3.5 Respiratory Pathophysiology.pdf

Respiratory Pathophysiology Lecture Outline I. Non-respiratory Functions of the Lung II. Hypercapnia and hypoxemic hypoxia III. Pathophysiology- Obstructive Diseases IV. Pathophysiology- Restrictive Diseases V. Pathophysiology- Vascular Diseases VI. Respiratory Failure and Treatment 1 Respiratory Pa...

Respiratory Pathophysiology Lecture Outline I. Non-respiratory Functions of the Lung II. Hypercapnia and hypoxemic hypoxia III. Pathophysiology- Obstructive Diseases IV. Pathophysiology- Restrictive Diseases V. Pathophysiology- Vascular Diseases VI. Respiratory Failure and Treatment 1 Respiratory Pathophysiology Objectives 1.Identify defense mechanisms of the lung 2.Describe how aerosols are removed by both impaction and sedimentation 3.Identify the function and location of the mucociliary escalator and alveolar macrophages 4.Explain how carbon monoxide and cigarette moke act as respiratory pollutants 5.Identify two causes of hypercapnia 6.Identify four main causes of hypoxemic hypoxia and give examples of each 7.Explain sources of hypoventilation 8.Identify the pathogenesis and signs and symptoms of obstructive, restrictive, and vascular diseases 9.Identify conditions that lead to respiratory failure 10.Explain management of respiratory failure with mechanical ventilation, PEEP, BiPAP, and CPAP 11.List potential hazards of oxygen therapy 2 References Assigned reading from your text Levitzky Chapter 10 for Nonrespiratory Functions of the Lung West’s Pulmonary Pathophysiology (book) 9th edition (selected content) Images referenced as West Pulmonary Pathophysiology with description The bulk of this lecture comes from this book Dr. John West’s lectures are available on YouTube; The two listed below are especially pertinent to this lecture Respiratory Failure from his Lectures in Pulmonary Pathophysiology Defense Systems of the Lungs from his Lectures in Respiratory Physiology 3 I. Non-respiratory Functions of the Lung 4 Non-respiratory Functions Of The Lung q Normal non-respiratory functions of the lung: Storage and filtration of blood for systemic circulation – Filters particles before they reach systemic circulation Particles may come from natural processes, trauma, or therapeutic measures – Can serve as a reservoir for the left ventricle when needed Average adult male has 500 ml in pulmonary circulation Metabolism of vasoactive substances – Vasoactive substances may be inactivated, altered, or removed in pulmonary circulation – Serotonin mostly removed – Epinephrine and histamine are unaffected after a single pass through lung (see table 10-2 Levitzky) Epi can be given down endotracheal tube Formation and release of substances – Surfactant – Mast cells release inflammatory mediators in response to anaphylaxis or pulmonary embolism e.g. histamine, lysosomal enzymes, prostaglandins, leukotrienes, serotonin, etc 5 Defense Mechanisms of the Lung q Defense against particulate matter Lungs are normally protected from inspired or aspirated contaminants Aspirated = accidentally inspired from oropharynx or nasopharynx 6 Clearance of Inhaled Particles q Lungs have a unique exposure to toxic, infectious, and inflammatory environmental insults 7500 L per day- increased with exertion 80% suspended aerosols exhaled Airway reflexes stimulate receptors in the: Nasopharynx to produce a sneeze Trachea/bronchi to produce a cough Mucociliary escalator removes inhaled particles down to level of the terminal bronchioles Mucus-covered ciliated epithelium lines respiratory tract from upper airways down to the terminal bronchioles Secretions produced by goblet cells and mucous glands Alveolar macrophages clear substances from the terminal airways and alveoli Most Pollutants Occur As Aerosols q Aerosols are solid particles or liquid droplets suspended in air or gas are mostly removed by impaction or sedimentation Large particles first filtered by vibrissae Deposited in mucus along airways Impaction- predominantly in tortuous airways; few particles > 10 um enter trachea Larger particles deposit in upper airways and down to bronchioles Sedimentation- occurs when airflow is low Brownian Motion- all gases and the smallest particles reach alveoli Masks q Common surgical masks- provide two-way physical barriers Reduce shedding and contamination Droplets suspended in mask instead of operative field N95 mask/filter/respirator- rated to filter 95% penetrating airborne particles (to 0.3 um) Filter efficiency varies regarding aerosolized particles (contaminants, viruses, etc) 9 Mucociliary Escalator q Occurs where cells are mucus-covered and ciliated along respiratory tract q Mucus occurs in an: Upper viscous gel layer that traps particles Lower liquid sol layer that allows cilia to propel the gel layer Particles deposited in mucus (by impaction, sedimentation) are moved continuously toward pharynx- from there they are removed by being swallowed, expectorated, or by blowing your nose Impaired mucociliary function: Mucus can change in volume or composition- bronchitis or cystic fibrosis Cilia may be paralyzed by toxic gases or destroyed Alveolar Macrophages q Most important innate immunity in the alveoli; they inhabit the alveolar surface Contain lysosomes to ingest foreign particles and bacteria Material toxic to macrophages will be redeposited when the macrophage dies Cigarette smoke inhibits their function Along with dendritic cells- secrete cytokines and other factors to activate immune response Macrophages migrate to the mucociliary escalator through the pores of Kohn to be removed Carbon monoxide q The largest pollutant by weight in the US Mostly from transportation Binds preferentially to hemoglobin Desflurane and sevoflurane are fluorinated hydrocarbons Cigarette Smoke q Cigarette smoke is a common pollutant Includes 4% carbon monoxide High inhaled concentrations exceed atmospheric pollutants May raise carboxyhemoglobin % to 10% in smoker’s blood- enough to impair cognitive and physical performance Tars (aromatic hydrocarbons) are carcinogenic A single cigarette increases airway resistance in nonsmokers Data evolving for vaping and marijuana use II. Hypercapnia and Hypoxemic Hypoxia 14 Hypercapnia q Two main causes of CO2 retention 1. 2. Hypoventilation Ventilation-perfusion inequality CO2 retention: – Increases cerebral blood flow – May result in headache, confusion, and decreased level of consciousness Hypoxemic Hypoxia q Common causes of hypoxemic hypoxia (covered on next several slides) 1. 2. 3. 4. Low Alveolar PO2 Diffusion impairment Shunt Ventilation-perfusion inequality Severity: – Mild hypoxemia produces few physiologic changes- slight impairment of mental performance, mild hyperventilation, and diminished visual acuity – Severe hypoxemia (PaO2 below 50 mmHg) causes mental confusion, tachycardia, lactic acidosis, proteinuria (from impaired renal function) Causes of Hypoxemic HypoxiaLow Alveolar PO2 is from Low FiO2 or Hypoventilation q Low FiO2 is from high altitude or low FiO2 q Hypoventilation -volume of fresh gas to alveoli per unit time is reduced Two cardinal features of hypoventilation: Always causes a rise in PCO2 Alveolar hypoxia can be abolished by increasing the FiO2 (alveolar gas equation) Hypercapnia – not hypoxemia- is the dominant feature of hypoventilation In isolated hypoventilation, CO2 retention and respiratory acidosis dominate Hypoventilation can double PCO2 to 80 mmHg and only decrease PAO2 from 100 to 60 mmHg Example of Hypoventilation- Sleep Apnea Causes Intermittent Hypoxia q Sleep apnea- Recurrent brief episodes of hypoxemia in sleep disordered breathing: Chronic sleep deprivation may cause daytime somnolence and impaired cognition Increases risk of CV complications (stroke, CAD, HTN, pulmonary hypertension) Two types of sleep apnea: – Central sleep apnea Apneic periods of no respiratory effort Likely due to instability in feedback control that regulates breathing patterns during sleep Common finding to have small periods of sleep apnea – Obstructive sleep apnea Apnea due to obstruction; effort without airflow More common During inspiration, airway pressure falls producing collapse – Muscles of the tongue and soft palate obstruct the airway (also occurs during sedation) Loud snoring often occurs CPAP raises pressure inside airways Surgical approach- uvulopalatopharyngoplasty Causes Of Hypoventilation q Causes of hypoventilation (and examples of each) include: 1. 2. 3. 4. 5. 6. 7. 8. 9. Depression of respiratory centers by drugs (opiates) Diseases of the medulla (hemorrhage) Spinal cord abnormalities (high cervical spinal cord injury) Anterior horn cell disease (poliomyelitis) Diseases of the nerves to respiratory muscles (Guillain-Barre) Diseases of the myoneural junction (Myasthenia gravis) Diseases of respiratory muscles (Duchenne muscular dystrophy) Thoracic cage abnormalities (crushed chest) Upper airway obstruction (obstructive sleep apnea) Causes of Hypoxemic Hypoxia 2. Diffusion impairment across the alveolar-capillary unit – – – – Equilibration does not occur between the PO2 in the pulmonary capillary blood and alveolar gas Impaired in patients with fibrotic changes, pneumonia, connective tissue diseases Lung normally has large reserve for time for equilibration at rest Hypoxemia caused by diffusion impairment can be corrected by administering 100% O2 3. Right-to-Left Shunt – – – Allows blood to reach the arterial system without passing through ventilated regions of the lung Shunts are the only cause of hypoxemia that do not respond to 100% O2 Does not usually result in a raised PaCO2 4. Ventilation-Perfusion Inequality – – – – – – Most common cause of hypoxemia True shunt and dead space rarely occur in normal physiology, most mismatch is an inequality Mismatch results in inefficient gas transfer of all gases- O2, CO2, anesthetic gases Responsible for most of the hypoxemia of COPD, interstitial lung disease, and vascular disorders (eg pulmonary embolism) All patients with V/Q inequality have a reduced PaO2 PaCO2 may be normal if amount inspired gas to alveoli is increased West lung zones- all lungs have some ventilation-perfusion inequality Exacerbated by 1) hypoventilation and 2) decreased cardiac output 21 NOT ON TEST 22 23 III. Pathophysiology- Obstructive Diseases 24 Obstructive Diseases q The fundamental physiologic problem in obstructive disease is increased resistance to expiratory airflow as a result of caliber reduction of the conducting airways Common obstructive diseases include asthma, bronchitis, and emphysema Increased resistance occurs by three main processes related to their location: – A. Within the lumen- bronchitis, secretions – B. In the airway wall - Edema or hypertrophy of smooth muscle cause a thickened wall – C. In the supporting parenchyma outside airway- Loss of radial traction in emphysema 25 Clinical Features of all COPDs q Clinical features common to all COPDs include: RV/TLC may be >40% Dynamic compression of airways limits expiratory flow rates PA pressures frequently raised Ventilation-perfusion inequality produces hypoxemia with or without CO2 retention – Chronic hypoxia (sleep apnea or at altitude) may blunt the hypoxic ventilatory response Increased work of breathing causes adaptation to CO2 retention – – – In chronic hypercapnia, brain pH is returned toward normal by compensatory changes in serum and tissue bicarbonate Central chemoreceptors become less sensitive to changes in PaCO2 A patient’s basal VE may depend on tonic stimuli from the carotid bodies – High FiO2 may depress carotid body output Treatment: – – – – – Smoking cessation most important Bronchodilators- B-agonists and anticholinergics are mainstays Inhaled corticosteroids reserved for severe disease Pulmonary rehabilitation may improve quality of life and exercise tolerance Lung volume reduction surgery removes diseased region and preserves health lung regions 26 Asthma Pathogenesis q This is a disease of airway inflammation and airflow obstruction Intermittent increased responsiveness of the airways to various stimuli Hypertrophied smooth muscle contracts to cause bronchoconstriction Mucus is thick and copious Subepithelial fibrosis is common Abundance of eosinophils in sputum may look purulent and be mistaken as infection US prevalence was 8.4% in 2019 500k hospital admissions and 4500 deaths annually Microbial exposure in childhood was shown to be inversely related to risk of asthma Atopy (production of IgE antibodies to allergens) is strongest predisposing factor Exposure to house dust mites and cockroach antigens are strong risk factors Children raised on farms have lower prevalances of atopy and asthma Pathogenesis r/t recruitment, multiplication, and activation of immune inflammatory cells through a network of locally released cytokines and chemokines Many triggers: allergy, exercise, environmental 27 Asthma Signs and Symptoms – Two common features of asthma related to a fundamental abnormality of smooth muscle tone Airway hyperresponsiveness Airway inflammation – Symptoms and signs: Dyspnea and chest tightness related to increased airway resistance and decreased lung compliance Wheezing from smooth muscle contraction and mucus hypersecretion and retention Cough from compressive airway narrowing, hypersecretion, high velocity of airflow Hypoxemia and changes in ventilation Obstructive defects and bronchial hyperresonsiveness 28 COPD Includes Chronic Bronchitis and Emphysema q Chronic obstructive pulmonary disease (COPD)- is an imprecise term denoting chronic bronchitis or emphysema (or both diseases) that leads to the development of airway obstruction Affects ~ 15 million people in the US Chronic bronchitis (predominates in 2/3 cases) involves inflammation of the airways; is defined by a clinical history of productive cough for 3 months of the year for 2 consecutive years – – “Blue bloater” Inflammation of airways: Blue bloater Emphysema (predominates in 1/3 cases) is a condition marked by irreversible enlargement of airspaces distal to the terminal bronchioles, accompanied by destruction of their walls – “Pink puffer” – Most often without obvious fibrosis Pink puffer 29 COPD- Chronic Bronchitis Pathogenesis q Inflammation of airways: – Larger airways- Hypertrophy of mucous glands with increased mucous hypersecretion and mucus obstruction of airways – Smaller airways- Principle site of inflammation and resultant increased airflow obstruction – Terminal respiratory units (alveoli) unaffected by bronchitis q Etiology is repeated exposure to irritants: – Cigarette smoking most common etiology in 90% patients – Dose-dependent relationship between tobacco smoke exposure and loss of lung function – In developing populations- etiology is indoor exposure to smoke from burning biofuels 30 COPD- Chronic Bronchitis Pathogenesis- Luminal Narrowing q Mucosal inflammation narrows the bronchial lumen – Mucociliary clearance function severely diminished or abolished – Normal ciliated pseudostratified columnar epithelium is frequently replaced by patchy squamous metaplasia – Excessive mucus production in the bronchial tree is sufficient to cause excessive expectoration of sputum Mucus hypersecretion contributes to luminal narrowing Semisolid plugs of mucus may occlude small airways q Bronchial smooth muscle hypertrophy is common in bronchitis – Causes hyperresponsiveness to nonspecific bronchoconstrictor stimuli Histamine and methacholine 31 COPD- Chronic Bronchitis Signs and Symptoms q Chronic bronchitis - clinical features related to chronic airway injury and narrowing – Cough with sputum production Purulent sputum from bacterial colonization and infection High viscosity of sputum due to presence of free DNA from lysed cells Cough is less effective due to narrowed airways – Wheezing – from airway narrowing and mucus obstruction- may be reversible – Inspiratory and expiratory coarse crackles from mucus in larger airways – Cardiac exam may reveal tachycardia, prominent P2 (pulmonary valve closing), elevated jugular venous pressure, and peripheral edema – Imaging reveals increased cardiac size – PFTs reveal reduced expiratory flows/volumes, increased RV and FRC – Arterial blood gas reveals hypoxemia at rest with an increased A-a gradient With increasing obstruction, expect hypercapnia and respiratory acidosis compensated by metabolic alkalosis – Polycythemia from chronic hypoxemia is mediated by erythropoietin (HCT may >50) COPD- Emphysema Pathogenesis q Emphysema Enlargement of parenchyma/air spaces distal to the terminal bronchiole with destruction of alveolar with loss of elastic recoil (anatomic definition) q Etiology of emphysema Chronic destructive process resulting from an imbalance of local oxidant injury and proteolytic (especially elasteolytic) activity caused by a deficiency of ⍺1-antitrypsin (an ⍺1protease inhibitor) Cigarette smoking most common cause of reduced elastase inhibitors Alveolar capillaries lost which results in diffusion abnormality 33 COPD- Types of Emphysema q Types of emphysema: – Centriacinar (central part destroyed) » usually from cigarettes – Panacinar (distension/destruction whole acinus) » from alpha 1-antitrypsin deficiency 34 COPD- Emphysema Signs and Symptoms q Emphysema- noninflammatory disease manifested by dyspnea, progressive nonreversible airway obstruction, and abnormalities of gas exchange, particularly with exercise – Breath sounds are decreased in intensity reflecting decreased airflow – Cardiac exam may reveal tachycardia, prominent P2 (pulmonary valve closing), pulmonary hypertension – Imaging reveals hyperinflation with flattened hemidiaphragms and bullae – PFTs reflect a loss of lung elastic recoil and parenchymal destruction. reduced expiratory flows/volumes, increased RV and FRC – Arterial blood gas reveals an increased A-a PO2 gradient Patients with high V/Q ratios increase their minute ventilation Hypercapnia, respiratory acidosis, and compensatory metabolic alkalosis common in severe disease – Polycythemia from chronic hypoxemia is mediated by erythropoietin (HCT may >50) IV. Pathophysiology- Restrictive Disease 36 Restrictive Diseases- Epidemiology and Pathogenesis q Less common than COPD- interstitial pulmonary fibrosis prevalence 14 per 100,000 q Diffuse parenchymal lung diseases is an umbrella term for interstitial and parenchymal processes that commonly involve infiltration of the lung by inflammatory cells and fluid, leading to scarring, fibrosis, and capillary obliteration Major risk factors include: Environmental exposure- tobacco smoke and organic/inorganic dust Systemic diseases include scleroderma, sarcoidosis, and hypersensitivity pneumonitis Genetics may play a role in a small number of cases- but are not the typical etiology Cellular events that mediate lung inflammation Initial tissue injury Vascular injury and endothelial cell activation with increased permeability, exudation of plasma proteins, and variable thrombosis and thrombolysis Alveolar epithelial cell injury and activation with loss of barrier integrity and release of proinflammatory mediators Damage to type II epithelial cells interferes with surfactant production Increased leukocyte adherence to activated endothelium Continued injury and repair processes alter cell population and increase matrix production 37 Restrictive Diseases- Signs and Symptoms q Signs and symptoms are related to increased lung elastic recoil, decreased lung compliance and volumes, and worsening V/Q Expansion of the lung is restricted either by alterations in the lung parenchyma or because of disease of the pleura (pneumothorax, effusion) chest wall (obesity), or neuromuscular apparatus Cough due to cellular alterations in both stimulatory and inhibitory nerve fibers of cough reflexes Dyspnea and tachypnea due to increased work of breathing From decreased lung compliance, lack of surfactant Increased stimuli from C fibers of fibrotic alveolar walls produce tachypnea sense increased force needed to breathe Inspiratory crackles due to successive opening of collapsed units (surfactant) Digital clubbing of unknown etiology Cardiac examination pulmonary hypertension, prominent P2, right heart overload, elevated JVP, and tricuspid murmur (S3) Imaging-the alveolar walls show marked infiltration with collagen and obliteration of capillaries Restrictive patterns have reduced TLC, FEV1, and FVC ABG shows hypoxemia in advanced fibrosis 38 V. Pathophysiology- Vascular Diseases 39 Vascular Diseases- Pulmonary Hypertension q Pulmonary Hypertension- An increased pulmonary artery pressure (>25 mmHg) – From diseases that cause structural changes in blood vessels – Involves three principal mechanisms: Increase in pulmonary vascular resistance Increase in left atrial pressure Increase in pulmonary blood flow – Idiopathic pulmonary hypertension and cor pulmonale are examples 40 Vascular Diseases- Pulmonary Edema q Pulmonary edema the accumulation of excess fluid in the extravascular compartment of the lungs- in the interstitium and alveolar spaces q Most commonly presents with dyspnea q In severe cases, pulmonary edema may cause acute respiratory failure q Etiology is related to many conditions: Hydrostatic pressure gradient increases – – Cardiogenic pulmonary edema Due to elevated pulmonary venous and left atrial pressures due to LV failure, mitral stenosis, or mitral regurgitation Vascular or alveolar epithelial cell permeability increases from cellular injury (eg ARDS) – Non-cardiogenic pulmonary edema Oncotic pressure gradient decreases- due to hypoalbuminemia or nephrotic syndrome Lymphatic drainage is impaired by malignancy or infection q Clinical manifestations include: Dyspnea Orthopnea Tachycardia Rales 41 Vascular Diseases- Pulmonary Embolism (PE) q Pulmonary circulation normally serves as a filter for gas bubbles, blood clots, fat cells, debris, etc q A PE consists of material that gains access to the venous system and then to pulmonary circulation English word “embolus” derives from Greek word for “plug” or “stopper” Most common emboli (95%) are from pulmonary thromboembolism from a lower extremity DVT Risk factors for DVT are risk factors for PE Amniotic fluid embolus - give “A-OK for AFE”. Atropine, ondansetron, ketorolac q Types of emboli include: 42 Vascular Diseases- Pathophysiologic Changes of PE qChanges accompanying PE may be difficult to identify/diagnose Inflammatory response can occur with any foreign substance blocking pulmonary capillaries No gas exchange occurs distal to the occlusion (embolism) Diffusing capacity of occluded area decreases for 4-5 days before returning to normal 43 VI. Respiratory Failure and Treatment 44 Respiratory Failure q Refers to the condition of the lung failing to oxygenate the blood adequately or prevent CO2 retention q Five groups of conditions lead to respiratory failure 1. 2. 3. 4. 5. Acute overwhelming lung disease Neuromuscular disorders Acute or chronic lung disease ARDS Infant respiratory distress syndrome 45 Management Of Respiratory Failure Treat the underlying cause- eg opioid overdose with Narcan Support oxygenation and ventilation – – Decrease airway resistance – – Respiratory failure is often precipitated by an increase in airway resistance Reduce the obstruction (chest PT, medications, adequate hydration) Improve compliance to decrease work of breathing – – May require resolution of disease, Pulmonary edema may respond to diuresis, – Pleural effusions respond to thoracentesis Treat infection and other contributing factors – Add supplemental O2 - effort determines negative/positive pressure breathing Most patients with hypercapnia require mechanical ventilatory support Noninvasively through a tight-fitting mask or through an LMA or endotracheal tube Two main physiologic factors of infections Increased secretions (bronchospasm may accompany) increase the work of breathing Worsening of ventilation-perfusion relationships to produce hypoxemia and hypercapnia Many patients with severe chronic lung disease also have compromised CV system46 O2 Therapy q O2 therapy is valuable and can often greatly increase the PaO2 The response of the PaO2 to inhaled (FiO2) O2 depends on the cause of hypoxemia Patients with large shunts will not respond well although increase in PaO2 can be helpful Various methods of O2 administration available Nasal cannulas are valuable for long-term treatment of patients with COPD- oxygen is pushed through nose and concentrated in the pharynx Highest FiO2s obtained with intubation and mechanical ventilation 47 Hazards of O2 Therapy q Hazards of O2 therapy include: O2 toxicity- formation of superoxide anions CNS, visual, and alveolar damage CO2 retention Excessive O2 can lead to hypercapnic respiratory failure in some COPD patients Absorption atelectasis Occurs when high FiO2 administered Consider when you can use reduced FiO2 48 Mechanical Ventilation q Mechanical ventilation is initiated based on the patient condition – Not an individual PO2 or PCO2 – Severity of the disease and rapidity of progression – Hemodynamic stability of the patient q Ventilatory support can be delivered invasively using positive pressure ventilation with a: – Secured airway- endotracheal tube Needed to protect against aspiration Deliver high pressures for poor compliance If high FiO2 required- it’s a secure airway – Unsecured airway- mask or LMA Less invasive Less stimulating for reactive airway Does not protect airway q Noninvasively with a tight-fitting mask – – – May be used in critical situations where duration expected to be short Does not protect airway 49 Not used in patients with excessive respiratory secretions or who are at high risk for aspiration Mechanical Ventilation May Be Combined With PEEP To Increase Pao2 And Decrease PCO2 Volume control delivers a preset volume at a specified rate – Advantage- delivers a known volume despite changes in the elastic properties of the lung or chest wall or increases in airway resistance – Disadvantage – high pressures (safety valve prevents dangerously high pressures) Pressure control delivers a preset pressure for a specified duration of time – Advantage- prevents development of excessive airway pressures – Chief disadvantage- volume of gas delivered per breath varies with changes in compliance – Disadvantage- increase in airway resistance may decrease the ventilation because they may be insufficient time for equilibration of pressure between the machine and alveoli – PaCO2 or end-tidal PCO2 must be monitored to determine effectiveness Pressure support delivers a preset pressure with no preset rate – Suitable only for patients initiating breaths – More comfortable mode when suitable - patient not working against the ventilator – Inspiratory pressure terminated once inspiratory flow falls below a certain threshold – Ventilators now combine PSV with SIMV-PC backup to prevent apnea (PSV-Pro) – Bilevel positive airway pressure (BiPAP) combines inspiratory and expiratory positive pressure For BiPAP- inspiratory pressure higher than expiratory pressure 50 CPAP and PEEP Continuous positive airway pressure or Positive-end expiratory pressure – Maintains airway pressure (aka intrapulmonic pressure) above zero cm H2O – CPAP used commonly for OSA patients Use postoperatively when possible Positive end-expiratory pressure – 5 cm H2o Pressure commonly applied during mechanical ventilation – High PEEP useful for raising the arterial PO2 in patients with respiratory failure – Values as high as 20 cm H2O can be used in severe hypoxemia – May allows the inspired O2 concentration to be reduced – May reduce venous return in compromised patients – May cause pneumothorax 51 1. A 63 yo woman is evaluated for dyspnea, 30 pack year smoking history, spirometry reveals FEV1 59%, FEV1/FVC ratio 0.62, CXR shows large lung volumes. Which PFT result do you expect? A. Decreased FRC B. Decreased RV/TLC ratio C. Increased diffusing capacity for CO D. Increased residual volume 2. The arterial hypoxemia of a patient with diffuse interstitial pulmonary fibrosis A. Typically worsens with exercise B. Is due to diffusion impairment C. Is associated with a large increase in diffusing capacity during exercise D. Is usually associated with CO2 retention 3. In addition to rapid, shallow breathing, which of the following applies to pulmonary edema with alveolar filling? A. Lung compliance is increased B. Airway resistance is unaffected C. Arterial hypoxemia cannot be abolished by inspiring 100% O2 D. Alveolar edema causes chest pain 4. A 65 yo female presents with hemorrhagic shock with an active GI bleed. After intubation to prevent aspiration of blood, vent settings are volume control ventilation with TV 450 mL, FiO2 0.5, breath sounds are equal, trachea is midline, and BP drops from 110/70 to 85/50. What is the most likely cause of her hypotension? A. Hypercarbia B. Atelectasis due to high FiO2 (absorption atelectasis) C. Right main stem intubation D. Decrease in venous return 52