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A Case of Dyspnoea
1. A Case of Dyspnea
Presented by Dr Shwet Dutta
Moderated by
Surg Capt Subhash Ranjan, NM, VSM,
Sr Advisor, Medicine & Oncology
2. Chief complaints
• 61 year old lady
• Resident of Manipur
• Presented with
Breathlessness on exertion X 02 years
Nausea
Upper abdominal discomfort
1
week
3. 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
4. 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.
5. Causes of Dyspnoea
System Acute dyspnoea Chronic exertional
dyspnoea
Cardiovascular system Acute pulmonary oedema Chronic CCF
Myocardial ischaemia
Respiratory system Acute severe asthma
Acute exacerbation COPD
COPD
Chronic asthma
Pneumothorax,
Pulmonary embolus
ARDS
Chronic pulmonary
thromboembolism , Large
pleural effusion
Pneumonia
Lobar collapse
Bronchial carcinoma
Lymphatic 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
6. History of Present illness (Contd/-)
• Nausea
• Decreased Appetite
• Occasional Vomiting (non bilious, non
projectile, gastric contents)
• Not relieved with PPI/ Antacids
• Dyspepsia?
7. Dyspepsia?
• Sleisenger: Rome III :- Pain /discomfort
centered in upper abdomen originating from
gastroduodenal region – include postprandial
fullness, early satiation, epigastric pain,
epigastric burning
8. 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)
9. 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
10. NYHA v/s Modified MRC
Functional
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 ground
pace
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
11. Negative history
• No h/o
Hemoptysis
Abdominal swelling
Swelling of feet
Syncope
TIA/Stroke
Weight loss
Worm infestation
14. 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
15. 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.
16. 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
19. 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.
20. 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.
21. 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)
24. 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)
25. 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
26. Pulsus tardus (delayed peak)
• AS – mechanical obstruction to left ventricular
ejection, accompanied by coarse systolic thrill
27. Hypokinetic (low volume and
amplitude)
•Hypovolemia / LV Failure 2 to myocardial
disease or myocardial infarction,
•Restrictive pericardial disease,
•Mitral stenosis
28. 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.
29. 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)
33. 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
34. 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.
35. 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.
36. 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
38. Pulsus bigeminus
• Regular alteration of pressure pulse amplitude
caused by a premature ventricular contraction
that follows each regular beat.
39. 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
42. • 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
43.
44. 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
45. 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
46. 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
50. 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
51. 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
52. Prominent x descent
• Presence of atrial relaxation with intact
tricuspid valve and good RV contraction
• Causes :
Cardiac tamponade
Constrictive pericarditis
53. 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.
54. 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
56. 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.
57. 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.
59. 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 .
60. 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
61. 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.
62. 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 normal
OS heard
Grade II/VI, Mid diastolic rumbling murmur,
heard best at apex in left lateral recumbent position
No PSE
63. Grading of murmurs
Grade 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
64. 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 pulse
3. Presence or absence of structural heart
disease
4. The amt of tissue, air or fluid between the
heart and the stethoscope.
65. Causes of Loud S1
1. If diastole is shortened because of
tachycardia
2. If AV flow is increased because of high CO
or prolonged because of MS
3. If atrial contraction precedes ventricular
contractions by unusually short interval (Short
PR interval)
66. Causes of Soft S1
1. Poor conduction of sound through the chest
wall.
2. Slow rise of LV pressure pulse
3. Long PR interval
4. Imperfect closure due to reduced valve
substance (MR)
5. Immobility of AMV leaflet due calcification
67. Splitting of S1
1. 10-30 ms (Normal)
2. M1 is followed by T1
3. Widening is most often due to RBBB &
resulting delay in onset of RV pr pulse
68. 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.
69. 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.
70. Splitting S2 (3/6)
• Splitting persisting in expiration is usually
abnormal in upright position.
71. Causes of wide split (4/6)
1. Delayed activation of RV (RBBB)
2. LV ectopic beat
3. LV pacing
4. 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
72. 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
73. Paradoxical Splitting (6/6)
• P2 precede A2
• Splitting is maximal in expiration & decreases
during inspiration
• Causes:-
1. LBBB
2. Delayed excitation of LV from RV ectopic beat
3. Severe Aortic outflow obstruction
4. Large Aortopulmonary shunt
5. Systolic Hypertension
6. IHD or CMP with LV failure
74. 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.
75. 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.
76. 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
77. 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
78. 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 function
ii) AV valve regurgitation
iii) Conditions that increase rate/volume of
ventricular filling
79. 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.
80. 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
82. 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
83. 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.
84. 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.
85. 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
86. 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
87. 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
88. 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
89. Criteria for Rheumatic Fever
Major 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
92. 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
93. 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)
94. 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)
97. Lab Investigations
Na+/K+ 139/3.6
S. Urea/ Creat 27/0.9
S. Bilirubin/
SGOT/SGPT/SAL
P
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
101. 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
102. 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
103. Haemoptysis
• Rupture of pulmonary vein–bronchial vein
shunts
• Pink frothy sputum with rupture of alveolar
capillaries
104. Ortner syndrome
• Compression of the left recurrent laryngeal
nerve by dilated left atrium, enlarged
tracheobronchial lymph nodes, and dilated
pulmonary artery causing hoarseness
105. 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
106. 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.
107. 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
108. 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
109. 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)
110. 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
111. Kerley A & B lines
Kerley 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.
117. Wilkins score
GRADE 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
118. 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.
119. 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)
120. Indications for Percutaneous Mitral
Balloon 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)
121. 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
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)
