Cardio, Neuro, Muscular Flashcards
Symptoms of cardiac dysfunction (many)
tachypnea
tachycardia
pale, clammy
fatigue
confusion
resp distress
poor weight*
not meeting developmental milestones*
Symptoms of cardiac dysfunction in infants
sleepy, fatigued
not gaining weight
tachycardia
Cardiac assessment
heart sounds - murmur
lungs sound - crackles
family history - infant deaths, heart disease
medical history
Cardiac tests
echo - structural abnormalities
ECG - rhythm
chest x-ray
Types of cardiac defects (2)
1) Congenital
2) Acquired
Congenital cardiac defect
anatomic - abnormal function
Acquired cardiac defect
disease process
-infection
-autoimmune response
-environmental factors
-familial tendencies
-medications
Medication that commonly causes acquired cardiac defects
chemo meds
need to monitor heart function!
Congenital Heart defect
not always symptomatic right away
one of the top causes of death in 1st year of life
often have another anomaly (trisomy 21, 13, 18, +++)
Most common congenital heart defect
ventricular septal defect (VSD)
Biggest change between prenatal and postnatal period in regards to circulatory system
breathing!
going from not breathing to breathing
Circulatory changes at birth (4)
1) umbilical vein; umbilical arteries
2) foramen ovale
3) ductus arteriosus
4) ductus venosus
umbilical arteries
carry blood from hypogastric arteries TO placenta
severed with the cord at birth
umbilical vein
carry blood AWAY from placenta –> ductus venosus and liver
severed with the cord at birth
foramen ovale
valve opening that allows blood to flow directly to left atrium
right –> left atrium
closes at birth due to increased pressure in right atrium and decreased pressure in left atrium
ductus arteriosus
shunting of blood from pulmonary artery to descending aorta
closes almost immediately after birth due to increased oxygen content in blood
ductus venosis
connection of umbilical vein to inferior vena cava
closes after birth due to loss of blood flow from umbilical vein
Older classification for congenital heart disease
altered hemodynamics
1) acyanotic
2) cyanotic
Current classification for congenital heart disease (4)
1) increased pulmonary blood flow
2) decreased pulmonary blood flow
3) obstruction to blood flow (out of the heart)
4) mixed blood flow (saturated and desaturated blood mix within the heart)
1) increased pulmonary blood flow
abnormal connection between two sides of heart
either septum or great vessels
increased blood volume on RIGHT side of heart
increased pulmonary blood flow
decreased systemic blood flow
Symptoms of increased pulmonary blood flow
tachycardia
decreased urine output
crackles
edema
weight gain
cool extremities
Exampes of increased pulmonary blood flow defects (3)
1) Atrial Septal Defect
2) Ventricular Septal Defect
3) Patent ductus arteriosus
Which defect is common in premature babies?
Patent ductus arteriosus
2) decreased pulmonary blood flow
pulmonary blood flow obstructed ANDAnatomical defect (ASD or VSD) between the R & L sides of the heart
blood has difficulty exiting R side of heart
pressure on R side increases
allows desaturated blood to shunt R –> L
results in desaturation in L side of heart & systemic circulation
decreased pulmonary blood flow defects (2)
1) Tetralogy of Fallot
2) Tricuspid atresia
Symptoms of decreased pulmonary blood flow defects
low oxygen saturation
cyanosis
cool limbs
decreased urine output
Unique sign of Tetralogy of Fallot
squatting
compensatory
3) obstruction to blood flow (out of the heart)
blood exiting the heart meets area of anatomical narrowing (stenosis) causing an obstruction to the blood flow
increased pressure PROXIMAL to defect
decreased pressure DISTAL to defect
usually near the valve
Examples of obstruction to blood flow defects (3)
1) coarctation of the aorta
2) aortic stenosis
3) pulmonic stenosis
How to check for obstruction to blood flow
BP!
arm BP will be HIGHER (proximal)
leg BP will be LOWER (distal)
4) mixed blood flow (saturated and desaturated blood mix within the heart)
fully saturated systemic blood flow mixes with desaturated pulmonary blood flow
causing relative desaturation of systemic blood flow
pulmonary congestion occurs
CO decreased
T or F: A child with a mixed blood flow heart defect will show signs right away.
FALSE
will look ok until PDA closes
Congestive Heart Failure (CHF)
inability of the heart to pump an adequate amount of blood into the systemic circulation
heart muscle becomes damaged if left untreated
Symptoms of CHF (many)
decreased urine output
crackles
decreased muscle strength
fatigue
tachycardia
tachypnea
edema
diaphoresis
poor feeding
resp distress
weight gain
Treatment Goals for CHF (many)
relieve symptoms
decrease morbidity (including risk of hospitalization)
slow progression of heart failure
improve patient survival and quality of life
Main meds/interventions given for CHF (5)
1) oxygen
-decrease demand
2) Digoxin
-improves contractility
3) Captopril (ACE inhibitor)
-decrease oxygen demand
4) Lasix
-remove excess fluid and sodium
5) Beta-blockers
What to teach parents related to Digoxin?
how to check HR before giving Digoxin
Nursing care management for CHF (lots)
assist in measures to improve cardiac function
monitor afterload reduction
decrease cardiac demands
reduce respiratory distress
maintain nutritional status
prevent infections
assist in measures to promote fluid loss
support child and family
What is a very important indicator of effective treatment in children with CHF?
weight!
Hypoxemia
symptom of many cardiac issues
state where insufficient oxygen to meet metabolic demands
can adversely affect every tissue in the body
Main signs of hypoxemia (4)
1) hypoxia
2) cyanosis
3) polycythemia
4) clubbing
polycythemia
increase in # of RBC
but can increase viscosity of blood
Good place to check for cyanosis in multiple different skin tones
centrally
in mouth!
Hypercyanotic Episode
SEVERE cyanotic episode
associated with Tetralogy of Fallot
can be spontaneous
can be precipitated by events associated with decreased systemic vascular resistance
T or F: Hypercyanotic episodes are usually self-limiting.
TRUE
What to teach parents to do with kids having hypercyanotic episodes?
knee-chest position
increases systemic vascular resistance
Endocarditis
caused by routine exposure to bacteremia associated with usual daily activities
also:
-dental work
-invasive procedures
-central lines
-IV drugs
T of F: Endocarditis is normally seen in healthy kids.
FALSE
most kids have other issues that increase their risk
Most common pathogens causing endocarditis (3)
1) Staphylococcus aureus
2) Streptococcus
3) Fungus
Endocarditis types (2)
1) acute
2) subacte
Signs of endocarditis
unexplained fever
malaise
weight loss
Janeway Lesions
Osler Nodes
Roth Spots
Janeway Lesions
nontender erythematous macules
on palms and soles
more common in ACUTE
Osler Nodes
tender subcutaneous violet nodules
mostly on pads of fingers and toes
Roth Spots
exudative, edematous hemorrhagic lesions of the retina with pale centers
Endocarditis diagnosis
CBC - elevated WBC
EST - inflammatory process
blood culture - which antibiotics or anti fungal
Endocarditis treatment
antibiotics
-high dose and lengthy treatment*
prophylaxis in high risk patient
surgery
Cardiomyopathy
refers to abnormalities of the myocardium in which the ability of the muscle to contract is impaired
Causes of cardiomyopathy (many)
familial or genetic cause
infection
deficiency states
metabolic abnormalities
collagen vascular disease
idiopathic
Hypertrophic Cardiomyopathy
one of most common forms of inherited cardiomyopathy
hypertrophy of left ventricle
In which age group are signs and symptoms of cardiomyopathy most common?
a) children under 1
b) older children
a) children under 1
older children can be asymptomatic
Clinical manifestations of cardiomyopathy
chest pain
syncope
palpitations
heartfailure symptoms
sudden cardiac arrest
physical exam may be normal
Diagnosis of cardiomyopathy
ECG
exercise testing
cardiac MRI
genetic testing
Treatment of cardiomyopathy
based on symptoms
correcting the cause
Therapies for cardiomyopathy
1st line: beta-blockers***
calcium channel blockers
CAUTIOUS use of diuretics
implantable cardioverter/defib
heart transplant
Child with hypertension normally have:
a) primary hypertension
b) secondary hypertension
b) secondary hypertension
secondary to structural abnormality or underlying pathology
renal disease
cardiovascular disease
endocrine or neurologic disorders
Symptoms of hypertension
vision, gait
headache - banging head*, holding head
crying, irritability
increased BP
Stage 1 hypertension
above 95th percentile for age group
Stage 2 hypertension
above 99th percentile for age group
Treatment for hypertension
find the cause
pharmacological - 1 med at a time
lifestyle
Kawasaki disease
aka monocutaneous lymph node syndrome
acute systemic vasculitis affecting medium sized arteries, especially coronary arteries
unknown cause
self-limiting
How long does Kawasaki disease last without intervention?
12 days
Why do we still want to treat it?
could result in coronary artery disease
want to identify early and treat
Diagnostic criteria for Kawasaki
1) at least 5 days of fever
PLUS
2) 4/5 of the CRASH criteria
CRASH criteria for Kawasaki
Conjunctivitis
Rash
Adenopathy
Strawberry tongue
Hands and feet
Phases of Kawasaki Disease (3)
1) Acute
2) Subacute
3) Convalescence
Acute phase
onset of high fever, unresponsive to antibiotics & antipyretics
Subacute phase
resolution of fever & lasts until all clinical signs disappear
Convalescent
clinical signs resolved but lab values are not normal
Kawasaki disease treatment (2)
1) IV immunoglobulin
2) Aspirin*
Types of shock (3)
1) hypovolemic
2) distributive
3) cardiogenic
Causes of hypovolemic shock
blood loss, plasma loss, extracellular fluid loss
Causes of distributive shock
reduction in peripheral vascular -
e.g. sepsis, anaphylaxis
Causes of cardiogenic shock
after surgery, dysrhythmias
Stages of shock (3)
1) Compensated shock
2) Decompensated shock
3) Irreversible or terminal shock
1) Compensated shock
initially compensated quite well, vital organs maintained
tachy, decreased urine output
2) Decompensated shock
more symptoms
may see changes in neuro status
3) Irreversible or terminal shock
NO urine
thready, weak pulse
very affected neurologically
Shock management
ventilation
fluids
-IV access super important!
improvement of cardiac function
How much fluid to give for shock
20 mL/kg bolus
then reassess
Cerebral palsy
group of permanent disorders of development of movement and postures
causes activity limitations
disturbances in the developing fetal or infant brain
abnormal muscle tone and coordination
Common co-morbidity with cerebral palsy
epilepsy
T or F: Most cases of cerebral palsy are caused by unknown brain abnormalities.
TRUE
Etiology of cerebral palsy
unknown
intrauterine exposure to chorioamnionitis
prematurity
periventricular leukomalacia
shaken baby syndrome
Types of cerebral palsy (3)
1) Spastic
2) Dyskinetic
3) Ataxis
Spastic cerebral palsy
increased muscle tone, poor control of posture, balance and coordinated movements
Dyskinetic cerebral palsy
slow, worm-like movements of extremities, trunk, face and tongue
Ataxic cerebral palsy
rapid repetitive movements; wide gait, unable to hold objects
What is the most common type of cerebral palsy?
spastic
Cerebral palsy diagnosis
assessment of at-risk infants
-e.g. difficult delivery, LBW, seizures, hypoglycaemia, emergency C-section, placental abnormalities
neurologic examination and history
neuroimaging
metabolic and genetic testing
Possible signs of cerebral palsy (many)
poor head control after age 3 months
clenched fists after age 3 months
no smiling age by 3 months
stiff or rigid limbs
arching back/pushing away
floppy tone
unable to sit without support at age 8 months
excessive irritability
persistent tongue thrusting
frequent gagging or choking with feeds
Goals of therapy for cerebral palsy
locomotion, communication, self-help
motor function
correct defects
education
socializaiton
Therapeutic management of cerebral palsy
ankle braces
surgery
drugs for pain and seizures (Baclofen)
botulinum A injections- localized spasticity
Baclofen – implanted pump
dental hygiene
OT
Why is dental hygiene especially important in those with cerebral palsy?
seizure meds can erode gum tissue
Spina bifida
failure of osseous spine to close
Spina bifida types (2)
1) spina bifida occulta
2) spina bifida cystica
Spina bifida occulta
not visible externally
Spina bifida cystica
visible defect
saclike protrusion
What condition is spina bifida commonly associated with?
hydrocephalus
increased fluid in the brain
associated with learning disabilities, seizures, UTIs, bowel dysfunction
Muscular dystrophy
genetic origin
GRADUAL
degeneration of muscle fibers, progressive weakness, and wasting of skeletal muscles
increasing disability and deformity with loss of strength
Duchenne Muscular Dystrophy (DMD)
SEVERE
X-linked inheritance pattern; one third are fresh mutations
develop normally until about age 3
Characteristics of Duchenne Muscular Dystrophy
onset between ages 2 and 7 years
progressive muscle weakness, wasting, and contractures
calf muscles hypertrophy
progressive generalized weakness in adolescence
death from respiratory or cardiac failure
Diagnostic evaluation of Duchenne Muscular Dystrophy
most reliable: muscle biopsy
elevated CK**
EMG
DNA test
characteristics
Clinical manifestations of Duchenne Muscular Dystrophy
waddling gait, frequent falls, Gower sign
lordosis
enlarged muscles, especially thighs and upper arms
profound muscular atrophy in later stages
varying degrees of mild cognitive impairment
Primary goal of management for Duchenne muscular dystrophy
maintain function in unaffected muscles as long as possible
Therapeutic management for Duchenne muscular dystrophy
NO effective treatment established
swimming!!*
physio
physical activity
genetic counselling
T or F: Spinal cord injuries are usually the result of INDIRECT trauma.
TRUE
MVA*
Paraplegia
complete or partial paralysis of lower extremities
Tetraplegia
lacking functional use of all four extremities (formerly called quadriplegia)
Which nerve do higher spinal cord injuries affect?
phrenic nerve
paralyzes diaphragm
ven dependent
