Ebook Respiratory physiology for the intensivist: Part 2
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Ebook Respiratory physiology for the intensivist: Part 2
CHAPTER 11Abnormalities of the Chest WallSome representative examples of abnormal respirator}' physiology for common representative diseases frequentl Ebook Respiratory physiology for the intensivist: Part 2ly seen in the practice of critical-care medicine will assist in understanding prior physiological principles and also in understanding abnormal physiology in specific disease states, bearing in mind the following definitions of ventilation/perfusion (V/Q) abnormalities based upon multiple inert gas Ebook Respiratory physiology for the intensivist: Part 2 elimination technique (MIGET) criteria: shunt physiology, represented by V/Q < 0.005; low V/Q, represented by 0.005 < V/Q < 0.1; high V/Q, representeEbook Respiratory physiology for the intensivist: Part 2
d by 10 < V/Q < 100; and dead space physiology, represented by V/Q > 100.Expansion of the intrathoracic space is not uniform in that the thoracic cageCHAPTER 11Abnormalities of the Chest WallSome representative examples of abnormal respirator}' physiology for common representative diseases frequentl Ebook Respiratory physiology for the intensivist: Part 2cesses that can result in structural and anatomic abnormalities and subsequent dysfunction, dys-synchrony, or dyscoordination of the normal coordinated mechanical coupling and function of the chest wall and their resultant deleterious effects upon ventilation. However, in relation to the intensivist Ebook Respiratory physiology for the intensivist: Part 2 and critical-care physician, the two most common musculoskeletal deformities of the chest that result in both chronic respirator}' insufficiency andEbook Respiratory physiology for the intensivist: Part 2
acute respiratory failure are severe kyphoscoliosis (KS) and flail chest (chapter 17). Both musculoskeletal abnormalities cause uncoupling of the coorCHAPTER 11Abnormalities of the Chest WallSome representative examples of abnormal respirator}' physiology for common representative diseases frequentl Ebook Respiratory physiology for the intensivist: Part 2luding the diaphragm, to shorten (below the ideal length-tension relationship), causing secondary muscle weakness.Abnormal respiratory mechanics inKYPHOSCOLIOSISKyphoscoliosis (KS) is a disease of the spine and its articulations, resulting in spinal buckling (Bergofsky 1959). The deformity of the sp Ebook Respiratory physiology for the intensivist: Part 2ine in this disorder characteristically consists of lateral displacement of spinal curvature (scoliosis) and vertebral anterioposterior angulation (kyEbook Respiratory physiology for the intensivist: Part 2
phosis) or both. The predominate curvature is a right major thoracic curvature extending from T4-6 to TD11-L1, resulting in the “typical” curvature ofCHAPTER 11Abnormalities of the Chest WallSome representative examples of abnormal respirator}' physiology for common representative diseases frequentl Ebook Respiratory physiology for the intensivist: Part 2tiple studies predominately in noncritically ill patients with KS and patients with KS undergoing orthopedic spinal/vertebral surgical corrective or stabilization procedures have shown three consistent mechanical and muscular pulmonary physiological abnormalities: (a) decreased chest-wall compliance Ebook Respiratory physiology for the intensivist: Part 2 (Ccw) or its inverse, increased chest-wall elastance (Ecw); (b) decreased lung compliance (Clung) or its inverse, increased lung elastance (Elung); aEbook Respiratory physiology for the intensivist: Part 2
nd (c) respiratory muscle weakness. In addition, the severity of these physiological abnormalities was directly correlated with the magnitude of spinaCHAPTER 11Abnormalities of the Chest WallSome representative examples of abnormal respirator}' physiology for common representative diseases frequentl Ebook Respiratory physiology for the intensivist: Part 2sely proportional to Cobb’s angle with more devastating abnormalities dependent upon the magnitude of deformity (Kafer 1975, Figure 5: Rochester 1988; McCool 1998, Figure 97-2).In general, patients with KS but minimal deformity as assessed by Cobb’s angle (less than 50 degrees) have barely perceptib Ebook Respiratory physiology for the intensivist: Part 2le effects in lowering Ccw to measured values of 136 mL/cmH2O (compared to normal healthy values approximately 200 mL/cmH20), but as Cobb's angle incrEbook Respiratory physiology for the intensivist: Part 2
eases above 100 degrees, Ccw may decline to as low as 31 mL/cmH20. In fact, equations have been derived relating the abnormally reduced Ccw to the angCHAPTER 11Abnormalities of the Chest WallSome representative examples of abnormal respirator}' physiology for common representative diseases frequentl Ebook Respiratory physiology for the intensivist: Part 2using approximate reductions in Ccw near 35 mL/cmH20 (Bergofsky 1995; McCool 1998). In addition, the subsequent disruption of normal mechanicothoracic coordination causes consistent reductions in virtually all lung volume measurements, causing KS patients to ventilate at rest on the relatively lower Ebook Respiratory physiology for the intensivist: Part 2 portion of the standard pressure-volume (P-V) curve with the bulk of tidal volume expansion now occurring during the relatively flat and hypocomplianEbook Respiratory physiology for the intensivist: Part 2
t portion of this curve with studies showing an absence of the normal “steep hypercompliant” S-shaped curve characteristics (Cooper 1984, Figure 6).TaCHAPTER 11Abnormalities of the Chest WallSome representative examples of abnormal respirator}' physiology for common representative diseases frequentl Ebook Respiratory physiology for the intensivist: Part 2Oml. 'cmHjOmL e:nH;ONormal (Rerjjofskyl 959)111.5193.8289(98-120)(138-280)(216-363)KS subjects (Bcrgoisky 1959)39.994.176.3(20 79)(54 138)(50 75)KS subjects (Kafer 1975)48 +/ 25177 +/- 11so +/ 12Normal (Cooper 1984)151 +/-56KS subjects (Cooper 1984)96+/- 13Similarly in a population of patients with Ebook Respiratory physiology for the intensivist: Part 2KS, elastance measurements (Ers, tot; Elung; Ecw) were also shown to be significantly increased above normal reference values (Ers, tot = 10 cmH2O/L;Ebook Respiratory physiology for the intensivist: Part 2
Elung = 5 cmH2O/L; Ecw = 5 cmH2O/L) as shown in the accompanying Table 11.2. (Baydur 1990).Table 11.2: Representative Values of Elastance (Total RespiCHAPTER 11Abnormalities of the Chest WallSome representative examples of abnormal respirator}' physiology for common representative diseases frequentl Ebook Respiratory physiology for the intensivist: Part 234+/-4.10KS subjects37.49.424.7 +/- 9.58.18+/-2.26Although some studies have demonstrated relatively normal airflow and airway resistance parameters, some cases of significant increases in Raw have been observed, but not universally in all KS patients. Raw, inspiratory (cmH2O/L/sec) = 5.34 +/- 4.10 Ebook Respiratory physiology for the intensivist: Part 2and 8.18 +/- 2.26 (normal values = 1.39) (Baydur, 1990).The combination of all these abnormal physiological effects creates risk factors for increasedEbook Respiratory physiology for the intensivist: Part 2
oxygen cost of breathing, at times approximately five times above normal. In a small subset of patients with severe KS, the oxygen cost of breathing CHAPTER 11Abnormalities of the Chest WallSome representative examples of abnormal respirator}' physiology for common representative diseases frequentl Ebook Respiratory physiology for the intensivist: Part 2 the inordinate amount of work required in moving the chest bellows; whereby WOB in KS in moving chest bellows accounted for 20-50 percent of the total WOB compared to only 18-20 percent in normal subjects (Bergofsky 1959).Abnormal gas exchange in kypi ioscoliosisDespite significant aberrations in l Ebook Respiratory physiology for the intensivist: Part 2ung and chest-wall mechanics, gas exchange, especially oxygenation, tends to be preserved in KS, given the absence of intrinsic lung disease per se (BEbook Respiratory physiology for the intensivist: Part 2
ergofsky 1959). In KS patients without hypercapnia, the alveolar to arterial oxygen gradient/difference (AaO2D) tends to remain normal or, if anythingCHAPTER 11Abnormalities of the Chest WallSome representative examples of abnormal respirator}' physiology for common representative diseases frequentl Ebook Respiratory physiology for the intensivist: Part 2percapnia the A-a 02 gradient still remains, either normal or again only mildly elevated with values between 14.9 mmHg and 25 mmHg (Bergofsky 1959; Kafer 1976).Physiologically from a gas exchange perspective, the onset, development, and progression of hypercapnia is predominately related to decrease Ebook Respiratory physiology for the intensivist: Part 2s in both tidal volume (Vt) and decreased overall minute ventilation (Ve) with preservation of relatively normal values for total pulmonary dead spaceEbook Respiratory physiology for the intensivist: Part 2
. Even with marked elevations in PaCO2, Vd/Vt remains less than 40 percent (PaCO2 = 38mmHg and Vd/Vt = 27%; PaCO2 = 45mmHg and Vd/Vt - 32%; PaCO2 = 60CHAPTER 11Abnormalities of the Chest WallSome representative examples of abnormal respirator}' physiology for common representative diseases frequentl Ebook Respiratory physiology for the intensivist: Part 2 area and resultant overaeration of alveoli insufficiently perfused with blood, the relatively mild to modest increases in Vd/Vt in patients with KS tend to be a reflection of their overall reduced vital capacity (VC) and thus a greater relative proportion of anatomic dead space compromising tidal v Ebook Respiratory physiology for the intensivist: Part 2olume (Vt) in relation to each individual breath. In a large group of patients with KS, Vt measured 360 +/- 114 mL and Vd/Vt 43 +/- 7 percent (with raEbook Respiratory physiology for the intensivist: Part 2
nge 30-54%) (Kafer 1975; Kafer 1976, Figure 3).ReferencesBaydur, A., s. M. Swank, c. M. Stiles, and c. s. H. Sassoon. 1990. “Respiratory Mechanics in CHAPTER 11Abnormalities of the Chest WallSome representative examples of abnormal respirator}' physiology for common representative diseases frequentl Ebook Respiratory physiology for the intensivist: Part 2ease: The Thorax Volume 85, edited by c. Roussos. New York: Marcel-Dekker, Inc. 1915-1949.Bergofsky, E. H., G. M. Turino, and A. p. Fishman. 1959. “Cardiorespiratory Failure in Kyphoscoliosis.” Medicine 38: 263-318.Cooper, D. M., J. Velasquez Rojas, R. B. Mellins, H. A. Keim, and A. L. Mansell. 1984 Ebook Respiratory physiology for the intensivist: Part 2. “Respiratory Mechanics in Adolescents with Idiopathic Scoliosis.” American Review of Respiratory Disease 130: 16-22.Gọi ngay
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