rt 141 week 3

copd def

heterogeneous, preventable condition characterized by chronic respiratory symptoms due to abnormality of the airways/alveoli causing airflow obstruction

spirometry for COPD

FEV1/FVC ratio marks exac risks, acuity levels, inflammation level

small airway disease

chronic inflammation of bronchioles, goblet cell hyperplasia and mucus hypersecretion, airway wall fibrosis and narrowing, loss of alveolar attachments

parenchymal disease

emphysema destruction of alveolar walls, loss of elastic recoil and gas exchange area, reduced tethering, air trapping and hyperinflation

chronic inflammation

noxious particle/gas exposure, neutrophils, macrophages and t-lymphocytes predominate, structural remodeling

chronic bronchitis

chronic productive cough for >3 months in 2 yrs, in airways (bronchi), symptoms as early as 36yrs, higher exac frequency, even without obstruction

emphysema

permanent enlargement of airspaces distal to terminal bronchioles with wall destruction w/o fibrosis, in lung parenchyma, progressive, loss of diffusing capacity (DLCO)

airway pathology

chronic inflammatory cell infiltration of airway wall, increased goblet cells + mucous gland hyperplasia, airway wall fibrosis with progressive narrowing, small airway reduction (#), airway collapse from loss of alveolar tethering (wall destruction)

lung parenchyma pathology

acinus - specific part affected by dilation/destruction defines emphysema subtype, loss of alveolar surface area, reduced DLCO (diffusing capacity for CO2), loss of elastic recoil

panacinar emphysema

enlargement/destruction of all parts of acinus, lung bases, involves the entire secondary pulmonary lobule, most commonly associated with alpha-1 antitrypsin deficiency

proximal acinar (centrilobar) emphysema

respiratory bronchiole (central position of acinus), upper lobe predominant, classically associated with smoking

distal acinal (paraseptal) emphysema

alveolar ducts predominantly affected, subpleural, may occurs alone (associated w/ spont pneumo) or combined w/ other subtypes

pulmonary vascular changes

intimal hyperplasia and smooth muscle hypertrophy/hyperplasia of small pulmonary arteries, though to result from chronic hypoxic vasoconstriction, causes loss of associated capillary bed (pruning)

cardinal symptoms

dyspnea, chronic cough, sputum production, less common → wheezing, chest tightness

systemic effects

weight gain (loss is more advanced, worse prognosis), activity limitation, cough syncope, depression, and anxiety (clubbing in COPD is not common, differential diagnosis likely)

gold standard diagnosing

spirometry required to confirm COPD, gold 1 mild, FEV > 80% predicted, moderate 80% > predicted, severe 50% > predicted, very severe 30% > predicted

DLCO

diffusing capacity, checks for interstitial disease, good inde of anatomic emphysema burden, not needed for COPD diagnoses

the BODE index

body mass index (low = worse), obstruction (FEV1, airflow limitation), dyspnea (mMRC dyspnea score, symptom burden), exercise capacity (6 min walk, cardiopulmonary reserve) → risk of death

x ray findings

rapidly tapering vascular shadows, increased lung radiotranslucency, flat diaphragm, bullae, prominent hilar vessels, pruning of distal pulmonary vasculature

gold ABE assessment tool

A - 0-1 moderate exac not leading to hospitalization, mmrc 0-1 / cat <10, B - 0-1 moderate exac not leading to hospitalization, mmrc >2 or cat >10, C- >2 moderate exac or >1 hospitalizations, any symptom level

end stage COPD

2+ respiratory related hospital admissions within 12 months, PaCO2 > 52mmHg, FEV1 <50% predicted, criteria should prompt earlier goals of care conversations, not only end of life

adjunctive agents

PDE4 inhibitors (roflumilast) chronic bronchitis + severe obstruction, chronic macrolide therapy (azithromycin) anti inflammatory + antibiotic, mucolytics/antioxidants in selected pts

anti inflammatory agents

eosinophils must be >300 cells per dL to add to COPD patient (ICS, biologics)

biologic therapy

for pts with continued exac despite maximal inhaled therapy with elevated eosinophils, dupilumab (anti IL-4Ra), mepolizumab (anti-IL-5), also given when LABA+LAMA do not work and eosinophils are low

acute resp failure COPD

first line recommendation is NIV (contraindications → nausea, sedation, respiratory arrest, inability to protect airway, secretions, hemodynamically unstable, refusal)

4Ms

matters (patient goals), medication (minimize polypharmacy), mentation (mental status), mobility

pneumothorax

restrictive lung disease, free air accumulates in the pleural space between visceral and parietal pleura, lowers functional lung volumes

closed pneumo

gas in the pleural space is not in direct contact w/ atmosphere

open pneumo

the pleural space is in direct contact with the atmosphere, so gas can move freely in and out (sucking chest would)

tension pneumothorax

intrapleural pressure exceeds intra alveolar (or atmospheric) pressure - a one way valve effect that builds pressure

pneumo presentation

sudden crisis onset, severe dyspnea, pleuritic chest pain, cough, cardiovascular collapse

pendelluft

during inspiration some rebreathed dead space gas moves back into the normal lung, paradoxical movement of gas between collapsed and normal lung

tachypnea in pneumo

deflation and irritant receptor activation, stimulation of j receptor, lung deflation triggers increase in RR

recognizing pneumo

tracheal deviation, jugular venous distension, hypotension, absent breath sounds, hyperresonant percussion on affected side, increased thoracic volume on affected side

ABG pneumo

small → high pH low PaCO2 from high RR, large → low pH, high PaCO2 cant sustain increased WOB

oxygenation indices severe pneumo

atelectatic, unventilated alveoli remain perfused → intrapulmonary shunt increases, reduced ventilation and cardiac output reduce O2 delivery, tissue O2 consumption stays roughly the same

radiograph pneumo

increased translucency on the side of pneumo, visible visceral pleural line w/ no lung markings peripheral, depressed diaphragm on affected side

suction of pneumo

negative pressure not exceed -12cmH2O, -5cmH2O is generally all that is needed

emergent needle decompression

5th ICS anterial/mid axillary line, 2nd ICS, midclavicular line

rib fracture signs

dyspnea, localized pain, chest wall instability, crepitus, pneumo/hemothorax

flail chest

two or more fractures in two or more places on at least three adjacent ribs creating a free floating segment, paradoxical chest wall motion is hallmark sign

aortic aneurysm

90% die within minutes, little external evidence of serious chest trauma, caused by sudden decelerations, massive blunt force (bp difference in R and L arms)