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pds 1

wwallace pds 1

QuestionAnswer
Anatomical differences of the upper airway in peds larger tongue and more lymphoid tissue, epiglottis is larger & less flexible, larynx higher, narrowest point is cricoid ring, trach narrower and shorter
Physiological considerations of upper airway larger tongue and lymph tissue make infants obligate nose breathers, causing secretions or inflammation to increase resistance and WOB, increased risk of occlusion, susceptible to trauma
Larger tongue and more lymphoid tissue causes increased risk of upper airway occlusion, is the reason infants are obligate nosebreathers
An infants epiglottis is susceptible to trauma because it is larger and less flexible than an adult, and lies more horizontal
An infant’s larynx is higher or lower in the neck in relation to the cervical spine? higher
The narrowest part of the infants larynx (airway) is the cricoids cartilage (ring), adult is glottis
Infants sternum and ribs are mostly made up of cartilage, less stability to chest (movement of diaphragm or RR determines VT)
Infants VE comes from increase in RR, not VT
Low pulmonary reserve in infants is due to 1 heart is large so lung volume is smaller, 2 instability of thoracic cage (VT not increased with chest expansion but RR), 3 proportionately large abdomen (pushing up diaphragm)
Infant Metabolism differences infants have higher BMR, infants have unpredictable response to medications do to BMR
Higher BMR in infants leads to higher caloric requirements and increased O2 expenditure in proportion to body size compared to adults
Infant BMR and Med dose caution unpredictable responses due to BMR means time and dose must be adjusted for each individual pt
Large surface area of skin compared to body weight in infants leads to prone to heat loss or difficult temperature control, and difficult maintenance of hydration
What percent of a newborns total body weight is H2O? 80
How many grams in 1 lbs? 454 grams per lbs
What weight of preemie is now considered viable? 500 grams
Barriers to good communication are language, culture and education level
Children presenting with what signs need to have a history taken? dyspnea and respiratory distress
Question to ask during history 1 chronic, 2signs of infection, 3fever, 4Rx, 5family Hx, 6 Hx of resp probs 7 Hx of GI reflux 8 character of cough 9 breathing pattern 10 Hx wheezing 11cyanosis 12 chest pain 13 sputum 14 growth 15 environment 16 meds
Cyanosis presence with O2 delivery indicates R-L shunting
Complaints of chest pains may be an indication of pneumonia
3 primary goals in assessment of the pulmonary system in pediatric patient are localize the disease, observe the adequacy of gas exchange, determine nature of pt’s respirations
How do we localize the disease gather Hx, additional testing ie CXR, auscultation, percussion, palpation, symmetric chest movement, trachea at sterna notch
How to we observe for adequacy of gas exchange ABG (not often, but sometimes heal stick), pulse ox, transcutaneous/end tidal CO2 monitors
How do we determine nature of pt’s respirations rate and pattern, increased WOB, LOC, skin color wheezing accessory muscles etc
Pediatric Asthma is reversible airway obstruction, airway inflammation and airway hyperresponsiveness to a variety of stimuli
The majority of ped pt’s have extrinsic or intrinsic asthma? extrinsic associated with allergies
Asthma exacerbation characteristics are dry hacking cough with wheezing on auscultation, with cough becoming wetter and productive, increased RAW, audible wheeze, decreased PaO2 early due to V/Q mismatch, decreased PaCO2 due to hypoxia and accessory muscle use
The best way to gage if therapy is working in asthma attack is % change in Peak Flow
Change in peak flow calc is (post – pre/ pre)x100 acceptable change is 12 to 15% so anything greater than 12% is good
If pt stops wheezing what does this mean? impending respiratory failure
Most common asthma allergens are pollutants, dust mites, feathers, smoke, pet dander, house dust, cockroaches, food preservatives (sulfurs)
Decreased PaO2 early in an acute asthma attack V/Q mismatch
What does RT look for to measure severity of asthma attack PaCO2, 35 or less is mild, 40 or less is moderate, above 40 is severe and resp is imminent
First line treatment for asthma 1. O2 (maintain SpO2 above 95%, 2. beta adrenergic (first two back to back then go to continuous neb) epi or terbutaline possible depends on doc 3 anti inflammatory (IV or inhaled) 4. Heli
Modality in ER to avoid intubation continuous neb with albuterol for enough for 8 treatments. Decreases need for intubation and perhaps decrease need for IV bronchodilators and terbutaline
Oxygen delivery or CAO2 equation CAO2 EQUALS (HGB*1.34*SAO2)+(PAO2*.003)
Why is the infant chest less stable? because the sternum and ribs are mostly cartilage
Adventitious BS wheezes, rhonchi, crackles/rales, stridor
Wheezes high pitched and musical sound, usually on expiration ( can be heard on inspiration with asthma), produced by air moving thru partially obstructed airways, seen in asthma, pulm edema, foreign body, airway tumor, external compression by vascular ring
Rhonchi produced by air moving through airways with a large amount of secretion, low pitched and rumbling (straw in milk) heard in bronchiectisis, pneumonia, CF
Crackles (rales) sounds like popping of bubble wrap or sandpaper, only heard on inspiration, caused by air moving through fluid filled alveoli, or deflated alveoli re expanding, associated with atelectasis and pulm edema
Stridor produced as air flow past the partial obstruction of the upper airway during inspiration, high pitched like wheezes, seen in croup, post exudation and foreign body aspiration
How do you tell the difference between stridor and wheezes listen over larynx and chest, stridor heard over trachea and wheezes heard over chest
Normal Vitals HR nb-100-180 inf 100-160 tod 80-110 sch 65-110, adol 60-90, BP age*2+80over .57 * syst, perfusion state equals capillary refill greater than 3 seconds is low rate, urine 1-2 ml/kg/hr, RR NB 30-60 inf 24-40 tod 20-30 sch 20-25 5-12 16-20 adol 12-16
CXR consolidation and infection is what color? white
CXR of airtrapping is what color? dark distal to plugging
Dull percussion note consolidation
High pitched “tympanic” percussion note hyperaerated (airtrapping)
What is the best way to evaluate gas exchange? ABG
What are the physical signs of hypoxemia tachycardia, cyanosis, labored breathing, deterioration in mental state
Peak flow change equation is change equals (post-pre)/pre* 100 (great than 12 % is acceptable change
Signs of hypercarbia are rapid, bounding pulse, confusion, muscular twitching
What are the steps in a pt scenario? History, examination (localization, accessing gas exchange, nature of respiration) diagnose and plan the treatment
Why does HGB saturation take so long to show signs of hypoxia? the lower the HGB count the longer it takes (5 grams)
When does a pt assessment start? as you enter the room
2 year old on peds floor is sleeping with RR of 70, what is the cause? Decreased PaCO2
(voice vibrations)that can be felt. increased by solids like consolidation and atelectasis fremitis
Heart Rate Normals NB 100-180, INF 100-160, TOD 80-110, SCH 65-110, ADOL 60-90
Resp Rate Normals NB 30-60, INF 24-40, TOD 20-30, SCH 20-25, age 5-12 16-20, ADOL 12-16
Adventitious Breath Sounds (abnormal Breath Sounds) Crackles/rales, Rhonchi, Wheeze, Pleural Friction Rub, Stridor, Diminished
Bronchial Breath Sounds (normal breath sounds) E
bronchophony (99 or 123 will be louder) increased intensity and clarity of vocal resonance, more tissue density than air (consolidation), easier to detect unilaterally, dull percussion, increased vocal fremitus bronchovesicular breath sounds
crackles/rales (adventitious BS) bubbling-crackling sounds, mainly on I, air flow through fluid, discontinuous-specific locations, does not clear with cough. caused by pulmonary edema, pneumonia, emphysema, atelectasis, pulmonary fibrosis
Created by: williamwallace