Cardio - 3 Flashcards

1
Q

What are the risk factors for subacute bacterial endocarditis?

A

In children:

Unlike in acute endocarditis, an underlying valvular heart disease is needed for streptococcus viridans to cause infection of the valve

Also VSD and ASD

Previous Hx of SBE

In adults, there are others such as valve surgery and IVDU

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2
Q

What are the causes for subacute bacterial endocarditis?

A

Normally streptococcus viridians (in mouth - dentition)
Also streptococcus intermedius

Less often:
enterococci (eg. from UTI)
Staphylococci

(gastro or pelvic procedures)

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3
Q

What is the management for subacute bacterial endocarditis?

A

If untreated, it can become fatal within 6weeks to a year

Minimum 4 weeks of iv penicillin + (aminoglycoside eg. gentamycin)

Rarely, valve repair/replacement via surgery.

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4
Q

What are the causes of myocarditis?

A

Viral infections (parvovirus B19, human herpes virus 6, enterovirus coxsackie virus)
Associated with respiratory tract infections.
Lyme disease

Autoimmune
Toxins (cocaine, metal, snake poison)
ADRs

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5
Q

What are the presenting features of myocarditis?

A

Usually signs and symptoms of acute decompensation of heart failure: tachycardia, gallop,mitral regurgitation, edema

SOB during exercise
Later also when sleeping
Fever, sweats, chills

Palpitations, syncope and even sudden cardiac death may develop! (20% of sudden death in young adults)

In viral myocarditis, there may be previous URTI, flu-like syndrome, arthralgia, tonsillitis

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6
Q

What is hypoplastic left heart syndrome?

A

Underdevelopment of entire left heart.

Mitral valve atretic, LV small, aortic valve atretic
Almost always with coarctation

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7
Q

What are the features of hypoplastic left heart syndrome?

A

Duct-dependent circulation

Profound acidosis +
Circulatory collapse around day 2 (duct closes)

Peripheral pulses absent/weak

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8
Q

How is hypoplastic left heart syndrome managed?

A

It is a duct-dependent lesion:

ABC
Prostaglandin infusion

Operations:
Norwood - Sano procedure (aorta connected to RV + huge Sano shunt from RV to pulmonary tree = provides circulation to body and lungs. Only works due to the presence of ASD)

Glenn at ca. 6 months (SVC connected to pulmonary tree and opening closed up)

Fontan at 3 years (IVC closed up and also connected to pulmonary artery). At this point, there is no mixing of oxygenated and unoxygenated blood - only oxygenated. Uses 1 ventricle.

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9
Q

What are the key features of Tetralogy of Fallot? (right-to-left shunt).

A

4 defects:

Pulmonary stenosis
RV hypetrophy (as a result of pulmonary stenosis)

Large VSD
Overriding Aorta

Blood from RV is more likely to enter Aorta than pulmonary artery (due to stenosis). Cyanosis
Also, RV too powerful and pushes blood across into LV

Loud, harsh ejection systolic murmur at left sternal edge from day 1. Usually picked up antenatally

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10
Q

What are characteristics of cyanotic spells? (eg in tetralogy)

A

rapid cyanosis, irritability, inconsolable crying because of severe hypoxia.

SOB/pallor because of acidosis.

Very short murmur

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11
Q

What is the infant management of Tetralogy of Fallot?

A

If very cyanosed: shunt - to increase pulmonary blood flow.

A modified Blalock-Taussig (BT) shunt is a tube placed between the subclavian artery and the pulmonary artery.

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12
Q

Describe complete correction of tetralogy of Fallot

A
In infancy (6 months??)
Most babies nowadays, apart from babies who are too weak to tolerate it. 

Widen pulmonary valve (ballon or replaced)
Patch VSD

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13
Q

Describe the parallel circulation and duct-dependence in transposition of great arteries

A

Pulmonary artery connected to LV
Aorta connected to RV

Unoxygenated blood pumped straight into the body, whereas oxygenated blood returns to the lungs

Means that there are 2 closed off circuits. A patent ductus arteriosus is required to pump oxygenated artery into the body! CYANOTIC

Often, there is concurrent VSD or ASD, so some blood mixes.

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14
Q

What is the immediate management of TPA?

A

Prostaglandin

Balloon atrial septostomy life-saving and required in 20%

A catheter with an inflatable balloon is passed through umbilical vein or femoral into RA and through foramen ovale. Balloon is inflated in LA and pulled back through atrial septum. Renders flap of foramen ovale incompetent and allows mixing of pulmonary venous and systemic blood.

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15
Q

Describe the arterial switch procedure (needed in all patients with TPA)

A

Usually performed in the first few days of life.

Pulmonary artery and aorta transsected above the arterial valves and switched over.
The coronary arteries also need to be transferred over to the new aorta

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16
Q

What are the features of supraventricular tachycardia?

A

HR 250-300
Can cause poor cardiac output and pulmonary oedema

Can present with symptoms of heart failure in neonate/infant

17
Q

What is the ECG finding on SVT?

A

Narrow-complex tachycardia (HR 250-300/min)

In heart failure, there may be T-wave inversion in lateral leads

In WPW syndrome, short P-R interval due to antegrade activation of ventricles + delta wave

18
Q

What is the aetiology of SVT?

A

Rarely due to structural heart problem.

Often re-entry tachycardia: an accessory pathway leads to premature activation of the atrium (there is a circuit of conduction)

Wolff-Parkinson White syndrome (genetic) can also cause it. (accessory pathway connecting atria and ventricles)

19
Q

What is the pharmacological and non-pharmacological management of SVT?

A

Manage ABC

Vagal stimulating manoeuvres - eg. carotid sinus massage, cold ice pack to face (80% success)

IV adenosine. Given in incrementally increasing doses.(breaks re-entry circuit between AV node and accessory pathway)

Electrical cardioversion with synchronized DC shock (0.5-2j/kg) if adenosine fails

20
Q

What is the maintenance management in SVT?

A

Flecainide or sotalol

If pre-excitation delta wave, propranolol can be added

If no pre-excitation delta wave, digoxin can be added

Treat for about 1 year. 90% will have no further attacks, even if resting ECG abnormal