CVP changes - peds and geriatric Flashcards

1
Q

cardiopulm changes from neonate to adult

A
  • 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
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2
Q

fetal circulation

A
  • 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

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3
Q

3 anatomic shunts in fetal circulation

A
  • 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

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4
Q

foramen ovale

A
  • allows blood to flow from R to L atrium, bypassing lungs
  • intracardiac
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5
Q

ductus arteriosus

A
  • intracardiac
  • allows blood flow from pulmonary artery to aorta, bypassing fetal lungs
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6
Q

ductus venosus

A
  • extracardiac
  • connects umbilical vein and inferior vena cava - bypasses portal circulation
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7
Q

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

A
  • 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
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8
Q

fetal circulation

A
  • 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
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9
Q

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

A
  • 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
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10
Q

more transition from neonate to newborn

A
  • 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)
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11
Q

newborn

A
  • 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
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12
Q

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

A
  • altered circulation and altered blood gases (PaCO2, PaO2)
  • altered blood gases will depend upon SVR:PVR - cyanosis versus acyanosis
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13
Q

congenital heart defects

A
  • PDA: patent ductus arteriosis
  • PFO: patent foramen ovale
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14
Q

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

A
  • fetal - normal fetal is R > L
  • post-natal - L > R
  • pressures determine direction
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15
Q

normal heart pressures

A
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16
Q

atrial septal defects (ASD)

A
17
Q

ventricular septal defects (VSD)

#1 most common congenital heart defects in newborns

A
18
Q

hypoplasia

congenital heart defect

A

hypoplastic left heart syndrome

19
Q

obstruction defects

congenital heart defect

A
  • aortic stenosis, pulmonary stenosis
  • coarctation of aorta
20
Q

septal defects

congenital heart defect

A
  • atrial septal defects (including patent foramen ovale)
  • ventricular spetal defects
21
Q

cyanotic heart disease

congenital heart defect

A
  • tetralogy of fallot
  • transposition of the great vessels - vessels out of R and L sides are switched
  • tricuspid atresia
22
Q

septal defects

A
  • atrial septal defects
  • patent ductus arteriosus
  • ventricular spetal defects
23
Q

atrial septal defect (ASD)

A
  • 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)
24
Q

ventricular septal defect (VSD)

A
  • 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)
25
Q

cyanotic heart disease

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

blue babies

26
Q

tetralogy of fallot

A
  • 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
27
Q

facts about tetralogy of fallot

A
  • 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
28
Q

CHD and general PT considerations

A
  • 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