CVP changes - peds and geriatric

Question 1

cardiopulm changes from neonate to adult

Answer 1

• HR down with age
• BP up with age
• RR down with age
• Vt up with age
• PaO2 up with age
• PaCO2 up with age
• pH up with age
• infant Hgb F - higher O2 affinity – carries O2 better, makes up for less overall O2

Question 2

fetal circulation

Answer 2

• pressure on R > L due to afterload/resistance to ejection (opposite of postnatal)
• R -> L shunt (increased pulmonary vascular resistance (PVR in RV) vs systemic vascular resistance (SVR in LV)
• only about 10% of combined ventricular output goes through lungs
• shunts: foramen ovale, ductus arteriosus, ductus venosus

TPR = PVR + SVR

Question 3

3 anatomic shunts in fetal circulation

Answer 3

• foramen ovale: between R and L atrai
• ductus arteriosus: PA (R) to aortic arch (L)
• ductus venosus: placenta to IVC

FO and DA are intracradiac, DV is extracardiac

Question 4

foramen ovale

Answer 4

• allows blood to flow from R to L atrium, bypassing lungs
• intracardiac

Question 5

ductus arteriosus

Answer 5

• intracardiac
• allows blood flow from pulmonary artery to aorta, bypassing fetal lungs

Question 6

ductus venosus

Answer 6

• extracardiac
• connects umbilical vein and inferior vena cava - bypasses portal circulation

Question 7

blood flows R to L before birth due to [ ] and switches after because

Answer 7

• due to vascular resistance and afterload
• switches after because fluid squeezed out of lungs in birth – PVR down, CO up, lungs take over for gas exchange

Question 8

fetal circulation

Answer 8

• high pulmonary vascular resistance (PVR) - RV pressures high
• low systemic vascular resistance (SVR) due to placenta circulation - LV pressures low
• right to left shunt via PFO and DA
• highly reactive to hypercapnia (increased CO2)/acidosis and hypoxemia (low O2)
• at birth: O2 in lungs cause pulmonary vasculature to dilate (PVR down)
• leads to pulmonary vascular vasoconstriction and increase PVR in utero

Question 9

transition from neonate to newborn (aeration and expansion of lungs)

Answer 9

• inflating lungs initiates gas exchange over 8 years
• opening of alveoli opens associated vascular units
• rising PaO2 leads to dilation of pulmonary arterioles – decreased PVR, decreases right heart pressure
• RA pressure decreases, prevents blood shunt - flap in LA

Question 10

more transition from neonate to newborn

Answer 10

• removal of placenta circulation increases SVR
• increased aorta and left heart pressures
• foramen ovale (FO) flap closes - increases blood flow to lungs
• shunting thru ductus arteriosus decreases
• functional closure associated with increased oxygenation (increased PaO2) and decreased production of vasodilator substances
• anatomic closure occurs later (week to months)

Question 11

newborn

Answer 11

• foramen ovale closes
• anatomical closure ~2-3 months
• left heart pressure > right heart pressure: SVR > PVR, LV compliance < RV compliance
• ductus arteriosus closes
• functional closure/constriction ~15-72 hours
• anatomical closure ~2-3 weeks

Question 12

in newborn, persistance of shunts (heart/vascular defect) can lead to

Answer 12

• altered circulation and altered blood gases (PaCO2, PaO2)
• altered blood gases will depend upon SVR:PVR - cyanosis versus acyanosis

Question 13

congenital heart defects

Answer 13

• PDA: patent ductus arteriosis
• PFO: patent foramen ovale

Question 14

right to left shunt is [ ]
left to right shunt is [ ]
factors that determine shunt direction [ ]

Answer 14

• fetal - normal fetal is R > L
• post-natal - L > R
• pressures determine direction

Question 15

normal heart pressures

Answer 15

Question 16

atrial septal defects (ASD)

Answer 16

Question 17

ventricular septal defects (VSD)

#1 most common congenital heart defects in newborns

Answer 17

Question 18

hypoplasia

congenital heart defect

Answer 18

hypoplastic left heart syndrome

Question 19

obstruction defects

congenital heart defect

Answer 19

• aortic stenosis, pulmonary stenosis
• coarctation of aorta

Question 20

septal defects

congenital heart defect

Answer 20

• atrial septal defects (including patent foramen ovale)
• ventricular spetal defects

Question 21

cyanotic heart disease

congenital heart defect

Answer 21

• tetralogy of fallot
• transposition of the great vessels - vessels out of R and L sides are switched
• tricuspid atresia

Question 22

septal defects

Answer 22

• atrial septal defects
• patent ductus arteriosus
• ventricular spetal defects

Question 23

atrial septal defect (ASD)

Answer 23

• patent foramen ovale (FO)
• allows blood flow between right and left atria
• fetal: right to left shunting through FO is normal
• birth/transitional circulation: FO should close due to increased left heart pressure (increased SVR, no shunt)

Question 24

ventricular septal defect (VSD)

Answer 24

• abnormal communication between right and left ventricular chambers of the heart
• most common CHD
• shunting depends on ventricular pressures – usually L to R shunt
• increased CO through pulmonary circulation - increase RV filling: can lead to RV failure
• may lead to HR and persistent pulmonary HTN of the newborn (PPHN) - overloads pulmonary circulation
• if increased PVR: right to left shunt (lung disease)

Question 25

cyanotic heart disease

Answer 25

• tetralogy of fallot
• transposition of the great vessels
• tricuspid atresia

blue babies

Question 26

tetralogy of fallot

Answer 26

• blue baby syndrome
• cyanotic heart disease
• tet spells: transient worsening of hypoxia f/b syncope (increased PVR) - child will often squat
• four heart defects:
  1. ventricular septal defect (VSD)
  2. pulmonary stenosis - pulmonary valve doesn’t open
  3. right ventricular hypertrophy
  4. overriding aorta

Question 27

facts about tetralogy of fallot

Answer 27

• 50-70% of cyanotic heart defects
• less obstruction: oxygenated blood L to R
• more obstruction: deoxygenated blood R to L –> O2 sats can < 80%, blue skin

Question 28

CHD and general PT considerations

Answer 28

• symptoms: fast breathing, respiratory distress, poor feeding and weight gain, failure to thrive, early fatigue, syncope, palpitations, pulmonary and peripheral edema
• may predispose: dysrhythmias (tachycardia), PPHN (persistent pulmonary hypertension of the newborn), heart failure (HF)
• children with cardiac disorders will frequently have reduced exercise capacity - residual hemodynamic abilities, sedentary lifestyle due to parents, children who have undergone a surgical correction may have a slight decrease to normal exercise capacity
• children can and should participate in cardiac rehab