patent ductus arterioSUS
name the average time for this to close
immediately or a few days after birth
dietary changes when on loop diuretics
eating foods that contain potassium (bananas, spinach), & hydration status = maintain electrolyte balances
describe a tet spell
little blood flow going out of pulmonary artery, less blood to oxygenate, this worsens during activity
(eating or playing), need more oxygen, can’t do it because they can’t force the blood flow (more cyanotic/hypoxic)
what type of flow problem is occurring here? try to explain what's happening.
obstruction of blood flow out of the heart, narrowing of the aorta creates a pressure point of blood flow of the L side of the heart, elevated pressure before the narrowing
describe what is happening with this
the aorta and pulmonary have completely switch places & connect to the wrong ventricles SO there is a recirculation of blood between pulmonary and systemic that is not passing through (without a septal defect, no blood mixing occurs) but there usually is so it would cause SOME
if the pulmonary pressure is high, what kind of shift will occur, & what kind of flow is increased EXPLAIN
a L to R shift, increased pulmonary blood flow
name complications of rheumatic fever and what causes it?
group strep A: bacteria migrates to joints, skin, brain, and heart = causing valvular damage & manifests as swollen & painful joints, weakness, a pink rash on the trunk & extremities, cariditis (chest pain, murmur, tachycardia, decreasing activity intolerance (HF)
what two things in the heart would be beneficial for this condition and why?
PDA or PTT shunt (allow oxygenated blood flow back into the lungs, even though it would be some mixed blood, it would increase the volume of blood into the lungs and throughout the body = overall increase oxygenation)
what would this manifest as that is a hallmark to this defect
high BP on arms than legs
signs you would see with this
hypoxia/respiratory depression/cyanosis (life-threatening)
what will atrophy from a L to R shift
R side, L will have an elevated preload from increased pulmonary circulation
what is the rationale for using a blaylock-taussig-thomas shunt?
takes a branch off the aorta, to allow blood flow to go from the aorta to the pulmonary artery (the larger more stable vessel that won’t close)
list the 4 defects
Pulmonic stenosis (not allowing a lot of blood flow to the lungs)
Overriding aorta (fills the hole - predisposed for blood to go into it)
Ventricular septal defect (a hole in the ventricle, mixed blood into aorta)
Right ventricular hypertrophy (RV is pumping against resistance of stenosed pulmonary valve = R→L shunt)
POV Right??
what will eventually occur from this condition (related to anatomy of the heart)
L ventricle will hypertrophy due to pumping against resistance
if a septal defect was present with this condition, what condition would present and why?
HF (from increased pulmonary pressures= ventricular hypertrophy)
how is a PDA kept open? why would it need to stay open
prostaglandins, might need to re-oxygenate/mix blood if another defect is present
define pulmonary hypertension & what us leads to:
paired with a lot of the defects, any resistance that is added to the lungs makes it difficult to oxygenate (usually not resistant)
leads to exercise intolerance, shortness of breath, chest pain, and syncope
explain how a child would handle a tet spell and why they are doing it?
By bending their knees, that increases pressure on lower half on descending aorta, so has to pump with resistance against pressure through aorta, it would back up to meet that resistance (where the ventricular septal defect is) = it will be easier to go out the pulmonary valve = increase blood flow to the lungs, more blood getting oxygenated (even if it's mixed blood)
other signs and symptoms of COA that don't involve BP
HA, epistaxis, & fainting from HTN
how quickly does this need to be managed and how could it be done appropriately? why would this be appropriate?
immediately - keep the DA open on a continuous prostaglandin drip until further treatment is done, allows mixed oxygenated blood flow (better than none at all)
what causes this to happen and what negative effects can this cause?
can cause pulmonary HTN from blood flow in the lungs, but not as symptomatic, some oxygen going to lungs = may feel hyper-oxygenated, might hear a machine-like murmur from blood going into opening
what are the RF for infective endocarditis (infection in the inner lining of the heart or valve) & how can it be prevented?
prevention: prophylactic antibiotics (penicillins) before dental procedures to reduce the risk
RF: children with valvular defects, central lines
what type of flow is occurring with this defect?
decreased pulmonary blood flow
treatements? maybe?
surgical repair & manage BP
what is the surgical procedure done for this defect?
"jatene" procedure (arterial switch operation)