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Pathophysiology and their
Anesthesia Management
Instructor: Paul Bennetts, PhD, CRNA
• I have no conflicts of interest.
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6
• Recognize / describe physiological and pathophysiological
respiratory events related to
• Obstructive lung diseases,
• Restrictive lung diseases,
• Pulmonary embolisms,
• Mediastinal masses,
• Acute respiratory distress syndrome (ARDS),
• Bronchospasm and
• Tension pneumothorax
• Manage anesthetics for patients with these disorders in
accordance with evidence-based practices.
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Emphysema, Chronic Bronchitis,
Asthma and Bronchospasm
• Pulmonary dysfunction marked by persistent airflow limitation
(outflow) in conducting airways
• 100,000 deaths per year in U.S.
• Not fully reversible
• Progressive in course
• Inflammatory response
• Types of COPD
• Emphysema
• Chronic Bronchitis
• Asthma
9
2
1
• Emphysema is characterized by an abnormal
permanent enlargement of air spaces distal to the
non-respiratory bronchioles
• Destruction of alveolar walls without obvious fibrosis
• Epidemiology
• Prevalence: 10% of the U.S. population
10
2, 3
• Etiology
• Principal causal factor is smoking
• May be result of α1- protease inhibitor deficiency
• Other environmental factors
• Exposure to chronic dust or chemical fumes
• Pathogenesis
• Destruction of lung elastic tissue
• Loss of surrounding supporting structures
• Small airway collapse resulting in obstruction to flow of air out of
the alveoli during exhalation
11
2, 3
2, 3
• Pathogenesis
• Protease (enzymes) secreted by alveolar macrophages and
neutrophils sequestered in pulmonary capillaries destroy
elastic fibers in the alveoli
• Inflammation results in ↑’d release of proteases &
recruitment of more neutrophils and macrophages
• α1- antitrypsin is an anti-protease (inhibits)
• Oxidative stress from smoking or other irritants
results in injury that inhibits α1-AT activity
12
13
• Higher levels of protease relative to α1-AT results
in elastic connective tissue destruction
• Outcomes:
• Increased compliance / diminished recoil
• Premature collapse of airways during expiration
• Destruction of alveolar septa with loss of septal walls
• Enlarged alveoli/airspaces
• Destruction of alveolar capillary walls
• Reduction in gas exchange surface area
14
• Centriacinar (Centrilobular):
• Commonly found in smokers
• Respiratory bronchioles are affected
• Distal Acinar (Paraseptal):
• Distal alveolar sacs are affected
• Emphysematous bullae
• Panacinar (Panlobular):
• Genetic (α1-antitrypsin deficiency)
• Both alveoli &respiratory bronchioles
15
2, 3
• “Barrel chest” appearance due to remodeling of the thorax from increased compliance and loss of recoil
• Chest x-ray – hyperinflation, with flattened diaphragm
• Dyspnea, little sputum production
• Individuals with genetic α1-AT develop emphysema at a younger age and particularly if they smoke
• At risk for development of pulmonary hypertension
• Probably due to vascular remodeling and not hypoxic vasoconstriction
16
17
Normal Emphysema
18McPhee & Hammer, p. 232, Fig. 9-20
Outflow obstruction
3
• Chronic bronchitis: chronic cough associated with
sputum production for more than 3 months of the
year for 2 or more consecutive years.
• Epidemiology: approximately 5.5% of U.S. adults
• 20-25% of men 40- to 65-years-old
• More common among smokers and urban-dwelling
adults
19
• Etiology: Tobacco smoke is a major factor
• Air pollutants
• Occupational exposures
• Previous infections
• Pathogenesis: Irritation results in inflammatory process
in the larger airways with mucosal thickening from
hypertrophy and hyperplasia of mucus glands &
goblet cells in the bronchi
• Mucus gland hypersecretion, resulting in airway narrowing
(obstruction) and secondary infection
20
• Lumen narrowing
• Further infiltration of the mucosa with inflammatory cells
→ more inflammation & narrowing
• Impaired clearance of airway secretions
• mucus plugging & infections
• Results in further bronchiolar inflammation:
wheezes, cough, thick sputum
21
• Pulmonary function testing
• Decreased expiratory flow (narrowed airways)
• Reduced FEV1 and FEV1/FVC (FEV1% ratio)
• Air trapping with increased RV
22
• Complications of chronic bronchitis
• Can be complicated by pulmonary hypertension and
cardiac failure
• Risk for the disorder to progress to the small airways
(bronchiolitis)
• Ongoing inflammation & fibrosis leads to obliteration of
bronchioles
23
• Exercise tolerance usually correlates well with
pulmonary function testing (PFT)
• PFTs do not reliably predict PPC
• Principals of medical management (mild to
moderate disease):
• Prevention, vaccination, pulmonary rehabilitation, long-
acting bronchodilators
• Severe disease → the patient may be on
corticosteroids and supplemental oxygen
24
1, 7
• Chest x-rays and CT chest only useful to rule out active infection or other disease (carcinoma)
• Not useful for routine screening
• ECG to detect right heart strain
• Patients with poor exercise tolerance should be evaluated for presence of coronary disease
• Routine labs of limited benefit
• Hypoxemia / hypercarbia (ABGs)
• Malnutrition (↓ albumin)
• Polycythemia (↑ Hgb /Hct)
25
1
• Goal in anesthesia management: prevent PPC
• Pneumonia, COPD exacerbation, bronchospasm, or
respiratory failure
• Smoking is well-defined risk factor for post-op
pulmonary complications (PPC)
• Smoking cessation has been shown to ↓ PPC
• No improvement in risk in patients who quit 2 to 4 weeks
before surgery
• Best benefit to reduce PPCs was quitting 8 weeks prior
26
• If possible, consider neuraxial techniques,
peripheral blockade or general anesthesia without
endotracheal intubation (i.e. LMA) as first-line
choices
• Review of over 100 randomized clinical trials suggests
decreased incidence of mortality, PPC & post-op cardiac
complications with regional anesthesia (RA) techniques
• A few studies did fail to show significant support for
epidural anesthesia/analgesia over GA
27
9
• Hausman et al. evaluated 2,644 matched pairs to determine benefits of RA for COPD
•Overall, GA patients had higher overall morbidity, including PPC
•Non-pulmonary complication rates were similar
• Epidural did not provide significant protection over GA, however spinal and peripheral anesthesia techniques did
• Improved outcomes not extended to patients with dyspnea at rest
28
9
• Presence of residual neuromuscular
blocking agents is a predictor of PPCs in
patients with COPD
• NMBDs should be used judiciously
• Short acting agents preferred
• Careful neuromuscular monitoring
• (Quantitative versus qualitative monitors)
• Full reversal of neuromuscular blockade prior
to extubation
• Sugammadex?
29
8
• Oxygen management in the COPD patient
• Higher FiO2 (100%) associated with reabsorption
atelectasis and increased O2 radical production
• FiO2 of 80%: less atelectasis (nitrogen splint)
• FiO2 of 60%: absorption atelectasis limited
30
• Fast-track tracheal extubation
• Avoidance of prolonged intubation / ventilation
• Effective pain relief critical for rapid recovery
• Concern with central effects of opioids as the sole
intervention for pain relief
• Use of regional techniques, catheters and long-acting
drug preparations such as liposomal local anesthetics
(Exparel)
• Multimodal analgesia: NSAIDS, IV acetaminophen
31
• Reactive airway disease (RAD) is highly relevant to
anesthesia providers because it may lead to
perioperative bronchospasm
• Commonly associated with asthma
• Frequently a lifelong condition
• Most common chronic respiratory disease
• Incidence of asthma up to 20% in westernized populations
(4 – 11% in the U.S.)
• Male > females
32
• Common cause of airway reactivity especially in
industrialized countries
• Asthmatics demonstrate variable degrees of airway
inflammation and remodeling
• Characterized by infiltration of eosinophils, mast cells and T-
helper lymphocytes into the peripheral airways
• Airway remodeling related to:
• Thickening of epithelial basal membrane
• Smooth muscle hypertrophy
• Hypertrophy of mucous-secreting goblet cells
33
2, 3
• Atopic (70%) – due to allergen sensitization
• Genetic predisposition to type I hypersensitivity
• Usually begins in childhood
• Often a positive history of asthma in the family
• Non atopic (30%)
• Pulmonary infection/viruses
• Environmental pollutants
• Stress, exercise
34
• Atopic individual
• Inflammatory response to allergen → type 2 helper T
cells (Th2) secretes
• IL-4 → stimulated B cells to produce IgE
• IL-5 → stimulates eosinophilic activity
• IL-13 → stimulates mucous production and promotes B cell
production of IgE
35
• Non-atopic individual
• Initial sensitization → Pulmonary infection/virus,
environmental pollutants, stress or exercise
inflammation of respiratory mucosa → lowers threshold
of response to irritants
36
• Immediate Phase Reaction (minutes)
• Antigen induced cross-linking of IgE activation of
mast cells on the respiratory mucosa
• Release of histamine and other substances which produce
prostaglandins and leukotrienes
• Opens mucosal intercellular junctions allowing
penetration of antigen to mucosal mast cells
37
• Vasodilation and increased vascular permeability
• Activation of more mast cells along the vascular walls
• Stimulates autonomic/other receptors resulting in
bronchoconstriction
• Edema (furthering airway narrowing)
• Smooth muscle contraction
• From activation of vagal nerve receptors and release of
leukotrienes
38
• Recruitment of additional inflammatory cells including
neutrophils, monocytes, lymphocytes, basophils and
particularly eosinophils to airway mucosa
• Mucus production → narrowing/airway occlusion
39
• Late phase reaction (2 – 24 hours)
• Inflammation and continued recruitment of eosinophils
• Results in injury to bronchiolar epithelium, increased penetration
of antigens to submucosal mast cells
• Secretion of cytokines:
• Growth and activation of mast cells & eosinophils
• Perpetuated inflammatory response
• Promotes IgE production in B cells
• Smooth muscle proliferation
40
• Long standing inflammation leads to:
• Damaged bronchial epithelium
• Diffuse luminal obstruction
• Hypersecretion of mucous
• Mucosal edema
• Thickened basal membrane
• Smooth muscle hypertrophy, remodeling
• Increase in interstitial collagen, submucosal fibrosis
41
• Reduced gas exchange leads to V/Q mismatch
• Outflow obstruction leads to air trapping, dynamic
hyperinflation and hypercarbia
• Expiratory wheezing
• Children are at increased risk of morbidity and
mortality from asthmatic obstruction due to smaller
airway diameters
42
• Surgery produces pro-inflammatory cytokines
• Higher levels in asthmatics may predispose them to
adverse events
• Reduction in ability to cough and mucociliary action
predisposes the asthmatic to problems
• Surgery site: closer to diaphragm = increased
respiratory complications
• Duration of intubation correlates with respiratory
complications
43
• Other Pharmacologic Adjuncts:• IV lidocaine before induction: not been demonstrated in
studies to be of benefit, however lidocaine 5 min. after induction did reduce airway resistance in patients with asthma
• Ketamine (bronchodilator) has been used to treat acute asthma, but data are insufficient
• Magnesium sulfate 1.2 - 2 Gm IV over 20 minutes has been reported in emergency treatment of bronchospasm
• Magnesium may promote bronchial smooth muscle relaxation
• Studies recommended
44
11
12
• Patients undergoing general anesthesia may develop
bronchospasm for multiple reasons
• History of respiratory disease
• Reaction to medications or contrast dye
• Spontaneous, possibly due to airway stimulation by
instrumentation secretions or aspiration
• Inadvertent esophageal or endobronchial intubation
• Inadequate depth of anesthesia
45
• Severe perioperative bronchospasm in asthmatics
reported in 0.17 - 4.2% of all general anesthetics
• Some estimates as high as 20%
• Asthmatic children can be especially prone to bronchospastic
events
• Also a common symptom of anaphylaxis (present in
19% of events)
• Especially related to the administration of water soluble
radiographic contrast media
46
13
• Mechanical: Tracheal and laryngeal sensory afferent
stimulation with efferent activation of vagal fibers
(parasympathetic)
• Anaphylactoid: Nonimmune-mediated medication
reaction
• Mast cell degranulation & histamine release
• Anaphylactic: Immune-mediated (IgE) reaction
• Also mast cell degranulation
47
• Idiopathic (airway manipulation) (55%)
• Especially laryngoscopy
• Allergy / anaphylaxis (21%)
• Esophageal intubation (12%)
• Aspiration (12%)
• Endobronchial intubation (2.5%)
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14
• Induction of anesthesia
• Airway irritation (oral airway, laryngoscopy, misplacement of
ET tube)
• Anaphylaxis
• Aspiration
• Maintenance of anesthesia
• Anaphylaxis
• Migration of ET tube
• No defined reasons
• Aspiration associated with the use of LMA
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14
• Emergence from anesthesia and recovery
• No defined causes
• Pulmonary edema
• Extubation
• Anaphylaxis
50
• Induction
• Increased ventilation pressures
• “Bronchospasm” with wheezing
• Low oxygen saturation
• Changes in capnography ( ↑ EtCO2, prolonged expiration)
• Maintenance
• Increased ventilation pressures
• Low oxygen saturation
• “Bronchospasm” with wheezing
• Reduction in tidal volumes
51
• Emergence and Recovery
• Low oxygen saturation
• “Bronchospasm” with wheezing
52
• Anaphylaxis/allergic reaction
• Latex, blood or fluid replacements
• IV administration of beta-blockers
• Irritation or secretions
• Pneumothorax
• Inadequate depth of anesthesia / failure of anesthetic
delivery system
• Bronchial obstruction
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• Increase FiO2 to 100% until spasm abates
• Cease stimulation or surgery
• Request assistance
• Deepen anesthesia (Propofol)
• Check tube position
• If LMA in place, consider possibility of aspiration
• Treat with beta-2 agonist
• Epinephrine (IV) 1 mcg/kg bolus
• Albuterol (salbutamol)
• Chest x-ray if not resolving
54
• Epinephrine 1 mcg/kg IV bolus
• 0.7 to 1 ml of 1:10,000 solution for 70-100 kg patient
• Albuterol (salbutamol)
• Metered dose inhaler 2 puffs (can be repeated)
• Nebulized in-line 0.5% solution, 1 ml in 3-5 ml NS
• 0.5% 0.1ml in 1 ml NS via ET tube
• Ipratropium bromide via inhaler (2 puffs) or nebulizer
(0.25 – 0.5 mg)
• Repeat twice, 20 minutes apart
55
• IV Corticosteroids (hydrocortisone 2-4 mg/kg)
• IV albuterol for adults and children > 12
• Bolus 3.5 mcg/kg over 5 - 10 minutes, infusion rate 0.04 -
0.29 mcg/kg/min
• IV Aminophylline – in severe asthma may improve lung
function over inhalers and steroids alone, but increases
risk of PONV
• Loading dose 4.6 - 6mg/kg over 20-30 minutes
• Maintenance 0.4 - 0.9 mg/kg/hr based on serum levels
• No differences between Aminophylline and IV beta-2s
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15
• Magnesium Sulfate either nebulized or intravenous
may also be of benefit
• Magnesium deficiency a risk factor in asthma
• MgSO4 has smooth muscle-relaxant effects, probably via
inhibition of calcium influx into muscle cells similar to calcium
channel blockers
• Other possible mechanisms include mast cell stabilization and
increased beta-receptor affinity
• Nebulized magnesium less effective for children
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Chronic Interstitial Parenchymal Diseases,
ARDS and Tension Pneumothorax
• Definition: Conditions that interfere with normal
lung expansion during inspiration
• Increased elastic recoil of lungs or chest wall
• Decreased compliance
• Decreased lung volume
• Total lung capacity below 5th percentile
• Other ventilation abnormalities
• Impaired diffusion
• V/Q mismatch
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• Classification of restrictive diseases
• Acute intrinsic
• Pneumonia
• ARDS
• Chronic intrinsic (Diffuse parenchymal disease)
• Idiopathic interstitial pneumonias
• Granulomatous diseases (including sarcoidosis)
• Environmental or toxin-induced, autoimmune
• Chronic extrinsic (conditions that inhibit normal excursion of the lungs)
• Traumatic injury (tension pneumothorax)
60
• Definition: ARDS is a clinical syndrome caused by
diffuse capillary and epithelial damage resulting
in increased permeability followed by interstitial
and alveolar edema
61
• Direct lung injury
• Pneumonia
• Aspiration
• Pulmonary contusion
• Fat embolism
• Near drowning
• Inhalational injury (burn victim)
• Reperfusion injury after lung transplantation
62
• Indirect lung injury (associated with a systemic
process)
• Sepsis
• Severe trauma with shock
• Cardiopulmonary bypass
• Acute pancreatitis
• Drug overdose
• Transfusion reaction
• Uremia
63
• Dyspnea
• Increasing Hypoxemia - Low V/Q
• Late hypercapnia
• Decreased compliance
• Development of infiltrates
• Increasing CXR opacity
• At least 30% to 40% mortality rate
64
• Direct or indirect lung injury
• Severe injury to alveolar epithelium
• Increased vascular permeability – fluids & proteins leak
from the pulmonary interstitium into the alveoli
• Alveolar flooding / loss of gas diffusion capacity
65
• Both pathways lead to:
• Activation of neutrophils and macrophages
• Capillary inflammatory response
• Release of cytokines and phospholipids from endothelium
• Reactive oxygen species, proteases
• Prostaglandin metabolites promote constriction of both airways and pulmonary vasculature
• Thromboplastin-triggered coagulopathy
• Microemboli → alveolar hypoxia, hypercapnia
• Damage to type II pneumocytes → surfactant abnormalities
66
• Increased pulmonary vascular resistance +
decreased compliance requires aggressive positive
pressure ventilation
• Increased workload on the right ventricle
• Right ventricular dysfunction → cor pulmonale
• 25% of cases
• Right to left shunt if patent foramen ovale is present
67
• Blum et al. reviewed 50,367 patient admissions
and identified specific preoperative risk factors
(decreasing order)
• ASA ≥ 3 (strongest risk factor)
• Emergent surgery
• Renal failure
• COPD
• Male gender
• Multiple anesthetics during the admission
68
• Intraoperative risk factors:
• PRBC transfusions
• Crystalloid administration
• Ventilator drive pressures
• Tidal volume not significant
• Large tidal volumes (pressure) should be avoided
• FiO2 (small effect)
69
18
• Intraoperative fluid therapy
• Fluid-induced lung injury
• Surgery patients with respiratory failure who received > 20
mL/kg/h were 3.8 times more likely to develop ARDS than
patients who received < 10 mL/kg/hr
• Goal directed fluid therapy with NICOM or PPV
70
• Supportive
• Correct hypoxemia (FiO2 and PEEP)
• Inotropic support
• Afterload reduction
• Corticosteroids
• Inhaled nitric oxide to control PA pressures
• Exogenous surfactant
• Extracorporeal membrane oxygenation (ECMO)
71
• Careful evaluation of cardiac, pulmonary & renal
status
• Judicious fluid replacement (avoid overload)
• Prevent IV entrainment of air (PFO)
• Risk of right to left shunt
• Monitoring should include invasive arterial and cardiac
output if available
• Transesophageal echo to evaluate RV function
• Protective lung ventilation (PLV) strategies
72
• Close attention to peak inspiratory pressures and
use of PEEP
• Objective: reduce atelectasis, promote alveolar
recruitment & avoid right ventricular overload
• “Permissive hypercapnia” to limit airway pressures
• Goal-directed strategy: Maintain target pH or PaCO2
while providing optimal lung protection
73
• Maintain target pH or PaCO2
• Use of higher PEEP to keep alveoli open and ensure
oxygenation at lower FiO2
• Lung protection
• Avoid barotrauma by using smaller volumes
• (VT ≤ 6 ml/kg)
• Limit plateau pressure to ≤ 30 cm H2O
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19
• Lung protective ventilation is insufficient – so what
now?
• Recruitment maneuvers: transiently increasing trans-
pulmonary pressures to recruit collapsed alveoli
• Airway Pressure Release Ventilation (APRV)
• High frequency oscillatory ventilation (HFOV)
• Inhaled pulmonary vasodilators
• Extracorporeal membrane oxygenation (ECMO)
• Prone positioning
75
• Sigh: VT or PEEP increased to a pre-specified plateau
pressure for one or several breaths per minute
• Sustained pressure: Airways pressurized and
maintained for a specific duration
• i.e. 40 cm H2O for 5 - 40 seconds or progressive increases in
PEEP
• Watch for hemodynamic instability
• Benefits of RMs limited to short term improvement in
oxygenation
• Survival rates unaffected
76
21
20
• Blood diverted from the patient and oxygenated
externally
• Controlled trial results were favorable but suffered from lack
of standard methods of ventilation in the control group
• “Last resort” in the management of ARDS
• Complications of ECMO:
• Bleeding,
• Thromboembolism,
• Vascular damage from cannulation
• Heparin-induced thrombocytopenia
77
• Heterogeneous group of pulmonary disorders characterized mainly by bilateral involvement of the lung connective tissues
• Categories
• Fibrosis
• Idiopathic interstitial pneumonias
• Environmental (exposure to asbestos, silica, coal dust)
• Collagen-vascular disease (scleroderma)
• Granulomatous
• Sarcoidosis
• Hypersensitivity pneumonitis (exposure to mold, dust)
78
• Primary characteristics: infiltration of inflammatory
cells & production of fibrous tissue leading to
decreased compliance & hypoxia
• Initial injury → activation of leukocytes
• Eosinophils, macrophages, neutrophils, immune cells accumulate
in alveolar walls & spaces
• Release of pro-inflammatory cytokines
• Leukocytes secrete proteases
• Damage to alveolar epithelia and connective tissues
• Macrophages activate fibroblast proliferation
• Connective tissue cells – collagen deposits
79
• Injury to Type I alveolar epithelial cells (removed by apoptosis)
• Type I cells replaced by abnormal type II cells
• Decreased production & turnover of surfactant
• Recruitment of inflammatory cells
• Production of more fibroblasts, deposition of collagen and elastin
• Alveolar destruction/distortion with widespread fibrosis
• Destroyed pulmonary vasculature / pulmonary hypertension
• Disrupted capacity for gas exchange
• Increased lung elastic recoil and decreased compliance80
• Intermittent, irritating non-productive cough
• Dyspnea, tachypnea, inspiratory crackles
• Clubbing of the digits
• Increased work of breathing
• Decrease VT offset by increased rate
• Abnormal blood gas values
• Lowered PaO2 due to thickened alveolar wall = ↓ diffusion
capacity
• Initially lower PaCO2 due to tachypnea (increased in later stages
due to increased work of breathing and hypoventilation)
81
• Chest radiography: Small volume, increased density,
honeycombed appearance
• Alteration in pulmonary function
82
• Meticulous pre-op evaluation
• 90% of GA patients will develop atelectasis
• 10 to 30% will experience PPC
• RLD prevalent in older patients
• Most important is a quality of life evaluation
• Focus on activity levels
• Ability to climb 2 flights without dyspnea is associated with
lower risk
83
• PFTs may be useful but have less of a role in
predicting PPC
• FEV1 > 40% associated with fewer PPC
• ABGs useful as baseline for patients with respiratory
disease
• Limited value for risk stratification
• Radiography useful in diagnosis of causes of
dyspnea
84
1
• Patients with RLD at risk for exaggerated
pulmonary dysfunction post-op
• Few EBP perioperative recommendations for
patients with RLD
85
• Honma et al. (2007) published a single case report
about perioperative management of a 68 year old
patient having low anterior resection of rectal CA
• H/O chronic interstitial pneumonia, FVC = 44% pred
• Anesthesia with combined spinal/epidural
• Spinal at L3-4; epidural catheter placed at T 10-11
• Combination of lidocaine and fentanyl
• Propofol IV for sedation (total 550 mg in 4 hours)
86
23
• Honma continued:
• Patient did well initially following resection
• Day 10: re-operation for anastomotic leak
• GA/endotracheal tube with minimal FiO2 (30%)
• No anesthesia-related problems with this surgery
• Recommendations:
• Neuraxial / regional anesthesia when possible
• Low FiO2 if GA required
• High FIO2 may exacerbate chronic interstitial pneumonia
87
88
• Spontaneous pneumothorax – may be
• Primary (no history of respiratory disease)
• Secondary (due to pre-existing disease)
• Traumatic pneumothorax
• Penetrating (stab or gunshot wounds)
• Blunt (often due to rib fractures)
• Surgical or procedural complication
89
• Frequently due to pulmonary bullae
especially at the apex of the lung
• Greater negative pleural pressures at
the lung apex in tall individuals result in
larger gradient in pleural pressures
within the thorax
• May stimulate development of sub-
pleural blebs
90
• Patient with pre-existing lung disease
• Most commonly COPD (70% of cases)
• Necrotizing pneumonia
• Lung cancers
• Tuberculosis (in endemic areas) is common cause
• Age > 55
• More severe symptoms than primary
• Great co-morbidities
• Higher mortality
91
• Pneumothorax occurs when lung is pierced
• May be caused by to surgical or procedural
interventions
92
• Laparoscopic cholecystectomy
• Colonoscopy with polypectomy
• Carotid endarterectomy
• Transthoracic needle biopsy
• Interscalene block for shoulder surgery
• Thoracic epidural placement
• Placement of central lines (subclavian approach)
• Local anesthesia injection into the chest wall (intercostal block)
93
• Have been reported during both intra- and extra-
peritoneal laparoscopic procedures
• Veress needle insertion, trocar insertion, CO2 insufflation
or gallbladder dissection
• Tracking of insufflated CO2 around the aortic and
esophageal hiatuses of the diaphragm into the
mediastinum with rupture into intra-pleural space
• Congenital diaphragmatic defect?
94
• Associated with substantial rate of mortality
• Diagnosis may be delayed or missed
• Failure to diagnose and treat tension pneumothorax
markedly increases likelihood of a fatal outcome
• Presentation differs between spontaneously
breathing individuals and those receiving positive
pressure ventilation
95
96
Mechanically ventilated patients have increased intra-pleural pressures
throughout the respiratory cycle, leading to hypotension and cardiac arrest
97
Pneumothorax
Tracheal and
Mediastinal
Shift
98
Right Lung
Re-expanded
• Symptoms: chest pain, dyspnea
• Physical signs: respiratory distress, tachypnea
• Decreased breath sounds (58%)
• Hyperresonance to percussion (26.7%)
• Contralateral tracheal deviation (17.9%)
• Subcutaneous emphysema (10.5%)
• Jugular venous distension (4.7%)
• Elevated CVP
99
• Cardiovascular signs:
• Tachycardia (HR > 100) (43%)
• Hypotension (MAP ≤ 60 mmHg) (16.3%)
• Bradycardia (HR < 60) (5.8%)
• Cardiac arrest (2.3%)
• Conclusion: Key signs of tension pneumothorax (awake
patient) appear to be chest pain, dyspnea,
tachycardia and decreased breath sounds
• tracheal deviation and hypotension less common
100
• Initial Signs:
• Need for increased FiO2 (86.6%)
• Decreased breath sounds (45.4%)
• Subcutaneous emphysema (30.9%)
• Hyperresonance (8.3%)
• Cardiovascular
• Hypotension (66%)
• Tachycardia (30.9%)
• Cardiac arrest (28.9%)
• Most common dysrhythmia was PEA (75%)
101
• Emergent CXR in a monitored setting is desirable but may not be feasible in the OR setting• Sensitivity of chest x-ray is as low as 36-48%
• Upright A&P chest x-ray seldom possible
• CT scan best but not possible in most ORs
• Ultrasonography a superior choice for OR• Readily available
• 80 to 90% sensitivity (supine chest x-ray only 50%)
• Can be done at bedside or in operating room
• Recommend Wilkerson & Stone, (2009) or Kline et al., (2013)
102
25, 26
• Ventilated patients with tension pneumothorax can
progress to symptoms of hypotension or cardiac
arrest often within minutes of first clinical
presentation
• Early recognition and intervention is important
• Confirmation with either chest x-ray or ultrasound if
readily available and patient is stable, but treatment
should not be delayed in the absence of diagnostic
reassurance
103
• If radiography or ultrasonography not available, or if
patient is deteriorating:
• Decompression as soon as tension pneumothorax is suspected
is the mainstay of treatment
• Chest tube thoracostomy if trained personnel present
• Alternative # 1: large bore (14 ga.) sheathed catheter over
a needle is acceptable temporary intervention
• Alternative # 2: Trans-diaphragmatic use of laparoscopic
trocars for chest decompression has been reported by Hatch
in 2014
104
27
• Traditionally, placement recommended at 2nd
intercostal interspace (ICS), midclavicular line
105
• Laan et al. (2015) suggest alternate locations at either
the 4th or 5th ICS, anterior or mid axillary lines
106
26
107
• Problems with needle decompression
• Higher failure rate than tube decompression
• Does not relieve tension pneumothorax physiology
• Subject to kinking and obstruction
• Prone to dislodgement
• 14 gauge catheters are sometimes ineffective due to
insufficient length (5 cm.)
• Needle length of at least 7-8cm has been recommended
108
29, 30
109
• Readily available in laparoscopy trays
• Rigid catheter with blunt trocar
• Overcomes kinking problems of plastic catheters or
lack of sufficient length
110
29
111
Pulmonary Embolism and Anterior
Mediastinal Masses
• Definition: Blockage in the one or more branches of
the pulmonary arteries by a substance that has
migrated from elsewhere in the circulation.
• Types of Embolism
• 95% Are venous thrombi from lower extremities
• Air, fat, amniotic fluid, septic emboli
112
Pulmonary
emboli
• Hereditary: Deficiencies of antithrombin, Protein C, Protein S and Factor V Leiden
• Acquired: older age, cancer, ↓ mobility, acute illness (CHF), IBD, nephrotic syndrome, trauma, SCI, obesity
• Virchow’s Triad: venous stasis, endothelial dysfunction, hypercoagulability
• Medications: heparins, HRT, oral contraceptives, chemotherapy and antipsychotics
• Surgery: “major,” trauma, joint arthroplasty, general anesthesia (in contrast with neuraxial)
113
32, 33
• PE responsible for between 150K and 200K
deaths per year in the U.S.
• In fatal PE, death usually occurs within one hour
• Higher risk of PE in hip fracture repairs
• Probably R/T distortion of the femoral vein during the
procedure
• Mortality can be as high as 12.9%
• Much lower if patient receives anticoagulant prophylaxis
• Increase in reports of PE probably due to
greater detection with spiral CT
114
32, 34
• If underlying cause still present, a patient with PE has
a 30% chance of a second embolus
• There is a 5-fold increase in the incidence of PE during
and after surgery
• 0.3 to 1.6% of the general surgical population
• Acute inflammatory reaction R/T tissue trauma
• Activation of clotting cascade
• Immobilization and venous stasis
115
33
• Impaired gas exchange → Hypoxemia
• Ischemia of down-stream lung tissue = increased dead
space (V/Q mismatch)
• Impaired CO2 removal → hyperventilation
• Over-perfusion of tissue still receiving circulation
• Decreased surfactant production by type II alveolar cells
→ alveolar edema & atelectasis
• Hypoxia worse if patent foramen ovale present
116
32
33
• Increased pulmonary vascular resistance (PVR)
caused by vascular obstruction , vasoconstriction
• Right ventricle sensitive to pressure ↑
• Decreased CO → catecholamine-induced tachycardia
• Limits LV filling, decreases CO
• Acute cor pulmonale
• Catechols may sustain B/P temporarily but as the RV fails,
CO falls further and systemic hypotension results
117
34
• Clinical Manifestations
• Dyspnea, pleuritic chest pain, hypoxemia, rales
• Non-productive cough with hemoptysis
• Possible hypotension
• Co-existing deep venous thrombosis (DVT)
• Diagnostics
• Abnormal chest x-ray.
• A segmental or larger perfusion defect on V/Q scan
• Positive spiral CT scan
• Elevated D-dimer level
118
32
• May be masked in patients under GA
• Hypotension and tachycardia are classic findings
• Significant hemodynamic instability including hypotension
requiring vasopressors, shock and CV arrest
• Elevated jugular venous pressure, ↑ CVP
• Wheezing is a frequent finding
• Decrease in EtCO2 (R/T ↑ physiologic dead space)
• Earliest means of PE detection under anesthesia
119
32, 33
120
• Sinus tachy and atrial dysrhythmias common
• 83% of patients
• ST segment and T abnormalities (50%)
• RBBB & pre-cordial T-wave inversion correlates with PE
• Right heart strain (S1Q3T3 pattern)
• S-wave in lead 1, Q-wave in lead 3, T-wave ↓ in lead 3
• A-fib/flutter, heart block less common
S1Q3T3 Pattern in Pulmonary Embolism121
33
• Arterial blood gases
• Hypoxemia: reduction in PaO2 may be the only indicator of
PE with obstruction less than 25%
• Hypocarbia: Varies with the amount of physiologic dead
space created by the PE
• D-Dimer level: protein fibrin degradation product
• Elevated value during excessive clotting,
• Greater amount of product from fibrinolysis
• Elevated D-dimer is sensitive to PE but not specific
• A negative D-dimer rules out PE
• Positive D- dimer test requires alternative confirmation
122
33
• Changes in other lab values
• Serum troponin-I and troponin-T may be elevated in less than 50% of cases
• Brain natriuretic peptide (BNP) may be elevated due to RV dilation
• Also elevated in other conditions i.e. CHF
• Chest radiograph
• Not very helpful, may confirm cardiomegaly
• Good for ruling out other causes such as pneumothorax, effusion, pneumonia, & atelectasis
123
33
• Confirmatory diagnostic tests
• V/Q scans commonly used in non-surgical settings
• Limited value: often non-diagnostic / indeterminate
• Angiography is the gold standard for PE diagnosis
• Expensive, invasive, may not be available, potential for major complications
• Spiral CT scan: sensitivity 85%
• Even greater sensitivity in the presence of RV overload
• Transesophageal echocardiogram (TEE)
• May be available in the OR, but limited sensitivity in milder cases. More helpful in conditions of RV strain
• Evidence of tricuspid regurgitation
124
• Initial therapy can be started before definitive
diagnosis is made (treat the symptoms)
• Vasopressors (maintain BP & coronary perfusion
pressures)
• Avoid excess treatment with fluids if PE suspected
• Norepinephrine (α1 vasoconstriction and β1 for contractility)
• Alternates: dopamine, epinephrine, dobutamine
• Caution with dobutamine due to β2 peripheral vasodilation
125
32, 33
• Anticoagulation (has been used since 1960s)
• In surgery or PACU, the potential risks of life threatening
bleeding must be considered
• Subcutaneous LMWH (100 IU/BID) recommended for
non-massive PE
• Extensive PE: unfractionated IV heparin may be better
choice if concern about subq absorption or if
thrombolytic therapy is being considered
• Bolus 80U/kg with maintenance dose of 18 U/kg/hr
126
32, 33
• Pulmonary vasodilators
• Milrinone
• Benefit of pulmonary vasodilation and increased myocardial
contractility
• May lower systemic B/P
• Inhaled nitric oxide
• May be used to ↓ PA pressures and increase RV function
• Improve gas exchange and cardiac output with little effect on
systemic B/P
127
33
• Further treatment which may or may not involve the
CRNA may include:
• Thrombolytic therapy
• Placement of vena cava filter
• Catheter-directed embolectomy
• Surgical embolectomy
• Mortality rates reported 6 to 27%
128
• 80 to 85% survival rate for acute PE
• Especially if adequate anticoagulant therapy is initiated
• Two main sequelae:
• Development of thromboembolic pulmonary hypertension
• Post-thrombotic syndrome (varicosities)
• Both due to chronic vascular changes
129
• May be benign or malignant
• Clinical signs & symptoms relate to compression of
vital structures of breathing and circulation
• Tracheal/bronchial compression:
• Cough, dyspnea
130
Thymoma (red area)
Spatially defined by: • The sternum (anterior) and
• The middle mediastinum (heart and great vessels) posteriorly, and diaphragm inferiorly
• MM = middle mediastinum
• PM = posterior mediastinum
131
35
• Thymic mass: thymoma, cyst, hyperplasia or
carcinoma
• Thyroid tumor
• Cystic hygroma (congenital lymphatic lesion)
• Seminoma (germ cell tumor)
• Lymphoma
132
36
• Superior vena cava (SVC) compression
• SVC syndrome – cardiac tamponade, syncope
• Facial / neck swelling with nosebleeds & cyanosis
• Orthopnea
• Esophageal compression
• Dysphagia
• Recurrent laryngeal nerve compression
• Hoarseness
133
• Chest x-ray and CT scan evaluation of the mass
and affected structures
• PFTs have been recommended for risk eval
• Mixed restrictive-obstructive pattern suggests
increased risk for post-op respiratory complications
• Restrictive: parenchymal compression
• Obstructive: tracheal/bronchial compression
134
• Symptomatic or radiographic evidence of tracheal
compression is of concern
• Risk of severe, even fatal airway compromise
• Patients with > 50% reduction in tracheal cross-sectional
area (CSA) are more likely to be symptomatic and have
complications
135
• Low Risk
• Asymptomatic or mildly symptomatic
• No postural symptoms or evidence of compression
• Intermediate Risk
• Mild to moderate postural symptoms
• Tracheal compression < 50%
• High risk
• Severe postural symptoms, stridor, cyanosis
• Tracheal compression > 50% with associated bronchial compression, pericardial effusion or SVC syndrome
136
35
• Consequences due to competition for space with
heart, vessels, lungs and air pathways
• Anesthesia with neuromuscular block (NMB) will affect
the balance
• Decreased FRC under GA
• Decreased trans-pleural pressure gradient under GA
promotes airway collapse
• Positive pressure ventilation increases intrathoracic
pressure
137
• Tracheal compression or deviation may complicate
airway management
• Posterior masses of concern due to absence of tracheal
cartilage posteriorly → obstruction
• Myocardial compression may result in tamponade
syndrome
• Anterior compression will affect the RV
• Posterior compression will affect the LV
138
• Individualized plan based on patient needs
• Multidisciplinary: CRNA, surgeon, intensivist, perhaps
even the oncologist
• Initial plan may involve biopsy procedure
• Evaluation to determine if steroids, chemotherapy or
radiation could be used to reduce the tumor size to lower
the risk and enhance patient safety
139
35 - 37
• Patients with low risk profile probably not at
significant risk of complications
• Standard general anesthesia and monitoring are
acceptable
• Patients at intermediate or high level of risk need
detailed case plan
• Based on symptoms and diagnostic imaging
140
• Most cases of severe complications occur in the
absence of spontaneous ventilation (SV)
• General agreement that SV should be maintained in
these patients
• Based on:
• Numerous case reports in which compromise followed NMB
and/or PPV, or….
• Reports / series of high risk patients where SV was
maintained and complications were avoided
141
• Pre-op considerations
• Have enough staff available
• Plan ahead for ICU admission
• IV access in a lower extremity
• Pulse oximeter on right hand
• No sedative premedication
• Consider invasive monitoring
• Alternative (backup) airway options
142
35 - 37
143
• Airway management
• Awake fiberoptic intubation with local/sedation or
• Inhalation induction, SV maintained, standard DL for intubation
• If tracheal obstruction: the surgeon may try rigid bronchoscopy (airway stent?)
• Then establish surgical anesthesia with patient ventilating spontaneously
• Consider use of dexmedetomidine or ketamine for minimal respiratory depression + analgesia
• Prepare for emergency airway maneuvers if
obstruction occurs prior to resection of the mass
• Options:
• Rapidly reawaken the patient
• Shifting patient to preplanned “rescue” position
• Rigid bronchoscopy
• Rescue position: should be selected pre-op based
on anatomy / location of the mass and anticipated
area(s) of compression
• Upright seated / lateral decubitus / prone
144
• If rigid bronchoscopy becomes necessary:
• Maintain anesthesia with IV infusions
• Jet ventilation
• Severe hypotension
• May respond to placement of patient in the rescue position
• Decreases in cardiac output
• Lighten depth of anesthesia
• Principals of tamponade management: plasma volume expansion, vasopressors, inotropes
145
• Use of heliox
• Decreased gas flow may be R/T increased turbulence in narrow airways
• Helium/oxygen mix may improve flow
• Required helium concentration will limit FiO2
• If all else fails….
• Emergency sternotomy to elevate the mass from compromised structures
• Final option is cardiopulmonary bypass (CBP).
• In high risk patients, CPB should be anticipated and cannulations of femoral vessels done in advance
146
147
1. Hong C, Galvagno Jr. S. Patients with chronic pulmonary disease. Med Clin N Am.
2013;97:1095-1107. doi.org/10.1016/j.mcna.2013.06.001.
2. Kumar V, Abbas A, Fausto N, Mitchell R, eds. Robbins Basic Pathology. 8th ed.
Philadelphia PA: Elsevier Saunders; 2007.
3. McPhee S, Hammer G, eds. Pathophysiology of Disease: An Introduction to Clinical
Medicine. 6th ed. New York, NY: McGraw Medical, 2010.
4. Csikesz N, Gartman E. New developments in the assessment of COPD: Early
diagnosis is the key. Int Journal COPD. 2014;9:277-286.
doi:10.2147/COPD.S46198.
5. Wong J, Lam DP, Abrishami A, et al. Short term preoperative smoking cessation
and postoperative complications: a systematic review and meta-analysis. Can J
Anaesth 2012; 59:268-279.
6. Quraishi SA, Orkin FK, Roizen MF. The anesthesia preoperative assessment: an
opportunity for smoking cessation intervention. J Clin Anesth 2006; 18:635-640.
7. Ruzzeh S, Kurup V. Respiratory Diseases in Hines R, Marschall K, eds. Stoelting’s
Anesthesia and Co-existing Disease. 6th ed. Philadelphia, PA: Elsevier Saunders;
2012.
148
8. Licker M, Schweizer A, Ellenberger C, Tschopp J, Diaper J, Clergue F.
Perioperative medical management of patients with COPD. Int Journal COPD.
2007;2(4):493-515.
9. Hausman Jr. M, Jewell E, Engoren M. Regional versus general anesthesia in
surgical patients with chronic obstructive pulmonary disease: Does avoiding
general anesthesia reduce the risk of postoperative complications? Anesth Analg.
2015;120(6):1405-1412. doi:10.1213/ANE.0000000000000574
10. Sylvanus MT, Groeben H, Peters J. Corticosteroids and inhaled salbutamol in
patients with reversible airway obstruction markedly decrease the incidence of
bronchospasm after tracheal intubation. Anesthesiol. 2004; 100:1052-1057.
11. Adamzik M, Groeben HG, Farahani R, Lehmann N, Peters J. Intravenous lidocaine
after tracheal intubation mitigates bronchospasm in patients with asthma. Anesth
Analg. 2007;104(168-172) doi:10.1213/ANE.0000247884.94119.d5
12. Kew, KM, Kirtchuk K, Michell, CI, Griffiths M. Intravenous magnesium sulfate for
treating adults with acute asthma in the emergency department (Protocol).
Cochrane Database System Rev. 2014; (1):CD010909.
doi:10.1002/14651858.CD01099.
149
13. Liccardi G, Salzillo A, Piccolo A, De Napoli I, D’Amato G. The risk of bronchospasm
an asthmatics undergoing general; anaesthesia and/or intravascular administration
of radiographic contrast media. Physiology and clinical/functional evaluation. Eur
Ann Allergy Clin Immunol. 2010;43(5):167-173.
14. Westhorpe RN, Ludbrook GL, Helps SC. Crisis management during anesthesia:
bronchospasm. Qual Saf Health Care. 2005;14:e7.
15. Travers A, Jones, A, et al. Intravenous beta-2 agonists versus intravenous
aminophylline for acute asthma. Cochrane Database System Rev. 2012;
(12):CD010256. doi: 10.1002/14651858.CD010256.
16. Das, U. Beneficial action of magnesium sulfate in bronchial asthma: How and why?
Am J Emerg Med. 2016; Online at
http://www.sciencedirect.com/science/article/pii/S0735675716301358
17. Blum J, Stentz, M et al. Preoperative and intraoperative predictors of postoperative
acute respiratory distress syndrome in a general surgical population. Anesthesiology.
2013; 118(1): 19-29. doi: 10.1097/ALN.0b013e3182794975
18. Joosten A, et al. Goal-directed fluid therapy with closed-loop assistance during
moderate risk surgery using noninvasive cardiac output monitoring: A pilot study. Br J
Anaesth. 2015; 114 (6):886-92. doi: 10.1093/bja/aev002. Epub 2015 Feb 17150
19. Uttman L, et al. Protective ventilation in experimental respiratory distress
syndrome after ventilator-induced lung injury: a randomized controlled trial. Br J
Anaesth. 2012; 109(4):584-594. doi:10.1093/bja/aes230.
20. Hartland BL, Newell TJ, Damico N. Alveolar recruitment maneuvers under general
anesthesia: A systematic review of the literature. Resp Care. 2015;60(4):609-620.
21. Mehta C, Mehta Y. Management of refractory hypoxemia. Ann Card Anaesth.
2016;91:89-96.
22. Sud S, Sud M, et al. High-frequency oscillatory ventilation versus conventional
ventilation for acute respiratory distress syndrome (Review). Cochrane Database
System Rev. 2016; (4):CD004085. doi:10.1002/14651858.CD004085.pub4.
23. Honma K, Tango Y, Honma K, Isomoto H. Perioperative management of severe
interstitial pneumonia for rectal surgery: A case report. Kurume Med Journal.
2007;54:85-88.
24. Roberts D, Leigh-Smith S, et al. Clinical presentation of patients with tension
pneumothorax: A systematic review. Ann Surg. 2015;261(6):1068-1078.
doi:10.1097/SLA.0000000000001073.
151
25. Wilkerson R, Stone M. Sensitivity of bedside ultrasound and supine anteroposterior
chest radiographs for the identification of pneumothorax after blunt trauma. Acad
Emerg Med. 2010;17(1):11-17. doi:10.1111/j.1553-2712.2009.00628.x.
26. Kline J, Dionisio D, Sullivan K, Early T, Wolf J, Kline D. Detection of pneumothorax with
ultrasound. AANA J. 2013;81(4):265-271.
27. Hatch Q, Debarros M, Johnson E, Inaba K, Martin M. Standard laparoscopic trochars
for the treatment of tension pneumothorax: A superior alternative to needle
decompression. J. Trauma Acute Care Surg. 2014;77(1):170-175.
doi:10.1097/TA.0000000000000249.
28. Laan D, Vu T, et al. Chest wall thickness and decompression failure: A systematic
review and meta-analysis comparing anatomic locations in needle thoracostomy.
Injury Int J. 2015;(in press): doi:10.1016/j.injury.2015.11.045.
29. Chang S, Ross S, et al. Evaluation of 8.0-cm needle at the fourth anterior axillary line
for needle chest decompression of tension pneumothorax. J Trauma Acute Care Surg.
2014;76(4):1029-1034. doi:10.1097/TA.0000000000000158.
152
30. Heckler M, Hegenscheid K, et al. Needle decompression of tension
pneumothorax: Population-based epidemiologic approach to adequate needle
length in healthy volunteers in Northeast Germany. J. Trauma Acute Care Surg.
2015;80(1):119-124. doi:10.1097/TA.0000000000000878.
31. Lubin J, Tank A, et al. Modified Veress needle decompression of tension
pneumothorax: A randomized crossover animal study. J Trauma Acute Care Surg.
2013;75(6):1071-1075. doi:10.1097/TA.0b013e318299563d.
32. Cox J, Jablons D. Operative and perioperative pulmonary emboli. Thorac Surg
Clin. 2015;25:289-299. doi:10.1016/j.thorasurg.2015.04.010.
33. Desciak M, Martin D. Perioperative pulmonary embolism: Diagnosis and
anesthetic management. J Clin Anesth. 2011;23:153-165.
Doi:10.1016/j.jclinane.2010.06.011.
34. Hall D. Perioperative pulmonary embolism: Detection, treatment and outcomes.
Am J Ther. 2012;20:67-72
35. Blank R, de Souza D. Anesthetic management of patients with an anterior
mediastinal mass: Continuing professional development. Can J Anesth.
2011;58:853-867. doi:10.1007/s12630-011-9539-x.
153
154
36. Gothard J. Anesthetic considerations for patients with anterior mediastinal masses.
Anes Clin. 2008;26:305-314. doi:10.1016/j.anclin.2008.01.002.
37. Erdös G, Tzanova I. Perioperative anesthetic management of mediastinal mass in
adults. Eur J Anaesthesiol. 2009;26:627-632.
doi:10.1097/EJA.0b013e328324b7f8.