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CVS - CONSOLIDATED

THEORY - ROADMAP

 March - Hemat, Endo, Rheumat


 APRIL 1st week : INTERNAL
 April- Nephro
 May – Cardio
 June – Gastro
 JULY – 1st half – Internal
 July – Neuro
 August – Infn diseases
 Sep – Respiratory system
 Oct – Critical care, Onco, Genetics, Skin, Psych etc.,
 Nov – 3rd Internal
 Dec, Jan - Revision
 Dec – Model, Medal exam
ROADMAP – CLINICAL

 Clinical methods – 5 days


 System theory – 16 days
 Case sheet writing – 14 days
 Disease theory – 25 days

 Total 60 days
 Xray, spotters, charts, ECGs- hearsay
BOOKS

 Hutchison’s, Mcleod’s – Examination methods


 Alagappan, Kundu, ?Mathew –System Theory,
Disease Theory
 Class Notes; ?PDF format

 Davidson’s +/- Slides – Theory


 Other subjects
PULMONARY HYPERTENSION

 a waves in JVP
 Prominent cv (s) waves in JVP due to
functional TR – venous corrigans
 Prominent pulmonary artery pulsations –
pulmonary area
 Palpable P2
 Parasternal heave
 Epigastric pulsations – tip of finger
PULMONARY HYPERTENSION

 Lateral displacement of Apex in the same space


 Exaggerated retraction of apical impulse (as RV forms
the apex)
 Closely split S2 or single S2
 Loud P2
 PSM of functional TR in Tricuspid area
 EDM of PR in Pulmonary area – Graham steel
murmur
 ESM in Pulmonary area
Atrial fibrillation

 Irregularly irregular pulse


 Varying volume pulse
 Absent a waves
 Variable intensity S1
 Absence of presystolic accentuation in MDM of MSM

 BP – average of 3 readings
Mitral stenosis

 Tapping apical impulse


 Diastolic thrill
 Loud S1
 Opening snap
 Low pitched rough rumbling MDM of grade
_ /4 intensity with presystolic accentuation
heard best with the bell of the stethoscope in
left lateral position with breath held in
expiration
 USUALLY ASSOCIATED WITH SIGNS OF PHT
LIKE:
 Palpable P2
 Parasternal heave
 Loud P2

 Other signs of PHT may be present


 Causes of soft S1 in MS?
 Silent MS?
 Absent presystolic accentuation?
 What OS indicate?
 Absent opening snap?
 When MS produces pandiastolic murmur?
 Why S1 loud?
Mitral regurgitation

 Large volume pulse (pseudocollapsing)


 Apical impulse shifted down and out
 Hyperdynamic apical impulse
 Soft S1
 Wide variable split S2
 S3
 Flow MDM at the apex
 Rarely OS best heard internal to apex
 Loud S1 in MR?
 Early systolic murmur in MR?
 Diastolic MR?
 What does intensity indicate?
AORTIC STENOSIS (Valvular)

 Pulsus parvus et tardus


 (diminished and delayed peaking slow rising,
small volume pulse)
 Heaving apical impulse
 Aortic area thrill
 Carotid thrill
 S4
 Valvular Aortic ejection click in BAV without severe
calcification
 A2 soft (loud A2 – BAV without severe
calcification)
 Single S2 or reverse splitting of S2
 Medium/mixed pitched rough rasping grade
_ /6 mid systolic or ejection systolic murmur
heard in the aortic area conducted to carotids
 Gallavardin phenomenon – high frequency
components of MSM/ESM better heard in the apex;
seen in AS of atherosclerotic etiology
Aortic regurgitation

 Peripheral signs of wide pulse pressure

 Aortic area, suprasternal, sternoclavicular,


epigastric pulsations
 Apical impulse shifted down and out
 Hyperdynamic apical impulse
Features of wide pulse pressure

 Light house sign (alternate flushing and blanching of


forehead)
 Landolfi’s sign (change in pupillary size in
accordance with cardiac cycle and not related to
light)
 Becker’s sign (Retinal artery pulsations)
 de Musset’s sign (head bobbing with each heart beat)
 Muller’s sign (systolic pulsations of uvula)
 Quincke’s sign (capillary pulsations detected by
pressing a glass on patient’s lip or nail bed
 Corrigan’s sign (Dancing carotids)
 Locomotor brachii
 Collapsing or water hammer pulse (large volume
pulse with rapid upstroke and rapid downstroke –
pulse pressure more than diastolic pressure
 Pistol shot femorals (Traube’s sign)
 Duroziez sign – systolic murmur heard over femoral
artery when it is compressed proximally and a
disastolic murmur when it is compressed distally
 Duroziez murmur -diastolic murmur heard with
diaphragm of stethoscope whe distal pressure is
applied
 Hill’s sign – popliteal pcuff systolic pressure exceeds
brachial cuff pressure by > 20mmHg
 Rosenbach’s sign – pulsations of liver
 Gerhardt’s sign – pulsations over enlarged spleen
AORTIC REGURGITATION

 S1 soft
 A2 soft in rheumatic; ringing in atherosclerotic;
tambour in syphilitic
 High pitched grade _/4 early diastolic
murmur heard in the aortic area heard better
in leaning forward position with breath held
in expiration
 Root causes of AR– better at the right side aortic
area and along the right sternal border
 Valve causes of AR– better at the neo aortic area
(Erb’s area) and along the left sternal border
 Flow ESM at the aortic area in severe AR
 Austin flint murmur – MDM due to premature
mitral valve closure obstructing mitral valve inflow
 Absence of signs of wide pulse pressure in AR?
 Duration of EDM?
ASD

 Prominent pulmonary artery pulsations


 Pulmonary area thrill may be present
 Loud P2
 Wide fixed split S2
 ESM heard at pulmonary area
 Tricuspid area OS
 Flow MDM in tricuspid area
 General examination findings in ASD?
 Congenital anomalies associated?
 What is the cause for murmur in ASD?
VSD

 Large volume pulse


 Hyperdynamic apical impulse
 Wide variable split S2
 Systolic thrill at left sternal border over 4th ICS
 Pan systolic murmur at the left sternal border over
4th ICS
 Early systolic murmur if very small muscular VSD or
VSD with PHT
 Flow MDM at the apex; rarely OS at apex
PDA

 Large volume pulse


 Hyperdynamic apical impulse
 Left infraclavicular pulsations
 Pulmonary area pulsations
 Machinery Continuous murmur at the
infraclavicular area reaching the acme at P2
 Flow MDM at the apex; rarely OS at apex

 Differential clubbing in PDA with PHT


 What happens to the murmur as patient develops
PHT?
 What are the other continuous murmurs?
TOF

 Central cyanosis
 Pan digital clubbing
 Absent P2
 Single loud A2
 Sytolic thrill may be present at left sternal border
 ESM/MSM at the pulmonary area
 What happens to the murmur in hypoxic spell?
 What is the cause for ESM in TOF?
EISENMENGER SYNDROME

 Cyanosis
 JVP elevated; prominent a waves
 Loud P2 and other features of PHT
 Single S2 – VSD
 Narrow split - ASD
 Closely split – PDA; Differential clubbing
Clues

 Down& out AI + Wide pulse pressure signs


EDM AA = AR
 Down & Out AI + PSM in MA (without wide pulse
pressure signs) = MR

 Same space AI + Loud S1 + OS + PHT signs + MDM


= MS
 Same space AI + ESM AA + Carotid thrill = AS
 All of the following can be seen except:

 OS in MR
 S3 in MS
 MDM in PDA
 Wide split S2 in VSD
 All of the following are true except:

 Left sternal border 4th space area thrill in VSD


 Single loud A2 TOF
 Loud A2 in calcific AS
 Loud S1 MVP
 All of the following are true except:

 PSM in Tricuspid area indicates PHT mostly


 ESM of AS can be conducted to MA
 ESM in PA in straight back syndrome
 Flow MDM in MA in ASD