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Flashcards in Twelve Deck (12):

What are 5 mechanisms of hypoxia including a distinguishing attribute of each.

Inadequate inspiratory partial pressure of O2-Low barometric pressure and/or FIO2

Hypoventilation-High PaCO2

Right to left shunt-Little improvement with supplemental O2

Ventilation-Perfusion Mismatch-Good response to supplemental Oxygen

Incomplete diffusion equilibrium-Good response to supplemental O2


What are the main causes of hypercapnia and hypercarbia?

Abnormal retention of CO2 causing hypercapnia (elevated PACO2) and thus hypercarbia (elevated PaCO2) is most often due to failures of a patient’s ventilatory apparatus that reduce VA (L/min) (Table 2). Among the causes of ventilatory pump failure, reduced central drive to breathe is usually attributable to CNS or PNS defects (c.f. RES-11, -12). More common are the obstructive lung diseases that increase respiratory work load by Ohm’s Law, and impair respiratory muscle performance as peripheral gas trapping increases residual volume (RV). An increased RV creates unfavorable muscle mechanics, notably a flattened diaphragm.


Explain what happens to pressure differences and thus flow rates during turbulent flow.

As presented in RES-6 and RES-8, the Poiseuille Equation restates Ohm’s Law and quantifies the impact of airway length and diameter on resistance to gas flow in each segment. Remember that this equation presumes ideal laminar flow that may never exist in the most distal airways, or when the diameters of larger ones are compromised. These deteriorations into transitional and turbulent flows are evident as declining airway pressure differences (PAW1 – PAW2 = PAW) and thus the maximal flow rates achievable (moving left to right in Figure 1).


Explain why forced expiration leads to less flow and constricted airways.

This normal tendency for flow patterns to deteriorate and for flow rate to decrease as airway dimensions shrink becomes most evident during forceful expirations (Figure 2). This occurs because distal alveoli must be compressed to expel their gas toward the trachea. Such gas moving toward the mouth within the airways exerts little outwardly-directed transmural PAW, leaving airways vulnerable to collapse by the Bernoulli Effect

This property of moving gases to exert little outwardly directed pressure (PAW) against the vessel walls that contain them occurs throughout normal breathing, including during forceful inspirations. As shown in Figure 3 however, the slightly negative PAW within airways during inspiration only adds to the negative intrapleural pressure (PIP) within the parenchyma exerted by the chest and diaphragm; thus airway diameters increase during inspiration. Conversely during expirations, high parenchymal pressures create large positive PAW gradients deep in the alveoli that must eventually decrease to 0 cm H2O (i.e., ambient barometric pressure) in the mouth. Thus all airways will decrease in diameter as gas moves through them during expiration, even in healthy persons without evidence of airways or parenchymal disease. Importantly, any airways without sturdy collagen support will eventually collapse completely; these often flutter open and closed as deeper pressures force them open momentarily, only to have them collapse again when both flow and the Bernoulli Effect resume. The smaller an airway’s internal diameter is, the sooner its collapse will occur during forced expirations.


Describe how obstructive lung disease leads to gas trapping. Describe how this can be alleviated.

Clearly, any obstructive disease process that reduces internal airway diameters will aggravate this airway instability during expiration and lead to premature airway closure. In turn, the persistent inability to expire as much gas as was just inspired will lead to peripheral gas trapping and thus an expansion of RV. While considering this dilemma, take a moment to re-examine panel D in Figure 3 to appreciate what would change if normal mouth pressure was not zero but was instead some small positive value, perhaps +5 to +10 cm H2O. This modest elevation in so-called “back-pressure” or “air stenting” could be achieved by pursed lip breathing, or by wearing of a continuous positive airway pressure (CPAP) mask as prescribed for many patients with obstructive sleep apnea (RES-16). However it is achieved, these slight elevations in oropharnygeal pressure to decrease P along the airways during expiration are remarkably effective in retarding premature airway closure. Not surprisingly, some persons afflicted with obstructive airways disease may self-discover pursed lip breathing as a simple strategy to alleviate their symptoms of dyspnea and respiratory fatigue.


Describe the basic clinical effects of COPD, as well as the clinical tests that can be done to diagnose it? What are the expected results?

As will be discussed in RES-L3 using patient data, many forms of chronic obstructive pulmonary disease (COPD) are quantified clinically by pulmonary function testing (PFT). Given the above discussion, it should be anticipated that in severe COPD both the filling and emptying of the lungs are compromised. As diagrammed in Figure 4, most COPD retards the timely filling of the parenchyma (line C) to a much greater extent than does a typical restrictive lung disease (line B). As was described in RES-6, remember that both obstructive and restrictive disease types will show abnormally low forced vital capacities (FVC). However, only restrictive diseases necessarily show an abnormally low total lung capacity (TLC) as well.

The effects of airways obstruction on both inspiration and expiration can be readily demonstrated during dynamic pulmonary function testing in which gas volumes are charted as their flow rates over time (Figure 5). A typical pattern for flow-volume loops as first described
in RES-6 is shown in Figure 5 at left for many forms of COPD, in which the areas under both flow curves are less than for normal subjects. The more unusual loops in Figure 5 at right feature abrupt “capping” or flattening of the flow loops caused by a fixed airway obstruction, such as neoplastic growth in the airway lumen or the presence of a foreign body there.


Explain how conductance and resistance change when going from RV to TLC. How does this change in COPD?

From the arguments made above regarding changes in airway diameters as a function of lung volume, it can be concluded that total airway resistance from trachea to respiratory bronchioles increases exponentially from TLC toward RV (Figure 6). The exponential relationship can be traced to the dependence of resistance in a tube with the fourth power of the tube’s radius. Furthermore, conductance was introduced in RES-9 as being equal to the inverse of resistance, and so conductance can be seen to increase linearly as the lungs expand from RV to TLC. This entire relationship will shift upward and to the right when airways obstruction is present (Figure 6); the afflicted COPD patient is challenged with potentially unsustainable resistance even at higher lung volumes where normal subjects have very little.


Describe how the work of breather is increased in COPD.

This effect of COPD on total airway resistance means that the overall work of breathing in such patients increases dramatically from that seen in non-affected individuals. You will recall that for normal subjects, only ~ 20-25% of their total work of breathing at rest is attributable to overcoming dynamic airway resistance and even less to overcoming tissue viscous drag (RES-6). As shown in Figure 7, the normal awake subject breathes at a rate and depth that minimizes their total work of breathing for any given VE (L/min), with the nadir or “sweet spot” occurring around their FRC. When normal subjects choose to breathe less often but more deeply (i.e., use a low f and a high VT), they will minimize their work to overcome tissue viscous drag and turbulent flow patterns. However they will utilize more energy overcoming elastic forces to stretch their lungs from very small to very large volumes with each breath. Conversely, when normal subjects choose to breathe more often but shallowly (i.e., use a high f and a low VT), most of their work of breathing will be expended overcoming the challenges of moving even small gas volumes back and forth rapidly through narrow tubes. For patients with airways obstructive disease, both their actual caloric expenditure to breathe the same VE as well as the fraction of that amount needed to overcome dynamic airway resistance will increase greatly. Furthermore, the peripheral gas trapping and expansion of RV that many COPD patients experience will force them into this latter inefficient mode of rapid, shallow breathing as they attempt to ventilate their lungs well above a normal FRC.


List 3 categories of obstructive lung diseases

Obstructions of epiglottis and upper airways

Obstructions of intermediate and distal airways

Obstructions caused by parenchymal destruction or consolidation.


In general, describe diseases that involve obstructions of the epiglottis and upper airways including treatment and in whom they occur. Describe 4 of these diseases individually.

Diseases within this subcategory can affect patients of almost any age from newborn to elderly. These diseases share the tendency for potentially catastrophic occlusions of the pharynx, trachea, or primary bronchi that may necessitate emergent surgical interventions and/or durable corrections of abnormal anatomy to provide lasting relief. They include:

1. Congenital pharyngeal, laryngeal, or epiglottic malformations as described in RES-4 and for which immediate interventional surgery may be both mandatory and curative. Students should review those lecture notes and recall the most frequently encountered breath sounds and other findings that provide definitive diagnoses.
2. Congenital tracheal stenoses and tracheomalacias as reviewed in RES-4. While the breath sounds made can resemble those for malformations listed above, surgical correction may not be possible, or if feasible may need to be done at multiple ages (e.g., placing of tracheal grafts or stents) or only when the affected patient is old enough to tolerate very invasive surgery (e.g., tracheal stenosis or strangulation caused by a vascular ring).
3. Tracheal or bronchial compression from external masses and lymphadenopathy (RES-21, -26, -27), or from internal reductions in upper airway diameters by invasive masses (RES-31, -32). Because the underlying disease is more often encountered in adult patients, their presentations by both breath sounds and degree of impairment vary greatly and can present as fixed obstructions on PFT loops.
4. Obstructive sleep apneas in which obesity, enlarged tonsils, mandibular defects, facial trauma, or other factors can occlude upper airways particularly when patients are sleeping in the prone position. The syllabus and book chapter for RES-16 contain considerable detail about this large and growing health threat. To the extent that certain CNS defects related to central sleep apneas can affect the tone of the pharyngeal and tongue musculatures, these too will present as obstructive diseases.


In general, describe diseases that involve obstructions of the intermediate and distal airways including treatment and in whom they occur. Describe 3 of these diseases individually.

Diseases in this subcategory are the most commonly encountered in clinical practice. They share profound increases in airway resistance that lead to gas trapping and expansion of RV due to premature airways closure during forced expirations (Figure 8). As such they can be ameliorated most effectively with timely diagnosis and management using combinations of modified behaviors (pursed lip breathing, stimulus avoidance), aerosolized drugs, respiratory therapy (including chest percussion and nasal O2), and other interventions. They include:

1. Purulent secretions that fully or partially occlude airways and lead to bronchitis and productive cough (Figure 8A). They are most often the result of normal host defenses to inhaled or aspirated pathogens (the pneumonias, see RES-10, -33 through -39), or to tobacco smoke, mineral powders, plant pollens, or agricultural dusts (as in pneumonitis, RES-17, -22). Chronic exposure to some stimuli causes lung fibrosis, leading to a mixed restrictive/obstructive pattern on presentation. As discussed in RES-10, a patient’s affected airways reflect the depth to which inhaled particles penetrate before being embedded in mucus and/or attacked by intra-luminal leukocytes. Treatments for many such acute processes are usually curative and so these types of obstructive disease are often transient.
2. Bronchial asthma, a chronic airways inflammation that occurs due to persistent irritation by stimuli that may be the same or different from those listed above (Figure 8B). As discussed in RES-14 and -15, therapeutic relief of such obstruction must necessarily involve both behavioral adjustments to avoid initiating stimuli, and the PFT-monitored administration of bronchodilators and anti-inflammatory agents directly into the upper airways in the most seriously affected patients.
3. Cystic fibrosis, a multi-organ disease with prominent manifestations in the lungs. Considered sufficiently important to warrant its own lecture (RES-19), CF represents one of the most studied but still challenging of all inherited disorders. The thick, tenacious mucous secretions in full-blown CF create the same problems seen in pneumonia and tobacco-related bronchitis, plus the high potential for irreversible airways remodeling or destruction as seen in asthma. Management is difficult and unremitting, with life expectancies still well short of those for the general population.


In general, describe diseases that involve obstructions caused by parenchymal destruction or consolidation including treatment and in whom they occur. Describe 2 of these diseases individually.

Diseases in this subcategory include those for which the distal parenchyma has not been spared, as well as those in which a genuine restrictive process is usually also present. Consequently, obstructed airflow and expansion of RV can occur because of factors extrinsic to the airways themselves. They include:
1. Emphysema or the irreversible replacement of alveolar parenchyma with cysts and enlarged open spaces that is most often associated with chronic use of tobacco products (RES-17) or more rarely found as a congenital defect (RES-4). The losses of septal collagen and elastin reduce normal tissue elastic recoil as well as the tethering of smaller airways that normally occurs during respiratory cycles (Figure 8C). Thus peripheral gas trapping is often severe, with RV’s that can approach 60-70% of predicted TLC (normally