Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 3a topics > paeds cardio > Flashcards

paeds cardio Flashcards

1
Q

continuous blowing noise heard just below the clavicles

A

venous hum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Low-pitched sound heard at the lower left sternal edge

A

stills murmur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

features of innocent murmurs

A

Soft
Short
Systolic
Symptomless
Situation dependent, particularly if the murmur gets quieter with standing or only appears when the child is unwell or feverish

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ddx for Pan systolic murmur

A

Mitral regurgitation
Tricuspid regurgitation
Ventricular septal defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ddx for ejection systolic murmur

A

Aortic stenosis
Pulmonary stenosis (+ tetralogy of fallot)
ASD
Hypertrophic obstructive cardiomyopathy
coarctation and bicuspid aortic valve (both in turners)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

when can splitting of the second heart sound be normal

A

can be normal with inspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Fixed splitting of second heart sound indicates?

A

ASD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Causes of PDA

A
  • genetic
  • maternal rubella
  • prematurity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pulse character in PDA

A

large volume, bounding, collapsing pulse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

continuous crescendo-decrescendo “machinery” murmur that may continue during the second heart sound, making the second heart sound difficult to hear

A

PDA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Diagnostic investigation heart murmurs

A

echocardiogram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Management isolated PDA

A

indomethacin or ibruprofen if symptomatic

may choose to monitor and do trans-catheter or surgical closure if still present at 1 year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What do you do to keep PDA open

A

prostaglandin E1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

ddx for diastolic murmurs

A

early diastolic:
- aortic regurg
- pulmonary regurg

mid diastolic:
- mitral stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Most common ASD

A

Ostium secondum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Complications ASD

A

Stroke in the context of venous thromboembolism (see below)
Atrial fibrillation or atrial flutter
Pulmonary hypertension and right sided heart failure
Eisenmenger syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

mid-systolic, crescendo-decrescendo murmur loudest at the upper left sternal border with a fixed split second heart sound

A

ASD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Management ASD

A

ASDs can be corrected surgically using a transvenous catheter closure (via the femoral vein) or open heart surgery.

Anticoagulants (such as aspirin, warfarin and NOACs) are used to reduce the risk of clots and stroke in adults.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is ebsteins anomaly

A

tricuspid valve is set lower in the right side of the heart (towards the apex), causing a bigger right atrium and a smaller right ventricle. This leads to poor flow from the right atrium to the right ventricle, and therefore poor flow to the pulmonary vessels. It is often associated with a right to left shunt across the atria via an atrial septal defect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

ECG wolff-parkinson white

A

short PR interval
wide QRS complexes with a slurred upstroke - ‘delta wave’
left axis deviation if right-sided accessory pathway*
right axis deviation if left-sided accessory pathway*

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Evidence of heart failure (e.g. oedema)
Gallop rhythm heard on auscultation characterised by the addition of the third and fourth heart sounds
Cyanosis

A

ebstein’s anomaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what can ebstein’s anomaly cause

A

wolff-parkinson white

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Management ebsteins anomaly

A

Medical management includes treating arrhythmias and heart failure. Prophylactic antibiotics may be used to prevent infective endocarditis. Definitive management is by surgical correction of the underlying defect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Causes ebsteins anomaly

A

lithium use in pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

ECG ASD caused by ostium secundum

A

RBBB with RAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

ECG ASD caused by Ostium primum

A

RBBB with LAD, prolonged PR interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Causes VSD

A

congenital VSDs are often association with chromosomal disorders:
Down’s syndrome
Edward’s syndrome
Patau syndrome
cri-du-chat syndrome

congenital infections

acquired causes
post-myocardial infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

failure to thrive, pan systolic murmur left lower sternal border. There may be a systolic thrill on palpation.

A

VSD. louder in smaller defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Management VSD

A
  • w&w
  • surgical closure: trans-catheter or open heart
  • antibiotic prophylaxis
30
Q

Cardiac assocations downs syndrome

A
  • endocardial cushion defect (most common, 40%, also known as atrioventricular septal canal defects)

ventricular septal defect (c. 30%)

secundum atrial septal defect (c. 10%)

tetralogy of Fallot (c. 5%)

isolated patent ductus arteriosus (c. 5%)

31
Q

Examination findings pulmonary hypertension

A

Right ventricular heave: the right ventricle contracts forcefully against increased pressure in the lungs
Loud P2: loud second heart sound due to forceful shutting of the pulmonary valve
Raised JVP
Peripheral oedema

32
Q

Complications VSD

A
  • aortic regurg
  • eisenmengers
  • pulmonary hypertension
  • infective endocarditis
33
Q

associations coarctation

A

more common in males Turner’s syndrome
bicuspid aortic valve
berry aneurysms
neurofibromatosis

34
Q

features of coarctation

A

weak femoral pulses

radio-femoral delay

ejection/mid systolic murmur heard at left infraclavicular space radiating to interscapular area

apical click from the aortic valve

35
Q

management coarctation

A
  1. prostaglandin E to keep PDA open
  2. Surgery
36
Q

Options for management congenital aortic stenosis

A

Limit exercise, regular follow ups and ECG
Percutaneous balloon aortic valvoplasty
Surgical aortic valvotomy
Valve replacement

37
Q

Associations congenital pulmonary stenosis

A

Tetralogy of Fallot
William syndrome
Noonan syndrome
Congenital rubella syndrome

38
Q

Complications congenital aortic stenosis

A

Left ventricular outflow tract obstruction
Heart failure
Ventricular arrhythmia
Bacterial endocarditis
Sudden death, often on exertion

39
Q

Management pulmonary stenosis

A

w&w
balloon valvuloplasty via a venous catheter

40
Q

4 things in tetralogy of fallot?

A

PROVE

Pulmonary stenosis
Right ventricular hypertrophy
Overriding of the aorta
VSD
Ejection systolic murmur

41
Q

Risk factors for ToF

A

RAID

Rubella infection
Alcohol consumption in pregnancy
Increased age of the mother (over 40 years)
Diabetic mother

42
Q

“boot shaped” heart

A

right ventricular hypertrophy - ToF sign

43
Q

Pathophysiology tet spells

A

Physically exertion –> generating a lot of carbon dioxide –> vasodilaton –> systemic vasodilation and therefore reduces the systemic vascular resistance –> Blood flow will choose the path of least resistance, so blood will be pumped from the right ventricle to the aorta rather than the pulmonary vessels, bypassing the lungs

can also occur with increased pulmonary vascular resistance

44
Q

Presentation tet spells

A

precipitated by waking, physical exertion or crying. The child will become irritable, cyanotic and short of breath. Severe spells can lead to reduced consciousness, seizures and potentially death.

45
Q

Management tet spell

A
  1. position with knees to chest to increase systemic vascular resistance
  2. O2
  3. beta bockers to decrease pulmonary vascular resistance
  4. IV fluids can increase pre-load

Morphine can decrease respiratory drive, resulting in more effective breathing.

Sodium bicarbonate can buffer any metabolic acidosis that occurs.

Phenylephrine infusion can increase systemic vascular resistance.

46
Q

In what conditions may you want to keep PDA open?

A
  • coarctation
  • tetralogy of fallot
  • transposition of the great arteries
47
Q

Management ToF

A
  1. Prostaglandin E1 infusion
  2. open heart surgery
48
Q

Management transposition of the GA

A
  1. prostaglandin E1
  2. Balloon septostomy
  3. Open heart surgery
49
Q

When does ToF present?

A

presents at around 1-2 months, although may not be picked up until the baby is 6 months old

50
Q

most common cause infective endocarditis

A

Staphylococcus aureus

51
Q

pathogen infective endocarditis after dental procedure

A

Streptococcus viridans

52
Q

pathogen infective endocarditis up to 2 months after valve replacement

A

coagulase-negative Staphylococci such as Staphylococcus epidermidis

53
Q

non infective causes endocarditis

A

systemic lupus erythematosus (Libman-Sacks)
malignancy: marantic endocarditis

54
Q

inheritance Hypertrophic obstructive cardiomyopathy

A

autosomal dominant

55
Q

Management hypertrophic obstructive cardiomyopathy

A

Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis*

56
Q

Pathophysiology hypertrophic obstructive cardiomyopathy

A

Usually due to a mutation in the gene encoding β-myosin heavy chain protein

57
Q

Echo findings hypertrophic obstructive cardiomyopathy

A

Echo findings include MR, systolic anterior motion (SAM) of the anterior mitral valve and asymmetric septal hypertrophy

mitral regurgitation (MR)
systolic anterior motion (SAM) of the anterior mitral valve leaflet
asymmetric hypertrophy (ASH)

58
Q

ECG pericarditis

A

the changes in pericarditis are often global/widespread, as opposed to the ‘territories’ seen in ischaemic events

‘saddle-shaped’ ST elevation

PR depression: most specific ECG marker for pericarditis

59
Q

Management pericarditis

A

NSAIDs
Colchicine

60
Q

chest pain: may be pleuritic. Is often relieved by sitting forwards
other symptoms include non-productive cough, dyspnoea and flu-like symptoms

A

pericarditis

61
Q

cyanotic CHDs

A

Tetralogy of fallot
Transposition of great vessels (TGA)
Tricuspid abnormalities eg ebsteins

Tricuspid atresia
Total anomalous pulmonary venous return
Truncus arteriosus

62
Q

Most common cardiac abnormality in turners

A

bicuspid aortic valve (ejection systolic murmur)

63
Q

Murmurs ebsteins anomaly

A

tricuspid regurgitation (pan-systolic murmur) and tricuspid stenosis (mid-diastolic murmur)

gallop rhythm, fixed splittng of second heart sound if ASD

64
Q

murmur grades

A

One- Very faint. Heard by an expert in optimum conditions

Two - Heard by a non-expert in optimum conditions

Three- Easily audible, no thrill

Four- A loud murmur, with a thrill

Five -Very loud, often heard over a wide area, with thrill

Six - Extremely loud, heard without a stethoscope

65
Q

management SVT

A

ABCDE

Cardioversion:
- syncronised eg defib
- adenosine
- amiadarone before 3rd shock

with appropriate sedation
+ analgesia (e.g. IM/intranasal
ketamine if delay in IV access)

66
Q

examples of vagal manourvres SVT

A

Vagal maneuvers – For infants, apply bag containing ice water to the face above the nose and mouth for 15 to 30 seconds. Do not obstruct ventilation. In older children, bearing down or blowing into an occluded straw for 15 to 20 seconds provides vagal stimulation.

67
Q

define SVT in children

A

Infant > 220 min-1
Child > 180 min-1
Abrupt onset

68
Q

Another name for wolff-parkinson white syndrome

A

AV reciprocating/bundle of kent

re-entry point is an accessory pathway

69
Q

pathophysiology SVT

A

Early depolarisation –> shortened PR interval and narrow QRScomplex

70
Q

what is considered a narrow QRS?

A

<0.12 seconds

Phase 3a topics (39 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions