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.
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)
Differential of Intraoperative Bronchospasm
Mechanical obstruction of ET tube: kinking, secretions, overinflation of cuff
Inadequate anesthetic depth
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
Pink Puffers/Emphysema: PaO2 >60mmHg and normal PaCO2. Minimal vasoconstriction and no secondary erythrocytosis.
Blue Bloaters/Bronchitis: PaO2 <60mmHg and PaCO2 >45mmHg.
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
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
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).
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.
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.
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).
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
Arterial vs. Venous CO2 tension
PvCO2: 40-50mm Hg
Acute Respiratory Failure/ ARDS: Treatment
Goals: 1.Correct hypoxemia, 2. Remove excess CO2, 3. Provision of a patent upper airway.
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.
Remove secretions: tracheal suctioning, chest physiotherapy, and postural drainage.
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
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.