CVP ISSUES- NEONATE AND CHILD

Question 1

Full term neonate HR, BP, RR, TV, paO2, paCO2, pH, and infant hemoglobin:

Answer 1

HR: 110-160 bpm

BP: 75/50

RR: 30-40/min

TV: 20 ml

PaO2: 75-80 mmHg

PaCO2: 33 mmHg

pH: 7.33

infant Hgb has a higher affinity for O2

Question 2

Fetal circulation:

Answer 2

-fetal heart pressure are the opposite of postnatal pressures
–> R heart > L heart (L>R postnatal)

-transition from R –> L shunt

-greater pulmonary vascular resistance compared to systemic vascular resistance
–> shunting of blood R to L
–> 10% of combined ventricular output goes through the lungs

Question 3

Pulmonary vascular resistance vs Systemic vascular resistance

Answer 3

IN CHILD
-increased pulmonary vascular resistance of blood trying to go through capillaries
–> why shunting occurs

–> pressure in the RA is greater than in the LA

–> forces systemic venous blood directly into systemic arterial circulation

Question 4

Why is there limited blood flow through the fetal lungs?

Answer 4

-in utero, lungs are filled with liquid and relatively collapsed, capillaries are also collapsed
and compressed

-Fetal lungs have limited blood flow because the fetus has evolved to divert blood away from the lungs and towards the placenta, which acts as the organ of gas exchange. This is achieved by maintaining high pulmonary vascular resistance (PVR) and low placental vascular resistance.

Question 5

Explain the typical “path of circulation” from umbilical vein to abdominal aorta

Question 6

3 anatomic shunts: intracardiac and extracardiac

Answer 6

1) Foramen ovale (intracardiac)
-shunt from RA to LA through foramen ovale
-directly into systemic circulation and never through the lungs

2) Ductus Arteriosus (intracardiac)
-allows blood to flow from the pulmonary artery to the aorta, bypassing the fetal lungs

3) Extracardiac (ductus venosus)
-connects the umbilical vein and IVC
-bypassing the portal circulation
-The ductus venosus is a shunt that allows oxygenated blood in the umbilical vein to bypass the liver and is essential for normal fetal circulation. Blood becomes oxygenated in the placenta and travels to the right atrium via umbilical veins through the ductus venosus, then to the inferior vena cava.

PATH: placenta–> umbilical vein–> through ductus venosus–> IVC–> RA–> LA–> LV–> pumonary artery–> through ductus arteriosus–> aorta–> descending aorta–>

Question 7

Risk of shunt when born premature:

Answer 7

-increased risk that foramen ovale and ductus arteriosus don’t close normally
-can have R–>L shunt due to elevated PVR

Question 8

Path of fetal circulation:

Answer 8

OPTION 1: Placenta–> umbilical vein–> ductus venosus–> inferior vena cava–> RA–> RV–> pulmonary trunk–> ductus arteriosus–> aorta–> systemic circulation –> umbilical arteries–> placenta

OPTION 2: Placenta–> umbilical vein–> ductus venosus–> inferior vena cava–> RA–> foramen ovale–> LA –> LV –> aorta–> systemic circulation –> umbilical arteries–> placenta

Question 9

Characteristics of fetal circulation:

Answer 9

-high PVR
-low SVR due to placenta circulation
-right to left shunt via PFO and DA
-highly reactive to high co2 levels (hypercapnia/acidosis) and hypoxemia
–> leads to pulmonary vascular vascoconstriction and increased PVR –> increased shunting

Question 10

Transition from neonate to newborn:

Answer 10

-upon birth, dramatic reduction in PVR
-lungs are immediately rung out and inflated at birth

AERATION AND EXPANSION OF LUNGS in newborn
-initiation of gas exchange
-opening of alveoli opens associated vascular units
-rising PaO2 leads to dilation of pulmonary arterioles–> decreased PVR and decreased R heart pressures

-if PVR and R heart pressures stays elevated after birth, flap doesn’t close–> continued shunting

-closure occurs when L side pressure exceeds R side pressure

Question 11

What happens in the case of L to R heart shunt?

Answer 11

-pulse ox will look normal
-blood coming from arterialized blood at L atrium
-decreased blood pressure bc extra volume going to the R side

-A left-to-right shunt is an abnormal connection between the right and left sides of the heart that allows oxygenated blood to leak from the lungs back to the lungs, instead of being pumped to the body. of heart and not into systemic circulation

Question 12

What happens to vascular resistance with removal of placenta circulation?

Answer 12

-increase in SVR

-increase aorta and L heart pressures

-FO closes; increasing blood flow to lungs

-shunting through ductus arteriosus decreases

-FUNCTIONAL closure of FO associated with increased oxygenation and decreased production of vasodilator substances (prostaglandins)

-ANATOMIC closure occurs later –> can take weeks to months

Question 13

What changes happen to the circulation in a newborn:

Answer 13

-FO closes
–> anatomical closure: 2-3 months
–> L heart pressure becomes greater than R
–> SVR> PVR
–> LV compliance < RV compliance

-DA closes
–> functional closure/constriction in 15 to 72 hours
–> anatomical closure in 2-3 weeks

Question 14

What can persistence of shunts lead to?

Answer 14

-altered circulation and altered blood gases
–> blood gases depends on SVR: PVR ratio

Question 15

What are some common congenital heart defects:

Answer 15

PDA: patent ductus arteriosus

PFO: patent foramen ovale
-atrial septal defect
-wall between atria don’t close completely

Hypoplasia- hypoplastic left heart syndrome

Obstruction defects-
- aortic stenosis; pulmonary stenosis
-coarctation of aorta (narrowing of aorta)

Septal defects
-atrial septal defects (PFO)
-ventricular septal defects

Cyanotic heart disease
-tetralogy of fallot
-transposition of the great vessels
-tricuspid atresia (when tricuspid valve does not develop)

Question 16

Adult circulation pressure gradients

Answer 16

LV: 100 pressure vs RV: 200 pressure (80 mmHg pressure gradient)

LA: 6 pressure vs RA: 4 pressure (2 mmHg pressure gradient)

Question 17

Description of ASD (PFO):

Answer 17

-allows blood flow between R and L atria

-Fetal: R –> L shunting through FO is normal, but not in an adult

Birth-transitional circulation:
-FO should close due to increased L heart pressure and increased SVR

Question 18

VSD - ventricular septal defect

Answer 18

-abnormal communication between the R and L ventricular chambers of the heart

** this is the most common congenital heart defect

-usually L –> R
–> increase of CO through pulmonary circulation, decrease CO through systemic
–> may lead to HF and persistent pulmonary HTN of the newborn PPHN

-if PVR increases: R–> L shunt and increased risk of lung disease (bronchopulmonary dysplasia; damage of alveoli)

Question 19

Tetrology of Fallot

Answer 19

“blue baby syndrome”

-a cyanotic heart disease

-Tet spells: transient worsening of hypoxia followed by syncope (increased PVR)
–> child often squats to avoid syncope

FOUR DEFECTS:
1) VSD
2) pulmonary stenosis (less blood reaching lungs)
3) RV hypertrophy
4) overriding aorta–> An overriding aorta is a congenital heart defect where the aorta is positioned above a ventricular septal defect (VSD) instead of the left ventricle.
–> This means that the aorta receives some blood from the right ventricle, which reduces the amount of oxygen in the blood

Question 20

CHD common symptoms and predispositions:

Answer 20

-fast breathing
-resp distress
-poor feeding and poor weight gain
-failure to thrive
-decreased exercise tolerance; early fatigue
-syncope
-pulmonary and peripheral edema
-palpitations

MAY predispose:
-dysrhythmias
-PPHN
-heart failure

Question 21

General PT considerations for children with CHD

Answer 21

REDUCED EX CAPACITY WITH CARDIAC DISORDERS IN CHILDREN:
–> – Residual hemodynamic abnormalities
–> Sedentary lifestyle (parent influence)
–> Children who have undergone a surgical correction may have slight
decrease to normal exercise capacity

CARDIAC REHAB- children can and should participate
–> mild CHD: permitted to participate in all competitive sports
–> extra caution for cyanotic and aortic defects, tachycardiaRE

Question 22

What is the AHA’s recommendation for aerobic activity for kids?

Answer 22

at least 60 minutes of moderate to vigorous intensity aerobic activity every day

Question 23

What type of illness accounts for >50% of all illnesses in children?

Answer 23

respiratory illness

accounts for 42% of hospitalizations

Question 24

Fetal lung development –> Why is 24-26 weeks of gestation a critical time?

Answer 24

-the resp system continues to develop throughout early childhood (8-10 years old)

TIMELINE:
-lung buds at 3.5 weeks gestation
-tracheo-bronchial tree - 16 weeks
-alveoli start forming at 20-24 weeks
–> surfactant at 24 weeks
-capillary networks continue forming and surround alveoli at 26-28 weeks (gas exchange)
-alveolarization continues postnatally

-lungs and surfactant mature at 35 weeks
–> if premature: immature lung architecture, inadequate surfactant and poorly developed diaphragm/chest wall

-normal term of pregnancy: 40 weeks

-lungs continue to develop until 8-10 years–> continued increase in alveolar number and thinning of alveolar-capillary membrane

Question 25

What are the different cell types in the lungs & why are they important in the developing lung?

Why is surfactant so important for viability?

Answer 25

TYPE I PNEUMOCYTES:
-majority of alveolar epithelium

TYPE II PNEUMOCYTES:
-produces surfactant
–> this cell develops around 20 weeks gestation

SURFACTANT:
-lipoprotein
-alveoli is air: liquid interface
-antimicrobial; immune defense; protect lung against invaders (surfactant proteins)
-prevents alveolar collapse and helps with lung inflation
-decreases surface tension to make the lungs more compliant; decrease muscular effort needed to ventilate lungs
-when lung deflates, surfactant lines up next to each other and prevents the alveoli from fully deflating

Question 26

Viability:

Answer 26

LIMIT OF VIABILITY: is the gestational age at which a prematurely born fetus/infant has a
50% chance of long-term survival

-FUNCTION OF :
–>baby’s gestational age and birth weight: increases 3-4% per day between 23 and 24 weeks of gestation and about 2-3% per day between 24 and 26 weeks of gestation
–>medical and tech capacity differs throughout the world: prenatal care, exogenous surfactant; mechanical ventilation, incubators, neonatology

Question 27

Difference between adult and newborn chest wall/rib cage?

Answer 27

NEWBORN
-Ribs oriented in parallel
-limited ability to increase thoracic volume during inspiration
-greater oblique orientation with standing and walking
-increased chest wall compliance –> increased risk of thoraco-abdominal coupling
-decreased mechanical efficiency

Question 28

What is thoraco-abdominal coupling?

Answer 28

Normally the contracting chest wall muscles stabilize the infant rib cage
–> minimizes inward rib cage displacement and allows effective volume change
–> promotes mechanical efficiency

ABNORMAL:
-hypercompliant rib cage coupled with reduced lung compliance
–> asynchronous chest wall movements
–> loss of mechanical efficiency (increased WOB)
-increased acidosis and hypoxemia
-limited pulmonary reserve

• may need to use breathing apparatus

Question 29

What exacerbates the risk of thoraco-abdominal coupling?

Answer 29

prematurity

Question 30

Diaphragm and its role in preterm infant vs infant

Answer 30

INFANT
-infant diaphragm continues to develop postnatally
-increased muscle growth and increased CSA
-increased force production and fatigue resistance

PRETERM VERSUS TERM INFANT
-preterm: relative fatiguability; decreased inspiratory reserve capacity
-increased WOB: high metabolic rate; high RR; decreased lung compliance; increased compliance of chest wall; thoraco-abdominal un-coupling

Question 31

What is a characteristic sign of neonatal respiratory distress?

Answer 31

-intercostal collapse
-blue baby

Question 32

Differences between the child and the adult

Answer 32

• Decreased lung surface area for gas exchange
• Horizontal rib alignment (infant)
• Decrease lung compliance; Increased chest wall compliance
• Increased RR with an irregular respiratory pattern
• Diaphragm continues to develop
• Limited airway clearance abilities
• Increased WOB
• predisposition of children to respiratory problems

Question 33

Infant respiratory distress syndrome is also called what, and description?

Answer 33

Hyaline Membrane Disease

CHARACTERISTICS:
-surfactant deficiency and lung inflammation
–> decreased compliance
–> atelectasis
–> hypoxemia low V/Q and R to L shunt physiology (bypass lungs)

AT RISK:
-babies <32 weeks gestation and weighing <1200 g

-often worsens over days 2-4–> progressive respiratory failure

-could lead to BPD
–> oxygen toxicity
–> thickened alveoli walls, lungs are edematous
–> mechanical ventilation

OTHER COMPLICATIONS:
-IVH
-developmental delay
-mitral regurgitation
-retinopathy of prematurity

Question 34

RISK of mechanical ventilation in an infant

Answer 34

-high pressure of air going into lungs–> can damage delicate infant lungs

Question 35

Bronchopulmonary Dysplasia (BPD)

Answer 35

-seen following IRDS
-Fibrotic changes resulting in reduced compliance & diffusion impairment
-usually hypercapnic and hypoxemic respiratory failure

-incidence is inversely related to birth weight (lower birth weight)

-TREATMENT:
– prevention: limit exposure to mech ventilation and o2 therapy
–> nutrition
–> airway clearance, positioning, mobilization
–> motor milestones

Question 36

Meconium Aspiration Syndrome

Answer 36

Meconium:
-early stool of infant; can be expelled prior to birth in amniotic fluid
–> aspiration
–> stickiness and tar consistency can block airways –> pneumonitis and/or pneumonia

Treatment:
-supportive med management
-mech vent. if resp. insufficiency (consider duration due to risk of BPD)
-airway clearance (postural drainage)

Common Complications
-tension pneumothorax: large air collection in the pleural space compromises respiration and cardiac function (DANGEROUS)
-pulmonary HTN

Question 37

Congenital Diaphragmatic Hernia

Answer 37

-developmental defect
-80% of hernias on L
-baby is: cyanotic, dyspneic, and tachycardic
-requires surgery; can be in utero
-outcome depends on lung development
–> could result in pulm. hypoplasia

-usually diagnosed at time of birth

** intestine herniates through the diaphragm

Question 38

Pulmonary hypoplasia

Answer 38

Pulmonary hypoplasia is a relatively uncommon medical condition characterized by incomplete development of the lungs that can affect the overall development of the child.

It can be either primary (idiopathic) or secondary to other congenital anomalies and usually leads to severe respiratory insufficiency in the fetus.

Question 39

Cystic Fibrosis characteristics:

Answer 39

-defective CF gene–> deficient CFTR protein–> decreased chloride secretion/altered ionic transport –> increased water absorption and abnormal mucus composition–> bronchial obstruction–> bacterial infections–> inflammation–> bronchiectasis and lung insufficiency

-chromosome 7 alteration

-90% of CF deaths are pulmonary related

Question 40

Other impairments among individuals with CF that is CFTR protein related:

Answer 40

PANCREAS
-DM, poor fat digestion
-pancreas can’t release enzymes into duodenum

DIGESTIVE TRACT
-malnutrition; blockage/obstruction

MSK
-arthropathy

Question 41

Characteristic of Airway surface liquid in cf:

Answer 41

In cystic fibrosis (CF), airway surface liquid (ASL) is dehydrated and acidic, and produces viscous secretions that are difficult to clear. This is due to defective anion transport, sodium and water compartmental shifts, and upregulated epithelial sodium channel (ENaC) activity

Question 42

Are survival rates for CF improving or decreasing in recent years?

Answer 42

Improving

Question 43

What kind of intervention might you use to clear mucous from an airway in patients with CF?

Answer 43

airway clearance techniques

Question 44

What is the most prevalent infection in CF patients, what is the most fatal?

Answer 44

P aeruginosa

MOST FATAL: B cepacia : 10-15 years of life

Question 45

Interventions/management for CF:

Answer 45

CORRECTION OF UNDERLYING DEFICIT
-meds
-gene therapy

REDUCTION IN THE MUCUS BURDEN
-airway clearance and
-exercise training
-DNA ase
-mucolytics
-hyperosmolar agents

CONTROL OF INFECTION
-Nebulised anti-pseudomonal antibiotics (AB)
I-V anti-pseudomonal ABs
-Oral antibiotics
-Vaccinations
-Long-term oral anti-staph antibiotics

CONTROL OF INFLAMMATION
-Oral corticosteroids
-Inhaled corticosterods
-NSAIDs
-Macrolides (antibiotic)

OTHER MANAGEMENT
-Bronchodilators
-Vaccinations
-Long term O2 therapy
-Non invasive ventilation (NIV)
-Lung transplantation

Question 46

Asthma etiology

Answer 46

ETIOLOGY: In asthma there is goblet cell hyperplasia/hypertrophy, subepithelial fibrosis, increased vascularity, and
smooth muscle hypertrophy and hyperplasia

-thickening of the airway basement membranes
-hypertrophy of submucous bronchial galnds and bronchial wall muscle
-edema and inflammation
-thick, firm mucous in airways
-lungs may be overinflated

Question 47

Asthma and exercise:

Answer 47

-can and should participate in PA

-can fully participate in physical activity
when they are symptom-free.

• Activity may need to be modified when a student’s asthma is not
  well-controlled
• so preventing asthma episodes and
  responding effectively to them are paramount.
• Pre-medication, if prescribed, and physical warm-ups are essential
  and can help prevent asthma episodes.

-Asthma Action Plans should include modified exercise recommendations from personal physician–> must be provided to school staff and individual asthma emergency protocol

-monitor environment for potential triggers

• Permit student to monitor breathing status using a
  Peak Flow Meter (see below) (gives you idea of flow rate)

Question 48

RED ZONE on asthma action plan

Answer 48

50% or less of peak flow with peak flow meter

-call doctor
-go to hospital or call ambulance

Question 49

Green vs yellow vs red zones asthma:

Answer 49

GREEN
80-100% peak flow

YELLOW
50-79% peak flow
-have student take meds
-consider activities that involve stopping and starting or a warm up in moist setting
-provide appropriate activity modifications, including rest periods

RED
0-49% peak flow
-STOP activity
-follow emergency plan
-inhaled meds
-call 911 if no improvement

Question 50

Pulmonary rehab approach for children:

Answer 50

• Observation for signs/symptoms of respiratory distress

– Symptoms/DOE: Borg RPE 4-6

– SpO2 (O2 saturation): as needed

– Be aware of the Asthma Action Plan