week 6 Flashcards
Cardiovascular problems - distal impacts
- growth and development
- learning
- cognitive function
Anatomy of the heart - pathway of blood through the heart
- superior vena cava, inferior vena cava (deoxygenated)
- right atrium
- tricuspid valve
- right ventricle
- pulmonary artery
- lungs
- pulmonary veins (oxygenated)
- left atrium
- mitral valve
- left ventricle
- out aortic valve
- to the body
blood flow in utero
- placenta helps facilitate blood flow
- umbilical vein - provides O2 blood into superior vena cava via ductus venosus
- O2 blood mixes with deoxygenated blood –> heart –> septum bipases non aerated blood into left atrium and left ventcicle
- umbilical arteries take deoxygenated blood from aorta
Blood moves through the body…
by pressure (blood moves away from pressure)
Fetal structures of cardiovascular (3)
- foramen ovale
- ductus arteriosus
- ductus venosus
Foramen ovale
small hole between R and L heart
allows oxygenated blood to the left side of the heart
Ductus arteriosus
connects pulmonary artery to aorta
shunts deoxygenated blood from RV to descending aorta bypassing nonaerated lungs
Ductus venosus
shunts oxygenated blood from umbilical to Inferior vena cava bypassing the liver
Causes of congenital heart disease
cardiac development begins on 18th day of life, completed by 45th = environmental influences during this time
- 90% are multifactorial causes (genetic and environmental)
Gestational and perinatal history - cardiac (2)
maternal infection
maternal medications
Gestational and perinatal history - cardiac - maternal infection (2)
- rubella in 1st trimester
- HIV in late pregnancy
Gestational and perinatal history - cardiac - maternal medications (2)
- amphetamines
- phenytoin/progesterone/warfarin/valpro acid
Cardiovascular assessment - respirations (3)
- rate depth effort
- dry unproductive cough presence
- mild/moderate/severe WOB
Cardiovascular assessment - pulse (2)
- rate rhythm quality
- compare pulse sites (upper/central/lower extremities)
Cardiovascular assessment - blood pressure (2)
- is it within normal range for age
- compare upper and lower extremities
Cardiovascular assessment - colour (4)
- pale/dusky/cyanosis (blue better than grey)
- compare colour in peripheral and central locations
- does crying help or worsen the colour
- pulse ox
Cardiovascular assessment - cap refill
press 3 seconds come back in 3 seconds
pulse assessment - babies
brachial pulse is easiest
dorsal foot
femeral
Cardiovascular assessment - heart auscultation (4)
- auscultate for heart sounds, quality, loud/soft, distinct/muffled
- any extra heart sounds
- normal is S1 (lub) S2 (dub)
- S3S4 abnormal
- murmurs abnormal (location radiation timing
quality)
Cardiovascular assessment - fluid status
- edema (periorbital, facial, peripheral)
- abdominal distension
- palpate liver for hepatomegaly (liver margin)
- monitor I/Os for fluid status
- cap refill (press 3 seconds comes back 3 seconds)
Cardiovascular assessment - activity and behaviour
exercise intolerance
Increased pulmonary blood flow - types of defects (3)
- patent ductus arteriosus
- arterial septal defect
- ventricle septal defect
Increased pulmonary blood flow - clinical manifestations (8)
- tachypnea
- tachycardia
- murmur
- congestive heart failure
- poor weight gain
- diaphoresis
- periorbital edema
- frequent respiratory infections
Decreased pulmonary blood flow - types of defects (4)
- pulmonary stenosis
- tetralogy of fallot
- pulmonary atresia
- tricuspid aterisia
Decreased pulmonary blood flow - clinical manifestations (4)
- cyanosis
- hypercyanotic episodes
- poor weight
- polycthemia
Obstructions to systemic blood flow - types of defects (5)
- coarctation of aorta
- aortic stenosis
- hypoplastic left heart syndrome
- mitral stenosis
- interrupted aortic arch
Obstructions to systemic blood flow - clinical manifestations (5)
- diminished pulses
- poor colour
- delayed cap refill
- decreased U/O
- congestive heart failure may occur with pulmonary edema
Mixed defects - dependent on the mixing of pulmonary and systemic blood - types of defects (4)
- transposition of great arteries
- total anomalous pulmonary venous connection
- truncus arteriosus
- double outlet right ventricle
Mixed defects - dependent on the mixing of pulmonary and systemic blood - clinical manifestations (4)
- cyanosis
- poor weight gain
- pulmonary congestion
- congestive heart failure may occur with increased shunting
Arterial septal defect (ASD) - what
- 5-10% of defects
- more in females
- sometimes late presentation - 5 years
- septum formed weeks 4-6
- before birth patent foramen ovale
Arterial septal defect (ASD) - pathophysiology
- at birth, left atrium pressure elevates and closes patient foramen oval
- if it doesn’t close, there is a L to R shunt
- RA dilation
- RV volume overload
- increase fluid to lungs
larger ASD = bigger flow = worse syumptmos
Arterial septal defect (ASD) problems
- Right atrium dilation
- right ventricle volume overload
- increase flow to lungs
Arterial septal defect (ASD) - larger ASD
bigger asd = bigger flow - worse symptoms
Arterial septal defect (ASD) - pressure
- pressure from left to right = blood stays in pulmonary circulation
- decreased perfusion to rest of body
Arterial septal defect (ASD) - clinical presentation (4)
- usually asymptomatic
- may present with congestive heart failure (5% <1 year…. cardiomyopathy, failure to thrive, Afib
- pulmonary edema (rarely pulmonary hypertension)
- may lack symptoms until late teens (fatigue SOBOE)
Arterial septal defect (ASD) - management
- 87% close spontaneously by 1 year
- congestive heart failure = digoxin, diuretics, fluid restriction
- cath lab closure (umbrella type device)
- surgical (stitch closure or patch)
Arterial septal defect (ASD) - complications (5)
- sinus node dysfunction
- 1st degree heart block
- bleeding
- tamponade
- residual shunts
Ventricular septal defect - what
- most common - 20% of defects
- mostly males
- Downs syndrome and other trisomies
- isolated defect
- associated with simple defects - ASD, patent ductus arteriosus
- associated with complex defects - TGA, TET, Truncus, DORV
- more pressure involved**
Ventricular septal defect - diagnosis (how and type)
- echo/ultrasound determines diagnosis and severity
- septum develops 4-8 weeks gestation
- birth = no shunting due to equal pressures of RV and LV
- 4-6 weeks significant L to R shunt
- perimembraenous - right below aortic valve
- muscular (swiss cheese closer to apex)
Ventricular septal defect - size and effect
- pinpoint to large
- 50% close by 2 years spontaneously
- L to R shunt
- smal defect = asymptomatic, large shunt - increased pulmonary vascular resistance
Ventricular septal defect - increased pulmonary vascular resistance (2)
- high flow
- increased pressure –> hypertrophy of pulmonary vessels
Ventricular septal defect - pathophysiology - how it causes damage
- increased pulmonary flow = pulmonary edema (high PVR, RV hypertrophy, LA dilation, LV volume overload
- ay be asymptomatic until 6 weeks when pulmonary vascular resistance (PVR) drops
- after 2-3 PVR les than systemic
Ventricular septal defect - development through childhood (4)
- small VSD may go undetected till pre school
- small restrictive - pressure gradient - loud murmur during systole
- 80% close spontaneously
- pulmonary vascular obstructive disease in 15% by age 20 (large VSDs)
Ventricular septal defect - management for small shunt
- asymptomatic =
- conservative
- closes spontaneously at 1 year of life
Ventricular septal defect - management for moderate shunt
- digoxin
- diuretics
- fluid restriction
Ventricular septal defect - management for severe shunt
- surgery recommended early
- suture or patch repair via right atrium
Ventricular septal defect - congestive heart failure symptoms
- feeding difficulties
- fatigue
- dyspnea, tachypnea, grunting
- pulmonary hypertension
- increased respiratory infections
- FTT
Patent ductus arteriosus - what (fequency, sex, risks, comorbidities, size)
- 10% of defects
- more in females
- maternal rubella, prematurity
- 15% associated with VSD, coarction of A
- connects the aorta to the pain Pulmonary Artery at its bifurcation
- approx. 1cm by 1cm
Normal development of Patent ductus arteriosus (4)
- birth = breathing increase in PO2
- begins closing within 10-15 hours of birth
- constricts by 24-72 hours
- structural closure 2-3 weeks
- fibrosed at 12 weeks
Patent ductus arteriosus - why it remains open (5)
- premature
- hypoxia
- scaring of ductus due to rubella
- acidosis
- PGE’s (we want it to stay open)
Patent ductus arteriosus - pressure
- blood shunts from aorta to lungs
- L to R shunt = pulmonary over circulation (LA dilation, LV hypertrophy, recirculates to left, volume loads LV
Patent ductus arteriosus - large
- congestive heart failure, cardiomegaly
- apnea, resp failure, recurrent infections
- systolic murmur at LT sternal border
- bounding peripheral pulses, wide pulses pressures with large PDAs
Patent ductus arteriosus - management
- CHF -> diuretics, fluid restriction, digoxin
- advil = PGE inhibitor –> close shunt
- surgical - suture ligation via L thoractomy, coil catheterization
Patent ductus arteriosus - diagnosis
- echo - size, progression etc.
Atrial ventricular septal defect - what
- 1-2% of all defects
- insufficiency of AV valves burdens the RV
- more common in downs syndrome
Atrial ventricular septal defect - types
- incomplete
- complete
Atrial ventricular septal defect - incomplete
- 2 seperate AV valves, often with a cleft mitral valve
Atrial ventricular septal defect - complete
common AV valves (5 leaflets), ASD and VSD
Atrial ventricular septal defect - shunting (4)
- atrial level is a L to R direction (LV to RA, incompetent mitral and tricuspid valve)
- L to R shunt to PVR drops so increased PVR over time
- risk of pulmonary vascular obstructive disease by 1 year
- shunt depends on : size of defect, PVR, AV valve competency
Atrial ventricular septal defect - volume load
- loads right and left side of heart
- CHF around 1-2 months, pulmonary hypertension, FTT
- varying degrees of AV regurgitation (BAD, not getting closing of valves = leaking and back up and fluid retension)
Atrial ventricular septal defect - ventricle sized
- balanced
- unbalanced
Atrial ventricular septal defect - balanced
- ventricles of equal size
Atrial ventricular septal defect - unbalanced
one ventricle larger than the other
Atrial ventricular septal defect - management (2)
- digoxin and diuretics
- antibiotics to prevent endocarditis
Atrial ventricular septal defect - surgery (complete vs incomplete)
- 3-6 months for complete AV
- 1-2 years for incomplete
Atrial ventricular septal defect - incomplete surgery
- patch ASD and suture cleft in the mitral valve
Atrial ventricular septal defect - complete
- pericardial patch repair of ASD and VSD and repair of cleft mitral and tricuspid valves (1 or 2 patch repair)
Atrial ventricular septal defect - post op
- push volume slowly, use of inotropes
- at risk for heart block, pulmonary edema, poor function
Right ventricular outflow tract obstructions
not getting oxygen or blood to pulmonary system
ex - tetralogy of fallot
Tetralogy of Fallot (4)
- pulmonary artery obstruction
- overriding aorta
- VSD
- right ventricular hypertrophy
- worse with crying (increases PVR –> Ted spells = purple)
Intervention for ted spells
put knees to chest
Left ventricular outflow obstructions example
- coarctation of the aorta
Coarctation of the aorta
- picked up in utero or at a well baby clinic (as decreased PVR starts)
- easily missed early on, picked up later
- decreased cap refil and pulse to feet
- gradient between BP in preductal (right arm) and postductal (legs)
- PGEs to keep duct open, two IVs at all times, then surgery, balloon dilations (cath lab)
Kawasaki’s disease - what (3)
- leading cause of aquired heart disease
- most children who contract illness are less than two years, 80% less than 5
- a generalized vasculitis of unknown etiology (attack coronary arteries)
Kawasaki disease - complications (7)
- coronary artery abnormalities (coronary aneurisms)
- 25% if untreated….
- may resolve or persist
- may lead to thrombosis
- evolve into segmental stenosis (narrowing)
- or rarely rupture
- cause of death = myocardial infarction
Kawasaki disease - child presentation
child is always miserable = keep them calm
Kawasaki disease - primary diagnosis criteria (3)
- fever persisting at least 5 days
- fever generally high and spiking (often to 40º)
- persists in untreated patients for one to two weeks or longer
Kawasaki disease - patient population
- Japanese descent
- typically male
- COVID –> MISC have similar findings
Kawasaki disease - presence of (5)
34
Kawasaki disease - diagnosis criteria (5)
4 of 5 of the following
- polymorphic exanthem (~5 days after fever onset)
- bilateral conjunctival injection
- changes in lips and oral cavity
- Desquamation of the fingers and toes (1-3 weeks after fever onset)
- cervical lymphadenopathy
Polymorphic exanthem
skin eruption of the trunk and extremities (several forms)
rash usually appears within five days of fever onset
Bilateral conjunctival injection (5)
- bulbar conjuntivae involved
- limbic region spared
- not usually associated with exudate
- usually painless
- aka redness of the eyes
Kawasaki disease - changes in lips and oral cavity (3)
- strawberry tongue
- redness and cracking of lips
- erythema of oropharyngeal mucosa (no ulcerative lesions)
Desquamination of fingers and toes
- acute distinctive changes in extremities (redness, swelling, induration of hands and feet)
- 1-3 weeks after onset of fever
- approx. 1-2 months after fever onset Beau’s lines (white lines on fingernails) may appear
beau’s lines
white lines on fingernails
Cervical lymphadenopathy (3)
- at least one lymph node with diameter of 1.5cm or greater
- usually unilateral
- firm and slightly tender nodes
Kawasaki disease - cardiac investigation findings
- pancarditis (esp coronary arteries)
- pericardial effusion (spontaneous resolve)
- myocarditis +/- CHF
- coronary artery abnormalities in 20-25% of patients
- diffuse ectasia or coronary aneurisms
Kawasaki disease - non-cardiac investigation findings (not including labs = 2)
- often very irritable
- arthritis and arthragia (first 2-3 weeks at knees ankles hips)
Kawasaki disease - non-cardiac investigation findings - Labs (7)
- elevated CRP
- elevated WBC >15,000,
- normocytic, normochromic anemia (normal number not normal amount at maturity)
- platelets >450,000, p
- pyuria (WBC in urine)
- ALT >50
- albumin <3
Kawasaki disease - treatment (6)
- not treated in 10 days, pts under 1yr have increased risk of coronary artery aneurisms
- initial therapy = reduce fever and inflammatory features
- treatment = helps prevent coronary artery abnormalities and myocardial ischemic injury
- Long term therapy = avoiding coronary thrombosis (prevent platelet aggregation)
- give an IVIG - antibodies to IV
- high dose asprin orally (prevents platelets) first dose, lower for 6-8 weeks
ECG’s - what they show (8)
- HR and rhythm
- abnormalities of conduction
- muscular damage (ischemia)
- hypertrophy
- bundle branch blocks
- electrolyte balance
- drug effects
- pericardial disease
SA node
primary pacemaker, initiates impulses
AV node
secondary pacemaker, conducts impulses
Bundle of His
purkenje cells rapidly impulse transmission
Purkenje fibres
rapid ventricular spread
Conduction (5) - ECG
P-wave
PR interval
QRS
ST segment
T wave
P-wave
contraction and depolarization of aorta
PR interval
spread and delay of electrical impulse form SA node to AV node
QRS
ventricular depolarization
ST segment
baseline
T wave
ventricular repolarization
Normal sinus rhythm - origin
SA node
Normal sinus rhythm - rhythm
regular +/-10%
Normal sinus rhythm - rate
- P to P
- R to R
Normal sinus rhythm - P waves
- present upright and uniform
- 1:1 conduction
Normal sinus rhythm - PR interval
constant within age related norms
Normal sinus rhythm - QRS
narrow, age related norms
QRS complexes are identical
Sinus bradycardia - rate
less than 80 bpm in newborns
less than 60 bpm in children
Sinus bradycardia - effect
rate dependent
- may decrease CO (low BP, dizzy, weak, decreased LOC, syncope, pale, underperfused)
Sinus bradycardia - cause (7)
- athletes
- electrolyte imbalances (hypokalemia)
- vagal stimulation
- hypoxia
- drugs (beta blockers, digoxin, etc)
- hypothermia
- increased ICP
Sinus bradycardia - treatment
- none, or treat the cause
- oxygen
- chest compressions for HR less than 60 bpm-
- meds = epinephrine, atropine
- pacing (transthoracic, transcutaneous, transesophogeal)
Types of bradycardias (4)
- sinus bradycardia
- nodal (junctional) rhythm
- second degree AV block
- third degree AV block
Sinus bradycardia - origin
SA node
Sinus bradycardia - rhythm
regular
Sinus bradycardia - rate
slower than normal for age
Sinus bradycardia - PR interval
constant, age related norms
Sinus bradycardia - QRS
narrow, age related norms
Sinus bradycardia 0 p waves
present upright and uniform, 1:1 conduction
bradycardias - general causes (2)
suppressed automaticity or conduction
bradycardias - impacts (6)
- decreased CO
- decreased BP
- decreased LOC
- increased tissue hypoxia
- increased anaerobic metabolism
- increased acidosis
Causes of bradycardias - specific (8)
- hypoxia
- SA node dysfunction
- heart block
- acidosis
- hypothermia
- increased vagal tone
- hyperkalemia
- drugs (digoxin)
Sinus tachycardia - rate
> 160 bpm in infants (usually lower than 200)
140 bpm in children
Sinus tachycardia - effect (2)
poor coronary filling, fatigue of myocardium
Sinus tachycardia - causes
- small stroke volume (tamponade, shock, CHF, hypovolemia)
- symptomatic stimulation (pain anxiety infection exercise, respiratory failure, myocarditis/pericarditis, fever, drugs, anemia, cardiac disease, shock
Sinus tachycardia - treatment (2)
treat cause
- if CO compromised = Digoxin, Ca channel blockers, beta blockers
Types of tachycardia (5)
- sinus tachycardia
- supraventricular tachycardia (SVT)
- ventricular tachycardia (VT)
- Atrial fibrillation (Afib)
- Atrial flutter
Sinus tachycardia - origin
SA node
Sinus tachycardia - rhythm
regular
Sinus tachycardia - rate
p to p (age related norms
Sinus tachycardia - R to R
faster than normal
Sinus tachycardia - p wave
present upright uniform
1:1 conduction
Sinus tachycardia - PR interval
constant age related norm
Sinus tachycardia - QRA
narrow, age related norms
Tachycardias - impacts (7)
- decreased cardiac filling time
- decreased stroke volume
- increased O2 demand
- decreased coronary artery diastolic filling time
- decreased BP
- increased hypoxia
- increased acidosis
Tachycardias - causes (7)
- congenital
- idiopathic
- drug toxicity
- surgical
- hypoxia
- acidosis
- infectious and inflammatory
SVT - what
rapid rate with normal QRS
- infants HR >220 bpm
- children HR >180 bpm
SVT - P waves
- may be buried in previous T wave and not visible
- not a rounded smooth sinus p wave
SVT - causes (9)
- fever
- catecholamines
- congenital heart disease
- cardiac surgery
- CHF
- hypoxia
- infection
- electrolyte imbalance
- idopathic
SVT - origin
atria or junctional (common term)
SVT - rhythm
regular
SVT - rate
p to p but often not seen
R to R normal
SVT - p wave
present upright and different than sinus, often not seen
SVT - PR interval
constant, sometimes longer (in accessory pathways is shorter)
SVT - QRS
narrow, age related norms
SVT - treatment (3)
- vagal stimulation (coughing gagging valsava knee to chest position suction ice to face carotid sinus massage (MD))
- atrial overdrive pacing, cardioversion
- adenosine, amiodarone, procainamide
Adenosine
a drug that stops the heart momentarily
Sinus arrythmia - rate
- HR increases with inspiration
- HR decrease with expiraciton
Sinus arrythmia - effect
- sign of good cardiac reserve
- indicates heart is unger vagal contral and not sympathetic
Sinus arrythmia - causes
normal varient in young and elderly
change in respiratory cycle -= change in intrathoracic pressure and change in sympathetic tone
Sinus arrythmia - treatment
none unless due to increased ICP or respiratory obstruction
Sinus arrythmia - origin
SA node
Sinus arrythmia - rhythm
regularly irregular (fluctuates with resp cycle)
Sinus arrythmia - rate
P to P, R to R age related norms
Sinus arrythmia - p waves
present upright uniform, 1:! conduction
Sinus arrythmia - PR interval
constant, age related norms
Sinus arrythmia - QRS
narrow, age related norms
Tetrology of Fallot - etiology (3)
- multifactorial (genes and environment)
- more common in trisomy 21 and others
- advanced maternal age, alc use, poor nutrition, viral illness
Tetrology of Fallot - structural abnormalities (4)
1) VSD
2) pulmonary stenosis
3) RV hypertrophy
4) overriding aorta
Pulmonary stenosis - what
narrowing of pulmonary valve
overriding aorta - what
an exist exists above both ventrivles
Tetrology of Fallot - pathophysiology (6)
1) pulmonary stenosis = decreased deoxygenated blood into pulmonary circuit
2) increased RV pressure (increased blood volume form shunting from VSD and less exiting to pulmonary)
3) increased RV pressure –> RV hypertrophy (increased work load to pump blood past stenosis)
4) VSD causes blood to be shunted L to R (severe pulm. stenosis will cause R to L shunting)
5) overriding aorta straddles VSD (deoxygenated blood shunted from RV to exit heart via aorta from LV to systemic circulation
6) deoxygenated blood enters systemic circulation = decreased O2
Tetrology of Fallot - initial symptoms
- murmurs at left mid-upper sternal border with posterior radiation
- Pre/post ductal SpO2 (decreased blood to R hand and both feet)
- Cyanosis/Tet spell
difference in pre and post ductal SpO2
pre - left hand
post = right hand and both feet
Tet spell
when a baby with Tetrology of Fallot turns cyanotic in lips or nail beds when they cry
Tetrology of Fallot - diagnosis (3)
- chest X ray (RV hypertrophy, boot shaped heart, decreased pulmonary vascular)
- echocardiograpm (visualize 4 structural defects)
- electrocardiogram (RV hypertrophy = right axis deviation, prominant P waves = atrial enlargment)
Tetrology of Fallot - diagnosis (3)
- chest X ray (RV hypertrophy, boot shaped heart, decreased pulmonary vascular)
- echocardiograpm (visualize 4 structural defects)
- electrocardiogram (RV hypertrophy = right axis deviation, prominant P waves = atrial enlargment)
Tetrology of Fallot - nursing priorites (6)
- managing tet spells
- risk for blood clots
- risk of endocarditis
- maintaining O2
- patient family education
- fluid balacne
Tet spell - Assessment findings (3)
- SpO2 - drastic decrease
- Respirations - increase in rate and depth
- skin colour - may appear cyanotic
Tet spell - treatment (6)
- knee to chest position (increase systemic vascular resistance= increased blood to lungs)
- administer o2
- IV fluids - improve preload and pulmonary blood flow
- narcotics
- beta blockers*
- vasoconstrictors*
Endocarditis (Tetrology of Fallot) - assessment findings (5)
- elevated WBC (if infection is cause)
- Anemia
- increased temp, respiratory rate, pulse
- blood culture positive
- chest x ray = heart inflammation
Endocarditis (Tetrology of Fallot) - treatment (3)
- prophylactic antibiotic treatment
- health teaching on aseptic techniques
- extra caution surrounding high risk procedures (ex dental surgery)
Tetrology of Fallot - treatment options (3)
- non-surgical (rare)
- palliative surgery
- complete surgical repair
Tetrology of Fallot - non surgical treatment (3)
- manage symptoms
- poorer outcomes or death
- will need surgery by 6 months to 1 year (not sustainable)
Tetrology of Fallot - palliative surgery (3)
- less invasive surgery, not open heart
- small tube placed between aorta and pulmonary artery to provide blood flow to lungs
- allow babies to grow strong enough for a complete surgical repair later
Tetrology of Fallot - complete surgical repair
- open heart surgery
- close VSD with patch, open obstructed pathway between RV and pulmonary artery
- most often done before an infant 1 year old
- prognosis excellent, following cardiologist necessary
Tetrology of Fallot - medication spotlight
- antibiotics
- narcotics
- beta blockers
- digoxin
- loop diuretic
coarctation of the aorta
present at birth
- narrowing or constriciton of descending aorta by a ridge formed by thickening of medial wall, tissues of aortic wall folding in
coarctation of the aorta - pathophysiology
- narrowing of aorta –> LV working harder to pump blood through body
coarctation of the aorta - severe narrowing symtoms (7)
- tachypnea
- problems eating (poor weight gain)
- irritability
- sleepiness and lethargy
- generalized mottling
- pale or gay skin colour, cyanosis
- heart failure and shock
coarctation of the aorta - mild symptoms (7)
- chest pain
- cold feet/legs
- dizziness, faintness
- decreased stamina
- poor growth/failure to thrive
- pounding headache
- SOB-
- can be asymptomatic
coarctation of the aorta - diagnosis
- echocardiogram
- chest X ray
- ECG
- CT scan
- CT angiogram
- MRI
- hyperoxia
- 4 limb BP
- blood tests
coarctation of the aorta - surgery
- interposition graft
- end-to-end anastomosis
- patch augmentation
- subclavian flap repair
- ascending to descending aorta bypass graft
- balloon angioplasty
- transcatheter stent therapy
coarctation of the aorta - other interventions (non surgical) (3)
- antihypertensives
- vasodilators
- promoting healthy lifestyle/preventing complications
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