Exam 2 Flashcards
A&P Respiration
diaphragmatic breathers (stomach rises & falls), ribs & sternum too pliable for intercostal muscles, less alveoli which increases exponentially, paradoxical chest movement, increased O2 consumption; biggest difference = airway is size of straw
Respiration – S/S
1 sign of change in oxygenation = restlessness
LOC, alteration in perfusion (color change, cap refill, decreased pulse ox, cool skin, mottling), increased HR & RR, nasal flaring, decreased urine output, dyspnea, grunting, retractions, stridor, wheezing, clubbing, intercostal bulging
Respiration – Assessment
LOC & response to environment, RR, resp effort (use of accessory muscles & work of breathing), color of skin/mucous membranes, lung sounds; hx including urine output, activity level
Retractions
usually starts lower & moves up (higher is worse); subcostal (below ribs), substernal, intercostal, suprasternal, clavicular
Respiratory distress
stridor (high pitched noisy respiration indicating upper airway narrowing), wheezing, grunting (body’s attempt to create PEEP), retractions (sinking in of soft tissue indicates use of accessory muscles to improve respiration
Resp distress – Moderate to Severe
anxious/restless, more retractions, color changes, wheezing/stridor, O2 going down w/ HR going up, head bobbing
Resp distress – Mild
mild retractions that start low, maybe a little pale, not much nasal flaring, responding to environment
O2
use nasal cannula but don’t go above 4L on little guys; only use mask if really need a higher O2% (kids will fight it)
Asthma
hyperresponsiveness of the airway = inflammation, constriction & mucus secretion
Asthma Peak Flow – Green
80-100% of kid’s personal best; no symptoms, continue maintenance tx
Asthma Peak Flow – Yellow
50-79%; acute exacerbation may be occurring, may need to increase maintenance tx, call Dr if kid stays here
Asthma Peak Flow – Red
less than 50%; medical alert b/c severe airway narrowing may be occurring, short-acting bronchodilator & notify Dr immediately if doesn’t come up to yellow or green
Croup
named by location of inflammation/infection (acute epiglottis/supraglottis, acute laryngotracheobronchitis (LTB), acute spasmodic laryngitis, acute tracheitis
Croup – S/S Acute Tracehitis
cough (brassy or barky sounds like a seal) & varying degrees of inspiratory stridor & resp distress (d/t inflammation/obstruction of larynx)
Croup – S/S Acute Epiglottis (Supraglottis)
more acute rapid onset w/ high fever, toxic looking, tripod position (w/ drooling); no throat inspection w/o prep to intubate
Croup – Tx Acute Epiglottis
IV antibiotics & corticosteroids
Croup – S/S Acute LTB
slower onset, less of a temp, usually a little older kids, usually viral & preceded by URI, most common form; tx by maintaining airway w/ cool mist (outside in winter), nebulized epinephrine (bronchodilate & open airways), steroids
Pneumonia – viral
supportive (fluids, cool mist, antipyretics, O2) & is more frequent than bacterial vs. bacterial = give antibiotics on time, antipyretics, O2, hydration, possibly thoracentesis (if pleural perfusion) teaching family w/ antibiotics
Suctioning
0.5-1cm beyond end of trach
babies 80 - 100 mmHg
2-3 = 100 mmHg
older kids 100-120 mmHg
CF – path and S/S
common organisms that cause infection are pseudomonas, streptococcus & pneumococcus; expect manifestations of long-term hypoxia (ie barrel chest & clubbing); increased risk for infection d/t depressed immune system & thick pulmonary secretions
CF – diet
high protein, low-moderate carbs & mod-high fat; need pancreatic enzymes before any meals/snacks; need fat-soluble vitamins
CV – health Hx
maternal rubella during PG, maternal ETOH or drugs, family hx of CHD (congenital heart defect), chromosomal abnormalities, presence of murmurs & age 1st detected, feeding problems (fatigue, FTT, diaphoresis during feedings), resp difficulties (tachypnea, DOE, SOB, cyanosis, frequent URIs), chronic fatigue/activity intolerance
CV – physical findings in child
FTT w/ minimal fat, cyanosis/dusky/pallor, periorbital & peripheral edema, pulse alterations, tachypnea & use of accessory muscles, hypotension or unequal BP b/w upper & lower extremities (coarctation of aorta), engorged neck veins, murmurs/bruits/thrills, abdominal distension, hepatomegaly, splenomegaly, decreased activity, diaphoretic
Murmurs
organic (CHD or acquired heart defect w or w/o physiologic abnormality)
innocent (no anatomic or physiologic abnormality)
functional (no cardiac defect but physiologic eg anemia)
Syndromes with high CHD
Trisomy 13, 18 & 21
Eisenmenger Syndrome
left to right shunt becomes right to left shunt = cyanosis which increases pulmonary vascular resistance (PVR); occurs after prolonged period of increased pulmonary blood flow & can lead to death
Increased pulmonary blood-flow (acyanotic)
ASD VSD PDA
ASD
left to right shunt so some of oxygenated blood goes back to r. side of heart & lungs; s/s: activity intolerance, fatigue & orthopnea, also resp issues (ie infections b/c lungs working harder)
ASD Tx
often spontaneous closure, supportive tx w/ diuretic until old enough for closure
VSD
most common, left to right shunt
s/s – overactive precordium, harsh systolic murmur, increased ventricular & pulmonary artery pressure, FTT, HF, dyspnea, frequent URIs, small = asymptomatic
VSD Tx
~1/2 spontaneously close, lg = managed w/ Dig & diuretics, sx closure before irreversible pulmonary disease (periodic caths to check pressures until repair d/t risk of Eisenmenger)
palliative tx – pulmonary artery banding (multiple VSDs or complex heart anatomy): assess for tightening of band
PDA
lg channel b/w pulmonary artery & descending aorta supposed to close at birth, increased incidence in premies (increased prostaglandins keep it open, may also have lung disease); sometimes w/ major defect must keep this open intentionally
s/s – sm may be asymptomatic, frequent URIs, premies present sooner, older kids slight growth retardation & activity intolerance
PDA Tx
some close spontaneously, admin Indomethacin to premie will close it, sx closure w/ ligation or VATS, nonsx w/ coils in cath lab
Decreased pulmonary blood-flow (cyanotic)
Tetraology of Fallot
Tricuspid atresia
TOF – patho
VSD
Overriding Aorta
Pulmonary Stenosis
R. Ventricular Hypertrophy
TOF – S/S
cyanosis, clubbing, dyspnea, thrill, resp distress during feedings, polycythemia (imp to prevent dehydration); infants = intense cyanosis when PDA closes, severe DOE, syncope, limpness, convulsions; older kids = squatting position
TOF – Tx
O2, Propranolol, Morphine, newborns get Inderal (BB) until sx repair (complex defects like this are staged repairs that start w/ palliative sx to get more blood to lungs
Hypercyanotic episode
intense cyanosis, extreme fussiness, pallor, tachypnea, flaccidity, possible LOC, common in AM, precipitated by crying, defecation & feeding (increases R-L shunting); can lead to seizures, CVA & death
Hypercyanotic episode – Tx
be calm & place sm kids & infants in knee-chest position (reduces desaturated venous return from legs & increases systemic vascular resistance which diverts more blood to pulmonary artery & lungs to get oxygenated)
Obstruction of blood-flow from heart (acyanotic)
Coarctation of Aorta, Aortic Stenosis/Atresia, Pulmonic Stenosis/Atresia; big issue is CHF
COA
narrowing of aorta near ductus arteriosus = increased pressure proximal & decreased pressure distally; s/s – high BP & bounding pulses in upper extremities, weak/absent pulses in lower extremities, BP difference 8-10mmHg b/w upper & lower needs to be evaluated, O2 sat differences b/w upper & lower extremities, present w/ s/s of CHF, infants present w/ near death state (severely acidotic & hypotensive), older kids present w/ dizziness, h/a, fainting & epistaxis
Mixed Blood Flow – patho
major heart defects
transposition of the great vessels (TGV), hypoplastic left heart syndrome (HLHS), truncus arteriosus
Mixed Blood Flow – Tx
O2 is of little benefit, may enlarge or create ASD for more mixing, Nitric Oxide (decrease PVR, increase pulmonary bloodflow & reduce cyanosis), Prostoglandin to dilate ductus arteriosus, sx (arterial switch – put the 2 great vessels where they’re supposed to go)
CHF – causes
CHD increased pulmonary blood-flow obstruction of blood-flow from heart also Cardiomyopathies Arrhythmias Hypertension Pulmonary Embolism or Chronic Lung Disease Severe Hemorrhage or Anemia
Right Ventricular Heart Failure
Less blood is oxygenated
Pressure increases in the right atrium and systemic venous circulation, which leads to edema of the extremities
Left Ventricular Heart Failure
Left Ventricle is unable to pump blood into systemic circulation
Pressure increase in the Left Atrium and the Pulmonary Veins
Lungs become congested with blood which leads to increased pulmonary pressure and pulmonary edema
CHF Nx
dig, antiHTN ie ACEIs (monitor BP), diuretics, fluid & Na restriction, decrease cardiac demands (neutral thermal environment, tx any infections, reduce effort of breathing, sedate fussy baby w/ Chloral hydrate, cluster care), improve oxygenation (used carefully in kids w/ complex heart defects b/c O2 is a vasodilator = decrease PVR = increased bloodflow to lungs)
Fluid restriction – may be on ½ maintenance d/t fluid retention to prevent further overload
Digoxin
ECG should be done before initial dose is given & always check for bradycardia; good for peds d/t rapid onset & short half-life
infants very rarely receive more than 1mL (50mcg) in 1 dose anything higher is warning of an error
Digoxin – good
inotropic
chonotropic
diuretic – inc renal perfusion = pee more
Rheumatic fever
systemic inflammatory disease caused by Group A Beta-Hemolytic Strep (GABHS) & Carditis is the big issue; s/s – carditis (tachycardia which is higher than would be expected w/ fever), arthritis, GI issues, thrombocytopenia, h/a, tinnitus; tx – lifelong antibiotic prophylaxis, anti-inflammatory (ASA), digoxin
SVT
HR 200-300; s/s – palpitations, dizziness, diaphoresis, infants: poor feeding, pallor & extreme fussiness; tx – vagal maneuvers (coughing, face in ice cold H2O), adenosine, cardioversion, propranolol, amiodarone, ablation (NPO & explain procedure)
Fe deficiency anemia
– s/s – fatigue, pallor, decreased O2, decreased Hgb/Hct, decreased SIC & increased TIBC; starting cow’s milk too early or too much (milk baby); tx – oral ferrous sulfate, Vit C, O2 by nasal cannula, Fe fortified formula & rice cereal
Digoxin alert
A decrease in serum potassium level enhances the effects of Digoxin, increasing the risk of digoxin toxicity.
An increase in serum potassium levels diminish digoxins’ effect – CHECK FOR HYPOKALEMIA
Therefore serum potassium levels (normal range 3.5-5.5) must be carefully monitored
Enemas
use NS; infant 120-240mL insert 1”, 2-4yrs 240-360mL insert 2”
Esophageal atresia & tracheoesophageal fistula
excessive mucus, continuous or sporadic resp distress, repeated regurgitations; 3 C’s of T-E fistulas = coughing, choking & cyanosis
Preop – NPO w/ frequent mouth suctioning, antibiotics, fluids & O2
pyloric stenosis
normal 1st 2 weeks of life then start vomiting or regurgitation initially progressing to projectile vomiting (hallmark symptom), vomit may occur during/right after feeding or be delayed & then infant will be very hungry
GERD – S/S
usually start during 1st week of life, chronic vomiting or regurgitation, cardiorespiratory symptoms, hematemesis; doesn’t become GERD until complications such as FTT, bleeding or dysphagia develop
GERD – Dx and Tx
dx – barium esophogram, esophageal pH monitoring, scintigraphic studies (radioactive nucleotide added to formula)
Tx – sm/slow feedings, frequent burping while feeding, formula thickened w/ rice cereal, upright prone (holding on shoulder), supine or side lying 1hr after heating, HOB elevated (reflux harness); antacids or H2 antagonists, PPIs, prokinetics (ie Reglan & Bethenechol
NISSEN
Calculating dehydration
Pre-illness weight in grams - illness weight in grams / pre-illness weight in Kgs = mls/kg loss
Mild Fluid Loss/Dehydration is < 50 mls/Kg
Moderate Fluid Loss/Dehydration is 51-99 mls/Kg
Severe Fluid Loss/Dehydration is > 100 mls/kg
Two Major Manifestations – CHD
Cyanosis
Becomes apparent when there is venous arterial shunting or obstruction of blood flow to the lungs
Congestive Heart Failure (CHF)
Occurs when Cardiac Output (C.O.) is unequal to body requirements. Blood dams up in the heart and the pulmonary vasculature become engorged
ACE
ACE Inhibitors block the conversion of Angiotensin I to Angiotensin II – So vasodilation occurs as opposed to vasoconstriction
ACE – effects
Decreased PVR, SVR and BP,
Reduction in Afterload
Decreased Right and Left Atrial Pressures
less preload and afterload
