Cardiology- Clinical Exam Flashcards
In a normal heart, increased splitting of S2 occurs in:
Inspiration
During inspiration, negative intrathoracic pressure causes increased venous return to the right heart, with increased right ventricular filling and therefore a relative delay in closing of the pulmonary valve after systole
Wide split S2 occurs in:
Wide split S2 occurs in:
ASD (fixed)- Right volume overload, so RV needs to stay open longer to expel all blood
Pulmunary stenosis - needs to stay longer open to push blood through narrow opening
Ebstein anomaly - R volume overload
RBBB- R side takes longer to depolarise, so contracts after left side, so pulmunary valve stays open longer
Narrow split S2 occurs in:
Pulmunary HTN (as pulmonary valve closes earlier due to high pulmonary resistance.
also pulm HTN causes LOUD S2
Single S2 occurs when:
a) If one of the semilunar valves is missing, as in pulmonary or aortic valve atresia, severe stenosis, truncus arteriosus, tricuspid atresia, hypoplastic left heart
b) If both valves close simultaneously as in double outlet single ventricle or in large VSD with equal ventricular pressures
c) In pulmonary hypertension with equal right and left ventricular pressures- Eisenmenger syndrome
d) If vessels are abnormally positioned- L transposition great arteries
Paradoxical splitting of S2 (P2 before A2) occurs in:
severe aortic stenosis
left bundle branch block
Parasternal heave
A parasternal heave is detected by placing the heel of the hand over the left parasternal region. In the presence of a heave the heel of the hand is lifted off the chest wall with each systole.
A parasternal heave is caused by RIGHT VENTRICULAR HYPERTROPHY
Eg ASD
Pulmonary regurg following repair of ToF
Thrill
A thrill is A palpable, and therefore loud, murmur, and has the same diagnostic significance as the murmur itself. Most thrills are more easily palpable when the patient is sitting up and holding his breath in full expiration.
Palpate in the suprasternal and supraclavicular regions
Suprasternal thrill - aortic stenosis
Upper right sternal border- aortic stenosis
Upper left sternal border- pulmonary stenosis
Left lower sternal border- VSD
Carotid arteries- aortic stenosis or CoA
Feel 3 locations:
https://www.youtube.com/watch?v=pcACFYqdOtY
Palpable pulmunary valve closure (P2) is felt in:
Palpation with the fingers over the pulmonary area may reveal the palpable tap of pulmonary valve closure due to PULMUNARY HYPERTENSION
Heart sounds
The first heart sound (S1) represents closure of the atrioventricular (mitral and tricuspid) valves as the ventricular pressures exceed atrial pressures at the beginning of systole . S1 is normally a single sound because mitral and tricuspid valve closure occurs almost simultaneously. Clinically, S1 corresponds to the pulse.
The second heart sound (S2) represents closure of the semilunar (aortic and pulmonary) valves . S2 is normally split because the aortic valve (A2) closes before the pulmonary valve (P2). The closing pressure (the diastolic arterial pressure) on the left is 80 mmHg as compared to only 10 mmHg on the right. This higher closing pressure leads to earlier closure of the aortic valve. In addition, the more muscular and stiff “less compliant” left ventricle (LV) empties earlier than the right ventricle.
The venous return to the right ventricle (RV) increases during inspiration due to negative intrathoracic pressure and P2 is even more delayed, so it is normal for the split of the second heart sound to widen during inspiration and to narrow during expiration.
The third heart sound (S3) is due to rapid ventricular filling- can be normal in children or a sign of heart failure (MR, VSD, dilated cardiomyopathy)
just after S2
* listen in left lateral position, apex of heart, with bell as it is in diastole*
The fourth heart sound (S4) is an abnormal late diastolic sound caused by forcible atrial contraction in the presence of decreased left ventricular compliance/stiff ventricle eg LVH.
** just before S1 in late diastole**
**listen in left lateral position **
The A2 sound is normally much louder than the P2 due to higher pressures in the left side of the heart; thus, A2 radiates to all cardiac listening posts (loudest at the right upper sternal border), and P2 is usually only heard at the left upper sternal border. Therefore, the A2 sound is the main component of S2
***CLINICAL PEARL: A split S2 is best heard at the pulmonic valve listening post, as P2 is much softer than A2.
***The S2 heart sound intensity decreases with worsening aortic stenosis due to immobile leaflets. In severe aortic stenosis, the A2 component may not be audible at all.
Cardiac cycle
Isovolumetric ventricular contraction (a-b): This phase marks the beginning of systole and starts with the appearance of the QRS complex on the EKG and the closure of the AV valves at point (a). With all valves closed, the ventricle generates positive pressure without any change in its volume (isovolumetric) to overcome the semilunar valves resistance that open at point (b). This phase usually lasts for 6% of the cardiac cycle.
Rapid ejection (b-c): As the semilunar valves open at point (b), there is a rapid ejection of blood due to increased ventricular contractility. The arterial pressure increases until reaching its maximum at point (c). This phase usually lasts for 13% of the cardiac cycle.
Reduced ejection (c-d): This phase marks the beginning of ventricular repolarization as depicted by the onset of the T wave on the EKG. Repolarization leads to a rapid decline in ventricular pressures and hence the reduced rate of ejection. However, some forward flow of blood continues secondary to remnant kinetic energy from the previous phase. This phase usually lasts for 15% of the cardiac cycle.
Isovolumetric relaxation (d-e): When the ventricular pressures drop below the diastolic aortic and pulmonary pressures (80 mmHg and 10 mmHg respectively), the aortic and pulmonary valves close producing the second heart sound (point d). This marks the beginning of diastole. The ventricles generate negative pressure without changing their volume (isovolumetric) so that the ventricular pressure becomes lower than the atrial pressure. This phase usually lasts for 8% of the cardiac cycle.
Ventricular filling (e-a): As the AV valves open at point (e), ventricular filling starts. The initial rapid filling is mainly augmented by ventricular suction which results from ventricular untwisting and the return of each ventricular muscle fiber to its slack length. The ventricular pressure gradually increases until it equals the atrial pressure and the AV valves close (point a). This phase usually lasts for 44% of the cardiac cycle.
Atrial contraction: Finally, near the end of ventricular diastole, the atrial contraction contributes about 10% of the ventricular filling volume. This is represented by the P wave on the EKG of the following cycle. This phase usually lasts for 14% of the cardiac cycle.
Bruits
Auscultate over the carotid arteries, abdominal aorta, renal arteries, and femoral arteries to detect bruits, which are vascular murmurs caused by turbulent, nonlaminar blood flow in a vessel.
Causes of bruits:
AV fistulae
Arteriovenous malformations
Aneurysms
Vascular stenosis
Hyperdynamic circulation E.g., pregnancy, fever, anemia, hyperthyroidism
May occur physiologically in adolescents
Apex beat
From birth to age 3 years the apex beat is located in the 4th intercostal space
With increasing age gradually moves into the 5th space, mid clavicular line
T21 common cardiac conditions
AVSD
VSD
TOF
Combo of AVSD + TOF almost diagnostic of T21 (would have superior axis, shunt murmur RVH on ECG)
Superior axis of AVSD remains post operatively, so should be seen in exam on ECG
Williams syndrome common cardiac conditions
Supravalvar aortic stenosis
Pulmunary stenosis (at any level)
Renal artery stenosis, coronary artery stenosis
HTN
DiGeorge common cardiac conditions
Conotruncal defects:
TOF
Pulmunary atresia + VSD
Truncus arteriosis
Interrupted aortic arch
+/-VSD
Turners syndrome common cardiac conditions
Scoliosis is more common after
Thoracotomy
Sternotomy
due to disruption of the chest wall
Noonans common ECG finding
Superior axis (regardless of their cardiac condition)
Noonans syndrome common cardiac conditions
Pulmunary stenosis or branch pulmunary stenosis
Hypertrophic obstructive cardiomyopathy (left sided murmur from outflow tract obstruction with right sided voltages on ECG)
ASD
Superior axis on ECG (regardless of cardiac anomalies)
Alagille syndrome common cardiac conditions
Pulmunary stenosis or branch pulmunary stenosis
VSD
Holt Oram Syndrome
ASD
VSD
Marfan syndrome
Aortic root dilatation (+/- regurgitation)
Mitral valve prolapse
Lesions in which you would not see a chest scar in an exam
Simple lesions: ASD, VSD, PDA, valvular lesions (but may have scars in groin from cardiac catheterisation)
Complex unrepairable lesions- usually accompanied by cyanosis and likely to have groin scars from cardiac catheterisation
Lateral thoracotomy
Left:
PDA ligation
Aortic coarctation/interrupted aortic arch
Left BT shunt (rare)
PA band (usually done from the front not the side)
Left lobectomy/pneumonectomy
Right:
Right BT shunt (more common)
Tracheo oesophageal fistula, oesophageal atresia
Right lobectomy/pneumonectomy
Median sternotomy
repair of complex cardiac lesions
ASD/VSD/AVSD
Some valvular lesions
Most CoA (some done via lateral approach)
PA band (rarely done via lateral approach)
(modified) Balock - Thomas-Taussig (BT) shunt
Gore tex shunt between subclavian artery and ipsilateral pulmunary artery
- usually on right side
Aim: provide adequate pulmunary blood flow
(but not excessive- we dont want pulmunary overcirculation–> pulmunary oedema! need to ensure the shunt is not too large for the patient to prevent this) - aiming balanced circulation with spO2 75-85% Qp:Qs 1:1
Uses: tetralogy of fallot, pulmunary atresia, tricuspid atresia, part of Norwood procedure in HLHS repair
Usually temporary shunt until definitive repair
* continuous murmur present- absence + worsening cyanosis means shunt obstruction*
Pulmunary artery band
reduces pulmunary overcirculation and therefore limits development of pulmunary HTN in L–> R shunts
Gives PS murmur
used in large VSD, AVSD, truncus
Surgery to repair HLHS
- Norwood procedure (newborn):
*aim: RV to pump to body rather than lungs
Pulmunary flow provided by shunt- atrial septostomy
- reconstruction of aortic arch (enlargement) to join to the origin of the pulmonary artery (so the right ventricle pumps blood to the body)
- closure of PDA
- BT shunt to supply pulmonary blood flow (aorta to pulmonary artery)/ Sano shunt (RV to pulmonary artery)
2. Glenn procedure (3-4 months): sends blood from upper body directly to the lungs - SVC is disconnected from the heart and connected to the pulmonary artery
- Removal of shunt (if previously had Norwood procedure)
- Arterial septectomy
3. Fontan procedure (3-4 years): all venous return from the body flows directly to the lungs - IVC is disconnected from heart and connected to the pulmonary artery using a conduit
- Fenstration (hole) between this conduit and right atrium allows some blood flow back to heart but prevents too much flow to the lungs initially
** first procedure changes according to single ventricle physiology, but second and third stages are the same for all single ventricle pathways
**first procedure is always arterial shunt to supply pulmunary blood flow
** child is BLUE until the Fontan procedure, only after this is completed do they become pink. Repercussions for neurodevelopment from chronic hypxia (ADHD, autism, inability to focus, learning difficulties, speech delay, behavioral disturbances)
Loud S2
increased pulm blood flow (eg asd, vsd, pda) or pulmunary HTN
Absent S2 in
TOF
PS
Fontan
ASD murmur
ESM murmur heard over pulmunary area
Diastolic murmur heard over tricuspid area (relative MS)
Fixed split S2
https://www.youtube.com/watch?v=W8gg2S-mvSQ
ECG: superior or left axis in primum asd/ right axis in secundum, complete or incomplete RBBB
VSD murmur
Systolic murmur (pansystolic or short systolic)
PDA murmur
Aortic stenosis
Harsh ejection systolic murmur heard loudest over the aortic area (RUSB)
Radiates to the carotid arteries
Loudest on expiration and when the patient is sitting forwards
Other clinical features of aortic stenosis may include:
Slow rising pulse with narrow pulse pressure
Non-displaced, heaving apex beat (if present indicates left ventricular hypertrophy)
Reduced or absent S2 (a sign of moderate-severe aortic stenosis)
Reverse splitting of S2: aortic valve closes after pulmonary valve (due to the longer time required for blood to exit the left ventricle)
DDx: hypertrophic cardiomyopathy (accentuates with Valsalva)
Pulmunary stenosis
Aortic regurgitation murmur
Diastolic murmur
Right upper sternal border
Pulmunary stenosis murmur
Ejection systolic murmur radiating to the back
Wide split S2
If severe- hepatomegaly and CCF
Pulmunary regurgitation murmur
Mitral stenosis murmur
Diastolic
5th intercostal space MCL
May have opening snap after S2 (slightly prior to diastolic murmur )- sudden opening of mitral valve
Causes: rheumatic heart disease
Relative stenosis in VSD
Use bell of steth
Mitral regurgitation murmur
Pansystolic
Loudest at apex
Radiate to axillae
Tricuspid stenosis murmur
Diastolic
LLSE
Tricuspid regurgitation murmur
Pansystolic
LLSE
Split S2 best heard in …
pulmunary area
Ejection click
Heard in systole over aortic or pulmunary areas
aortic click best heard at a[ex and may be only finding of bicuspid aortic valve
Due to aortic or pulmunary stenosis (BICUSPID AORTIC VALVE)
Followed by ESM of aortic or pulmunary stenosis
Causes pansystolic murmur
MR/TR
VSD
Bounding pulses seen in
Sig aortic runoff eg
PDA
Aortic regurgitation
Truncus arteriosus
Low volume leg pulses compared to arm seen in
CoA
Tapping apex beat
Palpable s1
Mitral stenosis
Pressure loaded apex beat
Vs
Volume loaded apex beat
Localised and forceful
Vs
Diffuse and slow rising
Coarctation of aorta
Systolic murmur loudest in LUSE, left infraclavicular area and the back below scapula
—> blood pressure difference between uppper and lower extremities 20 mmHg with HTN of upper limbs (must do 4 limb BP)
–> A systolic ejection click and systolic ejection murmur in the left upper sternal border is often found with a bicuspid aortic valve (often coexists with CoA)
–> diminished or delayed femoral pulses compared to radial pulses
—> radio radial delay
–> ECG: LVH (increased voltages in lateral precordial leads); echo: LVH + narrowing of the aortic arch
—> main association with Turners syndrome
–> treated with stent/balloon angioplasty but not complete cure and recoarctation is common
Syndromes associated with HTN
Turners
Williams
NF-1
Cardiac Short Case
Say pertinent positive and negative findings as you go
Sit patient to 45 degrees for JVP and chest exam, flat for abdominal exam
General inspection
- well or unwell
- colour, pink or cyanosed
- increased resp effort; as for vitals
- growth and nutritional status; height and wight
- oxygen, medical aids
- dysmorphism
Hands
- clubbing, cyanosis, anomalies (syndromic)
- pulse: rate, rhythm (even sinus arrhythmia), character, radioradial and radiofemoral delay
Face
- dysmorphism
- conjunctival pallor
- dentition
- uvula (LD syndrome)
- high arch palate
- central cyanosis (under the tongue- ensure good lighting)
Neck
- JVP (only in older kids after 4 years) - not big deal if dont do
- carotid pulse (only do in older kid)
Chest
- scars, chest deformities (and back, axillae)
- position of apex beat (exclude dextrcardia!)
- active or quiet precordium
- heaves or thrills
- suprasternal thrill (LVOTO/AS- but this doesnt make it 4/6 unlike other thrills)
- listen to back for crackles
“S1 and S2 were normal”
“there was a single S2”
“S2 physiologically split”
“fixed split S2”
“S2 was loud”
“no added sounds” or “ejection clic, mid systolic click, S3, S4 “ or if you dont hear a click, if your differential includes something that would give a click, say you would expect to hear this
Murmurs
- intensity (/6 if systolic, /4 if diastolic)
- ejection, pan/holo, mid (small vsd would give you short murmur not pansystolic)
- systolic vs diastolic
- location where loudest (RUSE, LUSE, LLSB, apex)
- radiation (axillae, neck, back)
Feel suprasternal notch
Sit forward for diastolic mumrus or innocent murmurs
Always listen left lateral decubitus position (MR which is often hard to head)
Abdomen
- scars
- hepato/splenomegaly
Legs
- femoral and pedal pulses (pedal if struggling to feel femorals- would effectively exclude CoA)
- lower limb BP
- muscle mass
- oedema (rare in kids in HF, much more common in adults)
Ask for CXR + ECG
**remember PS/PR murmur “to fro murmur” LUSE from conduit **
unlikely to have PDA wth continuous murmur as this is an indication for closure*
Common cardiology short cases
Simple cases:
* Bicuspid valve with AS +/- AR
* PS
* PPS
* PDA
* Unrepaired ASD and VSD
Complex:
* TGA – sp arterial switch with branch PS
* Sp transannular patch repair TOF
* Sp COA with clow acceleration through aorta
* Sp RV-PA condiut
* interstage single ventricle disease
Bell of stethescope
mitral murmurs of apex
HOCM
Murmur: LVOTO–> ESM crescendo decrescendo
Heard between apex and LLSE
Radiates to suprasternal notch NOT CAROTIDS
Louder with Valsalva (decreased preload), quieter with squatting (increased preload)
Holosystolic murmur at the apex and axilla (mitral regurgitation)
ECG:
-> LVH criteria
-> deep anterior lateral TWI
-> dagger-like (deep narrow) Q waves in infero-lateral leads
AVSD
can be either pink or blue child with sternotomy
residual murmurs (pansystolic, LLSE) will be heard post op as valves abnormal and cant be fixed
if unbalanced–> univentricular circulation (often cant proceed to fontan due to elevated pulmunary pressures so remain cyanotic and are palliative)
association with T21
ECG: superior axis (which persists even after surgery)
Murmur LUSE differentials
RVOTO-Pulmunary stenosis (valvular (has a click), subvalvular, supravalvular (thrill in suprasternal notch or Pulmunary area)
ASD
Pulmunary flow murmur
Aortic stenosis
CoA
PDA
TAPVR/PAPVR
Murmur LLSE differentials
VSD (early systolic if muscular, pansystolic if perimembranous)
HOCM
Tricuspid regurgitation
ToF (VSD)
Stills murmur (loudest lying down)
Murmur mitral area differentials
Mitral regurgitation
Mitral stenosis
[ aortic stenosis murmur may be loudest at the apex but doesnt radiate to the axilla]
Murmur RUSE
LVOT eg aortic stenosis which could be valvular subvalvular or supravalvular
i cant hear a click suggestive of vavlular obstruction
DDX PS (ESM at ULSE with radiation to back, soft P2, wide split S2)
Cyanonosis with continous murmur
MAPCAS (major aortopulmunary collateral arteries with PA + VSD
BT shunt
Mitral regurgitation murmur ddx
Pansystolic murmur apex –> L) axilla
No scar:
- rheumatic heart disease , post IE
- congenital: partial AVSD , MV cleft
Scar:
- rheumatic heart disease , post IE
- congenital: AVSD, congenital MS, post ALCAPA
Murmur LUSE ddx
Murmurs in LUSE (no scar)
RVOT which could be:
- PS (valvular, subvalvular, supravalvular)
- Branch PS (radiates to back)
- Pum flow murmur (soft murmur, increased with anemia or fever)
- ASD (soft murmur- secundum or primum)
- LVOT
Murmurs LUSE (+ scar):
- Severe/critical PS post valvotomy
- TOF (residual PS)
- PA + VSD
- TGA (if doing Rastelli for PA and VSD)
- Truncus arteriosus
- Post Ross procedure (for critical AS)- would see LVH on ECG
- All the above except PS and TOF would be due to RV-PA conduit= ES murmur or to fro murmur
- If no RBBB- all the ones associated with VSD (eg TGA, truncus, TOF) are much less likely
Pulmunary atresia + VSD: BT shunt until 2-3 years of age then definitive repair
PA + intact VS= BT shunt=>univentricular pathway
Cyanotic child with median sternotomy ddx
Univentricular circulation with staged palliative procedures
Which is most commonly HLHS
Other differentials include:
-Hypoplastic R heart syndrome
-Unbalanced AVSD
-PA with intact ventricular septum
-Double inlet left ventricle
-Severe Ebstein anomaly
Complications congenital heart disease
Delayed puberty
Poor growth
Protein losing enteropathy (fontan)
Congestive heart failure
Renal impairment
Arrythmias, heart block
Need for pacing
CNS complications:
- stroke
-cerebral abscesses
Operative:
- RLN palsy
- Horners syndrome
narrow egg on a string appearance w increased pulmunary blood flow on CXR
transposition great arteries
snowman sign with increased pulmunary blood flow on CXR
Supracardiac TAPVR
causes cyanotic child with median sternotomy and murmur
complex congenital heart disease with palliative surgery and residual disease
eg univentricular circulation
could be post norwood (shunt in situ) or post glenn (usually no murmur but may be murmur from MAPCAS)
DDX LLSE without scar
- VSD (pansystolic)
- AVSD (pansystolic)
- Mitral regurg (pansystolic)- radiates to apex, displaced apex
- Tricuspid regurg (pansystolic)- hepatomegaly, raised JVP
- HOCM (ESM)
- Stills (louder lying down, very quiet or absent when sitting up)
- Aortic regurg (diastolic)
Murmurs in LUSE (no scar)
RVOT which could be:
- PS (valvular, subvalvular, supravalvular)
- Branch PS (radiates to back)
- Pulm flow murmur (soft murmur, increased with anemia or fever)
- ASD (soft murmur- secundum or primum)
LVOT
Murmurs LUSE (+ scar):
RVOT:
- PS (valvular, subvalvular, supravalvular)
- TOF (residual PS)
- PA + VSD
- TGA (if doing Rastelli for PA and VSD)
- Truncus
- Ross procedure (for severe AS)- would see LVH on ECG
- All the above except PS and TOF would be due to RV-PA conduit= ES murmur or to fro murmur
- If no RBBB- rules out all the ones association with VSD (eg TGA, truncus, TOF)
Ejection systolic murmurs in RUSE (no scar)
LVOT
- AS (valvular, subvalvular, supravalvular)- radiates to carotids
HOCM- radiates to suprasternal notch, louder with Valsalva
Ejection click at RUSE:
Bicuspid aortic valve
Cyanotic child with median sternotomy:
- Univentricular circulation with staged palliative procedures
Which is most commonly HLHS
Other differentials include:
Tricuspid atresia
Unbalanced AVSD
PA with intact ventricular septum
Double inlet left ventricle
Double outlet rV
Severe Ebstein anomaly
“This could be due to a univentricular circulation with staged procedures, including….
Given that they are still cyanotic and their age, I would assume that they have completed two stages, and may be awaiting fontan repair OR have had a fenestrated Fontan (if child is >4 years) “
Continuous murmur:
PDA (unwell! Collapsing pulse/bounding pulse- wont be in the exam)
BT shunt (most common) - will either see lateral thoracotomy or median sternotomy
Venous hum
Mapcas (likely cyanotic child)
AV fistula
Ebsteins anomaly
Cyanotic or acyanotic if older
Single ventricular pathology
Scar
CXR: huge heart
ECG: superior axis, WPW , RBBB (and associated wide split S2), first degree heart block
Differentiating LVOTO
supravalvular AS has a thrill (and may be associated with Williams syndrome)
valvular AS has a click and thrill
Subvalvular AS has neither a click or a thrill
Diastolic murmur LUSE
pulmunary regurgitation
often post repair of TOF
VSD murmur is louder in
small defects
Increased pulmunary vascularity seen in
Truncus
TAPVD
TGA
Reduced pulmunary vascularity seen in
PA + intact ventricular septum
Tricuspid atresia
Ebsteins anomaly
TOF
Critical PS
RBBB occurs in
Post VSD repair
ASD
Causes RAH
Tricuspid atresia
Hypoplastic right heart
Ebsteins anomaly
Pulmunary atresia
Looks like peaked p waves on ECG
Causes LAH
Mitral valve disease
Cardiomyopathy
HTN
Any large L–> R shunt
Looks like wide bifid p waves on ECG
Deep, narrow (“dagger-like”) Q waves in lateral (I, aVL, V5-6) +/- inferior (II, III, aVF) leads indicate
HOCM
Would also see LVH with this
