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Types of Respiratory Diseases
- Upper Respiratory Tract Infection (URI)
- COPD (chronic bronchitis & emphysema)
- Acute Respiratory Failure
- Restrictive lung Disease
- Pulmonary Embolism
- Lung Transplantation
Acute URI: Info
- Systemic signs of infection such as fever, purulent rhinitis, productive cough, and ronchi
- Increases risk of adverse event
- Those with a URI for days o weeks and are stable or improving can be safely managed without postponing surgery
- Delaying surgery does no reduce indigence of respiratory events within 4 weeks of URI
- Airway hyperactivity may require 6 or more weeks to heal.
Acute URI: Intraoperative
- Adequate hydration, reduce sections, and limit manipulation of a sensitive airway
- LMA may be a good alternative to reduce the risk of bronchospasm.
- Adverse events: bronchosapsm, laryngospasm, airway obstruction, postintubation croup, desaturation, and atelectasis
- Def: Chronic airway inflammation, reversible expiratory airflow obstruction in response to stimuli, and bronchial hyperreactivity
- S/S: wheezing, cough, dyspnea, chest discomfort/tightness, and eosinophilia
- Status asthmaticus: Life-threatening bronchospasm that persists despite treatment
- 1. Allergens
- 2. Drugs (aspiring, NSAIDs, sulfiting agents, B-blockers)
- 3.Infections (resp virus)
- 5.Emotional stress (endorphins & vagal mediation)
- Tachypnea and hyperventilation do not reflect arterial hypoxemia, but neural reflexes in the lungs.
- Hypocarbia and respiratory alkalosis are the most common arterial blood gas findings in the presence of asthma.
- Hx of recent trauma, surgery, or tracheal intubation may be present in patients with upper airway obstruction mimicking asthma
- Congestive heart failure and pulmonary embolism may cause dyspnea and wheezing.
Emphasis on preventing and controlling bronchial inflammation with 2 components: 1.Controller treatments (corticosteroids, theophylline, and antileukotrienes), 2.Rescue agents for acute bronchospasm (B-agonists and anticholinergic drugs)
- Info: unresolving bronchospasm that persists despite treatment.
- Tx: repeated B2-Agonist, IV corticosteroids, supplemental O2, empirical broad spectrum antibiotics
- Emergency: Hypercarbia (PaCO2>50mmHg) despite aggressive anti-inflammatory and bronchodilator therapy is a sign of respiratory fatigue and requires tracheal intubation and mechanical ventilation
- MCV: high peak airway pressure may be needed to deliver acceptable tidal volumes, short inspiratory time and long expiratory time
- Therapy resistance: usually expiratory airflow is obstructed by airway edema and intraluminal secretion.
- Goal: Formulate an anesthetic plan that prevents or blunts expiratory airflow obstruction
- Eval: auscultation of the chest to detect wheezing or crepitation. Blood eosinophil counts, pulmonary function tests before and after bronchodilator therapy.
- Drugs: continue anti-inflammatory and bronchodilator therapy. Stress dose or corticosteroids may be indicated
- Suppress airway reflexes to avoid bronchoconstriction in response to mechanical stimulation of hyperactive airways.
- Induction: often IV. Ketamine may produce smooth muscle relaxation and decrease airway resistance. Sevoflurane is a less pungent volatile and preferred. IV or intratracheal lidocaine may suppress airway reflexes.
- Intubation: Depth of anesthesia that depress hyperreactive airway reflexes to permit intubation without precipitating bronchospasm
- Neuromuscular blockers: relieves ventilation difficulty but has no effect on bronchospasm. Choose one that does not cause histamine release.
Asthma: Intraoperative Bronchospasm
- Often due to other factors than asthma
- 1. Deepened anesthetic (may respond)
- 2. B2-Agonist
- 3. Corticosteroids
Differential of Intraoperative Bronchospasm
- Mechanical obstruction of ET tube: kinking, secretions, overinflation of cuff
- Inadequate anesthetic depth
- Endobronchial intubation
- Pulmonary aspiration
- Pulmonary Edema
- Pulmonary Embolus
- Acute Asthmatic Attack
Chronic Obstructive Pulmonary Disease (COPD)
- Chronic Bronchitis: obstruction of small airways
- Emphysema: enlargement of air sacs, destruction of lung parenchyma, loss of elasticity, and closure of small airways
- Risk Factors: smoking, respiratory infection, occupational exposure, genetic factors (alpha1-antitrypsin deficiency).
Anti-inflammatory drugs: Corticosteroids
- Drug: Beclomethasone, triamcinolone, flunisolide, fluticasone, budesonide
- Actions: decrease airways inflammation, reduce airway hyper responsiveness
- Adverse: dysphonia, myopathy are laryngeal muscles, oropharyngeal candidiasis.
Anti-inflammatory drugs: Cromolyn
- Drug: Cromolyn
- Action: inhibit mediator release from mast cells, membrane stabilization
Anti-Inflammatory Drugs: Leukotriene modifiers
- Drugs: Zafirlukast (Accolate), pranlukast (Ultair), montelukast (Singulair), zilueton (Zyflo)
- Action: Reduce synthesis of leukotrienes by inhibiting 5-lipoxygenase enzyme
- Adverse: Increase hepatic enzymes
- Drugs: Albuterol, metaproterenol, salmeterol
- Actions: Stimulate B2 receptors of tracheobronchial tree
- Adverse: Tachycardia, tremors, dysrhythmias, hypokalemia.
- DrugsL Ipratropium, atropine, glycopyrrolate
- Actions: Decrease vagal tone by blocking muscarinic receptors in airway smooth muscle
- Drugs: Theophylline
- Action: Increase cAMP by inhibiting phosphodiesterase, block adenosine receptors, release endogenous catecholamines
- Adverse: Disrupt sleep cycle, nervousness, nausea, vomtiing, anorexia, headache, dysrhythmias.
COPD: Signs and Symptoms
- S/S: orothopnea, chronic productive cough (bronchitis), progressive exercise limitations, dyspnea (emphysema).
- Pink Puffers/Emphysema: PaO2 >60mmHg and normal PaCO2. Minimal vasoconstriction and no secondary erythrocytosis.
- Blue Bloaters/Bronchitis: PaO2 <60mmHg and PaCO2 >45mmHg.
- Smoking cessation
- Supplemental Oxygen
- Anticholinergics (bronchitis)
- Inhaled corticosteroids
- Broad-spectrum antibiotics
- Lung Volume reduction surgery (emphysema)
- Preparation: smoking cessation (over 6 weeks), treatment of bronchospasm, and bacterial infection, tx evidence of respiratory airflow obstruction
- Pulmonary consultation: 1.Hypoxemia on room air, 2.Bicarbonate more than 44mEq/L or PCO2 over 50mmHg in a patient whose pulmonary disease has not been evaluated, 3.History of respiratory failure due to an existing problem, 4.Seere SOB due to respiratory disease, 5.Planned pneumonectomy, 6.Difficulty assessing pulmonary function by clinical signs, 7.Distinguishing among etiologies or respiratory compromise, 8.Determining the response to bronchodilators, and 9.Suspected pulmonary HTN.
- Flow-volume: Decreased expiratory flow rate at any lung volume. RV is increased. Restrictive lung disease has a decrease in all lung volumes.
Smoking Cessation Disadvantages
- Increased sputum production
- Fear of inability to handle stress
- Nicotine withdrawal symptoms including irritability
- Sleep disturbance
- Consider regional anesthesia and avoid surgical procedures over 3 hours.
- Anesthetic technique does not alter incidence of complications
- GA: often with volatiles (sevoflurane) which provide bronchodilation. N2O may cause passage into bullae (contraindicated). Opioids depress ventilation and aren't as useful. Humidification and low gas flows help keep airway secretions moist. Large tidal volumes and slow inspiratory rates minimize the likelihood of turbulent airflow and maintain optimal V/Q matching.
Effects of Smoking (cardiac, respiratory, other organs)
- Cardiac: 1.Risk factor for CV disease, 2.carbon monoxide decrease O2 delivery and increases myocardial work, 3. Smoking releases catecholamines and causes coronary vasoconstriction, 4.Smoking decreases exercise capacity
- Respiratory: 1. Major risk factor for COPD, 2.Decrease mucociliary activity, 3.Hyperreactive airway, 4.Decreases pulmonary immune function
- Other organs: Impairs wound healing
- Institute lung volume expansion maneuvers: Deep breathing, incentive spirometry, positive pressure breathing. Decrease atelectasis.
- Facilitate effective cough
- Maximize analgesia
- Maintain MCV: may be necessary after major abdominal/ intrathoracic surgery. Don't reverse hypercarbia too quickly (produce metabolic alkalosis)
- Localized, irreversible dilation of bronchus by destructive inflammatory process, reflecting impaired mucociliary activity and pooling of mucus in dilated airways.
- Tx: antibiotics and postural drainage.
- Anesthesia: double-lumen endobronchial tube to prevent spillage of the purulent sputum into the normal areas of the lungs.
COPD: cystic fibrosis
- Autosomal-recessive. Defective chloride ion transport in epithelial cells in the lungs, pancreas, liver, GI, and reproductive organs. Results in rehydrated, viscous secretions associations with luminal obstruction and destruction/scarring of various exocrine glands.
- Tx: Clearance of airway secretions, bronchodilator therapy, reduction in viscoelasticity of sputum, antibiotics
- Anesthesia: similar to COPD
COPD: Primary Ciliary Dyskinesia
- Impaired ciliary activity resulting in chronic sinusitis, recurrent respiratory infections, and bronchiectasis.
- Kartagener's syndrome: chronic sinusitis, bronchiectasis, and situs inversus (visceral organs are mirrored from normal).
COPD: Tracheal Stenosis
- Info: Typically develops after prolonged endotracheal intubation (tracheal mucosal ischemia that may progress to cartilagenous ring destruction and circumferential constricting scar formation).
- Dx: Peak expiratory rates are decreased. Stridor is usually audible. Flattened inspiratory and expiratory curves.
- Anesthesia: High frequency ventilation
Acute Intrinsic Restrictive Lung Disease
Info: Pulmonary edema due to leakage of IV fluid into the lung/alveoli interstitial due to increased capillary pressure or permeability (high protein and secretory products in the fluid).
Acute Intrinsic Restrictive Lung Disease: Aspiration Pneumonitis
- Increased permeability: Aspirated gastric fluid destroys surfactant producing cells and damages the pulmonary capillary endothelium.
- Leads to atelectasis and leakage of IV fluid into the lungs.
- Tx: Supplemental O2 and PEEP
Acute Intrinsic Restrictive Lung Disease: Neurogenic Pulmonary Edema
- Increased pressure: Follows acute brain injury. Sympathetic outpouring results in vasoconstriction and IV blood into the pulmonary circulation.
- Pulmonary HRN and hypervolemia can also injure BV in the lungs.
Acute Intrinsic Restrictive Lung Disease: Drug Induced Pulmonary Edema
- Increased permeability: Many drugs, especially opioids (heroin) and cocaine. High protein concentrations in the pulmonary edema fluid
- Tx: Naloxone does NOT speed resolution of the edema. Tx is supportive and may include tracheal intubation for airway protection and mechanical ventilation.
Acute Intrinsic Restrictive Lung Disease: Reexpansion of Collapsed Lung
Increased permeability: risk related to the amount of air in the pleural space, duration of the collapse, and rapidity of reexpansion. High protein edema.
Acute Intrinsic Restrictive Lung Disease: Negative Pressure pulmonary edema
- Info: May follow relief of acute upper airway obstruction due to postextubation laryngospasm, epiglottis, tumors, obesity, hiccups, or OSA
- Path: Due to vigorous inspiratory efforts against an obstructed upper airway. High negative intracellular pressure decreases interstitial hydrostatic pressure, increases venous return, and increases LV afterload.
Acute Intrinsic Restrictive Lung Disease: Anesthesia
- Preoperative: Delay elective surgery. Persistent hypoxemia may require MCV and PEEP
- Intraoperative: Ventilate with low tidal volumes and a high respiratory rate
Acute Respiratory Distress Syndrome (ARDS)
- Inflammatory lung condition with noncardiogenic pulmonary edema and impaired gas exchange
- Acute: arterial hypoxemia resistant to O2, influx of protein-rich edema due to increased permeability, pulmonary HTn due to vasoconsrtiction
Chronic Intrinsic Restrictive Lung Disease
Info: changes in the intrinsic properties of the lungs due to pulmonary fibrosis. Pulmonary HTN and for pulmonate develop as fibrosis results in the loss of pulmonary vasculature.
Chronic Intrinsic Restrictive Lung Disease: Sarcoidosis
- Systemic granulomatous disorder (mainly lymph nodes and lungs)
- Unilateral facial nerve palsy: most common near
- Laryngeal sarcoidosis in 5% of patients and may interfere with passage of adult tracheal tubes.
Chronic Intrinsic Restrictive Lung Disease: Other types
- Hypersensitivity pneumonitis
- Eosinophilic granulona
- Pulmonary alveolar proteinosis
- Lymphangioleiomyomatosis: proliferation of smooth muscle in airways, lymphatics, and BV
Chronic Intrinsic Restrictive Lung Disease: Anesthesia
- Preoperative: Present w/ dyspnea and nonproductive cough. Aryerial hypoxemia and normocarbia.
- Intraoperative: Do not tolerate apneic periods due to small FRC and low oxygen stores. Faster uptake of inhaled anesthetics due to small FRC. Keep peak airway pressures low to avoid barotrauma.
Chronic Extrinsic Restrictive Lung Disease
Info: Most often due to disorders of the thoracic cage/chest wall that interfere with lung expansion. Lungs are compressed and lung volumes are reduced, leading to increased work of breathing.
Chronic Extrinsic Restrictive Lung Disease: Obesity
Restrictive load of thoracic cage and decreases FRC.
Chronic Extrinsic Restrictive Lung Disease: Deformities of costovertebral skeletal structures
- Scoliosis: Lateral curvature of the vertebral column
- Kyphosis: anterior flexion of the vertebral column.
- Severe forms may lead to chronic alveolar hypoventilation, hypoxemia, secondary erythrocysosis, pulmonary HTN, and for pulmonate.
- Increased risk of pneumonia and hypoventilation induced by CNS depressant drugs.
Chronic Extrinsic Restrictive Lung Disease: Others
- Sternum deformities:
- Diaphragmatic Paralysis:
- Gullian Barre
- Myasthenia Gravis: disorder of neuromuscular transmission.
- Muscular dystrophy: Duchenne's muscular dystrophy, myotonic dystrophy, etc. Avoid CNS depressants
Chronic Extrinsic Restrictive Lung Disease: Flial Chest
- Info: paradoxical inward movement of the unstable portion of the thoracic cage while the remainder moves outward during inspiration.
- Tx: PPV until rib stabilization can occur.
Chronic Extrinsic Restrictive Lung Disease: Neuromuscular disorders
- Abnormalities of the spinal cord, peripheral nerves, NMJ, or skeletal muscles.
- Prevents generation of a forceful cough. Acute res[iratory failure likely when atelectasis is associated with pneumonia occurs or depressant drugs are administered.
Chronic Extrinsic Restrictive Lung Disease: Spinal cord Transection
- Breathing maintained by the diaphragm if transection is at or below C4.
- Usually no expiratory force and paradoxical inward motion of the upper thorax during inspiration (decreased tidal volumes).
Chronic Extrinsic Restrictive Lung Disease: Pleural
- Pleural Fibrosis:
- Pleural effusion: Increased fluid in the pleural space w/ as much as 25/50ml of pleural fluid (normal: <10ml). Blunt costophrenic angle.
- Pneumothorax: Gas in the pleural space. Ipsilateral chest pain and cough. Tachycardia. Tx w/ evacuation of air.
- Tension pneumothorax: Gas enters the pleural space during inspiration and is prevented from escaping. Common after central line placement, barotrauma from MCV, and rib fractures. Immediate evacuation of gas through a small bore catheter into the second anterior intercostal space may be lifesaving.
Chronic Extrinsic Restrictive Lung Disease: Mediastinum
- Mediastinal Tumors: Lymphoma, thyoma, teratomr,a and goiter are common anterior mediastinal masses. May lead to progressive airway destruction, loss of lung volumes, pulmonary artery or cardiac compression and SVC obstruction/syndrome.
- Mediastinitis: due to bacterial infection
- Bronchogenic cyst: Fluid/air filled cysts from the primitive foregut located in the mediastinum or lung . Caution with N2O and PPV
Superior Vena Cava (SVC) Syndrome
- Increased venous pressure leads to
- 1. Dilation of the collateral veins in the thorax and neck
- 2. Edema and cyanosis of the face, neck, and upper chest
- 3. Edema of the conjunctiva
- 4. Evidence of increased ICP (headache and altered mental status).
Chronic Extrinsic Restrictive Lung Disease: Anesthesia
- Preoperative: Consider preoperative radiation for tumors.
- Intraoperative: Does not influence choice of drug for induction or maintenance of anesthesia. MCV allows optimal oxygenation and ventilation. Increased inspiratory pressures may be required due to increased airway pressure. External edema sure to SVC syndrome may be accompanied by similar edema inside the mouth and hypopharynx.
Acute Respiratory Failure
- Info: Inability to provide arterial oxygenation/elimination of CO2
- PaO2: <60mmHg (90% saturation) despite supplemental O2 and in the absence of a R-L shunt.
- PaCO2: >50mmHg in the absence of respiratory compensation for metabolic alkalosis
- Decrease in pH can help distinguish from chronic respiratory failure since there is often renal compensation for acidosis.
- Often a decreased FRC and lung compliance w/ pulmonary HTN and respiratory failure.
Oxygen Saturation vs. Oxygen Pressure
- 1. 100% = 100mmHg
- 2. 95% = 80mmHg
- 3. 90% = 60mm Hg
- 4. 80% = 48mmHg
Arterial vs Venous Oxygen Tension
- PaO2: 75-100mmHg
- PvO2: 30-40mmHg
Arterial vs. Venous CO2 tension
- PaCO2: 35-45mmHg
- PvCO2: 40-50mm Hg
Acute Respiratory Failure/ ARDS: Treatment
- Goals: 1.Correct hypoxemia, 2. Remove excess CO2, 3. Provision of a patent upper airway.
- Supplemental O2
- Tracheal Intubation
- MCV: PaO2 60-80mmHg, Peak airway pressure not to exceed 35-40cmH2O. Inverse-ratio ventilation due to an end0inspiratory pause to maintain alveolar pressure at the plateau value.
- PEEP: added in 2.5-5cmH2O increments.
- Optimized IV fluid volume: fluid restriction to decrease magnitude of pulmonary edema.
- Diuretic Therapy
- Inotropic Support
- Remove secretions: tracheal suctioning, chest physiotherapy, and postural drainage.
- Possible corticosteroids
- Control Infection
- Inhaled B-agonists
- Nutritional Support: prevent skeletal muscle weakness.
Management of Patients Receiving Mechanical Ventilation Support
- Inadequate sedation can lead to self-extubation, deterioration in gas exchange, and barotrauma.
- Neuromuscular blockade vs. sedation
Patients Receiving Mechanical Support of Ventilation: Complications
- Infection: often tracheal intubation or sinusitis from nasotracheal tube.
- Alveolar overdistention: due to large tidal volumes (10-12ml/Kg) and high airway pressures (>50cmH2O)
- Barotrauma: Tension pneumothorax is the most common life-threatening manifestation.
- Atelectasis: common cause of hypoxemia w/ mechanical ventilation.
- Critical Illness myopathy: duration of drug-induced paralysis.
Patients Receiving Mechanical Support of Ventilation: Weaning from the Ventilator and Tracheal Extubation
- 1. Vital Capacity more than 15ml/kg
- 2. PAO2-PaO2 less than 350cmH2O while breathing 100% O2.
- 3. PaO2 more than 60mm Hg with FiO2 less than 0.5
- 4. Negative inspiratory pressure greater than -20cmH20
- 5. Normal pHa
- 6. RR less than 20 breaths/min
- 7. Dead-space ventilation/Tidal volume ratio (Vd/Vt) less than 0.6
- 1. Synchronized intermittent mandatory ventilation
- 2. Intermittent trials of total removal of mechanical support and breathing through a T-piece.
- 3. Use of decreasing levels of PSV
Patients Receiving Mechanical Support of Ventilation: Monitoring
- Supplemental oxygen: often needed after extubation.
- Oxygen exchange and arterial oxygenation: reflected by the PaO2. Arterial hypoxemia primarily caused by VQ mismatch, R-L intrapulmonary shunting, and hypoventilation.
- CO2 elimination: Reflected by PaCO2. Vd/Vt is usually less than 0.3 (ventilation/blood flow). Hypercarbia is PaCO2 over 45mm Hg
- Arterial pH:
- Intrapulmonary shunting: perfusion of alveoli that are not ventilated. Leads to decreased PaO2
Pulmonary Embolism: Diagnosis
- Info: Acute dyspnea, tachypnea, and tachycardia,Patent foramen oval or ASD may cause paradoxical embolism to occur.
- ECG: ST-T wave changes and RAD. Peaked P waves, AFib, and RBBB if it causes for pulmonate.
- Capnography: decreased end-tidal CO2 and increased alveolar-arterial CO2 difference due to increased dead space ventilation.
Pulmonary Embolism: Treatment
- Anticoagulation, thrombolytic therapy, IVC filter placement, and surgical embolectomy
- Heparin: cornerstone of tx.
- Warfarin: extended anticoagulation with an INR of 2-3.
- Positive inotropes: Dopamine and dobutamine to tx hypotension
Pulmonary Embolism: Anesthesia
- Support vital organ function
- Minimize anesthetic induced myocardial depression
- Phosphodiesterase inhibitors (Amrinone and Milrinone): increase contractility and pulmonary vasodilators
- Induction/maintenance: avoid arterial hypoxemia, systemic hypotension, and pulmonary HTN. N2O not likely due to increase in Pulmonary resistance. Non depolarizing NMB w/o histamine is best.
- Often seen after long-bone fractures.
- S/S: fever and tachycardia
Lung Transplant Recipients: Anesthesia
- Preoperative Focus: 1.Function of the transplanted lung, 2.Possibility of rejection or infection of the transplanted lung, 3.Effect of immunosuppressive therapy on other organ systems and the effect of other organ system dysfunction on the transplanted lung, 4.The Disease in the native lung, 5.Planned surgical procedure and its effect on the lungs.
- Preoperative meds: Antibiotic prophylaxis, antisialogogues, and corticosteroids
- Intraoperative: Diminished cough reflex under GA below anastomosis, so regional anesthesia is preferred. Central venous catheter is best on the side of the native lung. Volatiles are well tolerated and N2O is acceptable in the absence of bulls disease. Avoid endobronchial intubation. PPV may be complicated by differences in lung compliance.
- Intraoperative goal: Prompot recovery of respiratory function and early tracheal extubation.