class 10 congenital heart defects, kawasaki disease Flashcards
what side of the heart is oxygenated
left
what circulatory system has the highest resistance
systemic
on what side of the heart is the pressure the highest
left
the ______ the pressure gradient the _______ the rate of flow
higher
greater
why does blood flow from high pressure to low pressure
it takes the path of least resistance
the (higher/lower) the resistance the (higher/lower) the rate of flow
higher
lower
pulmonic resistance is (less/more) than systemic resistance
less
what is preload
the amount of blood returning to the heart (the volume of blood in a ventricle before systole)
what is afterload
the amount of pressure the heart needs to exert to eject blood during ventricular contraction
what is contractility
the efficacy of the heart muscles to pump (contract)
-assessed by looking for cyanosis in extremities
what are congenital heart defects
mild to severe defects arising from abnormal formation of heart or major vessels
-50% show s&s during 1st year of life
what is stenosis
narrowing or obstruction of the valves
what is atresia
abnormal (missing/malformed) valves
mild CHD:
common
may be asymptomatic & caught later in life
moderate CHD:
may be symptomatic, will need treatment
severe CHD:
discovered in utero
needs treatment once born
maternal risk factors for CHD
-medications (warfarin, antiepileptics, oral tretinoin)
-infections/illness(rubella)
-diabetes/lupus
-alcohol/drug use
infant risk factors for CHD
high or low birth weight
genetic risk factors for CHD
specific syndromes
-family hx
inspection findings for CHD
-failure to thrive (FTT)
-cyanosis
-pallor
-chest configuration
-pulsations (in neck veins)
-respirations
-clubbing
palpation and percussion findings for CHD
-crackles
-dim peripheral pulses
-hepato/splenomegaly
auscultation findings for CHD
-HR and rhythm (murmur)
-heart & chest sounds abnormal
CXR for CHD looks for
-heart size
-pulmonary blood flow
ECG for CHD looks for
-electrical activity
-conduction abnormalities
-heart rate/rhythm
echocardiography for CHD looks for
anatomy and structure (valves)
cardiac cath for CHD looks for
-diagnostic and interventional
-pressures & saturations
-monitor for complications
pre op for cardiac cath
-HT & WT
-allergies
-baseline o2
-pulses
post op from cardiac cath
-assess site
-monitor bleeding
-pulses
-o2
-extremity assessment
-vitals Q1
-hypoglycemia d/t NPO
Acyanotic defects with increased pulmonary flow
-atrial septal defect
-ventricular septal defect
-patent ductus arteriosus
-atrioventricular canal
“A-VAP”
Acyanotic defects with obstructive ventricular flow
-coarctation of the aorta
-aortic stenosis
-pulmonic stenosis
“CAP”
increased pulmonary blood flow
-connections along the septum or great arteries -> higher left-sided pressure causes left-to-right flow (shunt)-> increasing pulmonary blood flow causing increased pressure and stress in the lungs
acyanotic defects causes shunting from:
left to right
what is patent ductus arteriosus
the ductus arteriosus connecting the aorta and pulmonary artery fails to close after birth
what is ventricular septal defect
a hole in the septum seperating the ventricles allows blood to mix
-good prognosis
-loud murmur
what is atrial septal defect
a hole in the septum between the atrias allows blood to mix
-patched in cath lab then aspirin until 6m post-op
-s3 murmur
what is atrioventricular canal defect
a defect in which there is a hole between the 4 chambers of the heart
clinical manifestations ASD/VSD
-heart failure is common (left to right shunting)
-loud murmur at base of left sternal border
-risk for infective bacterial endo carditis
what is infective bacterial endocarditis
an infection of the inner lining of the heart in the endocardium, generally involves the valves which can potentially destroy heart valves
-all children with CHD are at risk
prevention of infective bacterial endocarditis in kids with CHD
-prophylactic antibiotic 30-60 mins before and up to 2 hours after procedures (surgical, dental, invasive)
-broad spectrum (amoxicillin, ampicillin, azithromycin)
what are patho of obstructive defects
narrowed valves or vessels obstruct blood from exiting heart->increased pressure on ventricules->decreased cardiac output
acyanotic obstructive defects in CHD
-aortic stenosis (AS)
-Pulmonic stenosis (PS)
-coarctation of aorta (CoA)
“CAP”
what is aortic stenosis
narrowing of the aortic valves (triple lumen becomes double lumen)
-blood backs up into the lungs
what is pulmonic stenosis
narrowing of the pulmonic valve due to malformation
-increases pressure, dc blood to the lungs and may be cyanotic at birth
-may give IV prostaglandins to keep PDA open to dec pressure
-surgery: stent
what is coarctation of aorta
narrowing defect in aorta
clinical manifestations of coarctation of aorta
-increased BP in arms but dec in legs (will have cool and weak pulses)
-may have bounding upper pulses, headaches, nosebleeds, and inc risk for stroke
-rt side has inc pressure= enlarged liver, heart, edema, and ascites
-could be asymptomatic but cyanotic
treatment for acyanotic defects
-surgery often indicated, infants must be minimum 10lbs before surgery
-FTT is common->can takes months to have surgery
-nutrition supplementation is primary tx until big and stable for surgery
-HTN is managed with beta blockers, angiotensin converting enzyme inhibitor (ACE) but can cause renal issues & drop bp
-medical management of HF
-may need o2
what is heart failure (HF)
-results from structural or functional cardiac disorders that impair the ability of the ventricles to fill or eject blood
-defects that cause obstruction or result in increased blood volume and pressure within the heart will eventually lead to HF
heart failure is characterized by
-ventricular dysfunction
-reduced exercise tolerance
-diminished quality of life
-shortened life expectancy
clinical consequences of rt sided heart failure
-increased pressure in RA & systemic venous circulation
-hepatosplenomegaly, peripheral edema, ascites
clinical consequences of lt sides heart failure
-increased pulmonary pressure, pulmonary congestion, dyspnea, cough
-inc risk for resp infection
3 major s&s groups of heart failure manifestations
- impaired myocardial function
2.pulmonary congestion
3.systemic venous congestion
how does impaired myocardial function present
-increased heart rate (+160)
-gallop on ascultation
-diaphoresis
-irritable
-FTT
-dec CO
-pallor
how does pulmonary congestion present
-difficulty expanding lungs
-inc resp (+60)
-SOB
-nasal flaring
-hypoxemia/cyanosis
-costal retractions
-inc metabolic demand=FTT
-orthopnea->HOB elevated
how does systemic venous congestion present
-rt sided failure
-hepatomegaly
-generalized edema
-ascites
-weight gain (early sign)
-distended neck veins
goals of treatment for CHD
-improve cardiac function (inc contractility and dc afterload) (digoxin, ACE inhibitors, beta blockers
-remove accumulated fluids and sodium (diuretics)
-decrease cardiac demands
-improve tissue oxygenation/decrease oxygen consumption
-dec stimuli in room, warm room,
medications for chronic heart failure
-digitalis
-angiotensin converting enzyme (ACE) inhibitors (dec afterload=dec BP. dc urine output d/t renal damage)
-beta blockers
-diuretics
digitalis toxicity s&s
-do not give to babies w heart rate less than 90-110 or kids less than 70
-EKG monitor
-dec heart rate
-nausea
-given in Mcg not Mg or babies
nursing considerations for HF
-possible fluid and sodium restriction, K + supplementation
-provide neutral thermal environment
-reduce work of breathing (o2, positioning)
-minimize rest, promote rest
-prevent/tx infections
-prevent skin breakdown from edema
cyanotic defects that decrease pulmonary flow
-tetralogy of fallot
-tricuspid atresia
cyanotic defects that mixes blood flow
-transposition of the great arteries
-total anomalous pulmonary venous return
-truncus arteriosus
-hypoplastic left heart syndrome
patho of decreased pulmonary blood flow
obstruction of blood flow-> decreased pulmonary blood flow-> increased pressure on the right side of heart-> right to left shunt
what is a tricuspid atresia (TA)
underdeveloped valve leads to underdeveloped right ventricle (no right valve)
what is tetralogy of fallot (ToF)
4 defects: Ventricular septal defect, pulmonic stenosis, aorta overriding ventricular septal defect, right ventricle hypertrophy
clinical manifestations in tetralogy of fallot
-may be acutely cyanotic at birth or mild cyanosis that progresses over first year
-characteristic systolic murmur; moderate in intensity
-acute episodes of hypercyanosis and hypoxia (tet spells) or anoxic spells (cyanosis during crying/feeding)
what is a mixed defect (cyanotic)
combined anomalies of heart structures - complex defects with abnormal connections and pressures = mixing of saturated and unsaturated blood
what are the 4 cyanotic mixed defects
-transposition of great vessels (TGA)
-total anomalous pulmonary venous return (TAPVR)
-truncus arteriosus (TA)
-hypoplastic left heart syndrome (HLHS)
what is transposition of great vessels (TGA) cyanotic
aorta comes off the RIGHT ventricle (deoxygenated blood being circulated) and pulmonary artery comes off the LEFT ventricle (oxygenated blood going to the lungs)
what is total anomalous pulmonary venous return (TAPVR) cyanotic
pulmonary veins return blood to the RIGHt side of the heart (oxygenated and deoxygenated blood mixing in the right atrium)
what is truncus ateriosus (TA) cyanotic
a ventricular septal defect and fusion of the aorta and pulmonary artery to be a single vessel (mixed blood going to both systemic and lungs)
what is hypoplastic left heart syndrome (HLHS)
the left side of the heart is underdeveloped at birth
clinical manifestations of transposition of the great arteries (TGA)
-s&s will depend on type and size of defect. infants with minimal communication are severely cyanotic and critical
-if a large septal defect or PDA is present they will have sone oxygenation but have s&s of hF
-heart sounds vary
-cardiomegaly is present a few weeks after bith
therapeutic management of Transposition of the great arteries (TGA)
-prostaglandins iV may be initiated to keep a PDA to allow for some oxygenation
-balloon septostomy may allow for cardiac mixing of blood done under cardiac cath
-surgical arterial switch procedure performed in the first few weeks of life
what does the paO2 need to be for cyanosis to be present
<80-85%
what is hypoxemia
decreased arterial oxygen saturation
what is hypoxia
reduction in tissue oxygenation results in impaired cellular processes
what is cyanosis
blue discolouration in mucus membranes, skins, nail beds with reduced o2 saturations
what is polycythemia
-clinical manifestation of hypoxemia
-increased # of RBC, increases o2 carrying capacity of the blood
what is clubbing
-clinical manifestation of hypoxemia
-thickening and flattening of tips of fingers and toes
infants with mild hypoxemia s&s
-may be asymptomatic
-mild cyanosis
-delayed or no growth and development
infants wth severe hypoxemia s&s
-fatigue with feeding
-poor weight gain
-tachypnea
-dyspnea
-tissue hypoxia and poor perfusion
hypoxemia management
-re-establish pulmonary blood flow
-treat hyper cyanotic episodes (tet spells)
-monitor for worsening hypoexmia, anemia
-maintain hydration
-prevent and tx infections
nursing care for cyanotic defects
-may always have low o2, may need o2 supp, HOB 45
-ensure adequate hydration( I&O, dehydration= inc risk of stroke)
-daily weight
-tx infections &prevent (i.e vaccines)
-nutritional support w NG
-cardiac and resp monitoring
-encourage rest and dec stimuli
-parent education
what is kawasaki disease (KD)
-systemic vasculitis of unknown cause (peak in toddlers)
-self limiting without treatment, 20-25% develop cardiac sequelae
cardiovascular systemic in kawasaki disease
-coronary arteries most susceptible
-dilation and/or aneurysm formation
-evident by day 7 - continued enlargement for 4-6 weeks
-potential for MI
diagnostic criteria for KD
-no specific test
-critical lab values (CBC, CRP, ESR)
-echo
-prolonged elevated temperature (>5 days) that is not responsive to antibiotics & not attributable to another cause + 4/5 acute phase symptoms
acute phase of KD
-high fever (unresponsive to antibiotics & antipyretics) and irritable
-develops conjunctivitis, polymorphous rash
-red cracked lips, “strawberry” tongue, rash
-edema/erythema of hands and feet
-single cervical lymphadenopathy
-early cardiac involvement
subacute phase of KD
-begins with resolution of fever and lasts until all s&s have disappeared
-irritability persists
-greatest risk for coronary artery aneurysms
-peeling of fingertips and toes
convalescent phase of KD
-begins when all clinical signs resolve
-ESR, CRP remain elevated, coronary complications
-phase ends when bloodwork is normal (6-8 weeks after onset)
management of KD
-IVIG: dec fever and s&s, single infusion 2g/kg over 10-12h
-aspirin; anti-inflamm dose: 80-100mg/kg/d divded q6
anti-platelet dose: 3-5mg/kg/d
-family education: disease process
-aspirin administration and toxicity
-follow-up care (echo’s_
nursing care of KD
-monitor cardiac and assess for HF
-I&O, daily weights, gallop rhythm, tachycardia, resp distress
-temperature
-monitor during IVIG
-symptom relief (dec skin discomfort, minimize mucosal inflammation (mouth care), promote rest to dec irritability (dec stimuli))
