1
Q
what are the changes in blood circulation of the baby after birth?
A
- as infant breathes and the lungs expand, blood flow to the lungs increases, pressure in the right side of the heart falls, and foramen ovale closes
- ductus arteriosus constricts as arterial O2 levels rise
- ductus venosus constricts when blood flow from the umbilical cord stops
- after birth, the ductus venosus and umbilical As and V become ligaments
2
Q
cardiac assessment
A
- ask about: meds, family hx, pregnancy and prenatal care/birth hx, gaining weight?, urine output?, color changes?, can they keep up with their friends?
- inspection
- palpation: palpate all pulses b/l (except carotid do one at a time)–are they equal in strength and rhythm?
- auscultate
3
Q
non-invasive and invasive procedures to assess cardiac system
A
- non-invasive:
- CXR: record size and shape of heart
- EKG
- echocardiogram
- CT/MRI: non-invasive unless contrast
- invasive:
- cardiac catheterization
4
Q
cardiac cath
A
- radiopaque catheter is inserted into large artery or vein (usually femoral) and threaded to the heart
- use of cardiac cath:
- diagnostic
- interventional
- electrophysiologic purposes
- biopsy
- if transplant, have to get biopsy
5
Q
nursing implications pre-cardiac cath
A
- NPO for 4-6 hours (need to be clear and specific about solids vs clear liquids)
- may pre medicate prior to cath
- stop anticoagulants
- assess for allergies, prior sedation hx, pregnancy
- check for baseline circulation in lower extremities and mark pedal pulses
- prepare child and family for what will occur
6
Q
nursing implications post cardiac cath
A
- lay flat and maintain pressure dressing for 4-8 hrs
- frequent V/S, assessment of pressure dressing and distal circulation, I/O
- adequate hydration
- check for hypoglycemia (b/c have been NPO for a while)
7
Q
complications of cardiac cath
A
- hemorrhage at site of infection
- loss of pulse in catheter extremity–distal to insertion site of catheter
- dysrhythmias
- fever
- n/v
8
Q
patient/parent education
A
- avoid strenuous activity for several days
- observe site for infection
- do not submerge site in water for one week
- may give acetaminophen/ibuprofen as needed
- if <6 mos, acetaminophen only
9
Q
critical weight gain or loss to be concerned about
A
- infants: 50 g/day
- toddlers/preschoolers: 200 g/day
- adolescents/adults: 500 g/day
10
Q
congenital heart dz (CHD)
A
- major cause of death in first year of life (other than prematurity)
- blood flows from area of high pressure to one of low pressure and takes path of least resistance
11
Q
hemodynamics of CHD
A
- shunt
- described in terms of ratio of pulmonary blood flow to systemic blood flow (Qp:Qs)–>normal is that Qp=Qs
- effects on pulmonary vasculature–3 stimuli can cause constriction of pulmonary vessels and inc pulmonary vascular resistance
- inc blood flow
- blood flow to lungs under inc pressure
- hypoxia
12
Q
Eisenmenger Syndrome
A
- situation in which a left to right shunt caused by a CHD causes increased flow thru pulmonary vasculature causing inc pressure on the right side which causes reversal of the shunt to become a right to left shunt, so deoxygenated blood goes out to periphery so child becomes hypoxic (blue)
- leads to a progressive inc in pulm vascular resistance (PVR)
- blood gets oxygenated by lungs, goes to left side of heart, but b/c of hole in heart, some blood foes back to R side of heart, so goes again to lungs and makes lungs work harder
- child will need heart/lung transplant
- occurs after a prolonged period of inc pulmonary blood flow
- can lead to death
13
Q
4 major categories of CHD
A
- inc pulmonary blood flow
- dec pulmonary blood flow
- obstruction of blood flow from the heart
- mixed blood flow
14
Q
name the defects with inc pulmonary blood flow
A
- ASD
- VSD
- PDA
- AV canal
15
Q
Atrial Sepal Defect (ASD)
A
- abnormal opening b/w the atria: L to R shunt
- S/S in infants: activity intolerance, fatigue, orthopnea
- mgmt:
- spontaneous closure occurs frequently
- supportive tx until child is in preschool
- direct closure or patch placement
16
Q
Ventricular Septal Defect (VSD)
A
- abnormal opening b/w ventricles: L to R shunt
- clinical manifestations:
- harsh systolic murmur
- inc ventricular and pulmonary artery pressures
- FTT
- dyspnea
- recurrent episodes of CHF: retaining fluid indicated by inc weight and dec UO
17
Q
therapeutic mgmt of VSD
A
- higher calorie, small frequent feedings
- spontaneous closure occurs in majority by first 2 years of life
- if small, usually asymptomatic
- if moderate to large, will show signs of CHF and FTT
- manage with digoxin and diuretics
- surgical closure done before irreverible pulmonary dz or Eisenmenger syndrome occurs
18
Q
VSD and pulmonary artery band (PA band)
A
- band is placed around main pulmonary artery to dec pulmonary blood flow
- usually done in patients with multiple VSDs or complex heart anatomy
- nurses must assess for tightening/loosening of PA band
- if band tightens, then not getting enough blood to lungs to get oxygenated, so becomes hypoxic
19
Q
patent ductus arteriosus (PDA)
A
- normal pathway in fetal circulation, but large channel b/w pulmonary artery and descending aorta
- functional closure usually shortly after birth
- permanent closure usually w/in 1st wk of life
- L to R shunt formed
20
Q
therapeutic mgmt for PDA
A
- PGs will maintain patency of ductus arteriosus
- administration of indomethacin/ibuprofen will close the ductus arteriosus
- surgical closure:
- PDA ligation
- visual assisted thorascopic surgery (VATS)
- nonsurgical: w/ coils in cath lab
21
Q
Atrioventricular Canal (AV Canal)
A
- large central AV valve is created, allowing blood to flow b/w all chambers
- inc incidence w/ Trisomy 21
- L to R shunt formed
22
Q
name the defects with obstruction of blood flow from the ventricle
A
- coarctation of the aorta (COA)
- aortic stenosis
- pulmonary stenosis
23
Q
coarctation of aorta (COA)
A
- localized narrowing of aorta near the insertion site of the ductus arteriosus
- can be before or after the DA
- results increased pressire proximal to the defect and decreased pressure distal to the defect
- hallmark sign: differences in BP in upper and lower body
- have to check BP on all 4 extremities
- high pressure in head: HA, epistaxis
- dec pressure in lower extremities: weak pulses, color change
24
Q
COA clinical manifestation and tx
A
- clinical manifestations:
- high BP and bounding pulses in UE, weak or absent pulses in LE (also usually cool to touch in LE)
- BP difference of 8-10 mmHg b/w upper and lower extremities needs to be evaluated
- oxygen saturation differences b/w UE and LE
- infants will present w/ signs of CHF: severely acidotic, hypotensive (shock)
- older children will present w/ dizziness, HAs, fainting, epistaxis from HTN
- tx: open coarcation w/ stent
25
aortic and pulmonic stenosis
* may correct in cardiac cath with balloon placement
* look for S/S of these narrowing down again as child ages
26
name the defects with dec pulmonary blood flow
* terrible "T's"
* tetralogy of Fallot (TOF)
* tricuspid atresia
* transposition of great vessels (TGV)
27
defects assoc with TOF
* VSD
* overriding aorta--aorta overrides VSD
* some of deoxygenated blood to periphery
* pulmonary stenosis
* right ventricular hypertrophy
* may not present at birth but will enlarge as child ages
28
S/S of TOF
* infants become acutely cyanotic at birth--once DA starts to close
* worsening of cyanosis for first year
* murmur
* fatigue with feedings--diaphoretic and cyanotic with PO feeds
* clubbing of fingers
* "tet" spells--hypercyanotic episodes
* squatting position in older children
* polycythemia--compensatory mechanoism to inc RBC to carry oxygen
* VERY IMPORTANT to prevent dehydration, but don't want to contribute to HF
29
"Tet" spells
* hypercyanotic episodes
* unusally occurs in the morning when waking up
* precipitated by crying, defecation, and feeding
* infant becomes acutely cyanotic
* dec pulmonary blood flow and inc R to L shunting
* so more deoxygenated blood being sent to periphery so they are blue
* leads to an inc in oxygen requirement which infant is unable to meet
30
therapeutic mgmt of TOF
* stay calm as not to make child anxious/upset
* place infants and small children in knee chest position--helps to decrease venous return from the legs which is deoxygenated
* increases systemic vascular resistance which diverts more blood into pulmonary A
* older children: squatting position
* administer oxygen: NC 5 L
* give morphine SQ or IV--slows RR and dec muscle spasms in heart
31
treatment of TOF
* palliative shunt: modified Blaclock Taussig shunt which provides blood flow to pulmonary As
* gives time for child to grow to be able to later get open heart surgery
* shunt MUST stay open so these kids are often on aspirin, but need to be attentive if child exposed to viral illness
* complete repair: consists of closing VSD and resecting the infundibular stenosis, placement of pericardial patch to enlarge the right ventricular outflow tract (RVOT)
* usually child leaves surgery on ventilatory support and chest tubes b/c want child to rest
32
tricuspid atresia
* tricuspid vave fails to develop, so have to keep the DA open to have blood flow to lungs
* there is no communication b/w right atrium and right ventricle
* pulmonary blood flow is diminished
* tx:
* keep PDA open with PG E1
* stages of surgical repair
33
important note about children with R to L intracardiac shunting
* children are at inc risk for air from venous sytem going directly to brain and resultin in air embolism
* all IV lines should have filters to rpevent air from entering the system
* entire tubing and any syringes used for flushing or medication administration are checked for air
* any air is removed and connections taped securely
34
transposition of the great vessels (TGV)
* pulmonary A leaves the left ventricle
* aorta leaves the R ventricle
* PDA must be kep open or it is not compatible with life
* patent foramen ovale
* manifestations:
* cyanosis always present at birth
* hypoxic spells--may be frequent esp when crying
* infants with large VSDs may present with CHF
35
therapeutic mgmt of TGV
* oxygen of little benefit
* may enlarge or create ASD to allow for more mixing
* nitric oxide can be used to dec PVR, enhance pulm blood flow, and reduce cyanossis
36
tx of TGV
* PG E1 administered to keep PG E1 open
* arterial switch: usually done 7-30 days after birth
* 2 great vessels are transposed to keep their correct ventricles and coronary arteries are transferred to ascending aorta
* ASD (all infants with TGV) and VSD closed at this time
37
what are the 2 defects considered mixed defects?
* TGV
* hypoplastic left heart syndrome (HLHS)
38
HLHS
* severe hypoplasia of L heart structures
* small L ventricle unable to sustain adequate CO in the presence of mitral valve stenosis/atresia or both
* only blood flow is through the PDA
* clinical manifestations
* cyanosis
* child may present in state of vascular collapse w/:
* tachypnea
* dyspnea
* dec BP in all extremities
* grunting
* nasal flaring
* hypothermia
39
therapeutic mgmt of HLHS
* stage reconstruction
* Norwood Procedure: anastomosis of pulm A to aorta to create new aorta
* also create large ASD
* Glenn Shunt: done at 6-9 mos to help get blood to lungs
* Fontan procedure
* heart transplant
40
w/ L to R shunt
* mostly pulmonary issues
* tachypneic
* resp illness
* dyspnea
41
w/ the terrible T's and HLHS
* usually have to keep DA open to make sure blood getting to lungs and out to periphery
42
who should transport a pt?
* the person with the highest ability to do something if something goes wrong
43
cyanosis
* when there is venous arterial shunting or obstruction of blood flow to the lungs
44
heart failure
* occurs when CO is unequal to body requirements
* body dams up in heart and pulm vasculature becomes engorged
* S/S: edema, shortness of breath, dec urine output, inc weight
* mainly occurs due to structural defects
* inc pulm blood flow
* obstructive defects
45
mgmt of HF
* improve cardiac fcn: digoxin, ACEI
* remove excess fluid
* furosemide, HCTZ, spirinolactone
* may require K+ supplements
* fluid restriction
* dec cardiac demand
* limit physical activity, minimize crying
* keep metabolic needs to a minimum: small frequent feeds
* cluster care
* improve tissue oxygenation: positioning, suctioning
* tx underlying cause
46
digoxin
* 3 major actions:
* inotropic: inc force of contraction
* chronotropic: dec HR
* dromotropic: slows conduction of impulses thru AV node
* indirectly enhances diuresis
* used in peds b/c of rapid onset/short half life
* ECG done before first dose
* bolus given IV or PO in divided doses over 24 hrs to bring child's levels to therapeutic range
47
digoxin as high alert med
* infants very raraly receive more than 1 mL in a single dose
* higher dose sign of error
* compare with another RN
* hypokalemia--\>inc risk of dig toxicity
* hyperkalemia--\>dec effects of digocin
* keep potassium in normal range
48
ACE inhibitors
* ACEI block the conversion of Ang I to Ang II--vasodilation occur
* effects:
* dec PVR, SVR, BP
* reduced afterload
* dec R and L atrial pressures
* reduces secretion of aldosterone--reduces preload by preventing volume expansion from fluid retention and dec risk of hypokalemia
* for this reason, this addition of potassium supplements to children taking diuretics is not necessary--may cause hyperkalemia
49
diuretics
* mainstay of therapy
* pay close attn to F/E
* begin to record output as soon as drug is given
* watch for dehydration
50
how to dec cardiac demands in HF
* neutral thermal env
* treat any infections (abx)
* reduce effort of breathing: suctioning, nebulizer
* use meds to sedate a fussy baby
* provide rest and quiet env
51
how to improve tissue oxygenation with HF
* supplemental cool, humidified oxygen
* use O2 carefully in children with complex heart defects (is a vasodilator and will dec PVR)
* will inc blood flow to lungs
52
how to d/c NG tube
* must clamp tube when pulling it out so baby doesn't aspirate the contents when crying
53
rheumatic fever
* systemic inflammatory dz that occurs as a result of naturally acquired immunity to group A strep infection
* carditis often occurs
* most common cause of acquired heart dz
* usually seen in children b/w 6-15, peak at 8 yo
* often seen in more than 1 family member
* onset usually about 3 weeks after untreated URI with Group A strep
* dx made with Jones Criteria
54
clinical manifestation of rheumatic fever
* positive strep test
* arthritis: most common
* carditis
* tachycardia--higher than normal even with a fever
* GI disturbances
* dec platelet count: inc risk of bleeding
* HAs
* tinnitus
* SEs of steroidal therapy if used
55
tx of rheumatic fever
* abx to tx strep infection and lifelong prophylaxis
* can be on daily PO meds or monthly IM injections
* anti-inflammatory meds: aspirin, ibuprofen
* digoxin: b/c the valves are affects by rheumatic fever--\>dec CO, so give digoxin to inc strength of contractility
56
Kawasaki Dz (Mucotaneous LN Syndrome)
* acute systemic vasculitis of unknown cause
* usually in those \<5 yo
* acute dz is self limited
* most common problem is dilatation of coronary As--\>aneurysms can develop
57
Kawasaki Dz clinical manifestations
* acute phase: first 10 days
* fever up to 104 (40 deg C)
* strawberry tongue--diffuse redness of oral mucosa, erythema of lips/gums
* erythema and edema of hands and feet
* polymorphous exanthema
* cervical lymphadenopathy (unilateral)
* sub acute phase: 11-25 days
* desquamation of hands/feet--skin sloughs off
* rash, fever, lymphadenopathy disappear
* CV changes occur--coronary dilations occur, so need serial echos
* convalescent phase:
* sed rate and platelet count return to normal
58
tx of Kawasaki Dz
* goal is to reduce inflammation in coronary A and prevent thrombosis
* give single dose of IV gamma globulin and aspirin w/in 10 days of onset
* reduces chance of coronary A inflammation
* then dec ASA dosage, but have to continue taking for 6-8 weeks or indefinitely if inflammation in coronary As
59
systemic HTN
* make sure using correct size BP cuff
* know baseline BP for that child
* smaller they are the lower the systolic pressure
* need to differentiate b/w primary HTN (not usual in kids) and secondary
* main cause of secondary HTN is renal dysfunction
* before a dx of HTN is made BP should be taken on 3 separate occasions
60
significant vs severe HTN
* significant: BP persistently b/w 95-99% for sex, age, height
* severe: BP persistently at or above the 99% for sex, age, height
61
mgmt of systemic HTN
* lifestyle modifications
* pharmacological agents
62
hyperlipidemia/hypercholesterolemia
* current research indicates that a presymptomatic phase of atherosclerosis begins in childhood
* preventive cardiology is trying ot identify at risk kids early and intervene
* mgmt:
* dietary changes
* if diet is not successful, drug therapy may be needed
* statins
* cholestyramine or chlestipol: bile acid binding resins
63
cardiac dysrhythmias
* bradycardia
* tachycardia
* conduction disturbances: irregular HR
* supraventricular tachycardia: one of most common
* HR b/w 200-300
64
SVT
* infants and young kids have trouble compensating for rapid HR
* S/S: poor feeding, pallor, extreme fussiness
* tx:
* vagal maneuvers
* administer adenosine
* children w/ minimal symptoms may receive digoxin
* transesophageal overdrive pacing or synchronized cardioversion
* used only on kids who don't respond ot above tx
* has to be done in ICU
65
digoxin toxicity
* halos in vision
* n/v
* bradycardia: late sign
Pediatrics Test II
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