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TAS > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the most common symptomatic congenital heart disease

A

VSD’s

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2
Q

Which genetic conditions have increase of VSDs

A

Downs syndrome
DiGeorge syndrome

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3
Q

What type of shunt is VSD

A

left to right

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4
Q

Types of murmurs in VSD

A

small - panystolic at left lower edge, ass. thrill

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5
Q

Medications to treat VSD

A

diuretics
ACEi

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6
Q

What is the pathophysiology of WPW

A

Normal heart - insulating fibre tissue between atria and ventricle - signal has to go via AVN node
In WPW - the band of fibre has myocardial cells which becomes accessory pathway

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7
Q

What is the delta wave?

A

conduction through accessory pathway leads to excitation of the ventricle before conduction of AVN = shortened PR interval
conduction is slower than AVN node which is why it is slurred upstroke of QRS

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8
Q

What is contraindicated in AF and WPW

A

Adenosine - could lead to VF

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9
Q

Treatment for WPW

A

slow conduction down

beta-blockers
amiodarone
flecainide
calcium-channel blocker

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10
Q

What is the most common cardiac condition ass. with Noonan syndrome

A

Hypertrophic cardiomegaly

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11
Q

What does hypertrophy fo LV cause?

A

reduces LV cavity volume
reduced ability of LV to fill in diastole

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12
Q

What does reduce filling in LV cause?

A

Rising left-atrial pressure
pulmonary oedema
congestive cardiac failure

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13
Q

What are the forms of hypertrophic cardiomegaly

A

Obstructive
Non-obstructive - most common

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14
Q

Why does obstructive cardiomegaly form?

A

Dynamic obstruction of LV outflow by anterior leaflet of mitral valve
Due to abnormality of papillary muscle insertion and abnormal flow in LV

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15
Q

What are most common symptoms in HOCM

A

angina
dizziness

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16
Q

Examination findings with patients with HCM

A

Displaced apex and heaving
additional heart sounds S3 S4

17
Q

ECG changes of ventricular hypertrophy

A

left axis deviation and large QRS complexes in chest leads = LVH ST segment changes and t wave inversion in V4-V6 left heart strain

right axis devotions and large qrs in II, III, avF, 1-3 = RVH

18
Q

medications for hypertrophy

A

beta blockers - slow heart rate, improve filling
diuretics
calcium channel blockers
ACE I

19
Q

When does ToF present if not detected antenatally

A

within 1 year with cyanosis and murmur

20
Q

what sign is seen on CXR for coractation of aorta

A

rib notching

21
Q

What murmur is coarctation of aorta associated with

A

ejection systolic murmur radiates to back

22
Q

What happens in TGA

A

Aorta rises from right ventricle
pulmonary artery arises from left ventricle

23
Q

What increases the incidence of TGA

A

DiGeorge syndrome
Infant of mum with diabetes

24
Q

What is CXR sign of TGA

A

egg on side appearance
pulmonary pleathora

25
Q

What type of discordance is TGA

A

ventriculoaterial discordance

26
Q

What is Marfan’s syndrome associated with?

A

Aortic root dilatation leading to aortic regurgitation

27
Q

Phase of cardiac action potential

A

Phase 0 - influx of sodium
Phase 1 - end of depolarisation - efflux of potatissium
pHASE 2 - Plateau phase - slow influx of calcium
Phase 3- rapid repolarisations - efflux of potassium
Phase 4 - diastole, calcium-sodium efflux, potassium influx

28
Q

Signs of servere aortic stenosis

A

Soft S2
second heart sound

So narrowed and calcified - 2nd here sound becomes inaudible

29
Q

Why is VT broad complex

A

rhythm starts from ventricle

30
Q

Is there P waves in VT?

A

No as SAN isn’t controlling the rhythm

If there is - they will be unrelated to ARS complex

31
Q

Which aortic arch forms right subclavian artery

A

right 4th aortic arch

32
Q

Which aortic arch forms internal carotid artery

A

third arches

33
Q

Adenosine doses for SVT

A

Start adenosine 0.1mg/kg

3mg -> 6mg > 12mg

If shocked - synchorous shock 1joules/kg

TAS (18 decks)

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