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patho lung

altered ventilation/diffusion

QuestionAnswer
ventilation regulation medulla/pons (autonomic) ANS tone lung receptors chemoreceptors
central chemoreceptors sense cerebrospinal fluid pH/PaCO2 which adjust rate/depth of breathing central indicating brainstem
what does CSF fluid represent PaCO2 -- remember lung buffer system
peripheral chemoreceptors carotid/aortic bodies sense PaO2 function to increase ventilation when low
PaO2 partial pressure of O2 in arterial blood, measured in mmHg
PaCO2 partial pressure of CO2
what effect does exercise and fever have on blood gas increased CO2 production resulting in increased drive
compliance (of lungs) ease of lung/chest expansion
decreased lung compliance seen in fibrosis edema ARDS
increased lung compliance seen in emphysema
elastic recoil spring force driving passive exhalation
what does loss of elastic recoil cause small airway collapse/air trapping
airway resistance is determined by airway radius (bronchus)
what causes increased airway resistance increased with bronchospasm, mucus/edema
pursed lip breathing gentle expiratory back pressure (as in PEEP) splint small airways open, slows flow and prolong exhalation = less air trapping + improve CO2 removal
tidal volume of adult around 500 mL resting
FEV1 forced expiratory volume in 1 second
FVC forced vital capacity, total volume exhaled
FEV1/FEV ratio decreased ratio (<1) = obstructive pattern normal/high ratio (>1) = restrictive pattern
restrictive FEV1/FEV ratio greater than 1
obstructive FEV1/FEV ratio smaller than 1
RV residual volume
TLC total lung capacity
VC vital capacity
what spirometry findings indicate air trapping increased residual volume (RV) increased RV/TLC ratio
type 1 alveolar cells structure/gas exchange
type II alveolar cells surfactant production
what does diffusion depend on partial pressure solubility membrane thickness surface area
what gene is affected in cystic fibrosis CFTR gene
SaO2 pulse oximetry % hemoglobin binding sites occupied
states of hypoxemia (SaO2) 91-94% = mild 86-90% = moderate <85% = severe
states of hypoxemia (PaO2) 80-100 = normal 60-80 = mild 50-60 = moderate <50 = severe
hyperoxemia levels in SaO2 and PaO2 100% (SaO2) >120 mmHg (PaO2)
hypercapnia elevated CO2
DLCO diffusing capacity for carbon monoxide measure how well O2 gas transfer across alveolar-capillary membrane
DLCO is low in fibrosis and emphysema
mechanisms of impaired ventilation airway narrowing/obstruction neural/muscular disruption
what results from impaired ventilation increased resistance ineffective clearance hypoventilation
low V/Q (what is it and conditions it can represent) shunting perfusion without ventilation PNA/atelectasis
high V/Q (what is it and conditions it can represent) dead space ventilation w/o perfusion Pulm embolus
mixed uneven V/Q COPD/Asthma
impaired diffusion decreased surface area increased thickness decreased partial pressure gradient increased CO2 production
causes of decreased partial pressure gradient altitude/low FiO2
FiO2 fraction of inspired oxygen % of O2 being breathed in
causes of increased membrane thickeness fibrosis, edema , ARDS (hyaline membranes)
causes of decreased surface area emphysema
hypoxemia leads to hypoxia - cellular O2 deficit
hypercapnia leads to respiratory acidosis
anaerobic metabolism leads to lactic acidosis -> organ dysfunction
pulm embolus work up V/Q scan or CT pulmonary angiography
POCUS point of care ultrasound checks pleural effusion, pneumothorax
bronchoscopy purpose remove foreign objects/obstruction lung biopsies
PEFR peak expiratory flow rate bedside trend for asthma
pneumonia pathophysiology infection of bronchiole/interstitium/alveoli inflammation -> exudate/consolidation -> impaired O2 diffusion dehydration risk
types of pneumonia typical vs atypical vs viral
PNA signs and symptoms fever/chills cough/purulent sputum (infection) pleuritic pain SOB and crackles confusion in older adults
diagnosis for PNA CBC CXR sputum culture pulse ox/ABG V/Q scan (as necessary)
treatment for PNA pathogen guided abx, O2 supplementation, IV fluids, CPT (chest physiotherapy) antipyretics/analgesia
COPD progressive irreversible airflow limitation common to have emphysema + chronic bronchitis (and or asthma)
alpha 1 antitrypsin deficiency is seen in emphysema
diagnosis for emphysema PFT hyperinflation in CXR low A1AT
emphysema irreversible alveolar destruction leading to decreased elastic recoil and air trapping
emphysema tx bronchodilators, smoking cessation, steroids, mucolytics, abx prn, O2 supplementation A1AT augmentation LVRS/transplant
LVRS lung volume reduction surgery, tx for emphysema
chronic bronchitis chronic cough of 3 months every year for 2 or more consecutive years
what causes bronchitis airway inflammation/edema, mucus gland hyperplasia, cilia loss, wall thickening/fibrosis
asthma triggers IgE mediated allergens, smoke, dust mites, exercise, cold air, illness, anxiety
ARDS acute respiratory distress syndrome severe lung inflammation (often sepsis, aspiration, trauma, toxic fumes)
ARDS pathophysiology increased permeability -> pulmonary edema/loss of surfactant -> atelectasis hyaline membranes thicken A-C barrier causing profound diffusion impairment
Created by: sleepingbear
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