Brainscape's Knowledge GenomeTM

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


See full index

Year 4 Paediatrics > Cardiology > Flashcards

Cardiology Flashcards

1
Q

State three causes of ‘Blue Baby Syndrome’

A

Cyanotic Heart Disease

Methaemaglobinaemia

RDS (more transient)

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

How is Blue Baby Syndrome investigates?

A

Pulse Oximetry (may be falsely elevated if cause is Methaemaglobinaemia so use Co-Oximeter)

If thinking cause is cardiac then do ECG, Echo, CXR

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

How is Blue Baby Syndrome secondary to Cyanotic Heart Disease treated?

A

Prostaglandin E1 to keep Ductus Arteriosus open
Oxygen Therapy

Definitive is corrective surgery

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

How is Blue Baby Syndrome secondary to Methaemaglobinaemia treated?

A

Methylene Blue

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

What is Methaemaglobinaemia?

A

Congenital or Acquired

Reduced oxygen carrying capacity of haemoglobin due to >1% being Methaemaglobin (iron in ferric instead of ferrous form)

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

Heart Murmurs can be described as ‘Innocent’ or ‘Flow’, what does this mean?

A

Caused by fast blood flow through various parts of the heart during systole

Typically soft, short, symptomless, systolic

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

When would you investigate an innocent murmur?

A

Murmur louder than 2/6
Diastolic
Louder on standing
Failure to thrive

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

How do you investigate murmurs?

A

ECG
CXR
Echo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Give two causes of Pan Systolic Murmurs. Where would these best be heard?

A 
Mitral Regurgitation (Apex in left lateral position)
Tricuspid Regurgitation (left lower sternal border)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Give three causes of an Ejection Systolic murmur and where they’d be heard

A 
Aortic Stenosis (Aortic Area)
Pulmonary Stenosis (Pulmonary Area)
HOCM (4th ICS, Left Sternal Border)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the pathophysiology or ‘Splitting the Second Heart Sound’

A

Inspiration increases negative intrathoracic pressure

This causes right side of the heart to fill more and faster therefore will take longer to empty

This causes pulmonary valve to close after aortic

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

How would an Atrial Septal Defect sound on auscultation?

A

Mid systolic crescendo decrescendo at upper left sternal border

Fixed split of second heart sound (fixed meaning unrelated to inspiration, as left to right shunt causes continuous increased blood on right)

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

How would a Patent Ductus Arteriosus sound on Auscultation?

A

If small, may not cause abnormalities

Normal first heart sound and machinery murmur for second

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

How would Tetralogy of Fallot sound on auscultation?

A

Ejection Systolic at left sternal edge

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

State three Acyanotic Heart Defects

A

ASD
VSD
PDA

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

What are the two types of ASD and how does it present?

A

Secundum (defect in central septum, involving foramen ovale)
Primum/Partial (bottom end of septum often involving abnormal leaky AV valves)

Asymptomatic, Arrhythmias, Recurrent chest infections

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

How would you investigate suspected ASD and what would you see?

A

CXR - Cardiomegaly, Enlarged Pulmonary Arteries
ECG - Secondum (partial RBBB and RA deviation), Partial AVSD (neg QRS in AVF)
Echo

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

When and how should ASDs be managed?

A

If defect is significant enough to cause RV dilation

Secundum - catheterisation and insertion of occlusion
Partial AVSD - Surgical Correction

Normally taken between 3-5 years to prevent RHF and arrhythmias later in life

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

Describe the types VSD in terms of location

A

Most common CHD (accounting for 30%)

Perimembranous are the most common (upper by the valves)

Muscular (lower portion of septum)

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

Describe the types VSD in terms of size - small

A

Asymptomatic, Loud Murmur, Investigations normal, Closes spontaneously

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

Describe the types VSD in terms of size - moderate

A

Increased flow in systole
May have some dilation of left heart
Excess sweating/Tachypnoea

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

Describe the types VSD in terms of size - large

A

Heart failure with breathlessness, faltering growth after one week, recurrent chest infections
Tachypnoea, Sweating

Same size or bigger than aortic valve

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

How would you investigate a suspected (large) VSD, and what would you see?

A

CXR - Cardiomegaly, Enlarged arteries
ECG - Biventricular Hypertrophy by 2 months
Echo

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

How would you manage a moderate/large VSD?

A

Diuretics
ACEI
Increased calories

Surgery at 3-6m (manage heart failure and prevent lung damage from pulmonary hypertension)

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

Define Patent Ductus Arteriosus

A

Ductus Arteriosus connects pulmonary artery to descending aorta

In term infants normally closes shortly after birth (therefore it is normal if preterm)

Classed as Patent if remaining open one month past expected delivery date

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

How does PDA present?

A

Continuous murmur beneath left clavicle

Normally asymptomatic but if large then heart failure

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

How should PDA be investigated?

A

ECG (presents like VSD if large)
CXR (presents like VSD if large)
ECHO

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

How is PDA managed?

A

Can try to close the PDA using Indomethacin (PGE1/COX1 inhibitor)

Closure with coil
Introduced by catheter

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

State three CYANOTIC Heart Defects

A

Tetralogy of Fallot
Tricuspid Atresia
Transposition of the Great Arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the Nitrogen Washout Test?

A

Determines presence of heart disease in a cyanosis neonate

Infant is placed on 100% Oxygen for 10 minutes and then right radial blood gas is taken (<15kPa qualifies as Cyanotic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What’s the acute management of a Cyanotic heart defect

A 
A to E Assessment 
Prostaglandin Infusion (can cause apnoea, seizures)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Tetralogy of Fallot is the most common cyanotic heart condition. What is involved in the tetrad?

A

VSD
Pulmonary Stenosis
RV Hypertrophy
Overriding Aorta (dilated and in severe cases collateral aortopulmonary arteries form)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Give four risk factors for Tetralogy of Fallot

A

Male
Teratogens (Alcohol, Warfarin)
First degree FH
Genetics (CHARGE, DiGeorge, VACTERL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Describe the three classifications of Tetralogy of Fallot

A

Mild - Pink TOF (usually asymptomatic, developing cyanosis in 1-3 years)

Mod to Severe - Presents in first few weeks with Cyanosis and Resp Distress, Recurrent chest infections

Extreme - usually detected in utero, if not presents within four hours. Completely dependent on PDA (pulmonary atresia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How would a TOF baby present OE?

A

General cyanosis and clubbing

Loud Single S2 (no pulmonary valve to close)
Pansystolic VSD murmur
Ejection click from dilated aorta

Post PG infusion - machinery murmur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Describe some investigations for TOF and what they would show

A

ECG - RA Deviation and RV Hypertrophy
CXR - Boot shaped heart and reduced peripheral markings
Echo - Gold Standard

Microarray - ?Genetic Syndromes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Describe the medical management of Tetralogy of Fallot

A

Encourage squatting

Prostaglandin Infusion (PGE1- Alprostadil, PGE2 - Dinoprostone)

Beta Blockers

Morphine (decrease Tachypnoea by decreasing resp drive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Why is squatting encouraged in TOF?

A

Increases venous return and systemic resistance

39
Q

Describe the surgical management of Tetralogy of Fallot

A

Palliative - Transcatheter stent in RV outflow tract, Modified Blalock Tausing Shunt (mimics PDA - connects blood flow from aorta to pulmonary artery )

Definitive - under bypass, from 3m to 4y

40
Q

State three complications of TOF

A

Polycythaemia
Stroke
CCF

41
Q

Define Transposition of the Great Arteries

A

Aorta arises from the right ventricle and pulmonary artery from left, creating a parallel circulation

42
Q

Describe the classification of Transposition of the Great Arteries

A

Dextrotransposition - Aorta is anterior and right to PA

Levotransposition - aorta is anterior and left to PA

43
Q

What is different about Levotransposition?

A

The ventricles have switched places rather than arteries therefore it is acyanotic

Right ventricle is not used to higher pressure of left side causing Hypertrophy and failure

44
Q

Give three risk factors for Transposition of Great Arteries

A

Maternal age >40
Diabetes
Rubella

45
Q

Describe the clinical features of Transposition of the Great Arteries

A

Cyanosis in first 24 hours (if no mixing)
CHF features over first 3-6 weeks
RV heave

46
Q

State four investigations for Transposition of the Great Arteries, and describe what they’d show

A

Oximetry - Cyanosis with discrepancy between upper and lower

ABG - Metabolic Acidosis

Echo - Definitive diagnosis

CXR - Egg on a string

47
Q

How is Transposition of the Great Arteries managed?

A

Emergency PGE1 infusion
Correct Acidosis
Emergency atrial balloon septostomy
Definitive surgical correction after four weeks

48
Q

State four complications of Transposition of Great Arteries

A

Neopulmonary Stenosis
Neopulmonary Regurgitation
Coronary Artery Obstruction
Sudden Cardiac Death

49
Q

Describe the pathophysiology of Infective Endocarditis

A

Triad of Endothelial Damage, Platelet Adhesion and Microbial Adherence

Organisms : Staph Aureus, Strep Viridans, Strep Pneumoniae

50
Q

How does Infective Endocarditis present?

A

Persistent low grade fever (without another clear focus)
New Murmur
Splenomegaly

Oslers Nodes, Janeway Lesions, splinter Haem

51
Q

How is Infective Endocarditis investigated?

A
  • Blood Cultures (from multiple sites over 24h)
  • Microscopic Haematuria
  • Echo (aids but doesn’t confirm or deny if vegetation’s are there/not)
52
Q

Describe the Major Duke’s Criteria

A
  • Positive blood cultures on two separate occasions

- Positive ECHO (oscillating intracardial mass, abscess)

53
Q

Describe the MINOR Dukes Criteria

A 
Predisposition
Fever
Vascular Phenomena
Immunological Phenomena
Echo and Bloods suggestive but not meeting criteria
54
Q

What is required via the Dukes Criteria to diagnose Infective Endocarditis?

A

Two Major
One Major and Three Minor
Five Minor

55
Q

Describe the Surgical Management of Infective Endocarditis

A

If highly mobile, valvular dysfunction, >1 embolic event in two weeks

56
Q

Describe the medical management of Infective Endocarditis

A

IV Amoxicillin (4 weeks) and consider adding Gentamicin (2 weeks)

57
Q

What is Acute Rheumatic Fever?

A

Systemic Illness occurring 2-4 weeks after Pharyngitis in some due to cross reactivity of Strep Pyogenes

B Cells produce Anti M Protein AB against S.Pyogenes which interacts with heart/joints/etc (antigenic mimicry)

58
Q

Give three risk factors for Rheumatic Fever

A

Children
Poverty
Overcrowding

59
Q

How does Rheumatic Fever present?

A

Recent Sore Throat/Scarlet Fever
New Murmur
Arthritis

60
Q

Describe the Jones Diagnostic Criteria

A

Positive throat culture and positive anti streptolysin titre
AND
2 major or 1 major 2 minor

61
Q

Describe the major criteria for Rheumatic Fever

A 
SPECS
Syndenhams Chorea
Polyarthritis
Erythema Marginatum
Carditis
Subcut Nodules
62
Q

Describe the minor criteria for Rheumatic Fever

A 
CAPP
CRP raised
Arthralgia
Pyrexia
Prolonged PR interval
63
Q

How is Rheumatic Fever investigated?

A 
Cultures
Rapid Antigen Test
Anti Strep Serology
ECG 
Echo
64
Q

How is Rheumatic Fever managed initially?

A

1) Benzathine Benzylpenicillin
2) NOT Asparin - simple analgesia
3) Assess valves/any carditis

65
Q

What is the long term management for Rheumatic Fever?

A

Antibiotic therapy for at least 5 years/ or until child is 21

IM Benzylpenicillin every 3-4 weeks

66
Q

What is Sinus Arrhythmia?

A

Normal in children

Cyclical change with respiration by up to 30 bpm

67
Q

What is the most common arrhythmia in children, and the underlying problem

A

SVT (rapid between 250-300bpm)

Rarely a structural problem, normally a re-entrant tachy

68
Q

What will be seen on ECG of Sinus Tachycardia in children?

A

Narrow complex tachycardia between 250-300 bpm

Potentially delta wave if WPW is underlying cause

69
Q

How is SVT managed in Children?

A

Circulatory and Respiratory support

Vagal Stimulating Manouvres
IV Adenosine (terminating re-entrant)

Maintenance with Flecainide/Sotalol if required

70
Q

What is Kawasaki Disease?

A

Systemic vasculitis mainly affecting children 6m-5y

71
Q

Diagnosis of Kawasaki is based on clinical findings, such as …?

A
  • Fever >5 days
  • Conjunctivitis
  • Mucous Membranes Changes (red or dry lips etc)
  • Cervical Lymphadenopathy
  • Polymorphous Rash
  • Red and Oedematous Palms and Soles
72
Q

Why do congenital arrhythmias occur?

A

Anti Ro/ Anti La bodies from mother prevent normal conduction of developing heart

73
Q

How is Kawasaki disease managed?

A

IVIG and Aspirin

If persistent then corticosteroids and infliximab

74
Q

Name two complications of Kawasaki

A

Myocardial Disease

Coronary Aneurysms

75
Q

What is Eisenmenger’s?

A

When blood flows from the right side of the heart to the left across a structural lesion

Associated with ASD,VSD,PDA

76
Q

When does Eisenmenger’s develop?

A

After 1-2y of large shunts, or in adulthood with small shunts

77
Q

Describe the pathophysiology of Eisenmenger’s

A

Overtime, increased blood flow from left to right leads to pulmonary hypertension

When pulmonary pressure>systolic, blood flows right to left

The cyanosis can lead to Polycythaemia (plethora, increased VTE risk)

78
Q

How does Eisenmenger’s appear OE

A

As pulmonary hypertension

Right Ventricular Heave
Loud S2
Raised JVP
Peripheral Oedema

79
Q

How is Eisenmenger’s managed?

A

Ideally the defect would be corrected before Eisenmenger’s has occurred

Only definitive management is heart lung transplant

Symptom management: Sildenafil, Anticoagulation, Prophylactic Abx, Venesection

80
Q

What is Coarctation of the Aorta?

A

Narrowing of the aortic arch, normally around the Ductus Arteriosus

Reduces pressure in distal vessels and increases pressure in the heart

81
Q

How does Coarctation of the Aorta present in the neonate?

A

Weak femoral pulses

Lower limb blood pressure < upper limb blood pressure

82
Q

How does Coarctation of the Aorta present in infancy?

A

Tachypnoea and increased work
Poor feeding
Grey and floppy

83
Q

Describe the murmur of Coarctation of the Aorta

A

Systolic murmur below left clavicle/scapula

84
Q

Describe the longer term effects of Coarctation of the Aorta

A

LV heave
Underdeveloped Left Arm
Underdeveloped Legs

85
Q

How is Coarctation of the Aorta managed?

A

Surgical correction

PGE keeps DA open until surgical correction and DA ligation

86
Q

What is Ebsteins Anomaly?

A

Tricuspid valve appears lower in the heart causing a large RA and small RV

Results in reduced blood flow from RA-RV and subsequently from RV to pulmonary vasculature

Often associated with a R-L shunt via ASD

87
Q

What condition can Ebstein’s Anomaly go on to cause?

A

Wolf Parkinson White

88
Q

How does Ebstein’s Anomaly present?

A

Evidence of Heart Failure

Gallop rhythm (addition of 3rd and 4th HS)
Cyanosis
Dyspnoes
Poor feeding

May appear soon after birth when PDA closes

89
Q

How does Ebstein’s Anomaly present on ECG?

A

RA enlargement
RBBB
LA deviation

90
Q

How does Ebstein’s Anomaly present on ECG?

A

Cardiomegaly

RA enlargement

91
Q

What is the definitive investigation for Ebstein’s Anomaly?

A

Echocardiogram

92
Q

When does PDA normally close

A

First 2 -3 weeks of life

Is non functioning long before that

93
Q

Give three risk factors for PDA

A

Rubella
Prematurity
Family History

94
Q

Name two diseases associated with VSD

A

Down’s Syndrome

Turner’s Syndrome

Year 4 Paediatrics (15 decks)

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