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Year 5 Specialties > Paediatric cardiac disorders > Flashcards

Paediatric cardiac disorders Flashcards

1
Q

Persistent cyanosis in an otherwise well infant is usually a sign of what?

A

Structural heart disease

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2
Q

Cyanosis in a newborn infant with respiratory distress (respiratory rate > 60) could be due to:

A

Cardiac disorders (congenital cyanotic heart disease)
Respiratory disorders (e.g RDS, meconium aspiration, pulmonary hypoplasia)
Persistent pulmonary hypertension of the newborn (failure of pulmonary vascular resistance to fall after birth)
Infection (e.g. septicaemia from GBS or other organisms)
Inborn errors of metabolism (metabolic acidosis and shock)

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3
Q

How congenital heart disease diagnosed?

A

If congenital heart disease is suspected, a CXR and ECG should be performed (these are rarely diagnostic but help demonstrate an abnormality)
Echocardiogrpahy with Doppler ultrasound enables almost all causes of congenital heart disease to be diagnosed
Specialist opinion should be sought if the child is haemodynamically unstable, evidence of heart failure, cyanosis, when oxygen saturation are <94% due to heart disease and when there are reduced volume pulses

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4
Q

2 main types of ASD

A

Secundum ASD 80%
Partial atrioventricular septal defect (AVSD or primum ASD)

Both cause similar symptoms and signs

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5
Q

Secundum ASD

A

Defect in the centre of the atrial septum

Involves the foramen ovale

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6
Q

Partial ASD

A

Defect in the atrioventricular septum
There is an interatrial communication between the bottom end of the atrial septum and the atrioventricular valves (primum ASD)
There are abnormal atrioventricular valves, with a left atrioventricular valve which has three leaflets and tends to lead (regurgitant valve)

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7
Q

Clinical features of ASD

A

No symptoms (common)
Recurrent chest infections/wheeze
Arrhythmias (4th decade on)

Ejection systolic murmur best heart at the upper left sternal edge (due to increased flow across the pulmonary valve because of left-to-right shunt)
Fixed and widely split second heart sound (often difficult to hear)- due to right ventricular stroke volume being equal in both inspiration and expiration
IN partial AVSD - an apical pansystolic murmur may be heard from atrioventricular valve regurgitation

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8
Q

Investigations for ASD

A

CXR: Cardiomegaly
Enlarged pulmonary arteries
Increased pulmonary vascular markings

ECG: Partial RBBB and right axis deviation secondary to right ventricular enlargement (in secundum ASD)
Superior QRS, due to a defect in the middle of the heart where the AV node is found. This displaced node then conducts to the ventricles superiorly, resulting in an abnormal axis (partial AVSD)

Echocardiography is essential

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9
Q

Management of ASD

A

Children with significant ASD (large enough to cause right ventricular dilatation) will require treatment

Secundum ASDs - managed by cardiac catheterisation with the insertion of an occlusive device (percutaneous closure/endovascular closure)  

Partial AVSD - managed by surgical correction  

NOTE: treatment is usually undertaken at 3-5 years of age
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10
Q

Eisenmenger syndrome

A

If high pulmonary blood flow due to a large left-to-right shunt is not treated early, the pulmonary arteries become thick walled and resistance to flow increases
Gradually, the symptoms reduce as the shunt decreases
Eventually, at around 10-15 years, the shunt reverses and the teenager becomes blue

The disease is progressive, and the patient will die of right heart failure (usually 30-40 years old)
Treatment is aimed at prevention with early intervention for high pulmonary blood flow

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11
Q

How can VSDs be categorised?

A 
Small = smaller than the aortic valve (usually <3mm diameter)
Large = larger than the aortic valve
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12
Q

Small VSD clinical features

A

Asymptomatic

Loud pansystolic murmur at lower left sternal edge (Loud murmur implies smaller defect)
Quiet pulmonary second heart sound

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13
Q

Investigations for a suspected small VSD

A

CXR and ECG are usually normal

Echocardiography demonstrates the precise anatomical defect

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14
Q

Management of small VSDs

A

The lesions will close spontaneously
This is demonstrated by disappearance of the murmur and a normal echocardiogram
Whilst the VSD is present, bacterial endocarditis should be prevented by maintaining good dental hygiene

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15
Q

Clinical features of large VSDs

A

Heart failure with breathlessness and faltering growth after 1 week old
Recurrent chest infections

Tachypnoea, tachycardia and enlarged liver from heart failure
Active precordium (precordium moves too much)
Soft pansystolic murmur or no murmur
Apical mid-diastolic murmur (from increased blood flow across the mitral valve)
Loud pulmonary second sound (P2)- from raised pulmonary arterial pressure

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16
Q

Investigations for large VSDs

A

CXR: Cardiomegaly
Enlarged pulmonary arteries
Increased pulmonary vascular markings
Pulmonary oedem

ECG: Biventricular hypertrophy by 2 months of age

Echocardiography: demonstrates the anatomy of the defect

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17
Q

Management of large VSDs

A

Heart failure is treated with diuretics (often captopril)
Additional calorie input

Surgery is usually performed at 3-6 months to:
prevent permanent lung damage from pulmonary hypertension and high blood flow (i.e. prevent Eisenmenger syndrome)
Manage heart failure and faltering growth

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18
Q

Patent ductus arteriosus

A

When the ductus arteriosus has failed to close by 1 month after the expected delivery date
Due to a defect in the constrictor mechanism of the duct
In preterm infants, the presence of PDA is due to prematurity and not due to congenital heart disease

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19
Q

Clinical features of PDA

A

Continuous murmur below left clavicle
Murmur continues into diastole (because pulmonary arterial pressure is always lower than aortic pressure)
Increased pulse pressure (causing bounding pulse)

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20
Q

Investigations for PDA

A

ECG and CXR are usually normal

Echocardiography

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21
Q

Management of PDA

A

CLosure is recommended to abolish lifelong risk of bacterial endocarditis and of pulmonary vascular disease
If a cyanotic disease is dependent on a PDA (e.g. transposition of the great arteries), the patient should start a prostaglandin infusion to keep the PDA open until corrective surgery can be performed
Usually closed through a coil or occlusive device introduced through a cardiac catheter at about 1 year of age

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22
Q

Left-to-right shunts

A

ASDs
VSDs
PDA

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23
Q

Right-to-left shunts

A

Tetralogy of Fallot

Transposition of the great arteries

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24
Q

How do right-to-left shunts present?

A

Cyanosis

Usually in the first week of life

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25
Q

Hyperoxia (Nitrogen washout) test

A

Used to determine the presence of heart disease in a cyanosed neonate
The infant is placed in 100% oxygen (head box or ventilator) for 10 mins
If the right radial arterial pressure of oxygen (PaO2) remains low (<15kPa) after this, a diagnosis of cyanotic congenital heart disease can be made (lung disease and persistent pulmonary hypertension must be excluded)
Blood gas analysis is necessary in this scenario because oxygen saturations are not reliable enough

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26
Q

Management of the cyanosed neonate

A

Stabilise the airway, breathing and circulation, with artificial ventilation if necessary
Start prostaglandin infusion (5ng/kg per minute)
- Most infants with cyanotic heart disease presenting in the first week of life, are duct dependent
- Maintaining duct patency is key to early survival
- Prostaglandins help maintain duct patency
- Side-effects of prostaglandins: apnoea, jitteriness, seizures, flushing, vasodilation, hypotension

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27
Q

What is the most common cause of cyanotic heart disease?

A

Tetralogy of Fallot

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28
Q

Clinical features of Tetralogy of Fallot

A

Large VSD
Overriding aorta with respect to the ventricular septum
Sub-pulmonary stenosis causing right ventricular outflow tract
Right ventricular hypertrophy

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29
Q

Symptoms of Tetralogy of Fallot

A

Most cases are diagnosed antenatally, or following the identification of a murmur in the first 2 months of life (cyanosis may not be obvious at this stage, but some may present with severe cyanosis)

The classical description of Tetralogy of Fallot includes:
Severe cyanosis
Hypercyanotic spells (important to recognise as they can lead to MI, cerebrovascular accidents and death. They are characterised by a rapid increase in cyanosis, usually with irritability and inconsolable crying because of severe hypoxia. Breathlessness and pallor because of tissue acidosis may also be present)
Squatting on exercise
NB: these features develop in late infancy and are rare in developed countries

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30
Q

Signs of Tetralogy of Fallot

A

Clubbing will develop in older children
Loud harsh ejection systolic murmur at the left sternal edge from day 1 of life (NB: as right ventricular outflow tract obstruction increases, the murmur will shorten and cyanosis will increase)

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31
Q

Investigations for Tetralogy of Fallot

A

CXR:
Relatively small heart
May have an up-tilted apex due to right ventricular hypertrophy
Pulmonary artery bay - a concavity on the left heart border where a normal pulmonary artery and right ventricular outflow tract should be
Decreased pulmonary vascular markings (due to reduced flow)

ECG:
Normal at birth
Right ventricular hypertrophy in older children

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32
Q

Management of Tetralogy of Fallot

A

Initially medical, with surgery at around 6 months

Surgery - involves closing the VSD and relieving right ventricular outflow tract obstruction

Very cyanosed neonates require a shunt to increase pulmonary blood flow
This can be done by inserting an artificial tube between the subclavian artery and pulmonary artery or by balloon dilatation of the right ventricular outflow tract

Hypercyanotic spells are usually self-limiting followed by a period of sleep
If this is prolonged, they need prompt treatment:
Sedation and pain relief (morphine)
IV propranolol (works as a peripheral vasoconstrictor and by relieving sub-pulmonary muscle obstruction)
IV volume administration
Bicarbonate to correct acidosis
Muscle paralysis and artificial ventilation to reduce metabolic oxygen demand

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33
Q

Transposition of the great arteries

A

A condition in which the main arteries are connected the wrong way (aorta –> right ventricle, pulmonary artery –> left ventricle)
This means that deoxygenated blood is returned to the body and oxygenated blood is returned to the lungs
This means that there are two parallel circulations (which is not usually compatible with life) However, this condition tends to be associated with some naturally occurring associated anomalies (e.g. VSD, ASD< PDA)

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34
Q

Clinical features of Transposition of the Great Arteries

A

Cyanosis (may be profound and life-threatening)
Present on day 2 of life when ductal closure leads to a reduction in mixing of saturated and desaturated blood

Second heart sound is often loud and single
Usually no murmur, but may be a systolic murmur from increased flow or stenosis within the left ventricular outflow tract

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35
Q

Investigations for Transposition of the Great Arteries

A

CXR: Narrow mediastinum with an egg on side appearance of the cardiac shadow (this is caused by the anteroposterior relationship of the great vessels,
narrow vesicular pedicle and hypertrophied right ventricle)
Increased pulmonary vascular markings (due to increased pulmonary blood flow)

ECG usually normal

Echocardiogrpahy is essential

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36
Q

Management of Transposition of the Great Arteries

A

In the sick cyanosed neonate, you need to improve mixing. Maintain patency of ductus arteriosus with a prostaglandin infusion.
Balloon atrial septostomy may be a life-saving procedure (breaks the flap valve of the foramen ovale and encourages mixing of blood)
ALL patients will require surgery (arterial switch procedure in the neonatal period): NB- the coronary arteries also need to be transferred to the new aorta

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37
Q

In what population is atrioventricular septal defect most commonly seen?

A

Children with Down syndrome

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38
Q

AVSD

A

Defect in the middle of the heart with a single five-leaflet valve between the atria and ventricles
It stretches across the entire atrioventricular junction and tends to leak
The large defect leads to pulmonary hypertension

39
Q

Features of atrioventricular septal defects

A

Present at antenatal ultrasound screening
Cyanosis at birth or heart failure at 2-3 weeks
NO murmur heard
Always a superior axis on the ECG

40
Q

Management of AVSD

A

Treat heart failure medically and surgical repair at 3-6 months

41
Q

What conditions are categorised under complex congenital heart disease?

A

Tricuspid atresia (MOST COMMON)
Mitral atresia
Double inlet left ventricle
COmmon arterial trunk (truncus arteriosus)

42
Q

Tricuspid atresia

A

Only the left ventricle is effective. The right ventricle is small and non-functional. This is due to complete absence of the tricuspid valve.

43
Q

Clinical features of Tricuspid atresia

A

Common mixing of systemic and pulmonary venous return in the left atrium
Cyanosis in the newborn period if duct-dependent
The child may be well at birth and hen become cyanosed or breathless

44
Q

Management of tricuspid atresia

A

Early palliation to maintain a secure supply of blood to the lungs at low pressure by:

  • Ballock-Taussig shunt insertion (between subclavian and pulmonary arteries)
  • Pulmonary artery banding operation to reduce pulmonary blood flow if breathless

IMPORTANT: complete corrective surgery is not possible in most cases because there is only one functioning ventricle

Operations can be performed to connect the SVC to the pulmonary artery (Glenn) and the IVC to the pulmonary artery (Fontan)

45
Q

Outflow obstruction in the well child

A

Aortic stenosis
Pulmonary stenosis
Adult-type coarctation of the aorta

46
Q

Aortic stenosis

A

The aortic valve leaflets are partly fused together, thus restricting the exit from the left ventricle
There could be 1-3 aortic leaflets
Aortic stenosis is often associated with mitral valve stenosis and coarctation of the aorta

47
Q

Clinical features of aortic stenosis

A

Reduced exercise tolerance
Chest pain
Syncope
NB: these only occur when stenosis is severe

Small volume, slow rising pulse
Carotid thrill
Ejection systolic murmur maximal at the upper right sternal edge and radiating to the carotids
Delayed and soft aortic second sound
Apical ejection click
48
Q

Investigations for aortic stenosis

A

CXR: Normal or prominent left ventricle (due to post-stenotic dilatation of the ascending aorta)
ECG: may be left ventricular hypertrophy

49
Q

Management of aortic stenosis

A

Regular clinical and echocardiographic monitoring
Balloon valvulotomy (if high resting pressure gradient or symptomatic on exercise)
Most children with significant stenosis will eventually need aortic valve replacement

50
Q

Pulmonary stenosis

A

Pulmonary valve leaflets are partly fused together and restricting right ventricular outflow

51
Q

Clinical features of pulmonary stenosis

A

Usually asymptomatic
Some may present with cyanosis

Ejection systolic murmur best heard at the upper left sternal edge
Ejection click best heard at the upper left sternal edge
Prominent right ventricular impulse (heave)- only if severe

52
Q

Investigations for pulmonary stenosis

A

CXR: normal or post-stenotic dilatation of the pulmonary artery

ECG: evidence of right ventricular hypertrophy

53
Q

Management of pulmonary stenosis

A

If the pressure gradient across the pulmonary valve is markedly increased (>64mmHg), intervention is needed
Transcatheter balloon dilatation is the treatment of choice

54
Q

Clinical features of adult-type coarctation of the aorta

A

Gradually gets more severe over many years
Asymptomatic
Systemic hypertension in the right arm
Ejection systolic murmur at the upper sternal edge
Collaterals heard with continuous murmur at the back
Radio-femoral delay

55
Q

Investigations for adult-type coarctation of the aorta

A 
CXR: rib notching (due to the development of large collateral intercostal arteries running under the ribs posteriorly to bypass the obstruction)
3 sign (visible notch in the descending aorta at the site of the coarctation)

ECG: left ventricular hypertrophy

56
Q

Management of adult-type coarctation of the aorta

A

A stent may be inserted when the condition becomes severe

57
Q

Examples of lesions causing an outflow obstruction in a sick infant

A

Coarctation of the aorta
Interruption of the aortic arch
Hypoplastic left heart syndrome

58
Q

Clinical features of outflow obstruction in a sick infant

A

Usually present sick with heart failure and shock in the neonatal period

59
Q

Management of an outflow obstruction in a sick infant

A 
Resuscitate (ABC)
Prostaglandin infusion (at the earliest opportunity)
Referral for early surgical intervention
60
Q

Coarctation of the aorta

A

Due to arterial duct tissue encircling the aorta just at the point of insertion of the duct
This causes severe obstruction to left ventricular outflow

61
Q

Clinical features of coarctation of the aorta

A

Examination may be normal on the first day

Neonates usually present with acute circulatory collapse at 2 days when duct closes

62
Q

Signs of coarctation of the aorta

A

Sick baby
Severe heart failure
Absent femoral pulses
Severe metabolic acidosis

63
Q

Investigations for coarctation of the aorta

A

CXR: cardiomegaly from heart failure and shock
ECG: normal

64
Q

Management of coarctation of the aorta

A

Surgical repair

65
Q

Interruption of the aortic arch

A

RARE
No connection between the proximal aorta and distal to the ductus arteriosus
Cardiac output is dependent on RIGHT-to-LEFT shunt via the duct
VSD is usually present

66
Q

Presentation of interruption of the aortic arch

A

Shock in the neonatal period

Complete correction with closure of the VSD and repair of the aortic arch within first few days of life
Associated with other conditions (e.g. Di George syndrome)

67
Q

Hypoplastic left heart syndrome

A

Characterised by underdevelopment of the entire left side of the heart
The mitral valve is small and atretic
Left ventricle is small
There is usually aortic valve atresia
The ascending aorta is also small
Usually accompanied by coarctation of the aorta

68
Q

Clinical features of hypoplastic left heart syndrome

A

May be detected antenatally
Children presenting after birth are the sickest of all neonataes presenting with duct-dependetn systemic circulation
There is no flow through the left side of the heart, so ductal constriction leads to profound acidosis and rapid cardiovascular collapse
Weakness or absence of all peripheral pulses

69
Q

Management of hypoplastic left heart syndrome

A

Surgery (Norwood procedure)

70
Q

Supraventricular tachycardia

A

Most common form of childhood arrhythmia
Rapid heart rate (250-300)
Can cause poor cardiac output and pulmonary oedema

71
Q

Presentation of supraventricular tachycardi

A

Symptoms of heart failure

It can cause hydrops foetalis and intrauterine death

72
Q

Investigations for supraventricular tachycardia

A

ECG:
Narrow complex tachycardia of 250-300bpm
It may be possible to discern P waves
May be features of myocardial ischaemia (e.g. TWI)
In Wolff-Parkinson-White syndrome, a delta wave may be visible

73
Q

Management of SVT

A

Prompt restoration of sinus rhythm is key to improvement

Circulatory and respiratory support

  • Tissue acidosis should be corrected
  • Positive pressure ventilation is needed

Vagal stimulating procedures (e.g. carotid sinus massage, cold ice pack to face)

IV adenosine:
Treatment of choice
Induces AV block after rapid bolus infusion
Terminates the tachycardia
Electrical cardioversion with synchronised DC shock if adenosine fails

Once sinus rhythm is restored, maintenance therapy will be required (e.g. flecainide or sotalol)
90% of children will have no further attacks after infancy
Children who relapse or are at risk usually treated with percutaneous radiofrequency ablation or cryoablation of the accessory pathway

74
Q

Congenital complete heart block

A

RARE

Usually related to the present of anti-Ro or anti-La antibodies in maternal serum  

The mothers will have latent or active connective tissue disease  

The antibodies seem to prevent the normal development of the electrical conduction system in the developing heart  

It can cause foetal hydrops, death in utero and heart failure in the neonatal period  

Most will remain asymptomatic for many years  

Some may present with syncope 

All children with symptoms require insertion of an endocardial pacemaker
75
Q

Long QT syndrome

A

May be associated with sudden loss of consciousness during exercise, stress or emotion
Usually presents in late childhood
It can be misdiagnosed as epilepsy
Sudden death from ventricular tachycardia can occur
Follows autosomal dominant inheritance
Associated with erythromycin therapy, electrolyte disturbances and head injury

76
Q

Causes of syncope

A

Neurally mediated syncope: In response to a range of stressors. Prodrome of dizziness and light-headed feeling and abnormal vision, along with pallor, nausea and sweating. In most people, there is a maladaptive drop in BP

Cardiac syncope: may be arrhytmic (e.g. heart block, SVT, ventricular tachycardia). May be structural (e.g. aortic stenosis, HOCM)

77
Q

Features indicative of a cardiac cause in syncope

A

Symptoms on exercise
Family history of sudden unexpected death
Palpitation

NB: check blood pressure and for signs of cardiac disease (e.g. murmur, femoral pulses, features of Marfan’s syndrome)
ALL patients presenting with a transient loss of consciousness should be investigated with a 12-lead ECG to check the corrected QT interval)

78
Q

Acute rheumatic fever

A

Rare in the developed world but is an important cause of heart disease worldwide

Acute rheumatic fever is a short-lived, multisystem autoimmune response to a preceding infection with group A b-haemolytic streptococcus
It progresses to chronic rheumatic heart disease in up to 80% of cases

79
Q

Clinical features of rheumatic fever

A

Symptoms manifest about 2-6 weeks after a pharyngeal or skin infection
Initial symptoms include polyarthritis, mile fever and malaise
Diagnosis is based on the Jones criteria

80
Q

Chronic rheumatic heart disease

A

MItral stenosis is the most common consequence of scarring and fibrosis of the valve tissue in the heart
This could occur at a relatively young age if the patient has repeated attacks of rheumatic fever with carditis
The other valves can also get affected

81
Q

Management of rheumatic fever

A

Acute rheumatic fever is treated with bed rest and anti-inflammatory agents (aspirin is very effective at suppressing the inflammatory response of the joints and heart, and should be given at a high dose)
Anti-streptococcal anitbiotics may be used if there is any evidence of a persistent infection (e.g. penicillin V, benzathine benzylpenicillin, amoxicillin)
If the fever and inflammation does not resolve rapidly, corticosteroids may be required
Symptomatic heart failure is treated with diuretics and ACE inhibitors

After the acute episode, recurrence should be prevented
The most effective prophylaxis is monthly injections of benzathine penicillin:
- Alternative: oral penicillin OD
- Most recommend prophylaxis either 10 years after the last episode of acute rheumatic fever or until the age of 21 years
- Lifelong prophylaxis is recommended for those with severe valvular disease

Surgical treatment with valve repair or replacement may be required

82
Q

Risk factors for infective endocarditis

A

ALL children with congenital heart disease are at risk of infective endocarditis
Highest risk groups= VSD, coarctation of the aorta, PDA or prosthetic materials

Should be suspected in any child or adult with:
Sustained fever
Malaise
Raised ESR
Unexplained anaemia
Haematuria
83
Q

Clinical features of infective endocarditis

A 
Fever
Anaemia and pallor
Splinter haemorrhages
Clubbing
Necrotic skin lesions
Changing cardiac signs
Splenomegaly
Neurological signs from cerebral infarction
Retinal infarcts
Arthritis/arthralgia
Haematuria (microscopic)
84
Q

Investigations for infective endocarditis

A

Multiple blood cultures should be taken before antibiotics are started
Detailed echocardiography may be able to confirm the diagnosis by the identification of vegetations NB: vegetations consist of fibrin and platelets and infecting organisms

85
Q

What is the most common causative organism of infective endocarditis?

A

Streptococcus viridans (a-haemolytic streptococci)

86
Q

Management of infective endocarditis

A

Involve the MDT: cardiologists, cardiac surgeons, infectious disease specialists, neurologists, neurosurgeons and microbiologists
50% of patients will require surgery

Empirical antibiotics should be given (varies depending on local epidemiology, presence of prosthetic valves and possibility of nosocomial infection) - an infectious disease specialist should be consulted

Native valves:
Penicillin-sensitive Streptococcus viridans= beta-lactam (benzylpenicillin sodium, ampicillin, ceftriaxone, amoxicillin) +/- gentamicin or vancomycin
MRSA= (beta-lactam OR vancomycin OR daptomycin OR co-trimoxazole) AND clindamycin

Prosthetic valves:
Penicillin-sensitive Streptococcus viridans = same as for native valves
Methicillin-sensitive Staphylococcus aureus = (nafcillin OR oxacillin OR cefazolin OR vancomycin) AND rifampicin AND gentamicin

In other words…high-dose penicillin with an aminoglycoside  
6 weeks of therapy  
If there is infected prosthetic material (e.g. valves), they may require surgical removal
87
Q

Prophylaxis for infective endocarditis

A

Good dental hygiene
Avoidance of body piercings or tattoos
Antibiotics prophylaxis is no longer recommended in the UK. However, it may be required in other countries for
Dental treatment
Surgery which is likely to be associated with bacteraemia

88
Q

Dilated cardiomyopathy causes

A

Inheritance
Secondary to metabolic disease
May result from direct viral infection of the myocardium

89
Q

How is dilated cardiomyopathy diagnosed?

A

Echocardiography

90
Q

Management of myocarditis/cardiomyopathy

A

Symptomatic with diuretics, ACE inhibitors and carvedilol

Myocarditis usually improves spontaneously

91
Q

Causes of pulmonary hypertension

A

Pulmonary arterial hypertension:
Idiopathic
Post-tricuspid shunts (e.g. VSD, VSD, PDA)
HIV infection
Persistent pulmonary hypertension of the newborn

Pulmonary venous hypertension:
Left-sided heart disease
Pulmonary vein stenosis or compression

Pulmonary hypertension with respiratory disease:
Chronic obstructive lung disease or BPD in preterm infants
Interstitial lung disease
Obstructive sleep apnoea or upper airway obstruction

Pulmonary thromboembolic disease

Pulmonary inflammatory or capillary disease

92
Q

Risks of untreated pulmonary hypertension

A

Can lead to changes to the pulmonary vascular bed which cannot be corrected other than with heart/lung transplantation

93
Q

Medications to reduce pulmonary hypertension

A

Inhaled nitric oxide
IV magnesium sulphate
Oral phosphodiesterase inhibitors

Year 5 Specialties (7 decks)

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