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Child Health > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Normal heart rates of children

A

<1y: 110-160 bpm
2-5y: 95-140 bpm
5-12y: 80-120 bpm
<12y: 60-100 bpm

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2
Q

Cardiac failure clinical presentation

A 
Poor weight gain/faltering growth
Tachypnoea
Tachycardia
Heart murmur, gallop rhythm
Cardiomegaly
Hepatomegaly
Cool peripheries
Breathlessness - particularly on feeding/exertion
Sweating
Poor feeding
Recurrent chest infections
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3
Q

Heart failure in the 1st week of life

A

Usually results from coarctation of the aorta
If obstructive lesion is severe then arterial perfusion may be predominantly R-to-L via patent ductus arteriosus
Closure of this duct leads to severe acidosis, collapse and death unless ductal patency is restored

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4
Q

Heart failure >1w of life

A

Progressive heart failure is most like due to L-to-R shunt
Pulmonary vascular resistance falls in first weeks which causes progressive increase in L-to-R shunt and increase pulmonary blood flow causes pulmonary oedema and breathlessness
Symptoms may improve >3m as pulmonary vascular resistance increases

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5
Q

What is Eisenmenger syndrome

A

Irreversible increased pulmonary vascular resistance
If L-to-R shunt left untreated
Can lead to reversal of the shunt (R-L) at 10-15 years and the teenager becomes blue
Treatment: heart-lung transplant

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6
Q

Neonatal causes of heart failure

A 
Obstructive duct-dependant lesions:
Hypoplastic left heart syndrome
Coarctation of the aorta
Critical aortic valve stenosis
Interruption of the aortic arch
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7
Q

Infant causes of heart failure

A

High pulmonary blood flow:
Ventricular septal defect
Atrioventricular septal defect
Large persistent ductus arteriosus

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8
Q

Causes of heart failure in older children/adolescents

A

R or L heart failure:
Eisenmenger syndrome
Rheumatic heart disease
Cardiomyopathy

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9
Q

Initial management of a child with heart failure

A

Underlying cause treated
General measures:
Bed-rest in semi-upright position
Supplemetal O2 (not in L-R shunt)
Sufficient calorie intake
Diuretics & ACEI (captopril): R-L shunt & high pulmonary flow
Beta-blockers and digoxin: to be considered
Prostaglandin infusion to keep ductus arteriosus patent in duct dependent lesions

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10
Q

Key features of a pathological heart murmur

A 
Diastolic or pansystolic
Late systolic 
Loud murmurs >grade 3/6
Continuous murmurs
Associated with cardiac abnormalities
Abnormal signs and symptoms: SOB, fatigue, failure to thrive, cyanosis, clubbing, hepatomegaly
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11
Q

Innocent heart murmur characteristics

A 
Systolic
Short duration &amp; low intensity
Intensifies with increased cardiac output: exercise/fever
May change intensity with posture/head position
No associated thrill/heave
No radiation
Asymptomatic patient
Left sternal edge
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12
Q

Types of innocent heart murmur

A

Venous hum: ‘machinery’ quality sound, upper left sternal edge, due to blood flow in great vessels
Flow murmur: short systolic murmur, mid left sternal edge, often heard during acute illness with fever
Musical murmur: systolic murmur, lower left systolic edge

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13
Q

Features of a venous hum

A

Common and harmless
Heard above right clavicle and over right jugular vein flow of blood causes the vein wall to vibrate causing a humming
Hum is heard throughout cardiac cycle
Placing finger on jugular vein will abolish the sound
Murmur may disappear if patient is supine or if the patient turns their head to one side

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14
Q

Types of left to right shunts

A

Atrial septal defects
Ventricular septal defects
Persistent ductus arteriosus

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15
Q

What are the 2 main types of ASD

A

Secundum ASD (80%): defect in the centre of the atrial septum involving the foramen ovale

Partial atrioventricular septal defect (pAVSD) defect of the atrioventricular septum characterized by:
Inter-atrial communication between bottom end of atrial septum and atrioventricular valves (primum ASD)
Abnormal atrioventricular valves, with L atrioventricular valve with 3 leaflets and often regurgitates (regurgitant valve)

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16
Q

ASD clinical features

A

Often asymptomatic
Recurrent chest infections
An ejection systolic murmur heard on ULSE due to increased flow across pulmonary valve
Fixed and widely split 2nd heart sound: due to right ventricular stroke volume being equal in both inspiration & expiration
With pAVSD apical pansystolic murmur from atrioventricular valve regurgitation

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17
Q

Small VSD clinical features

A

Smaller than the aortic valve in diameter (<3mm)
Asymptomatic
Loud pansystolic murmur at LLSE & quiet pulmonary 2nd sound

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18
Q

Large VSD clinical features

A

> 3mm
Heart failure with breathlessness and failure to thrive after 1w
Recurrent chest infections
Heart failure signs: tachypnoea, tachycardia, hepatomegaly
Active precordium: heave
Soft pansystolic murmur/no murmur (implies larger defect)
Apical mid-diastolic murmur: increased flow across mitral valve
Loud pulmonary 2nd sound: raised pulmonary arterial pressure

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19
Q

Persistent ductus arteriosus pathophysiology

A

The ductus arteriosus connects the pulmonary artery to the descending aorta it normally closes shortly after birth
In PDA it still hasn’t closed by 1 month old

The flow of blood across a PDA is from the aorta to the pulmonary artery (L-to-R) following the fall in pulmonary vascular resistance after birth

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20
Q

Persistent ductus arteriosus clinical features

A

Most present with a continuous murmur beneath the clavicle as the pressure in the pulmonary artery is lower than the aorta throughout the cardiac cycle
Pulse pressure is increased: collapsing/bounding pulse
Symptoms are unusual, however if large:
Increased pulmonary blood flow –> heart failure and pulmonary hypertension

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21
Q

Atrioventricular septal defect pathophysiology

A

Complete AVSD these is a large defect often found in the middle of the atrial septum down to the middle of the ventricular septum

No separate mitral and tricuspid valve: common atrioventricular valve of 5 leaflets guarding the atrioventricular junction
As there is a large defect there is pulmonary hypertension

Trisomy 21 with AVSD: complete AVSD is often found in conjunction with Down syndrome

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22
Q

Atrioventricular septal defect clinical features

A

Presentation on antenatal ultrasound screening o Cyanosis at birth or heart failure at 2-3 weeks of life
No murmur heard
The lesion can be detected on routine echo screening in a newborn baby with Down’s syndrome

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23
Q

Atrioventricular septal defect management

A

Small VSDs close spontaneously and is investigated via the disappearance of the murmur
Prevention of bacterial endocarditis: good dental hygiene
If large VSD:
Treat heart failure medically: diuretics & captopril
Surgical repair at 3-6m

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24
Q

AVSD features on ECG and CXR

A

CXR: Enlarged heart, enlarged pulmonary arteries, increased pulmonary vascular markings

ECG: negative deflection in aVF

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25
Q

Persistent ductus arteriosus investigations

A

CXR and ECG usually normal

If large: CXR = enlarged heart, enlarged pulmonary arteries, increased pulmonary vasculature

26
Q

Persistent ductus arteriosus management

A

Closure with coil/occlusion device introduced via a cardiac catheter at 1y
Occasionally surgical ligation is required

27
Q

ASD management

A

ASDs which cause RV dilatation require treatment to prevent right sided heart failure and arrhythmias
3-5y
Secundum ASD: cardiac catheterisation with insertion of an occlusive device
pAVSD: surgical correction

28
Q

Pathophysiology of coarctation of the aorta

A

Arterial duct tissue encircling the aorta at the point of insertion of the duct –> when the duct closes the aortic tissue also constricts causing severe obstruction to left ventricular outflow

Neonatal period: infants present at 48hrs when the duct closes

In older children: BP is elevated in blood vessels proximal to the obstruction and an extensive collateral circulation develops

More common in boys than girls (2:1) also common in Turner’s syndrome

29
Q

Coarctation of the aorta clinical features

A

Examination normal on 1st day of life
Then, sick baby with severe heart failure
Absent femoral pulses
Severe metabolic acidosis
CXR: possibly cardiomegaly from heart failure or shock
ECG: normal

30
Q

Syndromes associated with a bicuspid aortic valve

A

Turner’s (XO) syndrome: only occurs in females, only 1 X chromosome in each cell
Marfan’s syndrome: genetic connective tissue disorder
VSD
PDA
Coarctation of the aorta

31
Q

Coarctation of the aorta management

A

Surgical repair performed soon after diagnosis
Prostaglandins & medical management of heart failure
Angioplasty +/- stenting used to correct
Balloon angioplasty only buys time
Sometimes, open surgery is needed: techniques include resection & anastomoses, a bypass graft or a more tailored reconstructive approach

32
Q

Common types of duct dependant lesions

A 
Coarctation of the aorta
Transposition of the great vessels (TGA)
Hypoplastic left heart syndrome
Pulmonary atresia
Tricuspid atresia
33
Q

Pulmonary atresia pathophysiology and presentation

A

The pulmonary valve fails to develop –> blocks the outflow of blood from the heart to the lungs
In utero: no problem
When born: only thing providing oxygen to the lungs is the ductus arteriosus

Presentation: baby will usually turn blue rapidly = quick diagnosis

34
Q

Tricuspid atresia pathophysiology and presentation

A

The tricuspid valve is absent/abnormally developed –> blood flow is blocked from passing from the right atrium to the right ventricle
Right ventricle is small and non-functional

There is ‘common mixing’ of systemic and pulmonary venous return in the left atrium

Must have an ASD or VSD to survive, a PDA usually also persists to allow greater pulmonary flow

Presentation: cyanosis in the newborn period if duct dependent or the child may be well at birth and become cyanosed or breathless later

35
Q

Duct dependent lesion immediate management

A 
To maintain patency of the ductus arteriosus:
A prostaglandin (E) infusion (short term solution)
Formaldehyde infiltrated into the structure (longer term)
36
Q

Supraventricular tachycardia pathophysiology

A

Most common childhood arrhythmia
Re-entry within the AV node is most common cause
Re-entry tachycardia: a circuit of conduction is set up, with premature activation of the atrium via an accessory pathway
Rarely a structural heart problem (but should have echo to check)

37
Q

Supraventricular tachycardia on an ECG

A

Generally: narrow complex tachycardia
May be possible to discern P wave after QRS complex due to retrograde activation of the atrium
If heart failure is severe there may be changes suggestive of myocardial ischaemia T wave inversion in the lateral leads
In sinus rhythm short P-R interval may be discernible

Wolff-Parkinson-White (WPW) the early antegrade activation of the ventricle via the pathway results in a short P-R interval and a delta wave

38
Q

Supraventricular tachycardia management

A

Circulatory and respiratory support: correct tissue acidosis, positive pressure ventilation if required

Vagal stimulation manoeuvres: eg. carotid sinus massage, cold ice pack to face (80% successful), valsalva manoeuvre

IV Adenosine: (gold standard) safe and effective, inducing AV block after rapid bolus injection terminates the tachycardia by breaking the re-entry circuit that is set up between the AVN and accessory pathway, given incrementally in increasing doses

Electrical cardioversion with a synchronized DC shock if adenosine fails

Once sinus rhythm is restored: maintenance = flecainide or sotalol

Digoxin can be used on its own when there is no overt pre-excitation wave (delta wave)
Propanolol can be added in the presence of pre-excitation
Treatment stopped at 1y if no further attacks

39
Q

Tetralogy of fallot anatomical features

A

Large VSD
Overriding of the aorta: with respect to the ventricular septum
Subpulmonary stenosis: causing right ventricular outflow tract obstruction
Right ventricular hypertrophy: as a result of pulmonary stenosis

40
Q

Tetralogy of fallot presentation

A

Severe cyanosis with hypercyanotic spells
Characterised by: rapid increase in cyanosis
Irritability/inconsolable crying
Severe hypoxia and breathlessness
Pallor: tissue acidosis
Loud harsh ejection systolic murmur on LSE

41
Q

Tetralogy of fallot management

A

Initial neonatal period: prostaglandin E infusion & shunt fitted surgically between subclavian & pulmonary artery (to maintain pulmonary blood flow and oxygenation)

Definitive surgery (>4m): closure of VSD, relieving of right ventricular outflow tract obstruction

42
Q

Treatment of hypercyanotic spells in children with tetralogy of fallot

A

Usually self-limiting, followed by a period of sleep

If >15 minutes then require immediate treatment:
Sedation and pain relief morphine
IV propranolol: peripheral vasoconstrictor and relieves subpulmonary muscular obstruction
IV volume administration
Bicarbonate: correct acidosis
Muscle paralysis and artificial ventilation reduces metabolic demand

43
Q

Transposition of the great arteries pathophysiology

A

Aorta is connected to the right ventricle
Pulmonary artery is connected to the left ventricle:
blue blood is returned to the body and pink blood is returned to the lungs: two parallel circulations

Unless there is a mixing of blood between these two circuits, then this condition is incompatible with life

Naturally occurring associated anomalies/therapeutic interventions can achieve mixing in the short term –>
VSD, ASD and PDA

44
Q

Transposition of the great arteries presentation

A

Day 2 of life when ductus arteriosus begins to close leading to marked reduction in the mixing of desaturated and saturated blood –> cyanosis

45
Q

Transposition of the great arteries management

A

Initial management: prostaglandin infusion to maintain patency of ductus arteriosus

Balloon atrial septostomy (20%): catheter with an inflatable balloon tip is passed through umbilical/femoral vein and into RA and foramen ovale –> the balloon is inflated in LA and pulled back through the atrial septum, tearing it and rendering the flap valve of the FO incompetent; this allows the mixing of systemic and pulmonary venous blood within the atrium

Surgery for arterial switching in the neonatal period: arteries are transected above the arterial valves and switched over & transferring of the coronary arteries to the new aorta

46
Q

Turner’s syndrome features

A 
Turner's: 45,X
Incidence: 1/2500 live-born females
Features:
Neonatal lymphoedema in hands and feet
Short stature
Coarctation of the aorta/congenital heart defects
47
Q

Marfan’s syndrome features

A

Connective tissue disorder
Skeleton: tall, slim, long thin arms & legs, lose & flexible joints, small bottom jaw, high arched palate, deep-set eyes, flat feet, sternum protrudes and crowded teeth
Scoliosis, spondylolisthesis and dural ectasia can all occur
Eyes: short sighted, glaucoma, cataracts, detached retina
Cardiovascular: weakened walls of the aorta –> increasing risk of aneurysm and mitral/tricuspid regurgitation due to prolapse of valves

48
Q

Noonan’s syndrome features

A

Common features: short stature, characteristic facies, congenital heart disease severity can range from mild to life threatenting

Characteristic facies: broad forehead, wider distance between eyes, drooped eyelids, low set ears rotated backward, small jaw, short neck with excess skin folds, lower than normal hairline in the occipital region

Pulmonary stenosis affects ½ of people with Noonan’s Hypertropic cardiomyopathy affects 10-20% of children
Septal defects: ASD or VSD

49
Q

Hypoplastic left heart pathophysiology

A

Underdevelopment of the left sided heart structure: LV is small and non-functional, RV maintains both pulmonary and systemic circulations –> achieved by pulmonary venous blood passing through an ASD or patent foramen ovale OR via retrograde flow through a PDA

Mitral valve small or atretic
Left ventricle diminutive
Aortic valve atresia
Ascending aorta very small, associated with coarctation of the aorta

50
Q

Hypoplastic left heart presentation

A

HLHS can be detected antenatally via USS: allows for effective counselling and prevents baby from becoming sick after birth

Early onset (days) of cyanosis and heart failure --> collapse and death within a few days of life 
Sick baby with poor peripheral perfusion and weak peripheral pulses central cyanosis and evidence of heart failure will be present
51
Q

Hypoplastic left heart management

A

Prostaglandin infusion: maintaining patency of the ductus is necessary to support systemic blood flow

Neonatal surgical procedures (below) or a heart transplant

Norwood procedure
Glenn or hemi-Fontan: 6m
Fontan: 3y

52
Q

Myocarditis causes

A

Infections (normally viral): coxsackie B or EBV
Kawasaki disease
Drugs: adriamycin
Connective tissue disease: SLE, RA, rheumatic fever, sarcoidosis

53
Q

Myocarditis presentation

A

Vary depending on age/time-course of underlyong disease
CV: progressive worsening of dyspnea, congestive cardiac failure, sudden onset of ventricular arrhythmias
O/E: weak pulses, tachycardia, gallop heart rhythm, distant heart sounds

54
Q

Myocarditis investigations

A

Definitive diagnosis: histology from a percutaneous endomyocardial biopsy
Echo: poor ventricular function
CXR: cardiomegaly
ECG:reduced QRS complex size

55
Q

Myocarditis management

A

Treat underlying cause
Control symptoms of congestive heart failure
Treat arrhythmias

Cardiac transplant may be needed in patients with refractory heart failure

56
Q

Risk factors for bacterial endocarditis

A

Turbulent blood flow/insertion of prosthetic material
PDA or VSD
Coarctation of the aorta
Previous rheumatic fever

57
Q

Bacterial endocarditis common pathogens

A

Alpha-haemolytic Streptococcus viridans (50%): dental procedures
Staphylococcus aureus: central venous catheters
Group D streptococcus (enterococcus): after lower GI surgery

58
Q

Clinical features of subacute bacterial endocarditis

A

Early stages: mild symptoms, prolonged fever persisting over several months

Non-specific (B-) symptoms: myalgia, arthralgia, headache, weight loss, night sweats
Splinter haemorrhages
Osler’s nodes
Janeway lesions
Roth’s spots: retinal infarcts
Anaemia or pallor
Haematuria (microscopic)
Clubbing (late)
Necrotic skin lesions
59
Q

Subacute bacterial endocarditis investigations

A

Diagnosis: high index of suspicion

Bloods: FBC (raised WCC), ESR, CRP, repeated blood culture

Echo: vegetation of the valves made of fibrin & platelets and contain the infecting organism

60
Q

Subacute bacterial endocarditis management

A

Antibiotic therapy: immediate high dose IV penicillin/vancomycin for >6 weeks (delay may cause progressive endocardial damage and deterioration in cardiac function)

Bed rest is recommended and heart failure should be treated

Surgery only need to remove infected prosthetic material

Child Health (15 decks)

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