A & P 2 - Respiratory System 4

Front 1

What is the mechanism of Inspiration and expiration?

Back 1

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

Front 2

What happens in forced Inspiration and expiration?

Back 2

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

Front 3

What are Static Volumes and Capacities?

Back 3

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

Front 4

What is Spirometry?

Back 4

volume movement of air into and out of lungs

measures everything EXCEPT RV and FRC

Front 5

What is the Forced Vital Capacity (FVC), FEV, PEFR?

Back 5

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

Front 6

What are MV, RMV, and Maximal Voluntary Ventilation?

Back 6

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

Front 7

What are alveolar and dead space ventilation?

Back 7

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

Front 8

What are Obstructive and Resrtictive Respiratory disorders?

Back 8

Obstructive:
-increase in airway resistance due to narrowing of airways (asthma, chronic bronchitis, emphysema)

Restrictive:
-generalized decrease in lung compliance (pulmonary fibrosis, lung edema)

Front 9

What is Emphysema?

Back 9

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

Front 10

What is Asthma?

Back 10

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

Front 11

What is Pneumonia?

Back 11

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

Front 12

What is Atelectasis?

Back 12

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

Front 13

What are characteristics of Spirograms in Restrictive and Obstructive respiratory disorders?

Back 13

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 %

Front 14

What are the 2 characteristics that the rate of alveolar-capillary diffusion is a product of?

Back 14

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

Front 15

What is the Diffusion capacity of the lungs?

Back 15

D = rate of pulmonary gas transfer / driving P

Front 16

What are characteristics of the pulmonary exchange of oxygen and carbon dioxide?

Back 16

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

Front 17

What is the Ventilation-Perfusion ratio?

Back 17

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

Front 18

What are some disorders caused by high partial pressures of gases?

Back 18

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