- •Table of Contents
- •Copyright
- •Dedication
- •Introduction to the eighth edition
- •Online contents
- •List of Illustrations
- •List of Tables
- •1. Pulmonary anatomy and physiology: The basics
- •Anatomy
- •Physiology
- •Abnormalities in gas exchange
- •Suggested readings
- •2. Presentation of the patient with pulmonary disease
- •Dyspnea
- •Cough
- •Hemoptysis
- •Chest pain
- •Suggested readings
- •3. Evaluation of the patient with pulmonary disease
- •Evaluation on a macroscopic level
- •Evaluation on a microscopic level
- •Assessment on a functional level
- •Suggested readings
- •4. Anatomic and physiologic aspects of airways
- •Structure
- •Function
- •Suggested readings
- •5. Asthma
- •Etiology and pathogenesis
- •Pathology
- •Pathophysiology
- •Clinical features
- •Diagnostic approach
- •Treatment
- •Suggested readings
- •6. Chronic obstructive pulmonary disease
- •Etiology and pathogenesis
- •Pathology
- •Pathophysiology
- •Clinical features
- •Diagnostic approach and assessment
- •Treatment
- •Suggested readings
- •7. Miscellaneous airway diseases
- •Bronchiectasis
- •Cystic fibrosis
- •Upper airway disease
- •Suggested readings
- •8. Anatomic and physiologic aspects of the pulmonary parenchyma
- •Anatomy
- •Physiology
- •Suggested readings
- •9. Overview of diffuse parenchymal lung diseases
- •Pathology
- •Pathogenesis
- •Pathophysiology
- •Clinical features
- •Diagnostic approach
- •Suggested readings
- •10. Diffuse parenchymal lung diseases associated with known etiologic agents
- •Diseases caused by inhaled inorganic dusts
- •Hypersensitivity pneumonitis
- •Drug-induced parenchymal lung disease
- •Radiation-induced lung disease
- •Suggested readings
- •11. Diffuse parenchymal lung diseases of unknown etiology
- •Idiopathic pulmonary fibrosis
- •Other idiopathic interstitial pneumonias
- •Pulmonary parenchymal involvement complicating systemic rheumatic disease
- •Sarcoidosis
- •Miscellaneous disorders involving the pulmonary parenchyma
- •Suggested readings
- •12. Anatomic and physiologic aspects of the pulmonary vasculature
- •Anatomy
- •Physiology
- •Suggested readings
- •13. Pulmonary embolism
- •Etiology and pathogenesis
- •Pathology
- •Pathophysiology
- •Clinical features
- •Diagnostic evaluation
- •Treatment
- •Suggested readings
- •14. Pulmonary hypertension
- •Pathogenesis
- •Pathology
- •Pathophysiology
- •Clinical features
- •Diagnostic features
- •Specific disorders associated with pulmonary hypertension
- •Suggested readings
- •15. Pleural disease
- •Anatomy
- •Physiology
- •Pleural effusion
- •Pneumothorax
- •Malignant mesothelioma
- •Suggested readings
- •16. Mediastinal disease
- •Anatomic features
- •Mediastinal masses
- •Pneumomediastinum
- •Suggested readings
- •17. Anatomic and physiologic aspects of neural, muscular, and chest wall interactions with the lungs
- •Respiratory control
- •Respiratory muscles
- •Suggested readings
- •18. Disorders of ventilatory control
- •Primary neurologic disease
- •Cheyne-stokes breathing
- •Control abnormalities secondary to lung disease
- •Sleep apnea syndrome
- •Suggested readings
- •19. Disorders of the respiratory pump
- •Neuromuscular disease affecting the muscles of respiration
- •Diaphragmatic disease
- •Disorders affecting the chest wall
- •Suggested readings
- •20. Lung cancer: Etiologic and pathologic aspects
- •Etiology and pathogenesis
- •Pathology
- •Suggested readings
- •21. Lung cancer: Clinical aspects
- •Clinical features
- •Diagnostic approach
- •Principles of therapy
- •Bronchial carcinoid tumors
- •Solitary pulmonary nodule
- •Suggested readings
- •22. Lung defense mechanisms
- •Physical or anatomic factors
- •Antimicrobial peptides
- •Phagocytic and inflammatory cells
- •Adaptive immune responses
- •Failure of respiratory defense mechanisms
- •Augmentation of respiratory defense mechanisms
- •Suggested readings
- •23. Pneumonia
- •Etiology and pathogenesis
- •Pathology
- •Pathophysiology
- •Clinical features and initial diagnosis
- •Therapeutic approach: General principles and antibiotic susceptibility
- •Initial management strategies based on clinical setting of pneumonia
- •Suggested readings
- •24. Bacterial and viral organisms causing pneumonia
- •Bacteria
- •Viruses
- •Intrathoracic complications of pneumonia
- •Respiratory infections associated with bioterrorism
- •Suggested readings
- •25. Tuberculosis and nontuberculous mycobacteria
- •Etiology and pathogenesis
- •Definitions
- •Pathology
- •Pathophysiology
- •Clinical manifestations
- •Diagnostic approach
- •Principles of therapy
- •Nontuberculous mycobacteria
- •Suggested readings
- •26. Miscellaneous infections caused by fungi, including Pneumocystis
- •Fungal infections
- •Pneumocystis infection
- •Suggested readings
- •27. Pulmonary complications in the immunocompromised host
- •Acquired immunodeficiency syndrome
- •Pulmonary complications in non–HIV immunocompromised patients
- •Suggested readings
- •28. Classification and pathophysiologic aspects of respiratory failure
- •Definition of respiratory failure
- •Classification of acute respiratory failure
- •Presentation of gas exchange failure
- •Pathogenesis of gas exchange abnormalities
- •Clinical and therapeutic aspects of hypercapnic/hypoxemic respiratory failure
- •Suggested readings
- •29. Acute respiratory distress syndrome
- •Physiology of fluid movement in alveolar interstitium
- •Etiology
- •Pathogenesis
- •Pathology
- •Pathophysiology
- •Clinical features
- •Diagnostic approach
- •Treatment
- •Suggested readings
- •30. Management of respiratory failure
- •Goals and principles underlying supportive therapy
- •Mechanical ventilation
- •Selected aspects of therapy for chronic respiratory failure
- •Suggested readings
- •Index
assuming CO2 production remains constant. It is clear that is compromised either by decreasing the total (without changing the relative proportion of dead space and alveolar ventilation) or by keeping
the total constant and increasing the relative proportion of dead space to alveolar ventilation. A simple way to produce the latter circumstance is to change the pattern of breathing (i.e., decrease VT and increase frequency of breathing). With a lower VT, a larger proportion of each breath ventilates the fixed amount of anatomic dead space, and the proportion of alveolar ventilation to total ventilation must decrease.
In addition, if significant ventilation–perfusion mismatching is present, well-perfused areas may be underventilated, whereas underperfused areas receive a disproportionate amount of ventilation. The net effect of having a large proportion of ventilation go to poorly perfused areas is similar to that of increasing the dead space. By wasting this ventilation, the remainder of the lung with the large share of the perfusion is underventilated, and the net effect is to decrease the effective alveolar ventilation. However,
in many disease conditions, when such significant mismatch exists, any increase in PCO2 stimulates breathing, increases total minute ventilation, and can compensate for the effectively wasted ventilation.
Therefore, several causes of hypercapnia can be defined, all of which have in common a decrease in effective alveolar ventilation. Causes include a decrease in minute ventilation, an increase in the proportion of wasted ventilation, and significant ventilation–perfusion mismatch. However, by increasing the total minute ventilation, a patient often is capable of compensating for the latter two situations so CO2 retention does not result.
Decrease in alveolar ventilation is the primary mechanism that causes hypercapnia.
Increasing CO2 production necessitates an increase in alveolar ventilation to avoid CO2 retention. Thus, if alveolar ventilation does not rise to compensate for additional CO2 production, it will also result with hypercapnia.
As is the case with hypoxemia, pathophysiologic explanations for hypercapnia do not necessarily follow such simple rules so that each case can be fully explained by one mechanism. In reality, several of these mechanisms may be operative, even in a single patient.
Suggested readings
Cloutier M.M. Respiratory physiology 2nd ed. 2019; Elsevier Philadelphia.
Hsia C.C. Respiratory function of hemoglobin New England Journal of Medicine 1998;338: 239-247.
LoMauro A. & Aliverti A. Sex differences in respiratory function Breathe 2018;14: 131-140. Lumb A.B. Nunn’s applied respiratory physiology 8th ed. 2017; Elsevier Philadelphia. Petersson J. & Glenny R.W. Gas exchange and ventilation-perfusion relationships in the
lung European Respiratory Journal 2014;44: 1023-1041.
Mccormack M.C. & West J.B. Ventilation, blood flow, and gas exchange V.C. Broaddus, J.D. Ernst, T.E. King Jr., et al. Murray and Nadel’s textbook of respiratory medicine (7th ed.) 2021; Elsevier Philadelphia.
Robertson H.T. Dead space: the physiology of wasted ventilation European Respiratory Journal 2015;45: 1704-1716.
Schwartzstein R.M. & Parker M.J. Respiratory physiology: A clinical approach 2006;
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Lippincott Williams & Wilkins Philadelphia.
Wagner P.D. The physiological basis of pulmonary gas exchange: implications for clinical interpretation of arterial blood gases European Respiratory Journal 2015;45: 227-243.
Weinberger S.E, Schwartzstein R.M. & Weiss J.W. Hypercapnia New England Journal of Medicine 1989;321: 1223-1231.
West J.B. & Luks A.M. West’s pulmonary pathophysiology: The essentials 10th ed. 2022; Wolters Kluwer Philadelphia.
West J.B. & Luks A.M. West’s respiratory physiology: The essentials 11th ed. 2021; Wolters Kluwer Philadelphia.
aBy convention, a dot over a letter adds a time dimension. Hence, stands for volume of expired gas per minute—that is, minute ventilation. Similar abbreviations used in this chapter are (volume of CO2 produced per minute) and (blood flow per minute).
bThe units torr and mm Hg can be used interchangeably: 1 torr = 1 mm Hg.
cBy convention, A refers to alveolar and a to arterial.