Cardiology

Examination
 Greeting: Hand sterilization, Hello, Mr/Mrs …... while shaking hands, nice to meet you 

 Introduction: I am Dr ……, I was asked to examine your heart, is it ok with you? 

 Do you have any pain? … Kindly if you have any pain or discomfort, please let me know 

 1) General survey (inspection):

o Put your hands behind your back, then take few steps backward at the bed end, for inspection,
I will take a general look from your foot side, sir  ‫نظرة عامة من ناحية رجليين العيان من نهاية السرير‬
o Patient is comfortable/distressed.
o Can you elevated your arms up for me, sir 
o Surroundings: Oxygen, cannula.
o Facial dysmorphics:
 Down: VSD.
 Turner: Aortic: AS, Bicuspid, AR, and Coarctation.
 Noonan: (male turner): PS
 Marfan: AR, MR.
 2) Hands:
o Dorsum: Clubbing, Splinter Hge.
o Palm: Palmar erythema, Osler’s nodes, Janeway lesions.
 3) Pulse:
o Rate (…. /min): both radial pulsations together at the same time (radio-radial delay).
o Rhythm: regular / irregular.
o Radio-femoral delay (Ask firstly, Can I check you pulse here at your groin, sir )
o Collapsing pulse: (Ask patient firstly: Do you have any shoulder pain, sir )
 4) JVP & Carotid pulsations:
o Patient position at 45 degree.
o Ask the patient to turn his face to the left side.
o Hepato-jugular reflux: (+ve result = sustained rise ≥ 4 cm) (Ask firstly, Can I press here on
your tummy, sir ) 
o Palpate carotid pulsations: characters: visible in AR.
 5) Eyes:
o Look Up & look down.
o Jaundice.
o Xanthelasmas.
 6) Mouth:
o Cyanosis: evert your tongue ‫اللسان مقلوب‬
o High arched palate  Marfan $
 7) LL:
o LL oedema → pitting, level.
o Dorsalis pedis bilaterally.
o Scar: Saphenous vein harvesting scar.
 8) Inspection:
o Scars: mid-line sternotomy scar, mitral valvotomy scar, infraclavicular pacemaker scar.
o Chest wall deformity: pectus excavatum, carinatum.
o Cardiac bulge: denoting that it is a since childhood.
 9) Palpation:
o Apex:
 Site ‫هام جدا وكأنك بتعد الضلوع‬
 Size
 Character
 Thrill
o Lt Parasternal heave (by heel) & Thrill (by base of fingers)

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o P: Palpable P2 & Thrill.

o A: Thrill.
 10) Auscultation:
o Listen to each valve area in turn, then carotid area.
o Put your fingers on carotid pulse: not more than 5 seconds (I will put my fingers on your neck,
sir ) ‫االبهام على الكاروتيد‬
o Apex: MR, MS.
o Axilla: MS: Let patient lean to his Lt Side with elevation of Lt arm (Lt Lat position).
o Lower Lt Parasternal: TR.
o Upper Lt Parasternal: VSD.
o P: PHT, PS.
o A: AS.
o Carotids bilaterally.
o Use the bell for Apex & Axilla & Carotid.
 11) Let patient sit up and lean forward:
1. Could you please breathe in, breathe out & then hold it for me plz: better for AR (A2) area.
2. Back auscultation: lung base: clear/ bibasal fine end inspiratory crepitation.
3. Sacral oedema.
 12) End: Cover the patient, thank him with hand shaking 

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 Cardiology

Presentation
 Do not forget: Patient is comfortable at rest,/ signs of CHF:
 Do not forget: There is No peripheral stigmata of IEC (an important –ve finding):
o Splinter Hge.
o Osler’s nodes.
o Janeway lesions.

Inspection:
 ± Complexion:
o Anaemia: dt haemolysis, anticoagulation & IEC
o Jaundice: dt prosthetic valve haemolysis.
o Cyanosis: congenital cyanotic heart diseases.
 ± Clubbing:
1. Congenital cyanotic heart diseases → cyanotic clubbing, except: Pale clubbing: in Pink
Fallot (No overriding of Aorta) 
2. Other causes of clubbing: → atrial myxoma & IEC.
 ± Scars:
o Mid-line sternotomy scar,
o Mitral valvotomy scar (Lt lateral thoracotomy scar): easy to miss,
o Pacemaker scar (Lt infra-clavicular) with prominence.
o Radial artery harvest scar.
o Saphenous vein harvest scar.
 Gynecomastia: aldactone for CHF.

Pulse: (7 items):
1) Rate: …beats/ min
2) Rhythm: regular / irregular (AF)  MVD or ASD
3) Equality: Equal on both side/ unequal: aortic coarctation, dissection.
4) Volume:
a. Low volume: → AS
b. High volume: → AR
5) Special Character:
o Slow-rising: → AS.
o Collapsing: → AR, or any hyperdynamic causes.
o Jerky: → Severe MR
6) Radio-femoral delay.
7) Peripheral pulsation (Dorsalis pedis).

JVP:
 Not elevated.
 Elevated: …. cm,
o Giant systolic ‘v’ waves of TR, → so look for signs of PHT.
o Remember that: In AF: loss of ‘a’ wave & in AF: no S3 or S4.

Apex: (4 items):
1) Site:
o Undisplaced (normal): Lt 5th intercostal place at mid-clavicular line.
o Displaced (out & down): LVH of MR or AR.
o Displaced (out & in place): RVH of MS or TR.
2) Size:
o In one space: LVH.
o In 2 spaces: RVH.

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3) Character: ( by palm side of fingers tips):

o Tapping (Slapping) (=palpable S1): MS. HP = Heaving Pressure-loaded
o Heaving: AS, LVH, HOCM. TV = Thrusting Volume-loaded
o Thrusting (Hyperdynamic): AR, MR, VSD, TR & PDA.
4) Thrill: (by palm of the hand)
o Systolic: MR
o Diastolic: MS

Lt Parasternal heave / thrill:

 Lt Parasternal heave (denote RV pressure overload): PHT.
 Lt Parasternal systolic thrill (denote functional TR): VSD.

P area: Lt 2nd intercostal space:

 Palpable S2→ PHT.
 Thrill → PS/ ASD.

A area (A1): Rt 2nd intercostal space:

 Thrill → AS
 AS murmur: ejection systolic murmur, propagate to the root of the neck.
 If not propagate to the neck → so it is aortic sclerosis not stenosis.

A area (A2): Lt 3rd intercostal space:

 AR: early diastolic murmur: let the patient to sit up, lean forward with slightly deviation to his Lt side,
let him breath in then breath out then hold at the end of expiration.

S1:
 Normal: NS1
 Soft S1: MR.
 Accentuated (Loud) S1 ± Palpable S1 (= tapping apex beat): MS.

S2:
 Normal: NS2
 Soft S2: AS/ AR or PS.
 Reversed splitting of S2: AS/HOCM
 Loud pulmonary component of S2: PHT
 Wide splitting S2: PS
 Wide fixed splitting of S2 : ASD
Murmurs:
 Characteristics:
o Pansystolic: MR, TR & VSD.
o Ejection systolic:
 AS (crescendo-decrescendo)/ aortic sclerosis, HOCM
 PS , ASD
o Early diastolic: AR
o Mid diastolic rumbling with pre-sytolic accentuation: MS
 Time:
o Systolic.
o Diastolic.
 Best heard:
o ↑ During inspiration: (any Rt sided heart lesions): TR.
o ↑ During Expiration: (any Lt sided heart lesions): MR, AR.
 Patient position:
 Lt Lateral: MS, MR.

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 Sitting with leaning forward and slightly to the Lt side after end expiration: AR
You can say: I am unable to auscultate (I could not appreciate) any other valvular heart abnormalities.

Mention ± Malar rash (if MVD).

Mention severity of valvular lesion: MS, AS, MR, AR.

If prosthetic valve:
1) It appears to be functioning well (audible metallic click) / not 
2) ± Complications of anticoagulation: purpura.

Carotids:

Lung base: clear / bibasal fine end inspiratory crepitations.

LL: odema/ no odema

Signs of CHF (may be minimal if Pt on diuretics):

1) ↑ JVP
2) Basal crepitations → LVF,
3) Sacral odema,
4) LL oedema.
5) Congestive tender hepatomegaly.
6) Ascites.
7) Scrotal oedema

Signs of PHT:
1) ↑ JVP …. cm, with giant systolic ‘V’ waves of TR.
2) Lt Parasternal heave → denote RV pressure overload.
3) Lt Parasternal thrill → denote functional TR.
4) Palpable pulmonary component of S2 (P2) over P area.
5) Loud pulmonary component of S2 (P2) over P area.
6) Graham-steel murmur of PR: Very short early diastolic decrescendo murmur at P area (upper
Lt sternal edge), with the pt sitting forward, louder in inspiration, radiate down to lower Lt
sternal edge.
7) Functional TR: Pansystolic murmur at lower Lt sternal edge, louder in inspiration (Carvallo’s
sign).
8) ± Bibasal crepitations,
9) ± LL oedema.

If there is PHT >>> try to provide a possible cause: e.g.: COPD, ILD, RA, SLE, SS, Eisenmenger’s, MS.

I would like to complete my examination by checking the following:

 BP (in both arms).
 Peripheral pulsations.
 Urine dipstick for microscopic haematuria.

NB: A parasternal heave is often felt at the Lt sternal edge. However, in long standing PHT and RV dilatation,
the heave may be feltat the Rt parasternal edge.

NB: Sometimes a palpaple P2 can be difficult to confirm. It is best felt over P area, and coincides with S2.
This can be confirmed using one hand to palpate the carotid and other hand to feel over the P area. Knowing
that the carotid impulse coincides with S1, a palpable P2 will occur AFTER carotid impulse.
(Carotid impulse = S1).

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NB: A loud P2 may be herad all over the pericardium, but is loudest over P area. Although A2 occurs before
P2 (A2-P2), a separate P2 may be difficult to distinguish as often they merge as a loud S2, so you can present
it as “a loud S2”.
NB: The murmur of functional TR is often heard at the lower Lt sternal edge, and is louder in inspiration
(Carvello’s sign). Occasionally in case of severe RV dilatation with severe TR, the murmur can be heard over
the apex.

NB: Severe PHT (PASP ≥ 60 mmHg) → Pulmonary artery dilatation → Pulmonary valve dilatation → Loss
of coaptation of the pulmonary valve leaflets → Secondary Pulmonary regurgitation (PR): Graham-Steel
murmur.

NB: DD: pansystolic murmurs:

Pan-Systolic

Murmurs

TR MR VSD
↑ during Inspiration ↑ during expiration All over the precordium
propagate to the axilla

NB:
 Any murmur of RT sided of the heart: e.g. TR → ↑ during inspiration.
 Any murmur of LT sided of the heart: e.g. MR → ↑ during expiration.

NB: In any valve replacement: correlate the metallic click with the carotid pulsation:
 If coincide with carotid pulsation (S1) → MVR.
 If not coincide → AVR.

NB: Check the important peripheral signs of AR:

 Pistol shot.
 Corrigan sign.
 Capillary pulsation.

At the end of presentation:

 No signs of CHF
 No signs of PHT
 No signs of IEC
 No signs of over anticoagulation (if metallic valves)
I would like to complete my examination by checking BP, urine dipstick & observation chart

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AS & AR

Aortic stenosis (AS) Aortic regurgitation (AR)

 Ejection systolic murmur (ESM) at A area  Decrescendo early diastolic murmur (EDM)
(crescendo-decrescendo murmur) at the upper Lt sternal edge,
(Diamond murmur),  Loudest with the patient sitting forward and
 Louder during expiration, with end expiration.
 Radiate to carotids.

 NS1  NS1
 Soft S2, / reversed splitting of S2 (delayed  Soft S2 or NS2
A2).

 Apex:  Apex:
o Non-displaced. o Displaced (LVH),
o Heaving: (Sustained in Stenosis). o Thrusting.
(HP = Heaving Pressure loaded) (TV = Thrusting Volume-loaded)
o Thrill

 Pulse:  Pulse:
o Low volume. o Large volume.
o Slow-rising character. o Collapsing character.

 Systolic thrill palpable in A area  Visible carotid pulsation.

 Austin-flint murmur:
o It is a functional MS in Pt with AR.
o It is a marker of severity of AR.
o It is a soft low-pitched mid-diastolic
rumbling murmur at the apex.
o DD: from MS:
 Opening snap (OS).
 Loud S1.
 Palpable S1 (tapping apex
beat).
DD of AS: DD of collapsing pulse:
o Aortic sclerosis o AR.
o HOCM o Severe MR
o VSD o PDA.
o Aortic flow: high COP state: anaemia & o Paget’s D
pregnancy o Any hyperdynamic circulation:
o Fever
o Anaemia
o Thyrotoxicosis.
o Pregnancy.
o AVF.

Causes of AS: Causes of AR:

 Common:  Acute AR:
o Bicuspid aortic valve (young). o Aortic dissection.
o Sclerotic aortic valve (elderly). o IEC.
o RHD (Strept). o Rupture sinus of Valsalva aneurysm.
o Congenital: o Prosthetic aortic valve failure
 Supra-valvular AS: William  Chronic AR:
 Sub-valvular AS: HOCM o Bicuspid aortic valve (Turner).
 Rare: o RHD.

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o IEC. o HTN.
o Hyperuricaemia. o RA.
o Alkaptonuria. o SLE.
o Paget’s disease. o Aortitis:
 Syphilis.
 Takayasu’s arteritis.
 Anklosing spondylitis.
 Psoriatic arthropathy
 Reiter’s S.
o CT disorders:
 Marfan’s S.
 Pseudoxanthoma elasticum.
 Ehlers-Danlos S.
 Osteogenesis Imperfecta.
o Perimembranous VSD with prolapse
of Rt coronary cusp.
Clinical signs of severity of AS: Clinical signs of severity of AR:
1) Narrow PP. 1) Wide PP (collapsing pulse).
2) Slow-rising pulse. 2) Long duration of murmur.
3) Low pulse volume. 3) S3.
4) Heaving apex. 4) Austin Flint murmur (functional MS).
5) Systolic thrill. 5) Other clinical signs associated with
6) Reversed splitting of S2 (delayed A2). severe AR 
7) Soft S2/ absent aortic component of S2. 6) Signs of PHT.
8) S4. 7) Signs of LVF.
9) Late systolic peaking of a long murmur.
10) Signs of PHT.
11) Signs of LVF.

Indications for surgery: Indications for surgery:

 Symptomatic: Low COP: syncope, angina,  Symptomatic:
dyspnea: o Severe AR + symptoms of CHF.
o Severe AS: o Severe AR + angina.
 Mean PG > 50 mmHg &  Asymptomatic:
 AV area < 1 cm2. o EF ˂ 50%.
 Asymptomatic: o LV dilatation:
o Moderate/ severe AS with  LVESD ˃ 55 mm or
undergoing other cardiac surgery  LVEDD > 75 mm.
i.e. CABG. o Aortic root dilatation > 50 mm.
o Severe AS PLUS any of the
following:
1) LV systolic dysfunction 105 ‫القاعدة‬
(Mean PG >40 mmHg). ‫الميترالى يتغير بدرى عن األورطى‬
2) Abnormal BP response to
exercise treadmill test.
3) VT.
4) Valve area < 0.6 cm2.

Types of AVR surgery:

1) Open.
2) BAV = Balloon Aortic Valvoplasty.
3) TAVI = Trans-cutaneous Aortic Valve
Implantation

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 Cardiology

Mixed AVD
Predominant AS Predominant AR
Pulse o Low volume o Large volume.
o Slow rising character o Collapsing character
Apex beat o Minimally displaced. o Displaced.
o Heaving (sustained). o Thrusting.
Systolic thrill +ve no
Visible carotid pulsation no +ve
SBP Low High
PP Narrow Wide
Both Murmur of AS + Murmur of AR:
 AS: Ejection systolic murmur at A area, Louder in expiration, Radiate to carotids.
 AR: Early diastolic murmur at the upper Lt sternal edge, Loudest with the patient sitting forward and
with end expiration.

Associated peripheral signs findings in AR:

1) Corrigan’s sign = visible distension and collapse of carotid arteries

2) De Musset’s sign = head nodding with each heart beat
3) Quincke’s sign = pulsations are seen in the nail bed with each heart beat when nail bed is lightly
compressed
4) Duroziez’s sign = murmur (systolic or diasolic) over femoral arteries
5) Traube’s sign = pistol shot = sound heard when stethoscope placed over femoral arteries during
systole & diastole
6) Muller’s sign = uvula pulsations are seen with each heart beats

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MS & MR

Mitral stenosis (MS) Mitral regurgitation (MR)

 OS in early diastole, followed by  Pan-systolic murmur (PSM) at the apex,
 low pitched mid-diastolic rumbling murmur  Loudest on expiration.
(MDM) with pre-systolic accentuation at  Radiate to the axilla.
apex,
 loudest on expiration.
 Patient in Lt Lateral position.
 With bell.
 S1:  Soft S1
o Accentuated S1.
o Soft S1: only if mitral valve leaflets
calcifications or Mixed MVD.
o Palpable S1 = tapping apex beat.
o Variable S1 (if with AF).
 NS2  NS2
 Apex:  Apex:
o Undisplaced. o Displaced (LVH),
o Palpable S1 = tapping apex beat. o Thrusting.
o No heave. o No heave.
o No thrill. o Systolic thrill.
Causes of MS: Causes of MR:
o Rheumatic heart disease (RHD).  Acute MR:
o Congenital MS. o IEC.
o LA myxoma o Rupture of Chordae tendinae/
o MPS papillary muscles.
o RA. o Trauma.
o SLE.  Chronic MR:
o Carcinoid S. o RHD.
o Fabry’s D. o MVP.
o Whipples D. o Cardiomyopathy.
o LV dilatation (functional MR)
o RA.
o SLE
o CT disorders:
 Marfan’s S.
 Pseudoxanthoma elasticum.
 Ehlers-Danlos S.
 Osteogenesis Imperfeccta.

Clinical signs of severity of MS: Clinical signs of severity of MR:

1) Early OS, so greater LA pressure. 1) Systolic thrill at apex.
2) Increasing length of the murmur. 2) Signs of PHT: TR: parasternal thrill
3) Signs of PHT: PR Graham Steell murmur 3) Signs of LVH (pulm congestion).
4) Signs of LVH (pulm congestion). 4) Soft S1.
5) Low PP. 5) Wide splitting of S2.
6) S3.
7) S4.
NB:precordial thrill= (apex thrill + parasternal thrill)

Indications for surgery: Indications for surgery:

1) PHT. 1) Symptomatic: NYHA class III or IV.
2) LVF (pulmonary congestion) 2) Asymptomatic: Fup Echo/6m
3) Haemoptysis. o LV EF < 60%.

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4) Recurrent TE events despite AC. o LVESD > 45 mm.

The criteria for using mitral valvuloplasty: 105 ‫القاعدة‬

1) Mobile valve (loud S1 & OS). ‫الميترالى يتغير بدرى عن األورطى‬
2) No calcification.
3) No MR.
4) No LA thrombus (by TEE).

NB: In calcification of mitral valve: NB: DD: pansytolic murmur:

1) Soft S1. 1) MR.
2) No OS. 2) TR.
3) DOES NOT indicate severity. 3) VSD.

NB: MVP
The earlier OS, the greater LA pressure, thus more  NS1
severity of MS.  NS2
‫صعبة فى االمتحان لكن المعلومة مهمة‬  Murmur:
o Mid-systolic ejection click (EC) at
apex, followed by
o Late systolic crescendo-
decrescendo murmur
o Loudest at Lower Lt sternal edge.
o Murmur is accentuated by: Standing
from a squatting position or during
the straining phase of Valsalva.

Mixed MVD
Predominant MS Predominant MR
Pulse volume Small Sharp and abbreviated
S1 Loud Soft
S3 no +ve
Apex o Undisplaced. o Displaced.
o Palpable S1 = tapping. o Thrusting.
o No heave. o No heaves.
o No thrill. o Systolic thrill.
Both Murmur of MS + Murmur of MR:
 MS: OS in early diastole, followed by, Mid-diastolic rumbling murmur at apex, Best heard in
expiration. Patient in Lt Lateral position. With bell.
 MR: Pan-systolic murmur at the apex, Loudest in expiration, Radiate to the axilla.

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Prosthetic MVR Prosthetic AVR

 Mid-line sternotomy scar.  Mid-line sternotomy scar.

 Prosthetic click at S1.  Prosthetic click at S2.

 Prosthetic click can be heard with the unaided  Prosthetic click can be heard with the unaided
ears which coincides with S1. ears which coincides with S2.

 NS2.  NS1, followed by ejection systolic murmur.

NB: Functional flow murmur (like MS): NB: Functional flow murmur (like AS): ejection
Short mid-diastolic rumbling murmur at apex, best systolic, but not propagated to the neck. But if
heard in expiration & in Lt lateral position with bell. propagated →? ↑ valve gradient or fibrosis 

NB: Prosthesis dysfunction (like MR):

Apex: displaced, thrusting.

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 Cardiology

TS TR

 Mid-diastolic murmur (rarely audible)  Pansystolic murmur over T area

 Loudest Lt 3rd-4th ICS at sternal edge  Loudest during inspiration

 Loudest during inspiration  Elevated JVP (v wave)

 Signs of RA enlargement:  RT sided heart failure:

o Elevated JVP with giant “a” waves o Hepatic congestion & pulsation

o Peripheral oedema, ascites o Ascites

o LL oedema

 Causes of TS:  Cuases of TR:

o RHD o RHD

o IEC o IEC: IV drug abusers

o Congenital o RV dilatation: 2ry to PHT or PS

o Carcinoid $

o Congenital: Ebstein anomaly

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 Cardiology

ASD VSD

 Systolic thrill at upper Lt sternal edge (P).  Lt Parasternal thrill.

 NS1.  NS1.

 S2: fixed wide splitting of S2 (A2---P2).  NS2.

 Ejection click (dt pulmonary artery  Loud harsh pansystolic murmur, heard
dilatation). throughout the pericardium, loudest at lower
Lt sternal edge.
 Ejection systolic murmur at upper Lt sternal
edge (P area) (dt ↑ blood flow across P Maladie de Roger: Loudness of VSD does not
valve). (DD: PS: soft P2) correlate with the size, as loud murmur is dt high-
flow velocity through a small VSD.
 Mid-diastolic flow murmur at lower Lt
sternal edge (mimic TS) in large Lt to Rt If murmur disappear → so, Eisenmenger’s
shunt. develops 

 Mid-diastolic flow murmur at apex (mimic

MS) in large Lt to Rt shunt.

In large Lt-Rt ASD shunt: In large Lt-Rt VSD shunt:

↑ Pulmonary blood flow to RA → ↑ Blood flow ↑ Pulmonary blood flow to LA → ↑ Blood flow
across Tricuspid valve → mimic TS (mid-diastolic across Mitral valve → mimic MS (mid-diastolic flow
flow murmur) at lower Lt sternal edge. murmur) at apex.

RV heave & thrill  TR

If PHT  TR, PR (Graham steel murmur)

 No UL developmental deformities:
(hypoplastic thumb with an accessory
phalynx) = No Holt-Oram Syndrome).

 No scars (Ballon Mitral Valvoplasty).

 No PHT.
So, haemodynamicallly insignificant shunt
 No LVF

 No Cyanosis.
So, No Eisenmenger’s syndrome
 No Clubbing

ASD + MS:

1) Lutembacher syndrome = congenital ASD +

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acquired RHD (MS).

2) Iatrogenic ASD: at Balloon Mitral

Valvoplasty

Coarctation of the aorta

Examination & Presentation:

 Upper torso is better developed than lower torso.

 Radial pulse: → according to site of coarctation in relation to Lt subclavian artery:

o Equal volume bilaterally: as the site of coarctation is often distal to the origin of Lt
Subclavian artery.

o Lt Radial is diminished: If the site of coarctation is proximal to the origun of Lt Subclavian

artery or if repaires coarctation (check Lt Thoracotomy scar).

 Radio-femoral delay:

o Femoral pulse is delayed with low volume.

o No delay if with coarctation repair.

 Pulse:

o Large volume & normal character: (in Bicuspid aortic valve).

o Large volume & collapsing character: in (AR).

o Low volume & slow-rising: in (AS).

 Vigrous carotid pulsations of the neck (like AR).

 Collateral vessels developed over the scapula, anterior axillary line & Lt sternal border: with:

1) Visible arterial pulsation.

2) Palpable systolic thrill.

3) Auscultate bruits.

 Apex:

o Undisplaced & heaving: (LVH).

o Displaced & Thrusting: (AR).

 Murmurs:

o Ejection click (Bicuspid aorta).

o Ejection systolic murmur at A area: (AS).

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o Early diastolic murmur at A area: (AR).

o Harsh ejection systolic murmur over the Lt sternal edge & posteriorly over the thoracic spines:
(murmur of coarctation).

NB: The site of coarctation is often distal to the origun of Lt Subclavian artery.

NB: It is often associated with aortic valve disease: mainly Bicuspid aortic valve by 50%, AS & AR.

PS & PR

PS (Pulmonary stenosis) PR (Pulmonar regurgitation)

 JVP (promininent ‘a’ waves): severe PS.  JVP (promininent ‘a’ waves): severe PR.

 Apex: Undisplaced.  Apex: Undisplaced.

 Lt Parasternal heave.  No heave.

 Systolic thrill at the upper Lt sternal edge (P  No thrill.

area).

 NS1.  NS1

 S2: Widely splitting of S2 with diminished P  1ry PR: Splitting S2.

component (Soft P2).
 2ry PR dt PHT:

o Splitting S2 + loud P2.

o Palpable P2.

 Absent P2: if congenital absence of P valve.

 S4.  S3 & S4.

 Ejection click.  Early diastolic decrescendo murmur at the

upper Lt sternal edge (P area), which radiates
 Ejection systolic murmur (ESM), loudest at down the Lt sternal edge, louder in
the upper Lt sternal edge (P area), which inspiration.
radiates to the suprasternal notch, Lt
shoulder, Lt infra-clavicular region, and is
louder in inspiration.

Clinical signs of severity of PS: NB: 1ry or 2ry PR (dt PHT).

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1) Large ‘a’ waves. NB: check signs of PHT.

2) Widely splitting of S2. NB: PR (Graham Steel murmur): in MS with

PHT.
3) Soft/diminished P2.
NB: Search for other associated valvular heart
4) S4. diseases: MS, AR.

5) Early ejection click.

6) Long systolic murmur with late systolic

peaking.

7) RV dilatation: RV heave, Functional TR:

Systolic ‘cv” waves, parasternal thrill,
pansystolic murmur at lower Lt sternal edge
louder in inspiration.

Assocaition with PS:

1) Fallot tetralogy.

2) Turner’s, Noonan’s, Williams $

3) Carcinoid $

PDA

 Pulse: Large volume & collapsing character.

 BP: wide PP.

 Lt Parasternal heave.

 Lt Subclavian thrill (it reflects the flow through the PDA shunt).

 Apex: displaced & thrusting quality (LVH).

 Auscultation:

o Continuous machinery murmur with systolic accentuation in the Lt subclavian area

(Gibson murmur).

o NS1.

o S2 (usually obscured by the murmur):

 Loud PS in PHT.

 Reversed splitting of S2.

 Check for signs of PHT.

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 Check: Differential cyanosis and clubbing (i.e. cyanosis and clubbing of the toes NOT the fingers),
as PDA usually connect the pulmonary artery to the aorta distal to the origin of Lt subclavian artery.

 Associations:

o Turner’s syndrome (35% have coarctation of the aorta).

o Berry aneurysms

Fallot Tetralogy (F4)

 Central cyanosis.

 Clubbing. Due to: Blalock-Taussig shunt

 Lt Radial pulse: diminished.

 Lt arm appears smaller than the Rt arm. 1) VSD (Rt to LT shunt).

2) RV outflow tract obstruction (subvalvular) = PS.
 BP is lower in Lt arm. 3) RVH.
4) Overriding Aorta
 JVP: not elevated, absent ‘a’ waves.

 Apex:

o Undisplaced, normal character.

o Displaced, thrusting: in AR (prolapse of the Rt coronary cusp).

 Lt Parasternal heave.

 Systolic thrill at the upper Lt sternal edge (P area).

 S2:

o Palpable S2 (A2).

o Diminshed Pulmonary componenet of S2, so S2 manifests as a single A2.

 Murmurs:

1) Loud ejection systolic murmur at the upper Lt sternal edge (P area), louder in inspiration
(murmur of RV outflow tract obstruction, inverse relation with severity, not the VSD murmur).

2) Soft early diastolic murmur at the upper Rt sternal edge (A area), radiating down the sternal edge,
which is louder with the patient sitting forward in expiration (murmur of AR).

3) Continuous mumur throughout systole and diastole (to-and-fro murmur) in the Lt Subclavian area,
and can also be heard posteriorly (murmur of Blalock-taussing shunt). (DD: PDA murmur).

NB: Blalock-Taussig shunt:

o For correction of F4

o A shunt from the Lt Subclavian artery to the pulmonary artery, thus bypassing RV outflow
obstruction.

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o It is a palliative procedure not performed routinely nowadays due to possible total correction with
cardiopulmonary bypass. However, this shunt may be performed if the the anatomy is unfavourable
for total correction.

o Look for a thoracotomy scar: a Lt or Rt thoracotomy scar would suggest that the Lt or Rt subclavian
artery was used.

o There is absent radial pulse & thoracotomy scar.

o A modified Blalock-Taussig shunt is the interposition of a tubular graft between the two arteries.

o DD the continuous murmur of Blalock-Taussig shunt and that of PDA.

Eisenmenger’s syndrome

(PHT with shunt reversal, i.e from Rt to LT)

 Central cyanosis (NB: Differential cyanosis with PDA).

1) Central cyanosis.
 Clubbing. 2) Clubbing.
3) Signs of PHT.
 JVP: elevated, prominent ‘a’ and ‘v’ waves.

 Lt Parasternal heave.

 Lt Parasternal thrill.

 Palpable pulmonary component of S2.

 Apex: displaced (LVH).

 NS1.

 S2: ‫اهم حاجة للتحديد‬

o VSD: Single and loud S2 (A2 & P2 occur simultaneously).

o ASD: Widely Fixed split (A2-P2).

o PDA: Reversed splitting (P2-A2).

 Ejection click: (pulmonary artery dialatation).

 Early diastolic murmur at the upper Lt sternal edge (P area), radiating down to the Lt sternal edge,
louder in inspiration: (Graham –steel murmur of PR of PHT).

 Pansystolic murmur at the lower Lt sternal edge, which louder in inspiration: (murmur of functional
TR of PHT).

NB: The timing and charcteristics of S2 (A2 and P2) depend on the underlying shunt, and if correctly
identified will give clues to the underlying cause.

NB: Differential cyanosis and clubbing → PDA.

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Complications of Eisenmenger’s $:

1) RV failure
2) Angina
3) Arrhythmias: AF & flutter
4) IEC
5) Haemoptysis
6) Recurrent pneumonia
7) Paradoxical embolism (TIA, stroke)
8) Brain abscess
9) Polycythaemia & hyperviscosity $
10) Bleeding disorders
11) Hyperuricemia & gout

Management of Eisenmenger’s $:

1) IEC prophylaxis
2) Stop smoking, alcohol, avoid dehydration & hot conditions (↑ Rt to Lt shunt)
3) Contraception for females
4) TTT of CHF
5) Polycythemia with HCT > 65 %  Venesection & volume replacement (1st R/O dehydration)
6) Oxygen for cyanosis
7) Surgical repair of the 1ry cardiac defect ONLY if PHT is reversible
8) Heart-lung transplantation.

Hypertrophic Cardiomyopathy (HCM)

 Pulse: Jerky character.

 Double carotid arterial impulse.

 JVP: not elevated, prominent ‘a’ waves.

 Apex: displaced, with a marked presystolic impulse giving the impression of a double apical
impulse (palpable atrial & ventricular contraction), with heaving character.

 Lt Parasternal heave.

 Systolic thrill palpable at the lower Lt sternal edge.

 NS1.

 S2: reversed splitting.

 S4.

 Murmurs:

1) Ejection systolic murmur (ESM) at the lower Lt sternal edge, which radiates up the sternal
edge to suprasternal notch, not to the carotids or neck: (a murmur of LV outflow
obstruction), dynamic ESM accentuated by standing from squatting or during a strain phase
of Valsalva.

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2) Pansystolic murmur at the apex, which radiates to the axilla: (a murmur of MR: SAM Systolic
anterior motion of the mitral valve).

NB: HCM with AF, so: NO S4, No prominent ‘a’ waves, No double apical impulse.

Q: Associations with HOCM?

1) Friedreich’s ataxia.
2) Myotonic dystrophy.

Q: Investigations:

 ECG: LVH with strain pattern.

 CXR: normal
 Echo:
o ASH = Asymmetrical Septal Hypertrophy
o SAM = Systolic Anterior Motion of the anterior mitral leaflet across the LVOT
o LVOT gradient
 MRI heart: apical HCM
 Cardiac catheterization: gradient
 Genetic test.

Q: Management?

1) Non-pharmacological:
o Patient education.
o Avoid strenuous exercise, dehydration & vasodilators
o Genetic counselling of 1st degree relatives: AD
2) Pharmacological:
o BB
3) Surgical:
o Alcohol septal ablation
o Surgical myomectomy.
o ICD
o Heart transplantation.

Miscellaneous
Q: What are the causes of a collapsing pulse (bounding pulse)?

 AR.
 Severe MR
 PDA.
 Paget’s D
 Any hyperdynamic circulation:
o Fever
o Anaemia
o Thyrotoxicosis.
o Pregnancy.
o AVF.

Q: Target Levels of INR:

1) AF → 2-3
2) Valve replacement (aortic) → 2 – 3
3) Valve replacememt (mitral)  2.5 – 3.5

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Q: Complications of valve replacement?

1) Valve:
 Early: anaeasthesia complications, bleeding in OR.
 Late:
o IEC:
 Early (first 2 months)→ Staph epidermidis (skin)
 Late → Strept Viridans (blood spread)
o Thrombosis: stucked valve.
o Malfunction: Leak/dehiscence.
2) Systemic:
 Embolization → CVA.
 Haemolysis → Anaemia.
3) Drugs:
 Bleeding dt over anticoagulation.
3 blood samples from 3
different sites with 1 hour apart
Q: Duke’s criteria for IEC?
o Major:
1) Echo: abscess, vegetation, new murmur (regurgitation)
2) Blood culture: typical organism in 2 blood cultures 2 major
o Minor: OR
1) Echo  suggestive 1 major + 2 minor
2) Blood culture  with atypical organism OR
3) Pyrexia > 38 C 5 minor
4) Predisposed risks: e.g. prosthetic valve, IVD
5) Immunologic phenomena: GN, Osler’s, Roth’s spots, RF.
6) Vascular phenomena: Janway lesions, emboli, mycotic aneurysm, IC Hge.

Indications for AB prophylaxis against IEC:

1) Prosthetic valves
2) Previous IEC
3) Post cardiac transplant with valvoplasty
4) Partially corrected congenital heart disease.

Q: Modified Jones criteria for diagnosis of rheumatic fever?

o Major:
1) Carditis 2 major
2) Polyarthritis (migratory) OR
3) Chorea 1 major + 2 minor
4) SC nodules
5) EM (Eryhthema Marginatum)
o Minor:
1) Prolonged PR interval
2) Arthralgia
3) Pyrexia
4) Previous rheumatic fever
5) ↑ WBCs, ↑ ESR & ↑ CRP

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