Brainscape's Knowledge GenomeTM

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


See full index

FRACP Paediatrics > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the prevalence of CHD?

A
  • CHD occurs in approx. 0.8% of live births.

- The incidence is higher in premature infants (2% excl. PDA), stillborns (3-4%) and spont. abortions (11-25%)

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

What is the most common forms of CHD?

A
  • VSD (25-30% of all CHD)
  • ASD (6-8% of all CHD)
  • PDA (6-8% of all CHD)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What chromosomal abnormalities are associated with CHD?

A
  • Trisomy 13, 18 and 21
  • Turners syndrome
  • 22q11
  • Familial secundum atrial septal defect associated with heart block (transc. factor Nkx2.5)
  • Familial atrial septal defect without heart block (transc. factor GATA4)
  • Alagille syndrome (Jag1)
  • Williams syndrome (elastin of chrm. 7)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the risk of recurrence of CHD in subsequent children?

A
  • Incidence of CHD in the general population is 0.8%
  • In a second pregnancy after the birth of a child with CHD or if a parent is affected the incidence is 2-6%
  • Two 1st degree relatives with CHD risk for a subsequent child reaches 20-30%
  • When a second child is found to have CHD it will tend to be of similar class as their affected 1st degree relative
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What features are characteristic of a hypercyanotic episode?

A
  • Paroxysms of tachypnoea
  • Prolonged crying
  • Intense cyanosis
  • Decreased intensity of the murmur of pulmonic stenosis (ejection systolic) due to greater obstruction.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the action of prostacyclin?

A
  • Vasodilator derived from arachadonic acid via the cyclooxygenase pathway.
  • Acts to inhibit platelet aggregation and hence clot formation.
  • Antagonises effects of thromboxane A2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the ratio of right ventricular output: left ventricular output in a foetus?

A
  • 2:1 R:L
  • Blood enters the RA from the IVC and is directed across the foramen ovale by the eustacian valve. From here it is pumped to the LV and in to the aorta.
  • Blood entering from the SVC is directed to the RV and predominantly crosses in to the Ao through the ductus arteriosis supplying the lower half of the body.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What percentage of descending aortic blood flow in the foetus returns to the placenta for oxygenation?

A
  • Approx. 65%, the remaining 35% perfuses foetal organs and tissues.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the PO2 in the umbilical vein following gas exchange at the placenta?

A
  • 30-35mmHg - the placenta is not as efficient at gas exchange as the lung.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What percentage of blood in the umbilical vein enters hepatic circulation?

A

50%

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

What is the normal cardiac output of a neonate?

A
  • 350ml/kg/min
  • Falls in the first 2 months of life to 150ml/kg/min
  • More gradually after this falls to adult 75ml/kg/min
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

At what age is the foramen ovale functionally closed?

A
  • Usually by the 3rd month.

- It is possible to pass a probe through the overlapping flaps in alarge percentage of children and 15-25% of adults.

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

At what age is the ductus arteriosis functionally closed?

A
  • Usually complete by 10-15 hours in normal neonate.

- May remain open much longer in CHD, especially when associated with cyanosis.

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

What causes closure of the ductus arteriosis?

A
  • Ductus differs morphologically from the surrounding aortic and pulmonary artery in its large amount of circularly arranged smooth muscle in its medial layer.
  • In a full term neonate oxygen is the most important factor controlling duct closure.
  • When PO2 in the blood passing the duct reaches about 50mmHg ductal wall begins to constrict.
  • Ductus of a premature infant is less responsive to oxygen despite the musculature being developed.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do you calculate the Qp/Qs ratio?

A

Qp/Qs = Ao - MV/PV - PA

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

What are the normal oxygen saturations and pressures in each chamber of the heart on cardiac catheterisation?

A
  • Vena cava - SpO2 75%
  • RA - SpO2 75%, mean P 3mmHg
  • RV - SpO2 75%, P 25/3mmHg
  • PA - SpO2 75%, P 25/6mmHg, mean P 16mmHg
  • PV - SpO2 95%,
  • LA - SpO2 95%, mean P 8 mmHg
  • LV - SpO2 95%, P 100/8mmHg
  • Ao - SpO2 95%, P 100/60mmHg, mean P 83mmHg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the parthenogenesis of Eisenmenger physiology.

A

In a large VSD there may be little shunt or symptoms in the first weeks of life. When pulmonary vasculature resistance falls in the next several weeks , volume of the left-to-right shunt increases and symptoms begin to appear.
The increased volume to the lungs decreases pulmonary compliance and increased WOB. Fluid leaks in to the interstitial space and alveoli and causes pulmonary oedema.
The infant develops symptoms of heart failure (left ventricular output many times greater than normal but ineffective as being returned to the lungs).
To maintain high LV output, heart rate and stroke volume are increased, mediated by increased sympathetic activity.
The increase in circulating catecholamines, combined with the increased WOB, results in an elevation in the total body oxygen consumption, often beyond the oxygen transport ability of the circulation. Sympathetic activation leads to additional symptoms of sweating and irritability and the imbalance between oxygen supply and demand lead to failure to thrive. Remodelling of the heart occurs, with predominantly chamber dilatation and to a lesser degree hypertrophy.
If left untreated , pulmonary vascular resistance eventually begins to rise and, by several years of age, the shunt volume will decrease and eventually reverse to right-to-left (Eisenmenger physiology).

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

Which cyanotic congenital heart defects cause decreased pulmonary flow?

A

TOF, PA with intact septum, TA, TAPVR with obstruction

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

Which cyanotic congenital heart defects cause increased pulmonary flow?

A

TGA, single ventricle, truncus TAPVR without obstruction

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

What are the major causes of cardiomyopathy in children?

A
  • Viral myocarditis, metabolic disorders, and genetic defects.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the features of Horner syndrome?

A
  • Homolateral meiosis, mild ptosis, and apparent endophthalmos with slight elevation of the lower lid.
  • May have decrease facial sweating, increased amplitude of accommodation and transient decrease in intraocular pressure.
  • If paralysis of the ocular sympathetic fibres occurs before age 2, heterochromia iridis with hypopigmentation of the iris on the affected side may occur.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What percentage of small muscular VSDs close spontaneously in the first decade of life?

A
  • 80-90%

- Close due to growth of the ventricular myocardium which fills the defect.

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

What are the haemodynamic consequences of left-to-right shunt from a VSD?

A
  1. Excessive pulmonary blood flow and pressure overload which may lead to pulmonary oedema.
  2. Volume overload of left ventricle as it receives both the normal vena cavall blood from the right heartas well as the left to right shunted blood as it returns via the pulmonary veins to the left heart. This results in LV dilatation and hypertrophy over time. End-diastolic pressure will be elevated.
  3. Cardiac output is decrease as some of the LV blood is pushed to the RV through the VSD rather than the aorta. This leads to activation of the renin-angiotensin-aldosterone pathway as well as producing sympathetic stimulation, resulting in salt and water retention.
    - The magnitude of the left to right shunt is determined by the size of the defect and the pulmonary vascular resistance, rather than the location of the defect.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What auscultatory finding is an indication for surgery in VSD?

A
  • A mid diastolic rumble in the mitral area may be hear in moderate to large VSDs secondary to functional mitral stenosis (excessive flow through the mitral valve secondary to large left to right shunt)
  • The presence of a rumble is an indication for surgery.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the inheritance pattern of ASD?

A
  • Majority are sporadic.

- AD inheritance in Holt-Oram syndrome and families with secundum ASD and heart block.

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

What percentage of CHDs are accounted for by ASDs?

A
  • 7-10%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the significance of a patent foramen ovale in infancy?

A
  • Usually of no haemodynamic significance and is not considered an ASD.
  • If another anomaly is is causing increased right atrial pressure venous blood may shunt across the PFO leading to cyanosis.
  • In the presence of a large volume load or hypertensive left atrium (secondary to mitral stenosis) the foramen ovale may be sufficiently dilated to result in a significant atrial left-to-right shunt.
  • Isolated PFO does not require surgical treatment, although may be a risk for systemic embolisation .
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the most common type of ASD?

A

Ostium secundum (50-70% of ASDs)

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

What causes a widened and fixed split S2 in ASD?

A
  • Usually RV ejection time varies with respiration.
  • Inspiration increases RV volume leading to prolonged ejection and delay in pulmonary valve closure.
  • In ASD there is always increased volume, the ejection tims is constantly prolonged and S2 is widened and fixed through all phases of respiration.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the auscultation findings suggestive of a large ASD?

A
  • Widely split fixed S2 due to increased blood volume in RV.
  • 2-3/6 systolic murmur at LUSE due to increased flow across RV outflow tract in to PA.
  • Mid-diastolic rumble at LLSE due to functional TS with increased volume crossing the valve.
  • Mid-diastolic rumble suggests Qp:Qs at least 2:1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the ECG findings of ASD?

A
  • RAD
  • Mild RVH
  • RBBB or incomplete RBBB with rsR’ in V1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the most common associated anomaly in sinus venosus ASD?

A

Partial anomalous pulmonary venous return.

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

Describe the different types of partial anomalous pulmonary venous return.

A
  • R. pulmonary veins draining in to SVC. Usually associated with a sinus venosus ASD.
  • R. veins draining in to the IVC. Usually no associated ASD, but with bronchopulmonary sequestration.
  • L. lung anomalous veins usually drain to the coronary sinus or the innominate vein.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the prevalence of complete endocardial cushion defects in children with CHD?

A
  • 2% of all CHD.

- 30% occur in children with Down syndrome.

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

What are the ECG findings of complete endocardial cushion defect?

A
  • Superior axis
  • RVH or RBBB in all
  • Many have BVH
  • Most have prolonged pr interval (1st degree HB).
36
Q

What is the prevalence of ostium primum ASD in children with CHD?

A

1-2%

37
Q

What is the most common form of VSD?

A
  • Perimembranous (70%)

- Trabecular is next most common (5-20%)

38
Q

What syndromes are associated with pulmonary stenosis?

A
  • Noonan syndrome (PTPN11 gene).
  • LEOPARD syndrome (PTPN11, RAF1 and BRAF gene).
  • Alagille syndrome (Jag1 gene).
39
Q

What percentage of pulmonary stenosis is valvular?

A

90%

- thickened valve with fused or absent commisures and small orifice.

40
Q

What causes cyanosis in an infant with critical pulmonary stenosis?

A
  • RV is relatively hypoplastic with poor compliance.

Increased pressure pushes blood right-to-left through the patent foramen ovale.

41
Q

What are the characteristic auscultatory findings in PS without a VSD?

A
  • S2 may be widely split and P2 diminished in intensity.
  • Ejection systolic murmur (2-5/6) with or without systolic thrill is best audible at the ULSE and transmits to the back and axillae.
  • May be an ejection systolic click audible at ULSE in valvular PS
  • The longer and louder the murmur the more severe the stenosis
42
Q

What are the RV pressure criteria for severuty of PS?

A
  • Mild: <35-40 mmHg
  • Moderate: 40-70 mmHg
  • Severe: >70 mmHg
43
Q

What are indications for balloon valvuloplasty in PS?

A
  • Catheter pressure >40 mmHg whilst sedated in the cath lab.
  • Catheter pressure 30-39 = balloon procedure reasonable.
  • Symptoms attributable to PS (angina, syncope, presyncope) with catheter gradient >30 mmHg.
  • Reasonable to try on dysplastic valve (success rate 65%)
44
Q

What cardiac defects are more common in infants with congenital rubella syndrome?

A
  • Peripheral pulonary artery stenosis.
45
Q

Describe Shone syndrome.

A
  • Complete form consists of 4 left sided defects (supravalvular mitral membrane, parachute mitral valve, subaortic stenosis and coarctation.
  • Supravalvular mitral membrane is the first to occur and triggers development of the others.
46
Q

What is the prevalence of aortic stenosis in those with CHD?

A
  • Approx. 10%
47
Q

What are the examination findings in AS?

A
  • Ejection click may be audible with valvular AS.
  • A harsh ejection systolic murmur 2-4/6 is best audible in at 2RICS or 3LICS with transmission in to the carotids.
  • A high pitched, early diastolic decrescendo murmur of AR may be audible in those with bicuspid valve and those with discrete subaortic stenosis.
  • Systolic thrill may be palpable at the URSE, in the suprasternal notch or over the carotids.
  • In neonates with critical AS murmur may be absent or weak and peripheral pulses are weak and thready.
48
Q

Describe the Ross procedure.

A
  • Coronary arteries are excised from the aorta.
  • Aorta and pulmonary artery are transected with valves in situ.
  • Section of pulmonary artery including valve are placed in to aorte to give competent valve.
  • Allograft used for pulmonary artery or aortic valve placed in pulmonary artery (double Ross procedure).
49
Q

What percentage of those with AS develop AR?

A
  • 10-30%
50
Q

In what cardiac conditions is SBE prophylaxis recommended?

A
  • Prosthetic hear valves (mechanical or bio).
  • Rheumatic valvular heart disease.
  • Prev. endocarditis.
  • Unrepaired cyanotic CHD (incl. paliative shunts and conduits).
  • Surgical or catheter repair of CHD within 6/12 of procedure.
51
Q

What procedures is SBE prophylaxis required for?

A
  • All dental procedures (plus tonsillectomy/adenoidectomy) that require manipulation of gingival tissue or the periapical region of the teeth or perforation of the oral mucosa.
  • No longer recommended for non-dental procedures unless the procedure is at the site of an established infection.
52
Q

What is used for SBE prophylaxis?

A
  • Amoxicillin 50mg/kg PO 1h prior to procedure, or IV just prior to procedure, or IM 30m prior to procedure. Administer IV if IV access readily available.
  • Clindamycin (Clarithromycin orally) 15mg/kg PO 1h prior, IV over 20m just before or IM 30m prior.
  • If antibiotics are not administered inadvertently they can be given up to 2h following procedure.
53
Q

Widened splitting of the second heart sound with expiration is a feature of what?

A
  • May see paradoxical spliiting of S2 in children with severe AS.
54
Q

What is the most common cause of complete heart block in a neonate?

A
  • 90% are caused by maternal antibodies to Ro (SSA) or La (SSB).
  • Maternal antibody titre does not affect extent of disease in the neonate.
  • Most mothers of children with autoimmune CHB are asymptomatic.
55
Q

What is the most common location for a coarctation?

A
  • 98% origin of the ductus arteriosus just below the origin of the left subclavian.
56
Q

What percentage of children with coarctation have a bicuspid aortic valve?

A
  • 70%
57
Q

What is the most important factor in the pathogenesis of peripheral oedema in heart failure?

A
  • Sodium retention.
  • Reduced cardiac output leads to decreased juxtaglomerular perfusion. This stimulates the release of renin, which in turn results in aldosterone secretion.
  • Aldosterone causes retention of sodium and water.
  • Poor hepatic blood flow decreases the catabolism of aldosteron and potentiates the effect.
  • Sodium and water retention lead to an increase in plasma volume and elevated hydrostatic pressure in capillary beds producing peripheral oedema.
58
Q

What are features of postcoarctectomy syndrome?

A
  • Mesenteric adenitis.
  • Hypertension.
  • Abdominal pain.
  • May also have anorexia, nausea, vomiting, leukocytosis, intestinal haemorrhage, bowel necrosis and small bowel obstruction.
  • Occurs in the immediate post-operative period.
59
Q

What is the treatment for post coarctectomy syndrome?

A
  • Antihypertensives (nitroprusside, captopril).

- Intestinal decompression.

60
Q

What additional cardiac anomalies are associated with TOF?

A
  • Pulmonary valve atresia (10%)
  • Abnormal coronary artery (5%) - anterior descending originates from the right coronary.
  • Right aortic arch (25%).
61
Q

What are the typical auscultatory findings in TOF?

A
  • Ejection aortic click.
  • Single loud S2.
  • 3-5/6 systolic ejection murmur at middle and upper LSE (secondary to VSD anf RVOTO).
62
Q

What are the 4 characteristics of a tet spell?

A
  • Hyperpnoea.
  • Irritability and prolonged crying.
  • Increasing cyanosis.
  • Decreased murmur intensity.
63
Q

Describe the pathophysiology of a tet spell.

A
  • Pressure between left and right ventricles usually equal due to large VSD.
  • Decreased systemic vascular resistance or increased resistance at the RVOT leads to an increase in blood shunting right-to-left across the VSD.
  • Systemic and pulmonary mixing stimuates the respiratory centres (elevated CO2) and leads to hyperpnoea.
  • Hyperpnoea increases systemic venous return to the heart further increasing right-to-left shunting as increased blood is prevented from entering pulmonary circulation due to RVOTO.
64
Q

What percentage of children with tricuspid atresia have transposition of the great vessels?

A
  • 30%
65
Q

What is the most common variation of tricuspid atresia?

A
  • Small VSD with PS and hypoplastic PA.
  • Normally orientated great vessels.
  • 50% of TA.
66
Q

What is the medical agent used for terminating SVT?

A
  • Adenosine.
67
Q

Describe the heart sounds in Ebsteins anomaly.

A
  • Characteristic triple or quadruple rhythm.

- Splitting of S1 and S2 with added S3 and S4.

68
Q

What is D-TGA?

A
  • Aorta arises from the anterior RV and is positioned to the right of the PA.
  • PA arises posteriorly from the LV.
69
Q

What percent of children with L-TGA have dextrocardia?

A
  • 50%
70
Q

What is the most common form of double inlet ventricle.

A
  • Double inlet left ventricle with L-TGA and aorta arising from rudimentary RV.
71
Q

What is the most common cause of SVT in children?

A
  • AV re-entrant tachycardia.
72
Q

What are the differentials for a widely split S2?

A
  • Volume overload (ASD, PAPVR).
  • Pressure overload (PS).
  • Electrical delay (RBBB).
  • Early aortic closure (MR).
  • Occasional normal child.
73
Q

What are differentials for single S2?

A
  • Pulmonary or aortic atresia, severe stenosis, truncus arteriosus, TGA.
74
Q

What is the anatomy of a coronary artery fistula and what features do you find on examination?

A
  • Fistula between coronary artery and right ventricle or less often right atrium.
  • Continuous murmur bet heard at LLSE.
  • Murmur generally maximal in diastole with very high pitched components.
75
Q

To what event in the cardiac cycle does the 3rd heart sound relate?

A
  • Low frequency sound in early diastole due to rapid ventricular filling.
  • Can be normal in children but also seen in cardiac failure with ventricular dilatation.
76
Q

In which phase of the cardiac cycle is S4 heard?

A
  • Atrial contraction.

- Associated with a stiff ventricle with reduced compliance (ventricular hypertrophy).

77
Q

What is the best estimate of systemic blood flow?

A
  • 5L/min/m2 (pulmonary is the same).
78
Q

What percentage of children with tetralogy of Fallot also have 22q11?

A
  • 30%.
79
Q

During the cardiac cycle, what is the key trigger for onset of systole?

A
  • Release of Ca stored in the sarcoplasmic reticulum.
80
Q

What are the most common cardiac defects seen in Turner syndrome?

A
  • Aortic coarctation.
  • Bicuspid aorta.
  • Dilatation of the ascending aorta - unknown whether there is increased risk of dissection with this or not.
81
Q

Describe LQT2.

A
  • KCNH2 (HERG) affects potassium channels.
  • Females more commonly affected.
  • Triggers: excitement, sudden noises - especially on waking from sleep.
  • Can have warning events with syncope.
  • May see a low voltage duble bumps T-wave.
  • Reduction in rsk of sudden cardiac death with b-blockers - 50%,
82
Q

What change does hypocalcaemia cause on ECG?

A
  • Prolongation of Qtc.
83
Q

What ECG changes are seen in hyperkalaemia?

A
  • Narrow peaked T-waves, PR prolongation, QRS prolongation.
84
Q

What is the calculation for cardiac output using cath lab data?

A
  • Qs = VO2/(AO2 - MVO2)
85
Q

Describe Holt-Oram syndrome.

A
  • AD.
  • TBX5 gene.
  • Affects bones of the arms and hands.
  • Also causes cardiac anomalies - ASD/VSD or heart block.

FRACP Paediatrics (16 decks)

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