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pathology - Cardio notes
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congenital heart disease and murmur
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-TGV- trunks position of greater vessels (2 closedCongenital Heart Disease loops)
-PTA - patent truncus arteriosus
-Tricuspid Atresia
There are cyanotic vs acyanotic heart disorders.
-Cyanotic
-TAPVR (total anomalous pulmonary venous return) when the pulmonary veins drains… -TOF
(Tetrology of Fallot) its not the pulmonary valve getting stenoses but ventricular muscular hypertrophy
that’s behaving like the child has pulmonary stenosis. It’s sub pulmonary stenosis because it is below the
pulmonary valve.
-causes: sub pump ovary stenosis, RVH, Override of the atrium, VSD.
-Noncyanotic heart defect
-VSD (Most common)
-ASD
-Patent Ductus Arteriosum (PDA)
The upper 1/3 of the heart is made up of Enterchromaffin (EC) cells. If EC cells are damage, VSD, ASD and
valvular heart disorders are caused.
IF the spinosum membranosusm does not form, you will get persistent truncus arteriosus.
If there is VSD or ASD there is shunting of blood from the left side to right.
Ductus arteriosus is a shunt from the aorta to pulmonary shunt. If this has not closed when the baby is born, it
is PDA.
Patent ductus arteriosum, Patent ductus
venosum, and foramen ovale are responsible
for circulation of blood in fetal life.
Alprostadil maintains the PDA post fetal life.
This still results in sinosis.
There is a minute mixing of oxygenated and
deoxygenated blood due to veins on the left
atrium that causes the oxygen saturation to go
from 100-96%.
Babies who have TAPVR are kept alive by the
ASD and VSD defects.
What is the cause? What is the Pathogensis? What is the treatment?
The treatment for a baby with a cyanotic heart defect is surgical intervention.
The treatment for non-cyanotic with PGE1 antagonists.
We hear PDA in the left clavicle region.
If the baby is born with a possible cyanotic defect, first oxygenate, if there is no improvement, do an ECG.
The most common murmur in a newborn and athletes is S3. If eventually resolves itself.
, Smaller VSDs and ASDs resolve themselves around 1-2 years of age. Larger VSDs are harder to hear and
more detrimental. Smaller VSDs are easier to hear.
.
Eisenmenger syndrome (look at videos on this. It’s a condition where the right ventricle of the heart over
powered the left ventricle and there is mixing of oxygenated blood and deoxygenated blood).
*
MitrginIVCorsic ASDI
*
*
TOF: Cyanosis is present 3-4 months later called Tet spells. ->(babies who
have tetralogy of Fallot will suddenly develop deep blue skin, nails and lips
after crying or feeding, or when agitated)
When we are hyperventilating, there is an in increase in pulmonary vascular
resistance and the blood moves to an area of less resistance pathway
which is the aorta. This deoxygenated blood mixes with the oxygenated
blood, decreasing the oxygen saturation from 97% to 80%. This causes
cyanosis.
Systolic bp correlates to cardiac output. Diastolic bp correlates to peripheral
vascular resistance.
Squatting increases peripheral resistance which directly corelates to
diastolic pressure increase-> systolic pressure (cardiac output) and a
subsequent in aortic pressures. This forces the blood to go to an area of
less resistance which is now the pulmonary artery before heading to
the lungs.
TOF mostly cause idiopathically, trisomy 23, or alcohol fetal syndrome.
needed
surgicalinnervation in the state
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