structural cardiac disorders Flashcards
ductus venosus
structure in liver which allows most blood to bypass the liver and enter directly into the inferior vena cava
foramen ovale
opening between atria allowing some fetal blood to pass from right side of heart to left, bypassing right ventricle and lungs
ductus arteriosus
between the pulm artery and aorta which allows blood to bypass the lungs and enter directly into descending aorta
which side of the heart is more oxygenated and what %
left side- blood is returning from the lungs (about 95%)
right side- (72-80%)
atria pressure
thin walled chambers, low pressure
ventricle pressure
thicker walled with high pressure
left ventricle has what
the greatest presssure because it must pump blood into the high pressure systemic circulation
what is a cardiac shunt
an abnormal blood flow through the heart or great vessle
left to right shunt
oxygenated blood flow from the left side of heart goes to the right side, going through the lungs again
right to left shunt
less o2 blood goes from the right side of the heart to the left side skipping the lungs
what is a functional murmur
usually seen with stress in children and infants, mostly normal and goes away with age, usually not of great concern
what are the causes of congenital heart defects
- alcohol, antiseizure,
- maternal rubella
3heredity - diabetic mothers
- 10x greater change of siblings have defects
- environment
atrial septal defect
Left-> right
abnormal opening between atria leading to increased pressure and o2 on right side of heart
where do most of the atrial septal defects happen
90% occure at foramen ovale
clinical mani of atrial septal defect
usually asymptomatic
may show s/s of HF
ventricular septal defect
left-> right shunt
abnormal opening between the ventricles leading to increased pressure and o2 on R side of heart (RV)
clinical mani of ventricular septal defect
- usually asymptomatic (most close spontaneously)
- may see s/s increased volume or HF on R side
- most common CHD
patent ductus artheriosus
left-> right shunt
failure of fetal structure to close after birth
blood shunted from high pressure aorta to low pressure pulmonary artery
usually closes with higher o2 levels
clinical mani of patent ductus arteriosus
may see s/s of HF or increased volume of R side
coarctation of aorta
acyanotic heart disease
narrowing of aorta
what are the two types of coarctation of aorta
- pre-ductal
2. post ductal
pre-ductal coarctation of aorta
between the ductus arteriosus and subclavian artery (most severe)
post-ductal coarctation of aorta
distal to the ductus arteriosus
clinical mani of coartation of aorta on the proximal side
increased pressure proximal to the defect causes
- high BP
- bounding pulses in upper extremities
- dizziness, headache, fainting,
clinical mani of coarctation of aorta distal
decreased blood supply distal to defect causes:
- low BP
- decreased/absent femoral pulses
- muscle cramps, cool pale extremities
cyanotic heart disease
right-left shunt
desaturated venous blood flows into the left side of the heart, bypassing the lungs because the pressure on the right side is greater than the left or the vessels are misplaced
what are the 4 defects in tetralogy of fallot
- VSD- ventricle septal defect
- pulmonic valve stenosis
- overriding aorta (shift into right ventricle)
- R ventricle hyertrophy
what are the clinical mani of tetalogy of fallot
(related to degree of pulm stenosis)
- Polycythemia
- anoxic spells
- increases systemic vascular resistance
- shunted physical growth
- murmer
- squatting
- clubbing
what all happens with the tetralogy of fallot
increased pressure in the RV leads to right ventricle hypertrophy. Pulmonary valve stenosis and open VSD lead to blood being shunted into the overriding aorta and lV
where does the pressure increase and move to in tetralogy of fallot
high pressure on right pushing to the left
why does squatting help in tetralogy of fallot
increases systemic resistance thus increasing blood flow to the lungs and increase o2 to the tissues
what are the cyanotic heart diseases
- tetralogy of fallot
2. transposition of the great vessels
what is transposition of the great vessels?
the pulm artery and aorta are flipped.
- aorta leaves the RV
- pulm leaves the LV
what must happen to people with transposition of the great vessels in order to live
must have a defect present to allow communication between the 2 circulations in order to live!
(sometimes they will make a hole)
what are the clinical mani of transposition of great vessels
(depends on size and type of associated defects)
1. cyanotic manis
Congestive heart failure:
- tachy
- tachypnea
- cardiomegaly
- helatomegly
when do infants develop S/S of transposition of the great vessels
no symptoms for first few hours until the PDA closes
what is pedicarditis
inflammation of the pericardial mem and formation of a pericardial effusion
pericarditis can be
acute or chronic
what is the cause of pericarditis
infection injury immune response, metabolic disorders neoplasms
what is the patho of pericarditis
pericardial mems become inflamed and roughened
an exudate usually developes
what are the mani of pericarditis
- sudden onset of anterior/back pain
- dysphagia (trouble swallowing)
- weakness, malaise, restlessness, anx
- fatigue, exercise intolerance
- fever, tachy
- pericardial friction rub
- cardiac tamponade (cardiac compression and decreased CO)
what is cardiomyopathies
disease of the myocardium itself affecting the pumping ability of the heart because the fibers cannot contract well
degeneration of myocardial fibers
what causes cardiomyopathies
cost are idiopathic, we dont really know
may be secondary to toxins, infections, immunological disorders, nutritional disorders (alcoholism) and genetics
what are the 3 categories of cardiomyopathies
- dilated (congestive)
- hypertrophic
- restrictive
dilated cardiomyothies
enlarged heart due to degeneration of the heart fibers, balloons out
hypertrophic cardiomyothies
VENTRICULAR septum hypertrophy, and LV hypertrophy leads to altered shape of chambers and poorly coordinated contractions
restrictive cardiomyothies
myocardial fibers become infiltrated with abnormal substances (TOXINS) causing ventricular dysfunction
doesn’t allow LV to stretch and squeeze
clinical mani of dialated cardiomyopathies
both RVF and LVF
immense cardiomegaly (large heart)
clinical mani of hypertrophic cardiomyopthies
mostly LVF
clinical mani of dilated cardiomyopathies
RVF and LVF
mani of LVF and RVF cardiomyopathies
LVF:
- DOE
- orthopnea
- fatigue
- fluid in lungs
RVF:
- liver congestion
- edema
- JVD (jugular venous congestion)
what are the causes of valve diorders
- inflammation, infections
- trauma (HTN)
- degenerative
- connective tissue disorders
stanosis (valve)
doesnt open fully
valve orifice (opening) is narrowed and constricted
flow through that valve is impeded
increases pressure and workload of the chamber that is trying to eject blood through that valve
regurgitation (incompetence, insufficiency)
valve leaflets fail to close completely
blood can leak back through the valve when it is supposed to be closed
increases volume to pump because some is coming back in
with regurgitation, what has an increases workload
increased workload of both the chamber getting more volume and chamber trying to pump out
manifestations of aortic valve stenosis
increased pressure, workload, hypertrophy of LV
narrowed pulse pressure
SYSTOLIC murmur
mani of aortic valve regurgitation
increased volume to pump
LV volume overload due to backflow
LV hypertrophy, increased LV workload
DIASTOLIC MURMUR
