Respiratory Diseases

Question 1

Wakefulness & Sleep

Answer 1

wakefulness is accomplished by a brainstem neuronal pathway known as the ascending reticular activating system (ARAS)
Sleep is maintained by inhibition of the ARAS via a hypothalamic nucleus known as the ventrolateral preoptic (VLPO) nucleus.

There is reciprocal inhibition between the ARAS and the VLPO nucleus.

Question 2

Two Forms of Sleep are:

NREM

&

REM

Answer 2

NREM                                         
Slow eye movement            
Restful Sleep                        
Decreased metabolism       
Vital signs LOW                    
muscle tones maintained/relaxed    
NO vivid dreams                  

REM
Rapid eye movement
NOT restful
Increased metabolism
Vital signs Irregular
Muscle tone depressed/unresponsive
 Dreams Occur

Question 3

Obstructive Sleep Apnea

Answer 3

High % patients not clinically diagnosed
Patients at GREATER RISK:
with hypertension (including drug-resistant hypertension), type 2 diabetes mellitus, coronary artery disease, atrial fibrillation, permanent pacemakers, various forms of heart block, congestive heart failure, a history of stroke, and those coming for bariatric surgery

Question 4

Pathogenesis of Central Sleep Apnea

Answer 4

Central sleep apnea (CSA) refers to sleep apnea that is not associated with respiratory efforts during the apnea event. This absence of respiratory effort could be due to instability of neural control of respiration, weakness of respiratory muscles, or both. Instability of respiratory control may include increased, decreased, or oscillating respiratory drive.
Secondary CSA is narcotic-induced CSA
Central Sleep Apnea With Cheyne-Stokes Breathing
CSA with Cheyne-Stokes breathing was the first form of a sleep-related breathing disorder to be described.
Congestive heart failure, stroke, and atrial fibrillation are the three most common conditions during which CSA with Cheyne-Stokes breathing is encountered.
Four cyclical components: hypopnea, apnea, hypoxia, and hyperventilation

Question 5

Pathogenesis of Obstructive Sleep Apnea

Answer 5

The hallmark of OSA is sleep-induced and arousal-relieved upper airway obstruction.
Narrowing of the Upper Airway
Obesity
Genetic Factors
Physical Findings (large uvula, hyperplastic soft palate, nasal congestion & polyps, enlarged tonsils & tongue, small lower jaw, receded chin, neck >17”)

Question 6

Treatment of Obstructive Sleep Apnea

Answer 6

• Positive Airway Pressure Therapy
• Oral Appliance Therapy
• Surgical Therapy (Bariatric, surgical procedures target soft tissue and bony tissue to enlarge airway capacity—may not cure OSA) maxillomandibular advancement, laser-assisted uvulopalatoplasty, uvulopalatopharyngoplasty, and palatal implants
• Medical Therapy (Diet, exercise, positional therapy)

Question 7

High Risk for Obstructive Sleep Apnea Characteristics

Answer 7

1. Male
2. BMI > 25 kg/m2
3. Neck circumference (>17 inches in men, >16 inches in women)
4. Habitual snoring/gasping noted by bed partner
5. Daytime sleepiness
6. Hypertension

Question 8

Stop-Bang Scoring Model (8 Yes-or-No Questions)

Answer 8

1. Snoring: Do you snore loudly (loud enough to be heard through closed doors)?
2. Tired: Do you often feel tired, fatigued, or sleepy during the daytime?
3. Observed: Has anyone observed you stop breathing during your sleep?
4. Blood Pressure: Do you have or are you being treated for high blood pressure?
5. BMI: BMI more than 35 kg/m2?
6. Age: older than 50 years?
7. Neck circumference: >40 cm (17 inches)?
8. Gender: male?
   High risk of OSA: Yes to 3 or more questions
   Low risk of OSA: Yes to fewer than 3 questions

Question 9

What are some Obstructive Respiratory Diseases/Issues?

Answer 9

Acute Upper Respiratory Tract Infection
Asthma
COPD
Bronchiectasis
Cystic Fibrosis

Question 10

Describe Acute Upper Respiratory Tract Infection:

Should Surgery be Postponed?

What are management strategies for URI patient?

Answer 10

Most common responsible viral pathogens being rhinovirus, coronavirus, influenza virus, parainfluenza virus, and respiratory syncytial virus (RSV).

A patient who has had a URI for days or weeks and is in stable or improving condition can be safely managed without postponing surgery. If surgery is to be delayed, patients should not be rescheduled for about 6 weeks, since it may take that long for airway hyperreactivity to resolve.

The anesthetic management of a patient with a URI should include adequate hydration, reducing secretions, and limiting manipulation of a potentially sensitive airway. Nebulized or topical local anesthetic applied to the vocal cords may reduce upper airway sensitivity. Use of a laryngeal mask airway (LMA) rather than an endotracheal (ET) tube may also reduce the risk of laryngospasm.

Question 11

Asthma

What is the disease process of asthma?

Answer 11

One of the most common chronic medical conditions in the world and currently affects approximately 300 million people globally.
Prevalence of asthma has been rising in developing countries, attributed to increased urbanization and atmospheric pollution.
A disease of reversible airflow obstruction characterized by bronchial hyperreactivity, bronchoconstriction, and chronic airway inflammation.
Multifactoral: Genetic and environmental causes.

Question 12

Classification of Asthma Severity:

Intermittent

Mild

Moderate

Severe

Answer 12

Class Symptoms&B2use LimitActivity FEV1 (FEV1:FVC)

Intermittent: =2D/wk None >80% (normal)

Mild: >2D/wk (not daily) Minor <80% (normal)

Moderate: Daily Some <80%but>60% ( ↓ 5%)

Severe: Throughout Day Extreme <60% ( ↓ > 5%)

Question 13

Asthma Causes, Anatomy & Physiology

Answer 13

A chronic inflammatory condition affecting airways. Narrowing of airways, inflammation and mucous make it hard to breath. Many triggers (infection, flu, virus, allergy, exercise, weather changes, exposure to various things such as smoke, allergens, mold, smells/strong odors.

Question 14

Asthma Treatment & Managment

Answer 14

Focus is on preventing and controlling bronchial inflammation
As well as treating bronchospasm
Asthma treatments can be classified by their role in asthma management and by the timing of their effects (i.e., immediate relief or long-term therapy)

Question 15

Asthma Anesthesia Management

Answer 15

Factors that are more likely to predict the occurrence of severe bronchospasm include the type of surgery (risk is higher with upper abdominal surgery and oncologic surgery) and the proximity of the most recent asthmatic attack to the date of surgery.
Several mechanisms could explain the contribution of general anesthesia to increased airway resistance. Among these are depression of the cough reflex, impairment of mucociliary function, reduction of palatopharyngeal muscle tone, depression of diaphragmatic function, and an increase in the amount of fluid in the airway wall.
In addition, airway stimulation by endotracheal intubation, parasympathetic nervous system activation, and/or release of neurotransmitters of pain such as substance P and neurokinins may also play a role.

Question 16

Preoperative Evaluation of patients with Asthma

Answer 16

Assess Disease Severity & Effectiveness of Management
Assess patient
Review PFTs: A reduction in FEV1 or forced vital capacity (FVC) to less than 70% of predicted, as well as an FEV1:FVC ratio that is less than 65% of predicted, is usually considered a risk factor for perioperative respiratory complications.
Anesthetic plan: Prevents or blunts expiratory airflow obstruction
Optimize if possible:
Chest physiotherapy
Antibiotics
Bronchodilators
ABG’s
Anti-inflammatory continuation
Consider stress dose steroids

Question 17

Induction & Maintenance of Anesthesia in Asthmatic Patients

Answer 17

Suppress Airway Reflexes
Is Regional Anesthesia an Option?
Propofol (contributes to decreased airway resistance)
Sevoflurane use with induction ventilation to depresses hyper reactive airway reflexes sufficiently to permit tracheal intubation without precipitating bronchospasm.
Lidocaine (IV or intra-tracheal) LTA kit to suppress airway reflexes.
Opioids to suppress cough reflex & deepen anesthetic. (not prolonged 2* resp depression)
Neuromuscular blocker—relieve ventilaotory challenge w light anesthesia but has no effect on bronchospasm. (avoid histamine release drugs)
Provide sufficient time for exhalation to prevent air trapping.
Humidification & warming inspired gases may be useful.
Maintain hydration

Question 18

Chronic Obstructive Pulmonary Disease

Answer 18

A disease of progressive loss of alveolar tissue and progressive airflow obstruction that is not reversible.
Pulmonary elastic recoil is lost as a result of bronchiolar and alveolar destruction, often from inhaling toxic chemicals such as are contained in cigarette smoke.
The World Health Organization (WHO) predicts that by 2030 COPD will be the third leading cause of death worldwide.
Risk factors for developing COPD include
(1) cigarette smoking
(2) occupational exposure to dust and chemicals, especially in coal mining, gold mining, and the textile industry
(3) indoor and outdoor pollution
(4) recurrent childhood respiratory infections
(5) low birth weight. α1-Antitrypsin deficiency is an inherited disorder associated with premature development of COPD.
Intraoperative and postoperative pulmonary complications are more common in this patient population
Associated with an increased length of hospital stay and mortality.

Question 19

Review Lung Volumes in Obstructive Lung Disease Compared to Normal Lung Volumes (Slide #28 visual)

Answer 19

FIG. 2.4 Lung volumes in COPD compared with normal values. In the presence of obstructive lung disease, the vital capacity (VC) is normal to decreased, the residual volume (RV) and functional residual capacity (FRC) are increased, the total lung capacity (TLC) is normal to increased, and the RV:TLC ratio is increased. ERV, Expiratory reserve volume; IC, inspiratory capacity; VT, tidal volume.

Question 20

What are the Causes of COPD?

Answer 20

COPD Causes

(1) pathologic deterioration in elasticity or “recoil” within the lung parenchyma, which normally maintains the airways in an open position
(2) pathologic changes that decrease the rigidity of the bronchiolar wall and thus predispose them to collapse during exhalation
(3) an increase in gas flow velocity in narrowed bronchioli, which lowers the pressure inside the bronchioli and further favors airway collapse
(4) active bronchospasm and obstruction resulting from increased pulmonary secretions; and (5) destruction of lung parenchyma, enlargement of air sacs, and development of emphysema.

Question 21

What are the Signs and symptoms of COPD?

Answer 21

Signs and Symptoms
Signs and symptoms of COPD vary with disease severity but usually include dyspnea on exertion or at rest, chronic cough, and chronic sputum production.
COPD exacerbations are periods of worsening symptoms as a result of an acute worsening in airflow obstruction. As expiratory airflow obstruction increases in severity, tachypnea and a prolonged expiratory time are evident. Breath sounds are likely to be decreased, and expiratory wheezes are common.

Question 22

How can you Diagnose COPD?

Answer 22

Patients with COPD will usually report symptoms like dyspnea and chronic cough as well as a history of exposure to risk factors.
COPD cannot be definitively diagnosed without spirometry.
Pulmonary Function Tests (PFT’s)
Results of PFTs in COPD reveal a decrease in the FEV1:FVC ratio and an even greater decrease in the FEF between 25% and 75% of vital capacity (FEF25%–75%). An FEV1:FVC less than 70% of predicted that is not reversible with bronchodilators confirms the diagnosis. Other spirometric findings of COPD include an increased FRC and TLC (Fig. 2.4). Slowing of expiratory airflow and gas trapping behind prematurely closed airways are responsible for the increase in residual volume (RV). The pathophysiologic “advantage” of an increased RV and FRC in patients with COPD is related to an enlarged airway diameter and increased elastic recoil for exhalation. The cost is the greater work of breathing at the higher lung volumes.

Question 23

What are Causes, Anatomy & Physiology of COPD?

Answer 23

COPD is a disease of the lungs that over time limits the flow of air through airways making it progressively harder to breath. It’s not one condition but includes emphysema & chronic bronchitis (may have both).
Leading cause is tobacco smoke, through inhalation or 2nd hand smoke. Other causes pollution, industrial chemicals.
Healthy alveoli “grape like” shape, COPD “bullae”
COPD bronchi may be filled w mucus.

Question 24

Differential Diagnosis of Intraoperative Bronchospasm and Wheezing:

Answer 24

Mechanical obstruction of endotracheal tube  
Kinking  
Secretions  
Overinflation of tracheal tube cuff 
Inadequate depth of anesthesia  
Active expiratory efforts  
Decreased functional residual capacity 
Endobronchial intubation 
Pulmonary aspiration 
Pulmonary edema 
Pulmonary embolus 
Pneumothorax 
Acute asthmatic attack

Question 25

Treatment of Patients With COPD:

Answer 25

Smoking cessation
Annual vaccination against influenza
Vaccination against pneumococcus
Inhaled long-acting bronchodilators
Inhaled corticosteroids
Inhaled long-acting anticholinergic drugs
Home oxygen therapy if PaO2 < 55 mm Hg, hematocrit > 55%, or there is evidence of cor pulmonale
Diuretics if evidence of right heart failure with peripheral edema
Lung volume reduction surgery
Lung transplantation

Question 26

Treatment of patients with COPD Exacerbation:

Answer 26

Supplemental oxygen ± noninvasive positive pressure ventilation or mechanical ventilation
Increased dose and frequency of bronchodilator therapy
Systemic corticosteroids
Antibiotics

Question 27

Management of Anesthesia for COPD patients:

Answer 27

A complete history (causes, course, and severity of the COPD, smoking history, current medications (incl.steroid)
Exercise tolerance, frequency of exacerbations.
Noninvasive positive pressure ventilation (NIPPV) or mechanical ventilation is another key info.
h/o smoking, assess: presence & severity of concomitant diseases such as diabetes mellitus, hypertension, peripheral vascular disease, ischemic heart disease, heart failure, cardiac dysrhythmias, and lung cancer.
Long-acting bronchodilators, anticholinergics, and inhaled corticosteroids should be continued until the morning of surgery.
Elective surgery pts. need optimization prior to surgery to decrease morbidity & mortality after surgery.
PFT results and arterial blood gas analysis can be useful for predicting pulmonary function after lung resection, but they do not reliably predict the likelihood of postoperative pulmonary complications after nonthoracic surgery.
Even patients defined as high risk by spirometry (FEV1 < 70% of predicted, FEV1:FVC ratio < 65%) or arterial blood gas analysis (PaCO2 > 45 mm Hg) can undergo surgery, including lung resection, with an acceptable risk of postoperative pulmonary complications.
Right ventricular function should be carefully assessed by clinical examination and echocardiography in patients with advanced pulmonary disease.

Question 28

Management of Anesthesia for COPD patients AND PFT’s:

Answer 28

PFTs should be viewed as a management tool to optimize preoperative pulmonary function but not as a means to predict risk. Indications for a preoperative pulmonary evaluation (which may include consultation with a pulmonologist and/or performance of PFTs) typically include

(1) hypoxemia on room air or the need for home oxygen therapy without a known cause
(2) a bicarbonate concentration of more than 33 mEq/L or PCO2 of more than 50 mm Hg in a patient whose pulmonary disease has not been previously evaluated, (3) a history of respiratory failure resulting from a problem that still exists
(4) severe shortness of breath attributed to respiratory disease
(5) planned pneumonectomy
(6) difficulty in assessing pulmonary function by clinical signs,
(7) the need to distinguish among potential causes of significant respiratory compromise
(8) the need to determine the response to bronchodilators, and
(9) suspected pulmonary hypertension.

Question 29

Preoperative: Strategies to Decrease Incidence of Postoperative Pulmonary Complications for COPD

Answer 29

Preoperative
Encourage cessation of smoking for at least 6 weeks.
Treat evidence of expiratory airflow obstruction.
Treat respiratory infection with antibiotics.
Initiate patient education regarding lung volume expansion maneuvers.

Question 30

Intra-operative: Strategies to Decrease Incidence of Postoperative Pulmonary Complications for COPD

Answer 30

Intraoperative
Use minimally invasive surgery (endoscopic) techniques when possible.
Consider regional anesthesia.
Avoid surgical procedures likely to last longer than 3 hours.

Question 31

Post-operative: Strategies to Decrease Incidence of Postoperative Pulmonary Complications for COPD

Answer 31

Postoperative 
Institute lung volume expansion maneuvers (voluntary deep breathing, incentive spirometry, continuous positive airway pressure). 
Maximize analgesia (neuraxial opioids, intercostal nerve blocks, patient-controlled analgesia).

Question 32

Bronchiectasis: Pathophysiology

Answer 32

Pathophysiology
Localized irreversible dilatation of bronchi caused by destructive inflammatory processes involving the bronchial wall. (bacterial or mycobacterial infections can cause inflammation and destruction of medium-sized airways that can eventually lead to airway collapse, airflow obstruction, and an inability to clear secretions).
Increased susceptibility to recurrent or persistent bacterial infection, which reflects impaired mucociliary activity and pooling of mucus in dilated airways. Once bacterial superinfection is established, it is nearly impossible to eradicate, and daily expectoration of purulent sputum persists.

Question 33

Bronchiectasis: Diagnosis

Answer 33

Diagnosis
The history of a chronic cough productive of purulent sputum is highly suggestive of bronchiectasis. Patients may also complain of hemoptysis, dyspnea, wheezing, and pleuritic chest pain. Clubbing of the fingers occurs in most patients with significant bronchiectasis and is a valuable diagnostic clue, especially since this change is not characteristic of COPD.
Pulmonary function changes vary considerably (range from no change to alterations characteristic of COPD or restrictive lung disease).
CT provides excellent images of bronchiectatic airways and can be used to confirm the presence and extent of the disease. It will usually show dilated bronchi much larger in diameter than their adjacent blood vessels.

Question 34

Bronchiectasis: Treatment

Answer 34

Treatment
Bronchiectasis is treated with antibiotics and chest physiotherapy.
Also, Yearly immunization against influenza, bronchodilators, systemic corticosteroids, and oxygen therapy.

Question 35

Bronchiectasis: Management of Anesthesia

Answer 35

Management of Anesthesia
Much like patients with other types of obstructive airway disease, a detailed history should be elicited from the patient, including severity of disease, frequency of exacerbations, and the date of the most recent exacerbation. Home medications should be continued until the morning of surgery. Elective procedures should be delayed if there are signs of active pulmonary infection with respiratory compromise or systemic involvement. During general anesthesia, the patient may need to be suctioned frequently through the ET tube to manage secretions. If the patient is undergoing surgery for management of an empyema or hemoptysis, a double-lumen endobronchial tube must be used to prevent spillage of purulent sputum into normal areas of the lungs. Nasal endotracheal intubation should be avoided because of the high rate of concurrent chronic sinusitis in these patients.

Question 36

What is Cystic fibrosis (CF)?

Describe Pathophysiology of CF:

Answer 36

Cystic fibrosis (CF) is an autosomal recessive disorder. It affects an estimated 30,000 persons in the United States.
Pathophysiology
The cause of CF is a mutation in a single gene on chromosome 7 that encodes the cystic fibrosis transmembrane conductance regulator (CFTR). This regulator should produce a protein that helps salt and water move in and out of cells. The dysfunctional regulator blocks this movement and results in the production of an abnormally thick mucus outside of epithelial cells. Decreased chloride transport is accompanied by decreased transport of sodium and water, which results in dehydrated viscous secretions that are associated with luminal obstruction, as well as destruction and scarring of various glands and tissues. This causes damage to the lungs (bronchiectasis, COPD, sinusitis), pancreas (diabetes mellitus), liver (cirrhosis), gastrointestinal tract (meconium ileus), and reproductive organs (azoospermia). The primary cause of morbidity and mortality in patients with CF is chronic pulmonary infection.

Question 37

How is CF Diagnosed?

Answer 37

Diagnosis
The presence of a sweat chloride concentration greater than 70 mEq/L plus the characteristic clinical manifestations (cough, chronic purulent sputum production, exertional dyspnea) or family history of the disease confirms the diagnosis of CF. DNA analysis can identify the more than 90% of patients having the CFTR mutation. Chronic pansinusitis is almost universal. The presence of normal sinuses on radiographic examination is strong evidence that CF is not present. Malabsorption with a response to pancreatic enzyme treatment is evidence of the exocrine insufficiency associated with CF. Obstructive azoospermia confirmed by testicular biopsy is also strong evidence of CF. Bronchoalveolar lavage typically shows a high percentage of neutrophils, which is a sign of airway inflammation. COPD is present in virtually all adult patients with CF and follows a relentless downhill course.

Question 38

How is CF treated?

Answer 38

Treatment
Treatment of CF is similar to that for bronchiectasis and is directed toward alleviation of symptoms (mobilization and clearance of lower airway secretions and treatment of pulmonary infection), correction of organ dysfunction (pancreatic enzyme replacement), nutrition, and prevention of intestinal obstruction. Gene therapy is currently being investigated as a treatment for CF. This involves insertion of a normal CFTR gene into lung cells of CF patients.

Question 39

Describe the Standard Management of CF:

Answer 39

Clearance of Airway Secretions via chest physiotherapy with postural drainage.
Bronchodilator Therapy (considered if patients are known to have a response to inhaled bronchodilators). A response is defined as an increase of 10% or more in FEV1 after bronchodilator administration.
Reduction in Viscoelasticity of Sputum
The abnormal viscosity of airway secretions is due primarily to the presence of neutrophils and their degradation products.
DNA released from neutrophils forms long fibrils that contribute to the viscosity of the sputum.
Recombinant human deoxyribonuclease I (dornase alfa [Pulmozyme]) can cleave this DNA and increase the clearance of sputum.
Antibiotic Therapy

Question 40

Describe Cystic fibrosis Management of Anesthesia:

Answer 40

Management of anesthesia in patients with CF follows the same principles as outlined for patients with COPD and bronchiectasis.
Elective surgical procedures should be delayed until optimal pulmonary function can be ensured by controlling bronchial infection and facilitating removal of airway secretions.
Vitamin K treatment may be necessary if hepatic function is poor or if absorption of fat-soluble vitamins from the gastrointestinal tract is impaired.
Maintenance of anesthesia with volatile anesthetics permits the use of high inspired concentrations of oxygen, decreases airway resistance by decreasing bronchial smooth muscle tone, and decreases the responsiveness of hyperreactive airways.
Humidification of inspired gases, hydration, and avoidance of anticholinergic drugs are important to maintain secretions in a less viscous state.
Frequent tracheal suctioning may be necessary. Patients should regain their full airway reflexes and Ventilatory abilities before extubation to decrease risk of aspiration. Postoperative pain control is extremely important to allow for deep breathing, coughing, and early ambulation so that pulmonary complications such as pneumonia, hypoxia, and atelectasis can be prevented.

Question 41

List Restrictive Respiratory Diseases:

Answer 41

Acute Intrinsic Restrictive Lung Disease (Alveolar and Interstitial Pulmonary Edema) {Pulmonary edema, Aspiration}
Acute Respiratory Failure
Acute Respiratory Distress Syndrome
Chronic Intrinsic Restrictive Lung Disease (Interstitial Lung Disease) {Pulmonary Fibrosis, Sarcoidosis}
Chronic Extrinsic Restrictive Lung Disease {Thoracic Extrapulmonary Causes, Extrathoracic Causes}

Question 42

What are some Intrinsic Restrictive Lung Diseases?

Answer 42

Asbestosis
Radiation Fibrosis
Certain drugs (Bleomycin, methitrexate)
RA
Hypersensitivity pneumonitits
ARDS
Ideopathic pulmonary fibrosis/interstitial pneumonia
Sarcoidosis
Eosinophilic pneumonia
Alveolar and Interstitial Pulmonary Edema
Pulmonary edema
Aspiration

Question 43

Pulmonary Edema:

Answer 43

Pulmonary edema is due to leakage of intravascular fluid into the interstitium of the lungs and eventually into the alveoli.
Acute pulmonary edema can be caused by increased capillary pressure (hydrostatic or cardiogenic pulmonary edema) or by increased capillary permeability.
Typically appears as bilateral symmetrical perihilar opacities on chest radiography. This “butterfly” fluid pattern is more commonly seen with increased capillary pressure than with increased capillary permeability.
The presence of air bronchograms suggests increased-permeability pulmonary edema.
Cardiogenic pulmonary edema is characterized by marked dyspnea, tachypnea, and signs of sympathetic nervous system activation (hypertension, tachycardia, diaphoresis) that is often more pronounced than that seen in patients with increased-permeability pulmonary edema.
Pulmonary edema caused by increased capillary permeability is characterized by a high concentration of protein and secretory products in the edema fluid.
Diffuse alveolar damage is typically present with the increased-permeability pulmonary edema associated with acute respiratory distress syndrome (ARDS).

Question 44

Aspiration:

Answer 44

Aspirated acidic gastric fluid is rapidly distributed throughout the lungs and produces destruction of surfactant-producing cells and damage to the pulmonary capillary endothelium.
As a result, there is atelectasis and leakage of intravascular fluid into the lungs, producing capillary permeability pulmonary edema.
The clinical picture is similar to that of ARDS.
Arterial hypoxemia is present.
There may also be tachypnea, bronchospasm, and acute pulmonary hypertension.
Chest radiography may not demonstrate evidence of aspiration pneumonitis for 6–12 hours after the event. Evidence of aspiration, when it does appear, is most likely to be in the superior segment of the right lower lobe if the patient aspirated while in the supine position.

Question 45

What are Lung volumes in restrictive lung disease compared with normal values?

(Slide #48 See Visual Volumes)

Answer 45

FIG. 3.2 Lung volumes in restrictive lung disease compared with normal values. ERV, Expiratory reserve volume; FRC, functional residual capacity; IC, inspiratory capacity; RV, residual volume; TLC, total lung capacity; VC, vital capacity; VT, tidal volume.

Question 46

What are causes of restrictive lung disease—Acute Intrinsic Restrictive Lung Disease (Pulmonary Edema)?

Answer 46

Acute Intrinsic Restrictive:
Acute respiratory distress syndrome
Aspiration
Neurogenic problems
Opioid overdose
High altitude
Re-expansion of collapsed lung
Upper airway obstruction (negative pressure)
Congestive heart failure

Question 47

What are causes of restrictive lung disease—Chronic Intrinsic Restrictive Lung Disease (Interstitial Lung Disease)

Answer 47

Chronic Intrinsic Restrictive:
Sarcoidosis
Hypersensitivity pneumonitis
Eosinophilic granuloma
Alveolar proteinosis
Lymphangioleiomyomatosis
Drug-induced pulmonary fibrosis

Question 48

What are causes of restrictive lung disease—Disorders of the Chest Wall, Pleura, and Mediastinum. (Extrinsic Restrictive Disease)

Answer 48

Extrinsic Restrictive Disease:
Deformities of the costovertebral skeletal structures
 	Kyphoscoliosis
 	Ankylosing spondylitis
Deformities of the sternum
Flail chest
Pleural effusion
Pneumothorax
Mediastinal mass
Pneumomediastinum
Neuromuscular disorders
 	Spinal cord transection
 	Guillain-Barré syndrome
 	Disorders of neuromuscular 	transmission
 	Muscular dystrophies
Other
Obesity
Ascites
Pregnancy

Question 49

Management of Anesthesia in Patients With Pulmonary Edema:

Answer 49

Elective surgery should be delayed in patients with pulmonary edema, and every effort must be made to optimize cardiorespiratory function prior to surgery.
Large pleural effusions may need to be drained. Persistent hypoxemia may require mechanical ventilation and PEEP. Hemodynamic monitoring may be useful in both the assessment and treatment of pulmonary edema.
Patients with pulmonary edema are critically ill. Intraoperative management should be a continuation of critical care management and include a plan for intraoperative ventilator management.
The best way to ventilate patients with acute respiratory failure due to acute pulmonary edema has not been determined. However, because the pathophysiology is similar to that of acute lung injury and because there is the risk of hemodynamic compromise and barotrauma with the use of large tidal volumes and high airway pressures, it is reasonable to ventilate with low tidal volumes (e.g., 6 mL/kg) with a Ventilatory rate of 14–18 breaths per minute while attempting to keep the end-inspiratory plateau pressure at less than 30 cm H2O.
Typical anesthesia ventilators may not be adequate for patients with severe pulmonary edema, and more sophisticated intensive care unit (ICU) ventilators may be needed.
Patients with restrictive lung disease typically have rapid, shallow breathing. Tachypnea is likely during the weaning process and should not be used as the sole criterion for delaying extubation if gas exchange and results of other assessments are satisfactory.

Question 50

OBSTRUCTIVE

VS

RESTRICIVE

Answer 50

Obstructive Restrictive
Reduced Airflow Reduced Lung Volume
SOB in exhaling air Difficult taking air in
Air remains in lung Stiffness in lung tissue or in
after full exhalation chest wall cavity
COPD Interstitial Lung Disease
Ashtma Scoliosis
Bronchiectasis Neuromuscular cause
Marked Obesity

Question 51

Acute Respiratory Failure:

Answer 51

The inability to provide adequate arterial oxygenation and/or elimination of carbon dioxide.
Many causes.
Acute respiratory failure is considered to be present when the PaO2 is below 60 mm Hg despite oxygen supplementation and in the absence of a right-to-left intracardiac shunt.
In the presence of acute respiratory failure, PaCO2 can be increased, unchanged, or decreased depending on the relationship of alveolar ventilation to metabolic production of carbon dioxide.
A PaCO2 above 50 mm Hg in the absence of respiratory compensation for metabolic alkalosis is consistent with the diagnosis of acute respiratory failure.
Acute respiratory failure is distinguished from chronic respiratory failure based on the relationship of PaCO2 to arterial pH (pHa).
Acute respiratory failure is typically accompanied by abrupt increases in PaCO2 and corresponding decreases in pHa.
With chronic respiratory failure, the pHa is usually between 7.35 and 7.45 despite an increased PaCO2. This normal pHa reflects renal compensation for chronic respiratory acidosis via renal tubular reabsorption of bicarbonate.
Respiratory failure is often accompanied by a decrease in functional residual capacity (FRC) and lung compliance.
Increased pulmonary vascular resistance and pulmonary hypertension are likely to develop if respiratory failure persists. ARDS is a condition that falls within the spectrum of acute respiratory failure.
Treatment of acute respiratory failure is directed at initiating specific therapies that support oxygenation and ventilation.
The three principal goals in the management of acute respiratory failure are:
(1) a patent upper airway
(2) correction of hypoxemia
(3) removal of excess carbon dioxide.

Question 52

Acute Respiratory Failure & Mechanical Support of Ventilation

Answer 52

Supplemental Oxygen for spontaneously breathing patients (Venturi mask, non-rebreathing mask, progressing to CPAP
CPAP may increase lung volumes by opening collapsed alveoli and decreasing right-to-left intrapulmonary shunting.
Management of Patients Receiving Mechanical Support of Ventilation
Critically ill patients who require mechanical ventilation may benefit from continuous infusion of sedative drugs to treat anxiety and agitation and to facilitate coordination with ventilator-delivered breaths. Inadequate sedation or agitation can lead to life-threatening problems such as self-extubation, acute deterioration in gas exchange, and barotrauma. The need for neuromuscular blockade can be reduced by the optimum use of sedation. However, when acceptable sedation without hemodynamic compromise cannot be achieved, it may be necessary to produce skeletal muscle paralysis to ensure appropriate ventilation and oxygenation.

Question 53

Acute Respiratory Distress Syndrome Adult ARDS

Answer 53

ARDS is caused by inflammatory injury to the lung and is manifested clinically as acute hypoxemic respiratory failure.

Sepsis is associated with the highest risk of progression to ARDS
Rapid-onset respiratory failure accompanied by refractory arterial hypoxemia, with radiographic findings indistinguishable from cardiogenic pulmonary edema, are the hallmarks of ARDS.
The acute phase of ARDS usually resolves completely but in some patients may progress to fibrosing alveolitis with persistent arterial hypoxemia and decreased pulmonary compliance.
The focus of the new definition is on oxygenation, timing of disease onset, and imaging results.
The term acute lung injury is no longer used. Instead, ARDS is now classified as:
mild (200 mm Hg < PaO2/FIO2 ≤ 300 mm Hg),
moderate (100 mm Hg < PaO2/FIO2 ≤ 200 mm Hg) or
severe (PaO2/FIO2 ≤ 100 mm Hg).
The calculation of the PaO2/FIO2 ratio must now be calculated with CPAP or PEEP of at least 5 cm H2O.

Question 54

The Berlin Definition of Acute Respiratory Distress Syndrome ARDS

Answer 54

Lung injury of acute onset with 1 week of an apparent clinical insult and with progression of pulmonary symptoms
Bilateral opacities on lung imaging not explainable by other lung pathology
Respiratory failure not explained by heart failure or volume overload
Decreased arterial PaO2/FIO2 ratio:
Mild ARDS: ratio is 201–300
Moderate ARDS: ratio is 101–200
Severe ARDS: ratio is <101

Question 55

Acute Respiratory Distress Syndrome (Ards)–Treatment

Answer 55

Oxygen supplementation 
Tracheal intubation 
Mechanical ventilation 
Positive end-expiratory pressure 
Optimization of intravascular fluid volume 
Diuretic therapy 
Inotropic support 
Glucocorticoid therapy (?) 
Removal of secretions 
Control of infection 
Nutritional support 
Administration of inhaled β2-adrenergic agonists

Question 56

Chronic Intrinsic Restrictive Lung Disease (Interstitial Lung Disease) Pulmonary Fibrosis, Sarcoidosis &Hypersensitivity Pneumonitis

Answer 56

Management of Anesthesia in Patients With Chronic Interstitial Lung Disease
Patients usually have dyspnea and nonproductive cough. Cor pulmonale may be present. Coarse breath sounds with crepitations can be heard.
A chest radiograph may show a ground glass or nodular pattern. Arterial blood gas analysis reveals hypoxemia with normocarbia. Pulmonary function tests show restrictive ventilatory defects, and the diffusing capacity is decreased.
A vital capacity of less than 15 mL/kg indicates severe pulmonary dysfunction. Infection should be treated, secretions cleared, and smoking stopped preoperatively.
Patients with interstitial lung disease tolerate apneic periods very poorly because of their small FRC and low oxygen stores.
General anesthesia, the supine position, and controlled ventilation all contribute to further decreases in FRC.
Alterations in FRC and the risk of hypoxia continue into the postoperative period.
Uptake of inhaled anesthetics is faster in these patients because of the small FRC.
Peak airway pressures should be kept as low as possible to minimize the risk of barotrauma.

Question 57

Chronic Extrinsic Restrictive Lung Disease–Thoracic Extrapulmonary Causes

Answer 57

Chronic extrinsic restrictive lung disease is often due to disorders of the thoracic cage (chest wall) that interfere with lung expansion. Deformities of the sternum, ribs, vertebrae, and costovertebral structures include conditions such as ankylosing spondylitis, flail chest, scoliosis, and kyphosis. The lungs are compressed and lung volumes are reduced. The work of breathing is increased because of the abnormal mechanical properties of the chest and the increased airway resistance that results from decreased lung volumes. Any thoracic deformity may cause compression of the pulmonary vasculature and lead to right ventricular dysfunction. Recurrent pulmonary infection resulting from a poor cough is common.
Thoracic abnormalities such as those of the chest wall, pleura, and spine (e.g., pectus excavatum, kyphoscoliosis, pleural effusion, flail chest, bronchogenic cysts, pneumothorax, mediastinal tumors) can all cause extrinsic restrictive lung disease.
Idiopathic kyphoscoliosis accounts for 80% of cases.

Question 58

Pleural space accumulation (hemothorax, empyema, chylothorax pneumothorax & hydrothorax)

Answer 58

blood (hemothorax)
pus (empyema)
lipids (chylothorax) Is secondary to disruption or obstruction of thoracic lymph duct

serous liquid (hydrothorax)
Air (pneumothorax)

Question 59

Pneumothorax:

Answer 59

Medical emergency
Gas enters pleural space
Increase pressure/tension
Awake-see respiratory distress tachypnea, SOB, hypoxia, pleuritic chest pain
Anesthetized-, increased airway pressures and decreased tidal volumes can be observed
The trachea may be deviated to the side away from the pneumothorax.
Auscultation reveals decreased/absent breath sounds on the side of the pneumothorax, with hyperresonance on percussion.
Vital signs show tachycardia and hypotension.
When a pneumothorax occurs during anesthesia, immediate discontinuation of nitrous oxide and administration of 100% oxygen must commence. If the patient has a tension pneumothorax, needle/catheter decompression must be performed, followed by chest tube placement. Oxygen supplementation accelerates reabsorption of air from the pleural space.
Treatment of a symptomatic pneumothorax requires evacuation of air from the pleural space by aspiration through a needle or small-bore catheter or placement of a chest tube. Aspiration of a pneumothorax followed by catheter removal is successful in most patients with a small to moderate-sized primary spontaneous pneumothorax.

Question 60

Lung transplantation

Answer 60

Most often have restrictive lung disease and a large PAO2 − PaO2.
Posterolateral thoracotomy is performed for single-lung transplantation, and a clam-shell thoracotomy for bilateral or sequential lung transplantation.
A double-lumen endo-bronchial tube is used and its proper placement is verified by fiberoptic bronchoscopy. Place the endo-bronchial portion of the tube in the native bronchus so as to avoid contact with the tracheal anastomosis.
Potential intraoperative problems include hypoxia, especially during one-lung ventilation. CPAP to the nondependent lung, PEEP to the dependent lung, or some form of differential lung ventilation may be needed to minimize intrapulmonary shunting and hypoxia. Severe pulmonary hypertension and right ventricular failure can occur when the pulmonary artery is clamped. Infusion of a pulmonary vasodilator (e.g., prostacyclin) or inhalation of nitric oxide may be helpful in controlling pulmonary hypertension in this situation. If hypoxia cannot be controlled despite all of these maneuvers, support with partial cardiopulmonary bypass is required. Connection of the donor lung to the recipient is usually performed in the sequence of pulmonary veins to the left atrium, then anastomosis of the pulmonary artery, and finally anastomosis of the bronchus.
The principal effect of lung denervation from lung transplantation is loss of the cough reflex, which places patients at risk of aspiration and pulmonary infection. Only while awake will patients clear pulmonary secretions.

Question 61

Fat Embolism:

Answer 61

Appears 12-72 hours after long bone fractures (esp. febur or tibia)
Observed in acute pancreatitis, cardiopulmonary bypass, parenteral infusion of lipids and liposuction
Triad: Hypoxemia, mental confusion & petechiae
Pulmonary dyfunction may reveal hypoxemia or tachypnea to acute respiratory distress syndrome.
Source (disruption of adipose architecture of bone marrow)
Pathophysiology r/t obstructed vessels by fat particles
Treatment: Manage acute respiratory distress syndrome, immobilize fractures, corticosteroids

Question 62

Pulmonary Thromboembolism:

Answer 62

Surgery predisposes patients to Pulmonary thromboembolism (up to 1 month post op)
Clinical presentation vary from asymptomatic to mild dyspnea to shock.
Fatality range from 1-60%
Diagnosis: difficult (large differential) most consistent symptom acute dyspnea, pleuritic or substernal chest pain, cough, hemoptysis (? Pulm infarction), tachypnea & tachycardia.
Treatment: anticoagulation, throbolytic therapy, inferior vena caval filter placement and surgical embolectomy.
Mangement of Anesthesia: Supportive minimize myocardial depression, inotropic agents, phosphodiesterase inhibitors amrinone & milrinone increase myocardial contractility ad are excellent pulmonary artery vasodilators, avoid hypoxemia, hypotension or pulmonary hypotension. Avoid Nitrous Oxide (increases pulmonary vascular resistance & need high FiO2)

Question 63

______________ helps distinguish restrictive ventilatory defects from obstructive ventilatory defects

Answer 63

Spirometry

Question 64

What is FEV1/FVC?

Answer 64

A ratio which is useful in distinguishing between restrictive and obstructive diseases.

Question 65

What are main Lung Diseases categorized as Obstructive?

Answer 65

Asthma
COPD
   (emphysema-pink puffer)
    (chronic bronchitis-blue bloater)
*Airways are Obstructed

Question 66

What are the main Lung Diseases characterized as Restrictive?

Answer 66

Pulmonary fibrosis
Pneumothorax
Chest Wall Diseases
Neuromuscular Diseases

Question 67

What is considered a Normal FEV1/FVC Ratio?

Answer 67

The FEV1/FVC ratio, is a calculated ratio used in the diagnosis of obstructive and restrictive lung disease. It represents the proportion of a person’s vital capacity that they are able to expire in the first second of forced expiration (FEV1) to the full, forced vital capacity (FVC). The result of this ratio is expressed as FEV1%.

Normal values are approximately 80%. Predicted normal values can be calculated online and depend on age, sex, height, and ethnicity as well as the research study that they are based upon.

When FEV1 values make up less than 80% of the FVC, an obstructive lung disease is likely present.
In restrictive lung diseases, both the FEV1 and FVC measurements decrease proportionally.

Question 68

What are the muscles of Inspiration?

Answer 68

Diapragm (Most Important)

AND External Intercostals