Cardiology Flashcards

1
Q

Characteristics of a VSD on examination?

A

Loud, harsh, blowing pansystolic/holosystolic murmur, best heard at LLLE with thrill (should be L–>R shunt)

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2
Q

What is Eisenmenger syndrome?

A

Reversal of shunt through a defect to R–> L due to pulmonary hypertension - Cyanosis - murmur may disappear - accentuated S2 - cubbing

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3
Q

Normal foetal cardiac physiology x 4

A

1) Right –> Left shunting at the atrium through patent foramen ovale and from the arterial level thorugh the ductus arteriosis 2) High pulmonary vascular resistance 3) Low pulmonary blood flow 4) Ventricles work in parallel

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4
Q

What is this?

A

Ebsteins anomaly, cardiomegally, lung hypoplasia

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5
Q

TAPVD = total anomalous pulmonary venous drainage

A

Most commonly infra-cardiac and below the diaphragm

If also an obstruction to flow into LA = BAD, needs urgent surgery

Pulmonary blood flow goes into RA so RA saturations will be high

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6
Q

Causes of murmurs in first 24 hours of life?

A

Semi-lunar valve stenosis AV / tricuspid valve regurtiation Usually NOT ASD/VSD

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7
Q

Causes of cyanosis in the first 24 hours of life

A

Transposition of the great arteries single ventricle physiology

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8
Q

When do duct dependent lesions appear?

A

24 hrs –> 2 weeks of life

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9
Q

Cardiac lesions dependent on blood flow to lungs?

A

Present with cyanosis when duct closes eg) Critical pulmonary stenosis, pulmonary atresia, single ventricle with PS/PA

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10
Q

Cardiac lesions dependent on blood flow to body?

A

Present with low cardiac output (shocked) when duct closes eg) critical aortic stenosis, critical coarctation of the aorta, hypoplastic left heart syndrome

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11
Q

What is the hyperoxia test?

A

Place child in high oxygen environment - if sats / pO2 >150mmHg, likely lung pathology - If low sats / poor pO2, likely to be a cardiac issue with mixing of oxygenated and deoxygenated blood

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12
Q

Transposition of the Great Arteries (describe)

A

CXR - narrow upper/anterior mediastinum as aorta and pulmonary vessels are on top of each other, heart not huge, Present with cyanosis, M>F Mx - prostaglandin (keep duct open), septostomy (open ASD larger to mix blood, may need atrial switch procedure

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13
Q

Cyanotic neonate, what does this ECG show?

A

Small RV/TV large R waves

= ECG of pulmonary atresia

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14
Q

Management of pulmonary atresia

A

Mx: prostaglandin to keep duct open, If septum intact, associated with fistula to coronary artieries which when corrected, drop in pressure can cause myocardial ischaemia

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15
Q

Describe Truncus arteriosis

A

Large VSD

Single large outflow tract

CXR - pulmonary plethora

Well until pulmonary vascular resistance drops

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16
Q

Tetraology of fallot + pulmonary atresia

A

Large VSD

No pulmonary outflow tract (atresia) - maintain bronchial arteries from aorta

ADD INFO

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17
Q

Main signs and symptoms of heart failure in infants

A

*** Poor feeding

tachypnoea

tachycardia

**** poor growth

diaphoresis

hepatomegally

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18
Q

What percentage of children will have a systolic heart murmur?

+ most common

A

Up to 50%

15% will have a >2/6 murmur

Most do not have CHD and dont need any other investigation

  • Most commonly “functional” murmur, ASD, small VSD, AS/PS, rarely PDA or coart if child is well
  • minor lesions can wait until >3yrs
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19
Q

Older childen - common causes of heart murmurs?

A

1) innocent murmur
2) ASD - lound second heart sound, hyperdynamic praecordium, ,systolic flow murmur

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20
Q

Characteristics of coarctation of aorta?

A

Murmur heard best posteriorly (b/w scapular)

Hypertension

Difficult to palpate femoral pulses

associated with bicuspid aortic valve

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21
Q

Characteristics of an innocent murmuer in older kids? (x 5)

A

Healthy child, no exercise intolerance

No signs of heart failure / cyanosis

Normal praecordium

Murmur intensity varies with posture and fever

Normal second heart sound

* Pathological murmurs are almost never intermittent *

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22
Q

What is still’s murmur?

A

Vibratory murmur

A twanging sound, like that made by a piece of string

= aortic leave vibration

Almost always resolves when sitting

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23
Q

What is a venous hum and how can you elicit it?

A

Benign phenomenon

Heard loudest above the right clavicle

Continous, if loud, often confused with PDA

Assess my occluding ipsilateral internla juglar vein (if is disapears = venous hum)

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24
Q

Rheumatic heart disease

A

Mitral / aortic regurg

Valve thickening and deformity

pancarditis (pericardium, myocardium, epicardium)

Follow guildelines

* Can present in complete heart block *

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25
Q

Causes of Cardiomyopathy in a structurally normal heart (x 6)

A

Myocarditis

Familial dilated cardiomyopathy

Tachycardia induced

Mitochondrial

Myopathies

Metabolic

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26
Q

Heart failure management

A

Diuretics

ACE inhibitors

Spironolactone

betablockers

* may need inotropes eg) dobutamine, milrinone

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27
Q

What is the bernouli equation?

A

Change in pressure = 4 x (distal velocity2 - proximal velocity2)

Assume promimal velocity is low (except in coart)

therefore:

Change in pressure = 4 x (distal velocity2) mmHg

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28
Q

What is the noral expected fractional shortening?

A

30%

= diameter of ventricle in diastole minus diameter of ventricle in systole divided by VDD

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29
Q

What is the expected ejection fraction

A

60%

30
Q

$4yo M, well, 2/6 ESM LLSE, normal BP, RV lift

ECG (see below)

CXR - pulmonary plethora, prominent pulmonary artery, cardiomegally

A

ECG = borderline RAD, incompelte RBBB (narrow QRS)

= ASD

Should also have flixed spltting of S2

31
Q

4 yo M, well, normal puses and BP

2/6 vibratory ESM

ECG (see below)

Murmur goes away with head tilted back

A

iRBBB (RSR V1), high voltages, narrow QRS, normal rate and sinus rhythm

TWI V1-V3 (normal in age 4)

= Still’s murmur (aortic leaflet vibration)

32
Q

4 yo M, well, 4/6 pansystolc murmumr LLSE

A

ECG: Sinus rhythm, (upright p wave L I and aVf)

HR 120, normal axis (+60),normal pwave, PR 140ms,

High voltage R waves V6, , seep S V2 ? LVH

Dx: VSD (generous LV voltages)

33
Q

4 yo child, slim, recurrent chest infections

BP 95/60, normal pulses, overactive praecordium

2/6 low pitched pansystolic murmur lower LSE

2/4 diastolic murmur at apex

CXR - cardiomegally, pulmonary plethora, hyperexpanded lungs

A

Tall, dominant R wave V1-2 (RVH)

V5 - very high voltage (R-S)

Deep s-wave V6 (LVH)

= biventricular hypertrophy = Large VSD

If AVSD –> superior axis

34
Q

2 yo M, cyanotic (88%), loud systolic murmur

A

Sinus rhythm normal rate 160, QRS axis - right deviation +160

R wave dominant V1-2, S wave dominant V5-6, Upright t-wave V1 (usually inverted)

V4R - large R waves, no S waves)

= Right ventricular hypertrophy

= Tetralogy of Fallot

35
Q

Normal neonatal heart

Right heart T-wave

A

At birth, RVH is normal, upright t-wave in V1 because right ventricle is dominat

As soon as pulmonary vascular resistance falls, left ventricle dominates, RV regresses

Day 4 - 4 years, Normal to have TWI V1

36
Q
A

Sinus, rate 150, RWD

Half voltage sign at start!!

Very high voltages, biventricular hypertrophy

37
Q

8 month old

A

Tall p waves = right atrial dilataton

Pumonary atresia with small RV, large RA

On rhythm strip, first huge wave is the P wave

38
Q
A

Tall p wave V1,2

RVH (tall R wave V1, deep S V6, upright T V1 right axis)

= Total anomalous pulmonary venous connection (late diagnosis)

39
Q
A

Bifid P-waves, Too long

V1, deep wave

LA enlargement

40
Q

Bifid P-waves (tall)

+ causes

A

RA enlargement

> 3mm tall

Causes - large ASD, tricuspid anomalies

41
Q

Bifit p-waves (long) + causes

A

Left atrial enlargement

> 2.5mm long

Causes : mitral stenosis, mitral regurg, large VSD, large duct, cardiomyopathies

42
Q
A
43
Q

Murmur in a small but well 4 year old, modest murmur, Harrisons sulci, CXR pulmonary plethora

A

Rate - normal, ? sinus (can have more than one atrial foci)

Left axis deviation - 60

Upright T in V1, very large T in V4-6, iRBBB

= AVSD -or primum ASD

44
Q

Causes of leftward axis on ECG?

A

LVH (especially in large LVD with volume overload)

LBBB (broad QRS)

Left anterior hemiblock “superior axis”, narrow QRS - (Tricuspid atresia, AV canal defect, congenitally corrected TGA)

45
Q

Are Q waves in inferior leads in infants normal or worrying?

A

Usually normal in inferior and lateral leads (V5-6)

Key feature - thin (even if short)

Pathological in V1 (unless neonate)

Deep, wide Q-waves (esp post op) = BAD = infarction

46
Q

Which leads should you measure QTc? and what is the formula?

A

Meausre in lead 2 or V5

Normal is less than 450ms

QTc = QT(ms)/Squareroot R-R(ms)

47
Q

What are normal ST segment parameters?

A

Elevation up to 1mm normal in limb leads

Up to 2mm in V2-V4

Often early repolarisation (teenagers)

DDx: cardiomyopathies, myocarditis,

48
Q

Diagram of normal heart axis

A
49
Q

Haemodynamics in cardiac catheterisation

A

How does blood go round>

  • pressure/ pressure gradients
  • wave forms
  • saturations

-

50
Q

Angiography in cardiac catheterisation

A

” shaddow puppet” of the structure you are injecting the dyeinto

  • not cross sectinal like CT
  • Dynamic - nearly 4D

Great for vascular information - high spatial resolution <1mm (coronaries / tight stenosis

  • Absent or disconnected vessels

–> POOR for intracardiac info (atrial septim / inlet valves)

51
Q

Intervention in cardiac catheterisation

A

Evolved as an alternative to surgery / to defer surgery

  • narrow things are ballooned / stented
  • Holes / vessels get blocekd

Stent / valve impantation

52
Q

Who needs cardaic cath?

A

When you need precice info of pulmonary vascular resistace / shunt quantification

–> usually L–>R shunt (large VSD) - Eg - Eisenmengers

Complex lesions prior to single ventricle palliation

When you need precise / additional info on vessel anatomy

Increasing MRIs

53
Q

What pressure clasifies as pulmonary hypertension?

A

>25mmHg - Mild

>35mmHg - Moderate

>45 mmHg - severe

54
Q

Left –> Right shunt

A

Pink patient with extra pulmonary blood flow

Breathless, congested lungs, good saturations

Often present as pump failure but pump is working overtime

55
Q

RIght –> Left Shunt

A

Reduced pulmonary blood flow

Blue patient

Normal cardiac output to the circulation

Not breathlessness, normal ventilation but poor oxygenation

EG) tetralogy of fallots

56
Q
A

= ASD

normal pressures - no stenosis

LPA 30 = mild pulmonary HTN

57
Q
A

Step up at ventricular level

LPA 46mmHg - severe

RV pressure high

LPA (65mmHg)vs RV (85mmHg) - pessure gradient 20 mmHg between RV and LPA

= Large VSD, L–>R shunt + pulmonary hypertension + RV outflow tract obstruction (pulmonary stenosis)

58
Q
A

Very high pressure gradient between RV –> PA = PV outlow tract obstruction

Very high right ventricular pressure

Systemic sats are low (R –> L shunt)

= Tetralogy of fallot

59
Q

What is cardiac output (L/min)

A

Stroke volume x HR

= Q (Flow rate)

Mearure with MRI

Fick principle - calcualte cardiac output based on known input (O2) and uptake/use (VO2) and carrer (Hb)

Assume 120ml/metre squared

60
Q

Things that vary VO2

A

Activity, sedation, anaethetic (Ga reduced by 30%)

Muscle relaxants

Growth (Foetus VO2 30% higher)

Anabolic vs catabolic states

Sepsis

Surgery

61
Q

Equation for oxygen content

A

O2 sats x Hb x 1.36 + dissolved O2

eg (0.98 x 120 x 1.36)

Differnece in oxygenation between PV - PA

62
Q

Qp:Qs ratio

A

In normal person = 1:1

R–> L Shunt 0.5:1

L –> R shunt = 4:1

63
Q
A

Aortic stenosis

64
Q

What is resistance?

A

Resistance is a measure of how much pressure gradient is required ot generate a certain flow rate

= mmHg / Lirtre per minute

= Woods units

1-2 = normal PVR

2-4 WU/m squared = mild elevation

>7.9 WU/m square = severe elevation

65
Q

When would you use ECMO?

A

Patients with BIventricular dysfunction OR pulmonary hypertension

–> assists oxygenation

Not a great choice in overwhelming sepsis but used when back against the wall

66
Q

When and why do you use a Ventriculaar assist device?

A

Assists the ventricles

Does NOT assist in oxygenation

–> commonly used in ventricular dysfunction due to acute and reversible process (EG - myocarditis) or as a bridge to transplant or if cann not be separated from bypass following cardiacsurgery

Increased risk of blood stream infection

67
Q

What does this ECG show?

A

Wolff Parkinson white syndrome (during palpitation)

  • broad complex tachycardia

~280bpm

  • accessory pathway for initiation and maintenance of tachycardia
68
Q

What does this ECG at rest show?

A

Wolff Parkinson white

  • Short PR interval

Delta waves (Lead II, III, avF and V4)

= congenital cardiac pre-excitation syndrome with abnormal conduction through an accessory pathway

69
Q

What are the characteristiscs of an antidromic AVNRT?

A

ANTI = wrong direction of conduction but repeatable

= WIDE QRS

70
Q

What are the characteristics of an orthodromic AVNRT?

A

WPW, short PR, delta wave

Ortho = same direction as normal conduction

= narrow

71
Q

When do you measure serum calcium in a congenital cardiac defect?

A

DiGeorge (22.2 deletion) - ELEVATED calcium

William’s syndreom - LOW calcium