Paediatric cardiovascular Flashcards

1
Q

Atrial septal defect : definition

A

Opening between the right and left atrium of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Atrial septal defect : Normal foetal physiology of circulation

A
  1. Embryonic development : Foramen ovale is a one way valve between the right atrium and left atrium
  2. Oxygenated blood —>Placenta —> Umbilical vein **—> **Right atrium ->via foramen oval -> Left atrium -> left ventricle —>body
    -Lungs get bypassed
  3. Birth : Septum seconded and septum primum fuse and close off foramen oval
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Atrial septal defect : Pathophysiology of development

A

Atrial septal defect - the foramen ovale does not close after birth
* Blood shunted : Left atrium -> Right atrium
* Oxygenated blood enters pulmonary circulation } TWICE

-Most cases caused by ostium secundum (second opening) not closing fully

-Down’s syndrome : Osmium Primum not closing fully

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Atrial septal defect : Risk factors

A
  1. Down’s syndrome
  2. Fetal alcohol syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ASD : Murmur

A
  1. ‘splitting S2 sound’ + systolic murmur }
  • Increased blood volume entering the right side of the heart
  • Delays pulmonary valve close
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ASD : Complication

A

Embolism : if reaches the heart by travel via the ASD and enter systemic circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

VSD : definition

A
  • Ventricular septum gap between Right and Left ventricle
  • Most common congenital defect in babies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

VSD : Risk factors

A
  1. Fetal alcohol syndrome
  2. Down’s syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

VSD : Pathophysiology

A
  1. Oxygenated blood shunted from high to low pressure
  2. Left ventricle -> Right ventricle
  3. Oxygenated blood travels through pulmonary circulation } TWICE via ventricle septal defect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

VSD : Murmur

A

Murmur : Holosystolic murmur lower left sternal border

Cause : Left to right shunting of blood - leads to volume overload and increased blood flow leads to
Turbulence and vibration through the systolic phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

VSD : Complication

A
  1. Pulmonary hypertension
  2. Eisenmenger’s syndrome : Increase in RV pressure 2nd to pulmonary hypertension, shifts pressure gradient, thus shifting direction of blood shunting
    * Right —> Left } by passing oxygenation via lungs
    * Hypoxic blood circulated
    * Cyanosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Patent Ductus arteriosus : Risk factors

A

Congential rubella syndrome - Maternal infection of rubella in the first trimester

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Patent Ductus arteriosus : Definition

A
  1. Ductus arteriosus : connects Pulmonary artery to the Aorta on the aortic arch during fetal development
  2. Remains open after birth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Patent Ductus arteriosus : Normal foetal physiology of circulation

A

1. Ductus arteriosis function in utero; shunts oxygenated blood that doesn’t pass through the foramen ovale

2. Placenta -> ulmbilical vein -> right atria -> Right ventricle -> Pulmonary artery
-> Ductus arteriosus -> Aorta -> circulation
* Hence - bypassing the lungs

3. Ductus arteriosis closes after birth due to drop in prostaglandins

4. Becomes ligament - ligament arteriorsum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Patent Ductus arteriosus : Pathophysiology

A
  1. After birth; Remains open
  2. Shunts Aortic (oxygenated) blood back into the Pulmonary artery
  3. Enters pulmonary circulation } TWICE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Patent Ductus arteriosus : Complications

A
  1. Pulmonary hypertension } increased volume of blood in RV and pulmonary circulation
    Can lead to
  2. Eisenmenger’s syndrome :
    * RV pressure > LV pressure 2nd to Pulmonary HTN
    * Reverses shunt : RV —-> LV - Bypassing lungs
    * Hypoxic blood enters systemic circulation

3 . Cyanosis in lower extremities :
* Sx confined to lower extremities as PDA connects to the aortic arch below the arteries which supply the upper extremities e.g. head, arms etc

15
Q

Patent Ductus arteriosus : Management

A
  1. Indomethasin / ibuprofen (NSAID)
    * Inhibits prostaglandin release -> Closes PDA
  2. Prostaglandin E1: keeps PDA patent if mixing of blood is amenable in the context of another coexistent cyanotic congenital heart disease.
16
Q

Patent Ductus arteriosus : Clinical signs

A
  • Continuous ‘machinery’ murmur

-Due to continous shunting of blood between Aorta and Pulmonary artery throughout the cardiac cycle, turbulence of blood flow due to pressure gradient

  • Wide pulse pressure }

-2nd to increased stroke volume of the LV due to shunting increasing blood flow in the pulmonary artery
-Reduced peripheral resistance : runoff of aortic blood to the pulmonary artery
- Thus difference between systolic vs diastolic BP

  • Large volume, bounding, collapsing pulse
    -Wide pulse pressure and increased stroke volume
  • heaving apex beat
17
Q

Coarctation of the Aorta : Definition

A
  1. Narrowing of the aorta - after the aortic arch in infants
  2. Patent Ductus Arteriosus - just below level of coarctation
18
Q

Coarctation of the Aorta : Pathophysiology

A
  1. ‘Pre-ductal coarctation’
    Narrowing of the aorta : after the aortic arch
    Upper extremity circulation : unaffected as arteries are upstream from narrowing
  2. Patent ductus arteriosus
    * Connects to Aorta just after coarctation/narrowing
  3. Coarctation reduces Aortic Pressure
    * Narrowing of the aorta : reduces the blood volume and slows it down
  4. Pressure in Pulmonary artery > Pressure in Aorta post coarctation
  5. Deoxygenated blood from Pulmonary artery-> via ductus arteriosus -> Aorta -> Lower extremities circulation
    ( Bypassing lungs)
19
Q

Coarctation of the Aorta : Clinical features

A

Cyanosis in lower extremities - present at birth

20
Q

Coarctation of the Aorta : Risk factor

A

Turner’s syndrome - strong association

21
Q

Tetralogy of Fallot

A
  • Congential heart condition with 4 main abnormalities ; Narrowing of the RV outflow causes RV hypertrophy**
    Also; **
    VSD with the Aorta over arching it
  • Most common form of cyanotic heart condition
22
Q

Tetralogy of Fallot : Pathophysiology

A
  1. Stenosis
    Narrowing of the Right Ventricular outflow tract
    -The pulmonary valve
    -Narrowing of the infundibulum - the area below the pulmonary valve
    -> Harder for deoxygenated blood to enter the pulmonary circulation
  2. Hypertrophy of the Right ventricle
    -Myocardium contracts harder to push blood past the stenosis
    -> ‘Boot shaped’ on X-ray
  3. Large VSD -
    -Gap between ventricles which allows shunting of blood between them
    -> RV obstruction causes : RV pressure > LV pressure
    * Right (deoxygenated blood ) -> Left (Systemic circulation) shunt
  4. Aorta : Override ventricular septal defect**
    -May appear on right side of the heart

*The severity of symptoms depends on the degree of right outflow obstruction *

23
Q

Tetralogy of Fallot : Risk factors

A

Chromosome 22 deletion and di George syndrome

24
Q

Tetralogy of Fallot : Clinical symptoms

A

1 . At Birth : Cyanosis of lips and finger nails
* A few months : Clubbing of fingers and toes within months

2 . Episodic ‘Tet’ spells -
* Increase in activity -> increases CVS workload -> R-L shunt increases -> sudden increase in cyanosis due to prevalence of deoxygenated blood
* Often - sit down to squat during these spells
* Which increases peripheral vascular resistance thus increasing pressure L> R side of the heart

25
Q

Tetralogy of Fallot : Clinical signs

A
  • Ejection systolic murmur due to pulmonary stenosis
26
Q

Tetralogy of Fallot : Investigation

A
  1. Chest x-ray: shows a ‘boot-shaped’ heart - due to RV hypertrophy
  2. ECG shows right ventricular hypertrophy
27
Q

Tetralogy of Fallot : Management

A
  1. Surgical repair
28
Q

Transposition of the great arteries : Pathophysiology

A
  1. Left ventricle is connected to the pulmonary artery which takes it to the lungs
  2. Right ventricle is connected Aorta which takes it to the systemic circulation
  3. Two separate systems and blood does not mix
  4. In Utero - asymptomatic as lungs are not being used and shunts are available to allow mixing of blood
  5. At birth - Non survivable
    Unless there is a septal defect which allows for two circuits to mix
29
Q

Transposition of the great arteries : Complication

A

RV hypertrophy and LV atrophy } congestive heart failure

30
Q

Transposition of the great arteries : Risk factors

A

Diabetic mothers

31
Q

Transposition of the great arteries : Clinical features

A
  1. Cyanosis
  2. Tachypnoea
32
Q

Transposition of the great arteries : Clinical signs

A
  1. loud single S2 :
33
Q

Transposition of the great arteries : Investigation

A

Chest X-ray : ”Egg-on-Side” Appearance
* Abnormal cardiac silhouette : Right-sided bulge created by the aorta contributes to the larger, rounded aspect resembling the “egg,” while the left side appears narrower.

34
Q

Transposition of the great arteries : Management

A
  • Maintenance of the ductus arteriosus with prostaglandins
  • Surgical correction is the definite treatment.