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MBBS3-Pediatrics > Common cardiac diseases > Flashcards

Common cardiac diseases Flashcards

1
Q

what are some congenital structural lesions of the heart

A

septal defects (hole in the heart)- ASD, VSD, at the endocardial cushions

vessel abnormalities- transposition of the great vessels, coarctation of the aorta, pulmonary stenosis, PDA

valve abnormalities- tricuspid atresia, aortic stenosis

major structural abnormalities- fallot’s tetralogy, hypoplastic left heart

failure to transition- PDA, persistent fetal circulation

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2
Q

what are cyanotic congenital heart diseases

A

-transposition of the great arteries
-tetralogy of fallot
-critical pulmonary stenosis
-other complex structural defects

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3
Q

whats a duct dependent heart disease

A

its when the heart has structural abnormalities which are incompatible with life outside the womb once the ductus arteriosus closes

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4
Q

what can accelerate the closure of the ductus arteriosus

A

oxygen

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5
Q

what are the components of TOF

A

-pulmonary stenosis
-right ventricular hypertrophy
-perimembranous VSD
-overriding aorta

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6
Q

when does TOF present

A

infancy/ early childhood

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7
Q

how does a child with TOF look like from early life

A

dusky, gradually increasing over time

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8
Q

what are some physical signs of TOF

A

-persistent cyanosis
-ejection systolic murmur which corresponds to pulmonary stenosis
-hyper cyanotic spells

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9
Q

what happens to the blood cells of a child with TOF

A

polycythemia occurs

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10
Q

for TOF what does the CXR show

A

a boot shaped heart

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11
Q

how do you diagnose TOF

A

echocardiogram

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12
Q

whats the treatment for TOF

A

surgical

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13
Q

whats the management for TOF

A

-antibiotic prophylaxis
-anticoagulation
-treating hyper-cyanotic spells

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14
Q

what causes the hyper cyanotic spells to occur

A

right ventricular outflow obstruction, which gets worse over time and acute episodes of pulmonary infundibular spasm occur

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15
Q

what precipitates the hyper-cyanotic spells and how long do they last

A

activity like feeding/ playing and can last minutes and then resolve or progress

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16
Q

how do the hypercyanotic spells present

A

-deepening cyanosis
-agitation
-tachypnea
-pallor
-floppiness can occur
-loss of consciousness (where brain damage can occur)

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17
Q

how do older children terminate hyper-cyanotic spells

A

by squatting

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18
Q

how can you treat cyanotic spells

A

putting child in a squatting or knee to chest position- this increases systemic vascular resistance and promotes systemic venous return to the heart

giving oxygen- to decrease peripheral vasoconstriction (its a pulmonary vasodilator)

analgesia (e.g. morphine)- to decrease release of catecholamines hence decreasing HR, increasing filling time and relaxation of the infundibular spasm

i.v fluid bolus- to improve right ventricular preload

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19
Q

what are congenital lesions which may cause heart failure

A

-VSD
-ASD
-PDA
-coarctation of the aorta

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20
Q

what is a VSD

A

its where there is a connection between the 2 ventricles causing left to right shunt

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21
Q

whats the commonest cause of heart failure in infancy

A

VSD

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22
Q

what do you hear from a VSD

A

harsh pansystolic murmur louder at the left lower sternal edge

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23
Q

if the hole is big in VSD what is the murmur like

A

quiet

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24
Q

why is there no murmur in VSD in the newborn period

A

because the high pulmonary vascular resistance results in minimal shunting across the defect

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25
Q

how do you treat VSD

A

surgery

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26
Q

how do you manage VSD

A

-treat heart failure
-antibiotic prophylaxis

27
Q

what is ASD

A

its when theres a connection between the 2 atria, causing a left to right blood flow and an overloaded right side of the heart

28
Q

in ASD how do the children present

A

they are asymptomatic

29
Q

what do you hear in a child with ASD

A

an ejection systolic murmur loudest in the pulmonary area, caused by increase in blood flow through the pulmonary valve

30
Q

what does a CXR for ASD show

A

-big heart
-large pulmonary artery
-pulmonary plethora
-small aorta

31
Q

how do you treat ASD

A

surgically

32
Q

what is the medical management for ASD

A

-treat heart failure
-antibiotic prophylaxis

33
Q

where do you mainly see PDA

A

premature infants

34
Q

how does PDA occur

A

when there is failure to close the ductus arteriosus

35
Q

what happens in PDA

A

there is reversed flow from the aorta to the pulmonary circulation

36
Q

what do you hear in PDA

A

machinery murmur below left clavicle

37
Q

what is coarctation of the aorta

A

its when there is narrowing at a specific point in the aorta, usually before the point at which the ductus arteriosus

38
Q

when does coarctation of the aorta present

A

when the duct closes, with collapsed baby and heart failure

39
Q

what do you see in a child with coarctation of the aorta

A

-reduced or absent femoral pulses
-systolic murmur

40
Q

how do you treat coarctation of the aorta

A

surgically

41
Q

how do you manage coarctation of the aorta

A

-treat heart failure
-antibiotic prohylaxis

42
Q

what are acquired causes of heart failure

A

-rheumatic heart disease
-cardiomyopathy
-myocarditis
-bacterial endocarditis

43
Q

what does rhematic heart disease cause

A

episode/episodes of acute rheumatic fever leading to endocardium inflammation

44
Q

what does RHD mainly affect

A

mitral and aortic valves

45
Q

how does inflammation in RHD settle

A

with scarring, fibrosis and deformity of the valve which may lead to heart failure over time

46
Q

what happens in RHD-mitral regurgitation

A

during systole blood goes backwards through the incompetent valve from from the left ventricle to the left atrium and pulmonary veins

47
Q

what does mitral regurgitation caused by RHD result in

A

-reduced cardiac output causing pulmonary edema
-left ventricular hypertrophy to compensate

48
Q

how does a patient with mitral regurgitation present

A

they are easily fatigued and breathless as heart failure develops (symptoms do take a long time to develop though)

49
Q

what is cardiomyopathy

A

its weakened heart muscle commonly with dilation

50
Q

what causes cardiomyopathy

A

-idiopathic
-related to underlying metabolic or connective tissue disorders

51
Q

whats myocarditis

A

inflammatory process of heart muscle following viral illness (coxackie B virus)

52
Q

what is cardiomyopathy and myocarditis characterised by

A

poorly contracting large flabby heart with HF

53
Q

what does cardiomyopathy and myocarditis present with

A

-heart failure
-poor perfusion
-mitral regurgitation murmur

54
Q

where does bacterial endocarditis occur

A

in children with congenital or acquired heart defects

55
Q

what does bacterial endocarditis cause

A

-turbulent blood flow across a valve
-bacterial vegetations to form on damaged endothelium which shed infective emboli

56
Q

bacterial endocarditis is a differential for a child with what cardiac signs

A

-janeway lesions
-splinter hemorrhages
-roth spots

(these are from shed off infective emboli which block the microcirculation)

57
Q

whats the usual onset of bacterial endocarditis

A

insidious with fever, fatigue, loss of appetite and joint pains but it can be acute with fever, prostration and HF

58
Q

on examination what do you see with someone with bacterial endocarditis

A

-variable heart murmur
-petechial rash
-splinter hemorrhages
-osler nodes
-clubbing
-subconjunctival hemorrhages
-splenomegaly
-neurolgy

59
Q

why should you give antibiotics be given to children with heart lesions when they have any form of surgery/dental procedure as prophylaxis

A

to prevent infective endocarditis

60
Q

how do you treat heart failure

A
  • by reducing the amount of blood the heart has to pump
  • by making the heart pump harder
  • by supportive therapy
61
Q

how do you reduce the amount of blood the heart has to pump to treat HF

A
  1. with diuretics- frusemide and spironolactone (1-3mg/kg/day)
  2. with vasodilators to reduce the amount of work e.g. captopril (N.B captopril can cause hypotension espec in pts with ventricular dysfunction so measure BP before introducing captopril.)
62
Q

how do you make the heart pump harder to treat HF

A
  1. digoxin (10-30ug/kg/day)
  2. inotropes e.g. noradrenaline and adrenaline given on ICU/HDU
63
Q

how does supportive therapy treat HF

A
  1. feeding- tube feeding is helpful in babies if there are feeding difficulties and taking low salt in food
  2. nursing- nurse in a sitting position
64
Q

why would children with untreated VSD/ ASD eventually turn blue

A

this is because it will cause a chronic increase in pulmonary blood flow, which will cause irreversible damage to the pulmonary vasculature causing pulmonary damage. This then results in flow across the VSD/ASD to reverse causing the child to become cyanosed and polycythemia (N.B its now too late to fix the septal defect)

MBBS3-Pediatrics (2 decks)

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