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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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22. PDA – RF
- Genetic - Rubella - Prematurity
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23. PDA presentation
- Crescendo-decrescendo continuous machinery murmur - Shortness of breath - Difficulty feeding - Poor weight gain - Lower respiratory tract infections
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24. PDA pathophysiology
- 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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25. How is a PDA diagnosed ?
- Echocardiogram - Doppler flow studies can assess the size and characteristics of the left to right shunt
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26. Management of PDA
- 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
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27. Features of TOF
- Overriding aorta - VSD - Pulmonary stenosis - Right ventricular hypertrophy
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RFs for TOF
- Rubella infection - Increased age of mother - Alcohol - DM
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29. Investigations for TOF
- Diagnostic echocardiography - Chest X-ray – boot shaped heart
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30. Signs and symptoms of TOF
- 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
What is a tet spell ?
- 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
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32. Tet Spells non-medical management
- 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
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33. Tet spells medical management
- 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
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34. Why would prostaglandins be given in TOF ?
- 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
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35. Transposition of the great arteries
- 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
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36. What does immediate survival depend on in ToGA
- 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
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37. Management of ToGA
- 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
What is rheumatic fever ?
- An autoimmune condition triggered by Group A-haemolytic streptococcus bacteria - Typically streptococcus pyogenes - Type 2 hypersensitivity reaction
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39. Presentation of rheumatic fever ?
- Typically 2-4 weeks following a streptococcal infection such as tonsillitis - Fever - Joint pain - Rash - SOB - Chorea - Nodules
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40. What type of arthritis does rheumatic fever cause
- Migratory arthritis affecting the large joints, with hot swollen and painful joints - Migratory = joints will become inflamed and improve at different times
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41. What will be present in rheumatic fever on examination of the heart
- 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
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42. 2 key signs of rheumatic fever in the skin
- 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
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43. Investigations for rheumatic fever
- Throat swab - ASO antibody titres – ABs against streptococcus - Echo, ECG and chest x-ray
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44. Management for rheumatic fever
- 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
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45. Complications of rheumatic fever
- Recurrent RF - Valvular heart disease – MC mitral stenosis - Chronic heart failure
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46. What is endocarditis
- Infection of the endothelium (inner surface) of the heart - Most commonly affects the heart valves - Can be acute, subacute or chronic
50
47. RFs for endocarditis
- IV drug use - Structural heart pathology - CKD - Immunocompromised - PMHx
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48. What structural pathology can increase the risk of endocarditis
- Valvular heart disease - Congenital heart disease - Hypertrophic cardiomyopathy - Prosthetic heart valves - Implantable cardiac devices e.g. pacemakers
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49. What is the MCC of endocarditis
- Staphylococcus aureus
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50. What is the presentation of endocarditis
- Non-specific infection - Fever - Night sweats - Muscle aches - Anorexia
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51. Key exam findings for endocarditis
- 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
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52. Key investigations for endocarditis
- 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
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53. Dukes criteria for endocarditis
- One major plus 3 minor - Or five minor criteria
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54. Major criteria (Dukes) endocarditis
- Persistently positive on blood cultures - Specific imaging findings
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55. Minor criteria (Dukes) endocarditis
- 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
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56. Management endocarditis
- IV broad spectrum ABs e.g. amoxicillin and optional gentamicin - 4 weeks with native heart valves - 6 weeks for patients with prosthetic heart valves
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57. Complications endocarditis
- Heart valve damage, causing regurgitation - Heart failure - Infective and non-infective emboli - Glomerulonephritis causing renal impairment
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58. What is Eisenmenger syndrome
- When the right to left shunt of blood in the heart bypassing the lungs
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59. What 3 underlying conditions can lead to Eisenmenger syndrome ?
- ASD - VSD - PDA
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60. What is the pathophysiology of Eisenmenger syndrome
- 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
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61. Key exam findings for Eisenmenger syndrome - Associated with pulmonary hypertension
- Right ventricular heave - Loud P2: due to forceful shutting of pulmonary valve - Raised JVP - Peripheral oedema
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62. Key exam findings for Eisenmenger syndrome indicative of a underlying septal defect
- 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
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63. Key exam findings for Eisenmenger syndrome related to the right to left shunt and chronic hypoxia
- Cyanosis - Clubbing - Dyspnoea
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64. Prognosis of Eisenmenger syndrome
- Reduces life expectancy by about 20 years
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65. Definitive treatment for Eisenmenger syndrome
- Once pulmonary pressure is high enough to cause syndrome only definitive treatment is a heart-lung transplant

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