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Advan Physio Edu 27:34–40, 2003.)Poiseuille’s law applies to laminar flow of air but becomes lessprecise with turbulent flow. Laminar flow occurs in smallairways, whereas flow in the largest airways is turbulent; flowin the remainder of the system tends to be transitional, withsome turbulence (Fig. 14.6). Factors producing turbulent andlaminar flow are discussed in Section 3, in the context ofblood flow. In the largest airways, high velocity and airwaydiameter contribute to producing turbulent flow.
In small,peripheral airways, smaller diameter and lower velocity resultin laminar flow of air.Effects of Autonomic Nerves onAirway ResistanceAirway resistance is also affected by the autonomic nervoussystem:■■Activation of parasympathetic nerves innervatingsmooth muscle of conducting airways causes bronchoconstriction and promotes glandular secretions in thelungs.Activation of sympathetic nerves innervating smoothmuscle of conducting airways results in bronchodilation171CLINICAL CORRELATETreatment of Asthma with Sympathetic Adrenergic DrugsAsthma is a chronic respiratory disease, characterized by episodic bronchoconstriction and mucus secretion, resulting inincreased airway resistance and dyspnea (labored breathing).Asthma can be life-threatening in severe cases. Asthma attacksmay be initiated by a variety of factors, including inhaled allergens and irritants, cold air, stress, and exercise, which exacerbate the ongoing airway inflammation in asthmatics.
Drugsused to prevent asthma attacks are mainly aimed at reducinginflammation, whereas drugs used to relieve acute attacks aregenerally bronchodilators (e.g., inhaled β2-adrenergic agonistssuch as salbutamol or terbutaline). These drugs reduce airwayresistance by relaxing bronchial smooth muscle.and reduced airway resistance (through activation ofβ2-adrenergic receptor-linked pathways) in mammalianspecies, although human lungs have little sympatheticinnervation.
Release of epinephrine by the adrenalmedulla during sympathetic activation will also reduceairway resistance through activation of the pulmonaryβ2-receptor mechanism.Lung Volume and Airway ResistanceIn addition, there is a relationship between lung volume andairway resistance. At high lung volume, the diameter ofairways tends to be increased by the radial traction theexpanded lungs place on the airways. At low lung volumes, inthe absence of traction, small airways have a greater tendencyto collapse.DYNAMIC COMPRESSION OF AIRWAYSDURING EXPIRATIONAirway resistance is also affected by dynamic compression,which is the compression of airways during forced expiration.An expiratory flow–volume curve is illustrated in Figure 14.7(A, solid line), in which a subject performs a forced vitalcapacity maneuver, inspiring to total lung capacity and thenexhaling as forcibly as possible to residual volume.
Note thatin the expiratory flow–volume curve generated:■■The peak of this curve represents the peak expiratoryflow rate (PEFR).The downward slope (expiratory phase) of the flowvolume curve is effort-independent; during this phaseof the curve, flow is limited by dynamic compression ofthe airways.When less effort is exerted, lower peak flow is reached, but theassociated flow–volume curve converges with the maximumeffort curve and the downslope is the same, consistent withthe effort-independence of expiratory flow during active expiration (see Fig.
14.7A, dotted line).172Respiratory Physiologythe lung. Respiratory distress syndrome (previously known ashyaline membrane disease) is the most common cause of death inpremature infants, and is caused by a lack of surfactant production. Without surfactant, the negative pressure required to inflatethe lungs remains high (CL is low) and portions of the lung collapse, leading to respiratory distress and potentially respiratoryfailure and death. Treatment consists of ventilatory support andsurfactant therapy through the breathing tube.CLINICAL CORRELATERespiratory Distress Syndrome of the NewbornImmediately after delivery, a newborn takes its first breath.
Negative pressure of 40 to 100 cm H2O is required to draw air into thecollapsed airways and inflate the alveoli. During this first breath,in a healthy, normal, term infant, surfactant stored in type IIalveolar epithelial cells is released and forms a mononuclear layerat the air-fluid interface of the small airways and alveoli. By thethird breath, only a small negative pressure is required to inflateA. Risk factors for development of respiratory distress syndrome (RDS) of newbornPrematurityBirth wt.
⬎2.5 kg; RDS not likelyBirth wt. ⬍2.5 kg; likelihood ofRDS increases in relation tolower wt. (if viable)Perinatal asphyxia(2nd born of twins·· · more susceptible)Cesarean birthDrop of water mixed with householddetergent; surface tension reduced to 20dynes/cm and thus water spreads outB. Surfactant effects during lung inflation in the neonateDrop of water with surface tensionof 72 dynes/cm forms a globuleGlass sheetsRadius ⫽ 25 SurfactantabsentFluid-filledairwayTerminal sac(alveolus)Radius ⫽ 100 AirFluidNegative pressure of 40 to 100 cm H2Oneeded to inflate sac (alveolus) with air.Before 1st breathRadius ⫽ 25 SurfactantpresentDiabetes mellitus(maternal)Fluid-filled airwaySurfactant stored in type IIcells of terminal sac (alveolus)Negative pressure of 40 to 100cm H2O needed to inflate sac(alveolus) with air.Inflated terminalsac (alveolus)During 1st breathRadius ⫽ 100 Radius ⫽ 25 Air Fluid Collapsed terminal sac(alveolus)Minimum surface tension is 50 dynes/cm.As much as 20 cm H2O of negative pressureneeded to inflate sac (alveolus) during fourthand subsequent breaths.After 3rd breathRadius ⫽ 50 Air FluidSurfactant Inflated terminalsac (alveolus)Monomolecular layer of surfactant Surface tension is 5 dynes/cm or less.
Negativepressure of only 2 cm H2O needed to inflatelining fluid layer on surface ofsac (alveolus) to maximum diameter duringterminal sac (alveolus)fourth and subsequent breaths.AirFluidThe initial inflation of the collapsed lungs of a neonate requires large negative pressure (40 to 100 cm H20), but surface tension is reduced insubsequent breaths as surfactant lines the alveoli and small airways, reducing the work required to inflate the lungs. Premature birth is oftenassociated with surfactant deficiency and respiratory distress.During normal, quiet breathing, pleural pressure is alwaysnegative.
However, during active expiration, contraction ofexpiratory muscles results in elevation of pleural pressureabove atmospheric pressure (see Fig. 14.7). Under these circumstances, during expiration, alveolar pressure is the sum ofthe positive pleural pressure and the elastic recoil pressureof the lungs. Pressure in the airways falls between the alveoliand the opening of the mouth, reaching atmospheric pressureat the mouth. Thus, at some point downstream from thealveoli, an equal pressure point is reached, at which airwayThe Mechanics of BreathingLaminar flow occurs mainlyin small peripheral airwayswhere rate of airflowthrough any airway is low.Driving pressure isproportional to gas viscosity.Turbulent flow occurs athigh flow rates in tracheaand larger airways. Drivingpressure is proportional tosquare of flow and isdependent on gas density.Poiseuille’s law.
Resistance to laminar flow is inversely proportional to tuberadius to the 4th power and directly proportional to length of tube. When radiusis halved, resistance is increased 16-fold. If driving pressure is constant, flowwill fall to one sixteenth. Doubling length only doubles resistance. If drivingpressure is constant, flow will fall to one half.Transitional flow occurs inlarger airways, particularly atbranches and at sites ofnarrowing.
Driving pressureis proportional to both gasdensity and gas viscosity.r´ ⴝ 1rⴝ2Resistance ⬃16Resistance ⬃1Lⴝ2Resistance ⬃2173L´ ⴝ 4Resistance ⬃4Figure 14.6 Flow Airflow through large airways tends to be turbulent, whereas flow in smaller airwaystends to be laminar. Laminar flow is described by Poiseuille’s law. Airway diameter, according to this law,is the greatest factor in determining resistance and flow (flow is proportional to the fourth power of theradius of a tube).pressure is equal to pleural pressure. Beyond this point,airways will be compressed. This dynamic compression ofairways limits expiratory flow rate and accounts for the effortindependent nature of airflow in active expiration.
Whengreater effort is exerted, greater compression occurs, so thatairflow remains the same.OBSTRUCTIVE AND RESTRICTIVE PULMONARYDISEASES AND PULMONARY FUNCTION TESTSMeasurements of flow–volume relationships are important inassessing obstructive and restrictive pulmonary diseases (see“Compliance in Pulmonary Diseases” Clinical Correlate).Severe chronic obstructive pulmonary disease (COPD) ischaracterized by emphysema, in which inflammation leads todestruction of alveolar walls and capillaries, resulting in highlung compliance.
Reduced elastic recoil of the alveoli andairways also results in early formation of the equal pressurepoint (at a point closer to the alveolus) during expiration, and,as a result of this dynamic compression, “trapping” of airtakes place in the lung. These changes ultimately produce anincrease in total lung capacity (TLC), functional residualcapacity (FRC), and residual volume (RV). The changes inflow are clinically assessed by spirometry and related tests(Fig. 14.8). Notably, expiratory flow rate and FEV1 (the forced174Respiratory PhysiologyExpiratory Flow–VolumeCurves Performed withMaximal Effort (Solid Line)and Reduced Effort (Dotted Line)8Flow (L/sec)642010080A6040% VC200Determinants of Maximal Expiratory Flow⫹30Equalpressurepointⴙ2025ⴙ20ⴙAlveolarpressure+30press20Elastic recoilpressure oflung, ⴙ10⫹20BAt onset of maximal airflow, contraction of expiratory muscles at a givenlung volume raises pleural pressure above atmospheric level (+20 cm H2O).Alveolar pressure (sum of pleural pressure and lung recoil pressure) is yethigher (+30 cm H2O).
Airway pressure falls progressively from alveolus toairway opening in overcoming resistance. At equal pressure point of airway,pressure within airway equals pressure surrounding it (pleural pressure).Beyond this point, as intraluminal pressure drops further, below pleuralpressure, airway will be compressed.Pleuralⴙ35ⴙⴙ30Alveolarpressure+40ⴙ30ⴙ2530ⴙ ⴙ30ⴙ30⫹30pressureⴙ20ⴙ30ure15ⴙⴙ20⫹20PleuralEqualpressurepoint⫹20Force ofcontractionof expiratorymusclesⴙ30ⴙ30Elastic recoilpressure oflung, +10⫹30With further increases in expiratory effort, at same lung volume, pleuralpressure is greater and alveolar pressure is correspondingly higher.
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