a case of dyspnoea

A Case of Dyspnea

Presented by Dr Shwet Dutta

Moderated by Surg Capt Subhash Ranjan, NM, VSM, Sr Advisor, Medicine & Oncology

Chief complaints

• 61 year old lady• Resident of Manipur• Presented with Breathlessness on exertion X 02 years Nausea Upper abdominal discomfort

1 week

HISTORY OF PRESENT ILLNESS

• Breathlessness on exertion NYHA class II for 02 years

• Easy fatigability and dizziness for 02 years• Recently progressed to class IV; Orthopnea

for 07 days • Not associated with fever /cough /chest pain /

palpitations

Dyspnea

• Subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity. The experience derives from interactions among multiple physiological, psychological, social, and environmental factors and may induce secondary physiological and behavioral responses.

Causes of DyspnoeaSystem Acute dyspnoea Chronic exertional

dyspnoea

Cardiovascular system Acute pulmonary oedema Chronic CCFMyocardial ischaemia

Respiratory system Acute severe asthmaAcute exacerbation COPD

COPDChronic asthma

Pneumothorax,Pulmonary embolusARDS

Chronic pulmonary thromboembolism , Large pleural effusion

Pneumonia Lobar collapse

Bronchial carcinomaLymphatic carcinomatosis

Inhaled foreign body (especially in a child)Laryngeal oedema (e.g. anaphylaxis)

ILD: sarcoidosis, fibrosing alveolitis, extrinsic allergic alveolitis, pneumoconiosis

Others Metabolic acidosis Severe anaemia

Hyperventilation Obesity

History of Present illness (Contd/-)

• Nausea • Decreased Appetite• Occasional Vomiting (non bilious, non

projectile, gastric contents) • Not relieved with PPI/ Antacids• Dyspepsia?

Dyspepsia?

• Sleisenger: Rome III :- Pain /discomfort centered in upper abdomen originating from gastroduodenal region – include postprandial fullness, early satiation, epigastric pain, epigastric burning

Orthopnoea • Dyspnoea occurring in the recumbent position, relieved

by sitting upright or sleeping with additional pillows.

• Cause: Redistribution of fluid from splanchnic circulation and lower extremities into central circulation during recumbency, with a resultant increase in pulmonary capillary pressure

• Conditions: HF, obesity, ascites, pulmonary disease(lung mechanics favouring an upright posture)

Paroxysmal Nocturnal Dyspnea (PND)• Refers to acute episodes of severe shortness

of breath and coughing that generally occur at night and awaken the patient from sleep, usually 1–3 hours after retiring.

• Cause: Increased pressure in bronchial arteries leading to airway compression, along with interstitial pulmonary edema that leads to increased airway resistance.

• Persistent coughing and wheezing even after assuming upright position

NYHA v/s Modified MRCFunctional Capacity/Grade

NYHA (Objective Assessment) Modified MRC (Grade related to degree of breathlessness related to activities)

Class I/Grade 0 Patients with cardiac disease but without resulting limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitations, dyspnea, or anginal pain

No breathlessness except with strenuous exercise

Class II/Grade 1 Patients with cardiac disease resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain.

Breathlessness when hurrying on the level or walking up a slight hill

Class III/Grade 2-3 Patients with cardiac disease resulting in marked limitation of physical activity. They are comfortable at rest. Less than ordinary activity causes fatigue, palpitation, dyspnea, or anginal pain.

Walks slower than contemporaries on level ground because of breathlessness or has to stop for breath when walking at own

Stops for breath after walking about 100 m or after a few minutes on level groundpace

Class IV/Grade 4 Patients with cardiac disease resulting in inability to carry on any physical activity without discomfort. Symptoms of heart failure or the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort is increased.

Too breathless to leave the house, or breathless when dressing or undressing

Harrison’s Principles of Internal Medicine18 Ed

Negative history

• No h/o Hemoptysis Abdominal swelling Swelling of feet Syncope TIA/Stroke Weight loss Worm infestation

Family history

• Negative for:- Sudden death Valvular Heart Disease Ischemic Heart Disease

Personal history

No h/o• IV drug abuse• Tobacco/ Alcohol use• Disturbed Sleep• Mixed Diet

Past History

No 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 Breathing

Patients with advanced lung disease (in this case COPD) will often assume a tripod position (leaning forward, hands on knees) when breathing difficulties occur. This provides a position that optimizes respiratory mechanics.

General Examination

• Wt – 55 kg, Ht – 150 cm, BMI- 24.44 kg/m2 , • Pulse - 114/min, irregularly irregular, no

radio radial/ radio femoral delay, all peripheral pulses palpable

• BP – 108/64 mmHg right arm supine• 130/74 mmHg right lower leg• No pallor/ icterus/ cyanosis/ clubbing/ pedal

edema/ lymphadenopathy

Normal Pulse?

Normal Pulse?

Normal Pulse

• The normal central aortic pulse wave is characterized by a rapid rise to rounded peak.

• The anacrotic shoulder, present on the ascending limb, occurs at the time of peak rate of aortic flow just before maximum pressure is reached.

• The less steep descending limb is interrupted by a sharp downward deflection, coincident with AV closure, called incisura.

Pulse

• As the pulse wave is transmitted peripherally, the initial upstrokes becomes steeper, the anacrotic shoulder becomes less apparent.

• The incisura is replaced by the smoother dicrotic notch.

Pulse Rate/Rhythm

• Rate - > 100 / min - tachycardia < 50 / min - bradycardia• Rhythm • a)Regular – when every beat comes at the

expected time b) Irregular i)Regularly irregular(when the irregularities

can be predicted)

ii)Irregularly irregular (when they cannot)

Regular tachycardias

• 100-125 – Sinus tachycardia(CHF/High output state/Chronic lung disease/Rt. Sided hypertension)

• 125-165 – Atrial flutter with 2: 1 AV Block• 175-200 – Paroxysmal atrial tachycardia

Regularly irregular pulses

• 2nd degree AV Block • Sinus arrhythmia• Ectopic beats – bigeminy - digitalis

intoxication• Pulsus alternans ( + S3 = death rattles)

Irregularly irregular pulses

• Premature atrial contractions• Premature ventricular contractions• Atrial fibrillation( Delirium cordis – the only thing

predictable about the beat is its unpredictably)• Multifocal atrial tachycardia• Sinus arrest (If the pause b/w beats is less than 2 RR

intervals) • Sinus exit block v/s 2:1 AV Block(carotid sinus

pressure)

Pulsus Parvus

• The pressure is diminished, and the pulse feels weak and small, reflecting decreased stroke volume (e.g. heart failure), 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 ventricular ejection, accompanied by coarse systolic thrill

Hypokinetic (low volume and amplitude)

•Hypovolemia / LV Failure 2 to myocardial disease 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 significant

AR.• Seen in many conditions associated with increased

stroke volume: PDA, large arteriovenous fistula, hyperkinetic states, thyrotoxicosis anemia, and extreme bradycardia.

• Not seen in acute AR, since SV may not have increased appreciably.

Bounding Pulses (2/2)• Physical signs of aortic insufficiency are related to the high

pulse pressure and the rapid decrease in blood pressure during diastole due to the AI:

– Lighthouse sign (blanching & flushing of forehead) – de Musset's sign (head nodding in time with the heart beat) – Ladolfi's sign (alternating constriction & dilatation of pupil) – Becker's sign (pulsations of retinal vessels) – Müller's sign (pulsations of uvula) – Corrigan's pulse (rapid upstroke and collapse of the carotid artery pulse) – (Watson's) Water-hammer pulse – Quincke's sign (pulsation of the capillary bed in the nail) – Mayen's sign (diastolic drop of BP>15 mm Hg with arm raised) – Rosenbach's sign (pulsatile liver) – Gerhardt's sign (enlarged spleen) – Duroziez's sign (systolic and diastolic murmurs heard over the femoral artery when it is gradually

compressed) – Hill's sign (A ≥ 20 mmHg difference in popliteal and brachial systolic cuff pressures, seen in chronic

severe AI) – Traube's 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)

Water hammer

Bisferiens pulse – severe AR (+/- AS)

Bisferiens pulse - HOCM

Bisferiens pulse (2 systolic peaks)

• 1st peak – occurs as pulse wave upstroke rises rapidly and forcefully (percussion wave)

• A brief decline in pressure follows because of the sudden decrease in the rate of Left ventricular ejection during midsystole, when severe obstruction develops.

• 2nd peak – smaller and slowly rising positive pulse

wave(tidal wave) produced by continued ejection and by reflected waves from periphery

Pulsus Paradoxus (1/2)

• Pressure drop > 20 mmHg during inspiration.

• Normally, systolic arterial pressure falls 8-12 mmHg during inspiration.

• Evaluated with sphygmomanometer: – when the cuff is slowly released the systolic pressure at expiration is first

noted. With further slow deflation of the cuff, the systolic pressure during inspiration can also be detected.

Pulsus Paradoxus (2/2)• Causes:

– Cardiac Tamponade– COPD, hypervolemic shock– infrequently in constrictive pericarditis and rescrictive

cardiomyopathy.• Mechanism:

– Decreased LV-SV due to an increased RV-EDV and decreased LV-EDV during inspiration.

– In cardiac tamponade, the interventricular septum shifts toward the LV cavity during inspiration (reverse Bernheim’s effect) b/c of increased venous return to RV, decreasing the LV preload.

– Decrease in pulmonary venous return to the LV during inspiration also contributes to decreased LV preload.

Pulsus alternans

• Regular alteration of pressure pulse amplitude, despite a regular rhythm

• Due to alternating Left ventricular contractile force, which denotes severe left ventricular decompensation.

• May occur following/during paroxysmal tachycardia/ following a premature beat

• Poor prognosis

Dicrotic/ Bifid pulse

Peaks in systole and diastole – IABP, DCM

Pulsus bigeminus

• Regular alteration of pressure pulse amplitude caused by a premature ventricular contraction that follows each regular beat.

Apical-radial pulse deficit ?

• Simultaneously measure the apical ventricular rate and the radial pulse

• Put the stetho on apex and simultaneously count the dropped beats in the pulse for one minute.

• Conditions: AF, multifocal PACs and PVCs

JVP

• Jugular venous pulse is the oscillating top of the distended proximal portion of the internal jugular vein and represents volumetric changes that faithfully reflect the pressure changes in the right heart

Measurement of JVP

• Two scale method is commonly used • Normally JV pressure does not exceed 3- 4 cm of

blood above the sternal angle • Since RA is approximately 5 cm below the sternal

angle , the jugular venous pressure corresponds to 9 cm =7mmHg

• Elevated JVP : JVP of >3cm of blood above sternal angle

• CVP conversion factor 1.36 cm water equals to 1 mm Hg

a wave

• Reflects right atrial presystolic contraction and occurs just after the P wave, preceding S1

• Prominent a wave - reduced right ventricular compliance

• Cannon a wave - AV dissociation (right atrial contraction against a closed tricuspid valve)

• Absent with atrial fibrillation

Prominent a Wave • Forceful atrial contraction when there is resistance to RA

emptying or increased resistance to ventricular filling• RV inflow obstruction: Tricuspid stenosis or atresia RA myxoma • Decreased ventricular compliance:

Pulmonary stenosis Pulmonary hypertension of any cause RV infarction RV cardiomyopathy (HOCM) Acute pulmonary embolism

Large a wave

Cannon Waves• Whenever RA contracts against closed TV valve during RV

systole • Regular cannon waves: Junctional rhythm VT with 1:1 retrograde conduction Isorhythmic AV dissociation • Irregular cannon waves : Complete heart block AV dissociation with Ventricular tachycardia Ventricular pacing or ventricular ectopics .

Regular cannon waves

c wave

• Bulging of the tricuspid valve into the RA during RV isovolumic systole and by the impact of the carotid artery adjacent to the jugular vein

x descent

• Atrial relaxation, downward displacement of tricuspid valve during RV systole, and ejection of blood from both ventricles

• Most prominent motion of normal JVP which begins during systole and ends just before S2

• X descent more prominent during inspiration

Prominent x descent

• Presence of atrial relaxation with intact tricuspid valve and good RV contraction

• Causes : Cardiac tamponade Constrictive pericarditis

v wave

• Its height is determined by RA compliance and by the volume of blood returning to the RA, either antegrade from the vena cavae and/or retrograde through an incompetent TV

• With TR, the v wave will merge with the c wave because retrograde flow and antegrade RA filling occuring simultaneously.

Prominent v wave

• Increased RA volume during ventricular systole produce prominent v wave • Severe TR : giant v wave• ASD with mitral regurgitation • VSD of LV to RA shunt (Gerbode's defect)• RV failure

TR & cv wavecv wave/ ventricularized

y descent

• Tricuspid valve opening and the rapid inflow of blood into the RV.

• Resistance to ventricular filling in early diastole blunts the y descent, as in pericardial tamponade or tricuspid stenosis.

• The y descent will be steep when ventricular filling occurs early and rapidly, as with pericardial constriction or isolated severe TR.

Rapid y Descent

• Severe TR • Constrictive Pericarditis (Friedreich's sign)*:

Early rapid ventricular filling • Severe RV failure • ASD with mitral regurgitation

Friedreich's sign is the exaggerated drop in diastolic central venous pressure seen in constrictive pericarditis (particularly with a stiff calcified pericardium) and manifested as abrupt collapse of the neck veins or marked descent of the central venous pressure waveform. The sign is named after Nikolaus Friedreich.

Rapid y Descent

h wave • Small brief positive wave

following y descent just prior to a wave

• Described by Hieschfelder in 1907

• It usually seen when diastole is long

• With increasing heart rate, y descent immediately followed by next a wave .

Kussmaul's 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 upper quadrant, for at least 10 seconds.

• A sustained rise of more than 3 cm in the venous pressure for at least 15 seconds after resumption of spontaneous respiration is a positive response.

• Useful in predicting heart failure and a PA wedge pressure higher than 15 mm Hg.

SYSTEMIC EXAMINATION• JVP – raised• CVS – no visible pulsations/ heave no palpable thrill PMI – medial to left MCL S1 is loud,

S2 is normally split, P2 is normalOS heard

Grade 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 ideal

conditions)

Grade 2: Soft(faintest murmur that can be heard)

Grade 3 Intermediate between grades 2 and 4

Grade 4 loud with associated thrill

Grade 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 of systole.2. Rate of rise of left ventricular pressure pulse3. Presence or absence of structural heart disease4. The amt of tissue, air or fluid between the heart and the stethoscope.

Causes of Loud S1

1. If diastole is shortened because of tachycardia2. If AV flow is increased because of high CO or prolonged because of MS3. If atrial contraction precedes ventricular contractions by unusually short interval (Short PR interval)

Causes of Soft S1

1. Poor conduction of sound through the chest wall.

2. Slow rise of LV pressure pulse3. Long PR interval4. Imperfect closure due to reduced valve

substance (MR)5. Immobility of AMV leaflet due calcification

Splitting of S1

1. 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 Time

P2 is coincident with incisura of Pulm Artery pressure curve which is separated from RV pressure tracing by an interval termed the HANGOUT TIME.

Splitting of S2 (2/6)

3. The absolute value of Pulm Hangout reflects the resistance to pulm vascular bed.

4. The Hangout Time increases with RV Vol Overload & distensible pulm vascular bed

5. It decreases in increase in pulm vascular resistance with narrow splitting.

Splitting S2 (3/6)• Splitting persisting in expiration is usually

abnormal 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 RV

pressure load (PTE, PS)5. Delayed PV closure due to RV volume overload

associated with RV failure or diminished impedance of pulm 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 by LA & venae cavae varies reciprocally during the resp cycle so that RA inflow remains relatively constant.

2. Vol & duration of RV ejection remains same during Inspiration; leading fixed Splitting of S2

Paradoxical Splitting (6/6)

• P2 precede A2• Splitting is maximal in expiration & decreases

during 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 P2

Normally P2 is softer than A2 in second left ICS.P2 equal or greater than A2 in Pulm area suggests Pulm HTN; except in ASD where it is because of excess blood flow.

Ejection sound

• Sharp high pitched event occurring in early systole and closely following S1

• Occur with Semilunar valve stenosis, dilation of aorta/pulmonary artery

• Pulmonary ejection sounds, unlike aortic ones, tend to diminish or disappear in inspiration and the only right sided cardiac event to behave in this manner. It is better heard at lower left sternal border during expiration.

Non ejection clicks/Mid systolic clicks

• Occur with/without late systolic murmur denoting prolapse of one or both leaflets of mitral valve

• Results from chordae tendinae that are functionally unequal in length, best heard along left sternal border and at LV apex

• Systolic clicks occur later than systolic ejetion sound

Opening Snap

• Brief, High pitched, early diastolic sound due to AV valve stenosis (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 left atrial pressure. Ranges from 0.04-0.12 sec

• Tumor plop in patients with left atrial myxoma may have the timing of OS , but is usually lower pitched

S3

• Low pitched sound in ventricle 0.14-0.16 s after 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 of

ventricular filling

Pericardial Knock

• An S3 that is earlier (0.10-0.12 s after A2) and higher pitched than normal (pericardial knock in constrictive pericarditis) occurs due to restrictive effect of adherent pericardium which abruptly halts diastolic filling.

S4• Low pitched presystolic sound, best heard at LV apex

in left lat with bell during ventricular filling• Accentuated by mild isotonic/isometric exercise in

supine • It is associated with an effective atrial contraction

(Absent in AF)• Diminished ventricular compliance increases the

resistance 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

Common Murmurs and Timing

Systolic Murmurs• Aortic stenosis• Mitral insufficiency• Mitral valve prolapse• Tricuspid insufficiency Diastolic Murmurs• Aortic insufficiency• Mitral stenosis

S1 S2 S1

MDM

• Low pitched, MDM of MS follows OS. • Heard with bell at site of LV impulse(best

localised with the patient on the left side)• Increased with mild supine exercise• MDMs may be generated due to rapid flow

across the mitral valve in MR/PDA/VSD or across 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 to diastolic MR

• Severe chronic AR – MDM/Pre SM(Austin Flint) – originates at anterior mitral leaflet when blood enters LV simultaneously from both aortic root and LA.

Graham Steel Murmur

• High pitched EDM in Pulm area radiating down left sternal border.

• Seen in severe long standing Pulm Hypertension leading to secondary valve regurgitation.

P2 loud

• Its intensity exceeds that of A2 at the base• It can be palpated in the area of proximal

pulmonary artery (2nd left interspace)• Both components of S2 can be appreciated at

lower left sternal border or apex

Hill sign

• Brachial-popliteal systolic blood pressure gradient > 20 mm Hg

• With large stroke volume there is also a pressure wave at right angles to the forward wave. The two waves sum only in the lower extremities because the upper extremity vessels exit the aorta at right angles.

• Sensitivity 89% for moderate to severe AR

Müller's Manoeuvre

• Forced inspiration against closed glottis• The reverse of Valsalva manoeuvre• Positive result means site of upper airway

obstruction is below level of the soft palate

WHO Criteria for Diagnosis of Rheumatic Fever Diagnostic Categories Criteria

Primary episode of rheumatic fever Two major or one major and two minor manifestations plus evidence of preceding group A streptococcal infection

Recurrent attack of rheumatic fever in a patient without established rheumatic heart disease

Two major or one major and two minor manifestations plus evidence of preceding group A streptococcal infection

Recurrent attack of rheumatic fever in a patient with established rheumatic heart disease

Two minor manifestations plus evidence of preceding group A streptococcal infection

Rheumatic chorea Insidious onset rheumatic carditis

Other major manifestations or evidence of group A streptococcal infection not required

Chronic valve lesions of rheumatic heart disease (patients presenting for the first time with pure mitral stenosis or mixed mitral valve disease and/or aortic valve disease)

Do not require any other criteria to be diagnosed as having rheumatic heart disease

Criteria for Rheumatic FeverMajor manifestations Carditis

Polyarthritis

Chorea

Erythema marginatum

Subcutaneous nodules

Minor manifestations Clinical: fever, polyarthralgia

Laboratory: elevated erythrocyte sedimentation rate or leukocyte count

Electrocardiogram: prolonged P-R interval

Supporting evidence of a preceding streptococcal infection within the last 45 days

Elevated or rising anti-streptolysin O or other streptococcal antibody, or

A positive throat culture, or

Rapid antigen test for group A streptococcus, or Recent scarlet fever

Sydenham’s chorea

Mitral Facies

SYSTEMIC EXAMINATION (contd.)

• Abdomen – soft, tenderness + in right hypochondrium, liver is palpable 2 cm below Rt. MCL

• Chest – bilateral basal crackles + (left > right)• Central nervous system – within normal limits

Differential Diagnosis (1/2)

• Significant MR (murmur commences slightly later, evidence of LV enlargement, opening snap and increased P2 are absent, and S1 is soft or absent). Apical pansystolic murmur & S3 +

• Severe AR - Austin Flint murmur (not intensified in presystole and becomes softer with administration of amyl nitrite)

Differential Diagnosis (2/2)

• Atrial septal defect (fixed splitting of S2 with a grade 2 or 3 mid-systolic murmur at the mid to upper left sternal border)

• TS (murmur increases with inspiration)• Left atrial myxoma (features suggestive of

systemic disease + findings change with body position)

ECG

Chest Xray

Lab Investigations

Na+/K+ 139/3.6

S. Urea/ Creat 27/0.9

S. Bilirubin/ SGOT/SGPT/SALP

0.9/15/21/116

Hb/TLC/P/L/E/M 14.1/7300/65/27/03/05

PT/INR/APTT 25/2.0/49

S. Amylase 65

CK/MB 121/10

Echo

• Rheumatic Heart Disease – moderate Mitral Stenosis, mild PAH, mild TR, AF, mild AR, moderate LV Dysfunction

USG Abdomen

• Left Ovarian Cyst• Cholelithiasis• Grade II Fatty change

Mitral Stenosis - Etiology

• Rheumatic fever• Congenital• Annular calcification with extension onto

leaflets• Systemic Lupus Erythematosus, Rheumatoid

Arthritis

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 during exertion

• Severe MS - mitral valve opening <1 cm2 • ↑pulmonary venous and PAWP reduce

pulmonary compliance →→ exertional dyspnea

Pulmonary hypertension

(1) passive backward transmission of elevated LA pressure(2) pulmonary arteriolar constriction (reactive pulmonary hypertension)(3) interstitial edema in walls of small pulmonary vessels (4) organic obliterative changes in pulmonary vascular bed

Haemoptysis

• Rupture of pulmonary vein–bronchial vein shunts

• Pink frothy sputum with rupture of alveolar capillaries

Ortner syndrome

• Compression of the left recurrent laryngeal nerve by dilated left atrium, enlarged tracheobronchial lymph nodes, and dilated pulmonary artery causing hoarseness

Causes of AF

• Combination of mitral valve disease and atrial inflammation secondary to rheumatic carditis → left atrial dilation, fibrosis of atrial wall, disorganization of atrial muscle bundles → disparate conduction velocities and inhomogeneous refractory periods.

• Premature atrial activation, caused by automatic focus or reentry, may precipitate AF

Palpation

• Enlarged RV may displace LV posteriorly and produce RV apex beat that can be confused with a LV lift

• A palpable loud P2 (aka Diastolic shock) in second left ICS indicates severe pulmonary hypertension.

OS V/S S2

• OS occurs later, unless RBBB is present. • OS is loudest at apex, during expiration , S2 is

best heard at base. • OS is accompanied by accentuated S1.• OS - A2 interval varies inversely with left atrial

pressure

Associated lesions

• With severe PAH, a pansystolic murmur is heard (functional TR) along left sternal border, ↑during inspiration (Carvallo's sign)

• Graham Steell murmur of PR (a high-pitched, diastolic, decrescendo blowing murmur along left sternal border) ← dilation of pulmonary valve ring in patients with severe PAH

ECG

• Left atrial enlargement (P wave duration in lead II > 0.12 second and/or a P wave axis between +45 and −30 degrees)

• Correlate more with left atrial volume than pressure

• Criteria for RV hypertrophy(mean QRS axis > 80 degrees in frontal plane and R:S ratio greater than 1 in lead V1)

MS, CXR-PA view• The heart size is normal. • The enlarged left atrium (A)

displaces the left bronchus upwards (*) and creates a right retrocardiac double density.

• The left atrial appendage is enlarged (arrowheads). There is severe pulmonary venous 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.

2-D Echo showing heavily calcified Mitral valve leaflets and

Mitral stenosis

3-D Echo of Mitral Stenosis3-D Echo of Mitral Stenosis

LA viewLA view LV viewLV view

3-D measurement of Mitral valve area3-D measurement of Mitral valve area

MVA= 0.914 cmMVA= 0.914 cm22

LA viewLA view LV viewLV view

Real Time TTE of the Mitral Valve

LALA

A B C

D E F G

Real Time TTE of MS

Wilkins scoreGRADE MOBILITY THICKENING CALCIFICATION SUBVALVULAR

THICKENING

1 Highly mobile valve with only leaflet tips restricted

Minimal thickening just below the mitral leaflets

Leaflets almost normal in thickness (4-5 mm)

Single area of increased echo brightness

2 Leaflet mid and base portions have normal mobility

Thickening of chordal structures, extending up to one third of chordal length

Mid leaflets normal, considerable thickening of margins (5-8 mm)

Scattered areas of brightness confined to leaflet margins

3 Valve continues to move forward in diastole, mainly from the base

Thickening, extending to the distal third of the chords

Thickening extending through entire leaflet (5-8 mm)

Brightness extending into midportion of the leaflets

4 No or minimal forward movement of the leaflets in diastole

Extensive thickening and shortening of all chordal structures, extending down to the papillary muscles

Considerable thickening of all leaflet tissue (>8-10 mm)

Extensive brightness throughout much of the 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 increasing severity of regurgitation, advanced age, prior commissurotomy, absence of commissural fusion, and presence of commissural calcification merits surgical intervention.

Rx

• Penicillin prophylaxis of group A -hemolytic streptococcal infections for secondary prevention of rheumatic fever

• Restriction of Na+ intake , oral diuretics, Vasodilators

• Beta blockers, Calcium channel blockers (e.g., verapamil or diltiazem), digitalis for slowing the ventricular rate

• Warfarin (AF / h/o thromboembolism)

Indications for Percutaneous MitralBalloon Valvotomy

• Symptomatic patients, with moderate or severe MS (MVA < 1.5 cm2) and favorable valve morphology in absence of left atrial thrombus or moderate to severe MR

• Asymptomatic patients with moderate or severe MS with pulmonary hypertension (pulmonary artery systolic pressure > 50 mm Hg at rest or > 60 mm Hg with exercise)

Technique

• Advance a small balloon flotation catheter across interatrial septum (after transseptal puncture)

• Enlarge the opening• Advance a large (23- to 25-mm) hourglass-

shaped balloon (the Inoue balloon), and inflate it within the orifice

Percutaneous balloon mitral valvotomy

ThankYou