Cardiac Flashcards
How does ASD occur
Left to Right shunts
ASD (no association with pressure since pressure is the same in both atria, has an association with resistance)
Clinically
-Acynatic
Increased flow between R atrium & RV, there’s RA and RV enlargement.
-Fixed split second sound
-PS murmur
-TS murmur (rare)
How does VSD occur
Results from Pulmonary Vascular Resistance
-Flow from Left to right
-Acynotic
LA and LV enlarge first
-Small PSM only (pan systolic murmur)
-Medium ESM & MDM (Ejection systolic -too much blood on pulmo valve and mid diastolic- flow going over mitral valve)
-Large: Loud P2 (large volume of blood into lungs)vm
How is a VSD differ from a late VSD
With late VSd, theres increased pulmonary vascular resistance
RV hypertrophy occurs (this is after LA&RA enlarges) NB it doesnt enlarge in volume just the muscle gets bigger, so big heart on CXR. Eventually blood reverses and goes to the left
Now:
Very loud P2
RV Heave in epigastrium(kids)
Irreversible PHT
How to treat/reverse a VSD
- PAB- Pulmonary artery band)
-band put around pulmonary artery increasing resistance to flow, reduction of flow and flow reverses to right.
reduction in size of heart
Features
-Mild cyanosis
-ESM (over pulmonary band)
-Single S2
-No CCF
complication: stenosis/tightening overtime
constant cyanosis
not a definitive treatment
Outline the classification of cyanotic heart defects (4)
- RV outflow obstruction
- Mixing disorders
- Mixing disorders with RV outflow obstruction
- Parallel circulation
Common causes of cardiac cyanosis (5 Ts)
1. Tetralogy of Fallot
2. Transposition of great arteries
3. Tricuspid atresia
4. Total anomalous pulmonary venous return
5. Truncus arteriosus
Tetralogy of Fallop
1. RV Hypertropy
2. Aortic overide
3. Infindibular stenosis
4. VSD
Features
-Ejection systolic murmur
-Single S2
-No RV heave
Spelling can eventually occur
May have non or mild cyanosis!
(all structural changes in the heart are due to the anterior migration of infindibular septum between main pulmonary arteries and the aorta, that causes the above 4 lesions)
Management of cyanotic heart disease
- Increase systemic vascular resistance
- Relax infundibulum
- R modified Blalock-Taussig Shunt - from R subclavian artery to the R pulmonary artery (less resistance in pulmonary so blood flows from systemic to pulmonary vessels.)
palliation till child is repaired usually after 1y/o)
Shunts clinical features: Mild cyanosis, Lateral thoracotomy scar, Shunt murmur
what is spelling
A spell is a complication of cyanotic heart disease/Tetralogy of fallop
-Life threatening even which can cause hypercyanosis and death. Sub pulmonary infindibular outflow tract muscle becomes stenosed and it contracts. Increases RV outflow tract obstruction/stenosis further and very little blood enters main pulmonary artery into lungs.
-Systemic resistance can also cause a spell if it drops a lot such as in hypovolemia or pyrexia. Pt becomes hypoxic and acidotic causing further infundibular spasm, positively feedback causing more stenosis and then more hypoxia and cyanosis.
clinical features:
-Tachypnoea
-Severe cyanosis
-Absence of ESM
-Cardiac arrest then death
what is parallel circulation
TGA - Transporsition of Great Arteries
features: LA&LV enlargement
As these are 2 separate circuits:
Incompatible with life
No murmurs
Severe cyanosis
CCF
Management of TGA
Rashkind Atrial balloon Septostomy: Enlarge the shunting between LA towards RA so blood from Pulmonary veins can go into the aorta
Catheter through from IVC into LA then move it across to RA leaving a huge shunt between LA and RA. Remove ballon and the shunt serves to increase movement of oxygenated blood from LA into RA than to aorta and the child is perfused
Done in ICU with ECHO control
Later:
2. Arterial switch or mustard operation
Features of late VSD
Loud P2
RV heave
Irreversible PHT - Eisenmenger syndrome
Pathophysiology and clinal features of Tetralogy of fallop
Tetralogy of Fallop
1. RV Hypertropy
2. Aortic overide
3. Infindibular stenosis
4. VSD
Features
-Ejection systolic murmur
-Single S2
-No RV heave
-Spelling can eventually occur
May have non or mild cyanosis!
-squarting
-dyspnoea with exertion
(all structural changes in the heart are due to the anterior migration of infindibular septum between main pulmonary arteries and the aorta, that causes the above 4 lesions)
What are the hypercynotic spell features (pt in TOF may present with this)
Central cyanosis
Irritability
Hyperpnoea/tachypnoea
SOfter ESM (ejecction systolic murmur)
ISgns of trigger- dehydration, pyrexia
Management of Spells (from TOF)
- Keep child calm
-Sedate - Ketamine, chloral hydrate, morphine - Facemask or nasal prong oxygen
- Knee chest posture
- Fluids for IV volume expansion- Normal saline or Ringer
- Sodium carbonate
- Beta blocker - Propanolol PO, esmol IV
- DIscuss of refer urgently
If SATS nto improving
1. IIntubate and ventilate
2. Sedate/ paralysis
3. ICU admission
4. Alpha-agonists, noradrenalin or phenylephedrine
5. Surgery- Repair or Blalock Taussig shunt
