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3ayeeeee > Paeds Cardiac > Flashcards

Paeds Cardiac Flashcards

1
Q

Features of an innocent murmur

A
  • Short
  • Soft
  • Systolic symptomless
  • Situation dependent
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2
Q
  1. Features that would prompt the investigation of a heart murmur
A
  • Murmur louder than 2/6
  • Diastolic murmur
  • Louder on standing
  • Combined with – failure to thrive, feeding difficulty or SOB
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3
Q
  1. Investigation of an (innocent) heart murmur
A
  • ECG
  • Chest X-ray
  • Echocardiography
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4
Q
  1. What presents with a pan-systolic murmur, fifth intercostal space, mid-clavicular line)
A
  • Mitral regurgitation
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5
Q
  1. Pan-systolic murmurs
A
  • Mitral regurgitation
  • Tricuspid regurgitation
  • VSD
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6
Q
  1. What presents with a pan-systolic murmur, fifth intercostal space, left sternal border ?
A
  • Tricuspid regurgitation
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7
Q
  1. What presents with a pan-systolic murmur heard at the left sternal border
A
  • VSD
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8
Q
  1. How would a mitral regurgitation be heard ?
A
  • Pansystolic murmur
  • 5th intercostal space midclavicular line
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9
Q

How would a tricuspid regurgitation be heard ?

A
  • Pansystolic murmur
  • 5th intercostal space left sternal border
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10
Q
  1. How would a VSD be heard ?
A
  • Pansystolic murmur
  • Left sternal border
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11
Q
  1. Ejection-systolic murmurs can be caused by
A
  • Aortic stenosis
  • Pulmonary stenosis
  • Hypertrophic obstructive cardiomyopathy
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12
Q
  1. How does aortic stenosis sound ?
A
  • Ejection systolic murmur
  • Loudest at the second intercostal space, right sternal border
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13
Q
  1. How does pulmonary stenosis sound ?
A
  • Ejection systolic murmur
  • Loudest at the second intercostal space, left sternal border
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14
Q
  1. How does hypertrophic obstructive cardiomyopathy sound ?
A
  • Ejection systolic murmur
  • Loudest at the fourth intercostal space on the left sternal border
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15
Q
  1. What causes a second heart sound to be heard ?
A
  • Increased volume in the right ventricle causing it longer to empty during systole and delay to the pulmonary valve closing
  • Can occur is septal defects
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16
Q

How will a atrial septal defect sound in auscultation ?

A
  • Mild systolic crescendo-decrescendo murmur
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17
Q

How will a PDA sound on auscultation ?

A
  • A normal first heart sound and a continuous crescendo-decrescendo ‘’machinery’’ murmur that may continue during the second heart sound making the second heart sound difficult to hear
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18
Q
  1. How will Tetralogy of Fallot be heard on auscultation ?
A
  • Murmur in tetralogy of Fallot arises from pulmonary stenosis
  • An ejection systolic murmur heard loudest at the pulmonary area (second intercostal space, left sternal border)
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19
Q
  1. Cyanotic Heart Conditions
A
  • TOF
  • Tricuspid atresia
  • Transposition of the great arteries
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20
Q
  1. What is a complications of ASD ?
A
  • Stroke - when a patient normally has a DVT it travels to the lungs and becomes stuck
  • AF or atrial flutter
  • Pulmonary hypertension and right sided heart failure  Eisenmenger syndrome
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21
Q
  1. Typical symptoms of ASD
A
  • SOB
  • Difficulty feeding
  • Poor weight gain
  • Lower respiratory track infection
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22
Q
  1. Management of a ASD
A
  • Paediatric cardiologist referral
  • If small, watch and wight can be appropriate as may close by themselves
  • Can be closed surgically using a transvenous catheter closure (via the femoral vein) or open heart surgery
  • Anticoagulants such as aspirin
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23
Q
  1. Symptoms of VSD
A
  • Poor feeding
  • Dyspnoea
  • Tachypnoea
  • Failure to thrive
  • May be systolic thrill on palpation
  • Pan-systolic murmur more prominently heard at the left lower sternal border in the 3rd and 4th intercostal space
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24
Q
  1. VSD treatment
A
  • Refer to pediatric cardiologist
  • Small VSDs with no symptoms or evidence of pulmonary hypertension or heart failure can be watched over time and often close spontaneously
  • Can be corrected surgically using a transvenous catheter closure via the femoral vein or open heart surgery
  • Increased risk of infective endocarditis in patients with a VSD
  • AB prophylaxis should be considered during surgical procedures to reduce the risk
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25
Q
  1. PDA – RF
A
  • Genetic
  • Rubella
  • Prematurity
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26
Q
  1. PDA presentation
A
  • Crescendo-decrescendo continuous machinery murmur
  • Shortness of breath
  • Difficulty feeding
  • Poor weight gain
  • Lower respiratory tract infections
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27
Q
  1. PDA pathophysiology
A
  • Opening between the aorta and the pulmonary artery
  • Pressure higher in aorta so blood shunts into the pulmonary artery
  • Pressure is increased in the pulmonary vessels causing pulmonary hypertension leading to right sided heart strain as right ventricle has to contract harder
  • This leads to right ventricular hypertrophy
  • This leads to right to left shunt and left ventricular hypertrophy
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28
Q
  1. How is a PDA diagnosed ?
A
  • Echocardiogram
  • Doppler flow studies can assess the size and characteristics of the left to right shunt
29
Q
  1. Management of PDA
A
  • Pts monitored until 1 year of age using echo’s
  • After 1 year it is unlikely to close spontaneously
  • Trans-catheter or surgical closure can be performed
  • Symptomatic patients would need earlier closure
30
Q
  1. Features of TOF
A
  • Overriding aorta
  • VSD
  • Pulmonary stenosis
  • Right ventricular hypertrophy
31
Q

RFs for TOF

A
  • Rubella infection
  • Increased age of mother
  • Alcohol
  • DM
32
Q
  1. Investigations for TOF
A
  • Diagnostic echocardiography
  • Chest X-ray – boot shaped heart
33
Q
  1. Signs and symptoms of TOF
A
  • Cyanosis
  • Clubbing
  • Poor feeding
  • Poor weight gain
  • Ejection systolic murmur heart loudest in the pulmonary area (second intercostal space, lfet sternal border)
  • Tet spells
34
Q

What is a tet spell ?

A
  • Intermittent symptomatic periods where the right to left shunt becomes temporarily worsened, precipitating a cyanotic episode
  • This happens when the pulmonary vascular resistance increases or the systemic resistance decreases
  • For example if the child is physically exerting themselves they are generating a lot of carbon dioxide
  • CO2 is vasodilator that causes systemic vasodilation and therefore reduces the systemic vascular resistance
  • Blood flow will choose the path of least resistance, so blood will be pumped from the right ventricle to the aorta rather than the pulmonary vessels bypassing the lungs
  • Episodes may be precipitated by walking, physical exertion or crying
  • The child will become irritable, cyanotic and short of breath
  • Severe spells can lead to reduced consciousness, seizures and potentially death
35
Q
  1. Tet Spells non-medical management
A
  • Older children m ay squat when tet spells occur
  • Younger children can be positioned with their knees to their chest
  • Squatting increases systemic vascular resistance
  • This encourages blood to enter the pulmonary vessels
  • Any medical management of a tet spell should involve an experienced pediatrician, as they can be potentially life threatening
36
Q
  1. Tet spells medical management
A
  • Supplementary oxygen – treat hypoxia
  • Beta-blockers – relax right ventricle and improve flow to pulmonary vessels
  • IV fluids – can increase pre-load, increasing the volume of blood to pulmonary vessels
  • Morphine – decreases respiratory drive
  • Sodium bicarbonate – can buffer metabolic acidosis
  • Phenylephrine infusion – can increase systemic vascular resistance
  • Prostaglandin infusion to maintain PDA
37
Q
  1. Why would prostaglandins be given in TOF ?
A
  • In neonates a prostaglandin infusion can be used to maintain the ductus arteriosus
  • This allows blood to flow from the aorta back to the pulmonary arteries
38
Q
  1. Transposition of the great arteries
A
  • A condition where the attachments of the aorta and the pulmonary trunk to the heart are swapped (transposed)
  • RV pumps blood to the aorta instead of the lungs where it would become oxygenated
  • The LV pumps to the pulmonary artery and to the lungs becoming oxygenated but then returns to the LA preventing oxygenated blood traveling to the body
39
Q
  1. What does immediate survival depend on in ToGA
A
  • A shunt across a PDA, ASD or VSD
  • Can initially compensate by allowing blood to mix between the systemic circulation and the lungs however within a few weeks of life they will develop respiratory distress, tachycardia, poor feeding, poor weight gain and sweating
40
Q
  1. Management of ToGA
A
  • Prostaglandin infusion can be used to maintain the DA
  • Ballon septostomy – catheter into the foramen ovaleia and inflating a balloon to create a large atrial septal defect.
  • Open heart surgery is definitive management
41
Q

What is rheumatic fever ?

A
  • An autoimmune condition triggered by Group A-haemolytic streptococcus bacteria
  • Typically streptococcus pyogenes
  • Type 2 hypersensitivity reaction
42
Q
  1. Presentation of rheumatic fever ?
A
  • Typically 2-4 weeks following a streptococcal infection such as tonsillitis
  • Fever
  • Joint pain
  • Rash
  • SOB
  • Chorea
  • Nodules
43
Q
  1. What type of arthritis does rheumatic fever cause
A
  • Migratory arthritis affecting the large joints, with hot swollen and painful joints
  • Migratory = joints will become inflamed and improve at different times
44
Q
  1. What will be present in rheumatic fever on examination of the heart
A
  • Pericarditis, myocarditis and endocarditis leading to tachy or bradycardia
  • Typically mitral valve (pan systolic murmur hear loudest midclavicular line 5th intercostal space)
  • Pericardial rub on auscultation
  • Heart failure
45
Q
  1. 2 key signs of rheumatic fever in the skin
A
  • Subcutaneous nodules – firm painless nodules occurring over extensor surfaces of joints such as the elbows
  • Erythema marginatum rash – pink rings of varying sizes affecting the torso and proximal limbs
46
Q
  1. Investigations for rheumatic fever
A
  • Throat swab
  • ASO antibody titres – ABs against streptococcus
  • Echo, ECG and chest x-ray
47
Q
  1. Management for rheumatic fever
A
  • Phenoxymethylpenicillin (Penicillin V) for 10 days
  • Refer to specialist
  • NSAIDs for joint pain
  • Aspirin and steroids for carditis
  • Prophylactic ABs to prevent further streptococcal infection
  • Monitor and manage complications
48
Q
  1. Complications of rheumatic fever
A
  • Recurrent RF
  • Valvular heart disease – MC mitral stenosis
  • Chronic heart failure
49
Q
  1. What is endocarditis
A
  • Infection of the endothelium (inner surface) of the heart
  • Most commonly affects the heart valves
  • Can be acute, subacute or chronic
50
Q
  1. RFs for endocarditis
A
  • IV drug use
  • Structural heart pathology
  • CKD
  • Immunocompromised
  • PMHx
51
Q
  1. What structural pathology can increase the risk of endocarditis
A
  • Valvular heart disease
  • Congenital heart disease
  • Hypertrophic cardiomyopathy
  • Prosthetic heart valves
  • Implantable cardiac devices e.g. pacemakers
52
Q
  1. What is the MCC of endocarditis
A
  • Staphylococcus aureus
53
Q
  1. What is the presentation of endocarditis
A
  • Non-specific infection
  • Fever
  • Night sweats
  • Muscle aches
  • Anorexia
54
Q
  1. Key exam findings for endocarditis
A
  • New or changing heart murmur
  • Splinter hemorrhages
  • Petechiae – small non-blanching red/brown spots on the trunk, limbs, oral mucosa or conjunctiva
  • Janeway lesions
  • Osler’s nodes
  • Roth spots
  • Splenomegaly
  • Finger clubbing
55
Q
  1. Key investigations for endocarditis
A
  • Blood cultures are essential before starting antibiotics
  • 3 blood culture samples are recommended usually separated by at least 6 hours and taken from different sites
  • Echocardiography
  • Transesophageal echocardiography
56
Q
  1. Dukes criteria for endocarditis
A
  • One major plus 3 minor
  • Or five minor criteria
57
Q
  1. Major criteria (Dukes) endocarditis
A
  • Persistently positive on blood cultures
  • Specific imaging findings
58
Q
  1. Minor criteria (Dukes) endocarditis
A
  • Predisposition e.g. immune compromised
  • Fever above 38
  • Vascular phenomena e.g. Janeway lesions, ICHs
  • Immunological phenomena e.g. Osler’s nodes
  • Microbiological phenomena e.g. one positive culture
59
Q
  1. Management endocarditis
A
  • IV broad spectrum ABs e.g. amoxicillin and optional gentamicin
  • 4 weeks with native heart valves
  • 6 weeks for patients with prosthetic heart valves
60
Q
  1. Complications endocarditis
A
  • Heart valve damage, causing regurgitation
  • Heart failure
  • Infective and non-infective emboli
  • Glomerulonephritis causing renal impairment
61
Q
  1. What is Eisenmenger syndrome
A
  • When the right to left shunt of blood in the heart bypassing the lungs
62
Q
  1. What 3 underlying conditions can lead to Eisenmenger syndrome ?
A
  • ASD
  • VSD
  • PDA
63
Q
  1. What is the pathophysiology of Eisenmenger syndrome
A
  • Left to right shunts leads to increased pressure in the pulmonary vessels leading to pulmonary hypertension
  • When pulmonary pressure exceeds systemic pressure blood begins to flow across the lesion leading to a right to left shunt
  • With blood not entering the pulmonary circulation and becoming oxygenated this leads to cyanosis
64
Q
  1. Key exam findings for Eisenmenger syndrome - Associated with pulmonary hypertension
A
  • Right ventricular heave
  • Loud P2: due to forceful shutting of pulmonary valve
  • Raised JVP
  • Peripheral oedema
65
Q
  1. Key exam findings for Eisenmenger syndrome indicative of a underlying septal defect
A
  • Atrial septal defect – mid-systolic, crescendo-decrescendo murmur loudest at the upper left sternal border
  • Ventricular septal defect – pain systolic murmur loudest at the left lower sternal border
  • PDA: continuous crescendo-decrescendo ‘’machinery’’ murmur
  • Arrhythmias
66
Q
  1. Key exam findings for Eisenmenger syndrome related to the right to left shunt and chronic hypoxia
A
  • Cyanosis
  • Clubbing
  • Dyspnoea
67
Q
  1. Prognosis of Eisenmenger syndrome
A
  • Reduces life expectancy by about 20 years
68
Q
  1. Definitive treatment for Eisenmenger syndrome
A
  • Once pulmonary pressure is high enough to cause syndrome only definitive treatment is a heart-lung transplant

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