Pulm Flashcards
Conducting airway
Nose, pharynx, larynx (extra thoracic)
Trachea, bronchi, bronchioles (intrathoracic)
Respiratory zone
Terminal bronchi, alveoli, alveolar capillaries
Oxygenation
Factors that affect the muscles in the bronchi/bronchioles
-Transpulmonary pressure- keep smooth muscle areas open
-Smooth muscle- sympathetic (beta 2 receptors, relax smooth muscle and epi) and parasympathetic innerration, vagus nerve (acetylcholine causes contractions of bronchiolar smooth muscle and bronchoconstriction)
-Lung cells and endothelium=leukotrienes=constriction
-Histamine and substances from mast cells anaphylaxis and constriction
-Airway resistance-amp changes in diameters increase difficulty of breathing
Tidal volume TV
Volume of inspired and expired air with each normal breathe
Inspiratory reserve volume IRV
Max effort of air inspired after normal inspiration
Expiratory reserve volume ERV
Max effort of air expired after normal expiration
Residual volume
Air left in lungs at the end of expiratory reserve volume
Inspiratory capacity
Residual volume
Tidal vine plus Inspiratory reserve volume
75-120%
Functional residual capacity
Expiratory reserve volume plus residual volume
75-120%
Vital capacity
Inspiratory reserve volume plus tidal volume plus expiratory residual volume
(TV plus ERV is measurement)
Total lung capacity
Vital calcite plus residual volume
Max lung expansion.
80-120%
Forced expiratory volume
FEV and FEV1 (expired in one second)
80-120%
Normal PFT curve
Normal oval
Pressure necessary to get into lungs
Normal homeostasis
Increase in lung compliance in PFT
Wide oval curve
Increase pressure necessary for exhale
Obstructive disease-destruction of airway loss of elastin
COPD emphysema asthma
Decrease lung compliance curve in PFT
Compliance curve in side and narrow small curve
Increase pressure required to get air in and when air is in it’s usually less
Restrictive disease PNE, pulmonary edema, fibrosis
Intrathroacic pressure changes that result in air movement in and out of alveoli
-pleural pressure (between lining of pleura) negative -5 cm H20, inspiration (expansion) -7.5 cm H20 increase suction pulling lungs with ribs
-alveolar pressure- measure of respiratory tree, when glottis is open (atmospheric pressure is at 0) with chest expansion pressure decrease to 1cm H20 and air moves out, recoil-alveolar pressure increase to 1cm and air moves out
Transpulmonary- difference between pleural and alveolar pressure, elastic forces:PEEP, surfactant, and closed epiglottis
Pneumothorax
Breach of pleural spaces, atmospheric air enters and equalizes pressure to atmospheric at 0(-4 mm of Hg is lost) lungs cannot expand, air gets in but not out
S/s: SOB, tachypnea, deviated trachea, decreased breathe sounds on affected side, hyper resonance to percussion
Brain stem and breathing
Brain stem
Medulla-dorsal respiratory group (or neurons) for inspiration, ventral respiratory group (or neurons) for expiration
DRN-back and gloss pharyngeal nerve transmits signs from chemo baroreceptors which signals diaphragm and intercostal muscles
VRN basic autonomic rhythm of respiration, inactive during normal breathing, medullary rhythm of inspiration and expiration, fires during hypo ventilation and signals inspiration, which stimulates and muscle contraction for expiration
Pons
Pneumotaxic center responsible for respiratory rate and pattern
Pontine group modifies rhythm set by VRG
Chemoreceptors and breathing
-Center (near resp center)
Sense changes in pH of CSF, carbon dioxide crosses the BBB and H20, bicarbonate is formed, very sensitive to increase in CO2, and will change rate and depth of respiration, exceptions is in chronic conditions compensated acidosis by renal compensation
-Peripheral (aortic and carotid bodies)
Sense changes in O2 concentration decrease p02 and increase in RR
Lung intervention and breathing
-irritarion receptors (epithelium)
When lungs are irritated by inhalation of particulate matter-cough induced causes bronchospasms and increased RR
-stretch receptors
Smooth muscles stretch in bronchi, bronchioles, king parenchyma, signals DRN to switch off inspiration (prevents over inflation)
-pulmonary C fiber receptors (J receptors)
C fibers are sensitive to increases pulmonary capillary pressures (CHF) initiate shallow rapid breathing, laryngeal vasoconstriction, mucus secretion
Other mechanisms for breathing
Voluntary breathing with breathe techniques
CNS depression by brain injury or anesthesia
Blood flow zones
Deoxygenated RV->PA-> capillary bed
Oxygenated PV->LA
Bronchial vessels->systemic circulation->Trach->bronchi->lungs->esophagus->visceral pleura->PA
Not involved in gas exchange but maintain cellular function
Oxygen disassociation curve
Right
High pCO2, low affinity for 02, high hydrogen, low pH, high 2-3 DPG, high temp
Left
Low pCO2, low hydrogen, low 2,3 DPG, low temp
VQ mismatching
Failure in alveoli oxygen concentration
Shunts blood away from alveoli by constriction to higher concentrated oxygenated alveoli occurs within 10 minutes of hypoventilation
Results in differences in alveolar 02 concentration and paCO2, CO2 in expired air (end tidal CO2) and paCO2
Hypoxia pulmonary vasoconstriction maximizes ventilation and perfusion
Due to asthma, chronic bronchitis, PNE, atelectasis, PE
Physiological shunting
VQ less than normal and causes inadequate ventilation to oxygenated blood going to alveolar capillaries poor shunting
Minute ventilation
Air moved in and out in one minutes TVXRR
Alveolar ventilation:rate new air reaches alveoli for gas exchange
Dead space
Space in respiratory system where no gas exchange occurs
Conducting zone is about 30% of total lung capacity and is non wiring inherently all the time- anatomical dead space
Physiological draws space- anatomical dead space plus alveoli without blood flow due to pathology
On exhalation air in dead space is expired first before air from alveoli and causes CO2 harder to blow off
Pediatric respiratory system
Infants have no epiglottis flap movement between breathing and eating risk for aspiration
More susceptible to problems with restrictive distresses due to changes in diameter of lungs, airway
Child thoracic cage less pressures needed for expansion recoils and collapses easily
Adult respiratory system
Adults thoracic cage less expansion and construction restricted and limited recoil
Measure severity of respiratory failure
Alveolar arterial oxygen gradient: defines oxygenation disorders
PF ratio: most helpful, ratio of partial pressure of o2 in arterial blood to the fraction of Inspiratory oxygen concentration (Fi02), use this to classify ARDS
Obstructive lung diseases
Increase in lung volume
Croup, acute epiglottis, cystic fibrosis, chronic bronchitis (COPD), emphysema (COPD), asthma
Croup
Upper airway issue due to acute viral infection
Barky seal cough, strider
Subglottic edema narrows airway causes respiratory distress
Humidified 02 watch from away decrease stress
Acute epiglottis
Associated with H influenza
Inspiratory strider, drooling, tripod
Rapid edema of epiglottis and it is severe and life threatening
Protect airway
Cystic fibrosis
Autosomal recessive genetic disease that affects chloride ion transport in respiratory and GI tract
Cough, wheezing, expiratory sputum, PNE, clubbing, barrel chest, rales, recurrence infection like pseudomonas
Mucus plugs with submucosal glands and goblet cells
Chronic inflammation with excessive cytokines and neutrophil activation
Chronic bronchitis
Hyper secretion of mucus and chronic persistent cough (3 mths for 2 years)
Usually acquired, generic alpha 1 anti tripsin deficiency
Looks worse when exhaling, decreased FEV, wheezing in low airway strider in high airway, SOB, hypoxia, mild cyanosis, blue bloater, poor exercise tolerance, May cause polycythemia
Large airway but can affect all smooth muscles, bronchial inflammation causes edema causes increase number and size of mucosal glands, goblet cells, air trapping, VQ mismatch, chronic hyper capnia
Emphysema
Enlargement of respiratory zone and destruction of alveolar walls
SOB, barrel chest, tripod, purses lip breathing, wheezing, pink puffer, hyper resonance
Breakdown of elastin causes loss of recoil causes air trapping causes SOB causes decreased RR causes retention of CO2 and structural changes and loss of alveolar cells decreased area for gas exchange and bulbs and blend, VQ mismatch, hypoxia, inflammation and risk for infection
Asthma
Chronic inflammation bronchial mucosa, hyperresponse, constriction, and obstruction
Same ss as chronic bronchitis
Early in due to antigen response, cytokines reinsert; increase capillary permeability, mucosal edema, mucus production, bronchospasm
Late constriction VQ mismatch hypoxemia, CO2 retention, acidosis, resp failure
Pulmonary edema
In the lungs and alveoli
Differences in pressure gradient, excess fluid in alveoli including heart, pulmonary circulation, including pulmonary capillary permeability can’t drain to lymphatics
HF, ARDS, toxic gases
SOB, increased RR, crackles, pink frothy sputum, CP, orthopnea, PND
Gas exchange impaired due to decreased lung compliance fluid in pulmonary alveolar sacs
Pleural effusion
Excess fluid in pleural space, blocked by lymph node, heart failure, decreased oncotic pressure, increased vascular permeability of pleural membrane
Fatigue, SOB, high RR
Impaired gas exchange
Hypoxemia respiratory failure
Decreased pa02 with or without hypoxia
Resp failure less than or equal to 50 mm Hg
Tachycardia, cyanosis, confusion
Hypoventilation, VQ mismatch, increased alveolar capillary membrane thickness like in CHF, PE, pulm edema, PNE
Hypercarbic respiratory failure
Increases CO2 paCO2 over 50 mm Hg and decreased pH less than or equal to 7.25
Confusion, lethargy
Hypoventilation, decreased respiratory drive,, neuromuscular dz, airway obstruction, dead space, chest wall deformity
Restrictive disease
Decreased compliance and lung volume
Structural, aspiration, atelectasis, bronchiolitis, pulmonary fibrosis
Structural restrictive disease
Kyphosis, scoliosis, muscular, dystrophy, obesity,
increased shortness of breath, increase respirations, difficulty with secretion clearance, increased effort to expand lungs
Aspiration
Fluid or solid and lung, dysphasia
Bronchial inflammation causes decreased Cilia function, and bronchospasm, alveolar capillary membrane damage causes hemorrhagic, pneumonitis, and a stiff noncompliant lung
Atelectasis
Blockage of airway, pressure outside lungs, can’t expand, not enough, surfactant, common and bedbound patients, increase in pulmonary shunt increase in VQ mismatch, causing hypoxia and decrease compliance
Bronchiolitis
Inflammation of bronchioles, chronic bronchitis, viral, respiratory, illness, toxic gas
Atelectasis or emphysematous destruction of alveoli beyond area of inflammation, decrease VQ matching, decreased minute, ventilation, increase in carbon dioxide and tachypnea
Pulmonary fibrosis
Excess fibrosis and connective tissue in lungs
Scar tissue after pulmonary disease, such as ARDS or TB, autoimmune like RA or sarcoidosis, inhalation of toxins, or idiopathic
Chronic inflammation causes fibrosis of alveolar epithelium causes proliferation of myofibroblast, causes stiff alveoli, causes decrease compliance, VQ, mismatch and hypoxemia
Acute lung injury
Inflammatory process and lungs that leads to alveolar, epithelial and vascular endothelial injury in the lungs can be due to infection or non-infection
Onset oacute less than seven days
Bilateral infiltrates, respiratory distress that is not related to fluid overload
Acute lung injury, PF ratio less than or equal to 300
ARDS
PF ratio less than or equal to 200
When acute lung injury progresses
Causes can be direct, like pneumonia, aspiration, pulmonary contusion, fat, emboli, re-perfusion, near, drowning, inhalation injury, pulmonary edema post transplant, indirect, includes sepsis, trauma, cardiopulmonary, bypass, drug overdose, pancreatitis, blood transfusion
Symptoms include shortness of breath, decreased oxygen, poor response, to oxygen, hyperventilation, respiratory alkalosis, organ, dysfunction, metabolic, acidosis, decreased tidal, volume, increase, carbon dioxide, decreased, cardiac output, decreased blood pressure
Three phases exudative, proliferative, fibrotic
Exudative stage of ARDS
Inflammatory, first 72 hours, PF ratio 201 to 300, mild
Inflammatory and exudate, increase, capillary, permeability, surfactant, and inactivated or production impaired, compliance lost
Proliferative stage of ARDS
1 to 3 weeks after injury
PF ratio 101 to 200, moderate
Early healing, pulmonary Edema drain, increase, lymphatic drainage, increase, pleural effusion, exudates granulate and recovery of capillary, alveolar barrier, surfactant production restarts
Fibrotic stage of ARDS
14 to 21 days after injury overlaps with proliferative stage
PF ratio less than 100 and is severe
Does not occur in everyone fibroblast proliferate in alveoli, increased risk for pulmonary hypertension
Pulmonary embolism
Thrombus, fat, air, amniotic fluid postpartum
Increased respiratory rate, shortness of breath, chest pain, increase in dead space, VQ, mismatch, decreased and oxygen, pulmonary infection, pulmonary, hypertension, decreased cardiac output, hypertension, shock
Causes hypoxic vasoconstriction, which then causes decreased surfactant, which then causes release of neurohormones and inflammatory substances which causes pulmonary edema and atelectasis to the affected area
Diagnostics include D dimer CTA, MRA, EKG changes elevated troponins
Pulmonary artery hypertension
Increase in pulmonary artery pressure at greater than 25 mmHg normal is 15 to 18
Can be idiopathic, genetic, connective, tissue disease, chronic hypoxia, left, ventricular failure, valve disease, long-standing, hypertension
Shortness of breath, chest pain, increase respiratory rate, cough, JVD, fatigue, palpitations, right sided heart failure
Vasoconstrictors overwhelm vasodilators, causing resistance of blood flow to lungs, causing remodeling of right ventricle cor pulmonale
Pulmonary artery hypertension, and pulmonary artery hypertension crisis diagnostics include an echo and a right heart Cath
