Cardiology Short Cases Flashcards
Interpret the following physical findings:
Collapsing pulse
Wide pulse pressure
Displaced apex
Early diastolic murmur, high-pitch, blowing quality best heard at tricuspid area
+/- mid-diastolic, low-pitch rumbling murmur
Systolic flow murmur in aortic area
Thursting apex
Dx and ddx?
What maneuver next?
Aortic regurgitation
Ddx:
- Pulmonary regurgitation: no displaced apex, no collapsing pulse, not high-pitch murmur
- Mitral stenosis: has opening snap in diastole, loud S1, radiated to axilla from apex, tapping and non-displaced apex
Sit up and lean forward for murmur, best heard at tricuspid area
Causes of Aortic regurgitation?
Cusp disease:
- Rheumatic heart disease
- Infective endocarditis
- Congenital bicuspid aortic valve
- Degenerative
- Aortic dissection/ trauma
Causes of dilated aortic root/ aortic aneurysm:
- Marfan syndrome,
- syphilic aortitis,
- Seronegative arthritis: ankylosing spondylitis, psoriatic arthropathy…etc
Additional peripheral signs related to Aortic regurgitation?
→ Duroziez sign: to-and-fro murmur over femoral arteries heard
when apply pressure with stethoscope
→ Quincke’s pulse: capillary pulsation in finger tips or mucous
membranes
→ Traube’s sign: ‘pistol-shot’ systolic and diastolic sounds over
large arteries
→ De Musset’s sign: head bobbing with each heartbeat
(↑SV → transfer of momentum to head/neck)
Investigations for Aortic Regurgitation?
Investigations:
□ Blood: VDRL, blood culture (IE)
□ ECG: initially normal, later LVH + T wave inversion
□ CXR: dilated aortic arch, cardiomegaly
□ Echo: LV size and function, aortic size and Doppler for severity of regurgitant jet
Interpret the following physical findings:
Small volume and slow rising pulse Sustained and heaving apex Systolic thrill in aortic area Deceased/ soft S2 +/- S4 Ejection systolic murmur radiating to both sides of the neck, harsh
Dx/ ddx?
Why does the murmur sometimes radiate to the apex?
Aortic stenosis
D/dx:
- Aortic sclerosis: normal volume pulse,
normal/wide pulse pressure, intact S2 and no LVH
- HOCM: jerky pulse, normal S2, ↑murmur on standing
- MR: pansystolic murmur best heard at apex with radiation to axilla
Causes of aortic stenosis
Why does the murmur sometimes radiate to the apex?
Degenerative calcification
Rheumatic heart disease
Congenital bicuspid aortic valve
AS murmur radiating to apex may be more musical (high frequency vibration) and louder, known as Gallarvardin phenomenon.
It is easily confused with MR. However, in MR the S1 should be soft
Investigations for Aortic Stenosis?
□ ECG: LVH with ‘strain’ pattern
→ Strain pattern: downsloping ST depression + T wave
inversion in lateral leads
□ CXR: usually normal except in LV failure stage
□ Echo:
→ Restricted valve opening with concentric LVH
→ Mean valvular pressure gradient: ≥40mmHg = severe
→ Aortic valve area (AVA): ≤1cm = severe
Interpret the following physical findings:
JVP elevated Parasternal heave Fixed wide splitting of S2 Loud S2 Ejection systolic murmur at pulmonic area Mid-diastolic murmur at tricuspid area
Dx/Ddx?
Cause of the murmurs?
Atrial septal defect
D/dx:
Pulmonary stenosis: Soft S2 (very rare as isolated disease, usually part of Tetralogy of Fallot)
Pulmonary hypertension: Loud S2 without splitting/ Single S2
ESM at LUSB due to ↑PV flow
MDM at LLSB due to ↑TV flow
Causes of ASD?
Syndromes associated?
Failure to close foramen secundum → secundum ASD
Failure to close foramen primum → primum ASD
Down syndrome: Secundum ASD
Noonan syndrome
DiGeorge syndrome
Eisenmenger syndrome
Investigation for ASD?
Ix: can be normal in small ASD
□ CXR: cardiomegaly, RA/RV dilation, enlarged pA, pulm plethora
□ ECG: R axis deviation, RA/V dilation
→ Incomplete RBBB (in V1) due to RV dilation
→ L axis deviation + 1st degree HB in primum defect
□ Transesophageal Echo: diagnostic, evaluate size
Interpret the following physical findings:
Stunted growth Central cyanosis Digital clubbing Large A wave in JVP Left parasternal heave Loud S2 Early diastolic murmur in pulmonary area Pansystolic murmur in lower left sternal border
Causes?
Eisenmneger Syndrome
Triad of (1) congenital L-to-R shunt (2) pulmonary arterial disease (3) cyanosis
Causes of Eisenmenger syndrome and their signs:
VSD: single/closely split S2 (equalization of pressure)
ASD: fixed widely split S2
PDA: normally split S2, differential cyanosis and clubbing
Interpret the following physical findings:
Irregularly irregular pulse Lack of a wave in JVP S1 variable loudness ECG: □ No distinct P wave ± irregular baseline (fibrillation waves83) □ Narrow but irregular QRS complexes
Dx/Ddx?
Atrial fibrillation
Ddx:
Atrial flutter with variable block
Atrial tachycardia with variable block
Frequent multifocal ectopic beats
Causes of A-fib?
Mitral valve disease**
Ischemic heart disease
Thyroid heart disease
Alcohol
Hypertension
Interpret:
- Displaced Apex
- Systolic thrill
- Left parasternal heave
- Soft/ absent first heart sound + Pansystolic murmur at apex, radiation to axilla + Obscured S2
+/- ankle or sacral edema - Sinus rhythm, regular pulse
D/dx?
Causes?
Mitral regurgitation
D/dx: - VSD: murmur best heard at parasternal border and radiate to Rt sternum - TR: giant V wave in JVP, systolic murmur at Lt sternal border and pulsatile liver, accentuated by inspiration
Causes of Mitral regurgitation?
Causes:
Valvular leaflet diseases
→ Rheumatic: commonest, 50% a/w MS
→ Mitral valve prolapse due to myxomatous
degeneration of valvular leaflet
→ Infective endocarditis
→ HOCM with systolic anterior movement of mitral leaflet
□ Annulus dilatation due to LV dilatation (CAD, DCMP)
□ Ruptured chordae tendineae:
→ Degenerative or collagen disease
→ Infective, eg. IE
→ Acute rheumatic heart disease
□ Papillary muscle dysfunction: ischaemia or MI
Interpret:
Sacral or ankle edema Parasternal heave Tapping apex, not displaced Loud S1, +/- opening snap Mid-diastolic, rumbling/ low-pitch murmur at apex Redness of cheeks
Next maneuver for murmur?
D/dx?
Mitral Stenosis
Left lateral position to accentuate murmur
D/dx:
- Austin-Flint murmur of AR:
S1 soft, no Opening Snap, AR murmur
- Lt atrial myxoma
Causes of Mitral Stenosis?
Early vs late clinical outcomes?
Rheumatic heart disease (95%): less common nowadays
Others: congenital (infants), mitral annular calcification (elderly), radiation-associated (classically in
Hodgkin disease survivors), carcinoid valve disease, SLE/RA, mucopolysaccharidoses
Early: insidious onset of SOB
Late:
→ SOB at rest + orthopnoea + PND
→ Right heart failure with systemic oedema
→ Gross LAE: compression of RLN (hoarseness) and oesophagus
(dysphagia, also known as Ortner syndrome)
Interpret:
Mid to late systolic click + murmur
Best heard at apex
Next maneuvers to accentuate murmur?
D/dx?
Mitral valve prolapse
Sudden standing = earlier MVP click in systole
Sudden squatting = delayed MVP click in systole
D/dx:
- Other causes of MR, eg. DCMP
- TR
- AS
- HOCM: ESM at LLSB, non-displaced apex
Cause of MVP?
Degenerative: myxomatous degeneration
Congenital: primary AD inheritance
(Marfan’s syndrome), secundum ASD, Turner’s
syndrome, PDA …etc
Interpret:
Cyanosis and clubbing of toes
Large pulse volume or collapsing pulse
Continuous murmur across S1 S2 S1 +/- increased P2
D/dx?
Patent ductus arteriosus
D/dx: Coarctation of aorta Ruptured sinus of Valsalva aneurysm into right heart Coronary arteriovenous fistula Pulmonary arteriovenous fistula VSD and AR Venous hum
Causes of PDA?
Pulmonary trunk connected to aortic arch, causing LA, LV and PA dilation
Congenital: idiopathic or secondary to maternal rubella
Associated with other congenital heart diseases
Preterm, birth in high altitude
Interpret:
Visible, elevated JVP, one wave
Parasternal heave
Pansystolic murmur loudest in LLSB
Ankle edema
Next maneuver for murmur?
2 more classical signs?
D/dx?
Tricuspid regurgitation
Pansystolic murmur - Louder during inspiration, reduced during expiration
Pulsatile liver
Ascites
MR
VSD
Causes of Tricuspid regurgitation? (10)
Functional: right ventricular hypertrophy secondary to left ventricular failure
Rheumatic heart disease
Infective endocarditis
Pulmonary hypertension: cor pulmonale, ASD
Infarct of right ventricular papillary muscles
Tricuspid valve prolapse
Carcinoid heart disease
Trauma
Congenital
Endomyocardial fibrosis
Interpret:
Displaced apex Parasternal heave Raised JVP Systolic thrill Loud S2 Pansystolic murmur at LLSB Ejection systolic murmur at pulmonary area Mid diastolic murmur at apex
D/dx?
Causes (2)
VSD
MR, TR
Congenital: isolated or with other defects
Anterior myocardial infarction
List the cardiovascular diseases associated with: Turner's Marfan Down Cushing
Turner’s = coarctation of aorta
Down = AVSD, VSD
Marfan = MR, AR
Cushing’s = hypertension with LV hypertrophy
D/dx splinter hemorrhage
→ Most commonly due to trauma
→ Classically due to IE
→ Other causes: vasculitis (and other A/I), sepsis, haematological malignancy, profound anaemia
Differentiate Osler nodes and Janeway lesions
Osler’s nodes: red, raised, tender palpable nodules on pulp of fingers (or toes) or on thenar or
hypothenar eminence
Janeway lesions: non-tender erythematous maculopapular lesions on palms or pulps of fingers
4 types of xanthomas
→ Xanthelasma: yellowish collection at or around eyelids → Tendon xanthoma: papules/nodules in tendons of hands, feet and heel → Palmar xanthoma at palms → Tuberoeruptive xanthomas: red papules/nodules appearing inflamed and tend to coalesce
List locations of peripheral pulses (7)
Radial pulse: Distal forearm near the base of the thumb
Brachial pulse: Antecubital fossa immediately medial to
the biceps tendon
Carotid pulse: Lateral to the laryngeal prominence
(thyroid cartilage), medial to the SCM Usually use thumb of opposite hands
Femoral pulse: Halfway between the ASIS and pubic
symphysis
Popliteal pulse: In the popliteal fossa at the flexor
(posterior) compartment of the knees
Posterior tibial pulse: Midway between medial malleolus and heel
Dorsalis pedis pulse: On the dorsum of the foot lateral to the extensor hallucis longus tendon
Difference between pitting and non-pitting edema causes?
→ Pitting oedema: cardiac failure,
hypoalbuminaemia (usually refills more
quickly)
→ Non-pitting oedema: lymphedema (eg.
lymphatic obstruction), myxedema,
lipoedema
Causes of regularly irregular and irregularly irregular pulse
Regularly irregular
- Sinus arrhythmia
- Fixed ectopics
- 2o heart block (Mobitz type I)
Irregularly irregular
- AF (most common)
- AFL or AT with variable block
- Multifocal AT
- Frequent variable ectopics
Causes of radial- radial delay
subclavian artery stenosis/occlusion, thoracic aortic dissection
Causes of radial-femoral delay
coarctation of aorta, aortic dissection, severe UL/aortoiliac vasculopathy
Cause of slow rising pulse?
Aortic stenosis
Cause of Bisfiriens pulse/ jerky pulse with double peak?
AS+AR
HOCM
Causes of collapsing pulse
AR PDA Hyperdynamic circulation Aortic sinus rupture Peripheral AV fistula
Cause of Pulsus alternans/ Alternating strong and weak pulses
Advanced LV failure
Causes of Pulsus paradoxus
- Cardiac tamponade
- Constrictive pericarditis
- Hyperinflation of lungs
(eg. asthma, COPD)
Difference between JVP and Carotid pulse
JVP:
Non-palpable Obliterated by pressure Lower and more lateral Increase in amplitude with inspiration 2 peaks Decrease when upright Increase with hepatojugular reflex
Causes of raised JVP and decreased JVP
Normal JVP height
Normal: <4.5cm above zero point, below clavicle
Raised JVP:
□ SVC obstruction (loss of normal JVP waveform)
□ Circulatory volume overload (↑central venous
pressure)
□ RV failure and RV volume overload
□ Pericardial effusion or constrictive pericarditis
(look for +ve Kussmaul sign)
□ Severe bradycardia
Decreased JVP indicates ↓RA filling pressure
□ Hypovolemia
□ Dehydration
Cause of Cannon A wave
Indicates AV dissociation i.e. A and V contracting
together
- Complete heart block
- AFL, AT (due to heart block)
- Non-atrial rhythms
Nodal tachycardia
Ventricular ectopics
VT
Ventricular pacing
Cause of Giant A wave
Indicates ↓RA compliance or ↓RA outflow
- ↓RA compliance:
PS (∵chronic ↑RAP)
Pulmonary HTN - ↓RA outflow
TS
RA mass/thrombus
Cause of exaggerated x descent
Indicates pericardial compressive pathology
- Cardiac tamponade
- Constrictive pericarditis
Cause of large V wave./ dominant c-v wave
Indicates ↑RA inflow during ventricular systole (i.e. TR)
Tricuspid regurgitation
Cause of exaggerated y descent
Indicates ↑RA outflow during ventricular filling
- Severe TR
- Constrictive pericarditis11
Cause of slow y descent
Indicates ↓RA outflow during ventricular filling
- Cardiac tamponade
- TS
Procedures related to midline sternotomy scar
CABG, surgery requiring cardiopulmonary bypass (AV/MV replacement)
Procedures related to Lateral sternotomy scar
old previous mitral valvotomy (now rare)
Procedures related to subclavian scar
Pacemaker, ICD, defibrillator box
at Rt infraclavicular region
Defibrillator boxes larger than pacemakers (10×5×1cm)
List 4 characters of apex beat, list causes
Heaving = Pressure overload = AS, Hypertension
Thrusting = volume overload = AR, MR, Dilated cardiomyopathy
Tapping = MS
Double impulse = palpable A wave in concentric LV hypertrophy = HOCM
Cause of parasternal heave?
Heaving: RVH or severe LA enlargement (RV pushed anteriorly)
RVH due to RV volume overload → ASD, TR
RVH due to RV pressure overload → TS, pHT
→ LA enlargement → MR
What can be auscultated at the neck in cardiovascular exam?
AS radiation (bilateral)
Carotid bruit
Thyroid bruit
Split S1, Loud S1, Soft S1 causes
Split S1 = delayed RV systole → T close after M
- RBBB, right atrial myxoma
Loud S1 = limited atrial outflow, atrial outflow remains strong at onset of ventricular systole
- ↑HR, hyperkinetic states
- MS
Soft S1 = ↓atrial outflow or MV pathologies
- Increase PR interval e.g. first degree HB
- MR
- Severe, calcific MS
Explain physiological S2
closure of aortic (A2) and pulmonic (P2) valves
A2 normally a bit earlier than P2
Mechanism: inspiration → ↓intrathoracic pressure
→ blood attracted towards pulmonary vessels
→ early A2 (less blood in LV) + late P2 (more blood in RV)
Wide splitting S2 cause?
□ S2 split even during expiration
□ Mechanism: delayed RV systole → delayed P closure
□ D/dx:
→ Early A2: severe MR, WPWS type B
→ Late P2: RBBB, PS
Fixed splitting S2 cause?
S2 splitting unaffected by breathing
→ RV volume overload → delayed P closure
(obligatory flow volume from RV)
→ ↑VR offset by ↓L-to-R shunt
ASD
Reversed splitting S2 cause?
S2 splitting occurs during expiration
Mechanism: delayed LV systole → delayed A closure
→ normal inspiration-related P2 delay now abolishes splitting
D/dx:
→ Electrical A2 delay: LBBB, RV pacing
→ Mechanical A2 delay: PDA, severe AS
Loud S2 causes?
□ Loud both A2 and P2: hyperdynamic state
□ Loud A2:
→ Systemic HTN (↑aortic pressure)
→ Congenital AS (narrowed valve closed suddenly at the end of systole)
□ Loud P2: note that palpable P2 correlates better with pHT
→ Pulmonary HTN (↑pulmonary a. pressure)
Soft S2 cause?
□ Soft A2:
→ Calcified AS (↓mobility of aortic valve)
→ AR (incomplete closure of aortic valve)
□ Soft P2:
→ PS (↓mobility of pulmonic valve)
Single S2 cause?
□ Absent A2: severe AS
□ Absent P2: severe PS, ToF, pulmonary atresia
□ Reduced splitting: pulmonary HTN, eg. Eisenmenger syndrome
Cause of S3?
Mechanism: rapid filling → sudden tensing of ventricles → exaggerated in volume overload
D/dx:
→ Normal in children/young person, pregnancy, thyrotoxicosis
→ LV volume overload (apex, Lt lateral): congestive HF, MR, AR
→ RV volume overload (LLSB): RV failure, TR
Cause of S4?
atrial systole against a poorly compliant ventricle → vibration of ventricles always absent in A-Fib
D/dx: always pathological
→ ↓LV compliance (apex, Lt lateral): pressure overload (AS, HTN), IHD, ↑age
→ ↓RV compliance (LLSB): pressure overload (PS, pHT)
Changes to certain murmurs with sudden squatting?
→ Most murmurs become louder (↑preload → ↑CO)
→ HOCM murmur becomes softer (↑LV volume → relieved obstruction to outflow)
→ MVP murmur becomes softer and non-ejection click becomes later
(↑preload → ↑tension of chordae tendineae → prolapse occurs later)
How to perform isometric exercise maneuver?
sustained handgrip or repeated sit-ups for 20-30s
→ Most murmurs become louder (↑afterload → ↑backflow of blood)
→ AS murmur becomes softer (↑afterload → ↓ejection velocity)
→ HOCM murmur becomes softer (↑afterload → ↓ejection velocity + ↑LV volume)
→ MVP murmur becomes softer and non-ejection click becomes later (↑afterload → ↑LV volume → ↑tension of chordae tendineae → prolapse occurs later)
VSD and MR are associated with which myocardial wall infarct
VSD - Anterior wall infarct
MR - Inferior wall infarct causing papillary muscle dysfunction
Interpret:
Displaced apex
Grade 5/6 S2 at aortic area
Most likely dx, causes?
Mechanical aortic valve
Replaced due to aortic regurgitation or stenosis
How to differentiate multiple extrasystoles from A-fib
On exercise, multiple extrasystole is usually suppressed
A-fib remain irregular
4 causes of heart failure
Ischemic
Hypertension
Valvular
Idiopathic dilated cardiomyopathy
