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paeds > cardio > Flashcards

cardio Flashcards

1
Q

An innocent murmur is…?

A

Asymptomatic sensitive (changes w position) short soft sweet systolic single (no clicks/ gallops/ thrills/ radiation) e.g. Stills (musical/ twanging string)

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2
Q

cyanotic congenital heart diseases

A

TOF TGA tricuspid atresia

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3
Q

Heart failure symptoms

A

SOB breathless on feeding sweating poor feeding

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4
Q

Heart failure signs

A

poor weight gain gallop rhythm heart murmur enlarged heart hepatomegaly

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5
Q

signs of RHF

A

ankle/ sacral oedema ascites hepatosplenomegaly

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6
Q

breathlessness on feeding, sweating, poor feeding, recurrent chest infections, FTT, heart murmur, enlarged heart, gallop rhythm, hepatomegaly.

A

Heart failure.

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7
Q

causes of HF in older children and adolescents

A

Eisenmenger syndrome (RHF) Rheumatic heart disease Cardiomyopathy

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8
Q

causes of HF in infants

A

VSD AVSD Large PDA due to left to right shunt -> pulmonary oedema and breathlessness. if left untreated, will develop eisenmenger.

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9
Q

Causes of HF in neonates (duct dependent systemic circulation)

A

Critical aortic stenosis Severe coarcation of the aorta Interruption of aortic arch Hypoplastic Left Heart syndrome - no/ super small LV. blood flow supplied by ductus arteriosus

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10
Q

Atrial septal defect - what murmur

A

may get recurrent chest infections/ wheeze Soft midsystolic murmur best heard at upper left sternal edge + fixed and widely split 2nd heart sound

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11
Q

Atrial septal defect - Ix?

A

CXR - cardiomegaly, enlarged pulmonary arteries, increased pulmonary vascular markings ECG Echo

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12
Q

Atrial Septal defect - what mx

A

ASD causes a left to right shunt and volume overloading of the R atrium and ventricle. Long term complications after age 20 include pulmonary HTN, HF and atrial arrhythmias. Children w significant ASD require surgery. occlusion device/ corrective surgery

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13
Q

types of ASD?

A

secundum (80%) - in the middle of the atrial septum where the area of foramen ovale was

primum - at the bottom end of the atrial septum and affects the tricuspid and mitral valves -> regurgitation

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14
Q

complication of ASD?

A

paradoxical emboli

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15
Q

most common childhood congenital heart defect

A

VSD

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16
Q

VSD murmur

A

loud PSM at Lower left sternal edge (loud implies smaller defect) if large defect- soft or no murmur

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17
Q

Ix of VSD

A

CXR - cardiomegaly, enlarged pulmonary arteries, pulmonary oedema ECG - biventricular hypertrophy Echo - anatomy defect, haemodynamic effects may be normal if small defect.

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18
Q

persistent ductus arteriosus murmur

A

continuous machinery murmur beneath left clavicle.

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19
Q

persistent doctor arteriosus what happens

A

ductus arteriosus fails to close by 1 month of age. L-> R shunt. Pulse pressure is increased, causing a collapsing or bounding pulse.

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20
Q

Persistent ductus arteriosus Ix

A

CXR, ECG. usually normal. if PDA is large, features are indistinguishable from VSD. Echo- will clearly identify the patent duct.

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21
Q

patent ductus arteriosus Mx

A

IV Indomethacin or iv ibuprofen

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22
Q

hyperopia (nitrogen washout) test

A

to determine presence of heart disease in cyanosed neonate. measure PaO2. then put infant in 100% oxygen ventilator for 10 mins. If PaO2 still low (<15 kPa) then diagnosis of cyanotic heart disease can be made. if PaO2 high, then problem is with oxygenation/ ventilation.

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23
Q

Mx of cyanotic heart disease

A

Cyanosis, SaO2 <94% or collapse stabilise ABC, with airway ventilation if necessary. Start prostaglandin infusion (PGE).

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24
Q

most common cause of cyanotic congenital heart disease

A

tetralogy of fallot

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25
Q

Clinical features of TOF

A

VSD, overriding aorta, pulmonary stenosis, RV hypertrophy

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26
Q

presentation of TOF

A

most diagnosed antenatally severe cyanosis, hypercyanotic spells and squatting on exercise developing late in infancy. signs- clubbing of fingers and toes, loud harsh ESM at left sternal edge

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27
Q

TOF murmur

A

loud harsh ESM at left sternal edge

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28
Q

TOF ix

A

CXR- boot shaped due to RVH ECG - normal at birth, RVH when older Echo- will demonstrate the cardinal features

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29
Q

TOF mx

A

initial medical tx: prostaglandins to keep duct open repair surgery around 6 months- close VSD and relieve RV obstruction v cyanosed infants require shunt to increase pulmonary blood flow or sometimes balloon dilatation of RV outflow tract.

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30
Q

Tx of hypercyanotic spells in TOF

A

usually self limiting. if prolonged >15 min, prompt tx w sedation and pain relief, IV propranolol to relieve pulmonary muscular obstruction, IV fluids, bicarb to correct acidosis, muscle paralysis and artificial ventilation to reduce metabolic oxygen demand.

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31
Q

Eisenmengers

A

when there is a longstanding L-> R cardiac shunt caused by VSD/ ASD -> pulmonary HTN and eventually reversal of the shunt into a cyanotic R-> L shunt. * rare as congenital heart defects are often picked up earlier w echo Signs and Symptoms: cyanosis, polycythaemia, clubbing, syncope, HF

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32
Q

Eisenmenger’s Mx

A

heart-lung transplant or lung transplant w repair of the heart

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33
Q

Ebstein’s Anomaly RF

A

Lithium in Pregnancy

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34
Q

Ebsteins Anomaly

A

congenital heart defect in which valve leaflets are attached to the walls and septum of the R ventricle. -> leads to atrialization of a portion of the actual RV. Causes R atrium to be large and RV to be small in size. -> S3 and S4 heart sound Holosystolic / ESM along lower left sternal border due to tricuspid regurgitation.

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35
Q

Complications of Ebsteins Anomaly

A

RA hypertrophy, RV conduction defects, Wolff-Parkinson-White often accompanies

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36
Q

Ebstein Anomaly murmurs?

A

S3 and S4 heart sound Holosystolic / ESM along lower left sternal border due to tricuspid regurgitation.

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37
Q

transposition of great arteries

A

aorta connected to RV, and pulmonary artery to LV. cyanosis is predominant symptom, may be profound and life threatening. presentation usually on day 2 of life when duct closes, leading to marked reduction in mixing of desaturated and saturated blood. Cyanosis less severe and presentation delayed if there is more mixing of blood from associated abnormalities e.g. ASD.

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38
Q

Ix of transposition of great arteries

A

CXR - egg on side cardiac appearance, narrow upper mediastinum ECG - usually normal ECHO***- essential to show abnormal arterial connections and associated abnormalities

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39
Q

Mx of transposition of great arteries

A

maintain patent duct w prostaglandin infusion. Balloon atrial septostomy done as life-saving procedure. - where catheter is threaded into the foramen ovale and inflated so that more mixing can occur. Repair surgery within first few days of life.

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40
Q

AVSD assoc with?

A

Down’s

41
Q

features of AVSD

A

cyanosis at birth or HF at 2-3 days of life. no murmur heard, lesion being detected on routine echo in newborn with Downs.

42
Q

Mx of AVSD

A

tx HF medically and surgical repair at 3-6 months

43
Q

Pulmonary stenosis assoc w?

A

Noonan syndrome, TOF

44
Q

Pulmonary stenosis murmur?

A

ESM at Upper left sternal edge. thrill may be present. Ejection click at ULSE. when severe, RV heave.

45
Q

Ix of pulmonary stenosis

A

CXR- post stenotic dilatation of pulmonary artery ECG - evidence of RVH

46
Q

Mx of pulmonary stenosis

A

asymptomatic but when pressure gradient >64 mmHg, then balloon atrial septostomy

47
Q

aortic stenosis murmur?

A

ESM at upper right sternal edge, radiating to neck.

48
Q

Signs of aortic stenosis

A

slow rising pulse, carotid thrill, ESM at URSE radiating to neck, soft aortic HS2, apical ejection click.

49
Q

IX of aortic stenosis

A

CXR - prominent LV, post stenotic dilatation of ascending aorta ECG- may be LVH Echo

50
Q

Mx of aortic stenosis

A

regular clinical and echo assessment to assess when to intervene. Children with symptoms on exercise/ high resting pressure gradient (>64mmHg) across aortic valve will undergo balloon valvotomy. Most with severe AS with require AV replacement eventually.

51
Q

Presentation of Aortic stenosis

A

reduced exercise tolerance chest pain on exertion or syncope. in neonatal period, those w critical AS and a duct dependent systemic circulation may present w severe HF leading to shock.

52
Q

Ix of Coarctation of aorta

A

CXR- cardiomegaly ECG - normal

53
Q

Mx of coarctation of aorta

A

ABC, immediate prostaglandin infusion, referral to cardiac centre for early surgical repair.

54
Q

coarctation of aorta

A

LV outflow obstruction may lead to collapse. usually presents with acute circulatory collapse on 2nd day of life when duct closes.

55
Q

signs of coarctation of the aorta

A

sick baby w severe heart failure, absent femoral pulses, poor perfusion of the limbs, severe metabolic acidosis.

56
Q

causes of syncope

A

neurocardiogenic - prolonged standing and vasovagal situational - defecation, urination, cough, swallowing. orthostatic - BP fall >20mmHg after 3 minutes Ischaemic, arrhythmic.

57
Q

Ix of syncope

A

Check BP Signs of cardiac disease (murmur, femoral pulses) Ix w ECG.

58
Q

Rheumatic heart disease

A

after 2-6 wks following pharyngeal infection.

poly arthritis, malaise, mild fever.

chronic- scarring and fibrosis of valve tissue causing damage (Mitral stenosis)

59
Q

persistent fetal circulation aka persistent Pulmonary HTN of the newborn

A

condition caused by failure in the systemic circulation and pulmonary circulation to convert from the antenatal circulation pattern to the normal pattern.

In a fetus, there is high pulmonary vascular resistance and low pulmonary blood flow as fetus does not use the lungs for oxygen transfer.

when baby is born, lungs are needed for oxygen transfer and need high blood flow which is encouraged by LOW pulmonary vascular resistance.

this may result in cyanosis, usually w resp distress in the context of a newborn who has suffered a significant hypoxic, hypothermic or hypoglycaemic insult, who has pulmonary hypoplasia or sepsis, or sometimes for unknown reasons.

60
Q

most common cardiological cause of cyanosis in the newborn

A

transposition of great arteries.

vital organs not receiving oxygenated blood, rapid death if not for mixing in the atria via the foramen ovale and the patent ductus arteriosus vetween aorta and pulmonary arteries.

61
Q

emergency mx of transposition of great arteries

A

commence prostaglandin infusion to maintain patency of the ductus arteriosus, and to correct the metabolic acidosis. emergency balloon atrial septostomy will probably be needed to improve mixing of oxygenated and deoxygenated blood at the atrial level. ultimately, an arterial switch operation will need to be performed to provide anatomical correction.

62
Q

congenital cardiac lesions presenting w neonatal collapse

A

severe aortic coarctation

aortic arch interruption

hypoplastic left heart syndrome

critical aortic stenosis

L-sided obstructive cardiac lesions rely on the ductus arteriosus to perfuse the systemic circulation by passage of blood from the pulmonary arteries in the the distal end of the aortic arch. as the ductus arteriosus closes, the systemic perfusion becomes dramatically reduced, resulting in collapse and shock.

63
Q

mx in a collapsed neonate

A

emergency. call for senior help (neonatal resus team, anaesthetist)

ABC

airway should be maintained, high flow oxygen administered, iv access obtained and fluid resus for shock.

Blood glucose measurement must be checked early and corrected if low.

Arterial blood gas sample should be analysed. IV Abx should be given prompty as sepsis is a possible treatable cause.

If any suspicion of a duct dependent cardiac lesion, a prostaglandin infusion should be commenced, as this is life saving.

Early involvement of senior paediatricians, an anaethetic team and paediatric intensive care services will help appropriate mx.

64
Q
A

ECG shows narrow complex tachycardia with rate of approx 220/min and no p waves.

Diagnosis= SVT

supraventricular tachycardia.

commonest pathological arrhythmia in childhood.

it is usually secondary to a re-entrant tachycardia using an accessory pathway. Also associated with wolff-parkinson-white syndrome.

HR in SVT is typically 200-300 bpm.

Arrhythmias can last from a few seconds to days.

65
Q

presentation of SVT?

A

in older children: palpitations, light headedness and chest discomfort

In infants, inability to report symptoms leads to presentation w HF and shock.

in a third of cases this is assoc w CHD so an echo should be performed.

SVT needs to be differentiated from sinus tachycardia. In the latter, the HR is usually <220bpm, there is greater variability in HR and there is often a hx consistent w shock.

66
Q

what is the most common pathological arrhythmia in childhood?

A

SVT

HR 200-300bpm

67
Q

what is the commonest arrhythmia in childhood (a normal variant)?

A

sinus arrhythmia

68
Q
A

Wolff-Parkinson-White

short PR interval and slow upstroke of QRS (delta wave)

69
Q

features of HF

A

tachycardia

tachypnoea

hepatomegaly

poor feeding

sweating

acutely excessive weight gain

chronically poor weight gain

gallop rhythm

cyanosis

heart murmur

70
Q

tx of SVT

A

Standard resus call for help + ABC

secure airway, administer oxygen.

Specific tx comprises vagal stimulation, which will increase vagal tone, slow AV conduction and abort the tachycardia.

This can be done by placing a rubber glove filled with ice water over the baby’s face. If this fails, babys face can be immersed in iced water for 5s.

2nd line tx comprises IV adenosine that can be administered in escalating doses.

If this fails, synchronized DC cardioversion

Once sinus rhythm is achieved, maintenance tx using drugs such as amiodarone should be started following consultation w cardiologist.

Definitive tx comprises catheterization w radiofrequency ablation.

71
Q

why do children have innocent murmurs?

A

up to 40% of children will have a murmur heard at some time during childhood, particularly if examined at time of high cardiac output e.g. fever, anaemia or anxiety.

heart is structurally normal.

good practice to reexamine asymptomatic healthy children 1-2 wks later when they are well.

if the murmur persists, they should be referred.

72
Q

Pulmonary Valve stenosis

-features

A

common, accounting for 7-10% of congenital heart defects

children are healthy and asymptomatic unless stenosis is severe.

an opening click may be heard at the beginning of systole.

Pulmonary component of second heart sound dimishes and lower left sternal heave develops (RVH)

in severe PS -> RHF and hepatomegaly

ECG will show right axis deviation and evidence of RVH

73
Q

investigations of Pulmonary stenosis

A

ECG

CXR

Echo- definitive test to confirm the clinical diagnosis, assess severity to guide further investigation and tx and exclude any assoc cardiac lesions e.g. VSD

doppler echo measures velocity across the valve- the higher this is, the greater the need for intervention

74
Q

mx of Pulmonary stenosis

A

dependent on severity

Tx of choice in majority- catheter balloon valvuloplasty

if mild- regular monitoring

75
Q

DDx of a fit

A

epileptic seizure: aura, incontinence, tongue biting, fhx

cardiac arrhthymia: palpiations, sudden collapse, exercise related

vasovagal syncope: preceding stimulus, dizziness, nausea

panic attack: hyperventilation, paraesthesia, carpopedal spasm

breath holding attack: usually an upset/ crying toddler

reflex anoxic seizure: usually toddler, painful stimulus

pseudoseizures: psychological problems

hypoglycaemia

metabolic derangements

drugs/ alcohol

76
Q

most important investigation to perform after a seizure/ fit?

A

ECG

  • as this may show a potentially life threatening cardiac cause

EEG generally not performed after a first seizure, and adds little to prognosis at this stage.

Blood tests performed for glucose, electrolytes, calcium, magnesium.

77
Q

what is this?

A

long QT syndrome

The QT interval is measured from the start of the QRS complex to the end of the T wave. QTc is normally around 0.41s and should be less than 0.45s.

mx: anti-arrhythmic drug tx, may need implantable cardiodefibrillator.

78
Q

Definition of DKA

A

pH <7.30 and or bicarb <15 mmol/L

pt may have ketonuria but is not acidotic. -> **will not need IV fluids or IV insulin

79
Q

what to always be careful w in DKA?

A

dont overload pt with fluids/ rapid changes in blood glucose -> cerebral oedema

80
Q

T1DM mx

A

regular subcut insulin

  • background basal insulin once daily with rapid acting bolus insulin at mealtimes.

alternatives are twice daily injections of premixed long and rapidly acting insulins or insulin via a pump.

81
Q

T1DM breaking the diagnosis

  • what needs to be covered
A

child and family need to start a detailed education programme. education provided by MDT, including specialist nurses and dieticians.

  • how to give insulin
  • regular fingerprick testing
  • interpreting blood glucose results and altering insulin
  • recognition and tx of hypoglycaemia
  • mx of intercurrent illness e.g. flu
  • blood or urine ketones estimations
  • who to contact in emergency
  • diet and carbohydrate counting
  • school liaison
  • long term complications
  • using HbA1c to measure overall control
  • support groups
82
Q

Marfan syndrome

  • what protein is problematic?
A

connective tissue disease

inherited synthetic disorder of fibrillin-1, a glycoprotein constituent of the microfibrils of elastic fibres that anchor non-eleastic tissue such as the aortic adventitia and the suspensory ligament of the eye.

83
Q

DDx of tall stature

A

Familial tall stature

Marfan

Klinefelters (XXY)

growth acceleration due to endocrine cause e.g. GH excess, sexual precocity, thyrotoxicosis

physical examination, serial height measurements, parental height, skeletal age (bone age Xray of wrist)

84
Q

Marfans presentation

A

arm span to height ratio > 1.05

arachnodactyly (spider fingers) with a positive thumb sign

pectus excavatum

eyes - lens dislocation is a major criteria for diagnosis

*need slit lamp examination

heart - mitral valve prolapse, echo necessary for diagnosis and to moniotor aortic root dilatation.

85
Q

Important investigations for marfans

A

Slit lamp examination for lens dislocation

Echo - aortic root dilatation, mitral valve prolapse

86
Q

mx of marfans

A

referral to genetics team

for diagnosis and counselling

87
Q

Clinical signs suggesting a pathological cause for short stature

A

extreme short stature - < 0.4th centile

short for family size - outside of target range

short and relatively overweight - ?endocrinopathy

short and v underweight - poor nutrition and malabsorption

growth failure - crossing centiles

dysmorphic features

skeletal disproportion- skeletal dysplasia e.g. achondroplasia

signs of systemic disease- e.g. clubbing

88
Q

how to determine overweight/ obesity in children?

A

BMI >91st centile are overweight

and BMI >98th centile are obese

89
Q

commonest cause of obesity in children

A

simple obesity

caloric intake > energy expenditure

tend to be tall and overweight

if small and overweight - more likely to have an underlying pathology such as an endocrine disorder

90
Q

simple obesity

features

A

stretch marks- pink (violaceous stretch marks assoc w cushings)

large tonsils and obstructive sleep apnoea

always assess for comorbidities such as HTN, breathless on exertion, obstructive sleep apnoea, hyperinsulinaemia and type 2 diabetes, dyslipidaemia, PCOS and psychosocial dysfunction.

91
Q

acanthosis nigricans

A

thickening and darkening of skin in the axilla, neck or groin

usually a sign of insulin resistance.

92
Q

Ix for simple obesity

A

FBC, U+Es, LFTS, TFTs

Fasting glucose, insulin, cholesterol and triglycerides

BP

93
Q

DDx of obesity in children

A

simple obesity

genetic/ familial

endocrine disease e.g. hypothyroid, cushings, GH deficiency, pseudohypoPTH

drugs e.g. steroids, sodium valproate

syndromes e.g. Downs, Prader-Willi

Disorders assoc w immobility e.g. cerebral p0alsy

hypothalamic damage e.g. secondary to trauma or brain tumours

94
Q

mx of simple obesity

A

MDT - dietician, GP

children should be encouraged to exercise for 60 min/day.

sedentary activities such as playing computer games should be discouraged.

obesity can lead to low self esteem/ bullying -> psychologist who may also be able to initiate behavioural therapies

if enlarged tonsils -> sleep apnoea -> tonsillectomy may be indicated.

If HTN-> tx

if child >12 and severe physical or psychological co-morbidities: consider orlistat or sibutramine. Bariatric surgery/ gastric stapling post puberty in severe cases.

95
Q
A
96
Q

first step in mx of SVT

A

vagal manoeuvres

e.g. blowing a syringe like a balloon,

unilat carotid massage

putting head in ice

ideally, these should be carried out while child is on recorded cardiac monitoring to assess response

97
Q

mx of child w SVT after vagal manoeuvres have been tried?

A

adenosine

98
Q

mx of SVT in alert child when vagal manoeuvres/ adenosine have failed

A

sedated synchronised Cardioversion

if pt loses consciousness, then synchronized cardioversion can be carried out urgenly without waiting for sedation.

paeds (12 decks)

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