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274 Cards in this Set
- Front
- Back
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What are the 3 major components of the respiratory system?
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respiratory controller
ventilatory pump gas exchanger |
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What are the subcomponents of the respiratory controller?
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cortex
brainstem |
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What are the subcomponents of the ventilatory pump?
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chest wall muscles
chest wall skeleton chest wall connective tissue airways pleura spinal cord and peripheral nerves |
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What are the subcomponents of the gas exchanger?
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alveoli
pulmonary capillaries |
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What are the key anatomic components of the respiratory controller? What are the functions of each?
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Cortex: provides behavioral control of automatic centers in the brainstem
Medulla: central pattern generator Pontine respiratory group (PRG): assists the body in making a smooth transition from inspiration to expiration; may serve to coordinate information from higher centers with the activity of the central pattern generator. |
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What are the two respiratory components of the medulla? What does each do?
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Dorsal respiratory group (DRG): processes information from receptors in the lungs and vascular system; most activity is inspiratory in nature.
Ventral respiratory group (VRG): contains both inspiratory and expiratory neurons, as well as cells that innervate muscles that control the larynx and pharynx |
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Relate the role of afferent input, central integration, and output of the respiratory control system.
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Afferent input arises from the lungs, which contain flow, pressure, stretch, and irritant receptors; these receptors provide information about the movement of gas and distention of the lungs.
Chemoreceptors monitor O2, CO2, and pH in the blood and have fibers that extend to the medulla where the inspiratory neurons are located. This input reaches the DRG and is integrated to adjust the respiratory rate, and the output systems stimulate the respiratory movements. |
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Contrast autonomic control and voluntary control. Where is each located in the CNS?
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Autonomic control arises from the central pattern generator and is generally a consistent pattern that is continually adjusted for maintaining O2, CO2, and pH levels within the set ranges. It is located in the brainstem medulla and pons.
Voluntary control is a disruption of this autonomic pattern in order to properly execute behavior. It is located in the cortex. |
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What are the two major types of afferent information to the respiratory controller?
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Mechanoreceptors monitor flow, stretch, pressure, and irritants.
Chemoreceptors monitor O2 levels, CO2 levels, and pH. |
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Where are respiratory mechanoreceptors and chemoreceptors found?
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Mechanoreceptors: nose, pharynx, and lung airways and vasculature
Chemoreceptors: aortic arch, carotid bodies, and within the brainstem |
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What are the major muscles of inspiration?
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The diaphragm achieves the largest portion of normal inspiration. External intercostal muscles assist during normal and forced inspiration. The scalenus, SCM, and pectoralis muscles also contribute to forced inspiration.
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When do the pectoralis major muscles contribute to the work of breathing?
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During forced inspiration, but only when the person's arms are in a fixed position, such as when they assume the tripod position with their arms braced on their knees.
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Why are the pectoralis muscles not usually considered to be one of the normal muscles of ventilation?
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The pectoralis muscles move the arms, which are not usually in a fixed position.
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What is the "output" of the respiratory controller?
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The VRG of the medulla sends axons to the muscles via cranial and spinal nerves.
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What are the 2 variables of breathing set by the respiratory controller? What happens to ventilation if these variables change?
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Breathing rate and breath volume.
Ventilation is the volume of air going into and out of the lungs each minute. Increasing the volume and/or rate of breathing increases ventilation. |
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What are the origins of the peripheral nerves that drive the muscles of respiration?
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Diaphragm: C3-C5
Intercostals: T1-T12 Abdominals: Ts and Ls SCM: CN XI Scalenus: C3-C5 |
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How is the visceral pleural layer of the lungs connected to the parietal pleura of the chest wall?
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The pleural layers are continuous at their edges and separated by a potential space containing a very small amount of fluid.
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What are the consequences of gas getting into the intrapleural space?
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Air in the intrapleural space simultaneously allows the chest wall to expand and the lung to contract. This increases alveolar pressure and forces air out of the lungs, which stresses the ventilatory pump during inhalation.
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Contrast the sensitivity of central and peripheral chemoreceptors.
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Peripheral chemoreceptors (aortic arch and carotid bodies) are sensitive to hypoxemia (low PPO2) and hypercapnia (elevated CO2).
Central chemoreceptors (brainstem) are senstive to changes in arterial CO2 levels and pH. |
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What are mechanoreceptors sensitive to?
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Nasal mechanoreceptors are sensitive to flow.
Pharyngeal mechanoreceptors are sensitive to swallow stimuli and halt breathing. |
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What are pulmonary receptors sensitive to?
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Pulmonary receptors are sensitive to stretch and pressure.
Pulmonary chemoreceptors are sensitive to capsaicin, bradykinin, serotonin, and prostaglandin. |
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What physiological variable is only sensed by peripheral chemoreceptors?
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a decrease in the partial pressure of oxygen
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What 5 components are used to define the ventilatory pump?
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bones
muscles and soft tissues of thorax pleural lining of the chest wall and lungs peripheral nerves connecting the CNS to ventilatory muscles airways of the lungs |
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What are the three main functions of the ventilatory pump?
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Create negative intrathoracic pressure
Distribute gas throughout the lung Minimize expenditure of energy while achieving adequate ventilation |
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How do bones meet the functions of the ventilatory pump?
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The provide a superstructure for muscles and connective tissue.
They encase and protect internal organs. They provide a rigid cage that enables the muscles to generate a negative intrathoracic pressure during inspiration. |
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How do muscles meet the functions of the ventilatory pump?
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They contract during inspiration to generate negative intrathoracic pressure.
They relax during expiration, which helps minimize energy expenditure during the respiratory cycle. |
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How does the pleura meet the functions of the ventilatory pump?
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It links the motion of the chest wall and the lungs.
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How do peripheral nerves meet the functions of the ventilatory pump?
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They link the controller to the muscles of ventilation.
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How do the airways meet the functions of the ventilatory pump?
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They serve as a conduit for the flow of gas from the mouth to the alveoli and back out.
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What muscles are used during inspiration and expiration during a normal breath? Which are used during forced ventilation?
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During normal respiration, only the inspiratory muscles are required to contract; during forced inspiration, accessory muscles are recruited.
During normal breathing, expiration is passive with no muscle contraction. During forced expiration, the internal intercostal and abdominal muscles are recruited. |
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Describe the autonomic innervation of the airways. How does the ANS influence smooth muscle tone?
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Sympathetic fibers terminate near the airways and cause bronchodilation.
Parasympathetic fibers innervate the airways via cholinergic receptors and cause bronchoconstriction. The balance between the two determines the tone of the muscles of the airways and the resulting diameter of the conducting tubes - which determines the resistance to airflow within them. |
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If you wanted to test a patient for asthma, would you administer a beta-agonist or a cholinergic agonist? Why?
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A beta-agonist would stimulate receptors in the sympathetic nervous system and lead to bronchodilation. A cholinergic agonist would stimulate the parasympathetic receptors and cause bronchoconstriction. Have the patient inhale gradually increasing doses of methacholine, a cholinergic agonist. The patient has asthma if he develops significant bronchoconstriction at low doses of the inhaled agent.
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What are the components of the conducting airways of the lungs?
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The conducting airways are the tubes through which air flows but no gas exchange takes place.
Trachea, mainstem bronchi, lobar bronchi, segmental bronchi, subsegmental bronchi, and terminal bronchi |
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What are the components of the transitional zone of the lungs?
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Respiratory bronchioles
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What are the components of the respiratory zone of the lungs?
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alveolar ducts
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What is the dead space?
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The regions of the lung that receive air but do not participate in gas exchange; this includes the conducting airways and part of the transitional zone.
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Compare the composition and driving force for bulk flow of gas in the conducting airways with the composition and driving force for diffusion in the respiratory zone.
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The conducting airways have large diameters and are supported by cartilage; bulk flow is driven by pressure differences.
The bronchioles in the respiratory zone have small diameters but overall the respiratory zone has a large total cross-sectional area; diffusion is driven by concentration differences. |
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What is compliance?
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A measure of the stiffness of an object. It is equal to the change in volume that occurs in an object over the change in pressure across the wall of the object.
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How is compliance related to the work of breathing?
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The greater compliance of the unit, the less work is required for breathing.
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What are the key anatomic components of the gas exchanger?
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Alveoli
Pulmonary capillaries |
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What is oxygen saturation?
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The percentage of oxygen-binding sites on hemoglobin that are occupied by oxygen; the extent to which the entire oxygen-carrying capacity of hemoglobin is being used.
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What are the four requirements of the gas exchanger that make efficient gas exchange possible?
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Provide a large surface area for the diffusion of gas
Minimize distance for diffusion Maintain the structural integrity of the gas-exchanging unit to minimize the probability that the unit will collapse at low lung volumes Match ventilation and blood flow |
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Why can it be stated that there is a "tremendous capacity for diffusion" in the pulmonary capillary?
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In normal situations, RBCs are fully saturated by the time they have traversed 25-33% of the pulmonary capillary. During exercise, when cardiac output is increased and the speed with which the RBC traverses the alveolus increases, the blood will be saturated with oxygen by the time it exits the capillary.
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Is diffusion limitation a cause of hypoxemia in normal and/or diseased lungs?
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Rarely, because there should still be adequate time for the oxygen to diffuse into the RBCs. Diffusion limitation could cause hypoxemia in a person doing heavy exercise while breathing gas with low oxygen content.
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What is the relationship between gas flow and the distance over which diffusion of the gas must occur?
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The amount of gas that can diffuse across a surface (gas flow) is inversely proportional to the distance of diffusion (or the surface thickness).
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What is the role of the pores of Kohn in preventing atelectasis?
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The pores of Kohn permit the exchange of air between alveoli within a lobe and minimize the collapse of lung units if a more central airway is obstructed.
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What is the role of structural interdependence in preventing atelectasis?
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Connective tissue is interspersed between alveoli and the airways. As a result of this structural interdependence, forces imposed at the level of the alveolar wall are transmitted to adjacent alveoli and the rest of the lung, thereby providing a form of stabilization to individual gas-exchanging units.
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What is the role of surfactant in preventing atelectasis?
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Surfactant, produced by type II penumocytes, plays a critical role in reducing the surface forces within the alveolus, thereby contributing to the stability of the alveoli.
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What is hypoxic pulmonary vasoconstriction?
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Narrowing of precapillary pulmonary vessels in response to hypoxia in corresponding poorly ventilated alveoli. This phenomenon aids in directing blood flow preferentially to well-ventilated regions of the lungs.
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What is the physiological variable that signals vasoconstriction?
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Decrease in partial pressure of oxygen
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What is the most common physiological cause of hypoxemia in patients with cardiopulmonary disease?
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Mismatch of ventilation and perfusion (termed V/Q mismatch)
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What test gas is used to determine the diffusion capacity (DL) during PFT (pulmonary function testing)?
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carbon monoxide
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What are the parameters of the Fick equation that are reflected in the DL?
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The rate of diffusion of CO is limited by its diffusion coefficient, the surface area and thickness of the barrier.
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Why do interstitial fibrosis (a restrictive disease) and pulmonary edema decrease DL?
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DL is decreased because interstitial fibrosis and pulmonary edema increase the thickness for diffusion.
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Why does exercise increase DL?
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the surface area for diffusion increases
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Why does anemia decrease DL?
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There is not as much blood in the pulmonary capillaries in a patient with anemia. As a result, the CO concentration difference across the alveolar wall is not as great, so not as much CO will diffuse. Thus, the patient has a lower diffusion capacity.
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Contrast the elastic properties of the lungs and of the chest wall.
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The chest wall resists moving due to externally applied forces. If you apply a force to the chest wall to make it bigger or smaller, and then release the force, the chest wall will return to its resting volume. Normally, the chest wall is at a volume that is smaller than its isolated, unstressed position, and so it normally wants to spring out to resume its equilibrium configuration.
If you remove the lungs from the body, they collapse to their resting position - their smallest possible volume. In a live human being, the lungs are always stretched above their equilibrium position and exert a collapsing force. |
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What would happen to the pleural space if the chest wall and lungs did not change volume during inspiration and expiration?
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From a given unstressed position, if inspiration were initiated and the chest wall began to move outward to a larger volume, the pleural space would enlarge if the lungs did not also increase in volume. Similarly, during a passive exhalation, air exits the lungs, and the volume of the pleural space would enlarge during exhalation if the chest wall volume did not change.
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What is transmural pressure?
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The pressure across the wall of a structure. It is equal to the pressure inside an enclosed structure (intracavity pressure) minus the pressure on the outside of the structure.
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What limits the extreme volumes of the respiratory system to define TLC and RV?
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TLC is the volume of air in the lungs at the end of a full inspiration. RV is the volume remaining in the lungs at the end of a forced exhalation. The tension generated in a muscle when stimulated by a neurological impulse depends on the length of the muscle at the moment at which the neurological stimulus reaches the muscle. At low thoracic volumes (at the end of exhalation) the major inspiratory muscles are relatively long and thus the tension generated in them is high. In contrast, at high lung volumes (at the end of inhalation) the inspiratory muscles are shortened and are less effective at generating tension for a given neural stimulus. The opposite is true for expiratory muscles, but remember that these are only used during periods of increased ventilation.
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What is the resting position of the chest wall relative to TLC?
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The resting position of the chest wall is at a volume that is 75-80% of the TLC.
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Describe the resting position of the respiratory system. Name the volume in the lungs at this point. Relate this volume to a normal breath (tidal volume).
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At the resting position of the respiratory system, the forces exerted by the chest wall and the lungs are equal in intensity and opposite in direction. This state represents the FRC (functional residual capacity), the volume of air present in the lungs at the end of passive expiration. Tidal volume is equal to the volume inspired during a normal breath minus FRC volume.
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What is the relationship between airway diameter and lung volume?
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The diameter of small airways in the lung is determined partly by the volume of the lung: the higher the lung volume, the bigger the diameter of the airways.
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What is the mechanism for "air trapping" and an increase in RV? How is this increased as a part of the aging process?
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Energy is needed to exhale to RV (because the person has to force air out of the lungs). If the chest wall is stiff and the elasticity of the lung is decreased (as occurs with age), the pleural pressure may become positive as expiratory muscles are recruited. As the lungs become smaller (as they do during RV), the transmural pressure in the airways becomes negative, predisposing some of the these airways to collapse. When the airway collapses, gas distal to the point of collapse (gas in the alveoli) cannot exit and is trapped behind the collapsing or narrowed airway. The more air that is trapped in this manner, the greater the RV.
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What is compliance? How is calculated?
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Compliance is the relationship between the change in volume of an object and the change in pressure needed to achieve that change in volume.
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What changes in lung compliances occur with fibrotic lung disease?
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Inflammatory conditions lead to scarring or fibrosis with deposition of connective tissue in the lung and a decreased compliance.
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What changes in lung compliance occur in emphysema?
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Emphysema destroys lung tissue and reduces elastic recoil of the lung, leading to an increase in compliance.
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How is spirometry used to measure lung volume?
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The spirometer is a simple device for measuring gas volumes. As the person breathes in and out, gas enters and leaves the spirometer, tracing a pattern of the person's breathing pattern. The spirometer can only measure the lung volumes the subject can exchange with it.
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What is tidal volume?
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The volume of air inspired or expired in a normal breath. In the average person at rest, a normal tidal volume is approximately 450-500 mL.
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Which volumes can be measured by a spirometer?
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Tidal volume
Inspiratory reserve volume Expiratory reserve volume Inspiratory capacity Vital capacity |
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What is inspiratory reserve volume?
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the additional air that can be inhaled after a normal tidal breath in; the maximum volume of air that can be inspired in addition to the tidal volume.
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What is expiratory reserve volume?
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the maximal volume of air that can be expelled from the lungs after normal expiration; the difference in volume between the functional residual capacity and the residual volume
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What is inspiratory capacity?
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the maximal volume of air that can be inspired after normal expiration; the sum of the tidal volume and the IRV
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What is vital capacity?
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The maximal amount of air that can be moved into or out of the lungs in a single breath. The VC is the difference between the total lung capacity and the residual volume.
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What is a lung "capacity" equal to?
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it is simply the sum of two or more lung "volumes"
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What is the difference between vital capacity and forced vital capacity?
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Both are the measurement of the amount of air that can be forced out of the lungs after a maximal inspiration. However, with VC, the emphasis is on completeness of expiration. With FVC, the emphasis is on the speed of the expiration.
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Define the forced expiratory volume in one second (FEV1).
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FEV1 is the volume of air that is exhaled in the first second of FVC.
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How is the ratio of FEV1/FVC used to evaluate patients with obstructive disease?
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Individuals with obstructive lung diseases have abnormally low FEV1 because the high airway resistance results in abnormally low force generation during exhalation. FEV1/FVC should be greater than 0.7 in most healthy people and is used to diagnose airways disease.
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What volumes cannot be directly measured by a spirometer?
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Residual volume
Functional residual capacity Total lung capacity |
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What is residual volume?
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the volume at the end of a maximal expiration
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What is functional residual capacity?
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the volume at the end of a normal exhalation
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What is total lung capacity?
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the volume at the end of a maximal inhalation
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To know the values of the RV, TLC, or FRC, what must one know?
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One must know the absolute volume for at least on of them. with that information, the others can be derived from values obtained with spirometry.
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Which volume (TLC, FRC, or RV) is most reproducible? Why?
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FRC because its measurement is not dependent on the use of ventilatory muscles. It is the volume achieved at the end of a relaxed exhalation. To reach TLC requires the patient to make a maximal inspiration; to reach RV requires the patient to make a maximal exhalation. In either case, you must depend on the cooperation of the patient to achieve accurate measurements. If the individual gave less than maximal effort, all other volumes derived would be in error.
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What 3 techniques are used in pulmonary function testing to measure FRC? Which one can measure trapped gas in lung units that do not have communication with the central airways?
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Helium dilution
Nitrogen washout test Body plethysmography ** can measure trapped gas |
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Describe the helium dilution technique.
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The person breaths into a tube connected to a container with a known volume and initially known concentration of helium. By monitoring the concentration of helium as it distributes and comes to equilibrium across the combined volume of container plus lungs, the volume of the lungs (initially FRC when connected to the container) can be calculated.
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Describe the nitrogen washout test.
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The subject breathes a gas containing no nitrogen (typically 100% oxygen), and the volume and decreasing concentration of nitrogen in the exhaled gas are measured. The volume of the lungs (initially at FRC when the test is started) can be calculated in a similar manner to the helium dilution test.
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Describe body plethysmography.
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Used to measure trapped gas in lung units that do not communicate with central airways; person is seated within an airtight box. The body plethysmograph makes use of Boyle’s law to calculate the FRC based on changes in volume and pressure as the person attempts to inhale and exhale against a closed valve.
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How can the He dilution technique be used to measure RV?
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Derive RV from FRC by looking at changes in volume with a spirometer.
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How does pressure change in the alveoli and the intrapleural space during a normal breath?
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The inspiratory muscles are activated, pulling the chest wall outward, and pleural pressure becomes more negative. This negative pressure is transmitted to the alveolus. Alveolar pressure, which had been 0 an instant before, is now negative as well (Palv =Pel + Ppl, where Ppl is the pressure outside the pleura, and Pel is the elastic recoil of the lung). There is now a pressure differential between the airway opening and the alveolus, and air flows into the lung.
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What is surfactant? Where does it come from?
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It is produced by type II pneumocytes. It is a detergent, having a polar and nonpolar end. It is known chmically as dipalmitoylphosphatidyl choline, which is also called "lecithin". It has the lowest surface tension of any biological substance ever measured.
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What is used as an indicator of fetal lung maturity?
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A lecithin/sphingomyelin ratio > 2.0 in amniotic fluid.
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What are the three main functions of surfactant in the lungs?
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1) During lung inflation, molecules of surfactant move into the layer of molecules at the surface of the liquid lining the alveolus, reducing surface tension. This increases compliance and makes it easier to expand the lung.
2) During lung deflation, the density of surfactant molecules increases as surface area declines, decreasing surface tension. This allows pressure in the alveolus to decrease without leading to a significant reduction in the size of the alveolus. 3) Surfactant minimizes transudation of fluid from the pulmonary capillaries that line the alveoli (this is also a result of reduced surface tension). Thus, surfactant helps to keep the alveoli dry. |
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What is hysteresis?
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Hysteresis is the separation of the inflation and deflation segments of the pressure-volume curves of the lungs. In other words, the pressure corresponding to a given volume is different for inflation versus deflation. This property is characteristic of air-filled lungs and can be eliminated in experiments in which the lungs are filled with saline (suggesting that hysteresis is caused by the surface forces associated with an air-liquid interface).
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How are volume flow, pressure, and resistance related?
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Change in pressure = flow * resistance
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Compare laminar flow and turbulent flow.
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In laminar flow, all the molecules are moving in a direction that is parallel to the long axis of the tube. Fluid traveling in or near the center of the tube has a greater velocity than fluid near the wall of the tube. Under conditions of turbulent flow, some of the molecules in the fluid travel parallel to the long axis of the tube and other molecules travel in a variety of other directions, including perpendicular to the long axis.
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Describe the pressure gradients needed to drive laminar and turbulent flow.
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Under conditions of laminar flow, the change in pressure between two points within the tube is proportional to the flow of the fluid within the tube.
With turbulent flow, the change in pressure between two points in the tube is proportional to the square of the flow. |
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What is the relationship between the Reynolds number and flow?
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The larger the Reynolds number, the greater the likelihood that flow will be turbulent.
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Where in lungs is velocity the greatest?
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In the central airways, particular in the trachea. Thus, flow is turbulent in this region.
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Where does turbulent and laminar flow occur in the lungs?
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Turbulent flow is found in the central airways, where velocity is the greatest. Fully laminar flow probably only occurs in the small airways.
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What is the relationship between resistance and radius?
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Resistance is inversely proportional to the radius of the tube to the fourth power.
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How would resistance change if the radius of a tube is decreased by 1/2?
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Resistance would increase by a factor of 16.
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Which regions of the conducting airway have the greatest resistance to airflow?
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The central airways (trachea, mainly); the bulk of resistance resides in the first six to seven generations of airways.
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Why would the trachea not be predicted to have the greatest resistance if one were only to consider its radius?
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This would not be predicted because the radius of the trachea is the largest of all air tubes. However, the smaller airways are in parallel. For airways in parallel, the total resistance is less than the resistance of any of the individual tubes.
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What are the implications of the trachea having the greatest resistance when conducting PFT to examine disease processes that influence airway resistance in the central airways versus the small airways? What is the "silent zone"?
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Because most of the resistance in the lungs is attributable to the central airways, diseases that affect the central airways can easily be detected by tests that assess flow or resistance. In contrast, diseases of the small airways have relatively little impact on lung resistance and can be more difficult to detect with standard tests of pulmonary function. For this reason, the region of the lungs containing the small airways has been called the "silent zone" of the lungs.
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What is airway resistance versus tissue resistance? How does the work of breathing change with the speed of lung expansion?
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Airway resistance is determined by the principles above and accounts for 85% of the total resistance of the lungs. Tissue resistance is a manifestation of the forces that must be overcome by virtue of moving molecules as you stretch the lungs. To inflate the lung rapidly, you must overcome the resistance of the airways and the lung tissue. Initially, energy must be expended to accelerate the gas and to overcome the inertial forces of the lung. Thus, pressure changes with little change in volume at the outset of inflation. As higher flows are achieved, volume changes more rapidly than pressure, as the momentum of the gas carries it into the alveoli, until the desired volume is reached. The amount of work required for breathing in increases in relation to the speed of expansion.
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Describe the passive relationship between lung volume and airway resistance.
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As the lung expands, the diameter of the small airways increases; as the lung deflates, the diameter of the small airways decreases. Thus, lung size is one of the major determinants of the cross-sectional area of small airways (and therefore of resistance).
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What is the physical relationship between lung volume and airway resistance? In what region of the lung is this relationship most relevant?
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The small airways are supported by a latticework of connective tissue supplied by the surrounding lung. In a sense, the lung tethers open the small airways. Small airways in the periphery of the lung.
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What is the effect of the ANS on airway resistance? In what region is this relationship most relevant? How is the active control of airway resistance influenced by inflammatory processes?
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The parasympathetic system contracts the bronchiole smooth muscle (reducing their radii) by increasing secretion of inflammatory mediators. It does this in response to cold air, large particles, dust, and noxious fumes. The sympathetic system on the other hand relaxes bronchiole smooth muscle (increasing their radii) by downregulating the secretion of inflammatory mediators. This is most relevant in the medium-sizes bronchi that contain smooth muscle in their walls.
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How would the inhaled administration of a beta-agonist and corticosteroid be expected to result in bronchial dilation?
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The beta-agonists result in immediate relaxation of smooth muscle. The corticosteroids cause a slower reduction in inflammation.
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What is alveolar pressure? What is the relationship between alveolar pressure, pleural pressure, and elastic recoil pressure?
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The pressure in the alveoli in the lungs. Palv = Pel + Ppl where Palv = alveolar pressure; Pel = elastic recoil pressure; and Ppl = pleural pressure.
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Describe the components of the flow-volume loop.
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The flow-volume loop represents data obtained from a volume-time plot of exhaled gas in a different, more clinically useful manner. It plots flow (as determined from the slope of the volume-time plot) as a function of the actual lung volume at which it occurred. Flow is the volume per time, while volume is the volume at which the flow occurs. Normal breath is circular in shape. Max. inspiration (larger curve that reaches a plateau about midway) is followed by forced expiration (quickly rises to max. followed by linear decline to RV).
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What are the 4 factors that determine maximal expiratory flow?
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Elastic recoil of the lung and chest wall
Surface forces in the alveoli Force of contraction of the expiratory muscles Resistance |
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What is the "equal pressure point" (EPP)?
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The point at which transmural pressure of the airway is 0, that is, the pressure inside and outside are the same. When the EPP is reached in peripheral, unsupported airways, further increases in pleural pressure do not result in increased flow.
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What happens to pressure in the conducting airways, going from alveoli to the mouth, during expiration?
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As gas moves from the alveoli to the mouth during expiration, a loss of pressure occurs.
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What 3 factors are responsible for the loss of pressure as gas moves from the alveoli to the mouth?
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Airway resistance
Bernoulli's principle Transition from laminar to turbulent flow |
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Describe the patency of the conducting airway proximally and distally to the EPP during expiration.
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As pressure in the airway declines, you eventually reach EPP; any further loss of pressure within the airways leads to a negative transmural pressure and the collapse of the airway, causing flow in that airway to stop.
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Why is the location of the EPP important?
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The airway will not collapse if EPP is reached in the central airways, because the walls are largely supported by cartilage and the effects of a negative transmural pressure are minimized. However, if the EPP is reached in the small, peripheral airways (which may occur in diseased lungs) the development of a negative transmural pressure leads to the collapse of the airway.
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Why is the elastic recoil of the lung important to EPP?
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Whether EPP develops in a peripheral or central airway depends on the difference between the alveolar pressure and the pleural pressure at the beginning of the expiratory maneuver. The difference between these two pressures is the elastic recoil pressure. Thus, elastic recoil pressure is the determining factor for the location of the EPP.
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Explain the effects of emphysema on the location of the EPP.
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In disease states such as emphysema, in which the elastic recoil of the lungs is diminished, the likelihood of reaching EPP in the peripheral airways is increased for any lung volume.
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Emphysema results in lungs with very high compliance, so why is it classified as a "chronic obstructive disease"?
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Compliance is the change in volume as compared to the change in pressure required to achieve that change in volume. Emphysema minimizes the elastic recoil of the lungs, which increases compliance – a smaller change in pressure is required to change the volume of the lungs. However, reduced elastic recoil also causes the peripheral airways to collapse, obstructing airflow from these airways.
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Define the components of a flow-volume plot - where are TLC, FRC, and RV located?
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The patient begins by inhaling until he reaches TLC and then exhaling as hard and fast as he can until he is at RV; this is plotted as volume versus time. Once he has reached RV, he inhales as hard and fast as he can back to TLC, and this is also plotted. If he relaxes and breathes normally, you can plot a smaller curve enclosed by the maximal curves. FRC is represented by the end of expiration on this smaller curve.
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Compare the flow-volume curve for a normal breath with that obtained from a maximal inspiration followed by a forced expiration.
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The flow-volume curve for a normal breath is much smaller in amplitude and is more circular than the maximal curve – expiration and inspiration look like mirror images of each other.
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Describe effort-independent flow.
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Once EPP is established, further increases in pleural pressure do not lead to an increase in expiratory flow (an increase in pleural pressure increases alveolar pressure, but it also increases pressure surrounding airway with the result that transmural pressure remains constant).
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What is dynamic compression of airways? How does this relate to a patient with emphysema?
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Dynamic compression is the reversible narrowing of airways that results from changes in transmural pressure during exhalation. The reduction in elastic recoil (in emphysema) causes dynamic compression of the airways to occur at higher lung volumes than in normal individuals. Consequently, in a pt with emphysema, flow limitation may exist at any given lung volume between TLC and RV.
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What changes occur in flow-volume curves in obstructive and restrictive pulmonary diseases?
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1) In both, the curves have lower amplitude - lower expiratory flow overall.
2) In obstructive pulmonary diseases, the curve is shifted to the left – both TLC and RV are higher than normal but VC remains about the same as normal. 3) In restrictive diseases, the curve is shifted to the right – both TLC and RV are lower than normal, and VC is decreased as well. |
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What are the effects of obstructive lung disease like emphysema and asthma?
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Emphysema: max. insp. is normal, but expiratory flow is reduced at all lung vols.
Asthma: there is reduced expiratory and inspiratory flow at all lung volumes. |
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What is the relationship between alveolar ventilation, dead space ventilation, and minute ventilation?
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minute ventilation is equal to the sum of alveolar ventilation and dead space ventilation.
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What is alveolar ventilation?
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the volume of air per minute that enters or exits the alveoli of the lung
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What is dead space ventilation?
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the volume of air per minute that enters or exits the parts of the lung that do not participate in gas exchange.
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What is minute ventilation?
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the volume of air that can be inhaled or exhaled from one's lungs in one minute of ventilation
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What are the 2 types of dead space?
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Anatomic dead space: the volume of the conducting airways of the lung
Alveolar dead space: the volume of the alveoli that are not being perfused. |
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What are the relative proportions of each type of dead space in a healthy individual?
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Anatomic dead space can be estimated in the average person as equal to 1 mL per pound of body weight. Alveolar dead space in normal individuals is quite small, approximately 20-50 mL.
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What is the normal ratio of physiological dead space to tidal volume (VD/VT)?
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If the total dead space is roughly 175 mL, and the Vt is 450-500 mL, then the Vd/Vt is 175/500 or approximately 1/3.
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Why will rapid shallow breathing result in decreased alveolar ventilation when compared with a normal breathing pattern (assuming that minute ventilation is constant in both cases)?
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There is an increase in dead space ventilation
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Compare the PCO2 is expired air at the beginning of expiration and at the end of expiration (end tidal sample). How doe these contribute to the composition of a sample of mixed expired gas?
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The initial gas exhaled contains essentially no carbon dioxide. This gas represents the air in the anatomic dead space. As expiration continues, the PCO2 increases rapidly; this air arises from a mixture of anatomic dead space and alveoli. Eventually, the PCO2 stops increasing and plateaus; at this point, all air is coming from the alveoli.
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What will make (PACO2 – PECO2) increase?
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It increases if alveolar space decreases.
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Why can PaCO2 be substituted for PACO2 in the Bohr Method Equation?
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The blood in the capillaries that perfuse the alveoli quickly comes into equilibrium with the alveolar gas as CO2 diffuses from pulmonary arterial blood into the air sacs the blood surrounds. Thus, the arterial partial pressures of CO2 (PaCO2) is a reasonable approximation of the alveolar carbon dioxide.
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What is a normal value of PaCO2?
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40 mm Hg (range of 38-42 mm Hg); it is the primary regulated variable of the respiratory control system
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What will happen to PaCO2 if CO2 production doubles and alveolar ventilation stays constant?
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PaCO2 will also double
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What will happen to PaCO2 if CO2 production doubles and alveolar ventilation doubles?
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PaCO2 will not change (it will stay the same if both double)
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What will PaCO2 be if CO2 production is constant and alveolar ventilation doubles?
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PaCO2 will decrease by 1/2.
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What is hyperventilation?
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ventilation greater than the need excrete metabolic CO2 production (usually resulting in PaCO2 < 38 mm Hg)
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What is hypoventilation?
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ventilation less than that needed to excrete metabolic CO2 production (usually resulting in a PaCO2 > 42 mm Hg)
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Why is ventilation preferentially distributed to the base of the lungs in an upright individual?
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This distribution is a consequence of the varying pleural pressures from the bases to the apices of the lungs. In an upright person, because of the impact of gravity on the lung and the mechanical interactions between the lungs and the chest wall, pleural pressure is less negative at the base than at the apex of the lungs.
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Would you expect the pattern of distribution of ventilation to change if a person moved from an upright position to supine or side position?
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Yes; pleural pressure should vary less from the bases to the apices of the lung.
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Why is pulmonary blood flow preferentially distributed to the base of the lungs in an upright individual?
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In upright position, pulmonary blood flow preferentially is distributed to base of lungs because gravity and alveolar pressure compresses some arteries and/or veins (at apex: Palv > Pa > Pv, at middle: Pa > Palv > Pv; at base: Pa > Pv > Palv).
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Would you expect the distribution of blood flow in the lungs to change if a person moved from an upright position to a supine or side position?
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Yes; blood should become more evenly distributed in the lungs.
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What 2 properties of pulmonary circulation allow it to accommodate large changes in cardiac output without large changes in resistance?
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Closed capillaries open (recruitment)
Capillaries that are open distend (distension) |
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What is the influence of the ANS on pulmonary circulation?
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Unlike most capillary beds, there is little control of the pulmonary vasculature by the sympathetic and parasympathetic systems.
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What is hypoxic vasoconstriction? Contrast this to the effects of hypoxia on the systemic circulation.
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Hypoxic vasoconstriction refers to the narrowing of precapillary pulmonary vessels in response to hypoxia in corresponding poorly ventilated alveoli. This increases vascular resistance and reduces local blood flow, allowing blood flow to be preferentially directed to well-ventilated regions of the lungs.
This is in contrast to systemic circulation, which responds to hypoxia with vasodilation. |
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Is hypoxic vasoconstriction active at normal PACO2?
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yes
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What happens to pulmonary vascular resistance and the work of the right ventricle under conditions of hypoxemia?
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Pulmonary vascular resistance increases
Work of the right ventricle increases |
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What is the role of NO and prostacyclin in regulating pulmonary vascular resistance?
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they contribute to the tone and resistance of the pulmonary vessels. They dilate the pulmonary vessels.
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How do local changes in PACO2 and PaO2 result in changes that will tend to reestablish ventilation and perfusion matching?
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When there is too much ventilation for perfusion, PACO2 will decrease, causing bronchoconstriction that will reduce ventilation and restore matching.
When perfusion is greater than ventilation, PaO2 will decrease, causing vasoconstriction that increases vascular resistance and reduces local blood flow. |
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What are the 3 forms in which CO2 is trapped in the blood?
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CO2 bound to hemoglobin
CO2 dissolved in blood plasma in equilibrium with carbonic acid Carbonic acid dissociates into a proton and a molecule of bicarbonate |
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What is the normal range of CO2 content in the blood? What is the shape of the curve in this normal range?
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45-52 mL CO2/dL of blood; the shape of the curve in the normal range is relatively linear
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Describe the composition of blood leaving the left ventricle.
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It is a mixture of blood from different regions of the lung that may have quite different gas compositions. This is true for both CO2 and O2.
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Why does the linear shape of the CO2 content curve make it possible for well-ventilated regions of the lung to compensate for poorly ventilated regions to prevent hypercapnia?
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If an alveolus is receiving little ventilation, PaCO2 rapidly increases and stimulates the respiratory controller to increases ventilation. Maximal ventilation of a normal alveolus results in an alveolar PCO2 and PaCO2 of 10-12 mmHg. This process greatly reduces the CO2 content of the blood perfusing this alveolus. When this blood mixes with the blood from poorly ventilated alveoli, the final PaCO2 of the combined blood may be normal.
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What is the haldane effect? How does it relate to the transport of CO2 in the tissues and in the lungs?
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Hemoglobin has four heme sites that bind oxygen and a protein chain that binds carbon dioxide. In the presence of high levels of carbon dioxide in the tissues the increased binding to the protein chain alters the configuration of oxygen binding sites leading to the release of oxygen in the tissue. In the pulmonary capillary, the blood is exposed to high levels of oxygen in the alveolus, and the hemoglobin releases carbon dioxide and binds oxygen preferentially. The preferential binding of hemoglobin for oxygen and the resulting shift of carbon dioxide from being bound to hemoglobin to being dissolved in plasma is manifest as a shift to the right of the carbon-dioxide-hemoglobin dissociation curve.
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What are the 4 causes of hypercapnia?
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Decreased minute ventilation
Decreased alveolar ventilation caused by rapid, shallow breathing pattern Venitlation/perfusion mismatch Increased carbon dioxide production in the setting of a fixed ventilation |
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Describe the shape of oxyhemoglobin dissociation curve. How does it facilitate the transfer of oxygen in the tissues and alveoli?
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The shape is sigmoid. The PO2 in tissues is typically about 40 mmHg; at this partial pressure, oxygen leaves hemoglobin. In the alveoli, the PO2 is approximately 100 mmHg, and oxygen diffuses from the alveoli into the plasma and binds to the hemoglobin until the saturation reaches the value that corresponds to the PO2 in the plasma.
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Over what range of PO2s is oxygen content relatively independent of PO2 in the blood? (Hint: how does the shape of this curve act to ensure an oxygen saturation > 89% and a PO2 > 59 if possible?
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The relatively flat portion of the curve between a PaO2 of 60 and 100 mm Hg ensures that the hemoglobin will remain nearly fully saturated with oxygen even when the alveolar – and hence, arterial, PO2 – decreases to levels as low as 60 mmHG. Because most of the oxygen carried in the blood is bound to hemoglobin, this ensures that the oxygen content of the blood will remain high.
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What four factors cause a right shift in the oxyhemoglobin dissociation curve?
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Increased body temperature
Increased PCO2 Increased 2,3 diphosphoglycerate Decreased pH |
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What does a right shift in the oxygen saturation curve facilitate?
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O2 unloading from hemoglobin at any given PO2
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Compare the effect on oxygen content from an increased P50 at 100 mm Hg and 40 mm Hg.
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An increased P50 at 40 mmHg shows a significant decrease in hemoglobin’s affinity for oxygen; a significantly higher PO2 is required to reach the same saturation.
An increased P50 at 100 mmHg shows a less significant decrease in hemoglobin’s affinity for oxygen; a smaller rise in PO2 is required to reach the same saturation. |
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During exercise, an individual requires more oxygen in muscle tissue, produces more CO2 (pH of blood falls), and body temperature increases. Explain the benefit of changes in P50 under conditions of exercise in the tissues.
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These conditions cause unloading of oxygen at higher concentrations of oxygen, so more oxygen can be released into the tissues. Under normal (non-exercising) conditions, oxygen would not be released at these higher concentrations.
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What are the effects of CO on the oxygen-hemoglobin dissociation curve? What are the potential clinical ramifications of CO poisoning?
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CO competes with O2 for the heme-binding sites on hemoglobin, thereby reducing the amount of O2 carried by the blood to the tissues. In addition, CO alters the relationship between PO2 and O2 saturation. The oxygen-hemoglobin saturation curve loses its sigmoid shape and is shifted to the left. This change in the curve reflects the greater affinity of oxygen to hemoglobin in the presence of CO. Consequently, less O2 is released to the tissues than would be predicted based solely on the reduced O2 content of the blood. The effect of the combination of these two factors is to deprive metabolically active tissues of oxygen.
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What are the values of FIO2, Patm, PH2O, PACO2?
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FIO2 = fraction of oxygen in the inspired gas; 0.21 for atmospheric gas
Patm = barometric pressure (changes with altitude); 760 mmHg at sea level PH2O = water vapor pressure when the gas is fully saturated; 47 mmHg PACO2 is normally 40 mmHg |
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What is the respiratory quotient? Why is the respiratory quotient of a person who eats a typical American diet, a person who eats primarily carbs, and a person who eats a diet rich in fat?
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The respiratory quotient (R) represents the ratio between oxygen consumed and carbon dioxide produced by the body; it varies with diet.
Typical American diet: R = 0.8 Primarily carbs: R = 1.0 Diet rich in fat: R = 0.7 |
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What terms define a maximal PAO2?
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High Patm, low PACO2, and high R
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How does hyperventilation and hypoventilation influence PAO2?
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Hyperventilation increases PAO2
Hypoventilation decreases PAO2 |
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What term of the alveolar gas equation changes at high altitude? Why does hyperventilation at high altitude increase oxygen delivery to the tissues?
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Patm decreases at high altitude and therefore PAO2 decreases. Hyperventilation will therefore increase oxygen delivery to tissues by increasing PAO2.
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What is A-aDO2?
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Alveolar to arterial oxygen difference: the difference between PAO2 and PaO2; determines whether there is a problem with the gas exchanger. The A-aDO2 increases in normal people as they age because of changes in ventilation that relate to loss of elastic recoil in the lungs.
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How are PaO2 and PAO2 measured?
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PaO2 (and PaCO2) is measured from an arterial blood sample. You can use this information to calculate PAO2 using the alveolar gas equation.
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What is a normal value of A-aDO2? How does the normal value change with age?
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The normal A-a-DO2 is less than or equal to 10 mm Hg in people 30 and under. At ages older than 30 years, the normal A-aDO2 can be approximated by age*0.3.
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What is the diagnostic value of a high A-aDO2 or a normal A-aDO2 in the presence of hypoxemia?
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A high A-aDO2 in the presence of hypoxemia indicates a pathological problem with either the lung tissue or the pulmonary circulation. If the A-aDO2 is normal in the presence of hypoxemia, the gas exchanger is normal and an alternative explanation for hypoxemia must be sought.
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How is hypoxemia defined?
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As an oxygen saturation (SaO2) < 90% or from an ABG of PaO2 < 60 mm Hg (these are equivalent points on the oxyhemoglobin dissociation curve).
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What are the 5 physiological causes of hypoxemia?
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Decreased PIO2
Alveolar hypoventilation Ventilation-perfusion mismatch Shunt Diffusion abnormality |
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What is the most common pathologic cause of hypoxemia?
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Ventilation-perfusion mismatch
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Low VA/Q will result in hypoxemia. Why does the shape of the oxyhemoglobin dissociation curve not allow for compensation by increasing ventilation and VA/Q?
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A low V/Q ratio produces a PO2 that corresponds to the steep portion of the oxygen dissociation curve and thus significantly lowers the oxygen content of the outgoing capillary blood. In contrast, a high V/Q ratio produces a PO2 value that corresponds to the relatively flat portion of the oxygen dissociation curve and thus does not significantly elevate the oxygen content of the outgoing blood. Increasing V/Q ratio does not compensate for the significant decrease in oxygen content caused by the low V/Q ratio alveolus.
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What is shunt?
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A condition in which deoxygenated blood in the venous system is directed to the arterial system without receiving O2 from the lungs.
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How is shunt related to a low VA/Q?
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A pulmonary shunt is an extreme form of V/Q mismatch in which some of the alveoli of the lung completely collapse or fill with fluid. With a shunt, alveolar ventilation in the affected regions of the lung is 0. Conditions in which significant shunt is present are characterized by hypoxemia that does not respond to supplemental oxygen.
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Identify two organ circulations that comprise the “normal” right-to-left shunt.
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Normal anatomic shunt (blood flow from venous to arterial circulation or right-left shunt) occurs both in the lungs (bronchial circulation) and in the heart (Thebesian vessels).
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What are the two forms of oxygen content in the blood?
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Bound to hemoglobin
Dissolved in the plasma |
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How do you calculate oxygen content bound to hemoglobin?
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Amount of O2 bound to Hgb = 1.35(Hgb)(oxygen saturation)
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How do you calculate dissolved oxygen content?
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Amount of O2 dissolved in blood = 0.0003(PaO2)
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Compare oxygen content in each form while breathing room air and while breathing 100% oxygen.
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Breathing room air:
• Amount of oxygen bound to hemoglobin = 18.4mL/100mL of blood • Amount of oxygen dissolved in blood = 0.3mL/100mL of blood Breathing 100% oxygen: • Amount of oxygen bound to hemoglobin = 19.2mL/100mL of blood |
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What is normal range of hemoglobin concentration in healthy females and males and in anemic individuals?
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Healthy females: 12-16 gm/dL of blood
Healthy males: 13-16 gm/dL of blood Anemia is a [Hb] concentration below the range of normal. |
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Anemia can result in serious limitation in the ability to deliver oxygen to the tissues. Why wouldn't this be revealed using a pulse oximeter?
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Anemia reduces oxygen content significantly but does not change the PaO2. Pulse-oximetry specifically measures the PO2 of the blood.
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What is the one physiological cause of hypoxemia that does not have a significant increase in PaO2 when the patient breathes 100% oxygen?
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shunt
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What is the effect of breathing 100% oxygen on the mixed gas composition exiting the pulmonary vein?
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The shunted blood has a low O2 content. Alveolar blood has a high PO2 but not much extra O2 content. When the blood from these regions are mixed, the PO2 will be significantly lower despite the use of 100% oxygen.
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What is hyperventilation?
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increased ventilation greater than that required to meet metabolic needs, as reflected in the production of carbon dioxide, or increased alveolar ventilation relative to metabolic carbon dioxide production. If a person is hyperventilating, it means that his or her PaCO2 is less than normal, or less than 38 mm Hg.
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What is hypoventilation?
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decreased ventilation to a level that is less than that required to meet metabolic needs, as reflected in the production of carbon dioxide, or decreased alveolar ventilation relative to metabolic carbon dioxide production. If a person is hypoventilating, it means that his or her PaCO2 is greater than normal, or greater than about 42 mm Hg.
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What is tachypnea?
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rapid breathing; an increase in respiratory rate above the normal range (usually reserved for rates ≥ 20 breaths/min)
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What is bradypnea?
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abnormally slow breathing; a decreas in respiratory rate below the normal range (usually reserved for rates < 10 breaths/min).
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What are the 2 groups of neurons in the medulla that are responsible for the autonomic control of breathing?
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Dorsal respiratory group (DRG)
Ventrolateral respiratory group (VRG) |
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Describe the dorsal respiratory group.
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has inspiratory and expiratory neurons; plays an important role in processing information from receptors in the lungs, chest wall, and chemoreceptors that modulate breathing; important in the activation of the diaphragm
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Describe the ventrolateral respiratory group.
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has inspiratory and expiratory neurons; has a role in determining the rhythm of breathing; regulates the changes in diameter of the upper airway that occur with breathing by stimulating muscles to expand the upper airway during inspiration.
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Which medullary group processes afferent information from the lungs, chest wall, and chemoreceptors and is important in the activation of the diaphragm?
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DRG
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What medullary group is involved in setting the rhythm of breathing and controls upper airway diameter during inspiration?
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VRG
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Describe the central pattern generator responsible for autonomic rhythmic breathing.
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Consists of all the respiratory neurons responsible for autonomic rhythmic breathing. Some neurons in the medulla fire during inspiration; others have a role in transition from inspiration from expiration; others appear to fire during expiration, primarily serving an inhibitory role on the diaphragm. Neurons in the DRG increase their rate of firing during inspiration. Others in the VRG seem to increase activity during expiration.
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Compare the effects on ventilation of spinal chord damage at the mid-cervical (C3-C5) level with that in the thoracic spinal cord.
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The nerves that innervate the diaphragm exit the spinal cord in the mid-cervical (C3-C5) level. Thus people who sustain spinal cord injuries below this level can still inspire normally. The intercostals muscles may not function, but as long as diaphragmatic innervation is intact, inspiration can still take place.
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Identify the two populations of chemoreceptors.
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Peripheral chemoreceptors and central chemoreceptors.
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Identify where PCO2 and pH are sensed in the body.
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In the medulla, where central chemoreceptors monitor them in the CSF, which reflect changes in these variables in the arterial blood.
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Identify where PO2 is sensed in the body. Compare the response to changes in oxygen content with the response to changes in PaO2.
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By peripheral receptors in the carotid bodies and aortic arch. The stimulus for increased ventilation is PaO2, not the oxygen content of the blood.
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Identify the PaO2 threshold for increased ventilator activity. Compare this value with the oxyhemoglobin dissociation curve and the definition of hypoxemia.
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As PaO2 decreases below 60 mm Hg, the rate of firing increases rapidly. This is the start of rapid slope change in oxyhemoglobin dissociation curve, and defines hypoxemia.
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Compare the permeabilities of [H+], CO2, and HCO3- across the blood brain-barrier of the respiratory controller.
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The blood-brain barrier is highly permeable to lipid-soluble molecules like CO2 and not very permeable to ions, like H+ and HCO3-.
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Describe the integrated ventilator response to changes in arterial PO2.
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Ventilation changes little as PaO2 decreases from 95 to 60 mm Hg; at this point, the ventilation starts to increase.
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Identify the threshold for increased ventilation in response to hypoxemia.
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At moderate degrees of hypoxemia (PaO2 between 45 and 60 mm Hg), ventilation is only elevated to approximately twice the normal level. After PaO2 decreases below 40 mm Hg, ventilation increases sharply.
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Describe how is hypoxemia influenced by the PaCO2?
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When acute hypercapnia is present simultaneously with acute hypoxemia, there is a synergistic effect, and ventilation is substantially elevated.
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Describe the integrated ventilator response to changes in arterial PCO2.
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Ventilation increases linearly with acute increases in PaCO2. The normal range of response is between 2 and 5 L/min increase in ventilation for each 1-mm Hg increase in PaCO2.
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What is the threshold for increased ventilation due to increased PaCO2?
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An increase in PaCO2 from 40 to 50 mm of Hg may cause ventilation to increase from 5 to 40 L/min.
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Compare the sensitivity of the control system to increased PaCO2 with that for decreased PaO2 in the range of normal values for each.
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The control system is much more sensitive to changes in PaCO2 as compared to changes in PaO2.
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Describe acute on chronic respiratory failure.
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In the clinical setting in which the PaO2 decreases acutely (and the PaCO2 may increase above the baseline chronic levels) because of a respiratory infection or some other cardiopulmonary process, we describe the situation as acute on chronic respiratory failure.
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Identify the chronic changes that have occurred in blood, CNS, and respiratory drive as acute on respiratory failure develops.
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PaCO2 will be elevated, and the patient may experience chronic hypercapnia. Acutely, this leads to increased ventilation as a result of the stimulation of chemoreceptors. Within a few days, the pH of the blood and the fluid bathing the brain approaches normal levels, and ventilation comes back down. Because of increased levels of buffers now present in the blood and brain, further increases in PaCO2 have an attenuated effect on ventilation.
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Patients with chronic hypercapneic respiratory failure often have problems with hypoxemia as well. Sudden changes in clinical condition may result in acute worsening of these chronic gas exchange abnormalities. Classic teaching once said that these patients were dependant on their “hypoxic drive” to breath and discouraged the use of supplemental oxygen. Is this accurate?
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No.
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Describe the change in PaCO2 as the result of supplemental oxygen.
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On average, PaCO2 increases by approximately 20 mm Hg with the supplemental oxygen, but the patients do not stop breathing.
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Identify the mechanisms that result in the PaCO2 change that occur as a result of supplemental oxygen.
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o There is a small decrease in ventilation as hypoxemia is relieved
o V/Q mismatch is worsened by the administration of oxygen o Haldane effect; with the increase in PaO2, CO2 is displaced from hemoglobin and enters the liquid portion of the blood |
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Identify the implications for acid-base status of the chronically hypercapneic patient who receives supplemental oxygen, understanding that supplemental oxygen can [and should!] be applied to maintain a PaO2 > 60.
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Although a 20 mm Hg increase in PaCO2 is not good for the patient because it leads to cute acidosis (which may bring the level of hypercapnia near the point where it will have an anesthetic effect on the brain), acute hypoxemia can be a life-threatening problem and must be treated with supplemental oxygen. Use the lowest amount of oxygen necessary to raise the PaO2 to 60 mm Hg.
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Define the anaerobic threshold. Identify where it occurs relative to maximal oxygen consumption, VO2max.
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The level of oxygen consumption above which anaerobic metabolism leads to an accumulation of lactic acid in the blood. In normal individuals, it occurs between 40% and 60% of the maximal oxygen consumption.
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What are the three phrases of ventilatory response to exercise?
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Neurologic phase: ventilation increases almost instantaneously
Metabolic phase: ventilation increases linearly with the increase in oxygen consumption and carbon dioxide production that results from exercise Compensatory phase: energy needs in the muscles outstrip the ability of the CV system to supply oxygen for aerobic metabolism. |
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What drives the neurologic phase?
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o This may be a learned response, anticipating increased ventilation
o May result from stimulation of the controller by information arising from joint and muscle receptors in the limbs |
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What drives the metabolic phase?
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o PaO2 and PaCO2 remain normal
o Increase in ventilation = exercise hyperpnea |
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What drives the compensatory phase?
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o Cells increasingly shift to anaerobic metabolism, producing lactic acid
o Lactic acid lowers the blood pH, stimulating peripheral and central chemoreceptors to increase ventilation. o Ventilation increases at a faster rate than the increase in oxygen consumption, compensating for metabolic acidosis. |
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Describe the acute and chronic ventilator responses to the central and peripheral chemoreceptors when an acid is added to the blood.
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When acid is added to the blood, the peripheral chemoreceptors respond by increasing ventilation. This results in a PaCO2 decrease, which results in the diffusion of CO2 from the brain to the blood. As a result, the central chemoreceptor detects a lower PCO2 (but does not yet detect the elevated [H+] in the blood) and so it decreases ventilation. Eventually, the central chemoreceptor will be stimulated by the increased [H+].
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Describe the acute and chronic ventilator responses to the central and peripheral chemoreceptors when a base is added to the blood.
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• When a base is added, and arterial pH level increases, the peripheral chemoreceptor would decrease ventilation and the PaCO2 level would increase. CO2 would diffuse across the blood-brain barrier, causing the central chemoreceptor to increase ventilation in the short run.
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What is the ventilator response when PaCO2 is elevated chronically (such as in patients with COPD)?
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In cases where PaCO2 is elevated chronically (COPD), the activity of peripheral and central chemoreceptors decreases within a few days as pH is normalized. At extremely high levels of CO2, an anesthetic effect may be produced, and ventilation decreases rather than increases.
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Identify the normal pH of the extracellular fluid and the free hydrogen ion concentration that this value represents.
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Normal pH of extracellular fluid = 7.4
[H+] = 40 neq/L |
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Identify the extremes of pH that are compatible with life and the free hydrogen concentration of each value.
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pH: 7.80 – 6.90
[H+]: 16-126 neq/L |
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Identify the range of pH below which and above which major physiological problems will occur. Compare the [H+] of each with 40 nM at pH = 7.4.
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pH below 7.20 or above 7.55 results in major problems in multiple physiological processes.
pH of 7.2--> [H+] = 63 neq/L pH of 7.55 --> [H+] = 28 neq/L |
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Identify volatile acid production in mmol/day and the physiological system that maintains whole-body balance.
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Carbonic acid is referred to as volatile acid because we can eliminate it by breathing more, essentially driving the reaction to the left by increasing alveolar ventilation, thereby decreasing PCO2. Normal metabolism leads to the production of approximately 10,000-15,000 mmol of carbon dioxide a day.
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Identify fixed acid production in mmol/day and the physiolgocial system that maintains whole-body balance.
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About 50-100 meq of fixed acids are produced every day as a consequence of metabolism of protein; fixed acids consist mostly of phosphates and sulfates.
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What is a buffer?
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A molecule that is able to accept or release hydrogen ions so that changes in the free hydrogen ion concentration and, hence, the pH, are minimized.
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What are the major intracellular and extracellular buffers? What is the primary buffer of the extracellular fluid?
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Intracellular: proteins, phosphates, and hemoglobin in RBCs
Extracellular: bicarbonate (primary) Other: Serum albumin, bone (particularly, sodium and potassium ions on the surface of the bone) |
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What is the normal pH of extracellular fluid? What are the limits of a normal pH?
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Normal pH = 7.4, with a lower limit of 7.36 and an upper limit of 7.44.
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What is the difference between -osis and -emia?
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-osis: refers to the process that leads to a disturbance in the balance of acids or bases in the body
-emia: refers to the effect change on arterial hydrogen ion concentration that occurs when a process that alters the relative concentration of acids and bases alters the pH of the blood. |
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What are the normal values for pK, [HCO3], and PaCO2?
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• Normal pKa of carbonic acid is 3.5
o When adjusted for the use of dissolved CO2 as a marker, it is 6.1 • Normal [HCO3-] is 24 meq/L • Normal PaCO2 is 40 mmHg |
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What are the 2 major functions of the kidneys in maintaining whole-body acid-base balance?
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• They remove some chemicals from the blood via filtration in the glomerulus and secretion in the tubule
• They reabsorb some of these filtered molecules and ions at other portions of the tubule to maintain chemical, water, and acid-base levels |
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What are the two major buffers in the urine?
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• Phosphate: HPO42-
• Ammonia: NH3 |
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What are the two classes of acid-base disturbances? What systems are associated with each?
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• Respiratory disorders: respiratory system
• Metabolic disorders: problems with oxygen delivery to tissues, abnormalities in metabolic presses, ingestion of toxins, and diseases of kidney |
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What is the anion gap? What is its role in characterizing metabolic acidoses?
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The difference in concentrations between the commonly measured anions and cations in the blood. The anion gap can be altered by certain acids; thus, calculation of the anion gap serves as an aid to recognition and diagnosis of metabolic acidosis.
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What are the 4 causes of elevated anion gap acidoses?
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• Renal failure (in which reduced filtration capability of the kidney leads to the accumulation of sulfates and phosphates from the metabolism of proteins)
• Hypoperfusion of tissues leading to lactic acid accumulation • Uncontrolled diabetes leading to ketoacidosis • Ingestion of drugs such as aspirin and toxins such as ethylene glycol |
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What is a mixed acid-base disturbance?
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Occur when there is more than one primary acid-base disturbance present simultaneously. Frequently seen in hospitalized patients, especially the critically ill.
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Describe compensation for an acid-base disturbance.
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In order to maintain the pH of the blood and cells within a narrow range, the respiratory and renal systems provide compensatory mechanisms for the primary acid-base disturbances. However, the compensation never results in a pH that is all the way back to 7.4, with the exception of metabolic compensation for chronic respiratory alkalosis. Respiratory compensation for metabolic acid-base disturbances can occur within seconds to minutes. Metabolic compensation for respiratory disorders generally requires 2 to 5 days to be fully evident.
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List the key steps in approaching the analysis of an acid-base disturbance and apply these steps to interpretation of clinical scenarios.
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1. Is the pH abnormal? If so, in what direction?
2. Is the change inPaCO2 in the direction expected for a primary respiratory disturbance? (If the PaCO2 changes in the opposite direction from the pH, a primary respiratory disorder is present.) 3. If a primary respiratory disturbance is present, is it acute or chronic? 4. If a primary met. disturbance is present, is an abnormal anion gap present? 5. If a primary metabolic disturbance is present, is there an appropriate respiratory system response? |
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Why are acute and chronic phases of compensation for a respiratory disorder required?
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The pH change associated with an acute respiratory acidosis is greater than for a chronic respiratory acidosis because the kidney has not yet had time to compensate for lowered pH by retaining more bicarbonate and eliminating protons (as ammonium NH4+).
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Define the concept of corollary discharge and relate this to the sense of effort associated with the work of breathing.
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At the same time that the motor cortex sends efferent neural messages to the ventilatory muscles, it also sends a simultaneous message to the sensory cortex - this is called the corollary discharge. The corollary discharge is believed to be responsible for the sense of effort, or the perception of increased work of breathing, when ventilatory muscle activity is increased.
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Describe the hypothesis which has been developed to partially explain the association of dyspnea seen following an acute pulmonary embolism.
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Stimulation of RARs and C fibers in the lungs may contribute to the dyspnea experienced during acute pulmonary embolism. Patients who receive thrombolytic therapy to dissolve the clots often experience near-instantaneous relief of their breathing discomfort as the clots dissolve. This suggests that stimulation of pulmonary vascular receptors by the increased artery pressure associated with the embolism may be the source of the breathing discomfort in pulmonary embolism.
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Describe efferent-reafferent dissociation. Explain how this model concept can be used to incorporate a wide array of afferent information to result in modifications in the intensity of dyspnea.
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The mismatch of outgoing (efferent) signals to the ventilatory pump and returning (reafferent) signals from receptors in the lungs and chest wall. Allows for input from a vast array of receptors in the upper and lower airways, pulmonary parenchyma, and chest wall and modifies the intensity of dyspnea by increasing such sensations as “air hunger” and the effort or work of breathing.
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Describe the relationship between exercise, work, and oxygen consumption.
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Measurements of oxygen consumption during exercise show that oxygen consumption is linearly related to the work load up to the point at which maximal O2 uptakes is reached, VO2max. Beyond this point, only anaerobic metabolism can sustain further increases in work for a short time at the expense of developing lactic acidosis.
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Define the respiratory quotient (RQ).
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The ratio of carbon dioxide produced per unit of oxygen consumed by the body. The fuel used by the body determines this ratio; for carbohydrates, it is 1.0; for fats, it is 0.7; and for protein, it is 0.8.
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Identify the normal values for oxygen consumption, carbon dioxide production, and the respiratory quotient at rest.
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For someone who eats the average American diet, resting metabolism relies more on the consumption of fat than carbohydrates, and the RQ at rest is approximately 0.8.
Normal oxygen consumption at rest = 250 mL/min. Normal CO2 production is 200 mL/min. |
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Describe the changes in the respiratory quotient with increasing levels of exercise. Identify the metabolic basis for this change.
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During exercise, the body shifts to greater utilization of carbohydrates, and the RQ changes accordingly with greater production of carbon dioxide. Oxygen consumption may increase to as high as 3000 mL/min, and carbon dioxide production increases even more dramatically.
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Define the anaerobic threshold (AT) and describe the metabolic events that are occurring at this point. Explain why this shift in metabolism occurs.
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The level of exercise at which the body begins to rely on anaerobic metabolism to meet energy needs such that lactic acid accumulates in the blood; expressed in terms of the level of oxygen consumption at which lactic acid production can be detected.
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Identify where the AT occurs in untrained and high trained athletes relative to VO2max.
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Untrained people: AT occurs at 50-60% of his/her VO2max.
Highly trained athletes: AT occurs at 80-90% of his/her VO2max. |
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Explain how the AT is determined graphically.
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Ventilation is plotted as a function of oxygen consumption. The relationship between ventilation and carbon dioxide (as well as oxygen consumption) is linear through the metabolic phase of exercise hyperpnea. As one enters the compensatory phase of exercise ventilation, however, there is a need to increase ventilation at a greater rater because the body must accommodate the accumulation of metabolic acid. The level of oxygen consumption at which this shift occurs is the AT.
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Identify two sources of increased CO2 production that occur with strenuous exercise at work levels above AT.
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• Increased usage of carbohydrates
• Buffering of lactic acid, which produces CO2 |
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Describe the three phases of ventilatory response to exercise.
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Phase 1: Neurological Phase: breathing increases out of proportion to the metabolic needs of the body
Phase 2: Metabolic Stage: ventilation increases in concert with the increases in oxygen consumption and carbon dioxide production Phase 3: Compensatory Phase: compensation for acid produced by anaerobic metabolism |
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Identify the primary stimulus that drives each phase of the ventilatory response to exercise.
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Phase 1: studies suggest a central or peripheral neurological mechanism for this first stage of exercise hyperventilation; may also be do to joint or muscle receptors triggered by physical activity
Phase 2: body might have a mechanism for monitoring CO2 production or oxygen consumption, but there is no known receptor for this Phase 3: As protons accumulate and pH begins to decrease, the peripheral chemoreceptors respond by sending messages to the controller that result in an increase in ventilation |
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Explain the reason that “metaboreceptors” are hypothesized to exist in phase 2 of the ventilatory response.
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Some evidence suggests that there may be receptors sensitive to changes in the local metabolic environment at the tissue level located in skeletal muscles. These so called “metaboreceptors” could play a role in the increased ventilation during the metabolic phase of exercise.
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Explain why PaCO2 decreases during phase 3 of the ventilatory response to exercise.
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It decreases because the increased ventilation is more rapid than in stage 2.
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Identify the acid-base disturbance during phase 3 of the ventilatory response to exercise.
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Both aerobic and anaerobic processes lead to the creation of CO2 molecules that must be eliminated via the respiratory system. Anaerobic metabolism also leads to the production of protons that, when buffered by bicarbonate, lead to a further increase in CO2.
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Compare the mechanisms that allow for the initial increase in minute ventilation that occur at higher work loads.
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The respiratory system may generate the necessary ventilation during exercise by increasing the respiratory rate, increasing the tidal volume, or a combination of the two. The initial increase in ventilation is achieved primarily by enlarging the tidal volume. After doubling the tidal volume, the system relies to a greater degree on changes in respiratory ventilation.
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Describe the changes in dead space (VD), tidal volume (VT), and the VD/Vt ratio with increasing minute ventilation. Explain how this influences the efficiency of the work of breathing.
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The proportion of each breath that is composed of dead space ventilation – the ratio of dead space to tidal volume, or VD/VT – is also reduced. The absolute amount of dead space is smaller and the tidal volume increases during the early stages and typically doubles during moderate to very intense activity.
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How can the Fick equation be used to measure cardiac output in the laboratory setting?
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• We can measure VO2 by measuring difference in oxygen content of inspired and expired air
• We can measure CaO2 using the ABG • We can measure CvO2 using a catheter in the right atrium |
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Identify the increase in cardiac output that can be achieved in a healthy trained individual.
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Cardiac output can increase by 5-fold during exercise in a healthy trained individual.
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How does heart failure limit VO2max?
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Heart failure limits maximal oxygen consumption because blood cannot be delivered fast enough.
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Name the key variables in the cardiovascular system that would limit cardiac output and thus exercise tolerance.
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Heart rate and stroke volume
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Describe how the maximal ventilatory capacity of an individual is estimated from the value of FEV1.
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Based on exercise studies, we approximate the maximal ventilation that can be sustained in healthy individuals during exercise by multiplying the forced expired volume in 1 second (FEV1) by 40.
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How is maximal voluntary ventilation (MVV) measured in the laboratory?
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By having a patient breathe as deeply and rapidly as possible for approximately 12 seconds, measuring the volume expired, and converting this to a minute value. This is a useful test of the patient’s overall pulmonary function including muscle strength. The MVV can be estimated as 40*FEV1.
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Compare the MVV with the minute ventilation at maximal exercise tolerance.
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When minute ventilation at maximum exercise is compared with MVV, there is still ample reserve in the respiratory system.
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Identify the system that limits exercise tolerance in a normal health individual – the respiratory or cardiovascular.
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Cardiovascular system
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Define ventilatory reserve.
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The extra capacity of the respiratory system to deliver oxygen and remove carbon dioxide using the controller and ventilatory pump (about 30-35% of MVC (maximal ventilatory capacity)).
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