Lecture 10: Pediatric Cardiopulmonary Physical Therapy Flashcards
What does the placenta do?
Provides o2 and exchanges co2
when does the heart beat start?
22-27 days
which week of gestation is development primarily complete? (of the cardiac system)
10th week
fetal doppler US typically sheduled around 10-12 weeks of pregnancy
What is the foramen ovale?
Hole between the right and left atria
supposed to close post birth
What is ductus arteriosus?
Hole between aorta and pulmonary artery
this is supposed to close post birth
fetal cardiopulmonary circulation:
o2 rich blood from placenta enters via unbilical vein –> inferior vena cava –> right atrium –> left atrium (remember theres a hole [via foramen ovale) –> left ventricle –> aorta
* no need to go through lungs because they arent doing gas exchange at this point
Deoxygenated blood returns to the heart via the superior vena cava and coronary arteries –> right atria –> right ventricle –> pulmonary artery –> blood is shunted to descending aorta via ductus arteriosus –> umbilical arteries back tplacenta for o2 exchange
Blood traveling to the fetal lungs serve to nourish and develop lung tissue (not for gas exchange)
Cogenital heart defects
* most prevalent birth defect in newborns
* Defects are categorized as cyanotic or acyanotic
Explain an Acyanotic defect
* o2 sat
Fully oxygenated blood is shunted back into lungs and body (left to right shunting). Would present w/ >85% O2 saturation (L –> R shunting [o2 rich to non o2 rich] essentially over circulation of blood, but all the blood heading out does have enough o2 in it. essentially getting exposed to o2 twice)
* symptoms - sweating, increased resp rate, heart failure
* problems - low pao2 to periphery, low systemic stroke volume, increased work on heart
* surgery may or may not be required depending on size of defect
explain cyanotic defect
* o2 sat?
* what is there and increase in?
* do they need surgery?
Involve right-to-left shunting, where most of the blood bypasses the lungs (R –> L shunting, essentially missing the lungs aka missing the o2 saturation)
* decreased arterial o2 sat occurs (~70%)
* signals increase for red blood cell formation-polycythemia results
* increased risk for cerebrovascular insult
* cardiac surgery typically required within first year of life
think cyaniotic like posion
Acyanotic CHD
Patent ductus arteriosus (PDA)
* ductus arteriosus typically closes within the first 72 hours of life
* If it fails to close –> PDA and L to R shunting
* blood from aorta (oxygenated) is shunted to the pulmonary artery (mixed w/ deoxygenated blood) and circulated back to the lungs –> overcirculation of blood back to the lungs
* if ductus is large enough, could present with s&s of CHF within first 3 months of life
Acyanotic CHD
Ventricular Septal Defect (VSD)
* Most common CHD –> common to exist in certain conditions such as DS
* LV is a higher pressure system, will result in L to right shunting (acyanotic)
* increased blood through the pulmonary artery may result in pulmonary hypertension –> may result in s/s of CHF
so essentially blood is going from the L ventricle to the R which means the oxygenated it mixing w/ the deoxygenated
* blood flows this direction because the L side is a higher pressure system
Acyanotic CHD
Atrial Septal Defect (ASD) - hole between atria
* second most common CHD
* LA is a higher pressure system, will result in L –> R shunting (because the L side is a higher pressure system)
* may close spontaneously in first year of life
* may go undetected for a long time
* Can cause pulmonary HTN and RV hypertrophy
* may cause ex intolerance and arrythmias in late childhood
* Many adults may have asds and it may not be diagnosed until 3rd or 4th decade of life
just know they exist
Cyanotic CHD
Tetralogy of Fallot (ToF) one of the most common ones - surgery may not fully correct so they mey still have tet spells (moments of ex intolerance)
* 4 defects: (1) pulmonary stenosis, (2) Ventricular septal defect, (3) overriding aorta (coming over toward the middle line), and (4) right ventricular hypertrophy –> all this works to send deoxygenated blood to the rest of the body
* children can develop hypercyanotic spells called “tet spells” –> periods of profound systemic hypoxemia typically occuring in the context of crying, eating, or defecation
* decreased blood flow through the RVOT, right to left shunting across the VSD, and immediate desaturation
* PTs will note an abrupt deepening of cyanosis, increased RR and possibly syncope
* These tet spells can be relieved by increasing the systemic vascular resistance by bringing knees to chest or doing squats –> decreases the right to left shunting
* surgical intervention depends on pts symptoms
sometimes this defect isnt big enough to need immediate surgery. However they will still have periods of hypoxia = tet spells - think getting light headed or having ex intolerance
* can be hard to get them back to baseline
anytime you have to bare down and hold breath = will become moments of hypoxemia
Cyanotic CHD
Transposition of the Great Arteries
* Aorta and pulmonary artery are switched
* Aorta rises from RV and pumps deoxygenated blood to rest of body
* PA arises from the LV and pumps blood to the lungs immediate intervention is required to keep the PDA open, requires further surgical intervention
what they do is stop the closing of the foramen ovale - so blood can go back the other direction - until baby is strong enough to do cardiac surgery
chest wall retractions - babies are so small that when they take a deep breath and they’re struggling to breath - their skin will be pulled in through their ribs - thats a sign that they’re working really hard to breath
Sternal precautions in an infant: (happens w/ heart surgery)
* Avoid lifting baby from under their arms
* avoid pulling on babys arms when picking them up or dressing them - avoid abduction
* Avoid tummy time for a short period of time (usually first 2 weeks)
typical lung development
* when does terminal development occur?
* when do we have mature chemical levels of sarfactant?
* what is a full term pregnancy considered?
* how old to have adult # of alveoli
26-32 weeks
sarfactant = 34 weeks
full term pregnancy = 37-40 weeks
alveoli number increases to adult number by 10 years old
Pediatric Respiratory Conditions
Resp distress syndrome (RDS)
* common in premature infants
* caused by a deficient amount of pulmonary sarfactant
What happens w/ decreased sarfactant”
* Decreased lung complicance
* increased work of breathing
* leads to progressive diffuse microatelectasis, alveolar collapse, increased ventilation-perfusion mismatching, and impaired gas exchange
Pediatric resp conditions
bronchopulmonary dysplasia (BPD)
* Common in our very preterm infants who require prolonged mechanical ventilation (22 weeks or greater GA) - before the lungs fully develop (not just lack of sarfactant) - need lots of mechanical ventilation - issue is that were pumping a lot of blood into tiny blood = leads to lots of saccring which can lead to a lifetime impairment - little lungs cant handle the amount of o2 were feeding them through mechanical ventilation (to keep them alive)
* Chronic resp disorder characterized by scarring of lungs tissue, thickened pulmonary arterial walls, and mismatch between lung ventilation and perfusion
* Persistence of respiratory symptoms after 1 month, abnormal radiographic findings, depdence on supplemental o2
Cystic Fibrosis
* Genetic autosomal-recessive disease that affects exocrine gland function
* Na/Cl channel dysfunction creating thick mucus
* Thick secretions lead to ciliary collapse, leads to progressive airway obstruction and secondary infection
* Air trapping and atelectasis result in ventilation and perfusion mismatch, leads to hypoxemia
oscilating vest / manual drainage techniques utilized
* note babies have a really hard time coughing and dont have productive cough - need help getting all this out
notice the mucus
Asthma - glucosteriods
* characterized by airway inflammation, airway obstruction, and bronchial hyperresponsiveness to stimulation
* repeated inflammation from irritating stimuli can lead to airway remodeling and chronic inflammation –> important to manage medically with long acting and short acting medications
* increased use of accessory muscles can cause hyphotic posture
pediatric conditions with secondary cardiopulmonary issues - not just childhood disorders
DS: assocaited w/ endocradial cushion defect, ventricular septum defect, atrial septum defect, tetralogy of fallot
Marfan syndrome: Autosomal-dominant connective tissue disease commonly associated w/ aortic aneurysm and aortic/mitral insufficiency
Chromosomal deletion disorders such as DiGeorge syndrome and Williams syndrome
* Chromsoomal deletions can result in various cardiac anomalies
any neuromuscular or musculoskeletal condition that alters the alignment of the spine and thorax, or diminishes mobility has the potential to reduce cardiopulmonary function
Hr is higher in children than adults
RR is higher in children than adults
BP is typically lower than adults
because they’re smaller and there hearts working really hard to pump out the little bit of blood it is (so not as much blood = decreased bp)
MMT as erly as 2.5 as long as they are understanding and following directions
easier to breathe in prone - less wt on chest
* important for resp distress syndrome - work them up to supine
* think back to sleep
important to get that mobility before puberty - less ossified b4 = more ability for change
scar massage is important
at this age do body wt instead of free wts
focus on form
* form > progressive overload
trying to mobilize kids asap after surgery
early mobilization
remember kids dont understand why you’re doing interventions = make it as fun as possible
some kids cant read yet = complciates rpe/other scales
* different and standarized for kids
