Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
18 Cards in this Set
- Front
- Back
What is the mechanism of Inspiration and expiration?
|
Inspiration:
1. Excitation of medullary inspiration neurons 2. Excitation of the motor neurons to diaphragm and external intercostals (bursts of AP) 3. Flattening of diaphragm to increase vertical diameter of chest, elevation of ribs causes outward movement of sternum and increase transverse diameter of chest 4. Increase in thoracic size and decrease in intrapleural pressure (becomes negative -5 --> -7 or -8); Transpulmonary P exceeds elastic recoil leading to expansion of lungs 5. Increase in size of alveoli --> decrease in intra-alveolar P ( 0 mm Hg --> 1 mm Hg) 6. Air flows into alveoli under a P gradient between atmospheric environment and alveolar air Expiration: Opposite in everything -alveolar P exceeds atmospheric P --> air under P gradient flows out of lungs |
|
What happens in forced Inspiration and expiration?
|
Inspiration:
contraction of accessory inspiratory muscles elevates ribs intrapleural P becomes more negative than -8 cm H2O increase in volume of inspired air as well as velocity of air flow Expiration: contractions of expiratory muscles Intrapulmonary P can rise to +30 cmH2O increase velocity and magnitude of expansion |
|
What are Static Volumes and Capacities?
|
Inspiratory Reserve volume:
-3.3 M, 1.9 F -extra volume of air that can be inspired and above the normal tidal volume Inspiratory Capacity: -3.8 L M, 2.4 L F -Maximum volume of gas that can be inspired from end of expiratory position: IC = TV + IRV Tidal Volume: -0.50 L M, 0.35 L F -volume of air entering lungs during single quiet inspiration (equal to vlume leaving lungs during quiet expiration) Expiratory Reserve Volume: -1.0 L M, 0.7 L F -Maximal volume of air expelled by active expiration after end of quiet expiration - potential volume at the end of quiet expiration Vital Capacity: -4.8 L M, 3.1 L F -Maximal volume of air that person can expire after a maximum inspiration: VC = TV + IRV + ERV Residual Volume: -1.2 L M, 1.1 L F -amount of air remaining in lungs and air ways after a maximal expiratory effort Functional Residual Capacity: -2.2 L M, 1.8 L F -Normal end-expiratory volume: FRC = RV + ERV Total Lung Capacity: -6.0 L M, 4.2 L F -Maximal volume of air in lungs: TLC = VC + RV |
|
What is Spirometry?
|
volume movement of air into and out of lungs
measures everything EXCEPT RV and FRC |
|
What is the Forced Vital Capacity (FVC), FEV, PEFR?
|
volume of air expired when forced expiration with maximal speed is continued until no more air can be expelled from the lungs
may be lower than VC due to compression of airways Forced Expiratory Volume Timed (FEV): -fraction of FVC expelled from lungs over a period of time -normal is 80 % of FVC Peak Expiratory Flow Rate (PEFR): -maximal air flow developed by forced expiratory effort following a maximal inspiration, sustained for 10 ms -normal is 400-600 L/min |
|
What are MV, RMV, and Maximal Voluntary Ventilation?
|
Minute Ventilation (MV):
-total volume of air expired in one minute RMV = TV x RR (respiratory rate) = 500 ml x 12 = 6000 ml Maximal voluntary ventilation: -maximal breathing capacity for 15 sec -normal = 120-170 L/min |
|
What are alveolar and dead space ventilation?
|
Dead space:
1. Anatomical dead space - volume that is ventilated but does not take part in gas exchange, 150 ml 2. Alveolar dead space - ventilated but not perfused, 0 ml 3. Physiologic dead space (VD) - anatomical + alveolar Dead space ventilation = dead space volume x RR = 150 ml x 12 = 1.8 L/min Alveolar ventilation = (TV - dead space volume) x RR = 350 ml x 12 = 4.2 L/min |
|
What are Obstructive and Resrtictive Respiratory disorders?
|
Obstructive:
-increase in airway resistance due to narrowing of airways (asthma, chronic bronchitis, emphysema) Restrictive: -generalized decrease in lung compliance (pulmonary fibrosis, lung edema) |
|
What is Emphysema?
|
Pathophysiological changes:
-irritation of bronchi and bronchioles by smoke -inhibition of alveolar macrophages -increase mucous secretion with decreased movement -edema of bronchial walls Obstruction of smaller airways: -increased airway resistance and work of breathing -decrease expiratory flow --> entrapment of air in alveoli --> destruction of alveolar wall decrease lung diffusion capacity: -pulmonary hypertension --> air hunger |
|
What is Asthma?
|
contraction of bronchiolar smooth muscle leading to allergic reaction --> increase airway resistance
increase IgE Ab --> attaching to mast cells --> release of histamine and slow-reacting anaphylaxis leads to increase bronchialar reistance, decreased rate of expiration Beta 2 agonist used to treat bronchial spasm |
|
What is Pneumonia?
|
Inflammation of lungs with alveoli filled with fluid and blood cells
increase permeability of respiratory membranes --> filling of alveoli --> decrease alveoli surface available for gas exchange --> hypoxemia, hypercapnia |
|
What is Atelectasis?
|
collapse of alveoli due to:
1. Airway obstruction --> blockage with mucus or obstruction of major bronchus --> collapse of alveoli and compression of blood vessels 2. Respiratory distress syndrome --> decreased secretion of surfactant --> increased alveolar surface tension --> collapse of alveoli |
|
What are characteristics of Spirograms in Restrictive and Obstructive respiratory disorders?
|
Restrictive:
-rapid and shallow tidal breathing -decrease in ALL lung volumes -FEV % is normal or above normal -decrease resistance Obstructive: -prolonged expiration -increase RV and FRC -mild increase in TLC -decrease VC and FVC -FEV < 80 % |
|
What are the 2 characteristics that the rate of alveolar-capillary diffusion is a product of?
|
driving force:
-partial pressure difference betwen alveoli and pulmonary capillary blood for each gas; each species of gas moves along its own concentration gradient independent of other gases -concentration difference is NOT a driving force because O2 and CO2 are bound in another chemical form Ease of diffusion: alveolar area available for diffusion: -decreases in lung disease and pulmonary embolism diffusion distance: -pulmonary edema increases diffusion distance diffusion coefficient: -depends on MW of gas and water solubility (major factor) -CO2 is 24x more soluble than )2 and a higher MW --> much higher diffusion coefficient than O2 |
|
What is the Diffusion capacity of the lungs?
|
D = rate of pulmonary gas transfer / driving P
|
|
What are characteristics of the pulmonary exchange of oxygen and carbon dioxide?
|
Oxygen:
driving force = alveolar-blood partial P gradient = PaO2 - PvO2 = 100 mm Hg - 40 mm Hg = 60 mm Hg -for normal DO2 oxygen equilibration requires 0.25 seconds, since blood requires 0.75 sec normally oxygen equilibration is complete Carbon Dioxide: Driving force = PvCO2 - PaCO2 = 45 mm Hg - 40 mm Hg = 6 mm Hg high DCO2 almost always permits complete equilibration of CO2 |
|
What is the Ventilation-Perfusion ratio?
|
Degree of matching ventilation (VA) and Perfusion (Q)
Total ventilation = useful ventilation of alveoli + wasted ventilation (dead spaces) Total perfusion = useful perfusion of alveoli + wasted perfusion or shunts alveolar ventilation/CO = 0.9 - 1.0 Both ventilation and perfusion increase from apex of lungs to base due to gravity VA:Q in lung base = 0.6 (underventilated or overperfused) and in apex = 3.0 (underperfused or overventilated) VA:Q of non-ventilated = 0 VA:Q of non-perfused = infiniity |
|
What are some disorders caused by high partial pressures of gases?
|
Nitrogen narcosis:
-at sea level nitrogen is inert -under hyperbaric conditions nitrogen dissolves slowly - resembles alcohol intoxication and can have deleterious effects Decompression sickness: -solubility of N2 decreases as diver ascents -too rapid ascent causes formation of bubbles of nitrogen gas |