Iclination is required as level go below mandible in high jvp or below clavi in low pr. So start with 45 then tilt pt appropriately up or down . In patients with low jugular pressure , a lesser (<30‘) inclination is desirable In patients with high jugular pressure ,a greater (60-90‘) inclination is required to obtain visible pulsations
Shows the vertical course of the ijv which psses inbetween the two heads of the st mastoid under the medial end of clavicle
(Lanci sign) – ventricularization of atrial / jugular pressure
Elevated venous pressure from any cause. Constrictive pericarditis,(Friedreich’s sign) Severe TR, Severe RVF Severe RV infarction
Small brief positive wave following y descent just prior to a wave during period of diastasis It usually seen when diastole is long (as in slow heart rates)
A Case of Dyspnoea
A Case of DyspneaPresented by Dr Shwet DuttaModerated bySurg Capt Subhash Ranjan, NM, VSM,Sr Advisor, Medicine & Oncology
Chief complaints• 61 year old lady• Resident of Manipur• Presented withBreathlessness on exertion X 02 yearsNauseaUpper abdominal discomfort1week
HISTORY OF PRESENT ILLNESS• Breathlessness on exertion NYHA class II for02 years• Easy fatigability and dizziness for 02 years• Recently progressed to class IV; Orthopneafor 07 days• Not associated with fever /cough /chest pain /palpitations
Dyspnea• Subjective experience of breathing discomfortthat consists of qualitatively distinctsensations that vary in intensity. Theexperience derives from interactions amongmultiple physiological, psychological, social,and environmental factors and may inducesecondary physiological and behavioralresponses.
Causes of DyspnoeaSystem Acute dyspnoea Chronic exertionaldyspnoeaCardiovascular system Acute pulmonary oedema Chronic CCFMyocardial ischaemiaRespiratory system Acute severe asthmaAcute exacerbation COPDCOPDChronic asthmaPneumothorax,Pulmonary embolusARDSChronic pulmonarythromboembolism , Largepleural effusionPneumoniaLobar collapseBronchial carcinomaLymphatic carcinomatosisInhaled foreign body(especially in a child)Laryngeal oedema (e.g.anaphylaxis)ILD: sarcoidosis, fibrosingalveolitis, extrinsic allergicalveolitis, pneumoconiosisOthers Metabolic acidosis Severe anaemiaHyperventilation Obesity
History of Present illness (Contd/-)• Nausea• Decreased Appetite• Occasional Vomiting (non bilious, nonprojectile, gastric contents)• Not relieved with PPI/ Antacids• Dyspepsia?
Dyspepsia?• Sleisenger: Rome III :- Pain /discomfortcentered in upper abdomen originating fromgastroduodenal region – include postprandialfullness, early satiation, epigastric pain,epigastric burning
Orthopnoea• Dyspnoea occurring in the recumbent position, relievedby sitting upright or sleeping with additional pillows.• Cause: Redistribution of fluid from splanchniccirculation and lower extremities into centralcirculation during recumbency, with a resultantincrease in pulmonary capillary pressure• Conditions: HF, obesity, ascites, pulmonarydisease(lung mechanics favouring an upright posture)
Paroxysmal Nocturnal Dyspnea (PND)• Refers to acute episodes of severe shortnessof breath and coughing that generally occur atnight and awaken the patient from sleep,usually 1–3 hours after retiring.• Cause: Increased pressure in bronchial arteries leading toairway compression, along with interstitial pulmonary edemathat leads to increased airway resistance.• Persistent coughing and wheezing even after assumingupright position
NYHA v/s Modified MRCFunctionalCapacity/GradeNYHA (Objective Assessment) Modified MRC (Grade related to degree ofbreathlessness related to activities)Class I/Grade 0 Patients with cardiac disease but without resultinglimitation of physical activity. Ordinary physical activitydoes not cause undue fatigue, palpitations, dyspnea,or anginal painNo breathlessness except with strenuous exerciseClass II/Grade 1 Patients with cardiac disease resulting in slightlimitation of physical activity. They are comfortable atrest. Ordinary physical activity results in fatigue,palpitation, dyspnea, or anginal pain.Breathlessness when hurrying on the level or walking up aslight hillClass III/Grade 2-3 Patients with cardiac disease resulting in markedlimitation of physical activity. They are comfortable atrest. Less than ordinary activity causes fatigue,palpitation, dyspnea, or anginal pain.Walks slower than contemporaries on level ground becauseof breathlessness or has to stop for breath when walking atownStops for breath after walking about 100 m or after a fewminutes on level groundpaceClass IV/Grade 4 Patients with cardiac disease resulting in inability tocarry on any physical activity without discomfort.Symptoms of heart failure or the anginal syndromemay be present even at rest. If any physical activity isundertaken, discomfort is increased.Too breathless to leave the house, or breathless whendressing or undressingHarrison’s Principles of Internal Medicine18 Ed
Negative history• No h/oHemoptysisAbdominal swellingSwelling of feetSyncopeTIA/StrokeWeight lossWorm infestation
Family history• Negative for:-Sudden deathValvular Heart DiseaseIschemic Heart Disease
Personal historyNo h/o• IV drug abuse• Tobacco/ Alcohol use• Disturbed Sleep• Mixed Diet
Past HistoryNo h/o• Recurrent sore throat infections• Fleeting joint pains,• Erythematous rashes,• Subcutaneous nodules,• Abnormal involuntary movements• IV Penicillin use• Post menopausal Bleeding PV/PR
Tripod BreathingPatients with advancedlung disease (in thiscase COPD) will oftenassume a tripodposition (leaningforward, hands onknees) when breathingdifficulties occur. Thisprovides a position thatoptimizes respiratorymechanics.
General Examination• Wt – 55 kg, Ht – 150 cm, BMI- 24.44 kg/m2 ,• Pulse - 114/min, irregularly irregular, noradio radial/ radio femoral delay, allperipheral pulses palpable• BP – 108/64 mmHg right arm supine• 130/74 mmHg right lower leg• No pallor/ icterus/ cyanosis/ clubbing/ pedaledema/ lymphadenopathy
Normal Pulse• The normal central aortic pulse wave is characterizedby a rapid rise to rounded peak.• The anacrotic shoulder, present on the ascendinglimb, occurs at the time of peak rate of aortic flowjust before maximum pressure is reached.• The less steep descending limb is interrupted by asharp downward deflection, coincident with AVclosure, called incisura.
Pulse• As the pulse wave istransmittedperipherally, the initialupstrokes becomessteeper, the anacroticshoulder becomes lessapparent.• The incisura is replacedby the smootherdicrotic notch.
Pulse Rate/Rhythm• Rate - > 100 / min - tachycardia< 50 / min - bradycardia• Rhythm• a)Regular – when every beat comes at theexpected timeb) Irregulari)Regularly irregular(when the irregularities canbe predicted)ii)Irregularly irregular (when they cannot)
Irregularly irregular pulses• Premature atrial contractions• Premature ventricular contractions• Atrial fibrillation( Delirium cordis – the only thingpredictable about the beat is its unpredictably)• Multifocal atrial tachycardia• Sinus arrest (If the pause b/w beats is less than 2 RRintervals)• Sinus exit block v/s 2:1 AV Block(carotid sinuspressure)
Pulsus Parvus• The pressure is diminished, and the pulse feels weakand small, reflecting decreased stroke volume (e.g. heartfailure), restrictive pericardial disease, hypovolemia,mitral stenosis, and increased peripheral resistance (e.g.exposure to cold, severe CHF).• Pulsus Parvus et Tardus (weak and delayed):→Aortic Stenosis
Pulsus tardus (delayed peak)• AS – mechanical obstruction to left ventricularejection, accompanied by coarse systolic thrill
Hypokinetic (low volume andamplitude)•Hypovolemia / LV Failure 2 to myocardialdisease or myocardial infarction,•Restrictive pericardial disease,•Mitral stenosis
Bounding Pulses• A.K.A. water-hammer pulse or the Corrigan pulse.• Most commonly in chronic, hemodynamically significantAR.• Seen in many conditions associated with increasedstroke volume: PDA, large arteriovenous fistula,hyperkinetic states, thyrotoxicosis anemia, and extremebradycardia.• Not seen in acute AR, since SV may not have increasedappreciably.
Bounding Pulses (2/2)• Physical signs of aortic insufficiency are related to the highpulse pressure and the rapid decrease in blood pressureduring diastole due to the AI:– Lighthouse sign (blanching & flushing of forehead)– de Mussets sign (head nodding in time with the heart beat)– Ladolfis sign (alternating constriction & dilatation of pupil)– Beckers sign (pulsations of retinal vessels)– Müllers sign (pulsations of uvula)– Corrigans pulse (rapid upstroke and collapse of the carotid artery pulse)– (Watsons) Water-hammer pulse– Quinckes sign (pulsation of the capillary bed in the nail)– Mayens sign (diastolic drop of BP>15 mm Hg with arm raised)– Rosenbachs sign (pulsatile liver)– Gerhardts sign (enlarged spleen)– Duroziezs sign (systolic and diastolic murmurs heard over the femoral artery when it is graduallycompressed)– Hills sign (A ≥ 20 mmHg difference in popliteal and brachial systolic cuff pressures, seen in chronicsevere AI)– Traubes sign (a double sound heard over the femoral artery when it is compressed distally)– Lincoln sign (pulsatile popliteal)– Sherman sign (dorsalis pedis pulse is quickly located & unexpectedly prominent in age>75 yr)
Bisferiens pulse (2 systolic peaks)• 1stpeak – occurs as pulse wave upstroke rises rapidlyand forcefully (percussion wave)• A brief decline in pressure follows because of thesudden decrease in the rate of Left ventricularejection during midsystole, when severe obstructiondevelops.• 2ndpeak – smaller and slowly rising positive pulsewave(tidal wave) produced by continued ejectionand by reflected waves from periphery
Pulsus Paradoxus (1/2)• Pressure drop > 20 mmHg during inspiration.• Normally, systolic arterial pressure falls 8-12 mmHg duringinspiration.• Evaluated with sphygmomanometer:– when the cuff is slowly released the systolic pressure at expiration is firstnoted. With further slow deflation of the cuff, the systolic pressureduring inspiration can also be detected.
Pulsus Paradoxus (2/2)• Causes:– Cardiac Tamponade– COPD, hypervolemic shock– infrequently in constrictive pericarditis and rescrictivecardiomyopathy.• Mechanism:– Decreased LV-SV due to an increased RV-EDV anddecreased LV-EDV during inspiration.– In cardiac tamponade, the interventricular septumshifts toward the LV cavity during inspiration (reverseBernheim’s effect) b/c of increased venous return toRV, decreasing the LV preload.– Decrease in pulmonary venous return to the LVduring inspiration also contributes to decreased LVpreload.
Pulsus alternans• Regular alteration of pressure pulse amplitude, despite aregular rhythm• Due to alternating Left ventricular contractile force, whichdenotes severe left ventricular decompensation.• May occur following/during paroxysmal tachycardia/following a premature beat• Poor prognosis
Dicrotic/ Bifid pulsePeaks in systole and diastole – IABP, DCM
Pulsus bigeminus• Regular alteration of pressure pulse amplitudecaused by a premature ventricular contractionthat follows each regular beat.
Apical-radial pulse deficit ?• Simultaneously measure the apical ventricularrate and the radial pulse• Put the stetho on apex and simultaneouslycount the dropped beats in the pulse for oneminute.• Conditions: AF, multifocal PACs and PVCs
• Jugular venous pulse is the oscillating top ofthe distended proximal portion of the internaljugular vein and represents volumetricchanges that faithfully reflect the pressurechanges in the right heart
Measurement of JVP• Two scale method is commonly used• Normally JV pressure does not exceed 3- 4 cm ofblood above the sternal angle• Since RA is approximately 5 cm below the sternalangle , the jugular venous pressure corresponds to9 cm =7mmHg• Elevated JVP : JVP of >3cm of blood above sternalangle• CVP conversion factor 1.36 cm water equals to 1 mmHg
a wave• Reflects right atrial presystolic contraction andoccurs just after the P wave, preceding S1• Prominent a wave - reduced right ventricularcompliance• Cannon a wave - AV dissociation (right atrialcontraction against a closed tricuspid valve)• Absent with atrial fibrillation
Prominent a Wave• Forceful atrial contraction when there is resistance to RAemptying or increased resistance to ventricular filling• RV inflow obstruction:Tricuspid stenosis or atresiaRA myxoma• Decreased ventricular compliance:Pulmonary stenosisPulmonary hypertension of any causeRV infarctionRV cardiomyopathy (HOCM)Acute pulmonary embolism
Cannon Waves• Whenever RA contracts against closed TV valve during RVsystole• Regular cannon waves:Junctional rhythmVT with 1:1 retrograde conductionIsorhythmic AV dissociation• Irregular cannon waves :Complete heart blockAV dissociation with Ventricular tachycardiaVentricular pacing or ventricular ectopics .
c wave• Bulging of the tricuspid valve into the RAduring RV isovolumic systole and by theimpact of the carotid artery adjacent to thejugular vein
x descent• Atrial relaxation, downward displacement oftricuspid valve during RV systole, and ejection ofblood from both ventricles• Most prominent motion of normal JVP which beginsduring systole and ends just before S2• X descent more prominent during inspiration
Prominent x descent• Presence of atrial relaxation with intacttricuspid valve and good RV contraction• Causes :Cardiac tamponadeConstrictive pericarditis
v wave• Its height is determined by RA compliance and by thevolume of blood returning to the RA, eitherantegrade from the vena cavae and/or retrogradethrough an incompetent TV• With TR, the v wave will merge with the c wavebecause retrograde flow and antegrade RA fillingoccuring simultaneously.
Prominent v wave• Increased RA volume during ventricularsystole produce prominent v wave• Severe TR : giant v wave• ASD with mitral regurgitation• VSD of LV to RA shunt (Gerbodes defect)• RV failure
y descent• Tricuspid valve opening and the rapid inflowof blood into the RV.• Resistance to ventricular filling in earlydiastole blunts the y descent, as in pericardialtamponade or tricuspid stenosis.• The y descent will be steep when ventricularfilling occurs early and rapidly, as withpericardial constriction or isolated severe TR.
Rapid y Descent• Severe TR• Constrictive Pericarditis (Friedreichs sign)*:Early rapid ventricular filling• Severe RV failure• ASD with mitral regurgitationFriedreichs sign is the exaggerated drop in diastolic central venous pressure seen inconstrictive pericarditis (particularly with a stiff calcified pericardium) and manifested asabrupt collapse of the neck veins or marked descent of the central venous pressurewaveform. The sign is named after Nikolaus Friedreich.
h wave• Small brief positive wavefollowing y descent just prior to awave• Described by Hieschfelder in1907• It usually seen when diastole islong• With increasing heart rate, ydescent immediately followed bynext a wave .
Kussmauls sign• Rise or a lack of fall of the JVP with inspiration• Constrictive pericarditis• Severe right heart failure• RV infarction• Restrictive cardiomyopathy• Impaired RV compliance
Abdominojugular reflux• Firm and consistent pressure over right upperquadrant, for at least 10 seconds.• A sustained rise of more than 3 cm in thevenous pressure for at least 15 seconds afterresumption of spontaneous respiration is apositive response.• Useful in predicting heart failure and a PAwedge pressure higher than 15 mm Hg.
SYSTEMIC EXAMINATION• JVP – raised• CVS –no visible pulsations/ heaveno palpable thrillPMI – medial to left MCLS1 is loud,S2 is normally split, P2 is normalOS heardGrade II/VI, Mid diastolic rumbling murmur,heard best at apex in left lateral recumbent positionNo PSE
Grading of murmursGrade 1 very soft (only audible in idealconditions)Grade 2: Soft(faintest murmur that can be heard)Grade 3 Intermediate between grades 2 and 4Grade 4 loud with associated thrillGrade 5 very loud(with the chest piece tilted)Grade 6 heard without (stethoscope head held in front of patient’s chest)Davidson
Intensity of S1 is influenced by…1. Position of Mitral Valve leaflet at the onset ofsystole.2. Rate of rise of left ventricular pressure pulse3. Presence or absence of structural heartdisease4. The amt of tissue, air or fluid between theheart and the stethoscope.
Causes of Loud S11. If diastole is shortened because oftachycardia2. If AV flow is increased because of high COor prolonged because of MS3. If atrial contraction precedes ventricularcontractions by unusually short interval (ShortPR interval)
Causes of Soft S11. Poor conduction of sound through the chestwall.2. Slow rise of LV pressure pulse3. Long PR interval4. Imperfect closure due to reduced valvesubstance (MR)5. Immobility of AMV leaflet due calcification
Splitting of S11. 10-30 ms (Normal)2. M1 is followed by T13. Widening is most often due to RBBB &resulting delay in onset of RV pr pulse
Hangout TimeP2 is coincident with incisura of Pulm Arterypressure curve which is separated from RVpressure tracing by an interval termed theHANGOUT TIME.
Splitting of S2 (2/6)3. The absolute value of Pulm Hangout reflectsthe resistance to pulm vascular bed.4. The Hangout Time increases with RV VolOverload & distensible pulm vascular bed5. It decreases in increase in pulm vascularresistance with narrow splitting.
Splitting S2 (3/6)• Splitting persisting in expiration is usuallyabnormal in upright position.
Causes of wide split (4/6)1. Delayed activation of RV (RBBB)2. LV ectopic beat3. LV pacing4. Prolongation of RV contraction with increased RVpressure load (PTE, PS)5. Delayed PV closure due to RV volume overloadassociated with RV failure or diminished impedance ofpulm vascular bed & prolong hangout time (ASD)6. MR/VSD due to early Ao Valve closure
Fixed Splitting (5/6)1. In ASD proportion of RA filling contributed byLA & venae cavae varies reciprocally duringthe resp cycle so that RA inflow remainsrelatively constant.2. Vol & duration of RV ejection remains sameduring Inspiration; leading fixed Splitting of S2
Paradoxical Splitting (6/6)• P2 precede A2• Splitting is maximal in expiration & decreasesduring inspiration• Causes:-1. LBBB2. Delayed excitation of LV from RV ectopic beat3. Severe Aortic outflow obstruction4. Large Aortopulmonary shunt5. Systolic Hypertension6. IHD or CMP with LV failure
Loud P2Normally P2 is softer than A2 in second left ICS.P2 equal or greater than A2 in Pulm areasuggests Pulm HTN; except in ASD where it isbecause of excess blood flow.
Ejection sound• Sharp high pitched event occurring in early systoleand closely following S1• Occur with Semilunar valve stenosis, dilation ofaorta/pulmonary artery• Pulmonary ejection sounds, unlike aortic ones, tendto diminish or disappear in inspiration and the onlyright sided cardiac event to behave in this manner. Itis better heard at lower left sternal border duringexpiration.
Non ejection clicks/Mid systolicclicks• Occur with/without late systolic murmurdenoting prolapse of one or both leaflets ofmitral valve• Results from chordae tendinae that arefunctionally unequal in length, best heardalong left sternal border and at LV apex• Systolic clicks occur later than systolic ejetionsound
Opening Snap• Brief, High pitched, early diastolic sound due to AV valvestenosis (most often mitral valve)• Heard best at lower left sternal border, radiating to base.• A2-OS interval is inversely related to the height of mean leftatrial pressure. Ranges from 0.04-0.12 sec• Tumor plop in patients with left atrial myxoma may have thetiming of OS , but is usually lower pitched
S3• Low pitched sound in ventricle 0.14-0.16 safter A2, at the termination of rapid filling• Found in children, ↑ CO• > 40 yrs of age it indicates:i) Impairment of LV functionii) AV valve regurgitationiii) Conditions that increase rate/volume ofventricular filling
Pericardial Knock• An S3 that is earlier (0.10-0.12 s after A2) andhigher pitched than normal (pericardial knockin constrictive pericarditis) occurs due torestrictive effect of adherent pericardiumwhich abruptly halts diastolic filling.
S4• Low pitched presystolic sound, best heard at LV apexin left lat with bell during ventricular filling• Accentuated by mild isotonic/isometric exercise insupine• It is associated with an effective atrial contraction(Absent in AF)• Diminished ventricular compliance increases theresistance to ventricular filling• Causes: Systemic Hypertension, AS, HOCM, IHD,Acute MR, Acute MI, Delayed AV conduction• Rt sided S4 : RV hypertrophy secondary to PS/PAH
MDM• Low pitched, MDM of MS follows OS.• Heard with bell at site of LV impulse(bestlocalised with the patient on the left side)• Increased with mild supine exercise• MDMs may be generated due to rapid flowacross the mitral valve in MR/PDA/VSD oracross TV in cases of TR/ASD• TS – MDM localised along left sternal edge,louder during inspiration
Austin Flint Murmur• Acute severe AR – LV DP > LAP → MDM due todiastolic MR• Severe chronic AR – MDM/Pre SM(AustinFlint) – originates at anterior mitral leafletwhen blood enters LV simultaneously fromboth aortic root and LA.
Graham Steel Murmur• High pitched EDM in Pulm area radiatingdown left sternal border.• Seen in severe long standing PulmHypertension leading to secondary valveregurgitation.
P2 loud• Its intensity exceeds that of A2 at the base• It can be palpated in the area of proximalpulmonary artery (2nd left interspace)• Both components of S2 can be appreciated atlower left sternal border or apex
Hill sign• Brachial-popliteal systolic blood pressuregradient > 20 mm Hg• With large stroke volume there is also apressure wave at right angles to the forwardwave. The two waves sum only in the lowerextremities because the upper extremityvessels exit the aorta at right angles.• Sensitivity 89% for moderate to severe AR
Müllers Manoeuvre• Forced inspiration against closed glottis• The reverse of Valsalva manoeuvre• Positive result means site of upper airwayobstruction is below level of the soft palate
WHO Criteria for Diagnosis of Rheumatic FeverDiagnostic Categories CriteriaPrimary episode of rheumatic fever Two major or one major and two minormanifestations plus evidence of precedinggroup A streptococcal infectionRecurrent attack of rheumatic fever in apatient without established rheumatic heartdiseaseTwo major or one major and two minormanifestations plus evidence of precedinggroup A streptococcal infectionRecurrent attack of rheumatic fever in apatient with established rheumatic heartdiseaseTwo minor manifestations plus evidence ofpreceding group A streptococcal infectionRheumatic chorea Insidious onset rheumaticcarditisOther major manifestations or evidence ofgroup A streptococcal infection not requiredChronic valve lesions of rheumatic heartdisease (patients presenting for the first timewith pure mitral stenosis or mixed mitral valvedisease and/or aortic valve disease)Do not require any other criteria to bediagnosed as having rheumatic heart disease
Criteria for Rheumatic FeverMajor manifestations CarditisPolyarthritisChoreaErythema marginatumSubcutaneous nodulesMinor manifestations Clinical: fever, polyarthralgiaLaboratory: elevated erythrocyte sedimentation rate or leukocytecountElectrocardiogram: prolonged P-R intervalSupporting evidence of apreceding streptococcal infectionwithin the last 45 daysElevated or rising anti-streptolysin O or other streptococcal antibody,orA positive throat culture, orRapid antigen test for group A streptococcus, or Recent scarlet fever
SYSTEMIC EXAMINATION (contd.)• Abdomen – soft, tenderness + in righthypochondrium, liver is palpable 2 cm belowRt. MCL• Chest – bilateral basal crackles + (left > right)• Central nervous system – within normal limits
Differential Diagnosis (1/2)• Significant MR (murmur commences slightlylater, evidence of LV enlargement, openingsnap and increased P2 are absent, and S1 issoft or absent). Apical pansystolic murmur &S3 +• Severe AR - Austin Flint murmur (notintensified in presystole and becomes softerwith administration of amyl nitrite)
Differential Diagnosis (2/2)• Atrial septal defect (fixed splitting of S2 with agrade 2 or 3 mid-systolic murmur at the midto upper left sternal border)• TS (murmur increases with inspiration)• Left atrial myxoma (features suggestive ofsystemic disease + findings change with bodyposition)
Severity of MS• Normal mitral valve orifice area is 4–6 cm2• Mod MS (mitral valve orifice 1 cm2–1.5 cm2),CO is normal , but rises subnormally duringexertion• Severe MS - mitral valve opening <1 cm2• ↑pulmonary venous and PAWP reducepulmonary compliance →→ exertionaldyspnea
Pulmonary hypertension(1) passive backward transmission of elevatedLA pressure(2) pulmonary arteriolar constriction (reactivepulmonary hypertension)(3) interstitial edema in walls of smallpulmonary vessels(4) organic obliterative changes in pulmonaryvascular bed
Haemoptysis• Rupture of pulmonary vein–bronchial veinshunts• Pink frothy sputum with rupture of alveolarcapillaries
Ortner syndrome• Compression of the left recurrent laryngealnerve by dilated left atrium, enlargedtracheobronchial lymph nodes, and dilatedpulmonary artery causing hoarseness
Causes of AF• Combination of mitral valve disease and atrialinflammation secondary to rheumatic carditis→ left atrial dilation, fibrosis of atrial wall,disorganization of atrial muscle bundles →disparate conduction velocities andinhomogeneous refractory periods.• Premature atrial activation, caused byautomatic focus or reentry, may precipitateAF
Palpation• Enlarged RV may displace LV posteriorly andproduce RV apex beat that can be confusedwith a LV lift• A palpable loud P2 (aka Diastolic shock) insecond left ICS indicates severe pulmonaryhypertension.
OS V/S S2• OS occurs later, unless RBBB is present.• OS is loudest at apex, during expiration , S2 isbest heard at base.• OS is accompanied by accentuated S1.• OS - A2 interval varies inversely with left atrialpressure
Associated lesions• With severe PAH, a pansystolic murmur isheard (functional TR) along left sternal border,↑during inspiration (Carvallos sign)• Graham Steell murmur of PR (a high-pitched,diastolic, decrescendo blowing murmur alongleft sternal border) ← dilation of pulmonaryvalve ring in patients with severe PAH
ECG• Left atrial enlargement (P wave duration inlead II > 0.12 second and/or a P wave axisbetween +45 and −30 degrees)• Correlate more with left atrial volume thanpressure• Criteria for RV hypertrophy(mean QRS axis >80 degrees in frontal plane and R:S ratiogreater than 1 in lead V1)
MS, CXR-PA view• The heart size is normal.• The enlarged left atrium (A)displaces the left bronchusupwards (*) and creates aright retrocardiac doubledensity.• The left atrial appendage isenlarged (arrowheads).There is severe pulmonaryvenous hypertension
Kerley A & B linesKerley B lines (red arrows) are thickened horizontal linear opacities in the subpleural region, which meet the pleura at right angles.Kerley A lines (yellow arrows) are longer lines coursing diagonally toward the hila in the inner half of the lungs. Kerley lines are a sign seen on chest radiographs with interstitial pulmonary edema. They are thin linear pulmonary opacities caused by fluid or cellular infiltration into the interstitium of the lungs. They are named after Peter Kerley.
Wilkins scoreGRADE MOBILITY THICKENING CALCIFICATION SUBVALVULARTHICKENING1 Highly mobilevalve with onlyleaflet tipsrestrictedMinimal thickeningjust below the mitralleafletsLeaflets almostnormal inthickness (4-5 mm)Single area ofincreased echobrightness2 Leaflet mid andbase portions havenormal mobilityThickening of chordalstructures, extendingup to one third ofchordal lengthMid leafletsnormal,considerablethickening ofmargins (5-8 mm)Scattered areas ofbrightness confinedto leaflet margins3 Valve continues tomove forward indiastole, mainlyfrom the baseThickening, extendingto the distal third ofthe chordsThickeningextending throughentire leaflet (5-8mm)Brightnessextending intomidportion of theleaflets4 No or minimalforwardmovement of theleaflets in diastoleExtensive thickeningand shortening of allchordal structures,extending down tothe papillary musclesConsiderablethickening of allleaflet tissue (>8-10 mm)Extensivebrightnessthroughout much ofthe leaflet tissue
Wilkins score• Score < 8 - favorable response to valvotomy ,Score of 9 - 16 - surgical replacement.• Even in presence of low score, adverse baseline factors include increasingseverity of regurgitation, advanced age, prior commissurotomy, absenceof commissural fusion, and presence of commissural calcification meritssurgical intervention.
Rx• Penicillin prophylaxis of group A -hemolyticstreptococcal infections for secondaryprevention of rheumatic fever• Restriction of Na+ intake , oral diuretics,Vasodilators• Beta blockers, Calcium channel blockers (e.g.,verapamil or diltiazem), digitalis for slowingthe ventricular rate• Warfarin (AF / h/o thromboembolism)
Indications for Percutaneous MitralBalloon Valvotomy• Symptomatic patients, with moderate orsevere MS (MVA < 1.5 cm2) and favorablevalve morphology in absence of left atrialthrombus or moderate to severe MR• Asymptomatic patients with moderate orsevere MS with pulmonary hypertension(pulmonary artery systolic pressure > 50 mmHg at rest or > 60 mm Hg with exercise)
Technique• Advance a small balloon flotation catheteracross interatrial septum (after transseptalpuncture)• Enlarge the opening• Advance a large (23- to 25-mm) hourglass-shaped balloon (the Inoue balloon), andinflate it within the orifice