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Cardiology Notes

Medicine Notes > Paediatrics Notes

This is an extract of our Cardiology document, which we sell as part of our Paediatrics Notes collection written by the top tier of University Of Nottingham students.

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Cardiology 8 per 1000 live born infants have some significant cardiac malformation 12% of live births have some abnormality of the CV system The 9 common abnormalities listed below accoount for 80%
Left to Right Shunts (Breathless)

*

VSD

*

Persistent arterial duct (pulmonary aa to aorta reverses when pulmonary R falls)

*

Atrial septal defect

Right to Left Shunts (Blue)

*

Tetralogy of Fallot

*

Transposition of the great arteries

Common Mixing (Breathless and Blue)

*

Atrioventricular septal defect (complete)

Outflow Obstruction in a WELL Child (asymptomatic with a murmur)

*

Pulmonary stenosis

*

Aortic stenosis

Outflow Obstruction in a SICK Neonate (collapsed with shock)

*

Coarction of the aorta

*

(Hypoplastic LH syndrome)

Circulatory Changes At Birth

*

In the fetus the LA pressure is low very little blood returns from the lungs

*

Pressure in the RA is higher receives the systemic venous return (including blood from the placenta)

*

Flap valve of the foramen ovale is held open and blood flows into the LA and hence the LV

*

With the first breath pulmonary resistance falls and the volume of blood flowing through the lungs increases

o

Rise in LA pressure

*

Volume of blood returning to the RA falls due to exclusion of the placenta

*

Flap valve of the foramen ovale closes

*

Ductus arteriosus connects the pulmonary artery and aorta in fetal life hours/days of life

closes within the first few

o

Some circulations are duct dependent and a deterioration will be seen upon closureRx postaglandins maintain duct

Presentation of Congenital Heart Disease

*

Will be detected due to one of the following:

o

Antenatal

o

Murmur

o

Heart failure

o

Shock

o

Cyanosis

Antenatal Diagnosis

*

Fetal anomaly scan around 1820 weeks

*

70% of infants who will require surgery within the first 6 months of life are diagnosed

*

Abnormality or increased risk identified fetal echo

Heart Murmurs

*

30% of children have an innocent murmer

*

Hallmarks of an innocent murmur:

*

*

o

ASymptomatic

o

Soft blowing

o

Systolic only

o

Left Sternal edge

o

Normal heart sounds, non added

o

No parasternal thrill

o

No radiation

o

Innocent murmurs common during illness and situations of increased CO

Also

Pathological Murmurs

o

All diastolic

o

All pansystolic

o

Late systolic

o

Loud (>3/6)

o

Continuous

o

Abnormal clinical findings

*

NB; conditions such as VSDs or ductus arteriosus may only become apparent at several weeks of age when the pulmonary vascular resistance falls

Murmur Continuous

Region Left sternal edge

Diagnosis PDA

Features MACHINE murmur Bounding pulse

Systolic

Lower LSE (pansystolic)

VSD

Fixed split S2
+/ parasternal thrill LOUD implies SMALL SOFT implies BIG (>3mm) BIG

VSDapical

mid

diastolic murmu (inc. flow over mitral after circling lungs), LSE

ToF

loud P2 Cyanotic

ASD Secundum

Single A2
+/ parasternal thrill Fixed wide split S2 Mid

diastolic

murmur

(increased flow over mitral ASD Primum

nd

Ejection Systolic

2 IC space (PV)

valve)
+/ parasternal thrill Fixed wide split S2 Pansystolic

PS

murmur

regurgitation ) Radiates to back Parasternal heave

Maximum

between

shoulder blades Maximum in aortic area

CoA

Ejection click Weak/absent femorals

AS

Carotid thrill

radiating to the neck

Delayed soft S2 Apical ejection click Slow rising pulse

Heart Failure

*

Symptoms

o

Increased compensatory sympathetic driveSOBSweatingTachypnoea/tachycardia

o

Poor feeding

o

Recurrent chest infections

o

Symptoms of poor tissue perfusion fatigue, poor exercise tolerance and confusion

(AV

*

Signs

o

Poor weight gain

o

Tachypnoea

o

Tachycardia

o

Heart murmur, Gallop rhythm

o

Cardiomegaly, Hepatomegaly

o

Cool peripheries

o

(Typically few signs of systemic congestion as observed in adults)

*

Diagnosis CXR, echo, ECG, arterial blood gase

*

Rx rest in semi recumbent position, O2, diuretics, digoxin, vasodilators

*

In the first week of life typically left heart obstruction (coarction. Etc.)

o

Arterial perfusion may be predominantly by R to L flow of blood

duct dependent systemic

circulation

*

After the first week of life likely L to R shunt

o

As pulmonary resistance falls, progressive increase in L to R shunt

o

Pulmonary oedema and SOB

o

May subsequently improve as pulmonary vascular resistance rises in response to the L to R shuntUntreated = Eisenmenger syndrome

irreversibly raised pulmonary vascular

resistance

*

Now the shunt is from R to L and the teenager is blue

o

*

*

*

Rx Heart lung transplant

Neonates obstructed ( duct dependent) systemic circulation

o

Hypoplastic left heart syndrome

o

Critical aortic valve stenosis

o

Severe coarction

o

Interruption of the aortic arch

Infants (high pulmonary blood flow)

o

VSD

o

Atriventricular septal defect

o

Large persistent ductus arteriosus

Older children and adolescents (R or L heart failure)

o

Eisenmenger syndrome (R sided failure)

o

Rheumatic heart disease

o

Cardiomyopathy

Cyanosis

*

*

Peripheral cyanosis

o

Cold

o

Unwell

o

Polycythaemia

Central cyanosis

o

Fall in arterial blood oxygen tension

o

Only recognised if the concentration of reduced Hb in the blood is >5g/dlHarder to recognise in anaemic children

*

Check oxygen saturation with pulse oximetry (>94%)

*

Cyanosis in a newborn with respiratory distress (RR >60)

o

Cardiac disorders - cyanotic congenital heart disease (tetralogy of Fallot, transposition, Eisenmenger syndrome)

*

o

Respiratory disorders - surfactant deficiency, meconium aspiration, pulmonary hypoplasia

o

Persistent pulmonary hypertension - vascular resistance fails to fall after birth

o

Infection

o

Metabolic acidosis and shock

NB; nitrogen washout, if Pa02 is <15kPa likely heart Vs. resp

Left to Right Shunts (Breathless)

*

Atrial septal defects

*

Ventricular septal defects

*

Patent ductus arteriosus

Atrial Septal Defect

*

2 main types

o

Secundum ASD (80%)Defect in the centre of the atrial septum involving the foramen ovaleUsually isolated and well tolerated

*o

Typically present in 3rd decade

More common in girls

Partial / Primum AVSD

*Affects the endocardial tissue that gives rise to the AV valvesLocated in the lower septumAssociated with a cleft in the anterior leaflet of the mitral valve leaksCommon in Down's

Clinically

o

o

SymptomsCommonly noneRecurrent chest infections/wheezeArrhythmia (4th decade onwards)

SignsEjection systolic murmur best heard at upper left sternal edge due to increased flow across the pulmonary valveFixed split S2 the extra blood return during inspiration (due to negative intra thoracic pressure) gets equalized between the left and right atrium, pulmonary valve closes after aortic

*Primum apical pansystolic murmur from AV regurgitationSecundum mid diastolic murmur (increased blood flow across the mitral valve)

Investigations

o

o

Chest radiographCardiomegalyEnlarged pulmonary arteriesIncreased pulmonary vascular markings

ECG (see CP1)Secundum

Right bundle branch block (RSR V1; QRS V6), R axis deviation (RV

hypertrophy)Primum a

'superior' QRS complex, displaced AV node conducts to the ventricles

superiorly

o

Echo (see below; apex to the R, atria to the L)

*

Treatment

o

Secundum cardiac catheterisation and insertion of an occlusive device

o

Primum AVSD surgery

Ventricular Septal Defect

*

30% of all congenital heart disease

*

Classified based upon size

*

Small VSDs

o

Up to 3mm

o

Symptomso

Asymptomatic

Physical SignsLower left sternal edge loud pansystolic murmur

*o

o

Quiet P2

InvestigationsCXR - normalECG - normalEcho - demonstrates anatomy

Management*

LOUD implies SMALL

Will close spontaneously

Large VSDs

o

o

SymptomsHeart failure with breathlessness and FTT after 1 week oldRecurrent chest infections

Physical SymptomsTachypnoea, tachycardia and hepatomegalyCyanosis Eisenmenger's syndromeSOFT pansystolic murmurAplical mid diastolic murmur (increased blood flow across the mitral valve after blood has circled through the lungs)Loud pulmonary second sound (raised pulmonary arterial pressure)

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