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0.1 Paediatrics - RB > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Describe the three shunts of Foetal Circulation. What happens during birth to these shunts

A
  • Ductus Arteriosus (Connects Aorta to Pulmonary Artery, bypassing Pulmonary circulation)
  • Ductus Venosus (Connects Umbilical Vein to Inferior Vena Cava, bypassing liver)
  • Foramen Ovale (Connecting R and L atria)

During birth, air enters alveoli causing a decrease in pulmonary resistance. Blood takes path of least resistance and now enters pulmonary circulation. Also a drop in prostaglandins cause the foramen ovale to close, becoming fossa ovalis. Ductus arteriosis becomes Ligamentum arteriosus, and Ductus venosus becomes Ligamentum venosus

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2
Q

What is the murmur of Patent Ductus Arteriosis?

A

Systolic crescendo-decrescendo “machinery” murmur, with ability to hear S1 but not S2. Radiation to back / between scapula. Left subclavicular thill, large bounding and collapsing pulse, with a wide pulse pressure

a continuous crescendo-decrescendo “machinery” murmur

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3
Q

What are the risk factors of Patent Ductus Arteriosis?

A

High altitude, prematurity, rubella, hyaline membrane disease

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4
Q

Is Patent Ductus Arteriosis cyanotic or acyanotic?

What is the pathophysiology?

A

Acyanotic

The pressure in the aorta is higher than that in the pulmonary vessels, so blood flows from the aorta to the pulmonary artery. This creates a left to right shunt where blood from the left side of the heart crosses to the circulation from the right side. This increases the pressure in the pulmonary vessels causing pulmonary hypertension, leading to right sided heart strain as the right ventricle struggles to contract against the increased resistance. Pulmonary hypertension and right sided heart strain lead to right ventricular hypertrophy. The increased blood flowing through the pulmonary vessels and returning to the left side of the heart leads to left ventricular hypertrophy.

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5
Q

What is the murmur of Atrial Septal Defect?

A

FIXED SPLIT S2

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6
Q

What are the three types of Atrial Septal Defect? What are they associated with?

A
  1. Ostium Secundum (Holt-Oram syndrome)
  2. Patent Foramen Ovale (Migraine with aura)
  3. Ostium Primum (Down’s syndrome)

Ostium secondum, where the septum secondum fails to fully close, leaving a hole in the wall.
Patent foramen ovale, where the foramen ovale fails to close (although this not strictly classified as an ASD).
Ostium primum, where the septum primum fails to fully close, leaving a hole in the wall. This tends to lead to atrioventricular valve defects making it an atrioventricular septal defect.

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7
Q

Outline pathophysiology of Atrial Septal Defect. Is it cyanotic or acyanotic?

A

During development, the Septum primum travels down to the endocardial cushion, producing an Ostium primum as it does so. This however becomes redundant and an Ostium Secondum forms superior to it. A Septum secondum travels down also, forming a Foramen Ovale. This structure behaves as a valve between two atria, until they are ideally closed during birth

If it is not, there is communication still, causing a L -> R shift, pulmonary HTN and RVH. Acyanotic as deoxygenated blood does not enter systemic circulation

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During the development of the fetus the left and right atria are connected. Two walls grow downwards from the top of the heart, then fuse together with the endocardial cushion in the middle of the heart to separate the atria. These two walls are called the septum primum and septum secondum.
-
Defects this these two walls lead to atrial septal defects, a hole connecting the left and right atria. There is a small hole in the septum secondum called the foramen ovale. The foramen ovale normally closes at birth.
-
An atrial septal defect leads to a shunt, with blood moving between the two atria. Blood moves from the left atrium to the right atrium because the pressure in the left atrium is higher than the pressure in the right atrium. This means blood continues to flow to the pulmonary vessels and lungs to get oxygenated and the patient does not become cyanotic, however the increased flow to the right side of the heart leads to right sided overload and right heart strain. This right sided overload can lead to right heart failure and pulmonary hypertension.
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Eventually pulmonary hypertension can lead to Eisenmenger syndrome. This is where the pulmonary pressure is greater than the systemic pressure, the shunt reverses and forms a right to left shunt across the ASD, blood bypasses the lungs and the patient becomes cyanotic.

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8
Q

What are the ECG findings for an Ostium Secondum / Ostium Primum ASD?

A

Ostium Secondum - RBBB and RAD

Ostium Primum - RBBB and LAD

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9
Q

How is Patent Ductus Arteriosus treated?

A

Symptomatic -> Indomethacin (Prostaglandin Inhibitor)

Asymptomatic -> Echo monitoring upto 1 year old, followed by Transcatheter / Surgery to close

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10
Q

How is Atrial Septal Defect treated?

A
  • Anticoagulants (Warfarin, Aspirin, NOACs)

- Transcatheter Surgery

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11
Q

What are the associations with Ventricular Septal Defect?

A

Down’s syndrome
Edward’s syndrome
Patau syndrome
Turner’s syndrome

Post-myocardial infarction

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12
Q

What is the murmur of Ventricular Septal Defect?

A

Pansystolic murmur, heard best on the L lower sternal border with radiation to the RHS

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13
Q

Outline pathophysiology of Ventricular Septal Defect. Is it cyanotic or acyanotic?

A

Communication between R and L ventricle. Blood shifts from L -> R, causing pulmonary hypertension and RVH. Acyanotic because deoxygenated blood does not enter systemic circulation

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14
Q

What are the three causes of Eisenmenger’s Syndrome?

A
  1. Patent Ductus Arteriosus
  2. Atrial Septal Defect
  3. Ventricular Septal Defect
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15
Q

What is the Pathophysiology of Eisenmenger’s Syndrome?

A

PDA, ASD and VSD all cause L -> R shunts, leading to Pulmonary HTN and RVH. Over time however, the RVH causes the pulmonary pressures > systemic pressures, leading to a reversal of the L -> R shunt. As a result, deoxygenated blood enters systemic circulation causing cyanosis

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16
Q

Why do patients with Eisenmenger’s have a plethoric complexion?

A

Cyanosis causes stimulation of bone marrow to respond to hypoxia by releasing more RBCs, leading to polycythaemia, a plethoric complexion and an increased risk of DVT / PEs

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17
Q

What cardiovascular findings are present with Eisenmenger’s?

A

Loud P2
Right ventricular heave
Raised JVP
Clubbing

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18
Q

What is the non-definitive and definitive management for Eisenmenger’s?

A

Polycythaemia - Venesection
Pulmonary HTN - Sildenafil
Thrombosis prophylaxis - Anticoagulation
Infective Endocarditis - Prophylactic ABX

Definitive: Heart + Lung Transplant

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19
Q

What is Coarctation of the Aorta and its pathophysiology?

A

Congenital narrowing of the Aorta, commonly at the Isthmus near the ductus arteriosus. Causes reduced blood pressures distal to the coarctation and increased pressures proximal to narrowing

20
Q

What genetic condition is associated with Coarctation of the Aorta? What are other associations?

A

Turner’s Syndrome, 45 XO

Neurofibromatosis
Berry Aneurysms
Bicuspid Aortic Valve

21
Q

Why is notching of the Inferior Border of the Ribs seen in Coarctation of the Aorta?

A

Dilatation of collateral intercostal arteries

22
Q

What are the features of Coarctation of the Aorta?

A
  • Weak femoral pulses
  • High BP in limbs proximal to narrowing, and lower BP in limbs distal to narrowing
  • Underdeveloped left arm due to reduced flow through subclavian artery
  • Radiofemoral delay
  • Radio-radial delay
23
Q

What is the murmur associated with Coarctation of the Aorta?

A

Late systolic murmur, heard below left clavicle and left scapula. Left ventricular heave, with apical click over Aortic valve

24
Q

What is the murmur associated with Aortic Stenosis?

A

Ejection “click” systolic murmur, crescendo-decrescendo, heard loudest in the 2nd intercostal space, right parasternal, with radiation to carotids. Loudest on expiration, with a slow rising pulse and narrow pulse pressure

25
Q

What four things comprise Tetralogy of Fallot?

A
  • Pulmonic valve stenosis
  • Right ventricular hypertrophy
  • Ventricular septal defect
  • Overriding Aorta
26
Q

What condition is associated with Tetralogy of Fallot?

A 
Chromosome 22 deletion (DiGeorge syndrome)
Trisomy 21 (Down's Syndrome)
27
Q

What is the pathophysiology of Tetralogy of Fallot? Is it cyanotic or acyanotic?

A
  1. Pulmonary valve stenosis means deoxygenated blood cannot reach pulmonary circulation
  2. As a result, RVH occurs to increase the force of contraction to contract blood through stenosis
  3. There is also a VSD, and blood flows through a path of least resistance, causing a R -> L shunt
  4. Blood flows through overriding aorta and into systemic circulation, bypassing pulmonary circulation, causing cyanosis
28
Q

What are risk factors of Tetralogy of Fallot?

A
  • Rubella
  • Maternal age >40
  • Alcohol consumption during pregnancy
  • Diabetic mother
29
Q

What murmur is associated with Tetralogy of Fallot?

A

Ejection systolic murmur

30
Q

Explain why some babies only periodically become cyanotic with Tetralogy of Fallot, and why they squat

A

Cyanotic spells, aka Tet spells

A child may exert themselves, increasing oxygen demand. This causes the heart to increase cardiac output and in doing so, more deoxygenated blood into systemic circulation

Squatting is a compensatory mechanism of a Tet spell, where kinking of femoral arteries increases vascular / systemic pressures, causing pressure of the LV > RV and thus reversal of the R -> L shunt

31
Q

What is seen on a CXR of a patient with Tetralogy of Fallot?

A

Boot-shaped heart

32
Q

What is the treatment for Tetralogy of Fallot?

A

Prostaglandins to maintain opening of PDA, whilst waiting surgery

33
Q

What is the treatment for a Tetralogy of Fallot Tet spell?

A
  • Supplementary Oxygen
  • Beta blockers
  • IV fluids to increase pre-load
  • Sodium bicarbonate to buffer metabolic acidosis
  • Phenylephrine infusion to increase systemic resistance
34
Q

What is the murmur associated with Pulmonic Valve Stenosis?

A

Ejection systolic, heard loudest over the 2nd IC space, L parasternal, louder with inspiration. Right ventricular heave due to RVH, and a raised JVP with giant a-waves

35
Q

What four conditions are associated with Pulmonic Valve Stenosis?

A

Tetralogy of Fallot
Noonan syndrome
William syndrome
Congenital Rubella syndrome

36
Q

What is an Innocent Murmur?

A

Soft, short, systolic, situation dependent (quieter when standing) and symptomless

37
Q

What is Ebstein’s Anomaly? Outline pathophysiology and whether it is cyanotic or acyanotic

A

Congenital heart defect where tricuspid valve is inserted lower, towards apex of heart resulting in a large R atria and a smaller R ventricle. This causes poor flow from the R atria -> R ventricle, leading to deoxygenated blood to flow to the L atria through an Atrial Septal Defect and into systemic circulation causing cyanosis

38
Q

What are the two associations with Ebstein’s Anomaly?

A
  • Wolff-Parkinson White Syndrome

- Lithium use in-utero

39
Q

What are the findings on ECG / auscultation in a patient with Ebstein’s Anomaly?

A

ECG: RBBB and LAD
Auscultation: Gallop rhythm + S3/S4

40
Q

What is the most common cyanotic heart disease?

A

Tetralogy of Fallot

41
Q

Outline the anatomy of the Transposition of the Great Arteries. Is it cyanotic or acyanotic?

A

The attachments of the aorta and the pulmonary trunk are swapped. The right ventricle pumps deoxygenated blood into the aorta and into the systemic circulation, and the left ventricle pumps oxygenated blood into the pulmonary circulation causing cyanosis, aka Dextro-TGA. These are two closed circuits with little communication except for a Ventricular Septal Defect, which allows some blood to be oxygenated and enter systemic circulation

42
Q

What is Levo-TGA? Is it cyanotic or acyanotic?

A

The attachments of the aorta and the pulmonary trunk are swapped, but the left and right ventricles are also swapped. Termed “congenitally corrected” and is acyanotic.

43
Q

What are risk factors for Transposition of the Great Arteries?

A

Diabetes in mother
Rubella in mother
Mother >40 years
Alcohol consumption during pregnancy

44
Q

What is seen on a CXR for a patient with Transposition of the Great Arteries? What is heard on auscultation?

A

CXR: “Egg on side” appearance of heart
Auscultation: Loud single S2

45
Q

How is Transposition of the Great Arteries managed?

A
  • Prostaglandin to maintain Ductus Arteriosus
  • Balloon septoplasty in foramen ovale to create ASD
  • Open heart surgery
46
Q

How can we differentiate between Cardiac and Respiratory causes of Cyanosis in Neonates?

A

Nitrogen wash-out test:

Give neonates 100% oxygen for 10mins, followed by performing an ABG. If PaO2 <15kPA = cyanotic congenital heart disease

47
Q

What is the name of the Prostaglandin medication used to mantain a Patent Ductus Arteriosus?

A

Alprostadil

0.1 Paediatrics - RB (16 decks)

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