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51 Cards in this Set
- Front
- Back
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Describe the metabolism and/or production of O2 and CO2 with regards to ventilation.
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Metabolism consumes O2 and produces CO2. In the lungs, all CO2 leaving the blood can only enter the lungs via the alveolar space and NOT through the dead space. The volume of CO2 produced at rest is ~200 mL/min, and we must breathe to get rid of this.
No gas exchange occurs in the dead space. Thus, all the CO2 in exhaled air must come from alveolar gas. If the volume of gas exhaled (Vt) and the concentration of CO2 in the exhaled gas is measured (partial pressure), the VCO2 can be calculated. The same type of calculation applies to the volume of gas from the alveoli (VA). VCO2 (volume of CO2 produced/min)= VA x FACO2 Since PACO2= FACO2 x K (K=713), then FACO2=PACO2/K. Then, VCO2/VA=PACO2/K Because of the rapid equilibration of gases in alveoli, the PACO2 of alveolar gas is equivalent to PaCO2 of arterial blood. Thus: VCO2/VA= PaCO2/K. |
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What does the Alveolar Gas equation for CO2 (VCO2/VA= PaCO2/K) tell us?
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It emphasizes that the PaCO2 is determined by the amount of CO2 production and the amount of ventilation.
It says that the partial pressure of CO2 is inversely proportional to how hard you're breathing. |
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What is the relationship between Pa and PA for O2 and CO2 in the alveoli?
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In alveoli, PA is almost always equal to Pa for both O2 and CO2.
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In lung disease, what tends to happen to the ventilation rate and the PaCO2?
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In lung disease, there is a tendency to hypoventilate (decrease the rate of ventilation), which pushes PaCO2 up.
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What happens to PaCO2 and CO2 production with hyperventilation (2x the normal rate or tidal volume).
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PaCO2 is halved. CO2 production remains constant.
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What happens to PaCO2 and CO2 production with hypoventilation (1/2x the normal rate or tidal volume)?
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PaCO2 is doubled. CO2 production remains constant.
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Describe the relationship between PaCO2 and alveolar ventilation (VA).
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This relationship emphasizes that PaCO2 is set by the rate of ventilation and the rate of CO2 production. Normally, PaCO2 is maintained at ~40 mmHg with a ventilation rate of ~4-5 L/min. In exercise, the rate of CO2 production increases, therefore the PaCO2 does not change dramatically. However, if the individual hypoventilates (decreases VA), the PaCO2 rises; conversely, if they hyperventilate (increased VA), the PaCO2 falls.
Hypo- and hyper-ventilation also affect PAO2 but in reverse. However, it's a little more complicated because inhaled air always contains O2. With CO2, the relationship is simpler since inhaled air has effectively no CO2. Major point: with lung disease, pts frequently have a reduced Va, for example, due to obstructed airways, but their metabolic CO2 production remains constant. Therefore, the pt's PaCO2 is increased. |
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What is the respiratory quotient?
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Because of our metabolic pathways, the amt of O2 we consume is greater than the amt of CO2 we produce. About 250 mL/min of O2 is required for the 200 mL of CO2 released. This imbalance is referred to as the respiratory quotient (R) and represents the ratio of the volume or amt of consumed O2 to the amt of exhaled CO2. This imbalance is reflected in gas exchange:
R= VCO2/VO2=200/250=0.8. With this relationship, the effect of ventilation on PAO2 can be predicted, since the composition of inspired air and the respiratory quotient (R=0.8) are known. |
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What is the gas equation for PAO2?
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PAO2= PINO2 - (PaCO2/R), where R=0.8
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Describe the functional unit of the lung-chest in breathing.
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It consists of:
- Airways (conducting portion) - Soft expandable lung tissue: gas exchange sites- alveoli and BVs. - Chest wall (muscle and ribs) - Diaphragm (muscle) - Pleural cavity (imaginary space) |
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On what law is breathing based? Explain.
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Breathing is based on Boyle's law: PV=constant (nRT).
Inhalation of exhalation is achieved by developing a negative or positive pressure gradient, respectively, btwn the mouth and the alveoli to drive air movements. These pressure gradients are created by coordinated muscle movements within the chest wall that result in a change in lung volume. Muscle activity for breathing is controlled from the brain stem (in the medulla oblangata) and is usually autonomic. However, breathing muscles are striated and can be under voluntary control (by the cortex). The extent of inhalation is monitored by neural feedback from stretch-receptors in the lung and muscles. Breathing muscles are subject to fatigue and typical striated muscle force-tension relationships. |
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Describe the movements of lungs, chest wall, etc. and any changes in pressure associated with inhalation/
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At rest, with mouth open, Pb=Pi=0 mmHg (Pb=atmospheric pressure at mouth).
During inhalation: - increase in volume of rib cage - decrease the pleural cavity pressure (as chest wall expands outward) - Decrease pressure inside the lungs (Pi) - Pb outside is now greater than Pi - Air flows down the pressure gradient until Pi=Pb -At end of inhalation, with mouth open, Pb=Pi-0. |
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Describe the changes in pressure and chest wall, rib cage, and lung position during exhalation.
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At rest with mouth open, Pb=Pi=0.
During exhalation: - Opposite process from inhalation. - Decrease rib cage volume (chest wall contracts inward). - Increase in pleural cavity pressure. - Increase Pi. - Pi > Pb--> air flows down pressure gradient (i.e., out of lungs through airway) until Pi=Pb again. At rest, with mouth open, Pb=Pi=0 again. |
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Describe the major muscles used for breathing.
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1. Diaphragm: the most important muscle:
- Dome shaped, connects to the lower ribs. - Innervated by the phrenic nerve. - Upon contraction, moves downward. - Normal breathing: ~1 cm movement. - Forced breathing: ~10 cm movement. 2. External Intercostal Muscles: - Connect adjacent ribs. - Orientation down and forward. - Upon contraction, moves ribs upward and forward: bucket handle effect. 3. Accessory muscles: - Only used during forced breathing. - Include: nostrils, scale (1st and 2nd ribs), sternomastoids (sternum), and trapezius. |
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Is inhalation an active or a passive process?
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It is an active process that requires the activity of multiple muscles.
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Is exhalation a passive process or an active process? Explain.
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Exhalation is generally a passive process due to the elastic recoil of pulmonary tissue and the chest wall. The diaphragm relaxes and the abdominal wall pushes the diaphragm up.
However, forced exhalation is an active process that is used during exercise and hyperventilation. Abdominal muscles (internal obliques, rectus abdominus, and transverse abdominus) raise the intraabdominal pressure to push the diaphragm upwards. The internal intercostals that are oriented down and backwards then move the ribs down and back. |
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Describe the changes in pressure and volume during the breathing cycle.
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A reduction in pleural pressure (initially equal to -5 cm H2O) decreases alveolar pressure (initially zero) to inflate the lungs.
At full inspiration, pleural pressure is at its maximal negative value, but alveolar pressure returns to zero. The reverse occurs during exhalation. |
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How do lung diseases affect the muscles of respiration?
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When the work-load associated with breathing becomes excessive, muscle fatigue can result in acute ventilatory failure. This situation requires assistance from a mechanical ventilator, which allows the muscles to rest and recover.
Diseases with this potential problem include: 1. Asthma attack: increased airway resistance. 2. Chronic Obstructive Pulmonary Disease (COPD): increased lung resistance. 3. Pulmonary edema, ARDS: increased lung stiffness. 4. Emphysema: increased lung volume causes the diaphragm to drop, reducing it radius of curvature and contractile capacity. 5. Poliomyelitis: due to muscle function impairment. 6. Drug Over-Dose: Baclofen, a muscle relaxant. |
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Can you measure Residual Volume directly by spirometry?
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NO!
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What is tidal volume?
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The volume of air inhaled or exhaled during each breath with normal breathing. It is usually 500 mL at rest.
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What is Functional Residual Capacity?
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FRC is the volume remaining in the lung after normal exhalation.
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What is Vital Capacity (VC) or Forced VC?
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The volume of gas exhaled during a forced inhalation and exhalation.
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What is residual volume (RV)?
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The volume of air remaining in the lungs after a forced exhalation. Note: it cannot be measure directly by spirometry!
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What is Total Lung Capacity (TLC)? How is it calculated?
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TLC= Vital Capacity (VC) + Residual Volume (RV). It is the total volume of gas that can be held in the lungs.
Note: Since RV cannot be measured with a spirometer, TLC cannot be determined with a spirometer, either. |
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What techniques can be used to measure RV?
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Full body plethysmography or gas dilution techniques.
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Describe the Gas Dilution Technique and why it is used.
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RV or TLC cannot be measured directly with a spirometer.
Principle: By combining a known concentration of gas in a given volume with an unknown volume, the resulting gas concentration can be used to determine the unknown volume. V1 is helium with a known concentration, C1. V2 is the TLC. Inhalation combines the 2 volumes and dilutes the gas to C2. To prevent gas losses, helium is used, as this is virtually insoluble in blood. Several breaths are taken to fully mix gases, and the He concentration is re-measured in the expired air. Using gas laws (Boyle's law), PV=constant: C1V1= C2 (V1 + V2) Re-arranging: V2=V1*(C1-C2)/C2 Since V2=TLC, RV=TLC-VC. This technique only measures the ventilated air space. In diseases such as COPD, airway blockage may prevent helium from reaching all the alveolar space. Body plethysmography can also be used to measure TLC without using gases. |
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Describe how a spirometer works, and what it can measure.
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Spirometry refers to the measurement of amts of gases that are pumped in and out of the lungs. There are two commonly used spirometers: 1. obsolete: the water-sealed spirometer in which gases are collected in an inverted bucket over a vessel full of water, and 2. New technology: the solid state pneumotachographic spirometer.
The pneumotachograph is a device made up of a series of parallel tubes that have a low but finite (and known) resistance (R) to airflow. The patient blows into the device, and the pressure drop (P1-P2) is measured from the ends of the device. For (P1-P2)/R, you have Q, the rate of air flow. By integrating flow, you get volume. So this spirometer allows you to measure vital capacity, FEV1, etc. Furthermore, since both flow rate and volume measurements are simultaneously available in this spirometer, it is very easy to construct "flow-volume" loops, which are widely used to evaluate pts for respiratory disease. |
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What is PEF?
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PEF=Peak Expiratory Flow. It is a good estimate of airway function.
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Describe flow-volume loops for ventilation.
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The spirometer is also used to measure the rates of air movement in the lungs. It measures change in volume with time. The gradient of this function is the rate of change of volume, or the flow rate. By taking the gradient at each point on the curve, a flow-loop is generated. Modern spirometers measure flow directly and integrate to get volume.
On flow-loops, the lung volume on the x-axis is increasing from right to left (opposite from the normal orientation of graphs). Also, inhalation results in changes below the x-axis and exhalation causes changes above the x-axis. During tidal breathing, the central small loop is formed. This would be circular with multiple breaths. During deep inspiration, the curve moves below the axis to point 4, Total Lung Capacity. Upon forced expiration, the air flow very rapidly increases, peaks and declines at a steady rate to RV at full forced expiration. The curve will reconnect according to the next breath volume. The peak expiratory flow rate is a useful clinical parame |
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Describe Airway Resistance.
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The reduction in airway diameter also has a great consequence for the flow rate. According to Poiseuille's Law:
Flow Rate (Q)= Pressure Different (P1-P2)/Airway Resistance (R). Where R=8Lx gas viscosity/pi x r to the fourth power, where r= airway radius and L=airway length. Thus, a reduction of the airway radius by 1/2 will reduce the flow by 16, whereas doubling the airway length will only reduce the flow by 1/2. Maximum resistance occurs in the segmental airways. The decrease in radius of each airway is not offset by an increase in the number of airways. |
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What affect would narrowing the airways have on the velocity of the air flow? Does this occur in the lungs? Why or Why not?
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Narrowing the airways causes an increase in velocity. However, this does not occur in the lungs because the number of airway branches increases and the total cross-sectional area of the airways increases even though the airways narrow. (Velocity= Flow rate/Area).
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Describe Air Flow Velocity through the Respiratory System.
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Average Air Velocity= flow rate/ cross-sectional area
In the upper airways, air velocity is relatively high. The increased number of airways at the lung periphery greatly increases the cross-sectional area and, as a result, rapidly decreases the velocity of airflow to almost zero. Consequently, gas diffusion is the major mechanism for mixing and movement of gas in the alveoli. However, because the distances involved are very short, diffusion is sufficient. |
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What problem is associated with reduced air velocity?
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The deposition of particles on the airway surfaces. These particles can be removed by the lung defense mechanisms of mucocilliary clearance in larger airways with cilia and macrophage phagocytosis in smaller airways and alveoli.
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What problem is associated with increased air velocity?
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Increased air velocity has implications for airway collapse during forced exhalation because a faster airflow reduces the pressure inside the airway (a Bernoulli effect). This allows lower outside pressures to collapse the flexible small airways.
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How do diseases affect the airway?
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Because airflow is affected by small changes in the diameter of the airway lumen, it should be no surprise that many airway diseases have an abnormal narrowing of airway lumen due to obstruction from mucus or cell debris, inflammation, edema, and smooth muscle constriction.
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Describe the factors affecting airway lumen caliber.
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1. Location: the smallest airways have little or no cartilage and are more susceptible to collapse.
2. Low PACO2: a lung area poorly perfused: initiates a weak contraction of airway smooth muscle. 3. Reflex innervation: Sensory nerves detect irritants, which results in stimulation of parasympathetic nerves that release ACh and cause contraction of smooth muscle or cough reflex. This reflect loop results in areas of the airways that aren't exposed to the irritant to constrict. 4. Muscarinic, Endothelin, LTD4: G-Coupled Receptor Stimulation: Smooth muscle contraction. 5. Beta-2-Andrenergic Receptor Stimulation (albuterol, formoterol): causes relaxation of smooth muscle (asthma treatment), and reduces the release of mast cell products. 6. IgE receptors: allergic reaction: Causes release of histamine + other factors from mast cells--> edema. Also causes direct smooth muscle contraction. 7. Inflammation: continuous process of narrowing the airway. 8. Asthma Attack: the reduction of airway size leads to an increas |
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Describe the factors that increase airway resistance.
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If resistance is increased, it is more difficult to breath.
1. Allergy: asthma attack, smooth muscle contraction, reflex innervation (remote site). 2. Low PACO2: airway smooth muscle contracts (area with low blood perfusion--over-ventilated). 3. Inflammation or hypertrophy: wall thickening. 4. Obstructive disease: contents in the lumen OR collapse of airway. Increase in resistance reduces ventilation and increases the effort required to breathe. |
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What are Forced Expiratory Volume and forced vital capacity, and why are they important?
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After inhalation to TLC, the subject performs a forced exhalation towards RV. The rate at which the air is exhaled indicates the airway resistance. Because the exact time to reach RV is more variable, a comparative measurement is made after 1 second (FEV1). Similarly, the forced vital capacity (FVC) of individuals varies, so the measurement is normalized by dividing the FEV1 by the FVC.
In a normal pt, the FEV1/FVC is about 0.8 (80%). In obstructive lung disease, airway resistance is increased from either blockage or collapse. Thus, the air will be expelled more slowly, resulting in an FEV1/FVC less than 70%. The spirometer indicates that RV is usually increased, and TLC may be increased in diseases like emphysema. In contrast, a restrictive airway disease may have an increased FEV1/FVC (~90%). The airways have a smaller resistance because the disease affects the ability to inflate the lung and this often reduces the TLC. Thus, the amt of air that's expelled is less and the recoil forces are higher. |
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What is compliance?
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The ease with which ventilation/lung inflation occurs.
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What determines compliance?
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1. The elastic properties of the lung:
a. The material properties of the lung tissue: i. Elastic fibers: produce recoil ii. Collagen fibers: help withstand strain b. Surface tension forces within the lung: this is due to the fluid lining of the alveoli, and it contributes about 2x to the resistance to inflation as compared to elastic fibers. 2. The chest wall: a. Muscle: extent of contraction, force/length curve. b. Elastic properties of the rib cage. |
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Describe the pressure-volume relationship of lungs.
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Compliance is the change in volume per unit of pressure change:
C=(V2-V1)/(P2-P1) P-V of the lung is a non-linear relationship; the volume increase induced by equal pressure changes is less at high lung volumes than at small ones. When the intrapleural pressure (Ppl) is zero, the lung volume is not zero. In fact, even if Ppl becomes positive, the lung does not fully collapse. This occurs because when flexible airways collapse, they trap air in the alveoli. This phenomenon can also occur during forced ventilation. The inhalation and exhalation P-V curves are not identical; the volumes at deflation pressures are larger than at inflation pressures, a process called hysteresis. |
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Describe High, Normal, and Low compliance for the lung.
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High Compliance: the lung is extremely easily expanded or stretched BUT has little ability to recoil. Think of a paper bag: easy to inflate, but does not deflate.
Normal compliance: the healthy lung is considered to be very compliant (~200 mL/cm H2O), expanding pressure of only -2 to -10 cm H2O are required. Low compliance: the lung is difficult to expand. |
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Describe how different diseases change lung compliance.
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1. Reasons for a decrease in compliance are:
a. Fibrosis or swelling of the lung, which makes it difficult to inflate: PV shifts right and TLC is reduced. b. Similar effect when there's a loss of surfactant. 2. Reasons for an increase in compliance are: a. Emphysema, loss of elastic fibers, becomes easier to inflate (but harder to deflate): PV curve shifts left and TLC increases. b. Age: loss of elastic fibers. |
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What is elastance?
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Elastance or the ability to produce recoil is inversely proportional to compliance.
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What is specific compliance?
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Absolute compliance is related to lung size. Therefore, specific compliance is used to normalize and compare compliances of different lungs.
Specific compliance= Lung Compliance/Total Lung Volume. A good example is where one or more parts of a lung are surgically removed. Although the removal of the lung tissue doesn't affect the tissue's properties, compliance measurements that are not corrected for volume would indicate otherwise. |
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Positive vs. Negative pressures inside and outside of the lung.
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Some confusion can arise from the postive/negative signs of pressures on PV curves. This is because the pressures are expressed relative to the inside or outside of the organ. For example, pleural pressure is negative. However, is expressed as a transmural pressure of the lung=inside - outside of the lung= 0 - (-5)= positive 5.
So a positive pressure of 5 cm H2O inside the lung has the same effect as a negative 5 cm H2O pressure outside of the lung. |
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Describe the development of pleural pressure.
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Pleural pressure is required to provide the expanding force on the lung to fill the chest cavity. Resting pressure is generated by pumping of the fluid out of the pleural cavity. Openings of parietal lymphatics drain the fluid out of the cavity. These lymphatics have undirectional valves.
Most of the fluid is secreted by the parietal pleura, a little comes from the visceral pleura. |
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Describe the compliance curve of the lung and the chest, the Functional Reserve Capacity (FRC), and what it means.
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Normally, the lung and chest wall move together as a single unit. The intra-pleural space between the lung and chest wall is very small and filled with only a few mm of fluid. The intra-pleural space is a closed space and remains sealed during normal functioning. As a result, during chest movements, the size of the space remains unchanged and the lung effectively sticks to the inside of the chest wall. Sometimes the space is referred to as a potential space. The force maintaining the contact is a strong surface tension effect.
The combined motion of the chest/lung unit can be described by combining the individual P-V curves of the lung and chest. At the equilibrium point (Functional Reserve Capacity): - Lung Recoil= Chest Wall Expansion At lung volumes above the FRC, relaxing pressure is positive, and it recoils towards the FRC. At volumes below the FRC, relaxing pressure is negative, recoils towards the FRC. |
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Describe the compliance curve for the lung and the chest for emphysema.
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Due to emphysema, lung compliance has increased. The lung has become weaker, so the chest wall starts to win. This causes a barrell-chested effect. Since the chest wall has more influence, the lung-chest PV curve therefore shifts to the left. Importantly, the FRC occurs at a higher lung volume, thereby reducing the efficiency of inspirational effort and the capacity for inhalation.
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Describe the lung compliance and lung and chest PV curve in a fibrotic lung.
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Because the lung is stiff, you can't expand it as much, and it tends to pull the chest wall down. With decreased lung compliance due to fibrosis, the chest wall has less influence and the lung-chest PV curves shifts to the right. Now the FRC occurs at a lower lung volume.
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What is a pneumothorax? How is it caused?
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At FRC, the lungs and chest wall are held in equilibrium and a there is a negative pleural pressure (Ppl). A real pleural space forms upon puncturing the chest wall or lung. This allows air to enter the pleural space (pneuomothorax). When this happens, in the worst case, Ppl falls to zero, the lung collpases due to its recoil forces to its smallest volume (RV). Conversely, the chest wall expands to its resting position.
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