left atrium to the left ventricle can be assessed by pulsed wave (PW) Doppler using the apical 4-chamber view with the sample volume in the mitral inflow tract. This provides a good quality spectral trace. Inthe normal heart, the transmitral flow pattern (Fig. 6.7A) shows two discrete waves: stolic dysfunction. ies such as Ewave —: passive early diastolic LV filling Awave —: active late diastolic LV filling E:Aratio : greater than 1 When myocardial relaxation is impaired due to LV hypertrophy or myocardial ischemia, the A wave is large and E wave is smal e. E: A ratio less than 1 (Fig. 6.7B). The deceleration time (DT) of the E wave is prolonged (> 220 msec) (®) inpersons aged > 50 years, the E: A ratio should be less than 0.5 to qualify for diastolic dysfunction since the A wave is already dominant at this age. @ This is known as the “slow-relaxation pattern” and indicates reduced LV com nce. There is increase in atrial contribution to ventricular filling. ® When myocardial distensibility is impaired due to myocardial infiltration or pericardial constriction, the E wave is very tall and A wave is small (Fig. 6.7C). The deceleration time (DT) of the E wave is short (< 150 msec).“anem ajbuls ese seadde pue aun ates aye sn20 anem y pue anem 3 ay ‘yeasaiul Yd pa6uojoud uy ‘sawn wua!ayIp 1B 4ND30 anem y pUe nem a4} UONEDSSIP A-V YBIM y01q WeaY aa|dwWo> UI ‘BUIIIY 2e]N2!UAA Oo} UORNAHIUOD jeURe OU s! HY ‘UORE|WgY [eLNe UL ‘yeataiul y-d pabuojoid 2 10 0Iq UeaY arajduio> ‘uoRe|jLqy jeUIe Jo aouasaid ay Ut PIJeAUI! st ‘UOR2UNYSAP 2yOISeIp Jo 10Ve>IpUI UE se ‘one! Y:9 ay. = “eIpieaXpeig jo aduasaid ayy ul aduesytUBISs sayeaib saiie> anemy |J21 2 ‘10 J21944 (UOANGLNUOD jee 19sS—}) pabuojosd s1 Buy 2yorseip a2u1s jjeuss 51 anem y ‘eIpierpesg st auatp UayA (UORNgUIUOD jelne 1912946) pauaTJOYs s! 3]03seIp ay 2ouIS 1uaUIUONT a:UL S} anEM y ‘eIPseDAY>ED Jo aduasaid aD UY w “paseanout osje si yead anem 3 SUL Papuarsip AjjeunxeLU Apeasfe S1 3}>UIUIA aU JI MOY PIEMIOY saya IOUUe? UONeNUOD jeNNe aDUIS aneEM y ay saYeNUaNE uonew6inBe! snice 40 yeni 01 anp BuIpeopianc aWiNjoA = uonesidsas yo aseyd ay — won>uny a1orsAs jente Yor — wyrduy 2e1pie> pue ares ueaH — (peopaye pue peojaid) BuIpeo| awinjon — sapnpur waned moyur jentu ay? a2uaNYUL eUT S101>e4 “uoRDuNysAp 2yoISeIp (1 Jo 1018>1pUL ue se ones y: 3 uo Ajuo Ajai or arendosddeut si 11 ‘auojroyy “Amuqisuarsip pue uonexejas jeIpier0Kw sapisaq si013e) Jo saqunu ab.e ® Aq pasuanisul st Buy AT Jo Waned moyUH jen oy,» uon>unyshq >HoOIseIG AT JO SIsoUBeIG ayp UI S11esI1d sayLny Aue apunuan ay puaisip ouue> wine ayy pue ajorseIp Ajea UL Aypides sin>20 moyul Je]NDINUaA B4NUD YL “(d9A7) eNssoud DyorseIp-pua A] parenaje ue saje>!pul pue waned antio1se1, 242 Se UMOUYS!SIY ee wonsunysiq aeinstitusy, 31 Kian ‘waned aanoinsay (>) 19 1 oF E= Awith short deceleration time (DT), it indicates the presence of an elevated LV end-diastolic pressure (LVEDP). This is referred to as pseudo-normalization of MV inflow pattern. Causes of LV Diastolic Dysfunction- LV diastolic dysfunction is observed in: = Advanced age (> 50 years) » Left ventricular hypertrophy Coronary artery disease =” Restrictive cardiomyopathy = Myocardial infiltration »° Pericardial constriction ignificance of LV Diastolic Dysfunction = Diastolic dysfunction occurs due to increased stiffness of the LV wall, which impairs diastolic blood flow from the left atrium to the left ventricle. # The clinical features of left heart failure may occur in individuals with normal or near-normal LV systolic dysfunction as assessed by echo. These are often due to diastolic dysfunction. ™ Diastolic dysfunction is observed in a variety of cardiac conditions. It is more sensitive than systolic dysfunction to the effects of normal aging ® Abnormalites of diastolic function may occur in isolation, may coexist with systolic dysfunction or may be observed before ‘major systolic impairment becomes obvious. Heart failure may be predominantly diastolic in some cases. = LVsystolic and diastolic function have to be assessed separately since their causation and more importantly their treatment is considerably different. = Too simplistic a demarcation between diastolic and systolic dysfunction is often misleading. Systole and diastole are phases ofa continuous cardiac cycle and interactions do occur between them. = In mild systolic dysfunction with dyskinetic areas, some regions can continue contracting in diastole leading to shortening of the time available for ventricular filling. This leads to supervening dysfunction. = Conversely, a poorly compliant left ventricle that fai tofillade quately in diastole may cause a low stroke volume in systole. This, leads to additional systolic dysfunction. = Prominent A wave can be equated to the fourth heart sound (S,) on auscultation while a prominent E wave can be equated to the third heart sound (S,). RIGHT VENTRICULAR SYSTOLIC DYSFUNCTION = Whenever echocardiography is ordered or performed, the focus is always on the left ventricle. This is because the most common cardiac conditions namely systemic hypertension, coronary artery disease and valvular pathologies affect the left ventricle. Nevertheless, the importance of the right ventricle and its role in heart disease is being increasingly recognized. , Normal Indices "= RV free-wall thickness <5mm Echo Features of RV Dysfunction ® Right ventricular (RV) size and function can be evaluated by M-mode scan from the PLAX view and 2-D echo using the apical and subcostal 4-chamber views.uinidas qj ay} Jo Uonows jeD!Kopeled “a “Auned AY 240 Uo!sUBUUIp Pasea!dU} “y Buymoys a,>uNUAA IYBU ax JO Ue>s apoW!-W OL'9 “614 qunoD>8 oqul 101384 asap je BYe1 Pinoys uondury AY Jo siskjeuy ‘ainssaid jerpresuiadenut oy pue uorsinoxa jerdas pue Auyjn>eNU0> Aq ‘SuoRIPUO> BUIpEO| 01 O5|e ang Ayjn>eNUOD jeIpIEdOAW 01 4jUO OU BANISUAS SI UONIUNY AY siasqns iuaned asayp ul ueviodut 9104 ay) s1 UonDUNy AY Jo ApMs ‘Aye>KOpeLeg ‘K1aBins e104 snoInad pue sisoiqy Areuowynd ‘(ewaskyduia) uoneyutiadsy 6uny Jo aouasaid ayy UL yNdyyIp AeINotUed st AY ay Jo IuoLUSSassy eae euan par JoISUBUNp JPULON y (RRB cor0u0j560 seyn>10029 “winuias ay Japun kp2auip parer0} s1 Ay au 1anoa:0w ‘BulBeus| uo siaquiey> Jayio Yum deiano pue Arpxajduo> [e>119W09H 51) ‘uone|N2aqGeN Kaeay Jo asneraq 1n2ysIp Si AY B42 JO TUaLUssasse Oy] = uonsunyshq AY Jo sisouBeig ayp ut siete {01-9 B14) mara (xV1d) Sixe Bu] jeusarsered. aut Woy ueds apow-W UO (SAI) WUMdas 4ejNZ_QUAAIER ayi Jo UoNOW je>1Xopeied sasne> peojiano awN|OA AY a (6'9 614) uonendsur Gurinp ua>iad os aseape Aq, YPUISUOD 09 Sey YDIYM ‘WZ PUOKAg PAre}Ip S| EAD BUDA JOUAJUL au pue pabiejua st wine 1y611 ats ‘suny/e} Ay jo a2uasaid aya UY w -aseasip senajen papls-146u 10 1UNYs 1yBU-01-4a} © se ypns uon2UN|sép Ay Joasne> BuIxpapun ay [eandi AeL OY] @ sisouars Kieuowsjnd 40 uoisuayiadAy A1euownd ur se peopiano ainssaid jy 01 Atepuoras Aydoniodéy jy Jo auapiaa st Wu ¢ < Ssauy~>I [feM-2a4 AY “(g'9 614) adeys sejnBuern jeuoU sit 5250] pue Jejngo6 sawioeq py pabue|ud uy ‘|euOUge s141'smain -oypa ayp je Ul AT ay WEY 49B1ey 0 azIs aUIeS DY JO SI AYOUJL = ‘apunuan 1ybu snaUDjodAY pue (WU! €Z <) pare|Ip © YUM parerosse s1 UONDUN|SKP AY = apinuan pue wine 1ybu so uoney ip Buynoys maIA HOY B'9°BI4(SRE Echo Made Easy Ventricular Dysfunction i ES = Even in the most experienced hands, satisfactory echo RY infarction requires a different therapeutic approach than LV examination of the right ventricle is obtained in less than infarction. RV dysfunction due to post-Ml VSD in an important 50 percent of subjects. cause of mortality (see Coronary Artery Disease). = RV diastolic collapse is a reliable echo parameter of cardiac Causes of RV Dysfunction tamponade (see Pericardial Diseases) RV dysfunction is observed in: ® Left-to-right cardiac shunt: ASD, VSD Right-sided valvular disease: TR, PR Pulmonary hypertension: PRI, SEC Right ventricular infarction: INF. Ml Right ventricular dilatation: DCMP_ * ical Significance of RV Dysfunction = Assessment of RV dysfunction plays a critical role in certain congenital and acquired cardiac conditions where it is important for planning treatment, timing surgical intervention and for predicting prognosis. = Incongenital heart disease such as VSD, ASD or Fallot’s tetralogy, assessment of RV function before and after surgery is a useful prognostic marker. = Similarly, timing of surgery in valvular heart disease such as MS, PS or TR is determined by the presence or absence of RV dysfunction. = The long-term prognosis of patients with chronic lung disease (COPD, ILD) depends upon RV function. RV dilatation, pulmonary hypertension and cor-pulmonale are indicators of a poor prognosis. * Following myocardial infarction, RV dysfunction may be observed in the following situations: ~ Inferior wall infarction with rv infarction. — Anterior wall infarction with acute vsd.75 sp2e0x9 (A3A1) UoIsUaW.Ip >1]04SeIP-Pua se|NDUIUEAYE| aYL _"e1psedkyper A1oyesuadusos 01 anp jewuou aq, feat aia Je|nqo|6 a1ow e sawinsse Aqa1ayy Y>IYm ‘2)>ERUEA Ya} B41 JO 1ed siaquuey> DeIpse> Noy aug |Ie Jo UONEIE| ‘Kew (0D) 1ndyno >eIpse> ay 3nq Mo} SI (43) UONDeY UONafa SyL “(gaA7) Uon>ey UoNDafe pue (54) BuIUaTIOYs |eUON ey paonpay = “paseaiout st ajorsés-pua pue ajo1seIp-pua Ur Ja1aweIp seINDNIUAA ya] 4 UOSeA! WES B4LI04 paonpai ale Jem sO1NaISod JeIN>LNUIA Ya} a4 Jo pue WNidas JeINDINUAATaIUL ay Jo UOISsINDxa >11035Ks BYR ‘eIsaUrYodAY Jeqo|6 01 ang = paseasout axe (QQ3A1 pue qs3A7) SuOIsuaUIp 2eINDUNUAA aYL ‘MdAT PUL SAI ay JO UONOW paonpas s! YL uonen6inBas yeni jeuon>uny 01 spea} Y>iym Bul 1eInUUe Fen aya Jo Bulyrrans 0} anp sin290 wauia6ie|Ua JeUIe YO] uonereHp 7 Jo aa16ap ay 10) ayenbapeut st ypiya kydoniad(y py aq Kew aiayy io ump are sem AT2YL eISaUD{od Ky jeqo|B se UMOU Si si JeuoiBas wey sayper jeqo]6 40 pazije19Ua6 s} UoNOW jem A 1paanpa1 ay] paniasqo aie Uo |jem Jo apmiyjduse paonpa ue Buluax>in >HoIsAs paonpas ‘ssauy>IYp [Jem AT Panpay w= Auten: S!OrOUL a 0429 G-z pub apow-W dW2d Jo seanjeay 0423 EN CN OE ACEP NAL (W20H) Atpedokworpse> 1ydonsedéy (aWDY) Ayedokworpie> aanruasay > a (dW) Apedokwoypies pareyiq. :saitpedowiorpse> jo sadAi urews aaiyy aie a1ay, “Ayyedokwoipie> snaqeip Pue 2yoYo>Je ‘S!WAYDs! ‘aA!suarIadAY apnj>Ut suOMIPUOD YpNs Jo sajduiexg “asne> ajqeynuap! ue s} aru) UIB134yM SUO}IPUOD apn|>Ut 01 papuarxe uaag ‘abesn zeindod yBnouyp sey wai ay aASMOH ‘Aypedokwopies >143edo1p! ue se UmoUy 3! ase rey) Ul ‘asne> BuLapuN UMOUY OU sey IUD onspuod e 01 paridde aq fjuo pjnoys way ayp ‘asuas 91S SU UI . Papsndl Vesy sui jo sseasip © Subs Apedonwioypies)usay auL apunuan yo} 121NgGO|6 pue pabiejua Ue Buymoys moIA HOP LL BIS eevee (uon2unjskq 1eIn>;UeA aas) paonpar ae UoRDUNy ; JOrsAs 1eINDUIUAA Ja] JO Sa2IpUI ‘e!saurodAy jeqoj6 01 ang = —__- - _. “{wiu Zs 02 9¢€ St jeuuioU) Wu | ios a eto Made Easy i rw Fig. 7.2 M-mode scan of the left ventricle showing: + Increased size of left ventricular cavity + Reduced movement of IVS and LVPW + Increased E-point septal separation + Reduced excursion of mitral leaflets ® Increased E-point septal separation (EPSS) (Fig. 7.2). It is the distance between the farthest posterior excursion of the septum. and the E-point of the anterior mitral leaflet (AML). The normal EPSS does not exceed 5 mm. Note ~ The EPSS is reduced in hypertrophic obstructive cardio- myopathy (HOCM) due to systol n (SAM) of anterior mitral leaflet (AML). - Measurement of EPSS lacks utility in the presence of mitral valve disease in which case free motion of the AMLis already impaired. = Reduced anterior swing of aortic root during left atr (normal >7 mm) = Reduced AV cusp separation in systole (normal >15 mm) with premature closure of the aortic valve (Fig. 7.3). = Reduced MV anterior leaflet excursion in >20 mm) with rapid upstroke and downstroke. ™ Allthe above are signs of reduced cardiac output. ing jastole (normal Cardiomyoparhies QQ BEES M-mode scan of the aortic valve showing: Reduced aortic cusp sepa + Dilatation of the left atri = Associated non-specific findings in DCMP are: — Small pericardial effusion ~ Left ventricular thrombus. Doppler Echo = Functional mitral and tricuspid regurgitation (MR and TR) occur due to stretching of atrioventricular (A-V) rings, asa consequence of ventricular dilatation. Differential Diagnosis of DCMP. = It may be extremely difficult to differentiate myopathy from the following conditions: = Severe MR with LV dysfunction = Ischemic cardiomyopathy (ICMP). lated cardio- Severe MR with LV Dysfunction = Severe organic mitral regurgitation with volume overload and LV dysfunction can mimic DCMP with functional MR due to annular stretching. oo“(uw Zs 01 9¢ jeuioU) WL SE UeL S53} 01 paonpar s} (qa3/7) UoIsuaWiIp >o1SeIP-pUa 4eIN>INUAA 49] YL (pd 614) xode Ay pue A738 UONeZDMIGO Aner um ay pue 97 Jo azis Aune> pue suoisuaLUIp jeusaiu! parnpay = ‘aoueieadde sse/6-punos6, Guipyieds e saanpoid wnidas A241 OU! plo}Awe Jo OREN |YyUL “LUNIpIEDOAL aD UI BUIMIOW JO f pads jo sayaied ym wuNIpies0pua Jo Ay>}ueGoypa YG ww WI §< 5} Jem 905.AY UN JO vet pue WW Z| sp992xo 2]OISeIp UI SAI PUE MAT JO SSBUYDIY ayy “uinidas jj ay) pue sjjem aay AY pue AT ay Jo BuUayDIYL » 0y23.g-z pun apow-W WY JO Seanqea4 Oz COCCI P ERO SEL (vaVD1¥) Aiaue Aseuowjnd woy Buisuy = Aiauie Kieuoi05 ya} snojewouy euoe ayijouonei1e0) Anedofwiorpie> jeua6uoy squeyuy ul A] a61e7 jo sasne> “INLH ‘Sy) peopieno ainssaid Ay a (Vad ‘av YW) Peo}HaA© auINIORAT (aw) Aqpedoxwiorpie> sways} (Wy) Honaseyut perpieD0Kw JouaIUy (awa) Atnedokworpie> pare sunpy ul a7 26187 Jo sasne> paonpur-6nig jeuonminN = winuediiag = BB suiedoswopies Jeainasog “omyredorp dW2G jo sasne> ‘dWDd U! 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Very tall E The differentiation between the two conditions is important as it has crucial management implications. The following features are observed only seen in case of RCMP and not in constrictive: pericarditis: = Thickening of ventricular wal Reduction of ventricular cavity size — Impairment of LV systolic function ~ Mitral and tricuspid regurgitation latation of right and left atrium RCMP needs to be differentiated from apical cardiomyopathy, a sub-type of hypertrophic cardiomyopathy, where the hypertrophy is confined to the apices of the ventricles with obliteration of ventricular cavity. In both these conditions, the right and left atrium are enlarged. The only other cardiac condition in which both the atria are enlarged with normal or small ventricles is mitral stenosis with pulmonary hypertension and secondary tricuspid regurgitation. In dilated cardiomyopathy there is enlargement of chambers of the heart.