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Pediatric Perfusion defect notes

by: Pallavi Battar

Pediatric Perfusion defect notes NURS 410

Marketplace > San Francisco State University > NURSING > NURS 410 > Pediatric Perfusion defect notes
Pallavi Battar
GPA 3.75

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Pediatric Perfusion defect notes
Nursing Care of Children
Dr. Musselman
Study Guide
Pediatric Perfusion defect notes
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Popular in Nursing Care of Children

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This 9 page Study Guide was uploaded by Pallavi Battar on Saturday September 17, 2016. The Study Guide belongs to NURS 410 at San Francisco State University taught by Dr. Musselman in Fall 2016. Since its upload, it has received 19 views. For similar materials see Nursing Care of Children in NURSING at San Francisco State University.


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Date Created: 09/17/16
Pediatrics: Perfusion Notes Disorder/Disease Pathophysiology Diagnostic and Treatments and Nursing Assessment Interventions Findings Congenital Heart Defects > Shunting: >General CHD >PDA >classifications a. right to left S/Sx a. close PDA meds or a. inc. Pulmonary blood shunt blood a. Inc. HR, Inc. surgery flow (PDA, ASD, VSD) pumped to systemic RR, Retarded growth b. sometimes PDA is b. dec. Pulmonary circulation mixes w/ (special formula kept open to provide blood flow deO2 blood can given to provide adequate circulation  c. obstructive defects cause cyanosis more calories in meds used d. defects of the great b. left to right short period of c. Indomethacin vessels shuntblood time b/c child is a (prostaglandin inhibitor) e. defects w/functional pumped to systemic poor feeder), orally used in premies w/o single ventricle circ. is NOT mixed w/ dyspnea/ orthopnea, bleeding tendencies and deO2 blood  cause fatigue, URI good renal function for over circ. to lungs  >PDA (findings closure of PDA HF depend on age Ibuprophen can and size of shunt) encourage closure > PDA O2 blood a. large shunt = d. transcatheter closure causes ductus to inc. chance of HF in cath lab term babies constrict and close symptoms, frequent e. surgical ligation  if by 6 wks; failure = pulmonary child is NOT good candidate PDA. Should close infections, thinner, for closure complications w/in 24 hrs (Dr. continuous (rare): nerve damage, usually wants machinery-like diaphragmatic paralysis, newborn to stay in murmur heard @ 2 nd laryngeal nerve damage, hospital for > and 3 ICS, clyothorax (risk increased 24hrs) bounding peripheral due to incision), transient a. blood flows pulses from excess HTN, A-flutter from high pressure blood volume from f. Nursing in aorta through aorta to PA, widened Considerations: chest ductus arteriosus PP, cardiomegaly physiotherapy and excessive blood (seen on radiograph pulmonary toilet post-op, flow to lungs post toddlerhood) discourage splinting, b. small PDA is ok b. Dx confirmed encourage deep breathing but still at risk for and Tx through g. Prostoglandin E1 clots, air embolus, radiograph, 2D (PGE1): given if PDA is bacterial echocardiography, protective for infant acts endocarditis, and color flow Doppler as a natural shunt (allows pulmonary HTN studies blood flow to mix and (over time) bypass obstructed area) c. inversely > ASD potent dilator of DA used related to a. Dx can’t be for L sided obstructive gestational age made in utero b/c lesions (improves systemic (younger the child foramen ovale is perfusion), A-B balance, and is the more likely natural urine output they will have b. thinner, growth PDA premies!!!)  retardation, easily >ASD results from tired, repeat a. cardiac cath to close premature delivery, pulmonary b. patch closure for sinus therefore, infections, identified venosus only if cardiac cath situational defect as having only is not effective rather than murmur b/c of lack functional defect of S/Sx (must catch >VSD in early childhood), a. monitor for HF, poor >ASD b/w LA and HF (if severe), G/D, poor feeding RA; 3 classifications c. exact position b. if pt has HF diuretics based on location of (delineated) thru and digoxin (Lanoxin), defect echo, chest prophylactic antibiotics a. sinus radiograph shows against subacute bacterial venosus: opening cardiomegaly w/ endocarditis high in atrial septum enlarged RA + RV + c. palliative artery (junction of superior inc. pulm blood flow banding if kid is too small or vena cava and too ill RA)irregular >VSD (normally L d. surgery, cardiac cath pulmonary venous to R shunt) e. heart block is a SE b/c return a. small (smaller septal sutures can cause b. Ostium than aortic valve edema in close proximity to secundum: mid so that flow is conduction system septum closed w/ restricted and f. Inotropics support cardiac cath shunting is CO immediately post-op c. Ostium limited)asymptom g. Critical cases Primum low in atic sedation, hyperventilation, septum; inferior to b. Large  is inotropes (RHF), PGE1 (to foramen ovale unobstructed so it dec. PVR), NO (to dec. pulm associate w/ cleft in can equalize blood flow to manage P- mitral valve and pressure b/w RV and HTN) mitral insufficiency LV d. (shunts c. audible blood from LA to murmur 6-8 wks RA b/c pressure is after birth, HF greater on L develops after PVR side) amount of decreases, dec. blood shunted exercise tolerance, depends on size of repeat pulm defect big shunt = infections, slow/ excess volume on R impaired heart circulation and growth/dev, pulmonary bed cyanosis/ clubbing e. Unrepaired (indicates cardiac hypertrophy reversed shunt (R and L), risk on from inc PVR; is inc. PVR (inc. risk of now R to L shunt) Pulm HTN and PE), d. chest atrial arrhythmias radiograph (vary, depends on >VSD (most amount of common) shunting) pulm a. b/w RV and LV vascular markings, in the septum in cardiomegaly various places (patho depends on size, location, and effects on PVR). Bigger= more shunting= less systemic blood flow (excess flow through RV overworks ventricle and overcirculates pulm bed) b. Membranous: below aortic valve c. Muscular: w/in muscular septum multiple overlapping holes (Swiss cheese effect) makes it difficult for surgeon to find d. Supracristal: infundibular septum causes prolapsing aortic valve cusps. e. if unTx PVR can increases causing inc. pressures in RV than LV (pressure change causes reversal of shunt); severe P-HTN makes VSD inoperable, (sudden reduction of blood = fatality), RHF occurs b/c lungs stay constricted post-op high lung pressures over burdens RV which no longer has VSD as a release valve Tetrology of Fallot (VSD, >VSD is large > poor feeder, >Monitor SpO2, optimize PV stenosis, overriding diminished blood difficulty gaining oxygenation, Tx aorta, RV hypertrophy) flow to lungs, weight, cyanosis hypercyanotic spells (Tet therefore, DeO2 S/Sx (clubbing, Spells), encourage physical blood to systemic dizziness, loss of activity (determined by circulation consciousness, amount of R heart increases w/ activity pressure, RV volume >Pulm stenosis or during BM) overload, residual increases R-L shunting, presence of shunting through >may be acyanotic arrhythmias, degrees of VSD (lg. VSD w/ mild- pulm valve moderate pulmonary regurgitation) >normal G/D; if stenosis limits unTx cyanosis, intracardiac >Blalock-Taussig shuntdec. clubbing, mixing)Pink Tets shunting and eliminates tet polycythemia, spells for kids too ill/ small exercise intolerance > chest radiograph for corrective surgery noramal heart size and inc. pulm blood >surgical complications flow, RV hypertrophy bleeding, conduction problems, pulmonary valve > cardiac cath pre- regurgitation, residual VSD, op Dx tool, shows persistent RV failure, direction and amount of shunting >ECG, MRI, exercise testing, Holter monitoring lifelong Coarctation of the Aorta >located directly >manifestations >Balloon angioplasty in (deformity from localized opposite to the of depend on severity cath lab, surgery (different constriction + narrowing where ductus of narrowing types depending on lesion of aortic wall) arteriosus existed specifics), end-to-end can be preductal >decreases/absent anastomosis (most (narrowing proximal pulses in BLE; common), Darcon conduit to ductus) or measure BP gradient (subclavian flap aortoplaty) postductal difference b/w BUE in infants (obstruction distal to and BLE may ductus) indicate HTN >monitor BP immediately obstruction report pressure post-op (should be kept low usually occurs in gradient to avoid pressure on fresh upper thoracic >10mmHg in suture lines on aortic repair arch infants site); may have residual HTN even in surgery is > mechanically >FTT, HF, renal shut successful obstructs the down, and pumping and puts premature death in >complications strain on the LV. infant (if severe and (uncommon): infection, unTx) hemorrhage, renal >pulm. blood flow is dysfunction, paralytic ileus, normal and no spinal cord ischemia intracardiac mixing leading to paraplegia all unless kid has may occur from aortic coexisting lesion cross clamping (done w/o cardiopulmonary > blood flows to bypass) intra-op b/c of head and BUE @ lack of blood flow below high pressures but aorta. when rest of the blood meets the obstruction it flows @ lower pressure to the rest of the body through the descending aorta.  greater BP in BUE than in BLE >HTN develops, non-pulsatile flow through organs w/ COA caused by obstructed area RAAS stimulated when non- pulsatile blood renal flow causes arterial vasoconstriction Pulmonary Stenosis >obstruction of RV >findings depend on >balloon valvuloplasty (narrowing of valve or systolic ejection severity of stenosis in cath lab dilates and artery) a. mild ruptures deformed valve >3 types based on acyanotic w/ no thru circumferential stress location of RV activity restrictions outflow b. moderate >surgery pulmonary obstruction easily fatigued, valvuloplasty w/ muscle a. subvalvular exertional dyspnea resection and patch (infundibular) c. severe widening of pulmonary stenosis below cyanotic, S/Sx of HF, arteries pulm valve is pulm valve development of regurgitant post-op but pts b. supravalvular pulm arteries are are asymptomatic lifelong stenosis in pulm affected by various f/u arteries above pulm areas of valve congenital stenosisUrgent rubella and William’s surgical repair syndrome c. Valvular stenosis valve displasia > reduction of blood flow to lungs, increase RV pressure and RV SV workload  RV failure and HF over time Heart Disease and > circulating deO2 >hematological >Supplemental O2 Cyanosis hbg resulting in problem associated a. may destabilize kids hypoxemia w/ cyanosis w/ sever forms of CHD; cyanotic skins, nail (polycythemia, those w/ underlying pulm beds, and mucous dehydration, problems may improve membranesincreas bleeding, ed extraction of O2 clubbing, hypoxic >monitor CBC in cyanotic from peripheral spells, kids closely b/c blood can tissues neurological become too viscous injury, negative >don’t assume developmental >raise SVR when Tx cyanosis = cardiac outcomes) cyanotic spell problems as a. keep pt calm to primary issue; Chronic reduce O2 demand and other issues can hyperventilation cause cyanosis Hypoxemia and b. give O2 w/ morphine under perfusion (bronchopulmonary sulfate to relax RV dysplasia, causes the infundibulum which inc. pulmonary arterial following: blood flow which dec. R-L venous fistulas, >Polycythemia shunt neurological (chronic c. knee-chest position abnormalities) hypoxiemia d. hydrate stimulates inc. e. correct metabolic >2 anatomic RBC production) acidosis tx of underlying situations causes compensatory condition or bicarbonate cyanosis in CHD mechanism for body therapy (severity of cyanosis to more hgb f. palliative surgery depends on volume available to inc. O2 (establish shunt) of pulm blood flow carrying capacity g. corrective surgery/ and degree of and improve O2 to transplant shunting) tissues inc blood a. pulmonary viscosity = inc risk venous blood of strokes/ clots redelivery to a. if kid contracts pulmonary (polycythemic from circulation rather cyanosis) virus than flow to system vomiting = diarrhea; b. restricted monitor of pulmonary flow (R- dehydration (b/c L shunts) inc. risk of hemoconcentratio n) b. easy post-op bleeding, easy bruising, or epistaxis due to inc. hgb limiting vascular bed space for platelets and clotting factors c. clubbing from chronic arterial desat and polycythemia > tet spells occur if not yet surgically repaired (most common in 2-4 month old infants) cyanosis worsens w/ agitation, decreases/absent heart murmur intensity, fainting, convulsions a. prolonged/severe tet spells syncope, seizure, cardiac arrest >Neurological complications stroke, meningitis, brain abscesses, abnormal neurological development >Dx Tests (if severely anemic and w/ lg L-R shunt  may not appear cyanotic b/c severely low hgb level) a. H/H levels, CBC, ABGs, pulse ox, chest radiography, ECG >try to keep crying/ activities to a minimum especially in kids w/ intracardiac mixingmay worsen cyanosis Kawasaki Disease >common in >Clinical Criteria >Monitor for HFinc RR (generalized vasculitis; winter and spring; a. fever for 5+ and HR, dyspnea, rales, abd multiple organ system kids <5 y/o days distension disease of childhood) b. @ least 4 of >3 phases the following >comfort care frequent a. acute 1-11 1. bilat oral care, clear liquid diet, days progressive conjuntivitis w/o dec. environmental inflammation of sm. exudate stimulation (brain vessels vessels early 2. oral care also getting inflamed), arthritis, uveitis, mucosa dry, bed rest meningitis, cracked lips/tongue; perivasculitis, strawberry tongue; >Meds IVIG w/ high dose myocarditis, diffuse reddening of ASA during acute phase to pericarditis, mitral oral and pharyngeal reduce risk of coronary insufficiency, HF mucosa artery abnormalities anti- b. subacute11- 3. inflammatory and anti- 21 days medium extremities platelet effect size artery hand/foot edema, inflammation red palms/soles, >immunizations except coronary artery membranous measles/ varicella (b/c aneurysm, late- desquamation of these are viruses), annual onset arthritis, fingertips/toes flu gallbladder hydrops, 4. a. Measles + varicella fingertip + toe erythematous shouldn’t be given for desquamation, rash perineal area 11 months after high thrombocytosis, 5. non dose IVIG b/c mitral insufficiency, purulent swelling neutralizing antibodies coronary artery of cervical lymph will diminish thrombosis nodes  > or = 1.5 effectiveness of live c. cm in diameter vaccines early convalescent21- immunization and 60 days vessel wall >leukocyte count > reimmunization 11 + start to heal inward 15,000/uL, elevated months after IVIG should persistent arthritis, erythrocyte be done if child is @ high aneurysms, long- sedimentation rate, risk for measles term scarring in C-reactive protein affected walls  level 770 mg/L, child w/ prolonged platelets 500K to fever is most @ 1Mil/mm3, sterile risk pyuria Rheumatic Fever > immune response > 4 main signs >Tx depends on (sequalae of GABHS triggered by a. Regurgitant manifestations and severity respiratory infections) colonization of murmur absence of attack pharynx w/ group A make dx of streptococci rheumatic carditis >Management of unlikely; most carditis inotropes, >involves heart, common is mitral diuretics, vasodilators, joints, CNS, skin, regurgitation during corticosteroids (sometimes) and SQ tissues acute attack a. definitive Dx is (holosystolic, best important before ASA and > Characterized by @ apex and down corticosteroids b/c these exudate and left axilla, high anti-inflammatory drugs proliferative pitched, blowing, can mask other dx inflammatory unchanged by (arthritis) response of position, 2+/6 connective tissue intensity) >Chorea sedative, minor b. tranquilizers, quite Cardiomegaly can environment cause death in acute phase; effect endo + >eradication of GABHS tx pericardium strep throat before it gets c. HF worse d. Pericardial friction rubs >prevent reoccurrences >Other signs a. polyarthritis, erythema marinatum, SQ nodules, Chorea


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